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Cardiovascular System > Acute Heart Failure > Flashcards

Acute Heart Failure Flashcards

1
Q

What is heart failure?

A

The result of any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood

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2
Q

Overall five year mortality for heart failure?

A

60%

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3
Q

What is the biggest risk for HF

A

Age

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4
Q

What factors influence cardiac output?

A
  • Contractility
  • Heart Rate
  • Total peripheral resistance/wall stress
  • Preload
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5
Q

How does heart rate affect cardiac output?

A

Tachycardia decreases diastolic filling time which decreases stroke volume and eventually decreases CO

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6
Q

What is central venous pressure?

A

Pressure that increases with increased volume, peripheral resistance, or compliance - Reflects the amount of blood returning to the heart

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7
Q

How is Afterload related to Wall Stress

A

As afterload increases, so does wall stress, which is compensated with hypertrophy

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8
Q

What is the equation for wall stress?

A

Wall Stress = (Pressure x Radius)/(2x wall thickness)

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9
Q

What are some exacerbating factors in Acute Heart Failure associated with decreased contractility?

A

Acute MI

Negative inotrope

Alcohol

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10
Q

What are some exacerbating factors in acute heart failure associated with increased heart rate?

A
  • Increased metabolism
  • Fever
  • Infection
  • Tachycardia
  • Hyperthyroidism
  • Pregnancy

* slow heart rate is also exacerbating for AHF

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11
Q

What are some exacerbating factors in acute heart failure associated with increased preload?

A
  • Sodium content in diet
  • Excessive fluid intake
  • Renal failure
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12
Q

What are some exacerbating factors in acute heart failure associated with changes in afterload?

A

Uncontrolled hypertension

Pulmonary embolism

Severely dilated ventricle

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13
Q

What is the cycle of congestion in AHF

A

A process mediated by the kidneys: Myocardial oxygen demand → Myocardial ischemia → Worsening HF → Elevated Left Ventricular End Diastolic Pressure → Increased Wall stress → Myocardial oxygen demand →…

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14
Q

What are the goals of the physican in treating AHF?

A
  1. Identify the etiology of acute heart failure
  2. Appropriately treat acute heart failure to achieve a stable hemodynamic equilibrium
  3. Reverse (if possible) the exacerbating stimulus
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15
Q

What does the LVEDP directly increase in the heart?

A

Wall stress

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16
Q

What are methods of assessing a patient with Acute Heart Failure?

A

History and physical examination

Laboratory testing

Echocardiogram (Non invasive)

Swan-Ganz Catheter (Invasive)

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17
Q

Describe the Frank-Starling Relationship

A

Connects force and muscle fiber length - the more myosin actin cross bridges made to cycle, the more contractile force will be generated - as the fiber stretches, there is a greater number of bridges available and greater contraction but at some point the fibers can be stretched to a length where optimal cross bridging no longer happens

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18
Q

Physical exam findings with AHF: Murmurs

A
  • Mitral regurgitation
  • Crescedo-decrescendo murmur of aortic stenosis
  • S3 gallop
  • P2 “knock” suggests RV volume or pressure overload
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19
Q

Physical exam findings with AHF (besides murmurs)

A
  • Distended jugular veins
  • Pulmonary: tachypnea, inspiratory crackles
  • Lower extremity edema
  • Hypotension
  • Decreased pulses - intermittent pulses
  • Cold clammy skin
  • Tachycardia
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20
Q

How fast must tachycardia be to increase suspicion of AHF

A

Not very fast - even rates of 110 bpm should raise suspicion

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21
Q

What are the two most important physical exam findings in AHF?

A

Third heart sound and high jugular venous pressure (distended neck veins)

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22
Q

What lab tests do you perform in AHF? (what do you look for)

A
  • Brain natriuretic peptide (in atria and ventricles in response to stress)
  • Troponin: Risk stratification and diagnostic tool
  • Elevated BUN and Creatine
  • Basic metabolic panel (electrolyte imbalance)
  • CBC: evaluate for anemia or hemoconcentration
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23
Q

ELevated _______ in HF are common and predict death

A

Troponins

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24
Q

What estimates of hemodynamics are given by echocardiography in acute decomponsation?

