Cardiovascular System Lecture 5

Question 1

What is Intrinsic HR?

Answer 1

the natural rate at which the SA node generates electrical impulses to initiate heartbeats in the absence of external influences or neural inputs.

• ~100 bpm

Question 2

What is Cardiac Output (Q)?

Answer 2

The volume of blood pumped out of each ventricle per unit time (L/min)

Question 3

How to calculate Cardiac Output?

Answer 3

Q= HR x SV

where HR = bpm

Question 4

Stroke Volume

Answer 4

SV = EDV - ESV

Question 5

What is Extrinsic HR?

Answer 5

Need other influences beyond SA node to get a faster or slower heart rate, particularly the sympathetic and parasympathetic nervous sytems

Question 6

What is the Chronotropic effect?

Answer 6

Alters Heart Rate

Question 7

What is Positive Chronotropic?

Answer 7

• Positive chronotropic – increase HR
• Sympathetic nervous system, calcium

Question 8

What is Negative Chronotropic?

Answer 8

• Negative chronotropic – decrease HR
• Parasympathetic nervous system, sodium, potassium

Question 9

Answer 9

Question 10

What is a “Center”

Answer 10

A “center” is a cluster of neurons acting as a control area.
* Receives sensory input.
* Generates motor output (in this case alters HR)

Question 11

Where is the Cardiovascular Center?
What are the 3 Centers that it is composed of?

Answer 11

Cardiovascular (CV) center:
* In medulla oblongata.
* Composed of 3 smaller centers:
* Cardioacceleratory center.
* Cardioinhibitory center.
* Vasomotor center.

Question 12

What is the Sympathetic HR?
(7)

Answer 12

Cardioacceleratory center sends neural signal to heart.
* Releases norepinephrine (NE).
* Binds β1 receptors.

Cardioacceleratory center sends neural signal to adrenal gland (inner layer – adrenal medulla).
* Releases epinephrine into blood circulation.
* Travels to heart.
* Binds β1 receptors

β1 = beta1 receptors

Question 13

What is Parasympathetic HR?
(3)

Answer 13

Cardioinhibitory center sends neural signal to heart.
* Releases acetylcholine (Ach).
* Binds M receptors.

M = muscarinic receptors

Question 14

Stimulation of β1 Receptors on SA Node (5)

Answer 14

SA Node Response to β1 Receptors
* Pacemaker potential rises steeply.
* Reaches threshold quickly.
* More AP’s per unit time
* Increases heart rate (HR).
Occurs during “fight or flight” response.

Question 15

Stimulation of M Receptors on SA Node (5)

Answer 15

SA Node Response to M Receptors
* Pacemaker potential rises shallower.
* Takes longer to reach threshold.
* Less AP’s per unit time
* Decreases heart rate (HR).
Occurs during Rest and Digest.

Question 16

Stimulation of β1 Receptors in AV Node (4):

Answer 16

Alter length of AV Node Delay:
* Shortened time to get through the AV node.
* More action potentials (APs) transmitted per unit of time.
* Increases heart rate (HR).
Occurs during “fight or flight” response.

Question 17

Stimulation of M Receptors (M2) in AV Node:

Answer 17

Alter Length of AV Node Delay:
* Prolonged time to get through the AV node.
* Fewer action potentials (APs) transmitted per unit of time.
* Decreases heart rate (HR).
Part of “rest and digest” response.

Question 18

What is Intrinsic SV?

Answer 18

SA node pacemaker generated with no other influences.
* ~70 mL/beat

Question 19

What is Extrinsic SV?
What are the 3 Primary Influences?

Answer 19

Need other influences beyond SA node to get lesser or greater stroke volume.

Primary influences:
* Preload.
* Contractility.
* Afterload.

Question 20

What is “Preload”?

Answer 20

stretch on cardiac muscle fibers before systole
(by altering ventricular volume)

Question 21

What is Frank–Starling’s law of heart?

Answer 21

ventricle contracts more forcefully during systole when filled to a greater volume during diastole.

• More forceful contraction produces a greater SV
  Example:
  EDV 135 mL to 205 mL = SV 70 mL to 105 mL

Question 22

What is the Key to EDV?

Answer 22

Key to EDV is venous return (volume of blood returned from venous system back into heart).
* Controlled by venous pressure / ventricle filling time

Question 23

What is Contractility?

Answer 23

cardiac muscle fibers contraction strength
(by altering something other than ventricular volume)

Question 24

What is the Inotropic effect?

Answer 24

alters contraction strength

Question 25

What is Positive inotropic?

Answer 25

Positive inotropic – increase contractility
Norepinephrine, epinephrine, calcium

Question 26

What is Negative inotropic?

Answer 26

Negative inotropic – decrease contractility
Acetylcholine, potassium, anesthetics

Question 27

What is Ejection Fraction?

Answer 27

Ejection fraction (EF) –
way to quantify contractility
measure of the percentage of blood that is pumped out of the heart’s left ventricle during each contraction,

~50 – 75% at rest in healthy heart

Question 28

Ejection Fraction Example:

Answer 28

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 29

How do β1 and M Receptors Alter atrial cardiac muscle contraction?

Answer 29

• Bind β1 receptors on atrial cardiac muscle fibers – positive inotropic – increased SV.
• Bind M receptors on atrial cardiac muscle fibers – negative inotropic – decreased SV

Question 30

How do β1 and M Receptors Alter VENTRICULAR cardiac muscle contraction?

Answer 30

Bind β1 receptors on ventricular cardiac muscle fibers – positive inotropic – increased SV.

No M receptors on ventricle cardiac muscle fibers – no effect.

Question 31

What is “Afterload”?

Answer 31

how hard heart must work to eject blood into circulation.

Question 32

What 2 work (pressure) components does the heart do during afterload?

Answer 32

1. Overcoming Arterial Pressure
2. Ejecting Stroke Volume

Question 33

What occurs with an increase in afterload?

Answer 33

More of heart’s generated pressure has to go to overcoming an elevated arterial pressure so less pressure is available for ejecting blood.

Less pressure for ejecting blood means decreased SV or

To maintain same SV heart will have to work harder to generate same SV as would occur with a normal level of afterload

Question 34

What is the Main source of increasing afterload?

Answer 34

hypertension (high blood pressure)