MEDICAL-SURGICAL NURSING

PART I: ASSESSMENT AND DIAGNOSTIC EVALUATION

The heart pumps oxygenated blood to the body, LAYERS OF PERICARDIUM

moves a one-way flow providing oxygen and
1. Parietal - Outer layer
nutrients and regulates blood supply. The heart
2. Visceral - Inner layer
has different activities:
● Also known as epicardium
1. Circulation
● Adheres to the outside of the heart
● Systemic – Left
● Pulmonary – Right Pericardial space – Space between the
2. Cardiac conduction system – Conducts parietal and visceral layer
electrical impulse to the heart
3. Cardiac cycle ● Consists of at least 10 to 50 mL in order
● Complete heartbeat to lubricate the surface of the heart,
● Contraction and relaxation allowing easy movement during
4. Cardiac output contraction and expansion of the heart
● Volume of blood that is ejected from the ● Silent rapid filling as little as 100 mL can
heart compromise the cardiac function and
● Indicates the pumping functions of the cause cardiac tamponade
heart
THREE LAYERS OF CARDIAC MUSCLE
2 DIVISIONS
1. Endocardium – Inner layer
1. Systemic – Supplies oxygen and nutrients to ● Consists of endothelial tissue and
the body tissue and brings blood back to the lines inside the heart valves
heart ● Only layer that receives oxygen and
2. Pulmonary – Brings blood to the lungs for nutrients from blood circulating the
removal of carbon dioxide and oxygen update heart
2. Myocardium – Middle layer or
contracting layer
3. Epicardium – Exterior layer, also known
as visceral.
- Thickness of the cardium varies
according to the pressure generated to
move blood to its destination
- Left ventricle is thicker than right ventricle

CHAMBERS OF THE HEART

The heart has four chambers which functions as

a two sided pump:

1. Atria – Collecting chamber

2. Ventricles – Pumping chamber

STRUCTURE OF THE HEART

1. Pericardium – Has 2 layers

2. Valve
3. Arteries
HEART VALVES capillaries and function in controlling systemic
vascular resistance, which is referred to as
Valves - Ensures one-way blood flow and arterial pressure.
prevents back flow that produces heart sounds
Coronary arteries are the vessels that deliver
1. Atrioventricular valve oxygen-rich blood to the myocardium. Cardiac
● Produces S1 heart sounds that veins are the vessels that remove the
separates atria from the ventricle deoxygenated blood from the heart muscles.
● Contains mitral and tricuspid valve
Collateral circulation is a network of capillaries
2. Semilunar valve
that supplies myocardial cells. There are
● Produces S2 heart sounds
numbers of functional and nonfunctional
● Closure of the aortic and pulmonic
anastomosis that exist between the coronary
valve
vessels, which can enlarge by flow if one of the
arterial branches increases. Enlargement of
anastomosis can improve blood flow to
myocardial segment and provide collateral
circulation.

Arteries – High pressure

Arterioles – Response to ANS control

● Responsible for dilation or constriction

Coronary arteries – Delivers oxygen-rich blood

to the myocardium

Collateral circulation – Alternate circulation

around a blocked artery or vein via another path,
such as nearby minor vessels

MAJOR CORONARY ARTERIES

There are two major coronary arteries:

1. Right coronary artery, or RCA –

ARTERIES
Extends to the R and continues to R AV
Arteries are blood vessels that carry oxygenated sulcus to the posterior surface of the
blood away from the heart. They keep blood flow heart
away from the heart except pulmonary arteries 2. Left coronary artery, or LCA – Extends
which carry blood towards the lungs for to the L then divides into major branches
oxygenation.

The arterioles system is the higher-pressure

portion of the circulatory system. During heart
contraction it is called systemic pressure. When
the heart expands and refills it is called diastolic
pressure.

Arteries also help the heart pump blood. As blood

moves to the periphery, arteries subdivide to
become arterioles which can dilate or constrict in
response to autonomic nervous system control.

Dilation decreases resistance to flow.

Constriction increases resistance to flow.
Therefore the arterioles distribute blood to the
CO = HR × SV (4 to 8 LPM)

The average cardiac output in a resting adult is 4

to 6 L/min.

Stroke volume – Volume of blood ejected with

each heartbeat

Cardiac cycle is one contraction and one

relaxation of the heart to form one heartbeat.

The circulating volume of the blood to the heart

varies according to the needs of the tissue cells.
Increase in the work of the cell causes an
increase in blood flow and the subsequent
increase in the work of the heart and the
myocardial oxygen consumption.

The cardiac function is based on the cardiac

output. This is the total volume. Cardiac output
indicates how well the heart is functioning as it
pumps. It also depends on the stroke volume and
heart rate.

Stroke volume is the volume of blood ejected from

each heartbeat. The blood is ejected from each
ventricle due to the contractions of the heart
muscle which compresses the ventricles. Stroke
volume is expressed in mL per beat. Decrease in
stroke volume will decrease heart rate.

Cardiac Cycle – 2 phases

1. Diastole – Is the atrial contraction and

ventricular relaxation
2. Systole – Is the ventricular contraction
and atrial relaxation

Causes of Low CO:

1. Inadequate left ventricular ejection –

CAD, cardiomyopathy, HTN, aortic
stenosis, mitral regurgitation, drugs that
are negative inotropes, and metabolic
These pictures show how the coronary arteries
disorders
supply blood to the myocardium.
2. Inadequate left ventricular filling –
CARDIAC OUTPUT Hypovolemia, tachycardia, stenosis,
rhythm disturbance, high CO due to
Amount of blood pumped by the ventricles into exercise, fear, anxiety and sepsis
the pulmonic and systemic circulation per one
minute. Cause of High CO – Exercise, fear, anxiety and
sepsis
The average stroke volume in a resting adult is
about 60 to 130 mL. The average heart rate in a
resting adult is 60 to 100 bpm. Cardiac output is
computed by multiplying the stroke volume by the
heart rate.
FACTORS THAT REGULATE STROKE
VOLUME

1. Preload
● Gives the volume of blood that the
ventricle has available to pump
● Depends on the venous return
2. Contractility
● Is the force that the muscle can
create at a given length
● The force of the contraction is
generated by the myocardium
3. Afterload – Is the arterial pressure
against which the muscle will contract

These factors establish the volume of blood

pumped with each heartbeat

FACTORS THAT AFFECT CARDIAC OUTPUT

Cardiac output can increase or decrease by

changes in heart rate. This can lead to
dysrhythmia or arrhythmia. Increase in heart rate MEDICATIONS THAT LOWERS HR
reduces the time the heart is in diastole and 1. Adenosine
results in the decrease of left ventricular filling and 2. Beta blockers
coronary blood flow to the myocardium. Heart 3. Calcium channel blockers
rate and contractility are increasing factors. The 4. Digoxin
characteristics of the cardiac tissue are
influenced by the humoral and neural MEDICATIONS THAT INCREASES HR
mechanism. Preload and afterload depend on the
1. Epinephrine
characteristics of the heart rate and vascular
2. Norepinephrine
system.
3. Atropine
1. Heart rate, or HR – Changes in CO affects
CONDITIONS THAT INCREASE PRELOAD
HR
2. Preload – Starling’s Law There is an increase in blood returning to the
3. Afterload – Resistance of left ventricular heart
ejection
4. Contractility – Inotropic agents 1. Increase in circulating blood volume –
Overtransfusion, polycythemia
PRELOAD AND AFTERLOAD 2. Mitral or aortic insufficiency
3. Heart failure or hypovolemia
Preload is based on the principle of starling’s law
of the heart. The greater the volume, the greater Treatment:
the stretch of the cardiac muscle fibers and the
greater the force in which the fibers contract. ● Diuretics – Furosemide
Preload is affected by the venous blood pressure ● Vasodilators – Nitrates and morphine
and the rate of the venous return. There are
factors that affect preloading:

● Blood volume
● Distribution of blood
● Ventricular function
● Ventricular compliance
CONDITIONS THAT DECREASE PRELOAD CONDITIONS THAT AFFECT AFTERLOAD

There is a reduction in the volume of blood 1. Ventricular outflow obstructions – Aortic

returning to the ventricle. Very common example valve stenosis
is blood loss. 2. SNS stimulation – Epinephrine release
causes increase PVR
1. Decrease in circulating blood volume –
3. Hypertension
Bleeding, dehydration
4. Hypercoagulability
2. Mitral or aortic stenosis
3. Vasodilator Treatment:
4. Atrial fibrillation
If there is a decrease in afterload..
5. Cardiac tamponade
1. Vasodilators – Morphine, nitroprusside,
Treatment:
hydralazine, Clonidine, ACE inhibitors,
● Fluids – Isotonic solution, 0.9% NS, LR ARBs
● Blood and blood products
2. Intra-Aortic Balloon Pump, or IABP
● Vasopressor – Not effective if full tank
● Volume expander If there is an increase in afterload..
AFTERLOAD 1. Vasopressor – Dopamine, dobutamine,
norepinephrine, epinephrine
The resistance or pressure which the ventricle
must overcome to eject its volume of blood during Dopamine – Increases contractility and
contraction oxygen consumption
Right ventricle – Pulmonary Vascular Correct hypovolemia with volume
Resistance, or PVR – The right ventricle ejects replacement before considering
blood through the pulmonic valve against the low vasopressors
pressure of the pulmonary circulation, or
pulmonary vascular resistance

Left ventricle – Systemic Vascular Resistance,

or SVR – The left ventricle ejects blood through
the aortic valve against the high pressure of the
systemic circulation, also known as systemic
vascular resistance

Afterload is the resistance in blood flow as it

leaves the ventricle. Increase in vascular
resistance can increase ventricular contractility to Intra-aortic Balloon Pump – Increases
maintain stroke volume and cardiac output. myocardial perfusion, increasing cardiac output
and coronary blood flow
Afterload is directly related to arterial blood
pressure through ejection of blood in the systemic CONTRACTILITY
circulation. Increase in arterial pressure requires
Refers to the inherent ability of the myocardium
more energy to eject blood. Increase in energy
to contract normally and influenced by preload
requirement for ventricular systole increases
myocardial oxygen demand. May be affected by:

Vascular resistance must be overcome to push 1. Ventricular muscle mass

blood to the circulatory system. Systemic 2. Heart rate
vascular resistance is resistance by the systemic 3. Oxygen status
circulation. Pulmonary vascular resistance is the 4. Chemical or pharmacological effects
resistance by the pulmonary circulation.
Contractility is influenced by preloading. This is
sometimes called an inotropic state.
CONDITIONS THAT INCREASE TERMS
CONTRACTILITY
Ejection Fraction – Normal: 55% to 70%
1. Sympathetic stimulation – Fear or anxiety
Depolarization – Contraction
2. Calcium
3. Inotropes – Digitalis, epinephrine, and In depolarization, once electrical impulse is
dobutamine generated, movement of sodium into the cell exits
to the potassium. It is known as contraction of the
ventricle.
CONDITIONS THAT DECREASE
Repolarization – Relaxation
CONTRACTILITY
Repolarization – Return of ions to previous
1. Negative inotropes – Beta blockers, calcium
resting state which corresponds to relaxation of
blockers, barbiturates, and most
the myocardial muscles
antidysrhythmics
2. Infarction Action Potential – The change in electrical
3. Cardiomyopathy potential associated with the passage of an
4. Vagal stimulation impulse along the membrane of a muscle cell or
5. Hypoxemia nerve cell
6. Acidosis
Action potential is any stimulus that decreases
the permeability of the membrane to generate
electrical potential. It is the nerve impulse that
causes permeability of an ion to cross the cell
membrane.

ELECTROPHYSIOLOGIC PROPERTIES OF
CARDIAC MUSCLE

1. Automaticity or rhythmicity – Spontaneous

initiation of an impulse without control
- Automaticity and rhythmicity discharge
electrical impulse in the SA node where the
sodium moves into the cell. Rhythmicity
refers to the regular discharging of action
potentials

2. Excitability – Ability of the cell to respond to

an electrical impulse or stimulus
Ejection fraction is an indicator of the heart’s - Excitability indicates how well the response to
ability to maintain contractility. It is also the electrical stimulus. Conductivity is the ability
relationship between the diastolic volume and the of the cell to respond to an electrical impulse
stroke volume. from one cell to the next. Excitability and
Decrease in ejection fraction is a sign of conductivity are both related. Excitability
ventricular failure. refers to the ability to respond to a stimulus.
Conductivity allows the stimulus to pass from
Systolic Dysfunction – The ejection fraction falls one cell to the next
below 40%.
3. Conductivity – Propagate electrical
This is measured by echocardiogram, nuclear impulses *ability to transmit an electrical
studies, MRI, and CT scan. impulse from one cell to another

4. Refractoriness – Inability to respond to a

new stimulus while still in a state of
contraction from an earlier stimulus
- Refractory period is when the myocardial
cells depolarize before they can depolarize
again

2 phases:

● Absolute – Cell is complete

unresponsive to any electrical stimulus
and noncapable to initiate to any
depolarization; Normal
● Relative – Electrical stimulus is stronger
than normal, which can cause premature
contraction, placing the patient at risk

CARDIAC CONDUCTION SYSTEM

1. Sinoatrial node, or SA, or pacemaker – 60

to 100 bpm
● Primary or dominant pacemaker
● Located at the junction of the
superior vena cava and the right
atrium
2. Atrioventricular node, or AV, or junction – Pulse Pressure – Difference between systolic
40 to 60 bpm and diastolic pressure, 30 to 40 mm Hg
● Located at the lower portion of the
right atrium Mean Arterial Pressure – Average pressure
● The slow conduction of the AV node maintained in the aorta, 70 to 110 mm Hg
allows filling of the ventricle Peripheral Resistance – A resistance of all
3. Bundle of His or AV bundle – 40 to 60 bpm peripheral vasculature in the systemic circulation
● Fuse with the AV node to form
another pacemaker Pulse pressure reflects the stroke volume,
● It is divided into left bundle branch ejection velocity, and systemic vascular
and right bundle branch resistance. It indicates how well the patient can
4. Purkinje fibers – Inherent the rate of 30 to maintain cardiac output. Increase in pulse
40 bpm or less pressure increases stroke volume. It also
increases peripheral volume, increases in
● Not activated as a pacemaker unless vascular resistance, and reduces the sensitivity of
conduction through the bundle of His arteries due to high pressure in the aorta.
becomes blocked, or in a higher Examples include light exercise, fever, anxiety,
node such as SA or AV nodes atherosclerosis. Decrease in pulse pressure
reflects decrease in stroke volume. It means
there is a decrease in the left ventricular volume
and insufficient preloading. It also means
decrease in cardiac output. Examples include
hypovolemia, blood loss, heart failure, or shock.

Mean arterial pressure is the pressure at which

the blood moves for the cells to receive adequate
oxygen and nutrients needed to metabolize
energy in an amount sufficient to sustain life.
Decrease in mean arterial pressure indicates
decrease in blood flow which leads to decrease
perfusion to the vital organs. Increase in mean
arterial pressure increases cardiac flow.
Peripheral resistance is the resistance of
peripheral vasculature in the systemic circulation.
Blocked vessels and vasoconstriction can
increase peripheral resistance. Vasodilation can
decrease in peripheral resistance

VENOUS PRESSURE

Blood flows back to the heart via venous system

with assistance from vessel wall tone, pumping
action of the skeletal muscle

Central venous pressure – Approximation of

right atrial pressure; normal: 5 to 10 cm H2O

Brunner – 4 to 12 mm Hg

CAPILLARY PRESSURE

Capillary pressure is the pressure exerted by the CHANGES IN RESPONSE TO

blood against the capillary. The balance of the PARASYMPATHETIC AND SYMPATHETIC
interstitial fluid depends on the capillary pressure NERVOUS SYSTEM
and plasma oncotic pressure
Baroreceptor – Sends impulses to the medulla
25 to 30 mm Hg at arterial oblongata to stimulate either vagal response

10 to 15 mm Hg at venous ● Reports abnormal blood pressure to the

CNS, which responds by regulating the
REGULATION OF CARDIAC FUNCTION AND rate
BLOOD PRESSURE
Stretch receptors – Sends impulses to the CNS
1. Neural or ANS to stimulate HR and blood vessel constriction to
A. PNS – Inhibitory effects regulate circulatory volume status that affect BP
B. SNS – Acceleratory effects
2. Endocrine control – Hormones contribute to Chemoreceptor – Sensitive to hypoxemia and 2°
regulation of the circulation of the heart to ↑ CO2 and ↓ arterial pH
3. Local control or peripheral receptors – pH, O2
Baroreceptor is sometimes called a
and CO2 concentration
pressoreceptor. It is located in the wall of the
Parasympathetic nervous system releases neural aortic arch and carotid sinus. It is a sensory nerve
transmitter acetylcholine that can decrease the in the blood vessels that reports abnormal blood
rate of SA node firing or decrease in heart rate, or pressure to the CNS
even decrease in atrial or ventricular contractility
Stretch receptors respond to pressure changes
and conductivity
that affect circulating blood volume
Sympathetic nervous system releases neural
Chemoreceptor senses chemical changes in the
transmitter norepinephrine, producing
blood. Usually, chemical changes in blood
acceleratory effects on the heart, such as
including pH, carbon dioxide, and oxygen level
increase heart rate, increase conduction speed,
alters the cardiac and respiratory activity
or even increase in atrial or ventricular
contractility and peripheral vasodilation
HEALTH ASSESSMENT

SUBJECTIVE DATA

A. Chief Complaint
1. Chest pain or discomfort – SOCRATES
Angina pectoris – 5 to 15 min;
uncomfortable pressure, squeezing or
fullness in substernal chest area
Acute coronary syndrome, or ACS – >
15 min
Pulmonary disorders – Sharp, severe
epigastric pain or substernal arising from
inferior portion of pleura

● Location – Substernal or cordial

● Characteristics – Pressure, burning,
crushing
Categories of mechanism in the circulation in ● Intensity – Mild, moderate, or severe
addition to neural include: ● Onset – Sudden or gradual
● Duration – Intermittent or continuous
Autocrine Control. Several hormones contribute ● Precipitating factors – Emotion
to the regulation of the heart circulation.
Catecholamine are released in response to 2. Palpitations – Rapid or irregular
physical activity and stress, which influences heartbeat
heart rate, myocardial contractility, and peripheral 3. Dyspnea – EOD, PND, orthopnea
vascular resistance. Other hormones include such as ACS, cardiogenic shock, HF
angiotensin, adrenocortical hormones, and valvular heart disease
vasopressin, bradykinin, and prostaglandin. 4. Cough – Dry, paroxysmal with
Local Control. Meets all the metabolic needs of exertion
the surrounding cells 5. Unusual fatigue – Inability to perform
activities of daily living
6. Peripheral edema – Grading scale
7. Syncope – Medical term for fainting
or passing out, loss of
consciousness, because of decrease
blood flow to the brain, usually from 5. Pulse – PR, rhythm, quality,
low blood pressure configuration or contour, bruits, and
8. Weight gain palpation of arterial pulse
9. Hepatosplenomegaly, or HF –
Precordium
Common in patients with right-sided
heart failure 1. Inspection – Apical pulse, retraction
10. Dizziness in 5th ICS MCL
11. Postural hypotension Apical Pulse – Can indicate pericardial disease
2. Palpation – Thrills
B. Patient History Thrills – Palpable vibration over the precordium.
1. Past medical history It can indicate aortic stenosis or pulmonic
2. Medications history – Vitamins, herbal, stenosis
and other OTC medications 3. Auscultation – Murmurs, abnormal
3. Family history heart sounds
4. Diet and nutrition – Height and weight, 4. Jugular veins – 1 to 3 cm above the
food preferences and preparation level of manubrium
5. Elimination – Bowel and bladder habits 5. Blood pressure - SBP, DBP,
Nocturia – Very common in patients with heart pulse pressure
failure because of the increase in circulatory Patients might have postural hypotension in
volume during nighttime which there is a systolic increase of at least 20
Valsalva maneuver – Breathing method when mm Hg within 3 minutes of moving from lying,
the heart is beating too fast sitting, or standing, accompanied by dizziness
6. Socio-cultural – Education level, and lightheadedness due to reduced preloading
occupation, sleep pattern, exercise, which compromises the cardiac output
tobacco use, economic resources
Sleeping pattern – Recent changes such as There is a risk for coronary artery disease if
upright position is common in patients with heart abdominal fats are greater than 40 inches for
failure male and 35 inches for female
7. Psychological – Self-perception and
self-concept, coping and stress
strategies, prevention strategies;
depression, behavioral changes
JUGULAR VEIN
OBJECTIVE DATA

Head to toe physical exam – IPPA techniques

A. General Appearance
1. LOC, mental status, and the size,
height and weight, and BMI –
Normal, over-, or underweight,
cachectic
Cachexia – Weakness due to severe chronic
illness
2. Skin – Color, ecchymosis, turgor,
temperature, moisture – Pallor,
peripheral and central cyanosis
3. Nail – Color, shape, thickness,
symmetry, clubbing of fingers
Clubbing – Due to prolonged lack of oxygen,
which can activate local vasodilators that secrete
growth factors that causes changes in the distal
part of the fingers
4. Extremities – Edema, ulcerations,
capillary refill time
3. Aspartate Transaminase
● Serum Glutamic Oxaloacetic
Transaminase, or SGOT
● Heart failure can lead to generalized
swelling of the body that causes elevated
AST, which can result to liver damage or
an insult to the heart
● 10 to 40 u/L

4. Myoglobin
➔ Oxygen-binding protein found in striated
muscle
➔ Skeletal muscle injuries releases
myoglobin
➔ Increase within 2 hours after AMI
➔ Returns to normal about 12 hours
➔ 30 to 90 mcg/L
➔ Not specific in diagnosing MI but can help
in diagnosing the oxygen-carrying
capacity to the muscle tissue
➔ Hemoglobin transforms oxygen.
Myoglobin stores oxygen. Oxygen is the
carrying pigment of the muscle tissue

