N11

PHARMACOLOGY FOR NURSES

~ HEART FAILURE ~

HEART FAILURE
 Inadequate oxygen delivery by the heart or circulatory system to meet the demands of the body
o Oxygen delivery = O2 content of the blood x Cardiac Output
 Pathophysiology
o Insert picture here from slide
o Heart failure manifestations are primarily because of the compensatory mechanisms
o Problems lie on the compensatory mechanisms of heart failure  maladaptive
o Increase of sympathetic discharges  activation of alpha and beta receptors  increase in blood volume, peripheral resistance
(possible), heart remodeling
o Insert another picture here
 Treatment goals
o Eliminate the cause
 Surgical or cardiac catheterization
 Cardiac transplantation
o Optimize cardiac output
 Preload
 Contractility
 Afterload
o Enhance oxygen delivery
o Align metabolic demands of the body
o Prevent left ventricular remodeling and deterioration of cardiac function
o Enhance effects of natriuretic peptide systems
 BNP – promote natriuresis and vasodilation
 ANP – promote natriuresis and vasodilation
 Regulate detrimental effects of RAAS in HF-REF, inhibit secretion of AVP, nodulate autonomic nervous system
beneficial to the syndrome
 BNP analogue Nesiritide failed…..
 Cardiac output
o CO = HR X SV
 Where SV is determined by preload, contractility, afterload
 Decrease preload, increase contractility, decrease afterload (proper optimization)
 Treatment goals (physiologic/neurohormonal approach)
o Decrease effects of
 RAAS
 Angiotensin II
 Aldosterone
 Adrenergic system
 Epinephrine
 Norepinephrine
 AVP/ADH
 Pathophysiology
o Myocardial hypertrophy/LV remodeling
 Ultimately assoc. with alterations in cellular and subcellular phenotype reducing contractility
 Catecholamines
 For acute case, Beta agonist are used, but for long term, it is contraindicated as we do not want chronic
sympathetic activation
 Aldosterone
 Angiotensin II

PHARMACOLOGIC TREATMENTS OF HEART FAILURE

 Decrease preload
o Diuretics
 Furosemide (K sparing)
 Spironolactone (K sparing)
 Decrease afterload
o ACE inhibitors (captopril, enalapril)
o Vasodilators
 Except CCB  contractility will be compromised
 Augment contractility if necessary (severe heart failure)
o Beta-agonists
 Dobutamine
 Dopamine
 Epinephrine
 o Digoxin/lanoxin
o Decrease catecholamine/sympathetic effects – chronic, stable, heart failure
 Beta blockers – carvedilol
 Insert slide here
 Insert diagram
 Mnemonic
o Diuretics
o Inotropes
o Vasodilators
o ACE inhibitors
o Digoxin
o Ivabradine
o Beta blockers
o Aldosterone antagonists (Spironolactone, Eplerenone)
o ARNI (Sacubitril/Valsartan)
 Digitalis/Digoxin
 Cardiac glycosides
 Insert slide here
o Insert diagram here
 Insert explanation from Dr. Sison here
o Effects
 Increase contractility by increasing the free calcium concentration inside the cell
 Benefits r/t enzyme inhibition of noncardiac tissue
 Vagal afferent fibers….
 Insert slide here
 In theory, can reverese heart failure
 No net effect on mortality byt reduces hospitalization and death from progressive HF
 Increase in sudden death
 Mortality rate reduced if Serum level……….
o Other information
 75% bioavailability, 20-40% protein bound, 40 hours t1/2 (urinary excretion
 Many side effects
 Insert slides here
 Narrow therapeutic index
o Adverse effects/toxicity
 Arrythmia
 Bigeminal rhythm
 Serious digitalis-induced cardiac arrythmia in hypokalemia
 Cholinergic
 Vagal and chemoreceptor zone stimulation
 Disorientation, hallucination, visual disturbances
 Chronic intoxication – calcium overload
 Arrythmia more likely in
 Hypokalemia, hypomagnesemia, hypercalcemia
o Drug interaction
 Insert table here
 Beta Agonists
o Beta 1 receptor agonists
 Positive chronotropic effect (increase pacemaker activity)
 Positive inotropic effect
 Insert slides here
 Insert table here
o Medications
 Dobutamine
 Most widely used selective B1 agonist in HF
o 1-2 mins onset of action, half-life of 2 minutes, peak at 10 minutes
o Increase CO, decrease ventricular filling pressure
o Enhance automaticity of sinus node
o B2 receptor mediated ….?
 Dopamine
 Insert diagram here
 Bipyridines
o Inhibit PDE-3 which inactivates cAMP  increased cAMP
o Increase myocardial contractility
o Promote vasodilation
o Toxicity: nausea, vomiting, arrythmia, thrombocytopenia, liver enzyme changes
 o Medications
 Milrinone
 Most successful
 Oral and parenteral
 5-15 minutes onset……
 Insert slide here
 Amrinone
o Increase contractility, decrease afterload  increase CO (please confirm this)
 Vasodilators
o Decrease preload, decrease afterload
o Long-acting nitrates
 Most helpful in reducing filling pressures and the symptoms of pulmonary congestion
o Hydralazine (arteriolar dilator)
 Address fatigue due to low CO
 Diuretics
o Decrease preload, decrease afterload
o Not just diuretics but also vasodilators
o Reduce blood volume and direct vascular effects
o Deplete body soduium stores
o In heart failure
 Loop diuretics
 Insert slide here
o Insert diagram here
o Medications
 Loop diuretics
 Most potent
 Inhibit NaCl reabsorptions in the thick ascending loop of Henle
 Commonly used in patients with fluid overload, renal insufficiency, cardiac failure or cirrhosis
 Furosemide
o Onset: 2 hours for oral, 20 minutes for IV
o 2-3 hours duration
o Direct vascular effects
o Toxicity
 Ototoxicity
 Hypokalemia
 Dehydration
 Allergy (sulfa)
 Nephritis (intestinal)
 Gout
 Aldosterone antagonists
o Block aldosterone-stimulated NA reabsorption….
o Insert slide here
 Spironolactone
o Insert slide here
o Adverse effects
 Insert slide here
 ACE inhibitors
o Decrease afterload, decrease preload
o Insert slide here
o Captopril, mga -pril
o Toxicity
 Severe hypotension after initial doses
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 Angiotensin-receptor blockers
o Competitive angiotensin II receptor antagonists
o Effect same as ACEIs
 Vasodilation and decreased sodium retention
o Do not block bradykinin metabolism
o Same efficacy as ACEIs, more expensive
o Insert more
o Losartan, mga -sartan
 Nesiritide
o Acute heart failure
o Synthetic form of BNP
o Increase cGMP in smooth muscles
o Reduce venous and arteriolar tone in experimental drugs
 o Insert more
 ARNI
o Angiotensin receptor blocker neprilysin inhibitor
o Sacubitril/valsartan (combination drug of what???)
 Ivabradine
o If channel inhibitor (sinus node)
o Control spontaneous diastolic depolarization in the sinus node
o Slow down heart rate
o Increase diastolic filling and stroke volume
 Beta blockers
o Attenuate adverse effects of high catecholamines including apoptosis
o Upregulation of B receptors
o Decrease heart rate
o Reduce remodeling
o Insert more
o Selectivity
 Insert slide here
o Toxicity
 Blockade of cardiac, vascular, or bronchial B receptors
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 Binababa Chf Mortality
 Insert drugs here
 Aldosterone antagonists: spironolactone
o Competitive antagonist of aldosterone
o insert more
o mga -one

SUMMARY OF TREATMENT GOALS (MECHANISTIC)

 insert slides here