Heart Failure Flashcards
What is heart failure?
chronic, progressive condition; enlarged heart & inability to pump normally; impaired contraction of LV, organs not adequately perfused; can occur w/ low or high CO
What are the manifestations of heart failure?
dyspnea
fatigue/exercise intolerance
fluid retention/pulmonary congestion/peripheral edema
New York Heart Association quantification of HF
I: symptoms at levels of exertion that would limit normal individuals
II: symptoms on ordinary exertion
III: symptoms on less than ordinary exertion
VI: symptoms at rest
relate the Starling relationship to myocardial contractility
Increased sarcomere length during diastole increased the force of contraction. Muscle length is determined by end diastolic volume which is related to end diastolic filling pressure (preload). Preload recruitment augments CO.
*ppl w/ HF operate on a plateau phase of the Starling curve
factors affecting stroke volume
preload: increases stretch & engages Starling mechanism
afterload: ABP, increased resistance in small vessels
inotropic state: contractile state based on autonomic nerves & circulating catecholamines
How does calcium affect heart function?
promotes interaction of actin and myosin
steps of myocyte depolarization
Na enters via Na channel and changes membrane potential; Ca enters cell through VGCaC; Ca entry signals RyR to release more Ca from SR; Na/Ca exchanger reverses briefly to bring more Ca into cell; contraction happens; Ca pumped back into SR by SERCA for repolarization, also Ca ATPase & Na/Ca exchanger remove more Ca
systolic dysfunction
impairment in Ca-mediated contraction
diastolic dysfunction
problem with Ca re-sequestration needed for normal relaxation
What do myofibroblasts do?
maintain heart’s structural integrity; promote matrix formation by producing molecules promoting fibrosis (fibrotic remodeling)
compensatory responses for a decreased CO
*neurohumoral systems
baroreceptors activate SNS; SNS increases renin production; macula densa triggered by afferent arteriole
How does the SNS, AII, and aldosterone directly affect the myocardium?
promotes unfavorable remodeling via myocyte apoptosis and changes in gene expression
adaptation mechanisms in HF
abnormal baroreflex control: receptors interpret high pressure as normal so fail to inhibit SNS
cardiac hypertrophy
altered renal function: SNS vasoconstriction shunts blood from glomeruli, stimulates renin release
vasoconstriction: by SNS, RAS, vasopressin
edema
American College of Cardiology/AHA classification for HF
Stage A: at risk
Stage B: at risk
Stage C: existing HF
Stage D: existing HF
Stage A
risk of HF; no structural heart disease or symptoms; pts w/ HTN, atherosclerosis, DM, obesity, chemo, fam hx
therapy: treat HTN, dyslipidemia, smoking cessation
drugs: ACEIs or ARBs
Stage B
risk for HF; structural heart disease w/ no S/S; pts w/ prior MI, LV remodeling, asymptomatic vascular disease
therapy: everything under Stage A
drugs: ACEIs or ARBs, beta blockers
Stage C
HF; structural heart disease w/ prior or current symptoms; pts w/ known heart disease, dyspnea, fatigue, low exerc. tolerance
therapy: add a salt restriction
drugs: diuretic, ACEIs, beta blockers
addtl drugs: aldosterone antagonists, digitalis, hydralazine/nitrates
Stage D
refractory HF; requires specialized interventions; pts have symptoms at rest, may be hospitalized
therapy: same as others, add palliative care or transplant/mechanical support
drugs that reduced mortality of HF when used alone
*ACEIs, ARBs, beta blockers
other drugs for HF treatment
nitrates/hydralazine
loop diuretics/thiazides/spironolactone
adrenergic agonists, cAMP phosphodiesterase inhibitors, Dig
How do ACEIs treat HTN?
- -suppress AII, AII, aldosterone
- -increase Ang1-7
- -prevent degradation of bradykinin, a vasodilator
- -reduce afterload and increase SV & CO b/c they are potent arterial dilators
What is the first line of therapy for HF?
ACEIs
- for all HF and reduced LVHF
- often used in combo w/ beta blockers in stage A & B
mechanism of action of ARBs
competitive antagonism of AT1R suppressing effects of AII and AIII; allow residual AT2R stimulation by AII and AIII to promote vasodilation & natriuresis; increase Ang1-7 activity
Which diuretics are best for HF?
loops are preferred
thiazides preferred in HTN pts
How do beta blockers help in HF?
although they impair inotropic performance, they improve exercise tolerance & increase LVEF over a period of several mths; impair hypokalemia; prevent remodeling of heart; prevent hyperphosphorylation of RyR that causes Ca leak from SR
mechanism of action of digoxin
increases force of contraction by increasing intracellular Ca; increased CO decreases reflex SNS and increases renal perfusion; *inhibits Na/K ATPase
non-cardiac mechanism of action of digoxin
sensitizes cardiac baroreceptors (they sense pressure as higher); increases vagal tone and increases SA nodal cell sensitivity to ACh (decrease SNS activity on heart); inhibit Na/K ATPase in kidney which reducing renin release
mechanism of action of venodilators
decrease filling pressure & intracardiac volume
mechanism of action of arteriodilators
decrease SVR to increase CO; increase renal perfusion to promote diuresis (decreases filling pressure)
mechanism of action of isosorbide dinitrate
venodilation; increases venous capacitance to reduce preload; increases coronary artery flow
mechanism of action of hydralazine
reduces renal vascular resistance & increases renal blood flow
*added to ACEIs, dig, diuretics for HF
mechanism of action of sodium nitroprusside
reduces ventricular filling pressure & SVR; used in ICU setting
mechanism of action of nitroglycerin
selective for venous capacitance vessels
mechanism of action of positive inotropic agents
improve cardiac performance, facilitate diuresis, promote stability in the short term
mechanism of action of dopamine
- -stimulates beta receptors on heart to stimulate contractility
- -stimulates alpha receptors at high infusion rates to stimulate peripheral arterial/venous constriction (helps critical circulatory failure by increasing afterload)
mechanism of action of dobutamine
stimulates beta 1 (inotropic) & beta 2 (vasodilation) receptors; increase renal bloodflow to increase CO
mechanism of action of milrinone
stimulate myocardial contraction & accelerate myocardial relaxation by increasing cAMP (preventing degradation); cAMP activates protein kinase A (PKA) to increase Ca in the cell
