Cardiovascular system in its context Reverend Dr. David C.M. Taylor School of Medical Education

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 Percentage sarcomere length (100% = 2.2 µm) Tension developed %

Starling’s Law Percentage sarcomere length (100% = 2.2  m) Tension developed % 1.8  m 2.2  m 3.8  m

Contractility-”Inotropic effect” positive inotropic agents increase available intracellular Ca 2+ increase number of actinomyosin binding sites increase force of contraction positive inotropic agents sympathetic stimulation catecholamines glucagon thyroid hormones increased extracellular Ca 2+ 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 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 0mS300

Chronotropic effect 0 mV -70 0mS300

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: 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... 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 Chemicals Autonomic N.S. ADH 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) 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 capillary pressure veins

Shock David Taylor School of Medical Education

Shock Stage 1Compensated/Nonprogressive mechanisms work as planned Stage 2 Decompensation/Progressive if blood volume drops more than % Stage 3 Irreversible

Progressive shock depression of cardiac activity bp <60 mmHg poor flow through coronary arteries leads to ischemia depression of vasoconstriction bp mmHg increased capillary permeability caused by hypoxia clotting, cell destruction, acidosis