Asthma

Definitions:
Chronic inflammatory disorder of the airways in which
• many cells and cellular elements play a role.
• In susceptible individuals, this inflammation causes
recurrent episodes of wheezing, breathlessness, chest
tightness, and coughing, particularly at night or in the
early morning.
• These episodes are associated with widespread but
variable airflow obstruction that is reversible either
spontaneously, or with treatment.
• Usually associated with airflow obstruction of
variable severity.
• Airflow obstruction is usually reversible, either
spontaneously, or with treatment
• The inflammation associated with asthma
causes an increase in the baseline bronchial
hyper responsiveness to a variety of stimuli
 Classification
• Extrinsic – implying a definite external cause
more frequently in atopic individuals
(atopic – individual which tends to develop
hypersensitivity by contact with allergens)
often starts in childhood - accompanied by
eczema
Eg. Dust mites, mold spores, animal dander,
cockroaches, pollen, indoor and outdoor
pollutants, irritants (smoke, perfumes, cleaning
agents)
• Intrinsic/ Late onset
no causative agent can be identified
starts in middle age
Eg. Pharmacologic agents (ASA, beta-blockers)
Physical triggers (exercise, cold air)
Physiologic factors
Stress, viral and bacterial URI, rhinitis
 Clinical signs
• Feeling of chest tightness
• Dyspnea
• Non productive cough
• wheeze
severe imminent failure
• Breathlessness-
• On lying down
• Speaking-Words cannot speak
• Level of consciousness- confused
Always agitated
• Breathing rate->30/min
• Muscle retraction- Usually paradoxical
movements
• Wheezing- Very strong absent
• Pulse/minute->120 bradycardia
 Goal of asthma treatment
• Prevent and treat acute episodes of asthma
• Control chronic and nocturnal symptoms
• Maintain normal activity, including exercise
• Minimize ER visits and hospitalizations
• Minimize need for reliever medications
• Maintain near-normal pulmonary function
• Avoid adverse effects of asthma medications
Managing acute exacerbation of asthma
Main aim is to
• Relieve airflow obstruction
• Hypoxemia as quickly as possible, and to plan prevention
of future relapses.
• Oxygen administration to maintain SpO2 >90%
• Inhaled Salbutamol/Terbutaline preferably by nebulizer
• with spacer with/without facemask
• 1-2 puffs every 2-4 minutes upto 10 puffs and repeat
every 20-30 minutes
3. Ipratropium Bromide 250 mcg by nebulizer
with Salbutamol
4. Inj. Hydrocortisone 10mg/kg IV
5. Inj. Aminophylline 5 mg/kg bolus slowly
followed by
0.8-1.2 mg/kg/hr slow infusion
6. Inj. Magnesium sulphate 40mg/kg in 50 ml 5%
dextrose as slow infusion over 30 minutes
 Two major group of drugs
• Bronchodilator drugs to relieve bronchospasm
and improve symptoms.
• Anti inflammatory drugs to treat the airway
inflammation and bronchial
hyperresponsiveness, the underlying cause of
asthma, i.e. to prevent attacks.
• Monitoring the effects of treatment
 Repeat Puff 15-30min after initiating treatment
 Pulse oximeter monitoring: maintain SaO2 >92 %.
 Check blood gases within 2h if: initial PaO2 was
normal
 raised or initial PaO2 <8 kPa (60mmHg) or patient
deteriorate
 Pneumothorax
• Pneumothorax-
is Air in pleural cavity
• Etiology-
traumatic and non traumatic causes
• Tension and open neumothorax
• S/S :
 V/S changes
• Tachypnea , dyspnea, SOB, Tachycardia, decrease of CO &
BP
 Cyanosis
 Hyper resonant note
 Diminished breath sounds
 Tracheal shift
 Displaced heart sounds
 Increased thoracic volume on the affected side
Emergency management

