Phases of the cardiac cycle
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PHASE1: a) ventricular diastole - late: atrial contraction forces a small amount of additional blood into relaxed ventricles
b) atrial systole ends, atrial diastole begins
PHASE2: c) ventricular systole - isovolumetric phase: ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves
PHASE3: d) ventricular systole - ventricular ejection: as ventricular pressure rises and exceeds pressure in the arteries, the semilunar valves open and blood is ejected
PHASE4: e) ventricular diastole - isovolumetric relaxation: as ventricles relax, pressure in ventricles droops; blood flows back against cusps of semilunar valves and forces them closed. Blood flows into the relaxed atria.
PHASE5: f) ventricular diastole - early: all chambers are relaxed. Ventricles fill passively.
end diastolic volume, end systolic volume, stroke volume, ejection fraction
- end diastolic volume: when ventricular filling complete = max vol of ventricle
- end systolic volume: when ventricular ejection is complete = min vol in ventricle = is not 0
- stroke volume: EDV-ESV = how much blood gets ejected into the aorta
- Ejection fraction: SV/EDV = is a percentage = is what proportion of the blood that was in the LV got ejected into the aorta
Sounds of heart
- are due to heart valves closing
- S1: sound of your AV valves closing
- S2: sound of your aortic and pulmonary valves closing
Mechanical events of the cardiac
Phase 1: Late ventricular diastole
- ventricular diastole
- SA node depolarizes
- wave of depolarization sweeps over atria (which then contracts)
Phase 2: Isovolumetric contraction
- ventricular systole
- ventricular pressure rises
- atrioventricular valve closes
- When ventricular pressure exceeds aortic pressure → aortic valve opens
Phase 3: Ventricular ejection
- ventricular systole
- ejection most rapid during early part
- terminated by the end of ventricular contraction
- ventricular pressure falls rapidly & aortic valve closes
Phase 4: Isovolumetric ventricular relaxation
- ventricular diastole
- commences by closure of aortic valve
- all valves closed
- ventricular pressure falls
- aortic pressure falls much less rapidly than ventricular pressure
- because aortic run-off is much less rapid, being dependent on peripheral resistance
Phase 5: Ventricular filling
- ventricular diastole
- passive flow of blood into left atrium (& left ventricle through mitral valve)
- NOTE: ventricle is >80% full prior to atrial systole occurring (which is during late ventricular diastole - Phase 1)
extras
NOTE:
- Atrial pressure is normally low (close to zero)
- Ventricular pressure varies greatly during each cardiac cycle.
- Arterial pressure varies much less.
- Peak pressures in the right ventricle and pulmonary artery are much less (about 1/4 - 1/3) than peak pressures in the left ventricle and aorta.
heart rate, stroke volume, cardiac output, venous return
- Heart Rate (HR): the number of contractions per minute
- Stroke Volume (SV): the volume of blood ejected per contraction.
- Cardiac Output (CO): the volume of blood pumped out of the left ventricle (right ventricle) per minute.
- CO = SV x HR
- Venous Return: the volume of blood returning to the heart (right or left atrium) per minute.
How do we increase cardiac output?
By increasing heart rate
- Autonomic nervous system
- Sympathetic activation increases HR
- Parasympathetic activation decreases HR - Hormones (adrenaline, noradrenaline)
- Acting on adrenergic receptors (B1) - the same as sympathetic
- By increasing stroke volume
- Increasing pre-load (end diastolic volume)
- Decreasing after-load (blood pressure)
- Increasing contractility
Changes to Stroke Volume: (i) pre-load
- The higher the pre-load, the higher the stroke volume
- Pre-load: defined as the degree of stretch of the ventricular wall prior to contraction
- measured as the ventricular end-diastolic volume
Changes to Stroke Volume: (ii) after-load
- The higher the after-load, the lower the stroke volume
- After-load: defined as the pressure that the ventricles must overcome to eject blood. This is the aortic pressure (diastolic) at the time the aortic valve opens.
(i) Pre-load: The Frank-Starling Law of the Heart
+ consequences
- Frank-Starling Law: The greater the filling of the ventricle (i.e. end-diastolic ventricular volume), the greater will be the force of contraction (and hence stroke volume)
Consequences: - A change in return of blood to the left (or right) ventricle is immediately followed by a change in output (e.g. on changing posture when venous return suddenly decreases or increases).
- The cardiac output tends to be maintained in the face of changing aortic pressure (afterload).
Frank-Starling law: effects of change in venous return
Increase in venous return (such as when you lie down, when there is a rush of blood to the heart) –> increased end-diastolic volume (more efficient arrangement. Increases no. of cross bridges formed) –> increased force of ventricular contraction –> increased SV –> increased CO = this is the main way that SV is regulated - by changes in venous return
The effect of the Frank-Starling law on changes to (ii) after-load
Increase in after load (aortic pressure) –> reduced SV (1st effect) –> increased end-systolic ventricular volume (2nd effect) –> increased end-diastolic ventricular volume –> increased force of contraction –> SV increases, back towards original value (at the cost of increased cardiac work = this is the cause of cardiac hypertrophy in hypertension)
Changes to stroke volume: (iii) cardiac contractility
- Cardiac contractility is defined as the ability of the heart to contract, at any given end-diastolic ventricular volume
- Increases in cardiac contractility are caused by activation of cardiac sympathetic nerves, or an increase in circulating adrenaline.
- This effect is due to an increase in intracellular [Ca2+] in myocardial fibres. - Decreases in cardiac contractility are caused by activation of cardiac parasympathetic nerves that produces a decrease in myocardial intracellular [Ca2+].
- NOTE: The force of contraction of the heart therefore depends upon:
i. the end-diastolic ventricular volume
ii. extrinsic factors that affect contractility.
