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Mechanical Ventilation - Science topic

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Ventilation during adult cardiopulmonary resuscitation (CPR) is poorly understood. Therefore, guideline recommendations are limited. The use of waveform capnography is in part recommended to monitor frequency. Other ventilation measurements such as tidal volume or inspiratory pressure are not regularly obtained, especially when a bag-valve system is used. The use of new monitoring devices can improve guideline adherence and could lead to better understanding of ventilation during CPR. Different EMS systems have varying levels of training, equipment and resources during CPR of out-of-hospital cardiac arrest (OHCA) patients. To better understand the current state of ventilation monitoring during OHCA CPR researcher/practitioner feedback and international perspectives on this question are needed and very much appreciated.
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Current guidelines recommend giving the maximum feasible inspired oxygen during CPR based on the premise that restoring depleted oxygen levels and correcting tissue hypoxia improves survival.
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The study of ventilation during adult cardiac arrest remains challenging due to the unexpected nature of sudden cardiac arrest and the limited resources/personnel on site. This is especially true for interventions that influence outcomes when applied early in the cardiac arrest phase. Therefore, animal models (i.e. pigs, dogs), manikins, human cadavers and computer models have been used to study intra-arrest ventilation. Also, some data has been made available from registries and clinical studies in humans.
While the possible answers to my question heavily depend on the respective research question, personal perspectives on the well known experimental models, as well as lesser known models for this niche of cardiac arrest research, would be very much appreciated.
Please note, that I do not to intend to discuss airway management during cardiac arrest. Although, I'm aware that both intra-arrest ventilation and airway management are closely connected.
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Yet to be developed
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I am currently writing my dissertation on the use of non-invasive ventilation to deliver nitric oxide in neonates and I was wondering:
  • What are people‘s experiences of using non-invasive iNO with CPAP, Nasal cannula, oxygen hood etc?
  • Which gestational have you primarily used it with?
  • What were the indications/ underlying pathologies?
  • Have you found this has reduced the need for mechanical ventilation or ECMO?
  • Have you needed to deliver higher doses to achieve the same effect seen on mechanical ventilation?
  • Which countries have you seen this being practiced?
Any other insights or information would be greatly appreciated.
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I have used inhaled nitric oxide with non-invasive ventilation in a few infants with severe BPD- I must say, they did not stay extubated for long. Infants w BPD and concomitant pulmonary hypertension are probably served better by placed on sildenafil to manage their pulmonary hypertension and this has been our practice with our pulmonary colleagues.
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The preliminary report from the randomized RECOVERY clinical trial (NEJM JW Infect Dis Sep 2020 and N Engl J Med 2020 Jul 17; demonstrated that 10 days of dexamethasone resulted in a mortality benefit in hospitalized COVID-19 patients, especially those on mechanical ventilation. Investigators at a referral center in Brazil have now performed a double-blind, randomized, placebo-controlled clinical trial evaluating the efficacy of a 5-day course of methylprednisolone (MP) at reducing the mortality of patients hospitalized with COVID-19.
Of 416 patients randomized, 393 (mean age, 55 years) completed follow-up: 194 in the MP arm and 199 in the placebo arm. No patient received remdesivir, anti-IL-6, or anti-IL-1 agents. The most common comorbidities were diabetes, hypertension, and alcohol use disorder. One third of patients were mechanically ventilated. Mortality at day 28 was 37.1% in the MP group and 38.2% in the placebo group. No between-group differences were apparent in mortality at 7 days or 14 days, viral clearance in the upper airways, or need for mechanical ventilation at 7 days. In a subgroup analysis, day-28 mortality was significantly lower with MP versus placebo among patients older than 60 years of age (46.6% vs. 61.9%).
What is your thought on this ongoing debate? should we use it or not?
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Dear Shalendra Singh !! I'm also working in Covid-ward not in ICU. I agree with you. Those 2 really doing magic. Clinical Trial doesn't always goes hand in hand with Practical Experience.
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Hi fellow researchers and colleagues
I'm starting a new online peer review journal specific for the topic of mechanical ventilation. It will be free for authors and readers. Hoping for first issue in September 2020
Any suggestions how to promote it worldwide or feedback ?
Thank you
Ehab Daoud
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Hi colleagues
The first issue of the journal of mechanical ventilation is now online
Thank you for your support
Ehab Daoud
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Immune responses to infections with by a corona virus vary widely and are appear to be related to the development of most severe complication, acute respiratory distress syndrome. Since survival of patients respondingto the virus in this way depends on respirators support, mechanical ventilation and extracorporeal oxygenation, therapeutic methods which demand highly specialized medical and nursing staff, human resources which become scarce in an epidemic or pandemic. Since vaccination are not available in newly emerging corona virus epidemics it would be interesting to know if and which targeted pharmacological modulation of immune response early in the course of an infection could help to reduce the need for intensive care and/or improve the outcome of respiratory support.
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Detection of Immunoglobulin M (IgM), IgA, and IgG Norwalk Virus-Specific Antibodies by Indirect Enzyme-Linked Immunosorbent Assay With Baculovirus-Expressed Norwalk Virus Capsid Antigen in Adult Volunteers Challenged With Norwalk Virus
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As a consequence of the Noise Abatement Act, they were obligatory for many noise-loaded dwellings. Many types were developed.
Later, recently in fact, energy saving measures changed this: mechanical ventilation including heat exchangers and silencers made "suskasten" unnecessary.
