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Fam Med: CHF > Washington Manual > Flashcards

Washington Manual Flashcards

1
Q

How does furosemide work?

A

Reduces preload actuely by causing direct venodilation when admin IV, making it useful for managing severe HF or acute pulm edema

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2
Q

Which populations of CHF patients benefit from cardiac resynchronization therapy and why?

A

Patients with EF < or equal to 35%, NYHA class III-IV HF, and conduction abnormalities (LBBB and atrioventriular delay)

Improves quality of life and reduces risk of death in select patients

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3
Q

Which beta blockers are proven benefit on mortality?

A

Carvedilol

Metoprolol succinate

Bisoprolol

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4
Q

What diagnostic procedures should be performed in a CHF patient?

A
  • Coronary angiography in patients with angina or evidence of ischemia by ECG or stress testing unless patient isnt a candidate for revascularization
  • RH catheterization with placement of pulmonary artery catheter that may help guide therapy in patietns with HoTN and evidence of shock
  • Cardiopulmonary exercise testing with measurement of peak oxygen consumption (VO2) is useful in assessing functional capacity and inidentifying candidates for heart transplantation
  • Endomyocardial biopsy
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5
Q

How can thiazide diuretics be beneficial in CHF patients?

A

Useful in relief of acute sx of congestion and maintenance euvolemia

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6
Q

Why are ACE-I benefit in CHF?

A

Attenuate vasoconstriction, vital organ hypoperfusion, hyponatremia, hypokalemia, and fluid retention attributable to compensary activation of renin-angiotension system

First choice antagonism of RAAS

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7
Q

How does tx between regular CHF and HF with preserved ejection fraction differ?

A

Tx of HF with preserved EF is largely empiric and is directed toward improving sx with diuretic therapy and correcting precipitating factors (HTN, ischemia, tachycardia)

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8
Q

What reduces the specificity of BNP?

A

Patients with renal dysfunction

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9
Q

Discuss the pathophysiology of CHF

A

Begins with inital insult leading to myocardial injury which leads to pathologic remodeling which manifests as increase in LV size (dilation) and or mass (hypertrophy)

Compensatory adaptations initially maintain CO; activation of RAAS and vasopressin, which lead to increased sodium retention and peripheral vasoconstriction. SNS activated, which increased levels of circulating catecholamines, resulting in increased myocardial contractibility. Ultimately these neurohormonal pathways results in direct cellular toxicity, fibrosis, arrhythmias, and pump failure

Reduction in CO results in organ hypoperfusion and pulmonary and systemic venous congestion

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10
Q

What is the role of sodium nitroprusside in CHF?

A

Direct arterial vasodilator with less potent venodilatory properties

Reduces afterload and particularly effective in patients with HF who are hypertensive or with severe aortic or mitral valve regurg

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11
Q

What other tests are important in the workup of CHF and why?

A
  • Dx tests for HIV, hepatitis, and hemochromatosis
  • When clinically suspected:
    • Serum tests for rheumatolic dx (ANA, ANCA)
    • amyloidosis (serum protein electrophoresis-SPEP)
    • urine protein electrophoresis (UPEP)
    • Pheochromocytoma (catecholamines)
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12
Q

When do you need to be cautious with sodium nitroprusside?

A

Patients with myocardial ischemia due to its potential reduction in regional myocardial blood flow

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13
Q

Discuss fluid and free water restriction

A

<1.5L/d especially in hyponatremia (<130mEq/L) and volume overload

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14
Q

What is the definition of heart failure?

A

A clinical syndrome in which either structural or functional abnormalities in the heart impair its ability to meet the metabolic demands for the body

Progressive dx and is associated with extremely high morbidity and mortality

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15
Q

What is the etiology of HF with preserved ejection fraction?

A

Most have HTN and LV hypertrophy

Myocardial dx associated include RCM, obstructive and non HCM, infiltrative cardiomyopathies, and constrictive pericarditis

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16
Q

What is BNP?

A

B-type natriuretic peptide is released by myocytes in response to stretch, volume, overload, and increased filling pressure

Elevated with asx LV dysfunction as well as HF sx

Levels have been shown to correlate with HF severity and predict survival

>400 consistent with HF

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17
Q

Which CHF patients are candidates for a heart transplant?

A
  • Younger than age 65 years (although selected older patients may also benefit)
  • Advanced HF (NYHA class III-IV)
  • Strong psychosocial support system
  • Exhausted all other therapy options
  • Be free of irreversible extracardiac organ dysfunction that would limit functional recovery or predispose them to posttransplant complications
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18
Q

Why are beta blockers beneficial in CHF?

A

Work by blocking the toxic effects of chronic adrenergic stimulation of the heart

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19
Q

What are you evaluating with a CXR in a CHF patient?

A
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20
Q

What might you find on PE in a patient with CHF?

A
  • Systemic and pulmonary venous congestion –> LE edema, pulmonary rales, JVD, pleural and pericardial effusions, hepatic congestion, and ascites
  • In systolic dysfunction, S3 or S4 as well as holosystolic murmursof tricuspid or mitral regurg
  • Carotid upstrokes may be diminished
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21
Q

Which medications should be avoid in HF patients?

