Daily, thousands of patients with respiratory failure are kept alive by mechanical ventilation (MV). Simultaneously, MV with positive pressure is unphysiological, and can traumatize lungs.

Some understanding of balancing the benefit:risk ratio of MV comes from experience with Acute Respiratory Distress Syndrome (ARDS), an extreme form of lung injury. ARDS results from the body’s excessive innate immune response to a pathological insult, causing a dysregulated inflammatory process that damages the alveolar-capillary membranes patchily throughout the lungs. (Thompson et al, 2017)

Chest radiographs show diffuse bilateral infiltrates, so early workers thought ARDS lungs were uniformly “stiff”, needing high inflation pressures. CT scans show instead that ARDS lungs are inhomogeneous, containing variable proportions of three populations of alveoli. First, many alveoli are densely consolidated with exudative pulmonary oedema, are functionally lost to the lung for gas exchange, and act as sites for the intrapulmonary shunting that causes the severe hypoxaemia of ARDS. Second, many other alveoli appear normal, and still function for gas exchange. Because of the patchy nature of the disease, “normal” and consolidated alveoli may lie adjacent. As the consolidated alveoli are functionally removed from the lung, remaining “normal” alveoli collectively constitute a small residual lung. Protecting this “small lung” requires ventilation with reduced volumes of air. A key realization in our understanding was that the ARDS lung is small, not “stiff”. The improved safety of ventilating ARDS lungs with smaller Tidal Volumes (VT) was demonstrated by the seminal ARDS Network study in 2000, where intended VT of 6mL/kg instead of 12mL/kg predicted-weight-for-height reduced mortality by around 22% (Brower et al, 2000). With lower VT, mild/moderate hypercarbia is inevitable, but (except for patients with brain injury, major trauma or severe metabolic acidosis) seems well-tolerated.

The third population of alveoli are those that are collapsed (atelectatic). Atelectasis in ARDS has many causes, including surfactant destruction by the inflammatory response, and absorption atelectasis from supplemental oxygen. Collapsed alveoli also serve as sites of shunting. The proportion of collapsed alveoli varies between ARDS patients. Preventing initially “normal” alveoli from collapsing is vital to preserve oxygenation. Using enough Positive End-Expiratory Pressure (PEEP) to prevent alveolar collapse during expiration is essential. ARDS lungs may need very high levels of PEEP. It can be difficult to find the right balance of PEEP to prevent alveolar collapse while not overdistending the “normal” alveoli. Analysis of compliance curves, measurement of the End-Expiratory Lung Volume at various PEEP levels, or determination of Transpulmonary Pressure via oesophageal pressure measurement may help. For already-collapsed alveoli, re-opening may be possible by controlled application of airway pressures in the 40-60mmHg range. This is called “recruitment”, and numerous “Recruitment Manoeuvres” (RM) are described. Not all patients have recruitable alveoli, and recruitment may damage normal alveoli, so recruitment attempts must be individualized. For lungs that prove to be recruitable, the “Open Lung” approach – opening collapsed alveoli with a RM, then keeping them open with high PEEP – seems logical to reduce shunting and improve oxygenation. Prone positioning is another effective RM and atelectasis-reduction strategy in patients with severe ARDS (Santos et al 2015).

In ARDS lungs, any junctions between aerated and non-aerated alveoli are zones of intense stress, and are particularly vulnerable to injury, which in turn drives further inflammation; recruitment may reduce the number of these junctions. With severe ARDS it is advisable to initially prevent spontaneous patient respiration, if necessary by using muscle relaxants (Papazian et al 2010), as spontaneous breathing effort may increase the stresses across vulnerable junction zones.

