Major medications used to relieve chest pain include nitrates such as nitroglycerin and narcotic pain relievers such as morphine. Benzodiazepines, which are minor tranquilizers or antianxiety agents can help relieve anxiety.
Need To Know:
Nitrates, such as nitroglycerin, are used to treat chest pain associated with a heart attack as well as angina. Nitrates work by relaxing smooth muscle, including the smooth muscle in the walls of blood vessels. This causes them to dilate or open up, which improves blood flow to the heart and rest of the body.
This widening of arteries also lowers resistance to blood flow and blood pressure, which lowers the work of the heart. Dilation of veins decreases the amount of blood flow returning to the heart, which also decreases the heart's work load.
Nitrates improve blood flow to the heart and decrease work of the heart. Both of these events relieve pain due to inadequate blood flow (thus, oxygen supply) to heart muscle.
Nitrate medications comes in a variety of forms including:
Pills that dissolve under the tongue
Pills that are swallowed
Ointments or creams
Forms for intravenous administration
Intravenous nitroglycerin is recommended for the first 24 to 48 hours after a heart attack in patients with :
An acute heart attack complicated by congestive heart failure
A large heart attack affecting the front wall of the heart, called an anterior-wall myocardial infarction
Persisting insufficient blood flow to heart muscle, as detected by pain and ECG
Hypertension or high blood pressure
Use of nitroglycerin beyond 48 hours is useful if the chest pain returns or if persistent lung congestion due to heart failure occurs.
Individuals with an abnormally low blood pressure or slow heart rate should not receive nitrates because of their tendency to lower blood pressure. Side effects of nitrates include headache and occasional faintness.
Morphine and other narcotic pain relievers are used to relieve chest discomfort associated with a heart attack. Repeat dosages of morphine can be given intravenously frequently if breathing remains normal and no signs of toxicity occur. Side effects of narcotic pain relievers include nausea and pruritus (itching).
Medications To Limit The Size Of The Heart Attack: "Clot Busters"
During a heart attack, most damage to heart muscle occurs in the first six hours. Treating a heart attack during the first two hours is essential to preventing or reducing heart muscle damage.
Most heart attacks are caused by a blood clot blocking a coronary artery. Using thrombolytic agents or "clot busters" that can break down blood clots and restore blood flow through the artery can limit heart muscle damage.
Although these medications work slightly differently, they all activate an enzyme called "plasmin," which breaks down fibrin in blood clots.
Need To Know:
Giving a clot buster within several hours of an acute heart attack restores blood flow and significantly reduces damage in most cases where a coronary artery has been blocked by a blood clot. The earlier these drugs are used, the greater the benefit.
Giving thrombolytics within one hour after a Q-wave heart attack restores blood flow in up to 80 percent of cases.
Using thrombolytics within two hours of the onset of chest pain cuts the death rate to half that of patients who received therapy after six hours of pain.
Minutes count! The goal of many medical facilities is to have a "door-to-needle" time of 30 minutes of less - from when a patient enters to when he or she receives the clot buster medication.
Clot buster therapy is sometimes followed by treatment with blood thinners such as heparin to prevent future clot formation. Blood thinners can be given intravenously or under the skin, depending on type of drug and the patient's risk for future problems due to blood clots.
Thrombolytic treatment is appropriate for patients with an acute heart attack who:
Can begin treatment within 12 to 24 hours of the onset of symptoms (preferably less than 12 hours)
Have ST segment elevation in two or more leads on an electrocardiogram or ECG, consistent with an acute Q-wave heart attack affecting the entire thickness of heart muscle
Have other ECG changes consistent with a heart attack affecting the front wall of the heart
Thrombolytics probably do not help people
With pain that has lasted for longer than 24 hours
Who only have ST segment depression on ECG.This ECG finding is suggestive of a non-Q-wave heart attack, which often only affects the innermost layer of the heart muscle.
