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Rajesh Pande MD, PDCC

Sr. Consultant & Chairman Dept. of Critical Care Medicine & Emergency Medicine Dr. BL Kapur Memorial Hospital, New Delhi

Severe asthma and COPD exacerbations

causing respiratory failure remains a potentially reversible, life-threatening condition that imposes significant morbidity and mortality.
About 10% of asthmatics admitted to hospital

go to ICU, with 2% being intubated.

Admission to ICU & need for mechanical

ventilation are associated with morbidity & Am J Respir Crit Care Med 1998, 157:1804-1809. Ann Allergy Asthma Immunol 2004, mortality. (1-8 per 100 000 annually)

ICU admission identifies an asthmatic patient as a

member of a poor prognostic group.

Am J Respir Crit Care Med 1998;157:18049.

Chest 1992;101:6213,

Death is most commonly a result of one of the

complications of airflow obstruction & severe gastrapping.

These complications include barotrauma,

It is of paramount importance to properly triage patients hypotension and refractory respiratory acidosis. with COPD and asthma so that those who are at risk of It is of paramount importance to properly triage death benefit from an ICU environment patients with COPD and asthma so that those who are at risk of death benefit from an ICU environment

Initial assessment and management on ward/in ED

Impending respiratory arrest should be

ventilated immediately Warning signs of impending respiratory arrest are lethargy, obtundation, silent chest and cyanosis, bradycardia and hypotension. No current system that predicts survival or weaning failure for a particular patient with severe exacerbation of COPD - ventilatory support should be given to all patients with severe exacerbation of COPD requiring ventilatory assistance.

Severity assessment and risk assessment for respiratory exhaustion

Patient deterioration despite optimal treatment with progressive increase of PaCO2 is a sign of impending respiratory exhaustion and a predictor of fatal asthma, even before the occurrence of severe hypercapnia

Airflow Obstruction
Critical increase in airway resistance pressures required for airflow may overload

respiratory muscles (ventilatory pump failure).

Air trapping can not also function as Regions of lung& iPEEPproperly empty & a threshold load to trigger return to their resting volume (Air trapping)mechanical breaths. iPEEP/Auto PEEP further worsen respiratory muscle function.
Overinflated regions may compress healthy

regions V/Q mismatch.

Worsening airflow obstruction

Minute Ventilation - respiratory muscle


Hypercapnic respiratory failure. V/Q mismatch - regional lung compression &

regional hyperventilation.
Dead space & loss of capillaries - over Overload on right ventricle -hypoxic

distension & emphysematous changes.

Gas Trapping
Severe asthma exacerbation bronchoconstriction,

airway oedema and/or mucous plugging Severe airflow limitation.

WOB is significantly Expiration becomes active in an attempt by the

patient to force the inspired gas out of their lungs

inspiratory work d/t high airway resistance and

hyperinflation. Lungs and chest wall operate on a

Gas Trapping
Gas-trapping occurs because low expiratory flow

rates mandate long expiratory times if the entire inspired volume is to be exhaled.
If the next breath interrupts exhalation, then gas-

trapping results.
Trapped gas in lungs results in additional pressure at

end expiration (auto-PEEP or intrinsic PEEP) above applied PEEP, leading to dynamic hyperinflation.
Auto-PEEP, intrinsic PEEP and dynamic hyperinflation

are terms that are frequently used interchangeably.

Mechanism of dynamic hyperinflation in setting of severe airflow obstruction

Gas Trapping
Dynamic hyperinflation: Failure of lung to return to its

relaxed volume or FRC at end-exhalation.

Hyperinflation can be adaptive. With higher lung

volumes, the increase in airway diameter and elastic recoil pressure enhances expiratory flow
But excessive dynamic hyperinflation can cause

hypotension and barotrauma during mechanical ventilation of severe asthma.

These developments are the usual causes of excess

morbidity and mortality.

