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Therapeutics III > Sowinski Heart Failure Part 1 > Flashcards

Sowinski Heart Failure Part 1 Flashcards

1
Q

Definition of heart failure

A

-Although heart failure can be readily described as a clinical syndrome….an abnormality of myocardial function is responsible for the failure of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues
-Not a single disease state but the final common pathway for CV diseases

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2
Q

Type of heart failure

A

-Heart failure with reduced ejection fraction (HFrEF)
-Heart failure with preserved ejection fraction (HFpEF)

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3
Q

How do you define reduced ejection fraction?

A

EF < 40%

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4
Q

How do you define preserved ejection fraction?

A

EF > 50%

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5
Q

How do you define mildly reduced ejection fraction?

A

EF 41-49%

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6
Q

How do you define improved ejection fraction?

A

EF > 40% after previously having reduced ejection fraction

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7
Q

How is cardiac function impaired in HFrEF?

A

Systolic dysfunction: Decreased contractility

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8
Q

How is cardiac function impaired in HFpEF?

A

Diastolic dysfunction: Impairment in ventricular relaxation/filling

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9
Q

What causes HFrEF?

A

Dilated ventricle
-Ischemic dilated CM (~70% of cases)
-Non-ischemic dilated CM
-HTN, thyroid Dz, Obesity, Stress, Cardiotoxins, Myocarditis, Idiopathic, Tachycardic, Peripartum

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10
Q

Determinants of left-ventricular performance (Stroke Volume)

A

-Preload
-Myocardial contractility
-Afterload

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11
Q

Beneficial effects of increased preload due to Na/water retention

A

Optimize stroke volume via Frank-Starling mechanism

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12
Q

Detrimental effects of increased preload due to Na/water retention

A

-Pulmonary/systemic congestion and edema
-Increased MVO2

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13
Q

Beneficial effects of vasoconstriction

A

-Maintain BP in face of reduced cardiac output
-Shunt blood from nonessential tissues to the heart

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14
Q

Detrimental effects of vasoconstriction

A

-Increased MVO2
-Increased afterload decreases SV and further activates the compensatory response

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15
Q

Beneficial effects of tachycardia and increased contractility (SNS activation)

A

Maintain cardiac output

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16
Q

Detrimental effects of tachycardia and increased contractility (SNS activation)

A

-Increased MVO2
-Shortened diastolic filling time
-Beta-receptor downregulation and decreased responsiveness
-Ventricular arrhythmias
-Increased risk of myocardial cell death

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17
Q

Beneficial effects of ventricular hypertrophy and remodeling

A

-Maintain cardiac output
-Reduce myocardial wall stress
-Decrease MVO2

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18
Q

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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19
Q

Negative inotropes that can induce heart failure

A

-Antiarrhythmics (disopyramide, flecainide)
-Beta-blockers (atenolol, propranolol, metoprolol)
-Calcium channel blockers (verapamil, diltiazem)
-Itraconazole

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20
Q

Direct cardiac toxins that can induce heart failure

A

-Doxorubicin
-Epirubicin
-Daunomycin
-CYP
-Trastuzumab
-Bevacizumab
-5-FU
-Blue cohosh
-Imatinib
-Lapatinib
-Sunitinib
-Ethanol
-Cocaine
-Amphetamines

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21
Q

Drugs that cause sodium/water retention that can induce heart failure

A

-Glucocorticoids
-Androgens
-Estrogens
-NSAIDs/COX-2 inhibitors
-Rosiglitazone/pioglitazone
-Sodium-containing drugs (carbenicillin DiNa+, ticarcillin DiNa+)

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22
Q

Clinical presentation of heart failure

A

-Shortness of breath
-Swelling of feet/legs
-Chronic lack of energy
-Difficulty sleeping at night due to breathing problems
-Swollen or tender abdomen with loss of appetite
-Cough with frothy sputum
-Increased urination at night
-Confusion and/or impaired memory

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23
Q

Symptoms of right ventricular failure

A

-Abdominal pain
-Anorexia
-Nausea
-Bloating
-Constipation

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24
Q

Signs of right ventricular failure

A

-Peripheral edema
-JVD
-HJR
-Hepatomegaly
-Ascites

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25
Q

Symptoms of left ventricular failure

A

-DOE
-Orthopnea
-PND
-Tachypnea
-Bendopnea
-Cough
-Hemoptysis

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26
Q

Signs of left ventricular failure

A

-Rales
-S3 gallop
-Pulmonary edema
-Pleural effusion
-Cheyne-Stokes respiration

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27
Q

Nonspecific symptoms of heart failure

A

-Exercise intolerance
-Fatigue
-Weakness
-Nocturia
-CNS symptoms

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28
Q

Nonspecific signs of heart failure

A

-Tachycardia
-Pallor cyanosis
-Cardiomegaly

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29
Q

Major signs/symptoms of pulmonary congestion

A

-Exertional dyspnea (DOE)
-Orthopnea
-Paroxysmal nocturnal dyspnea (PND)
-Rales
-Pulmonary edema
-Bendopnea