B. Diagnostic Studies 5. Troponin

➔ Normal cardiac troponin level is very low.
Laboratory Tests
The level increases rapidly with
A. Serum Enzymes myocardial infarction
1. Creatinine Kinase, or CK – CK-MB ➔ Released only when myocardial
● Found in the heart necrosis occurs
● Rise within 6 hours of injury ➔ Preferred marker for myocardial injury.
● Peak at 18 hours post injury Physicians might suspect myocardial
● Returns to normal in 2 to 3 days. injury or ischemia in an elevated troponin
● Normal CK – 36 to 188 u/L. ➔ There are two levels. Troponin T might
● Normal CK-MB – < 25 u/L indicate myocardial ischemia. Troponin I
Creatine kinase is formerly known as creatine are for patients with unstable angina
phosphokinase. The three isoenzymes are CK- ➔ Increase within 3 to 12 hours from the
MM, CK-MB, and CK-BB. Elevated CK-MB might onset of chest pain
indicate myocardial infarction. Avoid IM injection ➔ Peak at 24 to 48 hours
prior to extraction
➔ Returns to baseline at 5 to 14 days
➔ Troponin level increase earlier than
2. Lactate Dehydrogenase, or LDH – L1 and
CK-MB level
L2
● Useful in diagnosis of MI ➔ Normal Troponin T – < 0.2 mcg/L
● Detected within 24 to 72 hours ➔ Normal Troponin I – < 0.35 mcg/L
● Peaks within 3 to 4 days
● Elevated 14 to 24 hours after onset of MI 6. C-reactive Protein, or CRP
● LDH – 90 to 176 units/L ➔ CRP is produced by the liver. It increases
● Returns to normal after 2 weeks in response to tissue inflammation or
injury
➔ Marker for systemic inflammation
➔ Identifies myocardial injury
➔ Better predictor for MI than cholesterol
➔ < 1 mg/dL ● Measures the seconds needed for a clot
to form. If there is prolonged PTT, then it
7. Lipid Profile will take longer for a clot to form and
➔ Cholesterol – < 200 mg/dL thrombus may not occur or develop
Required for hormone synthesis and
cell membrane formation, found in 9 Brain Natriuretic Peptide, or BNP – < 100
large quantities of the brain and ng/L
nerve tissue. ● BNP is a neurohormone that helps regulate
➔ Triglycerides – 100 to 200 mg/dL blood pressure and fluid volume
Free fatty acids and glycerol. Stored in adipose ● It is secreted from the ventricles to increase
tissue and it is a source of energy preload which can result in an increase in
Physical activities are needed to decrease ventricular pressure. If there is an increase in
triglycerides if it gets too high BNP, there is also an increase in ventricular
wall pressure. This is significant to patients
Lipoproteins with heart failure, acute MI, and hypovolemic
a. Low Density Lipoprotein, or LDL – < 160 state like renal failure
mg/dL ● Used to diagnose heart failure, MI, and
Primary transporters of cholesterol and pulmonary embolism
triglycerides into the cell ● Decrease in BNP decreases sodium
retention and decreases renin angiotensin
Harmful effect: secretion
Deposition of these substances in the walls of
arterial vessels, causes coronary artery disease 10. Homocysteine – Indicates high risk for CAD,
B. High Density Lipoprotein, or HDL stroke, and peripheral vascular disease. Normal:
M – 35 to 70 mg/dL 5 – 15 umol/L
F – 35 to 85 mg/dL ● Homocysteine is an amino acid that links to
Transport of cholesterol to the peripheral can the development of atherosclerosis
result to coronary artery disease ● Patients might indicate high risks for coronary
Triglycerides – Stored calories that provides the artery disease, stroke, and peripheral
body with energy vascular disease. This is to determine
HDL – Has a protective action in which it patients at risk for cardiovascular diseases
transports cholesterol away from the tissue and ● Increase in homocysteine indicates a risk for
cells of the arterial wall to the liver for excretion coronary artery disease due to genetic factor
and vitamins B6, B12, and folate deficiencies
8. Coagulation studies ● Vitamins B6, B12, and folate supplements
● Coagulation studies are performed before can lower homocysteine
invasive procedures
Prothrombin time – 10 to 14 seconds 11. Atrial Natriuretic Peptide, or ANP –
● Prothrombin time evaluates the extrinsic Controls body water, Na, and K release by the
coagulation system and screens coagulation atria in response to blood volume
deficiency factors 1, 2, 5, 7, 10 ● Regulates excess cellular volume. It reduces
● Monitor patients who take anticoagulants and water and sodium in the circulatory system to
screen patients with Vitamin K deficiency reduce blood pressure
● Measure the time to form a clot ● Counteracts secretion of aldosterone
If < 10 seconds – Patient is at risk for ● Patients with heart failure have high ANP
thrombus formation because of hypervolemic state
If > 30 seconds – Patient is critical and at 12. Electrolytes
risk for bleeding A. Sodium – Diuretic therapy; 135 to 145
Activated Partial Thromboplastin Time, or mEq/L
aPTT – 20 to 39 seconds Low or high sodium do not necessarily affect
● Evaluates intrinsic coagulation system cardiac function.
● Identifies bleeding and clotting disorders Decreased sodium may indicate fluid
● Monitors the effect of heparin excess, heart failure and administration of
diuretics. Increased sodium may indicate
fluid deficit, diarrhea, diaphoresis, loss of ● Necessary for absorption of calcium,
water. maintenance of potassium and metabolism
of ATP
Prolong use of diuretics may put pxs at risk ● Necessary factor for the conservation of
for Hyponatremia. potassium in the kidney
● Major roles include: Protein and
B. Potassium Carbohydrate synthesis, Muscular
● 3.5 to 5.5 mEq/L Contraction and Neuromuscular Activity
● Affects heart muscle ● Neuromuscular activity causes decrease in
● Ventricular dysrhythmias calcium and potassium
● Presence of U wave in the ECG tracing ● Mg is a factor for the conservation of
● Hypokalemia - may be caused by potassium in the kidney
administration of potassium excreting - ⬇ Mg could cause irregular
diuretic which may lead to heart rhythm, atrial or
dysrhythmia, ventricular tachycardia / ventricular tachycardia or v.
ventricular fibrillation. If the client is taking arrhythmia
digitalis, then hypokalemia may put client at - ⬆ Mg could depress myocardial
risk for digitalis toxicity. Presence excitability and contractility
of U wave is visible in ECG tracing. that will cause heart block,
● Hyperkalemia - may be caused by or worse, acistole as well as
increased intake of potassium, decreased hypotension and bradycardia
renal excretion of potassium, use of
● NORMAL VALUE: 1.8 to 3 mg/dl
potassium sparing diuretics eg. Aldactone.
Other Laboratory Tests:
Hyperkalemia may result in heart block,
acistole, ventricular dysrhythmia. Digitalis Basal Metabolic Panel > determine glucose
toxicity increases electrical instability. level in the blood;

NORMAL FASTING: 10 - 12 hours

Creatinine and BUN > assesses kidney

function and fluid balance .

CREATININE NORMAL VALUE: 0.7 to 1 mg/dl

BUN NORMAL VALUE: 10 to 20mg/dl
C. Calcium – 8.5 to 10.5 mg/dL Bicarbonate & Chloride
● Hypocalcemia – Dysrhythmia and prolong QT
interval 14. Complete Blood Count, or CBC
● Will slow nodal function and impair ● RBC – Hemoglobin and hematocrit
myocardial contractility which increases ● WBC
the risk for Heart Failure. ● Platelets
● Hypercalcemia – Could result from
administration of thiazide diuretics which Hemodynamics – Circulation
reduces renal excretion of calcium. ● Invasive procedure to closely monitor left
Shortens QT interval which results to ventricular pressure and cardiac output by
AV block/heart block. the use of Arterial Line and Pulmonary Artery
● Both Hyper/Hypocalcemia could result to Catheter
cardiac arrest ● Studies the movement and forces of blood in
D. Magnesium - 1.8 - 3 mg/dl the cardiovascular system
● Decreased Mg could cause irregular heart ● To test the effectiveness of cardiac
rhythm, atrial/ventricular tachycardia, or function
ventricular arrhythmia ● Used to patients in ICU
● Increased Mg could depress myocardial ● Close examination of cardiac function in
excitability and contractility that will cause acutely ill patients
heart block, or worse, asystole as well as ● Rapid identification of completions after
hypotensionand bradycardia MI
● Differentiates pulmonary disease from ● Assesses the right and left
left ventricular failure pumping action of the heart
● Guide in the management of low CO ● Could quantify cardiac output
● Calculation of oxygen level
between the arterial and venous
Methods that can be used to obtain ● Used to prevent overhydration
Hemodynamics and pulmonary edema during
open heart surgery
➔ Obtaining the Heart Rate - Use of ● Helps to improve conditions such
Dinamap or Doppler (Non invasive) as:
➔ Arterial Line, Swan-Ganz and - Cardiac tamponade
Pulmonary Artery Catheter (Invasive for - Myocardial infarction
Patients in ICU) - Cardiogenic shock
- Pulmonary Hypertension
- Restrictive cardiomyopathy

SWAN-GATZ CATHETERIZATION

PAP – Assess the left heart pressure, left

ventricle

PCWP – Indirectly measure left atrium

SWAN-GANZ MONITOR

Heart function – Right and left pumping action of

the heart

Blood flow – Quantitative measurement of

cardiac output

HEMODYNAMIC PARAMETERS Calculation of O2 level – Between arterial and

venous
1. Central venous pressure, or CVP –
Measures the blood volume and venous Radiographic Techniques
return; 1. Chest X-ray, or CXR
Indicates mean right atrial pressure; 5 to ● To assess contour, size and position of
10 cm H2O or 4 to 12 mm Hg the heart
2. Systemic intra-arterial pressure – ● Reveals any cardiac and pericardial
Allows continuous monitoring of systolic calcification
and diastolic blood pressure and mean ● Demonstrate physiology alteration in
arterial pressure, or MAP pulmonary circulation
2. Cardiac Catheterization – An invasive
MAP
procedure used to obtain details information
Systolic BP + (2 Diastolic BP) about structure and performance of the heart,
valves and circulatory system
3
● Visualize structure and performance of
Normal - 70 to 110 mm Hg the heart chambers, valves, great
vessels and coronary arteries and
Pulmonary Artery Pressure, or PAP and
circulation
Pulmonary Capillary Wedge Pressure, or
● Assesses the coronary artery patency,
PCWP
extent of atherosclerosis
Swan-Ganz catheter – A catheter is passed ● To determine the benefits of
through the right side of the heart and into the percutaneous coronary intervention
pulmonary artery ● Standard test for CAD
● Can be diagnostic and therapeutic 7. Determine the efficacy of a heart
intervention transplant
● Includes electrophysiologic studies,
For Evaluation of:
hemodynamic monitoring
● For percutaneous transluminal ● Any Coronary Heart Diseases with
angioplasty Unstable Angina that does not respond to
● Palliative procedure for congenital heart treatment of medications
defect ● The end of coronary artery surgery or
● Could diagnose pulmonary arterial Angioplasty
hypertension
To Diagnose:
Right – Myocardial biopsy and measure PAP
● Atypical chest pain
● More safe ● Complications for MI
● Inserted through basilica or femoral vein ● Aortic Dissection
● Potential complications may include:
- Dysrhythmia or arrhythmia To Assess for valvular function
- Venous spasm
To Determine the efficacy of heart transplant
- Infection
- Perspiration PREPARATION FOR CARDIAC
CATHETERIZATION
Left – Visualize coronary arteries and ventricular
function 1. Written consent
2. History taking – Allergies to shellfish
● Used to evaluate aortic arc and major
3. Laboratory results
branches
4. Baseline vital signs
● Monitor mitral and aortic valve function
5. NPO AMN
and shunting
6. Explain to patient the flushing sensation
● Inserted through brachial and femoral
during procedure
artery
7. Voiding; no jewelries and dentures
8. Pre-op medications – Antihistamine,
corticosteroids
9. Withheld Metformin 48 hours prior to
procedure
10. Shaving the operative site
11. Health teaching

POST PROCEDURE CARE FOR CARDIAC

CATHERTERIZATION

1. CBR - First 24 hours in hospital setting,

theoretically 6 to 12 hours
2. Monitor vital signs - Without hypertension,
hypotension, and bleeding which causes
elevated pulse rate
3. Immobilize the affected extremities
4. Elevate HOB at 30° angle
INDICATIONS OF CARDIAC
5. Check for the pressure dressing - Use 6 lbs
CATHETERIZATION
sandbag to prevent bleeding
1. Evaluate CAD with unstable angina 6. Refer chest pain, bleeding, dysrhythmias,
2. Diagnose atypical chest pain hematoma formation, and any untoward
3. Diagnose complications for MI signs and symptoms
4. Diagnose aortic dissection ● Manual pressure that is applied
5. Assess for valvular function during the removal of catheter may
6. Evaluate the end for coronary artery cause vagal stimulation could result
surgery or angioplasty
to bradycardia, hypotension, nausea - Patient is in supine position
and distended bladder with arm raised above the
● To reverse this effect, elevate the head while the camera move
lower extremities of the px higher around the patient chest in
than the heart, administer bolus of 180 to
intravenous fluid and atropine to treat - 360 degree to precisely
bradycardia identify areas of decreased
7. Hydration - Encourage increase fluid intake Myocardial perfusion.
for the excretion of contrast dye if it is not ● Positron Emission Tomography, or
contraindicated to the condition of the patient PET – Determine the blood flow in
the myocardium and metabolic
CONTINUATION OF RADIOGRAPHIC
function such as cardiac and tissue
TECHNIQUES
perfusion
3. Coronary Angiography – Technique of
- safer and faster than SPECT
injecting a contrast agent into the
due to lower exposure to
vascular system to outline the heart and
radiation
blood vessels
- Evaluate tissue and organ
● Visualizes coronary arteries
functions by identifying body
● Technique of injecting contrast agent
changes at the cellular level
into the vascular system to outline
which make a disease
the heart and blood vessels
evident prior to other
4. Radionuclide Testing – Uses
imaging tests.
radioisotopes to evaluate coronary artery
- Eg. Ischemia tissue,
perfusion
decreased blood flow and
● To evaluate coronary artery
increase metabolism
perfusion, left ventricular functions
using radioisotopes NURSING RESPONSIBILITIES
● Assess Myocardial Ischemia and
1. Assess patient for fear of closed spaces or
Myocardial Infarction
claustrophobia
Types of radionuclide testing:
2. Refrain from alcohol or caffeine 24 hours
● Thallium 201 - TI201; exercise
prior to PET
- Must be tested positive
3. ALARA Principle; explain that radiation
before undergoing Cardiac
exposure is safe and in acceptable levels
Catheterization
4. Monitor glucose level, or PET before the test
- Stress testing, to determine
5. IV access – Patent
Myocardial perfusion
6. Scan takes 1 to 3 hours to complete
immediately after exercise
and at rest GRAPHIC STUDIES
- Areas that doesn't show
current update may indicate 1. Echocardiography
Myocardial Ischemia or MI ● Evaluate internal structure and
● Technetium 99m – Tc99m; motions of the heart and great
sestamibi vessels; may be performed with an
- uses various chemical exercise and pharmacologic stress
compounds that gives test
affinity to different types of ● Doppler techniques are also used to
cell determine the direction of blood flow
- Can be taken during resting and velocity
period, before and after an
● may be performed with an exercise
exercise
and pharmacologic stress test
● Single Photon Emission Computed
Tomography, or SPECT ● Monitors overall cardiac
- provides 3D images of the performance including the
heart
chambers, size, motion and cardiac and determines whether the heart is
great vessels able to meet the increased oxygen
demand
● As well as the intraventricular
● Dipyridamole scan, or Persantine
septum, posterior left ventricular wall,
● Determines whether the heart is able
valve motion, the directions and
to meet increased oxygen demand
velocity of blood flow to determine
after physical activity
any leaking valve
Persantine Scan
● Monitor if there's an increased ● If the patient cannot exercise,
pericardial fluid. Dipyridamole/Adenosine (shorter
duration span) can be administrated for
● Modes: vasodilation that has the same response
after a physical activity
Motion Modes
● This scan will allow increased heart rate
- shows 1D view of the heart to the point of 85% of the maximum heart
- Shows an image of a narrow area heart rate
within the ultrasonic beam ● Eg. If the heart rate is 80 x 85% = 68 + 80
= 148 beats per minute, the final answer
2D Echo should not exceed beyond 148 beats per
- produces a cross sectional view minute
- Shows structure, lateral movement ● This scan is contraindicated with patients
and spatial relationship between the that has:
heart structure - Hypertension
- Doppler technique - to determine - Aortic stenosis
direction of blood flow and velocity - Coronary Artery Disease
- May be performed with an - Heart Failure
exercise and pharmacologic - Unstable Angina
stress test 3. Duplex Scan – Arterial and venous
● Visualize the flow or movement of a
Doppler Ultrasonography – Records the structure, typically used to image
direction of blood flow through the heart; detects blood within an artery
presence, direction, speed and character of ● Determine the flow velocities through
arterial or venous blood flow within the vascular a region of narrowing or resistance of
lumen; could be done in Carotid Area a vein or artery
● Is combined with doppler flow
Color Flow Doppler, or CFD – Records flow
information
frequencies into different colors
4. Electrophysiologic Studies
● Evaluate the electrical conduction
system of the heart
● Assess the effectiveness of anti-
arrhythmic medications and devices
● Treat certain dysrhythmias through
the destruction of the causative cells
● Identify the location and mechanism
● Assess function of SA and AV node

● To distinguish atrial from ventricular

tachycardia

● To treat dysrhythmias by destruction

of causative cells
2. Stress Test ● For patients who often experiences
● Increases the demand placed on the syncope, palpitations, dysrhythmia
heart by increasing physical activity
Assesses:
● Efficiency of Anti arrhythmic Evaluates cardiac status of px with
medications known heart disease during cardiac surgery.

● Function of Nodes (SA,AV,BoH,PF)

TEE NURSING RESPONSIBILITIES Pre-op
● The needs to alternate interventions 1. Obtain consent
like pacemaker, radiofrequency 2. Restrict foods and fluids - NPO for 6-8 prior
ablation, implantable cardioverter to procedure
defibrillator 3. IV access - No jewelry, Void before the
procedure, no dentures
4. Vital signs -
5. Lab result
6. Emotional support

POST-OP

1. Monitor vital signs

2. Position client at 45°
3. Monitor for dyspnea, LOC
4. Check for gag reflex - O2 saturation and
shortness of breath
5. Inform of sore throat and dysphagia for the
next 24 hours
6. Cool liquids - would soothe sore throat
5. Transesophageal Echocardiography, or 7. Avoid talking
TEE
● Gives higher quality picture of the heart
and useful in clients who have thickened 6. CT Scan – Determines cardiac masses
lung tissue or thick chest walls or who are and diseases of the aorta and
obese pericardium
● Provides higher quality image of the 7. Magnetic Resonance Angiography –
heart because the sound wave does not Evaluates physiologic and anatomic
need to pass through skin, muscle, or properties of the heart
bone tissue. - more higher technology than the
CT Scan
● Appropriate for patients who are obese, 8. Electrocardiogram – ECG, EKG
has pulmonary disease and ● Records the heart’s electrical activity
emphysema.
by detecting magnitude and direction
● Certain conditions of the heart that of electrical currents produced in the
could also be viewed under heart
TransEsophageal Echo: HOLTER MONITORING - >24 hrs monitoring of
the heart activity
a. Mitral valve disorder
b. Blood clots
c. Muscles inside the heart
d. Dissections of the lining of the aorta
e. Implanted prosthetic heart valve

Indications:

Assess heart function and structure

Evaluate the heart after heart surgery

procedure such as coronary artery
bypass / valve replacement.
ABNORMALITIES

1. Inverted P-wave
2. Wide P-wave – P mitrale
3. Peaked P-wave – P pulmonale
4. Saw-tooth appearance – Atrial flutter
5. Absent normal P wave – Atrial fibrillation

NORMAL P-R INTERVAL

• The time the impulse from the atria to the AV

node, the His-Purkinje system and through
the ventricles
• PR interval time 0.12 seconds to 0.20
seconds
➢ 0.20 sec – Delay in conduction from
SA node to the ventricle
• Three small squares to five small squares

PR ABNORMALITIES
ECG TRACING
1. Short PR interval – WPW syndrome
2. Long PR interval – First degree heart block

QRS COMPLEX

• Electrical depolarization and contraction of

the ventricles
• QRS duration 0.04 0.12 seconds
• Less than almost three small squares
• Morphology: progression from Short R and
deep S (rS)

QRS ABNORMALITIES

• Wide QRS Complex

• Tall R in V1
• Abnormal Q Wave – > 25% of R wave

ST SEGMENT

• The period between completion of

depolarization and the beginning of
repolarization of the ventricles
• Beginning of the ventricular repolarization
• Elevated or depressed indicates cardiac
ischemia
• ST elevation indicates myocardial injury; ST
depression changes in the ventricular wall
ECG WAVEFORM COMPONENTS

P WAVE
❏ Electrical activity associated with SA node
impulse and depolarization of the aorta
❏ Atrial depolarization and contraction
❏ Impulse is from the SA node
❏ In all leads except aVR
➔ Patient is conscious and
hemodynamically stable
● Pharmacologic / Chemical Cardioversion -
uses anti arrhythmic medications instead of
electrical shock
➔ If the cardioversion is elective,
not lasts not longer than 48 hrs
anticoagulation for few weeks
before cardioversion
➔ Digoxin is withheld for 48 hrs
prior to cardioversion > to assure
resumption of sinus rhythm and
conduction

