Cardiovascular System Lecture 5 Flashcards
What is Intrinsic HR?
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
What is Cardiac Output (Q)?
The volume of blood pumped out of each ventricle per unit time (L/min)
How to calculate Cardiac Output?
Q= HR x SV
where HR = bpm
Stroke Volume
SV = EDV - ESV
What is Extrinsic HR?
Need other influences beyond SA node to get a faster or slower heart rate, particularly the sympathetic and parasympathetic nervous sytems
What is the Chronotropic effect?
Alters Heart Rate
What is Positive Chronotropic?
- Positive chronotropic – increase HR
- Sympathetic nervous system, calcium
What is Negative Chronotropic?
- Negative chronotropic – decrease HR
- Parasympathetic nervous system, sodium, potassium
What is a “Center”
A “center” is a cluster of neurons acting as a control area.
* Receives sensory input.
* Generates motor output (in this case alters HR)
Where is the Cardiovascular Center?
What are the 3 Centers that it is composed of?
Cardiovascular (CV) center:
* In medulla oblongata.
* Composed of 3 smaller centers:
* Cardioacceleratory center.
* Cardioinhibitory center.
* Vasomotor center.
What is the Sympathetic HR?
(7)
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
What is Parasympathetic HR?
(3)
Cardioinhibitory center sends neural signal to heart.
* Releases acetylcholine (Ach).
* Binds M receptors.
M = muscarinic receptors
Stimulation of β1 Receptors on SA Node (5)
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.
Stimulation of M Receptors on SA Node (5)
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.
Stimulation of β1 Receptors in AV Node (4):
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.
Stimulation of M Receptors (M2) in AV Node:
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.
What is Intrinsic SV?
SA node pacemaker generated with no other influences.
* ~70 mL/beat
What is Extrinsic SV?
What are the 3 Primary Influences?
Need other influences beyond SA node to get lesser or greater stroke volume.
Primary influences:
* Preload.
* Contractility.
* Afterload.
What is “Preload”?
stretch on cardiac muscle fibers before systole
(by altering ventricular volume)
What is Frank–Starling’s law of heart?
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
What is the Key to EDV?
Key to EDV is venous return (volume of blood returned from venous system back into heart).
* Controlled by venous pressure / ventricle filling time
What is Contractility?
cardiac muscle fibers contraction strength
(by altering something other than ventricular volume)
What is the Inotropic effect?
alters contraction strength
What is Positive inotropic?
Positive inotropic – increase contractility
Norepinephrine, epinephrine, calcium
What is Negative inotropic?
Negative inotropic – decrease contractility
Acetylcholine, potassium, anesthetics
What is Ejection Fraction?
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
Ejection Fraction 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%.
How do β1 and M Receptors Alter atrial cardiac muscle contraction?
- Bind β1 receptors on atrial cardiac muscle fibers – positive inotropic – increased SV.
- Bind M receptors on atrial cardiac muscle fibers – negative inotropic – decreased SV
How do β1 and M Receptors Alter VENTRICULAR cardiac muscle contraction?
Bind β1 receptors on ventricular cardiac muscle fibers – positive inotropic – increased SV.
No M receptors on ventricle cardiac muscle fibers – no effect.
What is “Afterload”?
how hard heart must work to eject blood into circulation.
What 2 work (pressure) components does the heart do during afterload?
- Overcoming Arterial Pressure
- Ejecting Stroke Volume
What occurs with an increase in afterload?
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
What is the Main source of increasing afterload?
hypertension (high blood pressure)
