CARDIAC CYCLE

Definition: The sequence of pressure and flow changes occurring between two subsequent
ventricular/atrial contractions is called a cardiac cycle.
Normal duration: 0.8 s at HR=75/min
o Effect of HR on Duration of Cardiac cycle: diastole period is affected more therefore
end diastolic volume is most affected, very high heart rates may actually decrease
ventricular filling and thus, the cardiac output.
How a cardiac cycle is initiated (SAN), AVN delay allows atria to contract ahead of
ventricles, thereby pumping blood into ventricles before strong ventricular contraction occurs.
Beginning of cardiac cycle:
o All 4 cardiac chambers are relaxed, filled with blood due to venous return.
o AV valves are open therefore the pressure of the two chambers on one side is the
same.
o Now the SAN fires an impulse.
ATRIAL SYSTOLE [0.1 s]
2nd rapid filling phase
o Atrial muscle contracts; pressure in atria increases (4-6 mm Hg in RA, 7-8 mm Hg in
LA), and pressure in ventricles FOLLOWS.
o 30% additional blood is pumped primer pumps, heart can function without them
too since heart pumps 300-400% more blood than is required. Effect of atrial
dysfunction is only felt in stressful exercise
o The orifices of the SVC and IVC, pulmonary veins get narrowed but as no valves
present, so some regurgitation does occur.
o V.R. decreases
o a wave is caused in atrial pressure wave. Ventricular volume rises.
VENTRICULAR SYSTOLE [0.3 s]
o Isovolumic/Isometric contraction (0.02-0.03 s)
As atrial contraction passes and pressure falls in both atria and ventricles,
ventricular excitation occurs due to arrival of impulse at the Purkinje fibres.
Now contraction begins and p in ventricles exceeds atrial p very rapidly
causing AV valve closure at the BEGINNING of this phase, production of
HS1.
Now ventricular pressure rises ABRUPTLY but an additional period (0.020.03 s) is required to build up sufficient pressure to push the semilunar valves
open against the pressures in the aorta and pulmonary artery. Therefore
during this period, contraction is occurring but there is no emptying. Since
the ventricles are closed chambers, NO CHANGE IN VOLUME IS SEEN.
Onset of ventricular systole causes BULGING OF AV valves backward
towards the atria due to high pressure in the ventricles (c wave).
o Ventricular systole proper (0.27 s)
When the pressure in LV just exceeds 80 mm Hg and that in RV, 12 mm Hg,
the semilunar valves get opened by the pressure gradient and immediately,
blood begins to be poured out of the ventricles.
During this phase, ARTERIAL and ventricular pressures follow each other
closely.
Initial phase: Rapid ejection phase (0.09 s) Intraventricular
pressure rises to maximum (LV: 120 mm Hg and RV: 25 mm Hg) but
not as rapidly as in isovolumic phase; about 70% of the blood (i.e.
70% of the stroke volume) is emptied into the respective arteries,
whose pressure closely follows the ventricles since their walls get
stretched.

The summit (peak) of the pressure curve is reached when

aortic/pulmonary arterial pressure actually EXCEEDS the ventricular
pressure but for a short period, the blood keeps flowing forward due
to momentum.
Final phase: Slow ejection phase (0.18 s) Ventricular pressure
declines as the contraction begins to subside with slow ejection of
blood from ventricles into the arteries because there is still a gradient
since there is still 30% blood in the ventricles and blood from the
arteries is being continuously being transported away to the
peripheral circulation.
o Stroke volume (70-80 ml)
o This is 60% of the End-Diastolic Volume (110-120 ml, the volume that is normally
present due to normal filling in each ventricle at the end of ventricular diastole) 0.6 is
known as the ejection fraction (a measure of ventricular contractility), and the
remaining volume in each ventricle (about 40-50 ml) is called End-Systolic Volume.
o When the heart contracts strongly, the end-systolic volume can be decreased to as
little as 10-20 ml. Conversely, when large amounts of blood flow into the ventricles
during diastole, the EDV can become as great as 150-180 ml in the healthy heart. By
both increasing EDV and decreasing ESV, the stroke volume (and thereby cardiac
output) can be increased to more than double.
VENTRICULAR DIASTOLE [0.5 s]
o Protodiastole (0.04 s): At the end of ventricular systole, ventricular pressure drops
more rapidly than arterial pressure which is better sustained due to elastic recoil of
the vessel wall. Immediately as it exceeds the pressure of the ventricles, semilunar
valves close resulting in HS2.
o Isovolumetric ventricular diastole (0.08 s): Closure of semilunar valves, continued
relaxation of the ventricular muscle causes rapid fall in pressure but there is no
change in volume as the pressure is still higher than that of the atria. It ends when
ventricular pressure falls to basically zero. Atrial pressure demonstrates v wave
towards the end of ventricular contraction due to slow flow of blood into the atria
from the veins while the AV valves are closed.
o Ventricular diastole proper (0.28 s): Approximately 70% of the ventricular filling
occurs passively during this phase. It in turn has 2 phases.
1st rapid filling (0.1 s): AV valves open, ventricles continue to relax therefore
the pressure is low (rate of relaxation i.e. V increase = rate of inflow i.e. n
increase).
Slow filling (0.18 s) diastasis: occurs due to the continuous venous return
filling both the atria and ventricles and readjusting the EDV.
o 2nd rapid filling phase / Atrial systole
ATRIAL DIASTOLE [0.7 s]
o During this phase, atrial muscles relax and atrial pressure gradually increases due to
the continuous venous return (v wave) and drops to almost zero with the opening of
AV valves. Then the pressure again rises during the phase of diastasis and leads the
ventricular pressure.