Respiratory Therapy Blog

I recently attended the College and  Association of Respiratory Therapists of Alberta (CARTA) annual educational forum in Calgary, Alberta, Canada. I will over the next little while provide a little recap of the talks I attended each day. My recaps will mainly focus on some of the more key and interesting points that came up during the sessions.

Inhaled Nitric Oxide - Dr. Dean Hess

Assistant Director of Respiratory Care, Massachustets General Hospital - Boston MA

Dr. Hess presented inhaled nitric oxide (INO) from an evidenced based perspective and also covered its indications, contraindications and clinical application.

The best evidence for INO is in term and near term neonates with persistent pulmonary hypertension of the newborn (PPHN). In this population INO decreases the need for ECMO (with no change in mortality) and also there is a decreased development of chronic lung in these patients.

INO does not have any benefit in patients with congenital diaphragmatic hernia, it actually may increase mortality slightly. In the NINOS study published in Pediatrics (Ped 1997; 99:838), 70% of congenital diaphragmatic hernia treated with INO went on ECMO compared with 54% in the control group.

INO in pre-term infants has also been studied with some studies been published just a few months ago (4 studies in 2006). There is conflicting evidence to whether there is benefit in this patient population

When it comes to the possibility of long term adverse effects of patients treated with INO, there has been a number of studies that have followed newborns up to 5 years and there is no adverse effects what so ever.

In adults, the main interest for using INO is in patients with acute respiratory distress syndrome (ARDS) and there appears to be no real benefit. It seems about 2/3rds of ARDS patients will have a 20% improvement in their PaO2 that will last for only about 24 hrs with no improvement in survival.

When it comes to the dose of INO administered most studies report a positive response with 20 ppm or less. It is recommended use the lowest effective does as higher doses are more likely to increase adverse effects with little benefit.

When it comes to weaning of INO, the initial wean (e.g. 20 ppm to 5 ppm) occurs within the first 24 hrs of treatment. Additional weaning in then dependent on lung disease and response to therapy. INO is also weaned from 5 ppm to 1ppm for 30-60 minutes before discontinuation and FiO2 increased to help deal with any rebound response that may occur. Increasing FiO2 by 20% can help to blunt this rebound response.

The scavenging of NO is not necessary and the amount of exposure has bees studied (Phillips et al. Pediatrics 1995). The US Occupational Health and Safety Administration (OSHA) levels for NO exposure is a 25 ppm average throughout a 8 hour shift and for NO2 5 ppm at any time during work shift.

ARDS Update - Dr. Dan Zuege

ICU Medical Director, Peter Lougheed Center - Calgary, AB

There is a number of problems with the currently accepted definition of ARDS (American-European Consensus):

• range of severity, lung mechanics
• variability in chest x-ray interpretation
• assessment of left atrial pressure
• assessment of oxygenation independent of applied therapies

When it comes to chest x-ray interpretation, Rubenfeld (Chest 118;56:2000) had 21 experts review 28 films of patients with ARDS and only 43% had complete agreement with the ARDS diagnosis.

Oxygenation has dependence on therapy. Ferguson et al. (Intensive Care Medicine 30:2004) looked at 41 patients with ARDS that initially had a PaO2/FiO2 200.

Risk for ARDS in not uniform. Patients with severs sepsis have the highest risk and trauma patients have a low risk. Multiple risk factors increase the risk for ARDS. There are also a number of secondary risk factors including alcohol abuse and chronic lung disease.

Genetics and ARDS is currently a hot topic of study. Genetics may likely explain part of the ‘bad luck’ in ARDS. Genetics is the possible future for ARDS, giving us better understanding of pathophysiology and epidemiology. It may also help us better understand risk; nature versus nurture interactions …. Also genetics may help us to tailor therapy and the degree of intervention.

We have a very good understanding of how the lung is injured but we know little of how it heals in ARDS. A healing ARDS lung has a number of steps to go through:

• re-absorption of alveolar fluid
• removal of alveolar protein
• proliferation of Type II cells
• reduction of inflammation

A recent study, the Beta-Agonist Lung Injury Trial, looked at using IV salbutamol to try and improve lung liquid clearance. There was no difference in PaO2/FiO2 ratios or mortality but there was lower plateau pressures in the salbutamol group compared to the placebo group. Trying to improve lung liquid clearance will continue to be an area of study to treat ARDS.

When it comes to fluid management in ARDS, the ARDSnet group compared liberal and conservative fluid therapies (NEJM 354:2006). Dry patients had a (mean) 2 days less on the ventilator. There was no difference in the incidence of renal failure and there was no overall survival benefit between the two groups. It seems to hold true that a dry lung = a happy lung.

ARDS treatment principles:

• treat primary problem
• physiologic support
  •   of lungs
  • of other organs
• avoid complications
  • lung (barotrauma, VILI …)
  • sepsis (pnemonia, other …)
  • other (DVT, nutrition, ’stress’ ulscers…)
• disease modifiers

Dr. Zuege also discussed what we now know of the long term outcomes of ARDS survivors. It seems for these patients lung function does return to normal, usually within 6 months but they have long term functional deficits. Up to 2 years after hospital discharge patients still average only about 66% of predicted on walk tests with little or no improvement since 6 months of discharge. These patients also continue to complain about weakness and fatigue and this affects their ability to go back to work full-time and perform other duties that they once did.

