Research has shown that oxidation and the body’s inflammatory response contribute to atherosclerosis and heart disease. A hypothetical sequence of cellular interactions in atherosclerosis is shown in Figure 5-1. Oxidation is a normal chemical process in the body that is caused by the release of free radicals. Free radicals are oxygen atoms created during normal cell metabolism. Too many free radicals can seriously damage cells and impair the body’s ability to fight against illness. Examples of conditions that can cause an overproduction of free radicals include stress and exposure to cigarette smoke, pesticides, air pollution, ultraviolet light, and radiation.

Figure 5-1 Hypothetical sequence of cellular interactions in atherosclerosis. Hyperlipidemia and other risk factors are thought to cause endothelial injury, resulting in adhesion of platelets and monocytes and release of growth factors, including platelet-derived growth factor (PDGF), which lead to smooth muscle cell (SMC) migration and proliferation. Foam cells of atheromatous plaques are derived from both macrophages and SMCs—from macrophages via the very-low-density lipoprotein (VLDL) receptor and low-density lipoprotein (LDL) modifications recognized by scavenger receptors (e.g., oxidized LDL), and from SMCs by less certain mechanisms. Extracellular lipid is derived from insudation from the vessel lumen, particularly in the presence of hypercholesterolemia, and also from degenerating foam cells. Cholesterol accumulation in the plaque reflects an imbalance between influx and efflux, and high-density lipoprotein (HDL) probably helps clear cholesterol from these accumulations. SMCs migrate to the intima, proliferate, and produce extracellular matrix (ECM), including collagen and proteoglycans. IL-1, interleukin 1; MCP-1, membrane cofactor protein 1.

Antioxidants, such as Vitamins C and E, work by binding to free radicals and transforming them into nondamaging substances or repairing cellular damage. Oxidation causes injury to the inner (endothelial) layer of arteries. Low-density lipoproteins (LDL) become damaged when they react with free radicals. LDL may be responsible for a buildup of fat-like material on the artery walls.

Injury to the endothelial layer of an artery starts the body’s inflammatory response at the injury site. White blood cells are released at the site and oxidize LDL. Cytokines are also released. Cytokines attract even more white blood cells to the site. They also raise blood pressure and increase the tendency for blood to clot. Oxidation converts LDL to a foamy material, which sticks to the smooth muscle cells of the arteries. Over time, the foamy material builds up on artery walls and forms a hard plaque.

Atherosclerotic lesions include the fatty streak, the fibrous plaque, and the advanced (complicated) lesion (Figures 5-2 and 5-3). Fatty streaks are thin, flat yellow lesions composed of lipids (mostly cholesterol) or smooth muscle cells that protrude slightly into the arterial opening. They appear in all populations, even those with a low incidence of coronary artery disease (CAD). Fatty streaks do not obstruct the vessel and are not associated with any clinical symptoms.

Figure 5-2 The natural history, morphologic features, main pathogenic events, and clinical complications of atherosclerosis. ECM, extracellular matrix; SMC, smooth muscle cell.

Figure 5-3 Gross views of atherosclerosis in the aorta. A, Mild atherosclerosis made up of fibrous plaques, one of which is indicated by the arrow. B, Severe disease with scattered and complicated lesions.

Progression from a fatty streak to an advanced lesion is associated with injured endothelium that activates the inflammatory response. As the inflammatory response continues, the fatty streak becomes a fatty plaque, then a fibrous plaque, and finally an advanced lesion. Hemorrhage then occurs within the plaque and a thrombus forms.

Initially the walls of the blood vessel outwardly expand (i.e., remodel) as plaque builds up inside of it. This occurs so that the size of the vessel stays relatively constant, despite the increased size of the plaque. When the plaque fills about 40% of the inside of the vessel, remodeling stops because the vessel can no longer expand to make room for the increase in plaque size. As an atherosclerotic plaque increases in size, the vessel becomes severely narrowed (i.e., stenosed). Generally, arterial stenosis of 70% of the vessel’s diameter is required to produce anginal symptoms.

ACLS Pearl

The extent of arterial narrowing and the amount of reduction in blood flow are critical determinants of CAD.

