• intro
• indications for mechinal ventilation
• intubation (meds, etc.)
• strategies for ventilating
• complications
• weaning off
• Prognosis
• Non-conventional Interventions
• Post-ICU Management

• mortality rates for those requiring MV adults = up to 40%
  • children = up to 5%
  • MV usually for hours to few days
  • time on vent directly proportional to period from attack onset to MV
  • post MV prognosis (adult)
    • mortality: 1yr = 10%
    • 3yr = 14%
    • 6yr = 22%

indications

• absolute:
  • cardioresp. arrest
  • significant altered mental status
• other:
  • progressive exhaustion/ failure of maximal medical mgmt (most common)
  • ex: acidotic (<7.20 -7.25) who do not improve with aggressive tx.
  • pCO2 > 50 and rising by more than 5mmHg/hr
  • minimal chest movements
  • minimal air exchange
  • cyanosis and hypoxemia unrelievable by O2
  • PTX or pneumomediastinum
• adult studies:
  • 1/19, 4/27, 5/61 pts with hypercapnia on initial gas required intub.
  • pts with initial art. pCO2 > 50: 20% required MV
  • of those not intubated, pCO2 decreased with tx from mean 62 to 42 within 2 hrs
  • therefore give patients 2+ hrs. intensive bronchodilator trial first if possible
  • applies even to pts. with resp. acidosis

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intubation

• 100% O2 pre oxygenation
• NPO, NG to reduce risk of aspiration
• suction oral secretions
• prevent laryngospasm/bronchospasm, pretreat with:
  • atropine
  • topical anesthetic to hypopharynx/larynx
  • consider IV lidocaine
• sedative:
  • ketamine is ideal
  • benzos
  • propofol
  • avoid opiates may cause histamine release, worsen symptoms
• muscle relaxation:
  • rests fatigued resp muscles
  • eliminates ventilator-patient asynchrony
  • decreases pCO2 for any given level of minute ventilation
  • nondepolarizing - vecuronium - less cardiac SE
    • cisatracurium - more cardiac SE
  • depolarizing - succinylcholine - may cause histamine release
• maintenance:
  • benzo (ativan longer lasting) or ketamine
  • consider propofol
  • nondepolarizing muscle relaxant
• monitoring of side effects:
  • assess neuromuscular status daily by withholding muscle relaxants
  • neuromyopathy associated with intubated asthmatics receiving high dose steroids, nondepolarizing muscle relaxants (particularly vecuronium and pancuronium)

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ventilator management in general:

goals

• oxygenate and ventilate
• allow trapped air to escape -> avoid barotrauma
• rest respiratory muscles
• buy time for anti-inflammatory medications to work

strategy - oxygenate and ventilate while avoiding barotrauma

• controlled hypoventilation
• intentional hypoventilation
• controlled hypercapnia
• permissive hypercapnia

to understand strategies, must understand complications

• barotrauma: - Pneumothorax
  • pneumomediastinum, pericardium
  • retroperitoneal air
• hemodynamic: - hypotension due to intubation
  • decreased venous return, poor cardiac output
  • edema
  • arrhythmias
• mucus plugging
  • atelectasis
  • nosocomial infx
• Is hypotension due to DHI (dynamic hyperinflation) or other cause (Tuxen)?
• - slowly ventilate with 100% FiO2, 1-3 breaths/min
• - if BP increases and CVP decreases -> DHI is likely the cause

