Heart Failure 1

Question 1

a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood

Answer 1

HF

Characterized by s/s of reduced CO and volume overload

Question 2

what race/ethnicity is at highest risk of HF? why?

Answer 2

black pts
disparities in risk factors (obesity, HTN, DM), socioeconomic status, access to care.

Question 3

MCC of death with HF pts?

Answer 3

progressive HF or sudden cardiac death
Hospitalization and readmission is common

Question 4

risk factors for HF

Answer 4

CAD / Atherosclerosis
DM
HTN
Metabolic syndrome / Obesity

Question 5

Heart Failure Classification

Answer 5

1. Acute: sx within last few days to weeks
   - SOB, PND, orthopnea, and RUQ pain
2. Chronic: sx for months
   - Fatigue, anorexia, abd distention and edema
   - acute exacerbation in a chronic state
3. High: heart unable to meet demands of peripheral needs
   - sx of reduced CO > volume overload: Thyrotoxicosis, severe anemia, sepsis
4. Low: insufficient forward output
   - Reduced EF, hypovolemia

Question 6

HF with reduced left ventricular EF vs. HF with preserved EF

Answer 6

1. HFrEF → AKA HF w/ reduced EF (systolic)
   - EF ≤40%
2. HFpEF → AKA HF with preserved EF (diastolic)
   - EF ≥ 50%

Question 7

what are the 2 subtypes of HF with preserved ejection fraction (HFpEF) and their EF%?

Answer 7

HFpEF, borderline - 41-49%
HFpEF, improved - >40%

Question 8

Majority of cardiomyopathies
Leads to DOE, PND, orthopnea, fatigue

which side of HF?

Answer 8

left side HF

Question 9

RHF is MCC by what?

Answer 9

LHF
Also caused by lung disorders (COPD, PE, Pulm HTN), CAD, pulmonary and TC valvular disorders, ARVC, VSD w/ L–>R shunting

Question 10

s/s of JVD, hepatic congestion, ascites, anorexia, LE edema

are associated with what type of HF?

Answer 10

RHF

Question 11

s/s of LHF?

Answer 11

Question 12

HF Classification Based on sx

Answer 12

New York Heart Association (NYHA) functional classes I-IV - classification can change any time

I. no limitation of physical activity. Ordinary physical activity does not cause sx (dyspnea, fatigue)
II. slight limitation of physical activity. sx develop with ordinary activity but not at rest.
III. marked limitation of physical activity. sx develop with < ordinary activity but not at rest
IV. inability to do physical activity. sx at rest

Question 13

stages of HF

Answer 13

American College of Cardiology Foundation (ACCF) / American Heart Association (AHA) (A-D)

A. At risk, no structural heart disease or sx of HF.
B. Structural heart disease w/o s/s
- includes NYHA functional class I w/ no prior or current s/s of HF
C. Structural heart disease with prior or current sx
- Includes any NYHA class (including class I with prior sx).
D. Refractory HF requiring specialized interventions.
- NYHA IV with refractory sx

Question 14

what are 2 positive chronotropic agents that increases HR?

Answer 14

atropine
beta agonists

Question 15

what are 2 negative chronotropic agents that decreaes HR?

Answer 15

BB
CCB

Question 16

pathophys of HF

Answer 16

Neurohumoral Adaptations

1. Compensatory mechanisms to adjust for a reduction in CO
   - Maintain systemic pressure by vasoconstriction
   - Restores CO by increasing myocardial contractility and HR
2. Occurs with systolic and diastolic dysfunction

Question 17

what are Neurohumoral Adaptations for HF/reduced CO

Answer 17

1. Sympathetic NS
2. RAAS
   - ADH
   - Atrial (ANP) and Brain (BNP) Natriuretic Peptides

Question 18

how does the Sympathetic NS compensate for HF?

Answer 18

1. one of the first responses to low CO
2. increases release and decreased uptake of NOR
   - Increases ventricular contractility and HR
3. leads to vasoconstriction and enhanced venous tone, increasing preload
4. Stimulates proximal tubular Na reabsorption = Na retention
5. Results in increase of plasma NE concentration, which correlates to severity of HF and inversely with survival

Question 18

how does the RAAS compensate for HF?