 Needle chest decompression at mid clavicle at 2 nd ICS

 Chest tube at the 5th ICS…….definitive

 Mechanical ventilation protocol

 Oxygen therapy protocol

 If open- three sided dressing

 Respiratory failure
• “inability of the lung to meet the metabolic
demands of the body.
• This can be from failure of tissue oxygenation
and/or failure of CO2 homeostasis.”
Causes
 Asthma, Croup, Diphtheria
 Laryngeal spasm
 Swelling after burns of the face
 Swallowing of corrosive poisons
 Direct injury caused by a blow
Mechanical Obstruction
 Solid foreign objects lodging in the respiratory
passage
• e.g. choking of food
 Accumulation of fluids in the back of the
throat (mucous ,blood or saliva)
 Aspiration (Inhalation of any solid or liquid
substance)
• Brain stem compression or Ischemia (Head injury,
intracranial diseases ….)
• Drugs: opiates, diazepam, Barbiturates, alcohol,
muscle relaxants, organo phosphorus poison
• Muscle spasm-tetanus
• Neurological; fracture cervical spine
• Pneumothorax, haemothorax, effusion
• Fractured ribs including flail chest
• Diaphragmatic injury
Potential cause of respiratory failure
 Clinical manifestations
• Tachypnea
• Paradoxical breathing
• Tachycardia/BP changes
• Cyanosis - bluish color of mucous membranes/skin
indicate hypoxemia
• Decreased O2 saturation (< 85%)
• Dyspnea - secondary to hypercapnia and hypoxemia
• Confusion, and coma
• Convulsions
• Bradycardia accompanied by gasping respirations, which
warn of the impending cardiac arrest.
Some patients show signs of CO2 retention;
• peripheral vasodilatation
• Full bounding pulse ( possibly with HTN)
• sweating
• dilatation of the pupils
• drowsiness
• muscle twitching
• coma
 Management of RF
• ABCD evaluation
• Airway management
• O2 therapy
• IV Hydration
• Mechanical Ventilation
• Underlying cause
 Supportive management
A. Airway Management
• clear the upper airway (if necessary –coma care)
• extending the neck and pulling jaw forward
• O2 by face mask
• Ambu bag or Intubation
• ready for tracheostomy under local anesthesia
B. Posture
• sit up if conscious
• postural drainage for secretions
• coma position to protect airway
• chest physiotherapy
C. ventilation
•  Depends on the cause of respiratory failure
• Response to simple management
• O2 therapy for Patients with
 sever tetanus
 neuromuscular paralysis
 Flail chest
 Post operative Respiratory Failure
 Poisoning
 drug – related central depression
 septicemia, Fat embolism ,ARDS
 Specific treatment for different causes

Cause Treatment
•  CNS depression------Reverse opioids- naloxon
other causes – ventilate
• Muscle paralysis-------------------Ventilate
• Pleural space collection-----intercostals drain
• Flail chest---------------------------Analgesia,
physiotherapy, ventilate if large
 Obstructive airway
• Upper airway----------clear airway, correct
position, intubation, tracheostomy
• Foreign body--------suction, physiotherapy,
Drainage and bronchoscopy
• Bronchospasm--------Nebulise, salbutamol,
Aminophyline & hydrocortisone
 Inadequate gas exchange

• Pneumonia ------ Antibiotic, O2 therapy

• Pulmonary oedema------ Diuretics if renal function

normal, Dialysis if renal failure

• Pulmonary Embolus----- Anticoagulants, O2, morphine.

• ARDS------ Ventilation and PEEP

• Hypoxemia may cause death in RF
• Primary objective is to reverse and prevent
hypoxemia
• Secondary objective is to control PaCO2 and
respiratory acidosis
• Treatment of underlying disease
• Patient’s CNS and CVS must be monitored and
treated
 Artificial respiration
1. Negative pressure ventilation

was developed in 1929

a large elongated tank,
Vacuum creation
Used widely in 1940
polio epidemic
large portholes
Still in use in some
centers
Cuirass, biphasic cuirass
ventilation
2. Positive pressure ventilation
A. Mechanical ventilation:

on technical developments by the

military during World War II to
supply oxygen to fighter pilots in
high altitude.
polio epidemic in Scandinavia and
the United States in the early
1950s.
heroic intervention required the
continuous activity of 1400 medical
students recruited
decrease in mortality rate from
80% to 25%,
B. BiPAP- bilateral positive airway pressure
C. Ambubag – bag mask ventilation etc.
 Cardiopulmonary resuscitation
Pulmonary Edema:
• Pulmonary edema is an increase in
extravascular lung water
• Interstitial edema does not impair function
• Alveolar edema cause several gas exchange
abnormalities
Acute respiratory distress syndrome(ARDS):
• Diffuse damage to gas-exchanging surface
either alveolar or capillary side of membrane

