cardiac output 2

CARDIAC OUTPUT-

IIDR NILESH KATEASSOCIATE PROF

DEPARTMENT OF PHYSIOLOGY.

Wednesday, May 3, 2023

OBJECTIVES. Regulation of cardiac output. Control mechanisms. Extrinsic & intrinsic. Role of heart rate in cardiac output Integrated control. Heart lung preparation. Cardiac & vascular function curves.


REGULATION OF CARDIAC OUTPUT.

Since CO = SV × HR SO main factors

controlling are Venous return Myocardial

contractility Peripheral resistance Heart rate.


CARDIAC OUTPUT CONTROL MECHANISMS.

Intrinsic. Respiratory pump. Cardiac pump. Muscle pump. Blood volume. Sympathetic discharge. Standing body position. Resistance to venous

return.

Extrinsic. Sympathetic activity. Parasympathetic

activity.


INTRINSIC MECHANISMS. Based on Frank Starling’s

mechanism/law –

“Within Physiological limits the force of contraction of cardiac muscle is directly proportional to initial length of muscle fibre.”

Initial length of muscle fibre decided by condition of muscle before contraction – affected by End-diastolic Volume.


FRANK-STARLING CURVES LENGTH – TENSION RELATIONSHIP.


FACTORS AFFECTING END-DIASTOLIC VOLUME.

Respiratory pump. Cardiac pump. Muscle pump. Blood volume. Sympathetic discharge. Standing body position. Resistance to venous

return.


RESPIRATORY PUMP. Intrapleural pressure Diameter of IVC

increased – pressure decreased

Increased blood flow to right atrium during inspiration.


CARDIAC PUMP. VIS – A- TERGO Forward push from

behind. Due to myocardial

contraction during systole & elastic recoil of arterial wall (windkessel effect)

VIS – A – FRONTE. Suction force acting

from front which pulls the blood from great veins into right atrium. Ventricular systolic

suction Ventricular diastolic

suction.


MUSCLE PUMP. Working of muscle

pumps. During contraction During relaxation. With rhythmic

contraction – blood is squeezed to the heart.

Applied – Varicose Veins


BLOOD VOLUME. Mean circulating filling

pressure (MCFP) Mean systemic filling

pressure.(MSFP) – equilibrated pressure everywhere in circulation at rest.

It influences venous return. VR

More MSFP – More VR.

Relationship of MSFP & Venous Return.


BLOOD VOLUME. MCFP – depends upon

level of blood volume.

Relationship of MCFP & blood volume.


SYMPATHETIC DISCHARGE. Sympathetic stimulation Increase venous tone Decrease venous system

capacity- MCFP increases – increase VR

At normal blood volume sympathetic stimulation raises MCFP from 7 to 17 mm Hg & Inhibition lowers MCFP 7 to 4 mmHg.


STANDING BODY POSITION. Prolonged standing –

more venous pooling – decrease venous return.


RESISTANCE TO VENOUS RETURN. 2/3rd by Veins & 1/3rd by Arteries. Decrease resistance to half increases venous

return twice & vice –versa. Relation of VR & resistance.


EXTRINSIC MECHANISMSAUTONOMIC NEURAL MECHANISM.

Increase in stroke volume due to increase in myocardial contractility without change in initial muscle length.

Homometric mechanism.

Sympathetic activity. Parasympathetic

activity.


SYMPATHETIC ACTIVITY. Stimulation of

sympathetic nerves. Positive inotropic effect –

i.e. increase in maximal velocity of shortening.

Inhibition of sympathetic. When sympathetic

inhibited pumping decreases by 30%


CHARACTERISTICS OF INCREASED MYOCARDIAL CONTRACTILITY.

Mechanism – activation of B1 adrenergic receptors– activation of Adenyl cyclase – increase intracellular Camp – rapid intake of Ca via protein kinase.

Ventricle contracts more forcefully

EDV – Decreased.


PARASYMPATHETIC ACTIVITY. Negative Inotropic

Effect. Effect not much

pronounced as vagal fibres supply mainly atria not ventricles.


ROLE OF HEART RATE IN CARDIAC OUTPUT.

SINCE CO = HR × SV But if HR increased alones

CO not changes as increase HR decrease diastolic time & EDV

During exercise increase HR along with Chronotropic (Rate)effect increases CO.


INTEGRATED CONTRL OF CARDIAC OUTPUT.

Interaction of frank starling mechanism & myocardial contractility. Shift to left – Increased

myocardial contractility Shift to right - Decreased

myocardial contractility


INCREASED MYOCARDIAL CONTRACTILITY

Sympathetic stimulation – β adrenergic receptors.

Catecholamine. Xanthenes – caffeine,

Theophylline , inhibit breakdown of cAMP

Glucagon- increase cAMP Digitalis & related drugs –

Inhibitory effect on Na-K-ATPase.


DECREASED MYOCARDIAL CONTRACTILITY

Parasympathetic (vagal) stimulation.

Heart failure. Myocardial infarction. Hypercapnia, hypoxia &

acidosis decrease in cAMP Drugs – Quinidine,

Procainamide, Barbiturates


HEART LUNG PREPARATION. To demonstrate effect

of various factors on activities of Heart.


USES OF HEART LUNG PREPARATION

Effect of venous return on stroke volume ( Frank starling mechanism)

Effect of sympathetic stimulation on SV.

Combined effect of both. Effect of peripheral

resistance on CO. Cardiac Function Curves.


CARDIAC FUNCTION CURVES. It’s the graphical

analysis of CO, capacity of ventricles to pump & relationship between CO & CVP

Useful in patients with cardiac failure.

Normal cardiac function curve.


HYPER EFFECTIVE CARDIAC FUNCTION CURVE.

Sympathetic stimulation of heart.

Heart hypertrophy.


HYPO EFFECTIVE CARDIAC FUNCTION CURVE.

Reduced sympathetic discharge.

Decreased ventricular compliance, in MI, myocarditis.

Insufficient pumping ; valvular, septal defects

Reduced ventricular filling. Increased load


VASCULAR FUNCTION CURVES. Reflects relationship

between venous return & venous pressure.

Normal

Effect of increased blood volume.


CARDIOVASCULAR FUNCTION CURVES.

Normal During exercise In CCF.


Thank you.


cardiac output 2

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