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captopril
ACE inhibitors
suppress Ang II, Ang III and aldosterone production
suppress Ang-mediated effects on vasoconstriction, Na retention, SNS activity, and release of AVP and epinephrine
suppress aldosterone and AVP-mediated increases in Na/water retention
suppress Ang-mediated hypertrophy
more potent arterial than venous dilators, thereby reducting afterload and increasing stroke volume and CO
prevent degradation of bradykinin, a potent vasodilator
enalapril
ACE inhibitors
survival benefit in pts with mild to moderate and moderate-severe heart failure
suppress Ang II, Ang III and aldosterone production
suppress Ang-mediated effects on vasoconstriction, Na retention, SNS activity, and release of AVP and epinephrine
suppress aldosterone and AVP-mediated increases in Na/water retention
suppress Ang-mediated hypertrophy
more potent arterial than venous dilators, thereby reducting afterload and increasing stroke volume and CO
prevent degradation of bradykinin, a potent vasodilator
lisinopril
ACE inhibitors
suppress Ang II, Ang III and aldosterone production
suppress Ang-mediated effects on vasoconstriction, Na retention, SNS activity, and release of AVP and epinephrine
suppress aldosterone and AVP-mediated increases in Na/water retention
suppress Ang-mediated hypertrophy
more potent arterial than venous dilators, thereby reducting afterload and increasing stroke volume and CO
prevent degradation of bradykinin, a potent vasodilator
quinapril
ACE inhibitors
suppress Ang II, Ang III and aldosterone production
suppress Ang-mediated effects on vasoconstriction, Na retention, SNS activity, and release of AVP and epinephrine
suppress aldosterone and AVP-mediated increases in Na/water retention
suppress Ang-mediated hypertrophy
more potent arterial than venous dilators, thereby reducting afterload and increasing stroke volume and CO
prevent degradation of bradykinin, a potent vasodilator
candesartan
AT1 antagonist
competitive antagonism of AT1 receptors mediating effects of Ang II and AndIII thereby suppressing all of their actions
does not prevent bradykinin (vasodilator) degradation
losartan
AT1 antagonist
competitive antagonism of AT1 receptors mediating effects of Ang II and AndIII thereby suppressing all of their actions
does not prevent bradykinin (vasodilator) degradation
valsartan
AT1 antagonist
competitive antagonism of AT1 receptors mediating effects of Ang II and AndIII thereby suppressing all of their actions
does not prevent bradykinin (vasodilator) degradation
bumetanide
diuretics
central role in managing congestive sx. in PTS with heart falure.
increase in end diastolic filling pressure leading to ventricular remodeling, pulmonary venous congestion and edema
diuretics reduct fluid volume and preload.
pts in heart failure are on Frank-Starling plateu.
pre-load reduction happens w/o decrease in CO
furosemide
diuretics
central role in managing congestive sx. in PTS with heart falure.
increase in end diastolic filling pressure leading to ventricular remodeling, pulmonary venous congestion and edema
diuretics reduct fluid volume and preload.
pts in heart failure are on Frank-Starling plateu.
pre-load reduction happens w/o decrease in CO
metolazone
diuretics
central role in managing congestive sx. in PTS with heart falure.
increase in end diastolic filling pressure leading to ventricular remodeling, pulmonary venous congestion and edema
diuretics reduct fluid volume and preload.
pts in heart failure are on Frank-Starling plateu.
pre-load reduction happens w/o decrease in CO
thiazides
diuretics
central role in managing congestive sx. in PTS with heart falure.
increase in end diastolic filling pressure leading to ventricular remodeling, pulmonary venous congestion and edema
diuretics reduct fluid volume and preload.
pts in heart failure are on Frank-Starling plateu.
pre-load reduction happens w/o decrease in CO
torsemide
diuretics
central role in managing congestive sx. in PTS with heart falure.
increase in end diastolic filling pressure leading to ventricular remodeling, pulmonary venous congestion and edema
diuretics reduct fluid volume and preload.
pts in heart failure are on Frank-Starling plateu.
