Lecture 8: Heart Failure

Question 1

Cause of increased jugular venous pressure (jugular vein distention):

Answer 1

1. increased blood volume (CHF)
2. increased right atrial pressure

Question 2

What does a diminished S1 heart sound indicate?

Answer 2

• stiff left ventricle
• problem with contractility

Question 3

The two types of heart failure:

Answer 3

1. systolic
2. diastolic

Question 4

Systolic heart failure:

Answer 4

• impaired contractility.
• ejection fraction reduced.
• decreased cardiac output.

Question 5

Diastolic heart failure:

Answer 5

• impaired filling (stiff ventricle; diminished S1).
• same ejection fraction.
• decreased cardiac output.

Question 6

Draw ESPVR curve of heart failure with preserved EF:

Answer 6

diastolic dysfunction

• increased EDP
• decreased EDV
• same ESV and EF

Question 7

Draw ESPVR curve of heart failure with reduced EF:

Answer 7

systolic dysfunction

• reduced inotropy (NEW ESPVR LINE)
• reduced ESV
• increased preload and EDP

Question 8

Both systolic and diastolic heart failure have high demand for:

Answer 8

• oxygen
• Both have increased EDP; increased wall stress

Question 9

Cause of systolic heart failure:

Answer 9

1. hypertension/ischemia
2. unfavorable remodeling
3. necrosis
4. fibrosis
5. reduced ejection fraction
6. reduced cardiac output
7. reduced perfusion pressure
8. compensatory mechanisms (SNS; fluid retention)

Question 10

Draw cardiac function curve for non-compensated heart failure:

Answer 10

• decreased cardiac output leads to a decrease in MAP and an increase in RAP.

Question 11

What form of heart failure exhibits increased preload?

Answer 11

systolic heart failure

Question 12

Once the SNS becomes active in heart failure, what are its compensatory effects?

Answer 12

1. vasoconstriction (alpha-1)
   
   • increased TPR
2. splanchnic bed vasoconstriction (alpha-1)
   
   • increased venous volume/return/RAP
3. sodium and fluid retention (kidneys)
   
   • increased intravascular volume

Question 13

What is the effect of SNS splanchnic bed vasoconstriction in heart failure?

Answer 13

• shift of blood volume from arterial to venous
• increases venous return
• increased RAP

Question 14

Draw cardiac function curve for compensated heart failure:

Answer 14

• SNS causes increased RAP, MAP, and intravascular volume.

Question 15

Mechanism of peripheral edema in heart failure:

Answer 15

1. increased RAP leads to decrease in venous return.
2. increase in capillary pressures leads to edema.

Question 16

Mechanism of pulmonary edema in heart failure:

Answer 16

1. Impaired filling/ejection of LV increases LVP.
2. LAP increases, backs up into the pulmonary veins.
3. Increased pulmonary venous pressure leads to increase in pulmonary capillary hydrostatic pressure.
4. Pulmonary edema occurs.

Question 17

Heart failure treatment:

Answer 17

Decrease fluids, decrease heart rate, increase contractile force.

1. loop diuretic (furosemide)
2. beta-blocker (metoprolol; atenolol)
3. positive inotropic (digoxin)

Question 18

Draw the following cardiac function curves overlayed:

A: healthy
C: compensated HF
D: HF plus digoxin and furosemide

Answer 18

Question 19

How does total intravascular volume increase in euvolemic patients with congestive heart failure?

Answer 19

1. low pressure baroreceptors interpret decreased MAP due to decreased CO.
2. baroreceptors activate SNS, kidneys become activated.
3. fluid becomes retained on top of already normal fluid levels.

Question 20

What are the benefits and costs of having increased intravascular volume in congestive heart failure?

Answer 20

• benefit: increased preload and slightly increased CO.
• cost: peripheral and pulmonary edema.

Question 21

Mechanism of and hormonal response to heart failure:

Answer 21

1. high pressure baroreceptors fire at slower rate due to decreased MAP.
2. SNS activated (norepinephrine/epinephrine).
3. SNS stimulates arginine-vasopression secretion from hypothalamus.
4. Low renal BP stimulates AII secretion from kidney.
5. AII stimulates aldosterone secretion from adrenal cortex.