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Control of Cardiac Output: by Prof - Dr.Amna Al Dujeli PHD CV Physiology

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JAAFAR THE KING
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8 views29 pages

Control of Cardiac Output: by Prof - Dr.Amna Al Dujeli PHD CV Physiology

Uploaded by

JAAFAR THE KING
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PDF, TXT or read online on Scribd
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Control of cardiac output

By
prof.Dr.Amna Al Dujeli
PhD CV physiology
blood drains to the veins
• where pressure is determined by
balance between
– rate at which blood enters the veins
– rate at which the heart pumps it out
If total peripheral resistance
changes
• if TPR falls and CO does not change
• – arterial pressure will fall
• – venous pressure will rise

if TPR rises and CO does not change


– arterial pressure will
rise
– venous pressure will fall
If cardiac output changes
if CO rises and TPR does not change
• – arterial pressure will rise
• – venous pressure will fall

if CO falls and TPR does not change


– arterial
pressure will fall
– venous pressure will rise
Changes in demand for blood

• TPR is inversely proportional to the


body’s need for blood
• if metabolism changes, TPR will change and generate
‘signals’ in the form of changes in arterial and venous
pressure.
EXAMPLE
if we eat a meal the gut needs more blood
• local vasodilators dilate arterioles
• total peripheral resistance falls
• if CO does not change, arterial pressure will
fall and venous pressure will rise .
Demand-led pumping
• if the body needs more blood, the heart needs to pump more
• to meet the ‘demand’
• demand is expressed as changes in arterial and venous
pressure

Signals to the heart


• if the heart responds to falls in arterial pressure and
rises in venous pressure
by pumping more blood
• then it will meet the demand
• and bring arterial and venous pressures
back to normal
Determinants of Ventricular Function
Contractility

Preload Afterload
Stroke
Volume
•Synergistic LV Contraction
•Wall Integrity Heart Rate
•Valvular Competence

Cardiac Output
STROKE VOLUME
➢Is interaction of the:
➢ Preload
Control of stroke volume
• stroke volume is the
difference between
➢Inotropic state – end diastolic volume
– end systolic volume
•
➢Afterload heart fills in diastole
Ventricular filling
• the arteries, and connected to the veins
• • the ventricle fills until the walls stretch
• enough to
• • produce an intraventricular pressure
• equal to venous pressure
Venous pressure and ventricular
filling

the higher the venous pressure the


more the heart fills in diastole
• relationship between venous
pressure
and ventricularvolume known as
the ventricular compliance curve
End diastolic volume and force of
contraction
• like all muscle, if ventricular muscle is
• stretched before contracting
• • it contracts harder
• • Starlings law of the heart
Starlings Law
• the more the heart fills the harder it contracts
(up to a limit)
• the harder it contracts the bigger the stroke
volume
• rises in venous pressure automatically lead to
rises in stroke volume
• more in - more out!
The Starling curve
• relates stroke volume to venous pressure
• the slope is known as the contractility of
the ventricle
MYOCARDIAL CONTRACTILITY “INOTROPIC
STATE
• Being affected by sympathetic or vagal nerves
activity,drugs,receptors etc…

• Stimulation of the sympathetic nerves cause an


increase of myocardial contractility “+ve inotropic
effect”

• Stimulation of the vagal nerve causes decrease of


myocardial contractility “-ve inotropic effect
INOTROPIC EFFECT
End systolic volume

- how much the ventricle empties depends on


• – how hard it contracts
• – how hard it is to eject blood
Force of contraction determined by
– end diastolic volume (Starlings Law)
– contractility
• contractility increased by sympathetic
Difficulty of ejecting blood
‘aortic impedance’
• depends mainly on TPR
• the harder it is to eject blood the higher
the pressure rises in the arteries
End systolic volume
• the easier it is to eject blood, the more comes out
in systole
• so, if arterial pressure falls
• end systolic volume will fall
• and stroke volume rise
Direct effects of arterial and
venous pressures on stroke
volume
• if venous pressure rises
– stroke volume will rise
• if arterial pressure falls
– stroke volume will rise
Control of heart rate
autonomic outflow to the heart
• controlled by signals from baroreceptors
• carotid sinus senses arterial pressure
• sends signals to medulla which controls the heart
Falls in arterial pressure
• increase heart rate by
– reducing parasympathetic activity
– increasing sympathetic activity
• increase contractility by
– increasing sympathetic activity
Compensatory Mechanisms:
Sympathetic Nervous System
Decreased MAP

Sympathetic Nervous System

 Contractility Tachycardia Vasoconstriction

MAP = (SV x HR) x TPR


Compensatory Mechanisms:
Neurohormonal Activation –
Vasopressin
Decreased systemic blood pressure

Central baroreceptors

Increased systemic blood pressure Stimulation of hypothalamus, which produces


vasopressin for release by pituitary gland

Vasoconstriction Release of vasopressin by pituitary gland

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