Myocardial Injury: Contrasting Infarction and Contusion

Understanding the differences between acute myocardial infarction and myocardial contusion is important to facilitate healing, prevent complications, and provide accurate information to patients who have experienced one or both of these complications. This article uses a case study format to describe and contrast these 2 myocardial injuries.Acute myocardial infarction (AMI) and myocardial contusion both result in injury to the heart. The underlying pathophysiology, clinical findings, and interventions, however, differ markedly between the 2 disorders. Knowledge of these aspects can assist critical care nurses in facilitating healing, preventing complications, and providing accurate information to patients and patients’ families. Understanding the differences between AMI and myocardial contusion is particularly important when caring for a patient who has experienced both problems.In this article, we present 3 case studies to contrast AMI and myocardial contusion: H.N. with an AMI of the inferior wall, S.B. with a myocardial contusion, and L.R. with both an AMI and a myocardial contusion. Each of these patients is discussed in relation to his or her particular myocardial injury.H.N., a 57-year-old man, arrived in the emergency department with “excruciating” chest pain that he rated as 8 on a scale of 0 to 10 in which 0 equals no pain. Triage decisions were based on the patient’s history (pain, trigger events, and risk factors), results of initial diagnostic tests (expanded-lead electrocardiography [ECG] and measurement of creatine kinase–MB [CK-MB] level), and findings on physical assessment. We selected H.N.’s case to contrast the differences in pathophysiology between inferior AMI and myocardial contusion and the differences between the two in interventions for changes in hemodynamic status and heart rhythms.Myocardial infarction is due to extended ischemia and, if left untreated, leads to “ultimate cell necrosis.”1 Causes of AMI include thrombus formation, arterial spasm, and embolism; the primary cause is formation of a thrombus in the coronary artery. Although the mechanism of thrombus formation is not entirely understood, thrombi tend to form on unstabilized, ruptured atherosclerotic plaque. When a thrombus blocks blood flow to the myocardial muscle, muscle damage extends rapidly from endocardium to epicardium. Unless adequate blood supply is restored, necrosis of the myocardium may become complete and irreversible within 3 to 4 hours.2 Remodeling of the ventricle through expansion and dilatation of the infarct zone may continue for weeks, months, and years after the infarction.3 Most of the therapy and interventions for AMI are targeted toward restoring blood flow, reducing the risk of reinfarction, reducing oxygen demands on the injured ventricle, and altering dynamics to limit ventricular remodeling.2,4 Early administration of thrombolytic agents is one of the first-line interventions to establish reperfusion of an occluded artery.5H.N.’s known cardiac risk factors were his 20-year history of hypertension, his elevated cholesterol levels, and his male sex. He stated that he had experienced “some discomfort” in his chest earlier in the morning. In the afternoon while he was vacuuming, the pain increased, and he became diaphoretic and nauseated. He rested until his son came home and took him to the hospital’s emergency department, 5 hours after the onset of the severe pain. H.N.’s history is consistent with the experience of AMI. It is not unusual for pain or discomfort to start gradually just before a myocardial infarction, and nausea is often associated with an AMI.6 Triggering events, such as emotional stress or strenuous physical activity, occur in approximately 50% of persons who experience an AMI.7H.N.’s initial 12-lead ECG (Figure 1A) showed ST-segment elevations in the inferior leads II, III, and aVF. ST-segment elevation equal to or greater than 0.1 mV in 2 or more contiguous leads is considered indicative of AMI. An expanded ECG, obtained with either 15 or 18 leads, is recommended for all patients with inferior myocardial infarctions to check for associated right ventricular or posterior involvement.7–9 In this case, a right-sided 12-lead ECG (Figure 1BF2) showed no right ventricular ischemia or injury.H.N.’s creatine kinase level, level of isoenzymes (CK-MB), and relative index during the first 24 hours are given in Table 1. His CK-MB levels followed the predictable pattern of an AMI; they increased sharply and declined just as quickly, producing a pattern somewhat like a bell-shaped curve. After an AMI, the CK-MB level is markedly elevated above normal within 4 to 6 hours of the onset of signs and symptoms, maximum levels are reached between 18 and 24 hours, and levels return to normal in 72 hours.10 If creatine kinase levels do not follow this expected pattern within the first 48 hours, it may be assumed that the person did not have a myocardial infarction. A secondary increase in CK-MB level on the downward slope of the first increase in CK-MB level indicates a reinfarction.Because of the rapid washout of enzymes from the serum after thrombolytic therapy, CK-MB levels are expected to increase and peak more quickly when thrombolysis-induced reperfusion has been effective.10 For H.N., treatment with tissue plasminogen activator resulted in successful reperfusion; maximum plasma levels of creatine kinase were reached 10 to 15 hours after the infarction. The relative index, the relationship between the plasma level of CK-MB and the total plasma level of circulating