CHF (3/6) Flashcards
systolic vs diastolic HF
systolic LV, reduced EF
diastolic preserved LV EF
remodeling
adaptation to reduced CO
cardiac dilation, ^sympathetic tone, water retention and ^BV, natriuretic peptides
remodeling neurohormone systems
Renin angiotensin aldosterone, sympathetic nervous
CHF s/s
s3 gallop, cool pale cyanotic extremities, crackles, vBreath sounds (effusion), ^jugular venous pressure, LE edema, ascites, hepatomegaly, splenomegaly, displaced PMI
CHF diagnostics
echo (syst vs dias, valve disease), xray (cephalization pulm vessels, Kerley B lines), EKG (ischemic heart disease)
BNP level of exacerbation
100+
CHF tx
diuretics
(mod) Thiazide = vK( ^dig toxicity), w minimal edema
(large) Loop diuretics=vK(^dig toxicity), hypotension, work when gfr is low, for severe HF
(scant) K sparing diuretics-counteract K loss by other meds (vRisk for Dig tox), risk ^K*caution w ARBs/ACEi (dc diuretic)
which diuretic prolongs survival, why
spironolaction bc blocks aldosterone receptors (not bc diuresis)
ACEi AE
vBP, ^K, cough, angioedema, renal failure (bilateral renal artery stenosis) fetal injury
ARB
^LV EF, vHF sx, ^exercise tolerance, vHospitalization, vMortality
ARNI
angiotensin receptor blocker + neprolysin inhibitor
entresto
^natiuretic peptides, vAE of RAAS
used in place w ace/arb NOT w/
DRI
direct renin inhibitor
HTN only, not HF
B Blockers
1st line
protect from sympathetic stimulation and dysrhythmias
^LV EF, ^survival
AE: fluid retention, worse HF, fatigue, hypotension, vHR, heart block
Ivabradine
for stable chronic HF
EF <35%
NSR
70bpm on highest b blocker w/o improvement
Vericiguat
after hospitalization/outpt diuresis for HF <45%,
AE: vBP, xPD5i, xPregnant
SGLT-2i
Empaglifozin, Dapaglifozin
<40%, vMortality, improve sx,
Isosorbide+hydralazine effective for
AA
Digoxin and cardiac glycosides
inotropic (^contraction, alter electrical activity, favorable affect neurohormonal systems
2nd line, does not improve mortality, only sx
compete w K for binding
Digoxin hemodynamic benefits
vSympathetic tone, ^Urine, vRenin release
vHR, ^cardiac filling, vAfterload, vVenous pressure
Digoxin neurohormonal benefits
effect on vagus nerve
effect on kidney
supresses renin release=vNa sodium absorption, decreases sympathetic outflow=^`sensitivity cardiac baroreceptors= signal nervous system to reduce sympathetic traffic to periphery
ACEi
essential HF therapy**
block angiotensin2, vAldosterone, =benefit to cardiac remodeling (due to ^kinins)
arteriole dilation=^blood to kidney, vAftedrload, ^strokevolume/CO
=NA/ water excreted, venous dilation=vVenous pressure, pulmonary congestion, pulm edema, preload, cardiac dilation
aldosterone release suppresion=^sodium water release, ^K retention
CHF stage A
risk factors present
CHF stage B
structural heart disease-LV fibrosis, hypertrophy, LV dilation, hypocontractility, valv heart disease, previous MI
***try to prevent sx from appearing
CHF stage C
sx and structural heart disease
tx:diuretics, ACEi/ARB. B blocker, aldosterone antagonist for patients with severe sx after MI but monitor K/renal function
digoxin
isosorbide-hydralazine (AA)
CHF stage C drugs to avoid
antidysrhythmic agents, ca channel blockers, NSAIDs, aspirin
CHF stage D
b blockers can make HF worse, ACEi=hypotension/renal failure
heart transplant/palliative
ICD
biventricular pacemaker
EF<35%
helps ventricles pump together correctly (good for ascynchronus HF)
Refractory HF
inotropic drugs (dobutamine, dopamine, milrinone, nitro)
