cardiac output,

CARDIAC OUTPUT
 Stroke volume : amount of blood pumped by
each ventricle per beat. 70 -75ml
 Minute volume : amount of blood pumped by
each ventricle in one minute.
 SV × heart rate = 70×72 = 5 litres/min
 Cardiac index : amount of blood pumped out of
ventricle per minute per sq. mt. of body surface
area  2.8 – 3 L/ mt2. of body ( body surface area
of normal adult is 1.734 mt2 )

CARDIAC RESERVE
 maximum increase in
cardiac output above
normal value.
 e.g. excercise
 300 – 400 % in adults
 In cardiac disease :
reserve decrease or no
reserve

FACTORS AFFECTING CARDIAC OUTPUT
 Physiological:
1. Age
2. Gender
3. Diurnal variation
4. Environmental temperature
5. Emotions
6. Exercise, high altitude
7. Posture
8. Pregnancy
9. Sleep

PATHOLOGICAL FACTORS
 Increased CO:
Fever
Anemia
Hyperthyroidism
 Decreased CO:
Hypothyroidism
Heart block
Heart failure
Shock
Hemorrhage

DISTRIBUTION OF CARDIAC OUTPUT
 Liver : 1400 ml - 25%
 Kidneys : 1300 ml - 25%
 Skin, Subcutaneous tissue, Skeletal muscles :
1200ml - 25%
 Heart, lungs, brain : 1300 ml - 25%

REGULATION / FACTORS AFFECTING /
DETERMITANTS OF CO
CO = SV x HR
I. Venous return
II. Peripheral resistance control of SV (Intrinsic R)
III. Force of contraction
IV. Frequency of heart rate (Extrinsic R)

VENOUS RETURN (preload)  Frank Starling’s law
 Increased venous return,
increases cardiac output
 Respiratory pump : during
inspiration, venous return
increased, CO increases.
 Muscle pump : during exercise,
venous return increases, CO
increases
 Venomotor tone : sympathetic
stimulation  decrease volume of
capacitance vessels  increased
VR  increase CO.
 Gravity – upright posture decrease
VR
 Cardiac pump -

PERIPHERAL RESISTANCE
 Resistance offered by vessel wall
 Load (after load) against which heart has to pump the
blood.
 Afterload for the left ventricle is determined by aortic
pressure
 Afterload for the right ventricle is determined by
pulmonary artery pressure.
 Increased peripheral resistance (in old age &
atherosclerosis)  decreases cardiac output. (by
decreasing SV)

FORCE OF CONTRACTION
 Increase myocardial contractility increase CO.
 Sympathetic stimulation & increase circulating
catecholamines increase force of contraction of
myocardium. (Positive ionotropic effect)

FREQUENCY OF HEART BEAT
 CO directly proportional to HR (SV x HR)
 Adult HR is normally 80-100 beats per minute (bpm.)
 Heart rate is modified by autonomic, immune, and local
factors. For example:
a. An increase in parasympathetic activity via M2
cholinergic receptors in the heart will decrease the
heart rate.
b. An increase in sympathetic activity via B1 adrenergic
receptors throughout the heart will increase the heart
rate.
 But In extreme tachycardia, stroke volume decreased
(less diastolic filling), cardiac output decrease.

MEASUREMENT OF CARDIAC OUTPUT
A) Direct methods (animals):
Cardiometer, flowmeter
B) Indirect methods :
1. Fick’s principle
2. Dye dilution method
3. Thermodilution method
4. Echocardiography

FICK’S PRINCIPLE
Adolf Eugen Fick ( 1829 – 1901)
 Amount of substance taken per minute =
(A-V) diff. of substance blood flow/min
 Blood flow/min = amount of subst. taken per min
(A-V) diff. of that substance

 1) OXYGEN CONSUMPTION
 2) CO2 EVOLVED
1)CARDIAC = O2 CONSUMED (ml/min)
OUTPUT ARTERIOVENOUS DIFF.
O2 CONSUMED = BENEDICT ROTH APPARATUS
O2 CONTENT IN ARTERIAL BLD = FROM ARTERY
O2 CONTENT IN VENOUS BLOOD = CARDIAC
CATHETERISATION
CARDIAC OUTPUT = 250 * 100 = 5000ml/ min
20-15/100 ml 5