Plaque Rupture

Atherosclerotic plaques differ with regard to their makeup, vulnerability to rupture, and tendency to form a blood clot. A “stable” or “nonvulnerable” atherosclerotic plaque has a relatively thick fibrous cap that separates it from contact with the blood and that covers a core containing a large amount of collagen and smooth muscle cells but a relatively small lipid pool (Figure 5-4). A stable plaque may produce significant luminal obstruction, but has a lower tendency to rupture or erode.² Plaques that are prone to rupture are called “vulnerable” plaques because they have a thin cap of fibrous tissue over a large, soft, fatty center that separates it from the opening of the blood vessel. If the fibrous cap erodes or ruptures, the contents of the plaque (i.e., collagen, smooth muscle cells, tissue factor, inflammatory cells, and lipid material) are exposed to flowing blood.

Figure 5-4 Views of stable and vulnerable plaques. A, A stable plaque. Yellow, soft fatty material (gruel) is separated from the opening of the vessel by a thin fibrous cap. White radiographic contrast medium is visible in the vessel opening. B, A vulnerable plaque. This specimen was just a few millimeters distal to the one shown in A. In this specimen, the thin fibrous cap is ruptured, a big cap fragment and some of the soft atheromatous gruel are missing (from downstream embolization), and a clot has evolved where the fatty gruel has been exposed. White contrast medium has penetrated the soft gruel through the ruptured fibrous cap.

The rupture of a vulnerable plaque may occur after the following: extreme physical activity (especially in someone unaccustomed to regular exercise), severe emotional trauma, sexual activity, exposure to illicit drugs (e.g., cocaine, amphetamines), exposure to cold, or acute infection.³ Contributing factors to plaque rupture may include shear stress (i.e., the frictional force from blood flow), coronary spasm at the site of the plaque, internal plaque changes, and the effects of risk factors (see Chapter 1).

Plaque disruption (rupture) is most likely to occur at vessel bifurcations because of the speed of blood flow and turbulence created at these areas. Three vulnerable sites for plaque disruption within the coronary arteries have been identified and include the following ⁴:

• The proximal portion of the left anterior descending coronary artery

• Near the origin of the marginal branch on the right coronary artery

• Near the origin of the first obtuse marginal branch on the circumflex coronary artery

Thrombus Development

If the cap of a vulnerable plaque erodes or ruptures, platelets stick to the damaged lining of the vessel and to each other within seconds and form a plug (Figure 5-5). “Sticky platelets” secrete several chemicals, including thromboxane A₂. These substances stimulate vasoconstriction, reducing blood flow at the site. Aspirin, which is an antiplatelet agent, blocks the production of thromboxane A₂, slowing down the clumping (i.e., aggregation) of platelets and lowering the risk of complete blockage of the vessel.

Figure 5-5 Rupture of a vulnerable plaque results in adhesion of platelets at the site and activation of additional platelets (aggregation). The coagulation cascade then begins, resulting in additional platelet aggregation and thrombosis.

After the platelets are activated, glycoprotein IIb/IIIa receptors that are needed for platelet clumping appear on the surface of the platelet. Fibrinogen molecules bind to these receptors to form bridges (i.e., “cross-links”) between nearby platelets, allowing them to clump. Glycoprotein IIb/IIIa receptor inhibitors prevent fibrinogen binding and platelet clumping. As the process continues, fibrinogen cross-links between platelets, thrombin is made, and fibrin is formed; this ultimately produces a clot. Clots can be dissolved by a process called fibrinolysis. Fibrinolytics (i.e., “clot-busters”) are drugs that stimulate the conversion of plasminogen to plasmin, which dissolves the clot.

Coronary Artery Obstruction

The most common cause of a myocardial infarction is acute plaque rupture. The resultant thrombosis leads to acute closure of coronary arteries. When a temporary or permanent blockage occurs in a coronary artery, the blood supply to the heart muscle is impaired. An impaired blood supply results in a decreased supply of oxygen to the myocardium. When the heart’s demand for oxygen exceeds its supply from the coronary circulation, chest discomfort or related symptoms often occur. A decreased supply of oxygenated blood to a body part or organ is called ischemia.

