Lecture 14: Cardiac Output

Question 1

Cardiac output

Answer 1

Volume of blood each ventricle pumps per unit time
CO = HR * Stroke Volume

Question 2

HR control

Answer 2

Parasymp. + symp. to SA node (chronotropic)
Symp. to entire conducting system, parasymp. to atria/AV node conducting (dromotropic)

Question 3

Parasympathetic stimulation of SA node

Answer 3

Lowers heart rate by decreasing F-type Na+ channel permeability, increasing K+ permeability - pacemaker potential starts lower, rises slower

Question 4

Sympathetic stimulation of SA node

Answer 4

Increases HR by increasing F-type Na+ channel permeability - pacemaker potential reaches threshold faster

Question 5

Heart adrenergic receptors

Answer 5

Epi from adrenals (increases HR) and NE from ANS neurons interact with the same β adrenergic receptors to change HR

Question 6

Stroke volume control

Answer 6

SV is most important variable influencing CO - more force = more emptying
3 main factors for contractility:
1. Change in EDV (preload)
2. Change in symp. input magnitude to ventricles
3. Change in arterial pressure (afterload)

Question 7

Frank-Starling mechanism of the heart

Answer 7

Length-tension relation for cardiac muscle; more diastolic filling -> more forceful contraction. Thus increased venous return -> increased CO due to more EDV increasing SV

Question 8

Why does more cardiac stretch increase contractile force?

Answer 8

1. Change in thick/thin filament overlap (more stretch -> more overlap)
2. Decreased spacing between thick/thin filaments
3. Increased sensitivity of troponin for Ca++ binding
4. Increased Ca++ release from SR

Question 9

ANS innervation of the ventricles

Answer 9

Only sympathetic nerves are distributed to the entire myocardium; NE to β-receptors increases ventricular contractility at any EDV (inotropic effect)

Question 10

How does sympathetic stimulation affect cardiac contraction/relaxation speed?

Answer 10

Sympathetic stimulation increases speed of contraction and relaxation. Almost no parasympathetic stim. of ventricles

Question 11

Adrenergic GPCR cascade

Answer 11

Adrenergic symp. activation triggers a G-protein coupled cascade -> cAMP production -> PKA activation

Question 12

How does PKA activation increase cardiac contractility?

Answer 12

PKA phosphorylates several proteins to increase contractility
-L-type Ca++ channels more active
-RyRs more active
-Phospholamban less active (doesn’t close SERCA) (lusitropic)
-Decreased Ca++ affinity for TnC (lusitropic)
-Thick-f proteins assoc. w/ X-bridges
-Titin less stiff (easier filling)

Question 13

Overall net effect of PKA activity on contractile cardiomyocytes

Answer 13

Increased contractility due to:
1. Faster and greater Ca++ release
2. Faster Ca++ return
3. Accelerated X-bridge activation and cycling

Question 14

Preload

Answer 14

EDV; amount the heart gets filled

Question 15

Afterload

Answer 15

Arterial pressure; defines how hard the heart has to work to open valve and pump blood. Increased arterial P -> more vent P needed to start ejection -> longer latent period, slower ejection velocity

Question 16

Factors influencing CO

Answer 16

Primary: SV, HR
Secondary (SV): preload, afterload, contractility

Question 17

Why is Frank-Starling important for the CVS in series?

Answer 17

Length-tension maintains equal systemic/pulm. flow; more filling leads to more ejection

Question 18

How does an increase in cardiac contractility affect the Frank-Starling curve?

Answer 18

Increased contractility shifts the F-S curve upwards; i.e. more SV at a given EDV

Question 19

Law of Laplace

Answer 19

Wall stress σ = Pr / 2h where h = wall thickness

Question 20

How does the Law of Laplace affect the heart?

Answer 20

Increased radius increases wall stress i.e. more filling stresses the heart more. This is compensated by increasing the wall thickness, i.e. cardiac hypertrophy

Question 21

Fick’s method for measuring CO

Answer 21

CO = vO2 / C_a - C_v where vO2 = O2 inspired by body, C_a = [O2] leaving lung, C_v = [O2] entering lung

Question 22

Indicator dilution for measuring CO

Answer 22

Injection of dye to the heart; measuring concentration tells us flow aka vol. / time (V1C1 = V2C2)

Question 23

Thermodilution for measuring CO

Answer 23

Swan-Ganz catheter injects cold saline and a temperature detector measures how long it takes for the colder fluid to flow through

Question 24

Echocardiography

Answer 24

Mapping heart transthoracically with sound; allows us to measure ESV and EDV.