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54 Cards in this Set

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  • Back
1) Defince heart failure
a) HF is a condition with multiple causes that results ib Cardiac Output that is inadequate to provide O2 needed by the body
1) The primary signs and symptoms of Congestive heart failure are:
a) Tachycardia
b) Decreased exercise tolerance
c) SOB
d) Peripheral and pulmonary edema
e) Cardiac remodeling
1) Tx of heart failure is geared toward:
a) Extending life expectancy
b) Increasing quality of life
1) Role of exercise in tx of CHF
a) Benefits most pts when the HF has been stabilized
• Not used while unstable
1) What are the positive ionotropic drugs used in the tx of heart failure
a) Digoxin
b) Inamrione
c) Milrione
d) Dobutamine
e) Dopamine
1) What are the drugs used to tx heart failure that are not positively ionotropic?
a) Ace Inhibitors
• Captopril
• Enalapril
• Lisinopril
b) Angeotensin II receptor blockers
• Candesartan
• Losartan
• Calsartan
c) Vasodilator
• Hydralazine
d) Isosorbide dinitrate
e) BB
• Carvedilol
• Metoprolol
• Bisoprolol
• Atenolol
f) Diuretics
1) MOA of Digoxin
a) It is a Digitalis glycoside
• It Inhibits Na/K ATPase
1) Clinical Effects of Digoxin
a) Improves exercise tolerance (improving quality of life)
b) Reduces hospitalization
c) Withdrawal; of pts receiving digoxin leads to worsening heart failure
d) Does not decrease mortality
1) Cardiac effects of Digoxin
a) Positive ionotropic drug
• Inhibits Na/K ATPase which increases Na+ concentration in the cell which increases activity of the Na / Ca+ exchanger which increases Ca+ in the vicinity of the contractile proteins
• Increases the force and length of time the interaction between actin and myosin via increase free Ca in the vicinity of the contractile proteins during systole
• This is effective in CHF because it increased the ventricular performance
b) Increases Cardiac output
c) Reduce preload
d) Reduces risk of arrhythmia
e) No effect on HR
f) May or may not reduce afterload
g) Increases parasympathetic tone and Decreases sympathetic tone
• These actions slow the HR by decreasing the SA node automaticity
• Also slows the AV node conduction velocity, while increasing the AV node refractory period
-----Increases PR interval
• In ventricular tissue, digoxin shortens the action potential duration,  prolonged QT interval
1) How Can digoxin be used as an antiarrhythmic
a) Positive ionotropic and negative chronotropic effect (doesn’t cause bradycardia like BB)
b) Can use drug during pregnancy
c) Effects on the ECG
• Decrease HR
• Increase PR interval
• No effect on QRS
• Decrease QT
1) Onset of action of digoxin
a) 1 hour
1) DOA of digoxin
a) 24 hours
1) Elimination half life of digoxin
a) 36 hours
1) How is digoxin excreted?
a) 60% is excreted unchanged in the urine
• Possibility for digoxin toxicity
1) Common adverse effects of digoxin
a) Anorexia
b) Nausea
c) Vomiting
d) Arrhythmias
e) Blurred vision
f) Chromatopsia
g) Gynecomastia
h) Seizures
i) Hypokalemia induced arrhythmias
1) Common drug interactions of digoxin
a) Digitalis absorption is inhibited by antacids and cholestyramine
b) Digitalis clearance is reduced by:
• Dilitazem
• Quinidine
• Verapamil
c) Diuretic induced hypokalemia precipitates digitalis toxicity
• Toxic concentration of digoxin may evoke afterdepolarizations throughout the heart  extrasystole and tachycardia
1) Tx of digoxin toxicity
a) Discontinue the cardiac glycoside
b) Obtain serum K+ and digoxin levels
• Tx hypokalemia if present
c) Antiarrhythmic therapy
• For serious ventricular arrhythmias
d) Digoxin immune Fab:
• Antidote for life threatening toxicity
1) MOA of Inamrione
a) Selective for phosphodiesterase type III
• Which is found in cardiac smooth muscle
1) How is Inamrione used in Heart failure?
