course is designed to give an overview of the care and management
of the patient who has suffered an acute myocardial infraction (MI).
Focus will be placed on the pathophysiologic changes that occur during
an acute MI as well as differentiating the different types of
myocardial infarction (based on location). The prevalence, risk
factors, signs/symptoms and diagnosis of an acute MI will also be
presented. Potential complications associated with an acute MI
(including cardiogenic shock) as well as medical/pharmaceutical
interventions will be presented. Nursing care and management with NANDA
nursing diagnoses to include defining characteristics, nursing
interventions and patient/family education will also be presented.
Appropriate cardiac rehabilitation interventions will be the final
focus of this course. Course
completion of this course the student will be able to:
Understand and define
the pathophysiologic changes seen with an acute MI
different types of MI based on location of
Discuss the prevalence
associated with an acute MI
State the risk factors
associated with an acute MI
Explain the necessary
assessment/tests to diagnose an acute MI
Discuss the potential
complications associated with having an acute MI
management for the patient who has suffered and acute
List 3 appropriate
nursing diagnoses for managing the patient with and
Discuss the nursing
interventions appropriate for caring for the
patient who has suffered and acute MI (alteration in cardiac output,
pain, anxiety and ineffective coping)
Explain the important
aspects of patient education post MI
Describe the important
aspects of cardiac rehabilitation
Myocardial Infarction: An
acute MI occurs when myocardial cells have reached the threshold of
ischemia; which in turn cause the body’s myocardial cell
repair mechanism to first become overwhelmed and second to completely
fail. When this mechanism fails, myocardial tissue necrosis causing
irreparable tissue/cell death occurs. The
following are possible contributors to myocardial ischemia and
ultimately myocardial infarction (tissue necrosis and cell death):
metabolic demand which include:
Extremes in physical
Severe aortic stenosis
Other cardiac valvular
Low cardiac output
states associated with a decrease in aortic
Decreased delivery of
oxygen and nutrients to the myocardium (via the
An interruption in the
delivery of oxygen and nutrients to the
myocardium from a thrombus (that usually attaches itself to plaque).
A high grade (usually
> 75%) fixed coronary artery stenosis do
The most frequent cause
of an acute MI is a disruption in the vascular
endothelium that is associated with myocardial plaque (plaque occurs
over a period or years or decades). This combination causes the
development of an intra-coronary thrombus, which causes the coronary
artery affected to occlude. Within 20 to 40 minutes of an occlusion;
irreversible myocardial cell damage/death occurs.
The two primary
characteristics of plaque development are (1) a
fibromuscular cap and (2) an underlying lipid rich core. Plaque erosion
is thought to occur when there is a release of collagen and proteases
(within the plaque) which results in thinning of the overlying
fibromuscular cap. The action/release of proteases within the plaque
combined with hemodynamic pressure applied to the arterial segment,
causes continued disruption of the endothelium which leads not only to
continued thinning of the fibromuscular cap, but to actual cap rupture
(causing plaque erosion and/or ulceration).
The overall loss of
structural stability of the plaque usually occurs
at the junction between the fibromuscular cap and the vessel wall
(which is called the “shoulder region”). When this
occurs, a thrombus develops (due to the platelet-mediated activation of
the coagulation cascade), and partial or complete occlusion occurs
causing an acute myocardial infarction.
The severity of an
acute MI depends on the level of occlusion in the
coronary artery, the length of time of the occlusion and the patients
own collateral circulation. Myocardial cell death first occurs in the
portion of the artery that is most distal to arterial blood flow and as
the occlusion increases the damage spreads from the myocardium to the
endocardium and eventually to the epicardium. After cell death has
reached the epicardium, the tissue/cell death then moves laterally to
the areas of collateral perfusion.
Types of Acute MI (Based on Location): The
location of an acute MI is dependant on the coronary artery that
has been affected and what portion of the heart that artery feeds. The
following table describes the affected artery, a description of the
major areas and structures that supply blood to the area and the
primary infarction area.
and Structures Supplied
Area of Infarction
and AV nodes.
Bundle of HIS.
Left ventricle (inferior and diaphragmatic regions).
Posterior/Inferior portion of the Left bundle branch.
Inferior wall MI (leads II, III and AVF).
Inferoposterior wall MI.
Right ventricular MI.
major portion of the left ventricular region of the heart.
Anterior Descending Artery
Anterior wall of the left ventricle.
Anterior two thirds of the septum.
Bundle of HIS.
Right bundle branch.
Anterosuperior portion of the left bundle branch.
