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120 Cards in this Set
- Front
- Back
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3 factors affecting pulmonary capillary exchange
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starlings principle of cap exch
surface tension intrapleural pressure |
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Factors of starlings principle of capillary exchange favoring movement of fluid out of pulm cap?
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cap hydrostatic press
interstitial fluid hydro press interstitial fluid colloid osmotic pressure |
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Factors of starling's principle favoring movement of fluid into pulm cap?
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capillary osmotic pressure
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factors in starling's principle that predispose to pulm edema?
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-increased Kf
-increased Pc -decreased Pif -decreased interstitial fluid colloid osmotic pressure -increased interstitial fluid colloid osmotic pressure |
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factors increasing Kf
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oxygen toxicity
ARDS certain inhaled and circulating toxins |
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increased Pc is seen with anything causing pulmonary htn, what are these causes?
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left heart failure
excessive IVF's high altitude emphysema decreased alveolar oxygen increased alveolar co2 |
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decreased Pif is caused by what?
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anything that decreased IPP, such as laryngeal spasms, or too rapid evacuation of pneumo or hemo
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decreased cap osmotic pressure is caused by?
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starvation (decreased plasma protein formation)
nephrosis (proteins lost in urine) dilution of plasma proteins by IVF |
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increased interstitial fluid osmotic pressure is caused by?
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increase in Kf, therefore plasma protein concentration will be increased in the interstitium and will pull fluid out of capillary
-decreased IPP will also produce increased interstitial fluid osmotic pressure and allows for increased proteins in interstitium |
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increased surface tension has what effect on Pif?
what does this cause? |
decreased (makes IPP more negative)
-pulls water out of pulm cap and into interstitium, which leads to pulm edema |
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how does decreased IPP impact pulm edema?
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1. decreased in Pif and an increase in osmotic press of interstitial fluid
2. interrupts integrity of basement membrane |
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why does decreased IPP interrupt integrity of the basement memb?
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disrupts integrity by pulling connective tissue fibers apart, allowing plasma proteins to move across
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what is an example of decreased IPP and increased interstitial fluid osmotic press?
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laryngeal spasms
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what results from extubating at wrong stage, larynx becomes very narrow and a strong insp effort is required?
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non-cardiogenic pulm edema
neg press pulm edema |
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after NPPE, where does the fluid in the interstitium go?
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after the obstruction is removed, fluid will be squeezed down d/t return to less negative IPP.
You will see pink-frothy sputum |
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who do you see NPPE in?
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young, muscular men mostly
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how quickly does pulm edema resolve?
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usually w/i 24hrs
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2 concepts of the importance of pulm cap fluid dynamics:
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-helps keep alveoli dry by removing exogenous fluid
-facilitates rapid absorption of inhaled drugs...picked up by pulm blood, goes straight to left side of heart....immediate effect |
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3 parts to the regulation of the pulm circulation
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-nervous regulation
-chemical regulation -autoregulation of pulm blood flow |
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increased surface tension has what effect on Pif?
what does this cause? |
decreased (makes IPP more negative)
-pulls water out of pulm cap and into interstitium, which leads to pulm edema |
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nervous regulation of SNS to pulm circulation causes:
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-slight increase in resistance to pulm BF
-significant decrease in vascular capacitance (autotransfusion from pulm circ to systemic circ) |
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2 reflexes involving pulm circ
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carotid sinus baroreceptors
carotid body chemoreceptors |
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stimulation of carotid sinus baroreceptors by increased BP causes:
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inhibitory impulses sent to vasomotor center----causes fewer SNS impulses that cause vasoconstriction----pulm aa's and vv's vasoconstrict less---relaxation of smooth muscle
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inhibition of the vasomotor center causing vasodilation suggests that what two things will happen?
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-increased capacitance of pulm reservoir
-decreased blood volume in systemic circ---which decreases BP |
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primary cause of stimulation of carotid body chemoreceptors
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hypoxia
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stimulation of carotid body chemoreceptors by hypoxia causes what?