A
  • Right atrial pressure
  • Cardiac output
  • Left atrial pressure
  • Left ventricular dimensions and volumes
25
Q

How do Swan Ganz catheters work?

A

The catheter has a balloon at the tip which assists in moving the catheter through the right atrium, right ventricle, and pulmonary artery - can record hemodynamic tracings and pressures

26
Q

What is pulmonary capillary wedge pressure

A

The PCWP measures the pressure exerted by the pulmonary venous system - It can serve as an indirect measurement of the LVEDP (High wedge pressure means too much volume in left ventricle - too much preload or not enough stroke volume)

27
Q

When do you consider a PA catheter?

A
  • Uncertain status
  • Hypotension or worsening renal function
  • Evaluation for VAD or transplant
  • Presumed cardiogenic shock
  • Severe clinical decompensation - uncertain hemodynamic profile
  • Apparent inotrope dependence
28
Q

What is the distinction between pairings of…

Warm and Dry:

Warm and Wet:

Cold and Dry:

Cold and Wet:

A
  • Warm and Dry:
    • Dyspnea; lower extremity edema
  • Warm and Wet:
    • Increased weight, elevated JVD, Peripheral edema, dyspnea
  • Cold and Dry:
    • Dry mucous membranes, tachycardia, hypotension, cold extremities
  • Cold and Wet:
    • Hypotension, tachycardia, cold extremities, elevated JVD, dyspnea
29
Q

Profiles and hemodynamics for Dry, Wet, Warm and Cold?

A
  • Dry = PCWP <18 and RA pressure < 8
  • Wet = PCWP > 18 or RA pressure > 8
  • Warm = Cardiac Index > 2.2
  • Cold = Cardiac Index < 2.2
30
Q

What are hemodynamic goals for the following?

Right atrial pressure:

Pulmonary capillary wedge:

Systolic Blood pressure:

SVR:

Cardiac Output:

A

Right atrial pressure: < 8 mm Hg

Pulmonary capillary wedge: <16 mm Hg

Systolic Blood pressure: > 80 mm Hg

SVR (systolic venous return): if diastolic filling pressures are high consider reducing to 1000-1200 dynes/sec/cm

Cardiac Output: Not a goal in itself - summation of the above

31
Q

Cold and Dry based on filling pressure (PA catheter)

PCWP < 12 and RA < 6:

PCWP> 16:

PCWP 12-16 + normal RA pressure:

A

PCWP < 12 and RA < 6: DC diuretics, PO fluids

PCWP> 16: Profile C

PCWP 12-16 + normal RA pressure: Vasodialtors, IABP (intra-aortic balloon pump) and Inotrope are temporary fix

32
Q

Cold and Wet

Wet is synonymous with…

Cold is synonymous with…

Treatment?

A

Wet = congestion (PCWP > 18)

Cold = Inadequate perfusion (CI < 2.2)

  • Tx: You may need to warm the up before drying them out
    • Diuresis will improve cardiac output
    • Choose between vasodilator and inotrope (if impaired renal fusion don’t use vasodilator)
33
Q

Main functions of current treatments

Diuretics:

Vasodilators:

Inotropes:

A

Diuretics: Reduce fluid volume

Vasodilators: Decrease preload and/or afterload

Inotropes: Augment contractility

34
Q

How do you select a therapy based on the hemodynamic profile?

A

Vasodilators for warm and wet and cold and wet with high SVR

Inotropic drugs for Cold and Dry and Cold and wet with normal SVR

Both can be used for Warm and Dry

35
Q

What are the requirements for Inotrope Use?

A
  1. Advanced systolic heart failure + Low output syndrome + Hypotension
  2. Vasodilators either ineffective or contraindicated
  3. Fluid overloaded and unresponsive to diuretics or manifest deteriorating renal function
36
Q

Heart failure leads to impaired calcium handling and inotropes increase calcium - so what is wrong with inotropes?

A

Increased calcium leads to increase work and arrhythmia

37
Q

Starting doses of inotropes in ADHF

Dobutamine:

Milrinone:

Dopamine:

A

Dobutamine: 1-10 mcg/kg/min

Milrinone: 0.01 - 0.75

Dopamine: 1-4

38
Q

Milrinone - MOA and effect

A

Phosphodiesterase inhibitor administered as an iv infusion

Inotrope and vasodilator (Inodilator)

Increases contractility and decreases afterload

39
Q

Milrinone side effects?

