Cardiac output 2
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CARDIAC OUTPUT-
IIDR NILESH KATEASSOCIATE PROF
DEPARTMENT OF PHYSIOLOGY.
Wednesday, May 3, 2023
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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.
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REGULATION OF CARDIAC OUTPUT.
Since CO = SV × HR SO main factors
controlling are Venous return Myocardial
contractility Peripheral resistance Heart rate.
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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.
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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.
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FRANK-STARLING CURVES LENGTH – TENSION RELATIONSHIP.
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FACTORS AFFECTING END-DIASTOLIC VOLUME.
Respiratory pump. Cardiac pump. Muscle pump. Blood volume. Sympathetic discharge. Standing body position. Resistance to venous
return.
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RESPIRATORY PUMP. Intrapleural pressure Diameter of IVC
increased – pressure decreased
Increased blood flow to right atrium during inspiration.
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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.
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MUSCLE PUMP. Working of muscle
pumps. During contraction During relaxation. With rhythmic
contraction – blood is squeezed to the heart.
Applied – Varicose Veins
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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.
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BLOOD VOLUME. MCFP – depends upon
level of blood volume.
Relationship of MCFP & blood volume.
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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.
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STANDING BODY POSITION. Prolonged standing –
more venous pooling – decrease venous return.
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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.
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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.
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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%
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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.
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PARASYMPATHETIC ACTIVITY. Negative Inotropic
Effect. Effect not much
pronounced as vagal fibres supply mainly atria not ventricles.
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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.
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INTEGRATED CONTRL OF CARDIAC OUTPUT.
Interaction of frank starling mechanism & myocardial contractility. Shift to left – Increased
myocardial contractility Shift to right - Decreased
myocardial contractility
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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.
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DECREASED MYOCARDIAL CONTRACTILITY
Parasympathetic (vagal) stimulation.
Heart failure. Myocardial infarction. Hypercapnia, hypoxia &
acidosis decrease in cAMP Drugs – Quinidine,
Procainamide, Barbiturates
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HEART LUNG PREPARATION. To demonstrate effect
of various factors on activities of Heart.
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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.
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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.
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HYPER EFFECTIVE CARDIAC FUNCTION CURVE.
Sympathetic stimulation of heart.
Heart hypertrophy.
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HYPO EFFECTIVE CARDIAC FUNCTION CURVE.
Reduced sympathetic discharge.
Decreased ventricular compliance, in MI, myocarditis.
Insufficient pumping ; valvular, septal defects
Reduced ventricular filling. Increased load
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VASCULAR FUNCTION CURVES. Reflects relationship
between venous return & venous pressure.
Normal
Effect of increased blood volume.
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CARDIOVASCULAR FUNCTION CURVES.
Normal During exercise In CCF.
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Thank you.
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