This document discusses cardiac output and the factors that affect it. It defines key terms like stroke volume, minute volume, cardiac index and cardiac reserve. It describes physiological factors like age, gender, exercise and posture as well as pathological factors like fever, anemia and heart failure that can impact cardiac output. The document also covers methods of measuring cardiac output like Fick's principle, dye dilution and thermodilution techniques.
1. 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 )
2.
3. 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
4. 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
6. 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%
7. 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)
8. 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 -
9. 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)
10. FORCE OF CONTRACTION
Increase myocardial contractility increase CO.
Sympathetic stimulation & increase circulating
catecholamines increase force of contraction of
myocardium. (Positive ionotropic effect)
11. 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.
12.
13. 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
14. 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
15. 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
16.
17. 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
19. 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)
20. 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.
21. 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
22. Functions :
1. To maintain sufficient pressure to keep blood
flowing through the blood vessels.
2. To provide force of filtration at the capillaries.
24. 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
25. 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
26. 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.
27. REGULATION OF BP
Short term regulation : nervous
regulation
Intermediate regulation
Long term regulation : renal mechanism
Hormonal regulation
Local regulation
28. 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.
34. 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
37. 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
38. 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
39. 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.
40. 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
41. 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)
45. MEASUREMENT OF BP
DIRECT : insertion of canulla in to artery & connect it
to manometer.
INDIRECT : by Sphygmomanometer – two methods
# palpatory
# auscultatory
46. 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)
48. 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