chronic pulmonary diseases
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CHRONIC PULMONARY
DISEASES
ASTHMA, EMPHYSEMA &
CHRONIC BRONCHITISMartha Richter MSN, CRNA
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OBJECTIVES
The student will:
Compare/contrast the difference between
asthma, emphysema & chronic bronchitis List 3 anesthetic strategies in caring for this
population
Identify 3 pre operative tests desired for
anesthesia screening Describe intraoperative planning for
postoperative recovery in this population
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ASTHMA-what is it?
Chronic, inflammatory disease
Reversible obstruction (to a degree)
Increased airway reactivity Most common chronic illness in children
under 17 years
Complex; involves inflammatorycells,mediators, cells&tissues residing inthe airway
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ASTHMA-early response
Immed bronchospasm on exposure
Symptoms occur in 10-20 min
Resolves in 60-90 min
Antigen binds to IgE coated mastcells,bronchospasm .
Reversible with B2 agonist inhalers
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ASTHMA-Late Response
Onset 3-5 hrs after exposure
Involves inflammation&inc. airway
reactivity
May begin cycles of exacerbation
Chronic inflammation leads to airwayremodeling, which limits reversibilitydegree
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ASTHMA TRIGGERS
Infection (esp viral)-may last for weeks
Exercise-occurs 40-90% of pts. May be
due to loss of heat&moisture in theairway.Preventable withpretreat.B2agonist inhaler
Inhaled irritants-tobacco smoke,strongodors. Via irritant receptors & Vagus
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ASTHMA TRIGGERS
Emotional factors-via vagal pathways
Drug-induced NSAIDS (also called
aspirin induced), yellow food dyes,sulfites. Commonly see in pts withnasal polyps
There is a circadian influence ofheightened airway reactivity (4am)
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WHAT HAPPENS IN AN ASTHMA
ATTACK? Bronchospasm-bronch. Mucosa edema-
mucous plug-prolonged expir-FEV1&PEFR
dec (if
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ASTHMA & CHRONIC TREATMENT
Patients are already oninhalers,nebulizers,&/or po meds for
control(B2agonists,theophylline,corticosteroids)
Emotional issues may req use of
techniques for relaxation
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STATUS ASTHMATICUS
Severe, prolonged, refractory
Most deaths outside hospital
Death probably due to arrythmia &asphyxia secondary to severe obstruction
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CARDIAC ASTHMA
Due to heart failure
Chronic, nonproduct cough-becomes
worse when supine (autotransfusioneffect)
Bronchospasm occurs b/o congestion of th
bronchial mucosa
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WHAT WILL WE DO FOR THE
ASTHMATIC? Continue use of inhalers
Consider corticosteroids is appropriate
Listen to the chest & evaluate
Hydration, PT, baseline ABGs, additionalbronchodilator?
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ASTHMA-ANESTHETIC
CONSIDERATIONS Regional where appropriate
Induct-usual drugs are safe. Avoid drugs that
are histamine releasers (MSO4, Mivacron,Cisatracurium, etc)
Lidocaine 1-2mg/kg prior to instrumentation
Ventilator-slow(6-10)&deep(10-14cc/kg)
Hydrate Extubate when deemed safe;
?albuterol?Lidocaine
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ASTHMA-what else?
Skeletal muscle paralysis will not improvebronchospasm
Remember the differential for wheezingunder anesthesia
Mech. Obstruction,lightanesthesia,endobronch
intub,aspiration,pulm edema,pulmembolus,pneumothorax,acute asthma attack.
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COPD
A group of diseases characterized bychronic & recurrent obstruction to air flow
in the pulmonary airways. Usuallyassociated with emphysema (type A) andchronic bronchitis (type B). Common
cause=smoking. Also:inhaled toxins,inherited deficiency alpha1-antitrypsin
Porth, p.539
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EMPHYSEMA-what is it?
Loss of lung elasticity, abnormal permanentenlargement of air spaces distal to term
bronchioles with distention of alveolar walls &capillary beds without obvious fibrosis
Alpha1-antitrypsin normally protects lungagainst destruction caused by inflammatory
cells-diminished in this disease
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EMPHYSEMA-types
CENTRILOBULAR
-affects bronchioles & central part of resp.
lobule, preserving alveoli. Most common; seen in male smokers
PANACINAR
-begins in peripheral alveoli, extends tocentral bronchioles.
