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Control of the cardiovascular system

Control of the cardiovascular system. Reverend Dr. David C.M. Taylor School of Medical Education dcmt@liverpool.ac.uk http://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

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Control of the cardiovascular system

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  1. Control of the cardiovascular system Reverend Dr. David C.M. Taylor School of Medical Education dcmt@liverpool.ac.uk http://pcwww.liv.ac.uk/~dcmt/cvs09.ppt

  2. What is the role of the cardiovascular system?

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

  4. Which will give the greater flow ? Peripheral Resistance

  5. Which will give the greater flow ? Peripheral resistance 2

  6. End diastolic volume - End systolic volume Stroke volume Heart rate Cardiac output Cardiac Output • Heart rate x stroke volume

  7. Factors affecting stroke volume Preload Afterload Contractility

  8. 100 80 60 40 20 Tension developed % 40 60 80 100 120 140 160 Percentage sarcomere length (100% = 2.2 µm) Preload • increased end-diastolic volume stretches the heart • cardiac muscles stretch and contract more forcefully • Frank-Starling Law of the heart

  9. Starling’s 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)

  10. 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+ Contractility-”Inotropic effect”

  11. 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

  12. Stroke Volume Cardiac Output Heart Rate

  13. Heart Rate • Nervous system • increased sympathetic • decreased parasympathetic • Chemicals • catecholamines • thyroid hormones • moderate Ca2+ increase

  14. Heart Rate 2 • Other factors • age • gender • “fitness” • body temperature

  15. 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 Pacemaker activity

  16. 0 mV -70 0 mS 300 Chronotropic effect

  17. Hypertension David Taylor School of Medical Education

  18. 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”

  19. The story so far... • http://pcwww.liv.ac.uk/~dcmt/cvs09.ppt • intrinsic (Starling’s Law) • extrinsic (principally autonomic) Stroke volume Cardiac output Heart rate

  20. 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

  21. 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.

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

  23. 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

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

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

  26. Decreased renal blood flow Monitored by JGA cells Renin production Angiotensinogen Angiotensin I Converting enzyme Angiotensin II Sodium reabsorption Aldosterone Potassium secretion Local Blood Flow (kidney) Vasoconstriction

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

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

  29. Shock David Taylor School of Medical Education

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

  31. 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

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