Circulatory Adjustment Flashcards
how does graviety affecte pressure?
how does this correlate to orthostatic hypotension?
pressure: is a function of gravity (pull) and height
- the pressure at stadning in my legs will be higher than in my arm
this is because gravity – the pressure of all that liquid heading down to the feet adds to the pressure thats already being exerted by the heart (aorta)
Orthostatic Hypotension
- normally: from laying down to standing –> the blood will initially blood in the feet and be less in the head –> but your brain triggers constriction of the vessels in the LE to squeeze, therefore increasing the pressure to force against the “resistance” of gravity
- what happens in orthostatic hypotension – the body doesnt make that adaptation – the bloow flow to the brain remains low!! syncope
- HTN meds can cause this – as they work to decrease pressure there will be less “force” pushing the blood back up
aerobic v anaerobic exercise & oxygen demand
- how is oxygen consumption determined
- how is intensity determined
aerobic exercise: the amout of oxygen being delivered to the tissues = the amount of oxygen needed (dynamic)
anaerobic: the demand/need for oxygen in the tissue is higher than the amount thats being delivered (static)
O2 consumption of tissue: O2 content in arteries - O2 content in veins = how much the tissue is using
intensity: the amount of “work” –> determined in METS or metabolic equlivents –> a multiple of what your resting oxygen consumption would be
physiologically – what happens during exercise that allows for your body to deliver enough O2 to the tissues
- neural anticipation
- heart changes
- SNS changes
anticipation: the brain inhibits vagal stimulation (parasymp) & triggers sympathetic impulses
heart: increase HR (tachy) and therefore increases cardiac output (becuase CO = HR x SV)
SNS:
- increases vasoconstriction (resistance) to areas of the body where blood flow is not essential (kidneys, gut, muscles which arent important)
skin is complex: there is initial vasodilation to sweat but with increased O2 demand it constricts
majortiy of teh cardaic output is for the muscles during exercise (4x increase in CO)
how does cardiac output change during exercise?
how does resistance change?
does preload change?
how does blood pressure change?
cardiac output increase = because HR increases a LOT , SV increases
periperal resistance decreases: een with constriction of some vessels, there is so many capillary beds (muscles) that open the overall resistance goes down
preload: there is increased venous return – but there is decreased filling time so ther overall preload does not change (EDV remains)
increase in systolic pressure – overall MAP increases (because CO increases) even though resistance decreased!
how does training compensate for exercise and CV demands
decrease resting HR
increase (chronic) EDV
increase SV (getting more out of each squeeze)
more lean muscle mass with mitochondria
better V/Q ratio
what happens at the point of exhustion
ultiametly the pump cant pump any more
- the stroke volume plateaus
- dehydration –> triggers skin vasoconstriction
- the CO2 and lactic acid increase ( decrease pH)
- only so much o2 carrying capactiy of the RBC!!
what is the definition of shock?
inability to properly perfuse and deliver oxygen to the tissues
- a state of severely reduced blood supply and perfusion to the tissues
what is hypovolemic shock?
what is septic shock?
hypo - low volemic = volume
- a state of significantly reduced blood volume (hemmorage, dehydration, burn) which leads to a rapid decrease in blood pressure
septic shock: due to infection – these bacteria release toxins which cause vasodilation
- vasodilation long term like this causes a decrease in peripheral resistance & therefore a decrease in blood pressure
what is cardiogenic shock?
anaphylatic shock?
neurogenic shock?
cardiogeneic shock: (MI) a decrease in cardiac function, inability to produce cardiac output –> decrease in blood pressure
anaphylatic shock: immune reaction –> triggers immune mediators to flood to the site – a vasodilation occurs to let them get there
- sustained vasodilation - decreases resistance - decrease pressure
neurogenic shock: loss of vasal tone due to brain injury (like spinal cord damage)
- results in dilation of arterioles & veins
- decreased HR and ability to contract
- depressed CV system – decreased pressure
what are the body’s compensatory mechanisms to combat shock?
the negative feedback responses
- attempt to increased MAP
- baroreceptors fire
- chemoreceptors fire
- cerebral response
- release vasoconstriction molecules (NE,AGII) - increase blood volume
- reabsorption of fluid
- renal conservation of Na & water
- activated platelets– attempts to control blood pooling
increase CO: through E/NE, increase HR, increase preload
increase TPR: constrction
humoral players: E/NE/RAAS/ADH
how do the baroreceptors work in hemorrhage
noramally: they sit in carotid sinus and aortic arch — and respond to changes in blood pressure
when triggered in hemorrhage: they trigger an increase in sympathetic response (the baroreceptors STOP firing when the pressure is low)
- sympathetics kick in to increase resistance, constrict (especially in the resoviors of spleen (releases its RBCS to help) and to unnecessary organs)
describe vasoconstrction in the setting of shock
most? least?
what about renals?
- the vasoconstriction of arteries is not uniform
- MOST constriction: skin, splanchnic nerves, skeletal muscle
LEAST
- blood remains (might increase) to brain, and heart
renal?
- SHORT: counteracted by autoregulatory actions (the spleen temporarily releases RBCs to combat the loss)
- LONG: intense renal constriction, reduced GFR, reduced urine, leads to renal ischemia
how does the SNS response in hemorrhage?
how does the RAAS system?
- SNS: releases NE from the adrenal medulla & epi from the medulla and NE from Peripheral nerve endings
this triggeres vasoconstriction and triggers B1 on myocytes to increase HR (attempt to increase CO)
RAAS system:
renin released in response to the low pressure in the kidney follows pathway to produce the AGII and the constriction path
specifics of increasing blood volume during shock
- what is happening with hydrostatic/oncotic pressure
- what abour renal compensation for volume
- the body responds by increasing the absorbtion of fluid from the interstitum to the capillaries
- but this onyl works for so long – because once the fluid is in, theres not enough oncotic pressure to keep it in there — so its a temporary fix
- body attempts to push fluid from intracellular to interstital (extracellular)
Renal Comp. for volume
- GFR will be low — so theyll be a reduced abilit of the water and salt filteration
- ADH will trigger reabsorbtion of water
- aldosterone (from RAAS) will trigger salt and water reabsorbtion
what happens when shock leads to decompensation
what do we do as clinicians?
the negative mechanisms cant work forever — eventually the body cant sustain
- cardiac failure: the flow decreases so much that dec. CO and MAP – reduces TPR & no matter how much info from SNS – heart cant beat
- acidosis, CNS depression and loss of clot factors
we give
- fluid!!!!!!!!!!!!!!!!!
- stop the bleed
- then can consider pressors or inotropes