Blockage of a coronary artery by a thrombus may be partial or complete. Partial (incomplete) blockage of a coronary artery by a thrombus may result in no clinical signs and symptoms (silent MI), unstable angina, non-ST-segment elevation MI (NSTEMI) or, possibly, sudden death. Complete blockage of a coronary artery may result in ST-elevation MI (STEMI) or sudden death. The patient’s signs, symptoms, and outcome depend on factors including the following:

• The amount of heart muscle supplied by the affected artery

• The severity and duration of myocardial ischemia

• The electrical instability of the ischemic myocardium

• The degree and duration of coronary vessel blockage

• The presence and extent or absence of collateral coronary circulation

ACLS Pearl

The complete blockage of a coronary artery may cause an MI. However, because a plaque usually increases in size over months and years, other vascular pathways may enlarge as portions of a coronary artery become blocked. These vascular pathways (i.e., collateral circulation) serve as an alternative route for blood flow around the blocked artery to the heart muscle. Thus the presence of collateral arteries may prevent infarction despite complete blockage of the artery.

Other Causes of Acute Coronary Syndromes

Although a thrombus is the most common cause of blockage of a coronary artery, less commonly, an acute MI may occur as a result of coronary spasm (e.g., with cocaine abuse), abnormalities of coronary vessels, hypercoagulation, trauma to the coronary arteries, or coronary artery emboli (rare).⁵

Cocaine causes myocardial ischemia or MI by (1) increasing myocardial oxygen demand by increasing heart rate, blood pressure, and contractility; (2) decreasing oxygen supply via vasoconstriction; (3) inducing a prothrombotic state by stimulating platelet activation and altering the balance between procoagulant and anticoagulant factors; and (4) accelerating atherosclerosis.⁶ Although one study showed that two thirds of MI events occurred within 3 hours of cocaine ingestion,⁷ patients may not seek medical attention for hours to days after use.

The patient experiencing a cocaine-associated ACS may deny drug use and have atypical chest discomfort. Common cardiopulmonary complaints among cocaine users appear in Box 5-1.

Box 5-1 Common Cardiopulmonary Complaints among Cocaine Users ⁶

Anxiety

Chest pain described as pressure-like in quality (most common symptom)

Although there are no clear predictors for patients at risk of cocaine-associated ACS, the Cocaine-Associated Myocardial Infarction study retrospectively identified 130 patients who sustained a total of 136 cocaine-associated MI events. In this group, the majority of patients were young (mean age 38 years), nonwhite (72%), smokers (91%), and had a history of cocaine use in the preceding 24 hours (88%).^6,⁸ A 2003 study showed that patients with cocaine-associated chest pain and positive cardiac biomarkers for MI had significant angiographic stenosis and of patients without positive serum markers, 18% still had significant disease by angiogram.⁹ Cardiac biomarkers are discussed later in this chapter.

Prinzmetal’s angina which is also called Prinzmetal’s variant angina or variant angina, is the result of intense spasm of a segment of a coronary artery. This variant angina may occur in otherwise healthy individuals (usually in their 40s or 50s) with no demonstrable coronary heart disease or in patients with a nonobstructive atheromatous plaque. In some studies, coronary arteriography in patients with Prinzmetal’s angina showed one-vessel CAD in 39% of patients and multivessel disease in 19%.¹⁰

Although the episode of coronary artery spasm can be precipitated by exercise, emotional stress, hyperventilation, or exposure to cold, it usually occurs at rest, often occurs between midnight and 8 AM, and may awaken the patient from sleep.¹¹ Episodes may occur in clusters of two or three within 30 to 60 minutes. Although episodes usually last only a few minutes, this may be long enough to produce serious dysrhythmias including atrioventricular (AV) block and ventricular tachycardia (VT), as well as sudden death. If the spasm is prolonged, infarction may result.

It can be difficult to suspect Prinzmetal’s angina from the patient’s clinical presentation. Patients with Prinzmetal’s angina are generally younger and have fewer coronary risk factors (except for smoking) compared with patients with chronic stable angina. Prinzmetal’s angina has been associated with other vasospastic conditions such as migraine headache and Raynaud’s phenomenon.

The patient with Prinzmetal’s angina complains of chest pain that is often described as severe and may be accompanied by syncope. Chest discomfort is usually relieved by nitroglycerin (NTG). However, although typical angina produces ST-segment depression, Prinzmetal’s angina produces ST-segment elevation during periods of chest pain. After the episode of chest discomfort is resolved, ST segments usually return to the baseline. Because NTG is effective at relieving the coronary spasm, the ECG evidence of Prinzmetal’s angina may be lost if no pretreatment ECG is obtained.

ACLS Pearl

Obtain a baseline 12-lead ECG before initiating treatment in any patient presenting with a possible ACS.

Forms of Acute Coronary Syndromes

[Objective 2]

ACSs include unstable angina, NSTEMI, and STEMI.

