2. Respiratory Diseases
Obstructive Vs Restrictive
⢠Obstructive:
ďConditions that make it hard to exhale all the air in the lungs
⢠Restrictive:
ďPts will have difficulty fully expanding lungs with air.
ďShortness of breath during exertion is the common
symptom.
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3. Obstructive Lung Diseases
⢠Shortness of breath due to difficulty of exhaling air.
⢠Damage to lungs or narrowing of lung airways ď exhaled air
comes out more slowly than normal.
⢠Hard to breathe, especially during increased activity or exertion.
⢠At the end of a full exhalation, an abnormally high amount of air
may still remain in the lungs.
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4. OLDâŚ
⢠The most common causes of OLD are:
ďAsthma
ďCOPD (emphysema and chronic bronchitis)
ďBronchiectasis
ďCystic fibrosis
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5. Restrictive lung diseases
⢠Pts cannot fully fill their lungs with air
⢠Most often results from a condition causing stiffness:
ďźIn the lungs themselves
ďźThe chest wall,
ďźWeak muscles, or
ďźDamaged nerves
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6. RLDâŚ
⢠Common conditions classified under RLD:
ďInterstitial lung disease
ďSarcoidosis
ďObesity
ďNM disease, such as amyotrophic lateral sclerosis (ALS)
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7. Diagnosis of Respiratory Diseases
⢠Both OLD & RLD can cause shortness of breath, severe
coughing & chest pain.
⢠Almost all lung diseases are tested by using a pulmonary
function test (spirometry).
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8. Clinical Spirometry
⢠Vital Capacity
ďLargest volume measured after an individual inspires
deeply & maximally to TLC & then exhales completely to
residual volume (RV) into a spirometer.
ďSuspected of being abnormal if it < 80% of predicted value.
ďThe decreased VC is associated with restrictive disease.
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9. Clinical spirometryâŚ
⢠Time-Expired Spirogram
ďAfter a maximum inspiratory effort, a subject exhales as forcefully
and rapidly as possible, and the volume of gas is called FVC.
ďExhaled volume is recorded with respect to time.
ďRate of airflow indirectly reflects flow resistance properties of
AW.
ďWhen AW obstruction occurs, FVC tends to be < standard VC.
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10. Clinical spirometryâŚ
⢠The FVC is reduced by the same conditions that reduce VC.
⢠To identify AW obstruction, flow rates are determined by
calculation of volume exhaled during certain time intervals.
⢠Most commonly measured is volume exhaled in the first
second, called (FEV1).
⢠FEV 25%-75% --MMEF??
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11. Clinical spirometryâŚ
⢠FEV1 provides an even better perspective on degree of AWO
when it is expressed as a %age of FVC (FEV1/FVC).
⢠Normal, healthy subjects can exhale 75%-80% of FVC in the
first second.
⢠Obstructive airway diseases reduce expiratory flow rates and
therefore reduce FEV1 & FEV1/FVC.
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15. AsthmaâŚ
⢠Chronic lung disease characterized by inflammation &
narrowing of the airways ď reversible airflow obstruction
due to constriction of smooth muscle .
⢠An episodic disease with acute exacerbations interspersed with
symptom-free periods.
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16. AsthmaâŚ
⢠Most attacks are short-lived (for minutes-hrs) & clinically the
patient seems to recover completely after an attack.
⢠Status asthmaticus: is defined as life-threatening
bronchospasm that persists despite treatment.
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17. AsthmaâŚ
⢠Bronchial wall inflammation- fundamental
component of asthma, and results in:
ďMucus hyper-secretion
ďEpithelial damage, as well as
ďAn increased tendency for airways to constrict.
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24. Anesthesia for Asthmatic Patients
⢠Most well-controlled asthmatics tolerate anaesthesia & surgery.
⢠The frequency of complications is increased in patients with:
ďUnstable disease,
ďThose undergoing major surgery and
ďOver 50 years
5/18/2023 24
25. Anesthesia for Asthmatic PtsâŚ
⢠Poorly controlled asthmatics (current symptoms, frequent
exacerbations or hospital admissions)ď perioperative risk.
⢠Elective surgery should take place when the patientâs asthma is
optimally controlled.
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26. Preoperative evaluation
⢠Timing & goals: assess at least one week before.
ďź High risk of PO pul. complications procedures.
⢠Goal: optimization ď reduce perioperative pul. complications.
ďWell-controlled vs poorly controlled asthma
ďShould not be wheezing at the time of surgery.
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29. Important History
⢠Severity of asthma
⢠Allergies & atopy
⢠Asthma medication use
⢠Triggering factors
⢠Frequency of use of short-
acting beta2 agonist.
⢠Hx of hospitalizations &/or ED visits
⢠Hx of intubation with severe attack
⢠Frequency & most recent use of oral
glucocorticoids
⢠Recent URI, sinus infection, cough /
fever
⢠Baseline& current PEF or (FEV1)
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30. P/E & Ix
⢠P/E: RR, wheezing, signs of lung infection & air movement.
ďAcute severe bronchospasm ď diminished/ absent breath sounds.
⢠Preoperative testing: well controlled asthma (not steroid-
dependent).
ďBaseline pulse oximetry value should be noted.
ďPFT- For moderate to severe asthma âŚhigh-risk procedures
ďUse of asthma medications impacts lab. testing.
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31. Laboratory Testing
⢠Blood tests: similar to those for pts. without asthma.
⢠High-dose beta2- agonists ď hypokalemia, hyperglycemia &
hypomagnesaemia âŚpreoperative test.
⢠Oral or high-dose inhaled glucocorticoids ď HPA
suppression & adrenal insufficiency.
5/18/2023 31
32. Preoperative AssessmentâŚ
⢠Exercise tolerance
⢠Any allergies or drug sensitivities, especially effect of
aspirin or other NSAIDs on asthma.
⢠Prevalence of aspirin (or other NSAID) induced asthma
is 21% in adult asthmatics, and 5% in paediatric
asthmatics.
5/18/2023 32
33. Preoperative AssessmentâŚ
⢠Examination is often normal in a well controlled patient, but may
reveal chest hyperinflation, prolonged exp. phase & wheeze.
⢠Patients with mild asthma rarely require extra treatment.
⢠For symptomatic asthma, consider additional medication or
treatment with systemic steroids.
⢠Viral infections are potent triggers of asthma, so postpone elective
surgery if symptoms suggest URTI.
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34. Maintenance Medications
⢠Continue usual medication up to & including the day of
surgery except of theophylline.
⢠Supplemental steroids: poorly controlled with high-risk
surgery.
⢠Usually prednisone (40 mg once daily) for five days.
⢠IV hydrocortisone (100 mg QID), an alternative.
5/18/2023 34
35. Perioperative medications used to treat Asthma
Class of drug Examples Perioperative
recommendation
Notes
Beta 2 agonists Salbutamol,terbutaline,
salmeterol
Convert to nebulized preparation High doses may lower K+
Vagolytic drug Ipratropium Convert to nebulized
Inhaled steroids
Beclomethasone,
budesonide, flixotide
Continue with inhaled format If >1500 Âľg/day of
beclomethasone, adrenal
suppression??
Oral steroids Prednisolone Continue hydrocortisone until
take PO
If >10 mg/day, adrenal
suppression likely.
Leukotriene inhibitor (anti-
inflammatory)
Montelukast, zafirlukast Restart when taking oral
medications
Mast cell stabilizer Disodium cromoglycate Continue by inhaler
Phosphodiesterase inhibitor Aminophylline
Continue where possible Effectiveness in asthma
debated. In severe asthma
consider converting to an
infusion perioperatively.
35
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36. Premedication
⢠Anxiolytics ď reduce bronchospasm.To dry secretions.
⢠Short-acting beta2 agonist inhaler (2 to 4 puffs) or nebulizer
(albuterol 2.5 mg) 20 to 30 min prior to AW manipulation.