T WAVE ● Non-emergency basis

● Patient is sedated with either IV
• Recovery or repolarization phase of the diazepam or midazolam prior to the
ventricles procedure.
• Ventricular Repolarization
• Abnormal T wave indicates: myocardial 2. Defibrillation – Unsynchronized
ischemia or injury or electrolyte imbalances ● High energy shock
● Fall randomly anywhere within the
SUMMARY OF ECG TIMING
cardiac cycle – QRS complex
Seconds ● 200 to 360 J
P 0.06 – 0.12 ● AED
QRS 0.04 – 0.12 ● Emergency procedure - px is
ST Segment 0.12 unconscious
T 0.16 ● Delivers high energy shock randomly
PR Interval 0.12 – 0.20 within the cardiac cycle (QRS complex)
QT Interval 0.32 – 0.40 ● Discharge of unsynchronized impulse
● Most effective method in treating
ventricular fibrillation, dysrhythmia,
ADJUNCTIVE MODALITIES – Countershock ventricular tachycardia
● Initial Shock: 200 joules
1. Cardioversion – Treats tachydysrhythmias
● Secondary Shock: 200 - 300 joules
by delivering an electrical current that
● Third Shock: 360 joules
depolarizes a critical mass of myocardial cells
● Synchronized – Low energy
Defibrillator is the device both used in
➔ Use of electricity synchronized with cardioversion and defibrillation
the peak of QR ECG monitor is both needed in
➔ Option: Engage in Defibrillator cardioversion and defibrillation.
➔ Timing of electrical delivery should
be synchronized
➔ Used in patients with ventricular
tachycardia, atrial flutter and atrial
fibrillation
➔ Use of therapeutic dose of electrical
current to the heart using a rod at the
specific unit in the cardiac cycle
● Unsynchronized cardioversion - done in non-
emergency basis
NURSING CONSIDERATIONS IMPLANTED CARDIOVERTER-
DEFIBRILLATOR, OR ICD
1. Withheld digoxin 48 hours before
cardioversion • Similar with a pacemaker; implanted inside
2. NPO at least 4 hours before the procedure the body
3. Defibrillation: Epinephrine is given after initial • Delivers low level and high level of electrical
unsuccessful defibrillation impulses
4. Anti-arrhythmia: • Prophylaxis for patient who are at risk to have
➔ Amiodarone sudden cardiac death, ventricular fibrillation
➔ lidocaine
FUNCTIONS OF ICD
➔ magnesium
if ventricular dysrhythmia persists 1. To reset abnormal heart beat
5. Continuous CPR 2. Send high energy shock if an arrhythmia
➔ Two safety measure for the placement of become severe
Defibrillator paddle on the patient: 3. Treatment of certain fast rhythm
➔ Maintain good contact between the paddle 4. Detect sudden cardiac arrest or shock
and the skin of the patient
➔ No one should be in contact with the patient LINK OR CHAIN OF SURVIVAL
when the shock is being discharged

KEY POINTS TO REMEMBER WHEN ● Early access Early CPR

ASSISTING EXTERNAL DEFIBRILLATION ● Early defibrillation
● Integrated cardiac life support
1. Conducting medium – Gel – is used – DO ● Integrated post cardiac care
NOT use gel or paste with poor electrical
conductivity like UTZ gel
2. Paddles are placed on the chest wall –
One in the left of the pericardium and the
other on the right of the sternum just below
the clavicle
3. Apply 20 to 25 pounds of pressure to the
paddles
4. The operator calls ALL CLEAR

Adjunctive therapy and RFA will be discussed in

cardiac dysrhythmias
MEDICAL SURGICAL b) ​abnormal enhanced automaticity
CARDIOVASCULAR DISORDERS PART 2 ➔ Normally the SA node has a higher automaticity
Cardiac Arrhythmias than the rest of the heart, so any part of the heart
that initiates an impulse with outweighing the SA
Cardiac Dysrhythmias node is called ectopic focus. For a node open
than the SA node it can produce abnormal
★ A disturbance, irregularity or abnormal in the rhythm therefore every heartbeat that did not
electrical system of the heart. Dysrhythmias may originate from SA node is considered an ectopic
initially be evidenced by the hemodynamic effect beat. When the ectopic beat is early it is called
they cause (e.g., a change in conduction may extrasystole while if it is too late it is called
change the pumping action of the heart and escape.
cause decreased blood pressure), and are ➔ Factors the contribute to reduce resting
diagnosed by analyzing the electrocardiographic membrane potential:
(ECG) waveform ★ Ischemia, Hypokalemia, Hypoxia or
★ Also known as arrhythmia Effect of Drugs
​Heartbeat may be too fast or too slow, regular or
irregular
c)​ conduction disturbances
★ Primary disorder or secondary response to a
➔ It ​accounts​ for bradyarrhythmia
systemic problem or complications of drug toxicity
or electrolytes imbalance.
★ Heart rate influenced by the ANS which consists Classification of Arrhythmias by Site
of SNS and PNS 1.SA node (60 ​– ​100 bpm) ​– ​normal looking PQRST
complex
• Sinus bradycardia - Slow heartbeat, distant
Major Classification of Dysrhythmias • Sinus tachycardia - Fast heartbeat, close
• Sinus arrhythmia - Distance depends on respiration
❏ Cardiac Rhythm is identified according to the site > 1-3 they have a normal looking or normal PQRST the
of origin like SA node, AV node, conjunction, or difference is the rate.
ventricles
❏ It could be identified as a mechanism of 2. Atria ​– ​abnormal looking P wave, normal QRS complex
conductions like normal rhythm, bradycardia,
• Premature atrial contraction
tachycardia, dysrhythmia, flutters, fibrillation,
• Atrial flutter
premature complexes or conduction block.
1. Rate​ ​– ​very slow or very rapid • Atrial fibrillation
➔ Such as a patient who has hypoxia,
metabolic alkalosis, electrolytes 3. AV junction (40 ​– ​60 bpm) ​– ​prolong
imbalance. Imbalances like hypokalemia, PR interval > 0.20 seconds
hypocalcemia which cause prolonged • AV blocks
duty ​can lead to electrical instability.
2. ​Mechanisms ​– ​based on the electrophysiologic 4. Ventricles (30 ​– ​40 bpm) ​– ​abnormal wide QRS
mechanism complex
a. re-entrant > 0.20 seconds; serious life threatening
➔ electrical impulse travels in a ● Premature ventricular contractions (PVC)
tight circle within the heart ● Ventricular tachycardia
instead of moving from one end ● Ventricular fibrillation
to another
● Several conditions that may cause re-entry to
Causes of Cardiac Dysrhythmias
occur:
1. Myocardial Infarction (MI)
1. At a point where there are two conduction
❖ because of the conduction problem on the
pathways for an impulse to follow.
damage tissue
2. Because of the slow conduction through one
2. Rheumatic Heart Disease (RHD)
portion ​of that pathway.
3. There is a newly directional block at some 3. Heart failure
point along the conduction pathway. 4. Electrolyte Imbalances
5. Drug toxicity – esp. those taking digitalis, quinidine
6. Hypothermia 5. Antiarrhythmic drugs – lidocaine, β-adrenergic
7. Trauma blockers, calcium channel blockers, digitalis preparation
8. Coronary Artery Disease (COD)
Antiarrhythmic Drugs:
Class 1 – depress upstroke of action potential (lidocaine,
Sign and Symptoms of Dysrhythmias
quinidine, pronestyl)
1. Palpitations – most common
● pt. had a feeling of a skip heart beat ➢ It interferes with the sodium channel that
● some palpitations may be harmless but many of depresses the​ fasting wipe off of​ sodium
them predispose to adverse outcomes like a ● Quinidine - to treat fever, malaria and contain
higher risk of blood clotting or insufficient transfer antiarrhythmic properties at the same time it
of the blood because of the weak heartbeat could also suppress the supraventricular
● others are embolisation, stroke or sudden cardiac tachycardia and ventricular arrhythmia.
death ● Lidocaine - it is not widely used because of the
2. Lightheadedness or dizziness effect on ischemic tissue. It suppresses the
3. Syncope – fainting conduction more on ischemia tissue than on
4. Chest discomfort normal that why lidocaine is no longer routinely
5. Pounding chest used for the treatment of acute ventricular
arrhythmia.
6. Weakness or Fatigue

Class II ​– beta-adrenergic receptor blockers (effect on

DIAGNOSTIC STUDIES BP, HR and myocardial contractility) metoprolol

1. 12 lead ECG ❖ anti sympathetic nervous system agent that

2. 24-hour ambulatory ECG or Holter monitoring allows the SA node to fight ​spontaneously,
3. Electrophysiologic studies (EPS) therefore, it may decrease the blood pressure,
➔ This is to assess the electrical activity heart rate or myocardial contractility.
and conduction pathway of the heart. ❖ Ex. atenolol, metoprolol, propranolol or even
➔ need to investigate the location of origin carvedilol
are best treatment for various abnormal ➔ These drugs have the ability to inhibit
heart rhythm sympathetic activation of ​cardiac ​automaticity
➔ Stress Test - considered as one of the and conduction.
diagnostic studies for patients who have ➔ Beta Blockers also have an effect of decreased
cardiac arrhythmia or dysrhythmia. MI mortality, preventing recurrence of
tachyarrhythmia.
4.​ Laboratory test ➔ Propranolol - has a sodium channel blocking
effect
● Electrolytes – K, calcium, Mg and FBS
★ Fasting Blood Sugar - bc hypoglycemia can lead Class III – prolong duration of action potential (S/E:
to prolong heartbeat that may sidtubed blood flow hypotension and bradycardia)
to the heart which results in a lethal cardiac
event. ● it prolongs the repolarization and prevents
★ Test for digitalis and quinidine levels in order to re-entrance arrhythmia.
assess its toxicity level to the patient. ● It does not allow the permeability of this ion bc it
may cause stimulation on the contraction.
General Management for Cardiac Dysrhythmias ● Amiodarone - most common, it prevents the
1. Diet – SVT (Supraventricular Tachycardia) avoid repentance of arrhythmia, increases the PR
overuse of stimulants such as caffeine. interval and the QT interval.
2. Cessation of smoking – effects on ventricular ● it causes a slight prolongation of QRS duration
threshold which may be a basis for arrhythmias ● It is also a powerful inhibitor of ectopic
3. ​Oxygen therapy – low-flow oxygen may benefit pt pacemaker automaticity.
who has dysrhythmic or chest pain. ➔ Side effects are hypotension and
4.​Cardiac monitoring - in order to provide most efficient bradycardia.
and reliable method for detections of arrhythmia ➔ Usually treat ventricular tachycardia and
ventricular fibrillation
➔ It should not be used for AV block or any ● Lifespan of battery from 6 to 12 years
allergies to iodine.
➔ Contraindicated to patients who have Indications of Pacemaker Therapy
bradycardia and avoid eating grapefruits *The primary indications for symptomatic bradyarrhythmia
because it may increase the side effects and those who have a long ​(di ko maintindihan slide #14)
of the drugs ​by increasing the amount of syndrome.
this medicine in your body​.
1. Maintenance of adequate HR and rhythm during
➔ It also causes photosensitivity to
surgery and postoperative recovery.
ultralights and should instruct patients to
2. Irreversible bradycardia
avoid sun exposure and should use ➔ which is not responsive to medication
sunscreen. 3. Sinus node dysfunction.
4. Tachyarrhythmias
Class IV​ – calcium channel blockers 5. Symptomatic AV Heart Block
➔ esp. the second type on the third degree
❖ it may decrease the conduction into the AV node AV block
and shorten the phase two of the cardiac action ➔ patients who have fibrosis or sclerotic
potential therefore it prevents the calcium from changes of the cardiac conduction
entering the cell of the heart and blood vessels. system.
At the same time it also relaxes and widens the
blood vessels of the atrial node. Forms of Pacemaker Implantation
❖ Verapamil and Diltiazem​ - most common
➔ It is not appropriately used for those who • Temporary cardiac pacing ​– ​used for hemodynamic
had heart failure because it reduces the or life-support purposes.
contractility of the heart. INDICATION:
➔ Side effects: Reduce BP, headache 1. Complete heart block
(common), nausea and constipation. 2. Symptomatic Bradyarrhythmia
3. Acute MI
Unknown Mechanism Drugs: 4. Emergency measure for for malfunction of
implanted permanent pacemaker
❏ Digoxin ​- which decreases conduction of NOTE: This temporary cardiac pacing is not only for
electrical impulse to the AV node and increases controlling heart rate but also used in
fatal activity and increases in acetyl production electrophysiological laboratories to evaluate cardiac
which may decrease speed of conduction. dysrhythmia and interact with tachycardia.

❏ Adenosine - which is used intravenously for • ​Permanent cardiac pacing ​– ​indicated in the
supraventricular tachycardia. continuous presence of symptomatic bradyarrhythmias.
INDICATION:
❏ Magnesium Sulfate - decrease the calcium 1. Chronic Atrial fibrillation because of low
influx that prevents early depolarization.Widely ventricular response.
used for patient who have di ko maintindihan
sinabi ni Maam hehe Complications of Pacemaker Use:

6. Electrical countershock ​– terminate ventricular 1. Dislodgment of the pacing electrode ​– ​common

fibrillation. 2. Local infection
➔ because it is being inserted on the
7. Adjunctive therapy subcutaneous
3. Pneumothorax
a. Cardiac pacemakers ​– are battery-operated 4. Bleeding and hematoma
generators that initiate and control the heart rate 5. Hiccups ​– ​sign of phrenic nerve, diaphragmatic
by delivering an electrical impulse via an stimulation
electrode to the myocardium. ➔ because of irritation on the phrenic
● Burrowed within subcutaneous tissue below right nerves
clavicle 6. Hemothorax ​– ​puncture of the subclavian vein or
● Bed rest for 24 hours and gradual increase of internal mammary artery.
activity to prevent dislodging of the lid
Measures to Prevent Complications * this is one type of adjunctive
therapy
1. Prophylaxis antibiotics *very common for patient who has
➔ To prevent infection tachyarrhythmia and not
2. CXR ​– ​to check for placement and r/o responsive to medication
pneumothorax ➢ RFA ​– ​radiofrequency ablation
3. Continuous ECG monitoring ➔ Used in patient who has
4. Bed rest for 12 hours with minimal arm and atrial flutter, atrial
shoulder activity to prevent dislodgement of fibrillation and
implanted pacemaker lid. unresponsive to
medication therapy
NOTES: ➢ Cryoablation
1.If the patient is taking antiplatelets or antithrombotic ➔ Applied cold temperature
medications, it needs to be discontinued in order to to destroy the the selected
prevent the risk of bleeding or hematoma. cardiac cells
2. Use of plastic sheets in order to reduce the risk of ❖ Maze procedure
pneumothorax. ➔ A doctor creates a pattern
of scar tissue (the ​maze​) in
Health Teachings (for patient with pacemaker) the upper chambers of the
1. Wound care heart by applying heat or
2. Discuss activity allowances and limitations - NO cold. Or, the doctor uses a
strenuous exercise or lifting heavy objects, avoid scalpel to make several
contact sports; avoid arm and shoulder activity precise incisions.
● To avoid dislodgement of the lid ➔ To prevent reentry
3. Avoid near high voltage wires, power plants, conduction of the electrical
radio transmitters, microwave ovens, theft impulse
detectors
● Avoid those that contain magnets, stereo
speakers and jewelry should not be near
Sinus Rhythms
to the generator for longer than a few
seconds.
● The use of cellular phones is at least
6-12 inches away from the pacemaker
generator or opposite side, so the patient
needs to move from the area if they are
experiencing palpitation or dizziness.
4. Move away from the area if dizziness or
palpitations occur
5. Describe signs and symptoms of pacemaker
failure
● Dizziness
● Weakness
● Lightheadedness
● A drop in pacemaker set rate Disorders of Atria
6. Avoid traveling and driving for 1​st 4 weeks
following insertion 1. Sinus bradycardia
7. Explain the need for continuous medical follow-up
2. Sinus tachycardia
and for periodic battery check-up.
8. Avoid constricting clothing 3. Premature atrial contraction (PAC)
4. Supraventricular Tachycardia (SVT)
B. ​Cardiac Conduction surgery
5. Atrial flutter
★ Electrode catheter ablation ​–
radiofrequency energy “burn” the 6. Atrial fibrillation (AF)
areas or pathways of the abnormal
rhythm and promote normal
conduction of impulses or electrical
pathways between the atria and
the ventricle.
Sinus Bradycardia

❖ The conduction pathway is similar to normal Bradycardia & Hypotension Medical Management “IDEA”

sinus rhythm which has a normal PQRST but the

★ ISOPROTERENOL
SA node is discharging at a rate of less than 60
➔ Action: acts on beta 2 ​– ​adrenergic
bpm
receptors, causing relaxation on
❖ Rate: < 60 bpm
bronchial smooth muscles; acts on beta 1
❖ Causes of sinus bradycardia are:
– ​adrenergic receptors in heart, causing
a) low metabolic needs (athletes, sleeping,
positive inotropic and chronotropic effects
hypothyroidism)
and increasing cardiac output. Also,
b) vagal stimulation ​– ​vomiting, suctioning,
lowers peripheral vascular resistance in
severe pain, fever), and Valsalva maneuver
skeletal muscle and inhibits
means straining that reduces cardiac output
antigen-induced histamine release.
because of increased intrathoracic pressure
therefore decreasing the venous return and
★ DOPAMINE
cardiac output .
➔ Action: causes norepinephrine release
c) medications ​– ​calcium channel blockers,
(mainly on dopaminergic receptors),
amiodarone, beta-blockers
leading to vasodilation of renal and
➔ NOTE: If the patient is taking this
mesenteric arteries. Also exerts
medication then the nurse should check
ionotropic effects on heart, which
the heart rate prior to administration.
increases the heart rate,blood flow,
➔ If the patient has <60 bpm do not give the
myocardial contractility, and stroke
medication because it has an effect that
volume.
may reduce the heart rate of the patient
d) carotid sinus massage
★ EPINEPHRINE
➔ Or patient who has MI
➔ Action: stimulates alpha- and
beta-adrenergic receptors, causing
❖ 0.5 mg of AtSO4 (Atropine Sulfate) every 3 ​– ​5
relaxation of cardiac and bronchial
minutes for a maximum total dose of 3 mg
smooth muscle and dilation of skeletal
➔ If this drug is not responsive then Doctor
muscles. Also decreases aqueous humor
may have transcutaneous pacing or the
production, increases aqueous outflow,
use of dopamine or epinephrine.
and dilates pupil by contracting dilator
➔ Atropine may increase the heart rate and
muscle.
SA is charging so it blocks the vagus
nerve
★ ATROPINE
❖ Theophylline ​100 ​– ​200 mg SIVP (Slow IV Push)
➔ Action: inhibits acetylcholine at
who had a cardiac transplantation and acute
parasympathetic neuroeffector junction of
inferior MI or spinal cord injury
smooth muscle and cardiac muscle,
❖ It may increase the heart rate and contractility
blocking sinoatrial (SA) and
therefore it also relax bronchial smooth muscle
atrioventricular (AV) nodes. These
actions increase impulse conduction and
raise heart rate.
● These medications are used to increase heart
rate peripheral vaso pulsation.
● Another treatment is the use of a pacemaker. ➔ Serves as vasodilator
➔ Contraindicated to a patient who has
asthma because it could cause
Sinus Tachycardia bronchoconstriction due to the histamine
release and the relationship of this to
muscle.
3. Vagal maneuvers
➔ Because it may increase the
parasympathetic nervous stimulation
causing a slow conduction through the
AV node that blocks the re-entry of the
impulse.
➔ Example: Coughing, squatting, hold
breathe, carotid sinus massage, cold
● This is wherein the SA node is charging at a rate
application to the face, jogging and
of >100 bpm
straining.
● The result of inhibition of vagal reflex or
4. Beta-blockers and calcium channel blockers –
stimulation of sympathetic nervous system.
rarely used considering narrow QRS tachycardia
● If there is an increase in heart rate and reduction
➔ Class II Antiarrhythmic Agents like
in systolic filling time, it may reduce cardiac
metoprolol, atenolol
output.
➔ These agents are used to reduce heart
● If the rapid rate persists the heart cannot
rate and decrease Myocardial oxygen
compensate for the decreased ventricular filling
consumption, therefore it will decrease
therefore acute pulmonary edema may develop.
the heart rate, decrease the BP and
cardiac output. It also decrease the
Causes of Sinus Tachycardia
automaticity in the heart rate except it is
1. Physiologic and psychological stress – acute
rarely used if the patient has a narrow
blood loss, hypoglycemia (rt. to sympathetic
QRS tachycardia
nervous response that cause palpitations) ,
5. Procainamide, amiodarone ​– options for wide
hyperthyroidism, fever, anxiety, severe pain,
QRS tachycardia
hypoxia and MI)
6. Catheter ablation
2. Effects of medications – epinephrine,
norepinephrine, atropine, theophylline, nifedipine,
hydralazine
Sinus Arrhythmia
➔ These medications will increase the heart
rate of the patient
3. Autonomic dysfunction – postural orthostatic
tachycardia syndrome(POTS)
● It results from sinus tachycardia ​without
hypotension within 5-10 mins of standing
or sitting
● is an abnormal increase in heart rate that
occurs after sitting up or standing
● Treatment: Increase fluid intake, use of
compression stocking to prevent the
pulling of blood to the lower extremities.