Assoc with alpha1-antitrypsin def.
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EMPHYSEMA
Alpha1-antitrypsin deficiency
Inherited as autosomal recessive.
1% all cases; most common in children Scandinavians
People
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EMPHYSEMA-or Pink Puffers
Are able to compensate for hypoxicepisodes until late in disease
Barrel chest b/o hyperinflation
Weight loss b/o work of breathing
Pursed lipsmaintains distal airwayopening
Cough is not a feature
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EMPHYSEMA or Pink Puffers
Dyspnea may be severe FEV1/FVC decreased, inc. RV&FRC, inc CV&CC May have bullae Modest decrease SaO2 Normal PaCO2 Normal hct
Mild cor pulmonale 1 flight dyspnea Prone to respiratory infections
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EMPHYSEMA & ANESTHESIA
Encourage smoking cessation (8 weeks)
Continue inhalers
Preop CXR, ABG,PFT
?cor pulmonale/pulm hypertension
Chest infection? Consider antibiotics Listen to the chest
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EMPHYSEMA & ANESTHESIA
Normal induct drugs
May be dose sensitive (b/o nutritional
state, longstanding chronic dis,comorbidities)
Increase higher risk of
laryngo&bronchospasm Humidify & warm gases
Hydrate
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EMPHYSEMA & ANESTHESIA
Ventilator-slow & deep (allow for emptying)
Watch your PIP
Regional where indicated(keep sensory levelbelow T6; remember the poss complicationswith Interscalenes)
Emergence must include full, concise eval ofreturn from muscle relaxants, ability tomaintain Vt&sats.
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CHRONIC BRONCHITIS or Blue
Bloatersinflammation of major & small airways.
Edema & hyperplasia of submucous glands
with inc. mucous production. Chroniccough (3 mos) for at least 2 consecutiveyears in the absence of other diseases
Porth, p. 540
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CHRONIC BRONCHITIS
Simple
No obstructive component
Chronic obstructive Obstructive component
Usually middle aged male smokers who
have frequent respiratory infectionsMay have overlying emphysema
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CHRONIC BRONCHITIS-Blue
Bloaters Inc secretions lead to airway obstruction
which causes the VQ mismatch.
Hypoxemia occurs; they are not able tocompensate with increasing ventilation.Eventually they become hypoxic, cyanotic
(blue), and cor pulmonale with peripheraledema (bloaters) occurs
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CHRONIC BRONCHITIS
H&P will revealdyspnea with grad dec exercise tolerance
Rhonchi with prolonged exhalation
Clubbing
Polycythemia
Morning cough to clear secretions
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CHRONIC BRONCHITIS
What about the PFTs?
Increase in time for FVC
Dec FEV1/FVC
In advanced disease:
FVC markedly dec
Marked inc RV, inc TLC
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CHRONIC BRONCHITIS
Treatment will consist of:
Pulmonary toilet & rehab
Physical conditioning
Social support & education
Nutritional counseling (undernutrition
affects approx 25%; assoc with highmortality)
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CHRONIC BRONCHITIS
May be on home O2 (low flow). Thisindicates advanced disease.
Hypoxemia >55 mm Hg leads to pulmvasoconstriction & polycythemia
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CHRONIC BRONCHITIS &
ANESTHESIA REGIONAL
OK for extraperitoneal, sensory below T6
Careful sedation titration GA
Volatiles with humidity & warming of gases
Opioids may cause prolonged vent depression
May use N2O in absence of bullae
Vent-slow (6-10) & deep (10-15cc/kg)
To extubate or not
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DEALING WITH INCREASED
PHYSIOLOGICAL DEAD SPACE Shunt occurs when venous blood returns
to circulation without being oxygenated
Physiological shunt
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SHUNTS
Caused by
Hypoventilation
Pneumonia/atelectasis ARDS
Pulmonary edema
Acute lung injury (extensive)
Hypoxemia leads to dec. ventilation b/o V/Qmismatch
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SHUNTS
Three types:
Normal Anatomic
Intrapulmonary/alveolar Physiologic/Total
Anatomic + alveolar
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INTRAPULMONARY/ALVEOLAR
SHUNT Perfused with poor vent
Abnormal condition due to
Atelectasis Exten. Acute lung injury
Pulm edema
Consolidated pneumonia
COPD b/o secretions GETA
Airway collapse
Dependent atelectasis
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PHYSIOLOGIC/TOTAL SHUNT
Anatomic+alveolar shunt
Pulm bld not exp to alveoli/alv are
unperfused
Shunted bld is unoxygenated
Supplemental O2 does not help
Primarily inhibits art oxygenation
V/Q=0
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PHYSIOLOGIC SHUNT
Also called Pulmonary venous admixture
Sum of shunt + shuntlike states
Occurs where alveolar vent is deficientcompared to degree of perfusion
O2 therapy will improve
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ESTIMATING THE SHUNT
Perfect pt has same conc in arteries asalveoli
5% means that 5% of TGBF is not incontact with alveoli
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SHUNT SEVERITY
Normal = 15% (obvious SOB)
Severe = >30% (May need PPV)
Shunts >50% not uncommon in a verysick patient!