Measurement of Gas Trapping

It can be measured various ways involving

volume, pressure, or flow of gas.

Total exhaled volume during 20-60s of apnoea in a

paralyzed patient can give estimate of trapped gas.

VEI- volume of gas trapped, ( volume of gas at

end-inspiration above FRC)

VEI > 20 ml/kg predicts hypotension & barotrauma

in ventilated patients with severe asthma.

Measuring lung hyperinflation using VEI. VEI, volume of gas at end-inspiration above FRC

Measurement of Gas Trapping

PEEPi or auto PEEP Occlude expiratory port of ventilator at end-

expiration, the proximal airway pressure will equilibrate with alveolar pressure & permit measurement of auto-PEEP (end-expiratory pressure above applied PEEP) at the airway opening.
Expiratory muscle contraction can elevate auto-PEEP

without adding to dynamic hyperinflation. for accurate measurement patient should be relaxed.

Measureme nt of intrinsic PEEP.

Measurement of Gas Trapping

Observe the flow versus time graphics on the

If inspiratory flow begins before expiratory

flow ends, then gas must be trapped in the lungs.

Flow wave form demonstrates gas trapping. The decelerating expiratory limb fails to reach the baseline before the next breath begins (circled), preventing complete emptying of the lung

Measurement of Gas Trapping

Occult PEEP: All airways may not be in

communication with the proximal airway in severe asthma. (complete airway closure in those segments).
Occult auto-PEEP has all bad effect of auto PEEP

but it can not be quantified easily.

Good clinical judgement is important. Clinicians

should question low auto-PEEP measurements in

Measurement of Gas Trapping

Examples of Occult auto PEEP- When the

in Pplat is not explained by in respiratory system compliance during volume-cycled ventilation. paralyzed or heavily sedated for reliable measurements.

Do Pplat measurement. Patients must be

Pplat reflect gas-trapping- As lung volume

, the alveolar pressure also

assuming there is no other explanation, such as

adjustments to the ventilator or changes in respiratory

Measurement of end-inspiratory plateau pressure, an estimate of average end-inspiratory alveolar pressure.

Pplat is a reliable predictor of complications. Pplat < 30 cmH2O- reduces complications

Measurement of Gas Trapping

volumes during PCV- may indicate gas-


chest wall girth, hyperinflation on chest

efficiency of ventilation, patient effort unexplained patient agitation Barotrauma, hemodynamic compromise,

missed respiratory efforts (as patients attempt to trigger the ventilator

Gradient -5 0


Gradient -5 Auto PEEP +10


How to limit Gas trapping

Understanding how gas-trapping occurs is the

first step.
Controlled hypoventilation ( tidal volume, R/R)

[less gas to exhale] and [longer expiratory time]

Relieve expiratory flow resistance (airway

suctioning, bronchodilators, steroids, large-bore ET tube),

inspiratory time by inspiratory flow (70-100

l/min) or incorporating non-distensible tubing,

Role of External PEEP

Application of external PEEP in severe asthma is

Theoretical advantages:
the WOB & hence CO2 production, while limiting

gas-trapping by splinting the airways open. Intensive Care Med 2004, 30:1311-1318. inspiratory muscle effort required to overcome auto-PEEP & initiate an inspiration.

But in practice application of external PEEP may

increase total PEEP and worsen gas-trapping.

Rev Respir Dis 1989, 140:5-10.


Role of External PEEP

Useful in COPD with airflow obstruction: > 40% of

inspiratory muscle effort can be expended to overcome auto-PEEP.

By adding extrinsic PEEP, the inspiratory muscle

effort needed to trigger inspiration can be attenuated.

In such patients extrinsic PEEP must be titrated

individually, with an average of 80% of the autoPEEP being tolerated before the plateau pressures

Role of Extrinsic PEEP

Useful in patients breathing spontaneously and

capable of triggering the ventilator.

