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u DESCRIPTION
Ń A narrowing or obstruction of one or more
coronary arteries due to atherosclerosis, an
accumulation of lipid-containing plaque in the
arteries
Ń Causes decreased perfusion of myocardial
tissue and inadequate myocardial oxygen
supply
Ń Leads to hypertension, angina, dysrhythmias,
myocardial infarction, heart failure, and death

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| 
u DESCRIPTION
Ń Collateral circulation, more than one artery
supplying a muscle with blood, is normally
present in the coronary arteries, especially in
older persons
Ń The development of collateral circulation takes
time and develops when chronic ischemia
occurs to meet the metabolic demands;
therefore, an occlusion of a coronary artery in
a younger individual is more likely to be lethal
than in an older individual

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| 
u DESCRIPTION
Ń Symptoms occur when the coronary artery is
occluded to the point that inadequate blood
supply to the muscle occurs, causing ischemia
Ń Coronary artery narrowing is significant if the
lumen diameter of the left main artery is
reduced at least 50%, or if any major branch is
reduced at least 75%
Ń The goal of treatment is to alter the
atherosclerotic progression

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u ASSESSMENT
Ń Findings may be normal during asymptomatic
periods
Ń Chest pain
Ń Palpitations
Ń Dyspnea
Ń Syncope
Ń Cough or hemoptysis
Ń Excessive fatigue

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| 
u ECG
Ń When blood flow is reduced and ischemia
occurs, ST segment depression or T wave
inversion is noted; the ST segment returns to
normal when the blood flow returns
Ń With infarction, cell injury results in ST
segment elevation, followed by T wave
inversion

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| 
u CARDIAC CATHETERIZATION
Ń Provides the most definitive source for
diagnosis
Ń Shows the presence of atherosclerotic lesions

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u ’LOOD LIPID LEVELS
Ń May be elevated
Ń Cholesterol-lowering medications may be
prescribed to reduce the development of
atherosclerotic plaques

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| 
u IMPLEMENTATION
Ń Assist the client to identify risk factors that can
be modified
Ń Assist the client to set goals to promote
lifestyle changes that will reduce the impact of
risk factors
Ń Assist the client to identify barriers to
compliance with the therapeutic plan and to
identify methods to overcome barriers

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| 
u IMPLEMENTATION
Ń Instruct the client regarding a low-calorie, low-
sodium, low-cholesterol, and low-fat diet, with
an increase in dietary fiber
Ń Stress to the client that dietary changes are
not temporary and must be maintained for life;
instruct the client regarding prescribed
medications
Ń Provide community resources to the client
regarding exercise, smoking reduction, and
stress reduction

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| 
u SURGICAL PROCEDURES
Ń PTCA to compress the plaque against the walls
of the artery and dilate the vessel
Ń Laser angioplasty to vaporize the plaque
Ń Atherectomy to remove the plaque from the
artery
Ń Vascular stent to prevent the artery from
closing and to prevent restenosis
Ń Coronary artery bypass graft to improve blood
flow to the myocardial tissue that is at risk for
ischemia or infarction due to the occluded
artery

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| 
u MEDICATIONS
Ń Nitrates to dilate the coronary arteries and to
decrease preload and afterload
Ń Calcium channel blockers to dilate coronary
arteries and reduce vasospasm
Ń Cholesterol-lowering medications to reduce the
development of atherosclerotic plaques
Ń ’eta-blockers to reduce blood pressure in
individuals who are hypertensive

