-1 Lecture Medicine for Medical Students.ppt

1. Bronchial
Asthma

3. Reversible obstruction
of large & small airways
due to hyper-
responsiveness to
various immunologic &
non-immunologic
stimuli.

6. Epidemiology
Common chronic lung disease.
Before puberty twice boys as
girls,
at puberty sex incidence is equal.

7. TRIGGERS
Resp; infections (viral, mycoplasma).
Irritants(air pollution, cold air, cigarette smoke),
Exercise.
Inhaled (dust mite).
Ingested allergens.
Changes in weather.
Emotional stress.
Medications (aspirin).
Gastro-esophageal reflux,
Sinusitis.

9. RISK FACTORS
Poverty

11. Extrinsic (allergic) asthma
Exacerbations follow
exposure to
environmental factors
e.g; dust pollens.
↑ed total lgE & specific lgE
against allergen.

12. Something other than allergens
triggers-Clinically similar, no
evidence of lgE involvement,start
later in life,more common in
females.
Skin test –ve
& lgE low
Seen in 1st 2
yrs of life.

14. PATHOPHYSIOLOGY
Bronchospam (bronchoconstriction or smooth muscle contraction).
Mucus production.
Edema & inflammation of airway mucosa.
Infiltration of inflammatory cells (eosoinophils, neutrophils, basophils,
macrophages).
Desquamation of epithelial & inflammatory cells.
Obstruction during expiration as airway approaches closing volume & distal airway gas trapping.
More sever asthma diminished airflow during inspiration.
↑ed intrathoracic pressure due to hyperinflation interfere with venous return & ↓ cardiac output
manifested as pulsus paradoxus.
Mismatching of ventilation with perfusion causes hypoxia which interferes with conversion of lactic
acid to CO₂ & H₂O causing metabolic acidosis. Hypercapnia ↑ carbonic acid which dissociates in to
H₂ ions & HCo₃ causing resp; acidosis.

15. PATHOPHSIOLOGY
Allergic inflammatory response occur in airway mucosa resulting in
bronchial hyper-reactivity.
Early immune response
• results in bronchoconstriction.
• Treatable with β2 receptor agonists &
• prevented by mast cell-stabilizing agents e.g; cromolyn.
Late phase reactions,
• 6-8 hrs later, continued airway hyper-responsiveness with eosinophilic &
neutrophilic infiltration,
• treated & prevented with steroids,
• prevented by mast cell stabilizing agents.

17. CLINICAL FEATURS
Wheezing
Cough, shortness of
breath(dyspnea or
chest congestion)
tachypnoea &
exercise intolerance.
Persistent cough,
night cough,
exercise- induced
cough, post tussive
emesis, cough fol;
cold air exposure .
Airway patency ↓es
at night, many have
acute asthma at this
time.
If symptoms absent
or mild, chest
auscultation during
forced expiration →
prolonged expiratoy
phase & wheezing.
With severe
obstruction, wheeze
or rhonchi not heard
because of poor air
movement.

19. CLINICAL FEATURS
Flaring of nostrils, IC & suprasternal
retractions, use of accessory muscles of
respiration, hyper-inflated & hyper-resonant
chest →signs of severe obstruction.
Central cyanosis due to
severe hypoxia.
Tachycardia & pulsus
paradoxus
Agitation, lethargy, inability to speak,
tripod sitting position or diaphoresis,
→ early signs of resp; failure.
Between attacks may be N. With
chronic asthma ↓ average for height
& weight . Chest barrel shaped with
↑ AP diameter. Sternum prominent
& Harrison’s sulci
.

21. DIAGNOSIS
Clinical
CBC
↑ TLC in
acute severe
asthma
eosinophilia ↑ lgE blood.
Sputm eosinophilia
Chest X-ray
Hyper-inflated &
hyper lucent lungs.
↑AP diameter of chest
• (↑ed retro-sternal space on lateral
X-ray)
Flattening of
diaphragm.
More
horizontal ribs
Heart appears
narrow &
elongated.

