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Cardiovascular > Heart Failure 1 > Flashcards

Heart Failure 1 Flashcards

1
Q

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

A

HF

Characterized by s/s of reduced CO and volume overload

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2
Q

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

A

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

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3
Q

MCC of death with HF pts?

A

progressive HF or sudden cardiac death
Hospitalization and readmission is common

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4
Q

risk factors for HF

A

CAD / Atherosclerosis
DM
HTN
Metabolic syndrome / Obesity

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5
Q

Heart Failure Classification

A
  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
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6
Q

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

A
  1. HFrEF → AKA HF w/ reduced EF (systolic)
    - EF ≤40%
  2. HFpEF → AKA HF with preserved EF (diastolic)
    - EF ≥ 50%
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7
Q

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

A

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

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8
Q

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

which side of HF?

A

left side HF

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9
Q

RHF is MCC by what?

A

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

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10
Q

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

are associated with what type of HF?

A

RHF

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11
Q

s/s of LHF?

A
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12
Q

HF Classification Based on sx

A

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

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13
Q

stages of HF

A

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

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14
Q

what are 2 positive chronotropic agents that increases HR?

A

atropine
beta agonists

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15
Q

what are 2 negative chronotropic agents that decreaes HR?

A

BB
CCB

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16
Q

pathophys of HF

A

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
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17
Q

what are Neurohumoral Adaptations for HF/reduced CO

A
  1. Sympathetic NS
  2. RAAS
    - ADH
    - Atrial (ANP) and Brain (BNP) Natriuretic Peptides
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18
Q

how does the Sympathetic NS compensate for HF?

A
  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
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18
Q

how does the RAAS compensate for HF?

A
  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
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18
Q

how does ADH compensate for HF?

A
  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
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19
Q

how do Natriuretic Peptides compensate for HF?

A
  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
20
Q

which Natriuretic Peptides is preferred for testing and why?

A

BNP - has a longer half-life

21
Q

Maladaptive Consequences of HF

A
  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
22
Q

3 major determinants of the LV stroke volume

A
  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
23
Q

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

A

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
24
Q

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

possible dx?

A

HF

sx d/t low CO and fluid accumulation

25
Q

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

A
  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.
26
Q

PE of HF

A
  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
27
Q

how to properly assess for LE edema?

A

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

28
Q

Pathognomonic of severe LV failure
Characterized by evenly spaced strong and weak peripheral pulses

what PE finding of HF is this?

A

pulsus alternans

29
Q

what precordial palpation PE finding would indicate LV enlargement?

A

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

30
Q

which heart sound is associated with systolic HF

A

S3 gallop

31
Q

which heart sound is MC to find in diastolic HF?

A

S4 gallop

32
Q

PE Systems that should be covered:

A

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

33
Q

The goal of HF diagnostic studies is?

A

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

34
Q

initial testing for HF?

A
  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
35
Q

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

A

vascular congestion d/t HF

36
Q

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?

A

kerley B

just indicates there is fluid forsure

37
Q

initial lab findings for HF? (not including additional)

A
  1. CBC → anemia, pericarditis, leukocytosis
  2. CMP → lytes, BUN, Cr, Mg, LFTs
  3. Coags
  4. Fasting glucose
  5. Lipid panel
38
Q

additional lab testing for HF?

A

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
39
Q

what is the Best test for HF evaluation?

A

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
40
Q

Normal value of BNP and NT-proBNP?

A

< 100 pg/mL
NT-proBNP <300

41
Q

limitations of BNP and NT-proBNP

A
  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
42
Q

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

A
  • ACS, LVH, valvular disease, Afib, S/P - Cardioversion
  • Increased age, Severe anemia, Renal failure
  • PNA, Pulm HTN
  • Sepsis, Severe burns
43
Q

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

A
  • suggests ongoing myocardial injury or necrosis
  • Associated w/ increased mortality rate, whether present in acute or chronic HF
44
Q

diagnostic imaging for HF?

A

echo
- for all pts with new onset HF

45
Q

things that an echo can show for evaluating for HF?

A
  • 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
46
Q

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

A

CAD

47
Q

Denying what symptom is not reason enough to exclude CAD

A

chest pain

48
Q

how to r/o CAD in HF?

A

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
49
Q

Additional testing/imaging may be considered if necessary for HF

A

Cardiac MRI
Cardiac CTA
Endomyocardial biopsy

50
Q

tx recommendations for HF based on class?

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

Hefrf

Cardiovascular (24 decks)

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