Unstable Angina

Angina pectoris is chest discomfort that occurs when the heart muscle does not receive enough oxygen (myocardial ischemia). Angina is not a disease. Rather, it is a symptom of myocardial ischemia. Angina most often occurs in patients with CAD involving at least one coronary artery. However, it can be present in patients with normal coronary arteries. Angina also occurs in persons with uncontrolled high blood pressure or valvular heart disease.

The term angina refers to squeezing or tightening, rather than pain. The discomfort associated with angina occurs because of the stimulation of nerve endings by lactic acid and carbon dioxide that builds up in ischemic tissue. Common words used by patients experiencing angina to describe the sensation they are feeling are shown in Box 5-2. Some patients have difficulty describing their discomfort.

Chest discomfort associated with myocardial ischemia usually begins in the central or left chest and then radiates to the arm (especially the little finger [ulnar] side of the left arm), wrist, jaw, epigastrium, left shoulder, or between the shoulder blades (Figure 5-6). Ischemic chest discomfort is usually not sharp; it is not worsened by deep inspiration; it is not affected by moving muscles in the area where the discomfort is localized, nor is it positional in nature.

Figure 5-6 Common sites for anginal discomfort. A, Upper part of chest. B, Beneath the sternum radiating to neck and jaw. C, Beneath the sternum radiating down left arm. D, Epigastric. E, Epigastric radiating to the neck, jaw, and arms. F, Neck and jaw (common in women). G, Left shoulder and arm (common in older adults and women). H, Interscapular. (common in older adults and women).

Ischemia can occur because of increased myocardial oxygen demand (i.e., demand ischemia), reduced myocardial oxygen supply (i.e., supply ischemia), or both. If the cause of the ischemia is not reversed and blood flow restored to the affected area of the heart muscle, ischemia may lead to cellular injury and, ultimately, infarction. Ischemia can quickly resolve by reducing the heart’s oxygen demand (by resting or slowing the heart rate with medications such as beta-blockers) or by increasing blood flow by dilating the coronary arteries with drugs such as NTG. Early assessment that includes a focused history as well as emergency care are essential to prevent worsening ischemia. Serial ECGs and continuous ECG monitoring should be performed.

Stable (classic) angina remains relatively constant and predictable in terms of severity, signs and symptoms, precipitating events, and response to treatment. It is characterized by brief episodes of chest discomfort related to activities that increase the heart’s need for oxygen such as emotional upset, exercise or exertion, and exposure to cold weather. Possible related signs and symptoms are shown in Box 5-3. Symptoms typically last 2 to 5 minutes and occasionally 5 to 15 minutes. Prolonged discomfort (i.e., longer than 30 minutes) is uncommon in stable angina.

ACLS Pearl

Only 18% of MIs are preceded by longstanding angina.¹

Unstable angina, which is also known as preinfarction angina, is a condition of intermediate severity between stable angina and acute MI. It occurs most often among men and women 60 to 80 years of age who have one or more of the major risk factors for CAD.

Unstable angina is characterized by one or more of the following:

• Symptoms that occur at rest and usually last for more than 20 minutes

• Symptoms that are severe and/or of new onset (i.e., within the last 2 months)

• Symptoms that are increasing in duration, frequency, or both; and intensity in a patient with a history of stable angina

Unlike stable angina, the discomfort associated with unstable angina may be described as painful. Patients with untreated unstable angina are at high risk for a heart attack or death. During their initial presentation, distinguishing patients with unstable angina from those with an acute MI is often impossible because their clinical presentations and ECG findings may be identical. Early assessment, including a focused history, and emergency care are essential to prevent worsening ischemia. Serial ECGs and continuous ECG monitoring should be performed.

The diagnosis of unstable angina versus NSTEMI is made on the basis of the patient’s assessment findings and symptoms, history, presence of risk factors, serial 12-lead ECG results, blood test results (i.e., cardiac biomarkers), and other diagnostic tests.

ACLS Pearl

The time from symptom onset to emergency care can be shortened if patients, families, and bystanders are taught to recognize symptoms early and activate the Emergency Medical Services (EMS) system. Teach your patients and their families how to recognize the signs and symptoms of a heart attack. They should be taught to call 9-1-1 within 5 minutes of symptom onset. Let them know that not all heart attacks are accompanied by sudden, crushing chest pain and a loss of responsiveness. Symptoms may begin gradually or may come and go. Patients who have had a previous heart attack should be taught that the signs and symptoms of a second one might differ from those of the first.