creatine kinase, is useful in ruling out non-myocardial sources of CK-MB.11 The index is calculated by dividing CK-MB level (in micrograms per liter) by the total concentration of creatine kinase (in units per liter) and multiplying by 100. A relative index greater than 4.0 indicates myocardial damage.Measurement of cardiac troponin levels is an additional diagnostic test for AMI. Troponin T and troponin I are released from myocardial cells within 3 to 5 hours after the onset of ischemia. The specificity of troponin I for myocardial damage is very high; levels of troponin T are elevated with myocardial damage but not with skeletal muscle damage.12 The advantages of using troponin levels are that the troponin level increases earlier and remains elevated longer (up to 14 days) than do CK-MB levels. Troponin levels may be helpful in confirming suspected AMI, diagnosing difficult cases, and triaging patients with chest discomfort, and levels are easily measured at the patient’s bedside without specialized laboratory equipment. Troponin levels are not specific and diagnostic for myocardial contusion.12 In the cases described in this article, troponin levels were not measured because such measurements were not yet standard practice in the facility.H.N. was diaphoretic. He had no peripheral edema, and his jugular venous distention was normal (<4 cm above his sternal angle). His heart rate was 70/min, and his blood pressure was 120/80 mm Hg. He had an extra heart sound (S4), which often occurs soon after AMI because of decreased ventricular compliance and increased end-diastolic pressure in the left ventricle.H.N. was immediately given 3 L of oxygen by nasal prongs, aspirin, sublingual nitroglycerin, and intravenous morphine. Nitro-glycerin, tissue plasminogen activator, and heparin infusions were initiated per hospital protocol, and H.N. was admitted.After the intravenous infusions of nitroglycerin (30 μg/min) and tissue plasminogen activator, H.N. became hypotensive (blood pressure, 75/60 mm Hg) and bradycardic (heart rate, 40–50/min). This combination of events is most common in patients with volume depletion or inferior AMI and most likely is caused by venodilatation, low ventricular filling, and activation of receptors that trigger a vagal reflex arc and bradycardia. H.N. was given 250 mL of isotonic sodium chloride solution intravenously, and his blood pressure increased to 108/70 mm Hg and his pulse increased to 74/min. Life-threatening arrhythmias, such as heart block and ventricular tachycardia and fibrillation also may occur in AMI. Therefore, ECG monitoring is required immediately after AMI.Patients with AMI are at risk for arrhythmias and altered cardiac output. H.N. was treated with bed rest to decrease his oxygen demands and was transferred to the critical coronary care unit to be monitored for arrhythmias and hemodynamic status. His vital signs were stable, and he did not have any further documented arrhythmias.After an AMI, treatment with β-blockers is recommended to reduce myocardial oxygen demands, oppose the action of increased amounts of catecholamines, and provide antiarrhythmic effects.2 A β-blocker, metoprolol, was prescribed accordingly for H.N., but initially was withheld because of his bradycardia and hypotension. He received his first dose on the second day, when his heart rate and blood pressure had stabilized. He had no further chest pain; his ECGs and CK-MB levels indicated no reinfarction or extension of his AMI. H.N. was eager to learn about preventing further effects of his cardiovascular disease; he stated that the infarction “gave him an opportunity to focus on health.” His stay in the hospital was uncomplicated, and he was discharged to home 5 days later.S.B., a 53-year-old woman, was admitted to the medical-surgical critical care unit following a motor vehicle injury in which she collided head-on with another car in a highway intersection. The estimated speed of her car was 110 km/h (69 mph). Her car had no air bag, but she was wearing a safety restraint device. S.B. was transported via helicopter to the nearest trauma center, where she was treated for multiple injuries: myocardial contusion, fractured T6 vertebra, basal skull fracture, and pleural effusion. Her heart rate was 118/min, and her blood pressure was 90/70 mm Hg.Myocardial contusion is bruising due to rupture or hemorrhage of small vessels in the myocardium. Direct injury to myocytes may also occur, with rupture of cells and destruction of cell membranes. Cell injury and bruising may be marginal or extensive and can occur across diffuse areas of the myocardium. The right ventricle is at greatest risk in chest trauma, owing to its anterior location under the sternum.Myocardial injury due to contusion differs in several respects from injury that occurs in myocardial infarction. Although both types of injury may occur over a large surface area, contusion injury is due to the anatomic location of the injury within the chest and is not related to arterial distribution. Therefore, the injury of contusion is primarily epicardial rather than transmural or endocardial, and distinct ischemic zones do not occur.13 The cause of injury is external, and the area of injury is far less vulnerable to extension of injury.Several factors contribute to the decrease in cardiac function that occurs after myocardial contusion. Rupture of small vessels, hemorrhage into the interstitium and around the muscle fibers, and tearing of muscle fibers cause muscle dysfunction and diffuse hypoxia in the area of injury. Impediment of myocardial contractility and blood flow increases