cardiac output 2

27
II - Dr. Chintan

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Page 1: Cardiac output 2

CARDIAC OUTPUT - II- Dr. Chintan

Page 2: Cardiac output 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 recoilVis-a-fronte: suction force from front by,ventricular systolic suction + ventricular diastolic suction

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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

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Role of sympathetic systemHeart 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.

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Factors regulating Contractility↑ contractility:Sympathetic, CatecholaminesXanthine, theophylline - ↓ cAMPGlucagon - ↑ cAMPDigitalis

↓ contractility:ParasympatheticCCF, MIHypercapnia, hypoxia, acidosis - ↓ c AMPAntiarrhythmic, barbiturates

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Frank – starling curve

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Factors regulating Cardiac OutputIntrinsic frank – starling significance (Heterometric):Pulmonary insufficiencyLife saving in LVFPR, after load, BP ↑

Extrinsic (Homometric) – sympathetic system - ↑ contractility:EDV same, EF ↑More complete emptying – ESV ↓↑ SV, ↑ BP

Role of HR:↑ HR - ↓ diastolic time - ↓ EDV - ↓ SVDuring exercise - ↑ sympathetic activity – marked ↑ in HR + moderate ↑ in SV - marked ↑ in CO

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Parameters that Increase Cardiac OutputAtrial kickAdequate filling timeFrank-Starling law – more myocardial stretch - Increased preload (to a limit)Low afterload

Parameters that Reduce Cardiac OutputLack of atrial kickInadequate filling timeFrank-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.

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SUMMARY - REGULATION OF CARDIAC OUTPUT

Neural Regulation

( VMC, CVC )

Cardiac Hormones

Cardiac Reflexes

Chemoreceptors

Baroreceptors

Corticohypothalamic Descending Pathways

HEART RATE STROKE VOLUME

PRELOAD

CONTRACTILITY

AFTERLOAD

×

CARDIAC OUTPUT

SYMPATHETIC AND PARASYMPATHETIC

SYSTEM

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PathologicalCardiac Output is increased in fever due to increased oxidative process.

In anemia due to hypoxia. Hypoxia stimulates epinephrine secretion which increases over all heart activity.

Same happens at high altitude.

Increased metabolism in hyperthyroidism also increases cardiac output.

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PathologicalCO 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.

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PathologicalHeart attack, valvular disease, myocarditis, cardiac tamponade (filling of pericardial sac with fluid).

Decreased venous return caused by:Reduced blood volumeVenous dilatation Venous obstruction

Decreased tissue mass

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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.

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Methods for measurement of COElectromagnetic 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

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Electromagnetic flow meterA 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.

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The Oxygen Fick PrincipleTotal 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.

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The Oxygen Fick PrincipleCardiac output L / min

= O2 absorbed per minute by the lungs (ml/min) divided by Arteriovenous O2 difference (ml/L of blood ).

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The Oxygen Fick PrincipleCardiac 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.

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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 ).

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Indicator Should be non – toxicMix evenly in the bloodEasy to measure conc.Not alter CO or Blood flow

Evans blue (T-1824)Radioactive isotopes

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ThermodilutionThe 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.

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Disadvantages of Invasive tech.

• Infection

•Hemorrhage

•Arrhythmia•Ventricular fibrillation

•Higher values

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Doppler with EchoWall 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.

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Impedance Cardiography (ICG)

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THANQ…