22. • Reactive Airways Disease.
– (Top) Peribronchial thickening (white circles) seen en face shows small
donut-like rings in periphery of lungs, not normally seen.
• Contained in yellow circle are thickened bronchial walls seen in profile with a
"tram-track appearance.
– (Bottom) Close-up of left lower lung in same patient shows more donut
shaped thickened bronchial walls. (yellow arrows)

23. ABG’s: Hypoxemia from airway obstruction
RAST test:
In chronic asthma, skin test & radio-allergo
sorbent testing (RAST)
Pulmonary
function
tests:
PEFR
↓
VC
↓
FEV₁
↓
RV
↑
FRC
↑
TLC
↑ed
Diurnal variation in PEFR i.e between morning & evening of > 15-
20% used as defining features of asthma.

24. Differential diagnosis
Croup,
Acute bronchiolitis,
Penumonia,
Pertussis.
Foreign body in airway.
Endobronchial TB or
Lymph node pressing bronchi.
Cystic fibrosis.

25. COMPLICATIONS
Pneumothorax,
pneumomediastinum
Delayed maturation
& slowing of pubertal
growth velocity.

26. MANAGEMENT
O₂ therapy:
• 2-3 L/min by mask or nasal
prongs.
Nebulized salbutamol
•1st line therapy
•0.5 mg/kg/dose fol; by 0.1-0.5
mg/kg/dose at intervals of 20-30
min until adequate response
•5mg/ml, diluted with 1.5 ml N/S
•Nebulization with O₂ at 6 L/min
prevent salbutamol-induced
hypoxemia.
•↓ dose for HR>180/min.
•Adverse effects
•tachycardia,arrhythmias,
•CNS stimulation, hyperactivity
& irritability.
•hypokalemia
•Irritability
Adrenaline
• Is not used routinely
• 0.01ml/kg(1.1000 sol;)
subcutaneously.
• Once or twice at intervals of
20 min
• infants & small children ,0.05
ml
• still in distress after 3 doses,
do not give further doses.
• Not to be given if HR >
180/min in infants ,
>160/min in older children.
Side effects
• termors,
• pallor,
• anxiety,
• Palpitations
• Arrhythmias

27. Terbutaline
•Selective β₂
agonists.
•alternate to
adrenaline.
•0.01 ml/kg/dose
(1:100 sol;)
•Duration of action:
4 hrs.
Aminophylline
Considered
•Receving
maintenance
treatment with
theophyline.
•Unable to tolerate
maximal treatment
with inhaled β₂
agonist
•5mg/kg in IV slow
diluted for 5-15 min
•Repeated at 6-8 hrs
intervals total daily
dose 20mg/kg
•Rapid infusion
cardiac arrhythmias,
•Hypotension &
death.
Hydrocortisone
•To prevent late
phase reaction.
•IV 5-10 mg/kg every
4-6 hrs fol; by oral
(prednisolone 1
mg/kg/d for 5 d) or
inhaled
(beclomethasone
500 μg or 2 puffs
twice daily.
Adequate
hydration
•Dehydration
inadequate fluid
intake ,↑ed
insensible water
loss as a result of
tachypnea &
diuretic effect of
theophylline.
•20ml/kg N.saline
over 1-2 hrs &
continue 1⅟₂ times
the maintenance
rate for next 1-2 d.
•Circulatory
overloaded &
pulmonary edema
avoided β₂-agonists
produce
hypokalemia,
potassium added to
IV fluids after pt
voids.
Antibiotics:
•If bacterial infection
suspected
Ventilatory
support

30. SUBSEQUENT
MANAGEMENT

31. MANAGEMENT OF STATUS
ASTHMATICUS
Continuous resp; distress
despite sympathomimetic drugs
with or without theophylline.
Defined as ↑ severe asthma
not responsive to drugs that
are usually effective.
Admitt in ITC ,
CBC, S.electrolytes, ABG’s &
cardiac status monitored.
To prevent hypoxia, O₂ (2-
3L/min) to maintain 70-90
mmHg or O₂ saturation > 92% .
If previously on steroid therapy,
steriod given initially.
Others:
• salbutamol, nebulization,
• salbutamal+ ipratropium
nebulization,
• aminophyline infusion,
• adequate hydration , or
• steroids .
Mechanical ventilation resp;
failure inspite of measures.

