Chronic Pulmonary Diseases

7/31/2019 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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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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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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Chronic Pulmonary Diseases

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