Posteroinferior portion of the left bundle branch.
Anterior wall MI (Leads V1 through V6).
Anterolateral wall MI.
Inferoapical wall MI.
Apex (region) MI.
and AV nodes.
Inferior and diaphragmatic surface of the left ventricle.
Lateral wall of the left ventricle.
Posteroinferior portion of the left bundle branch.
Lateral wall MI (leads I aV1, V5 and V6).
Inferolateral wall MI.
Posterior wall MI (leads V1 and V2).
Inferoposterior wall MI.
An ST-segment elevation myocardial infarction (STEMI) can occur
when there is a “complete” blockage of any
artery(s). This type of MI is characterized by an upward shift in a
portion of the ST segment (seen on EKG). With this type of myocardial
infarction, quick interventions to reopen the occluded vessel or
vessels are imperative. The longer the myocardium goes without
oxygenated blood, the greater the damage. Prevalence:
is the leading cause of death in the United
States and is the most common cause of death in the industrial world as
The good news is that
the survival rate for patients who seek medical
treatment for an acute MI is up to 90% to 95%. This improvement in
survival is thought to be related to improved EMS responses and
With approximately 50%
of all acute MI’s in the United States
occurring to people under the age of 65; this disease is no longer
thought to be a “disease for the elderly” (as the
baby boomers age, this percentage is thought to again switch back to
show more people over the age of 65 with acute MI’s).
The actual incident of
suffering an acute MI depends on the number of
pre-disposing factors for atherosclerosis.
are six primary risk factors for developing
atherosclerosis/coronary artery disease and acute myocardial
infarction. The presence of any risk factor is thought to double the
relative risk for developing atherosclerosis/coronary artery disease
and acute myocardial infarction. These
risk factors include:
High Blood Cholesterol
(Hyperlipidemia) – An elevated
”total” cholesterol level is major component of
atherosclerotic plaque build up which causes the development of an
– Patients with DM have a substantially
greater risk of developing atherosclerotic vascular disease at an
accelerated rate. This acceleration occurs regardless of whether the
patient has insulin dependant or non insulin dependant diabetes.
– High blood pressure (squeezing of arteries and
veins) has consistently been associated with an increased risk of
developing an acute MI (both systolic and diastolic elevations).
Tobacco contains certain components that are known
to damage vessel walls. The body’s response to this damage
elicits the formation of atherosclerosis thereby increasing the risk of
an acute MI.
– The incidence of developing an acute MI is
greater for men than women however; with age this risk narrows.
– A family history of premature coronary
disease increases and individuals risk of developing atherosclerosis
and acute MI. Family history includes both genetic components and
learned behaviors (i.e. smoking and high fat diets).
an acute MI can either be a very straight forward process or
it can be a difficult process. The straight forward diagnosis usually
couples the patient’s risk factors with the presentation of
current symptoms (and past medical history). Once a diagnosis of acute
MI is suspected, the following confirmatory tests should be ordered: Electrocardiogram
(ECG) – Based on
electrical changes in the
coronary system during an acute MI; an ECG is the first test that
should be run. Laboratory Tests
– Because heart cells have specific enzymes
and proteins that are released when cell death occurs, drawing blood
levels to check for the presence and degree of these enzymes will
assist in diagnosing an acute MI. The following provides a description
of the major enzymes that are thought to assist with the diagnosis of
an acute MI.
Creatine Kinase (CK or
CPK) – Released from damaged muscle,
CK is an enzyme found in the heart, skeletal muscle and brain. It
consists of 3 isoenzymes; mm (found in skeletal muscle, MB (found in
cardiac muscle) and BB (found in brain tissue). Damage to any of these
tissues causes the release of CK into the blood stream and hence an
CKMB – After
cardiac injury, CK and the isoenzyme MB are
released into the blood stream at a predictable rate. Within a 4 to 8
hour window (post injury) the CKMB level rises above normal and within
12 to 24 hours this level elevates to approximately 5 to 15 times
normal. Within 2 to 3 days the CKMB returns to normal. Because the MB
isoenzyme is exclusive to cardiac muscle tissue, it is considered to be
a very definitive test for diagnosing an acute MI.
Troponin is a protein that helps regulate heart
muscle contraction and because it can be isolated in the blood, it is
considered to be a sensitive indicator of an acute MI. Troponin
consists of 3 separate proteins which are Troponin I, Troponin T and
Troponin C. The function of each of these specific proteins is as
Troponin I and T
– these levels are not normally found in the
blood stream so any detection of these protein in the blood indicates
the infarction or death of cardiac muscle/tissue.
