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Cardiac Output
Maryam Fida (o-1827)
Source: The Guyton and Hall Physiology
Cardiac Output
 The volume of blood pumped by each ventricle per
minute is called cardiac output
 Cardiac output = Stroke Volume X Heart Rate
 Normal value = 5 Liters /Minute
Regulation of Cardiac Output
 Cardiac output = Stroke Volume X Heart Rate
 The factors which regulate stroke volume and Heart
rate are basically regulating Cardiac output
Factors Regulating Stroke
Volume
 Volume of blood ejected by each ventricle in single systole; Normal Value
= 70 ml/beat
 Stroke Volume = End diastolic Volume – End Systolic Volume
 So stroke volume is mainly controlled by
 EDV
 ESV
Factors Regulating EDV
 VENOUS RETURN: What ever blood volume returns to the heart,
same is pumped forward through the Frank’s Starlings Law.
According to this law 13- 15 liters of blood volume can be pumped
out without cardiac stimulation.
 DURATION OF DIASTOLE OR FILLING TIME: ventricular filling occurs
during diastole, so there must be adequate ventricular filling time.
 DISTENSIBILITY OF THE VENTRICLES: Normally ventricles are
distensible to accommodate adequate blood volume. Infarction
decreases the distensibility which decreases the EDV.
 ATRIAL CONTRACTION: There must be adequate atrial contraction
to have adequate EDV. If atrial function is not adequate then EDV
will decrease.
Factors Regulating ESV
 E.S.V is basically CONTROLLED BY MYOCARDIAL CONTRACTION
 FORCE OF MYOCARDIAL CONTRACTION: It depends upon the
initial length of muscle fibers according to frank’s starlings
law.
 PRELOAD: The effect of EDV on initial length is called
preload. So EDV also effects the ESV.
 AFTER LOAD: Force of contraction is also dependant upon the
resistance against which the ventricles have to pump
 CONDITION OF THE MYOCARDIUM : It also effects the force of
contraction.
 AUTONOMIC NERVES : Sympathetic stimulation increases and
parasympathetic stimulation decreases force of contraction
 HORMONES: Catecholamines, thyroxine, glucagon, digitalis,
calcium, increased temp, caffeine, theophyline increase the
force.
 Force decreases by hypoxia, acidosis, barniturates,
procainamide and quinidine decrease the force of contraction.
Factors regulating Heart Rate
 Number of Heart Beats per minute is called Heart Rate.
 Normal Value = 70-80 beats / minute
 Generally with increase in heart rate, C.O increases.
 But this is upto 150 beats / minute.
 In the range of 150 – 180 beats / min there is no increase in C.O
with increased HR.
 When heart rate is increased above 180 beats / min there is
decrease in C.O because diastole is not adequate for filling.
Factors regulating Heart Rate
 Basically the heart rate is autonomous.
 In the body heart rate is modified by nervous mechanisms which
include the autonomic nerves and vasomotor centre.
 We can also include the afferent nerves which carry impulses to
vasomotor centre.
 Sympathetic stimualtion increases heart rate
 Parasympatehtic stimulation decreases heart rate
Factors Regulating Heart Rate
 In the body heart rate is modified by nervous mechanisms
which include the autonomic nerves and vasomotor centre.
We can also include the afferent nerves which carry
impulses to vasomotor centre.
 So heart rate is controlled by
 Parasympathetic nerves – Vagi
 Sympathetic nerves – Sympathetic chain
 Vasomotor centre
Effects of Parasympathetic
stimulation on Heart Rate
 Vagi i.e. right vagus mailnly controls the SA node and left vagus
mainly controls the AV node.
 Vagal fibers arise form Dorsal nucleus of Vagus and supply the atrial
muscle, SA NODE, AV NODE PURKINGE FIBER but not ventricular
muscle.
 PARASYMPATHETIC STIMULATION leads to :
Effects of Parasympathetic
stimulation on Heart Rate
 NEGATIVE CHRONOTROPIC EFFECT: decrease frequency of
heart beat
 NEGATIVE DROMOTROPIC EFFECT: Velocity of conduction is
slowed down. AV nodal delay is prolonged.
