Feature

Not All Heart Attacks Are the Same

Jaaska Lyn Cather, RN, BSN, MSN, staff nurse (Clinical RN-4), Cardiovascular Interventional Unit, Winchester Medical Center, Winchester, Virginia
Jaaska Lyn Cather, RN, BSN, MSN, staff nurse (Clinical RN-4), Cardiovascular Interventional Unit, Winchester Medical Center, Winchester, Virginia
A myocardial infarction occurs when an atherosclerotic plaque ruptures within the vessel wall of a coronary artery, resulting in formation of thrombus. The thrombus decreases the blood supply to a specific portion of the myocardium, resulting in myocardial necrosis from an unmet need for oxygen. Globally, acute myocardial infarction is the leading cause of death for both men and women.1 In the United States, one in five deaths is attributed to coronary artery disease.2 What are the signs and symptoms of a patient presenting with acute myocardial infarction? A great majority of patients have atypical presentations, which can be very confusing and can result in a misdiagnosis. These patients rarely use the word “pain,” instead offering descriptions such as “discomfort” or “squeezing” to describe their chief complaint. Patients may make statements such as “my bra is too tight” or compare the discomfort to a “burning sensation, toothache, or an elephant sitting on one’s chest.”3 Nausea and vomiting, or simply fatigue, may be the only complaint. Other symptoms can include pain or discomfort, either localized or radiating to areas such as the back, arms or epigastric area. Diabetics typically do not complain of chest pain, but will present with atypical symptoms. The patient may be anxious and have a feeling of “impending doom.” This is an ominous sign and should be taken seriously. Typical myocardial infarction symptoms include severe, prolonged chest pain, lasting more than 30 minutes, which may be described as squeezing, tightness or vise-like. The location is usually sub-sternal or retro-sternal, with radiation to the neck or jaw. Shortness of breath, nausea and vomiting, and diaphoresis commonly occur. A 12-lead ECG should be performed on all patients presenting with the previously mentioned symptoms. A 12-lead ECG shows 12 views, or a panoramic view, of the coronary arteries, and gives more complete information than just a single or even 3-lead ECG. ST elevations greater than 1 mm (one small box) in two or more anatomically contiguous limb leads, and 2 mm or more elevation in two or more contiguous precordial leads, is diagnostic of acute myocardial infarction.3 Proper assessment, diagnosis and treatment of the patient presenting with acute myocardial infarction will not only decrease mortality, but decrease morbidity as well. Properly indentifying the origin of the myocardial infarction by 12-lead ECG decreases complications such as arrhythmias, pump failure, hypo or hypertension, cardiogenic shock, congestive heart failure, and pulmonary edema. An inadequacy in the pump function of the right ventricle will result in right-sided heart failure, and the patient with left ventricular infarct will have symptoms of left-sided heart failure. Anterior wall myocardial infarction. Left ventricular infarct or anterior myocardial infarction involves the left anterior descending artery (LAD). This patient will have ST changes in leads V1-V6 and aVL.3 Physical exam will show findings that correspond with a high sympathetic tone, such as tachycardia and tachy-arrythmias. Complications may include a sudden onset of distal heart block (Mobitz type II second degree), complete heart block, or new onset bundle branch block, hypertension, and signs of left ventricular dysfunction such as congestive heart failure, pulmonary edema and in the most serious instances, cardiogenic shock.3 Left ventricle free wall rupture, ventricular septal rupture, ventricular aneurysm, left ventricle mural thrombus, systemic arterial embolism and pericarditis are all associated with anterior wall myocardial infarctions.3 Left ventricular filling pressures and cardiac output are optimized by the use of diuretics and vasodilators to decrease pre-load and after-load, and inotropes to improve contractility. This patient can very easily develop pulmonary edema or congestive heart failure. This patient often benefits from an intra-aortic balloon pump (IABP) to decrease the workload of the heart. Inferior wall myocardial infarction. In eighty percent of the population, it is the RCA that supports the posterior lateral branch (PLB), and twenty percent of the population have the PLB supported by the circumflex.3 ST changes will be seen in leads II, III, avF (if the RCA is the culprit lesion) or V4R (if the left circumflex artery is the culprit lesion).3 Physical exam will reveal clear lung fields. Bradycardia and marked hypotension are due to a high vagal tone,3 and will be exacerbated after the administration of nitroglycerin. Signs and symptoms of right-sided heart failure such as elevated jugular venous pressure, Kussmaul’s sign (inspiratory increase in jugular venous pressure), S4 and S3 gallops, systolic murmur of tricuspid regurgitation, pulsus paradoxus and pericardial friction rub may also be seen.3 A sign that your patient is experiencing a right ventricular myocardial infarction is a rapid and profound decrease in blood pressure after the administration of nitroglycerin. If this occurs, one should immediately suspect right ventricular infarct, and treat as such. Occlusion of the right coronary artery (RCA) will result in a decrease in blood supply to the sino-atrial node (SA), the natural pacemaker of the heart, and the A-V node, which is the natural electrical conduit between the atria and ventricles. Bradycardic arrhythmias and heart blocks are common.3 Temporary trans-venous pacing may be required. Fluid boluses and inotropes should be administered. Fluid boluses will augment right ventricular (RV) filling pressures and are beneficial for this patient, but can be detrimental to the patient with left ventricular (LV) infarct. Nitrates should also be avoided because they can produce profound hypotension. Reperfusion by means of percutaneous transluminal coronary angioplasty and stenting within 90 minutes of onset of symptoms is the gold standard set by the American College of Cardiology.1 Thrombolytic therapy is also utilized in areas in which a cardiac cath lab is not available within this time frame. As stated previously, the goal in the treatment of the patient presenting with acute myocardial infarction is reperfusion to the myocardium and prevention of co-morbidities. With proper diagnosis of the origin of the infarct and proper treatment, many co-morbidities and possibly mortality may be avoided. Every professional that cares for the patient with acute myocardial infarction should be strongly encouraged to take a 12-lead ECG class. This includes paramedics in the field, emergency department staff, cardiac cath lab teams and critical care nurses. Jaaska Cather can be contacted at jaaska@live.com
References
1) Kosuge M, Kimurak K, Ishikaura T, et al. Differences between men and women in terms of clinical features of ST-segment elevation acute myocardial infarction. Circulation Mar 2006; 70 (3): 222-226.

2) (PDF) The World Health Report 2004 – Changing History. World Health Organization. 2004 pp 120-4.x

3) Chizner M. Clinical Cardiology Made Ridiculously Simple. Miami, FL: MedMaster, Inc.; 79-105.

4) ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction – Executive Summary. Journal of American Cardiology 2004; 44: 671-719.