This document discusses the definition, diagnosis, treatment and management of asthma. It begins by defining asthma as a chronic inflammatory airway disease characterized by variable and recurring symptoms. It then discusses the diagnosis of asthma based on symptoms and evidence of variable airflow limitation. The document outlines treatment for acute severe asthma which focuses on relieving airflow limitation through bronchodilators and treating inflammation with corticosteroids. Key medications discussed include nebulized beta-agonists, ipratropium, systemic corticosteroids, and magnesium sulfate. Perioperative management and considerations are also reviewed.
A basic overview on the management of intra-operative bronchospasm: the risk factors, triggers, diagnosis, prevention and management. Includes a case scenario – discussion.
A basic overview on the management of intra-operative bronchospasm: the risk factors, triggers, diagnosis, prevention and management. Includes a case scenario – discussion.
Pre-oxygenation is: safe, simple, cheap, effective, well-tolerated. This article provides a compelling argument in favour of pre-oxygenation prior to all general anaesthesia.
mapleson circuits used in anesthesia practice, are in their way out but it is as important to know the mechanism with which the gases flow to and fro through them.
Asthma is a chronic inflammatory condition associated with airway hyperresponsiveness (an exaggerated airway-narrowing response to specific triggers such as viruses, allergens and exercise).
Physiotherapy can provide relief from symptoms of uncontrolled asthma, including coughing, wheezing, tightness in the chest, shortness of breath and QOL.
Pre-oxygenation is: safe, simple, cheap, effective, well-tolerated. This article provides a compelling argument in favour of pre-oxygenation prior to all general anaesthesia.
mapleson circuits used in anesthesia practice, are in their way out but it is as important to know the mechanism with which the gases flow to and fro through them.
Asthma is a chronic inflammatory condition associated with airway hyperresponsiveness (an exaggerated airway-narrowing response to specific triggers such as viruses, allergens and exercise).
Physiotherapy can provide relief from symptoms of uncontrolled asthma, including coughing, wheezing, tightness in the chest, shortness of breath and QOL.
Internal medicine review for national license examination 2 Santi Silairatana
Internal Medicine review, with focus on pulmonary medicine and critical care medicine including pneumonia, asthma, COPD, tuberculosis, and sepsis & septic shock. Intended to be used for medical students.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
2. Definition of asthma
A heterogeneous disease with
chronic airway inflammation
Defined by
- history of respiratory symptoms
(wheeze, SOB, chest tightness and
cough)
-that vary over time and in intensity
-variable expiratory airflow
limitation
GINA-2015
Airway inflammation
obstruction
3. one of the most common chronic diseases worldwide
(estimated 300 million affected)
Prevalence increasing especially in children
Mean age of onset- 4 years
a major cause of school and work absence
very high health care expenditure
Epidemiology
5. based on:
A history of characteristic symptom patterns
Evidence of variable airflow limitation,
( from bronchodilator reversibility testing or other tests )
Diagnosis of asthma
GINA 2015
6. Confirm presence of airflow limitation
reduced FEV1/FVC
healthy adults >0.75 – 0.80/ >0.90 in children
Confirm variation in lung function
greater the variation/ frequency of variation - greater
probability of diagnosis
Excessive bronchodilator reversibility (adults: FEV1>12%
and >200mL; children: >12% predicted)
Excessive diurnal variability from 1-2 weeks’ twice-daily
PEF monitoring
Significant increase in FEV1 or PEF after 4 weeks of controller
treatment
Diagnosis of asthma – variable
airflow limitation
GINA 2015, Box 1-2
9. Assessment of severity
Becker Asthma score
A score >4 is moderate acute severe asthma
score 7 and above is severe and needs ICU admission
10. Assessment of severity
Clinical Asthma score
A score >4 is impending Resp failure
Score 7 and above is Resp failure
11. Acute severe asthma
-Clinical Definition
Severe asthma that fails to respond to
inhaled β2 agonists
oral or IV steroids and O2
requires admission to the hospital for treatment
12. Pathophysiology in Acute severe
asthma
Pathologic changes in the airway airflow
obstruction premature airway closure on expiration
dynamic hyperinflation hypercarbia
Dynamic hyperinflation or “air-trapping” also leads to
ventilation / perfusion (V/Q) mismatching causing
hypoxemia
Prolonged respiratory acidosis- pulmonary
hypertension
13. Acute Asthma Management
Clinical and Laboratory Assessment
Assess clinically – accessory muscle use,
tachypnea, tachycardia, diaphoresis, pulsus
paradoxus, exhaustion.