 NEGATIVE BATHMOTROPIC EFFECT: Decreased excitability of
heart.
 SLIGHT NEGATIVE IONOTROPIC EFFECT: decrease force of
contraction of heart.
Effects of Parasympathetic
stimulation on Heart Rate
 The effect of vagi on the heart is continuous. This is called the vagal
tone. Vagi don’t allow the heart rate to increase.
 Vagal escape: When vagi are strongly stimulated, heart stops beating
but when strong vagal stimulation is continued, heart starts beating
again called vagal escape. The possible mechanisms of vagal escape
are:
 Exhaustion of acetylcholine stores
 Cardiac muscle becomes refractory to the action of acetyl choline
 Heart stops beating, blood pressure falls which stimulates the
baroreceptor reflex.
 Idioventricular rhythm, a focus in the ventricle starts the generation of
impulses.
Effects of Sympathetic
stimulation on Heart Rate
 Sympathetic nerves are called accelerator nerves.
 Effect of sympathetic is also continuous but not as
powerful as vagal tone.
 Preganglionic sympathetic fibers arise form T1 to T5.
These fibers go to the inferior cervical ganglion. And then
supply the heart.
 Sympathetic supply is mainly to ventricle musculature.
 POSITIVE IONOTROPIC EFFECT
 POSITIVE DROMTROPIC EFFECT
 POSITIVE BATHMOTROPIC EFFECT
 POSITIVE CHRONOTROPIC EFFECT
Vasomotor Centre
 The vasomotor center is a portion of the medulla oblongata that
regulates blood pressure and other homeostatic processes.
 The actions of the sympathetic and parasympathetic nerves is
coordinated by vasomotor centre.
 The medial part of vasomotor centre is cardioinhibitory through the
vagi supplying the heart
 The lateral part is cardioacceleratory through the sympathetic nerve
supplying the heart.
 The vasomotor centre is affected by impulses from different parts of
the heart to modify the heart rate.

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Cardiac output (The Guyton and Hall Physiology)

  • 1. Cardiac Output Maryam Fida (o-1827) Source: The Guyton and Hall Physiology
  • 2. Cardiac Output  The volume of blood pumped by each ventricle per minute is called cardiac output  Cardiac output = Stroke Volume X Heart Rate  Normal value = 5 Liters /Minute
  • 3. Regulation of Cardiac Output  Cardiac output = Stroke Volume X Heart Rate  The factors which regulate stroke volume and Heart rate are basically regulating Cardiac output
  • 4. Factors Regulating Stroke Volume  Volume of blood ejected by each ventricle in single systole; Normal Value = 70 ml/beat  Stroke Volume = End diastolic Volume – End Systolic Volume  So stroke volume is mainly controlled by  EDV  ESV
  • 5. Factors Regulating EDV  VENOUS RETURN: What ever blood volume returns to the heart, same is pumped forward through the Frank’s Starlings Law. According to this law 13- 15 liters of blood volume can be pumped out without cardiac stimulation.  DURATION OF DIASTOLE OR FILLING TIME: ventricular filling occurs during diastole, so there must be adequate ventricular filling time.  DISTENSIBILITY OF THE VENTRICLES: Normally ventricles are distensible to accommodate adequate blood volume. Infarction decreases the distensibility which decreases the EDV.  ATRIAL CONTRACTION: There must be adequate atrial contraction to have adequate EDV. If atrial function is not adequate then EDV will decrease.
  • 6. Factors Regulating ESV  E.S.V is basically CONTROLLED BY MYOCARDIAL CONTRACTION  FORCE OF MYOCARDIAL CONTRACTION: It depends upon the initial length of muscle fibers according to frank’s starlings law.  PRELOAD: The effect of EDV on initial length is called preload. So EDV also effects the ESV.  AFTER LOAD: Force of contraction is also dependant upon the resistance against which the ventricles have to pump  CONDITION OF THE MYOCARDIUM : It also effects the force of contraction.  AUTONOMIC NERVES : Sympathetic stimulation increases and parasympathetic stimulation decreases force of contraction  HORMONES: Catecholamines, thyroxine, glucagon, digitalis, calcium, increased temp, caffeine, theophyline increase the force.  Force decreases by hypoxia, acidosis, barniturates, procainamide and quinidine decrease the force of contraction.
