Control of the cardiovascular system

Reverend Dr. David C.M. TaylorSchool of Medical Educationdcmt@liverpool.ac.ukhttp://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 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/cvs09.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