Coronary heart disease (CHD) is the leading cause of death in the United States.^1,2 Almost 16 million Americans suffer from some form of CHD; almost half of these persons have experienced a myocardial infarction (MI).^1,2 Forty percent of people experiencing an MI this year will die,^1,2 most within the first hour after the symptoms begin (from ventricular fibrillation) and before the patient arrives at the ED.³ Patients who have a subsequent MI are four to six times more likely to die from sudden cardiac death than the population-at-large.¹

Acute Coronary Syndrome (ACS) is the term used to denote patients experiencing myocardial ischemia ranging from unstable angina to an acute MI. Acute MI is further divided into MIs that present with either ST-segment elevation (STEMI) or non-ST segment elevation (non-STEMI).⁴ According to the American Heart Association (AHA) Statistics Committee and Stroke Statistics Committee, 21% of patients with ACS will suffer STEMI.² Elevation of the ST-segment indicates injury to all three layers of the myocardial wall (aka a transmural MI) and, as such, presents a higher morbidity and mortality rate than non-STEMIs.⁴ Nurses in virtually every setting encounter people with CHD who are at risk for experiencing acute coronary artery occlusion. Victims of MI require rapid institution of appropriate diagnostic and treatment measures. The immediate goals of treatment are to provide pain relief, decrease myocardial oxygen demand, and enhance oxygen delivery to reduce the ischemia, thus limiting myocardial damage and extension of the infarct area, and stabilize cardiac function.⁵

Susan Martin, a 66-year-old retired schoolteacher, is admitted to the critical care unit following an acute inferior wall STEMI; physician’s orders included 150 mL per hour of IV fluid and a continuous inotropic infusion. Raymond Thomas, a 58-year-old computer operator, is in the next room having been admitted for an acute anterior wall STEMI. Yet his orders are radically different from Ms. Martin’s. Mr .Thomas is receiving IV fluids at a keep open rate, a diuretic, and a continuous infusion of inotropic and vasodilating agents. As you initiate the prescribed therapeutic measures, you wonder why the treatment strategies differ. After all, these patients both have an STEMI, don’t they?

The care we offer these two types of patients is based on the extent of damage to the heart muscle and the area of the heart affected by the ischemic process. To better understand why the treatment plans differ, we begin with a review of the coronary artery blood flow.

Coronary artery anatomy

The left and right coronary arteries originate from the base of the ascending aorta and are distributed over the epicardial surface of the heart. Their primary function is to provide oxygen and nutrients to the myocardium and to the electrical conducting structures located throughout the atria and ventricles.

The left main coronary artery divides into the left anterior descending (LAD) and the circumflex (CX) branches. Descending toward the apex of the heart, the LAD nourishes the anterior and inferioapical walls of the left ventricle, two-thirds of the interventricular septum, the papillary muscle, the Bundle of His, and the left and right bundle branches. Located between the left atrium and ventricle, the CX branch traverses posteriorly to supply the lateral and posterior myocardial surfaces.

At the right atrioventricular groove, the right coronary artery (RCA) divides into several branches supplying the sinoatrial (SA) node (in 55% of the population) and the atrioventricular (AV) node (in 90% of the population), the Bundle of His, the right ventricle, and the remaining inferior and posterior segments of the left ventricular muscle and conducting structures.

The three Is — ischemia, injury, infarction

Once we’ve visualized the blood supply to the heart muscle, we can better understand the mechanics when one of these vital vessels becomes blocked by a coronary atherothrombus or coronary vasospasm. Temporary interruption of blood supply by a partial occlusive thrombus will cause ischemia — from a decrease in oxygen delivery — which generally does not cause cell death. Reperfusion of the occluded vessel(s) within 20 minutes (if no collateral circulation is established) will replenish oxygen to the starved myocardial cells and reverse the ischemia.⁶

Prolonged loss of blood supply will result in tissue injury. Reperfusion of the injured myocytes may lead to a phenomenon of delayed ventricular recovery labeled myocardial stunning or a prolonged dysfunction of the myocardium named myocardial hibernation.⁷ Myocardial tissue necrosis, or infarction, occurs with prolonged vessel occlusion of as little as six minutes or as long as several hours. Within six to eight hours, irreversible damage to the cardiac myocytes will occur. Complete obstruction of a coronary artery occurs in almost 90% of myocardial infarctions.³

The extent of infarction depends on the area of muscle normally supplied by the obstructed coronary artery, the presence of collateral blood flow, and the oxygen demands of the tissues supplied by the artery. The wave of necrosis begins at the subendocardium, because there is little collateral blood flow, and advances through the ventricular wall.⁸ Necrotic tissue is replaced with nonfunctional, fibrotic scar tissue.⁹ On the ECG, myocardial ischemia, injury, and infarction alter normal depolarization and repolarization, which are reflected in the appearance of the QRS complex, ST segment, and/or T wave in leads corresponding to the affected area. These changes are classically depicted as symmetrical T wave inversion and ST segment depression with ischemia;⁶ ST segment elevation with injury; and abnormally wide and/or deep Q waves, which represent myocardial tissue death. However, not all acute MIs develop Q-wave changes (non-Q wave infarction) or have ST-segment elevation (non-ST elevation MI), and not all ECG wave changes are indicative of MI.^3,10,11 This realization has led to a new system of classifying all MIs as “Q-wave” or “non-Q-wave” contingent on their final morphology. The patient’s age, gender, and clinical condition need to be considered when interpreting the ECG. For example, T-wave inversions in leads V1 to V3 are more likely to represent a normal variant in a healthy young adult woman than in an elderly man with chest discomfort.¹¹ Nonspecific ECG abnormalities are also a possibility.³ Abnormal Q waves in the presence of a normal baseline ST segment suggest an old infarction.