⢠Sedatives & narcotics âŚover sedation & resp. depression.
⢠Midazolam or small doses fentanylâŚpainful procedures prior
to anesthetic induction (eg, placement of an intra-arterial or
epidural catheter), may be used.
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37. Choice of Anesthetic Technique
⢠Avoid of tracheal intubation if possible.
⢠Regional anesthesia
ďNeuraxial anesthesia
ďBrachial plexus blocks âparalyze diaphragm phrenic nerve block.
⢠General anesthesia âmechanical stimulation AW,
suctioning, inhalation of cold anesthetic gases, pulmonary
aspiration of stomach contents.
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38. Induction of Anesthesia
⢠AW management- A goal (minimize risk of a bronchospasm)
⢠LMA or mask ventilation vs ETT.
⢠Anesthetic agents- sufficient depth of anesthesia.
ďOpioid and/or lidocaine & NMBA.
⢠Propofol ⌠induction choice.
⢠Ketamine, etomidate, barbiturates (methehexital ,theopental
⢠Meperidine, morphine
5/18/2023 38
41. Ventilation Strategy
⢠Reduce air trapping
⢠Lung-protective ventilation strategies:
ďControlled hypoventilation with reduced Vt. (e.g, 6 mL/kg)
ďReduced RR with longer expiratory time
ďReduced inspiratory time (Reduce I:E ratio)
ďCautious use of PEEP
ďAdminister inhaled bronchodilator
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42. Intraoperative Bronchospasm
⢠Identification: Signs of bronchospasm under anesthesia;
ďWheezing on chest auscultation
ďChange in ETCO2: : Upsloping ETCO2 waveform
ďźSevere, decreased, or absent ETCO2 waveform
ďDecreased tidal volume
ďHigh inspiratory pressure
ďDecreasing oxygen saturation
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44. Mx of severe bronchospasm outside OR??
⢠Start high flow oxygen and gain IV access.
⢠Nebulised salbutamol 5 mg. May be given continuously at 5â10 mg/hour.
⢠Metered dose inhaler, preferably with a spacer. 5-10 puffs initially.
⢠Nebulised ipratropium 0.5 mg (4â6 hrly)
⢠IV salbutamol if not responding (250 mcg slow bolus then 5â20 mcg/min)
⢠Hydrocortisone 100 mg IV 6 hourly or prednisolone orally 40â50 mg/day.
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45. ⢠Magnesium sulphate 2g IV over 20 minutes
⢠Aminophylline 5mg/kg IV followed by infusion may be effective.
⢠In extremis (decreasing conscious level or exhaustion) adrenaline may be
used: nebuliser 5 ml of 1 in 1,000; IV 10 mcg (0.1 ml 1 : 10,000) increasing
to 100 mcg (1 ml 1 : 10,000) depending on response
ďź Beware arrhythmias in the presence of hypoxia and hypercapnia
ďź If IV access is not available, subcutaneous or IM administration (0.5â1 mg) may be
used, though absorption may be unpredictable due to poor perfusion.
45
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46. Postoperative Care
⢠Patients with severe asthma undergoing major abdominal or
thoracic surgery should be admitted to HDU/ICU.
⢠Usual medications should be prescribed after surgery.
⢠Pain relief âŚmajor abdominal or thoracic surgery
ďRegular administration of opioids is the most common technique,
epidural analgesia âŚthe best choice.
⢠Oxygen for the duration of epidural or opioids administration.
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49. COPDâŚ
⢠Most common pulmonary disorder encountered in anesthetic
practice & its prevalence increases with age.
⢠Strongly associated with cigarette smoking & has a male
predominance.
⢠Itis characterized by the progressive development of airflow
limitation that is not fully reversible.
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50. COPDâŚ
⢠Chronic airflow limitation of this disease is due to a mixture
of small & large airway disease (chronic bronchitis
/bronchiolitis) & parenchymal destruction (emphysema).
⢠Most patients are asymptomatic or only mildly symptomatic,
but show expiratory airflow obstruction upon PFTs.
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51. COPD..
⢠In many pts, obstruction has an element of reversibility, from
bronchospasmâŚimprovement in response to bronchodilator.
⢠With advancing disease ď low V/Q (intrapulmonary shunt), as
well as areas of high (V /Q ) (dead space).
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52. Chronic Bronchitis
⢠Defined by presence of a productive cough on most days of 3
consecutive months for at least 2 consecutive years.
ďCigarette smoking, air pollutants, exposure to dusts,
ďRecurrent pulmonary infections, familial factors
⢠Secretions from hypertrophied bronchial mucous glands &
mucosal edema (inflammation) of AWsď airflow obstruction.
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53. Chronic BronchitisâŚ
⢠âChronic asthmatic bronchitisââŚbronchospasm .
⢠Recurrent pul. infections are common & often ď
bronchospasm.
⢠RV is increased, but TLC is often normal.
⢠Intrapulmonary shunting is prominent & hypoxemia is
common.
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54. Chronic BronchitisâŚ
⢠In COPD, chronic hypoxemia ď erythrocytosis, pul.
hypertension, & eventually ď cor-pulmonale
⢠This combination of findings is often referred to as blue bloater
syndrome, but <5% of pts. with COPD.
⢠Pts. gradually ď chronic CO2 retentionď less sensitive
ventilatory & may be depressed by O2 administration.
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55. Emphysema
⢠Irreversible enlargement of the airways distal to terminal
bronchioles & destruction of alveolar septa.
⢠Mild apical emphysematous changes are a normal, clinically
insignificant & consequence of aging.
⢠Significant emphysema is more frequently related to cigarette
smoking.
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56. EmphysemaâŚ
⢠Less commonly, occurs at an early age & is associated with a
deficiency of Îą1 -antitrypsin.
ďźProtease inhibitor that prevents excessive activity of
proteolytic enzymes (mainly elastase);
ďźThese enzymes are produced by pulmonary neutrophils &
macrophages in response to infection & pollutants.
⢠Smoking associated emphysema may be due to similarly way.
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57. EmphysemaâŚ
⢠Loss of elastic recoilď premature collapse during exhalationď
expiratory flow limitation with air trapping & hyperinflation.
⢠Increases in RV, FRC, TLC & RV/TLC ratio.
⢠Alveolarâcapillary disruption & loss of acinar structure ď
decreased DLCO, V/Q mismatch & gas exchange impairment.
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58. EmphysemaâŚ
⢠Chronic CO2 retention occurs slowly & generally results in a
compensated respiratory acidosis on blood gas analysis.
⢠PaO2 is usually normal or slightly reduced.
⢠Acute CO2 retention is a sign of impending respiratory failure.
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59. EmphysemaâŚ
⢠Destruction of pul. capillaries ď pulmonary hypertension.
⢠Pul. HTN is usually low to moderate, rarely > 35-40 mm Hg.
⢠When dyspneic, pts. often purse their lips to delay closure of
the small airways, which accounts for the term âpink puffersâ.
⢠Most pts. diagnosed with COPD have a combination of
bronchitis & emphysema.
5/18/2023 59
61. Clinical Features of COPD
⢠Symptoms include:
ďWorsening dyspnea,
ďProgressive exercise intolerance &
ďChronic productive cough
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62. History
⢠Classic symptoms in the chronic bronchitis group:
ďProductive cough, with progression overtime to intermittent
dyspnea.
ďFrequent & recurrent pulmonary infections.
ďProgressive resp. & cardiac failure over time with edema.
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63. HxâŚ
⢠Classic symptoms in emphysema:
ďA long history of progressive dyspnea with late onset of
non-productive cough.
ďCachexia & respiratory failure.
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64. P/E
⢠Chronic bronchitis (blue bloaters)
ďPts may be obese
ďFrequent cough and expectoration are typical
ďUse of accessory muscles of respiration is common
ďCoarse rhonchi and wheezing
ďSigns of RHF (cor pulmonale)âŚedema & cyanosis.
