Acute Heart Failure - Lohr/Gaglianello Flashcards

1
Q

In a sentence, what is heart failure?

Does heart failure always mean impaired ejection?

A

Heart failure is a failure of the heart to pump blood.

This can be due to impaired filling or ejection.

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2
Q

What is the outlook for heart failure?

How many cases are there–how widespread is it?

A

Bad. 5-year mortality exceeds 50%.

Millions of cases (“550k/year), most common diagnosis for those aged 65+, largest expense for medicare.

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3
Q

Distinguish between the intrinsic and extrinsic factors that contribute to CO (& thereby heart failure).

A

Intrinsics: Contractility, Heart Rate.

Extrinsics: Preload, Afterload.

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4
Q

What effect does tachycardia have on stroke volume?

On cardiac output?

A

Increased heart rate decreases diastolic filling time, which means that stroke volume is reduced.

Cardiac output increases initially, then peaks and falls. Recall that CO = HR x SV.

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5
Q

How is CVP influenced by heart contractility?

By blood volume?

What should CVP ideally be?

A

CVP increases as heart contractility declines in heart failure.

Increased blood volume increases CVP.

CVP should ideally be 0-2mm Hg (*according to lecturer. According to outside sources, 2-6mm Hg).

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6
Q

Explain how ventricular dilation contributes to heart failure.

How does compensation change this process?

A

Ventricular dilation increases wall stress via Laplace’s Law. This increases myocardial oxygen demand & ischemia, weakening the heart further.

Compensation increases the thickness of the wall, reducing the stress.

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7
Q

Explain how each of the following factors can exacerbate heart failure:

Increased sodium intake

Uncontrolled hypertension

Acute MI

Hyperthyroidism

A

Increased Na >> Increased fluid retention >> Increased preload.

Hypertension >> Increased afterload.

Acute MI >> Loss of myocyte function >> Decreased contractility.

Hyperthyroidism >> Increased heart rate*

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8
Q

What are some important components of a heart failure patient’s history?

A

Changes to medication

Diet (observe salt intake)

Weight changes

Angina

Exercise tolerance

Orthopnea/PND

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9
Q

What findings are seen on physical exam in a patient with acute heart failure?

A

Murmurs (mitral regurg, crescendo-decrescendo, S3 gallop, P2 knock)

Jugular distension, lower extremity edema, painful hepatomegaly.

Tachypnea, inspiratory crackles.

Decreased pulses & cold, clammy skin.

Hypotension (predictive of increased mortality)

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10
Q

What is the signifiance of jugular venous distention?

How does this relate to CVP?

A

Jugular venous distention is a sign of right-sided heart failure–systemic congestion.

CVP can be estimated as JVP + 5.

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11
Q

Describe the lab findings in a patient with acute heart failure.

A

Elevated natriuretic peptides.

Elevated troponins.

Basic metabolic panel (BUN/Creatinine) suggesting renal dysfunction (indicative of mortality)

CBC: Possible anemia

CXR: Pulmonary edema

Venous oxygen saturation: <70%

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12
Q

What metrics can be measured by echocardiography in acute heart failure?

A

Hemodynamic parameters such as RAP, CO, LAP, EF. The cause of failure may be identified (wall/valve), and risk can be estimated.

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13
Q

A swan-ganz catheter is also called a PAC. Where is its sensor placed?

When is its use indicated?

A

In the pulmonary artery.

When there is uncertainty about hemodynamic parameters, to evaluate difficult cases (refractory, possible shock, decompensation), and to evaluate for VAD/transplant.

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14
Q

Describe the class of heart failure (dry/wet, warm/cold) each of the following patients best fits under.

Paroxysmal nocturnal dyspnea with hypotension despite use of an ACE-inhibitor

Mentally obtunded but otherwise normal

Lower limb edema with warm extremities

A

Cold & Wet

Cold & Dry

Warm & Wet

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15
Q

What does pulmonary wedge pressure estimate?

If PAWP is elevated, what can be said about the stroke volume of the left ventricle?

A

Wedge pressure estimates LVEDP.

Higher wedge pressure = elevated LVEDP. Stroke volume is probably elevated, but is certainly inadequate.

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16
Q

Is increased systemic vascular resistance a sign of “cold” or “wet” heart failure?

Is increased central venous pressure a sign of “cold” or “wet” heart failure?

Is decreased cardiac output a sign of “cold” or “wet” heart failure?

A

Increased SVR >> Cold

Increased CVP >> Wet

Decreased CO >> Cold

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17
Q

What hemodynamic parameters define heart failure as “wet” and/or “cold”?

What hemodynamic parameters are the goals of treatment?