Clinical presentation and associated pathophysiology

The differential diagnosis of MI is facilitated by considering a variety of evidence sources: the patient’s history and physical assessment findings, the results of the electrocardiogram (ECG), and the results of laboratory testing specific for cardiac damage (i.e., cardiac biomarkers such as troponin and CK-MB bands). The information gleaned from the patient history and physical examination will assist the advanced practice nurse (APN) to determine the next steps of which laboratory and diagnostic tests to be ordered. The chief complaint, history, and physical exam findings are key pieces of information used to aid in the diagnosis of acute MI. Chest pain is the hallmark of MI and the symptom most people recognize as indicative of MI.^2,12 Though the location, character, intensity, quality, and duration of the pain reported help in the general diagnosis of MI, these specifics do no assist in diagnosing the location of the MI. Even a thorough history that establishes a patient’s risk factors, such as male gender, and the presence of hypertension, hypercholesterolemia, low high-density lipoprotein, cigarette smoking, and/or diabetes, does not differentiate infarction location.

Though there are cardinal symptoms of ischemic heart disease, no physical assessment findings are considered pathognomonic for MI.^3,5,13 Complaints of chest pain and/or any of the common associated symptoms, such as nausea, diaphoresis, shortness of breath, weakness, or syncope, could be indicators of a variety of other cardiac and noncardiac disease states and are therefore not helpful differentiators when making the diagnosis of either a right or left ventricular infarction. In fact, many people do not even realize they are having (or have had) an MI: In the US, approximately 20% or 175,000 MIs per year are “silent” or present atypically, thus hindering diagnosis.^2,3 Up to one half of diabetic patients and the elderly may suffer silent MIs.³

Not all people experiencing an MI present with classic signs or symptoms; gender and age may play a role in the type of symptoms that are reported.^14,15,16 Though the studies are inconsistent, compared to men, chest pain is often not the chief complaint of women experiencing an MI. Instead, women tend to report shortness of breath; nausea and vomiting; pain in the back, jaw, and neck; cough; and fatigue.¹⁴ Women with atypical thoracic pain symptoms should be thoroughly assessed.¹⁵ Elderly patients experiencing an MI are also more likely to present a diagnostic challenge to APNs. Elders report atypical symptoms, tend to wait longer to seek treatment, have multiple comorbidities, and suffer a higher complication rate than younger patients.¹⁶ Knowing that women and older patients commonly have atypical clinical presentations during acute MI is extremely important information for the APN that should heighten awareness and lead to increased vigilance for recognizing acute MI among women and the elderly.^15,16

Certain clinical features can lead the APN to an accurate diagnosis of MI. Likelihood ratios (LRs) used in conjunction with the pretest probability of disease can help increase diagnostic certainty.¹⁷ LRs use sensitivity and specificity data to determine the probability that a specific test result (e.g., a positive stress test) or clinical symptom (e.g., a finding of an S3 heart sound) increases or decreases the likelihood of disease in a person with the result compared to a person without the result. Any test or sign/symptom with sensitivity and specificity data can have a positive and negative LR calculated. LRs close to 1 represent little change in disease probability. LRs greater than 10 or less than 0.1 cause large changes in disease probability. The positive LR is used to calculate posttest disease probabilities when the patient manifests the sign or symptom or has a positive test result. The negative LR is used when the patient is free of the sign or symptom or has a negative (normal) test result. For example, the LR for the symptom of chest pain radiating to both arms is 7.1; this is “translated” as the patient who complains of chest pain radiating to both arms is 7 times more likely to manifest this symptom (as a result of an acute MI) than a person who is not experiencing an MI. So, the odds of an MI being the cause of this symptom is 7 times higher than in persons who are not suffering an MI. Because the LR is not directly affected by the prevalence of the condition, it provides a clinically useful tool for diagnostic reasoning.¹⁷ Pretest probability is the APN’s suspicion of disease before additional diagnostic testing is initiated;¹⁷ pretest probability estimates based on age, gender, and symptomatology can be found in the literature and on the Internet for coronary artery disease and MI. Additional reading on the clinical utility of LRs is highly recommended for APNs.

