Exam 2: Ch 20 Heart Failure Flashcards
to meet the body’s needs, the heart adjusts its…
cardiac output
increased with exercise
decreased with sleep
calculate CO (cardiac output)
SV x HR
SNS can increase both SV and HR
calculate SV (stroke volume)
EDV - ESV
end diastolic volume - end systolic volume
calculate EF (ejection fraction)
SV/EDV
preload
EDV: increased EDV –> increased SV within limits
in HF EDV is very high and SV is low
afterload
SVR (systemic vascular resistance): high SVR –> increased work and/or low SV
contractility
ability of the heart to eject (SV at any EDV): low EF in HF
calcium from SR and ECF
L-type calcium channels opened by catecholamine binding to receptor
cardiac glycocides inhibit Na/K pump
athletes have a higher __ and lower __
SV, HR
heart failure definition
heart fails to pump the blood that it receives
veins of lungs and peripheral organs become congested
systolic HF
reduced EF: heart contracts poorly
often caused by ischemic heart disease, HBP, aortic stenosis
high EDV
low SV
EF less than 40%
Peripheral venous congestion
disatolic HF
preserved EF: heart relaxes and fills poorly
aggravated by tachycardia
low EDV, ESV, SV, CO
hypertrophic cardiomyopathy
Pulmonary congestion
right sided HF
high RVEDP –> high RAP –> high peripheral venous pressure
extremities and viscera become conjested –> peripheral edema & ascites
causes of right sided HF
Rt sided valve problems or MI
severe pulmonary disease
severe pulmonary HTN
left sided HF
low CO
high LVEDP –> high LAP –> high pulmonary venous pressure
lungs become congested and body tissues are inadequately perfused
causes of left sided HF
MI
HTN
left sided valve dysfunction
high output HF vs. low output HF
high output: CO is elevated but still inadequate
low output: pumping ability of the heart is decreased
Frank-Starling mechanism
low CO triggers Na + H2O retention to increase EDV & SV
HF –> high EDV at rest, nearly normal SV
compensatory mechanism partially exhausted so ability to exercise is limited
high LVEDP –> pulmonary congestion
______ are commonly helpful in HF
diuretics
SNS activity in HF
SNS nerve activity and catecholemine levels high in early HF
maintains CO and vital organ perfusion
downside is increased afterload –> low SV or increased work
down regulates beta receptors
more arrythmias
RAA system
stimulated by low renal blood flow or pressure
kidney secretes renin
renin turns renin substrate into angiotensin I
A I –> A II by ACE in lung capillaries
A II increases ADH/Aldo release
ADH/Aldo/A II
ADH: increases H2O retention
Aldo: increases Na retention
A II: vasoconstrictor, helps tissue remodeling
naturetic peptides
increased in HF
ANP (atrial natriuretic peptide), brain NP
ANP released when atria overstretched
BNP (brain) released from ventricles when stretched
both –> natriuresis (Na excretion by kidneys)
endothelins
vasoconstrictors released by endothelial cells
cause cardiac tissue hypertrophy and remodeling
is hypertrophy an initially helpful compensation for HF?
yes
eventually decreases cardiac pump function though
stimuli for hypertrophy
mechanical stress
A II, ANP, endothelin
ACEI
3 types of hypertrophy
symmetric
concentric
eccentric
symmetric hypertrophy
muscle length and wall thickness is increased (athletes)
concentric hypertrophy
wall thickens too much due to HTN
increased afterload
systolic function initially preserved, then leads to ischemia
eccentric hypertrophy
muscle length is increased (dilated cardiomyopathy)
decreased wall thickness
increased preload
6 manifestations of HF
edema and fluid retention
respiratory symptoms
fatigue and confusion
cachexia
cyanosis
arrhythmias and sudden death
edema and fluid retention
high capillary hydrostatic pressure causes edema
right sided failure –> peripheral edema
left sided failure –> pulmonary edema
nocturia
oliguria
nocturia
early in HF laying down
high venous return
low urine output
oliguria
late in HF
low CO and renal perfusion
low urine output
respiratory symptoms of HF
pulmonary congestion causes dyspnea
worst on exertion, when flat (orthopnea), and at night
cardiac asthma: stimulation of stretch receptors
fatigue and confusion is due to
decreased organ perfusion
cachexia (loss of weight)
GI involvement and general fatigue
cyanosis
arterial desaturation
pulmonary edema or O2 removal
arrhythmias and sudden death
AF (atrial fibrilation)
VT/VF (ventricular tachycardia/ventricular fibrillation)
acute HF syndromes
gradual or rapid change in HF signs and symptoms
worsening of chronic HF that responds to Rx
new onset HF from MI
worsening of end-stage HF that is refractory to Rx
acute pulmonary edema
dramatic and life-threatening symptom of AHFS and complication of left sided HF
severe dyspnea, cyanosis, confusion, frothy blood-tinged sputum
Rx: lower preload and afterload, increase contractility, give O2
case of a 51 yro male with SOB: PA chest radiograph demonstrates bilateral parahilar infiltrates resembling batswing o butterfly in which the hilum or medulla of the lungs are mainly involved with sparing of the periphery or cortex
pulmonary edema
“bats-wing” pattern
2 classification systems for diagnosing HF
functional classification of severity by NYHA
or ACC-AHA staging
Dx of HF: H&P, Labs, Echo, CXR
H&P: ask about dyspnea, nocturia, fatigue, cough, edema
Labs: BNP levels, electrolytes
echo: look at EF, hypertrophy, valve action, distinguish between systolic vs. diastolic failure
CXR: shows cardiac enlargement
functional classification system by NYHA
class 1 is best, no limitation of physical activity
class 4 is worst, can’t perform any physical activity without discomfort; symptoms present at rest
ACC-AHA staging
stage A: high risk for HF, no abnormalities yet
Stage B: no symptoms but developed structural heart disease that may lead to HF
Stage C: symptomatic HF associated with structural disease
Stage D: advanced structural heart disease, signs of HF at reset despite max therapy
pharmacologic treatment of HF goals
treat causes, reduce risk factors
slow or reverse dysfunction, relieve symptoms, improve quality of life
lower edema with Na restriction and diuretics
surgical repair of cardiac defects
pharmacology of HF treatment
diuretics: improve position of Starling curve
digitalis: poison Na/K pump, lower HR and up contractility
ACEI: lower afterload and aldosterone, slow remodeling
A II receptor blockers: similar as above
beta blockers: lower SNS activation to decrease mortality
vasodilators: isosorbide, hydralazine
Swan-Ganz catheter (invasive monitoring)
inserted in large vein (goes with flow)
when wedged (PCWP) ~ LVEDP
prolonged inflation causes pulmonary infarct
measures CO: thermodilution
measures MV O2
non pharmacologic treatments of HF
exercise program
Na/H2O restriction
O2 therapy
cardiac resynchronization
mechanical support
heart transplantation
O2 therapy
increases O2 saturation
CPAP - constant positive airway pressure
cardiac resynchronization
use of pacing leads in Rt and Lt ventricles
coordinates activity
mechanical support VAD
ventricular assist device
implanted percutaneously or open
augment pumping action of LV
heart transplantation
orthotopic technique: donor heart attached to retained posterior atrial walls of recipient
required continued immunosuppressants
5-yr survival rate is 2/3 –> 3/4
