Acute coronary syndrome is an umbrella term for a group of clinical symptoms indicative of acute myocardial ischemia. These conditions include non-ST-segment elevation myocardial ischemia (NSTEMI), unstable angina, and ST-segment elevation myocardial infarction (STEMI). These conditions are high-risk manifestations of atherosclerosis in the coronary artery and significant causes of utilization of emergency services and hospitalization (Kumar and Cannon, 2009). STEMI causes 30% of all acute coronary syndromes in Australia (Harper and Lefkovits, 2010). This paper will describe the expected presentation, pathophysiology, ECG findings, pre-hospital management, and initial 24-hour management of STEMI in hospitals settings. These aspects will be described in relation to a case study of a 35-year old patient named Bob who has complains of central chest pain radiating to the jaw and has pale, cool, and clammy skin.
Signs, Symptoms, and ECG Findings
The patient in this case is restless with pale, clammy skin. The patient is experiencing central chest pain that is radiating to the jaw. His skin is pale, cool, and clammy which are suggestive of a large area of ischemia and/or cardiogenic shock. Other physical examination findings that correlate with a large area of ischemia and are thus likely to be found in this patient include hypotension, sinus tachycardia, basilar rales, and a third or fourth heart sound. Tachycardia occurs due to the compensatory stimulation of sympathetic system following the drop in cardiac output that occurs as a result of ventricular dysfunction. Hypotension is suggestive of a large occlusion and is followed by cardiogenic shock. Basilar rales occur due to pulmonary congestion secondary to ventricular failure. Other symptoms expected in this patient are the typical signs that occur in nearly all types of acute coronary artery syndrome. These symptoms include dyspnea, diaphoresis, nausea and vomiting, and unexplained fatigue. Diaphoresis is due to sympathetic discharge while nausea results from stimulation of the vagal nerve. The vital signs expected in this patient are hypotension, tachycardia, tachypnea, and hypothermia (Bolooki and Askari, 2010).
Based on the physical findings presented, the patient is experiencing occlusion of blood to a large area of his heart and the occlusion is affecting the ability of his heart to supply blood to the rest of his body. Based on these facts, it is highly likely that the occlusion is affecting his left coronary artery which supplies blood to the left atrium and ventricle. The most likely diagnosis for this patient is, therefore, ST-segment elevation myocardial infarction (STEMI) of the anterior wall. STEMI results from complete occlusion of a major coronary artery by thrombus that leads to full thickness damage of myocardial muscles and is associated with more severe symptoms. The fact that the patient’s skin is cool and clammy suggests there is insufficient blood flow to the skin which may occur in the presence of cardiogenic shock secondary to occlusion of a major coronary artery (Mukau, 2011). The diagnosis of STEMI is further supported by the fact that the patient’s pain is centrally located and is radiating to the jaw.
STEMI is associated with ST segment elevations and pathological Q-waves on ECG as shown in the figure below. It is confirmed by presence of ST-segment depressions in contralateral ECG leads. ST-segment elevations denote full thickness injury of cardiac muscles while pathological Q-waves indicate muscle necrosis. T-wave inversions are sometimes found, they are a non-specific feature that denotes muscle ischemia (Deshpande and Birnbaum, 2014; American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, 2012). ST-segment elevations for anterior wall STEMI are seen in some or all of leads V1-V6 (Stroobandt, Barold, and Sinnaeve, 2016).
Pathophysiology
The primary cause of ACS is atherosclerosis. Myocardial infarctions frequently occur as a result of a disturbance in the vascular endothelium linked to an unstable atherosclerotic plaque. This disruption stimulates formation of a thrombus which then partially or completely occludes blood flow within the artery. If the occlusion lasts for > 20 minutes, it causes permanent myocardial cell damage and death. STEMI usually results from complete occlusion of a coronary artery after plaque rapture (Mukau, 2011).
Atherosclerotic plaques develop over a long period typically years to decades. Clinically symptomatic plaques have two chief attributes, a fibromuscular cap as well as an underlying core rich in lipids. Erosion of a plaque results from the effects of matrix metalloproteases produced by activated inflammatory cells as well as the release of other proteases and collagenases in the plaque that thin the overlying fibromuscular cap. Disruption of the endothelium and rapture or fissuring of the fibromuscular cap can occur due to the combined action of proteases and hemodynamic forces in the arterial segment. Loss of the structural stability of plaques often occurs at the shoulder region that is at the juncture between the fibromuscular cap and the wall of a blood vessel. Further disruption of the surface of the endothelium can trigger thrombus formation within the coronary artery through platelet-mediated activation of the coagulation cycle. MI results if the resultant thrombus is of adequate size to obstruct coronary blood flow (Mukau, 2011).
