Heart Failure Flashcards
What causes PND and orthopnea?
Left sided heart failure
When you lie back, you are increasing venous return into an already congested cardipulmonary circulation, exacerbating HF
What causes pulmonary crackles?
elevated pulmonary capillary hydrostatic pressure
there is more pressure in the pulmonary veins from left-sided heart failure
more fluid is in the interstitium
What secondary heart sound can dilated heart failure produce?
mitral regurgitation secondary to dilatation of the LV and mitral annulus
How does PV curvechange in HFrEF?
reduction in contractility causes a decrease in slope of the ESPVR
correspondingly, a decrease in contractility pushes the ESV to the right (greater ESV)
also have a decrease in stroke volume (width) and EDV also increases
Can viral myocarditis lead to heart failure?
yes
What are 2 things to check to rule out restrictive cardiomyopathy?
congo red stain (amyloid) and iron stains
is dilated cardiomyopathy HFpEF and HFrEF?
HFrEF due to systolic dysfunction
What is most common etiology of dilated CM?
idiopathic
Increased venous return leads to …
worse pulmonary edema
If you have increased volume, what type of hypertrophy do you get?
eccentric hypertrophy
What 3 processes are activated with heart failure? What do they do?
1) adrenergic system results in tachycardia (CO = SV * HR)
2) RAAS (causes vasoconstriction with decreased renal perfusion)
3) Increased secretion of ADH and aldosterone (retention of Na/H20)
When someone has acute heart failure, what is the first treatment decision you need to make?
if they are cold and wet, use an IV inotrope to increase CO before diuresis
if warn and wet, proceed directly to diuresis
What do you give for IV inotropic therapy?
1) beta agonist like dobutamine
2) Phosphodiesterase inhibitors like milrinone
What is the MOA of milrinone?
inhibits PDE inhibitor
this prevents conversion of cAMP to AMP and increases contractility
What drugs can you give to chronically manage HFrEF? (4)
B-blocker
aldosterone antagonist
ACE/ARB
SGLT-2 inhibitor
How does nitroglycerin change at different doses?
lower dose venous dilator decreases preload
higher dose arterial dilator decreases afterload
When is digoxin not indicated?
if you don’t have a problem with contractility, you don’t need digoxin
Why do you not see peripheral edema and hepatomegaly when someone acutely goes into heart failure?
there is not enough time (<24hr) to see full effects of Na/H2O retention
Which cardiac biomarker decreases first?
CK-MB
What do we call it when an MI prompts heart failure?
ischemic cardiomyopathy
How can diuretics help with supply-sided ischemia?
decrease intravascular volume
decreases preload which leads to a reduction in LV wall tension and O2 needed
Are lipid values during an MI accurate?
no
What are two other causes of right-sided HF besides left-sided HF?
Primary pulmonary arterial hypertension
Cor pulmonale
What is cor pulmonale?
enlarged right ventricle due to a pulmonary condition
What does the presystolic impulse on palpation indicate?
Non-compliant, stiff left ventricle
similar to S4
What type of heart failure can longstanding HTN cause?
diastolic dysfunction due to stiff, hypertrophied left ventricle
diastolic dysfunction = HFpEF
How will PV curve change in HFpEF? How does the PV curve remain the same?
shift upward and to the left
EDV goes down (left, decreased filling) and pressure goes up
stroke volume decreases
contractility has no change
What 4 factors can lead to an increase in wall tension of ventricle?
1) volume overload
2) increase in radius
3) increase in pressure
4) decrease in wall thickness
How do you treat HFpEF?
really only can give spironolactone and maybe SGLT-2 inhibitors long term
What patients tend to be older? HFpEF or HFrEF?
HFpEF
What is a difference in side effects between ACE inhibitors and ARBs why?
ACE normally breaks down bradykinin
if you inhibit ACE, you increase levels of bradykinin which can lead to cough and angioedema
What type of drug is spironolactone?
Aldosterone receptor anatogonist
prevents aldosterone from reabsorbing Na+
Is calcific AS a passive process?
No! Many studies have shown that it is associated with active inflammation
What does a soft aortic component of S2 indicate?
severe AS
the leaflets are not closing as well, leading to a reduction in sound
What does carotid pulse look like in aortic stenosis?
pulsation that is low in amplitude with a delayed upstroke
delayed upstroke is due to it taking longer for blood to get through the AV
pulsus parvus et tarvus
summation gallop
can occur when someone is tachycardiac
hard to distinguish between S3 and S4
What type of heart failure can aortic stenosis lead to?
Increased afterload leads to increased pressure
increased pressure = concentric hypertrophy
HFpEF as most of problem is from a stiff ventricle
Should you use verapamil / diltiazem in heart failure?
No! It has negative ionotropic and chrontropic effects which can lead to decreased CO
Aortic area of severe AS
< 1 cm2
What does a laterally displaced PMI tell you?
LVH (left ventricular hypertrophy) / cardiomegaly
How can you have decreased EF but still strong functional capacity?
some individuals are able to compensate better than others
When should you consider an ICD? (general rule)
EF < 30%
you are at a higher risk of sudden cardiac death in this scenario
4 levels of NY heart failure
1) cardiac disease but no symptoms and no limitations in ordinary physical activity
2) Mild symptoms and slight limitation during ordinary activity
3) Significant limitation in activity due to symptoms
4) Severe limitation. Symptoms even at rest
If you think a patient’s CM is idiopathic, what other testing should you do?
r/o ischemia, toxicity, or infiltrative causes of CM
What are 3 mainstay treatments in HFrEF?
ACE/ARB
B-blocket
aldosterone antagonist
2 aldosterone antagonists
Eplerenone
Spirinolactone
What is the hallmark of HF, even if EF is okay?
decreased CO
What is always high in left heart failure?
LVEDP
What does RAAS activation lead to?
increased TPR
How can BP stay normal in HF if CO is decreased?
the RAAS system vasoconstricts
BP = CO * TPR
What counteracts RAAS?
ANP / BNP
What does ANP signal?
tries to increase secretion of Na/H2O and increase urine output
What type of heart failure has reduced EF?
systolic since there is a problem with contraction in systole
Is dilated CM systolic or diastolic?
Systolic
cannot contract well
is dilated cardiomyopathy eccentric or concentric?
eccentric from increased fluid
What 2 scenarios really result in concentric hypertrophy?
aortic stenosis
htn
Concentric hypertrophy is normally systolic or diastolic dysfunction?
diastolic
What is the most common form of systolic HF?
MI / ischemic
What drug class can lead to acute HF?
NSAIDs
inhibit COX = decrease prostaglandins = increase Na/H2O
MOA of loop diuretics
inhibit Na-K-Cl pump in ascending loop of Henle
ACE inhibitors MOA
prevent conversion of angiotension I to angiotension II
angiotension II is main effector of RAAS system. So by decreasing angiotension II you prevent vasoconstriction
What is the only oral inotrope?
digoxin
What are digoxin’s 2 MOAs?
1) inhibit Na-K-ATPase pump which causes more Na and more Ca2+, therefore more contractility
2) suppress AV node / activate parasympathetic
ARB MOA
directly blocks the angiotension receptor
What do aldosterone antagonists do?
prevent Na+ reabsorption
Sacubitral MOA
inhibits neprilysin
neprilysin normally breaks down ANP / BNP
more ANP / BNP can counteract the RAAS system
Entresto MOA
combines sacubitral with ARB
How can Coxsackie cause heart failure? And what type?
can cause myocarditis which then can cause dilated CM
