Introduction
The case was chosen as ‘near fatal’ (BTS 1 definition) asthma poses significant ventilatory challenges which are vital to understand when dealing with such a case.
Clinical problem
A 40-year-old lady was admitted to hospital with a life threatening asthma attack. She had been previously fit and well until three weeks previously when she was admitted under the medics with shortness of breath (SOB) and wheeze. During that admission her symptoms were slow to settle and she had a thoracic CT scan which was normal. She gradually improved with bronchodilators and steroids and was sent home after twelve days with a diagnosis of adult onset asthma.
Ten days later she went to her GP after she had woken in the morning with SOB and wheeze. Her GP treated her with nebulised bronchodilators and 40 mg of oral prednisalone and admitted her to the medical admissions unit. She was treated by the medics with continuous nebulised salbutamol, IV magnesium and IV hydrocortisone but did not improve. She was referred to critical care thirty minutes after admission. A rapid examination and review of investigations revealed CO2 8, PO2 9, pH 7.2, HR 120, exhaustion and a silent chest. As there was no appropriate equipment, drugs or help on the medical ward she was immediately transferred to the Intensive Care Unit and intubated.
Management
The patient was commenced on volume controlled ventilation with a tidal volume (TV) of 350 mls (6mls/kg), a respiratory rate (RR) of 12, an I:E ratio of 1:3 and PEEP of 0. With these settings her peak pressure was 51, plateau pressure 28, intrinsic PEEP (PEEPi) 16 and total PEEP (PEEPt) 19. Constant and decelerating flow patterns were both tried (keeping the I:E constant) with no difference in plateau pressure or PEEPi. A decelerating flow was used from then on. External PEEP (PEEPe) was tried at 0, 5 and 10 cm H2O with the following effects:
0 PEEPi 16, PEEPt 19 (PEEPt = total PEEP)
5 PEEPi 12, PEEPt 19
10 PEEPi 10, PEEPt 21
A PEEPe of 5 was then selected and no other initial changes were made to the ventilator settings.
Deep sedation to prevent spontaneous breathing compromised her blood pressure so she was paralysed to prevent ventilator asynchrony. A low dose metaraminol infusion was used to maintain BP and UO. IV hydrocortisone and magnesium were continued.
The initial blood gas reading showed a pH 7.1. Despite a fall in CO2 from 13 to 10 it stayed around this level as lactate rose to 7 with a salbutamol infusion of 17 mcg/min. The salbutamol was reduced to 7 mcg/min and lactate fell to normal with an improvement in acidosis. After a few hours PEEPi and plateau pressures fell to 10 and 24 allowing a TV increase to 400 mls with further improvement in pH.
Next morning PEEPi was down to 5 with PEEPt 10 (PEEPt still 10 with PEEPe 0) and a plateau pressure of 19 so the RR was increased to 14 with no change in PEEPi or plateau pressure. A few hours later neuromuscular blocking agents were stopped with no adverse consequences. Extubation occurred successfully on day 3 and 2 days later the patient was discharged to the medical ward.
Discussion
This case demonstrates the ventilatory challenges that can be faced with near fatal asthma. Mucous plugging, bronchospasm and airway inflammation reduce the lung volume that can participate in ventilation and result in extreme airflow limitation, particularly in expiration. This is exacerbated by reduced driving force for expiration from low pulmonary elastic recoil (via an unknown mechanism) and outward recoil of the chest wall (persistent activation of inspiratory muscles during inspiration). The prolonged respiratory time constant leads to insufficient time for complete emptying (down to normal FRC) with the generation of PEEPi and lung hyperinflation. This leads to VQ mismatching, lung injury (from alveolar distension in normal lung units) and compromised haemodynamics due to reduced venous return. The figures below from the ICM article referenced 2 illustrate the inhomogenous ventilation that occurs.
pastedGraphic
A = normal lung
B = complete obstruction
C = obstruction in expiration
D = obstruction throughout respiratory cycle (less PEEPi than C)
Ventilation in such cases therefore requires strategies to minimise lung volumes and pressures. In 1987 Tuxen and Lane 3 demonstrated the key points below:
- If MV fixed; lung distension at end inspiration minimised with low TV and high RR.
- If TV fixed; distension minimised with prolonged exp time eg RR or I:E ratio
- If RR, TV and MV are constant then expiratory time (Te) can be increased at the expense of a shorter inspiratory time (with higher peak pressures).
Peak and Plateau Pressures
Peak pressures will be high in asthmatics because of proximal airway narrowing. The pressure measured by the ventilator is not alveolar pressure. This is self evident because flow is delivered to the end of inspiration thus meaning there is a pressure difference between ventilator tubing and the alveoli. It is only in conditions of no flow (an inspiratory pause) that alveolar pressures can be assessed. This does not mean however that peak pressures are not important. Looking at the illustration above demonstrates that flow and pressure is delivered to the least obstructed lung units first and an inspiratory hold gives time for units with longer time constants to fill (reducing pressure in less obstructed lung units). Thus alveolar pressures in normal lung units will be closer to peak pressure than other lung units and potentially be dangerously high with over distension. It is not possible to know to what extent this is occurring. However, it seems reasonable that plateau pressures are most important and high peak pressures acceptable (but not desirable). Plateau pressures should be as low as possible and certainly under 30 cmH2O.
