Heart Failure - Dahl 1 Flashcards
Pathophysiology of Heart Failure
What are diseases that occur before HF?
-problems with pericardium, heart valves, myocardium
-CAD: ischemic heart disease (narrow of arteries -> low blood supply to the heart), heart attack (MI) (clots blocking the blood flow to the heart)
HFpEF
-Preserved Ejection fraction: the pumping function of the heart worse fine -> FILLING problem
-stiffness of the ventricles
HFrEF
-reduced ejection fraction
Normal ejection fraction:
70ml out of 110 ml -> ~64%
Issues that affect HFreF and HFpEF patients
-pressure (fluid) overload in the heart -> compensation to upregulate the CO -> heart remodeling
Causes of HFpEF
stiffness of the ventricles
-ventricular hypertrophy
-infiltrative myocardial disease (amyloidosis, sarcoidosis, endomyocardial fibrosis)
-MI or ischemia
-mitral or tricuspid valve stenosis
-pericardial disease (pericarditis)
Causes of HFrEF
-75% due to CAD, infarction may affect the pumping function
-thin ventricles: dilated cardiomyopathies (drug-induced,
viral infections, postpartum)
- Pressure overload: vasoconstriction of the pulmonary artery -> heart works harder (pulmonary
hypertension or aortic valve or pulmonic
valve stenosis)
- Volume overload (valvular regurgitation,
shunts - hole in the ventricular -> fluids spills over)
What is SV determined by?
(CO = HR * SV)
-SV is determined by
Preload
Afterload
Force of contraction
What is an indicator of Preload?
LVEDV: left ventricle end-diastolic volume
LVEDP: left ventricle end-diastolic pressure
How is LVEDP estimated?
hemodynamically estimated by
PCWP (pulmonary capillary wedge pressure)
PAOP (pulmonary artery occlusion pressure)
Which ventricle does not affect SV?
If the LV is normal, the SV will not really be affected by afterload (aortic resistance)
What affects SV?
Systemic resistance -> Afterload
-negative effect predominantly in LV dysfunction
-Frank Starlin curve
-> SV is decreased with increased Afterload (resistance) in patients with LV dysfunction
What are the HFrEF compensatory mechanisms?
- increased sympathetic nervous system activation/tachycardia
- Frank-Starling mechanism (increase preload, increase SV)
- Vasoconstriction
- Ventricular hypertrophy and remodeling
->this helps short-term to maintain hemostasis, not long-term
What is the outcome of increased preload and which drug helps to treat the outcome?
-pulmonary and systemic congestion
-Aldosterone antagonist
What is the outcome of vasoconstriction and which drug helps to treat the outcome?
-Good: it keeps the BP from dropping and ensures that important organs (brain, heart keep getting blood)
BUT
-more oxygen supply needed, increased afterload decreases SV and potentiates further compensation
Drug: ACEi/ARBs
What is the outcome of sympathetic activation (tachycardia and contractility) and which drug helps to treat the outcome?
-more oxygen needed
-shortened filling time
-beta-1-receptor downregulation
-ventricular arrhythmias
Drug: ß-blocker
What is the outcome of ventricular hypertrophy and remodeling, and which drug helps to treat the outcome?
-diastolic and systolic dysfunction
-increased myocardial ischemia
-increased arrhythmias
-increased risk of myocardial cell death
Drug: Aldosterone antagonist, ACEi/ARBs, ß-blocker
HF Classification by Ejection Fraction
HFrEF: LVEF < 40% (0.4)
HFmEF: LVEF 41 - 49% (0.41 - 0.49)
HFpEF: LVEF > 50% (0.5)
HFimpEF:
Baseline of LVEF < 40% -> increased of more than 10 points > 40%
What is required to diagnose HFmEF and HFpEF (>50%)?
evidence of increased LV pressure
-elevated natriuretic peptide
-diastolic function on imaging
-invasive hemodynamic measurement
What are the ACC/AHA stages and NYHA classification referred to?
-ACC/AHA stage: development and progression of the disease
-NYHA classification: symptoms and functional status
ACC/AHA stages
A and B
Stage A: At risk for HF
No symptoms. No structural heart disease, no cardiac biomarkers, no stretch injury
Stage B: Pre-HF
No symptoms.