A
  • Hypotension: can be attenuated by withholding
  • Arrhythmia
  • Tachycardia
40
Q

Dopamine - MOA and function

A
  • Stimulates release of catecholamines
  • Lower doses exert effects on dopamine receptors AND ß receptors
  • At greater doses - tachycardia without increased inotropy
  • Afterload increases due to effects on alpha receptors at very high doses
41
Q

Dobutamine MOA and function?

A

Predominant action is a ß1 agonist with weak ß2 activity

Increases contractility with mild vasodilator effect

42
Q

What are the side effects of dobutamine?

A

Arrhythmia

Angina

Hypertension

Tachycardia

43
Q

Levosidmendan (not currently approved in US) MOA and Function

A

Acts on troponin C to increase its sensitivity to calcium

At high concentrations can be a phosphodiesterase III inhibitor

  • Decrease LVEDP
  • Decrease afterload
  • Increase stroke volume
44
Q

What are the negative effects of inotropes in ADHF

A
  • Arrhythmias
  • Hypotension
  • Increased Troponin release
  • Increase in hospital and 6 month mortality
  • Does not shorten hospitalization
45
Q

What are some challenges of diuretic therapy?

A
  • Threshold drugs - adequate dose is needed to achieve therapeutic effect
  • Braking phenomenon
  • Rebound - infrequent dosing may lead to sodium retention that exceeds natriuresis
  • Long term tolerance - tubular hypertropy to compensate for sodium loss
46
Q

What is the braking phenomenon?

A

Long term loop diuretic administration results in a reduced natriuretic response

47
Q

Diuretics used today?

A

Furosemide, Bumetanide, Torsemide

48
Q

What are some side effects of diuretics?

A
  • Electrolyte abnormalities (Hypokalemia, hypomagnesemia, hyponatremia)
  • Hypotension
  • Gout exacerbation
  • Hearing loss (rare)
  • Digoxin toxicity
  • Renal insufficiency
  • Muscle cramps - due to overly rapid diuresis
49
Q

What’s next if diuretics aren’t alleviating congestion?

A

Re-evaluate presence of congestion

Sodium and fluid

Increasing doses of loop diuretic, continuous infusion of a loop diuretic

Addition of a second type of diuretic orally or intravenously

Ultrafiltration

50
Q

Warm and Wet is the condition for most patients with ______ _______ _____ ______

A

acute decompensated heart failure

51
Q

IV vasodilators used in ADHF

A

Nitroglycerin

Nitroprusside

Nesiritide (no longer used)

52
Q

What are the effects of increasing doses of vasodilators?

A

Afterload decreases

Stroke volume increases

LVEDP decreases

Preload also decreases

53
Q

Hemodynamic effects of IV nitroglycerin?

A

Venodilator - arterial vasodilator at high doses

Decreases filling pressure at low dose; at high dose, decreases SVR and increases cardiac output

Increased coronary blood flow

54
Q

Major limitations of IV nitrglycerin?

A

Headache

Hypotension

Prolonged profound hypotension and bradycardia

Tachyphylaxis

55
Q

Nitroprusside hemodynamic effects?

A

Balanced vasodilator (both veins and arterioles)

Decrease filling pressures, SVR, PVR, and increases CI

56
Q

Major limitations to Nitroprusside?

A
  • Cyanide toxicity
    • Manifested by nausea and “feeling weird”
    • Occurs in setting of low hepatic perfusion due to low cardiac output
  • Accumulation of thiocyanate
    • Can occur over days during chronic use
57
Q

Use of adjunctive therapies beyond diuretics has not been demonstrated to improve outcomes in hospitalized ADHF patients with ____ and _____

A

Wet and Warm

58
Q

Choice of IV vasodilators or inotropes based on Systolic blood pressure?

A

SBP ≥ 85mm Hg: Vasodilator

SBP < 85 mm Hg: Inotrope +/- IABP

Cardiovascular System (35 decks)

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