Management of Sinus Tachycardia ● The ECG shows that there are changes in the
rhythm of the ECG depending on the respiration.
1. Synchronized cardioversion – hemodynamic
● The rhythm is irregular but it has a normal PQRS
instability
and interval is within normal.
2. Adenosine administration
➔ This would decrease the conduction of
the AV node
Sinus Arrhythmia ● Treatment: Withdraw from sources of stimulation
like caffeine or ​sympathomimetic ​ drugs
❖ One upright uniform p-wave for every QRS ● Beta blockers may be used to decrease
➔ The rate is within 60-100 bpm but the premature atrial contractions
rhythm is irregular depending on the ● PAC is not significant for a healthy person but
changes so the RR interval changes are with those heart diseases who have frequent
depending on the changes on respiration. premature atrial contraction or complex it
❖ Rhythm is irregular indicates enhanced automaticity of the atria or
➔ Rate increases as the patient breathes in the entry mechanism.
➔ Rate decreases as the patient breathes
out Supraventricular Tachycardia (SVT) or
❖ Rate is usually 60-100 (may be slower) Paroxysmal Atrial Tachycardia (PAT)
❖ Variation of normal, not life threatening
➔ There is no treatment ● In which the atria originating anywhere above the
➔ Common in children and young adult Bundle of HIS or anywhere above the ventricle.
● If the P wave cannot be identified then the rhythm
Premature Atrial Complex (PAC) may be called supraventricular tachycardia
(SVT).
➢ Also known as Premature Atrial Contraction or ● Rapid but regular heart rhythm that comes from
Atrial Extrasystole or Atrial Ectopic Beat the atria. Prevent the gating mechanism
➔ This is due abnormal electrical ​focal ➔ When an impulse is conducted to an area
➢ ​Early, extra heartbeats that originate in the atria in the Av node that causes the impulse
➢ 60 – 100 bpm and irregular re-acted back into the same area over
➢ P wave is abnormal and over again at a very fast rate.
➔ It has a different​ control ​wave ➔ Each time that the impulse is conducted
➔ It may be a notched or a negative thru this area it is also conducted down
deflection or hidden in the proceeding of into the ventricle cause extra ventricular
the P wave. rate of 150-250 bpm.
➢ P
​ R interval delayed or normal or shorter ➔ Normally, the ventricle is protected
➢ ​Result from emotional stress, use of caffeine,
against excessive heart rate arising from
nicotine or alcohol, low potassium level. supraventricular areas by making
➔ Hypermetabolic state like pregnancy mechanism at the AV node which
➔ Patient who has lung diseases prevents high rates, slowing the
proportion of the fast impulse to pass.
➢ ​Infection, hyperthyroidism, COPD, heart disease
● HR regular rhythm, rate 150 – 250 bpm
(CAD) and valvular disease
● Abnormal P wave present but may be hidden on
Premature Atrial Contraction (PAC) ST segment or T wave
● PAC are common in normal hearts.
● No treatment is necessary. BUT if they are
frequent of more than 6 per minute this may be
signs of atrial fibrillation
● Associated with overexertion, emotional stress,
RHD, digitalis toxicity, CAD, or cor pulmonale
➔ Symptoms can arise suddenly and
resolve without treatment such as stress,
exercise and emotion can precipitate
SVT.
➔ Stimulants like alcohol, caffeine or
nicotine.
● Those patients who have enlarged heart may ➔ Cor pulmonale - pulmonary heart
have premature atrial contraction although it is disease. An enlargement of the right
not necessary for any treatment but if it is ventricle of the heart as response to
frequent of more than 6 per minute then it will be increased vascular resistance or high
the sign of atrial fibrillation. pressure in the lungs.
● SVP is commonly seen in patient who have a ATRIAL FLUTTER
Wolff-Parkinson-White, a syndrome wherein it
bypass the gating mechanism, so that means it
avoid the north and its protection on passway
directly transmitted to the ventricle
● Tachycardia usually is a short duration resulting
in palpitation therefore a fast rate.
● That means Supraventricular tachycardia has a
fast rate or increase in heart rate that may cause
reduce in cardiac output resulting in significant
sign and symptoms.
● SX/ SY: Shortness of Breath, Restlessness,
Chest Pain, Pallor, Dizziness, Hypotension,
Rapid Breathing, and loss of consciousness

● Conduction defect in the atrium and causes rapid,

● HR: 150 - 250 bpm (Decreased Cardiac output regular atrial impulse at a rate between 250 - 400
with hypotension and Myocardial Ischemia). bpm.
● Abnormal P wave present but may be hidden ● More than one P-wave for every QRS complex
before T wave or ST Segment and has abnormal ● Atrial rate: 250 - 400 bpm; Ventricular rate: 75
contour and 150 bpm;
● PR interval is shortened ● PR Interval: Multiple F waves make the PR
● QRS complex normal or abnormal contour interval unidentifiable
● P wave: “​sawtooth​” appearance (F waves)
TREATMENT FOR PSVT OR PAT ● Atrial rhythm is regular. Ventricular rhythm will be
regular if the AV node conducts consistently. If
1. Vagal stimulation - Carotid massage to lower the pattern varies, the ventricular rate will be
heart rate. Instruct the patient to do valsalva irregular
maneuver to increase intrathoracic pressure that ● Not all atrial conduction conducted in the ventricle
affects para receptors. ● 250-300bpm
2. Drug therapy ● CAD, hypertension, mitral valve disorders,
a) Adenosine (Adenocard) – common pulmonary embolism, cor pulmonale,
● Given rapid IV then add 20 mL of saline hyperthyroidism
flush to promote rapid circulation. ● If atria cannot pump effectively, blood supply is
● This converts sinus to normal reduced
● Allow slow conduction of AV node to ● Signs and symptoms: Fatigue, palpitations, chest
allow visualization of P wave pain, light-headedness, syncope, SOB, low BP
● Prevents Ca reflux ● Treatment:
● Decreases SNS ○ Warfarin ​(risk of thrombus formation
● This has too short effects therefore if which then may lead to stroke)
drug not effective, Electrical ○ antiarrhythmic agents (converts atrial
Cardioversion must be done. flutter to sinus rhythm).
b) Diltiazem - Can use other beta adrenergic ○ Coumadin ​- 48 hours duration/ prevents
blockers. stroke.
c) Digitalis - Increase contractility to enhance ○ diltiazem, digoxin, β-adrenergic blockers
cardiac output. ○ Adenosine can be rendered (blocks
d) Amiodarone - Increase contractility to enhance SNS/ slows conduction therefore allows
cardiac output visualization). Give Intravenously by rapid
3. Radiofrequency Ablation therapy administration followed by 20mL saline
4. If the patient becomes hemodynamically unstable flush and elevation of the arm with the IV
– DC cardioversion (synchronized). line for rapid circulation.
○ RFA (Radiofrequency Catheter ATRIAL FIBRILLATION CLASSIFICATION
Ablation) – curative therapy; delivers
energy in the area heart muscles; Type Description
promotes normal conduction in the atria.
○ Electrical cardioversion - successful; Paroxysmal Sudden onset with termination that
used only in emergency situations. occurs spontaneously or after an
intervention lasts more than or equal to
ATRIAL FIBRILLATION 7 days, but may recur.

Persistent Continuous, lasting more than 7 days

Long -
Standing Continuous, lasting more than 12 days
Persistent

Permanent Persistent, but decision has been made

not to restore or maintain sinus rhythm

Nonvalvular Absence of mitral Stenosis, valve

replacement or repair

CLINICAL MANIFESTATIONS OF AF:

● Characterized by a total disorganization of atrial
electrical activity without effective atrial contraction 1. Palpitations
(Affects atrium/ ventricle) 2. Shortness of breath
● Causes are unknown. 3. Hypotension
● This causes electrophysiologic changes in the atrial 4. Dyspnea on exertion
myocardium (remodeling of the atrial electrical circuit) 5. Fatigue
and structural remodeling (fibrosis), which provides 6. Pulse deficit (the difference between radial and
the basis for continuance of the dysrhythmia
apical pulse)
● Results from abnormal impulse formation that occurs
7. Anginal symptoms due to myocardial ischemia
when structural or electrophysiological abnormalities
alter the atrial tissue causing a rapid, disorganized
DIAGNOSTIC FINDINGS:
and uncoordinated twitching of the atrial musculature.
● Most common sustained dysrhythmia 1. 12-lead ECG - verify atrial fibrillation rhythm and
● Shaking chaotic electrical impulses identify the presence or absence of left ventricular
● Prevalent in advance age (aged/ older people) hypertrophy, bundle branch block, prior myocardial
● Affects upper heart chambers ischemia.
● Not typically an emergency because ventricular 2. Transthoracic echocardiogram (TEE) - identify
fibrillation is much more dangerous. presence of valvular heart disease and check LV
● It does not completely empty the blood and RV size, function, and pressures
● Risk to: HF, myocardial ischemia, embolic events 3. Thyroid screening
such as stroke, cardiomyopathy; pericarditis, caffeine, 4. ​Renal clearance test
stress, alcohol use disturbances 5. ​Hepatic function test
● Blood pooling may result to thromboembolism (may 6. Chest X-rays – evaluate pulmonary vasculature
cause stroke) suspected for pulmonary hypertension
● Too fast - may cause low cardiac output 7. Exercise stress test – to exclude myocardial
● Without P wave ischemia
● PR interval not measurable 8. Holter monitoring
9. EP study – prior to catheter ablation
ATRIAL FIBRILLATION MANAGEMENT ○ Oxygen Support
○ Antidote: Digibind (Immunoglobulin fragment
● ANTICOAGULANTS ​– prevent embolization (Class that binds with digoxin)
II)
● BETA BLOCKERS – Antiarrhythmic drug, to block PREMATURE JUNCTIONAL CONTRACTION (PJC)
the effects of certain hormones on the heart to slow
down heart rate.
● CALCIUM CHANNEL BLOCKERS ​– Helps slow the
heart rate by blocking the number of electrical
impulses that pass through the AV node into the
lower heart chambers (ventricles). This increases
myocardial O2 supply and decreases afterload. This
has an acute alteration in the mental status.
Heart Rhythm P Wave PR QRS
● DIGOXIN ​– Helps slow heart rate by blocking the
Rate Interval
number of electrical impulses that pass through the (sec.) (Sec.)
AV node into the lower heart chambers (ventricles).
● ELECTROCARDIOVERSION ​– Procedure in which
Usually Irregular Premature, Short Normal<.12
electric currents are used to reset heart’s rhythm
normal abnormal, <.12
back to regular pattern. This is for patients that are may be
Hemodynamically unstable where medication is not inverted or
effective anymore. This resets the heart rhythm, hidden
converting it to a regular pattern.
● CATHETER ABLATION THERAPY – Destroys
specific cells that are the cause of a
tachydysrhythmia ● “​Premature Junctional Complex​”
● MAZE PROCEDURE – An open-heart surgical ● An impulse that starts in the AV nodal area before
procedure for refractory atrial fibrillation. Small the next normal sinus impulse reaches the AV
transmural incisions are made throughout the atria. node.
The resulting formation of scar tissue prevents ● Causes include digitalis toxicity, heart failure, and
reentry conduction of the aberrant electrical impulse. coronary artery disease.
● P wave: may be absent
JUNCTIONAL ARRHYTHMIAS ● QRS: less than 12 seconds

● Originate from the AV node FIRST DEGREE AV HEART BLOCK

● Idionodal rhythm occurs when AV node (instead of
the sinus node) becomes the pacemaker of the
heart.
● ​Abnormal P wave - inverted
● ​HR 40 – 60 bpm
● ​PR interval is ​< 0.12 sec ​(book: less than 0.12
seconds)
● P:QRS ratio: 1:1 or 0:1
● The ECG criteria for premature junctional complex
are the same as for PAC, except for the P wave
and the PR interval. The P wave may be absent
and PR interval of less than 0.12 seconds
● Associated with AMI especially inferior MI, digitalis
toxicity, open heart surgery
● Treatment: do not give atropine for digitalis toxicity, ● The duration of AV conduction is prolonged
β-adrenergic blockers, calcium channel blockers ● Occurs when all the atrial impulses are
and amiodarone conducted through the AV node into the
● DC cardioversion is NOT be used ventricles at a rate slower than normal
● Management for digitalis toxicity includes ● Every impulse is conducted to the ventricle
○ Hydration with IV Fluids ● delayed/ complete block
○ Correct electrolytes ● HR – normal and regular rhythm
● ​Pwave is normal ■ But remained fixed/ reconducted
● ​PR interval is prolonged > 0.20 second (5 small beats with intermittent dropped
sq) - Take note that PR interval is constant beat
● QRS complex has a normal contour ○ Serious type of block, occurs in the
His-Purkinje system
SECOND DEGREE AV BLOCK ○ ​Acute anterior MI, CAD, RHD
○ May progress to 3​rd​-Degree AV block
○ Presence of constant PR interval and
presence of more P waves than QRS.
○ QRS is usually abnormal, but may be
normal.
○ Treatment:
■ Permanent Pacemaker if block
persist
■ Temp: atropine, dopamine,
1. ​Type I (Wenckebach Phenomenon)
epinephrine
○ ​PR interval lengthen progressively (AV

conduction time that is prolonged until an

atrial impulse is not conducted and QRS
conduction is dropped)
○ Gradual lengthening of the PR
○ Dropped QRS
○ Occurs when there is a repeating pattern
through the AV node into the ventricles at a
rate slower than normal.
○ Treatment: atropine and temporary THIRD DEGREE AV BLOCK
pacemaker​.
○ Warning signs of impending AV conduction
disturbances
■ Transient
■ Well tolerated

● Sinus rate is 60 – 100 bpm, ventricular rate

depends on the site of the block
● PR interval is variable; no relationship between P
2. Type II second-degree AV block wave and QRS complex
○ Ventricular rhythm is irregular ● Result to ↓ CO with subsequent ischemia and heart
○ Less common but severe failure (Severe bradycardia/ asystole)
○ Occurs when only some of the atrial ● Complete heart block (no atrial impulse is
impulses are conducted through the AV conducted through the AV node into the ventricles).
node into the ventricles. ● Treatment: temporary pacemaker, for emergency
○ PR interval is prolonged (P = 2:1 or 3:1 to 1 basis; drugs (atropine, epinephrine, dopamine,
QRS) isoproterenol) - Acute Myocardial infarction
■ Constant unchanged prior to the
P wave
● However nurse should know that Atropine is not
responsive to complete AV block (lowers diastole
MAP, increases systole by HR and contraction)
● Isoproterenol produce vasodilation and cardiac
stimulation
● Having two impulses stimulate the heart results in a
condition referred to as AV dissociation which may
PVC ASSOCIATED TO VT
also occur during VT
1. PVCs are more frequent than 6 per minute
SUMMARY OF AV BLOCKS
2. Multifocal or polymorphic (having different shapes
● 1º - prolongation of PR Interval and rhythms)
● 2º - Mobitz I – Increasing PR Interval until 3. Occur two in a row (pair) - susceptible to VT
dropped beat is seen 4. Occur on the T wave - susceptible to VT
○ Mobitz II – Constant PR Interval with
more P waves to QRS II. Ventricular tachycardia (V- tach or VT)
● 3º - Complete dissociation between P waves &
QRS ● Defined as 3 or more PVC in a row with a rate of 100
– 250 bpm (book: 100 - 200 bpm)
DISORDERS OF THE VENTRICLE ● Severe decrease in Cardiac Output result of
decreased ventricular diastolic feeding time, leads to
I. Premature Ventricular Contractions / Complex atrial contraction loss, develops ventricular fibrillation.
(PVCs) ● VT is an emergency because the patient is nearly
● An impulse that starts in a ventricle and is always unresponsive or pulseless.
conducted through the ventricles before the ● P wave is absent
next sinus impulse ● PR interval is absent ( book: Very irregular if P waves
● Can occur with healthy people especially are seen)
with intake of caffeine, nicotine, or alcohol. ● QRS complex distorted and > 0.12 seconds
● P wave is rarely visible and lost in the QRS ● Pulmonary edema, shock, decreased blood flow to
complex of PVC the brain
● QRS complex is wide and distorted, > 0.12 ● Signs and symptoms (Severe)
seconds ○ altered level of consciousness
● T wave is generally a large and opposite ○ Pallor
direction to deflections of the QRS ○ Diaphoresis
(premature occurrence, wide, distorted in ○ Leads to cardiac arrest
shape). ● Signs and symptoms (Common)
● In the rhythm referred to as: ○ Palpitation,
○ Bigeminy - every other complex is a ○ chest pain,
PVC ○ syncope,
○ Trigeminy - every 3rd complex is a PVC ○ Tachypnea
○ Quadrigeminy - every 4th complex is a ○ Anxiety
PVC ○ Lightheadedness
● Mitral valve prolapse (MVP), CHF, CAD, MI, ○ Hypotension
hypokalemia, emotional stress ○ Diminished perfusion
● Treatment: hemodynamic assessment, ● Treatment:
correct electrolytes when there is ○ Determine if monomorphic (having consistent
hypokalemia, QRS shape and rate) or polymorphic (having
varying QRS shape and rate).
○ Determine the existence of a prolonged QT
interval before initiation.
○ Check if the patient is stable
○ Obtain 12 lead ECG
○ Amiodarone - Medication of choice for patient
with impaired cardiac function or acute MI.
○ Cardioversion - treatment of choice for Give patient ​MgSO4 ​( Magnesium Sulfate) - 2g over 1 to
monophasic VT in a symptomatic patient. 2 minutes over IV push for 4 to g hours or IV infusion to
○ For conscious patients - instruct patients to cough prevent recurrence. This slows SA node and prolong
for 1-3 seconds to prevent sinus rhythm. conduction time.
○ Defibrillation is action/ treatment of choice for
unconscious patients. Treatment: avoid offending odors, magnesium sulfate,
anti-arrhythmic drugs, electrical therapy (unsynchronized
defibrillation)

VENTRICULAR FIBRILLATION

● Most common dysrhythmia

● Form of cardiac arrest
● Rapid, disorganized ventricular rhythm that
causes ineffective quivering of the ventricles.
TORSADES DE POINTES ● MEDICAL EMERGENCY! GIVE CPR TO
PATIENT IF SEEN
● Polymorphic V-tach ● Rhythm is irregular and chaotic
● P wave is NOT visible
● Prolonged QT interval
● HR not measurable ( > 300 bpm)
● PR not measurable
● PR interval and QRS complex are NOT
● Wide QRS complex
measurable
● > 0.12 seconds ● Characterized by the absence of an audible
● Sy/sx: Palpitations, may lead to faintness, heartbeat, a palpable pulse and respirations
syncope (may lead to sudden death) ● Unconscious, apnea, seizures
● If not treated, patient will die

MANAGEMENT FOR VENTRICULAR FIBRILLATION

COMMON CAUSES OF TORSADES DE POINTES

● Early defibrillation
1. Diarrhea
● CPR and ACLS (as preparing defibrillator and 5
2. Hypokalemia
additional cycles of CPR, about 2 minutes of
3. Hypomagnesemia (may lead to malnourishment,
continuous chest compression
heart failure)
● Epinephrine
4. Chronic alcoholism
● One dose of vasopressin instead of epinephrine if
5. Certain drugs – cimetidine, haldol, amiodarone,
the cardiac arrest persists.
erythromycin which blocks Ca flow
● Other antiarrhythmic medications – amiodarone
6. Certain foods - grapefruit (may cause
and epinephrine (facilitates return of spontaneous
hypertension/ ischemia)
pulse after defibrillation) , lidocaine, magnesium
Magnesium helps in the movement of calcium, potassium as soon as possible after the 3​rd​ defibrillation.
and sodium in and out of the cell.
ASYSTOLE

● Total absence of ventricular electrical activity.

● End-stage CHF, advanced cardiac disease
● Commonly called “Flatline”

Treatment:

● CPR, ACLS measures which include intubation,

epinephrine and atropine
CORONARY VASCULAR DISORDERS
arterial walls that may decrease the dispensability
and elasticity of the vessel. More force is required
to pump blood through deceased arterial
Coronary Artery Disease
vasculature as it reflected in a higher BP. It
increases cardiac workload that causes left
ventricular hypertrophy and decreased stroke
volume with each contraction.

DM - Causes increased connective tissue

degeneration that may account for the
development of atheroma. Have alteration in lipid
metabolism, tends to have a higher cholesterol
and triglycerides level.

Hyperlipidemia - >200 mg/dl of cholesterol and

triglycerides is correlated to obesity, physical
inactivity, high caloric intake and intake of trans
fatty acids that can be found in junk foods such
as cookies, crackers, french fries, avoid these
Narrowing or obstruction of the coronary arteries,
foods to lower risk of development of CAD.
resulting in a reduction of blood supply to the
myocardium, then there will be ischemia, injury and
Lipoprotein - low density lipoproteins have an
infarction affinity for arterial walls. Whereas very low
density lipoprotein contains most of the
Atherosclerosis​-a disorder of the lipid metabolism
triglycerides that have correlation with heart
characterized by
disease. That's why it is necessary to maintain
HDL and to lower down the LDL or VLDL
a) development of fat-containing substances along
Example: fish oil at least twice a week that is rich
the intima of the blood vessels
in alpha linoleic acid (flaxid, canola, soy beans)
b) Smooth muscle cell proliferation
as these helps to lower down LDL and increase
HDL.

Elevations of homocysteine level -damages the

inner lining of the blood vessels. Promotes
plaque buildup which may alter the clotting
mechanism to make clot more likely to occur.
Supplementing vitamin B complex, B6, B12, folic
Atherosclerosis affects the intima of the large and acid lowers the blood level of homocysteine.
medium sized arteries.
Psychosocial factor - combined with high lipid
The intima lining of blood vessels accumulates the fatty level and smoking. Usually type A personality
deposits in the coronary arteries. Can be partial or which is very aggressive and competitive. They
completely blocked. are predisposed to develop CAD even sleep
apnea is one factor.
Risk Factors
Metabolic syndrome - have a greater risk factor
Modifiable
for cardiovascular diseases especially CAD
because it may increase in blood pressure that
1. Pathologic – hypertension, DM, hyperlipidemia,
high in triglycerides, increase insulin level, extend
elevated homocysteine, psychosocial factors,
body fats that may result in CAD. Diagnosis to
metabolic syndrome and premature menopause
this includes the following conditions like insulin
resistance which may damage the endothelium
Hypertension - related to the shearing stress
that causes thickening of the vessel wall and
causing denoting that causes injury to the
potential inflammation.
endothelial lining. Causes narrowed, thickened
Central obesity - waist circumference of >35 Genetics - has a major role in the development of
inches in female or >40 inches in male are at CAD.
great risk of developing CAD. Blood pressure
persistent of greater than 130/85 mmHg or even Race - CAD is common in patients who are African
the is a symptoms of lipidemia. Americans.