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u DESCRIPTION
Ń Chest pain resulting from myocardial ischemia
caused by inadequate myocardial blood and
oxygen supply
Ń Caused by an imbalance between oxygen
supply and demand
Ń Causes include obstruction of coronary blood
flow due to atherosclerosis, coronary artery
spasm, and conditions increasing myocardial
oxygen consumption


u DESCRIPTION
Ń The goal of treatment is to provide relief of an
acute attack, correct the imbalance between
myocardial oxygen supply and demand,
prevent the progression of the disease and
further attacks to reduce the risk of MI


u STA’LE ANGINA
Ń Also called exertional angina
Ń Occurs with exertion or emotional stress, and is
relieved with rest or nitroglycerin
Ń It usually has a stable pattern of onset,
duration, severity, and relieving factors


u UNSTA’LE ANGINA
Ń Also called preinfarction angina
Ń Occurs with an unpredictable degree of
exertion or emotion and increases in
occurrence, duration, and severity over time
Ń Pain may not be relieved with nitroglycerin


u INTRACTA’LE ANGINA
Ń A chronic, incapacitating angina that is
unresponsive to interventions
u POSTINFARCTION ANGINA
Ń Occurs after an MI, when residual ischemia
may cause episodes of angina


u ASSESSMENT: PAIN
Ń Can develop slowly or quickly
Ń Usually described as mild or moderate pain
Ń Substernal, crushing, squeezing pain
Ń May radiate to the shoulders, arms, jaw, neck,
back
Ń Usually lasts less than 5 minutes; however, can
last up to 15 to 20 minutes
Ń Relieved by nitroglycerin or rest


u ASSESSMENT
Ń Dyspnea
Ń Pallor
Ń Sweating
Ń Palpitations and tachycardia
Ń Dizziness and faintness
Ń Hypertension
Ń Digestive disturbances


u ECG
Ń Normal during rest, with ST depression or
elevation and/or T wave inversion during an
episode of pain
u STRESS TEST
Ń Chest pain or changes in the ECG or vital signs
during testing may indicate ischemia
u CARDIAC ENZYMES
Ń Normal findings in angina
u CARDIAC CATHETERIZATION
Ń Provides a definitive diagnosis


u IMMEDIATE MANAGEMENT
Ń Assess pain
Ń Provide bed rest
Ń Administer oxygen at 3 L via nasal cannula as
prescribed
Ń Administer nitroglycerin as prescribed to dilate
the coronary arteries, reduce the oxygen
requirements of the myocardium, and relieve
the chest pain
Ń Obtain a 12-lead ECG
Ń Provide continuous cardiac monitoring


u FOLLOWING ACUTE EPISODE
Ń Assist the client to identify angina-precipitating
events
Ń Instruct the client to stop activity and rest if
chest pain occurs and to take nitroglycerin as
prescribed


u FOLLOWING ACUTE EPISODE
Ń Instruct the client to seek medical attention if
pain persists
Ń Instruct the client regarding prescribed
medications
Ń Provide diet instructions to the client, stressing
that dietary changes are not temporary and
must be maintained for life
Ń Assist the client to identify risk factors that can
be modified


u FOLLOWING ACUTE EPISODE
Ń Assist the client to set goals that will promote
changes in lifestyle to reduce the impact of risk
factors
Ń Assist the client to identify barriers to
compliance with therapeutic plan and to
identify methods to overcome barriers
Ń Provide community resources to the client
regarding exercise, smoking reduction, and
stress reduction


u SURGICAL PROCEDURES
Ń Same procedures performed to treat CAD
u MEDICATIONS
Ń Same medications used to treat CAD
Ń Antiplatelet therapy may be prescribed to
inhibit platelet aggregation and reduce the risk
of developing an acute MI


u DESCRIPTION
Ń Occurs when myocardial tissue is abruptly and
severely deprived of oxygen
Ń Ischemia can lead to necrosis of myocardial
tissue if blood flow is not restored
Ń Infarction does not occur instantly, but evolves
over several hours
Ń Obvious physical changes do not occur in the
heart until 6 hours after the infarction, when
the infarcted area appears blue and swollen

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u DESCRIPTION
Ń After 48 hours, the infarct turns gray with
yellow streaks as neutrophils invade the tissue
Ń ’y 8 to 10 days after infarction, granulation
tissue forms
Ń Over 2 to 3 months, the necrotic area develops
into a scar; scar tissue permanently changes
the size and shape of the entire left ventricle

