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CARDIAC OUTPUT - II
- Dr. Chintan
Factors regulating EDV (VR)
Respiratory Pump:
Intrapleural pressure more negative – IVC diameter ↑ &
P↓
+
Descent of diaphragm - ↑ intra abdominal P
Cardiac Pump:
Vis-a-tergo: forward push from behind by,
systolic contraction + elastic recoil
Vis-a-fronte: suction force from front by,
ventricular systolic suction + ventricular diastolic suction
Factors regulating EDV (VR)
Muscle Pump:
One way, superficial to deep,
Presence of valves,
Contract – compression - ↑ pressure – proximal valve open,
Varicose veins – large, tortuous, bulbous
Mean Circulatory / Systemic Filling Pressure (MCFP / MSFP):
The pressure within the circulatory system when all flow is
stopped, (e.g. by stopping the heart or clamping large vessels),
Pressure gradient
Resistance to blood flow between the peripheral vessels and the
right atrium.,
Venous & arterial resistance
Cardiac output 2
Role of sympathetic system
Heart rate and contractility are influenced by sympathetic
innervation of the heart.
Sympathetic innervation which releases epinephrine and
norepinephrine, influences cardiac output through its alpha
effect (peripheral vasoconstriction) and its beta 1 effect
(increases heart rate and force of contraction).
The alpha effect provides more preload by shunting blood to
the core organs (including the heart). While the alpha effect
can also increase afterload, sympathetic stimulation usually
boosts cardiac output.
Factors regulating Contractility
↑ contractility:
Sympathetic, Catecholamines
Xanthine, theophylline - ↓ cAMP
Glucagon - ↑ cAMP
Digitalis
↓ contractility:
Parasympathetic
CCF, MI
Hypercapnia, hypoxia, acidosis - ↓ c AMP
Antiarrhythmic, barbiturates
Frank – starling curve
Factors regulating Cardiac Output
Intrinsic frank – starling significance (Heterometric):
Pulmonary insufficiency
Life saving in LVF
PR, after load, BP ↑
Extrinsic (Homometric) – sympathetic system - ↑ contractility:
EDV same, EF ↑
More complete emptying – ESV ↓
↑ SV, ↑ BP
Role of HR:
↑ HR - ↓ diastolic time - ↓ EDV - ↓ SV
During exercise - ↑ sympathetic activity – marked ↑ in HR +
moderate ↑ in SV - marked ↑ in CO
Parameters that Increase Cardiac Output
Atrial kick
Adequate filling time
Frank-Starling law – more myocardial stretch - Increased preload (to a
limit)
Low afterload
Parameters that Reduce Cardiac Output
Lack of atrial kick
Inadequate filling time
Frank-Starling Law – less myocardial stretch - Reduced preload (to a limit)
High afterload
Generally rates of 50-150/minute are associated with an acceptable
cardiac output.
Heart rates of less than 50/minute provide sufficient stroke volume but
often an insufficient heart rate results in poor cardiac output.
Rates of greater than 150/minute provide rapid heart rates but
insufficient filling times and poor stroke volume.
SUMMARY - REGULATION OF
CARDIAC OUTPUT
Neural
Regulation
( VMC, CVC )

PRELOAD
CARDIAC
OUTPUT

Cardiac
Hormones

Cardiac
Reflexes

HEART RATE

×

STROKE
VOLUME

CONTRACTILITY

Chemoreceptors
AFTERLOAD

Baroreceptors
Corticohypothalamic
Descending
Pathways

SYMPATHETIC AND
PARASYMPATHETIC
SYSTEM
Pathological
Cardiac Output is increased in fever due to increased
oxidative process.
In anemia due to hypoxia.
Hypoxia stimulates epinephrine
increases over all heart activity.

secretion

which

Same happens at high altitude.
Increased metabolism in hyperthyroidism also increases
cardiac output.
Pathological
CO is decreased in rapid arrhythmia due to incomplete
filling.
In Congestive Cardiac Failure due to weak contractions.

