ee CLASSES QO) Mild Haemorrhage = 10% of total blood volume. » This can be lost with no significant effect on arterial pressure. UO) Moderate Haemorrhage = 10 - 20% of total blood volume; >500 ml - 1L or 5-15mL/kg body weight > | PP but MAP may remain normal O Severe Haemorrhage = >30% of total blood volume; > 1.5L or >15mL/kg body weight » There is always a | in BP, (although BP changes vary from individual to individual).BLOOD-LOsS | Less return of blood to heart Less output from heart Lower blood pressure (pulse pressure, amount pressure rises with each, hheart beat, is particularly Low) | Less stimulation of baroreceptors Increased activity in sympathetic nerves Less activity in parasympathetic (vagal) nerves resistance vessels (small arteries) constrict heart rate increases capacitance vessels (veins) constrict, increasing flow of blood back to heart Increased secretion of vasapression heart rate and force increases reduces water loss by kadneys angiotensin formation increases: constricts blood vessels ancl promotes excretion of another hormone, aldosterone, which causes kidneys to retain salt and waterCompensatory Responses to Acute Blood Loss * 1. | blood volume — | mean systemic pressure — | in CO and | BP ¢ 2. | BP is sensed by the carotid sinus baroreceptors Carotid baroreceptor reflex then * — 7 sympathetic outflow to the heart and blood vessels * — | Parasympathetic outflow to the heart.Acute Haemorrhage Acute Haemorthage 4 | MAP 1 | Stretch on Carotid sinus baroreceptors 1 | firing rate of Carotid sinus N 4 Psymp outflow to heart 1 Symp outflow to heart and blood vessels THR THR + Contractility arteriolar constriction (t TPR) venoconstriction | unstressed volume fvenous retums mean sysmic P ee Figure: Role of the Baroflex in the Circulatory Responses to HaemorrhageAll these lead to: ? HR + CC 7 TPR (due to generalized arteriolar constriction; only brain and heart vessels spared; marked in the skin, kidneys and viscera) | Unstressed volume and } Stressed volume i.e. | blood in Vv 7 blood in arterial tree (due to venous constriction). Vasoconstriction occurs in skeletal, splanchnic and cutaneous vascular beds sparing vital organs only. This —> ¢ VR inspite of diminished blood volume+ When the sympathetic reflexes are functional, up to 30 — 40% of total blood volume has to be lost before the person will die, as opposed to 15 - 26% when the reflexes are not intact.Chemoreceptors * The peripheral chemoreceptors are very sensitive to hypoxia. ¢ The hypoxia, anaemia and acidosis occurring in haemorrhage stimulate them * They supplement the baroreceptor mechanism by + sympathetic outflow to the heart and blood vessels. * It results in stimulation of respirationMee CNS Ischemic Response * Cerebral Ischaemia (if present) causes an t PCO, which activates chemoreceptors in the VMC to ¢ sympathetic outflow. * CNS Ischemic Response is the elevation of arterial P. in response to cerebral ischemia. It can elevate the MAP for as long as 10mins and as high as 270mmHg. The effect is so great that some of the peripheral vessels become totally or almost totally excluded. The CNS ischemic response is however not activated until MAP falls below 50 mmHg.Kidneys i. Both afferent and efferent arterioles are constricted (Ea>>Aa) ii. GFR is reduced iii. Renal plasma flow is reduced >> GFR iv. Filtration fraction (GFR/RPF) increases v. Increased Na+ retention vi. Retention of nitrogenous waste products vii. Severe renal tubular damage may result from prolonged hypotension5. Reverse stress - relaxation of ne circulatory system ¢ . This causes the blood vessels to contract down around the diminished blood volume so that the blood volume that is available will fill the circulation more adequately.(st 6. Capillary Hydrostatic Pressure « Arteriolar vasoconstriction causes a | in Cap. Hydr. Pressure (Pc) so fat there is } capillary absorption since the colloid osmotic pressure is now higher * This helps to restore circulatory blood volume7. RAAS: This is activated by the | in renal perfusion pressure. Ang II is a potent vasoconstrictor, it therefore reinforces the stimulatory effect of the symp. N.S. on total periphral resistance Ang. II also stimulates the Adrenal cortex to produce Aldosterone which increases Na reabsorption in the kidney, thereby increasing circulatory blood volume Ang II also causes thirst by acting on the subfornical organ idAntidiuretic Hormone (ADH) * 8. ADH (Vasopressin) is released when arterial receptors detect the | in blood volume. ADH causes both vasoconstriction and + water reabsorption in the kidney, — f blood pressure.Acute Hg, | Aero Pressure 1 Renal prion presure Rerin release from the JG cols Plasma ACE lung) Angi 1 Constrictign of arterioles 1 Secration of aldosterone 1 Salt and H,0 reabsorption 1 a 1A. Pressure —» Norital Figure :Role of RAAS in the Circulatory Responses to Hemorrhage9. Catecholamines * The Adrenal medulla releases Epinephrine and Norepinephrine which supplement the actions of the Sympathetic N. System on the heart and blood vessels. Epinephrine and Norepinephrine are thought to have their major effect on the Retricular Activating System during haemorrhage, therefore — restlessness and apprehension. * When restlessness is present, there is t d motor activity and T resp. movements which f the muscular and thoracic pumping of venous blood — ft VR.Long Term Adjustments ¢ 1. Plasma volumes are restored in 12 - 72h ¢ 2. Preformed albumin enters the circulation from extra-vascular stores « 3. Dilution of the plasma proteins and cells due to the ¢ influx of fluid from the intestinal tract and from interstitial spaces. » This leads to td hepatic synthesis of plasma proteins over a period of 3 - 4 days.Ee ¢ 4. Erythropoiesis: The relative anoxia present in the tissue following hrrg — stimulation of erythropoietin production > f erythropoiesis. » f reticulocyte count (indicating erythropoiesis) reaches a peak in 10 days » Red cell mass is restored to normal in 4 - 8 weeks > Increased 2,3-DPG concentration in red blood cells leads to oxygen delivery to tissues inspite of low haematocrit 2gHaemerrhage | Arterial pressure 1 erorecobtor Reflex 7 Renin | + Symp outflow Tt i | Cap “T P e tHR Contracn VW TTPR 7TAldosterone 7 fluid absorption . of arterioles constriction 7cc Tt TPR 4 Blood in Vv 1 Nat reabsorption (unstressed volume) | t oem volume f Bloat “une 7 Arterial P — Normal Figure: Circulatory Responses to Haemorrhage+ Untreated severe haemorrhage is a threat to life: OCompensatory mechanisms fail OSympathetic activity cease (Vagus impulses to the heart increases » Fainting > Irreversible damage “Cause of death is kidney failure > Other probs: septicaemia, heart failure 2goaPron n= Signs of Hypovolemic Shock | BP Rapid thready pulse Cold clammy extremities Intense thirst Rapid respiration Sweatiness ag