CVS 2 Flashcards
Recording the Electrical Activity of the Heart with an Electrocardiogram
The electrocardiogram (ECG or EKG) is a non-invasive means of monitoring the electrical activity of the heart.
The ECG is a record of the overall spread of electrical current through the heart as a function of time during the cardiac cycle.
Because the electrical activity of the heart is highly synchronised, relatively large-amplitude electrical potentials that correspond to distinct electrical phases of the heart can be detected at the surface of the skin.
The ECG normally shows three characteristic waveforms:
- The P wave is an upward deflection that is due to atrial depolarization.
- The QRS complex is a series of sharp upward and downward deflections due to ventricular depolarization; it is correlated with phase 0 of the ventricular contractile cell action potential.
- The T wave is an upward deflection caused by ventricular repolarization; it is correlated with phase 3 of the ventricular contractile cell action potential. Atrial repolarization is generally not detected in an ECG recording because it occurs at the same time as the QRS complex.
first three Phases of the Cardiac Cycle
- Atrial Systole
SA node conducts electrical activity- spreads throughout the atria.
Causes atrial contraction – mitral/ bicuspid valve opens, aortic valve closes.
The ventricle will fill up with blood
- Isovolumetric contraction
Electrical activity spreads through ventricles – electrical depolarisation causes ventricular contraction; ventricular pressure spontaneously rises.
The mitral valve will consequently close (first heart sound).
With all valves closed, the ventricle is now a closed chamber; no change in intraventricular volume (isovolumetric).
During isovolumetric contraction AV valves bulge into atria (increasing atrial pressure).
- Rapid ejection phase ventricular systole
When LV pressure is slightly above aortic pressure, this will push the aortic valve open causing ventricular ejection.
70% of ejection occurs in the first 1/3 of the period of ejection (rapid ejection phase).
Aortic pressure increases as blood is ejected into the aorta.
Atrial pressure decreases as AV valves no longer bulge back into the atria.
Last three phases of the cardiac cycle
- Reduced ejection phase
Remaining 30% of ventricular emptying occurs so ventricular volume and pressure decreases.
Blood flow slows down so aortic pressure also decreases.
Repolarisation of myocardium occurs.
End of this phase represents end of ventricular systole.
- Isovolumetric relaxtion
Ventricular relaxation begins and so intraventricular pressure decreases.
Pressure in large arteries push blood back towards the ventricles – snaps aortic and pulmonary valves close = 2nd heart sound.
Both valves closed – no blood is entering or leaving ventricles.
Ventricular volume is at its lowest
- Rapid and reduced filling phases
Ventricular pressure is less than atrial so AV valves open.
Aortic and pulmonary valves are closed.
Blood fills into atria and then directly into ventricle – no atrial pressure.
Towards the end of this phase, atrial depolarisation starts and cycle repeats.
What is diastole and systole
Systole: contraction and emptying
Diastole: relaxation and filling
What is mean arterial pressure (MAP).
The average aortic pressure occurring during the cardiac cycle
Ventricular Volume
The volume of blood in the ventricle at the end of diastole, referred to as the end-diastolic volume (EDV), represents the maximum ventricular volume attained during the cardiac cycle, which is reached just before the beginning of ejection
The difference between end-diastolic volume and end-systolic volume represents the volume of blood ejected from the heart during one beat, which is the stroke volume (SV):
SV = EDV – ESV
The fraction of end-diastolic volume ejected during a heartbeat is known as the ejection fraction (EF):
EF = SV/EDV
Heart Sounds
Comparing the timing of the heart sounds to the events in the cardiac cycle reveals that the heart sounds occur at the beginning of systole (phase 2), when the AV valves close, and at the beginning of diastole (phase 4), when the semilunar valves close.
But contrary to what seems obvious, heart sounds are not caused by the valve cusps slapping together as they snap shut. Instead, the sounds are created by the turbulent rushing of blood through the valves as they are narrowing and about to close.
Cardiac Output and Its Control
The rate at which a ventricle pumps blood is called the cardiac output (CO), and it is usually expressed in litres per minute.
CO = HR x SV
The cardiac output of the left ventricle equals the rate of blood flow through the systemic circuit; the cardiac output of the right ventricle equals the rate of blood flow through the pulmonary circuit.
Over the long run, the left and right sides of the heart must have the same cardiac output, or else blood volume would shift from the pulmonary circuit to the systemic circuit, or vice versa. Because the heart rate and the cardiac output are the same for the right and left sides of the heart, both ventricles must also have the same average stroke volume.
Indicators used to measure different Volumes
Dye injected into large vein or RA – passes through right side of heart, lungs and left side of heart into arterial system.
The greater the blood flow (cardiac output), the greater the dilution of the injected dye.
Neural control of heart rate (factors affecting CO)
Increased activity in sympathetic neurons to the SA node increases the frequency of action potentials in the pacemaker cells. Sympathetic neurons release norepinephrine, which binds to β1 adrenergic receptors on the SA nodal cells and activates the cAMP second messenger system. In turn, cAMP augments the opening of funny channels and T-type calcium channels. The frequency of action potentials is thereby increased, causing an increase in heart rate, which tends to increase cardiac output.
Duration of diastole decreases more so than systole, there is ample time for the ventricles to fill.
Increased activity in parasympathetic neurons to the SA node decreases the frequency of action potentials. Parasympathetic neurons release acetylcholine, which binds to muscarinic cholinergic receptors on the SA nodal cells; this binding augments the opening of potassium channels and suppresses the opening of funny channels and T-type calcium channels.
Preload and Afterload
Preload: degree of stretching myocardium prior to contraction (end-diastolic volume).
Afterload: the force opposing myocardia contraction (degree of arterial pressure).
Because arterial pressure places a load on the myocardium after contraction starts, it is called afterload. Generally speaking, afterload increases as mean arterial pressure rises.
Physical Laws Governing Blood Flow and Blood Pressure
We know that the blood flow through the pulmonary circuit is identical to that through the systemic circuit. However how can they have the same blood flow is the pressure gradient is different?
It all comes down to resistance; the pulmonary circuit offers less resistance.
flow = pressure gradient / resistance
Define Resistance of Individual Blood Vessels
The resistance of any tube (including a blood vessel) is a measure of the degree to which the tube hinders or resists the flow of liquid through it.
I.e. blood flow is greater when resistance is lower.
What factors does resistance vary with?
- Vessel radius. Changes in resistance to blood flow in the cardiovascular system almost always result from changes in the radii of blood vessels: As radius decreases, resistance increases. A decrease in blood vessel radius is called vasoconstriction; an increase in vessel radius is called vasodilation.
- Vessel length. Even though longer vessels have greater resistance than shorter ones (all else being equal), changes in vascular resistance are rarely attributable to changes in vessel length; vessels do not change length except as a person grows.
- Blood viscosity. Vascular resistance increases as viscosity increases, but blood viscosity does not change appreciably under normal conditions.