Assess airflow limitation – peak flow
measurement.
Assess oxygenation – pulse oximetry.
Assess for hypercapnia –somnolent, fatigued,
difficulty with speech, elderly, concomitant use of
sedatives.
Imaging – chest X ray
Blood work – CBC, glucose
15. Preop assessment
History
frequency of symptoms/ sputum production
asthma triggers/Allergies
recent URTI
activity level/ exercise tolerance
previous history of surgery and anaesthesia
hospitalizations and emergency department
attendance
drug history-use and effectiveness of medication
NSAID/aspirin induced asthma
16. Examination
wheezing
Cough
Respiratory rate
use of accessory muscles
cyanosis
changes in mental status
Spo2 value as baseline
17. CXR
Limited role but indicated in-
First time wheezers
Clinical evidence of parenchymal disease
Suspected pneumothorax or pneumonia
underlying cause in doubt
suspected pulmonary hypertension ( + ECG)
18. ABG
Not routnely indicated
severe asthma (poorly controlled, frequent hospital
admissions, previous ICU admission)
major surgery
PaO2< 60 mmHg or PaCO2> 45mmHg- impending
respiratory failure
19. Preop optimization
mild asthma
- nebulized β2-adrenergic agonist 30 mnts prior to
surgery
moderate asthma
- additional optimization with any inhaled anti-
inflammatory agent and consistent use of nebulized
β2 agonists 1 week prior to surgery
severe persistent asthma
- optimize treatment with consultation with physician
- short-term oral corticosteroid therapy
Preop chest physiotherapy in major thoracic and
abdominal surgeries
22. Antibiotics
Not routinely indicated
Reserved for patients with evidence of bacterial
infection
High fever
Purulent secretions
Consolidation on X ray film
Very high leucocyte counts
23. Intraop management
Induction
Propofol
- inhibits bronchoconstriction
- increases central airway dilation by directly relaxing
the airway smooth muscle
- decrease the possibility of bronchospasm during
induction.
( may not be suitable for haemodynamically unstable
patients)
TPS ???
24. Ketamine
Direct bronchodilatory properties
decrease the possibility of bronchospasm with
induction
increases bronchial secretions
(an anticholinergic drug such as glycopyrrolate or
atropine is useful)
25. IV lignocaine
increases the histamine threshold
blocks the cough reflex
may be given to decrease the airway responses
associated with intubation(local spray as well)
29. Muscle relaxation
Vecuronium, Rocuronium, Cisatracurium and
Pancuronium
stimulate the M2 and M3 muscarinic receptors
evenly
do not cause bronchoconstriction
Atracurium and mivacurium
dose-dependently release histamine
trigger bronchoconstriction
Well controlled asthmatics –routine doses -OK
30. Intubation
avoidance of any stimulation of the airway
avoidance of tracheal intubation preferred unless
airway protection needed
LMA - less stimulating
ET insertion in a deep plane of anaesthesia
Avoiding carinal stimulation
31. Maintenance
Bronchodilatory inhalational agents
A method to administer another bronchodilatory
agent
Observe for bronchospasms
How?
Exclude other causes of airway obstruction
32. Severe bronchospasms during anaesthesia
Common following intubation
Exclude blocked tubes/circuits
100% O2
Deepen anaesthesia ( inhalational/ IV- ketamine preferred)
Higher inflation pressures may be needed
minimise build up of auto PEEP
( gas trapping and positive pressure build up in obstructed
alveoli in expiration)
- slower respiratory rates
( 6-8/min in adults)
Hypercarbia tolerated
33. B2 agonist inhaler 6-8 puffs with a special adaptor in to
ETT
IV salbutamol if not responding (250 mcg slow bolus
then 5–20 mcg/min)
Hydrocortisone 100 mg IV 6 hourly or prednisolone
orally 40–50 mg/day.