People at risk for bleeding should not receive thrombolytic agents. These include people
Recovering from recent surgery
With active bleeding from stomach ulcers
With very high blood pressure
With a history of a recent stroke, head injury, or a bleeding disorder
An alternative to thrombolytic therapy is coronary angiography followed by percutaneous transluminal coronary angioplasty (PTCA) referred to as "primary PTCA."
Other drugs can help limit the size of the damage by reducing the work load of the heart.
Medications To Reduce The Work Load Of The Heart
How well the heart works after a heart attack depends largely on how much heart muscle was damaged. Medications that decrease the work load and the oxygen needs of the heart can
Reduce the size of the area of dead heart muscle
Optimize the amount of remaining healthy heart muscle
Drugs that decrease the work load of the heart include:
Beta blockers have long been used in the treatment of angina and hypertension (high blood pressure).
Intravenous beta blockers given within the first several hours of the onset of a heart attack improve the prognosis (outcome) by:
Reducing the size of the infarct (area of dead muscle cells)
Lowering the chances of a repeat heart attack
Reducing the risk of deadly abnormal heart rhythms such as ventricular fibrillation
All of these benefits reduce the risk of death.
Treatment with beta blockers within the first 24 hours of the onset of a heart attack is recommended for all patients who can tolerate them. Beta blocker therapy is especially useful in individuals with continuing or recurrent pain or abnormally fast heart rhythms called tachycardias.
Beta blockers reduce the heart's work load by:
Slowing the heart rate
Reducing how hard the heart pumps, called contractility
All of these effects lower blood pressure as well as heart muscle oxygen requirements.
Due to the actions of beta blockers on the heart, blood vessels, and lungs, some people may not be able to tolerate beta-blocker therapy, including those with:
Abnormally low blood pressure or hypotension
Abnormally slow heart rate (bradycardia)
Asthma or chronic obstructive pulmonary disease (COPD)
Side effects of beta blockers may include:
Hyperglycemia or high blood sugar level
Undesirable changes in blood lipid levels, such as increased triglyceride levels and lower levels of "good" (HDL) cholesterol
Some of these side effects can be reduced by lowering the dosage.
Angiotensin converting enzyme (ACE) inhibitors
Angiotensin converting enzyme (ACE) inhibitors are drugs used in the treatment of:
Hypertension or high blood pressure
Diabetic nephropathy, which is kidney disease due to diabetes
Myocardial infarction or heart attack
Need To Know:
Using angiotensin converting enzyme (ACE) inhibitors after a heart attack:
Limits undesirable structural changes to the heart chamber that pumps blood through the body called "ventricular remodeling"
Lowers the frequency of complications such as recurrent angina and heart failure
Reduces the risk of death from the heart attack
Reduces the risk of a subsequent heart attack
The benefits of ACE inhibitor therapy add to the benefits of treatment with beta blockers (see above) and aspirin and are greatest in individuals with impaired ventricular function, which is inadequate heart pumping, and full-blown heart failure.
ACE inhibitors should be given 24 hours or more after stabilization with thrombolytic drugs and continued indefinitely in individuals with impaired ventricular function.
ACE inhibitors work by blocking the conversion of the inactive angiotensin I to active angiotensin II. The resulting lower level of angiotensin II circulating in the bloodstream reduces blood pressure and the work of the heart because of:
Less blood vessel constriction or narrowing caused by angiotensin II. TThis reduces resistance to blood flow through blood vessels, putting less strain on the heart.
Less retention of sodium and water by the kidneys in response to angiotensin II. This results in a lower volume of blood that has to be pumped by the heart.
The most common side effect of ACE inhibitors is a reversible dry cough. Other side effects may include:
Hyperkalemia or high potassium levels
Infrequent and rare side effects include a reduction in the number of white blood cells, called neutropenia, and a reversible skin rash with one type of ACE inhibitor.
Medications To Prevent And Treat Complications
This set of drugs includes an assortment of agents used to treat complications of a heart attack, including:
Drugs for heart failure
Anticoagulants or blood thinners
Aspirin decreases clot formation by reducing platelet adhesion. This is the "sticking together" of a type of blood cell involved in blood clot formation. Aspirin therapy has been shown to decrease the risk of death associated with a heart attack as well as reduce the risk of a subsequent heart attack.
