7. SIGNS AND SYMPTOMS
• Asthma is an episodic disease with acute exacerbations interspersed with symptom-free periods.
• Clinical manifestations of asthma include:
• expiratory wheezing
• productive or nonproductive cough
• dyspnea, chest discomfort or tightness that may lead to air hunger and
• Eosinophilia
• Most attacks are short lived, lasting minutes to hours, and clinically the person recovers
completely after an attack.
• Acute severe asthma is defined as life-threatening bronchospasm that persists despite treatment.
8.
9. DIAGNOSIS
The diagnosis of asthma is usually apparent from the symptoms of variable and intermittent airways
obstruction, but must be confirmed by objective measurements of lung function.
LUNG FUNCTION TESTS IN ASTHMA
Airflow limitation with a reduced FEV1 , FEV1 /FVC ratio, and PEF.
Reversibility is demonstrated by a >12% and 200-mL increase in FEV1 15 min after
an inhaled short-acting β2 -agonist (SABA; such as inhaled albuterol 400 μg) or in
some patients by a 2–4 week trial of oral corticosteroids (OCS) (prednisone or
prednisolone 30–40 mg daily).
Measurements of PEF twice daily may confirm the diurnal variations in airflow
obstruction.
Flow-volume loops show reduced peak flow and reduced maximum expiratory
flow
10.
11. Assessment of Airway Responsiveness
• Done in cases where pulmonary function tests
are nonconfirmatory and the diagnosis remains
in doubt.
• Methacholine, a cholinergic agonist, inhaled in
increasing concentrations is most commonly
used.
• A provocative dose producing a 20% drop in
FEV1 (PD20) is calculated, with a value ≤400 μg
indicative of airway reactivity.
ADJUNCTIVE ASSESSMENT TOOLS
• Eosinophil Counts:
• Patients not treated with ICSs will have
eosinophil counts ≥300 cells/μL
• Eosinophil counts correlate with severity of
disease in population studies.
• IgE, Skin Tests, and Radioallergosorbent Tests:
• Useful in considering whether patients
with severe asthma would be eligible for
anti-IgE therapy.
• Exhaled Nitric Oxide (FeNO):
• It is an approximate indicator of
eosinophilic inflammation in the airways.
• It is easily suppressed by ICSs and, thus,
can be used to assess adherence in
patients.
13. MEDICATIONS
1. Bronchodilators:
A. β2 –Agonists
Short acting Long acting Ultra long acting
Albuterol
Levalbuterol
Metaproterenol
Pirbuterol (Maxair)
ONSET: 3-5 mins
DURATION: upto 4 hours
Most commonly
administered by MDI
Salmeterol
Formoterol
DURATUON: upto 12 hours
Prophylaxis of exercise-
induced bronchospasm
iIndacaterol
olodaterol
vilanterol
DURATION:24-hours
They are only used in
combination with ICSs in
the treatment of asthma.
14. B. Anticholinergics
• Smooth-muscle relaxation by antagonizing the cholinergic nerve–induced smooth
muscle constriction.
• The long-acting agents in this class are known as long-acting muscarinic antagonists
(LAMAs).
2. Controller (Anti-Inflammatory/Antimediator) Therapies
A. Corticosteroids
• Reduce airway hyperresponsiveness, improve airway function, prevent asthma
exacerbations, and improve asthma symptoms.
• Corticosteroid use by inhalation (ICSs) minimizes systemic toxicity and represents a
cornerstone of asthma treatment.
15. ICS and ICS/LABA Oral Corticosteroids Intravenous
Corticosteroids
Intramuscular
Corticosteroids
• Cornerstone of
asthma therapy
• First-line therapy for
all forms of persistent
asthma.
• Their effects can be
noticeable in several
days, but continued
improvement may
occur over months of
therapy.
• Chronic oral
corticosteroids (OCSs)
at the lowest doses
possible (due to side
effects) are used in
patients who cannot
achieve acceptable
asthma control.
• OCSs are also used to
treat asthma
exacerbations,
frequently at a dose of
40–60 mg/d of
prednisone.
Intravenous preparations
are frequently used in
hospitalized patients.