In shock due to poor pumping & circulation.
In incomplete heart block due to defective pumping.
In hemorrhage due to reduction in blood volume.
In hypothyroidism due to decreased overall metabolism.
Pathological
Heart attack,
valvular disease,
myocarditis,
cardiac tamponade (filling of pericardial sac with
fluid).
Decreased venous return caused by:
Reduced blood volume
Venous dilatation
Venous obstruction
Decreased tissue mass
Disease States Lowering
Total Peripheral Resistance
Beriberi: insufficient thiamine–tissues starve
because they cannot use nutrients.
AV fistula: e.g. for dialysis.
Hyperthyroidism: Reduced resistance caused by
increased metabolism
Anemia (lack of RBCs): effects viscosity and
transport of O2 to the tissues.
Methods for measurement of CO
Electromagnetic or Ultrasonic Flow meter
The Oxygen Fick Principle
Indicator Dilution Method: Dye dilution & thermodilution
Doppler techniques (Transcutaneous Doppler &
Transoesophageal
Doppler)
combined
with
echocardiography.
Impedance Cardiography
Electromagnetic flow meter
A recording in a dog of blood flow in the root of the aorta shows that the blood
flow rises rapidly to a peak during systole, and then at the end of systole
reverses for a fraction of a second. This reverse flow causes the aortic valve to
close and the flow to return to zero.
The Oxygen Fick Principle
Total 200 millilitres of oxygen are being absorbed from the lungs into the
pulmonary blood each minute.
The blood entering the right heart has an oxygen concentration of 160 millilitres
per litre of blood, whereas that leaving the left heart has an oxygen
concentration of 200 millilitres per litre of blood.

Each litre of blood passing through the lungs absorbs 40 millilitres of oxygen.
Because the total quantity of oxygen absorbed into the blood from the lungs
each minute is 200 millilitres, dividing 200 by 40 calculates a total of five litre
portions of blood that must pass through the pulmonary circulation each
minute to absorb this amount of oxygen.
Therefore, the quantity of blood flowing through the lungs each minute is 5
litres, which is also a measure of the cardiac output.
The Oxygen Fick Principle
Cardiac output L / min

= O2 absorbed per minute by the lungs (ml/min) divided by Arteriovenous O2
difference (ml/L of blood ).
The Oxygen Fick Principle
Cardiac output L / min
= O2 absorbed per minute by the lungs (ml/min) divided by
Arteriovenous O2 difference (ml/L of blood ).
The rate of oxygen absorption by the lungs is measured by the rate of
disappearance of oxygen from the respired air, using any type of oxygen
meter.
Systemic arterial blood can then be obtained from any systemic artery in
the body.
Mixed venous blood is usually obtained through a catheter inserted up
the brachial vein of the forearm, through the subclavian vein, down to
the right atrium, and, finally, into the right ventricle or pulmonary artery.
Indicator Dilution Method
A small amount of indicator, such as a dye, is injected into a large systemic vein
or, preferably, into the right atrium.
This passes rapidly through the right side of the heart, then through the blood
vessels of the lungs, through the left side of the heart and, finally, into the
systemic arterial system.

The concentration of the dye is recorded as the dye passes through one of the
peripheral arteries, giving a curve.
Cardiac output ml / min
= Milligrams of dye injected × 60 divided by
( Average concentration of dye in each milliliter of blood for the duration of the
curve ) × ( Duration of the curve in seconds ).
Indicator
Should be non – toxic
Mix evenly in the blood
Easy to measure conc.
Not alter CO or Blood flow

Evans blue (T-1824)
Radioactive isotopes
Cardiac output 2
Thermodilution
The indicator used is cold saline.
The saline is injected into the right atrium through one side of a double lumen catheter, and the temperature change in the blood is recorded in
the pulmonary artery, using a thermistor in the other, longer side of the
catheter.

The temperature change is inversely proportionate to the amount of
blood flowing through the pulmonary artery, i.e., to the extent that the
cold saline is diluted by blood.
This technique has two important advantages :
(1) The saline is completely safe; and
(2) The cold is dissipated in the tissues so there is no problem arising
that of recirculation.
Disadvantages of Invasive tech.
• Infection
• Hemorrhage
• Arrhythmia
• Ventricular fibrillation
• Higher values
Doppler with Echo
Wall movement and other aspects of cardiac function can be evaluated
by echocardiography, a noninvasive technique that does not involve
injections or insertion of a catheter.
In echocardiography, pulses of ultrasonic waves, commonly at a
frequency of 2.25 MHz, are emitted from a transducer that also
functions as a receiver to detect waves reflected back from various parts
of the heart.
Reflections occur wherever acoustic impedance changes, and a recording
of the echoes displayed against time on an oscilloscope provides a record
of the movements of the ventricular wall, septum, and valves during the
cardiac cycle.
When combined with Doppler techniques, echocardiography can be used
to measure velocity and volume of flow through valves.
Impedance Cardiography (ICG)
THANQ…

