This chapter deals with a common cause of ICU admission, the wheezy COPD patient with some mixture of respiratory acidosis, hypoxic respiratory failure and biventricular dysfunction. After a rather long break from asking specifically about COPD, CICM examiners came back with a rather intelligent question in 2018, featuring one of the best-constructed model answers.
In total, the SAQs asking about COPD have been:
Question 29 from the second paper of 2005 asks about the assessment of the severity of COPD.
The BODE index
|Points on the BODE index|
|FEV1 (% of predicted)||>65%||50-64%||36-49%||<35%|
|Distance walked in 6 minutes||<350||250-350||150-249||<149|
|MMRC dyspnoea scale||0-1||2||3||4|
|Body mass index (BMI)||>21||<21|
Mortality accordidng to the BODE index
This graph is the slightly modified data from the original article; it demonstrates that among the most severe group, there is a 50% mortality at 36 months.
This comes in two flavours, distinguished by the extent of respiratory acidosis. You may either have hypercapneic respiratory failure, or your PaCO2 may be normal with hypoxia.
These are patients with chronic bronchitis. They are typically obese, and they may be obtunded not only by the hypercapnoea but also by the presence of CNS depressant medications. They will almost inevitably have some sort of obesity-related sleep hypoventilation. The right heart failure in these people may not play such a major role, but there will likely be increased pulmonary artery pressure.
These are the thin emphysema patients, with hyperxpanded chests and vigorously active accessory muscles. They are typically chronically hypoxic, and may be on home oxygen. Their right heart is failing, and pulmonary hypertension is almost inevitably present.
About a half of these patients have an "infective exacerbation" of COPD. Streptococcus pneumoniae and Haemophilus influenzae account for 80% of the pathogens. The rest are atypicals and viruses, such as Moraxella, Mycoplasma pneumoniae, Pseudomonas, RSV, adenovirus, influenza and parainfluenza. There may or may not be an actual pneumonia.
In either case, one can see from the above that most of the pathogens are either Gram-positive (covered by beta-lactams and cephalosporins) or atypicals (covered by macrolides). This promotes the use of the traditional cocktail of ceftriaxone and azithromycin/roxithromycin in these patients.
It is a well-known and lamented feature of emergency resident life that COPD patients get passed back and forth between the respiratory and cardiology teams. It is frequently difficult to distinguish where the CCF ends and the COPD begins. The lifestyle risk factors which predispose them to COPD also create a fertile soil for coronary artery disease, and some degree of ischaemic cardiomyopathy is almost mandatory.
In addition, BNP levels can be useful to differentiate between the cardiac and pulmonary causes of heart failure, assisting the beleaguered ED resident. BNP issues forth in volumes from the insulted over-stretched atria of the heart failure patient, whereas in the exacerbation of COPD these levels may be quite low. (Apparently this distinction is useful and holds true provided your patient is under 70 yrs of age and has normal kidneys).
Thankfully, in the ICU the question of "which team to admit them under" is pleasantly remote. One accepts that the heart failure is part of the spectrum, and both the pulmonary and cardiovascular components of the respiratory failure will respond to the same treatments. The left ventricle may be diseased, and there may be features of congestive heart failure which will respond to positive pressure. Relief of bronchospasm and the resulting decrease in intrinsic PEEP will improve the diastolic failure by improving left ventricular preload. The increased cardiac output demands to power respiratory pump muscles will also be remedied by interventions which decrease the work of breathing.
They do say that the chronic exposure to hypercapnia causes the hypercapneic respiratory drive to be suppressed, and that hypoxia is the primary driver of ventilation in severe COPD.
There are several other reasons as to why one may run into trouble with over-oxygenating their COPD patients. For instance, normoxia reduces their anxiety, and so their respiratory rate will decrease - which may be counterproductive. Similarly counterproductive is the effect of normoxia on the CO2-carrying capacity of hemoglobin (i.e. by the Haldane effect, the deoxygenated hemoglobin molecules have higher affinity for CO2).
In one Thoracic Society position statement, 100% O2 was administered for 15 minutes; an average 23mmHg rise in CO2 was recorded. Of this rise, only a 5mmHg rise was attributed to the Haldane effect. A major proportion was thought to be due to increased dead-space. How does this work?
Consider the emphysematous lung. Some emphysematous lung units a represented by eroded alveoli with little gas exchange surface, supplied by chronically obstructed bronchi. The pulmonary arteries running through these lung units are vasoconstricted because typically, the oxygen tension in these units is quite low. Consider what would happen if you wafted some oxygen though the obstructed bronchi and into these eroded alveoli. The ventilation has not become more vigorous- if anything, the reduced work of breathing associated with oxygen therapy has decreased the ventilation of these lung units. But the increased oxygenation has increased blood flow by decreasing the pulmonary vasoconstriction. The effect is that of increasing blood flow into lung units which have poor ventilation and limited gas exchange surface. That blood was being shunted way from effective lung units, and this decreased the overall rate of CO2 removal.
