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Cardiovascular system in its context
Reverend Dr. David C.M. TaylorSchool of Medical [email protected]://pcwww.liv.ac.uk/~dcmt/cvs06.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 Heart rate
Cardiac output
Factors affecting stroke volume
Preload Afterload
Contractility
Preload
increased end-diastolic volume stretches the heart
cardiac muscles stretch and contract more forcefully Frank-Starling Law
of the heart 40 60 80 100 120 140 160
Percentage sarcomere length (100% = 2.2 µm)
100
80
60
40
20T
ensi
on d
evel
oped
%
Starling’s Law
40 60 80 100 120 140 160Percentage sarcomere length (100% = 2.2 m)
100
80
60
40
20
Ten
sion
dev
elop
ed %
1.8 m2.2 m
3.8 m
Contractility-”Inotropic effect”
positive inotropic agentsincrease available intracellular Ca2+
increase number of actinomyosin binding sitesincrease force of contraction
positive inotropic agents sympathetic
stimulation catecholamines glucagon thyroid hormones increased
extracellular Ca2+
positive inotropic agents sympathetic
stimulation catecholamines glucagon thyroid hormones increased
extracellular Ca2+
Afterload
decreased arterial blood pressure during diastoledecreased afterloadsemilunar valves open sooner when blood pressure in pulmonary artery & aorta is lower
afterload
blood pressure viscosity of blood elasticity of
arteries
afterload
blood pressure viscosity of blood elasticity of
arteries
Stroke Volume
Heart Rate
Cardiac Output
Heart Rate
Nervous system increased sympathetic decreased parasympathetic
Chemicals catecholamines thyroid hormones moderate Ca2+ increase
Heart Rate 2
Other factors 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 TaylorSchool 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/cvs06.ppt
intrinsic (Starling’s Law)extrinsic (principally autonomic)
Stroke volume
Heart rateCardiac output
Postulated mechanism
Increased sympathetic activity 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 But, of course, drugs that decrease
sympathetic activity lower blood pressure.
Control
Volume
Pressure
Chemicals
Autonomic N.S.
ADH
Local BloodFlow
Angiotensin
Pressure
Sensed by baroreceptors in carotid arteries and aortic arch
an increase in pressure causes a decrease in sympathetic activitya 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 whichincreases sympathetic activity
Local Blood Flow (kidney)
Sodium reabsorption
Potassium secretion
Decreased renal blood flow
Monitored by JGA cells
Renin production
Angiotensinogen
Converting enzyme
Angiotensin I
Angiotensin II
Aldosterone
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
Fluid loss
Blood volume
Venous return
Cardiac output
Arterial pressure
Local blood flow
Blood volume
Venous return
Cardiac output
Arterial pressure
vol
baro
chemo
kidney renin/angiotensin aldosterone
ADH
CNS
sympathetic
heart rate
contractility
vasoconstriction
capillarypressure
veins
Shock
David TaylorSchool of Medical Education
Shock
Stage 1 Compensated/Nonprogressive mechanisms work as planned
Stage 2 Decompensation/Progressive 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 bp 40 - 50 mmHg
increased capillary permeability caused by hypoxia
clotting, cell destruction, acidosis