5/18/2023 64
65. P/EâŚ
⢠Emphysema (pink puffers)
ďPts may be very thin with barrel chest
ďHave little or no cough or expectoration
ďUse of accessory respiratory muscles
ďWheezing
ďHyper resonant chest
5/18/2023 65
66. COPDâŚ
⢠Three cardinal symptoms of COPD are
ď§ Dyspnea, chronic cough, and
ď§ Sputum production
⢠The most common early symptom is exertional dyspnea.
⢠Less common symptoms include wheezing & chest tightness.
5/18/2023 66
67. COPDâŚ
⢠Onset is slow & most pts. are symptomatic either with cough
or progressive dyspnoea long before they present to medical
services.
⢠Therefore a diagnosis of COPD should be considered in all
pts. over forty years old with a significant smoking history.
5/18/2023 67
68. Treatment
⢠Designed to relieve existing symptoms & slow dx. progression.
ďCessation of smoking
ďOxygen administration
ďDrug therapy: Bronchodilators, Antibiotics, diuretics
⢠Physical training
⢠Surgery
5/18/2023 68
69. Preoperative Assessment: Hx.& P/E
⢠A smoking history, exercise tolerance
⢠Frequency of exacerbations, hospital admissions & previous
requirements for invasive & non-invasive ventilation.
⢠Cough & particularly sputum production -independent risk
factor for PO pul. complications in COPD.
⢠A clear history regarding co-morbid conditions is vital.
5/18/2023 69
70. Investigations
⢠Chest X-ray - to exclude active infection & occult
malignancy
⢠ECG - may reveal right heart disease (right ventricular
hypertrophy or strain)
⢠Consider echocardiography
⢠Spirometry is used to clarify diagnosis & assess severity.
5/18/2023 70
71. GOLD Classification of COPD (post bronchodilator
FEV1)
Stage I: Mild FEV1/FVC <0.70
-FEV1 ⼠80% predicted
Stage II: Moderate FEV1/FVC<
0.70
-FEV1 50 - 80% predicted
Stage III : Severe FEV1/FVC <0.70
-FEV1 30 - 50% predicted
Stage IV: Very Severe
FEV1/FVC<0.70
-FEV1 <30% predicted
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73. Preoperative Optimisation
⢠Can be divided into four main areas:
ď§ Smoking cessation,
ď§ Optimization of drug therapy,
ď§ Treatment of infection, and
ď§ Respiratory physiotherapy
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74. Preoperative OptimisationâŚ
⢠Preoperative interventions aimed at correcting;
ďHypoxemia, relieving bronchospasm,
ďMobilizing & reducing secretions & treating infections may
decrease incidence of POP pul. complications.
⢠Long-acting bronchodilators & mucolytics should be
continued, including on the day of surgery.
. 5/18/2023 74
75. Intraoperative Management
⢠Regional anesthesia is often considered preferable to GA.
⢠High spinal or epiduralď decrease lung volumes, restrict use
of accessory muscles & produce ineffective coughď dyspnea
& retention of secretions.
⢠Interscalene blocks VS diaphragmatic paralysis
5/18/2023 75
76. Intraoperative Management
⢠Preoxygenation, selection of anesthetic agents & general
intraop. mx.
⢠Bronchodilating anesthetics improves only reversible AWO.
⢠PPVď air trapping, dynamic hyperinflation & elevated
intrinsic PEEP (iPEEP).
⢠Hyperinflation ď volutrauma, hemodynamic instability,
hypercapnia & acidosis.
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77. Intraoperative ManagementâŚ
⢠Interventions to mitigate air trapping include:
ď1) More time to exhale (decrease both RR & I:E ratio;
ď2) Allowing permissive hypercapnia;
ď3) Applying low levels of extrinsic PEEP;
ď4) Aggressively treating bronchospasm.
5/18/2023 77
78. Intraoperative ManagementâŚ
⢠Pneumothorax & right HF due to hypercapnia & acidosis ď
intraop. hypotension.
⢠A pneumothorax ď hypoxemia, increased PAP, decreasing Vt.
& abrupt CVS collapse unresponsive to fluid & vasopressors.
⢠Nitrous oxideâŚbullae & pulmonary hypertension.
5/18/2023 78
79. Intraoperative ManagementâŚ
⢠ABG analysis âŚintra-abdominal & thoracic procedures.
⢠Pulse oximetry, direct PaO2, PaCO2 measurement.
⢠Moderate (Paco2 up to 70 mmHg may be well tolerated in the
short term, assuming a reasonable CVS reserve.
⢠Hemodynamic support with inotropic agents.
⢠In pts. with pul. HTNâŚCVP reflect Rt, ventricular function.
5/18/2023 79
80. ManagementâŚ
⢠Extubation: bronchospasm vs respiratory failure.
⢠Successful extubation:
ďAdequate pain control, reversal of NMB,
ďAbsence of bronchospasm & secretions, absence of significant
hypercapnia & acidosis & absence of respiratory depression.
⢠Pts. with an FEV 1 < 50% may require a period of PO ventilation,
particularly following upper abdominal and thoracic operations.
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81. Restrictive Pulmonary Disease
⢠Characterized by decreased lung compliance.
⢠Lung volumes are typically reduced, with preservation of
normal EFR.
⢠Thus, both FEV1 & FVC are reduced, but the FEV1 /FVC
ratio is normal.
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82. RLDâŚ
⢠Include many acute & chronic intrinsic pul. disorders &
extrinsic (extrapulmonary) disorders (pleura, chest wall,
diaphragm, or NM function).
⢠Reduced lung compliance increases WOB ď rapid, but
shallow, breathing pattern.
⢠Respiratory gas exchange is usually maintained until the
disease process is advanced.
5/18/2023 82
84. Acute Respiratory Distress Syndrome
⢠ARDS is commonly encountered in critical care population &
is associated with a high mortality of between 27% and 45%.
⢠Diagnosed according to the Berlin definition & is
characterized as mild, moderate, or severe depending on
PaO2/FIO2 ratio.
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86. ARDSâŚ
⢠Potential causes of ARDS can be classified as;
ďPulmonary (pneumonia, pulmonary contusions, etc.) and
ďExtra-pulmonary (including burns, trauma, etc.).
⢠Pneumonia & non-pulmonary sepsis are the leading causes.
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87. ADRSâŚ
⢠End result of a complex interplay between various inflammatory
mediators ď diffuse alveolar damage, non-cardiogenic pulmonary
edema, surfactant dysfunction & atelectasis.
⢠Three overlapping phases ;
⢠Initially, exudative (or acute) phase ď hypoxaemia & a reduction in
pulmonary compliance (alveolar flooding with protein-rich fluid).
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88. ARDSâŚ
⢠Proliferative (or subacute) phase: from day 5 onwards with
further reduction in lung compliance & continued hypoxemia
⌠fibroproliferation & microvascular thrombus formation.
⢠Fibrotic or chronic phase, characterized by widespread fibrosis
& lung remodelling which may be irreversible.
5/18/2023 88
89. Management of ARDS
⢠Good supportive care & management of underlying causes of
illness of all critically unwell patients.
⢠Usually mandates intubation & mechanical ventilation.
⢠Previously, ICU practitioners attempted to ventilate with high
PP until normal gas exchange was achieved.
5/18/2023 89
90. ARDS MxâŚ
⢠Repetitive, cyclical lung overstretching & collapse generate
local & systematic inflammation & contribute to multi-organ
failure & death.
⢠PEEP is key ď collapse of alveoliď reducing shunt & V/Q
mismatch.
⢠An optimal level of PEEP not identified.
5/18/2023 90
91. ARDS MxâŚ
ďśHigh-frequency oscillation ventilation (HFOV)
⢠Now infrequently used in adults, (HFOV) delivers extremely
low VT (1â2 ml kgâ1) at very high rates (3â15 breaths/second).