2. Lifestyle – Smoking, obesity, elevated LDL, Theories of Atherogenesis

physical inactivity, Diet, Use of oral
contraceptives, Hormone replacement in women. 1. Endothelial injury – hyperlipidemia,
hypertension and chemical irritants
Smoking – increases 200% risk to develop CAD 2. Lipid infiltration – altered endothelial
because the tobacco contains nicotine that permeability
causes the release of catecholamines 3. Aging
(epinephrine and norepinephrine) that increases 4. Thrombogenic – RBC, platelets and lipids
heart rate, stroke volume, cardiac output and accumulation along the intima of the arteries
blood pressure. Carbon Monoxide directly 5. Vascular dynamics – increase intraluminal
damages the inner lining of the blood. pressure leads to altered membrane permeability
6. Inflammation
Peripheral vasoconstriction - increases systemic
changes that occur or may decrease the blood Endothelial injury - A normal intact endothelium, is
flow. It decreases the threshold of ventricular usually non-reactive to platelets, leukocytes, coagulation
defibrillation by interfering the oxygen combining even fibrinolytic. However, if the endothelial lining was
with hemoglobin therefore impairing O2 diffusion altered it may result in the chemical injury from
into the mitochondria. hyperlipidemia, hypertension may suggest certain
bacterial and various infections that play a major role in
Obesity - increased food intake is associated with the damage of the endothelium to the development of
elevation of LDL. Obese people have a high atherosclerosis.
tendency towards
With endothelial alteration the platelets are activated and
hypertension and glucose intolerance. It should they release growth factors that may stimulate smooth
not be greater than 20% of the ideal body weight. muscle proliferation so this may entrap the lipid which
may calcify over time and form an irritant to the
Physical inactivity - lack of exercise is directly endothelium on which platelets adhere or aggregate.
associated to the decrease of HDL. In diet, the
high intake of carbohydrates and fat leads to high Lipid infiltration - lipids from the circulations enter the
serum plasma cholesterol. endothelium and accumulate in smooth muscle in
response to the mechanical or inflammatory trauma.
Usage of oral contraceptive methods or Chromoprotein is trapped and damage occurs then
post-menopausal women – use of hormone endothelial permeability is altered.
replacement or birth control may affect the
cholesterol which is lowering the good cholesterol Aging - atherosclerotic changes occur to everyone and
and increasing the risk of blood clot. become more evident as one aged

Nonmodifiable Thrombogenic - Microthrombi form in intima lining of the

endothelium. It releases substances that may alter the
1. Age - middle-aged men endothelial permeability then thrombus extend and
2. Gender – attribute to sex hormones reactivate the cycle.
3. Family history
4. Race Vascular dynamics - mechanical factors like
hypertension, because of constant elevations in the blood
Aging - CAD in men are more prevalent than women pressure, it increases the rate of atheroma formation that
in the age of 60. Women’s advantage declines after alters membrane permeability which may increase lipid
menopause because of social and economic infiltration.
pressure and changes in lifestyle.
Inflammation – has a major role in the pathogenesis of enlargement of the plaque. The collagens are
atherosclerosis. Inflammatory reactions may be a also trapped forming fibrous plaque that appears
consequence of an infectious stimuli. grayish or whitish which may also narrow the
vessel lumen.
Developmental Stages in Atherosclerosis
❏ Complicated Lesion Phase Is the 3rd stage and
1. Fatty streaks the final stage in the development of
➔ Earliest lesions atherosclerosis with the incorporations of lipid,
➔ Characterized by lipid-filled smooth thrombus/thrombi, damaged tissue and
muscle cells accumulation of calcium. The growing lesions
become complex, as it grows the necrotic tissue
2. Raised fibrous plaque that is hardened in the arteries causing rigidity
➔ Beginning of progressive changes in the and hardening that may partially occlude the
arterial wall arteries, then thrombus formation may develop.
➔ Lipoproteins transport cholesterol and
other lipids into the arterial intima Complicated Lesion Phase
➔ Fatty streak is ​covered by collagen
forming a fibrous plaque that appears ❖ Continued inflammation can result in plaque
grayish or whitish instability, ulceration, and rupture
➔ Result = ​narrowing of vessel lumen ❖ Platelets accumulate and thrombus form
❖ ​Increased narrowing or total occlusion of lumen
➢ Raised fibrous plaque usually occurs at the age
of 30 or increases with age. Arterial wall changes Collateral Circulation
are initiated by chronic endothelial wall injury that
result from many factors; elevated BP, increase ● Arterial branching exists within the coronary
in cholesterol, hereditary, carbon monoxide circulation. Attributed to inherited predisposition
produced by smoking, or immune reaction with and presence of chronic ischemia.
toxic substances within the blood vessels.
● When an atherosclerotic plaque occludes the
➢ Normally, the endothelium repairs itself normal flow of blood through the coronary artery,
immediately but not in patients with CAD because the ischemia is chronic then increased collateral
it allows the LDL and growth factor from platelets circulations develop. Then occlusions of the
to stimulate smooth muscle proliferation and it coronary arteries occur slowly over a long period,
thickens the arterial wall. Once this endothelial is there’s a greater chance of adequate collateral
injured, the lipoprotein transport cholesterol and circulations developing and the myocardium may
other lipids into arterial intima. still receive an adequate amount of oxygen.

➢ In the 2nd stage, the lipid directly damages the ● However, rapid onset CAD or coronary spasm is
smooth muscle and contributes to plaque inadequate for collateral development and a
thickening and stability. As the lipids pass decrease in arterial flow results in more severe
through the vessel, they may adhere causing the ischemia or infarction. That’s why younger people
lesions build up or structure abnormalities. Even will have more severe M.I. because of inadequate
platelets also may acquire in the hypertrophy of collateral formation.
the smooth muscle cells. The large number of
platelets accumulate in the internal wall of the Pathophysiology of CAD
artery it may lead to thrombosis causing the
narrowing of the artery. Predisposing factors

Progression of Atherosclerosis ➔ arterial narrowing and ​occlusions of the arterial

wall​.
❏ Fatty Streak yellow thick appears in the intima ➔ Narrowing of the arteries/arterial blood
lining of the arterial wall so there are lipid lumen/arterial wall.
accumulations wherein the platelet also attaches ➔ There will be ​vascular changes which may affect
to the endothelium and the migrations of smooth the functional ability of the coronary arteries to
muscles into the intima. Then fibrous plaque, dilate, this leads to the decreased blood flow to
wherein the development of atheroma, there’s an the myocardium which may cause ​angina
insufficiency to the patient and will result in May increase luminal size of at least 20%
myocardial​ ischemia​.
➔ M. ischemia the patient may have angina
pectoris, acute coronary syndromes/ acute
myocardial infarction and sudden cardiac death.

Three Major Clinical Manifestations of CAD

1. Angina pectoris
2. Acute coronary syndrome (ACS)
3. Sudden cardiac death
4. Rapid pulse
5. Shortness of breath
6. Palpitations
7. Weakness

Diagnostic study Advantages of PTCA

●​ ​ECG 1. Provides an alternative to surgical procedure

●​ ​exercise stress test 2. Ambulatory 24 hours after the procedure
●​ ​2d-echo
3. Shortened the length of hospitalization
●​ ​coronary angiography 4. Rapid resumption of work in one week after the
●​ ​MRA procedure

Management of CAD Catheter is equipped with an inflatable balloon tip

which is inserted to the coronary arteries which pass
1. Reduce risk factors to the lesions and the atherosclerotic plaque is
❏ Stop smoking, regular exercise, diet, reduce compressed resulting in vessel dilations.
weight, control HPN, DM, and cholesterol
❏ Diet; reduce sodium/ low sodium intake, avoid ● ​Intracoronary stent placement – a stent used to
alcohol, avoid trans fatty acids maintain vessel patency by compressing the
❏ Restore blood supply (PCI) arterial walls and resisting vasoconstriction.
❏ ​Revascularization is the restoration of perfusion ●​ ​Usually in conjunction with Angioplasty
to a body part or organ that has suffered ●​ ​An expandable mesh like structure.
ischemia through Percutaneous Coronary ● ​Used to treat an abrupt closure and restenosis
Intervention (PCI) formally known as Angioplasty following PCI
and Stenting which may improve blood flow and Stent is thrombogenic – antiplatelet agents (aspirin,
restore blood supply clopidogrel (Plavix), ticlopidine (Ticlid)) is prescribed.

Complications: hemorrhage, vascular

injury and arrhythmias

✔ ​Percutaneous Transluminal Coronary

Angioplasty (PTCA) – restores luminal patency
by compressing atheromatous plaques within the
coronary arteries.
✔ ​Atherectomy – the plaque is shaved OFF ✔​ ​↓ strength of the heart muscle contraction
using a type of rotational blade. It decreases the
incidence of abrupt closure as compared with ✔​ ​Relax blood vessel
percutaneous coronary intervention (PCI).
4. Antiplatelet – aspirin (prevent platelet aggregation
☝ Limited to proximal and middle portion of a that impedes the blood flow), heparin (Prevent
vessel greater than 3 mm in diameter formations of blood clot)
➔ ​↓ contractility, cause arterial
☝​ L
​ ess than 15 mm long construction, ↓BP, peripheral vascular
resistance.
☝​ ​NOT heavily calcified
Surgical Management
☝ ​re..ing blocked vasculature via a needle
puncture in the skin. a) Myocardial revascularization or CABG – graft
from saphenous vein, internal mammary artery,
☝ ​Improves blood flow to the ischemic limb or radial artery, gastroepiploic artery.
peripheral arterial blood vessels
Construction of conduit between the aorta and
arteries to improve quality of life, good survival
and cardiac related mortality.

Palliative procedure only and is not a cure for

CAD

Indications:

➢ If the left main coronary artery stenosis is greater

than 50% may undergo CABG
➢ Stenosis of proximal left anterior descending and
proximal circumflex >70%
Pharmacologic therapy ➢ Three vessel disease which is asymptomatic with
mild or stable angina for patients with proximal
1. Vasodilator – Nitroglycerin (NTG) left anterior descending stenosis with poor left
➔ Reduce myocardial oxygen consumption ventricular functions
➔ Decrease ischemia and relieves pain ➢ ​Patients who have ongoing ischemia of non-ST
➔ ​Dilates vessels and ↑ perfusion segment elevation, MI that is unresponsive to
➔ Helps ↑ coronary blood flow, prevent medical therapy.
vasospasm
Contraindications:
2. β-adrenergic blocker – atenolol ➔ Asymptomatic patients who are at low risk of
➔ ​↓ myocardial oxygen consumption by MI or death
blocking the β-adrenergic sympathetic ➔ Advanced age is not a contraindication but is
stimulation of the heart less commonly done in the elderly because they
➔ ↓ HR, BP and myocardial contractility have a shorter life expectancy and CABG may
not be necessary to prolong survival. They may
➔ ​↓cardiac workload, excitability, ↓renin
likely to experience perioperative complications
release
after CABG
➔ Check BP and HR before administration
➔ B’s of β-adrenergic blocker​;
Preoperative tests:
B​radycardia, ↓​B​P, ​B​ronchial constriction, ❏ ​Full blood count; CBC
↓ ​B​lood glucose
❏ Screening for clotting, creatinine and electrolytes
to correct any abnormalities
3. Calcium channel blocker – nifedipine, diltiazem,
❏ Liver function test
verapamil
❏ Chest X-ray, ECG, 2D echo, coronary
✔​ ​↓ SA node automaticity and AV node angiography
➔ Stop all activity
➔ Bed rest
Nursing care: ➔ Observe signs of respiratory depression
➔ ​NTG
● Care for the 2 surgical sites; chest, arm, nape or ➔ Monitor vital signs
acromion 2. Reducing activity
● They use the radial artery so observe for the side 3. Health education on reducing risk factors
thumb and finger for the perfusion and oximetry 4. Teach stress reduction techniques
of the distal finger
● Monitor for hypertension because it may cause Relationship Between CAD, Chronic Stable Angina,
collapse of vein graft, if there’s increase in blood and ACS
pressure, it increases pressure that promotes
leakage from the suture line and may cause
bleeding
● May give Calcium channel blockers to decrease
the incidence of the arterial spasm of heart and
anastomosis sites especially the radial artery
● ​Prevent pulmonary complications
● Restrict fluids because clients usually have
edema

b) Transmyocardial laser revascularization

(TMR)
➢ Uses a laser to create a channel between the left
ventricular cavity and the coronary Angina Pectoris (chest pain)
microcirculation. The channel allows blood to flow
● A clinical syndrome characterized by episodes of
into the ischemic area.
➢ This can be done during cardiac catheterization pain or pressure in the anterior chest due to
and using elect anterior thoracotomy incision. insufficient coronary blood flow.
● The patients may experience A.P. due to
Complications: imbalance myocardial O2 supply and demand.
Usually occurs in coronary atherosclerosis.
● ​Ventricular arrhythmia
● Causes of Angina can also be: vessel factors;
● Post operative bleeding
atherosclerosis, arterial spasm from smoking or
● Cardiac tamponing emotional stress, circulatory factors; hypotension,
● Low cardiac output aortic stenosis because of ↓ in filling, ↓ venous
return, blood factors; anemia, hypoxemia,
CABG Surgery polycythemia.
● The mentioned factors contribute to the ↓ O2
supply.

PQRST Assessment of Angina

1. P​recipitating factors (activity, exercise, resting)

2. Q​uality (dull, aching, sharp, tight)
3. R​adiation of pain (back, arms, jaw, shoulder)
4. S​everity - using 0 – 10 pain scale
5. T​iming – 5 seconds to 30 minutes

Nursing Management

1. Treat pain
8. Circadian rhythm patterns
➔ related to the occurrence of stable angina
Location of Chest Pain (Angina) or prinzmetal angina or sometimes it may
MI or sudden death.
➔ Include the quality of Angina Pectoris
➔ how does it feel? (Quality) There’s a
sensation of pressures and heavy weight
on the chest.
➔ Burning sensation, feeling of tightness or
squeezing, choking or suffocating
sensation (Sensation)
➔ Patients who have Angina located in the
left shoulder, jaw, left interscapular/
suprascapular area, median aspect of the
left arm (Location)
➔ Duration is about 5 s -30 mins.
➔ The manifestation of CAD tends to occur
in the early morning after awakening
Precipitating Factors of Angina ➔ ​Severity of pain using pain scale

1. Physical exertion
➔ ​↑ HR that ↓ hearts time to diastole

2. Extreme temperature
➔ ​Cold ↑ workload of the heart, Blood
vessels constrict in response to a cold
stimulus; B.V. dilate and blood cools in
the skin in response to a hot stimulant

3. Strong emotion
➔ Stimulate the sympathetic nervous sys.
That may increase the workload of the
heart.

4. Consumption of heavy meal

➔ ↑ workload of the heart during the
digestive process, the blood is delivered Types of Angina
to the G.I. sys. Causing a ↓flow rate in
the coronary artery. 1. Stable angina
2. Unstable angina
5. Cigarette smoking 3. Intractable : severe incapacitating chest pain
➔ ​Nicotine stimulate catecholamine release 4. Variant angina – due to coronary vasospasm
it may cause vasoconstriction and ↑ HR, 5. Silent ischemia : objective evidence of ischemia
it may also ↓ 02 available by ↑ CO2 but patient reports no symptoms
6. Nocturnal : associated with rapid eye movement
6. Sexual activity sleep during dreaming
➔ ↑ cardiac workload and ↑ sympathetic 7. Angina decubitus - characterized by the onset of
stimulation, that’s why Nitroglycerin is chest pain when the patient is resting or lying
prescribed before engaging in this down.
activity.
Stable Angina
7. Stimulants
➔ cocaine, amphetamines ↑ HR and ❏ Described as a crushing, tightness or squeezing
subsequently myocardial O2 demand. sensation in the chest
❏ Down sloping ST segment indicate CAD
❏ Stress test or treadmill exercise test
❏ Characterized by effort induced chest discomfort ❏ Myocardial O2 demand and supply coronary
with or without radiation that lasts from 5 s – 15 artery spasm, and it is also stress related
mins. catecholamine release and platelet aggregation.
❏ Usually arises when the lumen stenosis is greater ❏ Unstable angina is the 1st clinical manifestation
than 70% which may incur blood supply to the of CAD
heart only during exertion or increase metabolic ❏ This unstable lesion ↑ the risk of complete
demands. thrombosis of the lumen with progressions to MI.
❏ Generally relieved by rest, removal of provoking That’s why patients with unstable angina require
factors, or taking of sublingual vasodilators immediate hospitalization for ECG monitoring and
❏ ​It is predictable; so, medications may be given to bed rest.
provide relief. So strenuous activities, cold
weather, heightened emotional stress may trigger VARIANT OR PRINZMETAL’S ANGINA
angina which can be relieved by NTG or rest
● NOT directly related to atherosclerosis but
Important Treatment /Elements of Stable Angina caused by coronary ​vasospasm
● NOT precipitated by exertion or stress
✔​ ​A – aspirin, antianginal therapy ● Occurs at the same time everyday
● Treatment – Nitrates, Calcium channel blocker
✔​ ​B – β-adrenergic blocker, blood pressure
❏ This is characterized by chest pain that occurs at
✔​ ​C – cigarette smoking, cholesterol rest in the early hours of the morning. It is often
associated with ST elevations in the ECG. And
✔​ ​D – Diet, diabetes the underlying cause is thought to be coronary
artery spasm due to the sudden reduction in
✔​ ​E – education, exercise
coronary blood flow brought on bi… spasm and
not on ↑ myocardial O2 demand.
Nursing Management (Stable Angina)
❏ It has been suggested that the spasm is caused
by a stroke (?) contraction of the smooth muscles
Acute Interventions for ​anginal attack
in coronary arteries, caused by ↑ intracellular
➢ Administration of supplemental oxygen calcium
❏ The ↓ in the myocardial consumptions that occur
➢ 12-lead ECG
➢ Prompt pain relief first with a nitrate followed by during sleep or rest may lead to coronary artery
an opioid analgesic if needed vasoconstriction that are responsible for the
➢ ​Auscultation of heart sounds spasm. Frequent between midnight and 8 am and
➢ Comfortable positioning of the patient to increase may disappear spontaneously or some point of
exercise, may have dysrhythmia and conduction
cardiac workload
abnormalities
Unstable Angina
Comparison of Types of Angina
➔ Pain last longer and more frequent and NOT
relieved by rest,
➔ Unpredictable
➔ Treatment: aspirin, heparin and antiplatelet
agents
❏ Also known as pre infarction or acute coronary
insufficiency
❏ Associated with deterioration of once stable
atherosclerotic plaque. Once the stable plaque
ruptured, exposing the intima to blood, and
stimulating the platelet aggregation and local
vasoconstriction with thrombus formation.
❏ It may be precipitated by factors other than effort
or activities. This is more severe than stable
angina. Frequency preceding with myocardial
infarction because of the imbalance between
Clinical Manifestation of Angina 10. Notify MD if Chest pain persists not relieved by
rest/Nitroglycerin
1. Chest discomfort and may experienced
epigastrium (upper central abdomen), back, neck
area, jaw, or shoulder ACUTE CORONARY SYNDROME
➔ When taking care of the elderly be sure
•A group of symptoms arise when vessel or coronary
to take the history properly because in
arteries becomes occluded or obstructed by thrombus
elderly with angina, it may not exhibit the
typical pain total, because of the ➔ When oxygen supply is decreased for a long
diminished responses of period of time which not immediately reverse,
neurotransmitters that occur with aging. then it can cause acute coronary symptoms
Most of the time the presenting symptom ➔ Usually precipitated by ​blood​ ruptured and blood
in the elderly is dyspnea. formation.
➔ Sometimes there are no symptoms ➔ Also associated with coronary thrombosis
making diagnosing and recognition as a
clinical challenge •Primary symptom is ​chest pain
2. Shortness of breath
➔ In which radiating from left arm or angle of the
3. Cold sweat
jaw which is very common and caused by
4. Weakness
atherosclerosis
5. Diaphoresis
➔ Cardiac chest pain can be precipitated by
6. Dizziness
anemia, bradycardia or tachycardia.
7. Nausea and vomiting
•​Etiology​: Atherosclerosis
Diagnostic Studies
NOTE: The acute ischemia is usually related to this
1. ECG or Holter monitoring syndrome raging from unstable angina to myocardial
2. Treadmill exercise test infarction with or w/o ST elevation
3. Nuclear imaging – myocardial perfusion
4. Positron Emission tomography Subtypes of ACS
5. 2-D echocardiography
Acute Coronary Syndrome - ​serve as an umbrella to the
6. Coronary angiography
7. Electron beam CT – assess CAD in all stages unstable angina, NSTEMI or STEMI.