the detrimental effects of muscle dysfunction and hypoxia.In addition, cardiac output may decrease because of valvular dysfunction, decreased preload, and increased afterload. Direct injury of the tricuspid or mitral valve may be caused by the external force and internal compression. Acute hemorrhage or mechanical ventilation may decrease right ventricular preload. Pulmonary contusion and mechanical ventilation may contribute to increased right ventricular afterload. Adequate left ventricular preload depends on total blood volume and right ventricular function. An extensive sympathetic nervous response to hemorrhage, pain, or shock causes vasoconstriction and increased left ventricular afterload.The mechanism and kinetic energy of the injury are significant factors in determining the risk for myocardial contusion and concomitant injuries. The mechanism of injury is the external force that is the cause of the event; the force may be blunt or penetrating. The direction, duration, and area of application of the force are associated with the mechanism of injury. Kinetic energy refers to the amount of energy transferred during the event. Myocardial contusion is usually due to blunt and direct injury, such as injuries caused by motor vehicle collisions, falls, or direct blows to the sternum. The primary cause of myocardial contusion is motor vehicle collisions. Wearing a safety restraint device may not prevent contusion; instead, the shoulder harness may increase the propensity for sternal fracture14 or pulmonary or cardiac contusion but may prevent more severe injuries.15 The mechanism of injury in S.B.’s case was blunt injury due to compression of the heart between the sternum and the spinal column. The kinetic energy was extensive because of the speed and type of collision.Because of S.B.’s head injury and decreased level of consciousness, her chest pain could not be assessed accurately. Persons with myocardial contusion may experience sternal pain, which is difficult to differentiate from the pain of infarction. Unlike the pain associated with infarction, the pain associated with contusion is not referred to other sites. Rib fractures, sternal fracture, or pulmonary contusion may also occur and contribute to chest pain. The person may experience shortness of breath (primarily due to concomitant pulmonary contusion), anxiety, and increased oxygen demands. Shortness of breath may occur with the decrease in cardiac output. Nausea may be present because of the stress response.Areas of injury in myocardial contusion may be reflected in diffuse changes in the ST segment or T waves on the ECG. Injury is not necessarily localized, and leads changes not necessarily be ECG changes due to contusion are more consistent with ECG changes that occur in than with the changes that occur in myocardial infarction. The ST segment may be elevated or The T may be or patients with myocardial contusion may have no ECG changes either injury or may also be on the or 12-lead ECG. occur because of increased levels, direct damage of the or areas of the myocardium. Most arrhythmias occur within the first 3 days after the injury. The of arrhythmias after myocardial contusion is with increased pulmonary contusion, fractures, and findings on the initial and blocks are the most arrhythmias other than fibrillation may The right is vulnerable to direct injury, and right block is more likely than left S.B.’s ECG changes are consistent with contusion. she had a right she had T waves (Figure had creatine kinase levels measured on days and without the of Troponin levels were not measured because such diagnostic tests were not at that of the levels of creatine kinase, isoenzymes (CK-MB), or troponin in patients with myocardial contusion have not been It is recommended that measurement of creatine kinase levels be to persons in AMI is suspected as either the cause or result of chest trauma because creatine kinase levels are and of required treatment or If levels are isoenzymes be because most patients have additional injuries that increase the total level of creatine The of the peak in creatine kinase levels is less predictable in myocardial contusion than in AMI, and creatine kinase levels may peak within the first 8 hours after injury or continue to increase over Troponin levels are not or diagnostic for myocardial initial showed normal left ventricular function and normal valve function. had a small and in right ventricular and left posterior and CK-MB levels, findings on are not of contusion or and is for patients with myocardial injury. For findings on contribute to between causes of low blood pressure related to coronary injury or S.B.’s on the was 4 of Her heart rate was to she had no and an blood had a on the left sternal at the to the left were bruising was over the left and was present from the to the In the emergency department, of the was and a chest was mL of was S.B. was and was treated with with a of oxygen of was given for the and her heart rate increased to Her blood pressure was mm Hg. sodium chloride solution was and infusions of per and per were initiated to increase blood pressure and S.B. had a and of a and was admitted to the medical-surgical critical care to the critical care S.B.’s and were from and to per and per the was and her blood pressure was with L of and mL of S.B. in right block and between and she from right block to normal Her blood pressure was mm and the was was treated with mechanical ventilation for an additional 10 days until of the pulmonary contusion and head patients with myocardial contusion to and therapy, such as administration