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strategies

• conventional - TV=10-12cc/kg
  • increase rate to normalize pCO2
  • increased MV => increased PIP => may lead toincreased barotrauma
    • (MV=TVxRR)
• Heiser and Downs - TV 18-24cc/kg
  • rate 1/2 that predicted for age
  • I:E = 1:2+
  • high TV can increase barotrauma
• Connors - increase inspiratory flow rate to increase gas exchange
• Pepe and Marini - minimize MV to decrease barotrauma
  • high inspiratory flow rates
• Tuxen - adjust I:E ratio (about 1:3) to decrease intrinsic PEEP, decreasing pulm. hyperinflation
  • demonstrated that pulm hyperinflation (defined by end-insp. lung vol) increased due to increased TV or decreased exp. time
  • PIP primarily related to insp. flow, did NOT reflect changes in hyperinflation
• Tuxen and Lane:
  • what correlates with barotrauma?
    • measure degree of lung hyperinflation
    • collect total amount of gas exhaled during prolonged apnea after tidal breath from ventilator. = VEI (vol at end insp)
    • VEI = TV + trapped gas exhaled during apnea
    • VEE (vol at end exp) = trapped gas exhaled after TV exhaled
    • when VEI is >20cc/kg -> barotrauma complications more likely
    • VEE and VEI are indicators of DHI (dynamic hyperinflation) which is related to barotrauma

• how do you decrease DHI?
  • increase Ve from 10l/min to 16l/min -> increased VEE, end insp. plateau pressure (Pplat) and PIP
  • increase Ve to 26l/min -> above + hypotension + increased CVP
  • for a given Ve, degree of DHI similar regardless of specific RR or specific Vt
    • absolute level of Ve was critical determinant of DHI
  • at constant Ve, decreased Vi (insp. flow) -> increases VEE, Pplat, but decreases PIP
  • gas trapping increases due to decreased Te
  • effect of diff. Vi on DHI is highly Ve-dependent
  • increase Vi from 40 to 100 l/min -> DHI decreases significantly at Ve of 16l/min, but little effect on DHI at Ve = 10l/min
  • concluded that decreasing Ve more beneficial than increasing Vi in lowering DHI, although both are helpful
  • at constant Vt, decrease RR or increase Vi to prolong Te
  • magnitude of reduction of gas trapping is related to Te lengthening, not I:E ratio (Leatherman)
  • methods to maximize Te at any given combo of Ve and Vi:
  • square wave flow - increases Te compared to decelerating wave (Ti is shorter)
  • PIP is increased but this is usually lost due to high resistance and is not clinically relevant
  • low compliance vent tubing less vol is lost expanding the tube, so you can use a smaller machine breath to generate the same effective Vt, so you can decrease your Ti
• Leatherman - measures/predictors of barotrauma risk:

• PIP - not accurate due to high airway resistance in asthma, causing large gradient between PIP and peak Palv.
• autoPEEP
  • measure of PEEP reflects P at prox airways and not necessarily at alveoli, as distal airways close on expiration in asthma, leaving air trapped in distal airways. To get accurate measurement, need communication between prox and distal airways measure of hyperinflation but does not correlate well with complications
• Pplat (plateau airway pressure) is best indicator of barotrauma risk, because it is a measure of alveolar pressure.
  • best estimate of end-insp. alveolar pressure
  • measured during 0.5 - 1 sec insp. pause
• strategy
  • keep Pplat < 30 cm H2O
  • if it increases -> decrease RR
  • if still increases -> decrease Vt
  • if acidosis < 7.15-7.20 and Pplat > 30 -> increase pH with buffer
  • PEEP - theoretically useful but no proven benefit
• Tuxen: - PEEP > 10 -> increased lung vol (deleterious)
  • PEEP < 5 -> no benefit

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weaning:

• start when airway resistance falls and PaCO2 < 45
• wean usually rapid
• IMV with PS can be used or T-tube with spontaneous breathing
• 15% require prolonged mech vent., associated with:
  • refractory airway obstruction
  • mucus plugging
  • nosocomial pneumonia
  • sepsis
  • brain injury due to hypoxic encephalopathy
  • weakness due to severe acute myopathy

acute severe myopathy:

• cause unclear
• assoc. with nondepolarizing muscle relaxants, mech. vent, steroids
• EM = selective loss of myosin filaments in many fibers
• paralysis can last hrs to days
• weakness can last weeks -> supportive care
• reversible in all cases eventually (may require rehab)

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Prognosis

Leatherman review

• prognosis post-MV (adults): - 1 yr. after intub = 10% mortality
• 3 yr. after intub = 14% mortality
• 6 yr. after intub = 22% mortality