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Simone Torresin : Of course people want to have the option of opening windows. The intention of "suskasten" is to avoid the dilemma: noise or fresh air. In particular in sleeping rooms this is important.
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Covid-19 cases, who are developing severe ARDS / respiratory failure are requiring mechanical ventilation, and the number of such cases is increasing during this pandemic. However, even in the countries having advanced and robust health care facilities are failing to provide an adequate number of ICU beds and Ventilators for such increasing numbers of patients. Healthcare providers of many areas are now using one ventilator for providing mechanical ventilation to multiple patients simultaneously. As most of the ventilators can not provide differential ventilation (even those which can, are designed for two lungs at most 2 patients), is it safe to do so? As the compliance of the lungs of the different patients will be different, their PS, Vt and MV required will be different, how it can be feasible? Isn't there a chance of cross-infection / super-infection? Please opine and guide..
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Everything in medicine balances risk and potential benefit.
In a crisis situation when I have to intubate a patient but there is no ventilator is available then I would share the ventilator rather than choose which patient should be ventilated.
Is sharing a ventilator less safe than using one ventilator per patient. Not ventilating a patient who needs it will inevitably result in death.
These are difficult times and difficult choices will have to be made.
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The entire world is now affected and the resources are getting exhausted. Even the best healthcare systems are failing to tackle the explosion of COVID-19. Judicious use of resources is therefore very essential. Many of the COVID-19 patients will be frail, terminally ill, etc. in whom intubation/mechanical ventilation or resuscitation may be futile. So, is it high time to adopt DNR/DNI for such patients? If yes, for which patients? Should the administrations/governments/ethical aspects be less rigid so that such rules can be adopted? What is the local rule/policy in your place?
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My opinion: As a physician, when you accept responsibility for the care of a patient, you must provide the best care possible for that patient, at the time, based upon your skills, resources and circumstances at the time. You are not the government and you are not God, don't try to be, focus on the best you can do to support the wishes and the outcome of that patient. If the patient requests DNR, then fine, but if the patient wants help, then you must do the best you can. I found a good test was, "Are you able to sleep that night?" If not, you are going to have problems (Unless the physician is a sociopath; but they should have been weeded out in premed)
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Anyone interested in exploring novel ways of monitoring the appropriate position of endotracheal tube (ETT) in mechanically ventilated ICU patients?
Traditionally this is done with repeated Chest X-rays. What about researching new available technologies, like ultrasound or wireless methods, without the potential hazards of repeated radiation?
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Dear Polly Dendy , yes, USG is already being used to detect ETT position in many centers with necessary expertise by the interventionists. Of course, the supportive options like direct visualization, capnography etc may be adopted in exclusively difficult plus suspected scenarios. You may please go through this related paper:
Regards- Rabiul
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This is the situation. A classification model with 5 groups with some kind of order has recently been published in adult patients under mechanical ventilation (http://bit.ly/33E3T2V) and I want to test if this classification also suits for pediatric patients in terms of similarity of proportions. I wonder if Chi2 (in a 2 x 5 table) vs. Cochran-Armitage test would be the best way to test this situation (I think the latter, because of the ordered classification) and also which would be the minimum sample size for each test. I found here (http://bit.ly/2OWB7Gz) that sample size in this scenario gets smaller when number of groups increases, and that with a five-group classification a n=400 would satisfy the requirements for a power near 80%.
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Yes, that was the paper I initially cited in the first question. With this, I can assume that a n=400 will provide 80% power and an alpha=0.05 as shown on table 4. Thank you for your invaluable advice.
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Occasionally we used to have transcutaneous CO2 monitors for selected ICU patients, especially those who are ventilated with HFOV.
However, with its poor correlation with the blood gas analysis and the complications of the electrode site burns, I think it is out of fashion?
Is anyone using similar products with better clinical experience?
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I'm a little confused by the comments about "burn sites" because modern transcutaneous oxygen and carbon dioxide monitors don't burn the skin. When I was an anesthesia resident at UCLA, I had the opportunity to try the earliest version of a transcutaneous oxygen monitor, and with these primitive machines there was some concern about leaving the sensor in the same location for prolonged periods of time due to the possibility of causing tissue damage. They warmed the skin to "arterialize" capillary flow, but the heating element was not regulated by a thermostat. It was impossible to calibrate these original monitors. They provided a numerical "readout" for oxygen concentration that rose with increased tissue oxygenation, but they could not actually measure the partial pressure. There has been considerable improvment in the technology during the 50 years since I was a resident. I have purchased one of the new machines. They now measure transcutaneous CO2 as well as oxygen, and can be calibrated to measure the partial pressures of both. However, they remain far from ideal. They are very "tricky" to use. Their main advantage is that they are non-invasive, and can provide continuous measurement of the partial pressures of oxygen and carbon dioxide. The sensors are not likely to cause tissue damage, because they are now governed by a thermostat that maintains the skin temperature around 45 degrees celsius, so patient injury is no longer a concern.
I am now working with the Plexus software company to enable automatic incorporation of TcO2 and TcCO2 data into my anesthetic records, and capture readings every five minutes.
