Presentation on theme: "Blood pressure regulation and tissue blood flow Reverend Dr David CM Taylor"— Presentation transcript:
Blood pressure regulation and tissue blood flow Reverend Dr David CM Taylor http:/www.liv.ac.uk/~dcmt
Define the term blood pressure – systolic, diastolic, mean arterial pressure Regulation of blood pressure (receptors and hormones) Fluids and fluid volumes Renin angiotensin system – what triggers renin Concept of negative feedback loop Learning outcomes
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
Putting this together Stroke volume Heart rate Cardiac output Cardiac output x Total peripheral resistance Blood pressure Chapter 18, p 207 in Preston and Wilson (2013) Chapter 11, p 525 in Naish and Court (2014)
Systolic pressure is the result of contraction (systole) Diastolic pressure is when the heart is relaxed (diastole) Pulse pressure is the difference between them Mean arterial pressure is estimated as Diastolic pressure + 1/3(pulse pressure) This is because the pulse is not a sine wave Strictly speaking we should include central venous pressure (but it is usually small enough to be ignored) Pressures Chapter 19, p 219 in Preston and Wilson (2013) Chapter 11, p 554 in Naish and Court (2014)
In a male 60% of body weight is due to fluid, in a female 55% 2/3 of the fluid is inside cells – intracellular fluid (ICF) 1/3 is extracellular (ECF) Of the ECF 80% is interstitial fluid And 20% is plasma Osmotic pressure and hydrostatic pressure determine the flow between interstitial fluid and plasma Fluids Chapter 3, p 30 in Preston and Wilson (2013) Chapter 2, p 20 in Naish and Court (2014)
Increased sympathetic activity Leads to increased cardiac output And peripheral vasoconstriction (to protect the capillary beds) Drop in blood flow Triggers renin-angiotensin system Postulated mechanism for hypertension
Cross transplantation studies show that essential hypertension has its origins in the kidneys. Human and animal studies So does renal denervation Little evidence that “stress” is involved in essential hypertension But, of course, drugs that decrease sympathetic activity lower blood pressure. Evidence Beevers, G., Lip, G. Y. H., & O’Brien, E. (2001). The pathophysiology of hypertension. BMJ: British Medical Journal, 322 (7291), 912–916.
Control Volume Pressure Chemicals Autonomic N.S. ADH Local Blood Flow Angiotensin
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 Pressure Chapter 20, p 236 in Preston and Wilson (2013) Chapter 11, p 554 in Naish and Court (2014)
Sensed by atrial volume receptors A decrease in volume causes an increase in ADH secretion and a decrease in ANF secretion Volume Chapter 20, p 244 in Preston and Wilson (2013) Chapter 11, p 556 in Naish and Court (2014)
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 Chemicals Chapter 20, p 238 in Preston and Wilson (2013) Chapter 11, p 555 in Naish and Court (2014)
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 Chapter 20, p 243 in Preston and Wilson (2013) Chapter 11, p 556 in Naish and Court (2014)
Angiotensin II is a vasoconstrictor Aldosterone increases vascular sensitivity to Angiotensin II ADH (anti-diuretic hormone) increases water reabsorption ANF decreases sodium reabsorption Hormones Chapter 20, p 244 in Preston and Wilson (2013) Chapter 11, p 556 in Naish and Court (2014)