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
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
Clinical Case
Notes:
- note that
Clinical Case
Decompensated CHF example
Notes:
- 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:
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
Notes:
- note that
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
Notes:
- note that
CHF - Viral / Infiltrative disease in Cardio myocytes
- coxsaccie virus causes myocarditis
- Hemachromatosis and amyloidosis
Clinical Cases
Clinical Case
Notes:
- note that
Clinical Case
Histology of viral myocarditis
- necrosis = large pink areas
- lymphocytic infiltrates
--> lymphocytes and macrophages
Aldosterone - STOP remodelling in systolic HF Treatment
- Spironalactone, Eplerenone
Clinical Cases
Clinical Case
Clinical Case
Notes:
- note that
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)
Clinical Cases
Clinical Case
Clinical Case
Notes:
- note that
Right Sided HF Edema Response mechanisms
- accessory lymphatic drainage system
Clinical Cases
Clinical Case
Notes:
- note that
Clinical Case
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
Notes:
- note that
Clinical Case
Clinical Case
Notes:
- note that
Clinical Case
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
Notes:
- note that
Clinical Case
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
