Acute Heart Failure - Lohr/Gaglianello

Question 1

In a sentence, what is heart failure?

Does heart failure always mean impaired ejection?

Answer 1

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

This can be due to impaired filling or ejection.

Question 2

What is the outlook for heart failure?

How many cases are there–how widespread is it?

Answer 2

Bad. 5-year mortality exceeds 50%.

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

Question 3

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

Answer 3

Intrinsics: Contractility, Heart Rate.

Extrinsics: Preload, Afterload.

Question 4

What effect does tachycardia have on stroke volume?

On cardiac output?

Answer 4

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.

Question 5

How is CVP influenced by heart contractility?

By blood volume?

What should CVP ideally be?

Answer 5

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).

Question 6

Explain how ventricular dilation contributes to heart failure.

How does compensation change this process?

Answer 6

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.

Question 7

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

Increased sodium intake

Uncontrolled hypertension

Acute MI

Hyperthyroidism

Answer 7

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

Hypertension >> Increased afterload.

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

Hyperthyroidism >> Increased heart rate*

Question 8

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

Answer 8

Changes to medication

Diet (observe salt intake)

Weight changes

Angina

Exercise tolerance

Orthopnea/PND

Question 9

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

Answer 9

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)

Question 10

What is the signifiance of jugular venous distention?

How does this relate to CVP?

Answer 10

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

CVP can be estimated as JVP + 5.

Question 11

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

Answer 11

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%

Question 12

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

Answer 12

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

Question 13

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

When is its use indicated?

Answer 13

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.

Question 14

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

Answer 14

Cold & Wet

Cold & Dry

Warm & Wet

Question 15

What does pulmonary wedge pressure estimate?

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

Answer 15

Wedge pressure estimates LVEDP.

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

Question 16

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?

Answer 16

Increased SVR >> Cold

Increased CVP >> Wet

Decreased CO >> Cold

Question 17

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

What hemodynamic parameters are the goals of treatment?

Answer 17

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.

Question 18

What is Cardiac Index (CI)?

Answer 18

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

Question 19

Which form of acute heart disease is least common?

Answer 19

Cold & Dry

(probably won’t be tested)

Question 20

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?

Answer 20

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

Question 21

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

Answer 21

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)

Question 23

Outline the requirements for inotrope use in acute heart failure

Answer 23

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

Question 24

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

Answer 24

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

Question 25

Describe the mechanism of action and primary effect(s) of milrinone

Answer 25

PDE inhibitor

Inodilator: increases contractility (inotropic) and decreases afterload (vasodilator) with no significant increase in oxygen consumption

Question 26

List some side effects of milrinone

Answer 26

• Hypotension
• arrhythmia
• tachycardia

Question 27

Describe the predominant action and effect(s) of dobutamine

Answer 27

• ß1 agonst, weak ß2 agonist
• increases contractility, mild vasodilator effect

Question 28

What are the primary side effects of dobutamine?

Answer 28

• arrhythmia
• angina
• hypertension
• tachycardia

Question 29

Diuretics - do they require increased or decreased dosing in the treatment of heart failure?

Answer 29

increased

Question 30

What are some key challenges of diuretic therapy in heart failure?

Answer 30

• 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

Question 31

Compare the relative potency of the following diuretics:

• furosemide
• bumetanide
• torsemide

Answer 31

furosemide > tosemide > bumetanide

Question 32

List some key side effects of diuretics

Answer 32

• electrolyte abnormalities (hypokalemia, hypomagnesia, hyponatremia)
• hypotension
• gout exacerbation
• hearing loss (rare)
• increased digoxin toxicity
• renal insufficiency
• muscle cramps

Question 33

Most patients with acute decompensated heart failure fall into what category?

(wet-temperature axis)

The majority of these patients require what primary therapy?

Answer 33

wet-warm

IV diuretics (may also require vasodilators)

Question 34

List some key caridac effects of vasodilators

Answer 34

• decreased afterload
• increased stroke volume
• LVEDP decreases
• decreased preload

Question 35

What are some side-effects or limitations of IV nitroglycerin use?

Answer 35

• headache
• hypotension
• prolonged profound hypotension and bradycardia (rare)
• tachyphylaxis
• 20% non-response among patients

Question 36

What are the dosing goals for IV nitroglycerin?

Answer 36

• SBP > 80
• SVR < 1200
• PCWP <= 16

Question 37

IV nitroglycerin exerts its therapeutic action though what primary hemodynamic mechanism(s)?

Answer 37

low dose: venodilation -> decreases filling pressure

high dose: arterial vasodilation -> decreases SVR, increases CO

Question 38

Does nitroprusside influence pre-load or after-load?

Answer 38

both (“balanced”)

decreases filling pressures, SVR, PVR, and increases CI

Question 39

What are the key dosing goals of nitroprusside?

Answer 39

• SBP > 80 mmHg
• SVR < 1200
• PCWP <=16

Question 40

What are the major limitations/side effects of nitroprusside therapy?

Answer 40

• 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)

Question 41

Which of the following therapies may be useful in ‘wet-warm’ heart failure?

• inotropes
• nesiritide
• endothelin anatgonists
• vasopressin antagonists

Answer 41

None. Use of adjunctive therapies beyond diuretics has not been demonstrated to improve outcomes.

Question 42

Which therapy is indicated with high vascular resistance and BP?

1. SBP >=85mmHg
2. SBP < 85mmHg

Answer 42

1. vasodilator
2. inotrope +/- IABP

Question 43

DO ACE Inhibitors target pre-load or after-load?

Answer 43

pre-load