In high-risk, poorly
adherent patients,
intramuscular
triamcinolone acetonide
has been used to achieve
asthma control and
reduce exacerbations.
16. B. Leukotriene Modifiers:
• Eg: Montelukast (Singulair)
Zafirlukast (Accolate)
Zileuton (Zyflo)
• Leukotriene modifiers are effective in preventing exercise-induced bronchoconstriction
without the tachyphylactic effects that occur with regular use of LABAs.
• Leukotriene modifiers are particularly effective in aspirin-exacerbated respiratory
disease, which is characterized by significant leukotriene overproduction.
• They have also shown modest effect as add-on therapy in patients poorly controlled on
high-dose ICS/LABA.
17.
18.
19.
20.
21. ACUTE SEVERE ASTHMA
• Acute severe asthma, previously called status asthmaticus, is defined as bronchospasm that does
not resolve despite usual treatment and is considered life threatening.
22. MANAGEMENT:
Initial assessment:
• Ability to speak
• Vital data
• ABG
• Measurement of PEF
Treatment
• Oxygen (goal: SaO2 > 92%)
• High dose of bronchodilators
(SABA via nebulisation)
• Systemic corticosteroids
• IVF
Subsequent management
• IV Magnesium sulphate
• IV β2 agonists
• IV Aminophylline
• IV LTRA
• Anaesthetics
23.
24. Management of Anaesthesia
• The occurrence of severe bronchospasm has been reported in 0.2% to 4.2% of all procedures
involving general anesthesia performed in asthmatic patients.
• Risk factors:
type of surgery (risk is higher with upper abdominal surgery and oncologic surgery) and
the proximity of the most recent asthmatic attack to the date of surgery
A. PRE OPERATIVE ASSESSMENT/MANAGEMENT:
• Emphasis should be on determining the severity and recent course of the disease.
• Preoperative evaluation begins with a history to elicit the severity and characteristics of the
patient’s asthma.
• PFTs (especially FEV1) performed before and after bronchodilator therapy may be indicated in
patients scheduled for major surgery.
FEV1:FVC ratio that is less than 65% of predicted, is usually considered a risk factor for
perioperative respiratory complications.
25. • Measurement of arterial blood gases is
indicated if there is any question about the
adequacy of ventilation or oxygenation.
• Chest physiotherapy, antibiotic therapy, and
bronchodilator therapy during the preoperative
period can often improve reversible
components of asthma.
• Bronchodilators should be continued up to the
time of surgery.
• If the patient is currently on or has been
treated with high doses of systemic
corticosteroids within the past 6 months,
supplementation with stress-dose
hydrocortisone or methylprednisolone may be
indicated.
26. B. INTRAOPERATIVE MANAGEMENT :
• The most critical time for asthmatic patients undergoing anesthesia is during instrumentation of
the airway.
• Pain, emotional stress, or stimulation during light general anesthesia can precipitate
bronchospasm.
• Drugs often associated with histamine release (e.g. atracurium, morphine, and meperidine)
should be avoided or given very slowly when used.
INDUCTION:
• Propofol is often used for induction in a hemodynamically stable asthmatic patient. It produces
smooth muscle relaxation and contributes to decreased airway resistance.
• Ketamine is a preferred induction drug in a hemodynamically unstable patient with asthma.
• Sevoflurane is the preferred inhalational anesthetic agent as it produces more profound
bronchodilation compared to isoflurane.
• An alternative method to suppress airway reflexes before intubation is IV or intratracheal
injection of lidocaine (1–1.5 mg/kg).
• Administration of opioids prior to intubation can help prevent increased airway resistance.
27. • Insertion of an LMA is less likely to result in
bronchoconstriction than insertion of an ETT.
• In asthmatic patients, sufficient time must be
provided for exhalation.
• Ventilation should incorporate warmed
humidified gases whenever possible.
• Severe bronchospasm is manifested by rising
peak inspiratory pressures and incomplete
exhalation.
• Tidal volumes of 6 mL/kg, with prolongation of
the expiratory time, may allow more uniform
distribution of gas flow to both lungs and may
help avoid air trapping.
