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.