Carbon dioxide chemistry and pathophysiology is very tricky stuff. I once had an engineer who helped design modern capnographs tell me that it was necessary to install a fan in the measurement chamber of the machines to constant stir the gas mixture, because carbon dioxide has a vexing tendency to "settle" and thereby frustrate accurate measurement. Transcutaneous CO2 measurement is similarly vexed by variables. The sensor is mounted in a small plastic cup that is pasted to the skin. About five drops of saline solution must be installed in the cup before the sensor is attached. The skin must be carefully "prepped" to prevent the water from leaking out of the plastic cup "chamber" where the measurement takes place. The temperature must rise to 45 degrees before the machine begins to operate. Too much or too little water in the chamber will disrupt measurement. The sensor must be calibated each time it is applied, and if you are using it in an ICU setting it's probably a good idea to re-calibrate the sensor every hour or so. I use the machine only during short dental surgeries, and must re-calibrate between each case. It's essential to have a clear understanding of the role of carbon dioxide in the pathophysiology of oxygen transport and delivery, and CO2 data alone is meaningless in the absence of O2 data.
Exactly what are you trying to accomplish in the ICU setting? Are you performing some sort of study, or are you using the machine to manage critically ill patients?
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I don'twant to use CFD method.
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Prof Liu Jing in HIT has deveploped a module in DEST for thermal energy analysis in underground buildings. You can contact him for more information.
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Waiting to read this article after reading the excellent article 'Ventilating the newborn and child.
I am interested in any model of lung physiology that can help with studying modes of ventilation in newborns.
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Hi David
We have developed a volume-controlled prototype platform for neonatal resuscitation and ventilation to mitigate volutrauma and BPD.
Please see www.kmmedical.co.nz for overview and comparative studies.
We are interested to license.
Regards
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Please take part to this international survey (3 minutes!). We want to know how you manage anticoagulation, including antithrombin supplementation, during veno-venous ECMO. Your contribution will be acknowledged in case of publication (this is why the survey is not anonymous).
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Dear Alessandro Protti,
VV-ECMO- Veno-Venous ExtraCorporeal Membrane Oxygenation is an artificial Membrane Lung, with its blood pump, placed in series with the failing Natural Lung (NL). The ML can totally or partially take over the functions of the NL in both carbon dioxide removal and oxygen intake. The delivery of O2 to the patient's metabolism and the removal of CO2 depend on a complex interaction between the ML, the NL and the metabolic status. Why anti-thrombin (AT) is needed during VV-ECMO?
-Bleeding is the most feared complication during ECMO and is associated with high dosing of heparin. Although, there is no consensus on antithrombin (AT) supplementation during ECMO, AT is needed by heparin to properly anticoagulate. Heparin is required during ECMO to avoid circuit thrombosis and its anticoagulant effect is strictly dependent on antithrombin (AT). AT also plays a central role in mediating inflammation. Acquired AT deficiency is common in patients on ECMO, arguably due to long term anticoagulation in addition to sepsis itself. AT supplementation increases anti-Factor Xa (anti-Xa) levels without increasing heparin dosage. This may have a clinical impact because risk of bleeding during ECMO is associated with higher heparin dosage. Clinicians strongly believe that maintaining normal antithrombin activity levels (80%-120%) during ECMO will potentially be associated with:
1. Less heparin dosage
2. More adequate level of anticoagulation
3. Less hemostasis related complications, and
4. A lower level of inflammation
See the links below:
Best wishes
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what is the best management in Acute exacerbation of COPD which is resistant to medical management :
A- CPAP ( Non invasive positve pressure ventilation )
B- Intubation and mechanical Ventilation .
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One must be selective in the post-surgical population with COPD. Although the morbidity and mortality is increased when a surgical patient is re-intubated, a thoughtful assessment of pathophysiology must be made. Residual muscle weakness associated with neuromuscular blockers, narcosis or residual anesthetic gases will exasperate COPD symptoms and may be best resolved with a short course of mechanical ventilation. I have had anecdotal experience of patients receiving NIV when tracheal intubation would have prevented significant gastric distention.
Regards,
Christopher
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We know the values of NOx, CO and soot production for vehicles based on the PIARC reports (for fluent traffic, as well as for traffic jams), the traffic flow from a detailed traffic forecast analysis and the age/fuel type of the cars as brackets from national statistics. This allows us to estimate mean/peak emissions within the tunnel with reasonable accuracy. We know what is the airflow velocity / ventilation capacity for all of the traffic scenarios as well. Now, we have to propose a filtration solution, for which we first need to know, how can we translate our emissions into PM2.5 / PM10.
A very easy assumption for our further modelling, would be that the most of the particulates generated in the tunnel are formed from the soot. I'm not sure if it is possible for larger particulates to form from NOx / O3, as the tunnel is constantly ventilated (either through traffic, or by mechanical ventilation in a traffic stop). I would also assume that mass of soot >>> mass of particulates emitted by breaks, tyres etc., which means we could ignore the latter (especially for traffic stop scenario).
Please share your experience in this (particulate) matter.
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When it comes to tunnel air filtration, there are a few studies available that may assist your work. although it is written in German, the following report may be of interest:
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 I am simulating a mechanical ventilation of a building floor space. Requesting help on how to define the Boundary Conditions (In general, I came across materials using P-Q curve of fans as inlet definition for electronic cooling applications. Is it similar for Jet fans/Propeller fans ? How should I do it inside FLUENT ?   Thanks for your help in advance!
PS: Is there any sample *wbpz files that any one can share so that I can take a look the Named Selection definition ?  This would be of great help!  
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I assume you are interested at the flow on the floor, and do not want to resolve the flow around the fan in detail?
One important issue: is the fan located inside  your domain (so, is it causing an internal recirculation), or is it on the domain edge (pumping air in, which leaves the domain elsewhere?)
