Generally, cardiac medications targeting hemodynamic properties are designed to affect afterload (vascular resistance), preload (circulating blood volume), or contractility (inotropic property).
[It should be emphasized that many of the antidysrhythmic medications also affect hemodynamic properties–particularly contractility. It should also be recalled that heart rate–especially influenced by antidysrhythmic medications–is also a property of hemodynamics.]
Drugs that affect afterload either enhance vasoconstriction or vasodilation. Vasodilators are intravenous medications that are ordered to decrease afterload on the heart by dilating arteries. The consequence of these drugs is decreased workload on the heart without decreasing contractility. Morphine and hydralazine are administered by slow IV pushes; nitroprusside is administered by intravenous infusion with calculated doses that are titrated to blood pressure. Nitroglycerin can be administered by a variety of routes with intravenous infusion the most easily regulated, but other routes may be sublingual, oral, or topical. Blood pressure and pulse must be monitored prior to initiating and during administration of vasodilators!
Drugs that enhance vasoconstriction increase afterload. These drugs are administered by intravenous infusion exclusively and must be regulated through dosage calculations and continuous monitoring of blood pressure and pulse. Most vasoconstrictors are alpha agonist sympathomimetic agents (e.g., dopamine, epinephrine, norepinephrine, or phenylephrine).
Sympathomimetic agents stimulate the sympathetic (adrenergic) nervous system. There are β1, β2, and α receptor sites associated with the sympathetic nervous system. β1 receptor sites are known as cardiac receptor sites; these receptors stimulate several myocardial properties such as contractility, heart rate, conductivity, and irritability. β2 receptors relax tubular smooth muscles; stimulation of β2 receptors result in vasodilation of arteries as well as dilation of bronchial airways in the lungs and relaxation of uterine muscle. α-adrenergic stimulation results specifically in vasoconstriction of the arteries. Usually sympathomimetic agents are administered by intravenous infusion monitored by calculated doses and hemodynamic monitoring. Below is a table revealing the effects of different sympathomimetic agents on hemodynamic properties:
|Sympathomimetic Agent:||Heart Rate(Chronotropic)||Contractility (Inotropic)||Vascular Tone (Afterload)|
|Epinephrine|||||| = vasoconstriction|
|Dopamine|||||| = vasoconstriction|
|Dobutamine||none||||↓ = vasodilation|
|Norepinephrine||minimal||at low doses|| = vasoconstriction|
|Phenylephrine||none||none|| = vasoconstriction|
|Isoproterenol||||||↓ = vasodilation|
Vasodilation can also be achieved with ACE inhibitors or angiotensin II receptor blockers (ARBs). Medications from these categories achieve a reduction in afterload–and consequently less myocardial workload–by promoting vasodilation. ACE inhibitors and ARBs work on the renin-angiotensin-aldosterone system (RAAS); ACE inhibitors block the formation of angiotensin 2, and ARBs block the receptor sites stimulated by angiotensin 2. ACE inhibitors produce the following therapeutic effects: 1) arterial dilation reducing afterload and increasing renal artery perfusion, 2) dilation of veins reducing the preload on the right ventricle, 3) suppression of the release of aldosterone limiting the retention of sodium and water from kidney elimination, and 4) increased levels of bradykinin by suppression of kinase II. Oral ACE inhibitor therapy is recommended by American Heart Association for acute myocardial infarction within the first 24 hours in order to reduce the extent of ventricular remodeling (changes in ventricular shape and function as a consequence of infarction). For heart failure, ACE inhibitors and ARBs reduce workload on the myocardium by reducing both preload and afterload.