In fact, this is exactly what happens in asthma, and for asthmatics the recommendation is to maintain a modest level of oxygenation, which permits good V/Q matching.
None of this means that oxygen should be withdrawn altogether if severe hypoxia persists. If the oxygen saturation remains below 88% one ought to up-titrate their oxygen delivery. Hypoxia is more rapidly fatal than hypercapnea.
Yes, the hypercapnea on the blood gas will be the dominant feature. Each 10mmHg chronic rise of CO2 from 40mmHg increases the HCO3- by 4mmol/L. In a patient with a random CO2 of 70, one ought to expect a chronic HCO3- level of around 36.
Apart from the obvious blood gas features, one who is asked by an examiner to comment on a COPD X-ray would be wise to mention something about the features of hyperinflation as well as the features of increased pulmonary arterial pressure.
One may also talk about the paucity of lung markings, about atrial enlargement, and about the presence of bullae (if there are any bullae to be seen).
The formal pulmonary function tests also lend us some information about the severity of COPD.
The TLCO (total lung carbon monoxide) uptake is a reflection of how much diffusing surface you have left; the fewer alveoli remain the lower the TLCO. In emphysema, this surface is destroyed, and the TLCO is usually ~ 80% below predicted.
Additionally, the plethysmographic lung volume measurements will demonstrate that the total lung capacity, FRC and residual volume are all increased ( the residual volume would be over 40% of total lung capacity!). This is a reflection of gas trapping ( the residual volume is all trapped gas).
This is somewhat helpful in differentiating the disorders. In asthma, the CO diffusing capacity will remain normal - alveolar tissue is not destroyed.
That's right, every COPD patient seems to get massive asthma-like doses of salbutamol in hospital. There is indeed some small element of reversible airflow limitation here. However, a meta-analysis has demonstrated that over the long term, the greatest mortality reduction is due to anticholinergic drugs like tiotropium, and that beta-agonists are essentially no better than placebo.
It is generally thought (and sometimes even demonstrated in studies) that drugs like aminophylline and theophylline improve outcomes in severe stable COPD. The therapeutic window is narrow; blood levels of the low effective range are usually targeted (55-85 mmol/L). However, the higher effective range (85-110mmol/L) is thought to be required for the diaphragm stimulation and respiratory drive increase which you want from these drugs. At this range, the balance of useful effects to side-effects becomes dangerously even.
If you cannot clear sputum, you cannot survive the exacerbation. Physiotherapy and those bubble-themed incentive spirometers tend to improve sputum clearance and encourage coughing. If all else fails, one may wish to suction these people's tracheas though a nasopharyngeal airway, or attempt actual bronchoscopy to remove large sputum plugs.
Theoretically, a low carb high fat diet should decrease the whole-body CO2 production (Ohs Manual reports that the decrease is by 15%). There is some evidence to support this, but strong recommendations are nowhere to be found. Overall, one can make a point for ensuring adequate nutrition in general, given how malnourished these people can get.
Lets face it, your first impulse is to blow off some CO2 with NIV, or to give some positive pressure and improve oxygenation. Additionally, the PEEP should decrease the work of breathing due to dynamic hyperinflation and bronchospasm.
There are several studies of NIV in COPD, which have demonstrated a survival benefit. Their entry criteria for NIV are as follows:
In short, NIV is your most useful tool in normalising respiratory function in this group.
This might seem like a completely valid practical question, which makes it all the more surprising to find it among the repertoire of CICM past paper SAQs. Question 8 from the second paper in 2018 presented the candidates with a severe COPD scenario, and asked: "Discuss in detail how you would make a decision about whether to offer invasive mechanical ventilation to this patient, should he fail the trial of NIV." The majority of these people don't have end-stage disease, and the mere fact that you have some COPD should not be a barrier to having a trial of mechanical ventilation to treat some sort of reversible pulmonary pathology. The patient in the CICM scenario has disease qualitatively described as "severe", but is not on home oxygen (which is generally viewed as a marker of the "end stage" of COPD), and is therefore in that horrible limbo where it is not completely clear whether to offer or withhold intubation.
In short, when deciding whether or not to offer intubation to a severe COPD patient, there are a few main questions to consider:
These will now be discussed in some detail.
Is there sufficient information to make a decision regarding whether or not to offer mechanical ventilation? If the answer is no, then it is generally better to err on the side of intubation. One buys time in this fashion. It is a broadly acknowledged fact that any plastic placed by an intensivist can be equally easily un-placed, i.e. if it emerges over the subsequent hours and days that the patient's background functional status and life expectancy is much worse than previously thought, a palliative one-way-extubation can be performed after some discussions with the family. Those discussions will also be much more civilised, as they will be performed in a calmer atmosphere - the decisions will not be urgent. In both Question 1b from the first paper of 2001 and Question 8 from the second paper in 2018 the college examiners are in favour of initial aggressive therapy (in the latter case, the actual phrase "buy time" is used in the model answer).