In case of the latter, what you can do is just create a surface on the location of the fan, and set it as a velocity inlet with the discharge velocity of your fan/ a mass flow inlet with the discharge flow rate. Set the locations where air leaves the domain as pressure outlets. In case of the former, the situation is a bit more tricky. One option may be to remove a small box from your domain at the fans location. Set one side of the box as  a velocity/mass flow inlet, the opposite site as a pressure outlet. Alternatively, you may specify a small cell zone region as "fan", and use fixed velocity values or a momentum source under cell zone conditions.
If you want to explicitly resolve the flow around the fan, you'll need to use multiple reference frames or sliding mesh, and resolve the fan geometry explicitly. Will be much more costly in terms of meshing. 
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Is there a positive effect on parallel canullamanegement and the weaning of ventilation? Or is there to less evidence of effectiveness?
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Less sedation, better suctioning, most probably earlier separation from the ventilator.
Tracman study compared early versus late trachy, where no mortality benefit had been shown
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Hello all,
In case of compressible fluids, where temperature can change due to changes in pressure, is there some threshold (or minimum) change in pressure required after which one can observe change in temperature. ( one may consider evaluating the phenomena on time scale of micro seconds)
Similarly, is the pressure change required to cause change in temperature in compression same as expansion i.e will the same change in pressure (increase or decrease) cause change in temperature or is it that for change in temperature in expansion, a little higher (or lower) change in pressure may be required as compared to compression. ( here also considering the processes being evaluated at micro second time scale)
Thanks
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@Zwan
In respect to your answer " It is equilibration time vs measurement time that is relevant here", if I talk in terms of typical Navier Stokes equation, then do you mean that there does not exist equilibrium between thermodynamic and mechanical pressure ? ( in other words stokes hypothesis is not valid)
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In my view the cause of lung damage during modern mechanical ventilation is due to the positive pressure. Positive pressure ventilation causes atelectasis, and subsequently all the other problems if mechanical ventilation is maintained for a long time.
Negative pressure (expanding the thorax and getting air to flow in by under-pressure e.g. by a quirass sytem, or natural breathing) takes away the atelectatis very rapidly. That is why in every manual of the Anesthesiogists it says: directly after surgery, when the patient is awake again, ask him/her to take e few deep sighs.
My question: is it possible by your thechnique to prove the development of atelectasis by positive pressure and removal of the atelectasis by negative pressure vetilation?
This is very important, because patients with severe lung problems should not be ventilated by positive pressure systems. The life of a category of patients will be saved by negative pressure ventilation, because of the above reasons. So, please show the world what is going on, for most of the ventilators still believe the "law" (spoken out as a proposition around 1900) that there can be no difference between negative and positive pressure; they claim that everything is determined only by the pressure difference. They claim this is just physics. But this is only true in a static situation. During dynamic pressure variation this is absolutely not true.
Jan van Egmond.
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If the respiratory system is modeled as a single compartment model (R and C) then of course there is no difference between "positive pressure ventilation" and "negative pressure ventilation" because all assisted ventilation is by means of a positive change in trans-respiratory pressure difference (pressure at airway opening minus pressure on the body surface). But of course the respiratory system is made up of millions of resistances and compliances in complex series and parallel combinations. Hence the paradoxical views expressed in the other comments.
To the extent that negative pressure ventilation attempts to mimic normal breathing, I would suggest that the issue is even more complicated than we think.
For example in a recent paper by Yoshida et al (Am J Respir Crit Care Med. 2013 Dec 15;188(12):1420-7. doi: 10.1164/rccm.201303-0539OC.Spontaneous effort causes occult pendelluft during mechanical ventilation. Yoshida T, Torsani V, Gomes S, De Santis RR, Beraldo MA, Costa EL, Tucci MR, Zin WA, Kavanagh BP, Amato MB.)
The conclusion was: "Spontaneous breathing effort during mechanical ventilation causes unsuspected overstretch of dependent lung during early inflation (associated with reciprocal deflation of nondependent lung). Even when not increasing tidal volume, strong spontaneous effort may potentially enhance lung damage."
See also
Am J Respir Crit Care Med. 2016 Oct 27. [Epub ahead of print]. Spontaneous Breathing During Mechanical Ventilation - Risks, Mechanisms & Management.Yoshida T, Fujino Y, Amato MB3, Kavanagh BP.
Concluding that: "Notwithstanding the central place of spontaneous breathing in mechanical ventilation, accumulating evidence indicates that this may cause -or worsen acute lung injury, especially if ARDS is severe."
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In respiratory research a breathing apparatus consisting of mouthpiece, filter, Pneumotachometer, and non-rebreathing valves plus some connectors are usually used. Although a non-rebreathing valve is used to reduce dead space, each of these devices has its own dead space. Though small, adding together they build a relatively large dead space sometimes. What is the max acceptable dead space in a breathing apparatus, for a study including healthy adults?
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I fully agree with the first answer. I would however like to suggest using two pneumotachographs, one in the inspiratory limb, one in the expiratory limb. The sum of flow rates of both gives you the total flow rate. This way, the pneumotachographs do not contribute to dead space. You may consider this principle also for filters etc.
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I’m working on project about the development of electronic communication device to be used with invasive mechanically ventilated patients who are not able to speak verbally, so beside I need to measure its impacts on patients outcomes , I am looking to measure the nurses experiences or satisfaction while using this new device.
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I am also interested to hear from colleagues if a Likert scale on this issue is available. Otherwise, you can use Visual Analogue Scale (VAS) for this purpose.
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How many times a week and for how many months should patients with Chronic LBP be trained in a hydrotherapy setup so as to improve core muscles, back extensor and gluteal muscle strength and endurance of core muscles and back extensors? Please provide any supporting articles as well if available.