The clinical manifestations that are most highly associated with the diagnosis of MI are chest pain radiating to both the left and right arm simultaneously (LR, 7.1); the presence of a third heart sound (LR, 3.2); and hypotension (LR, 3.1).¹⁸ The presence of pleuritic chest pain (LR, 0.2); chest pain reproduced by palpation (LR range, 0.2-0.4); sharp or stabbing chest pain (LR, 0.3); and positional chest pain (LR, 0.3) are most likely caused by a disorder other than MI.¹⁸

Raymond’s Left Ventricular MI: Anterior wall MIs occur following an LAD occlusion.^2,7,9 Because anterior wall infarctions involve the largest mass of myocardium, LV dysfunction can lead to a drop in cardiac output so severe that it fails to meet the oxygen demands of the body. Activation of the sympathetic nervous system — attributed to pain and anxiety and to chemical mediators emitted from damaged myocardial cells — produces compensatory vasoconstriction and rapid, irregular heart rates that further reduce stroke volume and cardiac output. Excessive sympathetic stimulation can cause transient hypertension as well. As LV failure worsens, pulmonary vascular congestion intensifies, vital organ systems are deprived of oxygen, and end-stage organ dysfunction may develop.

Patients with myocardial damage involving greater than 40% of the LV mass are at risk for cardiogenic shock, severe LV failure, and/or medically refractory dysrhythmias. Cardiogenic shock, one of the most serious complications of MI, is defined as life-threatening hypotension resulting from extensive myocardial damage (i.e.,Ž40% of myocardium) coexisting with signs and symptoms of inadequate systemic perfusion, such as cool skin, mental confusion, and oliguria.¹⁹ Cardiogenic shock typically appears about 24 hours to 72 hours after an acute anterior wall MI and is associated with a mortality rate of more than 70% On physical examination, Raymond appears acutely ill — short of breath with ashen skin that is cool and moist to touch. Other indicators of a poor cardiac output and LV failure include altered mentation; tachypnea; orthopnea; paroxysmal nocturnal dyspnea; moist bibasilar crackles; muffled heart sounds; decreased urinary output; pulsus alternans; frequent premature ventricular contractions; and an abnormal precordial impulse, which can be palpated between the left sternal border and apex.^3,6,9,10

Abnormal heart sounds are manifestations of diastolic dysfunction and extensive LV infarction. An S3 occurs during the early phase of ventricular filling and is one of the earliest and most subtle physical findings of ventricular dysfunction. Conversely, an S4 occurs during the later phase of ventricular filling due to atrial contraction against a rigid, noncompliant ventricle (i.e., the ventricle stiffens). When present during the acute infarction period, an S3 is an ominous sign associated with a poor prognosis and higher mortality.³ Left ventricular failure associated with anterior wall infarction can produce an abnormality in the papillary muscles preventing complete closure of the mitral valve during ventricular systole. As the ventricle becomes markedly dilated, a holosystolic murmur indicative of mitral regurgitation may be evident.

Susan’s Right Ventricular STEMI: Occlusions of the RCA are primarily responsible for infarctions involving the inferior wall of the left ventricle. With occlusion of Susan’s proximal RCA, the RV, as well as inferior walls, were damaged as demonstrated by ST elevation in leads II, III, and aVF, as well as V4R. RV infarction has been demonstrated in more than 50% of individuals experiencing an inferior wall infarction of the left ventricle and has been associated with a high incidence of morbidity and mortality.^2,13

Following RV infarction, the ventricle dilates and becomes dyskinetic, losing its ability to contract effectively. Impaired RV contractility reduces the amount of blood ejected to the left side of the heart, thereby reducing LV preload and, therefore, stroke volume. As LV stroke volume drops, cardiac output falls and hypotension results.^3,13 Susan’s injured right ventricle is unable to handle the incoming venous return (RV preload) which, in turn, causes an elevation in RV filling pressure and further impairment of RV contractility. As the right ventricle’s pumping effectiveness diminishes, right ventricular pressure rises shifting the interventricular septum into the LV obstructing LV performance.¹³ Right atrial pressure also rises as the blood backs up through the tricuspid valve; in this case, a holosystolic murmur of tricuspid regurgitation may be evident, as well as jugular venous distension.¹³ An RV infarction may be complicated by a ventricular septal rupture, evidenced by a pansystolic murmur associated with profound cardiac compromise.¹³ Because a RVMI is usually associated with an IWMI, the infarct area tends to be larger and, as such, a RVMI is correlated with a higher mortality in-hospital and within the first year after the event than patients with left coronary artery disease.²⁰ However, the RV tends to recover more quickly and more completely than a LV injury.^13,20

An evaluation of Susan reveals signs of peripheral hypoperfusion, including pale, cool, clammy skin; prolonged capillary refill time; and hypotension. She has mental status changes as well as a declining urinary output, a sign of a reduced cardiac output, and a widely split S2 — an indication of the delayed closure of the pulmonic valve resulting from prolonged RV emptying.

Susan is tachypneic but does not exhibit signs of pulmonary congestion despite the presence of neck vein distention. Because forward blood flow from the right ventricle is limited, her lungs remain clear. The chest radiograph will demonstrate clear pulmonary vasculature unless associated LV failure occurs.¹³ These findings often puzzle the most experienced clinician.

