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* @drdab
 #855774  
  cardio69 - 12/02/18 21:39
 
  Hi, hope all well on your end.
You're most welcome.

let see if you clear now:);

If intrapleural NEG to ensure lungs expansion & prevent “loss of lung vol”* by deflection of alveoli -> subsequently -> collapse of part of the lung (may cause by a variety of disorder as you know). Now you understand intrapleural/NEG is quite important to maintain a norm FRC, RT!!! In ‘newborns’, as you know kidos are predisposed “loss of lung vol”= (you recall what we call that in medical term as I just painted by words above?*) AND also, LOWER PaO2.

Now ans Q4 me, can you tell me HOW you can “INC” PaO2 let say from ~ 64 mmHg TO-> 100 mmHg in neonate’s base on what u learn from NEG intrapleural P?
 
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* Re:@drdab
#3375689
  drdab - 12/03/18 03:22
 
  Hi,
I am not clear about the 2nd last line that u've written but I shall try answering from what I have understood . I believe that ur suggesting newborns with respiratory distress.

Now the answer to your q-
If I wanted to increase the Pao2 in the neonate based on my comprehension of the -ve ipp, in the above case i wud need to provide surfactant (so as to decrease recoil & thus increase compliance)
& also provide positive pressure ventilation(so as to prevent alveolar collapse) . By doing this we wud increase the diffusion & ventilation so as to finally raise Pao2. Hope i am rt.

I have another q -
how exactly does increased surface tension in alveoli cause pull edema?

Thank u for ur time.
 
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* Re:@drdab
#3375721
  cardio69 - 12/03/18 20:38
 
  @time of kido walk to earth@birth wall of those grapes/alveoli are at 1st collapses (bz of surface T thick fluid that fills them). More thank 25mmHg of NEG inspiratory P in lung usually required to oppose the effect of surface T & open the alveoli for 1st time.
Once they are open more respiration can be affected with relatively weak respiration movements. The magic is that the 1st Inspiration of norm kido are thunder/very powerful (they able to create more than ~60 mmHg NEG P in intrapleural space😊 )
To norm pulmonary blood flow & ventilation ↑ both arterial & mixed venous O2 tensions, that been said; the PaO2 at 1st wk to a month of life can be low as 55 (but could range btw 65 & 85) a level lower than that of norm in children/older infants/adults (95-100)
The low PaO2 partially due compliant (cartilaginous neonatal chest wall) that really have a hard time to recoil outward @end of expiration ( as it happens in older children & adults). So you could say failure to recoil outward create intrapleural P of “0” cm water and NOT -5 P that u see in children/older infants or adults… Now bz NEG intrapleural P is important of maintaining norm FRC. Now that can jeopardize newborns to atelectasis & LOWER PaO2.
So if you could apply enough NEG P around the neonate’s chest -> to bring it -5 pleural P & INC PaO2 for that 64 -> 100. NEG intrapleural P expand -> lungs -> INC FRC and that can reduce atelectasis & improves the match of ventilation -> perfusion… and oxygenation
Now, that would be painted “Atelectasis” by word on my Q.

FIN.
_________________________________________
As For your Q, ↑ surface tension -> interstitial hydrostatic P? -> DEC -> favor movement of fluid -> alveolus.
 
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* Re:@drdab
#3375727
  drdab - 12/03/18 23:24
 
  Wow that was such an amazing concept, beautifully explained.
I am yet to touch upon atelectasis , so I guess that's why it didn't strike me.
Anyways lookin at the positive u've introduced me to it.

As for the answer to my q,
I can understand that increase surf tension causes increase recoil & so inc in neg ipp is required for lung expansion, which wud in turn act upon the alveolar capillaries & result in pulm edema.
But what I can't understand is that how an inc surf tension causes a decrease in interstitial hydrostatic pressure- is it cos the neg ipp gets transmitted to the interstitial space?????

Gracias😊
 
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* Re:@drdab
#3375771
  cardio69 - 12/04/18 18:50
 
  You kind of mixing it up;

Let say you got post obstructive pul edema ( NEG P pul edema following his/her acute upper airway obstruction* any cause epiglottitis, obesity, hiccups…
They related to dev high NEG intrapleural P by vigorous inspiratory effect against those* what happens, is that the high NEG intrapleural P goes down -> ↓ the interstitial hydrostatic P, and you know ↑ venous return & LV afterload ( + other factor I assume u know, Neg P -> rush of sympathetic kick in, HTN and central disp of blood vol. All those -> paint pic of Pul edema by ↑ the transpupillary P gradient.
You need to understand norm physio, pal Starling relationship & how to apply it.
So you understand one of major cause pul edema is a loss of surfactant? RT! so that cause high surface tension and follow my path my 1st path I draw for you above post (ARDS for ex).

