Asthma Ventilation Strategy 1

8/3/2019 Asthma Ventilation Strategy 1

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Rajesh Pande MD, PDCCSr. Consultant & Chairman

Dept. of Critical Care Medicine & Emergency MedicineDr. BL Kapur Memorial Hospital, New Delhi


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Introduction

Severe asthma and COPD exacerbationscausing respiratory failure remains a potentiallyreversible, life-threatening condition thatimposes 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 &

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


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IntroductionICU admission identifies an asthmatic patient as a

member of a poor prognostic group. Chest 1992;101:6213,Am J

Respir Crit Care Med 1998;157:18049.

Death is most commonly a result of one of thecomplications of airflow obstruction & severe gas-trapping.

These complications include barotrauma,

hypotension and refractory respiratory acidosis.It is of paramount importance to properly triage

patients with COPD and asthma so that those whoare at risk of death benefit from an ICU environment

It is of paramount importance to properly triage patients

with COPD and asthma so that those who are at risk of

death benefit from an ICU environment


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Initial assessment and

management on ward/in EDImpending respiratory arrest should be

ventilated immediately

Warning signs of impending respiratory arrestare lethargy, obtundation, silent chest andcyanosis, bradycardia and hypotension.

No current system that predicts survival or

weaning failure for a particular patient withsevere exacerbation of COPD - ventilatorysupport should be given to all patients withsevere exacerbation of COPD requiring

ventilatory assistance.


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Severity assessment and riskassessment for respiratoryexhaustion

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


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Airflow ObstructionCritical increase in airway resistance

pressures required for airflow may overload

respiratory muscles (ventilatory pump failure).

Regions of lung can not properly empty &

return to their resting volume (Air

trapping) iPEEP/Auto PEEP further worsenrespiratory muscle function.

Overinflated regions may compress healthy

regions V/Q mismatch.

Air trapping & iPEEP also function as

a threshold load to trigger

mechanical breaths.


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Worsening airflowobstruction

Minute Ventilation - respiratory muscleoverload.

Hypercapnic respiratory failure.

V/Q mismatch - regional lung compression &regional hyperventilation.

Dead space & loss of capillaries - overdistension & emphysematous changes.

Overload on right ventricle -hypoxic


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Gas TrappingSevere 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


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Gas TrappingGas-trapping occurs because low expiratory flow

rates mandate long expiratory times if the entireinspired volume is to be exhaled.

If the next breath interrupts exhalation, then gas-trapping results.

Trapped gas in lungs results in additional pressure atend expiration (auto-PEEP or intrinsic PEEP) aboveapplied PEEP, leading to dynamic hyperinflation.

Auto-PEEP, intrinsic PEEP and dynamic hyperinflationare terms that are frequently used interchangeably.


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Mechanism of dynamic hyperinflation in setting of severe

airflow obstruction


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Gas TrappingDynamic hyperinflation: Failure of lung to return to its

relaxed volume or FRC at end-exhalation.

Hyperinflation can be adaptive. With higher lungvolumes, the increase in airway diameter and elasticrecoil pressure enhances expiratory flow

But excessive dynamic hyperinflation can causehypotension and barotrauma during mechanicalventilation of severe asthma.

These developments are the usual causes of excessmorbidity and mortality.


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Measurement of GasTrappingIt can be measured various ways involving

volume, pressure, or flow of gas.

Total exhaled volume during 20-60s of apnoea in aparalyzed patient can give estimate of trappedgas.

VEI- volume of gas trapped, ( volume of gas atend-inspiration above FRC)

VEI > 20 ml/kg predicts hypotension & barotraumain ventilated atients with severe asthma.


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


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Measurement of Gas

TrappingPEEPi 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.


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Measurement of

intrinsicPEEP.


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Measurement of GasTrapping

Observe the flow versus time graphics on the

ventilator.

If inspiratory flow begins before expiratory

flow ends, then gas must be trapped in the

lungs.