Answer 18

1. Stimulated by decreased GFR and increased beta-1 adrenergic activity
   - Increases Na reabsorption
   - Induces systemic and renal vasoconstriction
2. act directly on myocytes = pathologic remodeling via hypertrophy, apoptosis, necrosis
3. as HF progresses, myocytes develop more AT₂ receptors = cell apoptosis

Question 18

how does ADH compensate for HF?

Answer 18

1. Low CO → activation of carotid sinus and aortic arch baroreceptors → release of ADH and stimulation of thirst
   - increase in systemic vascular resistance
   - Promotes water retention
2. Increased water retention and increased thirst, leads to reduced sodium level (due to dilution)
   - degree of hyponatremia = severity of HF

Question 19

how do Natriuretic Peptides compensate for HF?

Answer 19

1. ANP
   - Released from atria in response to volume expansion
   - ANP rises early in HF
2. BNP
   - Released from ventricles in response to high ventricular filling pressures
   - Present in chronic or advanced HF
   - Reduces systemic vascular resistance and central venous pressure, while increasing natriuresis, which reduces afterload

Question 20

which Natriuretic Peptides is preferred for testing and why?

Answer 20

BNP - has a longer half-life

Question 21

Maladaptive Consequences of HF

Answer 21

1. Elevation in diastolic pressures are transmitted to atria and pulm & systemic venous circulations
   - Results in pulm vascular congestion and peripheral edema
2. increased afterload = depress cardiac function and enhance deterioration
3. Catecholamine-stimulated contractility and increased HR can worsen coronary ischemia
4. Catecholamines and AT II promote myocyte loss = cardiac remodeling

Question 22

3 major determinants of the LV stroke volume

Answer 22

1. Preload – venous return and end-diastolic volume
2. Contractility – the force generated at any given end-diastolic volume
3. Afterload – aortic impedance, vascular resistance, wall stress
   - affects a normal heart less, but small changes in afterload in failing heart = large changes in SV

Question 23

With systolic dysfunction, there is a _reduction in myocardial contractility_ This is associated with a reduction in _____

Answer 23

SV and CO - Results in increasing SNS = increases contractility and HR - Promotes salt and water retention = expansion of blood volume = raising end-diastolic pressure and volume

Question 24

pt comes in with Dyspnea Fatigue Fluid retention - Lower extremity edema possible dx?

Answer 24

HF sx d/t low CO and fluid accumulation

Question 25

what part of the pt hx are possible identifiable source of HF?

Answer 25

1. Chest pain, flu-like sx, HTN, alcohol use, hx of murmurs 2. Family hx 3. Changes in meds (chemo, calcium channel blockers, flecainide) 4. PMH of autoimmune disorders, thyroid dz, DM, CAD, etc.

Question 26

PE of HF

Answer 26

1. VS - Resting sinus tach - narrow pulse pressure (< 25 mmHg) - diaphoresis - peripheral vasoconstriction - Suggests severity of cardiac dysfunction 2. volume assessment - Pulmonary congestion – Inspiratory rales or dull breath sounds at the bases - Peripheral edema – lower extremities, scrotum, ascites - Elevated JVP – present if edema is due to HF 3. pulsus alternans, Precordial palpation, Heart sounds

Question 27

how to properly assess for LE edema?

Answer 27

ALWAYS start at the feet, then work your way proximally to see how far the edema extends. Don’t forget about the sacral and scrotal areas

Question 28

Pathognomonic of severe LV failure Characterized by evenly spaced strong and weak peripheral pulses what PE finding of HF is this?

Answer 28

pulsus alternans

Question 29

what precordial palpation PE finding would indicate LV enlargement?

Answer 29

Laterally displaced apical impulse usually indicates LV enlargement May feel parasternal lift of RV with Pulmonary HTN

Question 30

which heart sound is associated with systolic HF

Answer 30

S3 gallop

Question 31

which heart sound is MC to find in diastolic HF?

