Control of the cardiovascular system

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Control of the cardiovascular system

• Reverend Dr. David C.M. Taylor
• School of Medical Education
• dcmt_at_liverpool.ac.uk
• http//pcwww.liv.ac.uk/dcmt/cvs09.ppt

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What is the role of the cardiovascular system?
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Blood Pressure

• Depends upon the amount of blood leaving the
  heart
• cardiac output
• and the resistance of the vasculature
• total peripheral resistance

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Peripheral Resistance
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Peripheral resistance 2
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Cardiac Output

• Heart rate x stroke volume

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Factors affecting stroke volume
Preload
Afterload
Contractility
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Preload

• increased end-diastolic volume stretches the
  heart
• cardiac muscles stretch and contract more
  forcefully
• Frank-Starling Law of the heart

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Starlings Law
2.2 ?m
3.8 ?m
1.8 ?m
100 80 60 40 20
Tension developed
40 60 80 100 120 140 160
Percentage sarcomere length (100 2.2 ?m)
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Contractility-Inotropic effect

• positive inotropic agents
• increase available intracellular Ca2
• increase number of actinomyosin binding sites
• increase force of contraction

• positive inotropic agents
• sympathetic stimulation
• catecholamines
• glucagon
• thyroid hormones
• increased extracellular Ca2

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Afterload

• decreased arterial blood pressure during diastole
• decreased afterload
• semilunar valves open sooner when blood pressure
  in pulmonary artery aorta is lower

• afterload
• blood pressure
• viscosity of blood
• elasticity of arteries

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Heart Rate

• Nervous system
• increased sympathetic
• decreased parasympathetic
• Chemicals
• catecholamines
• thyroid hormones
• moderate Ca2 increase

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Heart Rate 2

• Other factors
• age
• gender
• fitness
• body temperature

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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

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Chronotropic effect
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Hypertension

• David Taylor
• School of Medical Education

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Hypertension

• Excellent article
• ABC of Hypertension The pathophysiology of
  hypertension, Beevers G, Lip GYH and OBrien E
  (2001) BMJ, 322912-916
• Upto 5 of patients with hypertension have it as
  secondary to some other disease (e.g. renal
  disease)
• The rest have essential hypertension

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The story so far...

• http//pcwww.liv.ac.uk/dcmt/cvs09.ppt
• intrinsic (Starlings Law)
• extrinsic (principally autonomic)

Stroke volume
Cardiac output
Heart rate
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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

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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.

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Control
Autonomic N.S.
Volume
ADH
Pressure
Chemicals
Angiotensin
Local Blood Flow
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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

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Volume

• Sensed by atrial volume receptors
• A decrease in volume
• causes an increase in ADH secretion
• and a decrease in ANF secretion

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Chemicals

• A decrease in O2, or more usually an increase in
  CO2 or H2 causes an increase in chemoreceptor
  activity which
• increases sympathetic activity

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Local Blood Flow (kidney)
Vasoconstriction
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Hormones

• Angiotensin II is a vasoconstrictor
• Aldosterone increases vascular sensitivity to
  Angiotensin II
• ADH (anti-diuretic hormone) increases water
  reabsorption
• ANF decreases sodium reabsorption

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Overview
ADH
vol
baro
veins
capillary pressure
chemo
renin/angiotensin
aldosterone
kidney
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Shock

• David Taylor
• School of Medical Education

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Shock

• Stage 1 Compensated/Nonprogressive
• mechanisms work as planned
• Stage 2 Decompensation/Progressive
• if blood volume drops more than 15 - 25
• Stage 3 Irreversible

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Progressive shock

• depression of cardiac activity
• bp lt60 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