Pharmacology Week 5- Cardiac Review and Drugs

madamj2004's version from 2016-02-19 17:34

Section 1

Question Answer
CHFCongestive Heart Failure. Condition in which the heart is unable to pump sufficient blood to the tissues of the body..
CADCoronary artery disease. A general term for insufficient blood flow through the coronary arteries.
MIMyocardial Infarction. Death of cardiac muscle cells, usually caused by thrombosis.

Section 2

Question Answer
Cardiac Glycoside- OriginFound in the leaves of plants (eg. Foxglove). Contain compound glycoside.
Cardiac Glycoside- Used ForPrimarily Tx of CHF
Cardiac Glycoside- Pharmacological EffectsIncreased force of myocardial contraction (does not appreciably increase O2 consumption), improving efficiency of the heart. Decreases HR and AV conduction speed, stimulation of vagus nerve and depressing action of AV node.
Cardiac Glycoside- Characteristic ECG changesTherapeutic doses: ST depression, T wave alteration, increased PR interval=lengthened conduction time. Higher doses: Potential for heart conduction blockages.
Cardiac Glycoside- Mycardium ContractilityInhibits ATPase=no ATP to power Na+/K+ pump. Na+ accumulates inside the cell, resulting in more activity of the Na+/Ca++ pump bringing more Ca++ inside the cells. Allows for better contraction of the heart muscle. Contractions will also be SHORTER d/t alteration in Ca++ levels.
Cardiac Glycoside- AV ConductionInterference with Na+/K+ pump slows the return of K+ back into contractile cells after action potential. Slowed repolarization and prolonged REFRACTORY period.
Digoxin(Lanoxin) Cardiac Glycoside.
Digitoxin(Digitoxinum) Cardiac Glycoside.
Digitilazation"front loading" of a drug. Drug given at higher and more frequent doses in order to rapidly achieve therapeutic levels.
MaintenanceLow term usage. Lower and less frequent levels to maintain the therapeutic level.

Section 3

Question Answer
Cardiac Glycoside- Serum ElectrolytesCardiac Glycoside VERY affected by changes in serum electrolyte levels, particularly K+ and Ca++
Cardiac Glycoside- HypokalemiaThere is an INCREASED binding of glycosides to ATPase. Even more inhibition of the Na+/K+ pump. Increased incidences of ventricular ectopy and arrhythmias.
Cardiac Glycoside- HyperkalemiaAntagonistic to the therapeutic effects of cardiac glycosides.
Cardiac Glycoside- HypercalcemiaEnhance the action of cardiac glycosides- higher serum levels available for each contraction=arrhythmias.
Cardiac Glycoside- HypocalcemiaCan have a protective effect against the toxic (over excitation) of glycoside toxicity.
Cardiac Glycoside- Worse Case ScenarioArrhythmias and PVCs
Ectopic BeatsTypically PVCs (premature ventricular contractions) not associated with ischemic event.
Cause of Ectopic BeatsUsually caused by cardiac glycoside overdose.

Section 4

Question Answer
Diuretic Therapy- Primary RoleElimination of extra sodium and water by the urinary tract.
Reason For Diuretic TherapySodium and water retention leads to excess circulating blood volume and edema.
Indications for Diuretic TherapyCHF
Diuretic Therapy- CombinationCommonly used in combination with cardiac glycosides to rapidly decrease congestion and ease workload of the heart.
Furosemide(Lasix) Potent diuretic used in CHF emergencies.
Thiazide Family(eg. HCTZ) Milder diuretic typically for long term usage.

Section 5

Question Answer
Vasodilator Therapy- Primary EffectRelax and dilate blood vessels arteries and veins.
Reason for Vasodilator TherapyLower PVR. Decrease cardiac workload. Decrease cardiac oxygen consumption.
Vasodilator Therapy- ResultHeart able to pump MORE blood with LESS effort. Lowered blood pressure.
AfterloadThe amount of resistance against which the heart must pump blood out of the ventricles (aka PVR)
PreloadThe amount of blood entering the ventricles prior to systole.
Vasodilator Therapy- Effects on Preload/AfterloadDecreases the afterload= less PVR. Decreases the preload = less blood returning to heart.

Section 6

Question Answer
ACE InhibitorsAngiotensin-converting enzyme inhibitors
ACE Inhibitors- Primary EffectDecrease/Inhibit the formation of angiotensin
Angiotensin IIA potent vasoconstrictor formed at times of stress or decreased circulating blood volume.
ACE Inhibitors- Secondary EffectDilation of arterolar and venous vessels
Captopril(Capoten) ACE Inhibitor
Lisinopril(Zestril, Prinivil) ACE Inhibitor
Enlapril(Vasotec) ACE Inhibitor

Section 7

Question Answer
Angiotension Receptor Blockers (ARBs) Primary EffectBind to angiotensin II receptors to stop angiotensin II from taking effect
Angiotension Receptor Blockers- Secondary EffectVasodilation. Increased excretion of sodium and water.
Advantage of ARBs over ACE inhibitorsLess allergic responses
Candesartan(Atacand) Angiotension Receptor Blockers
Irbesartan(Avapro) Angiotension Receptor Blockers
Iosartan(Cozaar) Angiotension Receptor Blockers
Valsartan(Diovan) Angiotension Receptor Blockers

Section 8

Question Answer
Nitroglycerine- Venous effectPotent veno-dilator
Nitroglycerine- Arterial effectSome arterial dilation but not significant for tx of CHF
Nitroglycerine- Primary EffectDecrease venous return thus decreasing workload of the heart.
Nitroglycerine- MechanismContains nitrite ions which get converted to NO in the blood.
Nitric OxideA potent but short acting relaxant of smooth muscle, particularly in vascular tissue.