Myocardial Infarction Clinical Presentation
- Author: A Maziar Zafari, MD, PhD; Chief Editor: Eric H Yang, MD more...
The patient’s history is critical in diagnosing myocardial infarction (MI) and sometimes may provide the only clues that lead to the diagnosis in the initial phases of the patient presentation.
Patients with typical acute MI usually present with chest pain and may have prodromal symptoms of fatigue, chest discomfort, or malaise in the days preceding the event; alternatively, typical ST-elevation MI (STEMI) may occur suddenly without warning.
The typical chest pain of acute MI usually is intense and unremitting for 30-60 minutes. It is retrosternal and often radiates up to the neck, shoulder, and jaws, and down to the left arm. The chest pain is usually described as a substernal pressure sensation that is also perceived as squeezing, aching, burning, or even sharp. In some patients, the symptom is epigastric, with a feeling of indigestion or of fullness and gas.
In some cases, patients do not recognize the chest pain, have an unusually high pain threshold, or have a disorder that impairs pain perception and results in a defective anginal warning system (eg, diabetes mellitus). In addition, some patients may have an altered mental status caused by medications or impaired cerebral perfusion. Elderly patients with preexisting altered mental status or dementia may have no recollection of recent symptoms and may have no complaints whatsoever.
MI occurs most often in the early morning hours. Mechanisms that may explain this circadian variation include the morning increase in sympathetic tone leading to increases in blood pressure, heart rate, coronary vascular tone, and myocardial contractility; the morning increase in blood viscosity, coagulability, and platelet aggregability; and the increased morning levels of serum cortisol and plasma catecholamines leading to sympathetic overactivity, thereby resulting in increased myocardial demand.[42, 43]
Initial rapid evaluation should include obtaining a brief history and performing a focused physical examination. Important elements of the history, such as characteristics of the pain and important associated symptoms, and past history of or risk factors for cardiovascular disease, are used to determine the likelihood that these symptoms represent acute coronary syndrome (ACS) and to predict the likelihood of clinical outcomes.
Several risk assessment scores and clinical prediction algorithms are used to help identify patients with ACS at increased risk of adverse outcomes, such as TIMI (Thrombolysis In Myocardial Infarction) risk score, the GRACE (Global Registry of Acute Coronary Events) risk score, and the NCDR-ACTION (National Cardiovascular Data Registry-Acute Coronary Treatment and Intervention Outcomes Network) registry.[8, 30]
A high index of suspicion for MI should be maintained, especially when evaluating women, patients with diabetes, older patients, patients with dementia, patients with a history of heart failure, cocaine users, patients with hypercholesterolemia, and patients with a positive family history for early coronary disease (See Etiology). A positive family history includes any first-degree male relative aged 45 years or younger or any first-degree female relative aged 55 years or younger who experienced an MI.
Other symptoms of myocardial infarction include the following:
Anxiety, commonly described as a sense of impending doom
Pain or discomfort in areas of the body, including the arms, left shoulder, back, neck, jaw, or stomach
Light-headedness, with or without syncope
Nausea, with or without vomiting
Shortness of breath
Rapid or irregular heart rate
Fullness, indigestion, or choking feeling
The patient may recall only an episode of indigestion as an indication of myocardial infarction (see Physical Examination). In some cases, patients do not recognize chest pain, possibly because they have a stoic outlook, have an unusually high pain threshold, have a disorder that impairs function of the nervous system and that results in a defective anginal warning system (eg, diabetes mellitus), or have obtundation caused by medication or impaired cerebral perfusion. Elderly patients with preexisting altered mental status or dementia may have no recollection of recent symptoms and may have no complaints whatsoever.
Physical examination findings for myocardial infarction (MI) can vary; one patient may be comfortable in bed, with normal examination results, whereas another patient may be in severe pain, with significant respiratory distress and a need for ventilatory support.
Patients with ongoing symptoms usually lie quietly in bed and appear pale and diaphoretic.
The patient's heart rate is often increased (tachycardia secondary to sympathoadrenal discharge). The pulse may be irregular because of ventricular ectopy, an accelerated idioventricular rhythm, ventricular tachycardia, atrial fibrillation or flutter, or other supraventricular arrhythmias.
