Download Myocardial Infarction

Coronary Artery Disease and
Acute Coronary Syndrome
Myocardial Infarction
(relates to Chapter 33, “Nursing Management: Coronary
Artery Disease and Acute Coronary Syndrome,” in the
textbook)
Description
• Cardiovascular diseases are the major
cause of death in Canada
• Heart attacks are still the leading cause
of all cardiovascular disease deaths and
deaths in general
Etiology and Pathophysiology
Developmental Stages
• Complicated lesion
– Final stage in development
– The most dangerous
– Plaque consists of a core of lipid
materials within an area of dead tissue
Etiology and Pathophysiology
Developmental Stages
• Complicated lesion
– With the incorporation of lipids,
thrombi, damaged tissue, and
accumulation of calcium, the growing
lesion becomes complex
Etiology and Pathophysiology
Collateral Circulation
• Normally some arterial branching,
termed collateral circulation, exists
within the coronary circulation
Etiology and Pathophysiology
Collateral Circulation
• Growth of collateral circulation is
attributed to two factors:
– The inherited predisposition to develop
new vessels
– The presence of chronic ischemia
Etiology and Pathophysiology
Collateral Circulation
• When occlusion of the coronary arteries
occurs slowly over a long period, there is
a greater chance of adequate collateral
circulation developing
Collateral Circulation
Fig. 33-5
Clinical Manifestations of CAD
• Angina Pectoris
• Acute Coronary Syndrome
• Sudden Cardiac Death
Clinical Manifestations
• Stable Angina
– Results when the lack of oxygen supply
is temporary and reversible
Clinical Manifestations
• Acute Coronary Syndrome (ACS)
– Develops when the oxygen supply is
prolonged and not immediately
reversible
Clinical Manifestations
• ACS encompasses:
– Unstable angina
– Non-ST-segment-elevation myocardial
infarction (NSTEMI)
– ST-segment-elevation (STEMI)
Relationships Among CAD, Stable
Angina, and MI
Fig. 33-8
Etiology and Pathophysiology
• Myocardial ischemia:
– O2 demand > O2 supply
• Primary reason for insufficient blood flow
is narrowing of coronary arteries by
atherosclerosis
Etiology and Pathophysiology
• In CAD the coronary arteries are unable
to dilate to meet increased metabolic
needs because they are already
chronically dilated beyond the obstructed
area
Etiology and Pathophysiology
• For ischemia to occur, the artery is
usually 75% or more stenosed
• In addition, the diseased heart has
difficulty increasing the rate of blood
flow
Etiology and Pathophysiology
• Coronary spasm
– The constriction is transient and
reversible
– Causes either subtotal or total
narrowing
Etiology and Pathophysiology
• Myocardial cyanosis occurs within the 1st
10 seconds of coronary occlusion
• ECG changes
• Total occlusion  anaerobic metabolism
and lactic acid accumulation
Etiology and Pathophysiology
• Myocardial Infarction
– Occurs as a result of sustained
ischemia, causing irreversible cellular
death
Etiology and Pathophysiology
• Myocardial Infarction
– The degree of altered function depends
on the area of the heart involved and
the size of the infarct
Etiology and Pathophysiology
• Myocardial Infarction
– Contractile function of the heart stops
in the areas of myocardial necrosis
– Most involve the left ventricle (LV)
Etiology and Pathophysiology
• Myocardial Infarction
– Transmural MI
• Involves the entire thickness of the
myocardium
Transmural MI
Fig. 33-11
Etiology and Pathophysiology
• Myocardial Infarction
– Subendocardial MI
• The damage has not penetrated
through the entire thickness
Etiology and Pathophysiology
• Myocardial Infarction
– Infarctions are described by the area of
occurrence
Etiology and Pathophysiology
Healing Process
• Within 24 hours, leukocytes infiltrate the
area of cell death
• Enzymes are released from the dead
cardiac cells (important indicators of MI)
Etiology and Pathophysiology
Healing Process
• Proteolytic enzymes of neutrophils and
macrophages remove all necrotic tissue
by 2nd or 3rd day
• Development of collateral circulation
improves areas of poor perfusion
Etiology and Pathophysiology
Healing Process
• Necrotic zone identifiable by ECG
changes and nuclear scanning
• 10 to 14 days after MI, scar tissue is still
weak
Etiology and Pathophysiology
Healing Process
• By 6 weeks after MI, scar tissue has
replaced necrotic tissue
– Area is said to be healed
Etiology and Pathophysiology
Healing Process
• Ventricular remodeling
– In an attempt to compensate for the
infarcted muscle, the normal
myocardium will hypertrophy and
dilate
Types of Angina
Silent Ischemia
• Up to 80% of patients with myocardial
ischemia are asymptomatic
• Associated with diabetes mellitus and
hypertension
Types of Angina
Prinzmetal’s Angina
• When spasm occurs:
– Pain
– Marked, transient ST segment
elevation with angina (unlike with
AMI; ↑ST = MI)
– May occur during REM sleep
Clinical Manifestations
Myocardial Infarction
• Pain
– Severe, immobilizing chest pain not
relieved by rest, position change, or
nitrate administration
• The hallmark of an MI
Location of Chest Pain
Fig. 33-12
Clinical Manifestations
Myocardial Infarction
• Nausea and vomiting
– Can result from reflex stimulation of
the vomiting center by the severe pain
Clinical Manifestations
Myocardial Infarction
• Sympathetic nervous system stimulation