Detecting early signs of RV overload is key in staving off the severe, life-threatening complication of cardiogenic shock. Classic signs of right-sided heart failure are neck vein distention and peripheral edema. Additional signs include Kussmaul’s sign (a rise in jugular venous pressure during inspiration as the noncompliant RV is unable to accommodate the excess venous return), pulsus paradoxus (a fall in systolic pressure during inspiration of more than 10 mm Hg), and a rise in jugular venous pressure during palpation of the right upper quadrant (hepatojugular reflux).⁹ Elevation of jugular venous pressure may result in gastrointestinal edema and anorexia. RV infarction may occur in the aftermath of global LV dysfunction, especially if the patient has experienced a prior anterior wall MI. Noninvasive diagnostic tests, such as ECG and echocardiogram, can help distinguish between biventricular failure typical of ischemic cardiomyopathy and RV failure resulting from RV infarction.¹³

Diagnostics in brief

The standard 12-lead ECG is a simple, quickly performed, and cost-effective means for evaluating the electrical activity of the heart and provides the APN with additional data to increase diagnostic accuracy. ECGs should be done within 10 minutes for any patient presenting with chest pain or discomfort. If the patient’s symptoms are classic for MI, ST-segment elevation on ECG has a specificity of 90% and a sensitivity of 45% for diagnosing MI.²¹ ECG changes most likely associated with MI include new ST-segment elevation (LR range, 5.7-53.9) and new Q wave formation (LR range, 5.3-24.8).¹⁸ A normal ECG result (LR range, 0.1-0.3) greatly decreases the possibility of MI.¹⁸ Frequently clinical treatment decisions may be made with only the information gained from the history and physical exam coupled with the identification of normal and abnormal waveforms on the 12-lead ECG — “time is myocardium” and rapid reperfusion of the injured cardiac muscle is a major goal of treatment.

The ability to correctly use the LRs associated with specific ECG changes assumes that the clinician can accurately interpret the waveforms. Interpretation of the 12-lead ECG is a skill that needs to be learned and, like any skill, needs to be practiced. A recent study assessed the ability of nurses in the coronary care unit, ED, and telemetry units to accurately interpret myocardial ischemia and injury on 12-lead ECG strips and found that only 19% of the subjects correctly identified ischemia on all test strips and only 21% correctly recognized the nonischemic strips.²² This study highlights the importance of continuing education in ECG interpretation for nurses who care for potential ACS patients.²²

Raymond’s anterior wall infarction is evident in the precordial leads V1 through V4, which show ST segment elevation of more than 1 mm above baseline. A more extensive infarction would involve all six precordial leads as well as lead I and AVL (lateral leads). Observe for pathologic changes, including abnormal, persistent Q waves (> 0.04 seconds duration or one-fourth the R wave height).

While conventional ECG tracings are not extremely helpful in differentiating right from left ventricular infarction, identification of pathological Q waves and ST segment changes in the inferior wall (Leads II, III, and aVF) is the first step toward accurately diagnosing Susan’s RV infarction. A more sensitive and reliable indicator of RV infarction is the use of right-sided precordial leads (V1R-V6R).^13,23 If you can only do one right-sided lead, V4R is considered the most useful.²³ Because right-sided ST segment elevations are often transient and disappear a few hours after the onset of symptoms, individuals suspected of inferior wall infarction need initial, as well as serial right precordial tracings.¹³ However, right-sided ECG leads do not predict the magnitude of RV dysfunction or its hemodynamic consequences.¹³ In addition to the right-sided precordial leads, a, perhaps, subtle difference between an anteroseptal (AS) MI and a RVMI, is the magnitude of the ST elevations. In an ASMI, ST elevations typically increase in amplitude from V1 to V4; in RVMI look for the ST elevations to progressively decrease in these same leads. The smaller RV mass may make this subtle change hard to distinguish.²³

Cardiac-specific proteins called troponins (troponin I and T) can be detected within two to three hours of onset of ischemic symptoms and remain elevated for 5 to 14 days.³ These highly sensitive and most cardiac-specific biomarkers are useful in detecting individuals who present hours or days following their ischemic symptoms and thus have replaced LDH and its isoenzymes for MI diagnosis and monitoring. All patients experiencing chest pain should be evaluated for troponin levels. Troponin I levels of greater than 0.6 ng/mL or troponin T values greater than 0.2 ng/mL are considered positive. Troponin I levels are considered the test of choice in acute MI (75% sensitivity at 6 hours; 90%-100% at 12 hours; 98% specificity).³ Cardiac biomarkers released into the blood are useful in diagnosing MI; however, they cannot distinguish the area of damage.