Myocardial Infarction

Ischemia prolonged more than just a few minutes results in myocardial injury. Myocardial injury refers to myocardial tissue that has been cut off from or experienced a severe reduction in its blood and oxygen supply. Injured myocardial cells are still alive but will die (i.e., infarct) if the ischemia is not quickly corrected. If the blocked vessel can be quickly opened to restore blood flow and oxygen to the injured area, no tissue death will occur. Methods to restore blood flow may include giving fibrinolytics, performing a coronary angioplasty, or performing a coronary artery bypass graft (CABG), among others.

An MI occurs when blood flow to the heart muscle stops or is suddenly decreased long enough to cause cell death. The walls of the ventricles consist of an outer layer (the epicardium), middle layer (the myocardium), and an inner layer (the endocardium). The myocardium is subdivided into two areas. The innermost half of the myocardium is called the subendocardial area and the outermost half is called the subepicardial area. The main coronary arteries lie on the epicardial surface of the heart and feed this area first before supplying the heart’s inner layers with oxygenated blood. The endocardial and subendocardial areas of the myocardial wall are the least perfused areas of the heart and the most vulnerable to ischemia because these areas have a high demand for oxygen and are fed by the most distal branches of the coronary arteries. Transmural is a term used to describe ischemia, injury, or infarction that extends from the endocardium to the epicardium. For example, an infarction involving the entire thickness of the left ventricular wall is called a transmural MI. Possible locations of infarctions in the ventricular wall are shown in Figure 5-7.

Figure 5-7 Possible locations of infarctions in the ventricular wall.

In the strictest sense, the term myocardial infarction relates to dead heart muscle tissue. In a practical sense, the term myocardial infarction is applied to the process that results in the death of myocardial tissue. Think of the “process” of MI as a continuum rather than the presence of dead heart tissue (Figure 5-8). Infarcted cells cannot respond to an electrical stimulus or provide any mechanical function. If efforts are made to recognize the process of MI, patients may be identified earlier. If they are promptly treated, the loss of heart tissue may be avoided.¹²

Figure 5-8 Progression of a myocardial infarction (MI). When a coronary artery is blocked (usually by a thrombus), ischemia occurs immediately in the area supplied by the culprit artery, and subendocardial injury occurs within 20 to 40 minutes. Death of subendocardial tissue occurs in about 30 minutes and necrosis extends to about half of the myocardial wall by 2 hours. By 6 hours, necrosis involves about 90% of the myocardial wall and is complete by 24 hours. Healing begins within 24 to 72 hours. Within 2 to 8 weeks of the infarction, the necrotic tissue has been replaced by fibrous tissue.

In the past, an MI was classified according to its location (e.g., anterior, inferior), and whether or not it produced Q waves on the ECG (i.e., Q wave versus non-Q wave MI). However, because a pathologic Q wave may take hours to develop (and in some cases, never develops), the patient’s history and symptoms, cardiac biomarker results, and the presence of ST-segment elevation provide the strongest evidence for the early recognition of MI. ECG clues that may help to establish the presence, location, extent, and duration of an infarction are discussed in more detail later in this chapter.

Universal Definition of Myocardial Infarction

In 1999, the European Society of Cardiology (ESC) and the American College of Cardiology (ACC) convened a conference to revise jointly the definition of MI. The definition for MI was examined from seven points of view: pathological, biochemical, electrocardiographic, imaging, clinical trials, epidemiological, and public policy. The consensus committee findings were published in 2000 in the European Heart Journal and Journal of the American College of Cardiology. The ESC, ACC, and the American Heart Association (AHA) convened, together with the World Heart Federation (WHF), a Global Task Force to update the 2000 document and an updated expert consensus document was published in 2007.¹³ Classifications of MI are shown in Table 5-1 and the criteria for acute MI appear in Box 5-4.

