Cardiac Output 3.

Indicator dilution method

 Definition – amount of blood ejected by Fick Principle
each ventricle per minute
Amount of a substance taken up by an organ or
 Normal – 5 L/min (av)
by the whole body per unit of time is equal to the
 Cardiac output = Stroke volume x Heart
arteriovenous difference of the substance times
rate
blood flow.
Cardiac Index
 Cardiac output divided by body surface
area.

Regulation of Cardiac Output

 Used to standardize cardiac output among 1. Extrinsic autoregulation – Heart Rate

individuals of different body sizes.
a) By cardiac innervation by autonomic
Cardiac Reserve
nervous system – sympathetics increase
 Amount of blood that can be pumped by heart rate, parasympathetics decrease
each ventricle in excess of normal cardiac b) Cardiac centres in medulla
output.  Vasomotor centre (VMC)
 15 – 25 L/min – non-athletes  Cardiovascular centre (CVC)
 20 – 40 L/min – athletes
2. Intrinsic autoregulation – Stroke Volume
Variations in Cardiac Output
 No change: a) Heterometric regulation
o During sleep a. Preload – EDV
o Moderate changes in env temp i. Venous return
 Increase: ii. Ventricular filling
o Anxiety and excitement (50-100%) b. Afterload
o Eating (30%) i. BP – peripheral resistance
o Exercise (up to 100%) ii. Blood volume
o High env temp b) Homometric regulation
o Pregnancy a. Myocardial contractility – inc, dec
o Epinephrine Heterometric Regulation
 Decrease:
1. Preload
o Sitting or standing from lying posture
 End diastolic volume is considered as
(20-30%) – orthostatic hypotension
preload
o Rapid arrhythmias
 The extent to which ventricle is distended
o Heart disease
(stretched) depends on the degree of end-
Methods of Measurement diastolic filling of the ventricle
 Stroke volume varies at various
1. Doppler combined with echocardiography
ventricular muscle lengths - this is also
2. Direct Fick method
 known as heterometric autoregulation of 2. Elastic recoil of arterial wall (Windkessel
cardiac output. effect)
 The end diastolic filling of ventricle  Increases VR to heart
depends on venous return and ventricular
filling.  Vis-a-fronte
 Force acting from front (pulling
a) Venous Return force) to attract blood in veins
towards heart.
i) Skeletal muscle pump  Ventricular systolic suction:
 Movement results in rhythmic 1. In VS, AV junction descends and enlarges
contraction of skeletal muscle which atria and venae cavae
compresses veins and increases 2. Atrial pressure decreases and blood moves
venous return to heart. into atria from SVC and IVC
 Frequent, powerful rhythmic movt –  Ventricular diastolic suction:
muscle pumping, increases venous 1. In VD, opening of AV valves leads to rapid
return flow of blood from atria to ventricles.
 Standing - pooling of blood occurs in 2. Sudden decrease in atrial pressure pulls
the leg veins due to absence of blood from great veins.
muscle activity that decreases 3. Increases VR into atrium.
venous return.
iv) Total blood volume
ii) Thoracic or respiratory pump  Increase in TBV increases VR.
 Negative intrathoracic pressure: -2  Increased VR in pregnancy:
mmHg  Volume of plasma increases during
 During inspiration, the intrathoracic pregnancy – hemodilution
pressure becomes more negative  Constriction of veins decreases
due to expansion of thoracic cage. their capacitance.
 So, less pressure over larger veins  Size of venous reservoir decreases,
and arteries – increased pressure decreased venous pooling, so
gradient of blood flow towards heart. increases VR.
 Thus, VR to heart is increased.  Hypovolemic shock – decrease in TBV
 Less negative intrathoracic pressure leads to decrease in VR
– VR decreased  Distributive shock – normal blood vol,
 Descent of diaphragm increases but increased vasodilation leads to
intraabdominal pressure – squeezes decrease in VR
blood out of abdomen and towards
heart. Blood is not pushed towards v) Venous tone
leg veins as they are guarded by  Veins – capacitance vessels
venous valves. Thus VR increases.  Smooth muscles in walls of veins
determine venous tone.
