Status Asthmaticus

Dr Divya Jain
Definations
Asthma is a lung disease that is characterized by
inflammation, obstruction, and hyper responsiveness of
the airways
Status Asthmaticus
 Severe bronchospasm that does not respond to
aggressive therapies within 30-60 minutes
 Severe asthmatic attack with one or more of the

following:
◦ Dyspnea (precluding speech), accessory muscle use, RR
35/min
◦ Hr > 140/min
◦ Peak expiratory flow < 100 l/min
◦ Hypercapnea ( >= 50 mmHg)
Acute Severe Asthma
Critical limitation of expiratory flow

 Increased airway resistance

 Premature airway closure
 Lung and chest wall dynamic hyperinflation
 High intrinsic PEEP
 Respiratory muscle fatigue
Near-Fatal Asthma
 Respiratory arrest or respiratory failure (PCO2 > 50
mmHg)
Fatal Asthma
 Slow-onset
◦ Gradual deterioration of asthma symptoms over several days
◦ Usually associated with chronic poorly controlled asthma
◦ Eosinophilic predominance and mucus in submucosa

 Rapid-onset
◦ Symptom onset and progression to life-threatening status
within 3 hours
◦ “Greater” hypercapnea
◦ Neutrophilic predominance in airway submucosa
 Path physiology

Infla mma ti on Bro n ch o co n strictio n

submucosal edema,
plasma exudation, mucous plugging. Poor response to bronchodilators
Good re sponse t o bronchodi la tors
The Four Compartments
o
o
 Resistance to airflow strongly increased
 Driving force for expiratory flow is decreased
 Persistent activation of inspiratory muscles during
expiration
 Markedly prolonged expiration-Inspiration starts before

static equilibrium is reached-leads to Auto PEEP

Bronchial obstruction creates
 areas with low V/Q ratios-hypoxia
 alveolar distension causes high V/Q zones and

increased deadspace -hypercarbia.

 Increased oxygen consumption of respiratory muscles-

frank respiratory failure.

 Alveolar distension and hypoxic pulmonary

vasoconstriction- increase pulmonary artery pressures -

impair RV function.
 Intraventricular septal shift to the left may impair LV

function.
Dynamic Hyperinflation
 Incomplete alveolar emptying at
the end of expiration
◦ Intrinsic PEEP

 Increased ventilatory requirement

 Prolonged expiratory time
 Increased inspiratory threshold load
Dynamic Hyperinflation
 Mean pleural pressure becomes more negative
◦ Interstitial pressures are also lowered
◦ Vascular pressure is maintained
 The result:
◦ Interstitial edema and further increase in airway resistance
Risk factors for developing severe asthma
 previous severe attacks (i.e. previous intubation or
respiratory acidosis without intubation)
 multiple or recent hospital admissions
 recent steroid use
 deterioration while on steroids.
Clinical Features

 heart rate > 130

 paradoxical thoracoabdominal motion
 silent chest
 confusion, lethargy, fatigue
 can't speak
 bradycardia
Physical examination
 hyperinflation
 use of accessory muscles
 widespread wheezes
 tachycardia
 hypertension and pulsus paradoxus
 Decreased level of consciousness
 the inability to speak
 a silent chest
 hypoventilation
 bradycardia
 unremitting hypoxemia
Differential diagnosis

 pulmonary edema
 aspiration
 pneumothorax
 anaphylactic / anaphylactoid reactions,
 mechanical airway obstruction or compression
 congenital causes i.e. vascular ring
 pulmonary embolism
 In the intubated patient- misplaced or obstructed ETT,

and surgical compression.

Monitoring
 A CXR- an uncertain diagnosis, barotrauma or
pneumonia, and severe disease
 An ECG -may show signs of right heart strain,

myocardial ischemia, or dysrhythmias.

 ABG's-Normal or increased CO2 implies severe

disease
Lactic acidosis
Monitoring lung function
FEV1 /PEF.
low PEF values cannot distinguish between poor effort, restrictive
ventilatory disorders (e.g.,neuromuscular weakness, pneumonia)

Life-threatening asthma exacerbation- FEV1/ PEF not indicated

Any FEV1 or PEF value <25 percent of predicted that improves by <10
percent after treatment - indications for ICU admission.