TABLE 5-1 Myocardial Infarction—Classifications

Anatomic Classification¹⁴	Description
Transmural	Ischemic necrosis of the full thickness of the affected muscle segment(s), extending from the endocardium through the myocardium to the epicardium
Nontransmural	Area of ischemic necrosis is limited to the endocardium or endocardium and myocardium, it does not extend through the full thickness of myocardial wall segment(s)
Classification by Size¹³	Description
Microscopic	Focal necrosis
Small	Less than 10% of the left ventricular (LV) myocardium
Moderate	10% to 30% of the LV myocardium
Large	More than 30% of the LV myocardium
Pathological Classification¹³	Time Frame	Description
Evolving	Less than 6 hours	Minimal or no polymorphonuclear leukocytes may be seen
Acute	6 hours to 7 days	Presence of polymorphonuclear leukocytes
Healing	7 to 28 days	Presence of mononuclear cells and fibroblasts, absence of polymorphonuclear leukocytes
Healed	29 days or more	Scar tissue without cellular infiltration
Classification by Location
Anterior	Inferior	Septal
Lateral	Inferobasal (posterior)	Right ventricular
Clinical Classification¹³	Description
Type 1	Spontaneous myocardial infarction (MI) related to ischemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection
Type 2	MI secondary to ischemia due to either increased oxygen demand or decreased supply such as coronary artery spasm, coronary embolism, anemia, arrhythmias, hypertension, or hypotension
Type 3	Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischemia, accompanied by presumably new ST elevation, or new left bundle branch block, or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood
Type 4a	MI associated with percutaneous coronary intervention
Type 4b	MI associated with stent thrombosis as documented by angiography or at autopsy
Type 5	MI associated with coronary artery bypass graft

Data from Thygesen K, Alpert JS, White HD; Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction: Universal definition of myocardial infarction. J Am Coll Cardiol 2007;50:2173–2195.¹³ Data from Bolooki HM, Bajzer CT: Acute myocardial infarction. In Cleveland Clinic: current clinical medicine, Philadelphia, 2009, Elsevier.¹⁴

Box 5-4 Criteria for Acute Myocardial Infarction ¹³

The term myocardial infarction should be used when there is evidence of myocardial necrosis in a clinical setting consistent with myocardial ischemia. Under these conditions any one of the following criteria meets the diagnosis for MI:

• Sudden, unexpected cardiac death, involving cardiac arrest, often with symptoms suggestive of myocardial ischemia, and accompanied by presumably new ST elevation, or new LBBB, and/or evidence of fresh thrombus by coronary angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood.

• For percutaneous coronary interventions (PCI) in patients with normal baseline troponin values, elevations of cardiac biomarkers above the 99th percentile URL are indicative of peri-procedural myocardial necrosis. By convention, increases of biomarkers greater than 3 × 99th percentile URL have been designated as defining PCI-related MI. A subtype related to a documented stent thrombosis is recognized.

• For CABG in patients with normal baseline troponin values, elevations of cardiac biomarkers above the 99th percentile URL are indicative of peri-procedural myocardial necrosis. By convention, increases of biomarkers greater than 5 × 99th percentile URL plus either new pathological Q waves or new LBBB, or angiographically documented new graft or native coronary artery occlusion, or imaging evidence of new loss of viable myocardium have been designated as defining CABG-related MI.

• Pathological findings of an acute MI.

Criteria for Prior Myocardial Infarction ¹³

Any one of the following criteria meets the diagnosis for prior MI:

• Development of new pathological Q waves with or without symptoms.

• Imaging evidence of a region of loss of viable myocardium that is thinned and fails to contract, in the absence of a nonischemic cause.

• Pathological findings of a healed or healing MI.

History and Clinical Presentation ¹²

[Objective 3]

Patient History

The average patient experiencing an ACS does not seek medical attention for 2 hours or more after the onset of ischemic chest pain symptoms.^10,¹⁵ Women often delay longer than men do when seeking medical help. Common reasons that individuals delay in seeking medical care for ischemic-type chest discomfort are shown in Box 5-5.

Box 5-5 Common Reasons for Delays in Seeking Medical Care for Ischemic-type Chest Discomfort ^10,¹⁵

• Unaware of the importance of calling EMS or 9-1-1 for symptoms

• Unaware of the need for rapid treatment

• Mild discomfort began slowly rather than abruptly and with severe pain as depicted on television or in the movies

• Believed symptoms would go away or were not serious

• Believed symptoms were caused by another chronic condition (e.g., arthritis, muscle strain, influenza)

• Did not want to “bother” EMS personnel, physicians, or other healthcare professionals unless they were “really sick”

• Afraid of embarrassment if symptoms turned out to be a false alarm

• Wanted family approval before seeking medical care

• Felt they were not at risk for a heart attack (especially common among women or young, healthy men)

Note: Although these responses from 2004 and 2007 are still true today, the economy (i.e., lack of employment or medical benefits) is another common reason for delays in seeking care (i.e., “I can’t afford it”).

