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PHRM 845 > HF Pt1 > Flashcards

HF Pt1 Flashcards

1
Q

What percentage and total number of Americans have HF?

A

2-2.5% (6.7 million people)

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2
Q

What is the prognosis of HF?

A

Survival rate of about 50% in 5 years of HF

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3
Q

What is the definition of HF?

A

Failure of the heart to pump blood at a rate commensurate with requirements of metabolizing tissues

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4
Q

What is the impairment in cardiac function with HFrEF?

A

Systolic dysfunction: decreased contractility

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5
Q

What is the definition of HFrEF?

A

HF sx with EF <40%

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6
Q

What is HFrEF without Sx?

A

Asymptomatic reduced EF

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7
Q

What are the causes of HFrEF?

A

Dilated ventricle:
- Ischemic dilated CM
- Non-ischemic dilated CM
- HTN, obesity, stress, etc

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8
Q

What is the impairment in cardiac function of HFpEF?

A

Diastolic dysfunction: impairment in ventricular relaxation/filling

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9
Q

What is the definition of HFpEF?

A

HF Sx w EF >50%

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10
Q

What is the most common cause of HFpEF?

A

HTN

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11
Q

What is the definition of HFmrEF (mildly reduced)?

A

HF with EF 41-49%

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12
Q

What is the definition of HFimpEF (improved)?

A

HF w EF >40% and previously had HFrEF

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13
Q

What are the determinants of LV performance?

A
  • Preload
  • Myocardial contractility
  • Afterload
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14
Q

What are the compensatory mechanisms of HF?

A
  • Increased preload due to Na/water retention
  • Vasoconstriction
  • Tachycardia and increased contractility (SNS activation)
  • Ventricular hypertrophy and remodeling
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15
Q

What is the beneficial effect of increased preload due to Na/water retention?

A

Optimize stroke volume via Frank-Starling mechanism

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16
Q

What are the detrimental effects of compensation of increased preload due to Na/water retention?

A
  • Pulmonary/systemic congestion and edema
  • Increased MVO2
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17
Q

What are the beneficial effects of vasoconstriction?

A
  • Maintain BP in face of reduced CO
  • Shunt blood from nonessential tissues to heart
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18
Q

What are the detrimental effects of vasoconstriction?

A
  • Increased MVO2
  • Increased afterload: decreases SV and further activates the compensatory responses
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19
Q

What is the beneficial effect of tachycardia and contractility?

A

Maintain CO

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20
Q

What are the detrimental effects of tachycardia and contractility?

A
  • Increased MVO2
  • Shortened diastolic filling time
  • B-receptor downregulation and decreased responsiveness
  • Ventricular arrhythmias
  • Increased risk of myocardial cell death
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21
Q

What are the beneficial effects of ventricular hypertrophy and remodeling?

A
  • Maintain CO
  • Reduce myocardial wall stress: decreases MVO2
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22
Q

What are the detrimental effects of ventricular hypertrophy and remodeling?

A
  • Diastolic and systolic dysfunction
  • Risk of myocardial cell death and ischemia
  • Risk of arrhythmias
  • Fibrosis
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23
Q

What are some precipitating factors of HF in resource-limited hospitals?

A
  • Lack of compliance
  • With diet, drugs
  • Uncontrolled HTN
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24
Q

What are the precipitating factors of HF in “richer” hospitals?

A
  • Non-compliance with drug or diet
  • Cardiac ischemia
  • Inadequate therapy
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25
Q

What are the clinical presentations of HF?

A
  • SOB
  • Swelling of feet and legs
  • Chronic lack of energy
  • Difficulty sleeping at night due to SOB
  • Swollen or tender abdomen
  • Cough w frothy sputum
  • Increased urination at night
  • Confusion and/or impaired memory
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26
Q

What is right ventricular failure?

A

Primarily systemic venous congestion

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27
Q

What are the sxs of right ventricular failure?

A
  • Abdominal pain
  • Anorexia
  • Nausea
  • Bloating, constipation
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28
Q

What are the signs of right ventricular failure?

A
  • Peripheral edema
  • JVD, HJR
  • Hepatomegaly
  • Ascites
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29
Q

What is left ventricular failure?

A

Primarily pulmonary congestion

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30
Q

What are the sxs of left ventricular failure?