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Cardiac output 2

  • 1. CARDIAC OUTPUT - II - Dr. Chintan
  • 2. Factors regulating EDV (VR) Respiratory Pump: Intrapleural pressure more negative – IVC diameter ↑ & P↓ + Descent of diaphragm - ↑ intra abdominal P Cardiac Pump: Vis-a-tergo: forward push from behind by, systolic contraction + elastic recoil Vis-a-fronte: suction force from front by, ventricular systolic suction + ventricular diastolic suction
  • 3. Factors regulating EDV (VR) Muscle Pump: One way, superficial to deep, Presence of valves, Contract – compression - ↑ pressure – proximal valve open, Varicose veins – large, tortuous, bulbous Mean Circulatory / Systemic Filling Pressure (MCFP / MSFP): The pressure within the circulatory system when all flow is stopped, (e.g. by stopping the heart or clamping large vessels), Pressure gradient Resistance to blood flow between the peripheral vessels and the right atrium., Venous & arterial resistance
  • 5. Role of sympathetic system Heart rate and contractility are influenced by sympathetic innervation of the heart. Sympathetic innervation which releases epinephrine and norepinephrine, influences cardiac output through its alpha effect (peripheral vasoconstriction) and its beta 1 effect (increases heart rate and force of contraction). The alpha effect provides more preload by shunting blood to the core organs (including the heart). While the alpha effect can also increase afterload, sympathetic stimulation usually boosts cardiac output.
  • 6. Factors regulating Contractility ↑ contractility: Sympathetic, Catecholamines Xanthine, theophylline - ↓ cAMP Glucagon - ↑ cAMP Digitalis ↓ contractility: Parasympathetic CCF, MI Hypercapnia, hypoxia, acidosis - ↓ c AMP Antiarrhythmic, barbiturates
  • 8. Factors regulating Cardiac Output Intrinsic frank – starling significance (Heterometric): Pulmonary insufficiency Life saving in LVF PR, after load, BP ↑ Extrinsic (Homometric) – sympathetic system - ↑ contractility: EDV same, EF ↑ More complete emptying – ESV ↓ ↑ SV, ↑ BP Role of HR: ↑ HR - ↓ diastolic time - ↓ EDV - ↓ SV During exercise - ↑ sympathetic activity – marked ↑ in HR + moderate ↑ in SV - marked ↑ in CO
  • 9. Parameters that Increase Cardiac Output Atrial kick Adequate filling time Frank-Starling law – more myocardial stretch - Increased preload (to a limit) Low afterload Parameters that Reduce Cardiac Output Lack of atrial kick Inadequate filling time Frank-Starling Law – less myocardial stretch - Reduced preload (to a limit) High afterload Generally rates of 50-150/minute are associated with an acceptable cardiac output. Heart rates of less than 50/minute provide sufficient stroke volume but often an insufficient heart rate results in poor cardiac output. Rates of greater than 150/minute provide rapid heart rates but insufficient filling times and poor stroke volume.
  • 10. SUMMARY - REGULATION OF CARDIAC OUTPUT Neural Regulation ( VMC, CVC ) PRELOAD CARDIAC OUTPUT Cardiac Hormones Cardiac Reflexes HEART RATE × STROKE VOLUME CONTRACTILITY Chemoreceptors AFTERLOAD Baroreceptors Corticohypothalamic Descending Pathways SYMPATHETIC AND PARASYMPATHETIC SYSTEM
  • 11. Pathological Cardiac Output is increased in fever due to increased oxidative process. In anemia due to hypoxia. Hypoxia stimulates epinephrine increases over all heart activity. secretion which Same happens at high altitude. Increased metabolism in hyperthyroidism also increases cardiac output.
  • 12. Pathological CO is decreased in rapid arrhythmia due to incomplete filling. In Congestive Cardiac Failure due to weak contractions. In shock due to poor pumping & circulation. In incomplete heart block due to defective pumping. In hemorrhage due to reduction in blood volume. In hypothyroidism due to decreased overall metabolism.
  • 13. Pathological Heart attack, valvular disease, myocarditis, cardiac tamponade (filling of pericardial sac with fluid). Decreased venous return caused by: Reduced blood volume Venous dilatation Venous obstruction Decreased tissue mass
  • 14. Disease States Lowering Total Peripheral Resistance Beriberi: insufficient thiamine–tissues starve because they cannot use nutrients. AV fistula: e.g. for dialysis. Hyperthyroidism: Reduced resistance caused by increased metabolism Anemia (lack of RBCs): effects viscosity and transport of O2 to the tissues.
