Heart Failure Flashcards
what is heart failure
condition in which the heart cannot pump blood at a volume required ot meet the bodys needs
is heart failure a primary or secondary disease
secondary occurs after the heart becomes damaged or weakened
what is end diastolic volume or EDV
volume that is in the ventricles before the heart contracts
what does EDV tell us
preload
what is ESV
End systolic volume
amount of blood in te ventricles at the end of systole
what is a normal EF
60-80%
what is HFpEF
preserved EF >50%
What is HFmEF
mid-range EF 41-49%
what is HFref
reduced EF <40
recovered EF is
EF previously <40 now >40
what is systolic HF
dilated heart failure
problem with pumping and ventricular emptying
reduced contractility
what happens to the left ventricle in systolic HF
large dilated congested and overloaded
what type of remodeling is seen in systolic dysfunction
eccentric as cardiomyocgyes are elognated
what happens to contractility, EF and CO in systolic HF
reduced
what is the most common type of HF
systolic
what type of EF does systolic typically have
HFrEF <40%
what heart sound is likely heard in systolic HF
S3
what does BP typically look like in systolic HF
low
is systolic HF more common in men or women
men
what happens to preload, afterload and contracility in systolic Hf
increased preload
increased afterload - compsneatory
contractility decreased as heart stretched too far
what type of V/Q mismatch would you see in systolic HF
shunt like as increased hydostatic pressure in pulm capillaries causes fluid to back up into lungs
deadspace with decreased CO
what happens to lung compliance in systolic HF
decreased resulting in inc WOB
what type of meds are you likely to see in systolic HF
vasodialtors, diuretics, inotropes
what is diastolic HF
problems with inadequate ventricular filling d/t inability to relax/fill
what happens to the ventricles in diastolic HF
thick, stiff and noncompliant
what type of remodeling occurs in diastolic HF
concentric remodelling
cardiomyocytes increase in diameter not length
what happens to LVEDV and LVEDP in diastolic HF
LVEDV (preload) decrased
LVEDP increased
Causes of Diastolic HF
HTN
hypertrophic cardiomyopathy
aging
ER in Diastolic HF
Normal HFpEF
Ventricles in systolic HF vs Diastolic HF
S: large, dilated, overloaded problem with emptying/pumping
D: Thick, stiff, non compliant problem with filling adequately
remodeling in Systolic vs. Diastolic HF
S: eccentric and elongated
D: concentric and thicker diameter
Causes of systloic vs. Diastolic HF
S: CAD
D: Htn, aging, hypertrophic cardiomyopathy
Extra heart sounds heard in Systolic vs. diastolic Hf
S3 vs S4
preload in systolic vs diastolic HF
S: increased
D: normal - incrased
afterload in systolic vs diastolic HF
S: increased
D: incrased
contractility in systolic vs. diastolic Hf
S: decreased
D: normal-decreased
where is the increase in diastolic pressures in systolic and diastolic HF
LA, LA, pulmonary vessels
what are the three types of compensatory mechanisms for HF
neurological - ANS (SNS & PNS)
hormonal - RAAS
Chemical - chemoreceptors
Describe the pathway for ANS
medulla –> CN X (vagus) –> heart
what is the synapse for PNS
what neurotransmitter
cholinergic
ACetylcholine
where are the receptors for ANS
atria
AV junction
what effect does the PNS have on O2 supply and demand
decreases HR
slows impulse generation at SA
slows impulse through AV
what is the neural pathway for SNS
medulla –> spinal cord –> exits @ T1-L2
what type of synapse is in the SNS
what neurotransmitters
adrenergic
norepi, epi
what receptors are involved in SNS
alpha - smooth muscle, skin, gut, kidneys, peripheral circulation
B1 - SA/AV nodes and ventricles
B2 - bronchiole, smooth muscle, skeletal msucle, arterioles
how is the SNS triggered in HF
decreased CO/BP activates barorecpors in the aortic arch and carotid sinus -> stimulates medulla to activate SNS; also triggers RAAS
what happens when the SNS is triggered in HF
increased catecholmaines - vasoconstriction increase afterload, inc. HR/condution/contactility
increasecd myocardial O2 demand
How does HF trigger RAAS
dec CO poor kidney perfusion --> activates RAAS angiotensin II and aldosterone vasoconstriction and Na/H20 retention increases afterload and preload
what are the 2 types of chemorecepors and where are they located
Peripheral: carotid body, aortic arch
Central: brain ventral surface of medulla close to CSF
what are peripheral cehmoreceptors sensitive to
PaO2 <60 mm Hg
what are central chemoreceptors sensitive to
PaCO2 >40
what is endothelin
neurohormone invovled in ventricular remodelling in HF; produced by endothelin cells in the endotehlium of vessels
what does endothelin do
potent vasoconstrictor
can cause renal vasoconstriction and Na retention
what is apoptosis
controlled cell death w/o inflammation scarring
promoted by angiotenin II and catecholamines
decreases # and strength of myocytes contributing to remodelling
what remodeling process to ACE and Beta blockers slow down
apoptosis
why does ventricular remodeling place pts at risk for arrythmias
