EMS Pharmacology: Drugs That Affect the Cardiovascular System …

Drugs that Affect the Cardiovascular System

The heart is made up of many interconnected branching fibers that form the walls of the 2 atria and 2 ventricles. Some of these fibers are capable of, and responsible for, conducting electrical impulses while other fibers are mainly responsible for muscle contraction. These specialized fibers are nourished through a vast network of blood vessels known as the coronary vasculature. Medications that affect these fibers are classified by their specific effect on the tissue.

Cardiac glycosides are naturally occurring plant substances that have characteristic effects on the cardiac muscle. These specific compounds contain a carbohydrate molecule (sugar). When this molecule is combined with water, it is converted into a simple sugar plus 1 or more active substances. Glycosides may actually work by blocking certain ionic pumps in the cellular membrane. This action, indirectly increases the calcium concentration reaching the contractile proteins. A key cardiac glycoside is digoxin (Lanoxin); it is used to treat heart failure and to treat certain types of tachycardias.

Digitalis glycosides can affect the heart in 3 distinctive ways:

Many patients that take cardiac glycoside medication may develop side effects at one time or another due to the relatively small therapeutic value of these medications.

The symptoms associated with possible side effects include:

These symptoms are often vague and is easily attributed to a non-related viral illness by the patient.

The most common side effects of cardiac glycosides are:

The toxic effects of cardiac glycosides are mainly dose related. These effects can be increased by the presence of other medications such as diuretics and may cause cardiac rhythm disturbances.

The common dysrhythmias often associated with cardiac glycoside toxicity are:

For this reason, patients taking cardiac glycoside medication will require close monitoring during transport.Treatment for digitalis toxicity may include correction of underlying electrolyte imbalances and the use of certain antidysrhythmics.

Antiarrhythmic medications are used to treat and help prevent disorders of the cardiac rhythm. The pharmacological agents that suppress cardiac dysrhythmias may do so by its direct action on the cardiac cell membrane as seen with lidocaine, or the indirect action that affects the cells as seen with propranolol (a beta-blocker), or both.

The cardiac rhythm disturbances that this medication is intended to treat, may be caused by:

Dysrhythmias occur from disturbances in the impulse formation, disturbances in the impulse conduction or both.

Antidysrhythmic drugs have been classified into categories based on their fundamental mode of action on the cardiac muscle. Drugs that belong to the same class do not always produce an identical action. However, all antidysrhythmic drugs have some ability to suppress the automaticity of the tissues.

Sodium channel blockers arethe largest and most commonly prescribed group of antiarrhythmic drugs. These drugs bind to sodium channels when the channels are in the open and inactivate state, then they dissociate from the channels during the resting state. The sodium channel blockers have the most pronounced effect on cardiac tissue that is firing to rapidly. This occurs because these sodium channels spend more time in the open and inactivate state than in the resting state, calleduse-dependent blockade.Because of use-dependent blockade, sodium channel blockers suppress cardiac conduction more in a person with tachycardia than in a person with a normal heart rate.The drugs in Class I have been subdivided into three groups (Ia, Ib, and Ic). This is based on whether they have greater affinity for the open state or the inactivate state and based on their rate of dissociation from sodium channels called "rate of recovery".

Class II drugs are beta-blocking agents that reduce adrenergic stimulation of the cardiac muscle. Beta blockers were given their name because this class of medications counteracts the stimulatory effects of epinephrine (adrenaline) on the beta-adrenergic receptors found in the nervous system and the heart. Normal stimulation of the beta receptors leads to a faster heartbeat along with the constriction of blood vessels, resulting in an overall increase in blood pressure.Beta blockers, therefore, counteract stimuli that leads to an elevated blood pressure, resulting in a slower pulse rate and a reduction in the blood pressure. Both these effects reduce the workload of the heart, so beta blockers are of value in treating the symptoms of angina pectoris (chest painbrought on by narrowing of the coronary arteries that causes inadequate delivery of oxygen-rich blood to the heart muscle).

Examples of common Beta-blockers include:

Class III drugs are administered to cause a potassium channel blockade that increases the contractility of the heart. Unlike other antidysrhythmics, this type of medication does not suppress cardiac automaticity. It may not have any effect on conduction velocity, at all. This type medication is thought to work by blocking the inflow of calcium through the cell membranes of both, cardiac and smooth muscle cells. It helps cease the reentry of blocked impulses.The primary role of potassium channels in cardiac action potentials is cell repolarization. In non-nodal tissue, action potentials are initiated when a cell is depolarized to a threshold potential by an adjacent cell. This leads to rapid opening of fast sodium channels and a slower opening of some calcium channels, permitting calcium to enter the cell.As these channels become inactivated, potassium channels open permitting potassium ions to leave the cell, which causes repolarization of the membrane potential. Potassium channels remain open until the next action potential is triggered.

