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ketki asthma.pptx HDU/ICU care HDU/ICU care
1.
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
3. ⚫oneof the mostcommonchronic diseasesworldwide
(estimated 300 millionaffected)
⚫Prevalence increasing especially in children
⚫Mean ageof onset- 4 years
⚫a majorcauseof school and work absence
⚫very high health careexpenditure
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 presenceof airflow limitation
⚫ reduced FEV1/FVC
⚫ healthy adults >0.75 – 0.80/ >0.90 in children
⚫Confirm variation in lung function
⚫ greaterthevariation/ frequencyof variation - greater
probability of diagnosis
⚫ Excessive bronchodilatorreversibility (adults: FEV1>12%
and >200mL; children: >12% predicted)
⚫ Excessivediurnal variability from 1-2 weeks’ twice-daily
PEF monitoring
⚫ Significant increase in FEV1 or PEF after 4 weeksof controller
treatment
Diagnosis of asthma – variable
airflow limitation
GINA 2015, Box 1-2
11. Acute severe asthma
-Clinical Definition
⚫Severeasthma that fails torespond 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
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
25. IV lignocaine
⚫increases the histamine threshold
⚫blocks thecough reflex
⚫may be given todecrease theairway responses
associated with intubation(local sprayas well)
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 upof 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 puffswith 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 hourlyorprednisolone
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
36. ⚫Spinal anaesthesia or plexus/nerve blocks - safe
provided the patient isable to lie flat comfortably
37. ⚫Analgesic requirement post op similar to a normal
patient
⚫NOT in a higher risk of respiratory depression with
opiods
⚫NSAIDS’s avoided with patients who are sensitive
38. Post op management
⚫Patientswith severedisease/ majorthoracicand
abdominal surgeries- POST OP HDU/ICU care
⚫Adequateanalgesia- epidurals preferred( avoid dense
intercostal blockade)
- regularopioids/ pethidine
- NSAID’s if previously tolerated
⚫Supplemental O2
⚫Regular nebulisation/ b2 agonists sos/ Ipratropium?
⚫Continuesteroids
40. Treatment of Acute Severe Asthma
Principles and Primary Goals of care
⚫Relieve airflow limitation: bronchodilatortherapy
⚫Treat airway inf lammation: 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
⚫ 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
⚫ 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)
48. Corticosteroids
⚫ Mechanism:
⚫ Systemically reduce inflammation, decrease mucus production, and
enhance theeffects of B2-agonists
⚫ Prevents the sustained inflammatory phase which occurs 6-8 hours
afterallergen 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 severeasthma, steroids should beadministered IV toassure
adequatedrug delivery in a timely manner
49. Corticosteroid
s
⚫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
50. Corticosteroids: Side effects
⚫Short-term use of high-dose steroids
⚫Hyperglycemia
⚫Hypertension
⚫Acute psychosis
⚫Prolonged steroid
⚫Immunosuppression
⚫Hypothalamic-pituitary-adrenal axis suppression,
⚫Osteoporosis
⚫Myopathy
⚫Weakness
51. Magnesium Sulfate
⚫Mechanism:
⚫Inhibits Ca2+ influx into cytosol smooth muscle
relaxant
⚫Increases B2 agonistaffinity for its receptor, thereby
potentiating its effect
⚫Inhibits histamine release from mastcells
⚫40 mg/kg IV over 20-30 min with maxof 2 g
⚫Repeatonceor twiceafter 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).
⚫ Cardiacarrhythmia/ complete heart block
⚫ Respiratory failuredue to severe muscleweakness
⚫ Sudden cardiopulmonaryarrest
⚫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
54. Aminophylline Toxicity
-Narrow Therapeutic range -10 – 20 mcg/ml
⚫ Nauseaand vomiting
⚫ Tachycardia
⚫ Agitation
⚫ Severe toxicity (high serum concentrations)
⚫ Cardiacarrhythmias
⚫ Hypotension
⚫ Seizures
⚫ Death
⚫ Monitordrug level in blood:
⚫ 8hrafterdrug initiation and thenevery morning
58. Relative indications
⚫Poorresponse to initial management
⚫ fatigueand somnolence
⚫ cardiovascularcompromise
⚫developmentof a pneumothorax
⚫Hypercapnia???
