Term
What type of HF involves Thin dilated ventricular walls unable to contract, with
EF usually < 40%? |
|
Definition
|
|
Term
| Is diastolic or systolic HF more common? |
|
Definition
|
|
Term
Which type of HF involves Preserved left ventricular ejection fraction (EF > 40%)
Usually with stiff hypertrophied ventricle as a result of hypertension and
Few studies or guidelines – reduce risk factors and treat symptoms? |
|
Definition
|
|
Term
| What does acute or decompensated HF require? |
|
Definition
| hospitalization and use of vasodilators and inotropic agents |
|
|
Term
| Are more cases of HF acute, decompensated or chronic? |
|
Definition
Chronic failure – majority of cases (5 million people in 2003)-
Most treatment guidelines are for this group |
|
|
Term
| According to the new neuroendocrine model of HF, what increases as heart fails? This activates what system? |
|
Definition
Increase in sympathetic tone as heart fails.
Activation of renin-angiotensin-aldosterone system |
|
|
Term
| What drugs are used according to the new neuroendocrine model? How quickly do they take effect? |
|
Definition
Drugs: ACE inhibitors, beta-blockers, spironolactone.
Delayed but long term beneficial effect |
|
|
Term
| According to the RAA, low cardiac output stimulates what? |
|
Definition
| renin release from the underperfused kidney |
|
|
Term
| According to the RAA, what does renin stimulate. |
|
Definition
| Renin stimulates conversion of angiotensinogen to angiotensin I |
|
|
Term
| According to the RAA, to what is Angiotensin I converted? |
|
Definition
| Angiotensin I is then converted to angiotensin II via angiotensin converting enzyme (ACE) |
|
|
Term
| According to the RAA, what does Angiotensin II cause? |
|
Definition
| Angiotensin II causes vasoconstriction and also stimulates production of aldosterone to increase sodium and water retention |
|
|
Term
| Which stage of HF involves high risk but no structural heart dz or symptoms of HF? |
|
Definition
|
|
Term
| Which stage of HF involves structural heart dz w/o symptoms of HF? |
|
Definition
|
|
Term
| Which stage of HF involves structural heart dz w/prior or current symptoms of HF? |
|
Definition
|
|
Term
| Which stage of HF involves refractory HF requiring specialized interventions? |
|
Definition
|
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Term
| Are teh glomerulus, proximal renal tubule, and distal renal tubule part of the renal cortex or medulla? |
|
Definition
|
|
Term
| Are teh loop of henle and collecting tubule part of the renal cortex or medulla? |
|
Definition
|
|
Term
| What loop diuretic is the drug of choice for HF? |
|
Definition
|
|
Term
| Where and how do loop diuretics act? |
|
Definition
Inhibit sodium reabsorption in the loop of Henle in the kidney
Increase excretion of sodium by 20-25%
Also excretion of potassium, magnesium, and calcium |
|
|
Term
| What drugs for HF are effective when ClCr >5 mL/min? |
|
Definition
| loop diuretics effective even in renal failure |
|
|
Term
| What are the preferred diuretics for fluid overload in HF? |
|
Definition
|
|
Term
| How is furosemide administered? What are 2 other drugs that can also be used? |
|
Definition
Can give oral or IV (bioavailability ~ 60%)
Usual oral dose is 20-40mg
Also can use torsemide or bumetinide |
|
|
Term
| How are loop diuretics dosed? |
|
Definition
| Start at low dose (20mg) and titrate upwards until weight decreases by 0.5-1.0 kg/day. Can taper and stop when patient euvolemic |
|
|
Term
| On what does a maintenance dose of loop diuretics in HF depend? |
|
Definition
|
|
Term
| What are 9 adverse effects of loop diuretics? |
|
Definition
1. Hypovolemia and renal failure from hypoperfusion of kidney
2. Hypotension and syncope
3. Hypokalemia (must monitor potassium)
(May cause sudden death, especially if patient taking digoxin)
5. Hyponatremia, 6. hypomagnesemia, and 7. hypocalcemia
8. Metabolic alkalosis
9. Ototoxicity in high doses or if given too rapidly IV |
|
|
Term
| What is a drug interaction w/loop diuretics? |
|
Definition
| Drug interaction: NSAIDs decrease diuretic effect |
|
|
Term
| How and where do thiazide diuretics act? |
|
Definition
Inhibit sodium reabsorption in the distal tubule of the kidney.
