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Session 2 Pharm10
Pharm -10- CHF
| Question | Answer |
|---|---|
| What is Congestive Heart Failure | inability of cardiac muscles to pump sufficient blood to meet the peripheral metabolic demand -Can be from impaired ability of cardiac muscles to contract or by increased work load imposed on cardiac tissue |
| What is the result of CHF | increased blood volume and interstitial fluid |
| What can be causes of lower ventricular function | coronary artery disease hypertension dilated cardiomyopathy valvular disease congenital heart disease |
| What can be causes of restriction of ventricular filling | mitral stenosis restrictive cardiomyopathy pericardial disease |
| What do the following have in common Increased Na+ intake noncomliance with anti CHF meds Acute MI exacerbation of hypertension infections pulmonary emblolism infective carditis | all are precipitating factors for CHF |
| What are the symptoms of CHF | decreased exercise tolerance shortness of breath tachycardia pulmonary and peripheral edema cardiomegaly fatigue |
| What are the risk factors for CHF | Age Coronary Artery Disease Hypertension Smoking Alcohol Thyroid Disease Rheumatic heart disease cardiotoxic drugs |
| What is the bodies natural compensatory mechanism for CHF | increase sympathetic tone Activation of Beta adrenergic receptors of heart increases Heart Rate and CO, then you get vasoconstriction and enhanced venous return and increased CO |
| What is the bodies compensatory mechanism for the decreased CO in CHF that leads to fluid retention | decreased CO decreases GFR which increases Renin, aldosterone, and Angiotensin II, Increases TPR retention of Na and water increases blood volume |
| Why do you get ventricular hypertrophy and changes in cardiac size, shape and composition with myocardial structural and functional alterations in CHF | This is a compensatory mechanism of the body to deal with the decreased CO in CHF |
| What are the neurohormonal changes that occur in CHF to compensate for the decreased CO in CHF | increase in Angiotensin II, Aldosterone, Nor Epi, Endothelin, and Vasopressin |
| How many stages are there in CHF | 1-4 or A,B,C,D |
| what is stage 1 (A) of CHF marked by | Patient is at high risk for developing HF. Patient currently has no structural or functional abnormalities and never exhibited symptoms of HF |
| What is Stage 2 (B) of CHF marked by | patient has structural heart disease associated with HF but doesn't have s/sx |
| What is stage 3 (C) of CHF marked by | patients with current of past symptoms of HF with underlying structural heart disease |
| What is stage 4 (D) of CHF marked by | patient has progressive structural heart disease associated with HF and has marked symptoms even at rest, or with maximum therapy and require specialized intervention |
| What are the therapeutic goals of CHF tx | eliminate cause of symptoms manage HF symptoms Increase CO and enhance tissue perfusion modulate neurohormonal response |
| What is the tx schedule for CHF | diuretic Beta Blocker Angiotensin converting enzyme inhibitor digoxin |
| What are the diuretics commonly used in CHF | thiazides- Hydrochlorothiazide (Esidrex) Metolazone (Diulo) remember this drug Loop Diuretics- Furosemide (Lasix) 1st line drug Bumetanide (Bumex) Torsemide (Demadrex |
| What is the MOA of diuretics helping treat CHF | relieve pulmonary congestion and peripheral edema by reducing plasma volume and venous return to heart. Also reduces cardiac workload and oxygen demand reduces afterload and B/P |
| How do diuretic reduce edema | reduce preload |
| Which diuretics are most effective in treating CHF | those that act in the loop of hendle (furosemide and Bumetanide) |
| When shouldn't you use thiazides and why are they less effective in CHF | don't use thiazides if GFR is going down, thiazides are less effective than loop because of decreased renal perfusion can be used in mild CHF with hypertension |
| When are diuretics indicated for CHF | when systolic and diastolic heart failure is due to fluid overload, also for maintaining euvolemia in syptomatic and stages C & D of heart failure |
| When would you need to you combination diuretic therapy and what combinations are most common | use combination diuretics when patient is not responding to therapy of loop diuretic alone. Add metolazone or hydrochlorothiazide to furosemide |
| What is the tx protocol for diuretics in CHF | start slow and low adjust as needed for target weight loss of 2lbs/day then caution in tapering and withdrawl |
| Why are beta blockers effective in CHF treatment when it would be thought that they would have negative effects by reducing CO | low doses of beta blockers carvedilol and metoprolol have shown reduced mortality in HF patients. They stop remodeling of heart tissue, reduce hypertrophy to avoid reducing contractility give very small dose |
| When should you stop beta blockers in CHF therapy | when patient enters acute decompensated heart failure |
| in what class of CHF are beta blockers indicated | indicated in stage 2 & 3 patients |
| What are the advantages of using low dose beta blockers in CHF therapy | prevent adverse effect of nor epi on heart prevent myocardial remodeling (fibrosis and hypertropy) improve ventricular function improve exercise tolerance decrease renin release decrease oxidative damage prolong survival slow progression of heart |