a) ****Used only for the short term management of acute heart failure
b) Positive ionotropic drugs which increase contractility
• Inhibition of phosphodiesterase type III increases cAMP concentrations in the cell which increases cardiac muscle contractility and vasodilation
1) Cardiac Effects of Inamrione
a) Increase cardiac contractility
b) May or may not increase HR
c) Decreases preload
d) Decreases afterload
e) Has a risk of causing a cardiac arrhythmia
1) Onset of action of Inamrione
a) 3 min
1) Elimination half life of Inamrione
a) 4 hours
1) ROA of Inamrione
a) IV only
1) MOA for Milrione
a) Selective for phosphodiesterase type III
• Which is found in cardiac smooth muscle
1) How is Milrione used in Heart failure
a) ***Studies show that it increases mortality in patients with severe heart failure
b) ***Used only for the short term management of acute heart failure
c) Positive ionotropic drugs which ncreases contractility
• Inhibition of phosphodiesterase type III leads to increased cAMP concentrations in the cell which leads to increased cardiac muscle contractility and vasodilation
1) Cardiac Effects of Milrione
a) Increase cardiac contractility
b) May or may not increase HR
c) Decreases preload
d) Decreases afterload
e) Has a risk of causing a cardiac arrhythmia
1) Onset of action of Milrione
a) 3 min
1) Elimination half life of Milrione
a) 4 hours
1) ROA of Milrione
a) IV only
1) Common adverse effects of Milrione
a) Arrhythmias
b) Hypotension
c) Nausea
d) Vomiting
e) Thrombocytopenia
f) ***Do not mix milrione with furosemide in an IV line because a precipitate will form
1) MOA of Dobutamine
a) B1 selective agonist
b) B1>B2 >>>>Alpha
1) How is Dobutamine used in hearty failure
a) Positive ionotropic drugs  increase contractility
b) Used to tx acute heart failure or heart failure that does not respond to other agents
c) Must be administered by continuous infusion (IV)
d) Produces some vasodilation
1) Cardiac effects of Dobutamine
a) Increases cardiac contractility
b) May or may not increase HR
c) May or may not reduce preload
d) Reduces afterload
e) Increases risk of arrhythmia
1) Onset of action of Dobutamine
a) 1 minute
1) Duration of action of Dobutamine
a) <10 min
1) Elimination half life of Dobutamine
a) 2 minutes
1) How is Dobutamine excreted?
a) Not excreted in urine
b) Therefore probably good to use if pt has kidney problems
1) Common adverse effects of Dobutamine
a) Excessive vasoconstriction
b) Tachyarrhythmias
c) Hyper or hypotension
• Hypertension can occur as a reflex mechanism or sensitivity of the pt to the medication
1) Common drug interactions of Dobutamine
a) Activity affected by other agonists and antagonists
1) MOA of Dopamine
a) B receptor agonist
b) D1 = D2 >>Beta >>alpha
1) How is Dopamine used in heart failure?
a) Positive ionotropic drugs  increase contractility
b) Same indications as dobutamine…may be used if dobutamine was not successful
c) Must be administered by continuous infusion (IV)
d) Increases renal perfusion
1) Cardiac effects of Dopamine
a) Increases cardiac contractility
b) May or may not increase HR
c) May or may not reduce preload
d) Reduces afterload
e) ***Increases risk of arrhythmia
1) What Ace Inhibitors are used to tx heart failure?
a) Captopril
b) Enalapril
c) Lisinopril
1) How are ACE inhibitors used in heart failure?
a) Decrease in activation of cardiac angiotensin receptors leads to a decrease in cardiac remodeling and wall thinning which increases ventricular performance which decreases morbidity and mortality
b) Studies show that ACE inhibitors decreased the risk of CHF by 37% in post myocardial infarction pts with LV dysfunction
1) Adverse effects of AVE inhibitors
a) Chronic cough
b) Severe hypotension
c) Hyperkalemia
d) Rash
e) Acute renal failure in pts with bilateral renal artery stenosis
1) Cardiac effects of ace inhibitors
a) Reduce preload and afterload
1) What Angeotensin II receptor blockers are used to treat heart failure?
a) Candesartan
b) Losartan
c) Calsartan
1) Cardiac effects of Angeotensin II receptor blockers
a) Decrease preload and afterload
1) Cardiac effects of Hydralazine
a) Reflex tachycardia
b) Decrease afterload
1) Cardiac effects of Isosorbide dinitrate
a) Reflex tachycardia
b) Decrease preload and afterload
• Has more effect on preload
1) BB used to treat heart failure?
a) Carvedilol
b) Metoprolol
c) Bisoprolol
d) Atenolol
1) How are BB used in heart failure
a) They have a negative ionotropic effect which you wouldn’t think to be optimal for heart failure, However, these drugs have been shown to reduce mortality in patients with class II and class III heart failure
b) Increases cardiac output and LV ejection fraction???
c) Requires 2-3 months for improvement
d) Start with low dose and gradually work upward
e) Inhibits cardiac remodeling
1) What do studies show about Carvedilol and heart failure
a) Carvedilol has been shown to decrease mortality rate and improve ejection fraction
• Carvedilol reduces mortality more than metoptolol
b) Addition of candesartan to the ACE inhibitor (???)was shown to reduce mortality
1) How are Diuretics used in heart failure?
a) THiazides and loop diuretics increase the excretion of NaCL and water
• Leading to a reduction in plasma volume and ventricular preload
• Leading to a reduction in pulmonary and peripheral edema
• Leading to a reduction in cardiac size and improved pumping efficiency
• If pt is retaining Lg amount of fluid…Loop diuretic will deplete the water quicker than any other agent
b) Spirolactone (the aldosterone antagonist)has been shown to reduce morbidity and mortality in pts with severe heart failure
• Administered with other therapies
• Increases the excretion of Na and increase in potassium retention
• It was shown to decrease mortality by 30% at 24 months
c) Loop diuretics and thiazides decrease preload
• Reducing edema and congestion
d) K+ sparring diuretics may slightly reduce preload (they are the weakest of the diuretics)
• Used for severe HF