⢠This strategy is based on the theory that low VTs and higher
PEEP limit ventilator-associated lung injury.
5/18/2023 91
92. ARDS MxâŚ
⢠Prone positioning
⢠Extracorporal membrane oxygenation (ECMO)
⢠Fluid management: Conservative approach VS liberal strategy
ďUse of albumin
⢠Nutrition
⢠Pharmacotherapy: Steroids
5/18/2023 92
93. Pulmonary Edema
⢠Results from transudation of fluid, first from pul. capillaries ď
interstitial spaces & then from interstitial spaces ď alveoli.
⢠Fluid in interstitial space & alveoli is collectively referred to as
extravascular lung water.
5/18/2023 93
94. PEâŚ
⢠Movement of water across pul. capillaries is similar to what occurs
in other capillary beds & can be expressed by Starling equation:
ďź Q = net flow across capillary; PcⲠ& Pi = capillary & interstitial
hydrostatic pressures,
ďź ĎcⲠ& Ďi = capillary & interstitial oncotic pressures,
ďź K = filtration coefficient related to effective capillary surface area per
mass of tissue;
ďź Ď = reflection coefficient that expresses the permeability of the
capillary endothelium to albumin.
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95. PEâŚ
⢠Albumin is particularly important in this context.
⢠A Ď =1 implies that endothelium is completely impermeable to
albumin, whereas â0â indicates free passage of albumin. &
other particles/molecules.
⢠Net amount of fluid that normally moves out of pul. capillaries
is small (about 10â20 mL/h in adults) & is rapidly removed by
pul. lymphatics ď¨ central venous system.
5/18/2023 95
96. Pulmonary Edema..
⢠Stage I: Only interstitial PE is present.
ďAs pulmonary compliance decrease pts. often ď tachypneic.
ďX-ray: increased interstitial markings & peribronchial cuffing.
⢠Stage II: Fluid fills interstitium & begins to fill alveoli, initially
confined to angles b/n adjacent septa (crescentic filling).
ďNear-normal gas exchange may be preserved.
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97. PEâŚ
⢠Stage III: Many alveoli completely flooded & no longer contain gas.
ďFlooding is most prominent in dependent areas.
ďFlooded alveoli ď intrapul. Shuntingď Hypoxemia & hypocapnia
⢠Stage IV: Marked alveolar flooding spills into the airways as froth.
ďBoth shunting & AWOď compromised gas exchange ď
progressive hypercapnia & severe hypoxemia.
97
99. Causes of Pulmonary Edema
⢠Increase in net hydrostatic pressure across capillaries (hemodynamic
or cardiogenic PE) or
⢠Increase in permeability of alveolarâcapillary membrane (increased
permeability edema or non-cardiogenic PE).
⢠Protein content of the edema fluid can also help differentiate the two.
⢠Fluid due to hemodynamic edema has a low protein content, whereas
that due to permeability edema has a high protein content.
5/18/2023 99
100. Causes of PEâŚ
⢠Less common causes of edema include:
ďProlonged severe airway obstruction (-ve pressure PE),
ďSudden re-expansion of a collapsed lung, high altitude
ďPulmonary lymphatic obstruction & severe head injury.
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101. Less common causes of PEâŚ
⢠PE associated AWO: from an increase in transmural pressure
across pul. capillaries associated ď markedly -ve Pi.
⢠Neurogenic PE appears to be related to a marked increase in
sympathetic toneď severe pulmonary hypertension.
⢠The latter can disrupt the alveolarâcapillary membrane.
5/18/2023 101
102. Preoperative Considerations
⢠Reduced lung compliance: primarily due to an increase in EV
lung water (increase in pul. Pc or pul. capillary permeability).
⢠Increased pressure occurs with left ventricular failure.
⢠Fluid overload & increased permeability present with ARDS.
⢠Localized or generalized increases in permeability also occur
following aspiration or infectious pneumonitis.
5/18/2023 102
104. Anesthetic ConsiderationsâŚ
⢠Vasodilators & inotropes⌠heart failure.
⢠Drainage of large pleural effusions.
⢠Massive abdominal distention âŚNGT/drainage of ascites.
⢠Persistent hypoxemia may require mechanical ventilation.
5/18/2023 104
105. Anesthetic ConsiderationsâŚ
⢠Pts. with acute pulmonary disorders (ARDS, cardiogenic PE,
or pneumonia are critically ill.
⢠Anesthetic mx. should be a continuation preop. ICU care.
⢠High FIO2 & PEEP may be required.
⢠Decreased lung complianceď high PIP during PPV &
increases risk of barotrauma & volutrauma.
5/18/2023 105
106. Intraoperative ManagementâŚ
⢠Reduce VT (4â6 mL/kg) & increase RR (14â18 breaths/min).
⢠AW pressure should generally not exceed 30 cm H2O.
⢠Airway pressure release ventilation (inverse ratio ventilation)
may improve oxygenation in the ARDS patient.
⢠Anesthesia machine vs ICU ventilator.
⢠Aggressive hemodynamic monitoring is recommended.
5/18/2023 106
107. Chronic Intrinsic Pulmonary Disorders
⢠Are also often referred to as interstitial lung diseases.
⢠Generally characterized by an insidious onset, chronic
inflammation of alveolar walls & peri-alveolar tissue &
progressive pul. fibrosis.
⢠Inflammatory process: confined to lungs or part of a
generalized multiorgan process.
5/18/2023 107
108. Chronic Intrinsic Pulmonary DisordersâŚ
⢠Causes include hypersensitivity pneumonitis from
occupational & environmental pollutants, drug toxicity,
radiation pneumonitis, idiopathic pulmonary fibrosis,
autoimmune diseases & sarcoidosis.
⢠Chronic pulmonary aspiration, oxygen toxicity & severe
ARDS can also produce chronic fibrosis.
5/18/2023 108
109. Preoperative Considerations
⢠Patients typically present with dyspnea on exertion & sometimes a
nonproductive cough.
⢠Symptoms of cor-pulmonaleâŚonly with advanced disease.
⢠P/E may reveal fine (dry) crackles over lung bases & in late stages,
evidence of right ventricular failure.
⢠Chest X-ray progresses from a âground-glass opacityâď reticulo-
nodular markings & finally ď âhoneycombâ appearance.
5/18/2023 109
110. Anesthetic ConsiderationsâŚ
⢠ABG usually show mild hypoxemia with normocarbia.
⢠PFTs: restrictive ventilatory defect, reduced DLCO.
⢠Treatment: abating disease process & preventing further
exposure to causative agent (if known).
⢠Glucocorticoid & immunosuppressive âŚidiopathic pul.
fibrosis, autoimmune disorders & sarcoidosis.
⢠Chronic hypoxemia⌠oxygen therapy.
5/18/2023 110
111. Anesthetic Considerations
⢠Preoperative: degree of pul. impairment & underlying ds.
process.
⢠Potential involvement of other organs.
⢠Hx. of dyspnea on exertion (or at rest) , PFTs & ABG analysis.
⢠A VC < 15 mL/kg (severe dysfunction), (normal, >70 mL/kg).
⢠A chest radiograph is helpful in assessing disease severity.
5/18/2023 111
112. Anesthetic ConsiderationsâŚ
⢠Management is complicated by a predisposition to hypoxemia
& need to control ventilation to ensure optimum gas exchange.
⢠Reduced FRC (oxygen stores) ď rapid hypoxemia ff induction.
⢠May be more susceptible to oxygen-induced toxicity
(bleomycin) FIO2 should be kept minimum (achieving Spo2
>88% to 92%).
5/18/2023 112
113. Anesthetic ConsiderationsâŚ
⢠High PIP ď increase risk of pneumothorax & should prompt
adjustment of the ventilatory parameters.
⢠Severe restrictive diseas ⌠using an I:E ratio of 1:1 (or even
an inverse ratio ventilation) & dividing MV to a higher RR
(10â15 bpm)ď maximize inspiratory time per VT &
minimize peak & plateau ventilatory pressures.