Obstruction of coronary blood flow first causes ischemia and death to the myocardial cells in the endocardium as they are the ones most distal to the arterial blood supply. Continued occlusion results in an increase in the area of affected myocardium with extension from the endocardium to myocardium and lastly, epicardium. The region of myocardial cell death then extends laterally to include areas of collateral perfusion or watershed. After a period of 6 to 8 hours of coronary occlusion, a large area of the distal myocardium dies. The magnitude of an MI is determined by the degree of myocardial cell death. Restoration of blood flow to at-risk myocardium saves the remaining heart muscle from permanent damage or death (Bolooki and Askari, 2010).
Three factors determine the severity of an MI. These include the degree of occlusion in the affected coronary artery, duration of the occlusion, and collateral circulation. Proximal coronary occlusions put more extensive areas of the myocardium at risk of necrosis. Large myocardial infarctions, on the other hand, have a greater risk of death because of pump failure or a mechanical complication. Longer periods of vessel occlusion increase the probability of permanent myocardial damage to the area distal to the occlusion (Mukau, 2011).
Pre-Hospital Management of STEMI
The pre-hospital management of this patient will include assessment, oxygen, nitroglycerin, aspirin, morphine, 12-lead ECG, defibrillation, and prompt transfer to an appropriate hospital (Acute Coronary Syndrome Guidelines Working Group, 2006). Assessment of the patient will include measuring of vital signs. It is necessary to aid in diagnosis and facilitate determination of the severity of the MI. Supplemental oxygen is indicated for all patients with complains of chest pain and dyspnea, hypoxemia, or signs of shock or heart failure. Nonenteric aspirin is given early after the onset of symptoms unless the patient has already taken it or its contraindicated because of allergy or a bleeding disorder. The patient chews the aspirin for more rapid buccal absorption. Nitroglycerin can be given to the patient to a maximum of 3 doses at intervals of 3-5 minutes if the patient’s systolic blood pressure is not <90 mmHg or >30mmHg or more lower than the patient’s baseline. IV morphine, with close monitoring of blood pressure and respiratory rate, is indicated for patients who do not respond to nitroglycerin (Kumar & Cannon, 2009). A 12-lead ECG is performed on a routine basis for patients with complains of chest pains. Once the ECG confirms the diagnosis of STEMI, the information is communicated to a hospital with percutaneous coronary intervention (PCI) capabilities so as to avoid delays in initiation of reperfusion therapy. Because the patient has signs of cardiogenic shock, it is very important that he is transported to a PCI-capable hospital. Continuous cardiac monitoring using the 12-lead ECG should be provided enroute to the hospital to foster detection of life-threatening arrhythmias. Defibrillation and CPR would be indicated if the patient goes into cardiac arrest (O’Connor et al., 2010).
Hospital Management of STEMI within the first 24 Hours
Diagnostic investigations for the patient will include assays of cardiac markers of necrosis, 12-lead ECG, chest x-ray, and a full lipid profile. Prompt reperfusion that is restoration of blood flow to infarcted myocardium is the most effective and recommended treatment of STEMI. Reperfusion can be achieved be through PCI or thrombolysis. PCI entails balloon angioplasty for opening of the occluded artery as well as the insertion of a stent that maintains patency. Primary PCI is the preferred management modality for STEMI patients who can access hospitals with PCI-capability as it is associated with the best outcomes in several large meta-analyses (Australian Resuscitation Council, 2016a; Hoekstra, 2010). It has best outcomes when performed within two hours of onset of symptoms (Australian Resuscitation Council, 2016b). After PCI, antiplatelet therapy mostly aspirin and clopidogrel are continued indefinitely. In the absence of or anticipated delays with PCI exceeding 120 minutes, fibrinolytic therapy is administered instead. It is most effective when administered within 12 hours of onset of symptoms (O’Connor et al., 2010; ACCF/AHA Task Force Members, 2013). Notably, although PCI is the recommended management modality for STEMI, recent evidence suggests that prehospital thrombolysis when given within 2 hours of onset of symptoms of STEMI has better outcomes to primary PCI. When administered within 4 hours of onset of symptoms, fibrinotherapy has similar outcomes to primary PCI. Patients managed using prehospital thrombolysis, however, require angiography and PCI where indicated within 24 hours of onset of symptoms of STEMI for optimal results (Harper and Lefkovits, 2010).
Conclusion
In summary, a patient with STEMI is likely to present with signs suggestive of a large region of myocardial infarction, pulmonary congestion and sympathetic activation which include dyspnea, rales, tachycardia, abnormal heart sounds, and cool, clammy skin. STEMI is caused by the occlusion of a major artery by an atherosclerotic plaque. The ECG of a patient with STEMI shows ST-segment elevation in two or more leads and ST depression in contralateral leads. The Pre-hospital management of STEMI includes assessment, oxygen supplementation, nitroglycerin, aspirin, 12-lead ECG, defibrillation where indicated, and prompt transfer to a hospital. The mainstay management of STEMI in hospital settings is PCI. However, emerging evidence suggests that prehospital thrombolysis is more effective than PCI. The goal of therapy is to achieve reperfusion of ischemic myocardium in the earliest time possible.
References
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