In severe ARDS the small lung maybe even smaller than expected, and VT of 6mL/kg may still be too great. The Driving Pressure (DP) (the difference between PEEP and maximum airway pressure in pressure-targeted modes of ventilation, or between PEEP and plateau pressure in volume-targeted modes) might be an additional safety limit. Patients with DP of 15cmH2O or higher do worse, so perhaps after best attempts at recruitment and PEEP optimization, VT should be restricted further to keep DP below 15cmH2O – this warrants further investigation (Bugedo et al, 2017). Oxygen supplementation should probably also be restricted to keep the arterial saturations in the low 90% range – excessive oxygen generates damaging free radicals. There is no clear data that any mode of ventilation is better than another for ARDS; addition of extracorporeal CO2 removal makes PaCO2 management easier with low VT; full Extra-Corporeal Membrane Oxygenation limits deaths from hypoxaemia, but adds other complications. (Thompson et al 2017)

Most ventilated patients do not have severe ARDS, but all are at risk of lung injury from ventilation, which might be minimized if clinicians routinely incorporated the lessons from ARDS – reducing unnecessary oxygen, recruiting any already-collapsed areas of lung, using enough PEEP to prevent lung collapse, and protecting aerated lung from trauma by using constrained Tidal Volumes and Driving Pressures.

References

Brower, R.G., Matthay, M.A., Morris, A. et al. (2000). Ventilation with lower tidal volumes as compared with traditional tidal volumes for Acute Lung Injury and the Acute Respiratory Distress Syndrome. N Engl J Med, 342: 1301-1308.

Bugedo, G., Retamal, J., Bruhn, A. (2017). Driving pressure: a marker of severity, a safety limit, or a goal for mechanical ventilation? Critical Care, 21: 199-203.

Papazian, L., Forel, J.M., Gacouin, A. et al. (2010). Neuromuscular blockers in early acute respiratory distress syndrome. N Engl J Med, 363: 1107-16.

Santos, R.S., Silva, P.L., Pelosi, P., Rocco, P.R.M. (2015). Recruitment maneuvers in acute respiratory distress syndrome: the safe way is the best way. World J Crit Care Med, 4: 278-286.

Thompson, B.T., Chambers, R.C., Liu, K.D. (2017). Acute Respiratory Distress Syndrome. N Engl J Med, 377 : 562-572.

A key development in our understanding of Acute Respiratory Distress Syndrome was Luciano Gattinoni’s paradigm-shifting Baby Lung idea. In the mid-1990s it was thought that ARDS was a homogeneous lung-stiffening process. The “proof” was the uniform bilateral infiltrate on AP chest X-ray. Gattinoni’s innovative cross-sectional imaging studies showed instead that ARDS lungs were inhomogeneous, and showed various functional areas: some consolidated alveoli, some collapsed alveoli, and some open alveoli. Efforts could be made to recruit and open the collapsed ones, but the consolidated ones were temporarily lost. The patients survived by gas exchange in the remaining open alveoli. The total volume of the open alveoli added together to make up a smaller lung – the “Baby Lung”. Nobody would dream of ventilating a neonate with a 1litre Tidal Volume – obviously the lung would be ripped apart (though it would also appear to be “stiff” while it was being so ventilated – because it was being overstretched). So if we realized that an adult with ARDS no longer had a 5litre lung capacity, but only (say) 1litre of functional lung, it would make sense to ventilate them with a smaller Tidal Volume than the 10-15ml/kg Tidal Volumes commonly in use in 1995.

So the 2000 ARDSnet study helped, by showing that fewer ARDS patients died by ventilating with 6ml/kg (of predicted mass) rather than 12ml/kg. Somehow 6ml/kg then became the “ideal volume” – something ARDSnet never claimed to show. It could still be too big for some patients.

Amato’s 2015 study suggested a new scalable limit. The “Driving Pressure” is the difference between PEEP and Pmax (in a Pressure Mode) and PEEP and Pplateau (in a Volume Mode with a pause). Driving Pressure greater than 15cmH2O correlated with increased mortality.

So perhaps Driving Pressure is our scaleable limit. Start ventilating your ARDS patient at 6ml/kg predicted mass. But if the Driving Pressure required to do that exceeds 15cmH2O, we are exceeding the capacity of the available lung. By all means try recruitment, try to expand the available lung. But once you have done that, and you still have too high a Driving Pressure, scale back on your Tidal Volumes.