5/18/2023 113
114. Extrinsic Restrictive Pulmonary Disorders
⢠Alter gas exchange by interfering with normal lung expansion.
ďPleural effusions, pneumothorax, mediastinal masses,
ďKyphoscoliosis, pectus excavatum, NM disorders &
ďIncreased IAP (ascites, pregnancy/bleeding) marked obesity.
⢠Anesthetic considerations are similar to those discussed for
intrinsic restrictive disorders.
5/18/2023 114
116. Introduction
⢠TB is an infectious disesase usually caused by MTB bacteria.
⢠MTB spread: airborne transmission of small droplets (0.5-5 Οm).
⢠Usually, infection occurs b/n prolonged household contacts.
⢠Exposure to only a few bacteria is needed to establish infection.
⢠Primary site of infection is upper lobe of lung âŚhigh oxygen
tension,,, Ghon focus.
5/18/2023 116
117. IntroductionâŚ
⢠Bacteria invade & replicate within macrophages.
⢠Followed by a T- cell mediated response, which walls off
infected cells to form a granuloma.
⢠Bacteria within granuloma can become dormant ď latent
infection.
⢠At this stage, patient will be asymptomatic, but may show a
positive response to a tuberculin skin test.
5/18/2023 117
118. IntroductionâŚ
⢠Factors that increase likelihood of progression to active disease
include:
ďTime from exposure (most common in 1st year)
ďAge of patient (younger than five years old),
ďCompetency of the immune system.
5/18/2023 118
119. Patients may present in a number of ways:
⢠Pul. disease is most common
ďď a chronic productive cough & hemoptysis.
ďLymph nodes enlargement ď bronchial compression with
localized wheeze.
ďHematogenous spread ď widespread lung infection
(miliary TB).
5/18/2023 119
120. PresentationâŚ
⢠Constitutional symptoms secondary to production of proinflammatory
cytokines are commonly seen.
ďFever, night sweats, loss of weight, or failure to thrive in children.
⢠Activation of T-cell-mediated immunityď Hypersensitivity
ďźErythema nodosum, phlyctenular conjunctivitis & Poncetâs dx.
⢠Extrapulmonary disease
ďLymphadenitis (scrofula), bones and joints, abdominal TB &
meningitis.
5/18/2023 120
121. Diagnosis
⢠Traditionally: visualising acid-fast bacilli on sputum.
⢠Newer technology: such as XpertŽ M. TB/resistance to rifampicin or
GeneXpertÂŽ.
ďź Much quicker results (within 2 hrs).
⢠Children: sxs of TB, +ve contact & a +ve tuberculin skin test
(MantouxÂŽ).
⢠T cell interferon-γ (IFN-γ) release assays, which measure # of IFN-γ-
secreting T-cells, ⌠alternative to tuberculin skin test to detect infection.
5/18/2023 121
122. Treatment
⢠Cornerstone is directly observed treatment (DOT) for at least
six months.
⢠1st -line tx: rifampicin, isoniazid (INH), ethambutol &
pyrazinamide.
⢠Fixed dose combinations help to reduce pill burden.
⢠Steroids are given for six weeks in cases of TB meningitis,
pericarditis & AWO from lymph node compression.
5/18/2023 122
123. TreatmentâŚ
⢠Some of serious S/E, may have impact on anesthetist.
ďRifampicin may ď thrombocytopenia (high doses).
ďINH may ď sensory neuropathy, âŚregional blocks??
⢠This complication can be prevented by adding pyridoxine
(vitamin B6 ) in high-risk cases.
⢠Ethambutol has the potential to cause optic neuritis.
ďNot routinely given to children.
5/18/2023 123
124. TreatmentâŚ
⢠Drug-induced hepatitis is a worrying complication.
⢠Ant-TB plus concomitant RVI therapyď a mild liver enzymes
elevation.
⢠However, symptomatic hepatitis has a mortality of almost 5%,
& requires immediate halting of TB drugs, with careful re-
introduction under specialist care.
5/18/2023 124
125. TreatmentâŚ
⢠Wherever possible, surgery should be avoided during this
period.
⢠MDR and XDR TB require extended treatment for up to two
years with four or five drugs, depending on resistance patterns.
⢠Besides the added cost of treatment, there is also an increased
risk of life-threatening side effects.
5/18/2023 125
126. Anesthetic Implication
⢠The patient of TB may be require anesthesia for:
ďDiagnostic procedures (Lymphnode biopsies,
Brochoscopies),
ďComplications of TB (Hydrocephalus, Intestinal obstruction
requiring anesthesia) & elective /emergency surgeries.
5/18/2023 126
127. Anesthetic ImplicationâŚ
⢠Three major implications for the anethetist:
⢠1. General state of ptâs health & impact of the disease on organ
function.
⢠The tx. that pt. is receiving & considerable potential for drug
interactions.
⢠The risk of transmission of TB to staff & other patients.
5/18/2023 127
128. Patient Assessment
⢠The patient may be acutely ill, either with TB or a superadded
infection.
⢠Alternately, he or she may be chronically ill, malnourished &
frequently anemic.
⢠Long-standing TB.ď CLD with bronchiectasis & fibrosis.
⢠A full history, examination & relevant investigations.
5/18/2023 128
129. Drug InteractionsâŚ
⢠Drug interactions are mostly due to pharmacokinetic changes
full induction of liver enzymes.
⢠Rifampicin is responsible for most observed drug interactions.
⢠It is a potent inducer of CYP450 system ď Increased
metabolism.
⢠CYP3A4 is also found in small intestineď oral drugs more affected.
5/18/2023 129
130. Drug Interactions
⢠On the other hand, INH is a CYP450 inhibitor.
⢠However, due to differential effect on specific isoenzymes,
these two drugs do not simply cancel each other out.
⢠Greater potential for a drug interaction when a patient is also
taking ARI drugs & specifically protease inhibitors.
5/18/2023 130
131. Induction Agents
⢠TB therapy is unlikely to have an effect on a single induction
dose.
⢠However increased metabolism may be important in TIVA, with
a greater potential for awareness.
⢠While there is no evidence to support this, one should be
mindful of this risk & consider use of depth of anesthesia
monitoring in pts.
5/18/2023 131
132. Local Anesthetics
⢠As they exert their action primarily at the site of injection, LA
drugs are still likely to be effective & help to avoid many of the
other drug interactions seen with opiates.
⢠Increased metabolism may result in a decreased risk of local
anesthetic toxicity.
5/18/2023 132
133. Volatile Anesthetics
⢠Halothane is metabolized via isoenzyme CYP2E1 to trifluroacetic
acid.
⢠This molecule has potential to act as a hapten to trigger an immune
mediated hepatitis.
⢠CYP2E1 is induced by INH.
⢠Thus patients on anti-TB therapy are potentially at increased risk of
halothane hepatitis.
⢠The minimal metabolism of the newer volatile agents makes them a
better choice.
5/18/2023 133
134. Neuromuscluar Blocking Drugs
⢠Unless liver dysfunction results in decreased pseudocholinesterase
levels, effect of suxamethomium is unchanged.
⢠Similarly cisatracurium (organ independent metabolism) and
pancuronium (renal excretion) are minimally affected by TB therapy.
⢠While no trials specifically look at interactions with TB treatment, it
has been shown that effect of vecuronium is prolonged by cimetidine,
an enzyme inhibitor, and shortened by phenytoin enzyme induction.
5/18/2023 134
135. NMBâŚ
⢠Rocuronium is less affected but resistance to muscle blockade
has been shown with carbamazepine.
⢠Streptomycin may potentiate effects of non-depolarising
agents.
⢠NDNMD should, therefore, be titrated to response, with
frequent evaluation using a nerve stimulator.
