CARDIOVASCULAR SYSTEM

CARDIAC OUTPUT

• All body cells must receive a certain amount of oxygenated blood each
minute to maintain health and life. When cells are metabolically active, as
during exercise, they take up even more oxygen from the blood. During
rest periods, cellular metabolic need is reduced, and the workload of the
heart decreases.

• Cardiac output (CO) - Volume of blood ejected from the left ventricle (or
the right ventricle) into the aorta (or pulmonary trunk) each minute.
• Stroke volume (SV) - the volume of blood ejected by the ventricle during each contraction.
• Heart rate (HR) - the number of heart beats per minute.
• Cardiac output equals to the stroke volume (SV), multiplied by the heart rate (HR),
CO (mL/min) =SV(mL/beat) ×HR (beats/min)
• In a typical resting adult male, stroke volume averages 70 mL/beat, and heart rate is about 75
beats/min. Thus, average cardiac output is

CO = 70 mL/beat ×75 beats/min

= 5250 mL/min = 5.25 L/min

• Cardiac reserve is the difference b/w a person’s maximum cardiac output & cardiac output at rest.
The average person has a cardiac reserve of 4 or 5 times the resting value .
 REGULATION OF STROKE VOLUME

• A healthy heart will pump out the blood that entered its chambers during the previous
diastole. 3 factors regulate stroke volume and ensure that both ventricles pump equal
volumes of blood:

• (1) preload - the degree of stretch on the heart before it contracts;

• (2) contractility - the forcefulness of contraction of individual ventricular muscle fibers;

• (3) afterload - the pressure that must be exceeded before ejection of blood from the
ventricles can occur.
 PRELOAD

• Effect of Stretching

• A greater preload (stretch) on cardiac muscle fibers prior to contraction increases their force
of contraction. The more the heart fills with blood during diastole, the greater the force of
contraction during systole. This relationship is known as the Frank–Starling law of the heart.
• The preload is proportional to the end-diastolic volume (EDV).
• 2 key factors determine EDV:

• (a) the duration of ventricular diastole

• (b) venous return, the volume of blood returning to the right ventricle.
 FRANK – STARLING LAW OF THE HEART

• The Frank–Starling law of the heart equalizes the output of both ventricles & keeps the
same volume of blood flowing to both the systemic & pulmonary circulations. If the left
side of the heart pumps a little more blood than the right side, the volume of blood
returning to the right ventricle (venous return) increases.

• The increased EDV causes the right ventricle to contract more forcefully on the next beat,
bringing the two sides back into balance.
 CONTRACTILITY

• The 2nd factor that influences stroke volume is myocardial contractility, the
strength of contraction at any given preload.
• Substances that increase contractility are +ve inotropic agents; those that decrease
contractility are -ve inotropic agents.
• For a constant preload, the stroke volume increases when a +ve inotropic
substance is present. +ve inotropic agents often promote Ca2+ inflow during
cardiac action potentials, which strengthens the force of the next contraction.
 AFTERLOAD

• Ejection of blood from the heart begins when pressure in the ventricles
exceeds the pressure in the pulmonary trunk(20 mmHg), & the pressure in
the aorta (80 mmHg).

• The higher pressure in the ventricles causes blood to push the semilunar
valves open.

• The pressure that must be overcome before a semilunar valve can open is
termed the afterload.
 HEART SOUNDS
• During each cardiac cycle, there are 4 heart sounds.
• In a normal heart only the 1st & 2nd heart sounds (S1 & S2) are loud enough to
be heard through a stethoscope.
• The 1st sound (S1), which can be described as a lubb sound, is louder & a bit
longer than the 2nd sound. S1 is caused by blood turbulence associated with
closure of the AV valves soon after ventricular systole begins.
• The 2nd sound (S2), which is shorter & not as loud as the 1st, can be described as
a dupp sound. S2 is caused by blood turbulence associated with closure of the SL
valves at the beginning of ventricular diastole.
• S3 is due to blood turbulence during rapid ventricular filling, & S4 is due to blood
turbulence during atrial systole.
 REGULATION OF HEART RATE

• The cardiac output depends on both heart rate & stroke volume. The SA node initiates
contraction & would set a constant heart rate of about 100 beats/min.
• Stroke volume may fall if the ventricular myocardium is damaged or if blood volume is
reduced by bleeding. In these cases, homeostatic mechanisms maintain adequate cardiac
output by increasing the heart rate & contractility.
 AUTONOMIC REGULATION OF HEART RATE

• Nervous system regulation of the heart originates in the cardiovascular center in the medulla
oblongata. This region of the brain stem receives input from a variety of sensory receptors and
from higher brain centers (the limbic system & cerebral cortex).
• The cardiovascular center then directs appropriate output by increasing or decreasing the
frequency of nerve impulses in both the sympathetic & parasympathetic branches of the ANS.
• Chemoreceptors provide input to the cardiovascular center which monitor chemical changes
in the blood.
• Baroreceptors (arch of the aorta & in the carotid arteries), detect changes in blood pressure
& provide input to the cardiovascular center when it changes.
 CHEMICAL REGULATION OF HEART RATE

• Certain chemicals may also influence the heart rate. For example, hypoxia (low O 2level),
acidosis (low pH), & alkalosis (high pH) all depress cardiac activity. Several hormones
and cations have major effects on the heart.

Hormones

• Epinephrine and norepinephrine enhance the heart’s pumping effectiveness and they
increase both heart rate and contractility.

• Thyroid hormones also enhance cardiac contractility and increase heart rate.
Cations
•The differences b/w intracellular & extracellular concentrations of
several cations are important for the production of action potentials in
all nerve and muscle fibers.
•Elevated blood levels of K+or Na+ decrease heart rate & contractility.
Excess Na+blocks Ca2+ inflow during cardiac action potentials, thereby
decreasing the force of contraction, whereas excess K + blocks
generation of action potentials.
 
OTHER FACTORS IN HEART RATE REGULATION

• Gender , Age, physical fitness, body temperature etc.

•  Tachycardia- Increase in heart rate.

• Bradycardia- Decrease in heart rate.