Not all chest discomfort is cardiac-related. Obtaining an accurate history is important to help determine if a patient’s signs and symptoms are most likely related to ischemia as a result of CAD. Because time is muscle when caring for patients with an ACS, it is important to ask targeted questions to determine the patient’s probability of an ACS and to not delay reperfusion therapy, if indicated. Important information to obtain when eliciting a targeted history is shown in Table 5-2.

TABLE 5-2 Acute Coronary Syndromes—Targeted History

Historical Information to Obtain	Notes
Patient age, gender	Important risk factors
SAMPLE History
Signs and Symptoms	What prompted you to seek medical assistance today?
Allergies	Ask the patient about allergies to medications, food, environmental elements (e.g., pollen), and products (e.g., latex).
Medications	• What prescription and over-the-counter medications are you currently taking? • Do you take your medicine as prescribed? • Have you missed any doses or taken extra doses of any medicine? • Have you taken any medication for erectile dysfunction in the past 24 to 48 hours? • Do you take any herbal supplements or use recreational drugs such as cocaine? Ask about the use of cocaine in patients with suspected acute coronary syndromes, particularly in patients younger than 40 years of age.
Past medical history	• Are you currently under a physician’s care? • Do you have a history of a heart attack, angina, heart failure, high blood pressure, or abnormal heart rhythm? If the patient answers yes to this question, ask how his or her current symptoms compare to the previous episode. • Have you ever had a heart-related medical procedure such as a bypass (open-heart surgery), cardiac catheterization, angioplasty, transplant, valve replacement, or pacemaker? • Do you have a history of stroke; diabetes; lung, liver, or kidney disease; or other medical condition? Find out the patient’s risk factors for heart disease. Ask the patient if he or she smokes. If the answer is yes, ask how many packs per day. Ask the patient if a history of heart disease is in the family. If the answer is yes, ask whether anyone died of heart disease and at what age. Ask about a family history of high blood pressure, diabetes, and high cholesterol. • Have you been hospitalized recently? Any recent surgery?
Last oral intake	Ask the patient when he or she last had anything to eat or drink and if any recent changes in eating patterns or fluid intake (or output) have occurred.
Events leading to the incident	What were you doing when your symptoms began? Try to find out what precipitated the patient’s current symptoms. For example, did an event or activity cause the patient’s symptoms, such as strenuous exercise, sexual activity, or unusual stress?
OPQRST (Pain Presentation)
Onset	• When did your symptoms begin? • Did it begin suddenly or gradually? • Have you ever had this discomfort before? When? How long did it last? Were you seen, evaluated, or treated for it? If so, what was the diagnosis? How does the discomfort you are feeling right now compare with that?
Provocation/Palliation/Position	• What were you doing when your symptoms started? • What makes the discomfort better or worse? • What have you tried to relieve the problem? • Does a change in position lessen the discomfort?
Quality	• What does your discomfort feel like? Document the words the patient uses to describe discomfort.
Region/Radiation/Referral	• Where is your discomfort? Ask the patient to point to it. • Does it stay in one area? Do you have symptoms in a different area of your body?
Severity	• On a scale of 0 to 10, with 0 being the least and 10 being the worst, what number would you assign your discomfort?
Timing	• Is your discomfort still present? Is it getting better, worse, or staying about the same? • Does it come and go or is it constant?
Presence of associated symptoms?	Nausea, vomiting, difficulty breathing, sweating, weakness, fatigue
Special considerations	• Consider the possibility of potentially lethal conditions that mimic acute MI such as aortic dissection, acute pericarditis, acute myocarditis, and pulmonary embolism • Consider conditions that can produce ST elevation on the ECG (mimicking STEMI) including acute pericarditis, early repolarization, hyperkalemia, left ventricular hypertrophy, and bundle branch blocks

ACLS Pearl

When obtaining the patient’s history, use the patient’s words for the discomfort. For example, the patient may not consider their symptom “discomfort” or “pain” but instead have another appropriately descriptive term to describe their symptom. Whatever term the patient uses, continue to use that term when interacting with the patient.

ACLS Pearl

Patients with possible symptoms of ischemic chest discomfort should be taught the importance of calling 9-1-1, rather than arranging for their own transport to the hospital. Teach your patients that EMS professionals can provide life-saving care if complications develop en route to the hospital.