DYE DILUTION METHOD
 Based on how fast the flowing blood can dilute
the substances introduced into the circulation
 BLOOD FLOW = q
C (t2-t1)
q = CONCENTRATION OF DYE INJECTED
C = MEAN CONC. OF DYE
t1 = APPEARANCE OF DYE
t2 = DISAPEARANCE OF DYE

THERMAL DILUTION METHOD
 Indicator : cold saline  injected in to RA
 Temp. change in blood measure  in aorta by
thermostate
Temperature change in blood is inversely related to
blood flow from aorta. (depend on extent to which
cold saline diluted)

ECHOCARDIOGRAPHY
 Pulses of ultrasonic wave are used  frequency
2.25MHz
 Ultrasonic waves are emitted from a transdusers
which also act as receiver  to detect waves echo
from different parts of heart.
 Echoes are displaced against time on osciloscope.
 Recording of movements of ventricular wall,
septum, heart valves.
 Measurement of EDV, ESV, SV & ejection fraction.

BLOOD PRESSURE
 “ Lateral pressure exerted by column of blood
on wall of blood vessels ”
 Systolic pressure : maximum pressure during
systole = 100 to 140 mmHg
 Diastolic pressure : minimum pressure during
diastole = 70 to 90 mmHg
 Pulse pressure = SBP - DBP
 Mean BP = DP + 1/3 PP

 Functions :
1. To maintain sufficient pressure to keep blood
flowing through the blood vessels.
2. To provide force of filtration at the capillaries.

Normal blood pressure in different portion of
circulatory system

VARIATIONS IN BP
 Physiological factors affecting :
1. Age – SBP & DBP increase with age
2. Gender – male SBP more than female
3. Obesity – increase SBP & DBP
4. Diurnal variation – peak value in the evening
5. After meals – increase SBP
6. Sleep – decrease SBP
7. Exercise, emotions – increase SBP
• Pathological :
Hypertension : increased BP
Hypotension : decreased BP

FACTORS AFFECTING BP
1. Cardiac output
2. Heart rate
3. Peripheral resistance
4. Blood volume
5. Elasticity of blood vessels
6. Velocity of blood Flow
7. Diameter of blood Vessel
8. Viscosity of blood

BP = CO PR
 Cardiac output : Increased co, increases SBP
 Peripheral resistance:
Resistance offered in arterioles  Increase SBP
Elasticity of blood Vessels : inversely proportional
 Blood volume : directly proportional
 Venous return : directly proportional
 Velocity : inversely proportional (Bernoulli’s principle – in
tube or blood vessel some of kinetic energy of flow & pressure
energy is constant)
 Diameter of blood vessel : inversely prop.
 Viscosity : inversely proportional.

REGULATION OF BP
 Short term regulation : nervous
regulation
 Intermediate regulation
 Long term regulation : renal mechanism
 Hormonal regulation
 Local regulation

SHORT TERM REGULATION
 Nervous regulation can increase arterial BP to
double within 5-10 S & reduce to half within 10-40s
 Vasomotor center (VMC) : in medulla (anterolateral
part)  sympathetic outflow to CVS
(vasoconstrictor area-upper/ vasodilator area-lower )
 Cardiac vagal centre : in medulla in neucleus
ambigus  parasympathetic outflow to CVS (via
vagus nerve)
 Nucleus of tractus solitarius : receiving sensory
information from aortic & carotid baroreceptors &
chemoreceptors.

Autonomic outflow
to Cardiovascular
system

 Continuous Partial Constriction of the
Blood Vessels Is Normally Caused by
Sympathetic Vasoconstrictor Tone.