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30
Q

Major signs/symptoms of systemic venous congestion

A

-Peripheral edema
-Jugular venous distention (JVD)
-Hepatojugular reflex (HJR)
-Hepatomegaly, ascites

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31
Q

Other major non-specific finding inf heart failure

A

-Fatigue, weakness and exercise intolerance
-Nocturia
-Cardiomegaly

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32
Q

Laboratory assessments for heart failure

A

-CBC, serum electrolytes, BUN, Cr, TFTs
-Electrocardiogram
-Chest X-ray

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33
Q

Abnormal BNP

A

> 35 pg/mL

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34
Q

Abnormal NT-proBNP

A

> 125 pg/mL

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35
Q

How to evaluate LV function and measurements of EF

A

-Echocardiogram
-Nuclear testing
-Cardiac catheterization
-MRI and CT

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36
Q

How do you describe NYHA class I?

A

Patients with cardiac disease but without resulting limitations of physical activity (asymptomatic)

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37
Q

How do you describe NYHA class II?

A

Patients with cardiac disease resulting in slight limitations of physical activity (symptomatic)

38
Q

How do you describe NYHA class III?

A

Patients with cardiac disease resulting in limitations of physical activity (symptomatic)

39
Q

How do you describe NYHA class IV?

A

Patients with cardiac disease resulting in an inability to carry on any physical activity without discomfort (symptomatic)

40
Q

How do you describe AHA stage A?

A

High risk of developing HF. No identified structural or functional abnormalities of the pericardium, myocardium, or cardiac valves and have never shown signs or symptoms of HF

41
Q

How do you describe AHA stage B?

A

Structural heart disease that is strongly associated with HF but NO signs or symptoms of HF

42
Q

How do you describe AHA stage C?

A

Current or prior symptoms of HF associated with underlying structural heart disease

43
Q

How do you describe AHA stage D?

A

Advanced structural heart disease and marked symptoms of HF at rest despite maximal medical therapy and who require specialized interventions

44
Q

Examples of heart failure AHA stage A

A

-Systemic HTN
-CAD
-DM

45
Q

Examples of heart failure AHA stage B

A

-LVH or fibrosis
-LV dilation or hypocontractility
-Asymptomatic valvular heart disease
-Previous MI

46
Q

Examples of heart failure AHA stage C

A

-Dyspnea or fatigue due to LVSD
-Asymptomatic patients receiving treatment for prior HF symptoms

47
Q

Examples of heart failure AHA stage D

A

-Frequently hospitalized for HF and cannot be safely discharged from the hospital
-Patients in the hospital awaiting heart transplantation
-Patients at home receiving continuous intravenous support for symptom relief or being supported with a mechanical circulatory assist device
-Patients in a hospice setting for the management of HF

48
Q

Types of heart failure

A

-Heart failure with reduced ejection fraction
-Heart failure with preserved ejection fraction

49
Q

HFrEF impairment in cardiac function

A

Systolic dysfunction: decreased contractility

50
Q

HFpEF impairment in cardiac function

A

Diastolic dysfunction: impairment in ventricular relaxation/filling

51
Q

HFrEF definition

A

HF symptoms with ejection fraction below 40%

52
Q

HFpEF definition

A

HF symptoms with ejection fraction greater than 50%

53
Q

Causes of HFrEF

A

Dilated ventricle
-Ischemic dilated CM (~70%)
-Non-ischemic dilated CM
-(HTN, thyroid disease, obesity, stress, cardiotoxins, myocarditis, idiopathic, tachycardic, peripartum)

54
Q

Causes of HFpEF

A

HTN is most common cause ~60%

55
Q

Asymptomatic rEF definition

A

-Asymptomatic LV systolic dysfunction
-No heart failure symptoms with EF < 40%

56
Q

HFimpEF

A

Previous symptoms/rEF now improved

57
Q

HFmrEF

A

Heart failure with EF 41-49%

58
Q

Goals of therapy for treatment of rEF and HFrEF

A

-Slow disease progression
-Reduce symptoms and improve quality of life and prevent/reduce hospitalizations and need for emergency care
-Reduce mortality

59
Q

Dietary restrictions in patients with HF

A

-Sodium (2-3 grams/day as possible)
-Alcohol (men no more than 2 drinks/day; women no more than 1 drink/day)
-Fluid intake (< 2 L/day)