5/18/2023 135
136. Analgesics
⢠While metabolism of morphine predominantly involves phase II
reactions via UDP-glucuronosyltransferases, anti-TB therapy seems
to have an effect.
⢠A loss of analgesic effect of oral morphine has been demonstrated
following pretreatment with rifampicin.
⢠Fentanyl & alfentanil are both extensively metabolised by CYP450
3A4, therefore, also show potential for a shortened duration of
action.
⢠The metabolism of codeine is interesting.
5/18/2023 136
137. AnalgesicsâŚ
⢠The analgesic effect of codeine is mediated through its
metabolism to morphine via CYP450 2D6.
⢠One may, therefore, expect a greater analgesic effect following
enzyme induction.
⢠However, it is also metabolized to inactive norcodeine via
isoenzyme 3A4, resulting in an overall decreased effect.
⢠The effect of tramadol is unchanged.
5/18/2023 137
138. AnalgesicsâŚ
⢠Of NSAIDs, effect of diclofenac is decreased with rifampicin, while
that of ibuprofen is unchanged, making it a safer option.
⢠Analgesia should therefore be titrated to effect with the potential to
require more frequent dosing.
⢠Therefore, the choice of anesthetic depends on patient, procedure &
severity of disease.
⢠Regional anesthesia is often preferred in patients with CLD & to
avoid potential drug interactions.
⢠Hepatotoxic drugs must be avoided.
5/18/2023 138
140. Spread of Tuberculosis
⢠To immunocompromised patients & to theatre staff is an area
of concern.
⢠Airway during intubationď particular risk for anesthetists.
⢠Children are less likely to have cavitary dx. & are, therefore,
less infectious.
5/18/2023 140
141. Spread of TuberculosisâŚ
⢠Delay elective surgery until patient is no longer infectious.
ďOn treatment for 2-3 weeks, clinically getting better &
having had three negative sputa on different days.
⢠While practically, the third criterion might be difficult to
achieve, the first two should certainly be followed.
5/18/2023 141
143. Spread of TuberculosisâŚ
⢠Elective casesâŚlast case of day to allow decontamination.
⢠Transfer pt. wearing an N95Ž mask & brought straight to OR.
⢠Minimize OR inside traffic to essential staff.
⢠Theatre staff must wear N95Ž masks.
ďFor high-risk procedures, intubation & bronchoscopy.
ďAdequate anesthesia & muscle relaxation ď no cough on
intubation.
5/18/2023 143
144. Spread of TuberculosisâŚ
⢠Bacterial filter placed both by ptâs. airway & on the expiratory
limb of the circuit.
⢠These should be able to filter more than 99.97% of particles
greater than 0.3 Îźm.
⢠While not specifically advocated by ASA, it would be good
practice to sterilize the circuits after such a case.
5/18/2023 144
Restrictive disease is either intrinsic, such as pulmonary fibrosis related to rheumatoid arthritis or asbestosis, or extrinsic, such as caused by kyphoscoliosis or obesity. Oxygenation may be impaired at the alveolar level and because of poor air supply to it. Steroids are the usual treatment for fibrotic disease.
classify lung conditions as obstructive lung disease or restrictive lung disease. Obstructive lung diseases include.
People with restrictive lung disease have difficulty fully expanding their lungs with air.
Obstructive and restrictive lung disease share the same main symptom: shortness of breath with exertion
People with obstructive lung disease have shortness of breath due to difficulty exhaling all the air from the lungs.
As the rate of breathing increases, there is less time to breathe all the air out before the next inhalation
which includes
Bronchiectasis = loss of elasticity of wall of one or more bronchioles
Cystic fibrosis = is a disease of exocrine gland function that involves multiple organ systems but chiefly results in chronic resp infection, pancreatic enzyme insuficiency ( COPD like symptom)
People with restrictive lung disease cannot fully fill their lungs with air. Their lungs are restricted from fully expanding.
Restrictive disease is either intrinsic, such as pulmonary fibrosis related to rheumatoid arthritis or asbestosis, or extrinsic, such as caused by kyphoscoliosis or obesity
Restrictive lung disease most often results from a condition causing stiffness in the lungs themselves. In other cases, stiffness of the chest wall, weak muscles, or damaged nerves may cause the restriction in lung expansion.
Sarcoidosis = a chronic disease of unknown cause that is characterized by the formation of nodules resembling true tubercles esp. in the lymph nodes, lungs, bones, and skin
VC = TLC - RV
In healthy subjects, the two maneuvers usually result in almost equal measured volumes
To identify airway obstruction, flow rates are determined by calculation of the volume exhaled during certain time intervals. Most commonly measured is the volume exhaled in the first second, called the forced expiratory volume in 1 second(FEV1).
the remaining volume is exhaled in two or three additional seconds
Diseases such as asthma and bronchitis, which obstruct the airway, reduce expiratory flow rates and therefore reduce FEV1and FEV1/FVC.
Because the FEV1/FVC represents a ratio, it is important to realize that identical percentage values may not indicate equivalent degrees of lung dysfunction. For example, a patient with an FEV1 of 1.5 L and an FVC of 3.0 L does not have the same degree of impairment as a similar-sized patient with an FEV1 of 0.75 L and an FVC of 1.5 L, although both have an FEV1/FVC ratio of 50%.
TABLE 26-2-- Forced vital capacity (FVC) and 1-second forced expiratory volumes (FEV1) in disease states
Airway narrowing is assessed by asking patients to breathe in fully, then blow out as hard and fast as they can into a peak flow meter or a spirometer. Peak flow meters are cheap and convenient for home monitoring of peak expiratory flow (PEF) in the detection and monitoring of asthma but results are effort-dependent. More accurate and reproducible measures are obtained by maximum forced expiration into a spirometer. The forced expired volume in 1 second (FEV1) is the volume exhaled in the first second, and the forced vital capacity (FVC) is the total volume exhaled. FEV1 is disproportionately reduced in airflow obstruction, resulting in FEV1/FVC ratios of less than 70%. In this situation, spirometry should be repeated following inhaled short-acting β2 adrenoreceptor agonists (e.g. salbutamol); an increase of > 12% and > 200 mL in FEV1 or FVC indicates significant reversibility. A large improvement
in FEV1 (> 400 mL) and variability in peak flow over time are features of asthma (p. 567)
Bronchial asthma can occur at any age but typically appears early in life.
50% before 10yrs
In childhood, 2:1 male/female preponderance, but equalizes by age 30.
. However, there can be a phase in which the patient experiences some degree of airway obstruction daily. This phase can be mild, with or without superimposed severe episodes, or much more serious, with significant obstruction persisting for days or weeks.
- Bronchoconstriction may be triggered by a number of different mechanisms
Mild asthma is usually accompanied by a normal PaO2 and PaCO2. Tachypnea and hyperventilation observed during an acute asthmatic attack do not reflect arterial hypoxemia but rather neural reflexes in the lungs
Spirometry: for Dx, to determine severity & to check effectiveness of treatment
. The first is the use of âcontrollerâ treatments, which modify the airway environment such that acute airway narrowing occurs less frequently.
The other component of asthma treatment is the use of ârelieverâ or rescue agents for acute bronchospasm.
cromolyn sodium that inhibits the release of histamine from mast cells and is used usu. as an inhalant to prevent the onset of bronchial asthma attacks
cyclic AMP n a cyclic mononucleotide of adenosine that is formed from ATP and is responsible for the intracellular mediation of hormonal effects on various cellular processes (as lipid metabolism, membrane transport, and cell proliferation)
The incidence of perioperative bronchospasm in asthmatic patients undergoing routine surgery is less than 2%, especially if routine medication is continued
We assess patients with asthma at least one week prior to elective surgery to allow time for modification of treatment, if necessary, especially for those patients who are scheduled for procedures with a high risk of postoperative pulmonary complications. Postoperative pulmonary complications are most common following thoracic surgery, upper abdominal surgery, open aortic aneurysm repair, neurosurgery, and surgery on the head and neck.
