Complications of MI
Chronic Heart Failure
If a patient makes it through the acute phase, their heart’s ventricular muscle might become impaired, leading to chronic heart failure.
i. Loop diuretics such as Furosemide are used for all patients to alleviate symptoms and decrease volume overload.
ii. Initiate treatment with either an ACE inhibitor (ACEi) or beta-blocker (BB). Start with one medication at a time.
iii. If the symptoms continue, add the other drug (either ACEi or BB).
iv. If symptoms persist, incorporate Spironolactone, an aldosterone antagonist, into the treatment regimen.
Cardiac arrest is most often a result of patients developing complications following a myocardial infarction (MI), which makes it the leading cause of death post-MI. The standard management for these patients aligns with the Advanced Life Support (ALS) protocol, which includes defibrillation.
Ventricular fibrillation, as previously stated, is the leading cause of death post-myocardial infarction. Other types of arrhythmias, such as ventricular tachycardia, may also develop.
i. Examine the patient’s pulse. If there is no pulse, initiate the cardiac arrest protocol immediately, including prompt defibrillation.
Pericarditis typically develops within two days following a myocardial infarction. The condition is characterized by features such as pleuritic chest pain which worsens upon lying flat or during inhalation, a potential fever, and a pericardial rub.
As a result, pericardial effusion may develop, which may be seen as an enlarged globular heart on a chest X-ray. This diagnosis can be confirmed via an echocardiogram.
The ECG of these patients may show widespread, saddle-shaped ST elevation with upward concavity and PR depression.
For management, a full dose of NSAIDs should be administered. These can include aspirin (2-4 g/day), ibuprofen (1200-1800 mg/day), or indomethacin (75-150 mg/day). This treatment should be continued for at least 7-14 days.
Dressler’s Syndrome, while similar to pericarditis in its symptoms, typically occurs several weeks following a myocardial infarction.
The underlying pathophysiology is believed to be an autoimmune response to antigenic proteins formed as the myocardium recovers.
The condition is characterized by a combination of fever, pleuritic chest pain that worsens on inspiration and while lying flat, pericardial effusion, and an elevated ESR (erythrocyte sedimentation rate).
For treatment, nonsteroidal anti-inflammatory drugs (NSAIDs) are generally used.
An ECG may show widespread saddle-shaped ST elevation and potential PR depression.
Left Ventricular Aneurysm
A myocardial infarction (MI) can cause ischemic damage that weakens the myocardium, leading to a thinning of the muscle layer and the formation of a left ventricular aneurysm. This typically happens 4-6 weeks after the MI.
A persistent ST elevation and left ventricular failure are common associations with this condition.
The aneurysm can pose a risk of stroke as a thrombus may form within it. Therefore, anticoagulation therapy is used for these patients.
On an ECG, persistent ST elevation and signs of left ventricular failure can be observed. A chest X-ray may show an enlarged heart with a bulge at the left heart border, and an echocardiogram may reveal paradoxical movement of the ventricular wall.
Ventricular Septal Defect (VSD)
A ventricular septal defect, or VSD, typically results from a rupture of the interventricular septum, often happening within the first week after a myocardial infarction (MI). This complication is observed in about 1-2% of MI patients.
Patients with this defect may present symptoms of acute heart failure, characterized by a pan-systolic murmur.
An echocardiogram can provide a definitive diagnosis and can also rule out acute mitral regurgitation, which has a similar presentation.
Prompt surgical intervention is required to correct this condition.