Mechanical Ventilation - Science topic

There are several examples (a NATVENT conference paper is attached) showing that NV can provide a good indoor air quality at a lower energy and environmental cost than MV. Therefore, my replies ar as follows:

Mechanical ventilation plays a crucial role in the management of respiratory failure in the intensive care unit (ICU). Respiratory failure occurs when the respiratory system fails to maintain adequate gas exchange, leading to hypoxemia (low oxygen levels) and/or hypercapnia (high carbon dioxide levels) in the blood. Mechanical ventilation provides artificial support to the respiratory system, assisting or replacing spontaneous breathing to ensure adequate oxygenation and ventilation. Here's how mechanical ventilation is utilized in the management of respiratory failure in the ICU:

Overall, mechanical ventilation is a vital intervention in the management of respiratory failure in the ICU, providing essential support for oxygenation and ventilation while allowing time for the underlying condition to improve. The selection of ventilation mode and optimization of ventilator settings should be individualized based on the patient's clinical condition, underlying pathology, and ventilatory requirements. Close monitoring and adjustment of mechanical ventilation are essential components of critical care management in the ICU.

Firstly, the LVAD (Left Ventricular Assist Device) should be included in this discussion, because it can function as an artificial heart for years if necessary. Secondly, all these modalities are expensive and dangerous, and should be avoided in favor of safer and simpler measures.

The discovery of the mammalian stress mechanism (MSM), which functions continuously to repair tissues and regulate organs, provides a theoretical explanation for all forms critical illnesses, including eclampsia, ARDS, SIRS, SARS, MERS, COVID, MOFS, Sepsis, pneumonia, severe burn syndrome, Surgical Stress Syndrome, and major trauma.1 All of these “syndromes” are essentially the same because they are all caused by combinations of severe, unrelenting environmental stresses that induce MSM hyperactivity via combinations of nervous hyperactivity and tissue disruption. MSM hyperactivity wastes its substrates and produces excessive and defective versions of its products. This explains all the confusing manifestations of disease. The fundamental objective of medical treatment is to control and reduce stress mechanism hyperactivity to restore effective tissue perfusion and oxygenation and optimize organ function.

MSM hyperactivity can best be controlled as follows:

1. Elective endotracheal intubation to prevent aspiration and airway obstruction, enable monitoring and measurement of inhaled gas mixtures, and isolate medical workers from contagion.

2. ½ MAC general anesthesia with Isoforane to extinguish consciousness and eliminate fear and anxiety that exaggerates harmful sympathetic nervous activity. Propofol should be avoided on account of its dangerous toxicity. Anesthetic inhalation agent concentrations can be maintained at constant low levels that minimize toxicity, and they can be eliminated regardless of organ function.

3. Generous treatment with modern synthetic narcotics to maintain exhaled CO2 concentrations in the range of 50-100 torr to minimize microvascular flow resistance, optimize cardiac output, sustain respiratory drive, maximize tissue oxygenation, and control nociception that exaggerates harmful sympathetic nervous activity.

4. Antibiotics as needed to control bacterial infestation. The potency and penetration of antibiotics will be optimized by measures 1-3.

5. Spontaneous respiration is always preferable, but if mechanical ventilation becomes necessary care should be taken to avoid excessive pressures and volumes that cause “stretch injury” to lung tissues.

6. IV fluids should be minimized to avoid “wet lung” that undermines pulmonary gas exchange.

7. Measures 1-6 should be maintained even if IABP, LVAD, or ECMO is deemed necessary. ECMO is especially dangerous because it damages red cells and releases their toxic contents into systemic circulation.

1 Coleman, L. S. 50 Years Lost in Medical Advance: The Discovery of Hans Selye’s Stress Mechanism. (The American Institute of Stress Press, 2021).

You could take a look at Openmodelica and the Buildings library, might be a good fit for your task.

The follow up of the particular case that motivated my question has been spectacular. The crucial element was chronic malnutrition. Since the patient was adamant in her will to survive, eventually renutrition was started through an endoscopically placed gastrostomy tube. Within 4 weeks, partial weaning was accomplished. The patient was transferred to a. geriatric ward and after continued rehabilitation over 6 months was eventually able to move freely and finally to resume normal peroral nutrition and social activities. Minimal residual cognitive deficits were observed.