Flow wave form demonstrates gas trapping. Thedecelerating expiratory limb fails to reach the

baseline before the next breath begins (circled),reventin com lete em t in of the lun


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Occult PEEP: All airways may not be in

communication with the proximal airway in

severe asthma. (complete airway closure inthose 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

M t f G


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Examples of Occult auto PEEP- When thein Pplat is not explained by in respiratorysystem compliance during volume-cycledventilation.

Do Pplat measurement. Patients must beparalyzed or heavily sedated for reliablemeasurements.

Pplatreflect 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



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

pressure.Pplatis a reliable predictor of complications.

Pplat< 30 cmH2O- reduces complications

M t f G


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volumes during PCV- may indicate gas-

trapping.

chest wall girth, hyperinflation on chestimaging

efficiency of ventilation, patient effort

unexplained patient agitationBarotrauma, hemodynamic compromise,

missed respiratory efforts

(as patients attempt to trigger the ventilator



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0

-5

Gradient

0

-5


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0

Auto PEEP +10-5

Gradient

-15


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How to limit Gas trappingUnderstanding how gas-trapping occurs is the

first step.

Strategies

Controlled hypoventilation (tidal volume, R/R)

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

Relieve expiratory flow resistance (airway

suctioning, bronchodilators, steroids, large-boreET tube),

inspiratory time by inspiratory flow (70-100

l/min) or incorporating non-distensible tubing,


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Role of External PEEPApplication of external PEEP in severe asthma is

controversial.

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 overcomeauto-PEEP & initiate an inspiration.

But in practice application of external PEEP may

increase total PEEP and worsen gas-trapping.AmRev Respir Dis 1989, 140:5-10.


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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 auto-

PEEP being tolerated before the plateau pressures


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Role of Extrinsic PEEPUseful 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 withsevere asthma.Chest 2004, 125:1081-1102, Curr Opin Crit Care2002, 8:70-76.

If extrinsic PEEP is used: careful bedside

observation & weighing pro-cons (reductions in


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PEEP

10

Auto PEEP +105

Gradient

-5

h h ld hi k f


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When should we think ofventilation?

When severe asthma does not respond to

medical therapy

Intervene fast- Adequate oxygenation &ventilation.

Choices are

NIV

Invasive ventilation


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NIPPVIt 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 couldimprove lung function & possibly reduce the needfor hospitalization.

In COPD with severe airflow limitation a number ofprospective randomized trials have shown that NIVreduces the need for endotracheal intubation,

length of hospital stay and in-hospital mortality rate,


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NIVEmerg Med J 2006;23

The role of NIV in acute asthma is at bestcontroversial.

While no guidelines have been established, areasonable approach would be to use NIV inpatients who do not respond to initial medical

therapy, and have no contraindications for theuse of NIV.


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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.

(Many patients presenting with hypercapnia do

not require intubation)

Guidelines for the Diagnosis and Management of Asthma, National Institutes of Health;

1997.Am Rev Respir Dis 1988, 138:535-539.


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IntubationExplain & reassure the patient.

Pre-oxygenation.

Factors that may cause catastrophic

hypotension :Dehydration

PEEPi

Loss of endogenous catecholamines

Vasodilating properties of the anaesthetic/sedativeagents.

To avoid hypotension Volume resuscitationbefore anaesthesia, keep vasoconstrictors(ephedrine or metaraminol) handy.


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Thorax2003;58;81

-88


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Drug Therapy for intubation &

Mechanical VentilationEtomidate 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


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KetamineIt has sympathomimetic and bronchodilating

properties

It has been used before, during, and afterintubation in patients with acute severe

asthma.

Dose: 12 mg/kg, IV over 24 minutes. It mayBP, HR, seizure threshold, alters mood &

causes delirium.