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-causes them to send excitatory nerve impulses to vasomotor ctr, increasing SNS impulses in systemic and pulm and promotes vasoconstriction
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how does stimulation of carotid body chemoreceptors affect the capacitance of the pulm vasc?
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decreases cap of pulm reservoir: increases amt of blood in systemic, hopefully increasing BP which will deliver more oxygen to the body
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drugs causing vasoconstriction of pulm vasc?
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histamine
angiotensin II serotonin thromboxane epi NE |
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drugs causing vasodilitation of pulm vasc that we need to know for Reinke?
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Ach
Nitric Oxide --2 forms |
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what can be used to determine whether an incr in PVR is d/t to vasoconstriction or atherosclerosis?
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Ach...if they dilate, it isn't athero...duh
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nervous regulation of SNS to pulm circulation causes:
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-slight increase in resistance to pulm BF
-significant decrease in vascular capacitance (autotransfusion from pulm circ to systemic circ) |
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2 reflexes involving pulm circ
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carotid sinus baroreceptors
carotid body chemoreceptors |
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stimulation of carotid sinus baroreceptors by increased BP causes:
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inhibitory impulses sent to vasomotor center----causes fewer SNS impulses that cause vasoconstriction----pulm aa's and vv's vasoconstrict less---relaxation of smooth muscle
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inhibition of the vasomotor center causing vasodilation suggests that what two things will happen?
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-increased capacitance of pulm reservoir
-decreased blood volume in systemic circ---which decreases BP |
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primary cause of stimulation of carotid body chemoreceptors
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hypoxia
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endogenous NO is produced by?
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endothelial cells lining blood vessels
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another name for NO?
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endothelium derived relaxing factor
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MOA of NO
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Ach/Brady binds w/ receptors on capillary endo cell
-this activates NOS -NOS + L-Arginine=NO -NO diffuses out of endothelial cell into vasc sm mm -NO stimulates guanylate cyclase in cytoplasm -GC converts GTP to cGMP -cGMP decreases cystolic Ca and relaxes sm mm -vasodilation |
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exogenous inhaled NO acts as a ?
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selective pulm vasodilator
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why does exogenous NO not cause systemic vasodilation?
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because when it is picked up by pulm blood, it is rapidly inactivated by Hgb, so it never gets delivered to sm mm of systemic vasc
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exogenous NO can be used for the treatment of?
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pulm htn & arterial hypoxemia caused by:
ARDS PPHN (persistant pulm htn of the newborn) lung transplant |
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how does exogenous NO improve arterial oxygenation?
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-increases arterial oxygen by increasing perfusion to the well ventilated alveoli
-causes vasodilitation of the bv's serving the alveoli, which will increase pulm BF |
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most imp mechanism of control of pulm BF?
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autoregulation
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4 organs whose blood control is primarily under autoreg
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brain
lungs heart sk mm during exercise |
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what controls blood flow to resting skeletal mm?
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SNS
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2 factors to autoregulation of pulm blood flow
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-reg r/t alveolar oxygen (HPV)
-reg r/t alveolar CO2 |
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in alveolar hypoxia, what happens to the blood vessels serving the area?
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vasoconstriction
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why is vasoconstriction in response to low alveolar hypoxia in a certain area beneficial?
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you don't want to perfuse alveoli that aren't being well ventilated.
-You are diverting blood to better ventilated areas of the lungs -you are decreasing the magnitude of a shunt like condition that may be present -low alveolar oxygen immediately indicates inadequate vent |
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why is HPV not beneficial w/ widespread hypoxia?
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leads to:
widespread vasoconstriction increased PVR pulm htn pulm edema |
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when would you see widespread alveolar hypoxia?
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high elevations
COPD |
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describe progression of disease with widespread hypoxia?
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alveolar hypoxia...pulm vasoconstriction....increased PAP's, RV works very hard...eventually fails...cor pulmonale
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what are the causes of HPV?
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who knows:
-chemical mediator released in response to low oxygen that vasoconstricts -histamine -hypoxic air alone -not enough oxygen to make NO that causes vasodilation |
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HPV response is diminished by?
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inhalation agents
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an increase in pulm CO2 leads to pulmonary ______?