59. Intubation Tips
⚫ 50% of life threatening complications occur during induction
⚫ Carried outvia the most senior memberof anaesthetic team
⚫ Preoxygenatewith 100% oxygen
⚫ RSI
⚫ Anticipate hypotension – preload/ vasopressors readyat hand
⚫ If profound hypotension- disconnect from circuitand allow
passiveexpiration
⚫ Cuffed ET tube with the largestappropriatediameter
⚫ Avoid histamine-producing agents like morphineoratracurium
⚫ Ketamine: preferred induction agentdue to its bronchodilatory
action
⚫ Avoid overenthusiastic hand ventilation
60. Sedation, Analgesia and Muscle
Relaxants
Is sedation needed atall?
⚫ Propofol+fentanyl
⚫ Ketamine+midazolam
⚫ Morphine???
Initial muscle relaxation needed
⚫ Rocuroniumor pancuronium preferred
⚫ Vecuronium /atracurium
( Neuromyopathy with vecuronium
Histaminereleasewith atracurium)
- should discontinueas earlyas 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
⚫Attempt extubation as soon as possible
62. ⚫In Volume controlled ventilation
- P plat< 35cmH2o and pH>7.2
- P plat > 30cmH2 o – reduce minuteventilation( Vt or Rate)
-pH < 7.2 / P plat < 35cmH2O- increase MV
- pH<7.2/ Pplat > 35cmH2O- no change
⚫ minuteventilation is the most importantdeterminant
of hyperinflation
⚫the risk of barotrauma is proportional toend inspiratory
lung volume
63. Management of hypercarbia
⚫hypercapnia -well tolerated
⚫BUT- cerebral hypoxia secondary toa respiratory
arrest
ICP managementof hypercarbia
extracorporeal CO2 removal
64. Extra-corporeal support FOR CO2 elimination
⚫extra-corporeal membraneoxygenation
⚫Novalung
⚫Buffering- Bicarbonate/ Tromethamine (THAM)
⚫Measures to limit CO2 production-anti-pyretics /
activecooling
65. Dynamic hyperinflation (gas-trapping) due to
excessiveventilation — especially in the patientwith
bronchospasm.
Hypovolemia exacerbated bydecreased venous
returndue to positive intrathoracic pressure.
Vasodilation and myocardial depression due to the
inductiondrugs used forrapid sequence intubation
(e.g. thiopentone, propofol).
Tension pneumothorax due topositive-pressure
ventilation.
Hypotension following intubation !
66. Typical Ventilator Setting
⚫VT of 6–8 mL/kg,
⚫RR approximately half of the normal forage
⚫I: E ratioof 1:3 /1:4
⚫PEEP of 2–3 cm of H2O
⚫In infants, pressurecontrolled ventilation: adjust PIP
toachieve adequateventilation
67. Other complications of mechanical ventilation
⚫cardiac stunning
⚫Arrhythmia
⚫ rhabdomyolysis
⚫lacticacidosis
⚫Myopathy
⚫ CNS injury
69. Heliox
⚫ Mechanism:
⚫ Low-densitygas that increases laminar flow of oxygen and
decreases turbulent flow.
⚫ Reduce work of breathing in spontaneously breathing patients
⚫ Adjunct therapy
⚫ Forpatientsunresponsivetoconventional therapy
⚫ Children on high-pressure mechanical ventilatory support
⚫ Dosing: 60%/40% or 80%/20% helium/O2
⚫ No systemic sideeffects
-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
72. Chest Physiotherapy
⚫Useful in patientswith segmental or lobaratelectasis.
⚫In others no therapeutic benefit in thecritically ill
patientwith severeasthma.
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
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¶
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.
