Respiratory Medicine - Science topic

Just a personal opinion, based on 60 years experience.

From the 1950s, with analogue computers and calculating machines, there have been attempts at physical modelling of cardiovascular hydrodynamics and to a lesser mathematical extent respiratory fluid dynamics and gas exchange.

These have usually been motivated by inter disciplinary collaborations or in some rare cases by individual medical trained people who were also well educated in mathematics and physics ..

The topics chosen were usually the most amenable to mathematical modelling rather than the most clinically relevant.

With the development of digital computers and easy to use software packages requiring much less mathematical and physical knowledge, modelling has become more doable in medicine and especially in biomedical engineering. This has enabled more relevant problems to be addressed and has attracted a wider class of "mathephysicians", medical biophysicists and medical computing people and created its own academic niche.

However , many of the most important medical research developments have been due to mathematics/physics carried out by non medical people eg CT scanning, MRI, DNA sequencing, PCR, prosthesis design, neural net theory, drug design.

See Nobel prize winners.

Will this extension increase the dead space of the breathing system, and weaken the ventilation?

What is the infection risk with this arrangement?

Please take a look at the following RG links and PDF attachment.

Hello Matteo,

Here is the study that might be helpful:

Ng AS, Wong TK, Gohel MD, Yu WW, Chung JW, Fan KL. Using pulse oximetry level to indicate the occurrence of sleep apnoea events. Stud Health Technol Inform. 2006;122:672-5.

In brief, this research on ten people ( all men, mean age 45 /SD 8.9, body mass index 27/SD 3.3, apnea/hypopnea index 47/SD 15) attempted to select pulse oximetry (SpO2) level as an alternative parameter to indicate the occurrence of sleep apnoea. Time differences were compared between the "onset of nasal airflow cessation" and the "onset of three percent oxygen desaturation from the baseline" during sleep apnoea events. The results of this study showed there was around a twenty second delay after the onset of the cessation of nasal airflow. The paper provides results for each individual patient: the lowest time, in second (mean/SD) is 19.5/5.8, and the highest is 27.3/7.74.

These researchers concluded that the SpO2 level is not immediately sensitive to the occurrence of sleep apnea, where the time delay may be caused by: i) time utilized by the devise to process the signal, ii) time needed to carry deoxygenated blood to the finger, or iii) the desaturating of SpO2 level, which is affected by the last sleep apnea event and during the occurrence of repetitive events.

Hope this helps. Best wishes with your study,

Tatyana

Thanks @ Catia Cilloniz

there are some studies on this, e.g. reference mentioned below 

Am J Perinatol. 2001 May;18(3):169-74.

A prospective controlled trial of albuterol aerosol delivered via metered dose inhaler-spacer device (MDI) versus jet nebulizer in ventilated preterm neonates.

Khalaf MN1, Hurley JF, Bhandari V.

Author information

 

Abstract

The objective of this study was to identify the most efficient and cost-effective nebulizer device for delivery of albuterol aerosol as a bronchodilator in ventilated preterm infants. Bronchodilators are frequently used as part of the therapeutic regimen of ventilatedpreterm infants. This can be delivered by different types of nebulizers like the Jet or metered dose inhaler (MDI) spacer device. Fifty-three premature infants being ventilated for RDS (24 to 34 weeks of gestation) were studied just prior to extubation. Twenty-four of them received standard doses of albuterol aerosol via Jet nebulizer and 29 via MDI-spacer. Heart rate, respiratory rate, oxygen saturation, lung compliance, and airway resistance were monitored prior and 15 minutes after albuterol delivery. There were significant changes in the parameters studied between pre- and postnebulizer treatment. In both groups, there was a significant improvement in lung function as evidenced by 13-24% decreased airway resistance (RAWE) and 3-7% increased lung compliance (CDYN). There was also a beneficial clinical response as demonstrated by increased oxygen saturations. These findings suggest that both MDI-spacer and Jet nebulizer are equally effective in delivering the albuterol aerosol to the lower respiratory tract. Since a small dose of albuterol delivered via the MDI-spacer improved lung function as effectively as a higher dose via the Jet nebulizer, the MDI-spacer would be the preferred mode of aerosol administration, especially because it takes only 2 minutes to deliver it. Furthermore, it was also cost-effective as one MDI-spacer treatment costs 2 cents, while a Jet treatment costs 10 cents in our neonatal intensive care unit (NICU).

Nonsedating second generation H1 antihistamines (up to 4 times standard dose) ... no experience with onalizumab due to costs. 

Of Course professor.

In my country I am focusing specifically in young age, to start a primary prevention program at this early age inside Schools ! Thats why we just focus kids with this metabolic pattern !

Agree with your comment !