There is some evidence that jumping to conclusions does harm. Wilman et al (2007) found there was a significant amount of "prognostic pessimism" among ICU physicians who were asked to predict patient outcomes in this setting. "For the fifth of patients with the poorest prognosis according to the clinician, the predicted survival rate was 10% and the actual rate was 40%". The investigators concluded that some patients who might otherwise survive are probably being denied intubation. This is not helped by the fact that there are no strict criteria for this decisionmaking, and ICU specialists differ significantly in their opinion regarding the same patients (Wildman et al, again, this time 2003).
Does invasive ventilation meet any of the definitions of futility? Under certain circumstances, intubation may meet the broadly accepted definition of "operational" futility, being a therapy which is “so unlikely to succeed that many people... would consider it not worth the cost”. It remains to be debated what precisely "to succeed" means when it comes to intubating these people, but a sufficiently large number of people (both lay and professional) would probably agree that death is not "success". As such, patients should not be offered mechanical ventilation in any scenario where it will inevitably lead to death. That brings us to the next question.
Will invasive ventilation improve medium-term mortality? In other words, how likely is this patient to die if mechanical ventilation is offered, and what will that look like? This seems to depend on the pathology which drives the decision to intubate. Some scenarios and pathologies are associated with better outcomes. The following things can be confidently said:
Will invasive ventilation improve medium-term quality of life? This is the question most effectively answered by the severity rating scales.
Will invasive ventilation be a short-term process for this patient? And if not, what will be the likely outcome? This is a question often raised in discussion with respiratory physicians, who might recommend a "short-term trial" of invasive ventilation. Gadre et al (2018) found that the median duration of invasive ventilation in their cohort of 670 intubated COPD patients was 3 days, which certainly sounds like a short trial. The patients who were extubated early were mainly the "pure" COPD exacerbations, whereas the pneumonia were ventilated for longer. In general these authors found that the ICU mortality for their "pure" COPD cohort was actually lower than for other acute respiratory pathologies (9% ICU mortality, 17% hospital mortality). The authors concluded that the anxiety about intubating these people appears to be mainly driven by the results of older studies, from a bygone era of barbaric ventilator management.
But let's say they end up stuck on the ventilator, as you feared. What's the outcome? Quinnell et al (2006) reported on a cohort of 67 such patients, with median FEV1 of 0.6. Of these, 95% were weaned off the ventilator with a tracheostomy, and almost 90% survived to discharge. Their median post-discharge survival was 2.5 years, with one-year, 2-year, and 5-year survival rates were 68%, 54%, and 25%, respectively. ICU length of stay was relatively prolonged (around 30 days on average), and it was followed by another roughly 30-day stay in the "Respiratory Support and Sleep Centre", what sounds like some sort of ventilated nursing home designed for the purpose of weaning these people. In short, you're in for a long stay.
Is invasive ventilation something the patient would agree with? Often this becomes obscured by the fog of hypercapnic narcosis, but the patient's decisionmaking surrogates may be able to enlighten you on what the level of insight has been. It will have been influenced by what their respiratory physician has been telling them. Sullivan et al (1996) found there was some considerable amount of "spin" put on this, positive or negative (depending on what the "respirologist" expected for the patient).
When asked, months after their ICU experience, COPD patients who survived intubation seem relatively comfortable. In spite of the burden of their symptoms, Wildman et al (2009) found the majority rated their health as same or better, and 96% responded that they would be willing to undergo similar treatment again. Less is known about the slow-to-wean, two-month-in-hospital cohort. We can only assume that they are like all the other long-term ventilation survivors, who (according to Huttmann et al, 2018) who were all functioning poorly and feeling horribly depressed. Of these, 32% reported that they would have elected to die in hindsight rather than receive invasive ventilation for a prolonged period.
There are several features which promote intubation as a sensible step.
The objectives are to improve secretion clearance and to rest the respiratory muscles while removing as much CO2 as practical. Therefore, the less support you use the better the outcome.
There are a couple of tricks which may be useful in this scenario:
Expiratory pause to measure dynamic hyperinflation:
Match intrinsic PEEP with extrinsic PEEP
Steep inspiratory rise time
Extubate early, and on to NIV
But, even with the best intentions, some of these people go on to have a prolonged period of ventilation, which culminates in a tracheostomy.
The tracheostomy experience is a terrible thing for secretion clearance; without an epiglottis, one cannot cough properly, and the whole process becomes counterproductive.