During the late 1980's it was accidentally discovered that "permissive hypercarbia" improves outcome in nearly all forms of pulmonary disease, including asthma, pneumonia, and ARDS. This has actually been known for more than 100 years since Yandell Henderson discovered the therapeutic benefits of carbon dioxide. Try reading the attached review of CO2 pathophysiology. Mechanical ventilation is inherently dangerous because it depletes body reserves of CO2, which undermines oxygen transport and delivery to tissues, and it threatens mechanical damage to lung tissues. Ventilator management should focus on restricting tidal volumes and pressures to maintain hypercarbia in the range of 50-100 torr. This will minimize lung damage and promote tissue oxygenation and organ protection.

@H.A. Tillmann Hein, To change the authors in RG, open the paper and there is a 'more' option at far right at the top. Click it and a drop down menu opens which has 'edut'. Click this and it directs you to the paper's details which are editable which includes author names. However, if you made changes to author list recently, you have to wait for some time to revise the author details.

Farouk Kamal It depends...

A specific mode is rarely "the mode" for the patient. Oftentimes, patients with ILD (which covers a spectrum of pulmonary disorders, so I will focus on the primary pathophysiology) have very fast time constants (think quick to fill/quick to empty) with restrictive pulmonary physiology. Volume-control modes of ventilation have a constant flow rate, pressure controlled modes do not; the rate is variable and dictated by the patient. At this point in mechanical ventilator technology, both may be delivered with a decelerating waveform That said, a pressure-controlled mode of ventilation may meet the inspiratory flow demands of the patient, but the pressure required to inflate the lungs (in terms of Pplat) will be potentially similar to that of a volume control for the same tidal volume (if that is your primary concern). I think you are missing the big picture and should consider the independent ventilatory parameters.

For example, what do we know about "recruitability" or the fibrotic lung? It's pretty minimal, but FRC needs to be maintained. (see comment about time constants). "High PEEP" (≥ 10 cmH2O in this cohort), age, P/F ratio, and disease severity are associated with decreased survival in subjects with ILD (Fernandez-Perez, 2008)....just as a quick example. Keep in mind, as with any ventilatory parameter/study related to critically ill patients, those (and I mean this very, very generally) receiving relatively high levels of mechanical ventilator support (i.e., PEEP) may in fact be acutely sicker, have a more significant number comorbidities, or perhaps have not been managed correctly during their clinical course yet an intervention was associated with a measured outcome. Furthermore, flow and respiratory rate are two other drivers of lung injury that should be considered in terms of the "big picture." I'm not going to touch on tidal volume as that topic has been covered thoroughly in the literature. I suggest you venture into the world of mechanical power and take in the theoretical application of the energy/physics associated with that concept.

Long story short, there is not a "mode" that is best for a specific patient but rather one that (a) protects the lungs (as reasonably as possible; (b) promotes machine/patient synchrony (if not wholly passive); (c) meets reasonable physiologic goals for the specific patient. This is why a well-informed practitioner is the best "mode" of mechanical ventilation, but I may be biased as a respiratory therapist.

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.

Yet to be developed

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.

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.

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

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.

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.

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)

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

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.

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?

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

Richard rich@kmmedical.co.nz

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:

1. https://clinicaltrials.gov/ct2/show/NCT03208270 2.

2. www.euroelso.net/.../4-ecmo-for-severe-respiratory-failure.html

Best wishes

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

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:

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. 

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

@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)

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."

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.

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.

3 times per week. Each one 1 hour of duration session.

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.

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. 

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??

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.

see attached

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).

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.

 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.

Attached are clinical practice guidelines promulgated by the American Association for Respiratory Care

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

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).

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. 

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.

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

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.

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!

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.

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.

See article:

 Not so dificult,.In our depatrement anesthesiologist to do percutaneous tracheostomy. I agree- 5-10 supervised is enough to independently work.

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.).

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?

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.

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

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.

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

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.

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.

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.

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.