I had contacted him and continue to collect different data. Thank you.

I am not expert.

i assume that this relates to the aspect that - in the absence of shunting - all blood goes through the lung circulation, and consequently, this may act as a 'filter'

I am sorry to hear that this has happened to your mother. Hoping that she  will be better in near future. 

For the ARDS:

Ventilator aspects: recruitment maneuver, prone position ventilation, high PEEP

Drugs: diuretics, hormones, etc.

Extracorporeal Life Support: ECMO

Treatment of etiology: control of primary disease is very important.

Diagnosis is your key. Agreed procedures for post-mortem pathology and the persistence of pathologists to diagnosis may not be standardized.

Thanks for the reference.

here I am sorry I can not help

I think the answer depends on whether or not you want to increase respiratory muscle endurance or strength. Increasing respiratory muscle strength is best accomplished by a small number of repetitions, but very high tension/pressure. Endurance is increased by a much larger number of repetitions at a much lower force level. It's not any different than training a limb muscle.

You could use IBD2 (http://compbio.charite.de/tl_files/NGS/IBD2-tutorial.pdf), which computes haplotype blocks which are identical by descent (in case you've got several affected siblings).

A suitable option is to connect a 3-way connector in line with oxygen supply (nose prongs) and attach there the extremity of a pitot tube connected to a pressure sensor (this is a version of anemometer).

The cost of this setup is around 30 dollars.

Andre

Despite the already excellent and thorough  responses to your relevant question I would like to add some comments. 

Transition to spontaneous breathing in ARDS patients is one of the most difficult parts of their ventilatory treatment and the point in time to do so is still under debate. 

It is impossible to set fixed rules but was has been discussed so far are all good advices. It is important to have the precipitating cause of ARDS under good clinical control and to have witnessed an improvement in lung function such as less needs for FiO2, increasing compliance, decreased PEEP needs to maintain the same ventilation targets. It is very difficult to give general threshold values  as this vary from patient to patient. This improvement is generally seen after 2 - 3 days of controlled lung protective mechanical ventilation. 

The transition to spontaneous breathing has to be smooth as the lung is still  very susceptible to suffer from mechanical stress and it is essential to prevent a second hit mechanism at this stage. 

So independently of when it is decided to transit the patient to spontaneous breathing the following must be taken into account: 

Avoid patient-ventilator asynchrony by choosing modes or settings that enhance synchrony. 

Check for increased work of breathing. Prevent the patients from vigorous inspiratory efforts or high respiratory drive as this may cause large transpulmonary pressure changes in different regions of the lung. If this cannot be controlled it might be too soon to transition the patient to spontaneous breathing.   

Controlling tidal volumes is difficult as patients are contributing with their own Pmus Compliance is hard to interpret as the ventilator does not "see" the patient's contribution. In this circumstance a smooth breathing pattern and a low driving pressure may be the best indicators of an appropriate spontaneous breathing. 

In a randomized, double-blind, placebo-controlled clinical trial in 2011, conducted at Bastyr University Research Institute, Kenmore, WA and the Bastyr Center for Natural Health, Seattle, WA, reported that  short-term, oral intake (500 mg twice daily administered  to  volunteers for 4 weeks) GSH does not improve glutathione status or reduce markers of oxidative stress in healthy adults.  The authors indicated that routine supplementation might not offer health benefits in the absence of disease or oxidative challenge.

 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3162377/  

Thank you all: Waldemar Tomalak and Mike Czervinske.

 You can also see at https://www.ideals.illinois.edu/bitstream/handle/2142/7181/librarytrendsv30i1k_opt.pdf?sequence=1

You could have a look to Nijmegen questionnaire.

Dear Silvie,

maybe our study design (regarding a training program in lung cancer patients) is helpful in your context: http://linkinghub.elsevier.com/retrieve/pii/S155171441300195X

Use of high flow of oxygen does not necessarily mean use of high FiO2, because they are two different parameters (L / min of gaseous mixture versus O2% in the gaseous mixture). In any case, I believe that the target of 88-92% of SO2 in hypercapnic patients should always be respected.

In the case of secondary polycythemia due to COPD or smoking, the increase in red blood cell production is supposed to counterbalance the decrease in SpO2, so that Oxygen Delivery(and thus, consumption) remains stable. In cases like these, when polycythemia constitutes a physiological response, I believe an example can be drawn from other physiological responses, such as sinus tachycardia, a condition that may alarm the patient, yet seldom does it have a serious impact or consequences itself. Therefore, although I think such cases merit consideration and follow-up, no additional burden on thrombotic risk is usually carried with them. Of course, every patient is unique and given a heavy-burden history of thrombotic risk, measures might be necessary.  Secondary polycythemia due to other causes(erratic EPO production, for example) is a different story. 