–  catecholamines released during initial
phases of MI
– Results in diaphoresis and
vasoconstriction
Clinical Manifestations
Myocardial Infarction
• Fever
– May  within 1st 24 hours up to 100.4°
– May last as long as 1 week
Clinical Manifestations
Myocardial Infarction
• Fever
– Systemic manifestation of the
inflammatory process caused by cell
death
Clinical Manifestations
Myocardial Infarction
• Cardiovascular manifestations
–  BP and heart rate initially
– Later the BP may drop from  CO
Clinical Manifestations
Myocardial Infarction
• Cardiovascular manifestations
–  urine output
– Crackles
– Hepatic engorgement
– Peripheral edema
Complications of Myocardial
Infarction
• Arrhythmias
– Most common complication
– Present in 80% of MI patients
– Most common cause of death in the
prehospital period
Complications of Myocardial
Infarction
• Congestive heart failure
– A complication that occurs when the
pumping power of the heart has
diminished
Complications of Myocardial
Infarction
• Cardiogenic shock
– Occurs when inadequate oxygen and
nutrients are supplied to the tissues
because of severe LV failure
– Requires aggressive management
Complications of Myocardial
Infarction
• Papillary muscle dysfunction
– Causes mitral valve regurgitation
– Condition aggravates an already
compromised LV
Complications of Myocardial
Infarction
• Ventricular aneurysm
– Results when the infarcted myocardial
wall becomes thinned and bulges out
during contraction
Complications of Myocardial
Infarction
• Pericarditis
– An inflammation of the visceral and/or
parietal pericardium
– May result in cardiac compression, 
LV filling and emptying, and cardiac
failure
Complications of Myocardial
Infarction
• Dressler syndrome
– Characterized by pericarditis with
effusion and fever that develops 1 to 4
weeks after MI
Complications of Myocardial
Infarction
• Pulmonary embolism
– Source of the thrombus may be the
roughened endocardium or leg veins
Diagnostic Studies
Myocardial Infarction
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History of pain
Risk factors
Health history
ECG: ST elevation, greater than 1 mm above PR Interval; T Wave
inversion (flipped T Waves); Pathological Q-wave (Q wave greater
than ¼ size of R wave)
Serum cardiac markers:
CK-MB: indicates muscle damage (rises 3-12 hours post AMI –
returns to normal 2-3 days)
Triponen: is a myocardial muscle protein (rises as quickly as CK;
remains elevated for 2 weeks)
Myoglobin: rises 3 hours after AMI; lacks cardiac specificity
Collaborative Care
Angina
• Percutaneous coronary intervention
– Surgical intervention alternative
– Performed with local anesthesia
– Ambulatory 24 hours after the
procedure
Collaborative Care
Angina
• Stent placement
– Used to treat abrupt or threatened
abrupt closure and restenosis following
PCI
Collaborative Care
Angina
• Atherectomy
– The plaque is shaved off using a type of
rotational blade
– Decreases the incidence of abrupt
closure as compared with PCI
Collaborative Care
Angina
• Laser angioplasty
– Performed with a catheter containing
fibers that carry laser energy
– Used to precisely dissolve the blockage
Collaborative Care
Angina
• Myocardial revascularization (CABG)
– Primary surgical treatment for CAD
– Patient with CAD who has failed
medical management or has advanced
disease is considered a candidate
Collaborative Care
Angina
• MIDCABG procedure
– Minimally invasive direct coronary
artery bypass grafting (MIDCABG)
– Alternative to traditional CABG
Collaborative Care
Myocardial Infarction
• Fibrinolytic therapy
• Cardiac catheterization
• Percutaneous coronary intervention
Collaborative Care
Myocardial Infarction
• Drug Therapy
– IV nitroglycerin
– Antiarrhythmic drugs
– Morphine
Collaborative Care
Myocardial Infarction
• Drug Therapy
– -Adrenergic blockers
– Angiotensin-converting enzyme
inhibitors
– Stool softeners
Collaborative Care
Myocardial Infarction
• Nutritional Therapy
– Diet restricted in saturated fats and
cholesterol
– Low sodium
Nursing Management
Angina and Myocardial Infarction
Nursing Implementation: MI
• Acute Intervention
– Morphine
– Continuous ECG
– Frequent vital signs
– Rest and comfort
Nursing Management
Angina and Myocardial Infarction
Nursing Implementation: MI
• Acute Intervention
– Anxiety
– Emotional and behavioral reactions
• Communicate with family
• Provide support
Nursing Management
Angina and Myocardial Infarction
Nursing Implementation: MI
• Ambulatory and Home Care
– Rehabilitation
– Cardiac rehabilitation
– Physical exercise
Nursing Management
Angina and Myocardial Infarction
Nursing Implementation: MI
• Ambulatory and Home Care
– Resumption of sexual activity
• Emotional readiness
• Physical training
Nursing Management
Angina and Myocardial Infarction
Evaluation
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Pain level
Cardiac pump effectiveness
Anxiety control
Energy conservation
Health orientation
Women and
Coronary Artery Disease
• About 500,000 deaths occur in women per
year
• Kills almost 10 times more women than
breast cancer
Women and
Coronary Artery Disease
• Manifest CAD 10 years later in life than
men
• Most have symptoms of angina rather than
MI
Women and
Coronary Artery Disease
• Diabetes mellitus found to be the single most
powerful predictor of CAD in women