CARDIAC

CYCLE
Dr Noor Kamil
 ILOS

• After completion of this lecture you will be able to

• Define cardiac cycle
• Explain different events in each cardiac cycle
• Effect of autonomic nervous system on cardiac activity
• Mention factors affecting cardiac contractility
 DIASTOLE AND SYSTOLE

• The events that occur at the beginning of a heartbeat and last

until the beginning of the next heartbeat are called the
cardiac cycle.
• Each beat of the heart begins with a spontaneous action potential
that is initiated in the sinus node of the right atrium near the
opening of the superior vena cava.
• The action potential travels through both atria and the A-V node and
bundle into the ventricles.
• A delay of about 0.13 second occurs in the A-V node and bundle,
which allows the atria to contract before the ventricles contract.
 THE ATRIA FUNCTION AS PRIMER PUMPS FOR
THE VENTRICLES

• About 80 percent of ventricular filling occurs during diastole before

contraction of the atria, which causes the remaining 20 percent of
ventricular filling
• The atrial pressure waves include the following waves:
• The a wave, which is caused by atrial contraction
• The c wave, which occurs during ventricular contraction because of slight
backflow of blood and bulging of the A-V valves toward the atria
• The v wave, which is caused by in-filling of the atria from the venous
return
 FUNCTION OF THE VENTRICLES AS
PUMPS
• The Ventricles Fill With Blood During Diastole.
• The following events occur just before and during diastole:
• During systole, the A-V valves are closed, and the atria fill with blood.
• At the beginning of diastole is the period of isovolumic relaxation, caused by
ventricular relaxation.
• When ventricular pressure decreases below that of the atria, the A-V valves open.
• During diastole the higher pressure in the atria pushes blood into the ventricles.
• The period of rapid filling of the ventricles occurs during the first third of diastole
and provides most of the ventricular filling.
• Atrial contraction occurs during the last third of diastole and contributes about 25
percent of the filling of the ventricle.
• This contraction is commonly known as the “atrial kick.”
OUTFLOW OF BLOOD FROM THE VENTRICLES
DURING SYSTOLE
• The following events occur during systole:
• At the beginning of systole, ventricular contraction occurs, the A-V valves close,
and pressure begins to build up in the ventricle.
• No outflow of blood occurs during the first 0.2 to 0.3 second of ventricular
contraction (the period of isovolumic contraction).
• Note that isovolumic means “the same volume” and refers to the ventricular
volume.
• When the left ventricular pressure exceeds the aortic pressure of about 80
mm Hg and the right ventricular pressure exceeds the pulmonary artery
pressure of 8 mm Hg, the aortic and pulmonary valves open.
• Ventricular outflow occurs, called the period of ejection.
• Most ejection occurs during the first part of this period (period of rapid
ejection).
• The period of rapid ejection is followed by the period of slow
ejection.
• During this period, aortic pressure may slightly exceed the
ventricular pressure.
• During the last period of systole, the ventricular pressures fall
below the aortic and pulmonary artery pressures, and thus the
aortic and pulmonary valves close at this time.
• At the end of diastole, the volume of each ventricle is 110 to 120 milliliters; this
volume is called the enddiastolic volume.
• The stroke volume, which has a value of about 70 milliliters, is the amount of blood
ejected with each beat.
• The stroke volume of the heart can be doubled by increasing the end-diastolic volume
and decreasing the end-systolic volume.

• The end-systolic volume is the remaining volume in the ventricle at the end of
systole and measures about 40 to 50 milliliters.
• Ejection Fraction (EF) is the fraction of blood ejected by the ventricle relative
to its end-diastolic volume.
• Therefore, ejection fraction is calculated by dividing the stroke volume by
the end-diastolic volume; it has a value of about 60 percent.
𝑆𝑉
EF= ×100
𝐸𝐷𝑉
• where SV = stroke volume, EDV = end-diastolic volume
• Ventricular Ejection Increases Pressure in the Aorta to 120 mm Hg
(Systolic Pressure).
• When the ventricular pressure exceeds the diastolic pressure in the
aorta, the aortic valve opens and blood is ejected into the aorta.
• Systolic pressure in the aorta increases to about 120 mm Hg and
distends the elastic aorta and other arteries.
• When the aortic valve closes at the end of ventricular ejection, a slight
backflow of blood occurs, followed by a sudden cessation of flow that
causes an incisura, or a slight increase in aortic pressure.
• During diastole, blood continues to flow into the peripheral circulation
and the arterial pressure decreases to 80 mm Hg (diastolic pressure).
• The Heart Valves Prevent Backflow of Blood.
• The A-V valves (i.e., the tricuspid and mitral valves) prevent backflow
of blood from the ventricles to the atria during systole.
• In a similar fashion, the semilunar valves (i.e., the aortic and pulmonary
valves) prevent backflow of blood from the aorta and pulmonary artery
into the ventricle during diastole.
• The A-V valves have papillary muscles attached to them by the
chordae tendineae.
• During systole, the papillary muscles contract to help prevent the
valves from bulging back too far into the atria.
• The aorta and pulmonary valves are thicker than the A-V valves and do
not have any papillary muscles attached.
 WORK OUTPUT OF THE HEART

