Time (in milliseconds).
Blood flow = driving pressure / resistance.
The movement of blood through the heart and out the great vessels due to pressure changes generated by the muscular mechanical activity of the heart.
Cardiac AP > SAN AP > SAN AP Control > AVN > Ventricles.
Stroke volume decreases due to increased end-systolic volume (ESV).
Stroke volume increases due to decreased end-systolic volume (ESV).
Increased EDV leads to an increase in SV.
The higher pressure requirement in the left ventricle explains why its mass is larger than the right ventricle.
When Pventricular < Paortic.
Autorhythmic cells don't have a resting potential and instead contain a pacemaker potential.
To coordinate the electrical activity of the heart and regulate its rhythm.
They can be different.
The ventricles contract, forcing blood into the pulmonary and systemic circulations.
Potentially increased Ca2+ sensitivity of the contractile apparatus leading to more cross bridge formation at any given Ca2+ concentration.
Stroke volume.
Non-pacemakers (e.g. atria, ventricles).
The Frank-Starling mechanism states that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart. This mechanism ensures that the heart pumps out the same amount of blood that enters it, thus affecting stroke volume.
When the energy of ventricular blood is less than the energy of blood in the aorta, resulting in a decrease in pressure and momentum.
The amount of blood ejected by the left ventricle of the heart in one contraction.
The relationship between pressure and volume during a cardiac cycle for the left ventricle.
Stroke volume (SV) increases due to increased end-diastolic volume (EDV).
It decreases stroke volume.
It is very sensitive to changes in afterload.
Higher pressures are required due to the high Total Peripheral Resistance (TPR).
It lasts approximately the same length as the action potential, unlike skeletal muscle.
Cardiac Output = Stroke Volume x Heart Rate
Preload, Afterload, Inotropy.
Cardiac conduction system.
Cardiac muscle.
The sequence of events that occur in one heartbeat, including diastole and systole.
They change at different stages to facilitate blood flow through the heart.
K+ channels open, allowing K+ to exit the cell.
The phase of the cardiac cycle when the heart muscle contracts and pumps blood out of the chambers.
Rapid & passive filling, Atrial systole.
Blood is ejected from the ventricles into the pulmonary and systemic circulations.
Supplying blood flow to all organs except the lungs.
The number of heart beats per minute.
Electrical activity stimulating the mechanical activity (contraction/relaxation).
Generation of a single heartbeat.
The cardiac cycle in the left side of the heart.
Controlling stroke volume and matching left and right cardiac output.
Pressures in the heart and differences in the left and right sides.
The pressure that the ventricle must generate to eject blood into the aorta.
The autonomic nervous system.
It stretches.
To ensure ventricles relax and fill before the next ventricular contraction.
ECG, pressures (atrial, ventricular, aortic), ventricular volume, and heart sounds.
Left ventricle (LV).
Blood volume, skeletal muscle pump, respiratory pump, venous tone, and gravity.
To control the electrical impulse transmission to the ventricles.
The amount of blood ejected from the heart in one pump.
Vagal activity (parasympathetic nervous system).
It contracts with greater force.
Around 250ms.
PVR stands for Pulmonary Vascular Resistance, and lower pressures are required due to its low value.
Aorta or Pulmonary artery.
The cardiac cells are unable to respond to another stimulus.
It increases.
There is greater end-diastolic volume (EDV) and more ventricular stretching, leading to greater stroke volume.
Ventricular depolarisation, ventricular contraction, and rapid pressure changes.
To allow atrial depolarisation, contraction, and ejection to occur before ventricular depolarisation.
Due to compensatory changes in preload.
The contractile unit of a muscle cell.
Approximately 70mL.
Ventricles fill with blood while the atrium and ventricles are relaxed.
When Pventricular > Patrial.
Blood keeps flowing through the aorta due to high velocity and momentum of ejection.
Atrial contraction and heart rate.
Tetanus (sustained contraction).
When there is a pressure/energy gradient across them.
Due to a pressure gradient (Patrial > Pventricular).
Ventricular Diastole, Ventricular Systole, Isovolumetric relaxation, Isovolumetric contraction, Rapid & passive filling, Atrial systole, Ejection.
70 cardiac cycles.
Changes in contractility alter the rate of ventricular pressure development, affecting stroke volume.
In mL/minute or L/minute.
0-4mmHg (Right) to 0-10mmHg (Left).
The phase of the cardiac cycle when the heart muscle relaxes and allows the chambers to fill with blood.