● Unstable angina​ – when atherosclerotic plaque

May also include ​blood test​, ​lipid profile​ & ​cardiac enzyme
shoot of embolus downstream to cause
Goals for Management of Angina microinfarct
➔ Reduced blood flow in the coronary
1. Alleviate manifestations artery dues to ruptured of an
2. Prevent the progression of coronary heart atherosclerotic plaque
disease and myocardial infarction ➔ A plaque begin to form at top of coronary
3. Relieve acute attacks but artery not completely occluded
➔ This acute situation can result into chest
Nursing Management for Angina pain that may referred as preinfarction
angina because the patient is likely to
1. Oxygen as ordered have a myocardial infarction and
2. Pain relief – nitrates, narcotics, ​nitroglycerin interventions do not occur
(sublingual)
3. VS & assess cardiac function ● NSTEMI​ – when necrosis confined to endocardial
4. ECG layers (most susceptible to ischemia)
5. Semi-High fowler – to decrease myocardial ➔ Non-ST Segment Elevation Myocardial
demands Infarction
6. Emotional support – to reduce anxiety (eg. music ➔ If ECG does not show typical changes,
therapy) this called Non ST Segment Elevation
7. Minimize precipitating events ACS
8. Gradual increase in exercise ➔ However, patient may still suffered from
9. Allow for rest periods Non St elevation myocardial infarction
➔ Occlusion is about 25% or partial block in
Normal cardiac Elevated cardiac
the coronary artery but still there is blood
enzymes ST depression enzymes
perfusion to the block artery +/-
➔ The presence of collateral circulation is More severe
very important so no ST or P-wave T wave symptoms
alteration on the ECG when necrosis inversion on
confined​ to ​endocardial layer therefore,
more susceptible to ischemia ECG
➔ Can be a positive or negative cardiac
enzyme depending on the size that is Elevated cardiac
affected. enzymes
➔ TREATMENT: Conventional lifestyle
modification.
➔ MEDICATION: Aspirin, Clopidogrel or Signs and Symptoms of ACS
Heparin. Revascularization like
Percutaneous Transduminal Coronary 1. Palpitations - refers to patient with dysrhythmia
Angioplasty. 2. Pain – pressure, squeezing, or a burning
sensation across the precordium and may radiate
● STEMI ​– when full thickness necrosis of the to the neck, shoulder, jaw, back, upper abdomen,
ventricular wall occurs or either arm
➔ There is a sudden occlusion in the ➔ Cardinal signs of decreased blood flow to
coronary artery that caused ischemia the heart and pain radiates to the left
➔ There is a presence of clot arm. A pressure like in character or
➔ If the ECG confirm changes suggest associated with nausea and vomiting due
Myocardial Infarction to vagal stimulation. Sweating because of
➔ 30% of Transmural Infarction of the sympathetic discharge
Myocardium undergoes necrosis that 3. Exertional dyspnea that resolves with pain or rest
may results to ST Elevation in which also 4. Diaphoresis from sympathetic discharge
release cardiac enzyme 5. Nausea from vagal stimulation
➔ There is (+) cardiac enzyme and ST 6. Decreased exercise tolerance
changes in the ECG 7. Jugular venous distention
➔ P wave inversion and pathologic P Wave ➔ Also evidence also in patient who have
➔ This is emergency situation that needs acute coronary syndrome
Revascularization of the occluded artery 8. Cool, clammy skin
so it must done immediately ➔ Because of sympathetic system
➔ TREATMENT: Thrombolytic or stimulation
Angioplasty ➢ Patients might also experience the feeling of
acute ill.
NOTE: NSTEMI and STEMI are named according to the ➢ The presence of S3 and S4 in Heart sound.
appearance in the ECG classified as acute coronary ➢ Presence of rales in Pulmonary examination -
artery. suggestive of left ventricular dysfunction or mitral
devitations.
➢ HYPOTENSION - decreased in blood pressure
UNSTABLE NSTEMI STEMI indicates ventricular dysfunction due to
ANGINA myocardial ischemia or infarction.
➢ HYPERTENSION - it may precipitate angina or
elevated in catecholamine level due to anxiety or
exogenous​ sympathomimetic stimulation
Non occlusive Non-occlusive Complete
thrombus thrombus thrombus DIAGNOSTIC STUDIES
sufficient to occlusion
Non specific cause tissue 1. ECG
ECG damage & mild ST elevations ➔ Indicates acute heart damage
myocardial on ECG or new ➔ Elevation in the ST Segment or​ New Left
necrosis LBBB Bundle branch block
2. Chest X-ray
3. Troponin I and T
➔ Cardiac markers
➔ Pulmonary embolism is suspected - need
to place the patient in telemetry unit to
monitor the heartbeat
4. Brain natriuretic peptide (BNP) – provide
information to develop MI
5. C-reactive protein (CRP) – systemic inflammation
6. Interleukin-6 – major determinant of acute-phase
risk of unstable angina

MANAGEMENT OF ACS
THREE ZONES OF TISSUE DAMAGE
1. Monitor and treat arrhythmia
2. Correct electrolyte imbalances – potassium, 1. Ischemia – T wave inversion
magnesium ➔ There is a greater chance of viability of
3. Provide oxygen therapy – to correct hypoxemia the myocardial cells, unless the Ischemia
4. Pharmacologic therapy – aspirin, clopidogrel persists or worsens.
➔ It will take about 20 minutes
2. Injury – ST elevation
MYOCARDIAL INFARCTION (MI)
➔ Surrounding of necrotic tissue that
causes injury on the myocardial cells that
● Complete or nearly complete occlusion of a
potentially viable if adequate circulation is
coronary artery usually precipitated by rupture of
quickly restored
a vulnerable atherosclerotic plaque and
➔ ECG tracing - ST elevation, shows injury
subsequent thrombus formation with cause
in bipolar leads
abrupt cessation of blood and oxygen to the heart
3. Infarction – deep Q waves
➔ Myocardial - pertains to myocardium
➔ Sometimes called Central Area
➔ Infarction - there is a decrease in
➔ Consists of necrotic myocardial cells,
coronary p[erfusion that affect according
capillaries and connective tissue
to myocardial layer
➔ Causes the presence of the Q wave due
to the inability of this necrotic muscle to
Basic Types of MI Based on Pathology
conduct an impulse
1. Transmural – all layers is affected; complete
occlusion
➔ Extends from endocardium to
pericardium with results complete
occlusion of the areas blood supply
2. Subendocardial – small areas; susceptible to
ischemia
➔ Generally it confined a small part of
myocardium or the sub endocardial wall
of the left ventricle, ventricular septum or
papillary muscles
➔ Majority of this involve the left ventricle

NOTE: In the clinical picture of MI, if there is P wave

infarction that means it is a conversion of oxygen to the
cells therefore it becomes necrosis within 5-6 hours after
occlusion.
If there is a presence of deep P wave in the ECG training
that means it is permanent and also indicates sustained
coronary occlusion and extensive necrosis.
SITE OF INFARCTION

1. Anterior wall of the left ventricle near the apex –

common
➔ It results from thrombosis of the
descending arch branch of the left
coronary artery.
2. Posterior wall of the left ventricle near the base
➔ results from the occlusion of the right
coronary artery or circumflex branch of
the left coronary artery
3. Inferior surface of the heart
➔ Results from the right coronary artery The affected Myocardial cells do not regenerate after an
occlusion infarction so healing requires the formation of the scar
4. Lateral – left circumflex artery tissue that replaces the nuclotic myocardial muscles.

NOTE: The severity of MI depending on 3 factors: The morphology changes will be ranging from there is no
apparent cellular change within the first 6 hours total
1. The level of occlusion in the coronary arteries replacement by scar tissue.
2. The lent of time of occlusion
3. Absence collateral circulation When there is scar tissue it may inhibit the contractility
and cause slow conduction of electrical impulse that may
ETIOLOGY OF MYOCARDIAL INFARCTION trigger reentry mechanism that results in ventricular
defibrillation.
1. Coronary artery spasm can cause acute
occlusion
As the contractility falls, the failure of the myocardial to
2. Decrease oxygen supply from acute blood loss,
contract may cause heart failure so the body starts to use
anemia or low blood pressure the compensatory mechanism in attempt to maintain
3. Unstable angina
cardiac output.
4. Plaque rupture
CLINICAL MANIFESTATIONS OF MI
NOTE: The main problem is that there is insufficient blood
1. Chest pain – sudden and continuous (primary)
supply in the Myocardium so there is a decreased supply
➔ Substernal pain despite of medication
of oxygen and nutrients to the Myocardium.
and rest
If there is a deprivation of the Oxygen to the Myocardial
➔ Ask for the quality of chest pain, if it is
cells then Ischemia may develop because of prolonged
severe, squeezy, heavy, pressure
lack of oxygen it may result in Infarction of the death of
sensations or chest tiredness
myocardial cells.
➔ Usually, it is intense and not relievable for
The enzymes it may (​di ko maintindihan sorry​) the
about 30-60 minutes and there is
different intramyocardial cellular enzymes such as the
radiation from the substernal to the neck,
CGK or CK-MB, Myoglobin or Troponin that resulted in
shoulder, jaw and down the left arm.
patient develop or complaining of chest pain.
➔ Blood pressure is initially elevated bc of
chest pain, peripheral vasoconstriction
that results from adrenergic response to
pain ventricular dysfunction
2. Unexplained anxiety
3. Restless
4. Stomach, back and abdominal pain (epigastric
pain or indigestion)
5. SOB and dyspnea
6. Weakness
7. Diaphoresis or sweating
8. Syncope – without cause
9. Cognitive impairment – without cause
10. Sinus Bradycardia
11. Nausea and vomiting
assessment of the effect of perfusion
therapy.
❏ In this MRI, heart technology that
differentiate the reversible and
irreversible tissue injury.

4. Positron Emission Tomography (PET) scan​ –

cardiac metabolism and assess tissue perfusion
so it will evaluate the presence of coronary artery
disease, coronary flow reserve and even detect
MI.
*Some patients may experience Fever if it is greater than
1 degree celsius as early as 4-8 hours after the onset of 5. 2-D echo
the MI. ❏ Identify the different areas of abnormal
regional ​(di ko maintindihan hehe)
DIAGNOSTIC STUDIES IN MI ❏ Detecting complications associated with
MI
1. Laboratory test
6. ECG
❏ CK-MB​ ​- ↑ 4 – 6 hours after onset of ❏ ​ST elevation for AMI
chest pain (the peak is about 12 - 18 ❏ ST depression for ischemia
hours and normalize in 3-4 days)
❏ Troponin T and I​ ​(​Troponin T​ is about 1. Once the patient recovered from MI, the first to
84% sensitivity for MI, 8 hours after onset
return to the normal is the ​ST Segment; ​it takes
and this is very sensitive to detect 1 -6 weeks.
myocardial ischemia. Whereas, the 2. P​ waves ​become large and symmetric for the 24
Troponin I ​is about 90% sensitivity to
hours and invert within 1 to 3 days.
protect high risk and unstable angina). 3. P wave​ alteration that would be permanent.
❏ Myoglobin​ – indicate myocardial
damage (Elevated means myocardial P-Waves occur or notice changes in the ECG, usually
damage in the absence of skeletal following 36-48 hours then there would be changes in the
muscle but sensitivity may not be reliable P-waves if there is no PROMPT treatment to the patient.
after 10-12 hours because of the rapid
renal clearance). P Waves may persist as evidenced by an old infarction
❏ LDH​ (Increased in 12 hours after onset of and can be used to localize the effects throughout the
chest pain, peak is about 24-38 hours person's life.
and remains increased about 10 days
especially the isoenzyme L1 and L2 MANAGEMENT
which indicates myocardial damage.
❏ CBC​ – leukocytosis (bc of muscular 1. Hemodynamic monitoring
injury and subsequent ischemia and 2. Oxygen therapy
ESR (erythrocyte sedimentation rate is ➔ Need to measure the partial arterial
also elevated bc ​reflects​ the tissue oxygen if it is hypoxemia need to
necrosis. receives about 2-4 L per minute as per
❏ C-reactive protein (CRP)​ - for acute doctor's order
inflammation 3. Bed rest
➔ To decreased myocardial oxygen
2. Radionuclide imaging consumption
❏ Provides information in the presence of 4. Diet – liquid diet 1​st​ 4 to 12 hours (to decreased
coronary artery disease gastric distension); saturated fat restriction and
❏ Location of ischemic infarcted tissue low sodium
5. Pharmacologic therapy
3. MRI 6. Percutaneous coronary intervention (PCI)
❏ Help to provide or identify and extend the -Intra-aortic balloon pump, angioplasty, stent
MI and serves as the basis for the placement, etc.
➔ Intra-aortic Balloon Pump
➔ Angioplasty
O OXYGEN
➔ STEM Placement
To provide and improve oxygenation of
7. Cardiac rehabilitation
ischemic myocardial tissue ; enforced
➔ If the patient is already recovered from
together with bedrest to help reduce
Acute MI
myocardial oxygen consumption. Given via
➔ Long term program of medical evaluation,
the nasal cannula at 2 to 4 L/min.
indications to patients and even
counselling in order to limit the physical N NITROGLYCERIN
and psychological effect of cardiac illness First-line of treatment for angina pectoris and
and improve the pt’s quality of life. acute MI ; causes vasodilation and increases
➔ It has different phases blood flow to the myocardium.
➔ Theme: Improve functional mobility, and
decreased the risk factor through A ASPIRIN
medications that is related to cardiac First-line of treatment for angina pectoris and
inquiry acute MI ; causes vasodilation and increases
➔ Includes family that teaches how to blood flow to the myocardium.
manage the psychological effects that
may influence recovery after MI. T THROMBOLYTICS
To dissolve the thrombus in a coronary
INTRA-AORTIC BALLOON PUMP artery, allowing blood to flow through again,
minimizing the size of the infarction and
➔ Mechanical devices that increase the coronary preserving ventricular function; given in
perfusion and lowers systolic blood pressure. some patients with MI.
➔ Reduce the afterload and improve blood flow with
pt cardiac contractile functions. A ANTICOAGULANTS
➔ Increase the cardiac output by improving the Given to prevent clots from becoming larger
coronary blood flow. If there is an increased in and block coronary arteries. They are usually
coronary blood flow therefore, there is more given with other anti clotting medicines to
myocardial oxygen delivery help prevent or reduce heart muscle
damage.
❏ Usually it will inflate during the diastole and
ventricular filling that may increase the pressure S STOOL SOFTENERS
in the aorta therefore, it may increase the blood Given to avoid intense straining that may
flow through the coronary and peripheral arteries. trigger arrhythmias or another cardiac arrest.
❏ It is inflated just before ventricular contraction that
will lessen the pressure in the aorta before the S SEDATIVES
left ventricle contraction so that it may decrease In order to limit the size of infarction and give
the amount of resistance to the heart. rest to the patient. Valium or an equivalent is
usually given.

PHARMACOLOGIC INTERVENTION

1. Analgesics - ​Morphine
➔ Vasodilator that reduces the pain and
anxiety
➔ Reduces the blood flow of the heart, that
results into a decrease preload and
MYOCARDIAL INFARCTION “MONA TASS” afterload
➔ Help in relaxation of the bronchioles that
M MORPHINE
enhance oxygenation
Analgesic drugs such as morphine are to
reduce pain and anxiety, also have other
2. Thrombolytic – aspirin, heparin,
beneficial effects as a vasodilator and
streptokinase, tPA
decrease the workload of the heart by
a. Anti-platelet aggregating agents –
reducing preload and afterload.
aspirin
➔ Blocks the prostaglandin a. prevent conversion of angiotensin I to II
synthesis b. ​↓ BP, kidney excrete Na and fluid to ↓ O2
➔ Prevents additional platelets demand by the heart
activation that interferes to the
platelets adhesion 4. Beta blocker
➔ Limit formation of thrombus a. ​reduce pain, limit infarct size
➔ It should not be used in client b. ​↓ HR, reduce cardiac work and
with severe renal or liver
myocardial O​2​ demand
diseases
➔ Assess for presence of bleeding,
5. Nitrates
before administering this.
a. Reduce cardiac workload
➔ CLOPIDOGREL - adjunctive
b. Dilate coronary arteries and collateral
reperfusion therapy, beneficial
channels in the heart
combination with aspirin
➢ ​Adverse effect: tachycardia and
hypotension
b. I​ ndirect thrombin inhibitor​ - ​heparin
6. Dopamine​ – improves blood flow, prevent renal
(​Antidote: Protamine sulfate​)
ischemia
➔ HEPARIN:​ Increased the ability
of antithrombin, therefore it will NURSING MANAGEMENT
not activate the circulating
thrombin and limit the formation 1. Assess the characteristics of pain including the
of thrombus formation location, duration, quality, intensity and presence
➔ Monitor aPTT (activated partial of radiation.
thromboplastin time) levels 2. Maintain an IV access just incase of an
❏ STREPTOKINASE:​ Given during emergency situation.
the first attack of MI 3. Monitor ongoing assessment - lab test, cardiac
❏ Made from streptococcus enzyme, hemodynamic parameter if the pt is with
organism Swan-Ganz catheter
❏ Increased the amount of 4. Minimize anxiety - talk with the pt
plasminogen activator that 5. Minimize metabolic demands - provide a rest
increased the amount of both period
circulation clot ​blood 6. Assess vital signs and peripheral edema
plasminogen 7. Provide calm environment - quiet environment
❏ Not given to patient who has helps in early recovery of the patient
been exposed to recent 8. Limit visitors
streptococcal infection or just 9. Elevate legs and avoid pressure under the knees
received a streptokinase 10. Administer drug therapy as ordered (MONA)
❏ Not being used again after 4 11. Prepare for treatment (PTCA, CABG)
days of administration bc it might 12. Support system
cause allergic reaction, if allergic 13. Patient teaching
occurs need to administer tPA 14. Physical exercise - may used isometric and
❏ Need to monitor: Heart rate and isotonic
rhythm and observe for any 15. Resumption of sexual activity – use of nitrates
bleeding. before sexual activity
16. AVOID activities - always provide a resting period
c. Tissue-type plasminogen activator after exercise
(tPA) 17. Patient discharge - submit to cardiac
➢ Activate Plasminogen on the clot rehabilitation called care unit in hospital
➢ Heparin is used at the same time
➢ Ex. ​Alteplase​: breakdown the ➔ If the pt is still in the Hospital the pt needs to put
blood clots, conversion of the pt in ECG monitoring.
plasminogen to plasmin. ➔ Small frequent meals is one example to decrease
cardiac workload.
3. Angiotensin-converting enzyme inhibitor ➔ Avoid valsalva maneuver bc cause bradycardia
(Captopril)
COMPLICATIONS ➔ Weakened
➔ Cannot pump enough blood to supply the
1. Dysrhythmias body’s needs
➔ Bc of the damaged muscles which ● The heart is unable to provide sufficient pump
generates abnormal current causing action to maintain blood flow to meet the needs of
abnormal cardiac contractility and the the body.
infarct damaged of the conductive tissue ❏ The occurrence of circulatory congestion is from
➔ This also results in predisposing factors decreased myocardial contractility that results
like tissue injury, hypoxemia, lactic from inadequate cardiac output to maintain the
acidosis, hemodynamic abnormalities blood flow to the body organs that resulted from
and electrolytes imbalances. cardiac causes of congestive heart failure.
➔ Also, because of declines in cardiac it ❏ If it is not cardiac conditions like increased blood
increases the cardiac irritability which volume from sodium or salt retention of primary
further compromises myocardial or decreased peripheral resistance.
perfusion.
COMPENSATORY MECHANISMS FOR MAINTAINING
2. Congestive heart failure (CHF) CARDIAC OUTPUT
➔ Usually, the MI comprise the myocardial
function by reducing contractility and 1. Ventricular dilation - ↑ contraction leads to ↑ CO
producing abnormal wall ​motion, ​bc of and maintain perfusion
this pt may have have cardiogenic shock ➔ As the heart enlarges it can cause
bc of the failure of the heart to pump pressure in the left ventricle over a
adequately thereby reduces cardiac certain time, so the muscle fiber of the
output and compromised the tissue heart is stretched thereby, it increases
perfusion the contractile force.
➔ Usually occur in left ventricle ➔ Initially this may increased contraction
that may lead to increased cardiac output
3. Pericarditis – pericardial friction rub and maintaining arterial blood pressure
➔ Also known as Dressler Syndrome and perfusion therefore the dilation is an
➔ Usually pericardial is occur after a adaptive mechanism to cope with the
transmural infarction increasing blood volume but eventually
➔ Occur about 10-20% individual (after a this mechanism become inadequate bc of
week of infarction) elastic elements of the muscle fiber are
overstretched like a rubber band which
4. Ventricular aneurysm made it become no longer functional and
➔ Late complications of MI that involves not able to contract effectively then
thinning, ballooning and hypokinesis of resulting to a decreased cardiac output.
the left ventricular wall after transmural
infarction. 2. Myocardial hypertrophy – thickness response to
➔ Aneurysm often creates paroxysmal overwork and strain
motion of the left ventricular wall and ➔ Hypertrophy means there is an increase
ballooning of an aneurysmal segment of in the muscle mass and cardiac wall
the ventricular contraction. thickness
➔ Occurs slowly bc it takes time for this
CONGESTIVE HEART FAILURE (CHF) muscle tissue to develop
➔ Usually, it follows persistent or chronic
● Heart Failure is NOT a heart attack dilation and also increases the
❏ Associated with various type of heart contractive power of the muscle fiber that
diseases particularly with long standing will lead to increased cardiac output and
hypotension and CAD maintenance of tissue perfusion.
❏ Is a type of circulatory failure which ➔ Hypertrophic heart muscle has a poor
includes hypoperfusion resulting from contractility.
extra cardiac conditions like hypovolemia, 3. Sympathetic Nervous System activation -
peripheral vasodilation or inadequate release of epinephrine and norepinephrine ↑ HR,
oxygenation of hemoglobin myocardial contractility and peripheral vascular
● Heart failure means the heart is: constriction
➔ Vasoconstriction may cause an pulmonary pressure except pressure on the right
immediate increase in the preload that ventricle leading to hypertrophy of the right
initially increased the cardiac output. ventricle and failure
➔ However. An increased venous return ❏ Nutritional deficiency - ​decreases cardiac
(volume overload) can worsen ventricular function bc of decreased myocardial muscle
performance. mass and contractility
4. Neurohumoral response – Na and water retention ❏ Hypervolemia ​- it increases the preloading,
➔ Vasoconstriction secondary to therefore, causes an increased in blood volume
norepinephrine or epinephrine load in the right ventricle
➔ It may decrease the cardiac output by
stimulating the sympathetic nervous FACTORS THAT CAUSES INTERFERENCE WITH THE
system which increases the heart rate , NORMAL MECHANISM REGULATING THE CARDIAC
BP and contractility. OUTPUT:
➔ The release of the catecholamine
decreases renal perfusion or stimulation 1. Preloading bc of the amount of blood fills the
of RAAS (​Renin-Angiotensin-Aldosterone ventricle before contraction. (venous return and
System) that causes vasoconstriction, increased elasticity of the ventricle may results to
increased BP, vascular volume and hypertrophy or thickness of the myocardium)
decreases water and sodium restriction. 2. Afterload- amount of resistance to the ejection of
the blood vessels from the ventricle that related
If the cardiac output fails, blood flow to the kidneys to stroke volume
decreases glomerular blood flow therefore, the kidney ➔ Factors that determine after, the diameter
may release angiotensin 1 and 2 or also known as and distance ability of the great vessels
angiotensin system. like aorta and pulmonary artery and
➔ Even the opening of the aortic and
Adrenal cortex will release the aldosterone then increase pulmonic valve. If the valve open easily
in peripheral vasoconstriction and increase the arterial resistance is low therefore, hypertension
BP. may increased resistance
3. Heart rate, myocardial contractility, metabolic
RISK FACTORS OF CHF state of the individual - any alteration of these
factors can lead to decreased ventricular function
● ​High blood pressure and results in manifestation of heart failure.
● Myocardial Infarction
● High cholesterol ETIOLOGY OF CHF
● Damage to heart valves
1. Abnormal loading condition – ↑ preload
● ​Diabetes
(regurgitation of mitral or tricuspid valve); ↑
● ​Obesity
afterload (hypertension, aortic or pulmonic
● Advancing age stenosis)
➢ Even pt who have hypovolemia or pt who
Note: Precipitating factors:
has congenital defects like atrial or
ventricular septal defect
❏ Infection​ - increases oxygen demand of tissue
➢ High peripheral vaso resistance
then stimulating increased cardiac output
2. Abnormal muscle function – MI, cardiomyopathy
❏ Stress ​- has an effect in development of heart
➢ MI - bc of infarcted necrotic tissue
failure
myocardium that affects the function of
❏ Anemia​ - bc of decreased oxygen carrying
the heart
capacity of the blood then stimulating an increase
➢ Cardiomyopathy - disease in myocardium
in cardiac output to meet the tissue demands.
that affects contractility of the ventricles
❏ Thyroid disorders - ​bc of changes in tissue
➢ Ventricular aneurysm - bc of abnormal
metabolic weight that increases the heart rate
muscle function
and workload of the heart indirectly it predispose
3. Limited ventricular filling – cardiac tamponade,
to atherosclerosis thereby it decreases
pericarditis
myocardial contractility
➔ Cardiac tamponade - also known as
❏ Pulmonary embolism - ​bc of the blood clot in
pericardial tamponade, this a type of
the pulmonary vasculature therefore it increases
pericardial effusion in which the fluids
accumulate in the pericardium, so the ➢ Results from dysfunction, inability of the
pressure on the heart muscle which left ventricle to function normally that
occur when the pericardial space fill up causes to back up through the left atrium
with fluid faster than pericardial sac, if the ➢ If there is pressure in left atrium, the
amount of fluid increased slowly then the pressure affects the pulmonary vein
pericardial sac can expand a little then a ➢ In the pulmonary vasculature, it may
tamponade may occur cause an elevation of pulmonary
➔ If the fluid occurs rapidly as little as 100 pressure bc of this fluid extravasation
ml it can cause tamponade therefore, from the pulmonary capillary bed into the
increased in pericardial pressure but interstitium
decreased venous return and also ➢ Also affects alveoli which manifests
decrease in cardiac output depending on pulmonary congestion or edema
the determinants of the three ➢ Left sided may result to pulmonary
characteristics of ​extrayant in ventricular congestion that is why the patient
filling: experience dyspnea, exertion that
1. Distance heart sound - bc of the fluid inside the increases pressure on the blood vessels
pericardium on the lungs - called it as PULMONARY
2. Distended ​loop - ​bc of intravenous return of the HYPERTENSION bc of increased
heart pressure in the pulmonary area or
3. Decrease pulse pressure - bc of cardiac function vasculature
and decrease in stroke volume ➢ When the blood ventricle cannot pump
effectively then it blocks out the ventricles
TYPES OF VENTRICULAR FAILURE into the aorta to the systemic circulation
that affects the cardiac output and also
1. Systolic failure ​– common cause of CHF; ↓ the impair gastric change
left ventricular ejection fraction caused impaired
contractile function ● Right​: the right ventricle has reduced capacity to
➔ This means that inability of the heart to pump blood into pulmonary circulation causing
pump blood backup of fluid into the venous circulation
➔ There is a defect in the ventricular ➢ The right side of the heart cannot eject
contraction, so the left ventricle loses its blood forward to the pulmonary
ability to regenerate enough pressure to vasculature therefore it accommodates
eject blood forward to the high pressure all the blood in the right ventricles
aorta, the reason why it was called therefore there is a tendency that
SYSTEMIC FAILURE. backflow of blood to the right atrium and
mini circulation might happen.
2. Diastolic failure ​– impaired ability of the ➢ Patient that has right sided heart failure
ventricles to fill during diastole. ↓ filling of the primarily produces signs and symptoms
ventricles will result in ↓ stroke volume. like anxiety, hepatomegaly, peripheral
➔ Diastolic failure means there is a edema (Pitting edema) bc of vascular
decreased filling of blood in the ventricle congestion.
➔ Impair ability of the ventricle to fill blood ➢ Venous congestion causes Jugular Neck
during the diastole Vein Distension.
➔ Ventricle becomes less compliant or stiff.
Ventricular filling cannot relax because MAJOR ALTERATION IN CHF
of wall is thick and rigid therefore an
decrease in stroke volume 1. Diminished cardiac output – inadequate perfusion
of the vital organ result to deprivation
➔ Oxygen and nutrients are failed to meet
2. Pulmonary vascular bed no longer emptied
FORMS OF CHF effectively by left atrium and ventricle – engorged
pulmonary vessel (that also results to pulmonary
● Left​: Left ventricle has reduced capacity to pump hypertension and p. edema)
blood into systemic circulation -decreased CO 3. Increase venous pressure – engorged capillaries
and backup of fluid into the pulmonary circulation leading to ascites and peripheral edema
➔ Move backward that increased the however when the pt lies back at the night the
venous pressure that affects liver and fluid will move from interstitial space back to the
other organs will be congested circulatory system that increases renal blood
flow)