Only increase sodium excretion by 5-10% |
|
|
Term
| For what are thiazide diuretics preferred? |
|
Definition
Preferred agents for hypertension, but not heart failure.
Only effective during early stages of heart failure |
|
|
Term
| Which thiazide diuretic is the drug of choice? |
|
Definition
Drug of choice: hydrochlorothiazide.
For hypertension give 12.5-25mg once daily.
For heart failure need to give 25mg once or twice daily |
|
|
Term
| What is the preferred thiazide in combo w/furosemide? |
|
Definition
|
|
Term
| 5 ades of thiazide diuretics? |
|
Definition
Hypokalemia,
Metabolic alkalosis,
Hyperuricemia,
Mild hyperglycemia,
Mild hyperlipidemia |
|
|
Term
| What is the key to success of other drugs for HF? |
|
Definition
| diuretics: Need to avoid fluid retention from too low a dose or volume contraction from too high a dose |
|
|
Term
| What is the only class of drugs for HF that can control fluid retention? |
|
Definition
|
|
Term
|
Definition
| increase renal excretion of Na+ and H2O |
|
|
Term
| Do diuretics in HF stop dz progression or do they just tx symptoms of HF? |
|
Definition
Relieve *symptoms* of heart failure:
Decrease pulmonary and peripheral edema.
Faster benefits than other drugs.
Do not stop disease progression |
|
|
Term
| How does diuretic resistance arise w/HF? How does this effect dosing and drug choice? |
|
Definition
Increases as heart failure progresses.
High doses of loop diuretics necessary.
Use IV furosemide to bypass GI tract.
Use metolazone (a thiazide diuretic) with furosemide for synergistic effect.
Give 30 min before IV furosemide.
IV inotropic agents may be needed. |
|
|
Term
| What drugs should be avoided when confronted w/diuretic resistance? |
|
Definition
Avoid NSAIDs and COX-2 inhibitors!!
Antagonize diuretic effect |
|
|
Term
|
Definition
Block conversion of angiotensin I to angiotensin II;
Some angiotensin II can still be produced from non-ACE mechanisms. Also block bradykinin metabolism;
Appears to be additional benefit in HF patients.
However increased kinin responsible for cough |
|
|
Term
| What are 4 ACEI of choice? |
|
Definition
| Drugs of choice: enalapril, lisinopril, fosinopril, and quinapril are all generic |
|
|
Term
| What was first ACEI but is now rarely used due to short half-life and more adverse effects? |
|
Definition
|
|
Term
Most ACEI are pro drugs, metabolized to active form.
What is only ACEI that is not metabolized in liver? |
|
Definition
| Lisinopril: Need to reduce lisinopril dose if renal dysfunction |
|
|
Term
| What are ACEI effects on HF symptoms? |
|
Definition
Relieve dyspnea,
Prolong exercise tolerance,
Improve ejection fraction,
Decrease doses of diuretic, |
|
|
Term
| ACEI are effective for which stages of HF? |
|
Definition
| mild, moderate, or severe |
|
|
Term
| What doses of ACE were used in trials? |
|
Definition
|
|
Term
|
Definition
Optimal Dose:
*High doses used in trials*
Enalapril, lisinopril >20mg/day.
Start low and titrate slowly up to highest dose that doesn’t cause adverse effects.
Use QD or BID agent
-Captopril is too short acting (TID to QID) |
|
|
Term
| What must be avoided w/ACEI? |
|
Definition
Avoid NSAIDs-
Controversy about aspirin use but single dose probably OK |
|
|
Term
| What must be corrected for maximum effect w/ACEI? |
|
Definition
| Must correct fluid retention for maximum effect |
|
|
Term
|
Definition
1. Hypotension.
2. Renal failure, especially if:
Severe heart failure;
*Renal artery stenosis*;
NSAID use;
30% rise in serum Cr is OK.
3. Hyperkalemia.
4. Dry, non-productive cough (5-15%)-
Rule out pulmonary congestion.
5. Angioedema-
4 x more prevalent in black population.