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ESTIMATING THE SHUNT
There are 3 components needed:
PaO2/FiO2 ratio
a/A ratioA-a gradient
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PaO2/FiO2 ratio
Easiest calc & most common est
Normal = >286
Normal lowest PaO2 = 60 mmHg Room air = .21
60 div by 0.21 = 286
Lower value = worse shunt
Levels
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A-a gradient
Alveolar to arterial
Least accurate; requires PAO2 level
Normal =
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WHY DOES THIS MATTER?
How will your knowledge of the shuntseverity for an individual patient affect
your approach to their care? Will this help you anticipate problems?
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OBSTRUCTIVE AIRWAY DISEASEIN PACU
Atelectasis & pneumonia are the mostcommon problems
The closer to the diaphragm (surgicalprocedure), the greater the incidence
Goal is to restore lung volumes (esp FRC)& facilitate cough.
Mechanical vent for FEV1/FVC50mm
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What about other ObstructiveProcesses?
A few that we may encounter include:
Cystic Fibrosis
Bronchictasis Bronchiolitis Obliterans
Tracheal Stenosis
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CYSTIC FIBROSIS
Recessive gene on chromosome 7; 1:2500newborns
Bowels & pancreas affected: blockages &malabsorption
Lungs,bowels&pancreas have abn transportof salt & H20 across the cells
Defect in exocrine gland secretion leading toproduction of chemically abnormal sweat &viscous mucous.
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CYSTIC FIBROSIS S&S
Mucous is salty & THICK Obstruction to exp flow Dyspnea, chronic cough, recurrent infect Nasal polps Bowel obstructions Hemoptysis, pneumothorax
Pancreatic insufficiency = diabetes Malabsorption syndrome: Vit K def, failure to
thrive
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CYSTIC FIBROSIS
Pulmonary toilet/PT to optimize function
Vit K
Avoid anticholinergics
Volatiles are safe
Humidify and warm the gases
Will require freq suctioning during thecase
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BRONCHIECTASIS
Localized & irreversible dilation of abronchus caused by destructive
inflamm process. Usually untreatedpneumonia.
Impaired ciliary activity & pooling of
mucous in dilated airways.
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IDENTIFYING BRONCHIECTASIS
Purulent secretions
Cough
Hemoptysis
Clubbing
Recurrent/persistent bact infections
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TREATING BRONCHIECTASIS
Antibiotics
Postural drainage/PT
Surgical resection
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TRACHEAL STENOSIS
Seen after prlonged translaryngealintubation or tracheostomy
Mucosal ischemia leads to destruction ofcartilaginous rings b/o high pressure (highcuff pressure), infection and hypotension.
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TRACHEAL STENOSIS
Tracheal lumen may be decreased to 5mm
May not develop for several weeks
Dyspnea at rest, use of accessories duringall phases of resp
Ineffective cough with stridor
Slow RR in attempt to inc Vt
You can see this when you least expect it!
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TRACHEAL STENOSIS
ANESTHESIA CONCERNS
Narrowest part of airway is now below the
trachea, of unknown diameter May require tracheotomy/translaryngeal ETT
High frequency jet vent
May require addition of helium (50-75%) toimprove flow beyond the stenotic point
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OBSTRUCTIVE AIRWAY DISEASE
The principals are the same whoever youare taking care of.
Be safe. Be thorough. Pay attention.Know your basics.
Thank you.
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