A

Wet: PCWP > 18 or RAP > 8

Cold: CI < 2.2

Keep CI above 2.2, PCWP above 16 (18?), and RAP above 8. Try to reduce SVR below 1200.

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18
Q

What is Cardiac Index (CI)?

A

Cardiac index (CI) = Cardiac output (CO) / Body surface area

19
Q

Which form of acute heart disease is least common?

A

Cold & Dry

(probably won’t be tested)

20
Q

A patient presents in acute heart failure with RAP 25, PAWP 30, and SvO2 < 30%.

What class of heart failure is this, and how can you tell?

A

Cold & Wet. Wet because of the apparent congestion (elevated RAP, PAWP), cold because of the inadequate perfusion (low venous oxygen saturation)

21
Q

What is the treatment of choice for cold & wet acute heart failure?

A

To correct the “wet”: Diuretics.

To correct the “cold”: Vasodilator or inotrope, depending on MAP.

(renal impairment means that perfusion may have to be reestablished before diuretics may take effect)

23
Q

Outline the requirements for inotrope use in acute heart failure

A
  • Advanced systolic heart failure + low output syndrome + hypotension
  • Vasodilators either ineffective or contraindicated
  • Fluid overloaded and unresponsive to diuretics or with deteriorating renal function
24
Q

Why are inotropes a ‘double-edged sword’ in the treatment of acute heart failure?

A

Inotropes increase calcium release, which increases cardiac workload and risk of arrhythmia

25
Describe the mechanism of action and primary effect(s) of milrinone
PDE inhibitor Inodilator: increases contractility (inotropic) and decreases afterload (vasodilator) with no significant increase in oxygen consumption
26
List some side effects of milrinone
* Hypotension * arrhythmia * tachycardia
27
Describe the predominant action and effect(s) of dobutamine
* ß1 agonst, weak ß2 agonist * increases contractility, mild vasodilator effect
28
What are the primary side effects of dobutamine?
* arrhythmia * angina * hypertension * tachycardia
29
Diuretics - do they require increased or decreased dosing in the treatment of heart failure?
increased
30
What are some key challenges of diuretic therapy in heart failure?
* Threshold - need adequate dose to achieve effect (difficult and time-consuming to find right dose) * Braking phenomenon: long-term loop diuretic use results in a reduced natriuretic response * Rebound: infrequent dosing leads to excess sodium retention * long-term tolerance, resulting in tubular hypertrophy
31
Compare the relative potency of the following diuretics: * furosemide * bumetanide * torsemide
furosemide \> tosemide \> bumetanide
32
List some key side effects of diuretics
* electrolyte abnormalities (hypokalemia, hypomagnesia, hyponatremia) * hypotension * gout exacerbation * hearing loss (rare) * increased digoxin toxicity * renal insufficiency * muscle cramps
33
Most patients with acute decompensated heart failure fall into what category? (wet-temperature axis) The majority of these patients require what primary therapy?
wet-warm IV diuretics (may also require vasodilators)
34
List some key caridac effects of vasodilators
* decreased afterload * increased stroke volume * LVEDP decreases * decreased preload
35
What are some side-effects or limitations of IV nitroglycerin use?
* headache * hypotension * prolonged profound hypotension and bradycardia (rare) * tachyphylaxis * 20% non-response among patients
36
What are the dosing goals for IV nitroglycerin?
* SBP \> 80 * SVR \< 1200 * PCWP \<= 16
37
IV nitroglycerin exerts its therapeutic action though what primary hemodynamic mechanism(s)?
low dose: venodilation -\> decreases filling pressure high dose: arterial vasodilation -\> decreases SVR, increases CO
38
Does nitroprusside influence pre-load or after-load?
both ("balanced") decreases filling pressures, SVR, PVR, and increases CI
39
What are the key dosing goals of nitroprusside?
* SBP \> 80 mmHg * SVR \< 1200 * PCWP \<=16
40
What are the major limitations/side effects of nitroprusside therapy?
* cyanide toxicity -\> nausea, 'weirdness'. Develops with high dose (\>250 mcg/min for \>2 days) or with low hepatic perfusion due to low CO * accumulation of thiocyanate (with chronic use and impaired renal function)
41
Which of the following therapies may be useful in 'wet-warm' heart failure? * inotropes * nesiritide * endothelin anatgonists * vasopressin antagonists
None. Use of adjunctive therapies beyond diuretics has not been demonstrated to improve outcomes.
42
Which therapy is indicated with high vascular resistance and BP? 1. SBP \>=85mmHg 2. SBP \< 85mmHg
1. vasodilator 2. inotrope +/- IABP
43
DO ACE Inhibitors target pre-load or after-load?
pre-load