4. Integumentary​ – pallor or cyanosis ​(bc of

decreased supply of O2)​, cool and clammy skin,
diaphoresis ​(bc of stimulation of SNS)

5. Respiratory​ – DOE, SOB, tachypnea, orthopnea,

dry cough​ (blood stain sputum bc there is a
presence of alveoli edema herein the alveoli
lining cells are destructed and contain RBC move
in alveoli)​ ,crackles in lung base
➢ pt should be in semi or high fowler's
position to facilitate breathing bc of the
pressure in the pulmonary vasculature,
this position should be done to avoid
impaired gas exchange

6. Gastrointestina​l​ – anorexia, nausea, abdominal

distention, liver enlargement, RUQ pain

7. Musculoskeletal​ – fatigue and weakness​ (lack of

oxygen and blood supply in the muscles)

8. Metabolic processes ​ - peripheral edema and

weight gain ​(bc of fluid retention)

DIAGNOSTIC STUDIES

1. ECG​ – clue to the cause of left ventricular failure

➔ Changes in the ECG tracing
2. CXR​ – shows enlarged cardiac silhouette,
pulmonary congestion
3. 2-D echo​ – provide cardiac chamber size and
ventricular function (EF - > 55% to 70%)
4. ABG ​– respiratory alkalosis or acidosis
➔ Usually occurs in patient who have
pulmonary edema due to hyperventilation
then it may results to respiratory alkalosis
➔ Hypoventilation - acidosis
CLINICAL MANIFESTATIONS PER SYSTEM 5. Laboratories​ – electrolytes ​(check the sodium,
potassium)​, blood chemistry (​increased creatinine
1. Cardiovascular​ – activity intolerance ​(bc of the
bc of decrease glomerular filtration and liver
reduced CO & blood circulation)​, tachycardia ​(​bc
function value is the liver is affected that results
of reduced CO & stimulation of SNS)​,
to increased liver enzyme)​ ,urine studies
palpitations, S3 and S4 heart sounds ​(in normal
(decreased urine output)
pt it cannot hear)​, elevated CVP, neck vein
➔ Hyponatremia due to water retention,
distention, hepatojugular reflux, splenomegaly
urinary sodium loss in response to
diuretics to relieve the congestions.
2. Neurologic​ ​– confusion, impaired memory,
➔ Hypokalemia bc of excessive use of
anxiety, restlessness, insomnia
diuretics or secondary to manifestation of
aldosteronism
3. Genitourinary​ – decreased urine output, nocturia
(bc of the imapired renal perfusion during the day
6. Nuclear imaging studies ​- areas of myocardial maintain arterial blood pressure of >60
perfusion mmHg), thiocyanate toxicity

7. Cardiac Catheterization ​may be done 3. Morphine​ – dilates pulmonary and systemic

blood vessels to improve gas exchange
MANAGEMENT ❏ Reduction of anxiety

1. Oxygen therapy Recommended by Expert:

2. Intubation - severe case​ (severe pulmonary
edema) 4. Diuretics​ - help control symptoms
3. Positioning – High Fowler’s ​(in order to increase ➢ Increased the rate of urine output with
venous return and increase thoracic capacity patient fluid overload
allowing for improve ventilation) ➢ Reduces pulmonary venous pressures
4. Monitor I and O, weigh daily and preloading
5. Fluid restrictions - less than Liter per day to ➢ Furosemide​ - acts on the ascending loop
prevent more fluid that may ​ampere​ the functions of henle to promote sodium chloride and
of the heart water excretion. It is more predictable in
6. Decrease Na in diet each response.
7. Rest - bc they get easily get fatigue due to ➢ SIDE EFFECTS: Reduces serum
decreased CO potassium level
8. Auscultate heart and lung sounds ➢ THIAZIDE​ - for chronic heart failure.
9. Hemodynamic monitoring (PCWP) Treat edema secondary to heart failure. It
10. Surgery - heart transplant; cardiomyoplasty is also controlling hypertension. Inhibits
(severe type of heart failure) sodium reabsorption in the ​distal tubule
11. Intra-aortic balloon pump - it assists the heart by and also promotes excretion of sodium
decreasing afterload or increased coronary artery and water another example of this is
perfusion. Hydrodiuril - oral
➢ Potassium-sparing diuretics -
promotes water and sodium excretion but
blocks potassium excretion (​Aldactone​)

5. Digoxin​ - helps control symptoms

➔ Increases the strength and force of
cardiac contraction
➔ It has a inotropic action which reduces
the conduction speed within the
myocardium and slows the heart rate
➔ Allows the complete emptying of
ventricles during diastole
➔ Need first to check the heart rate of the
patient before administering this drug.
➔ If less than 60 bpm do not give the
medication bc it slows the heart rate
12. Drug Therapy furtherly
➔ DIGITALIS - increases cardiac output
1. Nitroglycerin (NTG)​ (vasodilator)​ – improve and stroke volume and contractility
coronary artery circulation
❏ Reduce preload, slightly reduce afterload 6. ACE Inhibitors​ - can slow disease progression
and increased myocardial oxygen supply ➔ Treatment for all stages of heart failure
2. Nitroprusside (Nitrate)​ (vasodilator)​ – reduces ➔ Useful systolic and diastolic heart failure
preload and afterload ➔ First line therapy in the treatment bc this
❏ Improve myocardial contraction promotes vasodilation, increasing urine
❏ Increases cardiac output output by decreasing afterload and
❏ Reducing pulmonary congestions preload.
❏ COMPLICATIONS of IV nitrate: ➔ Ex. ​Captopril and Enalapril
Hypotension (needs dopamine to
7. ​Beta-adrenergic Agonist ​ - can slow disease 1. Primary (​essential or idiopathic​)
progression a. Common form
➔ Epinephrine in which increases b. Unknown cause/ usually asymptomatic
myocardial contractility and blood flow to c. Theories:
the renal​ (di ko maintindihan)​ and i. Neural ​- contributive factor because of
coronary and cerebral vascular excessive neuro humoral stimulation
➔ Highly effective to patients who have that may increase muscle tone
heart failure because it increases the CO ii. CNS activation - increased central
and promotes diuresis. nervous activity may increase bp by
increasing the renin via releasing the
HYPERTENSION catecholamine
iii. Renin-angiotensin-aldosterone
● Abnormal elevation of the systolic arterial BP with system - (RAAS) stimulation and
age related differences. production of high plasma level of renin
● Intermittent/ sustained elevation of systolic or that result the production of angiotensin
diastolic blood pressure and conversion of angiotensin I to
● Major cause of cerebrovascular accident (stroke/ angiotensin II (vasoconstricting
cardiac diseases or renal failure) substance) which may stimulate
● Labile hypertension – a phenomenon when BP can aldosterone result to retention of water
be markedly elevated at one time and normal at salt
another. iv. Vasodepressor ​- decrease
● Isolated systolic hypertension – ↑ in systolic concentration of vasodilating substance
pressure without diastolic elevation. such as prostaglandin or kinins
● May occur in elderly person or in the presence of d. Associated: Advancing age, Obesity, neural
hyperdynamic circulation or aortic insufficiency mechanism,
2. Secondary – elevated BP is related to underlying
Causes of condition such as kidney disease:
Hypertension a. A known cause: chronic renal disease, disease
of adrenal gland, BC pills, preeclampsia,
1. Nonmodifiable
hyperparathyroidism, diet pills, migral
factors – (cannot
medications
change) genetics, b. Increased peripheral resistance mainly
family history, age,
attributed to structural narrowing of arterial
race which may increase venous return, increase
2. Modifiable factors: cardiac preload, and cause diastolic
○ Inactivity
dysfunction
(Low physical fitness - may engage in
exercise)
○ Stress
○ Obesity
○ Alcohol
○ High Sodium Diet
○ Tobacco Use
○ Menopausal Medications
○ Low fiber diet

Types of Hypertension
Secondary Hypertension Causes
1. Chronic kidney disease CLINICAL MANIFESTATIONS
2. Disorders of the adrenal gland (pheochromocytoma or
Cushing syndrome) 1. Headache in occipital area (most common)
3. Pregnancy (preeclampsia) 2. Lightheadedness
4. Medications such as birth control pills, diet pills, some 3. Tinnitus – buzzing in the ears
cold medications, and migraine medications 4. Early morning vertigo
5. Narrowed artery that supplies blood to the kidney 5. Flushed face
(renal artery stenosis) 6. Epistaxis ( doesn’t mean the px w/ HPT may result to
6. Hyperparathyroidism this, depends on stage II or stage III or how high the
pressure is, and response of the body because of too
JNC7 Parameters
much pressure in the capillaries of the nasal area may
result to epistaxis)
7. Altered vision or fainting
8. Nausea and vomiting
9. Oliguria

MANAGEMENT

1. Lifestyle modifications
a. Diet and
exercise
(Lifestyle
modification)
b. Limit alcohol and
● Join national committee tobacco use
● Classification of BP c. Reduce stress
● JNC8 parameters, there are changes factor = teach patients how to reduce stress
(feedback, meditation, relaxation).
AMERICAN HEART ASSOCIATION (AHA) 2018 d. Sodium restricted diet
e. DASH DIET = dietary approach to stop HPT
(low sodium, high potassium and high calcium)
f. Health teach = use of ketchup (high sodium
BP Systolic BP Diastolic (mm
content), limit or stoppage of alcohol content
Classification (mm Hg) Hg)
and cigarettes
g. Control weight of the patient.
h. Engage regular exercise
Normal 120 - 129 80 - 84 2. Drug therapy
a. Thiazides – promotes excretion of Na, Cl, and
water
Elevated 130 - 139 85 -89 ■ Cause photosensitivity
■ Sunscreen
■ Hypokalemia
■ Eat banana
Stage 1 HTN 140 – 159 90 – 99
b. Aldosterone blocking diuretics (Aldactone) –
inhibits reabsorption of Na, Cl, while retaining K
in the distal loop of Henle
Stage 2 HTN 160 - 179 100 - 109 ■ Potassium sparing diuretics
c. Furosemide (Lasix) – inhibits reabsorption of
Na, Cl in the ascending loop of Henle.
Stage 3 >​180 > 110 ■ Predictable
d. Calcium channel blockers - anti diuretic effect
■ Reduce peripheral vascular resistance
■ Decrease blood pressure, relax vascular
Isolated >​ 140 < 90 smooth muscle, cause vasodilation
■ Nifedipine
e. Adrenergic blocking agents - blocks
sympathetic activity at beta or alpha receptor
sites
f. Angiotensin converting enzyme (ACE) Inhibitor
- suppress the renin-angiotensin mechanism
(ex. capotet)
■ Reduces arterial pressure and venous
pressure
■ Lowers bp by decreasing vascular
resistance
■ Cause dry cough = elevations of
bradykinin levels
g. Anti-hypertensive drugs
■ Do not stop abruptly stop
antihypertensive drugs, may cause
rebound hypertension ● Heart​: cause HF, Left ventricular hypertrophy
■ Rebound HTN= difficult to control because of increase workload that may result to
■ Goal: Decrease peripheral resistance of myocardial hypertrophy = may experience angina,
the blood volume, strength and rate of HF, ventricular hypertrophy, and eventually may
contraction result to ischemia
■ Beta blockers: metoprolol ● Brain: decrease flow of blood to the brain because
of peripheral vasoconstriction, reduce O2 supply,
Diagnostic Test to Consider​:
transient ischemic attack or TIA (thrombosis,
● CHECK: BUN + creatinine, proteinuria (urinalysis) aneurysm, hemorrhage = alter mobility, paralysis,
= check kidneys memory, speech).
● Endocrine: Thyroid stimulating hormone ● Eyes​: decrease blood flow, increase pressure in the
(Hyperthyroidism, Hyperparathyroidism) arterioles, causes retinal vascular sclerosis and
● Cholesterol, FBS (Fasting blood sugar) = visceral disturbances (presence of spots), if it's not
associated with the development of hypertension controlled, result to blindness
● Check electrolytes: K. Na, Ca ● Peripheral Vascular​: blood pressure in the
● Chest x-ray and ECG arterioles, causes gangrene may result = pain upon
walking
● Renal​: Decrease in the perfusion of blood flow to the
kidney, cause secretion of the renin (convert
angiotensin I and angiotensin II) = increase bp and
may experience proteinuria and polyuria, activation
of your RAAS, sodium and water absorption will
occur, O2 supply is also reduced, kidney capabilities
are reduced (Azotemia may happen).