Answer 31

S4 gallop

Question 32

PE Systems that should be covered:

Answer 32

General Cardio_vascular_ Respiratory Abdomen Skin Neuro – general assessment to determine orientation/level of consciousness Thyroid

Question 33

The goal of HF diagnostic studies is?

Answer 33

not only to confirm that sx are due to HF but then to **determine CAUSE** of the HF

Question 34

initial testing for HF?

Answer 34

1. ECG - Can detect findings that specify a cause - arrhythmia that is the cause or result of HF 2. CXR - evaluate for pulmonary edema, cardiopulmonary structural abnormalities, etc - Pulmonary vascular congestion, cardiomegaly, Kerley B lines, pleural effusions

Question 35

for looking for cause of HF, radiological evaluation will most likely state “patchy infiltrate” on CXR which in this case is due to ?

Answer 35

vascular congestion d/t HF

Question 36

on CXR are thin, 1-2 cm lines, virtually always at the lungs bases and at lung periphery lying perpendicular to pleural surface to which they contact what are these findings?

Answer 36

kerley B just indicates there is fluid forsure

Question 37

initial lab findings for HF? (not including additional)

Answer 37

1. CBC → anemia, pericarditis, leukocytosis 2. CMP → lytes, BUN, Cr, Mg, LFTs 3. Coags 4. Fasting glucose 5. Lipid panel

Question 38

additional lab testing for HF?

Answer 38

Only consider if beneficial in supporting or determining etiology of HF 1. Thyroid function 2. Iron studies 3. ANA 4. Viral serology 5. Genetic testing

Question 39

what is the Best test for HF evaluation?

Answer 39

BNP and NT-proBNP - Released from ventricles while in HF - Useful in supporting dx and establishing severity - Used to _exclude HF_ as a cause of sx, because it has a **very high negative predictive value** - Limited studies/data to support serial BNP levels to monitor HF therapy, in an acute or chronic setting

Question 40

Normal value of BNP and NT-proBNP?

Answer 40

< 100 pg/mL NT-proBNP <300

Question 41

limitations of BNP and NT-proBNP

Answer 41

1. Pt w/ **>1 cause** for dyspnea, ex. PNA and HF 2. Pts with severe chronic HF may have **persistently elevated levels of BNP** 3. other causes for elevated BNP

Question 42

causes for elevated BNP that causes limitations in BNP and NT-proBNP testing?

Answer 42

- ACS, LVH, valvular disease, Afib, S/P - Cardioversion - Increased age, Severe anemia, Renal failure - PNA, Pulm HTN - Sepsis, Severe burns

Question 43

why Can troponin I/T be elevated with severe HF, without CAD/ myocardial ischemia?

Answer 43

- suggests ongoing myocardial injury or necrosis - Associated w/ increased mortality rate, whether present in acute or chronic HF

Question 44

diagnostic imaging for HF?

Answer 44

**echo** - for _all pts_ with new onset HF

Question 45

things that an echo can show for evaluating for HF?

Answer 45

- shows **ventricular size and function** --- Also detects LV diastolic function - Can detect **regional wall motion abnormalities** --- Usually suggests CAD, but segmental abnormalities are possible with nonischemic dilated cardiomyopathies - Pericardial thickening or effusion can be seen - Valvular disease is evaluated - RV function and pulm pressures can be measured

Question 46

what condition is typically needed to be excluded, especially in pt’s with new reduced LVEF and no other identifiable causes for HF?

Answer 46

CAD

Question 47

Denying what symptom is _not_ reason enough to exclude CAD

Answer 47

chest pain

Question 48

how to r/o CAD in HF?

Answer 48

stress test 1. Even if stress test normal, if no other cause is identifiable, coronary angiography should be considered - May also perform left ventriculogram during cardiac catheterization to evaluate LV function

Question 49

Additional testing/imaging may be considered if necessary for HF

Answer 49

Cardiac MRI Cardiac CTA Endomyocardial biopsy

Question 50

tx recommendations for HF based on class?

Answer 50

1. Class I - do it 2. Class II - conflicting evidence - IIa - should be considered - IIb - may be considered 3. Class III - don't Hefrf