Integrated Circulatory Control: Hypotension And Hemorrhage Flashcards
Hypotension
. Low blood pressure . Symptoms: blurry vision, confusion, dizziness, light-headedness . Sleepiness . Nausea . Weakness . SBP under 90, diastolic under 60 mmHg
General causes of hypotension
. blood loss: hemorrhage, excessive sweating/loss of fluids from burned skin, loss of fluids rom GI or kidney
. Excessive dec. in CO: depressed cardiac contractility from cardiac mm. Damage
. Excessive dec. in TPR: excessive vasodilation from allergic rxn or responses to infection
. Orthostatic hypotension: impaired neural compensatory responses to falling bp, hypovolemia, drugs causing arterial vasodilation
Shock
. Profound and widespread reduction of effective tissue perfusion leads first to reversible and then prolonged to irreversible injury
. Cause of poor perfusion is prolonged hypotension )but is not required for state of shock)
Categories of shock
. Hypovolemic shock due to loss of whole blood or fluids
. Los resistance shock: septic shock falls in this category
. Cardiogenic shock
What occurs w/ blood when moving from horizontal position to an upright vertical posture
. Causes shift in BV from the central circulation to the more distensible veins in the legs
. Weight of the column of blood is accommodated by the compliant v. Walls so venous return is immediately reduced (venous pooling)
. Physiological compensatory responses similar to those engaged for mild hemorrhage
Initial response to standing
. Dec. in venous return -> dec. CO ->. Dec. bp
Compensatory response when standing
. Unloading of arterial baroreceptors activates arterial baroreflex
. Inc. HR
. SNS to visceral organs inc. TPR
. Keeps bp from falling too far, if compensatory responses are insufficient, cerebral perfusion will fall and the person may feel dizzy or faint
What occurs w/ prolonged standing
. Use muscle pump to break up column of blood
. Mm. Contraction assists venous return by moving blood out of the compliant vv.
. Dec. venous pressure in the leg reduces the amount of capillary filtration in the ankles/feet so less fluid leaves vascular space
Emotional responses causing vasovagal syncope
. Person is in upright position when emotional stress occurs
. Activation of cerebral cortex
. Cortex activates the hypothalamus
. Hypothalamus tells the CV centers in medulla activate vagal tone to the heart -> abruptly dec. HR and CO
. Withdraw sympathetic tone from visceral and skeletal m. Vessels -> abruptly dec. TPR
. Result: sudden drop in bp -> dec. cerebral perfusion -> faint
Initiation of shock
. Loss of over 30% of total BV leading to hypovolemic shock state
. During shock, SBP is under 90 mmHg, and MAP is under 70 mmHg
Common clinical signs of shock
. Hypotension . Tachycardia . Oliguria . Slowed thought processes (confusion) . Cool skin w/ mottled appearance due to reduced skin blood flow . Thirst
Initial CV response due directly to hypovolemia
. Dec. in venous return, SV, CO, and MAP
. Compensatory response: rapid reflex effects (mediated by inc. in peripheral SNS activity) directed to heart and vasculature to partially restore CO and raise TPR
. OR slower, neurohumoral effects: conserve body fluids via kidney and passive fluid shifts from intracellular/interstitial spaces into vascular space
. In some cases shock transitions to irreversible state and blood transfusion will not prevent further fall in bp
Until response to shock from arterial baroreceptor
. They are unloaded (dec. stretch) so arterial baroreflex activated
. Withdraw vagal one from heart and inc. SNS to heart, visceral organs, skin and skeletal m. Arterioles
. Inc. HR
. Inc. TPR
. Inc. venous constriction: shifts blood out of compliant vv. And help replenish the effective circulating volume
Cardiopulmonary baroreceptors response to shock
. Sense dec. in BV
. Inc. HR
. Inc. release in vasopressin
. Inc. synthesis of AII and then aldosterone
. Neurohumoral responses will attempt to conserve body water and also will enhance arteriolar vasoconstriction
Peripheral arterial chemoreceptors initial response to shock
. Dec. in MAP reduces perfusion of carotid and aortic bodies
. Local dec. PO2, elevation in PCO2, and inc. acidosis stimulates arterial chemoreflex
. Causes resultant reflex sympathetic activation to heart and vasculature
Central chemoreceptors initial response to shock
. If cerebral perfusion is reduced (MAP under 40 mmHg)
. Results in inc. brain PCO2 and local acidosis
. Acidosis then activates the central chemoreceptors
. Result is inc. SNS to periphery
CO initial response to shock
. Redistribution will occur
. SNS activity is higher to renal and mesenteric circulations: heart and brain favored
. Over time and if severe this can lead to acute renal failure and breakdown of the GI mucosal lining
. Can lead to bacterial sepsis
Capillary fluid shift response to shock
. Slower response but Major compensatory effect
. Shift fluid from interstitial to vascular spaces bc of dec. capillary pressure
. Initially results in hemodilution by lowered capillary oncotic pressure
. Eventually rate of capillary fluid shift into vasculature slows down
. Liver albumin synthesis inc. and more plasma proteins begins to appear in blood
. Intracellular fluid begins to shift into interstitial compartment as new osmoles appear in interstitium which were released from ischemic-damaged tissue
Shock affect on fluid retaining hormones
. AII, aldosterone, vasopressin all inc.
. Activation of hormonal synthesis and/or release by neural reflexes (from cardiopulmonary baroreceptors; arterial baroreceptors)
. Low perfusion pressure in kidney will also activate renin release
. Inc. AII and vasopressin contributes to inc. TPR
Decompensation
. Poor tissue perfusion can initiate time-dependent processes that cause pathophysiologic changes in cardiac and vascular function and CNS depression
. At a point can be positive feedback bc they amplify the initial insult (dec. MAP) rather than return it towards the homeostatic level as in compensatory or neg. feedback mechanisms
Cardiac failure from shock
. Reduction in ventricular performance (depression of contractility)
. Acidosis depresses contractility (result of poor peripheral tissue perfusion)
. Poor perfusion of heart promotes necrosis
. Poor pumping performance further dec. MAP and this tissue perfusion
Vascular control failure in shock
. Return of TPR towards resting level
. Accumulation of vasodilator metabolites in poorly perfused tissues
. Damage to GI system Allows bacterial endotoxins to enter bloodstream
. Endotoxins can cause massive vasodilation by introducing NO production
. Excessive activation of inflammatory processes can lead to capillary damage
. Results in extravasation of plasma protein and fluid into the interstitial space
CNS depression when in shock
. Severe hypotension can lead to. Reduction in cerebral perfusion
. Resultant CNS depression causes inhibition of SNS outflow to the periphery
. Reduction in TPR aggravates the hypotension