• The PaCO2 may increase, which is acceptable if
there is no contraindication from a
cardiovascular or neurologic perspective.
28. REVERSAL:
• Reversal of nondepolarizing neuromuscular blocking agents with anticholinesterase agents
generally does not precipitate bronchoconstriction if preceded by the appropriate dose of an
anticholinergic agent.
• Sugammadex avoids the issue of increasing acetylcholine concentration; however, cases of
allergic reaction to sugammadex have been reported.
• Deep extubation (before the return of airway reflexes) reduces the risk of bronchospasm on
emergence. Lidocaine as a bolus (1.5–2 mg/kg) may help to obtund airway reflexes upon
emergence.
29. COPD
Chronic obstructive pulmonary disease (COPD) is defined as a disease state characterized by
persistent respiratory symptoms and airflow obstruction (https://goldcopd.org/2021-gold-reports/).
• INCLUDES:
• Emphysema (an anatomically defined condition characterized by destruction of the lung
alveoli with air space enlargement).
• Chronic bronchitis (a clinically defined condition with chronic cough and phlegm)
and/or
• Small airway disease (a condition in which small bronchioles are narrowed and reduced in
number)
30. CHRONIC BRONCHITIS
• The clinical diagnosis of chronic
bronchitis is defined by the
presence of a productive cough on
most days of 3 consecutive
months for at least 2 consecutive
years.
• In patients with COPD, chronic
hypoxemia leads to
erythrocytosis, pulmonary
hypertension, and eventually right
ventricular failure; this
combination of findings is often
referred to as the “blue
bloater” syndrome.
EMPHYSEMA
• Characterized by irreversible
enlargement of the airways distal
to terminal bronchioles and
destruction of alveolar septa
• Significant emphysema is more
frequently related to cigarette
smoking. Less commonly,
emphysema occurs at an early age
and is associated with deficiency
of α1 -antitrypsin.
• When dyspneic, patients with
emphysema often purse their lips
to delay closure of the small
airways, which accounts for the
term “pink puffers” that is often
used.
34. TREATMENT OF COPD
• The first and most important step in treating COPD is
reducing exposure to smoking and environmental
irritants.
• Smoking cessation in particular can significantly
decrease disease progression and lower mortality by
as much as 18%.
• Symptoms of chronic bronchitis can diminish or
entirely disappear.
• Pharmacologic treatment usually begins with
inhalers, specifically long-acting muscarinic
antagonist.
• If dyspnea persists, long-acting β2 agonist can
be added.
• A third therapy with inhaled glucocorticoids is
most effective when symptoms are associated
with asthma, rhinitis.
35. MANAGEMENT OF ANAESTHESIA
A. Preoperative Management
• Questioned about recent changes in dyspnea,
sputum, and wheezing.
• Any previous need for noninvasive positive
pressure ventilation (NIPPV) or mechanical
ventilation should also be determined.
• Patients should also be questioned on the
presence and severity of concomitant diseases.
• PFTs should be viewed as a management tool
to optimize preoperative pulmonary function
but not as a means to predict risk.
36. Risk Reduction Strategies:
Preoperative strategies :
1. Smoking cessation:
• The maximum benefit of smoking
cessation is not usually seen unless
smoking is stopped more than 8 weeks
prior to surgery.
• However, patients should always be
counseled to stop smoking irrespective of
the time of encounter before surgery.
• Cessation of smoking for as little as 24 h
has theoretical beneficial effects on the
oxygen-carrying capacity of hemoglobin.
Effects of smoking cessation:
• The adverse effects of carbon monoxide on
oxygen-carrying capacity and of nicotine on
the cardiovascular system are short lived.
• Within 12 hours after cessation of
smoking, the PaO2 at which hemoglobin is
50% saturated with oxygen (P50) increases.
• Improvement of ciliary and small airway
function and decreased sputum production
occur slowly over weeks after smoking
cessation.
37. 2. Nutritional status:
• Poor nutritional status with a low serum albumin
level (3.5 mg/dL) is a powerful predictor of
postoperative pulmonary complications in COPD
patients.
• Malnutrition can increase the risk of prolonged
postoperative air leaks after lung surgery.