Creatine kinase (CK) and its specific isoenzyme — CK-MB — are present in the blood three hours following the onset of an acute MI. CK-MB peaks within 12 to 24 hours and returns to normal in about 36-48 hours, depending on infarct size and/or use of fibrinolytic agents for myocardial reperfusion.³ CK-MB levels greater than 7.0 ng/mL are indicative of acute MI (65% sensitive at 6 hours; 95% at 12 hours; specificity 95%).³

Finally, serum myoglobin analysis allows for early, rapid identification of acute MI within one to two hours of the event;³ it is rapidly metabolized and returns to normal in approximately 18 to 24 hours. Myoglobin is highly sensitive (85% at 6 hours; 90% at 12 hours),³ but lacks cardiac specificity (80%) and requires other biomarkers to confirm myocardial ischemia. Normal myoglobin values are <90 ng/mL. With an acute MI, levels are greater than 90 ng/mL or increased by two times the previous value. Myoglobin analysis is useful in detecting early presentations. Other routine blood test results helpful before the initiation of standard therapies include a complete blood count; blood chemistries, including lipids; and hematologic tests.³

A chest radiograph should be obtained on all MI patients to assist in the differential diagnosis of chest pain.³ For example, paired with their corresponding signs and symptoms, radiographic findings of a widened mediastinum, lobar pulmonary infiltrates, or an enlarged heart may lead toward a diagnosis of dissecting aneurysm, pneumonia, or heart failure, respectively.

During the nonacute period of an infarction, invasive and noninvasive techniques are used to identify the specific areas of myocardial damage and to differentiate new from old infarcts. Two-dimensional echocardiography is useful for assessing the presence and severity of ventricular dysfunction, wall motion abnormalities, chamber enlargement, and/or valvulopathy.^3,5,13,24 Echocardiography may be used to clarify STEMI and aid in risk stratification patterns with chest pain, especially if the diagnosis of STEMI occurs in the presence of a left bundle branch block or ventricular pacing.²⁵

Cardiac catheterization and coronary angiography are useful in assessing the heart’s hemodynamic status; performance of the left and right ventricles; the presence, severity, and/or distribution of atherosclerotic coronary heart disease; and valvular function. These tests may be indicated for a patient who is experiencing limiting or escalating symptoms of myocardial dysfunction or myocardial ischemia; or when objective measures such as echocardiography or exercise testing suggest the patient is at risk for functional deterioration, MI, or other adverse events.⁹

The standard treatments

Many evidence-based guidelines are available for care of the patient with acute MI from professional organizations dedicated to cardiovascular health.^5,25 The APN’s consistent use of these guidelines should foster positive patient outcomes.²⁶ Early administration of aspirin (162 mg to 325 mg dose) following the onset of acute MI symptoms reduces the risk of recurrent infarction and death by diminishing the aggregation of platelets, thereby sustaining coronary perfusion (Class 1 recommendation).^3,5,25 The initial dose should be chewed^5,7 and continued with daily doses of the same strength in the hospital.₇ According to major randomized trials, taking 162.5 mg of aspirin for 30 days, beginning on the first day of the STEMI, provides a 23% reduction in the 30-day vascular mortality rate and does not increase the stroke risk during this time frame.⁷ Both Raymond and Susan will receive doses of 162 mg to 325 mg of oral aspirin daily and will need to continue it indefinitely at a daily dose of 81 mg to 325 mg.^3,25 There are, however, risks for gastrointestinal (GI) upset, gastritis, and the development of asthma with aspirin administration. Enteric coated aspirin is not recommended by the European Society of Cardiology (ESC).⁵ Using a 325 mg aspirin suppository is a safe alternative and is recommended for a patient with severe nausea, vomiting, or an upper GI disorder. Ticlopidine or clopidogrel are alternative medications for the patient who is aspirin-sensitive.²⁹ Unless contraindicated, all MI patients should receive aspirin.^3,5,25

More than half of all MI patients entering the hospital have ST segment elevation making it likely that the acute injury process is caused by an obstructive coronary thrombus.³ All patients presenting with STEMI require rapid evaluation for reperfusion therapy and should have a reperfusion strategy implemented promptly.^5,25 Clot-dissolving fibrinolytic therapy in the form of IV streptokinase (SK), alteplase (tPA, Activase), reteplase (rPA, Retavase), and Tenecteplase (TNKase) can reduce mortality and rapidly restore blood flow to both the right and/or left coronary arteries.^3,5,25,29 However, data from several large-scale trials indicate that the choice of fibrinolytic agent is not as important to survival as the timeliness in treatment from the onset of symptoms.²⁷ Fibrinolytic therapy within 6 hours of symptom onset for STEMI patients saves 30 lives/1000 treated; the number of deaths prevented decreases as the time to reperfusion increases: 20 lives saved per 1000 treated between 6-12 hours and no significant benefit after 12 hours.⁵ Because “time is myocardium,” the administration of fibrinolytic agents by pre-hospital personnel is being trialed and championed.^5,30 STEMI patients presenting to a facility without the ability to provide expert, prompt intervention with a primary percutaneous coronary intervention (PCI) within 90 minutes should under undergo fibrinolysis unless contraindicated.²⁵

Fibrinolysis can be beneficial regardless of the patient’s age, gender, or presence of conditions such as diabetes mellitus.^16,25 In elderly patients, reperfusion strategies are not used to the extent possible.¹⁶ Reasons noted for this underuse in the elderly include clinician fear of the effects of the drug on the patient and the fact that elderly patients have higher complication rates, thus negating the benefit of these drugs. According to the ACC/AHA guidelines, thrombolytic therapy in the elderly is a Class 2a intervention; 25 reports indiciate that elderly patients do have an increased risk of intracranial hemorrhage (ICH) (from an increased risk of 50% of ICH to an increased risk of 170%-330% more risk).^16,25 These agents interrupt the infarction process, reduce myocardial necrosis, and improve ventricular function and survival if delivered within 12 hours of the onset of symptoms.²⁵

