Ivonne
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A 79 yo M, weighting 75kg with emphysema is intubated in the ICU due to respiratory failure after developing ARDS secondary to E coli bacteremia. His ventilator is set to a RR of 20/min, tidal volume of 450ml and pO2 100%. If these setting are continued for 72 hours he is at risk of developing which of the following complication?
a.-CHF
b.-Jugular venous distension
c. Pulmonary embolus
d.-Pulmonary fibrosis
e.-Pneumothorax
Explain your answer pz
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| farnsworth
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(D) pulmonary fibrosis --> oxygen is pretty reactive and high partial pressures (not oxygen saturation!!!) lead to cell membrane damage. Usually reactive oxygen radicals are detoxified by catalase, glutathion synthetase and superoxide dismutase (the latter is often damaged/down regulated in patients after chemotherapy with bleomycin. This is the reason why young patients who underwent chemotherapy for testicular cancer are prone to developing ARDS when ventilated with a FiO2 of 50% for elective surgery)
Theoretically (B) could happen, but this a very, very remote option: FiO2=1.0 leads to resorption atelectasis, especially in ZEEP conditions, thus promoting shunt, thus eventually leading to pulmonary hypertension and to right sided heart failure.
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| farnsworth
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BTW: mortality of ARDS is around 30 - 50% (ARDSNet 1999: 38-48%), despite all progress in intensive care medicine. Most deaths are attributable to multi organ failure; even if the patients survives, the quality of life is reduced (due to pulmonary fibrosis, impaired oxygen exchange, and right sided heart failure etc).
Indeed, the ARDSNet study is almost the only study that could prove a benefit regarding the outcome attributable to a specific therapy regime: limitation of the tidal volume to 6mL/kg predicted body weight. It is also one of the most controversal studies (it is common practice to limit the peak pressure to 32mbar, even if the tidal volume is further reduced, e. g. to 4mL/kg PBW and to reduce the FiO2, aiming at a SaO2 of 88-95% and a PaO2 of 55-80mmHg, hypercapnia is tolerated, as long as pH>7.2).
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| hero
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probably before pt will develop fibrosis (that's correct, but it will take time), he will have pulmonary edema (RR 20 and 100% O2) and ans probably is not D.
i would say B
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| farnsworth
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hero: you are right, fibrosis develops later in the course of ARDS, whereas edema formation within hours, so the answer might as well be (B).
Although: edema formation has not been shown to be dependent on neither RR nor FiO2. Cyclic stretch (caused by high VT) imposed on the lungs leads to activation of alveolar macrophages and release of inflammatory mediators 1) into the lung and 2) into the system circulation (translocation). The release of inflammatory mediators leads to an increase in alveolar cell permeability and edema formation.
However, this patient has most likely an indirect (extrapulmonary) ARDS secondary to E. coli bacteremia, so edema may already be present at initiation of ventilator therapy.
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| arlete
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No idea. I am posting so I'll come back to check the answer. 
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| lampard
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Why no takers for tension / simple pneumothorax?
High inrapulmonary pressur=> increased intraalveolar pressure => plus the patient is generally vulnerable to pneumothorax = > rupture of an alveolus/ bronchiole into pleural cavity
PEEP increases the intrathoracic pressure => pressure on the heart => Hypotension => No JVD Hence B ruled out.
Pulmonary Fibrosis is a chronic event. I dont think , it would develop over a period of 72 hours.
I would greatly appreciate if I am corrected...
Ref:
Kaplan vids
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| Ivonne
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Hi lampard I thought like you....barotrauma...but i was wrong. i learnt that the if the tidal volume is the weight(kg) times 6 the risk for tension pneumothorax is low.
in this case tidal volume---------->75kg times 6 = 450---------->low risk for tension pneumothorax.
Keep trying 
Edited by Ivonne on 01/29/08 - 08:05 PM
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| hero
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lampard wrote:
PEEP increases the intrathoracic pressure => pressure on the heart => Hypotension => No JVD Hence B ruled out.
Why you assume PEEP?
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| drshvetasm
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i wud have picked pneumothorax too...
so wats the consensus Ivonne...whats the answer given? we all gng with pulmonary fibrosis?
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| Ivonne
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Ok the correct answer is pulmonary fibrosis.
High concentrations of inspired oxigen through a ventilator may lead to pulmonary fibrosis, which becomes irreversible. In the setting of ARDS if the inspired fraction of oxigen can not be lowered without producing hypoxia, the adition of PEEP is indicated.
Therefore another point to remember:
PEEP is indicated to prevent the development of oxigen toxicity, which may result in irreversible pulmonary fibrosis.
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| lampard
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Hi Ivonne,
I was under a wrong impression that 72 hours is short duration for development of pulmonary fibrosis ( duely corrected by my study partner )
I would like to make a correctinon too:
In the kaplan vids, he mentions the normal tidal volume to be 10 cc/kg, which doesnt sound appropriate. Your value of 6 cc/ kg seems more acceptable ( 70 * 6 = 420 cc )
Thanks mate...
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| farnsworth
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in 'real life' no patient is ventilated without PEEP. The ARDSNet (NEJM 2000) suggested the following FiO2 and PEEP setting (for ARDS patients):
FiO2 0.3 0.4 0.4 0.5 0.5 0.6 0.7 0.7 0.7
PEEP [mbar] 5 5 8 8 10 10 10 12 14
FiO2 0.8 0.9 0.9 0.9 1.0 1.0 1.0 1.0
PEEP [mbar] 14 14 16 18 18 20 22 24
a more recent study investigated the effects or a higher PEEP vs the ARDSNet settings, but failed to show any benefit (Brower, NEJM 2004).
PEEP is generally used to counteract de-recruitment caused by suppression of spontaneous breathing, leading to a relative increase in blood flow to shunt and low V/Q areas. A PEEP of 5mbar is definitely not sufficient to recruit collapsed areas, in most ICU pts it is not even effectively preventing de-recruitment ('opening the lung' and 'keeping the lung open' are two different buzzwords in the world of ventilation specialists).
My personal opinion is, that this question is more suitable for the board exam in intensive care medicine, than for the USMLE.
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| farnsworth
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Regarding 'barotrauma': most authorities now speak of 'volutrauma' (high VT), 'atelectotrauma' (cyclic opening and closing of alveoli, mainly caused by insufficient PEEP), and 'biotrauma' (caused by mechanical stress of alveolocytes due to ventilation distribution heterogeneity in ARDS, leading to macrophage activation, and .....).
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| Ivonne
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farnsworth wrote:
My personal opinion is, that this question is more suitable for the board exam in intensive care medicine, than for the USMLE.
Well it is one of the new questions in kaplan Qbank for CK...
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