Depressed heart rate may also be present in some cases. Bradyarrhythmias may be attributable to impaired function of the sinus node. An atrioventricular (AV) nodal block or infranodal block may also be present.
Unequal palpable pulses can be suggestive of the presence of aortic dissection, which commonly presents with chest pain radiating to the back, accompanied by a blood pressure difference of 15 mm Hg or greater between both arms and an aortic regurgitation murmur.
In general, the patient's blood pressure is initially elevated (hypertension because of peripheral arterial vasoconstriction resulting from an adrenergic response to pain, anxiety, and ventricular dysfunction). However, it is not uncommon to have increased blood pressure as the precipitant of acute MI.
Alternatively, hypotension can also be seen. Usually this indicates either right ventricular MI or severe left ventricular dysfunction due to a large infarct area or impaired global cardiac contractility.
The respiratory rate may be increased in response to pulmonary congestion or anxiety.
Fever is usually present within 24-48 hours, with the temperature curve generally parallel to the time course of elevations of creatine kinase (CK) levels in the blood. Body temperature may occasionally exceed 102°F.
In patients with acute inferior-wall MI with right ventricular involvement, distention of neck veins is commonly described as a sign of failure of the right ventricle. Impaired right ventricular function also leads to systemic venous hypertension, edema, and hepatomegaly.
On palpation, lateral displacement of the apical impulse, dyskinesis, a palpable S4 gallop, and a soft S1 sound may be found. These signs indicate diminished contractility of the compromised left ventricle.
Paradoxical splitting of S2 may reflect the presence of left bundle-branch block or prolongation of the pre-ejection period with delayed closure of the aortic valve, despite decreased stroke volume.
A new mitral regurgitation murmur (typically holosystolic near the apex) indicates papillary muscle dysfunction or rupture, or mitral annular dilatation; it may be audible even when cardiac output is substantially decreased.
A holosystolic murmur that radiates to the midsternal border and not to the back, possibly with a palpable thrill, suggests a ventricular septal rupture; such a rupture may occur as a complication in some patients with full-thickness MIs. With resistive flow and an enlarged pressure difference, the ventricular septal defect murmur becomes harsher, louder, and higher in pitch than before.
A pericardial friction rub may be audible as a to-and-fro rasping sound; it is produced through sliding contact of inflammation-roughened surfaces.
Rales or wheezes may be auscultated; these occur secondary to pulmonary venous hypertension, which is associated with extensive acute left ventricular MI. Unilateral or bilateral pleural effusions may produce egophony at the lung bases.
Patients frequently develop tricuspid incompetence; hepatojugular reflux may be elicited even when hepatomegaly is not marked.
A pulsatile abdominal mass may suggest an abdominal aortic aneurysm.
Peripheral cyanosis, edema, pallor, diminished pulse volume, delayed rise, and delayed capillary refill may indicate vasoconstriction, diminished cardiac output, and right ventricular dysfunction or failure. Pulse and neck-vein patterns may reveal other associated abnormalities, as previously discussed.
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|Absolute Contraindications||Relative Contraindications|
|CPR = cardiopulmonary resuscitation; INR = international normalized ratio; STEMI = ST-elevation myocardial infarction; US = United States of America.
Table modified from 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.
|Fibrinolytic Agent||Dose||Fibrin Specificity||Antigenic||Patency Rate|
|Streptokinase (no longer marketed in the US)||1.5 million units IV given over 30–60 min||No||Yes||60%–68%|
|30 mg for weight <60 kg
35 mg for 60–69 kg
40 mg for 70–79 kg
45 mg for 80–89 kg
50 mg for >90 kg
|Reteplase (rPA)||10-U IV boluses given 30 min apart||++||No||84%|
|Alteplase (tPA)||Bolus 15 mg followed by infusion 0.75 mg/kg for 30 min (maximum 50 mg), then 0.5 mg/kg (maximum 35 mg) over the next 60 min; total dose not to exceed 100 mg.||++||No||73%-84%|
|IV = intravenous; rPA = recombinant human tissue plasminogen activator; STEMI = ST-elevation myocardial infarction; tPA = tissue plasminogen activator; US = United States of America.
Table modified from 2013 ACCF/AHA guidelines for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.