Risk of such complications in well-controlled asthmatics is low, whereas poorly controlled asthma increases such risk [3,4]. The asthmatic patient should not be wheezing at the time of surgery.
The history given by the patient at the time of preoperative evaluation can help determine the severity of asthma and level of control and can help predict the likelihood of perioperative bronchospasm.Â
Perioperative bronchospasm and laryngospasm are more likely in patients who used asthma medications, noted asthma symptoms, or visited a medical facility for asthma treatment within the past year, particularly if within 30 daysÂ
Preoperative evaluation of patients with asthma requires an assessment of disease severity and the effectiveness of current pharmacologic management and the potential need for additional therapy prior to surgery.
Preoperative .evaluation begins with a clinical history to elicit the severity and characteristics of the patient's asthma.
Atopy refers to the genetic tendency to develop allergic diseases such as allergic rhinitis, asthma andatopic dermatitis (eczema). Atopy is typically associated with heightened immune responses to common allergens, especially inhaled allergens and food allergens.
Preoperative testing â Patients who have well controlled asthma that is not steroid-dependent generally do not need additional testing beyond that performed for patients without asthma. Baseline pulse oximetry value should be noted. Preoperative pulmonary function testing is usually reserved for patients with moderate to severe asthma undergoing particularly high-risk procedures. In addition, use of asthma medications impacts preoperative laboratory testing.
Theophylline has the potential to cause serious arrhythmias and neurotoxicity at a level just beyond the therapeutic range, and theophylline metabolism is affected by many common perioperative medications.
cAMP
Dexmedetomidine, an alpha2Â agonist, achieves anxiolysis, sympatholysis, and drying of secretions without respiratory depression, and may be useful during preoperative procedures. Dexmedetomidine is given by continuous infusion and requires continuous monitoring of vital signs.
Neuraxial anesthesia â Mid-thoracic or higher levels of neuraxial anesthesia can result in paralysis of accessory muscles of breathing. Asthmatic patients may depend on active exhalation for adequate gas exchange, and high levels of sensory or motor block may provoke anxiety and precipitate bronchospasm.
 Ventilatory strategy during controlled ventilation should be designed to reduce air trapping [56-58]. Patients with airflow obstruction need prolonged expiration. Stacked breaths, which occur when a breath starts before the prior exhalation is complete, can result in air trapping, hyperinflation, and, in the extreme, barotrauma. Reduction of the inspiratory/expiratory ratio is an important strategy to reduce air trapping, but the most effective maneuver is to reduce minute ventilation by reducing both rate and tidal volume. The use of PEEP for ventilation in asthmatics is controversial. Extrinsic PEEP may actually worsen air trapping and exacerbate hyperinflation. Conversely, PEEP may prevent airway collapse by stenting airways open, thereby decreasing air trapping. When PEEP is used in asthmatic patients, it should be used cautiously, monitoring for signs of hyperinflation.
Extracorporeal membrane oxygenation is reserved for the most severe bronchospasm that is refractory to maximal medical and mechanical ventilatory therapy.Â
Chronic obstructive pulmonary disease (COPD) is a common respiratory condition involving the airways and characterized by airflow limitation [1,2]. It affects more than 5 percent of the population and is associated with high morbidity and mortality. It is the third-ranked cause of death in the United States, next to heart ds n cancer, COPD, accident, stroke .. It costs $50bln every year
In Africa AIDS, lower RTI (pneumonia), diarhea, malaria, stroke
Alpha 1-antitrypsin (A1AT) is produced in the liver, and one of its functions is to protect the lungs from neutrophil elastase, an enzyme that can disrupt connective tissue: the pathopysiology of emphysema is always an imbalance b/n protease and anti protease activity!
Balance b/n protease/elastase (destructive) and antiprotease (protective) = elastic fibers of alveolus and bronchioles destruction if protease secretion increase
Chronic bronchitis â Chronic bronchitis is defined asâŚThe Global Initiative for Chronic Obstructive Lung Disease (GOLD
Chronic bronchitis is overproduction of mucus to remove irritants
âChronic asthmatic bronchitisââŚbronchospasm (major feature). Recurrent pulmonary infections (viral & bacterial) are common and often associated with bronchospasm. RV is increased, but TLC is oft en normal. Intrapulmonary shunting is prominent, and hypoxemia is common.nic asthmatic
In patients with COPD, chronic hypoxemia leads to erythrocytosis, pulmonary hypertension, and eventually right ventricular failure (cor pulmonale); this combination of fi ndings is oft en referred to as the blue bloater syndrome, but <5% of patients with COPD fi t this description ( Table 24â4 ). In the course of disease progression, patients gradually develop chronic CO 2 retention; the normal ventilatory drive becomes less sensitive to arterial CO 2 tension and may be depressed by oxygen administration (below).
Emphysema is defined by abnormal and permanent enlargement of the airspaces distal to the terminal bronchioles that is accompanied by destruction of the airspace walls.
Marked by distension & eventual rupture of the alveoli with progressive loss of pulmonary elasticity ď shortness of breath with or without cough.
Less commonly, emphysema occurs at an early age and is associated with a homozygous deficiency of Îą 1 -antitrypsin. This is a protease inhibitor that prevents excessive activity of proteolytic enzymes (mainly elastase) in the lungs; these enzymes are produced by pulmonary neutrophils and macrophages in response to infection and pollutants. Emphysema associated with smoking may similarly be due to a relative imbalance between protease and antiprotease activities in susceptible
individuals.
Loss of the elastic recoil that normally supports small airways by radial traction allows premature collapse during exhalation, leading to expiratory
flow limitation with air trapping and hyperinflation. Patients characteristically have increases in RV, FRC, TLC, and the RV/TLC ratio. The FRC is shifted rightward along the compliance curve of the lungs, toward the fl at portion of the curve, in detriment of the pulmonary mechanics.
Disruption of the alveolarâcapillary structure and loss of the acinar structure ď decreased diffusion lung capacity (DLCO), V/Q mismatch & impairment of gas exchange.
Due to the higher diffusibility of CO2, its elimination is well preserved until V/Q abnormalities become severe.
Chronic CO2 retention occurs slowly & generally results in a compensated respiratory acidosis on blood gas analysis.
Pao2 is usually normal or slightly reduced.
Acute CO2 retention is a sign of impending respiratory failure.
Emphysema in AAT deficiency (AATD) is thought to result from an imbalance between neutrophil elastase in the lung, which destroys elastin, and the elastase inhibitor AAT, which protects against proteolytic degradation of elastin. This mechanism is called a "toxic loss of function." Specifically, cigarette smoking and infection increase the elastase burden in the lung, thus increasing lung degradation [4]. In addition, the polymers of "Z" antitrypsin are chemotactic for neutrophils, which may contribute to local inflammation and tissue destruction in the lung [8].
A chronic productive cough and progressive exercise limitation are the hallmarks of the persistent expiratory airflow obstruction characteristic of COPD
In addition some important clinical and hstorical differences can exist b/n types of COPD
and weight gain
About 25% of patients with COPD will develop cachexia (females)). This is associated with approximately 50% reduction in median survival
.. âblue bloatersâ (PaO2 usually less than 60 mm Hg and PaCO2 chronically increased to more than 45 mm Hg).
Blue bloaters develop pulmonary hypertension because arterial hypoxemia and respiratory acidosis evoke pulmonary vascular vasoconstriction. They also develop secondary erythrocytosis due to the hypoxemia. Chronic pulmonary hypertension may produce right ventricular hypertrophy and cor pulmonale. Right ventricular failure results in systemic venous congestion, jugular venous distention, peripheral edema, hepatic congestion, and, occasionally, ascites
âpink puffersâ (PaO2 usually higher than 60 mm Hg and PaCO2 normal) or
(home oxygen therapy) is recommended if the PaO2 is less than 55 mm Hg, the hematocrit is more than 55%, or there is evidence of cor pulmonale
Bronchodilators may alleviate symptoms by decreasing hyperinflation and dyspnea
An additional benefit of β2-agonists may be fewer infections since these drugs decrease the adhesion of bacteria such as Haemophilus influenzae to airway epithelial cells
Diuretic therapy may be considered for patients with cor pulmonale and right ventricular failure with peripheral edema.