iii) Cardiac pump  Increased sympathetic activity →
 Vis-a-tergo increases venous tone → increases VR
 Force from behind which drives → increased cardiac output
blood forward (pushing force). vi) Posture and gravity
 Types  Standing – peripheral venous pooling
1. Contraction of heart during the time when → decreases VR
blood passes through it (systole)  Lying down posture – maximum VR
 vii) Myocardial compliance i. Heart must make a greater
 Compliance refers to stretchability of effort to pump into a high-
myocardial tissue. pressure area
 After myocardial infarction, dead part ii. This causes muscle cells to
of myocardium becomes fibrotic and proliferate and enlarge →
non-functional → affects wall mobility hypertrophy
 So ventricular compliance decreases  Aortic stenosis
and VR decreases → cardiac output i. Narrowing of opening of valves
decreases. ii. Intra-ventricular pressure if not
 Infiltrative diseases of the heart – decreased → systolic volume
decreased VR due to increased intra- decreases → decreased cardiac
pericardial pressure output
 Aortic regurgitation
b) Ventricular Filling – decreased myocardial i. Blood comes from aorta into
distensibility decreases VF chamber → increased EDV →
increased systolic volume
i) Atrial contraction – 30% of ventricular ii. Little change in aortic
filling impedance
ii) Intrapericardial pressure – pericardial
Heart-Lung Preparation
effusion increases intrapericardial
pressure → decreases VF  Method to study cardiac output – to study
effects of preload and afterload.
2. Afterload o Isolate the heart and lungs and
 Afterload is the resistance to flow against connect to reservoir – right atrium →
which the ventricle has to pump. right ventricle → lungs
i) Blood pressure o Systemic circulation is bypassed
 Lateral pressure exerted on wall of o Only pulmonary circulation is
arteries by blood maintained
 Transmitted pressure o Respiration is maintained by
 Directly related to CO intubation
ii) Peripheral resistance o Brain is removed
 In the left ventricle, aortic o Changes:
impedance is afterload  Adjust the calibre of the tubing
 Aortic pressure = 7 x pulmonary  Adjust the volume in the
artery pressure reservoir
 Stroke work of LV = 7 x stroke work o Length of muscle fibres increases
of RV with increase in blood volume →
 Aortic impedance – hydrostatic increase in force of contraction →
pressure of blood in aorta which increased systolic volume →
opposes ventricular ejection increased cardiac output
i. Acts as a load against  Preload is more important than afterload
ventricular shortening in stroke volume regulation.
(resistance against which
ventricles pump blood)
 Long standing systemic Homometric Regulation
hypertension → LV hypertrophy
 Cardiac output is changed without change
in initial length of muscle fibres
  Myocardial contractility  During respiratory phases - Sinus
o Affected by factors acting on heart Arrhythmia
from outside o HR is increased during inspiration
o Myocardial contractility in increased and decreased during expiration
without any change in muscle length o Causes:
o Neural factors –  Impulses from the respiratory
 Sympathetics (↑) system act on Nucleus Tractus
 Parasympathetics (↓) Solitarius (NTS) and decrease
 Higher centres, spinal cord, the vagal tone.
medulla, spinal cord,  Increased intra-thoracic
hypothalamus etc pressure increases atrial filling
o Chemical factors – and thus increases HR.
 Blood chemistry (hypoxia,  Bainbridge reflex
acidosis, hypercapnia ↓)  After meals & during pregnancy - HR
 Catecholamines (↑) increases
 Glucagon, thyroxine  Effect of posture- standing increases HR
 Xanthines, quinidine,  HR is lower in athletes and in sleep
procainamide, digitalis (↑),  Tachycardia – infancy, excitement, anger,
propranolol, calcium (↑), exercise, inspiration, increased temp (10
calcium channel blockers (↓), β- beats increase for every 1o F rise), high
blockers (↓) altitude, extreme pain, in females
 Bradycardia – sleep, expiration, well-
Ejection Fraction
trained athletes
 Percentage of EDV that is ejected with