pre-load reduction happens w/o decrease in CO
bisoprolol
b-receptor antagonists
B1 blocker
carvedilol
b-receptor antagonists
a1, B1, B2 blocker
more reduced mortality than metoprolol
metoprolol
b-receptor antagonists
B1 blocker
sustained release
digoxin
cardiac glycosides
naturally occuring steroid
non-cardiac tissue benefits
treats arrythmias
digitoxin
cardiac glycosides
eplerenone
aldosterone antagonists
short term tx with ACEIs and ARBs can lower aldosterone
cant sustain suppression with long term tx
exerts adverse effects on structure/function of heart, indep of and in addition to deleterious effects of AngII
addition of atag should be considered in pts with moderately severe heart failure or with l. ventricular dysfunction after MI
spironolactone
aldosterone atagonists
short term tx with ACEIs and ARBs can lower aldosterone
cant sustain suppression with long term tx
exerts adverse effects on structure/function of heart, indep of and in addition to deleterious effects of AngII
addition of atag should be considered in pts with moderately severe heart failure or with l. ventricular dysfunction after MI
hydralazine
vasodilator
arterial vasodilator with little effect on venous tone and cardiac filling pressure
effective in reducing renal vascular resistance and increasing renal blood flow, therefore can be used in pts who cannot tolerate ACEIs
used in combo with siosorbide dinitrate and abailable as combo prep called BIDIL
alone may provide hemodynamic improvements in pts with advanced heart failure already being treated with ACEI, digoxin and diuretics
SE: h/a GI complains, prevent many pts from continued treatment
hydralazine/isosorbide dinitrate together increase survival but not as effectively as the ACEI enalapril
isosorbide
vasodilator
isosorbide dinitrate - short acting
isosobide mononitrate - long acting oral
venodilation by supplying NO and thereby activating guanylyl cyclase
increase venous capacitance and thereby preload
increase coronary artery fow by vasodilation which may enhance ventricular function
less effective as arteriodilator (not good monotx for heart failure)
used in combo with hydralazine
nitrate tolerance limits long term use
blood levels musy be allowed to fall to neglible levels for 6-8 hours/day
SE: h/a hypotension
nitroglycerin
vasodilator
tablets - quick acting
IV nitroglycerin is a vasoactive NO source
relatively selective for venous capacitance vessels. indicated for treatment of l. sided heart failure due to acute MI or when prompt reduction of ventricular filling pressure is required.
SE: h/a and nitrate tolerance
dobutamine
beta agonist
for pts with systolic dysfunction and congestion associated with heart failure
doesnt activate dopamine receptors
stimulates B1 (inotropic) and B2 (vasodilation)
inotropic predominates typical infusion rates, little chronotropy
increase in renal blood flow is proportional to increase in cardiac output
infused initially for several days but tolerance limits efficacy with long term use
SE: tachycardia and arrythmias which require dose reduction
dopamine
beta agonist
stimulates b-adrenergic receptors on heart to stimulate cardiac contractility (chronotropic, inotropic) at intermediate infusion rates
stimulates a-adrenergic @ high infusion rates
- stimulates peripheral arterial and venous constriction which may be desirable to support critically reduced Pa in pts with circulatory failure, but which does not help heart failure (increased afterload)
tachy from dopamine can provoke ischemia in pts with CAD
inamrinone
PDE inhibitors
short term support for circulation in advanved heart failure
stimulate myocardial contraction and accelerate myocardial relaxation by increased cAMP
stimulate balanced arterial and venous dilation
cardiac output increases by stimulated contractility and decreased l ventricular afterload
milrinone
PDE inhibitors

short term support for circulation in advanved heart failure
stimulate myocardial contraction and accelerate myocardial relaxation by increased cAMP
stimulate balanced arterial and venous dilation
cardiac output increases by stimulated contractility and decreased l ventricular afterload
more favorable SE, shorter half life, more selective for PDE3 and best among PDEs for short term parenternal inotropic support
ACE inhibitor mechanism
suppress Ang II, Ang III and aldosterone production
suppress Ang-mediated effects on vasoconstriction, Na retention, SNS activity, and release of AVP and epinephrine
suppress aldosterone and AVP-mediated increases in Na/water retention
suppress Ang-mediated hypertrophy
more potent arterial than venous dilators, thereby reducting afterload and increasing stroke volume and CO
prevent degradation of bradykinin, a potent vasodilator
ACE inhibitor tx
heart failure
often first line of therapy
should be prescribed to all pts with heart failure with reduced LVEF
CI in pts with adverse rxns (angiodema), impaired renal fxn (angII helps maintain kidney perfusion, or if pregnant
often used in combo with B-blocker
ACE inhibitor SE
hypotension
hyperkalemia
cough (bradykinin)
renal failure (if impaired renal rxn)
ACE inhibitor survival
improves survival in pts with heart failure, systolic ventricular dysfunction (40%) reduction in mortality after 6 months in pts with severe heart failure treated with enalapril
also survival benefit in pts with mild moderate and moderate-severe heart failure taking enalapril compared to isorbide dinitrate/hydralazine
prevent progression of heart failure in pts after MI
ARB Mech
competitive antagonism of AT1 receptors mediating effects of Ang II and AndIII thereby suppressing all of their actions
does not prevent bradykinin (vasodilator) degradation
ARB tx
reasonable alternative to ACE inhib.
commonly used in pts with heart failure with reduced LVEF
risks of tx are same as those attributed to ACEI but w/o cough and angiodema
ARB survival
provide comparable mortality benefits to ACEIs
no incremental benefit with combo tx of ACEIs and ARBs
diuretics
central role in managing congestive sx. in PTS with heart falure.