In conjunction with these fibrinolytic agents, Susan and Raymond will receive anticoagulation with IV unfractionated heparin (UFH) to minimize the incidence of early coronary reocclusion and mortality. Heparin also prevents formation of LV thrombi resulting from anterior wall infarction. Heparin, administered either IV or subcutaneously, is less beneficial in individuals who receive selective fibrinolytic agents such as streptokinase or anisoylated plasminogen streptokinase activator (APSAC).²⁵ When alteplase is infused in combination with IV heparin, improved infarct-related arterial patency has been demonstrated angiographically. Low-dose subcutaneous UFH may be prescribed to prevent post-MI complications of venous thrombosis related to bed rest and inactivity. Using a low-molecular weight heparin (LMWH), such as enoxaparin (Lovenox), for anticoagulation appears to be superior to UFH for reducing myocardial ischemia and mortality for the patient with an acute MI without ST segment elevation.^{3, 29} However, LMWHs have not proven to be efficacious as an adjuvant therapy to fibrinolysis.²⁵ Careful monitoring is essential because the combination of aspirin and UFH or LMWH may increase the likelihood of bleeding. People with known heparin-induced thrombocytopenia may receive bivalirudin (Angiomax), a direct thrombin inhibitor, as an alternate to UFH when used in conjunction with streptokinase for STEMI.²⁵

Early primary PCI is a recommended reperfusion strategy if performed in a timely fashion by physicians skilled in the procedure and supported by experienced personnel in high-volume centers.^5,7,25 According to the ACC and the AHA guidelines, primary PCI is a Class 1 alternative to fibrinolytic therapy for patients with an STEMI (including true posterior MI) or MI with new or presumed new left bundle branch block (LBBB) within 12 hours of symptom onset or beyond 12 hours if ischemic symptoms persist.²⁵ Primary PCI is considered reasonable for selected patients who are within 36 hours of an ST segment elevation/Q wave or new LBBB MI, are more than 75 years old and in whom revascularization can be performed within 18 hours of shock onset.^16,25 Primary stent placement for STEMI continues to be evaluated and there is a growing body of evidence to suggest that it is beneficial.²⁵

Glycoprotein IIb/IIIa inhibitors target platelet-rich thrombi and prevent platelet aggregation, which can lead to thrombus formation and coronary artery occlusion. They are useful for preventing thrombotic complications such as reocclusion following successful fibrinolytic therapy and for patients with an acute MI undergoing a percutaneous coronary procedure.²⁹ The ACC/AHA Guidelines indicate that these agents are useful for patients with acute MI without ST segment elevation who have some high-risk features and/or refractory ischemia and do not have a major contraindication to the drug due to bleeding risk.²⁵ A combination pharmacologic reperfusion strategy with the antithrombotic abciximab (ReoPro) and half-dose reteplase or tenecteplase (TNKase) may be considered for prevention of reinfarction complications of STEMI in the following instance: anterior wall MI, age greater than 75 years, and no risk factors for bleeding.²⁵

Another adjunctive measure designed to protect the myocardium is the initiation of beta-blocker therapy which reduces the risk for future MI and death, especially in anterior wall infarctions, reversible LV failure, moderate depression of LV ejection fraction, in the elderly, and in those who continue to have myocardial ischemia with little effort.^2,25 The immediate use of beta-blockers, followed by long-term oral administration, slows the heart rate and decreases contractility, lessening myocardial oxygen demand.^5,29 These drugs are relatively contraindicated during an acute MI when marked bradycardia, AV block, congestive heart failure, bronchospasm, and/or hypotension are present. However, study evidence suggested that individuals who have these relative contraindications to beta-blockers fare significantly better following acute MI after receiving these drugs than those who do not.²⁸ Beta-blockers must be used with caution in patients with insulin-dependent diabetes mellitus as these drugs may cause a blood sugar shift and an alteration in insulin requirements.²⁵ Both Susan and Raymond will have frequent blood glucose monitoring. Intensive insulin therapy will be used for strict glucose control following STEMI.²⁵

Angiotensin-converting enzyme (ACE) inhibitors used within 24 hours following an acute MI or a suspected acute MI with ST segment elevation in two or more precordial leads should be initiated in all hemodynamically and clinically stable patients.^5,25 ACE inhibitors prevent ventricular dilation and remodeling with subsequent reduction in the occurrence of heart failure and cardiovascular morbidity.⁷ Blood pressure should be monitored frequently, especially with the initial dose, as hypotension can occur.

