Transcript Document

Definition of asthma: reversible
airway obstruction caused by airway
inflammation, increased mucus
production, and bronchial smooth
muscle contraction to a variety of
stimuli.
Epidemiology
•prevalence 5-12%
•runs in families, atopy associated with chromosomes 5 and 11
•1-2% of patients with severe asthma die
•mortality increasing since around 1980
•reasons for increased mortality rate:
•improper assessment of severity of illness by pt. and physician
•inadequate hospital treatment
•inadequate access to health care (esp. inner city where mortality
is highest)
•increased exposure to indoor allergens (possibly due to better
insulated homes)
•use of more potent bronchodilators may enable longer exposure
to triggers and prolonged inflammation
•asthma deaths in 51 patients under age 20 years Robertson
•33% had "trivial or mild" asthma
•32% had no previous hospitalizations
•63% had sudden collapse within minutes of developing
dyspnea
•78% died before reaching hospital
•final attack was <2hrs for 50% of those dying
•other studies have found that a minority of patients
have rapid onset of severe asthma with death within 1-3
hours (15-29% of asthma deaths)
•characteristics of those dying from asthma:
•severe disease - hx intubation, hypoxic SZ's, rapid
progression of attacks
•attacks precipitated by foods
•lack of perception of severity of attacks
•self weaning of meds, especially corticosteroids
•lack of parental and/or medical support systems
•psychologic disease, depression
•decreased dyspneic sensation, decreased hypoxic
response, +/- Ø hypercapneic response (Kikuchi,
unpublished)
•African-American, urban boys < 15 yrs have 50% higher
mortality rate than females of same age
•death from:
•hypoxic cardiac arrest
•pneumothorax
Pathophysiology
•components:
•airway inflammation with wall thickening and increased
vascular permeability
•mucus hypersecretion
•bronchial smooth muscle contraction
•stimulus causes cascade of inflammatory cell migration and
activation, with numerous cytokines and other mediators
involved.
•major players:
•mast cells
•eosinophils
•T cells
•airway mechanics:
•airway obstruction
•narrowing of bronchioles
•upstream obstruction causes premature closure of
airways with expiration as pleural pressure becomes
greater than pressure inside airway (equal pressure
point, EPP), causing downstream airways to become
compressed with expiration, causing air trapping.
•complete obstruction from mucus plugs or edematous
airways causes atelectasis.
•atelectasis (micro to segmental to lobar) causes V:Q
mismatch which causes desaturation.
•air trapping
•reduced respiratory muscle efficiency and function
due to:
•lung hyperinflation, thoracic hyperexpansion results in:
•altered resp. muscle mechanical advantage
•flattened diaphragm = shortened muscle fibers
•pneumothorax, pneumomediastinum, subQ emphysema
•increased intrathoracic pressure which causes decreased
venous return, causing both decreased R and L
ventricular preload, causing hypotension
•this can lead to tissue hypoperfusion and hypoxia
•hypoxia leads to increased RR which decreases
dynamic compliance of the lungs.
•[C = DV/DP] where C=compliance, DV=change in
volume, DP=change in pressure
•normally, major impedance to DV is elastic recoil of
lungs
•at high RRs, major impedance to DV is flow resistance,
which is high in the condition of narrowed airways,
therefore making dynamic compliance lower.
•lower compliance means stiffer lung
Hospital presentation
•history of acute onset of symptoms, often with known
stimulus, or
•indolent course with increased use of bronchodilators over
days to weeks
•Signs:
•cough, wheeze, SOB, fatigue, HA, fever, URI c/o's
•Symptoms:
•tachypneic, hypoxic, uncomfortable, difficulty speaking
long phrases, wheezes, crackles, decreased air entry,
increased exp phase, retractions, flaring, unable to lay
recumbent
•Labs:
•blood gas - NL to high pH, low to NL pCO2, low pO2
•metabolic acidosis possible due to hypoxemia or IV Bagonists
•WBC - demarginated PMNs due to stress, steroids
•electrolytes - hypokalemia due to B-agonists (drives K+
intracellularly)
•bicarb low due to met. acidosis
•CXR:
•hyperinflated - flat diaphragms, large AP diameter, lucent,
PTX/mediastinum
•peribronchial cuffing
•atelectasis - volume loss
Indicators of severity on initial
presentation
•Position and Diaphoresis Brenner et al
•a continuum of signs and
symptoms
sitting and diaphoretic
recumbent
sitting
increased heart rate
increased respiratory rate
increased pulsus paradoxus
=>
=>
decreased arterial pH
decreased pO2
increased pCO2
least severe
=>
most severe
•if able to lay recumbent, these pts not acidotic,
normal pulsus, did not need ABG
•may need O2 though
•all diaphoretic patients were upright
•continuum between recumbent, sitting, sitting and
sweating
•sweating due to increased WOB, sympathetic
stim
•upright position allows increased use of accessory
inspiratory muscles and max. diaphragmatic
excursion
•may allow for maximized use of abd. muscles
for expiration
•Initial Oxygen Saturation on presentation- Geelhoed (Australia
1994)
•SaO2 in ED as predictor of outcome
•SaO2 < 91% -> poorer outcome (sens 100%, spec 84%)
•Not a cutoff though - number of poor outcomes increased
gradually with decreasing SaO2
•good outcome = sent home without cont. problems
•poor outcome = admitted or sent home but had to return
•worst outcome = IV steroids and aminophylline
Inpatient therapy
Non pharmacologic:
•O2 - most patients are hypoxemic (PaO2:FiO2 <400) due
to V:Q mismatch
•mismatch due to:
•atelectasis
•B-agonist vasodilation (B2, aminophylline.)