6. Teratogenic – avoid in pregnancy (Category D) |
|
|
Term
| Which drug for HF causes *renal aa stenosis?* |
|
Definition
|
|
Term
| Where and how do ARB act? |
|
Definition
| Block action of angiotensin II at cell receptor sites (AT1 receptors). |
|
|
Term
| What drug for HF affects bradykinin? |
|
Definition
ACEI. ARBs Do not block AT2 receptors or affect metabolism of bradykinin-
May be less benefit than ACEI in HF patients |
|
|
Term
| What are the Only two ARBs approved for heart failure? |
|
Definition
Diovan (valsartan) and Atacand (candesartan)-
Only after ACE inhibitor has been tried |
|
|
Term
| What are teh Drugs of choice in HF if patient has developed cough or angioedema secondary to ACEI? |
|
Definition
|
|
Term
|
Definition
Still can cause hypotension, hyperkalemia, and renal failure.
Teratogenic – avoid in pregnancy |
|
|
Term
| What have studies shown re: combining ACEs and ARBs? |
|
Definition
Theoretically should increase efficacy in heart failure because the effects of angiotensin II are being blocked by two different mechanisms.
Clinical trials have been inconclusive so far.
Can expect additive adverse effects on potassium levels and kidney function |
|
|
Term
| How do Beta-Adrenergic Blockers act? |
|
Definition
Block effects of sympathetic nervous system (norepinephrine).
Blocking stimulation of beta1-receptors in heart can cause decrease in heart rate, contractility, and cardiac output |
|
|
Term
| What was first beta-blocker to demonstrate long term beneficial effect (1996)? |
|
Definition
| coreg (carvedilol); Slowed clinical progression, decreased hospitalization and death |
|
|
Term
| What pts should be selected for beta-blockers? With which pts should beta-blockers be avoided? |
|
Definition
Mild-moderate CHF (Class II-III);
*Stable* on ACEI, diuretics, +/- digoxin. Avoid if acutely ill, unstable, hypotensive |
|
|
Term
| How should beta blockers be dosed? |
|
Definition
Start with *very* low doses and titrate up slowly every 1-2 weeks.
Carvedilol (Coreg) 3.125mg BID;
New dosage form: Coreg CR 10mg QD (= 3.125mg BID);
Metoprolol (Toprol XL) 12.5mg QD;
Bisoprolol 1.25mg QD |
|
|
Term
| What are 3 ADE of beta blockers? |
|
Definition
Worsening heart failure,
Hypotension,
Bradycardia |
|
|
Term
| Beta-blockers should be used w/caution w/which pts? |
|
Definition
| Caution in patients with asthma, COPD, diabetes, heart block |
|
|
Term
| Which beta blockers are cardioselective? Which are not? |
|
Definition
Metoprolol and bisoprolol are cardioselective.
Carvedilol is not cardioselective |
|
|
Term
| What is teh action of spironolactone? |
|
Definition
Aldosterone antagonist.
Potassium-sparing diuretic-
Increases potassium reabsorption at distal tubule |
|
|
Term
| How should spironolactone be dosed when combined w/ACEI? What ADE should be monitored w/this combo? |
|
Definition
RALES trial confirms that ACEI may not completely suppress aldosterone levels.
Only need 25mg daily.
*Reduce* diuretic dose due to synergistic effect.
Monitor for hyperkalemia:
Risk with renal failure, ACE inhibitor use;
Recent study documents 100% increase in hospital admissions due to hyperkalemia |
|
|
Term
| What is an important ADE of spironolactone? |
|
Definition
| Androgen antagonist: can cause gynecomastia and impotence |
|
|
Term
| When is spironolactone not recommended? |
|
Definition
| Not recommended if K+ > 5.0 mg/dL or CrCl < 30 ml/min |
|
|
Term
What is a New aldosterone antagonist also indicated for heart failure and
Also reduces all-cause and cardiovascular mortality? |
|
Definition
|
|
Term
| Which has more anti-androgenic adverse effects: spironolactone or eplerenone? |
|
Definition
|
|
Term
| What can be Used in patients intolerant to endocrine adverse effects of spironolactone? |
|
Definition
|
|
Term
| What ADE does Eplerenone (Inspra) share w/spironolactone? |
|
Definition
| Still causes hyperkalemia |
|
|
Term
| What is the dosing/cost of Eplerenone (inspira)? |
|
Definition
Give 25-50 mg orally once daily.