• The Volume-Pressure Diagram of the Left Ventricle Determines the

Cardiac Work Output.
• The cardiac cycle can be depicted in a volume-pressure diagram that
plots intraventricular pressure as a function of left ventricular volume.
• The phases of the cardiac cycle are as follows:
• Phase I: Period of filling during which the left ventricular volume increases
from the end-systolic volume to the end-diastolic volume, or from 45 to 115
milliliters, an increase of 70 milliliters.
• Phase II: Period of isovolumic contraction during which the volume of the
ventricle remains at the end-diastolic volume but the intraventricular
pressure increases to the level of the aortic diastolic pressure, or 80 mm Hg.
The volume-pressure diagram demonstrating changes in intraventricular volume and pressure during a single
cardiac cycle (red line).
The shaded area represents the net external work (EW) output by the left ventricle during the cardiac cycle.
 • Phase III: Period of ejection during which the systolic pressure
increases further because of additional ventricular contraction and
the ventricular volume decreases by 70 milliliters, which is the stroke
volume.
• Phase IV: Period of isovolumic relaxation during which the ventricular
volume remains at 45 milliliters but the intraventricular pressure
decreases to its diastolic pressure level.

• Preload is usually considered to be the end-diastolic pressure,

and the afterload is considered to be the pressure in the
artery exiting the ventricle (aorta or pulmonary artery).
 RELATIONSHIP OF THE ELECTROCARDIOGRAM
TO THE CARDIAC CYCLE
• The Spread of the Action Potential in the Heart Initiates Each
Heartbeat.
• The electrocardiogram is a recording of the voltage generated by
the heart from the surface of the body during each heartbeat
• The P wave is caused by spread of depolarization across the atria, which
causes atrial contraction.
• Atrial pressure increases just after the P wave.
• The QRS waves appear as a result of ventricular depolarization about 0.16
second after the onset of the P wave, initiating ventricular contraction; then
the ventricular pressure begins to increase.
• The ventricular T wave is caused by repolarization of the ventricle.
Events of the
cardiac cycle for left
ventricular function,
showing changes in
left atrial pressure,
left ventricular
pressure, aortic
pressure, ventricular
volume, the
electrocardiogram,
and the
phonocardiogram.
A-V, atrioventricular.
 REGULATION OF HEART PUMPING

• Pumping Ability. When venous return of blood increases, the

heart muscle stretches more, which makes it pump with a
greater force of contraction.
• The Frank-Starling Law states that “the stroke volume of the
left ventricle will increase as the left ventricular volume
increases due to the myocyte stretch causing a more forceful
systolic contraction”
 THE AUTONOMIC NERVOUS SYSTEM
AFFECTS CARDIAC PUMPING
• Under strong sympathetic stimulation, the heart rate of a young adult increases from a
resting value of 72 beats/min up to 180 to 200 beats/min, and the force of contraction
of the heart muscles increases dramatically.
• Sympathetic stimulation therefore can increase cardiac output two- to threefold.
• The heart has a resting sympathetic tone; therefore, inhibition of the sympathetic
system decreases the heart rate and the force of contraction of the heart, and thus
cardiac output decreases.
• Parasympathetic stimulation mainly affects the atria and can decrease the heart
rate dramatically and the force of contraction of the ventricles slightly.
• The combined effect decreases cardiac output by 50 percent or more.
CARDIAC CONTRACTILITY IS AFFECTED BY
SEVERAL FACTORS
• Among the factors that affect cardiac contractility are the
extracellular electrolyte concentrations.
• Effect of Potassium Ions. high potassium concentration in the extracellular
fluids decreases the resting membrane potential in the cardiac muscle fibers,
• Excess potassium in the extracellular fluids causes the heart to
become dilated and flaccid and also slows the heart rate.
• Large quantities of potassium also can block conduction of the cardiac
impulse from the atria to the ventricles through the A-V bundle.
• Elevation of potassium concentration to only 8 to 12 mEq/L—two to
three times the normal value—can cause severe weakness of the heart,
abnormal rhythm, and death.
CARDIAC CONTRACTILITY IS AFFECTED BY
SEVERAL FACTORS

• Effect of Calcium Ions.

• Excess calcium ions cause effects almost exactly opposite to those
of potassium ions, causing the heart to move toward spastic
contraction.
• This effect is caused by a direct effect of calcium ions to initiate the
cardiac contractile process
• Conversely, deficiency of calcium ions causes cardiac weakness,
similar to the effect of high potassium.
 EFFECT OF TEMPERATURE
ON HEART FUNCTION
• Increased body temperature, such as that which occurs when one has
fever, greatly increases the heart rate, sometimes to double the normal
rate.
• Decreased temperature greatly decreases heart rate, which may fall to
as low as a few beats per minute when a person is near death from
hypothermia in the body temperature range of 60° to 70°F.
• Heat increases the permeability of the cardiac muscle membrane to
ions that control heart rate, resulting in acceleration of the self-
excitation process.
AVERAGE/NORMAL INTRACARDIAC AND VASCULAR PRESSURE (mmHg)