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Acute Coronary Syndrome (ACS) - 4 Nursing CEs
Acute Coronary Syndrome (ACS) - 4 Nursing CEs
Author: Kristi Hudson RN, MSN CCRN

Course Description
This 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 Objectives
Upon completion of this course the student will be able to:
  • Understand and define the pathophysiologic changes seen with an acute MI
  • Differentiate the different types of MI based on location of ischemia/infarct
  • 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
  • Describe medical management for the patient who has suffered and acute MI
  • List 3 appropriate nursing diagnoses for managing the patient with and acute MI
  • 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
Defining 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):
  • Increased myocardial metabolic demand which include:
  1. Extremes in physical exertion
  2. Severe hypertension
  3. Obstructive Cardiomyopathy
  4. Severe aortic stenosis
  5. Other cardiac valvular disorders
  6. Low cardiac output states associated with a decrease in aortic diastolic pressure
  • Decreased delivery of oxygen and nutrients to the myocardium (via the coronary circulation).
  • 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 to atherosclerosis.
  • 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.
Different 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.


Coronary Artery

Area and Structures Supplied

Primary Area of Infarction

Right Coronary Artery

1. SA and AV nodes.

2. Bundle of HIS.

3. Right atrium/ventricle.

4. Left ventricle (inferior and diaphragmatic regions).

5. Septum (1/3rd).

6. Posterior/Inferior portion of the Left bundle branch.

1. Inferior wall MI (leads II, III and AVF).

2. Inferoposterior wall MI.

3. Right ventricular MI.


Left Coronary Artery

1. The major portion of the left ventricular region of the heart.

Left ventricular MI.

Left Anterior Descending Artery

1. Anterior wall of the left ventricle.

2. Anterior two thirds of the septum.

3. Bundle of HIS.

4. Right bundle branch.

5. Anterosuperior portion of the left bundle branch.

6. Posteroinferior portion of the left bundle branch.

1. Anterior wall MI (Leads V1 through V6).

2. Septal MI.

3. Anterolateral wall MI.

4. Inferoapical wall MI.

5. Apex (region) MI.

Left Circumflex Artery

1. SA and AV nodes.

2. Inferior and diaphragmatic surface of the left ventricle.

3. Lateral wall of the left ventricle.

4. Left atrium.

5. Posteroinferior portion of the left bundle branch.

1. Lateral wall MI (leads I aV1, V5 and V6).

2. Inferolateral wall MI.

3. Posterior wall MI (leads V1 and V2).

4. Inferoposterior wall MI.

Note: 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.
  • Myocardial infarction is the leading cause of death in the United States and is the most common cause of death in the industrial world as well.
  • 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 treatment strategies.
  • 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.
Risk Factors/Causes:
There 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 acute MI.
  • Diabetes Mellitus – 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.
  • Hypertension – 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).
  • Smoking – 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. 
  • Male Gendered – The incidence of developing an acute MI is greater for men than women however; with age this risk narrows.
  • Family History – 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).
Diagnosing 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 elevated level.
  • 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 – 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 follows:
  • 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 tissue/death.

Cardiac Enzyme Normal Values


Normal Value

Creatine Kinase

50 – 80 U/L

Total Creatinine Phosphokinase (CPK)

30 - 200 U/L

CPK MB (Fraction)

0 - 8.8 ng/ml

CPK MB (Fraction with percent of total CPK).

0 - 4 %

CPK MB2 (Fraction)

Less than 1 U/L

Troponin 1

0 – 0.4 ng/ml

Troponin T

0 – 0.1 ng/ml


Echocardiogram – 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

Premature Ventricular Contraction


Ventricular Fibrillation

2% - 4%

Supraventricular (thought to produce worse outcomes than ventricular dysrhythmias)

< 10%

Bradyarrhythmias (including AV block and sinus brady).

20% of patients with acute RV infarction

Embolic Complications – 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).
Note: PTCA is contraindicated in patients with left main coronary artery disease (especially those who are thought to be poor surgical candidates).
Complications of PTCA include the following:
Acute coronary occlusion (requiring emergent surgical intervention).
  • Dissection of the artery.
  • Allergic reaction to contrast.
  • The development of bleeding or a hematoma at the femoral insertion site (or retroperitoneal bleeding).
  • Decrease in circulation below the femoral insertion site (diminished or absent pulses).
  • Vasovagal reaction (when sheath is removed).
  • The development of a pseudo aneurysm of the artery.
  • Re-stenosis or occlusion of the artery with in 6 months.
  • A blood clot breaking away and causing a stroke (or other embolic event).
Contraindications for PTCA include:
  • A bleeding disorder (anti-coagulation should be stopped prior to procedure).
  • Renal insufficiency
  • Severe uncontrolled hypertension
  • Severe peripheral vascular disease
  • Untreated active infections
  • Severe anemia
  • Uncorrected electrolyte imbalances
  • Endocarditis
PTCA (with “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
  • Intracranial neoplasm or recent brain surgery
  • Prolonged traumatic cardiopulmonary resuscitation
  • Allergy to streptokinase
  • Recent trauma or surgery (within the past 2 weeks)
  • Pregnancy
  • A history of hemorrhagic or non-hemorrhagic stroke
Dopamine – 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 Characteristics:
  • Dysrhythmias (tachycardia, bradycardia, electrocardiographic changes).
  • Altered Preload (jugular vein distention, fatigue, edema, increased/decreased central venous pressure (CVP), increased/decreased pulmonary artery wedge pressure (PAWP).
  • Altered Afterload (cool clammy skin, shortness of breath/dyspnea, oliguria, prolonged capillary refill, decreased peripheral pulses)
  • Altered Contractility (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).
  • Behavioral/Emotional (anxiety or restlessness).
Nursing Interventions:
  • Monitor for symptoms of heart failure/decreased cardiac output (VS, heart sounds, and S3 gallop).
  • 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 stress tests).
  • Watch laboratory data closely (ABG’s, serial enzymes, electrolytes, B-type natriuretic peptide, serum creatinine).
  • Monitor oxygen saturation and provide O2 as ordered and necessary.
  • Monitor blood pressure/pulse before and after the administration of cardiac medications.
  • 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.

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