Magnesium 2g IV over 20 minutes
Aminophylline 5mg/kg IV followed by infusion
34. Adrenaline - in extremis (decreasing conscious level or
exhaustion)
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
S/C or IM administration (0.5–1 mg) if IV access not
available
risk of arrhythmias in the presence of hypoxia and
hypercapnia
35. Extubation
Elective cases- deep extubation unless contraindicated
Emergency/ full stomach situations
- fully awake extubation with prior redosing of inhaled
β2-agonists
Avoid reversal agents
( Neostigmine/pyridostigmine- increased secretions and
air way hyperactivity)
36. Spinal anaesthesia or plexus/nerve blocks - safe
provided the patient is able to lie flat comfortably
37. Analgesic requirement post op similar to a normal
patient
NOT in a higher risk of respiratory depression with
oipiods
NSAIDS’s avoided with patients who are sensitive
38. Post op management
Patients with severe disease/ major thoracic and
abdominal surgeries- POST OP HDU/ICU care
Adequate analgesia- epidurals preferred( avoid dense
intercostal blockade)
- regular opioids/ pethidine
- NSAID’s if previously tolerated
Supplemental O2
Regular nebulisation/ b2 agonists sos/ Ipratropium?
Continue steroids
39. Worsening dyspnoea/ wheezing post op
- Exclude heart failure/ pul. Embolism/ pneumothorax
40. Treatment of Acute Severe Asthma
Principles and Primary Goals of care
Relieve airflow limitation: bronchodilator therapy
Treat airway inflammation: steroids
Treat hypoxemia or hypercapnia if present
Life threatening asthma
42. Nebulized b2 agonists
Mainstay of therapy
Salbutamol and terbutaline have relative β2-selectivity.
Short-acting b2-agonists (e.g. salbutamol) - given repeatedly in 5 mg
doses or by continuous nebulization at 10 mg/ h driven by oxygen
No difference in clinical response to treatment with racemic salbutamol
vs lev-salbutamol in acute severe asthma in children
Qureshi F. et al. Ann Emerg Med. 2005;46:29–36.
MDI
4-8 puffs (100 mcg each) per dose
MDI with a holding chamber is at least as effective as nebulized
salbutamol in young children with moderate to severe asthma
exacerbations
Continued until a clinical response seen or side effects occur
Oral/s/c / IV routes
43. Intravenous β2-agonists
Not to give routinely in acute exacerbations
Travers A. et al. Cochrane Database Syst Rev. 2001; (2): CD002988.
Use in patients unresponsive to inhaled β2-agonists
Those in whom nebulization is not feasible
Intubated patients
patients with poor air entry
IV Salbutamol 5-20mcg/min
IV Terbutaline
Loading 10 mcg/kg IV over 10 min, followed by continuous infusion at
0.1–10 mcg/kg/min.
70% develop lactic acidosis 2-4hrs after IV therapy
44. Subcutaneous β2 agonist
Primarily used for children with no IV access
As a rapidly available adjunct to inhaled β2 agonist.
Subcutaneous terbutaline 0.01 mg/kg/dose (max of 0.3
mg)
May be repeated every 15–20 min for up to three doses
Not recommended for acute severe asthma!
