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20 Cards in this Set
- Front
- Back
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Issues with Upright Posture
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Gravity exerts force on column of blood within vasculature
75% of blood volume in compliant veins 70-75% of total blood volume below the level of the heart, must be driven back to RA |
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Orthostatic Intolerance
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Characterized by a fall in CVP & decreased CO
if severe enough a fall in MAP accompanied by dizziness, lightheadedness, & nausea When MAP falls below 60 mmHg (syncope) |
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Hydrostatic Indifference Point (HIP)
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Point in vasculature where pressure is independent of posture
represents center of gravity for the vascular system Approximately at level of diaphragm in humans Determined by distribution of compliances in upper & lower body reduce compliance or reduce pooling in dependent limbs will result in cranial shift of HIP & restrict fall in CVP requires large increase in blood volume to shift HIP |
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2 Major Problems of Upright Posture
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Most of the blood volume is below venostatic level in distensible/compliant vessels rather than stiff vessels
Blood volume is too small to fill the entire vascular container in upright posture If veins were as noncompliant as arteries, hydrostatic effect of upright posture would be minimal vascular system would be more like a rigid container hemorrage is a benefit of having compliant venous system in upright posture |
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Counteract Pooling: Venous Compliance
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Shape of venous compliance curve is of crucial importance
Steep, compliant portion is primary reason for orthostatic intolerance Veins relatively stiff at high pressures pooling limited at highest transmural pressures without stiff portion, upright posture would be impossible |
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Counteract Pooling: Venous Valves
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Acute upright posture
hydrostatic column of blood from veins in feet to heart is broken up by series of valves Over time blood flows from arteries into dependent veins forcing valves open creates uninterrupted hydrostatic column between RA & feet With all valves open 600 ml of blood is displaced away from central concentration to dependent veins of legs Patients with incompetent or congenitally absent venous valves suffer from sever orthostatic intolerance uninterrupted hydrostatic column upon standing (abrupt pooling, no time dependent effect) sudden loss of filling pressure results in inability to maintain CO (immediate syncope) Maintain MAP in water/tight elastic stocking cancels hydrostatic increase in transmural pressure below heart level |
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Mechanical factors- The 2nd Heart
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Passive upright posture is a potentially lethal stress for humans
blood continues to pool due to delayed compliance high capillary pressure results in net filtration decline in ventricular filling pressure causes CO to fall below levels required to maintain MAP loss of consciousness & lethal effects of cerebral ischemia if supine posture is not restored quickly |
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The Muscle Pump
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Must have competent valves & hydrostatic column
Creates 90 mmHg driving pressure CVP & SV rapidly restored with modest muscle contractions Resting muscle tone can determine volume of blood displaced into legs in upright humans rhythmic changes in antigravity muscles intramuscular pressure is reduced with prolonged bed rest, surgery, spaceflight |
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Responses to Upright Posture
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Substantial reduction in blood volume & CVP preced any significant decrease in PP, MAP, or tachycardia
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HR Changes
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Pharmacological denervation of the heart
atropine & propranolol CO fell 25% before blockade & 50% after blockade during 70 HUT, MAP did not change before OR after blockade peripheral vascular factors rather than cardiac mechanisms are essential to maintaining MAP in upright posture Remember that CVP 0 mmHg in upright posture the only way to increase CO with CVP close to 0 is to raise RAP by activating muscle pump or with blood infusion vasoconstriction increases TPR, but may not alter CVP |
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Reflex Control: Cardiopulmonary BR
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Low pressure baroreceptors in atria, pulmonary artery & great veins
Hydraulically isolated from arterial pressure signal, receives no input or feedback about MAP Reflex adjustments to selective inhibition of cardiopulmonary baroreceptors slow ramp of LBNP (1 mmHg min) gradually reduce RAP from 5 to 0 mmHg Arterial baroreflex appear to be activated when aortic pulse pressure begins to fall |
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Normal Responses
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Inverse relationship between CO & CVP
CO & relationship between flow & volume in the peripheral circulation Increase in peripheral vascular blood flow (maldistributioin of CO) in upright posture leads to immediate hypotension |
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Post-Exercise Orthostatic Intolerance
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Immediately (& up to 2 hr) there is a decrease in MAP
persistant muscle vasodilation not compensated by an equal increase in CO resulting in fall in MAP CO falls faster than vsodilation wears off slow reversal of muscle vasodilation & high CO with no muscle pump decreases CVP & SV MAP Fall increasing HR does not help CVP approaches 0 mmHg & nothing can be done to raise CO the heart cannot pump what it does not receive unless muscle pump is activated or supine position supine posture will raise CVP & prevent syncope but hypotension will persist |
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Heat -Induced Orthostatic Intolerance
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Severe heat stress is prime example of CO maldistribution
increases skin blood- highly compliant circulation CO not distributed to withstand orthostatis or many other severe stressors CO well distributed for temperature regulation Lowers CVP close to 0 mmHg CO can inrease up to 12 l/min during supine heat stress skin can receive up to 8 l/min of the CO during supine heat stress Decrease in RAP due to high skin blood flow Decrease in TPR due to whole body cutaneous vasodilation Normally CO can increase 2-3 l/min by pacing the heart or with drug infusion large increase in CO due to ionotripic effect on heart, hyperventilation, & vasoconstriction of splanchnic vasculature |
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Heat-Induced Orthosatic Intolerance (2)
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To prevent fall in CVP during upright posture in heat
must vasoconstrict cutaneous & splanchnic vasculature both vascular beds normally constricted in upright posture even with vasoconstriction, skin blood flow remains significantly elevated above baseline CO cannot increase enough & MAP falls with upright posture muscle pump may not help nothing to pump in the skin & very little blood flow to the leg passes through the muscle |
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Autonomic Dysfunction
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Responses to HUT 45
much different than those with autonomic neuropathey MAP falls rapidly with partial recovery to levels above syncope muscle spasms & increase in angiotensis II due to decrease in afferent arteriole pressure resulting in splanchnic & lower body vasoconstriction appears cerebral circulation shifts autoregulatory range to a lower pressure so cerebral perfussion pressure is adequate despite decrease in MAP patients with autonomic neuropathy have persistent fall in MAP & reach syncopal levels unless they activate muscle pump Diabetic Neuropathy long term leads to degeneration of sensory & autonomic nerves MAP fell to 50 mmHg decrease in CO & increase in HR not different than control subjects inability to increase vascular resistance due to nerve degeneration contrast with tetraplegics who can still vasoconstrict |
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Cardiovascular Responses to HUT 45
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Decreased CVP
Increased sympathetic activity plasma norepinephrine vasoconstriction |
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Cardiovascular Responses to HUT 90
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Decreased CVP
Decreased Arterial PP Increased sympathetic Activiy plasma NE HR vasoconstriction aldosterone |
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Cardiovascular Responses to HUT Prolonged 90
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Decreased
CVP arterial PP arterial mean pressure Increased sympathetic activity plasma NE HR vasoconstriction aldosterone vasopressin |
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Cardiovascular Responses to HUT Syncope
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Increased
plasma Epi vagal activity Bradycardia decreased sympathetic activity Vasodilation decreased aldosterone decreased vasopressin |