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Non conventional interventions

• manual chest compression
• inhalational anesthetics
• bronchoscopy
• heliox
• NO
• ECMO
• CPAP/ non-invasive positive pressure ventilation

manual chest compression - studies from Australia, Great Britain

• usually intub, but can be breathing spont.
• intub pt. - give breath of 100% O2
• disconnect from vent
• at end exp. apply firm pressure laterally, toward midline, on lower chest wall for 15-20 sec's
• then another breath, continue for 10-15 min - if no benefit in 10-15 min. -> discontinue
  • (PIP, autoPEEP, etc.)
• most useful in pts with rapid deterioration in whom edema and mucus plugging are not established yet
• no complications reported

inhaled anesthetics- halothane, ether, isoflurane, enflurane

• use only in severe pts on vent.
• can be used through conventional vent circuitry
• can be beneficial even when B2 therapy failing
• mechanism unclear but may be due to:
• relaxation of sm. muscle directly
• inhibition of bronchoreactive mediators
• inhibition of vagally mediated bronchospasm
• always SE's (hypotension), but less with isoflurane
• rapid onset of action
• start at low dose
• give IV fluids
• PVC's can occur
• can see rapid changes in compliance, pCO2, PIP
• usually only required for several hours
• very few case reports in children

bronchoscopy

• to remove mucus plugs, relieve atelectasis
• acetylcystine, saline, NaHCO3, DNase all described
• problems:
  • can cause bronchospasm
  • vent will pressure-limit -> need to decrease Vi, which will then decrease Te
  • scope may also directly limit exp. flow by occlusion
  • therefore, must be willing to accept lower pH during procedure
  • RARELY indicated

heliox

• helium is less dense than O2 and N2 -> lessens frictional resistance when gas flow is turbulent
• lose effect when FiO2 > 40% (helium < 60%) -> seldom useful in asthma

NO

• no proven benefit
• may worsen V:Q mismatch by vasodilation
• Pfeffer (U of UT) showed no benefit in children (measured spiro), but spirometry was performed immediately after, and 10 min after NO inhalation for 15 min. Was not measured during inhalation

ECMO - described in adults, rarely required

CPAP/non-invasive ventilation

• may be an option, more studies being done
• used to decrease WOB in pts not improving but not ready for intub
• may decrease insp. and exp WOB -> decreases muscle fatigue -> decrease need for MV
• studies:
  • Shivaran - decreased dyspnea and RR with CPAP 5-7.5 cmH20
  • Meduri - CPAP with PS via full face mask -> improvement in pCO2 and RR in 2 pts. (used NG to deflate stomach)
• complications:
  • severely dyspneic pts report claustrophobia
  • increased incidence of aspiration
  • do not use in pts with encephalopathy and difficulty with secretion mgmt.

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Outpatient management

• PICU to floor to home
• goals:
  • treatment
  • education
  • follow-up

treatment

• antiinflamm
  • depends on age, severity, triggers, home environment, etc
  • intal, inhaled steroids (MDI vs. nebulized), systemic
• viral (RSV, Adeno, etc.) can cause lung damage that can take 6 weeks to repair
  • need extra protection during that time, especially if still during viral season
• bronchodilator - goal is for prn only, except to prevent Exercised Induced Bronchospasm and occas nocturnal cough
  • can be weaned in hospital as tolerated
  • switch to MDI in hospital
• treat exacerbating factors (GER, sinusitis, allergies, etc.)

education - pts and families must be taught:

• signs/symptoms of asthma and how to detect them
• Peak Flows
• detection, control, elimination of triggers
• what to do if an attack occurs
• recognize importance of maint. med. use
• recognize increasing bronchodilator use

follow-up regularly with spirometry in many cases

over 125 therapies for asthma currently under investigation, including CSA, Ginseng, Baclofen, Menthol, eucalyptus oil, etc.

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This page last updated 1/14/99 at 1135