-Starting to have signs of heart failure such as structural heart disease, evidence of increased filling pressures
-patients with risk factors and increased concentrations of BNPs
-persistently elevated cardiac troponin
ACC/AHA stages
C and D
Stage C: Symptomatic HF
Structural heart disease with current OR previous
symptoms of HF
Stage D: Advanced HF
Marked HF symptoms that interfere with daily life
and recurrent hospitalizations despite guideline
directed medical therapy optimization
NYHA classification
Class I: No limitation of physical activity;
ordinary physical activity does not cause undue
fatigue, palpitation, or dyspnea
Class II: Slight limitation of physical activity;
comfortable at rest, but ordinary physical activity
results in fatigue, palpitations, or dyspnea
Class III: comfortable at rest, less ordinary activity leading to fatigue, palpations, dyspnea
Class IV: symptoms at rest, uncomfortable doing physical activity - struggling to do their daily activities
Signs and Symptoms of HF
Symptoms: fatigue, palpitations, dyspnea
Signs: can’t do physical activities, fluid retention (pulmonary congestion, peripheral edema, JVD)
Left VS Right-sided HF
-Left can cause right and vice versa
-patients may have isolated left or right HF
-both ventricles affected: Biventricular failure
Where does blood back up in LV and RV HF?
LV is the “main” ventricular so blood backs up to the lungs (pulmonary edema)
in RV HF blood backs up to the systemic circulation
Common symptoms of LV HF
-Pulmonary edema/ congestion
-Dyspnea
-Orthopnea: SOB when laying flat, venous blood in the legs and the GI moves up
-Crackles/rales on auscultation of the lungs
Common symptoms of RV HF
-back up into the systemic circulation
-enlarged spleen and liver (liver can become cirrhotic)
-JVD (jugular vein distention, vein in the neck is swollen)
-pitting edema (legs - gravity pulls fluid down)
Signs (physical exam)
-edema
-cardiac enlargement
-JVD
-Rales
-Ascites
-Displaced PMI (point of maximum impulse murmurs)!
-cool extremities (not perfused)
Labs for HF
-BNP > 100 pg/ml
-NT-pro BNP > 450 pg/ml if less than 50yo
-NT pro BNO > 900 pg/ml if 50-74yo
-NT pro BNO > 900 pg/ml if > 75yo
if BNP is low HF is probably not the problem, no evidence for measuring serial measurement (decrease is not an indicator for decreased risk of HF)
-Echocardiography: structure and function of the heart, for diagnosis (looking at valves, EF, diastolic dysfunction)
Acute Decompensated HF (ADHF)
-decompensation episode (more frequently as the disease progresses)
What are events that result in a de novo HF?
-sudden elevated BP
-MI
-25% of cases with sudden elevated BP or MI
-70% of patients experience an exacerbation of chronic HF
Signs and symptoms of ADHF
-Volume overload
pitting edema
low BNP or NT-pro BNP rules out ADHF
low Na < 130
elevated alk phosph
elevated GGT
Symptoms of Low output
-more end organ damage
-altered mental status
-fatigue
-low UOP
-GI symptoms
Signs: elevated transaminases, SCr, lactate
-Hypovolemic (intravascular)
Meaning of intravascular Hypovolemic condition
-no fluid intravascularly -> the kidney thinks there is no perfusion -> upregulation of the RAAS system
-the fluid is in the lungs, periphery,
Therapy at Stage A (ACC/AHA)
-At risk for HF -> Goal is prevention
-if T2DM + CVD (cardiovascular): SGLT2i
-manage other comorbidities
Therapy at Stage B (ACC/AHA)
-Pre-HF
-ACEi or BB only if their LVEF is below 40
-ARB if ACEi is not tolerated (LVEF < 40 + MI)
Therapy at Stage C - HFpEF
-Symptomatic -> Look at the Ejection fraction
-SGLT2i
-MRA (Spironolactone) and/or ARNI if LVEF is <55-60%
-ARB if ARNI is not tolerated
-Loop diuretic PRN
Therapy at Stage C HFmrEF
-consider SGLT2i
-consider MRA, ACEi/ARB/ARNI, and BB -> especially when close to HFrEF (<40%)
-Loop diuretic PRN
Therapy at Stage C HFrEF
!!!
-biggest evidence for symptomatic HF (reduced EF < 40%)
-ARNI/ACEi/ARB
-BB
-SGLT2i
-MRA
-Loop diuretic PRN
-GDMT (even if asymptomatic): get drugs on board, monitor, and titrate them up