Preload is the initial stretching of the heart muscle, afterload is the pressure the heart must work against, and inotropy is the contractility of the heart. They affect stroke volume by influencing the amount of blood pumped out of the heart.
Ventricle relaxed, filling occurs, and the majority of filling is passive.
Changes in stroke volume.
The pressure in the ventricle falls until it is lower than the pressure in the atrium.
The heart rate at the AV Node is slower, at only 40 beats per minute (BPM).
To allow atrial depolarisation, contraction, and ejection to occur before ventricular depolarisation.
Because Pventricular < Paortic.
The ventricles are relaxed and filling with blood.
850 milliseconds.
Sympathetic activation increases stroke volume and decreases end-systolic volume.
The amount of blood (mL) ejected per beat by the left ventricle into the aorta.
4-24mmHg (Right) to 4-120mmHg (Left).
Any changes in the components can result in SV being affected.
To illustrate the cardiac cycle and the relationship between electrical and mechanical events in the heart.
Left ventricular end-diastolic pressure.
It shortens.
The resistance to blood flow offered by all the systemic vasculature, excluding the pulmonary circulation.
Diastole.
Systole.
They change together.
Depolarization.
They decrease.
Balancing of inward Ca2+ movement with outward K+ movement.
Frank-Starling Mechanism.
Ventricle contracting and pressure generated for ejection.
100 beats per minute (BPM).
Myocardial infarction/heart failure.
2/3 (600ms).
The ventricle is in a closed system, undergoing isovolumetric relaxation as the volume of blood in the ventricle remains the same.
The volume of blood the heart pumps per minute, calculated as stroke volume times heart rate.
(End Diastolic Volume - End Systolic Volume).
It is the change in electrical potential associated with the passage of an impulse along the membrane of the cardiac myocyte.
Stretching the whole heart during diastole leads to a greater force of contraction.
Inward Na+ movement through voltage-gated ion channels.
The aortic valve opens, allowing for ventricular ejection of blood into the aorta.
Pulmonary resistance (25mmHg).
The ventricles relax, and all four heart valves are closed, preventing blood from entering or leaving the ventricles.
The atrium is stimulated to contract with greater force, allowing greater blood volume to enter the ventricle.
The Frank-Starling curve shifts up and left, resulting in an increase in stroke volume and left ventricular end-diastolic pressure.
It reduces the intrinsic rate to 60-80 beats per minute (BPM).
The phase of relaxation of cardiac muscle and filling of blood.
It is the blood flow to and from the lungs.
The resistance that the right ventricle must overcome to pump blood through the pulmonary circulation.
From an area of high pressure/energy to an area of lower pressure/energy.
The momentum of blood leaving the left ventricle is greater than that in the aorta, allowing ejection to continue.
Due to K+ leaking out.
ABP = Stroke Volume (SV) x Heart Rate (HR) x Total Peripheral Resistance (TPR).
Pressure multiplied by momentum.
In a closed system as the volume of blood remains the same.
Systemic resistance (90mmHg).
Passively down a pressure gradient.
Ventricular filling, isovolumetric contraction, ventricular ejection, and isovolumetric relaxation.
2.
Voltage-gated Ca2+ channels open, Ca2+ enters, and there is a further decrease in K+ conductance via L-type (long-lasting) Calcium channels.
It decreases.
Pacemakers (e.g. SAN).
Heart failure decreases stroke volume and increases end-systolic volume.
EDV = 120mL, ESV = 50mL.
The ventricles contract, but all four heart valves are closed, preventing blood from entering or leaving the ventricles.
10-25mmHg.
Ventricular repolarization, isovolumetric relaxation, and rapid filling occur.
80-120mmHg.
The phase of contraction of cardiac muscle and ejection of blood.
Because the pressure in the ventricle is still greater than the pressure in the atrium.
Passive and does not require atrial muscle contraction.
Blood rapidly enters the ventricle as the pressure in the ventricle becomes lower than the pressure in the atrium.
An increase in the force of contraction.
The strength of the heart's contraction.
By subtracting End Systolic Volume (ESV) from End Diastolic Volume (EDV).
Inward movement of Na+ via If channels.
Cardiac output.
Atrial depolarization followed by atrial contraction.
Inactivation of Ca2+ channels and outward movement of K+.
Haemodynamics.
Usually 70mL.
1/3 (300ms).
The pressure exerted by circulating blood upon the walls of arteries.
