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M2 Cardiovascular > Heart Failure - Auchampach > Flashcards

Heart Failure - Auchampach Flashcards

1
Q

What is heart failure?

A

Inability of the heart to pump blood equal to the metabolic rate of the body

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2
Q

What is the formula for cardiac output?

A

CO=heart rate*stroke volume

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3
Q

What factors influence stroke volume? Do they increase or decrease stroke volume?

A

Contractility- Increase
Preload-Increase
Afterload-Decrease

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4
Q

How is ‘preload’ measured?

A

Left Ventricle End Diastolic Volume (or pressure?)

IE: how much blood can be loaded into the left ventricle

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5
Q

What is afterload?

A

Resistance the ventricle overcomes to empty it’s contents

IE: the pressure in the aorta

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6
Q

What can change contractility?

A

Availability of intracellular calcium

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7
Q

What is compliance?

A

The change in pressure caused by an increase in volume

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8
Q

When does isovolumic contraction occur?

answer for the left side of the heart

A

After the closure of the mitral valve

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9
Q

When does isovolumic relaxation occur?

answer for the left side of the heart

A

After the closure of the aortic valve

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10
Q

What are three general causes of heart disease?

A

Impaired Ventricular Contractility
Increased Afterload
Impaired Relaxation/Filling

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11
Q

What are two ways to classify heart failure? Which typically combine?

A

Diastolic dysfunction vs Systolic dysfunction
Reduced Ejection Fraction vs Preserved Ejection Fraction

Diastolic dysfunction usually pairs with preserved EF
Systolic dysfunction usually pairs with reduced EF

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12
Q

What are some causes of increased afterload?

A

Hypertension

Aortic Stenosis

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13
Q

What are some causes of impaired contractility?

A

Coronary Ischemias (transient or infarction)
Overload caused by regurgitations
Cardiomyopathy

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14
Q

What are some causes of impaired relaxation/filling?

A

Left ventricle hypertrophy
Myocardial fibrosis
Pericardial constriction/tamponade

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15
Q

What is unique about the right side of the heart? What does this mean in terms of heart failure?

A

RV has high compliance

Right-sided heart failure typically due to an increase in afterload and is SECONDARY TO LUNG DYSFUNCTION

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16
Q

What are some examples of neurohormonal activation in response to decrease cardiac output?

A

Sympathetic activation
Renin-Angiotensin-Aldosterone activation
Anti-diuretic hormone

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17
Q

Why is neurohormonal control not a viable long-term solution to heart failure?

A

CV system is a closed loop! You can not increase preload without eventually increasing afterload, leading to decrease cardiac output.

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18
Q

What are some (very general) causes of heart failure?

A 
Increased metabolic demand
Increased circulating volume
Increased afterload
Decreased contractility
Bradycardia
19
Q

What would increase metabolic demand?

A 
Fever
Infection
Anemia
Hyperthyroidism 
Pregnancy
20
Q

How does the heart association classify heart failure?

A

Class I- no limitation in physical activity
Class II- dyspnea, fatigue with moderate exertion
Class III- dyspnea with minimal exertion
Class IV- dyspnea at rest

21
Q

What is the prognosis of heart disease?

A

5 year mortality rate is 45-60%

Class II or high is 60% mortality rate

22
Q

What are the 4 goals of treating systolic heart failure?

A

Fix underlying causes
Manage symptoms
Modulate neurohormonal response
prolong survival

23
Q

What are 5 classes of drugs used to treat heart failure with preserved ejection fraction? Why are these used?

A 
Diuretics 
Renin-Angiotensin-Aldosterone Inhibitors
Beta-blockers
Vasodilators
Positive Inotropic agents

Decrease afterload

24
Q

What is an example of a positive inotrope?

A

Digoxin

25
Q

What are Digoxin’s primary effects? Secondary effects?

A

Primary

  • Increases contractility
  • Increases Stroke Volume
  • Slows Heart Rate

Secondary

  • Arterial and Venous Dilation
  • Normalized Arterial Baroreceptors
26
Q

What is the mechanism of action for digoxin?

A

Inhibits the Na/K ATPase

The decreased Na gradient decreases the power for the Ca/Na exchanger, meaning that Ca stays in the cell longer

27
Q

How does digoxin affect heart rate?

A

Increased activity of the vagal nerve leading to reduced firing at the SA node and decreased conduction at the AV node.

28
Q

What is seen on an ECG of a patient taking Digoxin?

A

Increased PR interval

29
Q

What are some negative effects of Digoxin?

A
  • Affects all electrical systems (GI, visual, neuro, muscular)
  • Increased toxicity with hypokalemia
  • Multiple drug interactions
30
Q

When is Digoxin used?

A
  • Heart failure patients with LV systolic dysfunction AND atrial fibrillation
  • Heart failure patients who have sinus rhythm despite maximal doses of other therapies
31
Q

How does Milrinone work?

A

Phosphodiesterase Inhibitor

Positive inotrope that also produces vasodilation

32
Q

How do dobutamine and dopamine work?

A

Dobutamine
-Beta1 receptor agonist, positive inotrope

Dopamine
-Simpathomimetic, positive inotrope

33
Q

Why are diuretics used to treat heart failure?

A
  • reduced preload
  • reduced heart size
  • reduced edema
34
Q

What are three classes of diuretics? What is the main drug associated with each class?

A
  • Loop diuretics (furosemide)
  • Thiazide diuretics (chlorothiazide)
  • K sparing diuretics (amiloride, triamterene)
35
Q

What is the main side effect of diuretic therapy? What can be done to prevent it?

A

hypokalemia

prescribe K-sparing diuretics

36
Q

What does angiotensin do? What does aldosterone do?

A

Angiotensin causes aldosterone secretion; aldosterone causes water and sodium retention

37
Q

What are common ace inhibitors? Why are they prescribed for heart failure?

A

captopril, lisinopril, enalapril

Decrease afterload and preload
Increase survival rate

38
Q

What are some potential side effects of ACE inhibitors?

A

Dry cough
Decreased renal function
hyperkalemia when used with aldosterone antagonists

39
Q

What is an alternative for patients who can not tolerate ACE inhibitors?

A

Angiotensin Receptor blockers

40
Q

What do aldosterone antagonists do? What are some examples?

A

Block aldosterone to reduce edema, decrease fibrosis

Spironolactone, eplerenone

41
Q

What do beta-adrenergic receptors antagonists do?

A

Decrease BP, arrythmias
Increase ventricular function
Decrease mortality rate

42
Q

What is important about dosing for beta-adrenergic receptor antagonists?

A

They can initially worsen cardiac function, so dose must start low and then increase.

43
Q

What is Neprolysin?

A

peptidase that degrades vasoactive peptides

M2 Cardiovascular (40 decks)

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