Thanks David. Yes we have looked at HPLC. Would be keen to know if anybody has a protocol/SOP for this?

Hello Adam,

I hope to help you

Silvia

In South Africa, virtually all people should show a positive skin test - in our context, I would say no. 

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. 

Here we experience the same problem. As we have no proper therapeutic measures to apply, we end up administering salbutamol (in our case) to almost all infants. However, we've been using saline in almost all cases, with apparent good results. 

You can use a Complete Lung Function equipment as

Medical Graphics Corporation, CareFusion (Jaeger), Medisoft and also a Spanish company SIBEL that provide a Spirometer together with MIP and MEP (see link)

Regards

Not my area of expertise. Sorry

Dear Lawrence, this is an interesting question for which there are some (but not all)  answers.

As you indicate there is a balance of risk between "primum non nocere" and early resection resulting in cure of a malignant process. 

I would refer you to the attached papers

a. Fleischner Society recommendations for the management of a solid nodule - Radiology (2013)

b. Furman et al (2013) Future Oncol. 2013;9(6):855-865.

c.  American Association for Thoracic Surgery guidelines for lung cancer screening

In addition to growth rate and SUV on PET, which you mention, there are other the factors:

1. Those which increase pre- test probability, namely smoking burden, current and remote history of malignancy,  family history, exposure to radon gas, asbestos and certain metals (e.g., chromium, cadmium and arsenic), pulmonary fibrosis, HIV infection, asbestosis, haemoptysis and constitutional symptoms.

2. Shape (Spiculation)

3. Contrast enhancement

4. Location - upper lobe increases risk

5. Ground glass opacity

6. Absence of a polygonal shape, Thickness of a cavity wall > 15mm

There are separate guidelines for ground glass opacities

Hope this helps

Best wishes

MAC lung disease can be difficult to treat and can have difficult to tolerate side effects.  Having said this, most experts in this area do not start with injectable agents.  For MAC lung disease a typical regimen would include a macrolide, rifampin and a fluoroquinolone or ethambutol 3x per week (daily if severe or cavitary disease).  Injectable agents are generally reserved for severe cases that are resistant to oral therapy or have become complicated (extensive pleural disease for example).

The goal is to continue therapy for at least 12 months after the last negative sputum culture, and patients need to understand that prolonged therapy is essential.  In many patients, achieving a cure may not be realistic and it may be necessary to treat to achieve control rather than cure.  You will find the ATS guidelines for non tuberculous mycobacterial lung disease useful:

Dear Hassan,

Many thanks for this answer. Attached is a link to the paper which was eventually published. http://www.hcaf.biz/2014/Respiratory_CMV.pdf

Any thoughts welcome.

Cheers

Rod

There is a big difference clinically between tension pneumothorax in spontaneous breathing patients and those on a ventilator - the latter usually developing much more rapidly. Once " tension"  has developed, however, they are the same and usually easy to diagnose clinically. A chest X-ray is of course desirable, but by definition a tension pneumothorax is an emergency and definitive action precludes prior investigation.

Peter

I am working in KSA in Dr. Soliman Fakeeh Hospital in Jeddah and the case discovered to have the first diagnosed Mers-Cov was my patient in May 2012. 

since then all cases were discovered in Al-Ahsa were in 2013 during the same period of  April May and June 2013, the burst of cases this year were in the same months of April May and June 2014.

after tat period there is no recorded cases in the whole Kingdom during July and August

The amount of pressure generated by the CPAP fan decreases with altitude due to lower gas density.  For this reason, an increase in fan speed is needed to compensate for the modest drop in pressure at altitude.  Older machines have adjustable "altitude" settings in them.  Newer machines have internal correction for altitude so that no adjustments are necessary. 

The following article describes this phenomenon in greater detail:

Hi Gregory,I would like to share my thoughts. You can look for NSAIDS called meloxican. We ran a trial last year in which animals that received meloxican had better imune response (decrease cortisol and acute fase proteins) compared with cohorts. Those imune response are related with BRD problems. Other ingredients you can look for are polyunsaturated fatty acids which are related to decrease immune response and cortisol concentration.

I hope that informations were useful

histoplasmin is uavailable in Cameroon, so I need somebody to help me to buy it. Thanks

MLST is a method to categorize MRSA strains and is a method with higher discraminatory by epidemiological studies.

In our institutional experience, when the biopsy is done for a patient who is in an outpatient setting it usually provides useful information and a therapeutic change for over 50% of the patients. For critically ill and mechanically ventilated patients that require high PEEP and FiO2, perhaps it is too late and surgical intervention not only adds insult to injury but also doesnt change much in terms of therapy. Our mortality rate for outpatients is 0% and for ICU patients jumps to 45%.