Pressure or volume control
There is little evidence for one over another but respiratory compliance can change rapidly meaning controlled volumes are potentially safer (avoidance of severe respiratory acidosis or alkalosis). It is important to monitor airway pressures in volume control.
Constant vs decelerating flow
Some texts advocate using a constant inspiratory flow (square waveform) 4. The rationale they site is that changing to a square wave doubles the inspiratory flow and therefore prolongs expiratory time. This, however, is merely a function of I:E ratio rather than waveform (if the I:E ratio is held constant, a decelerating pattern will start with twice the flow rate of a square wave). Moreover, if TV and Ti are held constant (which will therefore hold Pplat constant), Ppeak will be greater with a square waveform (in decelerating flow Ppeak and Pplat are the same). This is undesirable for the reasons cited above.
Tidal volume
As above smaller tidal volumes cause less hyperinflation. 6 mls per kg would seem a sensible starting point.
Respiratory rate and I:E ratio
As above, for a fixed MV, lower TV and higher RR leads to less hyperinflation. Once, however, TV has been set, distension is minimised with a longer expiratory time. One way to achieve this is with a lower RR. The other way is to increase expiratory time at the expense of inspiratory time. Peak pressures will rise (see above). Expiratory flow is exponential with most flow occurring early in expiration and getting progressively less. Extending expiration beyond about 4 seconds therefore leads to very little further emptying and will only serve to lead to higher airway pressures.5 There is therefore little point in RRs of <12 and I:E ratios of >1:4. For the same reason, TV reduction will give ever decreasing returns in lung emptying.
Pasted Graphic
This figure illustrates constant flow ventilation and the difference between Ppeak and Pplat and how this is related to airway resistance. From Drager website.
Extrinsic PEEP
In COPD, dynamic airway compression (airway closure) increases the work of breathing and extrinsic PEEP will counteract this with no increase in lung volume (provided PEEPe is set at < PEEPi). In an asthma attack the main problem is narrowed airways rather than weakened (compressible) airways. Increased resistance will of course lead to a rapid pressure drop with potential for airway closure (pleural pressures > airway pressures). However, the predominant site of increased airway resistance in acute asthma is in proximal non compressible airways meaning distal compressible airways maintain positive pressure and stay open.6 This means any PEEPe would be applied to the whole airway down to the alveoli and thus increase lung volume. In practice, some patients (particularly with longstanding, chronic asthma) have lung disease more similar to patients with COPD and PEEPe can be of benefit. Whilst in controlled ventilation PEEPe will have no effect on work of breathing (which is of course zero), maintaining the patency of distal airways will result in better VQ matching and improved CO2 clearance.
It seems sensible therefore to experiment with different levels of PEEPe (starting at zero). It was demonstrated in this patient that 5cm PEEPe reduced PEEPi with no increase in PEEPt showing that airway compression was occuring. 10cm PEEPe was too much as it resulted in increased PEEPt.
Assessment of hyperinflation
Hyperinflation can be assessed by prolonged apnoea with measurement of expiratory volume (rarely done as paralysis needed). The expiratory portion of the flow graph can be examined to see if it returns to baseline. Pplat and PEEPi can also be used. Measured PEEPi is influenced by the length of the expiratory pause, compliance of the ventilator tubing, expiratory muscle activity and dynamic airway compression (pressure behind closed airways cannot be measured). Pplat is therefore best remembering the inspiratory pause must be long enough for equilibration of lung units and that there must be no leaks.
Lessons learnt
Ventilation of asthmatics requires meticulous attention to detail to prevent lung injury and potentially fatal haemodynamic compromise. I will use the above principals in future for ventilating patients with near fatal asthma.
References
1. British Guideline on the Management of Asthma. 2009. British Thoracic Society.
2. Management of Mechanical ventilation in Acute Severe Asthma: Practical Aspects. Oddo, M Feihi, F Schiller, M D Perret, C. Intensive Care Medicine (2006): 32: 501 -510
3.The effects of ventilatory pattern on hyperinflation, airway pressures, and circulation in mechanical ventilation of patients with severe air-flow obstruction. Tuxen DV, Lane S: Am Rev Respir Dis 136:872–879, 1987
4.Principals and Practice of Mechanical Ventilation. 2nd ed. Tobin 2006 McGraw-Hill.
5. Effects of prolonging respiratory time on dynamic hyperinflation in mechanically ventilated patients with severe asthma. Leatherman et al: Crit Care Med 32:1542-5, 2004
6. McFadden ER Jr, Ingram RH Jr, Haynes RL, Wellman JJ (1977) Predominant site of flow limitation and mechanisms of postexertional asthma. J Appl Physiol 42:746–752