Pulse oximetry-
severe distress
have FEV1 /PEF <40 percent of predicted
unable to perform lung function measures.
Classification of Severe Asthma
Principal goals and Expert Panel
recommendations
 Correction of significant hypoxemia
 Rapid reversal of airflow obstruction
 Reduction of the likelihood of relapse of the

exacerbation or future recurrence of severe airflow

obstruction by intensifying therapy
Recommended Drugs
• Short acting selective beta 2 agonists
• Inhaled ipratropium bromide

• Systemic corticosteroids
ADJUVANTS :
intravenous magnesium
Heliox
Controvertial-
intravenous beta 2 agonists
Intravenous leukotriene antagonists
Non invasive ventilation
Not recommended

 Methylxanthines are not recommended

 Aggressive hydration is not recommended for older

children and adults

 Chest physical therapy is not generally recommended
 Mucolytics are not recommended
Inhaled Short-Acting Beta2-Agonists (SABA)

Salbutamol
 Nebulizer solution (0.63 mg/3 mL,1.25 mg/3 mL,2.5

mg/3 mL,5.0 mg/mL)-

2.5–5 mg every 20 minutes for 3 doses,
then 2.5–10 mg every 1–4 hours as needed,
or 10–15 mg/hour continuously
MDI
(90 mcg/puff)
4–8 puffs every 20 minutes up to 4 hours, then every
1–4 hours as needed
Levalbuterol(R-albuterol)
Nebulizer solution
1.25–2.5 mg every 20 minutes for 3 doses, then 1.25–5
mg every 1–4 hours as needed.
MDI
(50mcg/puff)
4–8 puffs every 20 minutes up to 4 hours, then every
1–4 hours as needed
Action of beta 2 agonists-
relax bronchial smooth muscle
inhibit the release of mast cell mediators.

About beta 2 agonists-

Which is the better means
-inhalational or parentral
- MDI or Nebulization
Systemic (Injected) Beta2-Agonists
Parentral beta 2 agonists
Parenteral therapy may be given SC OR IV

Epinephrine- intravenous
S/C- .3-.5 mg
via ETT- 5ml of 1:10,000
Salbutamol- iv-4mg/kg load-infusion .1-.2mg/kg/hr
Terbutaline (1 mg/mL)
0.25 mg every 20 minutes for 3 doses.
Ipratroprium
 Anticholinergic, muscarinic – M1, receptors mediate
bronchoconstriction
 Dosing: 0.25 – 0.5 mg nebulized x 24 hours after

admission
 MDI (4-8 puffs every 15 min.)
 Advantages: has no systemic anticholinergic action
 Other: unilateral pupillary dilation can occur
Corticosteroids
Mechanism of action:
 effective in preventing the sustained inflammatory

phase which occurs 6-8 hours after allergen exposure

 Dosing: Methyl-prednisone: Loading dose: 2 mg/kg IV

& Maintenance dose: 0.5mg/kg IV q 6hr
 Other: Steroids should be administered IV to assure

adequate drug delivery in a timely manner.

Magnesium Sulfate
 Mechanism of action: smooth muscle relaxant
 Dosing: 50 mg/kg IV over 20 min with max of 2 gm
 Advantages: has been shown to be effective in “severe”

(FEV1<25% predicted) asthma

 Side effects: hypotension, respiratory depression & muscle

weakness can be treated with IV Calcium Gluconate

 Other: respiratory depression & muscle weakness are

noted only at levels >12mg/dL. Normal Mg levels are

1.5-2mg/dL and minimal increase in level is noted with a
single dose.
Terbutaline
 Mechanism of action: IV β2 agonist
 Dosing: Loading dose: 5 - 10mcg/kg IV over 10 min &