of of cardiac output usually occurs within 3 days of and blood pressure is If hemodynamic increases or severe right ventricular or be S.B.’s myocardial contusion and right block to her of cardiac function. Her pulmonary and not the focus of this article, were of greater to her than was the myocardial a man, was admitted to the trauma critical care unit after a motor vehicle with a of the particularly the mechanism of injury, the initial for cardiac injury were to myocardial contusion. L.R. was with decreased blood A was to cardiac status on the of results of diagnostic and findings on physical the of injury, L.R. stated that he had sternal chest pain on The pain did not to other and was not associated with was because L.R. was with and it was not if he had experienced chest pain before the L.R. had no history of coronary His known risk factors were his male and his his indicated that had at the of of a myocardial infarction. L.R. was at an estimated speed of more than km/h and was not wearing a safety restraint device. He was through the and was was (30 initial 12-lead ECG (Figure showed significant ST-segment elevation in the anterior and leads, with T waves in the inferior kinase and CK-MB levels were elevated findings are more consistent with AMI than with blood tests a complete blood cell measurement of and levels, and arterial blood level was 24 of was suspected on the of his level of his level of his level of and his L.R. had both and with an initial of 10 L of oxygen via a was mm oxygen was and level was chest showed fractured 4 to and a large on the left injuries are consistent with the of the the and the that L.R. the changes in cardiac function were on with and across the and the anterior and changes in left ventricular function are consistent with his ECG creatine kinase levels, and the of a large AMI. mitral and tricuspid also The combination of these valvular findings is more consistent with direct trauma than with ischemia from coronary was with a heart rate of and had a decreased blood pressure of mm Hg. is a common in a of factors for L.R. the stress of the motor vehicle related to and the of an anterior AMI. is a of levels of circulating and present after was with and was a that an accurate assessment. His heart were and with no extra or blood through the injuries and was to per and a of mL of solution were to blood rate at He had a chest and decreased breath with breath in the left of the over the sternum was from the to the L.R. was and treated with with a of oxygen of and a volume of His decreased to chest were on the left both had air and L.R. was immediately to where the were An indicated multiple of the and which had to was was to per to a arterial pressure of mm Hg. has a on the coronary artery. μg/min) was to prevent of the coronary had a of but the to than no other arrhythmias were L.R. was by a and a large AMI was It is the AMI was the cause of or a result of the motor vehicle vehicle and other events occur if the person an AMI or by the discomfort caused by the AMI. Myocardial infarction with thrombus formation in the injured may occur at the of chest trauma when either direct or injury of the coronary of his heart an The ECG showed waves in the L.R. had of He chest pain with and ECG changes with the chest pain, which most likely was due to the pulmonary and injuries. of via a was with a rate of 2 and a maximum rate of 4 pulmonary was the initial findings were venous pressure, mm pulmonary pressure, mm index, and cardiac index, index was calculated as in per to the by surface area in index was calculated as cardiac output in per by surface area in arterial pressure was to mm Hg. His index decreased to administration was increased to per and nitroglycerin was The for the low index was tachycardia his heart rate was at to was given to oppose the elevated levels, reducing heart rate and myocardial oxygen demands. arterial pressure was 72 to mm and the index was output was less than normal serum levels of and were not consistent with and were can blood vessels and decrease the concentration of this was and administration was output over the of L.R. treatment with an and The of with has effects on ventricular after a large infarction, reducing the of the and the risk of and heart L.R. was and metoprolol, and was transferred out of the critical care cause of AMI is not however, he did have myocardial After L.R. was discharged from the trauma care his care was assumed by the The of aspirin, and was consistent with recommended for myocardial infarction. L.R. required further to his but was required to 6 to his cardiac status to It was recommended to L.R. that he complete the cardiac after his L.R. was about risk of chest discomfort, activity, and In to cardiac and him at risk for additional injury, and he have or about his of myocardial injury and The pathophysiology, findings, and interventions for myocardial contusion and infarction have and AMI is injury due to decreased or myocardial contusion results from both injury due to the mechanism of injury and injury due to in pain, pressure, and discomfort are expected with type of injury, but tests for AMI, ECGs changes in contiguous leads and blood tests elevated levels and are more specific and accurate than are tests for myocardial contusion. Understanding type of myocardial injury can nurses to provide and type of injury, the focus is on and cardiac while cardiac and myocardial oxygen This focus preventing complications, facilitating healing, and providing accurate information to patients and patients’ families.

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