Troponin C binds to
calcium ions and is not used to determine cell
Cardiac Enzyme Normal
– 80 U/L
Creatinine Phosphokinase (CPK)
(Fraction with percent of total CPK).
0 - 4 %
than 1 U/L
– 0.4 ng/ml
– 0.1 ng/ml
– An echocardiogram can assist with diagnosing
which portion of the heart has been damaged and which coronary arteries
have been affected. An echocardiogram can also help determine cardiac
muscle movement/contraction and cardiac wall abnormalities. Potential
Complications Associated with an Acute MI: Dysrhythmias
– A dysrhythmia is the most common complication
after an acute MI. Dysrhythmias after an acute MI are caused by the
formation of re-entry circuits between the still healthy and necrotic
myocardium. The following table describes the percentage of time
specific dysrhythmias occur post acute MI.
Percentage of time present
post acute MI
2% - 4%
Supraventricular (thought to
produce worse outcomes than ventricular dysrhythmias)
AV block and sinus brady).
20% of patients with acute
The incidence of clinical significant systemic embolism post acute MI
is less than 2% (this percentage increases in patients who have
suffered and acute anterior wall MI). Mural thrombus formation is
however more prevalent post acute MI with numbers ranging in the 20%
range and increasing as high as 60% in patients with large anterior
wall MI’s (development of emboli comes from myocardial wall
motion deficits or atrial fibrillation). The most common time post
acute MI for the development of embolism is within the first 10 days.
Patients who suffer from the complication of embolism are at risk of
developing limb ischemia, renal infarction, intestinal ischemia but the
most common clinical presentation after an embolic event is a stroke. Pericarditis
– The incidence of early Pericarditis after and acute MI is
approximately 10% with inflammation developing within the first 24 to
96 hours after MI. Late Pericarditis occurs in 1% to 3% of post acute
MI patients between weeks 1 and 8 (after MI). The cause of Pericarditis
after acute MI is due to an inflammatory reaction that occurs secondary
to the presence of necrotic tissue (acute Pericarditis occurs most
often in patients who have suffered a transmural MI). Cardiogenic Shock
(secondary to acute MI)
– Simply stated; cardiogenic shock occurs when the bodies
needs for oxygen are not met for a prolonged period of time. When this
occurs; the body attempts to compensate for the decreased oxygen supply
by increasing heart rate, stroke volume and contractility.
Unfortunately as this continues, the workload of the heart becomes too
much and the result; total cardiac decompensation begins. When
decompensation begins the patient shows signs of shock, low blood
pressure, increased or decreased heart rate and decreased oxygen
saturations. Other symptoms mimic those that are seen with congestive
heart failure and/or pulmonary edema. This condition is critical and
must be addressed emergently. In addition to other medical and
pharmaceutical therapies; patients in cardiogenic shock are often
helped with the addition of a balloon pump (IABP). The major advantage
of a balloon pump during cardiogenic shock is the decrease in
myocardial oxygen demand by decreasing myocardial workload, and the
increase in coronary artery perfusion. Medical/Interventional
Management: PTCA –
A percutaneous transmural coronary angioplasty (PTCA) is an effective
revascularization procedure that is used to increase the diameter of an
artery that has been stenosed due to coronary artery disease. With the
use of fluoroscopy, a cardiologist can insert a catheter (through the
femoral artery) and guide it through the arterial circulation through
the ascending aorta and into the ostium of the right or left coronary
artery. A balloon tipped catheter is then passed into the area of
blockage and inflated (no more than 30 to 129 seconds) which in turns
helps to compress plaque against the lumina of the artery. The balloon
can also help to stretch the lumina itself which also improves blood
flow. Of note: when the balloon is inflated, there is an occlusion of
coronary blood supply, so patients often experience a degree of chest
pain during balloon inflation. The degree of chest pain experienced and
the difficulty in compression plaque may require that the physician
inflate and deflate the balloon several times during the procedure. The
following is a list of patients who are thought to be good candidates
for percutaneous transmural coronary angioplasty:
Patients with acute,
chronic or unstable angina.
Patients with an acute
MI or post acute MI.
Patients with angina
post coronary artery bypass grafting (CABG).
Patients with single of
double vessel disease.
Patients with at least
50% vessel stenosis.
Patients with a
blockage that is concentric and located away from bifurcations.
Patients who are
thought to be good candidates for the survival of emergency cardiac
surgery (if there are procedural complications).
