A myocardial infarction (MI), more commonly known as a heart attack, is a medical emergency where a section of the heart muscle begins to die. This occurs when the flow of oxygen-rich blood to the heart is abruptly reduced or cut off, usually by a blockage in a coronary artery. Without swift restoration of blood flow, the affected heart tissue sustains permanent damage. Diagnosing this condition involves clinical assessments and specialized tests to confirm the event and determine its severity.
Patient Symptoms and Clinical Presentation
The most widely recognized finding of a myocardial infarction is chest pain. Patients often describe this as intense pressure, squeezing, or heaviness in the center of the chest, rather than a sharp pain. This discomfort is persistent, lasting longer than 15 minutes, and does not subside with rest. The pain frequently radiates from the chest to other areas of the upper body, including the left arm, jaw, neck, back, or shoulders.
Other common symptoms include shortness of breath, as the heart’s compromised pumping function affects the lungs. Many individuals experience profuse sweating (diaphoresis), which may present as a cold sweat. Nausea, sometimes leading to vomiting, and feelings of lightheadedness or dizziness are also frequently reported.
Not everyone experiences these classic symptoms, and presentations can vary. Women are more likely to present with atypical symptoms such as profound fatigue, indigestion-like discomfort, and shortness of breath, sometimes without any noticeable chest pain. Elderly individuals might exhibit signs like confusion or sudden weakness. Patients with diabetes may experience a “silent MI,” where nerve damage blunts or eliminates chest pain.
Physical Examination Findings
A physical assessment can reveal objective signs of a myocardial infarction. The patient may appear anxious, distressed, pale, and sweaty. These signs reflect the body’s intense physiological stress response to the cardiac event.
Changes in vital signs offer further evidence. The heart rate can be abnormally fast (tachycardia) or slow (bradycardia). Blood pressure may be elevated from pain and anxiety or dangerously low if the heart is too damaged to pump effectively, a condition known as cardiogenic shock. The respiratory rate may also increase.
Listening to the heart and lungs with a stethoscope can reveal specific abnormalities. A new heart murmur might indicate a mechanical complication, such as the rupture of a muscle that controls a heart valve. Extra heart sounds, like an S3 or S4 gallop, can suggest heart failure. Crackles in the lungs are sounds indicating fluid backup from the heart’s inability to pump blood forward efficiently.
Electrocardiogram (ECG) Indicators
The electrocardiogram (ECG) is a primary tool used to diagnose a myocardial infarction by recording the heart’s electrical activity. Specific patterns on the ECG can indicate that the heart muscle is suffering from a lack of oxygen. This interpretation helps clinicians quickly determine the type and location of the heart attack, guiding immediate treatment.
One of the most definitive ECG findings is ST-segment elevation. This pattern signifies an ST-Elevation Myocardial Infarction (STEMI), a serious event where a coronary artery is completely blocked. This finding is a clear signal for emergency procedures to restore blood flow.
In contrast, other ECG changes may point to a different type of heart attack. ST-segment depression or an inversion of the T-wave can indicate a Non-ST-Elevation Myocardial Infarction (NSTEMI). These findings suggest that a coronary artery is only partially blocked, and the immediate treatment protocol for NSTEMI differs from that of a STEMI.
Over time, the ECG can also show evidence of a past myocardial infarction. The development of deep and wide Q waves is a significant indicator. These Q waves represent dead heart tissue that has become electrically inert scar tissue and often remain on the ECG permanently.
Cardiac Biomarkers in Blood Analysis
Blood tests that measure specific cardiac biomarkers are used to confirm heart muscle damage. When heart muscle cells die, they release their internal proteins into the bloodstream. Detecting these proteins allows for a definitive diagnosis of a myocardial infarction.
The primary biomarkers are cardiac troponins, specifically troponin I (cTnI) and troponin T (cTnT), which are highly specific to cardiac muscle. Following an MI, troponin levels in the blood begin to rise within two to four hours and peak around 24 to 48 hours. Their concentration remains elevated for several days, making them a reliable indicator.
Historically, another enzyme, Creatine Kinase-MB (CK-MB), was used to diagnose an MI. While its levels also rise after a heart attack, it is less specific to the heart than troponin. Because troponins offer greater sensitivity and specificity, they have largely replaced CK-MB as the preferred biomarker.
Confirmatory Imaging Results
Advanced imaging techniques are used to confirm a diagnosis, evaluate the extent of heart muscle damage, and identify the cause of the myocardial infarction. This information guides both immediate and long-term treatment strategies.
An echocardiogram uses ultrasound waves to create images of the heart. A primary finding after a heart attack is a wall motion abnormality, where a segment of the heart muscle does not contract normally. An echocardiogram also measures the heart’s overall pumping strength, known as the ejection fraction.
A coronary angiography is the definitive procedure for identifying the cause of a myocardial infarction. It involves guiding a catheter to the heart and injecting dye into the coronary arteries. X-ray images then highlight the location and severity of any blockages.