Very expensive ($110/mo) compared to spironolactone |
|
|
Term
What is A digitalis glycoside with an
Active ingredient from foxglove? |
|
Definition
|
|
Term
|
Definition
Positive inotropic agent;
Increases systolic contraction. |
|
|
Term
| When is digoxin contraindicated? |
|
Definition
| Do not use for diastolic failure |
|
|
Term
| What is the usual digoxin dose? What is the dose in elderly and pts w/reduced renal function? What is the t1/2? |
|
Definition
*0.125 mg/day*. Give 0.125mg QOD or less if elderly and/or reduced renal function.
Half-life = 1-2 days |
|
|
Term
| How can digoxin help HF pts? |
|
Definition
| Can improve symptoms and quality of life |
|
|
Term
| What is an antibody to treat severe digoxin toxicity? |
|
Definition
|
|
Term
| What ADEs must be avoided w/Digoxin, as these potentiate arrhythmias? How are levels monitored? |
|
Definition
Avoid *hypokalemia*, hypomagnesemia.
(Potentiate arrhythmias)
Must order periodic serum digoxin levels |
|
|
Term
| 7 ADRs associated with serum levels > 1 ng/ml |
|
Definition
Arrhythmias, heart block, gastrointestinal complaints, visual disturbances, confusion.
Avoid hypokalemia, hypomagnesemia
(Potentiate arrhythmias) |
|
|
Term
| What are 4 drugs that increase digoxin levels? |
|
Definition
| Increase in digoxin levels with addition of quinidine, verapamil, diltiazem, and amiodarone |
|
|
Term
| What are 2 traditional vasodilators? |
|
Definition
Part of traditional drug therapy using the hemodynamic model.
Nitrates-
Venous dilation – reduces preload;
Isosorbide dinitrate (Isordil), nitroglycerin.
Hydralazine-
Dilates arterioles – reduces afterload;
Hypotension, reflex tachycardia |
|
|
Term
| What is the benefit of traditional vasodilators (nitrates, hydralazine) and how are they used? |
|
Definition
Only short term symptomatic benefit.
Used in combination if intolerant of ACE inhibitors |
|
|
Term
| To what ethnic group was Hydralazine/Isosorbide (BiDil) marketed and what was the primary ADE? |
|
Definition
| african-americans. HA (47%) |
|
|
Term
| What are 2 Drug classes Used for Acute, Decompenstated Heart Failure |
|
Definition
Vasodilators (Nitroprusside;
Nesiritide (Natrecor))
Inotropic agents (Dobutamine;
Milrinone (Primacor)) |
|
|
Term
Which vasodilator for Acute, Decompenstated Heart Failure is given as IV infusion to reduce afterload
(Can get cyanide toxicity with overuse)? |
|
Definition
|
|
Term
| Which vasodilator for Acute, Decompenstated Heart Failure is a recombinant B-type natriuretic peptide (BNP) causes vasodilation and sodium excretion when given as IV infusion? |
|
Definition
|
|
Term
| Which vasodilator Used for Acute, Decompenstated Heart Failure has a controversial Place in therapy due to recent reports of increases in renal failure and mortality compared to placebo? |
|
Definition
|
|
Term
| Which inotropic agent for Acute, Decompenstated Heart Failure can increase CO in short-term but effect blunted if patient taking B-blocker? |
|
Definition
|
|
Term
| Which inotropic agent for Acute, Decompenstated Heart Failure is a phosphodiesterase inhibitor which increases cardiac contractility by increasing intracellular calcium concentrations? |
|
Definition
|
|
Term
| What are 3 ADEs that must be monitored w/ diuretics? |
|
Definition
| Electrolytes, renal function, weight |
|
|
Term
| What are 3 ADEs that must be monitored w/ ACE inhibitors? |
|
Definition
Renal function, potassium, blood pressure
Beta-blockers |
|
|
Term
| What 2 ADEs must be monitored w/ beta-blockers? |
|
Definition
| Heart rate, blood pressure |
|
|
Term
| What 2 ADEs must be monitored w/ spironolactone? |
|
Definition
|
|
Term
| What 2 ADEs must be monitored w/ digoxin? |
|
Definition
| hr, k+, serum levels occasionally |
|
|