You understand the basic, the abnorm gone be easier to understand.

If I tell you got pat with mitral stenosis/or LHF, how they dev Pul edema?; you would say ↑capillary hydrostatic P, a result of abnorm high pulmonary venous P…. and so on

Try to understand pul edema caused by what mech... I touch 2 mech, you need 2 more cause.
 
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* Re:@drdab
#3375785
  drdab - 12/05/18 00:17
 
  Hmm 🤔
The other 2 causes wud be decrease oncotic press & obstructed lymphatics, rt??

As always thank u for helping me out.
 
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* Re:@drdab
#3375818
  cardio69 - 12/05/18 15:46
 
  That’s RT, my recommendation to you think if you can place the scenario or your pat in the real world in cardiogenic or not (noncardiogenic divide them exogenous^ or endogenous/sepsis for yourself).

If cardiogenic or hydrostatic pul edema -> then hydrostatic pul edema (hydrostatic P gradient up/ or pulmonary capillary hydrostatic P).

If vascular endothelial cell &/or alveolar epithelial cell permeability is UP that setting place it non-cardiogenic /or ↑ permeability pul edema

If you got ↓plasma colloid osmotic P (i.e. hypoalbuminemia/nephrOtic…)

and if lymphatic drainage is impaired (i.e. lymphoma or infection TB or radiation* & yellow nail S…)
You may see indirect injury let say narcotic OD and last not least can be undetermined origins or let say direct injury* or in gas^/O2, phosgene, smoke or chlorine… or pat near drowning. Or the undetermined origin of edema like high altitude. Keep all these causes in your ddx.

Glad I could help.
 
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* Re:@drdab
#3375824
  cardio69 - 12/05/18 17:26
 
  Let’s make sure you got it


You are called for a 26 y/o F, possible OD, unknown if breathing. On arrival, the pat is unresponsive on her bathroom floor. Sis reports they found her on the floor not breathing just prior to calling 911. They had last seen her well 20 minutes prior. She has a known history of heroin use, and you notice an empty syringe next to her. On exam, pat is unresponsive, cyanotic, with agonal respirations and has a pulse of 40. You immediately commence resuscitative measures. The airway is positioned, a nasopharyngeal airway is inserted, and +/pressure ventilations are initiated via a bag-valve-mask connected to high-flow oxygen, with a resultant resolution of cyanosis. 4 mg intranasal naloxone is adm. About 3 minutes later, the pat wakes and you start to notice copious pink, frothy secretions. You suction, but it continues, and even seems to increase. The pat is now alert, complaining of shortness of breath and hypoxic to 78% despite a non-rebreather mask flowing at 15 L/min. Your partner asks you, “did she aspirate?”

The scenario here is cardiogenic or non?

 
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* Re:@drdab
#3375923
  drdab - 12/07/18 23:09
 
  That's a tough q
umm i am guessing its non cariogenic cos i read that heroin causes histamine release
 
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* Re:@drdab
#3375945
  cardio69 - 12/08/18 16:28
 
  RT,

My preach of teaching prove that you learn it well. No matter how hard the Q would be.

That is a case of opioid related NON-cardiogenic Pul edema/NCPE Osler dissected 1st ~ 150 yr ago. Can be OD of heroin/or methadone. You see it mostly in M shoter duration of heroin & mostly w/in hrs of injection.

Pathophys hazy combo of direct toxicity/hypoxia*/acidosis 2ndry to hypOventilation &/or cerebral edema + what I just mention the most favorite theory ↑ pulmonary capillary permeability related to* &/OR as u mention histamine release -> leaky pulmonary vasculature
Other side pic we can blame naloxone, dependent pat opioid/OD, and repaid reverse with high dose of naloxone -> experience rush of catecholamine (particularly if your pat combo that with cocaine) and as I just dissected the previous post you can blame naloxone following a long period near/or complete apnea -> inspiratory effort to complete opening of glottis -> excess NEG P w/in lung, drawing in fluid from the pulmonary pipe/vasculature ( adm POS P ventilation before naloxone therapy may soften pic😊

Regardless of underlying etiology, you learn my preach and that’s all important 4 me.
 
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* Re:@drdab
#3375951
  drdab - 12/08/18 22:23
 
  U r truly an encyclopedia on this forum.
Thank u for being so insightful.
😊😊😊😊
 
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