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vasoconstriction
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in autoregulation, what is the direct source for vasoconstriction?
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-release of H+ as a result of CO2....(carbonic acid dissoc into bicarb and H+)
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what are the two problems that emphysema pts face that leads to severe vasoconstriction?
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alveolar hypoxia
alveolar hypercapnia |
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what is used to quantify the relationship b/t alveolar vent and pulm blood flow?
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ventilation perfusion ratios
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normal V/Q ratio for the lung as a whole
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0.8
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how do you determine V/Q ratio?
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alveolar vent (4L/min)/normal pulm perfusion (5L/min)
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normal tensions in a V/Q ratio of 0.8
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PaO2=100
PCO2=40 |
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what kind of ratio indicates ventilation in excess of perfusion?
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>0.8
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Tensions of a V/Q >0.8
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PaO2>100
PaCO2<40 |
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a V/Q > 0.8 results from ?
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-increase in alveolar vent
-decrease in pulm BF -both factors |
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in a V/Q > 0.8, gases are becoming more like ?
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ambient air
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what type of work does a V/Q > 0.8 represent?
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wasted work to hyperventilate alveoli: ventilation is > than BF to area
-alveolar units characteristic of alveolar dead space |
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what type of V/Q ratio indicates perfusion in excess of alveolar vent?
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<0.8
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tensions in a V/Q of <0.8
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PaO2<100
PCO2>40 |
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V/Q < 0.8 results from:
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decrease in ventilation
increase in perfustion combination of both |
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a V/Q < 0.8 will result in gases being more like?
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mixed venous
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a ratio of <0.8 represents what type of work and what type of alveolar cap units?
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wasted work of heart
alveolar cap units that have shunt like characterisitics |
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where do you see high V/Q ratios > 0.8?
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apical areas
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in apex, what are the tensions of the ratio is >0.8?
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PAO2=130
PCO2=30 (<40) |
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where do you see lower V/Q ratios, <0.8
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basilar areas
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in base, what are tensions if the ratio is <0.8?
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PAO2=90
PACO2>40 (42) |
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why is arterial oxygen tension=100torr?
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not a simple avg:
d/t quantitiy, more perfusion to base, so greater BF coming from base with oxygen tension of 90 -combo of apical and base areas gives us a mean of 100/104 |
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why does the apex have a higher V/Q ratio?
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well, despite a decrease in both vent and perfusion, the ratio is higher b/c the decrease in blood flow is greater than the decrease in perfusion
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if the base is better ventilated than the apex, why is the V/Q ratio lower?
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the increased perfusion is greater than increased vent
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4 ventilation perfusion disturbances
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-normal perf w/ NO vent
-normal perf w/ decreaed vent -normal vent w/ decreased perf -normal vent / no perfusion |
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describe vent and perf of an absolute shunt
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normal perfusion w/ No vent
-V/Q is 0 |
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in an absolute shunt, tensions in arterial blood will resemble?
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mixed venous blood
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describe V/Q when you have normal perfusion w/ decreased vent?
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0<V/Q<0.8
shunt-like characteristics |
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describe V/Q when you have normal vent w/ decreased perf
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0.8<V/Q<infinity
alveolar dead space LIKE |
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describe V/Q in normal vent w/ NO perfusion
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V/Q approaches infinity
alveolar dead space |
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2 compensatory mech assoc w/ abnormal V/Q ratios
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HPV response
Bronchiolar constriction |
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if you have a low V/Q ratio....perfusion in excess of ventilation, what will you see occur?
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HPV, blood flow is diverted to well ventilated areas, V/Q ratio brought back to normal in area
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when you have a high V/Q ratio...vent in excess of perfusion, what will you see occur?
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low alveolar CO2 resulting in bronchiolar constriction.
this diverts air to alveoli being better perfused...brings V/Q ratio back to normal in area |
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what two mechanisms can lead to a silent unit?
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HPV and bronchiolar constriction
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both compensatory mech associated w/ abnormal V/Q ratios start off with?
