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Heart Failure Drugs

Determinants of oxygen demand by heart (4): Diastolic filling pressure, affected by blood volume and venous tone. Resistance to ejection of stroke volume during systole, which depends on BP and arterial tone. Heart Rate. Contractility
Types and examples of groups of drugs that decreases oxygen demand by lowering determinants (3): Beta blockers: eg. proponolol, atenolol and labetalol. Calcium channel blockers: eg. verapamil, nifedipine Nitrates: eg. nitroglycerin.
Beta blockers: mode of action on heart Affected largely by B2 recept. activated B2 receptors release cAMP -> influx of Ca into cells -> ^ contractility. Also ^ HR by stimulating SA&AV node. B blockers antagonise these effects and also help w/ hypertension by reducing renin pdtn by kidney.
Beta blockers: mode of action on lungs and smooth muscle Affected predominantly by B1 receptors, therefore should not use non-selective on asthmatic patients, as it may precipitate asthma attacks due to bronchoconstriction.
Beta blockers: uses CHIG: Cardiac arrythmias (since catecholamines ^ HR), Hypertension (v renin pdtn and contractility), Ischaemic heart disease (decreasing oxygen demand from heart) and Glaucoma (reduces intraocular pressure by reducing aqueous humour production)
Beta blockers: toxicity and contraindications WEBS: Withdrawal symptoms (drug dose must be tapered off), Erectile dysfunction, Bradycardia (presents as coolness of extremities) and Sedation (since catecholamines increases anxiety)
Calcium channel blockers: summary (refer to anti-hypertensives for more detailed questions) Eg. Verapamil and Nifedipine. Blocks Ca channels, decreases Ca influx into cells -> relaxes smooth muscle. Vascular muscle particularly affected, esp arterioles, and so does not cause orthostatic hypotension. reduce contractility and SA AV node conduction
Nitrates: Mode of action & example Nitroglycerin. Taken up into smooth muscle cells and de-nitrated. Nitrite ion is then released and converted into NO, which relaxes all types of smooth muscle
Nitrates: Uses Relaxes all vascular smooth muscle, which ^ venous capacitance and v ventricular preload -> reduces oxygen demand of heart and CO. Increases coronary blood flow as epicardial coronary arteries affected. Decreased preload and afterload good for angina.
Nitrates: toxicity Major vasodilation -> hypotension -> baroreceptors activated -> tachycardia. Also increases tolerance
Signs & symptoms of heart failure Tachycardia, dyspnoea, orthopnoea, nocturnal paroxysmal dyspnea, pulmonary edema, peripheral edema, cardiomegaly, decreased exercise tolerance.
Drug used in heart failure: Cardiac glycosides/ Digitalis
Cardiac glycosides: mode of action Inhibits Na/K ATPase, increasing intracellular [Na] -> less Ca efflux (^ free Ca in sarcomere during systole) -> stronger systolic contractions. Affects both normal and failing heart.
Cardiac glycosides: effects on heart: digoxin -> ^ contractility -> ^CO -> ^carotid sinus receptor & renal blood flow -> decreased sympathetic activity & deactivation of RAAS -> decreased preload & afterload. There is a decrease in QT & ST interval, inversion of T.
Cardiac glycosides: uses Heart failure and atrial fibrillation, back up choice after ACEI and diuretics.
Cardiac glycosides: toxicity Cardiac problems eg. a&v fib, premature ventricular depolarisation. GIT (nausea, vomiting, anorexia), Headache, confusion, fatigue, blurred vision. Rarely, gynecomastia.
Cardiac glycosides: treatment of toxicity Reduce or stop treatment if side effects include vision & GIT. Correct K or Mg deficiency and anti-arrythmatic drugs to prevent cardiac arrest.
Cardiac glycosides: drug interactions K+ & digitalis inhibit each other's binding to Na/K ATPase, therefore hypokalemia will increase effect of digitalis. HyperCa might worsen action as ^ Intracellular Ca. Mg has opposite effect of Ca. Verapamil ^ [digoxin]. Interaction w corticosteroids.
Created by: Aurorahx



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