Acid Base Q, .......................NBME 2,3,14,15 - forever07

[ArchivalUser]

going to sleep...

[ArchivalUser]

My ans,
1) If co2 become normal instead of low level in B. Asthma... means respiratory muscles become fatigue and respiration become slow, so...co2 retain and co2 level rise to normal...But that is indication for intubation in asthma exercerbation.

2) Yes, if you give Badrenergic agonist in severe asthmatic child, it can cause pulmonary oedema.Mechanism???


3)Magnesium™s pharmacological action is ......to inhibit the release of calcium from vesicles in the sarcoplasmic reticulum, resulting in bronchial smooth muscle relaxation.
so, beta agonist will start action within minutes, steroid will be within hours. Mg can be used as an alternatives to above tm.

Am i right? TQ

[ArchivalUser]

1)Q where i ask how does metabolic acidosis occurs in a asthma
ans is hypoxia and increase work of breathing lead to lactic acidosis...

2)mechanism of pulmonary edema in severe asthmatic childeren not after starting treatment but basic pathophysio behind it..

ans-Spontaneous breathing in severe asthmatic children have negative Intra pleural pressure,as low as -35cm h2o during almost the entire respiratory cycle,so negative IPP causes increase left ventricle afterload resulting in pulm edema..and hypoxic vasoconstriction would increase the resistance pulm artery and can worsen the scenario..Pulmonary edema with acute asthma is a rare pathologic condition because the associated trapped air tends to maintain a positive intraalveolar pressure, thus decreasing the hydrostatic pressure gradient. Its pathogenesis can be associated with the severity of the maneuver done by patients so as to inhale (ie, forced inspiration as the patient struggles to inhale)..the lowered pleural pressure results in decreased interstitial pressure, whereas intravascular pressures are only minimally influenced. The airway obstruction in acute asthma is not uniform throughout the lungs, resulting in heterogeneous extravascular fluid accumulation...but in very rare scenarios..over all i think pulm edema mechanism in various conditions is very high yield topic...

yes beta2 agonists too can cause PE..

3)u said absolutely right...

[ArchivalUser]

1)due to hypoxia and increase work of breathing,promote lactate accumulation so lactic acidosis...so MAcidosis in Acute asthma and met alkalosis in chronic as we know due to RA in Ch asthma

2)yes beta 2 agonist also can cause P edema in severe asthmatics but without giving any t/t

MECHANISM-Actually spontaneous breathing children with sever asthma have negative Pleural pressure(as low as-35cm of h2o)during almost the entire expiratory cycle,so -IPP causes increased Left Ventricle afterload resulting in pulmonary edema..and the lowered pleural pressure results in decreased interstitial pressure, whereas intravascular pressures are only minimally influenced. The airway obstruction in acute asthma is not uniform throughout the lungs, resulting in heterogeneous extravascular fluid accumulation.
pulmonary edema with acute asthma is a rare pathologic condition because the associated trapped air tends to maintain a positive intraalveolar pressure, thus decreasing the hydrostatic pressure gradient. Its pathogenesis can be associated with the severity of the maneuvers done to get enough amount of inspired oxygen like forced inspiration as the patient struggles to inhale...

3)u said absolutely correct.

[ArchivalUser]

Thanks for your correction...
Any Q, info, explanation whatever u want me to know ,please Leave your message here..
I will answer you after next 10hrs, today my schedule is tight.
Appreciate u support!

[ArchivalUser]

I ll definitely let u know if something..
ok one more for you on acid base

Q,A 30 year old male is brought to ED from prison,where he works in the paint shop.He is barely arousable but has no focal abnormaltiies.He has no past medical history.CT scan of head is normal.Urine toxicology screen is negative.Ethanol and acetaminophen are not detectable.Lab data;-
Na:138meq/l
K=4.2meq/l
HCO3-=5meq/l
Cl-=104meq/l
BUN=14mg/dl
Ca=10mg/dl

ABG-po2=96,pco2=20,pH=7.20
Bl glucose=90mg/dl
urineanalysis=normal,without blood,protein or crystals.
Physical examination is BP 100/60,with no orthostatic change.
Which of the following is the most likely acid-base disorder?
a)Non-anion gap metabolic acidosis
b)Respiratory acidosis
c)Anion-gap metabolic acidosis
dAnion gap metabolic acidosis plus respiratory alkalosis

[ArchivalUser]

AG-29, so increased
D,anion gap metabolic acidosis plus respiratory alkalosis.
Please give some moreQ.

[ArchivalUser]

@ forever but the answer is C.
a bit strange though..but as explanation to this i read they mentioned the point that anion-gap metabolic acidosis PLUS resp alkalosis is excluded because the PCO2 of 20 is APPROPRIATE compensation,not TRUE respiratory alkalosis,so ans was C according to the KIND of options they gave..i also made it wrong first.

[ArchivalUser]

WOW! so then how can i different that appropriate compensation?
A/t Winter's formula, co2 should be 15.8 for compensation, right?
now, it's 20... I am confused...

[ArchivalUser]

,,