Unless contraindicated, aspirin should be started immediately and continued indefinitely on a daily basis.
Other drugs that reduce platelet adhesion may be substituted if the person is allergic to aspirin or does not respond to treatment.
Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) are useful for treating chest pain due to pericarditis (inflammation of the sac that encloses the heart), which may occur after a heart attack.
Antiarrhythmic agents refers to a variety of drugs used to treat abnormal heart rhythms or arrhythmias associated with a heart attack.
These drugs are divided into four classes:
Class I: These are sodium channel blockers including drugs such as quinidine, procainamide, and lidocaine. These agents must be used with caution as they can also depress left ventricular function (heart pumping) and promote or cause arrhythmias.
Class II: These drugs are beta-blockers and examples include atenolol and metoprolol. These agents are used to control supraventricular tachycardias (arrhythmias originating above the ventricles) and also help to suppress dangerous ventricular arrhythmias such as ventricular tachycardia and ventricular fibrillation.
Class III: Examples of these drugs are amiodarone and sotalol. Amiodarone is the most powerful antiarrhythmic drug, but its side effects limit its use. Sotalol is also a beta-blocker, with side effects and other actions similar to those of other beta-blockers. It is used to treat atrial fibrillation and atrial flutter as well as ventricular arrhythmias.
Class IV: These drugs are calcium channel blockers, which slow the heart rate and dilate or open up blood vessels. These drugs are used to control abnormally rapid rhythms such as atrial fibrillation as long as signs of heart failure or heart block are not present. Examples include verapamil and diltiazem.
In addition to the above four classes of antiarrhythmic drugs, there are also some miscellaneous drugs:
Digoxin - This medication increases the strength of heart muscle contractions and is useful in the treatment of heart failure. Because digoxin also slows conduction of the heart's electrical impulses, it is also useful in controlling atrial fibrillation, atrial flutter, and atrial tachycardia.
Adenosine - This drug slows or blocks the conduction of electrical impulses. Since it is only available in intravenous form and only works for a short time, adenosine is only used as acute treatment for supraventricular tachycardias.
Most of the above drugs treat rapid or irregular heart rhythms. Slow heart rhythms (bradycardia) or asystole (cardiac standstill) are treated with atropine or similar drugs. In some cases, a pacemaker may be necessary.
Need To Know:
The selection of the antiarrhythmic drug depends on the type of abnormal rhythm and clinical circumstances. Another way of treating arrhythmias is electrical cardioversion. This involves application of electrical shocks to the chest to convert the abnormal heart rhythm to a normal rhythm.
Electrical cardioversion is used to stop all life-threatening tachycardias or rapid heart rhythms. Cardioversion of ventricular fibrillation to sinus rhythm is referred to as defibrillation. Cardioversion is also used to stop atrial flutter or atrial fibrillation associated with cardiovascular instability or ischemia.
Drugs for Heart failure
Drugs commonly used to treat heart failure that may occur with a heart attack include:
Diuretics, which reduce the blood volume by causing the kidneys to get rid of more sodium and water
Individuals with very low blood pressure due to cardiogenic shock may require treatment with inotropic agents, which are drugs that increase the force of heart contraction. Two examples are dopamine and dobutamine.
These drugs increase the vigor of heart pumping, which in turn increases the amount of blood pumped. The higher cardiac output increases blood pressure and allows more body tissues to receive adequate blood flow.
Anticoagulants or blood thinners differ from thrombolytic agents in that they prevent blood clots from forming as opposed to dissolving them.
Good candidates for treatment with anticoagulants such as heparin after a heart attack include those who are:
Undergoing percutaneous or surgical revascularization - the reestablishment of the blood supply to a portion of muscle
People receiving nonselective thrombolytic agents who are not at high risk for such blood clots may still benefit from subcutaneous heparin, which is heparin administered under the skin instead of in the veins. The routine administration of intravenous heparin does not appear to benefit these individuals.