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u LOCATION OF MI
Ń Obstruction of the left anterior descending
(LAD) artery results in anterior and/or septal
MI or both
Ń Obstruction of the circumflex artery results in
posterior wall MI or lateral wall MI
Ń Obstruction of the right coronary artery results
in inferior wall MI

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u TOTAL CK LEVELS
Ń Rise within 3 hours after the onset of chest
pain
Ń Peak within 24 hours after damage and death
of cardiac tissue
u CK-M’ ISOENZYME
Ń Peak elevation occurs 12 to 24 hours after the
onset of chest pain
Ń Levels return to normal 48 to 72 hours later

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u TROPONIN LEVELS
Ń Rise within 3 hours
Ń Remain elevated for up to 7 days
u MYOGLO’IN
Ń Rises within 1 hour after cell death, peaks in 4
to 6 hours, and returns to normal within 24 to
36 hours or less

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u LDH LEVELS
Ń Rise within 12 to 24 hours after MI
Ń Peak between 40 and 72 hours and fall to
normal in 7 days
Ń Serum levels of LDH1 isoenzyme rise higher
than serum levels of LDH2
u WHITE ’LOOD CELL (W’C) COUNT
Ń An elevated count of 10,000 to 20,000
cells/mm3 appears on the second day following
the MI and lasts up to a week

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u ECG
Ń ST segment elevation, T wave inversion,
abnormal Q wave
Ń Hours to days after the MI, ST and T wave
changes will return to normal but the Q wave
usually remains permanently abnormal

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u DIAGNOSTIC TESTS FOLLOWING ACUTE
STAGE
Ń Exercise tolerance test or stress test: prescribed to
assess for ECG changes and ischemia and to evaluate
for medical therapy or identify clients who may need
invasive therapy
Ń Thallium scans: prescribed to assess for ischemia or
necrotic muscle tissue
Ń MUGA scans: Used to evaluate left ventricular function
Ń Cardiac catheterization: Performed to determine the
extent and location of obstructions of the coronary
arteries

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u ASSESSMENT: PAIN
Ń Crushing substernal pain
Ń May radiate to the jaw, back, and left arm
Ń Occurs without cause, primarily early in the
morning
Ń Is unrelieved by rest or nitroglycerin, and
relieved only by opioids
Ń Lasts 30 minutes or longer

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u ASSESSMENT
Ń Nausea and vomiting
Ń Diaphoresis
Ń Dyspnea
Ń Dysrhythmias
Ń Feelings of fear and anxiety
Ń Pallor, cyanosis, coolness of extremities

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u COMPLICATIONS OF MI
Ń Dysrhythmias
Ń Heart failure
Ń Pulmonary edema
Ń Cardiogenic shock
Ń Thrombophlebitis
Ń Pericarditis
Ń Mitral valve insufficiency

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u COMPLICATIONS OF MI
Ń Postinfarction angina
Ń Ventricular rupture
Ń Dressler¶s syndrome (a combination of
pericarditis, pericardial effusion, and pleural
effusion, which can occur several weeks to
months following an MI)

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u ACUTE STAGE
Ń Obtain a description of the chest discomfort
Ń Assess vital signs
Ń Assess cardiovascular status and maintain
cardiac monitoring
Ń Obtain a 12-lead ECG
Ń Administer nitroglycerin as prescribed
Ń Administer morphine sulfate as prescribed to
relieve chest discomfort that is unresponsive to
nitroglycerin

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u ACUTE STAGE
Ń Administer oxygen at 2 to 4 liters by nasal
cannula as prescribed
Ń Place the client in semi-Fowler¶s position to
enhance comfort and tissue oxygenation
Ń Establish an IV access route
Ń Administer IV nitroglycerin and
antidysrhythmics as prescribed

