216a heart failure

heart failure

any functional or structural disorder that decreases the hearts ability to fill &/or eject blood can cause

can cause hf

CAD, HTN, pulmonary HTN, arrhythmias, MI, cardiac tamponade, renail failure/disease

cardiomyopathy

cardiac muscle dysfunction reducing EF

-enlarged heart, thick walls, smaller volume, hard to squeeze

-can be from infection, drug effects, genetics, autoimmune disease, htn

restrictive/hypertrophic cardiomyopathy

excessive wall thickening of cardiac muscles

cardiac valve insufficiencies

like mitral valve prolapse- wont close properly, backs up and fills up in atrium, less flow to aorta

right hf

impaired ability to pump deoxygenated blood from the body (venous system) to the lungs (pulmonary circulation)

-reduction in mvmnt of blood to pulmonary circulation

-blood backs up into the systemic circulation

right hf s&s

peripheral edema, jvd, enlarged liver, enlarged abdomen, weight gain, fatigue

left hf

impaired mvmnt of blood from the pulmonary circulation (lungs) to systemic circulation

-blood backs up into pulmonary circulation

left hf s&s

pulmonary edema, dyspnea/sob, crackles, cyanosis, fatigue, loc effects

central cyanosis

caused by arterial hypoxia, where there is a low level of oxygen in the red blood cells leaving the heart

peripheral cyanosis

rarely a emergency, most commonly due to reduction of blood flow in peripheral circulation

circumoral (perioral) cyanosis

bluish discoloration of the mouth or the lips, and other mucous membranes. it is most commonnly caused by constricted blood vessels in response to cold temps

compensation

sns activation - tachycardia, water retention → worsening of CO

release of endothelial enzymes

as compensation for hf

induce smooth muscle cell and fibroblast proliferation → over time: hypertrophy of smooth muscles & fibroblasts (not myocardial cells) → thick and stiff cardiac wall

risk of cardiac arrhythmias

vtach, vfib, bundle branch block

condition where electrical signals in the heart are delayed or blocked as they travel to the ventricles, causing the right and left sides of the heart to beat out of sync

risk of low output failure

hypoxemia, hypoxia, hypotension

systolic dysfunction

low EF (normal ~ 70%)

diastolic dysfunction

cannot fill → reduced pre load

preload

the degree to which the myocardial fibers are stretched, loading of each ventricle at the end of diastole

afterload

the force of the contracting heart must overcome to eject blood

contractility

the strength of the contraction of the heart

reduction of preload

as tx of hf

diuretics

vasodilators

beta blockers (alpha specific eg)

reduction of afterload

vasodilators and beta blockers (eg alpha specific)

as tx of hf

for improved contractility use these

beta blockers (eg beta 1) -slow hr, improve filling time

phosphodiesterase inhibitors (pde 3)

cardiac glycosides

catecholamines (increase hr, increase contractility, rescue drugs)

neprilysin inhibitors

neprilysin is the enzyme which breaks down NPs which are endogenous vasodilators

-so when inhibited = high natriuretic peptide presence → vasodilation

high NPs

stimulate RAAS

• + ARB to inhibit compensation via RAAS

Sacubitril/valsartan

a neprilysin inhibitor and a ARB for vasodilation

cardiac glycosides moa

for contractility

-block na/k atpase = blocks exit of Na = high Na in cell activates Na/Ca exchanger = increased Ca in = increased contractiliy

cardiac glycosides

Digoxin, digitoxin for contractility

cardiac glycosides monitor

hr 1min prior to admin

serum levels (pk: narrow ti)

cv assessment

toxicity: n&v 1st sign

digibind

antidote for digoxin and digitoxin

catecholamines action

sympathomimetics

-rescue drug for severe hf

potent

iv continuous, titrate

short 1/2'

continuous monitoring CV

catecholamines

dobutamine and dopamine hcl

continuous iv drip

dobutamine

direct sympathomimetic

high cardiac (B1) specificity (increased contractility)

dopamine

indirect sympathomimetic (precursor to NE)

non-selective (contractility, bp, vasoconstriction)

CRT

cardiac resynchronization therapy aka bi ventricular pacing

-dial chamber pacemaker

-can be combined w/ a defibrillator (ICD)

-communicates electronic data to cardiologist

-battery life 10 years

hf guidlines

change often, based on EF (>40%, <35%)

acute HF tx

potent and IV admin drugs

lasix, nipride, dobutamine, milrinone, O2

chronic hf

po and for at home

-neprilysin/arb, beta blockers

-drugs to enhance remodelling of cardiac muscle and vasculature

-anticoagulant/antiplatelet