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STUDY GUIDE

CHAPTER 26

QuestionAnswer
Congestive heart failure Due to weakening of d contractile function of d heart. Blood/fluid accumulate in d heart, lungs, abdomen, and lower extremities because d heart fail to pump well. Decrease cardiac output/ b/p are unable to meet body requirements.
CHF CONT. BAD Cardiovascular reflexes cause vasoconstriction,tachycardia, and sodium and fluid retention which try to maintain b/p, but usually fail.
Mechanism of action Cardiac glycosides inhibit Na/k adenosine triphosphatase, d "sodium pump" which causes more Na to remain inside myocardial cells.
Mechanism of action CONT. Increased intracellular Na stimulates Na/Ca exchanges that brings more Ca inside heart cell to increase the force of contraction.
Mechanism of action Cont. Cardiac glycosides also stimulate the vagus nerve which decreases heart rate.
Cardiac Glycosides Drug orignially obtained from plant source, Digitalis purpurea and Digitails lanata. Digoxin and digitoxin are the only cardiac glycosides currently available.
Cardiac Glycosides CONT. Main pharmacologic effect of cardiac glycosides is to increase d contractile force of myocardial contraction.CARDIA GLYCOSIDES ALSO DECREASE HEART RATE AND ATRIOVENTRICULAR CONDUCTION. (Test)
Pharmacokinetic and dosing Digoxin is water soulbe and eliminated mostly unmetabolized by d urinary tract,Digitoxin is more lip soluble,requires metabolism, and has a longer half-life.
Pharmacokinetic CONT: In acute CHF, initial digitalization doses are administered to rapidly attain effective therapeutic concentration. Lower daily maintenance doses are then given to maintain desired therapeutic concentrations.
Adverse Effect Common complaints include headache, dizziness, nausea, and vomiting. visual disturbances halo effect around lights often signals overdosage
Adverse effect CONT: Bradycardia, ectopic beats and a variety of other cardia arrhythmias can occur and can be life-threatening.* check d heart rate b/4 you give heart medication.* if d HR is below 60 you can not give digoxin.
Electrolyte and cardiac glycoside interactions Low serum potassium (K) level "Hypokalemia" increase drug toxicity and can cause cardiac arrhythmias. people we be toxicity
Electrolyte CONT: High serum potassium level hyperkalemia decrease d actions of d cardiac glycosides. increase serum calcium level hypercalcemia can increase d actions/ toxicity of d cardiac glycosides.
Ace Inhibitors Increase cardiac output, cardiac rate, cardiac contractility. Causes Dizziness, orhostatic hypotension, Gl distress, nonproductive cough, headache.
Vasodilator Therapy of CHF Vasodilator drugs relax and dilate blood vessels,it make blood easier to pump d the heart, vasodilation decreases peripheral resistance, allows more efficient blood flow, and usually increases cardia output.
Vasodilator CONt: Angiotension-converting enzyme inhibitors and angiotensin receptor blocking drug are particulary useful in CHF. Angiotensin-converting enzyme inhibitors the are vasodilator.
Cardiac Arrhythmias Arrhythmias are disturbances in the normal electrical activity of the heart- make heart work effectively. Arrhythmias can be detected on a recording of d ECG.
Cardiac Arrhythmias CONT: Supraventricular arrhythmias occur above d ventricles in d atria, SA node, and AV node. ventricular arrhythmias occur in d ventricles and purkinje fibers and are usually more serious and life threating.
SA and AV If is not working well is called Arrhythmias. SA node is a peacemarker (Excitability)
Electrophysiological properties of the heart Excitability, Automaticity,Refractory period, PVCs
Excitability associated with membrance depolarization and the influx of Na ions
Refractory Period Associated with repolarixation and the efflux of K ions.
Automaticity ability of the SA and AV nodes to initiate membrane depolarizations. under conditions of hypoxia and excessive sympathetic stimulation, the ventricles can also demonstrate automaticity to cause extopic beats or PVCS
PVCs is the only kind of ventricular arrhythmias that is not fatal. EKG- measure electrical conduction in d heart.
Quinidine and Procainamide Classified as CLASS 1 antiarrhythmic drugs (impact d heart), posses local anesthtic activity and block d influx of Na. ions during depolarixation.
Quinidine and Procainamide CONT: Main effects are to decrease excitability, slow coduction and prolong the refractory period' ECG: prolong the PR< QRS< and QT intervals .EXam : Used for both supraventricular and ventricular arrhymias.
Lidocaine Class 1 local anesthetic-type antiarrhythmic used only for ventricular arrhythmias, must be admiistered IV by infusion, d drug of choice in acute and emergency ventriclar arrhythmias
Lidocaine CONT: Main effect is to decrease automaticity. Mexiletine and tocainide are similar to lidocaine and can be administered orally.
B-Blockers Decrease heart rate, force of contraction, rate of A-V conduction. effect: bradycardia, lethargy, gl disturbance CHF, decrease BP and depression.
Propranolol Classified as a class 2 antiarrhythmic drug, primarily blocks cardiac beta receptors to slow heart rate, AV conduction, and prolong d refractory period.
Propranolol CONT:(BLOCKER) ECG: mainly increases the PR interval, used for both supraventricular and ventricular arrhythmias
Amiodarone Classified as a Class 3 antiarrhythmic drug. is used during emergency. ADENOSINE only used during the emergency.
Calcium Antagonists Blocks calcium access to cells, decrease contractility plus decrease conductivity of the heart , decrease demand for Oxygen. Effect- decrease p/p, bradycardia, may precipitate A_V block, headache, abdominal discomfort, peripheral edema.
Verapamil and diltiazem Classified as class 4 antiarrhythmic drugs act by blocking calcium ions, maineffects are to decrease heart rate and AV conduction, increase the PR interval.
Verapamil and diltiazem Mainly used t treat supraventricular arrhythmias, may cause cardiac depression at higher doses.
Created by: 100000888879579
 

 



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