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a decrease in alveolar gas tensions
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an alveolar cap unit that has little to no ventilation and perfusion
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silent unit
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two mech of a silent unit
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1.absolute shunt: alveolus perfused but not ventilated...HPV
2. alveolar dead space: alveolus vent and not perfused...bronchiolar constriction |
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shunt in which poorly oxygenated blood is mixing w/ well oxygenated blood
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R to L shunt
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physiologic shunt=
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anatomical + intrapulmonary shunts
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intrapulmonary shunts are composed of:
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-capillary shunts
-perfusion in excess of ventilation |
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that portion of systemic venous blood that enters into systemic arteries w/o having passed through pulm capillaries is?
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anatomic/absolute/true shunts
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2 examples of normal anatomic shunt
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bronchial circulation
thebesian veins |
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a pathological anatomic shunt and its description
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tetralogy of fallot is an intra-cardiac shunt where poorly oxygenated blood from RV mixes with well oxygenated blood from LV, consists of:
intraventricular septal defect right vent hypertrophy pulm artery stenosis dextroposition of aorta |
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in right to left shunts, do we usually see a change in arterial CO2?
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no, b/c if severe enough, it will stimulate resp centers and peripheral chemoreceptors and you will increase RR, and lower arterial CO2
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that portion of RV CO perfusing pulm cap, but NOT undergoing gaseous exchange or equilibration of alveolar air?
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intrapulmonary shunt
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that portion of RV CO perfusing pulm capillaries in contact w/ totally unventilated alveoli or collapsed alveoli?
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capillary shunt
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with a capillary shunt, what will your tensions be like when blood leaves alveoli?
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like mixed venous
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that portion of RV CO perfusing pulm capillaries to a greater extent than ventilation
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perfusion in excess of ventilation...V/Q mismatch
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causes of V/Q mismatch/perfusion in excess of ventilation
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poorly ventilated alveoli
greater than normal pulm blood flow impedance to oxygen diffusion d/t grossly abnormal alveolar membrane |
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what is responsible for most of the defective gas exchange seen in resp problems?
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V/Q mismatch
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what is the result of a V/Q mismatch?
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equilibration never occurs, so poorly oxygneated blood will eventually mix with well oxygenated and have a "shunt-like" effect
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which shunts are true shunts?
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anatomic or capillary
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does breathing 100% oxygen correct an absolute/true shunt?
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no
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does breathing 100% oxygen correct perfusion in excess of ventilation?
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yes
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how do you determine b/t an absolute shunt and perfusion in excess of ventilation?
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breathing 100% oxygen
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difference b/t PO2 in alveolar air and PO2 in arterial blood is expressed as?
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A-aDO2
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which oxygen tension will always be first when figuring out oxygen difference of alveoli and arterial blood?
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alveoli will always be first b/c it will always be equal or greater than arterial oxygen tension
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normal range of A-aDO2
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5-15 torr
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A-aDO2 for physiologic person
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104-100=4torr
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causes of > 15 A-aDO2?
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-may be d/t a shunt: mixing poorly Oxy blood w/ well Oxy blood
-V/Q mismatch -impedance to O2 diffusion |
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when will you see a reduction of A-aDO2 after breathing 100% oxygen?
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in a pt w/ perfusion in excess of ventilation
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when will you see an increase in A-aDO2 after breathing 100% oxygen?
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in a pt w/ an absolute shunt
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when breathing 100% oxygen, an A-aDO2 of 15 torr represents a shunt of?
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1%
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what can occur during the administration of 100% oxygen?
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denitrogenation absorption atelectasis
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what happens to nitrogen in poorly ventilated alveoli?
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nitrogen will eventually pass from poorly ventilated alveoli into blood....and be exhaled as it passes by well vent alveoli.
-as this happens, this decreases gas vol of alveoli, causing decreased size of alveoli |
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what happens to poorly ventilated alveolus after giving 100% oxygen?
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increased oxygen causes increase in BF and HPV response will stop. This causes vasodilation and greater quantities of Oxygen are removed. This leads to decreased Oxygen, decreased volume.
SO: now you have decreased N and Oxygen, collapse of alveoli |
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what is nitrogen splinting?
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administering a little nitrogen w/ oxygen to help keep the alveolus from collapsing
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