Control of Blood Volume - Lecture Notes PDF

8. Control of blood volume MD3001 Dr Alun Hughes 1 Lecture overview Long term regulation of blood volume Vasopressin Renin-angiotensin-aldosterone system Hypovolemia 2 Long-term regulation of blood pressure Control of body fluid volume by the kidneys – Renal-body fluid feedback system • When...

8. Control of blood volume MD3001 Dr Alun Hughes 1 Lecture overview Long term regulation of blood volume Vasopressin Renin-angiotensin-aldosterone system Hypovolemia 2 Long-term regulation of blood pressure Control of body fluid volume by the kidneys – Renal-body fluid feedback system • When arterial pressure increases, urine production increases • When arterial pressure decreases, urine production decreases Guyton p217 12th ed, p231 13th ed Long-term regulation of blood pressure Two primary determinants –The renal output curve for salt and water –The level of salt and water intake Impossible to change long-term mean arterial blood pressure without changing one or both of these! How are changes in blood volume and blood osmotic pressure sensed and altered? Effect of arterial pressure on urinary volume Guyton p214 12th ed, p228 13th ed Effect of water and salt intake or output on arterial pressure Guyton p214 12th ed, p228 13th ed Antidiuretic hormone (a.k.a. ADH, arginine vasopressin) Released by the pituitary gland in response to – ↑ osmo2c pressure • Hypothalmic osmoreceptors – Hypovolemia (10% loss or greater) • Atrial baroreceptors normally inhibit ADH release • ↓ volume leads to ↓ firing rate  ↑ ADH release – Hypotension • ↓ arterial baroreceptor firing • ↑ sympathe2c ac2vity and ↑ ADH release – Angiotensin II Antidiuretic hormone (a.k.a. ADH, arginine vasopressin) Increases blood volume by – ↑ water permeability in renal collecting ducts •  ↓ urine produc2on In severe hypovolemic shock – ADH release is high – Causes vasoconstriction • ↑ total peripheral resistance Regulation of blood osmolarity ↓↓ Blood volume ↑Blood osmo2c pressure ↓ Atrial baroreceptor rate Hypothalamus Hypothalamic thirst centre Posterior pituitary ↑ Fluid intake ↑ An2diure2c hormone output ↓ Kidney fluid (water) loss Renin-angiotensinaldosterone system (RAAS) Renin • Proteolytic enzyme released from the kidneys in response to: – Sympathetic nerve activation • Mediated by baroreceptor feedback – Renal artery hypotension • Independent of baroreceptor feedback – Decreased sodium in kidney distal tubules • More about that in MD3002! RAAS and regulation of blood volume Medullary cardiovascular control (CVC) centre ↓ Baroreceptor rate ↓ Blood volume ↓Kidney blood flow Renal sympathetic nerves ↓Urine formation ↑ Kidney renin output RAAS Renin released from kidney juxtoglomerular cells Angiotensin II acts on resistance vessels – ↑ total peripheral resistance Angiotensin II acts directly on the kidneys – Constricts renal arteries  ↓ blood flow via kidneys Angiotensin II causes release of aldosterone from the adrenal glands – ↑ Na+ and water reabsorption Angiotensin II stimulates release of ADH from pituitary Guyton p220 12th ed, p235 13th ed Atrial-natriuretic hormone (a.k.a. Atrial-natriuretic peptide) 28-amino acid peptide synthesised and stored in muscle cells of the atria – Released in response to stretch of the atria – Helps oppose the effects of the RAAS system May help counteract volume overload Excessive loss of blood volume Hypovolaemia – Loss of blood volume • ↓ whole blood, e.g. hemorrhage • ↓ plasma, e.g. burns • ↓ sodium, e.g. vomitting – ↓↓ in blood pressure Classification of shock – – – – Class 1, 10-15% blood loss Class 2, 15-30% blood loss Class 3, 30-40% blood loss Class 4, >40% blood loss Hemorrhage Immediate (reflex) SV response to hypovolemia Baroreceptor reflex – Degree of volume loss affects how successful SV = stroke volume HR = heart rate CO = cardiac output (SV x HR) TPR = total peripheral resistance MABP = mean arterial blood pressure (CO x TPR) Haemorrhage Reflex compensations HR CO TPR MABP Time Later response to hypovolemia Arteriolar constriction – ↓ hydrosta2c pressure in the capillaries – Favours fluid reabsorption – Temporary redistribution Decreased renal blood flow Baroreceptors plus thirst Severe hypovolemia If volume of fluid lost can’t be compensated for – Damage to tissues and organs can occur – Heart fails Fluid replacement required – Resuscitation fluids • • Colloid (gel/starch/albumin) or Hartmann’s Blood – Fluid challenge algorithm • Whilst monitoring central venous pressure Integrated control of blood pressure Posture, movement etc Respiratory movements CSF pH Cortex Hypothalamus, thalamus Blood hormone levels Medullary CVC centre Carotid chemoreceptors Baroreceptors Blood pO2 Blood pressure Other factors affecting blood pressure control Cortex – Conscious effects of emotions • Nerves from cortex to medullary CVC centre Time of day – Diurnal variations due to hormones and cortical input Respiration – Via mechanical movements – Via chemoreceptors • Aortic and carotid bodies detect changes in pO2 • If ↓ pO2 then rate of firing ↑ Summary points Long term control of blood pressure is through control of blood volume Blood volume and blood osmotic pressure are detected Hormonal regulation of kidney function, combined with direct effects of flow, mediate blood volume 21 Learning outcomes To describe the hormonal mechanisms involved in long-term regulation of blood pressure (i.e. vasopressin, the renin-angiotensin-aldosterone system and atrialnatriuretic peptide) and how their involvement is regulated. To predict the short-term, intermediate and long-term physiological changes in the cardiovascular system in response to increased/decreased plasma volume, or changes in plasma osmolarity. To identify other systems that integrate with the cardiovascular system and can influence blood pressure.