daira
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Hypoxemia in Pulmonary embolism is a result of
a. tachycardia
b. inc. right heart filling pressure
c. increased dead-space ventilation in the area of vascular occlusion
d. perfusion of areas poorly ventilated becuz of airway constriction
e. inadequate time for oxygenation diffusion secondry to reduction in capillary bed
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| lucky
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(e) i think
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| daira
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Its D lucky.
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| Ahab
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Sure it is not C?
A pulmonary embolus will occlude the vessels, not the airways, leading to a ventilation/perfusion mismatch (V/Q) i.e. increase in dead space ventilation
D would appear to be true in the case of an acute asthma attack
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| dimps
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qalander can u explain this answer as i thought of c
how pul embolism is causing airway obs
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| daira
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Bronchoactive mediators are released which cause bronchoconstriction, another factor may be atelactasis. Both these may cause decreased ventilation to the areas which are perfused well, leading to hypoxemia.
Increased dead-space ventilation wont be a cause of hypoxemia in PE.
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| dimps
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still could not get ur answer
in pul emolism there is perfusion defect ,ventilation is normal
then how answer is d
just check this http://www.emedicine.com/med/topic1958.htm
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| msashraf
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hello,
i think the answer is c bcoz i read in current that vascular obstruction creates a physiologic dead space ventilation but no perfusion leading to shunting of the blood from right to the left side.
bronchoconstriction would cause wheezing and increased work of breathing not hypoxia.
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| dmnz
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I think ans- (c)
High probability V/Q mismatch - occurs in PE
Segment of PA is blocked --> no blood flow --> no gas exchange.
All oxygen is wasted in "alveolar"dead space.
CO2 retention occurs --> results in hypercarbia --> actually increases ventilation by stimulation of respiratory centre ( recollect- these patients are tachypneic - not primarily because of broncho spasm but becoz of CO2)
This increased ventilation washes out CO2 but does not improve hypoxemia due to inadeqate oxygen exchange , because available hemoglobin can only take that much of oxygen.
Actually speaking the PE results in activation of intrapulmonary reflexes that releases primarily vasoconstrictive substances (not bronchoconstrictive)- histamine,serotonin,prostaglandins- --> further vasoconstriction throughout the lung - places RV under strain- basic mechanism of RV strain pattern in ECG [ S1,Q3, T-inv in V1-3].
Remember most sensitive ABG finding for PE is = increased A-a DO2 gradient and not Hypoxemia or hypercarbia.
I hope you got it. :wink:
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| dmnz
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Sorry I submitted answer early-
So in early part of pathophsiology - answer -(c) is correct
What qualander means may be ??? that vasoactive substances also leads to bronhoconstriction is prime mechanism due to intrapulmonary reflexes . In that aspect - probably answer (d) is right.
?????Do we get that much time to think in exam. :?:
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| dimps
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dmnz what is the 1 correct answer
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| dmnz
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I WOULD GO FOR [C]
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| daira
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This q is from Harrison, the answer is D.
Thanks
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| mdwannabe
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Why would airway constrict?? I thought i was vise-versa... once ventilation goes down...vessels constrict..that is the mechanism explaining pulm hypertension in COPD pts.
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| mdwannabe
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so, no responces to my question?
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| daira
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Airway constriction is due to Bronchoactive mediators (probably Leukotrienes). Atelectasis may play a role as well. (Harrison - selfassessment and board review, 15th ed. P. 191).
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| mdwannabe
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But what do "broch. active mediators" have to do with PE. There is no time for inflamation. Hypoxia is a rather acute event in PE.
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| mdwannabe
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So no explanation? Just a page referral? Unfortunatelly i don't have that book. So I would definitely appreciate if someone would share the info with me. Coz it does not make sence as of yet. Not according to pulmonary phisio, as far as my understanding of it goes.
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| daira
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Dear! I put this question here for discussion. I already wrote what the explanation said, I am looking for some detailed explanation as well. I ll post if I find something.
Thanks
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| mdwannabe
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I d appreciate it. Thank you.
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