A

Negative iontropes (verapamil, diltiazem-CCB) in pt with impaired ventricular contractibility along with OTC beta stimulants (ephedra, pseudoephedrine hydrochloride)

NSAIDs: antagonize the effect of ACE-I and diuretic therapy

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22
Q

What are the 4 AHAdi stages of heart failure and how do you treat each stage?

A
  • Stage A: No structural heart dx and no sx, but risk factors: CAD, HTN, DM, cardio toxins, familial cardiomyopathy
    • Tx: lifestyle modification-diet, exercise, smoking cessation; treat hyperlipidemia and use ACE for HTN
  • Stage B: Abnormal LV systolic dysfunction, MI, valvular heart diease but no H sx
    • Tx: lifestyle modifications; ACE-I and beta-adrengeric blockers
  • Stage C: Structural heart dx and HF sx
    • Tx: lifestyle modifications; ACE-I, beta blockers, diuretics, digoxin
  • Stage D: Refractory HF sx to maximal medical management
    • Tx: Therapy listed under A, B, C and mechanical assist device, heart transplantation, continuous IV inotropic infusion, hospice in select patients
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23
Q

How long does it take to see a response to a beta blocker in CHF?

A

2-3 months of therapy for significant effects on LV function

May occur much earlier for reduction of cardiac arrhythmias and incidence of sudden cardiac deaths

24
Q

Which CHF patients should get an ICD?

A

An EF < or equal to 35% for primary prevention of sudden cardiac death

25
Q

Discuss lifestyle modification in CHF patients

A
  • Dietary counseling for sodium and fluid restriction
  • Smoking cessation strongly encouraged
  • Abstinence from alcohol recommended in sx HF patients with low EF
  • Exercise training recommended in stable HF patients as adjunct to pharm tx
    • Improves exercise capacity (peak VO2 max as well as 6-min walk time), QOL, and decrease neurohormonal activation
    • Individualized, warm up period, 20-30 mins of exercise and cool down 3-5 days a week
  • Weight loss as appropriate
26
Q

What is the role of coronary revascularization in CHF patients?

A

reduces ischemia and may improve systolic function in some patients with CAD

27
Q

When would you order a cardiac MRI in a CHF patient?

A

Previous MI

Also to assess ventricular fuction and presence of valvular heart sx, infiltrative cardiomyopathy, and myocarditis

28
Q

In what specific population of CHF patietnts is hydralazine useful, in conjunction with other medicaitons?

A

African American patients

Hydralazine and isosorbide dinitrate when added to standard therapy with beta blockers and ACE-I

29
Q

What labs should be ordered for inital workup?

A
  • CBC
  • CMP
  • BUN
  • Creatinie
  • Calcium
  • Magnesium
  • Fasting glucose
  • LFTs
  • FLP
  • UA
  • Thyroid function test
30
Q

When do you need to be cautious using hydralazine in CHF patients?

A

Patients with ischemic heart disease- can cause reflex tachycardia and increased myocardial oxygen consumption

31
Q

How do you need to monitor someone on inotropes?

A

Increased risk for arrhythmias and higher mortality rates

32
Q

What is the preferred vasodilator in CHF?

A

Sodium nitroprusside

33
Q

What it the epidemiology of HF with preserved ejection fraction?

A

Almost half of patients admitted to the hospital with HF have normal or near-normal EF

Most prevalent in elderly women (most with HTN and/or DM) and also CAD and/or afib

34
Q

What type of history might a patient give you presenting with CHF?

Sx

A
  • Sx including:
    • Dyspnea (exertion and/or rest)
    • Fatigue
    • Exercise intolerance
    • Orthopnea, paroxysmal nocturnal dyspnea
    • Systemic or pulmonary venous congestion (LE swelling or cough/wheeze)
    • Presyncope, palpatations, and angina
  • Other presentations:
    • Incidental detection of asx cardiomegaly
    • Sx related to coexisting arrhythmia, conduction disturbance, thromboembolitic complications or sudden death
  • Clinical manifestations vary depending on the rapidity of the cardiac decompensation, underlying etiology, age, and comorbidities
    • Extreme decompensations may present as:
      • Cardiogenic shock (hypoperfusion of vital organs, leading to renal failure-decreased UO, mental status change changes-confusion and lethargy, or “shock liver”-elevated LFTs)
35
Q

How can digitalis be beneficial in CHF patients?

A

Increases myocardial contractibility and may attenuate the neurohormonal activation associated with HF

Decreases number of HF hospitalizations without improving overall mortality

36
Q

What is a rare complication of treatment with nitroprusside?

A

Methemoglobulinemia:

Occurs when RBCs contain methemoglobin at levels higher than 1%

Methemoglobin results from presence of iron in the ferric form instead of normal ferrous form

37
Q

What is the most common cause of heart failure?

A

Coronary artery disease

over 50% of cases

38
Q

What is the main purpose of pharm therapy in CHF?