It is occasionally difficult to measure auto-PEEP

reliably. If extrinsic PEEP > auto-PEEP, gas trapping will worsen. Recommendations: Use extrinsic PEEP minimally, or not use it at all in patients with severe asthma. Chest 2004, 125:1081-1102, Curr Opin Crit Care
2002, 8:70-76.

If extrinsic PEEP is used: careful bedside

observation & weighing pro-cons (reductions in

PEEP 10 Gradient 5 Auto PEEP +10


When should we think of ventilation?

When severe asthma does not respond to

medical therapy
Intervene fast- Adequate oxygenation &

Choices are
NIV Invasive ventilation

It is possible that some patients with severe asthma

may benefit from NIV . Evidence:

Chest 1996;110:76774. Meduri et al (n=17) Intensive Care Med 2001;27:48692. (n=33) Chest 2003;123:101825. (n=13) Acad Emerg Med 2001;8:112835.

Interpretation: in selected patients, NPPV could

improve lung function & possibly reduce the need for hospitalization.
In COPD with severe airflow limitation a number of

prospective randomized trials have shown that NIV reduces the need for endotracheal intubation, length of hospital stay and in-hospital mortality rate,


Emerg Med J 2006;23

The role of NIV in acute asthma is at best

While no guidelines have been established, a

reasonable approach would be to use NIV in patients who do not respond to initial medical therapy, and have no contraindications for the use of NIV.

When to intubate?
The decision to intubate should be based on

clinical judgement.
Signs of deterioration: CO2 levels (+

normalization in a previously hypocapnic patient), exhaustion, mental status depression, hemodynamic instability & refractory hypoxemia.
Decision should not be based solely on ABG.
Guidelines for the Diagnosis and Management of Asthma, National Institutes of Health; 1997. Am Rev Respir Dis 1988, 138:535-539.

(Many patients presenting with hypercapnia do not require intubation)

Explain & reassure the patient. Pre-oxygenation. Factors that may cause catastrophic

hypotension :
Dehydration PEEPi Loss of endogenous catecholamines Vasodilating properties of the anaesthetic/sedative

agents. To avoid hypotension Volume resuscitation before anaesthesia, keep vasoconstrictors (ephedrine or metaraminol) handy.

Thorax 2003;58;81 -88

Drug Therapy for intubation & Mechanical Ventilation

Etomidate and thiopentone, propofol. Propofol is useful for intubation and

intermediate term sedation

rapid onset and offset of action easily titrable for intubation Provides deep sedation rapidly,

Problems: vasodilatation & hypotension in

dehydrated patients.
Longer term sedation by infusion of midazolam

It has sympathomimetic and bronchodilating

It has been used before, during, and after

intubation in patients with acute severe asthma.

Dose: 12 mg/kg, IV over 24 minutes. It may

BP, HR, seizure threshold, alters mood & causes delirium.

Inhalational anaesthetics: Advantage of

Opioids & Muscle Relaxants

Opioids : useful addition to sedatives, provide

Avoid Morphine- causes histamine release &

may worsen bronchoconstriction & hypotension.

Fentanyl: better, inhibits airway reflexes,

causes less histamine release but large boluses may cause bronchospasm and chest wall rigidity.

Topical drug delivery to the ventilated patient

Invasive as well as non invasive ventilation

compromise the delivery of bronchodilator aerosols.

The drug delivery varies from 0% to 42%,

depending on nebuliser design, driving gas flow, ventilator tubing, and size of ET tube.
Humidification may reduce drug deposition by

40%, which may be reversed by addition of a spacer device.

Ultrasonic & jet nebulisers are effective in

Thorax 2003;58;81 -88

Goals of Mechanical Ventilation

Select modes that provide muscle

Reduce TV as much as possible to limit the

peak pressures & avoid barotrauma.

pH, PaCO2 is an acceptable trade off. The role of PEEP to recruit alveoli is less

than in parenchymal disease.