FACTORS AFFECTING VMC
1. BARORECEPTOR REFLEX
2. CHEMORECEPTORS REFLEX
3. CNS ISCHEMIC REFLEX
4. HIGHER CENTERS

BARORECEPTOR REFLEX Spray type nerve endings
 Stretch receptors  at bifurcation of common
carotid A & arch of aorta.
 Respond to change in mean BP
 Carotid sinus : IX cranial nerve  from CCA BR
 Arch of aorta : X cranial nerve  from AA BR
 Function:
Increased BP -> baroreceptors activated ->
suppresses VMC -> Stimulates cardioinhibitory
center -> vasodilatation -> decreased BP
 Response mainly to rapidly changing pressure than to
a stationery Pressure

Pressure
“Buffer”
Function of the
Baroreceptor
Control System

CHEMORECEPTORS
 Carotid body & aortic body.
 Nerve supply via IX and X nerves.
 Respond to change in chemicals in blood
(PaO2 , PaCO2 , H+ ION concentration)
 Decrease BP (<80mmHg)  decrease blood
supply  decrease O2 & increase CO2 
stimulate chemoreceptors that excites VMC 
increase BP

CNS ISCHEMIC REFLEX
 Emergency pressure control system
 operates between 15-50 mmHg SBP
 Cerebral ischemia  strong sympathetic
stimulation  to increase blood pressure up to 250
mmHg for 10-15 minutes.
 “Last ditch stand” mechanism
 Cushing’s reaction

HIGHER CENTERS
 In response to emotion
 Cerebral cortex area 13 (limbic A.) 
 To Hypothalamus (cortico - hypothalamic
descending pathway)  posterolateral portion of
hypothalamus causes excitation of VMC.
 Anterior hypothalamus cause mild excitation or
inhibition.

Intermediate regulation
 Begin to act within few minutes & reach full
function within a few hours.
I. Capillary fluid shift mechanism – mean
capillary pressure directly proportional to ABP
 change in fluid filtration & reabsorption at
capillary level.
II. Stress relaxation & reverse stress relaxation
mechanism : by local vascular tone adjustment
in blood storage organ like veins, liver, spleen,
lungs  in response to change in ABP

LONG TERM (RENAL) REGULATION OF BP
By regulation of extracellular fluid volume
* ABP more excretion of water and salt by
kidneys
Pressure diuresis (water exc.)
Pressure natriuresis (Na+ exc.)
 ABP retention of salt and water by kidneys
(by direct mechanism & indirect mechanism –
renin angiotensin mechanism)

SEC. OF
ALDOSTERONE
Renin angiotensin
mechanism
Presure diuresis &
pressure natriuresis

HORMONAL REGULATION
Increase BP
 Adrenaline, noradrenaline
 Thyroxin
 Aldosterone
 Vasopressin
 Angiotensin
 Serotonin

Decreased BP
 VIP
 Bradykinin
 Prostaglandins
 Histamine
 Acetylcholine
 Atrial natriuretic peptide

MEASUREMENT OF BP
 DIRECT : insertion of canulla in to artery & connect it
to manometer.
 INDIRECT : by Sphygmomanometer – two methods
# palpatory
# auscultatory

HYPERTENSION
 Hypertension is a sustain increase of systemic
arterial blood pressure.
 Two types :
 Primary or essential HT: benign, malignant
 Secondary HT:
1. CVS - atherosclerosis
2. Endocrine - Cushing syndrome
3. Renal - tumour of JG cells & stenosis of renal
arteries
4. Neurogenic - increased intracranial pressure
(Cushing’s reaction)
5. During pregnancy (eclampsia)

One kidney “Goldblatt
hypertension”

 Primary or essential HT :
 When ABP is persistently more than 150/90 mmHg
 benign : in early stages increase up to 210/110
during stress condition. In late stages remain above
210/110.
Malignant : ABP increase up to 260/150. so death
occurs within 6M to 2Yr.
Compensatory cardiac hypertrophy
Thickening of wall of small arteries & arterioles.
Myocardial infarction
Renal failure

MANIFESTATIONS
 Renal failure
 Left ventricular failure
 Myocardial infarction
 Cerebral hemorrhage
 Retinal hemorrhage

TREATMENT
 Beta blockers – B1 blockers – Atenolol, Metoprolol
 Calcium channel blockers – Verapamil, Amlodipin
 Vasodilators- Nitroglycerin
 Diuretics – Furosemide, Thiazide, Spironolactone
 ACE inhibitors – Analapril, Captopril

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