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3 times per week. Each one 1 hour of duration session.
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Can the use of different types of mechanical ventilatory modes cause peripheral vasoconstriction?
During the cares of a patient on BIPAP ASB it was noted that the patients fingers were both cold on both hands, and mottled on the left hand. After changing the ventilatory mode to CPAP ASB, both hands and fingers warmed up, and return of normal colour appeared.
But on returning the patient back to BIPAP ASB, after an hour the patients fingers became cold again!
Has anyone got any specific reasoning as to why, if any, the reason for the peripheral vasoconstriction due to different modes of mechanical ventilation, be it increased Peak Pressures etc?
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Without knowing more about the patient history, or assessment, I am going to a take a tentative stab at it.
With normal ventilation the intra-thoracic pressure (inhalation/exhalation close to 0 i.e. ranges about -5 to +2 cmH20) therefore there is no resistance for blood return to the heart. Whenever you expose a person to positive pressure ventilation, be it intubated and mechanically ventilated or even the positive pressure of BIPAP, it creates a positive pressure in the thoracic cavity (roughly whatever the BIPAP is set at so if its 10 and 5, the intra-thoracic pressure ranges from +5 to +15), which impacts the preload of the heart. Now there is resistance for blood return. A strong heart, with a good hemodynamic status easily compensates for this change in preload by increasing the rate. BUT on the edge of hemodynamic stability, if increasing the heart rate is not enough, the body tries to increase preload by vasoconstriction. which is why you might see the physical evidence of vasoconstriction. This would have been nice to have tested by a small fluid bolus, if that was something appropriate for that patient. 
The other possible cause or co-cause would be something like Raynaud's disease, which is a disorder affecting the blood vessels. When the patient is either exposed to cold or stress (like the stress of needed BIPAP or the hemodynamic stress of BIPAP - who knows) this results acute vasoconstriction especially in the hands and feet. Again, worth reviewing the patient history to see if there is evidence of, or a family history of Raynaud's.
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Many  Intensivists   straight  away intubate  and  mechanically  Ventilate the  patients.  In  my  personal  experience  > 100  instances majority  of  the  patients  in  Myasthenic  crisis  recover  completely  with Inj. Neostigmin  Slow  IV  bolus upto  1 to 1.5 mg over  5  minutes  period  without  intubation. Soon they  needed  IM  Neostigmin  with  oral  Pyridostigmin. Some  of  these  patients  also  received IV Ig. Rarely 2 - 3 % crisis  patients  needed intubation  and Mechanical  Ventilation.
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In developing countries , ventilators may not be easily available to treat myasthenic crisis . Therefore , Neostigmine is a valuable drug to treat this complication . In addition , a similar complication due neurotoxic cobra snake bite envenomation can be treated similarly . This is very useful in rural areas & has been included in the protocol of treatment of snake bite. 
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We do intraoperative contrast enhanced ultrasounds of the liver with Sonovue. When reaching the liver there seem to be too many bubbles destroyed.
- We use the same technique/device on prostates (transrectal, in awake non ventilated patients in the outpatient clinic). This works fine.
- In the operating room we do them during liver resections before the resection phase. We pre-oxygenate patients and pause the mechanical ventilation for a second. We give a fast bolus of 2.4ml and a slow one (5-10 sec) in which we do a flash 3 times.
Any ideas or experience with the intraoperative use? 
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Thank you both! We paused the ventilation during the examination for a few minutes (mentioned it wrong..) and got these results. Making the bubbles according to protocol, which works fine in the prostate examination..
Or maybe I should raise the dosage??
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As lung protective strategy you prefer volume control or pressure control ventilator mode?!
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PC protects from high airway pressure. Lung damage comes from high trans-alveolar pressure, which may happen if there is a large inspiratory effort (ie, Pmus adds to Paw). We are talking about simple, set-point targeting of PC modes. You could choose to use adaptive targeting in PC (eg, PRVC or VC+ modes). It all depends on what your goal is. There are only 3 goals of ventilation, safety (gas exchange and lung protection), comfort (patient-ventilator synchrony), and liberation (minimize time on vent). The choice of mode, not just PC vs VC depends on your assessment of the patient's need and hence your clinical goal. There is a rational approach to selecting modes. See attached paper.
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During controlled mechanical ventilation as compared to spontaneous breathing, less gradient of pressure in the system exists helping with repetitively opening and closing of the alveoli. When lungs are ventilated e.g. using the positive pressure mode, by application of positive end expiratory pressure (PEEP) it prevents alveolar over distension during cycles by avoiding its repetitive opening and closing. The systemic venous blood return still depends on a pressure gradient between the extrathoracic veins and the RA (the right pressure gradient) to create adequate RV preload, but with lesser amount....(can this be quantified, and how?). AM I COMPLETELY WRONG by saying that: during controlled mechanical ventilation the inspiration does not significantly increase this gradient to the level as observed in case of spontaneous breathing to accelerate venous return while enhancing the preload? 
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Do you have any publications/books where I can find the information about duration of a single respiratory rehabilitation intervention on a mechanically ventilated patient in Intensive Care Unit? 
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It will depend on specific objectives you aim and for how long the patient remained intubated. I think that for a safe extubation more tham a single respiratory rehabilitation will be needed and for more median of 2 to 4 weeks of muscle training. But I agree that there is a lack of evidence, mainly because these situations are too much variable (time of intubation, clinical condition and performance status of the patient, team skills,  etc).