Predisposing Factors

Studies have shown that the peak incidence of acute cardiac events is between 6 AM and noon.¹⁶^–¹⁹ The early morning hours are associated with increases in blood pressure, heart rate, sympathetic nervous system activity, cortisol, and platelet aggregability. Some studies have shown that an MI is more likely to occur on Monday (as the patient transitions from weekend to work week) and during the winter months.^16,²⁰^–²²

A predisposing factor (i.e., trigger) is present in about 50% of patients experiencing an acute cardiac event.²³ Examples include moderate to heavy physical exertion, unusual emotional stress, lack of sleep, overeating or use of alcohol, acute respiratory infection, or pulmonary embolism.^19,²⁴^–²⁷ Cocaine use may be a factor, particularly in patients younger than 40 years of age.

Typical Symptoms

[Objective 4]

Chest discomfort is the most common symptom of infarction. It is present in 75% to 80% of patients with acute MI. Patients experiencing a heart attack may describe the sensation they are feeling as similar to angina, or use words such as “heartburn,” “indigestion,” “dull,” “squeezing,” “gnawing,” “aching,” “tightness,” or “pressure.” The patient may describe his or her discomfort with a clenched fist held against the sternum (Levine’s sign). The discomfort typically lasts longer than 30 minutes. It may be constant or come and go, and occasionally may be relieved with belching.¹⁵

The ACC/AHA guidelines list the following as pain descriptions that are not characteristic of myocardial ischemia ¹⁰:

• Pleuritic pain (i.e., sharp or knife-like pain brought on by respiratory movements or cough)

• Primary or sole location of discomfort in the middle or lower abdominal region

• Pain that may be localized at the tip of one finger, particularly over the left ventricular apex

• Pain reproduced with movement or palpation of the chest wall or arms

• Constant pain that persists for many hours

• Very brief episodes of pain that last a few seconds or less

• Pain that radiates into the lower extremities

Atypical Presentation

[Objective 6]

Not all patients experiencing an ACS present similarly. Atypical presentation refers to uncharacteristic signs and symptoms that are experienced by some patients. Atypical chest discomfort is localized to the chest area but may have musculoskeletal, positional, or pleuritic features. Examples of atypical presentations of STEMI are listed in Box 5-6.

Patients experiencing an ACS who are most likely to present atypically include older adults, diabetic individuals, women, patients with prior cardiac surgery, and patients during the immediate postoperative period after noncardiac surgery.⁵

Older adults may have atypical symptoms such as dyspnea, shoulder or back pain, weakness, fatigue, a change in mental status, syncope, unexplained nausea, and abdominal or epigastric discomfort. They are also more likely to present with more severe preexisting conditions, such as hypertension, heart failure, or a previous acute MI than a younger patient. Individuals with diabetes may present atypically due to autonomic dysfunction. Common signs and symptoms include generalized weakness, syncope, lightheadedness, or a change in mental status.

Women who experience an ACS report acute symptoms including prodromal chest discomfort, unusual fatigue, sleep disturbances, dyspnea, nausea or vomiting, indigestion, dizziness or fainting, sweating, arm or shoulder pain, and weakness. When chest discomfort is present, it is often described as “aching,” “tightness,” “pressure,” “sharpness,” “burning,” “fullness,” or “tingling.” The location of the discomfort is often in the back, arm, shoulder, or neck. Some women have vague chest discomfort that tends to come and go with no known aggravating factors.

ACLS Pearl

Researchers compared African-American, Hispanic, and Caucasian women’s prodromal and acute symptoms of MI.²⁹ Symptom severity and frequency were compared among racial groups. Among the women, 96% reported prodromal symptoms. Unusual fatigue (73%) and sleep disturbance (50%) were the most frequent. Eighteen symptoms differed significantly by race. African-American women reported higher frequencies of 10 symptoms than did Hispanic or Caucasian women. Thirty-six percent reported prodromal chest discomfort. Hispanic women reported more pain/discomfort symptoms than did African-American or Caucasian women. Minority women reported more acute symptoms. The most frequent symptom, regardless of race, was shortness of breath (63%); 22 symptoms differed by race. In total, 28% of Hispanic, 38% of African-American, and 42% of Caucasian women reported no chest pain/discomfort. These researchers concluded that prodromal and acute symptoms of MI differed significantly according to race.