Asthma in the intensive care unit

Impaired ventilatory response to hypoxia associated with near-fatal cases P0.1-- airway occlusion pressure 0.1 second after the start of inspiration against an occluded airway... Increas

Asthma in the

Intensive Care Unit

Sean M CaplesAssistant Professor of Medicine

College of Medicine

Mayo Clinic

Acute exacerbation of asthma

Most cases are slow-onset

• Infectious, allergic, irritant triggers

• Autopsy: airway mucus plugging /

obstruction; generalized airway thickening

• Poor compliance with outpatient asthma meds

Pathophysiology

Small, controlled trial of etanercept

Berry, NEJM, 2006

What Constitutes A Severe Case of

Asthma?

• Not based solely on organ impairment

• According to consensus guidelines, ≥ 1 of the following:

– Accessory muscle use

– HR > 110

– Resp rate > 25-30

– Pulsus paradoxus > 25 mmHg

– Limited ability to speak

– FEV1 < 50% predicted (or peak flow)

The Response to β-agonists

• Their presence or absence do NOT predict

outcomes

• About half of those considered to have

“life-threatening attacks” were discharged from the emergency department

• Severity may best be based upon outcomes rather than presentation

Differential Diagnosis ( Misdiagnosis: 8 – 25% of admissions)

• PE

• Pneumonia

• Glottic dysfunction

ICU Admissions

• About 20 papers over 25 years

• Criteria for admission rarely stated

• Wide range (3 to 70%) reported on need for ventilatory assistance; estimated about one-third

• 2.7% death rate

• 8.1% in those intubated

• In the USA, minorities living in large cities are disproportionately at risk of morbidity and mortality

Clinical Features

• No sign or symptom is uniformly present

• Wheezing absent 5% (a concerning

finding)

• Dyspnea absent up to 20% of the time

Impaired ventilatory response to hypoxia

associated with near-fatal cases

P0.1 airway occlusion pressure 0.1 second after the start of inspiration against an occluded airway

Impaired perception of dyspnea associated with near-fatal cases

Increased airway resistance (non-uniform)

Diminished flow Air-trapping / Hyperinflation Increased work of breathing Changes in elastic recoil

(Muscle weakness / fatigue not common)

• Mild hypoxemia due to V/Q mismatch

• Slow to resolve

• Marked hypoxemia is uncommon

• Quantitated only in small studies

• Residual volume 400% normal

• Functional residual capacity 200% normal

• Total lung capacity slightly increased

Auto-PEEP

– Increases inspiratory threshold for airflow

– Decreased radius of curvature puts

diaphragm at mechanical disadvantage

– At some point, deflation no longer passive— accessory expiratory muscles

Measure auto-PEEP with end-expiratory pause

Blood Gases

• Hypocapnia

• Mild hypoxemia

• Respiratory alkalosis

Blood Gases

• CO2 retention in about 10%

– Modest: 10-15 mmHg over normal – Indicates FEV1 < 20%

– May recover without intubation

• Normocarbia: 15 to 20% cases

– FEV1 20 to 30%

– Impending respiratory failure

Blood Gases

• Metabolic Acidosis

– Compromised cardiac output—lactic acidosis

– Increased oxygen consumption of respiratory muscles

– Aggressive sympathomimetic use

• Tremor and tachycardia usually mild

• Subcutaneous epinephrine or terbutaline of little added benefit

Additive effects of ipratropium bromide

(anticholinergic) in more severe disease with

prolonged symptoms

The effects of ipratropium are not always replicated

in other studies

Systemic Corticosteroids

• Conflicting results over whether these

result in physiologic changes in first 6 hrs

• May improve outcome (rates of

hospitalization) when used early

Cochrane Systematic Review:

Reduces Hospitalization, especially in those with more

severe disease, not already on steroids

9 Trials have compared dose of drug in

severe asthma: No evidence for an Optimal

(Or higher) Dose

National Institutes of Health (NIH)

Expert Consensus, 2002

• 120 – 180 mg/day (prednisone, methylpred,

prednisolone) in 3 or 4 divided doses for 48 hours then

60 – 80mg/day until peak flows improve

• Oral dosing probably as good as IV if no GI upset and intubation not planned

• Inhaled corticosteroids may have some added benefit

Theophylline / Methylxanthines

• No positive impact on multiple outcomes (peak flow, hospitalization) dependent of use of steroids

• May increase adverse effects: GI, tremor, arrhythmia

• May be some benefit in children

Magnesium Sulfate

• Conflicting study results

• May have bronchodilatory properties via effects on

Nebulized MgSO4 may have additive bronchodilatory

properties when given with β-agonist

Hughes, Lancet, 2003

• Mixture of oxygen and helium (minimum 60% Helium)

• Reduced density promotes more efficient gas flow characteristics

• Good for upper airway obstruction

• May increase flow rates and pulsus paradoxicus, but available trials don’t support routine use

• In theory, may

Heliox may improve delivery of aerosolized

bronchodilators

Kress, AJRCCM, 2002

2002 Expert Consensus: Not indicated in the absence of evidence for pneumonia or

sinusitis

Mechanical Ventilation

POSITIVE AIRWAY PRESSURE MAY:

• overcome inspiratory threshold imposed by auto-PEEP

• Improve gas exchange

• Enhance delivery of bronchodilators to peripheral airways

• Bi-level may be more comfortable than CPAP in the face of expiratory delay

Invasive Mechanical Ventilation

Absolute indications:

mental status changes

impending respiratory arrest

Larger diameter tube preferred to minimize resistance to airflow (≥ 8.0)

About 4% of hospital admissions

Ventilator Settings Key Concepts

• Peak airway pressures

– a function of flow characteristics

– likely to be elevated early

– can be aggravated by high inspiratory flow rates, dried

secretions in tube, dys-synchrony / biting

• Plateau pressure measured with end-inspiratory breath hold

• Threshold level (i.e < 30 to 35 cm H2O) not consistently correlated with outcomes

• Give adequate exhalation time

– Respiratory rate / minute ventilation, flow rates

Plateau pressure Peak pressure

Auto-PEEP measured here Reasonably reliable in the non-paralyzed patient

Lower inspiratory flow rates (100 L/min to 40) decrease expiratory time

causes increase in end expiratory volume (VEE)

• No consensus on ventilator mode

Permissive Hypercapnia

• A “consequence” of low tidal volume ventilation

• May have therapeutic role (inflammatory, oxidative) in research models

anti-• Slow rise in PaCO2 well tolerated

Laffey et al, Lancet 1999

• Little data to support buffering (bicarbonate or THAM) but it is probably not uncommon

• Theoretical risk of worsening CO2 with Bicarbonate

HCO3- + H+ H2CO3 H2O + CO2

(THAM is a non-bicarbonate buffer)

• Might avoid hypercapnia in brain injury and myocardial depression

One proposed algorithm

Corbridge and Corbridge

Use of Bronchodilators with Ventilator

• NO controlled trials to support recommendations

• MV patients tend to have higher dose requirements (may relate to their disease or to technical considerations)

• MDI use

– Activate close to circuit near patient

– Use a spacer

– Temporarily turn humidifier off

– Temporarily turn down flow rate to reduce turbulence