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  #1  
Old 12-06-2011
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Lungs Acid base status in pulmonary embolism!

Whats the acid base disturbance in a person with a Pulmonary embolism??
Is it respiratory acidosis or respiratory alkalosis?

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  #2  
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respiratory alkalosis for sure
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well i think it depends on the level of embolization,,
if saddle embolism,,then acidosis,bcz no site for gas exchange otherwise, respiratory rate will increase that cause alkalosis . .

don't know for sure . .
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Old 12-06-2011
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Always remeber..
watever causes Dyspnea, Hyperventilation.. RESP ALKALOSIS.. u r losing CO2
includes Anxiety, PE, Panick Attacks, Pregnancy ( stimulation of central resp drive)
n remebr Hyperventilation can decrease Intracranial Pressure, by decreasing CO2 ,cerebral blood flow decreases... so ppl Hyperventilate in setting of Cerebral Edema!

n to contrast ,watever suppresses ur resp system.. like OPIODS, or THORACIc Muscle problems, u kno paralysis n stuff, COPD .. causes RESP ACIDOSIS and cuz u r retaining CO2
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  #5  
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Ok i agree with you but i was wondering if it also depends on whether its perfusion or a ventilation defect
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Also u can solve it with physiology concept
V/Q.. wen there is PE, acts like SHUNT!! no blood flow in presence of ventilation.. so the PaCo2 rises and PaO2 decreases!
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Quote:
Originally Posted by indigo View Post
Ok i agree with you but i was wondering if it also depends on whether its perfusion or a ventilation defect
there u go! perfusion defect!!
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well i feel there is a question in uworld in which a person presents with leg swelling and dyspnoea and answer is respiratory alkalosis . .actually when we consider alkalosis or acidosis,we should take lungs as a whole yes there is perfusion defect in an alveolus,but overall effect is dyspnoea so alkalosis . .but if saddle embolus then i think acidosis . .well again i don't know for sure . .

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  #9  
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Thanks Shyangel that was the very needed reply.
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Quote:
Originally Posted by shyangel18 View Post
Also u can solve it with physiology concept
V/Q.. wen there is PE, acts like SHUNT!! no blood flow in presence of ventilation.. so the PaCo2 rises and PaO2 decreases!
WOULDN'T T ACT LIKE A DEAD SPACE?
SHUNT IS INCASE OF AIRWAY OBSTRUCTION..
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Hyperventilation is the mechanism in ALL cases
Hyperventilation (ie increased alveolar ventilation) is the mechanism responsible for the lowered arterial pCO2 in ALL cases of respiratory alkalosis.
This low arterial pCO2 will be sensed by the central and peripheral chemoreceptors and the hyperventilation will be inhibited unless the patientís ventilation is controlled.

Causes of Respiratory Alkalosis
1. Central Causes (direct action via respiratory centre)
Head Injury
Stroke
Anxiety-hyperventilation syndrome (psychogenic)
Other 'supra-tentorial' causes (pain, fear, stress, voluntary)
Various drugs (eg analeptics, propanidid, salicylate intoxication)
Various endogenous compounds (eg progesterone during pregnancy, cytokines during sepsis, toxins in patients with chronic liver disease)
2. Hypoxaemia (act via peripheral chemoreceptors)
Respiratory stimulation via peripheral chemoreceptors
3. Pulmonary Causes (act via intrapulmonary receptors)
Pulmonary Embolism
Pneumonia
Asthma
Pulmonary oedema (all types)
4. Iatrogenic (act directly on ventilation)
Excessive controlled ventilation
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http://www.anaesthesiamcq.com/AcidBaseBook/ABindex.php
Most kickass Acid base explanations
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  #13  
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Quote:
Originally Posted by indigo View Post
Hyperventilation is the mechanism in ALL cases
Hyperventilation (ie increased alveolar ventilation) is the mechanism responsible for the lowered arterial pCO2 in ALL cases of respiratory alkalosis.
This low arterial pCO2 will be sensed by the central and peripheral chemoreceptors and the hyperventilation will be inhibited unless the patient’s ventilation is controlled.

