Myocardial Infarction is a condition resulting from decreased blood and oxygen supply to the heart, causing cell death. The major cause is sudden blockage of coronary arteries.
Coronary arteries are blood vessels that supply the heart muscle with blood and oxygen. Blockage of a coronary artery deprives the heart muscle of blood and oxygen, causing injury to the heart muscle causing chest pain and chest pressure sensation. If blood flow is not restored to the heart muscle within 20 to 40 minutes, irreversible death of the heart muscle will begin to occur. Muscle continues to die for six to eight hours at which time the heart attack usually is "complete." The dead heart muscle is eventually replaced by scar tissue.
The Classic symptoms are sudden chest pain, breathlessness, palpitation, sweating and anxiety.
Major risk factors include previous cardiovascular disease (such as angina, a previous heart attack or stroke), older age (especially men over 40 and women over 50), tobacco smoking, high blood levels of certain lipids (triglycerides, low-density lipoprotein or "bad cholesterol") and low levels of high density lipoprotein (HDL, "good cholesterol"), diabetes, high blood pressure, obesity, chronic kidney disease, heart failure, excessive alcohol consumption, the abuse of certain drugs (such as cocaine and methamphetamine), and chronic high stress level.
The primary goal of the treatment is to first open the blocked artery and restore blood flow to the heart muscle. This process is called reperfusion. As the reperfusion takes place the patient is slowly relieved from the pain. The early reperfusion i.e. within 4-6 hours of the heart attack can not only prevent further damage to the heart but also preserves the pumping action of the heart. The damage to the pumping action of the heart develops heart failure, decreased ability to exercise, and abnormal heart rhythms.
Emergency agents: MONA- Morphine, oxygen, Nitroglycerine, aspirin
Emergency agents are used in the process of reperfusion of the heart muscle. These agents basically help in relieving the severe heart pain, cause Vasodilatation to open the blocked artery, restore the oxygen supply and prevent the further damage of the heart muscle.
Treatment overview in heart attack:
Anti-platelet medications to prevent formation of blood clots in the arteries. The NSAID, Aspirin inhibits cyclooxygenase-1 enzyme and thus prevents blood clotting by blocking the production of thromboxane A-2, by platelets, the chemical that causes platelets to clump. In addition to thromboxane A-2, platelets also produce adenosine diphosphate (ADP), which when acts on its receptor causes clumping of the platelets. The thienopyridines, clopidogrel, block the ADP receptor thus preventing the platelets from clumping.
Anti-coagulant medications to prevent growth of blood clots in the arteries. Anti-coagulants such as intravenous or subcutaneous heparin, subcutaneous low molecular weight heparin, and oral warfarin (Coumadin), prevent the formation of blood clots either by inhibiting the production of clotting factors or by interfering with the action of the clotting factors.
- Coronary angiography with either percutaneous transluminal coronary angioplasty (PTCA) with or without stenting to open blocked coronary arteries.
Fibrinolytic or thrombolytic agents are known as clot dissolving agents used to open blocked arteries and dissolve the existing clots. Intravenous administration of clot-dissolving drugs such as tissue plasminogen activator (TPA) or TNK can open up to 80% of acutely blocked coronary arteries. Drugs such as Streptokinase can be used to breaking up or dissolving the clots, by converting the intrinsic plasminogen present in the fibrin clot to its active agent form plasmin.
- Supplemental oxygen to increase the supply of oxygen to the heart's muscle.
- Medications to decrease the need for oxygen by the heart's muscle.
Beta-blockers act by decreasing the workload of the heart. Decrease in the workload decreases the demand for oxygen by the heart and limits the amount of damage to the heart muscle. Long-term administration of beta-blockers following a heart attack has been shown to improve survival and reduce the risk of future heart attacks.
- Medications to prevent abnormal heart rhythms.
Beta-blockers decrease the workload of the heart by slowing the heart rate and decreasing the force of contraction of heart muscle.