Continuous infusion: 0.4 - 4 mcg/kg/min IV

 Advantages: effectively reaches areas of lung by IV

infusion that salbutamol does not due to airway

obstruction
 Disadvantages / side effects: tachycardia,

hyperglycemia, hypokalemia, cardiac ischemia

Aminophylline
 Mechanism of action: phosphodiesterase inhibitor which
allows for smooth muscle relaxation and augments
mucociliary clearance
 Dosing: Loading dose: 6 mg/kg over 20 min IV &
Continuous infusion: 0.6 - 1 mg/kg/min IV
 Advantages: may prove very effective in patients resistant
to above treatments given the different MOA
 Disadvantages / side effects: N/V, agitation, arrhythmias,
seizures
 Other: A theophylline level q8hr after drug initiation and
then every morning. Therapeutic levels are 10 – 20 mcg/ml.
Heliox
 MOA: low-density gas that increases laminar flow and
decreases turbulent flow.
 Dosing: 60%/40% or 80%/20% helium/O2
 Advantages: has no systemic side effects
 Other: Data suggests prevents intubation. In intubated

patients, heliox has been shown to decrease the PIP

requirements.
Non invasive ventilation in asthma
Concerns
◦ Worsen hyperinflation and air trapping,
◦ Increase intrathoracic pressure
◦ Decrease venous return and contribute to
barotrauma
NIPPV
 Causes bronchodilation and decreases airway
resistance
 Reexpands atelectasis and promotes removal of
secretions
 Rests the diaphragm and inspiratory muscles and may
offset PEEPi
 Decreases the adverse effects of large negative peak
and mean inspiratory pleural pressures
NIPPV
 Respiratory muscles rapidly unloaded
 Dyspnea improved
 RR improved
 Gas exchange improved with low inspiratory pressure
 12% of patients with NIPPV were intubated
When to intubate
 Progressive exhaustion
 respiratory arrest
 decreased level of consciousness,
 persistent respiratory acidosis (pH<7.2)
 unremitting hypoxemia
 Intubation -a marked stimulus for bronchospasm.
 When positive pressure is initiated -the markedly

negative pleural pressures-becomes positive- venous

return drops-hypotension may occur.
 Large bore IV's and vasopressors should be available.
 Avoid agents that may release histamine.
 A large ETT is preferred to facilitate suctioning and

possible bronchoscopy
Mechanical Ventilation
 Minimize high airway pressures and barotrauma
 Minute ventilation < 10 L/min
 Permissive hypercapnea
 Low tidal volumes (6-10 cc/kg)
 Low ventilation rates ( <= 10 /min)
 Plateau pressures < 30 cm water
 Inspiratory flow rate 60-80 l/min
 No PEEP

Oddo, Intensive Care Med 2006;32:501-10

Role Of PEEP
 Theoratically - PEEP will splint open airways during
exhalation.
 If the applied external PEEP < auto-PEEP-obstructed

units could empty due to decreased dynamic airway

compression- risk is increased DHI.
 No role in the sedated, paralyzed, mechanically

ventilated patient.
 May be an advantage to using moderate levels of

PEEP in spontaneously breathing patients as it

decreases WOB.
General Anesthesia
 Considered with:
◦ Elevated airway pressures
◦ Persistent hypoxemia
◦ Continued bronchospasm
Thiopental: Large doses may block bronchospasm
induced by an irritating ETT but increase the risk of
hypotension.
 Avoided in a patient with severe status

Ketamine:bronchodilation due to its sympathomimetic

effects
Lidocaine: Intravenous lidocaine reduces irritant
induced bronchospasm.
IV infusions of 1-4 mg/min
Propofol: Propofol's effect on airway tone and
reactivity are not clear
good choice for sedation of the ventilated asthmatic
patient.
Benzodiazepines: used for intubation and sedation and
appear to be safe
Neuromuscular Blocking Agents
 NMBs that cause histamine release (atracurium), or
that block M2 muscarinic receptors be avoided in the
treatment of the acute asthmatic.
 profound muscle weakness -NMBs and corticosteroids
 monitor CPKs
 minimize the dose and duration of NMBs
Extracorporeal Life Support
 Despite institution of hypoventilation and while
tolerating increased peak inspiratory pressure
◦ pH < 7.2
◦ PCO2 > 100
◦ Life threatening conditions due to hypoxemia, hypotension or
barotrauma
Extracorporeal Life Support
 Since 1988- venovenous access and perfusion
◦ Percutaneous cannulation of:
 Right atrium via the jugular vein ( 16F)
 IVC via femoral vein ( 22F Heartport long venous catheter)
 Connected to the ECLS circuit
 Femoral-atrial flow at 3.5 L/Min
 Passive support of gas exchange and perfusion
 Low pressure, low oxygen ventilator settings