PTCA is contraindicated in patients with left main coronary artery
disease (especially those who are thought to be poor surgical
of PTCA include the following: Acute
coronary occlusion (requiring emergent surgical intervention).
Dissection of the
Allergic reaction to
The development of
bleeding or a hematoma at the femoral insertion site (or
Decrease in circulation
below the femoral insertion site (diminished or absent pulses).
(when sheath is removed).
The development of a
pseudo aneurysm of the artery.
occlusion of the artery with in 6 months.
A blood clot breaking
away and causing a stroke (or other embolic event).
for PTCA include:
A bleeding disorder
(anti-coagulation should be stopped prior to procedure).
“stent” placement) –
In addition to using angioplasty as an intervention for compressing
plaque and stretching the lumina of the artery; the procedure can also
be used to place a stent into the artery. A stent is a small stainless
steel tube that can be attached to the end of the balloon tipped
catheter and placed into the artery immediately after PTCA in an
attempt to more permanently prevent re-occlusion of the artery. For
patients who have undergone PTCA and suffered an arterial re-occlusion;
the placement of a stent is an alternative (benefit has been shown for
patient who suffer re-narrowing or re-occlusion). Laser Angioplasty
– Laser angioplasty
is a technique that can be used to open coronary arteries that are
blocked by plaque. With this procedure, the catheter that is inserted
has a small laser at the tip. When the catheter is in place; the laser
emits small pulsating beams of light that vaporize the plaque that is
blocking the artery. This procedure can be used alone or in conjunction
with balloon angioplasty. Pharmaceutical
Treatment Options: Morphine
– Because catecholamines are released in response to the
anxiety and pain associated with suffering an acute MI (increasing the
workload of the heart), Morphine can be used. Morphine is also
beneficial in reducing the hemodynamic workload by increasing venous
capacitance and reducing systemic vascular resistance (therefore
decreasing myocardial oxygen demand). Nitroglycerin
– Nitrates such as Nitroglycerin cause vasodilation of the
vessels and help to decrease cardiac oxygen demand, cardiac preload and
afterload while increasing cardiac output. Aspirin –
Antiplatelet therapy (specifically aspirin) is now a standard therapy
for the treatment of angina and acute MI. The primary mechanism is
believed to be related to irreversible inhibition of the cyclooxygenase
pathway of platelets (blocking the formation of thromboxane A2 and
thromboxane A2-induced platelet aggregation). It is strongly
recommended that all patients who have suffered and acute MI be given a
non-enteric coated aspirin (160mg to 325mg) to chew and swallow as soon
as possible. Anticoagulants
(ReoPro) – ReoPro
is a platelet glycoprotein II/b/IIIa receptor inhibitor that has been
proven to be effective for the management of any coronary ischemic
syndrome. It is starting during a PTCA procedure and in most cases is
used as an adjunct for stent placement. ReoPro is given as an IV bolus
of 0.25 mg/kg and followed by a continuous infusion rate of 10 mcg/min
for the following 12 hours. The use of ReoPro is thought to reduce
platelet aggregation by approximately 80%. Anticoagulants
(Ticlid) – Ticlid
is given in 250 mg doses BID and is also an Antiplatelet agent. Unlike
aspirin, Ticlid does not block cyclooxygenase but instead interferes
with the platelet “activation” mechanism that is
mediated by adenosine diphosphate (ADP) which in turn interferes with
the fibrinogen receptor glycoprotein IIb/IIIa. It takes approximately 2
weeks of therapy with Ticlid before the full benefit is achieved. Heparin
– Heparin is an anticoagulant that inhibits activated factors
IS, S, SI and XII (which are all involved in the conversion of
Prothrombin to thrombin). By inhibiting these activated factors,
Heparin is thought to keep the blood thinner and prevents clotting.
This is turns allows for easier blood travel through the vessels that
are affected by narrowing and atherosclerosis. Beta Blockers
– A beta blocker acts by blocking the B-adrenergic responses
to catecholamine stimulation. Beta blockers decrease heart rate, blood
pressure, contractility and myocardial oxygen demand. Being able to
decrease the work load of the heart assists with improving cardiac
output and lessens the severity of the damage caused by the acute MI.