[From Nature.com]

It appears that cholesterol drugs called statins could protect smokers lungs from some of the damage caused by smoking.

Statins are a group of drugs known for lowering cholesterol and helping to prevent heart disease. But they also seem to reduce inflammation and animal tests have suggested that they may protect the lungs.

A study from the University of Oklahoma Medical Center examined the medical records of 485 smokers and former smokers, they compared medical tests of the patients’ lung health. They found that smokers and former smokers that took statins were 35% less likely to require hospitalization or an emergency room visit for lung-related illness compared to those not taking statins. The patients who were taking statins had their lung volumes decline by just 1% each year compared with a 10% drop in the comparison group.

Statins work by blocking an enzyme called HMG-CoA reductase, which works to produce various fatty acid molecules, blocking this enzyme lowers cholesterol levels. It also reduces the concentration of molecules that promote inflammation from irritants such as smoke.

This needs to be now tested in a rigorous randomized clinical trial. It is important to note that statins will never be as good as quitting smoking altogether. The drugs may be used to help protect smokers’ lungs against diseases such as chronic obstructive pulmonary disease and a few studies are already testing this idea.

The URL for this site is now just resptherapy.com. For many this won’t make much of difference as the URL resptherapy.wordpress.com still works and will continue to work in the future, you will just be redirected to the new URL.

Old permalinks and bookmarks will still work. The same redirection will apply to RSS feeds but you might want to update to the new URL. Most feed readers will happily follow the directions to the new URL but some might not.

Have you ever heard that a cylinder can turn into a rocket that will go through a concrete wall if the regulator breaks off?

Well this settles the discussion.

The New England Journal of Medicine in their Videos in Clinical Medicine section have released a video that covers performing a thoracentesis.

Thoracentesis is used diagnostically to establish the cause of a pleural effusion. It can also be performed to drain large effusions that lead to respiratory compromise.
Topics covered in the video include:

• Indications
• Contraindications
• Equipment
• Preparation
• Pleural fluid aspiration
• plural fluid analysis
• Complications

The video is 8 mins 51 seconds in length and can be viewed and downloaded at the NEJM (you will need to be a registered user or active subscriber to view). The video also has a PDF summary to accompany it.

Some previous Videos in Clinical Medicine include arterial line insertion, nasogastric tube insertion and lumbar puncture.

Feel free to contact me if you would like more info on these great learning/teaching tools.

Tuberculosis was rampant in North American mastodons during the late Ice Age and may have led to their extinction, researchers say. [via National Geographic News]

http://www.rtcorner.net

RT Corner is a site created by the husband and wife team of Ken and Tammy Kane. Together their experience covers adult care , pediatric care, neonatal care and respiratory education.

The site has something for everyone. There is info on guidelines, products, calculations and a forum for discussion. They also have a RT Word of the Day, articles about being on the job and more.

Check out the site and gather in the forum to have your questions answered or maybe answer a question for someone else.

Mechanical ventilation is associated with a number of risks and recognizing when the patient has adequately recovered from their illness that caused their intubation is key to minimizing their time on the ventilator and these risks. It has become common practice throughout the past number of years to use some bedside physiologic measurements (weaning predictors) to decide if the patient is ready to breathe spontaneously.

Some weaning protocols measure the ratio of frequency to tidal volume (f/VT) during 1 min of spontaneous breathing as a final step before beginning a prolonged spontaneous breathing trial (SBT). The f/VT ratio is used to predict the success of weaning for that day and if a patient has a poor f/VT they may be spared having to perform a SBT. These patients are spared performing a SBT because of the possible risks associated with a failed SBT such as excessive anxiety, hemodynamic instability and it may require greater than 24 hours for muscle strength to recover.

In this month’s Critical Care Medicine (Oct 2006), Tanios, Nevin, Hendra et al. (1) looked at the impact weaning predictors (f/TV) had in weaning protocols to assess a patient’s readiness to advance to a SBT. They looked at 304 patients that had been ventilated for greater than 24 hrs, every patient under went a weaning screen daily at 7 am, half had the f/TV measured but not included in the weaning readiness assessment while the rest had the f/TV measured and included in the weaning assessment.

The criteria to pass the daily screening:

• PaO2/FiO2 ratio ≥ 150 or SaO2 > 90% at FiO2 ≤ 40%
• PEEP ≤ 5 cm H2O
• mean arterial pressure ≥ 60 mmHg without vasopressors (low-dose dobutamine or dopamine allowed)
• awake or easily arousable
• adequate cough and not requiring suctioning more than every 2 hours
• for patients randomized to the f/VT group, the f/VT could not exceed 105 breaths/min/L

If any of these are not met the patient would not go on to a SBT and would be continued to be screened daily. The SBT consisted of a 2 hour trial on a continuous positive airway pressure (CPAP) of 5 cmH2O and a pressure support (PS) of up to 7 cmH2O after which, if successful, the patient was extubated.

