Transcript Cardiovascular response to extreme circumstances

Control of the cardiovascular
system
Reverend Dr. David C.M. Taylor
School of Medical Education
[email protected]
http://pcwww.liv.ac.uk/~dcmt/cvs09.ppt
What is the role of the
cardiovascular system?
Blood Pressure
Depends upon the amount of blood
leaving the heart

cardiac output
and the resistance of the vasculature

total peripheral resistance
Peripheral Resistance
Which will give the greater flow ?
Peripheral resistance 2
Which will give the greater flow ?
Cardiac Output
Heart rate x stroke volume
End diastolic volume - End systolic volume
Stroke volume
Cardiac output
Heart rate
Factors affecting stroke
volume
Preload
Contractility
Afterload
increased enddiastolic volume
stretches the heart
cardiac muscles
stretch and contract
more forcefully

Frank-Starling Law of
the heart
Tension developed %
Preload
100
80
60
40
20
40 60 80 100 120 140 160
Percentage sarcomere length
(100% = 2.2 µm)
Tension developed %
Starling’s Law
2.2 m
1.8 m
3.8 m
100
80
60
40
20
40
60
80
100
120
140
160
Percentage sarcomere length (100% = 2.2 m)
Contractility-”Inotropic effect”
positive inotropic
agents
increase available
intracellular Ca2+
increase number of
actinomyosin
binding sites
increase force of
contraction
positive inotropic
agents
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
sympathetic
stimulation
catecholamines
glucagon
thyroid hormones
increased
extracellular Ca2+
Afterload
decreased arterial
blood pressure
during diastole
decreased afterload
semilunar valves
open sooner when
blood pressure in
pulmonary artery &
aorta is lower
afterload

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blood pressure
viscosity of blood
elasticity of arteries
Stroke Volume
Cardiac Output
Heart Rate
Heart Rate
Nervous system
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
increased sympathetic
decreased parasympathetic
Chemicals
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catecholamines
thyroid hormones
moderate Ca2+ increase
Heart Rate 2
Other factors
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age
gender
“fitness”
body temperature
Pacemaker activity
The rhythm of the
pump is provided by
the pacemaker
activity of some
specialized muscle
cells in the wall of
the right atrium -
the sinoatrial node
0
mV
-70
0
mS
300
Chronotropic effect
0
mV
-70
0
mS
300
Hypertension
David Taylor
School of Medical Education
Hypertension
Excellent article:

ABC of Hypertension: The pathophysiology
of hypertension, Beevers G, Lip GYH and
O’Brien E (2001) BMJ, 322:912-916
Upto 5% of patients with hypertension
have it as secondary to some other
disease (e.g. renal disease)
The rest have “essential hypertension”
The story so far...
http://pcwww.liv.ac.uk/~dcmt/cvs09.ppt
intrinsic (Starling’s Law)
extrinsic (principally autonomic)
Stroke volume
Cardiac output
Heart rate
Postulated mechanism
Increased sympathetic activity

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Leads to increased cardiac output
And peripheral vasoconstriction (to protect
the capillary beds)
Drop in blood flow

Triggers renin-angiotensin system
Evidence
Cross transplantation studies show that
essential hypertension has its origins in
the kidneys.

Human and animal studies
Little evidence that “stress” is involved
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But, of course, drugs that decrease
sympathetic activity lower blood pressure.
Control
Autonomic N.S.
Volume
ADH
Pressure
Chemicals
Local Blood
Flow
Angiotensin
Pressure
Sensed by baroreceptors

in carotid arteries and aortic arch
an increase in pressure causes a
decrease in sympathetic activity
a decrease in pressure causes an
increase in sympathetic activity
Volume
Sensed by atrial volume receptors
A decrease in volume
causes an increase in ADH secretion
and a decrease in ANF secretion
Chemicals
A decrease in O2, or more usually an
increase in CO2 or H2 causes an increase
in chemoreceptor activity which
increases sympathetic activity
Local Blood Flow (kidney)
Decreased renal blood flow
Monitored by JGA cells
Renin production
Angiotensinogen
Angiotensin I
Converting enzyme
Angiotensin II
Sodium reabsorption
Aldosterone
Potassium secretion
Vasoconstriction
Hormones
Angiotensin II is a vasoconstrictor
Aldosterone increases vascular
sensitivity to Angiotensin II
ADH (anti-diuretic hormone) increases
water reabsorption
ANF decreases sodium reabsorption
Overview
ADH
Fluid loss
Arterial pressure
Blood volume
Venous return
heart rate
vol
sympathetic
contractility
vasoconstriction
Cardiac output
baro
Arterial pressure
chemo
CNS
Cardiac output
Venous return
veins
capillary
pressure
Blood volume
Local blood flow
kidney
renin/angiotensin
aldosterone
Shock
David Taylor
School of Medical Education
Shock
Stage 1 Compensated/Nonprogressive

mechanisms work as planned
Stage 2 Decompensation/Progressive
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if blood volume drops more than 15 - 25%
Stage 3 Irreversible
Progressive shock
depression of cardiac activity

bp <60 mmHg poor flow through coronary
arteries leads to ischemia
depression of vasoconstriction
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bp 40 - 50 mmHg
increased capillary permeability

caused by hypoxia
clotting, cell destruction, acidosis