Cardiovascular System, Lecture 5

Question 1

Cardiac Output (Q̇)

Answer 1

• volume of blood pumped out of each ventricle per unit time (L/min)
  composed of:
• heart rate (HR): number of heart beats per unit time (beats/min or bpm)
• stroke volume (SV): volume each ventricle ejects during each heart beat (mL/beat; SV = EDV - ESV)
  -> Q̇ = HR x SV
• training can induce changes in cardiac output, stroke volume and heart rate at resting, submaximal and maximal levels
• regulation of cardiac output involves regulation of heart rate and stroke volume

Question 2

Heart Rate

Answer 2

intrinsic HR:
- SA node pacemaker with no other influences generates a heart beat
~100 bpm
extrinsic HR:
- provides regulation of HR (slower or faster) beyond the SA node influence
- chronotropic effect - something that alters HR
- positive - increase HR
- negative - decrease HR (not a negative effect just negative chronotropic effect in that in decreases heart rate)
- neural
- sympathetic - increases HR
- parasympathetic - decreases HR
- ions
- calcium - increase HR
- sodium, potassium - decrease HR

Question 3

Heart Rate - regulation

Answer 3

a “center” is a cluster of neurons responding to a specific input by generating a specific output
- cardiovascular (CV) center in medulla oblongata incudes a cardioacceleratory center, cardioinhibitory center and vasomotor center
sympathetic - cardioacceleratory center sends:
- in cardioacceleratory nerves (thoracic spinal nerves); releases norepinephrine (NE) that binds B1 (beta) receptors (can have effects on both atria and ventricles)
- in cardioacceleratory nerves to adrenal gland; releases epinephrine into blood circulation that circulates to heart and binds beta1 receptors
parasympathetic - cardioinhibitory center sends:
- in vagus nerves; releases acetylcholine (Ach) that binds M (muscarinic) receptors (atria)

Question 4

Heart Rate - regulation (alter SA node firing & alter length of AV node delay)

Answer 4

alter SA node firing
- bind beta1 receptors on SA node - pacemaker potential steeper rise - shorter time to get to threshold - more APs per unit time - increased HR
- bind M receptors on SA node - pacemaker potential shallower rise - longer time to get to threshold - less APs per unit time - decreased HR
alter length of AV node delay
- bind beta1 receptors on AV node - shorter time to get through AV node - more APs per unit time - increased HR
- bind M receptors on AV node - longer time to get through AV node - less APs per unit time - decreased HR

Question 5

Stroke Volume

Answer 5

“intrinsic” SV
- SA node pacemaker with no other influences generates basic ventricular filling and ejection events (SV = EDV – ESV).
“extrinsic” SV
- provides regulation of SV (lesser or greater) beyond SA node influence.
- primary effects:
- preload
- contractility
- afterload

Question 6

Stroke Volume - preload - regulation

Answer 6

preload - degree of stretch on cardiac contractile muscle fibers before systole (by giving more volume)
frank-strarling’s law of the heart:
- ventricle contracts more forcefully during systole when filled to a greater volume during diastole
- more forceful contraction produces a greater SV
example:
EDV 135mL to 205 mL = SV 70mL to 105mL
2 key interrelated factors determine EDV:
- filling time (duration of ventricular diastole; very heart rate dependent)
- venous return (volume of blood returned from veins back into heart)

Question 7

Stroke Volume - contractility - regulation

Answer 7

contractility - contraction strength of cardiac contractile muscle fibers (something other than volume)
inotropic agents:
positive - increase contractility - norepinephrine, epinephrine, calcium
negative: decrease contractility - acetylcholine, potassium, anesthetics
ejection fraction (EF) - quantify contractility
- EF = SV/EDV report as percentage
~50-75% at rest in healthy heart
example:
- EDV 135 mL to 135 mL (no change in EDV; not effecting preload)
- apply positive inotropic agent
- SV 70 mL to 105 mL/ EF 52% to 78%

Question 8

Stroke Volume - contractility - regulation

Answer 8

alter atrial cardiac muscle contraction:
- bind beta1 receptors on atrial cardiac muscle fibers - positive inotropic effect - increased SV
- bind M recepetors on atrial cardiac muscle fibers - negative inotropic effect - decreased SV
alter ventricular cardiac muscle contraction:
- bind beta1 receptors on ventricular cardiac muscle fibers - positive inotropic effect - increased SV
- no M receptors on ventricle cardiac muscle fibers

Question 9

Stroke Volume - afterload - regulation

Answer 9

afterload – how hard the heart must work to eject blood into circulation.
- when heart ejects blood out into arteries some of the pressure generated is used to overcome arterial pressure.
- in a healthy heart the level of afterload is such that there is enough pressure generated to both overcome the arterial pressure and provide for stroke volume
- with an increase in afterload more of the heart’s generated pressure has to go to overcoming an elevated arterial pressure so less pressure is available for actually ejecting blood
◦ less pressure for ejecting blood means decreased SV
◦ if the heart wants to maintain the same SV it will have to work harder to generate the same SV as would occur with a normal level of afterload
- main source of increasing afterload = hypertension (high blood pressure)