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Cardiology - CHF = Congestive Heart Failure (dropped image link (CHF Body…
Cardiology - CHF = Congestive Heart Failure
*HFpEF vs HFrEF
HFpEF = HF with preserved EF (50%)
HFrEF = HF with reduced EF (<50%)
Preserved EF = diastolic failure
--> stiffend LV
Non-Preserved EF = systolic failure
--> dilated LV
HFrEF = HF with reduced EF
EF < 50%
HFrEF = reduced EF *Treatment
for Systolic HF --> Keep it simple
ABC Treatments improve systolic HF survival
(Betas = low CO and ACE / Aldosterone = remodelling)
--> Aldosterone system drugs (ACE, ARBs, Aldosterone blocking Spiron and Eplerenone)
--> Beta blockers
--> (Carvedilol and ACE)
main goal = inhibit the RAAS system immediately with both DIRECT (ACEIs) and INDIRECT (K Sparing Diuretics = K+ STAys)
add spironalactone to ACEIs
--> reduce mortality specifically in reduced HF --> Aldosterone remodels the heart
--> need to stop this anyway possible
Aldosterone - STOP remodelling in systolic HF Treatment
Spironalactone, Eplerenone
Clinical Cases
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HFpEF = HF with preserved EF
EF > 50%
CHF = Compensated (acute response) vs. *decompensated
decompensated = think of as DEGRESS in compensation
note that compensated = refers to the cardiorenal response syndrome
Decompensated CHF
chronic CHF leads to constant RAAS activation
urine sodium / K+ ratio low < 1%
--> since RAAS not activated
Clinical cases
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Clinical Case
Decompensated CHF example
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note that decompensated CHF is a renal response to CHF having low CO and blood volume
renal response is to increase the Blood volume and renal perfusion
activation of the RAAS system
higher sodium reabsorption, aldosterone from adrenal gland = zona glomerulus and Angiotensin 2 at PCT
higher free water reabsorb from ADH at CDs
Example
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Compensated CHF
RAAS not activated
urine sodium / K+ ratio normal > 1%
--> since RAAS not activated
CHF Body Response
increased Epi, Angiotensin 2, ANP and BNP (work against them)
CHF and bodies response case
Clinical Case
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CHF Body Response
carotid baroreceptors --> epinephrine and SNS
juxtaglomerular cells / low renal perfusion --> RAAS system
ANP (atrium walls) and BNP (brain) --> try to counteract Epi and RAAS system
Neurohormone Response to Heart failure
Neuro = SNS --> contractility of the heart
Hormonal = RAAS / ANP, BNP (Nepryilysin)
Body's own PRIL for ACE lysis
:
Neprilysin breaks down both peptide hormones of RAAS and ANP/BNP
sacubitril is used to stop it along with an ACE since it stops the body from shutting down both pathways
Secubitril / valsartin combo
Neprilysin inhibitor / Arb
Neprilysin breaks down both RAAS and ANP/BNP systems
CHF *Causes
rarer causes = amyloidosis from transthyretin protein
Transthyretin amyloidosis CHF
transthyretin is THE CRETIN of Heart Failure
Transthyretin amyloidis CHF case
Clinical Case
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CHF - Viral / Infiltrative disease in Cardio myocytes
coxsaccie virus causes myocarditis
Hemachromatosis and amyloidosis
Clinical Cases
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Histology of viral myocarditis
necrosis = large pink areas
lymphocytic infiltrates
--> lymphocytes and macrophages
Left vs Right CHF
Isolated *Right Sided HF
blood backs up to the Veins and Portal System
can happen with RCA occlusion and inferior MI with LV sparring
Right sided HF *Sequalae
Congestive Hepatopathy (Liver)
3 zones of the liver
go inward to outward 3,2,1
--> radiate out from the central vein
congestive liver disease from Right sided HF
--> effects Zone 3 only
--> hydrostatic blood and edema from the central veins
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Right Sided HF Edema Response mechanisms
accessory lymphatic drainage system
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Isolated *Left Sided HF
can be either rEF or pEF
blood backs up to the lungs
left sided CHF Histopathology of Lungs
pulmonary HTN and pulmonary edema that is constant
blood leaks into the lung parenchyma and avleoli
alveolar macrophages eat up the RBCs
Chronic CHF caused pulmonary edema = Hemosiderin-laden macrophages
--> look like reddish brown rust
--> Fe iron from RBCs stored in the macrophages as hemosiderin
Clinical Cases
Clinical Case
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Chronic CHF Histopathology of Lungs
pulmonary HTN and pulmonary edema that is constant
blood leaks into the lung parenchyma and avleoli
alveolar macrophages eat up the RBCs
Chronic CHF caused pulmonary edema = Hemosiderin-laden macrophages
--> look like reddish brown rust
--> Fe iron from RBCs stored in the macrophages as hemosiderin
Clinical Cases
Clinical Case
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