d/t atrial/ventricular stretching and dilation –> disrupts conduction pathways
what is the most common arrhythmia seen in remodeling
Afib
what does an EF <30 and a hx of ventricular arrythmias predict might happen to a person
sudden death
what are the 2 natriuretic peptides and where are they released from
ANP - atrial natriuretic peptide - atrial wall in response to stretch
BNP - brain natriuretic peptide - ventricle wall in response to stretch
what do natriuretic peptides do
counter effects of compensatory mechanisms
promote vasodilation reduce Na and H2O retention via diuresis
promote balanced vasodilation
reduce preload and afterload
limit hypertrophy from injury or ischemia
what do we call an acute worsening of chronic heart failure
acute decompensated HF
what would cause acute decompensated HF
MI, myocarditis
dysrhtymias, ischemia
not adhering to diet restrictions
what are some common medical issues that lead to chronic HF
DM kidney disease atherosclerosis COPD valve dysfunction
what occurs in left sided HF (3)
left ventricle ineffective contractile fn
low CO –> inc. afterload
pulmonary congestion decreased perfusion to peripheries
what occurs in rt sided HF (3)
rt ventricle has ineffective contractile fn
can be caused by an acute condition such as a PE or rt ventricular infarction
most commonly caused by left sided HF
what are 3 specific to HF lab values
BNP, CK, trop
other than HF what else can cause inc. in BNP
pulmonary HTN, CKD, sepsis, burns, COPD, OSA
what are 4 imaging tests for HF
CXR, TTE, angio, 12 lead
2 types of valve dysfunction
stenosis
regurg
what is valve stenosis
can be congenital or calficifation
narrowing
results in mechanical obstruction
limits blood flow
what does valve stenosis do to afterload
permanent increase
what are signs and symptoms of valve steonsis
dyspnea fatigue waekaness resp symptoms angina activity intolerance edema
what is valve regurgitation
leaflets dont close adequately causing backflow during systole
increases pressure in chambers before affected vlave
does valve regurgitation cause hypertorphy
yes to maintain adequate stroke volume and forward flow
what caues regurg
dilated poorly contractile ventrilce
stretching of valvular tissue as dilation and remodelling occur
what are signs and symptoms of valve regurgitation
fatigue
dyspnea
palpations
pulmonary edema
what are some medicatoins we can use to decrease or redirect preload
diuretics - decrease total ciculating volume
vasodilators - inc. venous capitance decrease preload
improves contractility and reduces afterload
aside from medication what can e do to reduce preload
CRRT
uses osmosis to remove water directly from pts blood
what medication can we give to eliminate anxiety associated with pulmonary edema
morphine
what are 4 ways we can improve oxygenation in HF
O2 therapy - inc driving pressure
CPAP or BiPAP - pushes fluid out decrease preload from pressure
high fowlers - dependent portions more perfused and better ventilated
diuretic - decreases preload improves oxygenation and ventilation
3 medications for improving contractility
dobutamine -inotrope and vasodilator beta 1 and some beta 2
milrionoe -phophodiesterase III inhibitor with vasodilation effect
digoxin - HR control in acute HF as an inotrope for chronic HF
what are 3 short term devices that can be used in the management of HF
intra aortic balloon pump
ECMO
Impella
what is the goal with IABP
increase coronary artery perfusion and decrease afterload
should only be used for 5-7 days
what does the impella do
sucks blood from LV and transfers to aorta offloads the LV allowing it to rest and recover
what does ECMO do
functions as a heart and lungs giving organs a chance to recover
What is the NYHA and what are the 4 classes
new york heart association heart failure classification
I no limitation
II slight limitation comfortable at rest
III comfortable at rest but any movement causes symptoms
IV SOB even with bedrest
what do ACEI and BB do
slow remodelling and progression of HF
what does Ivabradine do
SA node modulator slows HR
reduces hospilizations for HF and reduces mortality
used in comination with BB
what are 3 devices that can be used for HF
implantable cardioverter defibrillators (ICDs)
Cardiac REsynchronization Therapy (CRT)
Left ventricular assistive device (LVAD)
what is an ICD? when is it indicated
implantable cardioverter defibrillator EF < 30 narros QRS hx of sudden cardiac arrest can overdrive pcae, cardiovert and defibrillate
can an ICD cause PTSD
yes
when would you implant CRT
for prolonged QRS or BBB any asyncrhonous contraction of ventricals
it uses biventricular pacing to synchroinize contraction and improve LV fn
pateints who have what 3 things should get a cRT
LBBB EF <35 and NYHA class II/III
what is an LVAD
left ventricular assistive device
provides CO or flow using an outflow cannula in the left atrium or ventricule
bypasses ventricle and augments/replaces pumping
do pts with an LVAD have a palpable pulse
no
when should a HF pt call for help
weight gain >5lbs in a week increaseing SOB with regular activities increasing orhtopnea waking up in the night SOB increasing edema
