Cardiac output 2

CARDIAC
OUTPUT-
II
DR NILESH KATE
ASSOCIATE PROF
DEPARTMENT OF PHYSIOLOGY.
Thursday, February 4, 2016

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 MECHANISMS
AUTONOMIC 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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