Lecture 14: Cardiac Output

Question 1

End Diastolic Volume

Answer 1

~135 ml
the amount of blood in the heart’s ventricles after they are fully filled with blood, but before the heart contracts

Question 2

End Systolic Volume

Answer 2

~65 ml
the amount of blood remaining in the ventricles of the heart after the heart contracts, or at the end of systole

Question 3

Stroke Volume

Answer 3

~70 ml
SV = EDV - ESV

Question 4

Ejection Fraction

Answer 4

EF = SV/EDV
* 50-67% at rest
Ejection Fraction can increase upon exercise (from 50-65% to ~85%)

Question 5

Cardiac Output (CO)

Answer 5

CO = HR × SV
* Typical resting CO is about 5 L/min
(72 beats/min × 0.07 L/beat = 5.0 L/min)

Can rise 4-5X with exercise
* Resting heart rate is 60-100 beats/min.
* Can rise 3-4x (> 200 bpm)

Question 6

In the pressure-volume loop, where is ESV, EDV, and SV? Where does the aortic valve open and close?

Answer 6

A = EDV
D = ESV
A-D = SV

The aortic valve opens at point B and closes at point C

Question 7

Preload

Answer 7

The amount of stretch on the heart muscle due to the end-diastolic volume.
End diastolic pressure in the ventricle.

Question 8

What relationship is shown in the Frank-Starling Law of the Heart?

Answer 8

The more blood the heart gets during filling, the more it ejects
Intrinsic to cardiac muscle
Maintains equal flow in systemic and pulmonary circulation

Question 9

What is the effect of increased Preload on PV Loop?

Answer 9

EDV ↑
ESV same
SV = EDV - ESV ↑
EF = SV/EDV ↑

Question 10

How does a failing heart shift the Frank-Starling curve?

Answer 10

Failing heart can result in a shift of the Starling curve downward
Increased EDV through fluid retention can compensate

Question 11

Afterload

Answer 11

The arterial pressures against which the ventricles pump

Ventricle cannot shorten until
sufficient pressure is generated to
eject blood

Increased afterload = increased diastolic pressure
Needs to generate higher
pressure to eject blood and
shorten

Question 12

Effect of Afterload on SV

Answer 12

• Increased aortic pressure (more ventricular pressure needed to eject blood)
• Increases latent period (more pressure needs to be generated)
• Decreases ejection velocity (greater load during shortening)
• Less shortening leads to lower SV (larger ESV)

EDV same
ESV ↑
SV = EDV - ESV ↓
EF = SV/EDV ↓

Question 13

How does increased contractility (sympathetic stimulation) affect the SV?

Answer 13

• Increases in contractility shifts the Starling curve upward
• Greater SV at same EDV
• Family of Starling curves – heart can access many SVs

Question 14

How does increased contractility (inotropy) affect the tension curve?

Answer 14

Higher and shorter curve

• Increases tension development (rate and amount)
• Decreases time of contractile period –> lusitropy
• Can be quantitated (max dP/dt)
• Interval-duration relationship

Question 15

Effect of epinephrine on cardiac muscle cell
contractility (1st method)

Answer 15

Stimulation β-1 receptor:
* ↑ cAMP
* Activate PKA
* PKA phosphorylates many proteins

PKA phosphorylates
L-type Ca2+ channel (LTCC):
* ↑ activity
* ↑ release of Ca+2 from SR (more interaction w/ ryanodine receptor, more possibilities of cross bridges happening)
* ↑ tension (inotropic effect)

Question 16

Effect of epinephrine on cardiac muscle cell
contractility (2nd method)

Answer 16

PKA phosphorylates Phospholamban
↓ inhibition of Ca+2 –ATPase –> now SERCA stays open
↑ sequestration into SR (faster)
↓ duration of contraction
(lusitropic effect)

Question 17

SERCA

Answer 17

Sarcoendoplasmic reticulum calcium ATPase (SERCA) is a pump that moves calcium ions from the cytoplasm of cells into the sarcoplasmic reticulum (SR).

Kept closed/inhibited by phospholamban

Question 18

Effect of epinephrine on cardiac muscle cell
contractility (3rd method)

Answer 18

PKA phosphorylates Troponin I:
↓ Ca+2 affinity TnC
↑ sesquestration into SR
↓ duration of contraction (lusitropic effect)

Question 19

Effect of epinephrine on cardiac muscle cell
contractility (4th method)

Answer 19

PKA phosphorylates Titin:
↓ stiffness of titin in cardiac muscle
Helps with filling

Question 20

Effect of Contractility on PV Cycle

Answer 20

EDV ↓
ESV ↓
SV =EDV - ESV ↑
EF = SV/EDV ↑

Question 21

What is the Law of Laplace? How does it contribute to the preload and afterload?

Answer 21

P = Pressure
r = radius
h = wall thickness
T = tension
σ = stress

T = 𝑃 𝑟/2

σ =𝑃 𝑟/2 ℎ

• Capillaries (small radius = small stress), even though when we stand, we put a lot of pressure/stress on our capillaries, since the r is so small, the stress is not too much
• Increase EDV = increased r = increase in wall stress –> heart will increase wall thickness to compensate
• Dilated cardiomyopathy (↑ radius, ↓ thickness, ↑ stress)
• Hypertrophy (↑ thickness, ↓ stress)

Question 22

What is Fick’s method to determine cardiac output?

Answer 22

Cardiac Output = Oxygen Consumption / (Arterial Oxygen Content - Venous Oxygen Content)

CO = VO2/(Ca-Cv)

Determine blood flow to the body:
VO2 = oxygen taken in by the body (spirometer)
Ca = [O2] leaving the lung, radial arterial blood sample
Cv = [O2] entering the lung, catheter or mixed venous blood

Question 23

What is the indicator dilution method to determine cardiac output?

Answer 23

• Indicator dye injected into circulation
• Dye is mixed and diluted in the heart
• Detector measures [indicator] over time
• Volume = Quantity of dye/Concentration of dye
• Flow = volume/time

V1C1=V2C2

Question 24

What is the thermodilution method to determine cardiac output?

Answer 24

• Swan-Ganz catheter inserted into the jugular vein, it goes down into the heart
• Inject cold saline or dye
• Time to pass detector
• Can determine flow (L/min)

Question 25

What is the echocardiography method to determine cardiac output?

Answer 25

- Uses sound to map the heart - Transthoracic - Measures left ventricular volumes at the end of systole and diastole - (EDV - ESV = SV) - CO = SV x HR