| How do ACE inhibitors help in CHF | they decrease Angiotensin II, Bradykinin inactivation, aldosterone secretion, vascular resistance, venous tone, B/P and ultimately decrease CO |
| How do ACE inhibitors reduce afterload and preload | reduce afterload by decreasing vascular resistance reduce preload by reducing salt and water retention |
| How do ACE inhibitors cause vasodilation | increase bradykinin levels which cause vasodilation |
| When are ACE inhibitors indicated for CHF | indicated as cornerstone of therapy indicated in patients with LV systolic heart failure Indicated in diabetic patients, post myocardial infarction, slows renal disease progression reduces mortality rates |
| What is the protocol for administering ACE inhibitors | start low does of captopril (has shorter half life) then switch to longer acting agent for maintenance (enalapril) Evaluate renal function and serum potassium |
| When are ACE inhibitors Contraindicated | angioedema, bilateral renal artery stenosis, and pregnancy also somewhat CI in patients with unilateral renal artery stenosis, cough, renal insufficiency, hypotension, and hyperkalemia |
| What are the following drugs Captopril (Capoten) Enalapril (Vasotec) Lisinopril (Zestril) Quinapril (Accupril) Ramipril (Altace) Fosinopril (Monopril) Trandolapril (Mavik) | ACE inhibitors |
| What are the following drugs Candersartan Losartan Valsartan | Angiotensin Receptor blockers |
| What is the MOA of angiotensin receptor blockers | inhibit binding of angiotensin II reducing plasma volume, vasodilation and reducing TPR antiproliferative effects |
| If your patient is intolerant or contraindicated to take ACE inhibitors what would you most likely prescribe them in their place | Angiotensin Receptor Blockers |
| What are the advantages to ACE inhibitors and ARBS | provide balanced vasodilation improve myocardial function improve cardiac workload and stroke volume reduce blood pressure improve exercise tolerance slow disease progression (decrease myocardial fibrosis and hypertrophy) improve survival |
| What are Spironolactone (Aldactone) Eplerenone (Inspra | Aldosterone Antagonists |
| How do aldosterone antagonists work | prevent aldosterone from binding neurohormonal inhibition inhibit Na+ and Fluid Retention inhibit ventricular remodeling reduction of mortality |
| What should you combine aldosterone antagonists with and when is it indicated | indicated in class 3 and 4 CHF and should be combined with loop diuretic, beta blocker, digoxin and ace inhibitor |
| Why would you use eplerenone in place of spironolactone even though it is a strong cyp3a4 substrate | does not have adverse effects of spironolactone on endocrine |
| What are the advantages of spironolactone in CHF | assist in sodium/fluid excretion prevent myocardial remodeling which improves heart function prevent myocardial fibrosis which reduces likelihood of arrhythmias reduce vascular fibrosis |
| HOw are vasodilators helpful in CHF | Impaired contractility of heart is exacerbated by compensatory increase in preload and afterload vasodilators help reduce excessive preload and afterload |
| What is the only vaso-dilator that has shown improved survival in CHF during clinical trials | Hydralazine-isosorbide |
| What type of vasodilator are nitrates | venous vasodilators increase venous capacitance decrease venous return to heart to reduce preload |
| what type of vasodilator is hydralazine | arteriolar vasodilator- reduces systemic vascular resistance and therefore afterload increases forward cardiac output |
| Positive inotropic effect Inhibits Na/K ATPase (reversible) Increased intracellular sodium Increased cardiac contractility Reduced sympathetic activation Reduced renin-angiotensin-aldosterone activation | Digoxin |
| what is another name for digoxin | digitalis |
| When is digoxin indicated | indicated in persistently symptomatic patients indicated in atrial fibrillation |
| What effect does digoxin have on ventricle | reduces ventricular size |
| Should digoxin be used in combination with ACE inhibitors, diuretics and beta blockers | yes |
| What is the half life of digoxin | 36-48 hours |
| what is the half life of dogoxin in renal failure patient | increase from 36-48 hours to >4days |
| Why do you have to be very careful in protocol for administering digoxin | Digoxin has a very narrow therapeutic window |
| Why do you need to monitor patients on digoxin for other drug use and warn them before taking any drugs | Other drugs such as quinidine, verapamil,m amiodarone can displace digoxin off of plasma carriers increasing plasma concentration of digoxin Cholestyramine- decrease absorption of digoxin |
| What frequently precipitates digitoxin intoxication | often precipitated by depletion of serum K caused by diuretic therapy |
| what are the s/sx of digitalis toxicity | anorexia nausea, vomiting headache, delirium ventricular tachycardia |
| what is the tx for digitalis toxicity | dc digoxin maintain serum [K+] between 4-5mmol/L treat ventricular arrythmias with lidocaine treat AV block with atropine Antidigoxin antibodies for overdose |
| What is B-Natriuretic peptide administered for in CHF | given to hospitalized patients IV for decompensated heart failure |
| what are the effects of giving B-Natriuretic peptide | Rapid Vasodilation increases CO promotes diuresis antagonizes effects of Renin-angiotensin-aldosterone system and endothelin and ADH |
Created by:
smaxsmith
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