60
Q

Pharmacologic strategies

A

-Reduce intravascular volume (diuretics, SGLT2i)
-Increase myocardial contractility (positive inotropes)
-Decrease ventricular afterload (ACEIs, vasodilators, SGLT2i)
-Neurohormonal blockade (ARNIs, beta-blockers, ACEIs, ARBs, MRAs, SGLT2is)

61
Q

GDMT for stage A

A

-Drug therapies for routine use if atherosclerotic vascular disease is present
-ACEI/ARB

62
Q

GDMT for stage B

A

-Drug therapies for routine use if previous MI or asymptomatic rEF
-ACEI/ARB
-Beta-blocker

63
Q

GDMT for stage C

A

-ARNI/ACEI/ARB (ARNI preferred)
-GDMT beta-blocker (metoprolol, bisoprolol, carvedilol)
-Aldosterone antagonist (Eplerenone, spironolactone)
-SGLT2i (dapagliflozin/empagliflozin)
-Loop diuretic for volume overload
-ISDN/hydralazine (if black and persistently symptomatic on GDMT; or if ARNI/ACEI/ARB intolerant)
-Ivabradine
-Digoxin

64
Q

Which HF patients are candidates for diuretic treatment?

A

All HF patients with signs/symptoms of fluid retention (SYMPTOMATIC)

65
Q

Effects of diuretics on HF patients

A

-Reduce hospitalizations but do not have an impact on mortality or natural progression of HF
-Reduce symptoms associated with fluid overload, improve exercise tolerance and improve QOL

66
Q

How do you determine dosing of diuretics?

A

-Lowest dose that maintains euvolemia
-Weight is good indicator of fluid status

67
Q

Short term benefits of diuretics

A

Reduce fluid retention via . . . decreased edema, pulmonary congestion and JVD by reducing preload and cardiac filling pressure

68
Q

Long term benefits of diuretics

A

Reduced daily symptoms and improve ability to exercise

69
Q

Diuretic mechanism of action

A

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

70
Q

Which diuretics are most often used in HF patients?

A

Loop diuretics

71
Q

Loop diuretics clinical pearls

A

-Enhancing renal release of prostaglandins (increases renal blood flow and enhancing venous capacitance)
-Blocked by NSAIDS
-Patients with impaired renal function may require higher doses
-Furosemide has erratic bioavailability, torsemide may have an advantage in some patients

72
Q

Initial dose of oral furosemide

A

20-40 mg QD or BID

73
Q

Max dose of furosemide

A

160 mg QD or BID

74
Q

Initial dose of oral bumetanide

A

0.5-1 mg QD or BID

75
Q

Max dose of bumetanide

A

2 mg QD or BID

76
Q

Initial dose of oral torsemide

A

10-20 mg QD

77
Q

Max dose of torsemide

A

80 mg QD

78
Q

Initial dose of oral ethacrynic acid

A

25-50 mg QD or BID

79
Q

IV equivalent doses of the loop diuretics

A

F 40 mg = B 1 mg = T 20 mg = E 50 mg

80
Q

Loop diuretics mechanism of action

A

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

81
Q

Thiazide diuretics mechanism of action

A

Relatively weak agents, block Na and Cl reabsorption in the DCT

82
Q

When are thiazide diuretics recommended to be used?

A

-May be used in patients with mild HF and small amounts of fluid retention
-HCTZ and MTZ are frequently used in combination with loop diuretics in patients who become resistant to single drug therapy

83
Q

Initial dose of hydrochlorothiazide

A

25 mg/day

84
Q

Max dose of hydrochlorothiazide

A

100 mg/day

85
Q

Initial dose of metolazone

A

2.5 mg/day

86
Q

Max dose of metolazone

A

10 mg/day

87
Q

Adverse effects of thiazide and loop diuretics

A

-Decrease in magnesium
-Decrease in potassium
-Volume depletion, decreased renal function, pre-renal azotemia
-Decreased sodium
-Postural hypotension
-Increased uric acid
-Increase in calcium (thiazide)
-Decrease in calcium (loop)

88
Q

Loop diuretics initiation

A

-Initiate at low-doses, then double and titrate
-Dosage adjustments based on weights and symptoms
-If fluid overload, reduce weight 1-2 pounds/day
-Patients should report if there is weight gain
-Hypotension and increased SeCr or BUN/Cr ratio may be indicative of volume depletion
-Dose adjustments may be required during ACEI/ARB/ARNI and/or beta-blocker titration

89
Q

When to monitor after initiation of loop diuretics

A

1-2 weeks and increase

90
Q

What to monitor in patient after initiation of loop diuretics

A

-Fluid intake and urinary output; body weight; S/S of congestion, JVD
-Blood pressure
-Serum electrolytes (especially K and Mg)
-Replace K (4 mEq/L or more) and Mg (2 mEq/L or more) as necessary
-Renal function

Therapeutics III (42 decks)

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