3. Preoperative incentive muscle training:
• Patients should be advised to do deep breathing
exercises or incentive spirometry, which may
improve respiratory function postoperatively.
Intraoperative strategies :
• Regional anesthesia is preferred over general
anesthesia in patients with COPD.
• However, an interscalene block can cause
ipsilateral phrenic nerve palsy and should be
avoided in patients with severe COPD.
• General anaesthesia:
• desflurane may cause irritation of the bronchi
and increased airway resistance, thereby
limiting its usefulness during induction and
emergence in patients with severe airway
reactivity.
• Goals of mechanical ventilation should be to avoid
dynamic hyperinflation of the lungs and prevent
development of auto-PEEP.
• Interventions to mitigate air trapping include:
(1) allowing more time to exhale by decreasing
both the respiratory rate and
inspiratory/expiratory (I:E) ratio
(2) allowing permissive hypercapnia
(3) applying low levels of extrinsic PEEP; and
(4) aggressively treating bronchospasm.
38. Postoperative strategies:
• Prevention of postoperative pulmonary
complications is based on maintaining
adequate lung volumes, especially FRC, and
facilitating an effective cough.
• Lung expansion maneuvers:
Lung expansion maneuvers (deep breathing
exercises, incentive spirometry, chest
physiotherapy, positive pressure ventilation)
have proven benefits in preventing
postoperative pulmonary complications in
high risk patient.
• Continuous positive airway pressure (CPAP) is
reserved for the prevention of postoperative
pulmonary complications in patients who are
not able to perform deep-breathing exercises
or incentive spirometry.
• Patients with an FEV1 below 50% may require a
period of postoperative ventilation, particularly
following upper abdominal and thoracic
operations.
• When continued mechanical ventilation is
necessary, FiO2 and ventilator settings should
be adjusted to keep the SpO2 around 90% and
the PaCO2 in a range that maintains normal
arterial pH (7.35–7.45).
• Early mobilization postoperatively can decrease
pulmonary complications by promoting deeper
breathing, lung expansion, and cough.
GINA defines asthma as “heterogenous disease, usually characterised by chronic airway inflammation”.
Others:
family history of asthma, maternal smoking during pregnancy, viral infections (especially with rhinovirus and infantile RSV)
; TSLP, thymic stromal lymphopoietin
Regular use has been associated with tachyphylaxis of the bronchoprotective effect.
at higher doses, they can produce tremor, tachycardia, palpitations, and hypertension. They promote potassium reentry into cells, and at high doses, they can produce hypokalemia.
Lama e.g. aclidinium, darotropium, tiotropium
GINA, as part of a comprehensive strategy of asthma management, recommends ICS/formoterol be used as the reliever in all steps of asthma severity, including intermittent asthma
GINA, as part of a comprehensive strategy of asthma management, recommends ICS/formoterol be used as the reliever in all steps of asthma severity, including intermittent asthma (Step 1). NAEPP guidelines utilizing evidence-based studies recommend that ICS/ formoterol be used as the reliever medication in patients requiring step 3 and 4 therapy
Ketamine should probably not be used in patients with high theophylline levels, as the combined actions of the two drugs might precipitate seizure activity.
but muscle rigidity caused by an opioid could decrease lung compliance and impair ventilation. Opioid-induced muscle rigidity can be decreased by the combined use of IV anesthetics and neuromuscular blocking drugs.
Note that intratracheal lidocaine itself can initiate bronchospasm if an inadequate dose of induction agent has been used.
but less than 5% of patients with COPD fit this description.
Upon long-term exposure to cigarette smoke in genetically susceptible individuals, lung epithelial cells and T and B lymphocytes recruit inflammatory cells to the lung. Biological pathways of protease-antiprotease imbalance, oxidant/antioxidant imbalance, apoptosis, and lung repair lead to extracellular matrix destruction, cell death, chronic inflammation, and ineffective repair
Physiologic Testing:
The BODE index is a grading system that takes into account the patient’s body mass index, degree of airflow obstruction, level of dyspnea, and exercise tolerance to assess overall prognosis. Higher BODE scores indicate greater risk of COPD exacerbations, hospitalizations, and death as a result of pulmonary complications.