Diuretic-induced chloride depletion may produce a hypochloremic metabolic alkalosis that depresses the ventilatory drive and may aggravate chronic carbon dioxide retention
Physical training programs can increase the exercise capacity of patients with COPD
Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines as either GOLD 1 (mild), GOLD 2 (moderate), GOLD 3 (severe), or GOLD 4 (very severe)
Smoking Cessation: Current smokers are at far greater risk of developing postoperative pulmonary complications. Smoking should be stopped at least 8 weeks before surgery in order to obtain maximum benefit
Optimal drug treatment: Some patients with COPD have a degree of reversible airways disease and even in those patients with no demonstrable reversibility, bronchodilators are indicated as they increase exercise tolerance even if there is no change in FEV1. Almost all patients with COPD benefit from at least one dose of nebulised bronchodilator preoperatively.
Treatment of infection/ exacerbation: Current infection or exacerbations are a contraindication to elective anaesthesia.
They should be treated with both β-agonist and anticholinergic therapy.
Physiotherapy: Preoperative physiotherapy is important in sputum producing COPD patients to clear any retained sputum that may cause intraop bronchial plugging or pneumonitis
Bronchospasm - induction, AW instrumentation & extubation. Whilst in some pts. this may be mild & transient, others may need aggressive administration of bronchodilators to prevent or treat acute hypoxemia & hypercarbia.
High spinal or epiduralď decrease lung volumes, restrict use of accessory muscles & produce ineffective coughď dyspnea & retention of secretions
Bronchodilating anesthetics improves only reversible AWO; significant expiratory obstruction may still present, even under deep anesthesia.
PPVď air trapping, dynamic hyperinflation & elevated intrinsic PEEP (iPEEP).
Dynamic hyperinflation ď volutrauma, hemodynamic instability, hypercapnia & acidosis
Inhibition of hypoxic pulmonary vasoconstriction by inhalation anesthetics is usually not clinically significant at the usual doses. However, due to increased dead space, patients with severe COPD have unpredictable uptake and distribution of inhalational agents, and the end-tidal volatile anesthetic concentration is inaccurate.
Inhibition of hypoxic pulmonary vasoconstriction by inhalation anesthetics is usually not clinically significant at the usual doses..
The role of angiotensin II has been recognized as being of particular interest because of its ability to induce alveolar apoptosis and fibrosis, highlighting its future research potential.
Three overlapping phases are recognized
Prone positionin: Underlying principles of reducing V/Q mismatching, increasing FRC & recruitment of atelectatic lung underpin prone positioning strategy
The pulmonary endothelium normally is partially permeable to albumin, such that interstitial albumin concentration is approximately one half that of plasma; therefore,under normal conditions Ďi must be about 14 mm Hg (one half that of plasma). Pulmonary capillary hydrostatic pressure is dependent on vertical height in the lung (gravity) and normally varies from 0 to 15 mm Hg (average, 7 mm Hg). Because Pi is thought to be normally about â4 to â8 mm Hg, the forces favoring transudation of fl uid (Pcâ˛, Pi, and Ďi) are usually almost balanced by the forces favoring
reabsorption (Ďcâ˛).
Pulmonary lymphatic obstruction & severe head injury although the same mechanisms (ie, changes in hemodynamic parameters or capillary permeability) also account for these diagnoses.
Reexpansion pulmonary edema (RPE) is a rare complication that may occur after treatment of lung collapse caused by pneumothorax, atelectasis or pleural effusion and can be fatal in 20% of cases. The pathogenesis of RPE is probably related to histological changes of the lung parenchyma and reperfusion-damage by free radicals leading to an increased vascular permeability. RPE is often self-limiting and treatment is supportive.
A number of mechanisms have been proposed to mediate reperfusion injury. These include: cellular calcium loading; the occurrence of a no reflow phenomenon due to cell swelling, impaired vascular relaxation or the formation of white cell plugs; and perhaps most importantly the formation of oxygen radicals.
Sarcoidosis is a disease involving abnormal collections of inflammatory cells that form lumps known as granulomas.[2] The disease usually begins in the lungs, skin, or lymph nodes.
In radiology, ground glass opacity (GGO) is a nonspecific finding on computed tomography (CT) scans that indicates a partial filling of air spaces in the lungs by exudate or transudate, as well as interstitial thickening or partial collapse of lung alveoli.
Honeycombing or "Honeycomb lung" is the radiological appearance seen with widespread fibrosis[1] and is defined by the presence of small cystic spaces with irregularly thickened walls composed of fibrous tissue. Dilated and thickened terminal and respiratory bronchioles produce cystic airspaces, giving honeycomb appearance on chest x-ray. Honeycomb cysts often predominate in the peripheral and pleural/subpleural lung regions regardless of their cause.
Plateau pressure (PPLAT) is the pressure applied to small airways and alveoli during positive-pressure mechanical ventilation.[1] It is measured during an inspiratory pause on the mechanical ventilator.[2] In ARDS maintain plateau pressure <30cm of water measured on ventilator.
Peak inspiratory pressure (PIP) is the highest level of pressure applied to the lungs during inhalation.[1] In mechanical ventilation the number reflects a positive pressure in centimeters of water pressure (cmH2O). In normal breathing, it may sometimes be referred to as the maximal inspiratory pressure (MIPO), which is a negative value.[2]
Peak inspiratory pressure increases with any airway resistance. Things that may increase PIP could be increased secretions, bronchospasm, biting down on ventilation tubing, and decreased lung compliance. PIP should never be chronically higher than 40(cmH2O) unless the patient has acute respiratory distress syndrome
IAP-Intraabdominal pressure
Pectus excavatum is a structural deformity of the anterior thoracic wall in which the sternum and rib cage are shaped abnormally. This produces a caved-in or sunken appearance of the chest. It can either be present at birth or develop after puberty.
Kyphoscoliosis describes an abnormal curvature of the spine in both a coronal and sagittal plane. It is a combination of kyphosis and scoliosis. This musculoskeletal disorder often leads to other issues in patients, such as under-ventilation of lungs, pulmonary hypertension, difficulty in performing day-to-day activities, psychological issues emanating from anxiety about acceptance among peers, especially in young patients. It can also be seen in syringomyelia, Friedreich's ataxia, spina bifida, Kyphoscoliotic Ehlers-Danlos Syndrome (kEDS), and Duchenne muscular dystrophy due to asymmetric weakening of the paraspinal muscles
Diagnosis Traditionally, diagnosis is made by visualising acid-fast bacilli on sputum. Newer technology, such as the XpertÂŽ M. tuberculosis/resistance to rifampicin or GeneXpertÂŽ, make use of real-time polymerase chain reaction to detect specific DNA sequences. They can provide much quicker results (within two hours), as well as information on rifampicin resistance.9 Obtaining a sputum sample can be difficult in children, and the diagnosis is usually made on the basis of signs and symptoms of tuberculosis, positive contact and a positive tuberculin skin test (MantouxÂŽ).8 Gastric aspirates can be used, but have a pick-up rate of less than 40%.10 T cell interferon-Îł (IFN-Îł) release assays, which measure the number of IFN-Îł-secreting T cells, have been developed as an alternative immune-based approach to the tuberculin skin test to detect infection.
A full history, examination & relevant investigations are needed, as dictated by the clinical condition of the patient, to determine the extent of organ dysfunction.
Delay elective surgery until the patient is no longer infectious.
The ASA defines this as having been on treatment for 2-3 weeks, clinically getting better, and having had three negative sputa on different days.