COMPLICATIONS OF HTN

1. Hypertension crisis – severely and abrupt/ sudden

elevated BP of > 180 mm Hg (systolic)
○ Hypertensive emergency – direct damage to
one or more organs are as a result of ↑ BP
(affect kidney, heart, eyes, brain function etc.).
Px is non compliance of medications and
asymptomatic (severe headaches/ dizziness)
○ Hypertension urgency - ↑ BP but there is no
evidence of impending or target organ damage
2. .Aortic aneurysm
○ 3.5 C’s -CAD, Cerebrovascular disease,
Chronic renal disease, CHF and Cardiac arrest
COMPLICATION OF HYPERTENSION “THE 5 C’s” ○ Thoracic Aneurysm = Abnormal bulging of the
portion of the aorta, hardening of the arteries
● CORONARY ARTERY DISEASE – Can lead to common in male; 40 to 70 years of age.
narrowing of blood vessels making them more likely ○ Abdominal Aortic Aneurysm = “Triple A”,
to block from blood clots. prevalent in the elderly; enlarged area in the
○ Weakens the wall. aorta.
● CHRONIC RENAL FAILURE – Constant high blood ○ Peripheral = located commonly popliteal,
pressure can damage small blood vessels in the femoral, carotid, occurs in the legs behind the
kidneys, making it not to function properly. knee along the joint.
● CONGESTIVE HEART FAILURE – Pumping blood ○ Aortic aneurysm = occurs in the major artery
against the higher in the vessels causes the heart from the hearts because of the constant stress
muscles to thicken in the wall and absence of penetrating vaso
● CARDIAC ARREST – high blood pressure can cause vasorum in the medial layer.
CAD, damaged arteries cannot deliver enough
oxygen to other parts of the body eventually leading
to heart attack
● CEREBROVASCULAR ACCIDENT – Hypertension
leads to atherosclerosis and hardening of the large
arteries, This, in turn, can lead to blockage of small
blood vessels in the brain

VALVULAR DISORDERS
Inflammatory and Valvular Heart Disease

AORTIC ANEURYSM

Basic Classification

1. True aneurysm – 3 layers (intima, media,

adventitia) wall of artery forms the aneurysm
(asterosclerotic, syphilitic, congenital and
ventricular aneurysm) which follow transmural MI
and subdivided into:
○ Fusiform
○ Saccular
2. False aneurysm or pseudoaneurysm – complete
tear of all three arterial coats
○ results in bleeding that fills the
● Result of localized weakness and stretching of the surrounding tissues producing a pulsatile
arterial walls hematoma.
● Unknown cause but of atherosclerosis (theory) ○ Collection of blood that leaks out
● Atherosclerotic plaque deposit beneath the intima completely of the artery or vein but is
(inner layer of the arterial wall). confined next to the vessel by the
● Plaque formation = cause degenerative changes in surrounding tissues.
the media leading to loss of elasticity, weakening and ○ False aneurysm may be the result from
even dilation of the aorta trauma, infection or after peripheral artery
● Types: bypass graft surgery at the site of the
graft-to-artery anastomosis.
Categories of True Aneurysm Risk factors

1. Saccular – outpouching on one side of an artery. 1. Age of the patient (>65)

Looks like a berry 2. Elevated BP
when they occur 3. Hypertension history
on the arteries of 4. Smoking (Abdominal Aneurysm high risk)
the blood vessel 5. Hypercholesterolemia
and frequently 6. Atherosclerosis (susceptible to aortic aneurysm)
arise on the 7. Peripheral vascular disease
ascending and
Clinical Manifestations
descending
thoracic aorta 1. Chest pain – common (px with thoracic aneurysm
2. Fusiform - balloon on all sides (Circumferential because of the location, in the ascending aorta and
arterial dilation). All of the sides are affected, filled the aortic arch that can sometimes produce forceness
with necrotic debris and thrombus. Ca may because of laryngeal nerve, chest pain may radiate to
infiltrate the area, sac may dilate because of the neck to back and shoulder)
weakened media layer 2. Dysphagia – compression of the esophagus
3. Aortic Dissection - “​dissecting aneurysm​”, theory (common in thoracic aneurysm)
and degeneration of the 3. Pulsatile mass in the periumbilical area slightly to the
medial layer allows the left of the midline during PE (abdominal aortic
blood to separate the aneurysm) - do not do deep palpation
arterial intimal layer from 4. Bruits audible with a stethoscope
the adventitial layer , 5. Abdominal or back pain – result from compression of
cause is unknown but nearby anatomic structures. (Abdominal aortic
exposure to hypertension is susceptible to this, aneurysm)
causing the degeneration and necrosis. ○ Blue toe syndrome = mattling of the feet and
Pregnancy (increased blood volume and hormonal toe of the patient. (common with Triple A)
changes and hypertension that leads to
degeneration) , traumatic dissection (direct injury Diagnostic Studies
due to procedure or even in arteriography)
1. CXR
CLASSIFICATION OF ANEURYSM 2. ECG – to r/o evidence of MI
3. Echocardiography
4. Ultrasound
5. CT scan
6. Angiography – mapping of the aortic system by
contrast image

Management

1. Risk factor modification

a. Diet – sodium restriction
b. Use of Anti-hypertensive drugs
■ Does Not cure aneurysm but controls HTN
c. Monitor the size of aneurysm every 6 months
2. Hemodynamic monitoring
3. Pain management
a. Morphine Sulfate
Etiology of Aortic Aneurysm
4. Surgery - repairs the artery by closing/ application of
1. Unknown a synthetic patch drop over the arterial defect.
2. Atherosclerosis – plaques formation cause a. open - suturing
degenerative changes in the middle layer of the b. Endovascular aortic repair - newest alternative
arterial wall procedure (EVAR)
3. Genetic predisposition (hereditary)
4. Congenital
5. Mechanical, traumatic, infection (syphilis that may
affect arterial wall) – least common
ENDOVASCULAR AORTIC REPAIR ○ Postoperative care

INFECTIVE
ENDOCARDITIS

● An infection of the inner

layer (endocardium) of the
heart. It may affects the
cardiac valves (normal
heart is resistant to
infection because bacteria
do not adhere easily
because of constant blood
flow)– mitral and tricuspid
valves
● Bacterial endocarditis
● Mouth, spread through
● Fixation of the ruptured abdominal aortic aneurysm
the bloodstream
(5.5 cm or 2 inches)
● Repair is done by resecting the vessel and sewing the Predisposing Factors
bypass graft in place
1. Aging – degenerative heart disease (invasive
● Become a mainstay of therapy for treating an
testing)
infrarenal abdominal aortic aneurysm and involves the
2. Intravenous drug abuse (Tricuspid valve; Cocaine
transluminal placement and attachment of a sutureless
aortic graft (Stent graft) prosthesis across an Abuse)
3. Structural heart or valves defect – increase
aneurysm
● Performed under a local or regional anesthesia number of platelet and fibrins in the endothelium
a. Etiology:​ presence of microorganism in
● May be performed if the patient's abdominal aorta or
the body; Streptococcus and
iliac arteries are not extremely tortuous, small, calcified
or filled with thrombi Staphylococcus, portal of entry (UTI,
catheter, etc.)
● Complication includes bleeding, hematoma, wound
infection, distal ischemia or embolization; dissection or
perforation of the aorta; graft thrombosis or infection,
graft migration, proximal or distal graft leaks, bowel
ischemia.
● MANAGEMENT:
○ Px must lie supine for 6 hrs
○ HOB may be elevated (45 degrees after 2 hrs)
○ Bedpan
○ Vital signs and doppler assessment (peripheral
pulses are performed every 15 mins)
○ Check access site (femoral artery)
○ Assess for bleeding, pulsation, swelling, pain,
and hematoma formation
○ Temperature should be monitored every 4 hours
○ Check for any signs of postimplantation
syndrome (begins usually 24 hours of stent graft
placement; sy&sx: spontaneous occurring fever,
leukocytosis, and occasionally transient
thrombocytopenia.
○ Notified of persistent coughing, sneezing,
vomiting, or systolic blood pressure >180mm Hg
○ IV infusion may be continued until the px can
drink normally
○ 6 hours after the procedure, the px may roll from
side to side and may be able to ambulate with
assistance to the bathroom
4. Echocardiography - evaluate for diagnosis
5. Chest X-Ray – detect the presence of an enlarged
heart
6. ECG – shows 1​st​ or 2​nd​-Degree block
7. CRP - detect presence of inflammation and infection

Management

1. Antibiotic includes prophylaxis (Specific cardiac

condition)
a. Ceftriaxone (Rocephin) – streptococcus
b. Vancomycin (Vanocin) – staphylococcus
2. Antipyretic for fever
3. Rest (bed rest)
4. Anti-embolic stocking – prevents thrombus formation
(Applied early in the morning)
5. Restrict normal activity 4 – 6 weeks
6. Surgery – repair or replacement for severe valvular
damage (replacement is needed)

MAJOR TYPES OF VALVULAR HEART DISEASE

Clinical Manifestations 1. Stenosis – heart valve leaflets fused together, opening

narrow, stiff, unable to open or close properly
1. Fever and chills – 90% a. Scar of the valves from endocarditis or infarction
2. Fatigue and weakness b. Constriction of the valve
(malaise, anorexia) c. Cannot fully open or close (Funnel like/ rigid)
3. splinter hemorrhage – d. Calcium deposits - impedes the forward flow,
occur in nail bed of the blood decreasing cardiac output (lesser blood
vascular (block and lack of ejection), impaired ventricular feeling
longitudinal) 2. Regurgitation – improper or incomplete or incompetent
4. Petechiae – fragmentation closure of heart valves, resulting in back flow of blood
and microembolization of a. Common cause: Deformity of valve cusps caused
vegetative lesions (also by vegetative lesions caused by the bacterial
common in conjunctiva, endocarditis
buccal mucosa) b. Do not close completely = Too loose
5. Osler’s nodes – painful, c. Cause: Scarring/ tearing of MI or cardiac dilation
tender, red pea-size d. Contraction = backflow where it just left
lesion found in the e. Heart enlarges = streched valve
fingertips or toes f. Excess blood volume behind
6. Janeway’s lesion – flat, painless, small red spots
found on the palms and soles
7. Roth’s spot – hemorrhagic retinal lesion through MITRAL STENOSIS
examinations
8. Murmur - noted 80% of the cases ( cardiac vault is ● Thickening and
shortening
affected)
9. Splenomegaly - embolization to the spleen result in between the
the sharp LUQ pain commissures
10. Embolization to the brain (40%) - causes neurologic (junctional
problem (hemiplegia, ataxia, aphasia), change in the areas) of the
leaflets that
level of consciousness
obstruct the
Diagnostic Studies flow of blood
from the left
1. Blood culture – primary tool
atrium into the left ventricle.
2. Leukocytosis around 11,000 unit/ liter
● Cause: Rheumatic endocarditis
3. Erythrocyte sedimentation rate (ESR) - > 30 mm/hour
● Narrowing of the cardiac valve
because the presence of infection
● Reduced CO
● affectleft atrium, because of the pressure and dilation,
may cause atrial hypertrophy
● Pulmorary hypertension
● Problem: inflow of the left ventricle
● Group A hemolytic Streptococcus
● Look like a funnel

Clinical Manifestations

1. Dyspnea sometimes accompanied by hemoptysis

(reduced lung compliance because increase pressure
caused transudation of lung fluid in interstitium)
2. Palpitations – from atrial fibrillation and fatigue (prone
to form blood clots)
3. Chest pain - ↓ CO
4. Seizures (from emboli because of stagnation of blood
in the left atrium)
5. Hepatomegaly
Nicole: Slide 111 onwards.
6. Peripheral edema (Back up pressures not only to the
LA but also affect RV)
MANAGEMENT
7. Crackles - because problem of gas exchange,
pulmonary congestion and hypertension 1. Sodium restriction
8. Cyanosis 2. Oral diuretics – Relieve pulmonary congestion
3. Digitalis and anti-arrhythmic drugs – AF
4. Antibiotic – AHA guidelines do not recommend
PATHOPHYSIOLOGY infective endocarditis prophylaxis for most
patients with rheumatic heart disease. Some
doctors prescribe prophylactic antibiotics before
dental procedures. However, the maintenance of
optimal oral health care remains an important
component of an overall healthcare program
5. Anticoagulant – Prevent and treat emboli
6. Beta blockers – Control long-term use of oral
beta blockers, ↓ HR, ↑ tolerance to exercise
7. Percutaneous Transluminal Balloon Valvuloplasty
– Open narrowed cardiac valves, contraindicated
in px with left atrial thrombus or left ventricular
thrombus, beneficial to px with no complications
or additional conditions
8. Surgery – Mitral Commissurotomy – Surgical
incision of a commissure, relieve constriction
9. Avoid strenuous exercise or activity – Prevent ↑
HR
Digitalis – Slows HR → prevents atrial fibrillation, 5. Digitalis
administers IV 6. ACE inhibitors

MITRAL REGURGITATION VALVULOPLASTY PROCEDURES

Backflow of blood from the left ventricle into the left atrium Annuloplasty​ – Repair of the valve annulus
during systole

Etiology:

1. Inflammatory and infective – Rheumatic heart

disease and endocarditis
2. Degenerative changes or calcification of the
mitral annulus – MVP
3. Process that dilates the papillary muscles or the
chordae tendineae – Left ventricular hypertrophy,
MI
4. Congenital defects - Systemic lupus
erythematosus, cardiomyopathy

Chordoplasty – Repair of the chordae tendineae,

involves the mitral valve

MITRAL VALVE PROLAPSE – MVP

● One or both mitral valve cusps buckle back into

the left atrium during ventricular systole –
Displacement of the thickened mitral valve leaflet
● Structural abnormalities of the mitral valve reflex

Etiology:

1. Unknown
2. Familial incidence – First degree relatives,
CLINICAL MANIFESTATIONS echocardiogram
3. Excess collagen tissue in the valve leaflets
1. Systolic murmur
2. Cool, clammy extremities
4. Elongated chordae tendineae – Causes the
buckle back of leaflets
3. Dyspnea
4. Palpitations – First symptom 5. Infective endocarditis
5. Fatigue
6. Cough from pulmonary congestion
7. Shortness of breath on exertion

DIAGNOSTIC STUDIES

1. ECG
2. 2-D Echo

MANAGEMENT

1. Restrict physical activities

2. Reducing sodium intake
3. Diuretics
4. Nitrates
Etiology:

1. Congenital leaflet malformation

2. Inflammatory changes rheumatic endocarditis –
Stiffening of the valve
3. Cusp calcification

CLINICAL MANIFESTATIONS

1. Murmur – Very common, best heard at the apex,

accentuated by standing and Valsalva maneuver
which ↓ venous return
2. Palpitations
3. Light-headedness
4. Dizziness
5. Chest pain – Px does not respond to nitrates,
responds to beta blockers or calcium channel CLINICAL MANIFESTATIONS
blockers
6. Activity intolerance Similar to mitral stenosis, difference is the affected valve
7. Syncope
1. Angina pectoris
8. Dyspnea
2. Syncope
9. Surgery – Valve replacement – Depends on the
3. Heart failure
condition
4. Pulmonary edema
10. Health teaching
5. Narrow pulse pressure
● Practice oral hygiene
● Avoid sharp objects in the oral cavity 6. Dyspnea on exertion – Encourage bedrest, give
● Avoid OTC medications that contain antibiotics
alcohol or caffeine
Digitalis and diuretics – Not effective in mitral stenosis, for
Aspirin – Prevent blood clots px with left ventricular failure

Beta blockers – Relieve palpitations and chest pain Beta blocker – Induce left ventricular failure

AORTIC STENOSIS AORTIC REGURGITATION

Narrowing of the orifice that obstructs the flow of blood ● Flow of blood back into the left ventricle from the
from the left ventricle and the aorta during systole aorta during diastole
● There is a leak in the aortic valve 6. Austin-flint murmur – A low frequency diastolic
● 25% regurgitation ↓ diastolic blood pressure, ↑ murmur at the cardiac apex
pulse pressure, assessment reveals bulging
radial pulse MANAGEMENT

Etiology: 1. Diet – Low sodium to avoid volume overload for

asymptomatic px
1. Inflammatory lesions that deform the leaflets of 2. Activity – Avoid physical exertions and
the aortic valve competitive sports
2. Trauma – Congenital anomalies, rheumatic 3. Medications – Calcium channel blockers, ACE
endocarditis inhibitors
3. Congenital abnormality 4. Prosthetic valve replacement
4. Rheumatic conditions ● For childbearing age women to avoid
potential complications from long-term
anticoagulants
● Perform before left ventricular failure
occurs
● ​Lasts for 7-15 years

Different types of mechanical valve:

● Tissue valve – Autograft – Px pulmonic

valve and portion of pulmonary artery as
aortic valve
● Bioprosthesis – 4 seal
● Pig valve
● Equine – Horse

5. Homograft – Anagram
● Human valve
● From tissue donations for aortic and
pulmonic valve replacement
● Lasts for 10-15 years

Porcine Heterograft Valve​ –Carpenter Edwards

MECHANICAL VALVE REPLACEMENT

CLINICAL MANIFESTATIONS
Bileaflet​ – St. Jude
1. Weakness
2. Severe dyspnea
3. Hypotension
4. Palpitations – Can cause dysrhythmia
5. Corrigan’s pulse – Forceful and sudden collapse
of pulse
● Very common in px with aortic ● More durable than tissue prosthetic valve
regurgitation
● For younger patients with endocarditis
● Sometimes called as water hammer
● Can cause thromboembolism
pulse
● Requires long-term use of anticoagulant Palpation

Caged Ball Valve​ – Starr Edwards ❖ Temperature – Bilateral

❖ Pulses – Note the rhythm, amplitude and
symmetry of pulses
➢ Bilateral
➢ Except in carotid pulse –
Stimulates carotid sinus
❖ Allen’s Test – Assess patency of radial
and ulnar arteries
➢ Before ABG
❖ Homan’s sign – Compress the
PERIPHERAL VASCULAR DISEASE gastrocnemius muscle of the calf for
tenderness

Auscultation ​– Assess for bruits

DIAGNOSTIC EVALUATION

● Doppler Ultrasonography – Detects blood flow

● Ankle Brachial Index – Compares blood pressure
in the upper and lower limbs
● Exercise Test
● Duplex Ultrasonography – Px with deep vein
thrombosis

PERIPHERAL ARTERIAL OCCLUSIVE DISORDERS

ASSESSMENT ● Affects men and involvement of the upper

extremities
● Health History – Intermittent claudication
● Hallmark symptom is intermittent claudication

Intermittent claudication – Symptom that describes

muscle pain on mild exertion in the calf muscle, which
occurs during exercise, and is relieved by short rest

● Physical examination

Inspection

❖ Capillary refill – Less than 3 seconds

➢ < 3 seconds – Diminish blood
flow
❖ ​Edema – Press skin for 5 seconds
➢ Pitting edema​ – + Indentation
➢ Grading scale ● Distal occlusion – Common in elderly and px with
❖ Elevation pallor – Reddish-blue diabetes
discoloration of the extremities, occurs ● Extremities are cold and pale when in an
within 20 seconds-2 minutes after elevated position
extremities are placed in elevated
position Peripheral Vascular Disease – Commonly affects elderly
➢ Rubor – Redness, means there and px with diabetes, there is disturbance in flow to
is damage to the arteries peripheral vessels, leads to ischemia and excessive
❖ Clubbing fingers – Due to prolong lack of accumulation of fluid which causes venous and lymphatic
oxygen stasis
❖ Trendelenburg’s Test – Indicates
weakness in the hip
Cellular anaerobic metabolism – Build-up of lactic acid
and pyruvic acid waste products

● Clinical manifestations – Muscle atrophy, bruit,

diminish or absent peripheral pulse
● Lack of treatment and intervention leads to
changes in skin and nails, gangrene, and
ulceration
● Palpation – Bilateral

MANAGEMENT

● Exercise
● Do not apply heat in px with arterial insufficiency
● Medications – Pentoxifylline (Trental), cilostazol
● Surgery – Endarterectomy, bypass graft

Pentoxifylline – ↑ erythrocyte flexibility, ↓ fibrinogen, has

antiplatelet effect

Cilostazol – Vasodilator, inhibit platelet aggregation,

contraindicated in px with congestive heart failure

Endarterectomy – Surgical incision in the artery to

remove atheromatous obstruction
Distal to proximal

Bypass Graft – Reroute the blood flow around the

BUERGER’S DISEASE
stenosis
● Tobacco smoke stains on male patient's fingers
THROMBOANGITIS OBLITERANS – Buerger’s
suggest diagnosis of thromboangiitis obliterans –
Disease
Buerger’s Disease
● A condition in which the small arteries and
● Patient presented with small, painful ulcers on
tips of thumb and ring finger
arterioles constrict in response to various stimuli
● Affects the medium-sized arteries, veins and
nerves of the upper and lower extremities – Only
affects hands and feet
● Large arteries – Not involved, very rare
● Cause is unknown – Theories related to smoking,
familial tendency, autoimmune
● More common in younger men ages 25-40
➢ Postoperative – ↑ BP without
bleeding
❖ A
​ rterial bypass graft

STEPS OF BUERGER ALLEN EXERCISE

1. Elevate feet on padded chair or board for ½ to 3

minutes
2. Sit in a relaxed position while each food is flexed
and extended then pronated and supinated for 3
minutes. The feet should become entirely pink. If
the feet are blue or painful, elevate them and
relax as necessary
3. Lie quietly for 5 minutes, keeping legs warm with
CLINICAL MANIFESTATIONS
blanket
4. Pharmacologic therapy
1. Redness along the lines of the veins and arteries
2. Spasm of the digital arteries that result to pallor
3. Diminished sensation
4. Paresthesia – Sensation of tickling, tingling,
burning or numbness
5. Skin is shiny and thin
6. Nails are thickened and malformed

Intermittent claudication – Calf pain during activities

❖ P​allor
❖ ​P​ulses decreased

❖ ​P​erishing cold
❖ ​P​ain

❖ ​P​aresthesia

❖ ​P​aralysis

No diagnostic studies

MANAGEMENT

1. Smoking cessation
2. Keep extremities warm
3. Managing stress
4. Keeping affected extremities in a dependent
position
5. Regular exercise
6. Wound care
7. Buerger’s Allen exercise – Promote circulation
and establish collateral circulation
8. Calcium channel blockers to ↓ the blood viscosity RAYNAUD’S PHENOMENON
and ↑ RBC flexibility to improve peripheral blood
flow to relief symptoms ● A spasm of arteries causing blanching of ​fingers
9. Surgery – Depends on the condition and toes​ and affects young women ages 15-40
❖ A
​ mputation – If px has gangrene ● Vasospasm induce color changes – Fingers,
❖ Sympathectomy – If there is interruption toes, ears, nose
of SNS input to the affected vessels ● Also known as white-red disease
● Unknown cause
❖ Emerge hands in warm water to reduce
spasms
6. Measures to avoid injury to the hands
7. Vasodilators
❖ Calcium channel blockers such as
nifedipine – Relax smooth muscles,
reduce vasospastic attack
❖ Alpha blockers such as minipress –
Counter norepinephrine
8. Surgery – Sympathectomy – For advance cases

THEORIES OF RAYNAUD’S PHENOMENON

A. Vasospasm occurs secondary to SNS stimulation

B. Abnormalities in the endothelium -
Endothelium-derived vasoactive substance
C. Other contributing factors: Occupation related
trauma and pressure on the fingertips
D. Exposing to heavy metals

PRECIPITATING FACTORS

1. Exposure to cold
2. Emotional upset
3. Caffeine intake
4. Tobacco use

Buerger’s Disease – Strong relationship to smoking

Raynaud’s Phenomenon – Response to cold and stress

CLINICAL MANIFESTATIONS

1. Sensory changes – Numbness, stiffness,

decreased sensation and aching pain
2. Thickened fingertips and nails become brittle
3. Pallor
4. Skin becomes bluish
5. Hyperemia
6. Ulcerations and gangrene – Serious
complications

Hyperemia​ – Is an excess of blood in blood vessels

MANAGEMENT

1. Loose, warm clothing

2. Avoid extreme temperature
3. Smoking cessation
4. Avoid caffeine and drugs with vasoconstrictive
effects
5. Stress reduction management