A

Aimed at blocking neurohormonal pathways that contribute to negative re modeling and the progression of HF, while reducing sx, hospitalizations, and mortality

39
Q

What is the role of nitrates in CHF?

A
  • Predominately venodilators and help relieve sx of venous and pulmonary congestion
  • Reduce myocardial ischemia by decreasing ventricular filling pressures and directly dilating coronary arteries
  • May precipitate HoTN in patients with reduced preload
40
Q

Why can’t you use CCB in HF?

A

Non-dihydropyridine CCB (diltiazem and verapamil) worsen HF and increase risk of death in patients with advance LV systolic dysfunction due to their negative inotropic effects

41
Q

When would you order an endomyocardial biopsy?

A

Useful in making diagnosis of infiltrative cardiomyopathy if suspected

42
Q

What are the 4 NYHA classes?

A
  • I (mild): No sx or limitation while performing ordinary physical activity (walking, climbing stairs)
  • II (mild): mild sx (mild SOB, palpitations, fatigue, and/or angina) and slight limitation during ordinary physical activity
  • III (moderate): marked limitation in activity due to sx, even during less than ordinary activity (walking short distances). Comfortable only at rest
  • IV (severe): severe limitations with sx even while at rest. Mostly bebound patients
43
Q

What is a ventricular assist device?

A

Surgically implanted devices that shuttle blood from the left ventricle to the aorta to augment cardiac output.

May be indicated for patients with severe HF after cardiac surgery, individuals with intractable cardiogenic shock after acute MI, as a “bridge to transplantation” for patients awaiting heart transplantation, and as a permanent or “destination” therapy for select patients with refractory end stage HF and an estimated 1-year mortality over 50% with medical therapy

44
Q

How do you dx HF with preserved ejection fraction?

A

Based on echocardiographic criteria and Doppler findings of normal LV systolic function with impaired diastolic relaxation and elevated filling pressures

45
Q

What should dopamine be primarily used for in the setting of HF?

A

Stabilization of HoTN

46
Q

What should ICD therapy be deferred?

A
  • Advanced age
  • life-shortening comorbidities
  • end stage HF who are not candidates for transplantation
47
Q

What is the role of aldosterone antagonists in CHF patients?

A

Improve survival and decrease hospitalizations in NYHA class III-IV patients with low EF and indicated in patients if creatinine <2.5mg/dL and potassium is <5.0mEq/L

48
Q

When do you need to avoid ACE-I in CHF patients?

A

Pregnant women

Careful dose titration in patietns with renal insufficiency

49
Q

What can precipitate a CHF exacerbation?

A
  • Dietary and medication noncompliance
  • Myocaridial ischemia
  • HTN
  • Arrhythmias (e.g. a fib)
  • Infection
  • Volume overload
  • Alcohol/toxins
  • Thyroid dx
  • Drugs (NSAIDs, CCBs, doxorubicin)
  • PE
50
Q

How can digoxin be beneficial in CHF patients?

A

Exerts positive inotropic effects through binding sodium and potassium activated ATP pumps, leading to increased intracellular sodium concentrations and subsequently more available intracellular calcium during systole

Also neurohormonal blocking effects that may be related to restoration of baroreceptor sensitivity and reduced sympathetic outflow

51
Q

How can loop diuretics be beneficial in CHF?

A

Increase sodium and water excretion and induce a prostaglandin-mediated increase in renal blood flow which contributes to their natriuretic effects

Useful in relief of acute sx of congestion and maintenance euvolemia

52
Q

What separates metolazone from other thiazide diuretics?

A

Exerts its action at the proximal and distal tubule that may be useful in combo with a loop diuretic in patients with low GFR

Maintains activity in setting of low CrCl

53
Q

What is the definition of HF with preserved ejection fraction?

A

Diastolic heart failure

Clinical syndrome of HF in the presence of preserved systolic function (LV EF >40)

54
Q

List other causes of HF

A
  • Valvular heart disease
  • Toxin induced (alcohol, cocaine, chemo)
  • Myocarditis (infectious or autoimmune)
  • Familal cardiomyopathy
  • Infiltrative dx (amyloidosis, sarcoidosis, hemochromatosis)
  • Peripartum cardiomyopathy
  • Hypertrophic cardiomyopathy
  • Constrictive pericardial disease
  • High-output states (Ateriovenous malformation or fistula)
  • Generalized myopathy (Duchenne or Becker muscular dystrophy)
  • Tachycardia- induced cardiomyopathy
  • Idiopathic cardiomyopathy
55
Q

What is the role of inotropic agents in CHF?

A

Act via increasing intracellular cyclic adenosine monophosphate (cAMP) concentrations through different mechanisms which leads to enhanced phospholipase activity, which then increases the rate and extent of calcium influx by sarcoplasmic reticulum which improves cardiac relaxation

56
Q

What effect can dobutamine have on CHF patients?

A

Increased mortality in patients treated continuously

No signficant role in tx of HF resulting from diastolic dysfunction or high-output state

Fam Med: CHF (1 decks)

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