  • 15. Methods for measurement of CO Electromagnetic or Ultrasonic Flow meter The Oxygen Fick Principle Indicator Dilution Method: Dye dilution & thermodilution Doppler techniques (Transcutaneous Doppler & Transoesophageal Doppler) combined with echocardiography. Impedance Cardiography
  • 16. Electromagnetic flow meter A recording in a dog of blood flow in the root of the aorta shows that the blood flow rises rapidly to a peak during systole, and then at the end of systole reverses for a fraction of a second. This reverse flow causes the aortic valve to close and the flow to return to zero.
  • 17. The Oxygen Fick Principle Total 200 millilitres of oxygen are being absorbed from the lungs into the pulmonary blood each minute. The blood entering the right heart has an oxygen concentration of 160 millilitres per litre of blood, whereas that leaving the left heart has an oxygen concentration of 200 millilitres per litre of blood. Each litre of blood passing through the lungs absorbs 40 millilitres of oxygen. Because the total quantity of oxygen absorbed into the blood from the lungs each minute is 200 millilitres, dividing 200 by 40 calculates a total of five litre portions of blood that must pass through the pulmonary circulation each minute to absorb this amount of oxygen. Therefore, the quantity of blood flowing through the lungs each minute is 5 litres, which is also a measure of the cardiac output.
  • 18. The Oxygen Fick Principle Cardiac output L / min = O2 absorbed per minute by the lungs (ml/min) divided by Arteriovenous O2 difference (ml/L of blood ).
  • 19. The Oxygen Fick Principle Cardiac output L / min = O2 absorbed per minute by the lungs (ml/min) divided by Arteriovenous O2 difference (ml/L of blood ). The rate of oxygen absorption by the lungs is measured by the rate of disappearance of oxygen from the respired air, using any type of oxygen meter. Systemic arterial blood can then be obtained from any systemic artery in the body. Mixed venous blood is usually obtained through a catheter inserted up the brachial vein of the forearm, through the subclavian vein, down to the right atrium, and, finally, into the right ventricle or pulmonary artery.
  • 20. Indicator Dilution Method A small amount of indicator, such as a dye, is injected into a large systemic vein or, preferably, into the right atrium. This passes rapidly through the right side of the heart, then through the blood vessels of the lungs, through the left side of the heart and, finally, into the systemic arterial system. The concentration of the dye is recorded as the dye passes through one of the peripheral arteries, giving a curve. Cardiac output ml / min = Milligrams of dye injected × 60 divided by ( Average concentration of dye in each milliliter of blood for the duration of the curve ) × ( Duration of the curve in seconds ).
  • 21. Indicator Should be non – toxic Mix evenly in the blood Easy to measure conc. Not alter CO or Blood flow Evans blue (T-1824) Radioactive isotopes
  • 23. Thermodilution The indicator used is cold saline. The saline is injected into the right atrium through one side of a double lumen catheter, and the temperature change in the blood is recorded in the pulmonary artery, using a thermistor in the other, longer side of the catheter. The temperature change is inversely proportionate to the amount of blood flowing through the pulmonary artery, i.e., to the extent that the cold saline is diluted by blood. This technique has two important advantages : (1) The saline is completely safe; and (2) The cold is dissipated in the tissues so there is no problem arising that of recirculation.
  • 24. Disadvantages of Invasive tech. • Infection • Hemorrhage • Arrhythmia • Ventricular fibrillation • Higher values
  • 25. Doppler with Echo Wall movement and other aspects of cardiac function can be evaluated by echocardiography, a noninvasive technique that does not involve injections or insertion of a catheter. In echocardiography, pulses of ultrasonic waves, commonly at a frequency of 2.25 MHz, are emitted from a transducer that also functions as a receiver to detect waves reflected back from various parts of the heart. Reflections occur wherever acoustic impedance changes, and a recording of the echoes displayed against time on an oscilloscope provides a record of the movements of the ventricular wall, septum, and valves during the cardiac cycle. When combined with Doppler techniques, echocardiography can be used to measure velocity and volume of flow through valves.