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Cardio > Heart Failure - Dahl 1 > Flashcards

Heart Failure - Dahl 1 Flashcards

1
Q

Pathophysiology of Heart Failure

A
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2
Q

What are diseases that occur before HF?

A

-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)

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3
Q

HFpEF

A

-Preserved Ejection fraction: the pumping function of the heart worse fine -> FILLING problem

-stiffness of the ventricles

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4
Q

HFrEF

A

-reduced ejection fraction

Normal ejection fraction:
70ml out of 110 ml -> ~64%

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5
Q

Issues that affect HFreF and HFpEF patients

A

-pressure (fluid) overload in the heart -> compensation to upregulate the CO -> heart remodeling

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6
Q

Causes of HFpEF

A

stiffness of the ventricles
-ventricular hypertrophy
-infiltrative myocardial disease (amyloidosis, sarcoidosis, endomyocardial fibrosis)
-MI or ischemia

-mitral or tricuspid valve stenosis
-pericardial disease (pericarditis)

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7
Q

Causes of HFrEF

A

-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)

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8
Q

What is SV determined by?

A

(CO = HR * SV)
-SV is determined by
Preload
Afterload
Force of contraction

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9
Q

What is an indicator of Preload?

A

LVEDV: left ventricle end-diastolic volume
LVEDP: left ventricle end-diastolic pressure

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10
Q

How is LVEDP estimated?

A

hemodynamically estimated by
PCWP (pulmonary capillary wedge pressure)

PAOP (pulmonary artery occlusion pressure)

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11
Q

Which ventricle does not affect SV?

A

If the LV is normal, the SV will not really be affected by afterload (aortic resistance)

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12
Q

What affects SV?

A

Systemic resistance -> Afterload
-negative effect predominantly in LV dysfunction
-Frank Starlin curve

-> SV is decreased with increased Afterload (resistance) in patients with LV dysfunction

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13
Q

What are the HFrEF compensatory mechanisms?

A
  1. increased sympathetic nervous system activation/tachycardia
  2. Frank-Starling mechanism (increase preload, increase SV)
  3. Vasoconstriction
  4. Ventricular hypertrophy and remodeling

->this helps short-term to maintain hemostasis, not long-term

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14
Q

What is the outcome of increased preload and which drug helps to treat the outcome?

A

-pulmonary and systemic congestion

-Aldosterone antagonist

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15
Q

What is the outcome of vasoconstriction and which drug helps to treat the outcome?

A

-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

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16
Q

What is the outcome of sympathetic activation (tachycardia and contractility) and which drug helps to treat the outcome?

A

-more oxygen needed
-shortened filling time
-beta-1-receptor downregulation
-ventricular arrhythmias

Drug: ß-blocker

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17
Q

What is the outcome of ventricular hypertrophy and remodeling, and which drug helps to treat the outcome?

A

-diastolic and systolic dysfunction
-increased myocardial ischemia
-increased arrhythmias
-increased risk of myocardial cell death

Drug: Aldosterone antagonist, ACEi/ARBs, ß-blocker

18
Q

HF Classification by Ejection Fraction

A

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%

19
Q

What is required to diagnose HFmEF and HFpEF (>50%)?

A

evidence of increased LV pressure
-elevated natriuretic peptide
-diastolic function on imaging
-invasive hemodynamic measurement

20
Q

What are the ACC/AHA stages and NYHA classification referred to?

A

-ACC/AHA stage: development and progression of the disease

-NYHA classification: symptoms and functional status

21
Q

ACC/AHA stages

A and B

A

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

22
Q

ACC/AHA stages

C and D

A

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

23
Q

NYHA classification

A

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

24
Q

Signs and Symptoms of HF

A

Symptoms: fatigue, palpitations, dyspnea

Signs: can’t do physical activities, fluid retention (pulmonary congestion, peripheral edema, JVD)

25
Q

Left VS Right-sided HF

A

-Left can cause right and vice versa
-patients may have isolated left or right HF
-both ventricles affected: Biventricular failure

26
Q

Where does blood back up in LV and RV HF?

A

LV is the “main” ventricular so blood backs up to the lungs (pulmonary edema)

in RV HF blood backs up to the systemic circulation

27
Q

Common symptoms of LV HF

A

-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

28
Q

Common symptoms of RV HF

A

-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)

29
Q

Signs (physical exam)

A

-edema
-cardiac enlargement
-JVD
-Rales
-Ascites
-Displaced PMI (point of maximum impulse murmurs)!
-cool extremities (not perfused)

30
Q

Labs for HF

A

-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)

31
Q

Acute Decompensated HF (ADHF)

A

-decompensation episode (more frequently as the disease progresses)

32
Q

What are events that result in a de novo HF?

A

-sudden elevated BP
-MI
-25% of cases with sudden elevated BP or MI

-70% of patients experience an exacerbation of chronic HF

33
Q

Signs and symptoms of ADHF

A

-Volume overload
pitting edema
low BNP or NT-pro BNP rules out ADHF
low Na < 130
elevated alk phosph
elevated GGT

34
Q

Symptoms of Low output

A

-more end organ damage
-altered mental status
-fatigue
-low UOP
-GI symptoms

Signs: elevated transaminases, SCr, lactate
-Hypovolemic (intravascular)

35
Q

Meaning of intravascular Hypovolemic condition

A

-no fluid intravascularly -> the kidney thinks there is no perfusion -> upregulation of the RAAS system

-the fluid is in the lungs, periphery,

36
Q

Therapy at Stage A (ACC/AHA)

A

-At risk for HF -> Goal is prevention

-if T2DM + CVD (cardiovascular): SGLT2i
-manage other comorbidities

37
Q

Therapy at Stage B (ACC/AHA)

A

-Pre-HF

-ACEi or BB only if their LVEF is below 40
-ARB if ACEi is not tolerated (LVEF < 40 + MI)

38
Q

Therapy at Stage C - HFpEF

A

-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

39
Q

Therapy at Stage C HFmrEF

A

-consider SGLT2i
-consider MRA, ACEi/ARB/ARNI, and BB -> especially when close to HFrEF (<40%)
-Loop diuretic PRN

40
Q

Therapy at Stage C HFrEF
!!!

A

-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

Cardio (27 decks)

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