The average weaning time for the group that had f/VT included in the weaning protocol was 3 days, for the group that had f/VT omitted the weaning time was 2 days. The patients that had weaning decisions made without f/VT did not have a higher reintubation or mortality rate.

While the purpose of weaning protocols is to assess when patients are ready for a SBT and to avoid premature SBTs that lead to failure, they may actually lead to a longer weaning period. Failed SBTs may cause respiratory muscle fatigue that can take >24 hours to recover but there is no definitive evidence that a failed SBT adversely affects weaning outcome.

The role of the weaning predictors such as f/VT may need to be moved further along down the weaning process. At our institution we typically now use the f/VT ratio at the end of a SBT to help with deciding whether to extubate, instead of using it as a tool to see if the patient is ready to progress to a SBT. We may need to begin to reevaluate the use of weaning predictors such as f/VT and the role they play in the weaning process.

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(1) Tanios MA, Nevins ML, Hendra P et al. A randomized, controlled trial of the role of weaning predictors in clinical decision making. Crit Care Med. 2006 Oct;34(10):2530-35.

Scientists at the University of Edinburg, UK and at the National Instutute of Advanced Industrial Science and Technology in Tsukuba, Japan have discovered the crystal structure of solid red oxygen that forms at high pressures.

From Nature.com: 

As a gas, oxygen molecules (O2) normally float around with only passing attraction to each other. But increasing pressure forces the molecules together, turning oxygen into first a magnetic, pale blue liquid, then a pale blue solid at 54,000 times atmospheric pressure (5.4 GPa).

In 1979, chemists discovered that, at pressures above 10 GPa, oxygen becomes a red solid. At 96 GPa, oxygen molecules are so close that electrons flow freely between them, in a metallic phase seen in 1990.

Instead, it appears that oxygen gangs up under pressure into groups of four pairs, in a shape like a squashed cube. These clumps of four O2 molecules could also be called a single O8 molecule — but they aren’t in a ring. The result demands a rethink of theoretical calculations about the behaviour of dense oxygen.

Exciting as it is, solid red oxygen seems, for the moment, useless. It is made in tiny amounts and vaporizes as soon as the pressure lifts. Nor will it be found in nature: despite the high pressures found in places such as inside the Earth, non-gaseous oxygen almost always joins to other elements, as an oxide or in water.

The annual College and Association of Respiratory Therapist of Alberta (CARTA) educational conference will take place November 1- 4, 2006 in Calgary, Alberta.

There will be prominent speakers from all over North America. For more information click on one of the pictures below or go to the CARTA website at:www.carta.com

Hope to see you there!

It has been awhile since I last posted anything but now I’m back after a little hiatus. I have been away on vacation for the past month and there hasn’t been much to post about lately.

As you can see I recently changed the look of the site and added a neat little feature where you can chat with me live when I am online. I’m looking forward to see how this new feature will work.

Another respiratory care related site has popped up on the web, snotjockeys.blogspot.com. It is still very fresh but it is nice to see another RT blog.

Hopefully there will be more to post about soon!

Patients who have an endotracheal tube (ETT) in place are possibly at risk for post-extubation stridor due to things such as airway inflammation, edema, and airway mucosal ulceration. Post-extubation stridor has an incidence that ranges between 2% and 16% in patients that have been intubated for longer than 24 hours. One technique used to attempt to predict the occurrence of post-extubation stridor is the ETT cuff-leak test.

There are two types of cuff leak tests that can be performed, the auscultation cuff leak test and the cuff leak volume test. The auscultation cuff leak test classifies the leak into three categories:

• no leak, where no sound of leak was heard by using stethoscope detection

• mild leak, where a leak is heard using a stethoscope

• significant leak, where the sound of a leak was heard without using a stethoscope

In the cuff leak volume (CLV) test the actual tidal volume at expiration during six consecutive breaths in the Assist Control mode is measured before and after deflation of the ETT cuff, the difference in the tidal volume before and after cuff deflation is the cuff leak volume. This can be shown as an absolute volume or as percentage of tidal volume. When cuff leak volume is less than 140 ml or less than 10-20% the risk for post-extubation stridor is significantly elevated.

Dr. Cheng and colleagues(1) recently looked at IV methylprednisolone to reduce the incidence of post-extubation stridor and they also looked for agreement between qualitative (auscultation) and quantitative (CLV) measurement of cuff leak. They found that 18% of CLV was the optimal predictor for stridor and there was excellent agreement between the auscultation and CLV tests. There does appear to be a lot of false positives (cuff leak predicts stridor but it does not always occur), in 128 patients with a CLV of less than 24%, 70% of patients did not develop stridor and 81% did not require reintubation.

There seems to be a nice correlation between auscultation and CLV tests in assessing for the possibilty of post-extubation stridor. I tend to use the auscultation cuff leak test solely and so do alot of my colleagues. Although it is somewhat subjective it is nice to know that it correlates well with the CLV test.

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(1) Cheng KC, Hou CC, Huang HC, Lin SC, Zhang H. Intravenous injection of methylprednisolone reduces the incidence of postextubation stridor in intensive care unit patients. Crit Care Med. 2006 May;34(5):1345-50.