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Cardiff university adult nursing student
interested if there is any welsh studies or policies regarding this topic.
In need of direction of the best way to direct my literature review.
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Excellent question!!  An article from one of the journals from AACN (Critical Care Nurse. 2013;33[3]:68-79), Stites, M, revealed that CPOT had a higher and more consistent inter rater reliability than the BPS, however dementia or chronic illness may effect the scoring.  The assessment of pain needs to be an effective culmination of the observational behavior of the patient, the self-report of the pain, the physical findings of the patient, as well as the situational background causing the patient's pain.  My suggestion is to start w/ this study and take note of all of the studies that are sited in this article--you will find that it is comprehensive.
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Patient has major stroke on the left middle cerebral artery, right side no sensation except the foot, with atrial fibrillation and polymyositis. Would the intercostal muscles be strong enough to allow breathing ? Patient is 79 year old female.
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 in this particular sceinario percutaneous tracheostmy will be right answer. this patient as somebody has already mentioned must be needing mechanical ventilation and will need it for pretty long time .You can always get benefits of right time tracheostomy in such cases.RE intercostal muscle weakness this patient will need tracheostomy for early weaning and preventing resp infections with good tracheal toilette.
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The guidelines recommend change each 72-96hs in the overall patient, and every 48 hours in patients with COPD, but the practice is very different between different hospitals
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Attached are clinical practice guidelines promulgated by the American Association for Respiratory Care
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PTP is usually measured to determine the inspiratory effort of the patients with spontaneous breathing. The static recoil of the chest wall has to be added in the calculation. My question is how to get the static recoil of the chest wall? Or please provide a reference.
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Are the patients being ventilated in pressure support? If they are breathing without assistance (i.e. spontaneous breathing trial with a T piece) it would be better to measure work of breathing, using an esophageal baloon there are some equipments that can build a Campbell diagram to evaluate work of breathing
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Whereas in the ninety’s blind nasotracheal intubation (NTI) was the gold standard for medical ICU’s patients (more than 90%; Vassal et al, Intensive Care Med 1993) and the surgical ICU’s patients suspected or requiring mechanical ventilation more than 48 H (Aebert et al Intensive care Med 1988), after the implementation of rapid sequence induction (RSI), NTI’s use became confidential (less than 1% in a recent survey). Therefore, NTI is no longer taught in the ICU’s, whereas it may be necessary in some particular cases (inability to open mouth, to move the neck…) and reduces at least the risk of unplanned extubation. Moreover RSI is not so safe and easy according to the recent meta-analysis of Hubble et al (Prehosp Emerg Care 2010).
So should we save nasotracheal intubation?
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  • Its a very good question. Now a days, in today's Anaesthesiologists blind nasal intubation (BTI) is a dying art. Its a great technique in the armamentarium of anesthesiologist specially in the scinario of NIL mouth opening and there is a lack  of advanced airway gadgets ( FOB ) at your centre. In some of Asean countries, even now FOB is not available in 60-70 % teaching Hospital. In the given scinario, it becomes  a greatly useful technique.
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I am currently interviewing SCI patients for my research study and some report the lack of mouthcare in critical care as being particularly upsetting. This should be provided routinely as part of a daily care bundle, however these patients have had to ask for it - despite being non-verbal at that time due tracheostomy/vent.
I'd like to find out about practices elsewhere.
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I work in a residential facility with individuals who have dual diagnosis (MR and other diagnoses, i.e., CP; ASD; Blind; Deaf; Deafblind; Nonverbal, etc.) and I am the chair of the Dysphagia team.
The standard in our facility is to ensure oral hygiene twice daily (morning and night).  I, of course, do not feel that this is adequate; especially for those who have or are at risk for aspiration and aspiration pneumonia.  Our team directs that all individuals who are under the care of the Dysphagia team receive mouth care pre and post-oral consumption with pre-consumption mouth care being defined as "checking mouth for any foreign matter and clearing mouth of all debris as well as providing a sip of a cool fluid to ensure that the mouth is not too dry to consume" and post-consumption mouth care as full hygiene including tooth brushing.
I believe that a lot more needs to be done in the area of oral hygiene--people tend to forget that the mouth is one of the best places to start in decreasing the risk of aspiration pneumonia (as well as allowing a free water protocol to be put in place which I would not feel comfortable beginning until I knew that appropriate mouth care is being provided to all who reside in this facility).
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Is there a correlation between the number of days premature infant required mechanical ventilation increase chance of requiring or needing bronchodilator therapy?
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Thank you for the reply. I am doing a research on number of days neonatal infants received Albuterol treatments while placed on conventional vent versus high frequency oscillator.  If the mode of ventilation does play a role on these infants that require bronchodilator therapy. 
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Hi to all,
I construct a plant including a way for passing of air. I can measure pressure at the start and end of tube and flow rate and maybe temperature. I add an extra artificial orifice as resistance Intentionally. How can i calculate airway resistance of this combination with these measures ?
As you know, the relation between Pressure, flow and airway resistance are obtained as below : R = (P_end - P_start) / (Flow_av) where  Flow_av=(Flow_end + Flow_start)/2.
1- I have done numerous experiments with different flow rate. In every flow rate, resistance is different but i expect the airway resistance (based on electrical analogous) is constant ! isn't it ?! 
2- Also i have done numerous experiments with constant flow rate and different artificial orifice. When i add a orifice with R=5 cmH2O/lit/s, the airway resistance (obtained from above eq.) was 6 cmH2O/lit/s. Then I add another orifice with R=5 cmH2O/lit/s and repeated the experiment again, but this time the value of airway resistance was 7 cmH2O/lit/s. What is wrong ?!!
