Download CARDAIC OUTPUT AND ITS REGULATION

CARDAIC OUTPUT AND ITS
REGULATION
Learning Objectives
By the end of this lecture, the students should be able to understand:
• The terminology of cardiac function: Cardiac output, venous return,
stroke volume and ejection fraction
• The factors regulating cardiac output
• Effect of preload, contractility, and afterload on stroke volume and
cardiac output.
• Positive and negative chronotropic and inotropic effects
Cardiovascular System
• The goal of the cardiovascular system is to maintain adequate blood flow
to all body tissues
– The heart works in conjunction with cardiovascular centers and
peripheral blood vessels to achieve this goal
Definition of Cardiac Output
Cardiac output is the volume of blood pumped by heart each minute.
• It is product of heart rate and stroke volume and averages about
5.25L/min.
Cardiac output = heart rate x stroke volume
Heart Rate=number of beats per minute
Stroke volume=amount of blood ejected in each beat
•
Venous Return
• Quantity of blood flowing from the veins into the right atrium per minute
• In steady state, the heart pumps blood at the same rate at which blood
enters the heart ;
Cardiac Output (CO)=Venous Return (VR)
• For the normal heart, CO is largely determined by events in peripheral
circulation
• Venous Return derives Cardiac Output
Factors Affecting Cardiac Output
Heart rate
• Heart rate is no. of beats /min.
• It is typically 70 to 80 beats/min in young adults but higher in children
and elderly.
• Adjustments in HR are important in the short term control of CO and BP.
• A persistent high resting HR above 100bpm is called tachycardia and a
persistent low resting rate below 60bpm is called bradycardia
Cardiovascular Center
• Nervous system regulation of heart originate in the cardiovascular
center in medulla oblongata
• This region of the brain stem receives input from variety of sensory
receptors and from higher brain centers, such as limbic system and
cerebral cortex
• The cardiovascular center then directs appropriate output by increasing
or decreasing the frequency of nerve impulses in both sympathetic and
parasympathetic branches of ANS
Autonomic Activity
•
•
Sympathetic stimulation
– Positive inotropic effect
– Increases HR and SV
– Releases NE
– Dominant during exercise and stress
Parasympathetic stimulation
– Negative inotropic effect
– Decreases HR and SV
– Releases Ach
– Dominant at rest
Stroke Volume
• The amount of blood that leaves the heart with each beat or ventricular
contraction.
– Not all blood ejected
– Normal Adult 70 ml / beat
Stroke volume = end-diastolic volume – end-systolic volume
• End-diastolic volume = volume in ventricle before ejection (ml).
• End-systolic volume = volume remaining in the ventricle after ejection
(ml)
• Ejection fraction: The fraction of end-diastolic volume ejected in each
stroke volume
Ejection fraction = stroke volume/End- diastolic volume
Preload/Afterload
• Determinants of stroke volume
• Preload
tension on ventricular muscle before contraction
determined by left ventricular end diastolic volume
• Afterload
pressure against which ventricles pump blood
determined by total peripheral resistance
Frank-Starling Mechanism
“within physiological limits, the heart pumps all the blood it receives
without allowing excessive damming of blood in the veins”
• Increased Venous return
• Increased cardiomyocyte contractility
• Increased stroke volume
Frank-Starling Mechanism
•
•
•
•
•
Increased venous return increases
the ventricular filling (end-diastolic
volume) and therefore preload
Myocyte stretching increases the
sarcomere length
The myocardial fibers are stretched,
the force of contraction is increased
The length of the fiber is determined
primarily by the volume of blood in
the ventricle, thus
EDV is the primary determinant of
preload
This mechanism enables the heart
to eject the additional venous return,
thereby increasing stroke volume.
End Diastolic Volume
• Two factors determine :
1- The duration of ventricular diastole.
2- Venous return
• When HR increases, the duration of diastole is shorter. Less filling means
a smaller EDV.
• When venous return increases, a greater volume of blood flows into the
ventricles and EDV is increased.
• SV is directly proportional to EDV
Contractility
• Second determinant of SV
• Contractility of the myocardium
refers to its contraction force for
a given preload.
• An increase in tension resulting from
increased stretch and increase that
make the myocytes more responsive
to stimulation.
Contractility
• Factors that increase the contractility are called positive inotropic agents
• positive inotropic agents produce increase in SV and cardiac output for a
given end diastolic volume.
• Thus a larger fraction of the end diastolic volume is ejected and there is
increase in ejection fraction.
• Agents that decrease contractility have negative inotropic effect.
• They produce decrease in SV and cardiac output for a given end diastolic
volume.
• So smaller fraction of the end diastolic volume is ejected per beat and
there is decrease in ejection fraction
Afterload
• It is the load against which myocardial fibers contract or shorten during
systole.
• It includes:
• aortic pressure
• peripheral resistance
• blood volume
• viscosity of blood
Measurement of Cardiac Output
•
•
The oxygen Fick method
Indicator dilution method
Fick method of measuring cardiac Output
Cardiac output = O2 absorbed per minute by the lung (ml/min)/ Arteriovenous O2
difference (ml/L of blood)
REFERANCE
MEDICAL PHYSIOLOGY
GUYTON & HALL
12TH EDITION
Pg # 229 – 231
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