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u ACUTE STAGE
Ń Monitor thrombolytic therapy, which may be
prescribed within the first 6 hours of the
coronary event
Ń Monitor for signs of bleeding if the client is
receiving thrombolytics
Ń Monitor laboratory values as prescribed
Ń Administer beta-blockers to slow the heart rate
and increase myocardial perfusion, while
reducing the force of myocardial contraction, as
prescribed

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u ACUTE STAGE
Ń Monitor for complications related to the MI
Ń Monitor for cardiac dysrhythmias, since
tachycardia and PVCs frequently occur in the
first few hours after MI
Ń Assess distal peripheral pulses and skin
temperature, since poor cardiac output may be
identified by cool, diaphoretic skin and
diminished or absent pulses

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u ACUTE STAGE
Ń Monitor I&O
Ń Assess respiratory rate and breath sounds for
signs of heart failure, as indicated by the
presence of crackles or wheezes or dependent
edema
Ń Monitor the ’P closely after the administration
of medications; if the ’P is less than 100
systolic or 25 mmHg lower than the previous
reading, lower the head of the bed and notify
the physician
Ń Provide reassurance to the client and family

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u FOLLOWING ACUTE STAGE
Ń Maintain bed rest for the first 24 to 36 hours
Ń Allow the client to stand to void or use a
bedside commode if prescribed
Ń Provide range-of-motion exercises to prevent
thrombus formation and maintain muscle
strength
Ń Progress to dangling at the side of the bed or
out of bed to the chair for 30 minutes three
times a day as prescribed

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u FOLLOWING ACUTE STAGE
Ń Progress to ambulation in the client¶s room and
to the bathroom, then in the hallway, three
times a day
Ń Monitor for complications
Ń Encourage the client to verbalize feelings
regarding the MI
u CARDIAC REHA’ILITATION
Ń Process of actively assisting the client with
cardiac disease to achieve and maintain a vital
and productive life within the limitations of the
heart disease

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u DESCRIPTION
Ń The inability of the heart to maintain adequate
circulation to meet the metabolic needs of the
body, due to an impaired pumping capability
Ń Cardiac output is diminished, and peripheral
tissue is not adequately perfused
Ń Congestion of the lungs and periphery may
occur
 

 


u ACUTE
Ń Occurs suddenly
u CHRONIC
Ń Develops over time; however, a client with
chronic heart failure can develop an acute
episode

 

 

u RIGHT-SIDED/LEFT-SIDED HEART
FAILURE
Ń ’ecause the two ventricles of the heart
represent two separate pumping systems, it is
possible for one to fail alone for a short period
Ń Most heart failure begins with left ventricular
failure and progresses to failure of both
ventricles
Ń Acute pulmonary edema, a medical emergency,
results from left ventricular failure
Ń If pulmonary edema is not treated, death will
occur from suffocation as the client literally
drowns in own fluids

 

 

u FORWARD FAILURE/’ACKWARD FAILURE
Ń In forward failure, an inadequate output of the
affected ventricle causes decreased perfusion
to vital organs
Ń In backward failure, blood backs up behind the
affected ventricle, causing increased pressure
in the atrium behind the affected ventricle

 

 

u LOW OUTPUT/HIGH OUTPUT
Ń In low-output failure, not enough cardiac
output is available to meet the demands of the
body
Ń High-output failure occurs when a condition
causes the heart to work harder to meet the
demands of the body

 

 


u SYSTOLIC FAILURE/DIASTOLIC FAILURE

Ń Systolic failure leads to problems with
contraction and the ejection of blood
Ń Diastolic failure leads to problems with the
heart relaxing and filling with blood
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u Include increased heart rate, improved stroke
volume, arterial vasoconstriction, sodium and
water retention, and myocardial hypertrophy
u Act to restore cardiac output to near normal
levels
u Initially these mechanisms increase cardiac
output; however, they eventually have a
damaging effect on pump action
u Contribute to an increase in myocardial oxygen
consumption and when this occurs, myocardial
reserve is exhausted and clinical manifestations
of heart failure develop
 