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What is your length scale? And is the flow laminar? If so, I would suggest you check your pressure drop using the Hagen-Poiseuille equation: delta P = (8uLQ)/(pi*r^4) . This would be how air flow in the lungs can be modeled. Similarly you can modify the equation to estimate the resistance directly: R =  (8uL)/(pi*r^4) . This may be a good check during a control experiment without the additional orifices to see if your pressure meters give an accurate answer. Also to address your first point, I don't think your resistance will necessarily be constant, as by changing your flowrate you could be moving into different flow regimes where wall effects play a greater or lesser role. For your second point, I think doing a control experiment as I mentioned above would help determine what the problem is, for instance, whether it is a meter problem, or the orifice resistances are not correct.
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Performing tracer decay testing in non-well mixed spaces.
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Dear David,
I mentioned mass balance equation means that, although the air temperature and tracer gas concentration may not be uniformly distributed in a displacement ventilated room, however, the mass balance or energy balance principle should be conserved between inlet, outlet, sources/sinks and boundary conditions. By this we can validate or measure the corresponding temperature or tracer gas concentrations. In my opinion, only this case could be simply analyzed. Otherwise we have to measure the distribution with multiple sensors or analyze with CFD tools.
To me, I have did some analysis for particulate matter contaminant with mass balance equations.
Hope above answer helpful.
Bin
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Why not use a MULTIVIB mattress for transferring sound stimuli to these patients?
It can transfer music as well at VAT stimuli, and will aid the process of ventilation significantly.
Olav Skille
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For those of you who maybe interested in holistic medicine, some anaesthetist use in animal an acupuncture point which, apparently may help with ventilation: GV 24...but it seems they use to stimulate breathing during recovery from anaesthesia, while weaning from the ventilator...not sure it will halp in terms of increasing ventilation in an alrady breathing aptient.
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Need responses for an article to be published in a respiratory care magazine.
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The suggestions above are excellent.  Here is a peds reference (which has the same recommendations) from the Solutions for Patient Safety Group that has the references included (that you can site in your paper).  Hope it helps!
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Do you use heat moisture exchangers or active humidifiers? Do you know if there is a guideline or a suggested material and values for optimal results?
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Another resource for guidance on the use of these devices can be found at AARC.org. Search for the clinical practice guideline on heated humidification during mechanical ventilation.
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In acute myocarditis with severe LV dysfunction, worsening pulmonary edema leading to progressive hypoxemia requires mechanical ventilation. Higher Peep can help in improving oxygenation which in turn is beneficial for failing myocardium. On the other hand, it will decrease cardiac output in already compromised status. What should be the aim in such patients and is there any role of permissive hypocapnea with higher ventilation rate to maintain alkalotic environment?
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In the setting of severe LV dysfunction, the diminished cardiac preload resulting from elevated intrathoracic pressure is potentially desirable.  As Todd Carpenter mentioned, increased intrathoracic pressure also improves LV afterload.  RV afterload may be increased or decreased by PEEP, depending on whether there is atelectasis or hyperinflation.  I titrate PEEP with a goal of keeping the lung open and avoiding hyperinflation.  The optimal number will depend on the lung and total respiratory compliance.
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Hi all, I am investigating on different ways to increase the efficiency of Iranian wind towers. Right now, I am doing a research on contemporary buildings having passive wind tower(or Cool tower) like Animal Campus Dog Adoption Park project design by tsk (http://www.aiatopten.org/node/154). I wonder if you know any other project like this.
Looking forward to hear from you.
Thanks in advance.
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Are there any specific number of these procedures you need to perform under supervison to achieve competency? How many you need to do to maintain this competency?
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 Not so dificult,.In our depatrement anesthesiologist to do percutaneous tracheostomy. I agree- 5-10 supervised is enough to independently work.
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For Mechanical ventilation in laparoscopic in Trendelemburg positioning.
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PRVC or VCV can be used. In most of the ventilators in anesthesia machine, PRVC mode is not available so VCV is the most common option. RR (respiratory rate) should be adjusted (increased) accordingly to keep the ETCO2 within normal range. In Trendelenburg position, head is lowered and abdominal contents pushes the diaphragm upward so small tidal volume is preferred (6-8 ml/ Kg of ideal body wt.).
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Dual modes of ventilation seem to be more physiological.
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Although we also consider PRVC our mode of choice for the previously stated reasons, it also comes with some caveats. When using lung protective strategies during ALI or ARDS with tidal volumes adjusted for PBW, it is not uncommon for patients to generate tidal volumes far greater than the set parameter. This may cause a decrease in mean airway pressure, thus affecting oxygenation. I also believe the jury is out on whether spontaneous volumes greater than 8 cc/kg lead to VILI despite the low plateau pressures generated by spontaneous efforts. Does this make APRV a better option?
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In a patient under sedation and paralytic agent on mechanical ventilation, is there any difference between pressure control mode and SIMV PS mode? What would be the preferred mode?
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I agree with Thomas. If the breath type in SIMV is PC then it will be similar to AC-PC breath when there are no patient triggered breaths.
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Can anyone tell the negative airway pressure in the trachea during inhalation, during calm respiration but also in a forced deep inhalation, model human 60 - 80 kg?