Causes of Respiratory Alkalosis
1. Central Causes (direct action via respiratory centre)
Head Injury
Stroke
Anxiety-hyperventilation syndrome (psychogenic)
Other 'supra-tentorial' causes (pain, fear, stress, voluntary)
Various drugs (eg analeptics, propanidid, salicylate intoxication)
Various endogenous compounds (eg progesterone during pregnancy, cytokines during sepsis, toxins in patients with chronic liver disease)
2. Hypoxaemia (act via peripheral chemoreceptors)
Respiratory stimulation via peripheral chemoreceptors
3. Pulmonary Causes (act via intrapulmonary receptors)
Pulmonary Embolism
Pneumonia
Asthma
Pulmonary oedema (all types)
4. Iatrogenic (act directly on ventilation)
Excessive controlled ventilation
that's what i m trying to say, although perfusion defect, but still due to hyperventilation, it's alkalosis. . .PO2 will be low . .
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Quote:
Originally Posted by aiminghigh View Post
WOULDN'T T ACT LIKE A DEAD SPACE?
SHUNT IS INCASE OF AIRWAY OBSTRUCTION..
yes u rright !!! uggh i mixed that up.. its deadspace cuz ventilation going on without perfusion like happens in apex of lungs!!
and shunt is wen BLOOD IS being shunted because of airway obsstruction!!
but then. if its acting as DEAD SPACE.. mean the Alv Co2 shud Increase and Alv O2 will Decrease!! did i jus confuse myself even more?
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  #15  
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I think it all depends on whether hyperventilation is present or not,no matter what the cause is. Even Copd can have either respi alkalosis or acidosis and depends on the severity of it, I think
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Quote:
Originally Posted by indigo View Post
I think it all depends on whether hyperventilation is present or not,no matter what the cause is. Even Copd can have either respi alkalosis or acidosis and depends on the severity of it, I think
whenever you see dyspnea click alkalosis . .
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  #17  
Old 12-20-2011
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Default It depends on the level of perfusion defect

If the level of embolization is huge and if it is in the large arteries like the pulmonary arteries ( saddle embolus ), even though you try hard to hyperventilate and flush the co2 off your blood, you cannot, because your blood is not reaching the alveoli at all (ALMOST IT DOESN'T REACH, when you have a big embolus ). When the embolus is small and if it is mild-moderate, your Pco2 would definitely increase first. Then, your central receptors trigger, hyperventilation. But now since you have enough circulation to your alveoli, using that flow, you can flush the co2 out and so you end up in low pc02 and so alkalosis.
--------------------------------------------------

BOTTOM LINE :: It depends on the degree/level/size of the embolus. In case of a saddle embolus, it causes ACIDOSIS that cannot be corrected. In case of a small embolus, for a very very transient period, it causes acidosis which is rapidly reversed by hyperventilation that finally results in low pc02 and ALKALOSIS.

Because most of the emboli are small, you would have to consider that the embolus is small, when the stem of the question has no data regarding the size/position of he embolus and so you would have to answer it as RESPIRATORY ALKALOSIS.

Last edited by docchitra; 12-20-2011 at 11:02 PM.
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  #18  
Old 12-21-2011
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Thanks doc that was very well explained
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Old 12-21-2011
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You're welcome.
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Thumbs Up super duper high yield acid-base principle

Quote:
Originally Posted by shyangel18 View Post
Always remeber..
watever causes Dyspnea, Hyperventilation.. RESP ALKALOSIS.. u r losing CO2
includes Anxiety, PE, Panick Attacks, Pregnancy ( stimulation of central resp drive)
n remebr Hyperventilation can decrease Intracranial Pressure, by decreasing CO2 ,cerebral blood flow decreases... so ppl Hyperventilate in setting of Cerebral Edema!

n to contrast ,watever suppresses ur resp system.. like OPIODS, or THORACIc Muscle problems, u kno paralysis n stuff, COPD .. causes RESP ACIDOSIS and cuz u r retaining CO2
I should just remember:
Any problem causing one to hypoventilate = RESP ACIDOSIS
Any problem causing one the hyperventilate = RESP ALK
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