Inhalational anaesthetics: Advantage of

Opioids & Muscle


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Opioids & MuscleRelaxants

Opioids : useful addition to sedatives, provide

analgesia

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.


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Topical drug delivery to the

ventilated patientInvasive 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 & et nebulisers are effective in


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Thorax2003;58;81

-88


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Goals of Mechanical

VentilationSelect modes that provide muscle

unloading.

Reduce TV as much as possible to limit thepeak pressures & avoid barotrauma.

pH,

PaCO2 is an acceptable trade off.

The role of PEEP to recruit alveoli is lessthan in parenchymal disease.


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Mechanical Ventilation-

Pressure assisted modalities

Offers high flow initially that vary with patientefforts.

Helps to keep inspiratory time short(expiratory long).

Better synchrony with patients spontaneousbreathing efforts.


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Mechanical Ventilation-Reducing Minute Ventilation

Appropriate medical therapy

Reduce Minute Ventilation to dynamic

hyperinflation/gas-trapping.

tidal volume, frequency, or set pressure.

It may result in CO2 retention.

Permissive hypercapnia is generally considered well

tolerated.

Permissive hypercapnia: pH > 7.20, PaCO2 < 90

mmHg has gained widespread acceptance.

The technique has been used successfully in


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Reducing Gas TrappingExpiratory timeHigher 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 10l/min or less & R/R is low.

Changing I/E ratio is important to gas-trappingbut single most effective way is by MV.


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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).


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Ventilatory SettingStart with pressure control mode

Thorax

2003;58;81


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BronchoscopySevere mucus impaction could be an issue instatus asthmaticus, bronchoscopicexamination 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 therisk for pneumothorax [Thorax 1986,41: 459-463. 55]

Bronchoscopy is not recommended.


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Mucus cast of bronchial tree coughed up by

an asthmatic patient during an


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Difficult weaning &

extubationThe endotracheal tube induces

bronchoconstriction as the sedation is

withdrawn in preparation for extubation.

Inhalational anaesthetic agent allows ETto be removed under anaesthesia with the

confident expectation of rapid recovery

once the anaesthetic is discontinued.


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Conclusion

While the prevalence of asthma has increased,outcomes of severe asthma appear to beimproving, with lower complication rates and

fewer in-hospital deaths.

Ventilation management in acute severeasthma is difficult & challenging.

Clinicians managing these patients shouldunderstand why gas-trapping occurs, how tomeasure it and how to limit its severity. Theyshould em lo a strate to minimise as


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A 63-year-old man is brought by hisdaughter to the emergency departmentof your hospital because of progressive

difficulty in breathing. On arrival, the patientis non-responsive and has a dark purplecolour, without perceptible breathingmovements or any perceptible pulse.

What is your immediate action


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You intubate the patient and ventilate him byhand. After one dose of epinephrine 1 mgintravenously, you have a good carotid pulse

and the purple colour is disappearing. Youtransfer the patient to the ICU. The daughtertells 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 sayshis condition has worsened over the past tendays. As well as having increasing difficultybreathing, in the last two days he could no

longer walk and he was coughing up a lot of


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The initial electrocardiogram (ECG) showedregular QRS complexes.

There is no pulse - ?

cause of the respiratory arrest?

Most important complication suspected ?


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Considering severe air trapping, how do youset the ventilator parameters?

Ventilating the patient eight times/min with500 ml (the patient weighs 70 kg), zero PEEP,

and FiO2 of 1.0, you measure a PaO2 of 200mmHg, a PaCO2 of 60 mmHg, and a pH of 7.3.

The peak airway pressure is 60, the plateaupressure 35 cmH2O.

Why peak and plateau pressures are high


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In the deeply sedated and relaxed patient,you measure a total PEEP of 18 cmH2O.

What next ?


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Following tidal volume and respiratory ratereduction, the plateau pressure drops to 30cmH2O and the pH to 7.2.

Role of PEEP

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Asthma Ventilation Strategy 1

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