Ventilation Strategies for COPD
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.
- Question 29 from the second paper of 2005
- Question 30 from the second paper of 2005
- Questions 1a, 1b, 1c and 1d from the first paper of 2001
- EUC / CMP / FBC / CRP /BNP
- Chest Xray - looking for pneumonia
- Transthoracic echo - to assess the contribution from heart failure
- Blood/sputum cultures
- Urinary pneumococcal and legionella antigens
- Atypical pneumonia serology
- Oxygen therapy, aiming at a SpO2 around 90%
- Anticholinergic bronchodilators in combination with beta-agonists, eg. ipratropium bromide plus salbutamol - at first 2-hourly, and gradually de-escalating
- Think about methylxanthines
- Think about antibiotics (3rd generation cephalosporin and a macrolide)
- Steroids IV (100mg of hydrocortisone q6h)
- Attack them with a physiotherapist and an incentive spirometer.
- Manage their heart failure. Consider digoxin in cor pulmonale, and be careful with diuretics (as right heart failure may worsen in the absence of adequate preload).
- Attention to electrolytes, particularly phosphate
- Nutrition, preferably low-carb and high-fat
- NIV to reduce respiratory muscle workload, correct respiratory acidosis, improve oxygenation.
- Consider intubation if their functional capacity suggests the possibility of a return to independence
- Intubate them if they are comatose, not benefitting from NIV, or unable to clear secretions
- Use a minimum level of support, and aim for longer expiratory time
- Match intrinsic PEEP with extrinsic PEEP
- Extubate them onto NIV as soon as is practical.
Assessment of severity of COPD
Question 29 from the second paper of 2005 asks about the assessment of the severity of COPD.
- exercise tolerance
- breathlessness with everyday activities
- presence of chronic cough
- high volume of sputum, suggestive of bronchiectasis
- haemoptysis, suggestive of malignancy
- home O2 requirement
- home CPAP requirement
- pattern of bronchodilator use
- pattern of steroid use
- frequency of hospitalisations
- previous mechanical ventilation
- anorexia and weight loss
- features of malnutrition
- features of obesity (sedentary lifestyle)
- features of chronic steroid use
- central cyanosis
- breathlessness at rest
- hyperexpanded chest
- degree of air entry
- signs of right heart failure
- Bicarbonate levels
- Hb (polycythaemia)
- Spirometry, pre and post bronchodilator
- Formal lung function tests
- ABGs to determine degree of hypoxia and hypercapnea
- TTE (pulmonary pressures)
- High-resolution CT to assess the severity of emphysematous changes
The BODE index
- Predicts mortality among COPD outpatients
- According to the original article, "is better than the FEV1 at predicting the risk of death from any cause and from respiratory causes among patients with COPD"
- Consists of 4 categories, each worth a certain number of points, up to a maximum score of 10 moints (being the worst chances).
|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|
- The MMRC breathlessness scale is basically a subjective report of how breathless the patient feels; 0 is "doin fine" and 4 is "can't leave the house"
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.
Acute respiratory failure in COPD
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.
Hypercapnic respiratory failure in COPD
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.
Normocapnic respiratory failure in COPD
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.
Infective exacerbation of COPD
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.
Does it matter if there is also left heart failure?
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.
Do I really need to restrict oxygen for these people? What is the evidence?
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.
The relevant features of their investigations
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 relevant features of their formal lung function tests
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.
Everybody seems to get bronchodilators, but is the obstruction not chronic and irreversible?
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.
The role of methylxanthines
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.
The importance of sputum clearance
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.
The COPD diet
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.
The goal of non-invasive ventilation
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:
- Resp rate > 28
- Respiratory acidosis: PaCO2 > 45mmHg and pH < 7.35
In short, NIV is your most useful tool in normalising respiratory function in this group.
When NOT to intubate the COPD patient
A Cochrane review of NIV in the COPD patient group has demonstrated that in comparison to the invasively ventilated group, patients treated with NIV have greatly reduced mortality (by half), reduced hospital stay, and reduced risk of pneumonia. This implies that the decision to intubate these people tends to reflect a more severe disease, and the prognosis is proportionally worse.
Question 1b from the first paper of 2001 presents such a patient. "The history from her daughter reveals that Mrs X lives independently but is limited by severe breathlessness with exercise. Does this change your management?" The college, in their answer, are aggressively in favour of actively managing this patient.
However, the functional capacity should factor in the decision to intubate. People who are house-bound and partially dependent, and people who are chair-bound or bed-bound, are poor candidates for intubation. Not just because the end-stage nature of their disease may not justify aggressive intervention, or that there is a risk of permanent ventilator dependence (as you decondition the respiratory muscles) but because mortality in this group demonstrably increases in the 12 months following extubation. A recent study from Thorax (Hajizadeh et al, 2015) retrospectively observed a cohort of 4791 end-stage oxygen dependent COPD patients who were itnubated, and foud that 23% died in the hospital, and 45% died in the subsequent 12 months, with 26.8% discharged to a nursing home within 30 days.
However, the majority of these people don't have end-stage disease; and the mere fact that you have COPD should not be a barrier to having a trial of mechanical ventilation to treat some sort of reversible pulmonary pathology.
Which COPD patients should be intubated
There are several features which promote intubation as a sensible step.
- Failure of NIV: The patient is already on NIV, but it has failed to reduce the work of breathing, and the patient is beginning to become fatigued which makes the ABG results look terrible.
- Coma: Level of consciousness does not permit NIV, or the airway reflexes are not preserved
- Pneumonia: There are copious secretions, and an ineffective cough (which is made worse by NIV- its very hard to clear secretions by coughing against a 10cm positive pressure)
- Their hypoxia is worsening, and NIV is not contributing usefully
How to ventilate the COPD patient
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:
- The expiratory pause manoeuvre measures intrinsic PEEP. As this rises to 8-10 cm, one might consider changing the I:E ratio to increase the duration of expiration
Match intrinsic PEEP with extrinsic PEEP
- Having established which the intrinsic PEEP is, one should set the machine to deliver a similar level of pressure, thereby neutralising the effect of intrinsic PEEP on the work of breathing.
Steep inspiratory rise time
- If you have little control over the I:E ratio (eg. in a patient-triggered mode) you may consider using a higher inspiratory flow rate (which on some ventilators is represented by a "rise time" inspiratory flow ramp). The greater the inspiratory flow, the shorter the inspiratory time; thus more time is allowed for expiration for any given respiratory rate. A good quick flow rate is about 100L/min.
Extubate early, and on to NIV
- As soon as practical, these people should be extubated and supported with NIV. This Cochrane review suggests this strategy can halve mortality and reduce the rate of VAP to one third. .
But, even with the best intentions, some of these people go on to have a prolonged period of ventilation, which culminates in a tracheostomy.
When and why to decannulate the tracheostomy
The tracheostomy experience is a terrible thing for secretion clearance; without an epiglottis, one cannot cough properly, and the whole process becomes counterproductive.
- As soon as you confirm the upper airway reflexes are intact
- When the secretions are under control (i.e. you suction the tracheostomy only every 2-4 hours)
- When the respiratory muscle strength has recovered sufficiently to make good cough efforts
- Obviously, when the patient is free from their dependence on the ventilator for PEEP and oxygen(i.e. they are on humidified blow-over room air)