increase in end diastolic filling pressure leading to ventricular remodeling, pulmonary venous congestion and edema
diuretics reduct fluid volume and preload.
pts in heart failure are on Frank-Starling plateu.
pre-load reduction happens w/o decrease in CO
diuretcs mech
interfere with sodium retension of heart failure but inhibiting reabsorbtion of Na+ or Cl- at sites in the renal tubules
loop diuretics are preferred diuretics in most patients with heart failure although thiazides may be preferred in hypertensive pts due to persistence anti-hypertensive actions
diuretics tx
pts with evidence of fluid retension shoudl take a diuretic until euvolemic state is acheived and diuretic tx should be continued to prevent recurrence
produce symptomatic benefits more rapidly than any other drug for heart failure -within hours or days vs weeks or months for clinical effects of ACEIs, b-blockers or digitalis
should not be used alone in pts with stage C heart failure
diuretics adverse effects
electrolyte and fluid depletion
hypotension
azotemia (increased nitrogen compounds, ie urea in blood)
diuretics survival
no mortality benefit in heart failure
b-adrenergic receptor antagoinst
heart failure is characterized by sympathetic hyperactivation, an adaptive response that can increase cardiac performance
- increasing inotrophy, chronotrophy, ventricular volumes, vasoconstriction, impairing Na+ excretion by kidney
used to use SNS stimulants (now only for short term tx) but they increased mortaility
impair inotropic performance, they improve symptoms, excercise tolerance, increase LVEF in pts with heart failure over months
b-adrenergic receptor antagonist mechanism
not fully understood
anti-arrythmic benefit, possibly by impairing SNS-mediated increases in automaticity and hypokalemia
improved LV structure and fx by preventing remodeling of heart during heart failure
improvement of abnormal Ca2+ handling in heart failure, possibly by preventing hyperphosphorylation of ryanodine receptor
b-adrenergic antag tx
all pts with heart failure to reduce LVEF (Stage C) unless they have bradycardia or reactive airway diseaes
initiate at low doses and gradually increase
2-3 months for effects
b-adrenergic SE
fluid retention
fatigue
weakness
bradycardia
heart block (only if lightheaded - if so, reduce dose)
hypotension
b-adrenergic antag survival
reduce death from heart failure
digoxin mechanism
increases force of cardiac contraction but increasing intracellular free Ca2+
increased cardiac output decreases reflex SNS activity and increases renal perfusion
inhibits Na+/K+ ATPase
produces an increased accumulation of Na+ in cell which reduces gradient for Na+/Ca+ exchange
reduced Ca2+ efflux and repeated entry of Ca2+ uptake into the SR (by SERCA) and increased Ca2+ release from SE during next cycle of excitation/contraction

non-cardiac actions:
-sensitizes cariac baroreceptors (sense Pa as being higher) (also increase vagal tone and by increasing SA nodal cell sensitivity to ACh. decreases sympathetic and increases parasympathetic activity
inhibiting Na+/K+ ATPase in kidney, digoxin reduces renal tubular reabsorbtion of Na+, increasing Na+ delivery to distal tubules thereby reducing renin release
digoxin tx
only glycosde evaluated so dont use others
no longer a first line tx
use in pts with heart failure who are in atrial fibrillation or in pts with persistent or severe symptoms of heart failure during tx with diuretics, an ACEI (or ARB) and B-blocker
digoxin toxicity
related to electrical properties of the heart
inhibition of the Na+/K+ ATPase reduces membrane potential from -80 to -60 mV increasing possibility of abnormal beat
reduced Na+ gradient results in decreased Vmax of depolarization which causes re-entry arrythmias
increase automaticity can lead to extra systoles, v. tachycardias, and v fib.
toxicity increased with hypokalemia (caused by most diuretics), hypercalcemia, or hypothyroidism
also concomitant use of other drugs increase serum digoxin conc.
tx range may be deleterious in the long term
GI (anorexia, vomiting, nausea), CNS (spontaneous depol = altered behavior, disorientation, hallucinations, and muscle pain/fatigue
toxicity treated with anti-digoxin immunotherapy
aldosterone antag
short term tx with ACEIs and ARBs can lower aldosterone
cant sustain suppression with long term tx
exerts adverse effects on structure/function of heart, indep of and in addition to deleterious effects of AngII
addition of atag should be considered in pts with moderately severe heart failure or with l. ventricular dysfunction after MI
aldosterone antag safety
not known in absence of concomitant diuretic tx.
not recommended to give these w/o concomitant diuretics
risk is life-threatening hyperkalemia due to inhibition of potassium excretion
in pts with class III or IV failure, low doses of spironolactone added to ACEI tx reduce mortality
vasodilators
reduce preload, afterload or both
allow heart to fx more efficiently
venodilators decrease filling pressure and intracardiac volume
arteriodilators decrease systemic vascular resistance to increase cardiac output, increase renal perfusion to promote diuresis which also results in decreased filling pressure
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