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hi karen,
interesting question ...
i don't know how detailed you want/need to know this. as far as i remember according to typical physiology books: normal intrathoracic negative pressures during spontaneous respiration are between -5 to -20 cmH2O, and i assume it will be similar in the trachea, however, i do not know the exact pressurue gradient lowering this value in the trachea, apparently it has to be higher than in the alveoli to keep air flowing. however in obstruction maximum numbers such as -140 cmH2O have been observed.
christoph
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In a standard shunt model, blood oxygen content is decreased by venous admixture. Saturated capillary blood mixes with blood from the shunt. Because of the nature of the blood dissociation curve, higher FiO2 and, hence, higher alveolar partial O2 pressure will increase saturation only slightly above a FiO2 of about 30%. Hence, it will only increase SaO2 slightly if the shunt fraction is constant.
So why does increasing FiO2 above 30% in a real patient still increase SaO2 efficiently? I thought it could be based on increased diffusion, but did not find any literature about it.
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Another angle on this question is to consider the cause of the shunt. If it is an anatomical shunt then additional oxygen will have a lesser effect (other than increased transport in solution and possibly some pulmonary vasodialtion). However, if the shunt effect is "physiological" say due to V/Q mismatch the additional oxygen may promote pulmonary vasodilation that creates improved V/Q matching and hence improved PaO2.
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There are studies on higher mortality in burn patients with inhalation injury. Cancio 2004 found out, that inhalation injuries were linked to higher volumina of fluids applied, only when artificially ventilated. Could it be possible that the higher mortality of inhalation injuries at least partially is linked to the fact of hyperbaric ventilation, increasing the level of natriuretic peptide and causing capillary leakage in a higher amount than in non-ventilated, followed by higher needs of fluid?
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Cancio LC, Chávez S, Alvarado-Ortega M, Barillo DJ, Walker SC, McManus AT, et al. Predicting increased fluid requirements during the resuscitation of thermally injured patients. The Journal of trauma [Internet]. 2004 Mar [cited 2012 May 30];56(2):404–13
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I have heard of people using APRV, which seems a little odd in the absence of inspiratory efforts. My impression is that there is not much research on this topic. Any thoughts?
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Accordingto the data published by Mascia (JAMA, 2010, 304, 2620),we use volume control ventilation with VT 6 to 8 mL/Kg, PEEP 8 to 10 cm H2O (according to the hemodynamic tolerance and respiratory mecanics (we use the stress index). We use CCS for trachal aspiration and performed the apnea test in CPAP. RM were performed after each disconnection.
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Positive end-expiratory pressure(PEEP) is usually applied during mechanical ventilation to improve lung compliance and oxygenation, and then elevate oxygenation index in patients with respiratory failure, meanwhile, PEEP could increase intrathoracic pressure and influence the accurate measurement of hemodynamic parameters. But current studies to explore the effect of PEEP on hemodynamics were mostly performed in patients with acute respiratory distress syndrome or with acute lung injury,and the results drawn from these studies were influenced by multiple factors. Our study is to determine the impact of PEEP on such hemodynamic parameters as central venous pressure(CVP), mean arterial pressure (MAP) and heart rate in patients with central respiratory failure in neurological ICU, aiming to supply some quantitative guide in the acurate evaluation of some hemodynamic parameter levels measured during PEEP application in mechanically ventilated patients.
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Yes, it will be important to get this piece of information. My only concern will be the ethical issue. Patients in neurological ICU without lung problem have relatively normal lung and heart function and can provide us the effect of PEEP on other physiological parameters but to do invasive monitor with changing ventilatory setting without clinical indications will fall into ethical concerns unless wriiten consent from family can be obtained.
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Were you surprised by the two studies published in the NEJM, Oscar and Oscillate? Is the benefit of HFOV lost in the era of low volume, pressure limited ventilation for ARDS? Will you continue using HFOV for rescue therapy or jump to extracorporeal support instead? Why do you think Oscillate had a higher mortality in the HFOV group?
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The problem with treating ARDS using mechanical ventilation is that treatment starts too late in the disease process. We have recently published two papers in a high fidelity clinically applicable animal model showing that preemptive application of the appropriate ventilation strategy actually PREVENTS ARDS. In our first paper (Roy S et al J Trauma 2012) we tested early application of airway pressure release ventilation (APRV) using very precise settings immediately post injury (peritoneal sepsis plus gut ischemia/reperfusion) and showed that we could prevent the development of ARDS. In the second paper (Roy S et al Shock 2013) we compared preemptive APRV with the standard of care ARDSnet low tidlal volume (Vt) ventilation, which was applied late after injury developed. Again APRV prevented ARDS while the low Vt did not stop disease progression and all animals in the ARDSnet group developed established-ARDS. Our efforts should not be at treating established ARDS because it is refractory to treatment. In the recent ALIEN paper by Villar he showed even with low Vt ventilation mortality is still greater than 40%, clearly showing that low Vt is not very effective. Indeed, nothing is very effective at treating established ARDS therefore we must attempt to prevent the disease from occurring. In the paper by Roy et J Trauma we discuss ARDS being a staged disease similar to cancer and the key to reducing ARDS mortality is application of treatment in an early ARDS stage, similar to reducing mortality for cancer.
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The number of patients under mechanical ventilation increases, but we have limited health professionals in our ICU so, it would be better to have the automated MV, to protect the patients.
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Good point Dave. And another benefit of applying protocols consistently is that we can learn from our mistakes and evolve better protocols. That is how artificial intelligence was able at last to beat humans at chess. The way we practice medicine now, by word of mouth, it is very hard to learn what works and what does not in a way that consistently improves patient care.