Nitrates are used primarily to relieve pain associated with acute MI and only slightly impact mortality. Intravenous, oral, and topical nitrates are used to prevent ischemia (the cause of pain) and ventricular remodeling.^7,25 Due to a lack of convincing evidence of the efficacy of nitrates in the early stage of MI, the ESC guidelines do not recommend nitrate administration.⁵

Aldosterone blockers, such as spironolactone (Aldactone) and eplerenone (Inspra) post STEMI have proven beneficial for people with heart failure, an ejection fraction of 40% or less, or both. However, these agents should not be used if hyperkalemia or renal insufficiency is present.²⁵

Long-term pharmacologic treatment of the post-MI patient should include aspirin, ß-blockers, and an ACE inhibitor.²⁹

For those on the left

Fluid restriction and diuretics are used to treat Raymond’s LV failure. Their mechanisms of action reduce LV preload, lessen myocardial work, and minimize the risk of pulmonary edema. Nesiritide, a recombinant B-type natriuretic peptide, has not been investigated sufficiently in the occurrence of STEMI.²⁵ However, IV nitroglycerin causes venous vasodilation, which is also useful in reducing preload and improving myocardial oxygenation. Beta-blockers are contraindicated at this time, but should be initiated when the patient has stabilized, and there are no further signs of heart failure. Raymond should receive treatment with an ACE inhibitor, provided he is not significantly hypotensive, or there are no other contraindications.

Vasodilating agents like nitroprusside reduce the resistance to LV ejection (afterload), decrease myocardial oxygen consumption, and increase stroke volume resulting in improved organ perfusion. Caution must be used when administering this drug, because it also enhances venous dilatation, reduces preload, and ultimately affects cardiac output. Dobutamine, a positive inotropic agent, is an appropriate choice for low cardiac output states, as it enhances contractility and reduces afterload. Meticulous physical assessment and physiologic monitoring are necessary to detect the effects of impaired coronary perfusion and drug-related hypotension.

For those on the right

Administration of crystalloids and/or colloids is the mainstay of treatment for RV infarction.¹³ Maximizing myocardial muscle fiber stretch through volume expansion, up to a certain physiologic limit, creates a greater contractile force. Through distension of the RV chamber with volume, a stronger systolic contraction and improved stroke volume result. This improves blood flow to the lungs for oxygenation facilitating the delivery of oxygenated blood to the left ventricle and enhancing cardiac output.

Therapeutic management of STEMI with RV infarction and ischemic dysfunction should include early reperfusion, maintenance of AV synchrony, and correction of bradycardia; optimization of RV preload using a fluid challenge; optimization of afterload with measures designed to treat LV dysfunction; and use of inotropic support for hemodynamic instability unresponsive to fluid challenge.^5,13,25

An important aspect of Susan’s care is to make certain that preload reducers (e.g. diuretics, nitroglycerin) are avoided. These medications decrease venous return, impair ventricular filling pressure, reduce cardiac output, and can cause significant hypotension. IV morphine, which is frequently used to treat physical discomfort and anxiety, can also reduce preload and must be given with extreme caution. With the exception of oxygen, interventions routinely used to treat LV infarction may prove disastrous when used to manage RV infarction.

Unraveling the inotropics

Inotropic agents such as intravenous dopamine and dobutamine may be used in treating complications of RV and LV STEMI. Both drugs enhance myocardial contractility, which improves stroke volume and cardiac output reflected by blood pressure. Dopamine directly stimulates alpha (peripheral vasoconstriction) and beta 1 receptor cells (increased myocardial strength and heart rate) but its physiological effects are dose related. Its beta effects dominate when dopamine is infused at 5 mcg/kg/min to 15 mcg/kg/min, which is recommended for significant hypotension (systolic B/P 70 mmHg to 100 mmHg) in the presence of the signs and symptoms of shock. At doses of 2 mcg/kg/min to 4 mcg/kg/min, dopamine has little inotropic effect nor does it significantly augment renal and splanchnic perfusion as once believed.³¹ However, it may occasionally promote diuresis and therefore, should be used cautiously in the case of RV infarction as enhanced diuresis can lead to excess volume loss, which negatively affects stroke volume. In doses 10 mcg/kg/min to 20 mcg/kg/min, dopamine’s alpha receptor effects dominate;³¹ and the resulting systemic and splanchnic arteriolar vasoconstriction and tachycardia may be significant enough to compromise systemic, cardiac, and peripheral perfusion.

Dobutamine directly activates beta-1 and beta-2 (vasodilation) receptor sites when infused at 2.5 mcg/kg/min to 10 mcg/kg/min. It’s indicated for the treatment of LV dysfunction and severe systolic heart failure,³¹ complications of acute MI. Caution must be exercised with dobutamine  because an increase in stroke volume frequently induces a reflex peripheral vasodilatation that may or may not cause a decreased blood pressure.³¹ Doses in excess of 10 mcg/kg/min may induce an unwanted hypotension and tachycardia,² which may cause or exacerbate myocardial ischemia.³¹ In practice, inotropic agents are titrated to optimize physiological response while avoiding an altered sensorium, a declining urine output, an increasing tachycardia, or a new dysrhythmia.

