Cardiovascular System Part 2 Flashcards
Cardiac output
Total blood flow, the volume of blood that circulates through the blood vessels each minute
Cardiac output equation
CO = heart rate x stroke volume
How the cardiac output becomes distributes into circulatory routes that serve various body tissues depends on two more factors:
1) The pressure difference that drives the blood flow through a tissue
2) the resistance to blood flow in specific blood vessels
Frank-Starling law of the heart
The law states that the stroke volume of the left ventricle will increase as the left ventricular volume increases due to myocyte stretch cause a more forceful systolic contraction
Preload
The amount of sarcomere stretch experienced by cardiac muscle cells, called cardiomyocytes, at the end of the ventricular filling during diastole
Contractility
The inherent strength and vigor of the heart, contraction during systole.
According to Starling’s law, the heart will eject a greater stroke volume at greater filling pressures.
Afterload
The pressure against which the heart must work to eject blood during systole (systolic pressure). The lower the afterload, the more blood the heart will eject with each contraction.
Stroke volume =
End diastolic volume - end systolic volume
Average stroke volume at rest:
70ml -> amount of blood being pumped out per cardiac cycle
Stroke volume is regulated by:
Preload, contractility, and afterload
Cardiac reserve
Is the heart’s ability to increase cardiac output to meet the metabolic requirements during exercise
The difference between resting level and max we can achieve
Contractility (Inotropy)
Contractility is important for the balance between the left and right sides of the heart
Positive inotropy agents:
Increase forcefulness of a contraction (Ca2+)
Negative inotropy agents:
Reduce forcefulness of contraction (K+)
In blood plasma, key components that drive contractility are:
Na+, Ca2+, and K+
Factors that affect inotropy (contractility) of the heart include:
Heart rate
afterload
sympathetic activation
parasympathetic activation
At very high rates, stroke volume is _______, this can result in a ________ of cardiac output.
Decreased
Decrease
Increasing heart rate ______ ventricular filling time.
The heart compensates by being more efficient at relaxation.
Stroke volume is ______
_______ cardiac output and efficiency of contraction.
reduces
decreased
decreases
Ejection fraction: pumping efficiency usually between __-__%
60-70%
Ejection fraction goes ___ with high BP/hypertension (140/90mmHG), extra _____, can lead to heart failure.
down
afterload
What does the heart’s conducting system consist of?
Cardiac muscle cells and conducting fibers that are specialized for initiating impulses and conducting them rapidly through the heart.
The sequence of contraction:
1) The SA node signals the atria to contract
2) The signal travels to the AV node, through the bundle of His, down the bundle branches, and through the Purkinje fibers
3) Causing the ventricles to contract
The AP will be fired when the _______ reaches about ___mV (the threshold)
depolarisation
-55
ECG: P-wave
depolarisation of atrial contractile fibers produces P-wave
ECG: QRS complex
the onset of ventricular depolarisation
depolarisation of ventricular contractile fibers produces QRS complex
ECG: T wave
ventricular repolarisation
repolarization of ventricular contractile fibers produces T wave
ECG
A summation of the action/electrical potentials
ECG: After P-wave
atrial systole (contraction)
ECG: S-T segment
Ventricular systole (contraction)
ECG: After T wave
Ventricular diastole (relaxation)
Parasympathetic system on the heart
- affects the heart via the vagus nerves
- if reduced increases heart rate
- relaxation, slows the heart
- can change heart rate very quickly
Sympathetic system on the heart
- increase in the rate of spontaneous SA node depolarisation
- affects the heart via cardiac accelerator nerves
- sympathetic nerves run down the spinal cord and to the heart
- increases heart rate
chronotropic:
the heart rate
contractility/inotropy:
The force of energy of heart muscular contraction
Vagus nerve
Innervates the SA node to slow the rate of spontaneous depolarization, decreasing heart rate. It does not have any fibers that innervate and relax cardiac myocytes
Sympathetic nerves
Innervate both the SA node (accelerating spontaneous depolarization and therefore heart rate) and the cardiac myocytes (increasing contractility and stroke volume)
Time length of cardiac AP
300ms
Time for nerve AP
1-2ms
Phases of cardiac action potential
1) Rapid depolarization
2) Early repolarization
3) Plateau
4) Repolarization
5) Restoration of the resting membrane potential
Rapid depolarization:
Na+ channels open in the cell membranes -> rapid influx of Na+ ions into the cell
The membrane potential changes from -90mV - 30mV within 1-2ms
Early repolarization:
Na+ channels closed -> membraine potential stops esculating -> some K+ channels are activates -> produces small outward possitive current