Mechanical VentilationPressure assisted modalities

Offers high flow initially that vary with patient

Helps to keep inspiratory time short

(expiratory long).
Better synchrony with patients spontaneous

breathing efforts.

Mechanical VentilationReducing Minute Ventilation

Appropriate medical therapy Reduce Minute Ventilation to dynamic

tidal volume, frequency, or set pressure.

It may result in CO2 retention. Permissive hypercapnia is generally considered well

Permissive hypercapnia: pH > 7.20, PaCO2 < 90

mmHg has gained widespread acceptance.

The technique has been used successfully in

Mechanical VentilationReducing Gas Trapping

Expiratory time
Higher inspiratory flow (70100 l/min) Shorter inspiratory time respiratory rate, and eliminate inspiratory pause.

Prolongation of expiratory time dynamic

hyperinflation, seen as in Pplat. Benefit is modest when the baseline MV is 10 l/min or less & R/R is low. Changing I/E ratio is important to gas-trapping but single most effective way is by MV.

Mechanical Ventilation Gas Trapping

Apply adequate sedation and analgesia to lower

CO2 production & ventilatory requirements.

The use of NMB should be limited to short

periods of time and only when absolutely necessary ( patient ventilator asynchrony).

Ventilatory Setting
Start with pressure control mode

Thorax 2003;58;81

Severe mucus impaction could be an issue in

status asthmaticus, bronchoscopic examination of the airways and removal of secretions may be beneficial [Crit Care Med 1994,
22:1880-1883 54].

As the presence of the bronchoscope may

worsen lung hyperinflation and increase the risk for pneumothorax [Thorax 1986, 41: 459-463. 55]

Bronchoscopy is not recommended.

Mucus cast of bronchial tree coughed up by an asthmatic patient during an

Difficult weaning & extubation

The endotracheal tube induces

bronchoconstriction as the sedation is withdrawn in preparation for extubation.

Inhalational anaesthetic agent allows ET

to be removed under anaesthesia with the confident expectation of rapid recovery once the anaesthetic is discontinued.

While the prevalence of asthma has increased,

outcomes of severe asthma appear to be improving, with lower complication rates and fewer in-hospital deaths.
Ventilation management in acute severe

asthma is difficult & challenging.

Clinicians managing these patients should

understand why gas-trapping occurs, how to measure it and how to limit its severity. They should employ a strategy to minimise gas

A 63-year-old man is brought by his

daughter to the emergency department of your hospital because of progressive difficulty in breathing. On arrival, the patient is non-responsive and has a dark purple colour, without perceptible breathing movements or any perceptible pulse. What is your immediate action

You intubate the patient and ventilate him by

hand. After one dose of epinephrine 1 mg intravenously, you have a good carotid pulse and the purple colour is disappearing. You transfer the patient to the ICU. The daughter tells you that her father is a heavy smoker, that he doesn't like to go to the doctor, and that he doesn't take any medicine. She says his condition has worsened over the past ten days. As well as having increasing difficulty breathing, in the last two days he could no longer walk and he was coughing up a lot of

The initial electrocardiogram (ECG) showed

regular QRS complexes. There is no pulse - ?

cause of the respiratory arrest? Most important complication suspected ?

Considering severe air trapping, how do you

set the ventilator parameters?

Ventilating the patient eight times/min with

500 ml (the patient weighs 70 kg), zero PEEP, and FiO2 of 1.0, you measure a PaO2 of 200 mmHg, a PaCO2 of 60 mmHg, and a pH of 7.3. The peak airway pressure is 60, the plateau pressure 35 cmH2O.
Why peak and plateau pressures are high

In the deeply sedated and relaxed patient,

you measure a total PEEP of 18 cmH2O.

What next ?

Following tidal volume and respiratory rate

reduction, the plateau pressure drops to 30 cmH2O and the pH to 7.2.

Role of PEEP