A
  • DOE, orthopnea, PND, tachypnea
  • Bendopnea, cough, hemoptysis
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31
Q

What are the signs of left ventricular failure?

A
  • Rales, S3 gallop, pulmonary edema
  • Pleural effusion, Cheyne-Stokes respiration
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32
Q

What are the sxs of nonspecific findings?

A
  • Exercise intolerance, fatigue, weakness
  • Nocturia, CNS sxs
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33
Q

What are the signs of nonspecific findings?

A

Tachycardia, pallor cyanosis, cardiomegaly

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34
Q

What are the major s/sxs of pulmonary edema?

A
  • Exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, rales
  • Pulmonary edema, bendopnea, peripheral edema
  • Jugular venous distension, hepatojugular reflux, hepatomegaly, ascites
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35
Q

What are other major non-specific findings of pulmonary edema?

A
  • Fatigue, weakness, and weakness intolerance
  • Nocturia, cardiomegaly
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36
Q

What are clinical assessment of HF?

A

H/P, med hx, s/sx, cardiac risk factors

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37
Q

What are initial laboratory assessment of HF?

A
  • CBC, serum electrolytes, BUN, Cr, TFTs
  • Electrocardiogram
  • Chest x-ray
38
Q

What are abnormal natriuretic peptide levels?

A
  • BNP (>35 pg/mL)
  • NT-proBNP (>125 pg/mL)
39
Q

What tests evaluate LV function and measure EF?

A
  • Echocardiogram
  • Nuclear testing (single photon emission computed tomography, MUGA)
  • Cardiac cath
  • MRI and CT
40
Q

What is the gold standard of nuclear testing?

A

MUGA

41
Q

What is NYHA FC 1?

A

Pts w cardiac disease but wo resulting limitations of physical activity (asx)

42
Q

What is NYHA FC 2?

A

Pts w cardiac disease resulting in slight limitations of physical activity

43
Q

What is NYHA FC 3?

A

Pts w cardiac disease resulting in limitations of physical activity

44
Q

What is NYHA FC 4?

A

Pts w cardiac disease resulting in inability to carry on any physical activity wo discomfort

45
Q

What is AHA stage A?

A
  • High risk of developing HF
  • No identified structural or functional abnormalities of pericardium, myocardium, or cardiac valves, and have never show s/sxs of HF
46
Q

What is AHA stage B?

A

Structural heart disease that is strongly associated w HF but no s/sxs of HF

47
Q

What is AHA stage C?

A

Current or prior sxs of HF associated w underlying structural heart disease

48
Q

What is AHA stage D?

A

Advanced structural heart disease and marked sxs of HF at rest despite max med therapy and who require specialized interventions

49
Q

What is the definition of asx rEF (aka asx LV systolic dysfunction)?

A

No HF sxs w EF <40%

50
Q

What are the goals of therapy?

A
  • Slow disease progression
  • Reduce sxs and improve QOL and prevent/reduce hospitalizations and need for emergency care
  • Reduce mortality
51
Q

What FC/stage goes w high risk for HF?

A

Stage A

52
Q

What FC/stage goes w asx rEF?

A

Stage B; NYHA FC 1

53
Q

What FC/stage goes w HFrEF?

A

Stage C, D; NYHA FC 2-4

54
Q

What are general measures for HF?

A
  • Tx underlying causes (HTN, CAD)
  • Remove precipitating causes
  • Exercise (caution during acute sxs)
55
Q

How should exercise be approached?

A

Dynamic exercise to increase HR to 60-80% of maximum for 20-60 min 3-5/week

56
Q

What is the measures for sodium?

A
  • Intake be restricted to 2-3 g/day
  • Pts w severe HF may require diets w <2 g/day
57
Q

What is the measures for alcohol?

A
  • Pts w alc induced HF: totally abstain
  • In others, no more than 2 drinks/day for men and 1 drink/day for women
58
Q

What is the measures for fluid intake?

A

Restrict to <2 L/day in pts w hyponatremia (<130 mEq/L) or if tx w diuretics is difficult in maintaining fluid volume

59
Q

What are other general measures?