•always use humidified oxygen
•IVF - most pts with severe asthma are dehydrated due to:
•increased metabolism
•increased insensible losses
•decreased intake
•vomiting
•dehydration can: increase viscosity of secretions, thereby
increasing bronchiolar plugging and atelectasis.
•worsen already poor cardiac output due to decreased preload,
esp. with PPV
•overhydration can: cause pulm edema due to accumulation
around bronchioles due to increased neg. intrapleural pressure
and increased ADH secretion
•Therefore:
•correct dehydration, then provide maintenance, remembering
that insensible losses will be high. Monitor and react.
•NPO due to risk of aspiration
Pharmacologic Therapy
Medications
•bronchodilators
•inhaled B-agonists
•subQ anticholinergics
•IV methylxanthines
•anti-inflamm
•inhaled
•PO
•IV
Bronchodilators:
•Beta-agonists - drug of choice, best bronchodilator
•non selective - efficacious but many side effects (epinephrine,
ephedrine, isoproterenol)
•risks: tachyarrhythmias, myocardial ischemia, death
•selective B2 - fewer side effects (isoetharine, metaproterenol,
terbutaline, albuterol (salbutamol), fenoterol, bitolterol,
pirbuterol, salmeterol)
•route: inhaled -intermittent vs. continuous
•usually albuterol (salbutamol)
•fewest side effects
•some studies show it to be more effective than SQ epi
•studies split on inhaled vs. IV effectiveness
•if little effect with inhaled, IV also will likely have little effect
•Metered Dose Inhaler vs. nebulization: - little difference if
spacer and good technique
•if unable to breathe deeply (i.e. poor technique), neb
more effective
•switch to MDI in hospital during resolution (effective
and less cost) continuous neb
•if B-agonist needed q30 min or more, continuous neb
shown to be more effective
•0.1 to 0.3 mg/kg/hr to max 10-15mg/hr
•10-15 mg/hr - fewer side effects than IV
•> this range = same side effects as systemic
•use > 6 l/min O2 to correct hypoxemia
•IV - continuous infusion (terbutaline, isoproterenol, albuterol)
•good drug delivery
•use when no improvement with inhaled bronchodilators
•dosing (terbutaline) - bolus 10mcg/kg over 30 min, infuse
with 0.1mcg/kg/min
•increase by 0.1mcg/kg/min q30min to effect
•max. 4mcg/kg/min or side effects
•rebolus with each increase
•decrease starting dose by half if theophylline also used
•side effects: dysrhythmias rhabdomyolysis
•HTN lactic acidosis
•myocardial ischemia hypophosphatemia
•hyperglycemia
•- need close monitoring: CR, oximeter
•frequent ABG's, lytes, glucose
•consider arterial line (ABG's, BP)
•SQ - systemic, if no other route available/acceptable
•epinephrine, terbutaline
Anticholinergics
•atropine, ipratropium bromide (Atrovent), glycopyrrolate
(Robinul) - inhaled
•bronchodilate but not as effective as B-agonists
•additive effect to B-agonists
•side effects: tachycardia, dry/thick secretions
•effectiveness: B agonist and anticholinergic > B-agonist alone
>> anticholinergic alone
•dosing - Atrovent - 250mcg (1cc) neb q3-6 hr
•Robinal - 1mg neb q3-6 hr
•atropine - 0.01 - 0.03 cc/kg q3-4 hr
Aminophylline - drip
•bronchodilates by:
•phosphodiesterase inhibition
•intracellular calcium modulation
•prostaglandin antagonism
•more recent studies have shown that it does not add significant
bronchodilatory effect to patient on aggressive B-agonist therapy for
acute exacerbation (DiGiulio - J. Peds 1993, others) - did not look at
ICU patients though
•may be useful by:
•increasing diaphragm contractility
•increase mucociliary clearance
•+/- anti-inflammatory properties
•so it may be of some added benefit in patients with poor response to
B-agonist
•dosing?
Anti-inflammatory - corticosteroids
•the most important drug in treating asthma
•inhaled vs. PO vs. IV
•some new literature suggests inhaled therapy
may be effective acutely
•if patient can take PO steroid without
emesis/diarrhea, etc. , it may be as effective as IV
(still debated)
•high dose vs. low dose still debated
•I start with 1-2mg/kg/dose q6hrs of solumedrol
(methyprednisolone) , then back off depending on
clinical course (any benefit in > 40mg q6hrs is
questionable)
•similar dose PO but usually bid-tid
•actions:
•decreases recruitment and activation of inflammatory cells
•up-regulates B2 receptors
•decreases microvascular permeability
•decreases mucus production
•side effects (short burst)
•hyperglycemia
•hypertension
•depression, psychosis
•hyperactivity
•increased appetite
•fluid retention
•myopathy (+ mech vent + paralytics)
antibiotics - no role for routine use
•indications: - sputum/trach aspirate predominantly PMNs
•evidence of sinus infx.
