Congestive Heart Failure Flashcards
Define heart failure
HF: inadequate cardiac output (contrast w/ ischemia w/ is inadequate myocardial o2)
Describe a typical presentation of congestive heart failure
(4)
Typical presentation of CHF:
Dyspnea on exertion
Orthopnea (having to prop oneself up to sleep)
Paroxysmal nocturnal dyspnea
Swelling in the legs
What are the typical physical exam findings of CHF? (4)
PE findings:
Rales
S3, s4 gallops
Elevated JVP (high left or right sided atrial pressures
Dependent edema
***look for things that suggest volume overload***
Describe the classes of CHF (4) (hint: each ass’d with physical activity)
Class I: no real CHF symptoms
Class II: symptoms with more activity than usual
Class III: symptoms with less than normal activity
Class IV: symptoms @ rest (worst prognosis)
List some causes of HF symptoms (hint: think of things that can cause reduced cardiac output) (7)
There are 2 phenotypes of congestive heart failure, namely ___ (hint: related to systole and diastole)
Systolic dysfunction (heart failure w/ reduced ejection fraction - HFrEF)
Diastolic dysfunction (heart failure w/ preserved ejection fraction - HFpEF)
**note that the difference between these is based on left ventricular ejection fraction**
How do you calculate ejection fraction?
Systolic dysfunction is considered an EF of ___. What is the range of normal EF?
EF = stroke volume/end diastolic volume
Systolic dysfunction = EF
Normal EF = between 55-70%
***
EF 40-50% = Mildly reduced
EF 30-40% = Moderately reduced
EF 15-30% = Severely reduced
EF < 15% = Awful
Describe the difference between systolic dysfunction and diastolic dysfunction
Systolic dysfunction - can’t/impaired pump blood out of LV
Diastolic dysfunction - can’t/impaired fill blood inside LV
Review how plumonary edema occurs
Recall that the pressure in the LV will be reflected back to the left atrium, and that’ll be the same as that of the pulmonary veins (the interstitial pressure in the lungs is a little higher)
When the pressure in the left ventricle (and thus in the left atrium and pulm veins) increases beyond that of the interstitium (>25mmHg), that develops into pulmonary edema (b/c of fluid leakage)
What are 5 common causes of systolic dysfunction HFrEF?
Myocardial infarction
Chronic severe HTN
Familial cardiomyopathy (genetic)
Valvular heart disease
Idiopathic
In systolic heart failure, the body can compensate for the decreased ejection fraction. Name 3 mechanisms that the body does this
Frank Starling mechanism
Sympathetic nervous system activation
RAAS activation
Describe the neurohormonal response to heart failure (hint: there’s 2 parts to it, and both are about addressing the decreased CO)
Neurohormonal response:
Short term and long term:
Short term – baroreceptor response to decreased CO; long term – vasoconstriction, Na+/water retention etc (all efforts to increase CO again because your body doesn’t know that you actually don’t have a volume problem. As soon as your body sees low CO, it thinks you’re having a volume problem)
What 5 molecules will be elevated in the plasma in response to low ejection fraction?
Molecules that will be elevated in the plasma include
norepinephrine
renin
atrial natreuretic peptide
endothelin
vasopressin
**all are in response to the low CO**
Explain the neurohormonal response to HFrEF below
Essentially this entire process is so you can raise your BP again, raise blood volume and increase renal perfusion back to normal levels
Explain the Starling curve changes that occur when a pt has a decreased CO, and when that pts body responds to the decrease in CO (i.e. what’s happening below?)
Basically:
When a pt has something like an MI that lowers their CO, they are lower on the starling curve. The response to decreased CO (the vasoconstriction to raise HR, BP, increased renin to retain more volume etc) will cause a shift in the curve such that at higher filling pressures, the pt can have a better CO
Problem is that response is unregulated so the pt can actually have increased filing pressure (and continued compensation) >> pulmonary congestion symptoms
Explain what orthopnea is and what the pt will be trying to achieve by that
Orthopnea – the pt is decreasing the amount of blood going back to the heart (i.e. decreasing venous return) so they can breathe more comfortably
What is this below?
Pitting edema - sign of CHF
What condition does this pt have? (hint: suggestive of HF)
Pulmonary edema (right)
Explain the Frank-Starling compensation that happens in heart failure
Basically when you stretch out your myocardium too much, the strength of the contraction will continue to increase until it levels off and actually starts decreasing
Describe the changes in the P-V loop that occur with congestive heart failure
Lower stroke volume
Reduced contractility – slope of the line lowers
Preload increases (remember this is due to those compensatory mechanisms
Decreased compliance
What causes diastolic dysfunction? (HFpEF) (i.e. what’s the mechanism?)
Diastolic dysfunction is a problem of decreased compliance – the heart muscle is stiffer so it’s less receptive to filling during diastole
What are some causes of diastolic dysfunction? (3)
LV Hypertrophy
Coronary artery disease
Restrictive cardiomyopathy
***
Restrictive cardiomyopathy
Decreased compliance of ventricular endomyocardium >> restricted filling during diastole
Various causes: amyloidosis; endocardial fibroelastosis; hemochromatosis; Loeffler syndrome; sarcoidosis
Presents as congestive heart failure; ECG = low voltage; diminished QRS amplitudes
Poor compliance leads to (increased/decreased) LVEDP
Describe the pressure-volume loop changes seen with diastolic dysfunction
Poor compliance leads to increased LVEDP
**see below**
Describe the differences in stroke volume and resulting symptoms between people w/ normal function and folks w/ HFpEF
**see below**
People with diastolic dysfunction will have similar symptoms as folks with impaired LV function
Note that the stroke volume decreases in the pt with the stiff ventricle because their end diastolic volume was low to start with (coz of resistance to filling)
T/F: A pt with HFpEF and HFrEF will present similarly
True. *see below*
Explain the slide below
**HFrEF is basically a never ending cycle of reduced cardiac output, the body trying to increase the CO but that results in even more reduced CO**
What classes of drugs are used in the Rx of HFrEF? (5)
Diuretics
Vasodilators (ARBs/ACE inh; nitrates; hydralazine)
Beta blockers
Aldosterone antagonists
Glycosides
Of the drugs used to Rx hfref, which ones improve survival? (3 classes)
Vasodilators
Beta blockers
Aldosterone antagonists
Describe the action of vasodilators in hfref
Vasodilators work by reducing afterload, which increases stroke volume (and thus cardiac output) w/o affecting contractility (so curve B)
Why are aldosterone antagonists better drugs than ARBs for HFrEF?
Aldosterone antagonists improve survival by preventing angiotensin escape (other means for angiotensin to be generated and bind to the receptor)
What are the drug therapies shown to improve survival in HFrEF pts? What Rx is there for HFpEF?
**see below**
for hfref, basically everything except diuretics coz those have NO effect on mortality but they do improve congestion
hfpef has NO Rx as of yet
