BIOL 200 - Lecture 05

BIOL 200 - Lecture 05 - Unit 5 Drugs of the Cardiovascular...

Info iconThis preview shows page 1. Sign up to view the full content.

View Full Document Right Arrow Icon
This is the end of the preview. Sign up to access the rest of the document.

Unformatted text preview: Unit 5 Drugs of the Cardiovascular System Cardiotonic drugs • Drugs that increase the strength of the heart. • Drugs for a failing heart. The heart becomes weaker as a pump. Can happen over many years or rapidly in response to injury • Goals for treatment: increase CO and increase pumping efficiency while reducing cardiac work (increase preload and decrease afterload) Cardiac Glycosides (digoxin) • MOA: increases contractility in the heart muscle Increases intracellular calcium ion concentration and increases the force of contraction. Increases CO and relieves edema if it is present • S/E: narrow therapeutic window, long half life Development of arrythmias Can induce AV block Arrythmias • Abnormal pacemaker activity: a cell takes over the pacing of the heart at a rate that is different from what it ought to be. Ectopic pacemakers: cells generating impulse outside of the SA node The first cell to reach threshold will begin to pace the heart. 4 classes of drugs for Arrythmias • Sodium channel blockers: delay the upward spike which then will take longer to trigger the action potential. Delay phase 4 to spike of AP Calcium channel blockers: same MOA as above Blocking beta receptors: slows automaticity Potassium channel blockers: will cause the cell to take longer to get back to resting membrane potential and slows the heart rate. Makes the whole AP process take longer • • • Class 1: Sodium channel blockers • Bind to channels in the inactive and active state, they prolong the period in which these channels don’t work. These drugs will lengthen the time it takes for the channel to go back to the resting state. Especially effective in sites of ischemia. Quinidine • A sodium channel blocker, not widely used. There is an antimuscarinic effect. • Blocks open & active sodium channels. It will stop an arrythmia. • Effective orally • Problem: potential for generating arrythmias due to lengthening of the action potential. Lidocaine • Also sodium channel blocker; used for ventricular arrythmias (esp. v-fib) • Effective with less tendency for cardiotoxicity • Used intravenously; first pass metabolism Amiloridorane • Potassium channel blocker & sodium channel • • • • blocker. Also blocks calcium channels & betaadrenergic receptors. Effective in orally suppressing arrythmias. Less likely to produce arrythmias. Has a very long half life and has a tendency to go crystalize in the tissue Pulmonary fibrosis is the limiting side effect Class 2: Beta adrenergic antagonists • Slow the heart down and suppresses arrythmias • Decrease catecholamine induced automaticity Class 3: Potassium channel blocker (sodalol) • Prolongs the action potential and refractory period. • If you lengthen the AP it takes longer to get back to the resting potential and longer until the cells can fire again. • Produces the same arrythmias as quinidine. Class 4: Calcium channel blockers (verapamil) • Works the same way as the sodium channels blockers, they have a preference for open/active channels. But they works at the SA & AV node, places where calcium currents are driving the current • Effective for atrial arrythmias and circus movements • Can weaken the cardiac muscle over time Hypertension • CVD #1 killer in the US • Essential hypertension: no identifiable cause that • • you can treat. Treatment aimed a symptoms. Symptoms are unnoticeable. Risk factors: weight, sex, family history, genetics Targets for treatment • CO: sympatholytics • Vascular resistance: sympatholytics, direct acting vasodilators, drugs that interfere with the RAA system • Fluid volume: diuretics Damage to the Cardiovascular System • Hypertrophy of the heart. The heart is stretched and leads to remodeling cardiomyopathies The bigger the heart, the more wall tension the heart has to generate to push blood against the pressure • Vascular damage Elevate pressure can damage the blood vessels Centrally acting sympatholytic (clonidine) • MOA: alpha-2 adrenergic agonist in the brain. When those receptors are turned on it decreases sympathetic outflow. When that happens you see a decrease in vascular resistance and decrease in CO. • Uses: HTN • S/E: sedation & depression Rebound HTN Centrally acting (guanefidine & reserpine) • MOA: prevents the release of nor-epi from nerve terminals Decrease vascular resistance and a decrease of CO 2nd line drug • S/E: severe hypotension Reserpine can cross the BBB & can cause depletion of catecholamines, commonly causes depression Alpha (1) Blockers (prazosin) • MOA: block alpha receptors in peripheral arterioles. The arterioles dilate and the BP falls. Drugs are very useful in lowering BP • S/E: 1st dose hypotension --> dizziness (postural hypotension) Drowsiness Fluid retention tachycardia Beta Blocker (propranolol) • MOA: blocks beta adrenergic receptors, decreasing cardiac output and heart rate--> decreasing BP Decrease in vascular resistance and dilation arterioles • Indications: HTN, arrythmias • S/E: decrease in contractility of heart, rebound • HTN Contraindications: asthma (b-2 receptors) Calcium channel blockers (verapamil) • MOA: blocks the calcium channels in smooth muscle and cardiac muscle. Not all Ca++ channel blockers are the same; same work better for arrythmias (verapamil), some are better for the blood vessels (nifedipine) • S/E: decrease contractility in the heart ACE inhibitors • MOA: inhitbits angiotensin converting enzyme Decreases BP in practically everyone • Indications: HTN • Adverse effects: common dry cough • C/I: pregnancy due to tendency toward renal stress and potential renal failure Angiotension 2 receptor blocker • Same action as ACE inhibitor • No cough Calcium Channel Blockers • MOA: cause vasodilation • Therapeutic uses: HTN, suptraventricular tachycardia, angine • Note: better antihypertensive agent for African Americans (in combo w/ diuretics • CI: not for patients with CHF Diuretics • Often first line therapy • If one drug only is being used, it is usually a diuretic • MOA: reduces hypervolemia Also appears to relax blood vessels Antihypotensive Agents • These drugs increase blood pressure • How? Increase peripheral resistance (ie; alpha agonist) Increase CO (ie; beta agonist) Increase (replace) fluid volume (ie; whole blood) • Therapeutic uses: chronic symptomatic hypotension, acute hypotension, replace bllod volume Antianemic / Hemopoietic Drugs • Drugs that replace missing factors for blood formation Iron, vitamin B12, folic acid • Therapeutic uses: treat anemias Drugs affecting Coagulation • Hemostatics - speed up blood clotting Used to treat hemorrhage • Anticoagulants - slow down blood clotting, decrease risk of clotting Work by blocking the formation of thrombin & fibrin, decreases platelet aggregation Therapeutic uses: venous thrombosis, prevent coronary thrombosis, any condition that results in blood remaining in heart after systole • Thrombolytics: drugs that dissolve clots MOA: cause plasminogen to convert to plasmin Therapeutic use: any clot Antilipemic Agents • • • • Fibroic Acid Derivatives Niacin Bile sequestrant Statins Statins • MOA: inhibit enzyme for cholesterol synthesis Can greatly reduce LDL cholesterol (30-40%) • Adverse effect: May negatively affect the liver Muscle pain, weakness ...
View Full Document

Ask a homework question - tutors are online