Accumulating evidence suggests a role of obstructive sleep apnoea (OSA) as a risk factor for cardiovascular diseases. Here are some of the latest articles:

1. Association of obstructive sleep apnea with subclinical coronary atherosclerosis.

2. Independent association between obstructive sleep apnea and subclinical coronary artery disease.

3. Obstructive sleep apnea in obese adolescents and cardiometabolic risk markers.

4. Sleep-disordered breathing and glucose metabolism in hypertensive men: a population-based study.

5. Cardiovascular morbidity in patients with obstructive sleep apnea in relation to the severity of respiratory disorder.

Ventilation settings can have an impact on respiratory mechanics outcomes, as shown in the following article:

ACE is known also as kininase II, consequently ACE contributes to degradation of kinins (brady and takykinins); these kynins may cause bronchoconstriction and cough if orally administered ; the levels of kynins may increase as consquence of ACE inhibitors intake, either as usual by mouth or presumably by aerosl. That's wy, in my opinion, the use of ihaled ACE inhibitors do not have EBM data and is not easy to be introduced as alternative way

Dear Sheila

As a part of CPT we manage and treat not only the disease itself but its clinical consequences as well.

One of the consequences of pleural effusion is lung volume reduction which could couse ventilation-perfusion mismach, hypoxemia and increasd work of breathing.

It means that Pleural effusion by itself is not an absolute CI

But several PT interventions may be contraidicated in case of Pleural effusion.

Some possible interventions that can improve ventilation-perfusion ratio are positioning: side lying (abdomen free) with unaffected lung down, modalities to decrease stress and WOB (music, massage, , appropriated breathing pattern) , and maintain the general mobility.

You can find some suggestions for treatment in the following textbooks:

1. Physiotherapy in respiratory care (by Alex Hough)

2. Emergency physiotherapy (edited by Beverly Harden)

I think you are better off getting rapid tests for influenza A and B at your site. Really, they are extremely economical, and very reassuring. It's unwise to initiate oseltamivir after a course of antibacterial agents (such as amoxicillin) because the therapeutic effect of oseltamivir is greatest early in the course of the disease, ideally in the first 2-3 days of symptoms. In contrast to the rapid tests, a course of oseltamivir is expensive, as is a course of azithromycin. Parents really appreciate a rapid test diagnosis that confirms or rules out on their first visit influenza.

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.

I think the answer depends upon the service model that you are using. If you are using a substitutive model, for example if home visits are replaced by telehealth visits or home monitoring, then the appropriate criteria is non-inferiority. If you have demonstrated non-inferiority, then one can go on to do a cost-comparison study; can we deliver the demonstrably same service with greater staff efficiency or lower costs? But if you are using an additive model, whereby the patients get their usual care plus telehealth then the appropriate research paradigm is cost-effectiveness. So, can we achieve better patient outcomes (however measured, ie physiological measures, service utilisation etc) by adding this extra service?

Large-scale implementation has its own particular problems. I have just been looking at this as part of my PhD. I'm not quite ready to be definitive, but one of my preliminary conclusions is that where it has worked the implementation model has been flexible, such as the Veterans Health Administration in the US, and where it is deeply problematic the implementation has been attempted via a large cluster RCT, such as the Whole System Demonstrator project in the UK. Look at the work of Carl May and Penny Hawe; they have both pointed out that large RCTs on health technology interventions with no flexibility often, years after commencement, produce weak, unconvincing findings, which do not convince decision makers or practicing clinicians. I think the WSD has fallen into precisely this trap.

The H1N1 Virus is a very invasive virus, high morbidity but with very low mortality. In the absence of any complication one can manage the case at home with non pharmaceutical interventions. It is only when the disease has complications in risk group, the case needs to be hospitalized,

A K Prasad.

.

Ok, thanks for you reply, but, which factor determine that the inflammatory process is finished? why such this inflammatory process is finished in a short time period in some disorders such as viral bronchitis and some process such as detergent injuries continue for long time?

In Taiwan, national health insurance didn't cover long term use bronchodilator inhalation. Sometimes, we prescribed oral beta adrenergic agonist instead of inhalation one. As young as 3 months old baby could tolerate it. But you should start it from lowest dose and the response was variable.

Me ha encantado encontrar un comentario en Español. El proyecto se va a llevar a cabo por un equipo de psicológos de la universidad de Granada e informáticos de la universidad de Málaga. Queremos evaluar si la exposición a música diaria, permite disminuir la dosis de sedoanalgesia en pacientes de intensivos. Hemos pensado en aplicarlo a pacientes en ventilación mecánica bajo sedo-analgesia. Ya veremos los resultados. yo confío en que irá bien. Atentamente.