45. Adverse effects of β2-agonists
Cardiovascular system
Tachycardia
Increased QTc interval
Dysarrhythmia
Hypertension
46. Adverse effects of β2-agonists
Excessive CNS stimulation
Hyperactivity
Tremors
Nausea with vomiting
Hypokalemia
Hyperglycemia
Long acting B2 agonists- NO PLACE in acute severe
asthma ( associated with increased mortality)
47. Nebulized ipratropium bromide
for all patients with life-threatening asthma
added to nebulized b2 agonists treatment (500 mcg 4
hourly)
Mechanism:
Muscarinic agonist (anticholinergic)
M1 receptor decrease cGMP decreases intracellular Ca2+
Synergistic effects with beta agonists
Minimal side effects
( Dry mouth, bitter taste, flushing, tachycardia, and
dizziness, unilateral pupillary dilation (local effect)
48. Corticosteroids
Early as possible- improve survival
Parenteral: preferred for critically ill
Oral: equal efficacy if it can be given
Aerosolized: limited role in severe asthma
Effect starts in 1–3 h and reach at max in 4–8 h
49. Corticosteroids
Mechanism:
Systemically reduce inflammation, decrease mucus production, and
enhance the effects of B2-agonists
Prevents the sustained inflammatory phase which occurs 6-8 hours
after allergen exposure
Dosing:
Hydrocortisone: 10 mg/kg followed by 5 mg/kg 6hrly
Methylprednisone: 0.5–1 mg/kg IV 6h (2-4 mg/kg/day)
Dexamethasone: 0.15 mg/kg/dose 4-6 hrly
Prednisolone: 1-2 mg/kg/day
Duration 5-7 days
In severe asthma, steroids should be administered IV to assure
adequate drug delivery in a timely manner
51. Magnesium Sulfate
Mechanism:
Inhibits Ca2+ influx into cytosol smooth muscle
relaxant
Increases B2 agonist affinity for its receptor, thereby
potentiating its effect
Inhibits histamine release from mast cells
40 mg/kg IV over 20-30 min with max of 2 g
Repeat once or twice after 4–6 h
Nebulised form- no benefit
52. Magnesium -Side effects
Hypotension
CNS depression
Muscle weakness
Flushing
Very high serum magnesium levels (usually >10–12 mg/dL).
Cardiac arrhythmia/ complete heart block
Respiratory failure due to severe muscle weakness
Sudden cardiopulmonary arrest
Treatment: IV Calcium Gluconate
53. Aminophylline
Mechanism
Xanthine derivative
Decreases intracellular Ca2+
Inhibits TNF-alpha and leukotriene synthesis
Loading dose: 5 mg/kg over 20 min IV
Continuous infusion: 0.5–0.75mg/kg/min IV
Limited role in unresponsive to steroids, inhaled and IV β2
agonist, and O2 with severe asthma
Ream RS et al. Chest 2001;119:1480–8.
54. Aminophylline Toxicity
-Narrow Therapeutic range -10 – 20 mcg/ml
Nausea and vomiting
Tachycardia
Agitation
Severe toxicity (high serum concentrations)
Cardiac arrhythmias
Hypotension
Seizures
Death
Monitor drug level in blood:
8hr after drug initiation and then every morning
58. Relative indications
Poor response to initial management
fatigue and somnolence
cardiovascular compromise
development of a pneumothorax
Hypercapnia???
59. Intubation Tips
50% of life threatening complications occur during induction
Carried out via the most senior member of anaesthetic team
Preoxygenate with 100% oxygen
RSI
Anticipate hypotension – preload/ vasopressors ready at hand
If profound hypotension- disconnect from circuit and allow
passive expiration
Cuffed ET tube with the largest appropriate diameter
Avoid histamine-producing agents like morphine or atracurium
Ketamine: preferred induction agent due to its bronchodilatory
action
Avoid overenthusiastic hand ventilation
60. Sedation, Analgesia and Muscle
Relaxants
Is sedation needed at all?
Propofol+fentanyl
Ketamine+midazolam
Morphine???
Initial muscle relaxation needed
Rocuronium or pancuronium preferred
Vecuronium /atracurium
( Neuromyopathy with vecuronium
Histamine release with atracurium)
- should discontinue as early as possible
61. Ventilation Principles
Maintain adequate oxygenation
permissive hypercarbia with arterial pH of >7.2
Adjust minute ventilation
Slow ventilator rates
Avoid air trapping
Prolonged expiratory phase, short inspiratory time
Minimal PEEP< 5cmH2o
Stewart TE, Slutsky AS. Crit Care Med. 1996;24:379–80
Attempt extubation as soon as possible
62. In Volume controlled ventilation
- P plat< 35cmH2o and pH>7.2
- P plat > 30cmH2 o – reduce minute ventilation( Vt or Rate)
-pH < 7.2 / P plat < 35cmH2O- increase MV
- pH<7.2/ Pplat > 35cmH2O- no change
minute ventilation is the most important determinant
of hyperinflation
the risk of barotrauma is proportional to end inspiratory
lung volume
63. Management of hypercarbia
hypercapnia -well tolerated
BUT- cerebral hypoxia secondary to a respiratory
arrest
ICP management of hypercarbia
extra corporeal CO2 removal
64. Extra-corporeal support FOR CO2 elimination
extra-corporeal membrane oxygenation
Novalung
Buffering- Bicarbonate/ Tromethamine (THAM)
Measures to limit CO2 production-anti-pyretics /
active cooling
65. Dynamic hyperinflation (gas-trapping) due to
excessive ventilation — especially in the patient with
bronchospasm.
