Cardiovascular system in its context

Reverend Dr. David C.M. Taylor School of Medical Education [email protected]

http://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 100 80 60 40 20 40 60 80 100 120 140 160 Percentage sarcomere length (100% = 2.2 µm)

Starling’s Law

1.8  m 2.2  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 Ca actinomyosin binding sites contraction 2+ increase number of increase force of positive inotropic agents   sympathetic stimulation catecholamines    glucagon thyroid hormones increased extracellular Ca 2+

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

Stroke Volume Heart Rate Cardiac Output

Heart Rate

Nervous system   increased sympathetic decreased parasympathetic Chemicals    catecholamines thyroid hormones moderate Ca 2+ 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

mV 0 -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/cvs06.ppt

intrinsic (Starling’s Law) extrinsic (principally autonomic) Stroke volume Heart rate Cardiac 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 Autonomic N.S.

ADH 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 O 2 , or more usually an increase in CO 2 or H 2 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

Fluid loss ADH Arterial pressure Blood volume Venous return Cardiac output Arterial pressure heart rate vol baro sympathetic contractility vasoconstriction CNS veins chemo capillary pressure Local blood flow kidney renin/angiotensin Cardiac output Venous return Blood volume aldosterone

Shock

David Taylor School 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