9 side effects after a heart attack
Heart attacks cause permanent damage and death of an area of the heart muscle cells due to a lack of enough blood supply and oxygen to the cells. It is highly necessary to restore the blood supply to the heart to minimize the damage.
Following a heart attack, the patient may develop certain complications that may be life-threatening, which include:
The heart’s normal electrical rhythm may be disturbed due to a heart attack. This is known as arrhythmia.
- Early arrhythmias, which occur within the first 24 to 48 hours after MI, are caused by myocardial ischemia. Arrhythmia usually does not reoccur, and even if it does, it does not indicate a poor prognosis.
- Late arrhythmias develop after 48 hours and represent the amount of ventricular injury. They are prone to reoccur, indicating a poor prognosis. Arrhythmias that develop after MI may be attributable to additional problems such as a ventricular aneurysm or heart failure.
A special device known as a pacemaker may be implanted for a few days to correct arrhythmias. Sometimes, the patient may require a pacemaker for the rest of their life, which a small device is inserted under their skin.
The risk of mortality increases following MI with 50 percent of patients dying within the first hour of symptom onset, following an acute coronary blockage.
- The most common cause of death is due to ventricular fibrillation (irregular and rapid heartbeats that are initiated in the lower chambers of the heart).
- The risk of death is high in the initial hours following MI that reduces gradually over the next few days.
- This is the reason the patient needs immediate access to defibrillators and other life-saving drugs.
Chest pain or angina
Angina, which may occur when the blood vessels are damaged, is a type of chest discomfort caused by a lack of blood flow to the heart muscle.
Because one or more of the coronary arteries may be constricted, angina can develop before or after a heart attack. The doctor may recommend an angiography to examine the coronary arteries in greater detail.
Cardiogenic shock refers to a complicated illness characterized by insufficient perfusion (blood circulation) of essential organs, such as:
Cardiogenic shock is caused by significant irreparable damage to the myocardium; hence, treating arrhythmias early may help prevent them from developing. Early thrombolysis and beta-blockers, for example, maybe effective in reducing the size of MI.
- Cardiogenic shock affects 15 percent of MI patients, and 90 percent of these individuals will die despite recent breakthroughs in treatment.
- Patients who have had anterior MI or lost more than 40 percent of functional myocardium are at risk of cardiogenic shock.
- The majority of deaths occur within the first 24 hours, whereas a small proportion of individuals may die up to seven days later.
Cardiac rupture is seen in 10 percent of acute MI patients and may occur throughout healing stages, which last for five to nine days.
- The risk appears to be greater in people who have hypertension or have had large MI, and it is four times more likely in women than in men.
- Death occurs quickly due to hemopericardium and the resulting cardiac tamponade, resulting in a pulseless electrical activity cardiac arrest.
However, after the development of thrombolytic treatment, the greatest danger appears to have shifted to the first 24 hours. Early therapy with beta-blockers has been tried to lower the risk.
One of the most serious consequences of MI is heart failure. When a significant region of the heart muscle has been severely damaged, the heart's pumping function reduces and may not meet the body's demands for blood and oxygen.
- When this occurs, it is referred to as heart failure because the heart is unable to function properly.
- Heart failure complicates 25 to 50 percent of acute MI caused by a decrease in contractility in the injured myocardium because of left ventricular remodeling.
- Symptoms such as fluid retention, fatigue, and shortness of breath may occur.
Thromboembolism is caused by the formation of a mural thrombus in the severely inflamed endocardium, frequently following a massive Q-wave infarction (from the endocardium to epicardium), or the development of a ventricular aneurysm. It usually occurs one to three weeks after the infarction and accounts for three percent of all fatalities.
There is a risk of systemic embolism, which is one of the major concerns post-MI. The use of prophylactic anticoagulation is useful after the evidence of mural thrombus in the echocardiogram.
Pericarditis is generally acute and occurs within 24 to 72 hours, following MI and occurs in 20 percent of individuals following Q-wave MI.
It is normally short, harmless, and self-limiting although the symptoms can be upsetting, which include:
- Pain: Usually felt around the heart, gets worse with inspiration and is reduced by sitting up or leaning forward
- Pyrexia: Often present
- Pericardial rub: Discomfort is so common that it should be suspected based only on the history
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