Congestive Heart Failure Flashcards
What is CHF?
Inability of the heart to pump enough blood to provide the O2 needed by the body, LV is not efficently pumping to meet metabolic needs
What is stroke volume driven by?
preload, afterload, and contractility
Ejection
amount of blood pumped out of heart during each beat
Fraction
the volume of blood expelled vs remaining volume after pumping
Normal EF
55-75%
Systolic heart failure is caused by
decrease in ventricular EF, impaired contractility, increased afterload, aortic stenosis, cardiomyopathy, mechanical abnormalities
Diastolic heart failure is caused by
decrease in ventricular relaxation during diastole, chronic hypertension, pulmonary hypertension
Mixed heart failure pts will have
low EF, high pulmonary pressures, dilated cardiomyopathy
Drugs that cause HF
antiarrhythmics, CCBs, chemotherapy, Na and H2O retention by steroids, NSAIDs, some diabetic drugs
Cardiovascular symptoms
tachycardia, cardiomegaly, dysrhythmias, fatigue, exercise intolerance
Repiratory symptoms
SOB, orthopnea, pulmonary edema, cyanosis
GI symptoms
epigastric fullness, anorexia, ascites, cardiac cachexia, hepatomegaly
Renal symptoms
peripheral edema, hypernatremia, hypomagnesemia, decreased urine output, hypokalemia
Class I
no limitation of activity, activity does not induce fatigue, dyspnea, angina
Class II
slight limitation of activity, no symptoms at rest, ordinary activity results in fatigue, angina, dyspnea
Class III
Marked limition of activity, comfortable at rest, activity causes angina, dyspnea, fatigue
Class IV
inability to carry on any physical activity w/o discomfort, cardiac insufficiency or angina present at rest, discomfort increased with activity
Stage A
Patients at high risk of developing dysfunction because of existing conditions
Stage B
Patients develop structural heart disease but do not show symptoms
Stage C
patients have current or prior symptoms associated with underlying heart disease
Stage D
advanced structural heart disease and marked symptoms of HF at rest despite intervention, end stage disease
Goals of therapy
prevent disease progression, reduce morbidity/mortality, reduce hospitalizations
Non-pharmacological approaches
remove precipitating causes, exercise if able, Na restriction, fluid restriction, weight control
Focus of medical treatment
inhibit compensatory processes, ACE inhibitors, BB, aldosterone antagonists, prevent cardiac remodeling, vasodilators, diuretics, inotropic agents, Symptom control!
Most common treatment
Furosemide, bumetanide, LOOP diuretic, end stage will include thiazide too
Diuretic key points (4)
daily dose adjustment based on weight, keeps pts out of hospitals, increase dose with decrease kidney, K sparing used for activity of aldosterone
ACE-I key points (5)
used to prevent cardiac remodeling, use with caution with K sparing, sudden fluid changes can drop BP, NO pregnant pt, renal artery stenosis or angioedema, can cause hyperkalemia or hypotension
ARB key points (2)
usually used as alternative to ACE-I when not tolerated, used for SE
Hydralazine/isosorbide dinitrate combo
acts on artery and vein, reduces pre and afterload, hard to tolerate, limits use, African american pt use as adjunct therapy
BB key points (3)
improve outcome because effect NE, EPI, and angiotensin II, Metroprolol DOC, use low dose
Spironolactone (4)
only use 25 mg, only benefit for NYHA III or IV, also benefit post-MI, watch K+
Digoxin (6)
no benefit on outcome, mild positive inotropic, Never discontinue once start, decrease node conduction, only HF and Afib, TDM required
Digoxin toxicity presents as
anorexia, N/V/D, abdominal pain, visual disturbances, fatigue, confusion, arrhythmias, AV block, tachycardia
Acute decompensated heart failure
CV function becomes so impaired it requires hospital admission for aggressive treatment and monitoring
Cardiogenic shock
profound hypotension and low CO
What causes AHF
uncontrolled HTN, poor compliance, Afib, environmental factors, inadequate therapy, pulmonary infection, arrhythmias, CCB, ibuprofen, naproxen
Diagnosing AHF
BNP, ECHO, BP, pulmonary artery catheters, central venous pressure (2-6), MAP (80-100)
Warm and wet
pt has normal cardiac index, good bp, high PCWP, fluid in lungs or other lung symptoms
Cool and dry
poor perfusion, low crdiac index, PCWP normal, no lung symptoms
Cool and wet
worst case scenario, poor perfusion, lung symptoms, requires ICU admission
Loop diuretic treatment for AHF
use with caution, too rapid diuresis can decrease CO, usually give furosemide or bumetanide IV, chronic therapy can lead to resistance
Vasodilators treatment for AHF
Nitroprusside reduces preload and SVR, but decrease BP and reflex tachy; Nitroglycerin most beneficial for pt with MI; Nesiritide used as 2nd or 3rd after nitro and diuretics, $$$$; enalaprilat only for stable pt; Hydralazine limited because of variances with pts
Dopamine for AHF
primarily a B and a agonist to increase CO, dose dependent, too low= inc renal blood flow and urine output, intermediate= inc HR, CO, high= vasoconstriction and inc BP; DOC for low BP/HF, no use for MI, vesicant
Dobutamine for AHF
B1 agonist w/ some B2 no a, inc CO, no effect on BP, short T1/2, give continuous infusion, first line for AHF
Milrinone for AHF
PDE-3 inhibitor, inhibits cGMP breakdown, inc contractility, artery and vein vasodilation, dec SVR, no change BP, reserved for pt who don’t respond to other meds, T1/2=2-4 hours; continuous infusion, gets complicated
Goal for warm and wet/ treatment
reduce PCWP, diuretics and/or vasodilators, always IV because don’t have time to wait
Goal for cool and dry/ treatment
inc CO, fluid and inotropic agents, start with fluids, once hydrated start inotrope, normotensive- dobutamine or milrinone; hypotensive- dopamine; if not at goal CO- vasodilator (IV)
Goal for cool and wet/ Treatment
reduce preload to reduce pulm congestion, incr CO to improve perfusion