  • 7. Factors regulating Heart Rate  Number of Heart Beats per minute is called Heart Rate.  Normal Value = 70-80 beats / minute  Generally with increase in heart rate, C.O increases.  But this is upto 150 beats / minute.  In the range of 150 – 180 beats / min there is no increase in C.O with increased HR.  When heart rate is increased above 180 beats / min there is decrease in C.O because diastole is not adequate for filling.
  • 8. Factors regulating Heart Rate  Basically the heart rate is autonomous.  In the body heart rate is modified by nervous mechanisms which include the autonomic nerves and vasomotor centre.  We can also include the afferent nerves which carry impulses to vasomotor centre.  Sympathetic stimualtion increases heart rate  Parasympatehtic stimulation decreases heart rate
  • 9. Factors Regulating Heart Rate  In the body heart rate is modified by nervous mechanisms which include the autonomic nerves and vasomotor centre. We can also include the afferent nerves which carry impulses to vasomotor centre.  So heart rate is controlled by  Parasympathetic nerves – Vagi  Sympathetic nerves – Sympathetic chain  Vasomotor centre
  • 10.
  • 11. Effects of Parasympathetic stimulation on Heart Rate  Vagi i.e. right vagus mailnly controls the SA node and left vagus mainly controls the AV node.  Vagal fibers arise form Dorsal nucleus of Vagus and supply the atrial muscle, SA NODE, AV NODE PURKINGE FIBER but not ventricular muscle.  PARASYMPATHETIC STIMULATION leads to :
  • 12. Effects of Parasympathetic stimulation on Heart Rate  NEGATIVE CHRONOTROPIC EFFECT: decrease frequency of heart beat  NEGATIVE DROMOTROPIC EFFECT: Velocity of conduction is slowed down. AV nodal delay is prolonged.  NEGATIVE BATHMOTROPIC EFFECT: Decreased excitability of heart.  SLIGHT NEGATIVE IONOTROPIC EFFECT: decrease force of contraction of heart.
  • 13. Effects of Parasympathetic stimulation on Heart Rate  The effect of vagi on the heart is continuous. This is called the vagal tone. Vagi don’t allow the heart rate to increase.  Vagal escape: When vagi are strongly stimulated, heart stops beating but when strong vagal stimulation is continued, heart starts beating again called vagal escape. The possible mechanisms of vagal escape are:  Exhaustion of acetylcholine stores  Cardiac muscle becomes refractory to the action of acetyl choline  Heart stops beating, blood pressure falls which stimulates the baroreceptor reflex.  Idioventricular rhythm, a focus in the ventricle starts the generation of impulses.
  • 14. Effects of Sympathetic stimulation on Heart Rate  Sympathetic nerves are called accelerator nerves.  Effect of sympathetic is also continuous but not as powerful as vagal tone.  Preganglionic sympathetic fibers arise form T1 to T5. These fibers go to the inferior cervical ganglion. And then supply the heart.  Sympathetic supply is mainly to ventricle musculature.  POSITIVE IONOTROPIC EFFECT  POSITIVE DROMTROPIC EFFECT  POSITIVE BATHMOTROPIC EFFECT  POSITIVE CHRONOTROPIC EFFECT
  • 15. Vasomotor Centre  The vasomotor center is a portion of the medulla oblongata that regulates blood pressure and other homeostatic processes.  The actions of the sympathetic and parasympathetic nerves is coordinated by vasomotor centre.  The medial part of vasomotor centre is cardioinhibitory through the vagi supplying the heart  The lateral part is cardioacceleratory through the sympathetic nerve supplying the heart.  The vasomotor centre is affected by impulses from different parts of the heart to modify the heart rate.