Note that the above assumes no problem with the chest wall – it assumes the chest wall is soft and stretchy, and that all the Driving Pressure goes into stretching the lung. If the chest wall is stiff (eg: an obese patient, or a patient with abdominal hypertension), then we have to make allowances for the chest wall. The best way then is to get an estimation of pleural pressures by measuring oesophageal pressures. This enables one to work out the pressure over the chest wall and separate out the pressure over the lung only (the transpulmonary pressure). The aim must be then to keep the Transpulmonary Driving Pressure below 15cmH2O.

(This is also only relevant in alveolar lung disease – in patients with bronchospasm MUCH bigger Driving Pressures will be required to move air through the narrowed airways. Different pathology, different limits.)

So, although not everyone yet agrees, I think Driving Pressure limitation is the way to properly scale our Tidal Volumes to the size of the residual Baby Lung in ARDS.

Cardiac arrest resuscitation is stressful. For the Team Leader, it is difficult to keep track of everything. This is especially true in real-world situations where there is no pre-assembled team.

I have developed the “I Call a CAB DRIVA” mnemonic to help me with this.

It is described in the document below.

ICallaCABDRIVA poster 20171116

Stabilizing a critically ill patient requires effective co-ordinated interventions.

The first hour is critical. The longer it takes to fix key problems, the more the patient’s body is damaged.

The ABCD3E3 PITCHER mnemonic is my personal guide to remind me of how to stabilize a patient with critically ill patient with multiple organ dysfunction. It incorporates the Universal Resuscitation Algorithm (ABCDE) and seven further priorities that I feel need to be addressed for all critically ill patients in the first hour. Specific therapy of the patient’s initiating pathology should be added to these interventions.

The chart brought up by the link below summarizes the goals for first-hour stabilization of a critically ill adult patient who is not in cardiac arrest.

ABCDEPITCHER poster 20171115

Ensuring patient comfort in ICU is important.

Most patient’s memory of ICU is dominated by memories of pain.

Adequate ANALGESIA is therefore the first thing that must be ensured.

DELIRIUM – a reversible, acute brain dysfunction – is often brought on by the ICU environment (sleep deprivation is a major factor in causing it), and is exacerbated by pain. The disorders of thinking, and potential for hallucinations, are more reasons for patient suffering.

DEPRESSION is also a debilitating factor.

Only when all the above have been addressed, should the patient receive SEDATION. If the ADD have been appropriately managed, only a minority of patients (those needing neuroprotection, or extreme ventilation, or those with profound neurological or metabolic abnormalities), require deep sedation. For the remainder, light sedation, to a defined target, regularly lightened and re-assessed, is more appropriate.

 

These are the slides for the lecture on Haemodynamic Support of the Elderly presented by Richard von Rahden at the 2016 South African Society of Anaesthesiologists’ Conference.

Cardiovascular Support of the Elderly VON RAHDEN publishable

Here is the 2015 ILCOR-compatible update to 3-health care professional Basic Life Support for use in the wards of Grey’s Hospital, Pietermaritzburg.

Ward Resus 04p

Here is the updated Adult Cardiac Arrest algorithm for Grey’s Hospital, incorporating 2015 ILCOR updates.

General Adult Resus 03p

General Adult Resus 02p (2)

Dr RP von Rahden made this flowchart as an all-in-one one-pager for Grey’s Hospital in Pietermaritzburg.

It is based on the 2010 ILCOR guidelines, and will be reviewed when the 2015 ones come out.

For years it has been standard practice to give oxygen to patients with Myocardial Infarctions, even if they are not hypoxaemic. The logic seemed obvious: the heart muscle was short of oxygen, so bonus oxygen could only help. 

Or could it? We know also that excess oxygen generates free radicals, which are a key driver of reperfusion injury.

An article in the May 22 issue of Circulation may help. A multimeter trial enrolling 441 patients with confirmed ST Elevation MI, who were not hypoxaemic. Giving oxygen worsened outcomes: higher peak CK,  increased recurrent MI (5.5% vR 0.9%), more arrhythmias, and a 50% bigger infarction size at 6 months.

Note that these were vessel occlusion type MIs – things may be different in non-STEMI infarcts where global oxygen supply is reduced,  but there is no absolute flow occlusion. But still,  this study means that oxygen should be carefully prescribed, and in the setting of STEMI, should only be given to patients who actually have hypoxaemia.