Hypovolemia exacerbated by decreased venous
return due to positive intrathoracic pressure.
Vasodilation and myocardial depression due to the
induction drugs used for rapid sequence intubation
(e.g. thiopentone, propofol).
Tension pneumothorax due to positive-pressure
ventilation.
Hypotension following intubation !
66. Typical Ventilator Setting
VT of 6–8 mL/kg,
RR approximately half of the normal for age
I: E ratio of 1:3 /1:4
PEEP of 2–3 cm of H2O
In infants, pressure controlled ventilation: adjust PIP
to achieve adequate ventilation
69. Heliox
Mechanism:
Low-density gas that increases laminar flow of oxygen and
decreases turbulent flow.
Reduce work of breathing in spontaneously breathing patients
Adjunct therapy
For patients unresponsive to conventional therapy
Children on high-pressure mechanical ventilatory support
Dosing: 60%/40% or 80%/20% helium/O2
No systemic side effects
-Colebourn CL et al. Anaesthesia 2007;62:34–42.
70. Noninvasive Mechanical
Ventilation
An alternative to conventional mechanical ventilation
in early phase
While weaning off conventional ventilator
Only found to be effective in mild to moderate asthma
No place in life threatening asthma
-Carroll CL, Schramm CM. Ann Allergy Asthma Immunol. 2006;96:454–9.
72. Chest Physiotherapy
Useful in patients with segmental or lobar atelectasis.
In others no therapeutic benefit in the critically ill
patient with severe asthma.
73. Leukotriene Modifiers
Little data to suggest a role for leukotriene modifiers in
acute asthma
It is not part of standard management of severe
asthma
Silverman RA et al. Chest 2004;126:1480–9.
TodiVK, Lodha R, Kabra SK. Arch Dis Child. 2010;95:540–3.
74. Bronchial thermoplasty
Controlled thermal energy to airway wall
Aim to reduce hyperresponsiveness and smooth
muscle mass
Found to be effective in long-term (5-year) and
relatively safe in severe asthma¶
¶ J Allergy Clin Immunol. 2013 Aug 30.
75. Anti-IgE therapy
Omalizumab
monoclonal antibody that blocks IgE
used in treatment of selected patients with moderate to
severe allergic asthma.
No place in life threatening asthma
More potent anti-IgE antibodies - in development
§ J Allergy Clin Immunol. 2003 Sep;112(3):563-70.
76. Humidified oxygen titrated to SpO2 90-92%
Nebulised beta-agonist bronchodilators
Nebulised anticholinergic drugs
Steroids: IV hydrocortisone or oral prednisone
First-tier therapies with strong supporting evidence
Second-tier therapies with weak supporting evidence
Intravenous beta-agonist bronchodilators for refractory bronchospasm
Methylxanthines
Nebulised adrenaline
Magnesium sulfate
Helium-oxygen mixture
Third-tier therapies without any supporting evidence
Ketamine
Volatile anaesthetics
ECMO in asthma
77. References
British Guideline on the Management of Asthma
-A national clinical guideline revised in 2012
GINA Guidelines for asthma management- revised in 2015
The ICU BOOK- 6TH EDITION 2012
Kumar & Clerk- 7th edition
Anaesthesia tutorial of the week –asthma and anaesthesia-
2005.05.16
Preoperative considerations for the patient with asthma
and bronchospasm:woods B.D Sladen R.N BJA103 I 57-65
78. Questions-
MD part II Anaesthesiology
1991-– Long essay
- Describe the assessment and preoperative preparation of a
severly asthmatic patient for elective abdominal surgery
2006- SAQ
- How would you asess a patient presenting with acute severe
asthma?
2011- SAQ
- A 19 year old patient with acute severe asthma is admitted
with severe respiratory distress to ICU
a) Describe your immediate management
b) What are the indications for mechanical ventilation?
c) How would you intubate and ventilate this patient?