• Increased vascular permeability causes

pulmonary edema
• Pathology: fluid and RBC in interstitial space,
hyaline membranes
• Loss of surfactant: alveolar collapse
Management of PE and ARDS:
• Mechanical ventilation corrects
hypoxemia/respiratory acidosis
• Fluid management correction of
anemia and hypovolemic
• Pharmacological intervention Dopamine to
augment CO. Diuretics
Antibiotics
Corticosteroids - no demonstrated benefit
early disease, helpful 1 week later
• Mortality continues to be 50 to 60%
• Supportive management
 Oxygen administration(therapy)
Why oxygen required?
• O2 is required for the aerobic metabolism
– Oxidative phosphorylation in mitochondria
– Glucose + 6O2 → 6H2O + 6CO2 + 36ATP
• Lack of O2 causes
– Anaerobic metabolism in cytoplasm
– Glucose → lactic acid + 2ATP
↓
H+ + lactate-
O2 Therapy : CLINICAL OBJECTIVES
1. Correct documented or suspected
hypoxemia
2. Decrease the symptoms associated with
chronic hypoxemia
3. Decrease the workload hypoxemia imposes
on the cardiopulmonary system
 O2 Therapy : Indications
• Documented hypoxemia as evidenced by
– PaO2 < 60 mmHg or SaO2 < 90% on room air
– PaO2 or SaO2 below desirable range for a specific clinical
situation
• Acute care situations in which hypoxemia is
suspected.
• Severe trauma
• Acute myocardial infarction
• Short term therapy (Post anaesthesia recovery)
 O2 Delivery systems
DESIGNS
Low- flow system
Reservoir systems
High flow system
  Low flow system
• The gas flow is insufficient to meet patient’s
peak inspiratory and minute ventilatory
requirement
• O2 provided is always diluted with air
• FiO2 varies with the patient’s ventilatory
pattern
• Deliver low and variable FiO2 → Variable
performance device.
Eg:  A plastic disposable device
consisting of two tips or prongs 1
cm long, connected to oxygen
• Nasal cannula tubing
 Inserted into the vestibule of the
nose
 FiO2 – 24-40%
 Flow – ¼ - 8L/min (adult)
< 2 L/min(child
  FiO2 – 35-45%
• Nasal catheter:  Flow – 1 - 10L/min (adult)
< 2 L/min(child
  High Flow System
• The gas flow is sufficient to meet patient’s peak
inspiratory and minute ventilatory requirement.
• FiO2 is independent of the patient’s
ventilatory pattern.
• Deliver low- moderate and fixed FiO2 →
Fixed performance device
EG: Air entrainment devices/venturi mask
Blending systems
  Reservoir system
• Reservoir system stores a reserve volume of
O2, that equals or exceeds the patient’s tidal
volume.
• Delivers mod- high FiO2
• Variable performance device
• To provide a fixed FiO2, the reservoir volume
must exceed the patient’s tidal volume
  Reservoir mask
Commonly used reservoir system
• Three types
1. Simple face mask
2. Partial rebreathing masks
3. Non rebreathing masks
Simple face mask
Reservoir - 100-200 ml
Variable performance device
FiO2 varies with
 O2 input flow,
 mask volume,
 extent of air leakage
 patient’s breathing pattern
FiO2: 40 – 60%
Input flow range is 5-8 L/min
Minimum flow – 5L/min to
prevent CO2 rebreathing
 Partial rebreathing mask
No valves
Mechanics –
Expiration: O2 + first 1/3 of exhaled gas (anatomic dead
space) enters the bag and last 2/3 of exhalation escapes
out through ports
Inspiration: the first exhaled gas and O2 are inhaled
FiO2 - 60-80%
FGF > 8L/min
The bag should remain inflated to ensure the highest
FiO2 and to prevent CO2 rebreathing
 Non-rebreathing mask
Has 3 unidirectional valves
Expiratory valves prevents air entrainment
Inspiratory valve prevents exhaled gas flow into reservoir bag
FiO2 - 0.80 – 0.90
FGF – 10 – 15L/min
To deliver ~100% O2, bag should remain inflated
Factors affecting FiO2
 air leakage and
 pt’s breathing pattern
Thank you for your attention!!!