 

u ASSESSMENT: RIGHT-SIDED HEART
FAILURE
Ń Signs will be evident in the systemic circulation
Ń Pitting, dependent edema in the feet, legs,
sacrum, back, buttocks
Ń Ascites from portal hypertension
Ń Tenderness of right upper quadrant,
organomegaly
Ń Distended neck veins
 

 

u ASSESSMENT: RIGHT-SIDED HEART
FAILURE
Ń Pulsus alterans (regular alteration of weak and
strong beats noted in the pulse)
Ń Abdominal pain, bloating
Ń Anorexia, nausea
Ń Fatigue
Ń Weight gain
Ń Nocturnal diuresis


 





 


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u ASSESSMENT: LEFT-SIDED HEART
FAILURE
Ń Signs will be evident in the pulmonary system
Ń Cough, which may become productive with
frothy sputum
Ń Dyspnea upon exertion
Ń Orthopnea
Ń Paroxysmal nocturnal dyspnea
Ń Presence of rales or crackles on auscultation
Ń Tachycardia
 

 

u ASSESSMENT: LEFT-SIDED HEART
FAILURE
Ń Pulsus alterans
Ń Fatigue
Ń Pallor
Ń Cyanosis
Ń Confusion and disorientation
Ń Signs of cerebral anoxia

 

 



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u ASSESSMENT: ACUTE PULMONARY EDEMA
Ń Severe dyspnea and orthopnea
Ń Pallor
Ń Tachycardia
Ń Expectoration of large amounts of blood-
tinged, frothy sputum
Ń Wheezing and rales
Ń ’ubbling respirations
 

 

u ASSESSMENT: ACUTE PULMONARY EDEMA
Ń Acute anxiety, apprehension, restlessness
Ń Profuse sweating
Ń Cold, clammy skin
Ń Cyanosis
Ń Nasal flaring
Ń Use of accessory breathing muscles
Ń Tachypnea
Ń Hypocapnia evidenced by muscle cramps,
weakness, dizziness, and paresthesias
 

 

u ACUTE STAGE
Ń Place the client in high-Fowler's position with
the legs in a dependent position to reduce
pulmonary congestion and relieve edema
Ń Administer oxygen in high concentrations by
mask or cannula as prescribed to improve gas
exchange and pulmonary function
Ń Prepare for intubation and ventilator support if
required; monitor lung sounds for rales and
decreased breath sounds
 

 

u ACUTE STAGE
Ń Suction as needed to maintain a patent airway
Ń Assess level of consciousness
Ń Provide reassurance to the client
Ń Monitor vital signs closely noting tachycardia or
pulsus alterans
Ń Monitor for hypotension due to decreased
tissue perfusion, or hypertension due to
anxiety or history of hypertension
 

 


u ACUTE STAGE
Ń Monitor heart rate and dyrhythmias using a
cardiac monitor
Ń Assess for edema in dependent areas and in
the sacral, lumbar, and posterior thigh region in
the client on bed rest
Ń Insert a Foley catheter as prescribed and
monitor urine output closely following
administration of a diuretic
Ń Monitor I&O
 

 

u ACUTE STAGE
Ń Avoid the administration of unnecessary IV
fluids
Ń Administer morphine sulfate as prescribed to
provide sedation and vasodilation, and monitor
for respiratory depression or hypotension after
administration
Ń Administer diuretics as prescribed to reduce
preload, enhance renal excretion of sodium and
water, reduce circulating blood volume, and
reduce pulmonary congestion
 

 

u ACUTE STAGE
Ń Administer digitalis as prescribed to increase
ventricular contractility and improve cardiac
output
Ń Administer bronchodilators as prescribed for
severe bronchospasm or bronchoconstriction
Ń Administer additional inotropic medications
such as dopamine (Intropin) or dobutamine
(Dobutrex) as prescribed to facilitate
myocardial contractility and enhance stroke
volume
 