A
  • Weight monitoring, smoking cessation, immunizations
  • Mx and replace electrolytes
  • Appropriate thyroid disease management
  • Herbal products and nutritional supp education
60
Q

What are the 4 drug therapy strategies?

A
  • Reduce intravascular volume
  • Increase myocardial contractility
  • Decrease ventricular afterload
  • Neurohormonal blockade
61
Q

What drug classes reduce intravascular volume?

A

Diuretics, SGLT2i

62
Q

What drug class increase myocardial contractility?

A

Positive inotropes

63
Q

What drug classes decrease ventricular afterload?

A

ACEi, vasodilators, SGLT2i

64
Q

What drug classes cause neurohormonal blockade?

A

ARNIs, BBs, ACEi, ARBs, MRAs, SGLT2i

65
Q

What pts should receive diuretics?

A

All HF pts w s/sxs of fluid retention (symptomatic) should be managed w diuretics

66
Q

What do diuretics do for HF?

A
  • Reduce hospitalizations but do not have an impact on mortality or natural progression of HF
  • Reduce sxs associated w fluid overload, improve exercise tolerance, improve QOL
67
Q

What dose of diuretics should be used?

A

Lowest dose that maintains euvolemia

68
Q

Which pts should not receive diuretics?

A

Pts who do not have sxs of volume overload should not receive diuretics

69
Q

What are the short term benefits of diuretics?

A

Reduce fluid retention via:
- Decreased edema, pulmonary congestion, and JVD by reducing preload and cardiac filling pressure

70
Q

What are the longer term benefits of diuretics?

A

Reduced daily sxs and improve ability to exercise

71
Q

What is the general MOA of diuretics?

A

Increase sodium and water excretion by reducing sodium reabsorption at a variety of sites in nephron

72
Q

What is important for diuretics in terms of their pharmacologic response?

A

Must get to their site of action to elicit a pharmacologic response

73
Q

What is the MOA of loop diuretics?

A

Potent diuretics block Na and Cl reabsorption in ascending limb of LOH

74
Q

What % of Na is reabsorbed in the LOH?

A

20-25% of filtered Na

75
Q

What are additional benefits of loop diuretics?

A
  • Enhancing renal release of PGI2 (increases renal blood flow and enhancing venous capacitance)
  • Blocked by NSAIDs
76
Q

What is a problem w furosemide?

A
  • Furosemide has erratic bioavailability
  • So torsemide may have advantage in some pts
77
Q

What is the MOA of thiazides and thiazide like diuretics?

A

Block Na and Cl reabsorption in DCT

78
Q

What is the strength of thiazides and thiazide like diuretics?

A

Relatively weak agents

79
Q

What are the use of THZs?

A

Used in pts w mild HF and small amounts of fluid retention

80
Q

What are the use of thiazide like diuretics (ex. HCTZ and MTZ)?

A

Frequently used in combo w loops in pts who become resistant to single drug therapy

81
Q

When are higher doses required for THZs and THZ like diuretics?

A

Higher doses generally necessary when GFR is decreased (<30 mL/min)

82
Q

Why does K sparing diuretics work in HF?

A

Blocks aldosterone, so not necessarily used bc of their diuretics effects

83
Q

What drugs are traditionally considered K sparing diuretics but will be considered MRAs in HF?

A

Spironolactone and eplerenone

84
Q

How are loops initiated?

A

Initiate at low doses, then double and titrate

85
Q

How are loops dose adjusted?

A

Based on weight and sx

86
Q

If the pt is fluid overloaded, what is the weight reduction goal?

A

Reduce weight 1-2 lbs/day

87
Q

What should pts do if they have weight gain?

A

Report the weight gain (3-5 lbs/week)

88
Q

What may be indicative of volume depletion?

A

Hypotension and increased SCr or BUN/Cr ratio

89
Q

What BUN/Cr ratio is normal?

A

15:1

90
Q

What BUN/Cr ratio may indicate pt is volume depleted?

A

20:1

91
Q

What is another lab to assess volume depletion?

A

Hemoglobin and hematocrit:
- Their levels increase as volume decrease

92
Q

What are the monitoring parameters of loops?

A

1-2 wks after initiation:
- Fluid intake, urinary output, body weight, s/sx of congestion, JVD
- BP, serum electrolytes
- Renal function

PHRM 845 (48 decks)

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