Examples of common potassium channel blockers include:

Calcium channel blockers prevent calcium from entering cells of the heart and blood vessel walls, resulting in a lower blood pressure. Calcium channel blockers relax and widen blood vessels by affecting the muscle cells in the arterial walls. Some calcium channel blockers have the added benefit of also slowing the heart rate, which can further reduce blood pressure, relieve chest pain (angina), and control an irregular heartbeat. This action depresses automaticity, and in some cases, depress conduction velocity.Some calcium channel blockers are available in short-acting and long-acting forms. Short-acting medications work quickly, but their effects last only a few hours. Long-acting medications are slowly released to provide a longer lasting effect.

Examples of calcium channel blockers include:

High blood pressure affects as many as 50 million Americans alone and has been directly related to many incidence of stroke, cerebral hemorrhage, heart failure, renal failure, and cardiovascular disease. The exact mechanism of action of many of the antihypertensives is unknown.

The ideal antihypertensive agent should accomplish the following for the patient:

Certain medications are used to reduce blood pressure in patients with chronic hypertension. These drugs are usually given in low dose combinations and then titrated to reach the desired effect.

These drugs include:

Diuretics are the drug of choice for the treatment of hypertension and are often used in conjunction with other medications to reach the desired BP range. Diuretics cause a loss of salt and water from the body through the kidneys. This decrease in plasma and extracellular fluid volume decreases preload and stroke volume. The decrease in fluid volume has a direct effect on the diameter of the arterioles, resulting in a reduced BP. The response causes an initial decrease in cardiac output followed by a decrease in peripheral vascular resistance.

Sympathetic blocking agents may be classified as beta-blocking agents and adrenergic-inhibiting agents. Adrenergic blocking agents are effective antihypertensives that work by modifying the action of the sympathetic nervous system. Arterial pressure is influenced through various mechanisms of the heart, blood vessels, and the kidneys. Sympathetic stimulation increases the heart rate and force of myocardial contraction, constricts arterioles and venules, and cause the release of renin from the kidneys. Blocking this sympathetic stimulation can and will reduce blood pressure.Adrenergic-inhibiting agents are classified as centrally acting adrenergic inhibitors or peripheral adrenergic inhibitors. The exact mechanism of action for many of these agents is unknown, but it is believed they have several points of action.

Examples include:

Centrally acting adrenergic inhibitors

Peripheral adrenergic inhibitors

Vasodilator medications act directly on the smooth muscle walls of the arterioles, veins or in some cases both, causing an overall decrease in peripheral vascular resistance. This in turn lowers the patients overall blood pressure. This action stimulates the sympathetic nervous system and activates the baroreceptor reflexes, leading to an increase in heart rate, cardiac output, and renin release. Medications that are given to inhibit the sympathetic response are usually given in this form.In addition to their usefulness as powerful antihypertensives, some vasodilators are very effective in the case of ischemic chest pain (angina pectoris). For example; nitrates are given to cause the veins/arteries to dilate, this leads to venous pooling and reduces the amount of blood returning to the heart. Thereby reducing left ventricular end-diastolic volume which subsequently lowers blood pressure. The decrease in wall tension helps to reduce myocardial oxygen demand and reduce the associated ischemic chest pain. Vasodilator drugs are classified as arteriolar and arteriolar/venous dilators.

Examples of each class include:

Arteriolar dilator medications

Arteriolar and Venous dilators medications

As we recall from A and P, the renin-angiotensin-aldosterone system plays a key role in maintaining blood pressure and fluid/sodium balance. A disturbance in this system can cause hypertension. In addition, kidney damage may result in an inability to regulate the release of renin through normal feedback mechanisms, causing an elevated blood pressure in some patients. Angiotensin II is a strong vasoconstrictor that raises the blood pressure. Angiotensin II also cause the release of aldosterone, which contributes to water and sodium retention.

Examples of ACE Inhibitors include:

Calcium channel blocking agents reduce peripheral vascular resistance by inhibiting the contractility of vascular smooth muscle and dilate the coronary vessels in the same manner. The effects of these drugs are important in treating hypertension, decreasing the oxygen requirements of the heart through decreased afterload. The various drugs in this class differ in the degree of selectivity for the coronary and peripheral vasodilators or decreased cardiac contractility.

Examples of calcium channel blockers include:

A new class of antihypertensive agent. They block the renin-angiotensin-aldosterone system more completely than ACE inhibitors. This medication lowers blood pressure by selectively inhibiting the actions of the angiotensin II receptors that include vasoconstriction, renal sodium reabsorption, aldosterone release, and stimulates the central/peripheral sympathetic activity. These drugs are normally administered to patients that can not tolerate the effects of ACE inhibitors.

Drugs in this class include:

Antihemorrhagic Agents are used to treat peripheral vascular disorders caused by pathological or physiological obstruction as seen with arteriosclerosis. These medications improve the blood flow and the oxygen delivery to the ischemic tissue. They do this by restoring red blood cell flexibility and reducing the blood's viscosity. An example of of an anti-hemorrheologic agent is pentoxifylline (Trental).

Medicationsused to treat Dysrhythmias

Medicationsused to Optimize Cardiac Output/Blood Pressure

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EMS Pharmacology: Drugs That Affect the Cardiovascular System ...