Beta blockers can actually interrupt an evolving MI, limit the infarct
size and decrease the risk of ventricular arrhythmias by decreasing
oxygen demand. Calcium Channel
Blockers – Calcium
channel blockers prohibit the entry of calcium into smooth muscle. This
assists with dilating coronary arteries and veins which in turn
provides an increase in overall cardiac blood flow. Calcium channel
blockers also decrease systemic blood pressure, total peripheral
resistance and cardiac afterload. ACE inhibitors
– An Angiotensin converting enzyme; ACE inhibitors block to
the conversion of Angiotensin I to Angiotensin II (which is a potent
vasoconstrictor). The goal of and ACE inhibitor is to decrease blood
pressure and afterload without increasing heart rate or the workload of
the heart. tPA (Ateplase)
– tPA is a human protein that is manufactured by genetic
engineering. Tissue plasminogen activator is one of several drugs not
approved for use in certain patients who are suffering from and acute
MI. tPA is designed to dissolve the blood clots (in the arteries) that
are responsible for causing the majority of acute MI’s. tPA
is given in an initial 15 mg IV bolus then 0.75 mg/kg (maximum of 50
mg) over 30 minutes. This is then followed by 0.5 mg/kg (maximum 35 mg)
over 60 minutes for a total of 100 mg over 90 minutes. Signs of
reperfusion include pain relief; reperfusion arrhythmias (accelerated
idioventricular rhythm, ventricular ectopy and bradycardia). Contraindications
for the use of tPA:
Active internal bleeding
or recent brain surgery
Allergy to streptokinase
Recent trauma or
surgery (within the past 2 weeks)
A history of
hemorrhagic or non-hemorrhagic stroke
– Dopamine has both a and b-adrenergic effects (as well as
dopaminergic effects). At low doses (2-5 mcg/kg/min) it increases renal
and mesenteric blood flow. At moderate doses (5-10 mcg/kg/min) it has a
positive inotrope affect which increases blood pressure and cardiac
output. At larger doses (10-20 mcg/kg/min) it exhibits a pure alpha
stimulation which causes peripheral vasoconstriction with both
increased systemic vascular resistance (SVR) and afterload. Dobutamine
– Dobutamine stimulates B-receptors of the heart and provide
a direct acting positive inotrope effect. Dobutamine increases stroke
volume and cardiac output by increasing cardiac contractility while
decreasing SVR. By increasing contractility and cardiac output; there
is more oxygen rich blood available for damaged tissue. Nursing
Care/Management and Patient Education (Based on NANDA diagnosis): Decreased
Cardiac Output: Definition
– Inadequate blood pumped by the heart to meet the metabolic
demands of the body. Defining
(crackles at the lung bases, cough, orthopnea/nocturnal dyspnea,
cardiac output less than 4 liters/min, cardiac index less that 2.5
liters/min, decreased stroke volume, decreased left ventricular stroke
work index (LVSWI), S3 or S4 heart sounds present).
(anxiety or restlessness).
Monitor for symptoms of
heart failure/decreased cardiac output (VS, heart sounds, and S3
Observe for symptoms of
cardiogenic shock (cool clammy skin, hypotension, decreased peripheral
pulses, and pulmonary congestion).
If shock present,
monitor hemodynamic parameters for increased PAWP and increased
systemic vascular resistance.
Titrate inotropic and
vasoactive medication within defined parameters to maintain adequate
contractility, pre/afterload and blood pressure.
For complaints of chest
pain, medicate and note severity, location, radiation, what were
contributing factors (getting up, participating in ADL’s for
example) and report findings.
Monitor intake and
output (IV fluid, urine output, PO intake (fluid overload increases the
workload of the heart and decreased cardiac output can cause a decrease
in perfusion to the kidneys).
Note results of
diagnostic imaging studies (EKG, radionuclide imaging, and Dobutamine
Watch laboratory data
closely (ABG’s, serial enzymes, electrolytes, B-type
natriuretic peptide, serum creatinine).
saturation and provide O2 as ordered and necessary.
pressure/pulse before and after the administration of cardiac
HOB should be at 30
degrees to decrease the work of breathing and decrease preload.
Provide a proper
rest/activity balance to assure that cardiac output is not compromised
(gradually increase activity as condition warrants).
Order small sodium
restricted diet (sodium restriction helps to avoid fluid overload).
Monitor bowel function
(a stool softener should be ordered to avoid unnecessary pushing).
Provide a peaceful
environment that minimizes stressors to promote healing.
Weigh patient daily
(same time each day, same equipment).
Assess for the presence
of anxiety (keep environment free of unnecessary stressors, educate
patient to the rationale for interventions and procedures).
Assess for the presence
of depression (depression is common after and acute MI and can result
in increased mortality).
Refer patient to
cardiac outpatient program and support groups. Assist with organizing
cardiac rehabilitation efforts post discharge.