Inamrinone (amrinone) and milrinone (Primacor) are bipyridine derivatives, inotropic agents that also cause vascular smooth-muscle relaxation. These drugs improve cardiac output; however, they should be used cautiously, and usually after more standard treatments for severe heart failure and cardiogenic shock have been unsuccessful.³² Inamrinone’s hemodynamic effects are similar to dobutamine, but it causes serious adverse effects, such as thrombocytopenia (with large doses), increased myocardial ischemia, and ventricular dysrhythmias.³² Milrinone is 20 times more potent than amrinone and is used for ventricular dysfunction related to acute MI, as well as chronic heart failure. Adverse effects include dysrhythmias, hypotension, lightheadedness, nervousness, headache, and rarely thrombocytopenia.³³ Vigilant ECG monitoring is necessary throughout the infusion. Should dysrhythmias or hypotension occur, stop or slow the infusion, as directed by the physician.

Intraaortic balloon pump (IABP) counterpulsation is a Class 1 recommendation for STEMI when cardiogenic shock is not quickly reversed with pharmacologic therapy. The IABP is useful as a stabilizing measure for angiography and prompt revasculization.^5,25

Watch for complications

Both Raymond and Susan will require vigilant ST segment monitoring in the leads overlying their infarcted areas to detect changes indicative of improvement or extension of myocardial damage. ST-segment monitoring is an evidence-based intervention shown to have a positive effect on patient outcomes;^34,35 yet only 50% of critical care units report routine monitoring of the ST segment.³⁴ Patients who have suffered an acute MI should be continuously monitored for ST-segment changes for a minimum of 24 hours.³⁴ Continuous cardiac monitoring is essential because lethal ventricular dysrhythmias (ventricular tachycardia and ventricular fibrillation) and conduction disturbances associated with anterior MIs are difficult to treat and occur without warning. Other complications of acute anterior MI include congestive heart failure, papillary muscle rupture, rupture of the interventricular septum, infarct extension, LV aneurysm, pericarditis, and cardiogenic shock.^3,5

Because the RCA supplies the sinus and AV nodes in most people, there is a strong possibility that Susan will experience symptomatic bradycardias, ventricular escape rhythms, and progressive heart block.¹³ Atrial fibrillation frequently accompanies RVMI and should be corrected rapidly as the loss of atrial kick and AV synchrony further decreases right ventricular preload.⁵ Mortality related to complete heart block approaches 80% and is directly related to necrosis of the electrical conduction system below the level of the AV node. You must be prepared to detect subtle signs of hemodynamic instability and intervene promptly to abolish hemodynamically stable ventricular tachycardia; accelerate symptomatic bradycardias, junctional, or slow ventricular rhythms with atropine; initiate emergency transthoracic pacing; or perform synchronized cardioversion according to institutional protocols. The use of the rate-pressure product or double-product (heart rate x systolic blood pressure), is an easy calculation and clinically useful tool for the estimation of myocardial workload (oxygen demand) and therefore myocardial oxygen consumption.³⁶ A value over 12,000 indicates increased cardiac workload, an undesirable outcome for the injured heart and an alert for a need for therapeutic intervention. This calculation can help the APN assess the patient’s response to the effects of therapy.³⁶ Online calculators are available such as www.clinicalcalculator.com

Physiologic complications are not the only types of complications for which you should be vigilant. Depression has been implicated as a trigger for MI, as well as a predictor of adverse outcomes; the effects of depression may affect the patient’s quality of life for up to 5 years after the event.³⁷

Knowledge is Power

Patients surviving an acute MI have a higher risk of death than the general population ranging from 1.5 times to 15 times higher risk! Patient education is an important intervention for health maintenance and the prevention of another MI. Cardiac rehabilitation after acute MI has produced positive outcomes in patients and should be started as soon as possible.⁵ Yet a large majority of MI survivors do not use cardiac rehabilitation.² Compared to men and patients under age 70, respectively, women and elderly patients are less likely to be involved in cardiac rehabilitation programs.²

An international study on cardiovascular health, the INTERHEART study www.cihr-irsc.gc.ca/e/26489.html, identified nine risk factors that were responsible for the vast majority (90%) of initial MIs. In addition to the traditional modifiable and nonmodifiable risk factors for CHD, recent publications have emphasized the risk of MI from psychosocial or emotional stressors, such as earthquakes and terrorist acts.³⁷ Do not assume that your CHD patients are informed about risk reduction strategies; be sure to include risk assessment and counseling and referrals, as appropriate. Strategies, such as anger and stress management classes and social networking groups, may be useful to reduce your patients’ risks of future cardiac events.³⁷

Reinforcing the need for immediate action if the patient experiences signs and symptoms of another MI is imperative to excellent patient care. Ensuring that your patients are aware of the classic signs and symptoms is essential, but educating your patients to be aware of the atypical signs and symptomatology of acute MI, is also critical. Twenty percent of patients delay seeking treatment for at least two hours;¹⁵ a symptom not normally associated with MI is one reason patient’s delay. Patient delay in accessing treatment for an acute MI has been shown to increase morbidity and mortality.^14,26,38 Ten to fifty people per 1,000 population will die for every hour due to delay to treatment for acute MI.³⁸

Differentiating left from right ventricular MI affords you an opportunity to anticipate expected complications and promptly institute appropriate therapeutic measures to reduce oxygen consumption and improve oxygen delivery. Ultimately, your efforts can positively influence patient outcomes and long-term survival.