each heartbeat. 2. Pathological
 EF = SV/EDV x 100 = 60-65%  Increased HR – shock, hemorrhage, fever,
 Measure of ventricular contractility. hyperthyroidism
 Decreased HR – intracranial tension, heart
Heart Rate
block, myxedema, in viral infections
 Normal – 60-90 beats/min, average – 70
Applications
beats/min
 Ejection Fraction - Amount or Percentage of
Variations
blood ejected out per minute = stroke
1. Physiological volume/end diastolic volume
 Species – rat – 300/min, elephant –  A normal ejection fraction is about 50% to
25/min 75%, Av: 65% (American Heart Association).
 Age  A borderline ejection fraction can range
o In utero- 150-160 beats/min between 41% and 50%.
o At birth- 130-140 beats/min  Heart Rate Variability is an important
o At 10 years- 100 beats/min marker of Baro-Receptor Sensitivity and is
o Adolescence-72 beats/min used routinely to assess Cardiac Autonomic
o Old age- higher HR Neuropathy (CAN) Cardiovascular Risk in
 Gender – females have higher HR than metabolic, endocrine and cardiovascular
males disorders.
 Exercise - HR increases due to increased
sympathetic activity, decrease in vagal
tone, increase in temperature, release of
adrenal medullary catecholamines Regulation of Heart Rate
1. Neural Factors increases Ca2+ permeability, decreases
K+ efflux.
a) Autonomic Regulation o Effect –
 Positive chronotropic effect - ↑
I. Cardiac Innervation HR
 Positive inotropic effect - ↑ force
 Both parasympathetic and sympathetic of contraction
divisions of autonomic nervous system  Positive dromotropic effect - ↑
influence heart rate. rate of conductivity
 The intrinsic heart rate is the rate of  Positive bathmotropic effect - ↑
discharge of SA node when the heart is excitability
completely denervated. It is about 110 per o Sympathetic tone – to blood vessels,
minute. This indicates that the heart rate is maintains BP, increased in fright, flight,
more in the absence of neural influences. fight and haemorrhage.
 Sympathetic nervous system
o Sympathetic vasomotor nerve fibres  Parasympathetic nervous system
leave the spinal cord through T1 to T5 o Carried through two vagi: right vagus –
– cardiac nerves. SA node, left vagus – AV node.
o They then pass immediately into a o Pre-ganglionic fibres – long, myelinated.
sympathetic chain, one of which lies o Arise from nucleus ambiguous in
on each side of the vertebral column. medulla, dorsal nucleus of vagus (CIC).
o Superior and middle cardiac ganglia o Synapse in ganglia located within
supply SA node – mainly right superficial and deep cardiac plexuses
sympathetic nerves. and walls of atria.
o Inferior cardiac ganglion supplies AV o Post-ganglionic fibres – short,
node – mainly left sym nerves. unmyelinated
o Via cardiac nerves, sympathetics o No motor fibres from vagus to
supply nodal tissues and muscles of ventricles.
atria and ventricles (mainly by left sym o Fibres are endocardiac.
nerves) o Neurotransmitter – acetylcholine
o Effect –
 Negative chronotropic effect – ↓
HR
 Negative inotropic effect - ↓ force
of contraction (in atria only)
 Negative dromotropic effect - ↓
rate of conduction
 Negative bathmotropic effect - ↓
excitability (atria only)
o Mechanism - ↑ K+ , ↓ Ca2+ permeability

Vagal Tone
 Continuous stream of inhibitory impulses
to heart from CIC via vagus.
 Keeps HR constant
o Norepinephrine released from post-  Strong stimulation of vagus – heart stops
ganglionic sympathetic nerve endings in diastole; heart starts pumping 10 sec
activates β1 – adrenoceptors →
 later at a slower rate called idioventricular
rhythm – vagal escape.
 If vagus is cut – HR ↑ to 150 – 180/min
 If sympathetics also cut – HR ↑ to
100/min
 Effect of sympathetic and
parasympathetic stimulation on HR

 Vagal tone ↑ - HR ↓ (athletes)

 Vagal tone ↓ – HR ↑
 Vagus is blocked by atropine – HR ↑ from
70/min to 150 – 180/min
 Vagal tone is controlled by sino-aortic
reflex.

I. Peripheral Vascular Innervation

1. Vasoconstriction
 By sympathetic vasoconstrictor
nerves arising from IMLC from T1 to
L2 spinal segments