 


u ACUTE STAGE
Ń Administer vasodilators as prescribed to
reduce afterload, increase the capacity of the
systemic venous bed, and decrease venous
return to the heart
Ń Monitor weight to determine a response to
treatment
Ń Assess for hepatomegaly and ascites and
measure and record abdominal girth
 

 


u ACUTE STAGE
Ń Monitor peripheral pulses
Ń Analyze arterial blood gas results and evaluate
electrolyte values for imbalances
Ń Monitor potassium level closely, which may
decrease due to diuretic therapy, and
administer potassium supplements as
prescribed to prevent digitalis toxicity
 

 


u FOLLOWING ACUTE STAGE

Ń Encourage the client to verbalize feelings about
the lifestyle changes required as a result of the
heart failure
Ń Assist the client to identify precipitating risk
factors of heart failure and methods of
eliminating these risk factors
 

 

u CLIENT EDUCATION
Ń Prescribed medication regimen, which may
include digoxin (Lanoxin), a diuretic, and
vasodilators
Ń Notify the physician if side effects occur from
the medications
Ń Avoid over-the-counter medications
Ń Contact the physician if unable to take
medications due to illness
 

 

u CLIENT EDUCATION
Ń Avoid large amounts of caffeine found in
coffee, tea, cocoa, chocolate, and some
carbonated beverages
Ń Prescribed low-sodium, low-fat, and low-
cholesterol diet
Ń Provide the client with a list of potassium-rich
foods because diuretics will cause hypokalemia
(except for potassium-sparing diuretics)
 

 

u CLIENT EDUCATION
Ń Fluid restriction, if prescribed, advising the
client to spread the fluid out during the day,
and to suck on hard candy to reduce thirst
Ń Space periods of activity and rest
Ń Avoid isometric activities that increase pressure
in the heart
Ń Monitor daily weight and report signs of fluid
retention such as edema or weight gain
u DESCRIPTION
Ń Failure of the heart to pump adequately,
thereby reducing cardiac output and
compromising tissue perfusion
Ń Necrosis of more than 40% of the left ventricle
occurs usually as a result of occlusion of major
coronary vessels
Ń The goal of treatment is to maintain tissue
oxygenation and perfusion and improve the
pumping ability of the heart

|
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u ASSESSMENT
Ń Hypotension: ’P less than 90 mmHg systolic or
30 mmHg less than the client¶s baseline
Ń Urine output of less than 30 ml/hour
Ń Cold, clammy skin
Ń Poor peripheral pulses
Ń Tachycardia, tachypnea
Ń Pulmonary congestion
Ń Disorientation, restlessness, and confusion
Ń Continuing chest discomfort

|
| |
u IMPLEMENTATION
Ń Administer IV morphine sulfate as prescribed to
decrease pulmonary congestion and relieve
pain
Ń Administer oxygen as prescribed
Ń Prepare for intubation and mechanical
ventilation
Ń Administer diuretics and nitrates as prescribed
while monitoring blood pressure constantly

|
| |
u IMPLEMENTATION
Ń Administer vasopressors and positive inotropics
as prescribed to maintain organ perfusion
Ń Prepare the client for insertion of an intraaortic
balloon pump (IA’P), if prescribed, to
facilitate emptying of the left ventricle and
improve cardiac output
Ń Prepare the client for immediate reperfusion
procedures such as PTCA or CA’G

|
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u IMPLEMENTATION
Ń Monitor urinary output
Ń Monitor arterial blood gas levels and prepare to
treat imbalances
Ń Assist with the insertion of Swan-Ganz catheter
to assess heart failure
Ń Monitor distal pulses and maintain the
transducer at the level of the right atrium if the
client has a Swan-Ganz catheter

|
| |