•evidence of pneumonia (lobar, no vol loss, effusion)
•suspicion of Mycoplasma or Chlamydia
Characteristics of life-threatening asthma:
Indications to transfer to PICU:
•disturbed consciousness
•exhaustion
•recumbent position accompanied by diaphoresis
•markedly decreased air entry
•interrupted speech
•rising, near normal, elevated pCO2
•air leak syndromes
•severe hyperexpansion
•previous hx resp failure
•drug toxicity
•failure to improve with standard aggressive tx
•cardiac/resp arrest
•metabolic acidosis
•worsening PFT's despite tx
•inadequate staffing on general ward
Indicators of impending respiratory
failure:
•Level of Consciousness (LOC)
disturbance
•inability to speak
•markedly decreased or absent breath
sounds
•central cyanosis
•marked sternocleidomastoid retractions
•pulsus paradoxicus > 10mm Hg
Less reliable indicators of impending respiratory failure
•wheezing
•dyspnea - slight increase airflow may make large decrease in
dyspneic sensation, esp. if obstruction long term
•may be rate of change of obstruction that effects dyspnea, not
absolute amount
•leads to false sense of tx efficacy
•McFadden study - patients reported TOTAL resolution of
symptoms even when:
•their FEV1 rose only from 30 to 49% of pred.
•or their Peak Flows rose only from 20 to 43% of pred
•helpful to measure PFT's
•caution: reported cardiopulmonary arrest in pts performing
forced exp. maneuvers while in acute severe asthma attack
•ABG helpful only in severe obstruction:
•McFadden - hypercapnia not seen in pts with PF>25% or
FEV1>20%
•mild to mod airflow obstruction:
•usually hypocapneic with resp alkalosis
•Normal PaCO2 indicates deterioration
•hypercapnia indicates life-threatening obstruction
•does not always mean intubation
•metabolic acidosis indicates severe obstruction, whether in
combo with resp alkalosis or acidosis
•may be due to overburdened resp muscles, hypoxemia
(presumed lactic acidosis)
•may be due to high doses IV B-agonists (even without
hypoxemia)
•CXR - limited usefulness in asthma
•obtain if clinical exam suggests barotrauma or pneumonia or if
dx of asthma not clear
Further ICU therapies - after IV bronchodilators, continuous nebs,
anticholinergics, steroids, O2
•Base therapy (NaHCO3, THAM (tromethamine), Carbicarb) - to
decrease acidosis
•acidosis
•increased lactic acid production by resp. muscles
•decreased utilization of lactate by underperfused liver and
skeletal muscle
•B-agonist (IV) direct effect on muscle tissue produces lactic
acidosis even in absence of hypoxemia, mech. unknown
(Raimondi, unpubl, Buenos Aires)
•acidosis causes: - myocardial depression
•decreased effectiveness of B-agonists
•stimulates ineffective rapid/shallow breathing
•bicarb therapy - correct metabolic acidosis
•may increase B-agonist effectiveness
•may decrease dyspnea
•be cardiac protective
•may decrease CSF pH initially
•may lower potassium
•as obstruction improves -> resp and metabolic alkalosis may
develop
•indications - persistent/worsening metabolic acidosis
•dyspneic sensation with improved air entry, +acidosis
•concerns of cardiac dysfunction
•intubated patient in whom permissive hypercapnia used
•unclear
•dosing - partially correct (keep pH > 7.20) in most cases, not to
normal (permissive hypercapnea)
•ex. 1 meq/kg or partially correct deficit, no specific
guidelines
•Magnesium SO4 - bronchodilator - mech. unclear but may be due
to:
•inhibition of Ca++-mediated smooth muscle contraction
•direct inhibition of smooth muscle contraction
•adult studies with mixed results, no controlled studies in children
•given IV, onset minutes, duration about 2 hrs
•side effects - facial flushing/warmth, malaise
•hypotension/bradycardia only with rapid infusion
•dosing - 30-70 mg/kg IV over 20-30 min. (max=2g)
•bronchodilation proportional to serum levels
•Sedatives - dyspnea-> anxiety -> worsening
bronchoconstriction -> ineffective ventilation ->
interference with aerosol med. use
•can depress resp. effort/drive
•use only in PICU setting
•can use any, but may as well use those with
bronchodilating effect
•droperidol - alpha-adrenergic antagonist, therefore may
bronchodilate
•may cause hypotension, be ready with fluid
•dose = 0.2 mg/kg IV
•ketamine - relaxes smooth muscle directly, also increases
chest wall compliance
•sympathomimetic properties
•has been used in unintubated asthmatics to avoid intubation
successfully
•side effects: arrhythmias
•increased secretions
•laryngospasm
•use benzodiazepines to decrease emergence reactions