32. LONG TERM MANAGEMENT
OF CHRONIC ASTHMA.
Pt
education
• Improvement pt skill in use of spacer devices (MDIs).
• Use of peak flow monitoring.
• Use of self management & envirnomental control measure.
• Assessment & monitoring of asthma severity.
• Avoidance of control of asthma triggers.
• Establishment comprehensive plans of pharmacologic therapy.
cromolyn :
• Inhibit early & late phases allergen –included bronchospasm ac bronchospasm. Useful as
prophylactic agents with mild to moderate asthma no known side effects.
Inhaled
corticosteroids
• Safe & extremely effective for chronic asthma.
• ↓ airway hyper-reactivity & need for rescue broncho dialator therapy.
• Long term oral use reserved for chronic asthma only if other therapies fail; preferable
with an alternate day schedule. Side effects with

34. β₂
adrenergic
agonists:
Ac & chronic asthma
alone do not give LT
control because not
affect airway
inflammation .
Relax airway smooth
muscle enhance
mucociliary clearance.
↓mediator
release from mast
cells & basophils.
Short acting
inhaled β₂
agonists
e.g; salbutamol
Ac exacerbations
of asthma.
pretreatmnt of
exercise inhaled
asthma.
Rescue (quick
relief) therapy
chronic asthma.
Long term
inhaled β₂
agonists:
Duration of action
> 12hr
Useful for chronic
asthma
unresponsive to
inhaled anti
inflammatory
agents
Night time cough.
Must not be used
for ac
exacerbations.
Sustained
release
theophyline:
Bronchodilator
with mild anti
inflammatory
effects.
LONG TERM MANAGEMENT OF
CHRONIC ASTHMA.

35. Anti-cholinergic
agents,e.g;Ipratropium
potent bronchodilator,
block reflex
bronchoconstriction
caused by inhaled
irritants.
less effective as
bronchodilators than β₂
agonists.
Leukotriene antagonists:
Anti inflammatory agents
not bronchodilators.
Montelukast
2-5yrs= 4mg/d
6-14 yrs =5 mg/d
>15yrs =10mg/d

36. PROGNOSIS
Aggressive
therapy is
instituted early.
Death always a
result of under
treatment.
Ultimate
remission 50%
free of symptoms
within 10-20yrs.
5% severe disease
. Recurrence may
occur in
adulthood.

37. PREVENTION
Reduce risk
allergies.
breast feeding ↓
wheezing episodes 1st
mon of life.
Benefits persist 1st 6
yrs of life.
Esp; useful in
symptoms in exposed
tabacco smoke.
Once a child is known
for repeated attacks
↓ triggers.

38. Clinical features before
treatment
Symptoms Night time symptoms Lung function
Step 4
Severe persistent
Continual symptoms
Limited physical activity
Frequent FEV₁ or PEFR < 60%
predicated
PEFR variability > 30%
Step 3
Moderate persistent
Daily symptoms .
Daily use of inhaled
Short-acting β₂-agonist.
Exacerbations affect
activity.
Exacerbations > 2 times a
Week: may last days.
>1 time a week FEV₁ or PEFR >60%-80%
predicated.
PEFR variability > 30%
Step 2
Mild persistent
Symptoms > 2 times a
week
But < 1 time a day
Exacerbations may affect
activity.
> 2 times a mon FEV₁ or PEFR >80%
predicated.
PEFR variability 20-30%
Step 1 mild intermittent. Symptoms < 2 times a
week.
Asymptomatic & N.
PEFR between
exacerbations brief (from
a few hrs to a few days)
Intensity may vary.
< 2times a mon FEV₁ or PEFR > 80%
predicated.
PEFR variability < 20%.
The presence of 1 of features of severity is sufficient to place a pt in that category.An individual should be assigned
to most severe grade in which any feature occur.characteristics noted in this figure are general & may overlap
because asthma is highly variable .furthermore, an individual classification may change over time

39. Stepwise approach for managing asthma in children 0 to 4 years of age. National
Institutes of Health. National Heart, Lung, and Blood Institute. National Asthma
Education and Prevention Program. Expert Panel Report 3: Guidelines for the diagnosis
and management of asthma. August 2007. NIH publication no. 07-4051. Available at:
http://www.nhlbi.nih.gov/guidelines/asthma/index.htm. 3 Accessed December 30,
2007. PRN, As necessary.

41. SEQ-1
A 4 years old boy, brought to emergency with
breathing difficulty. He has rhinorrhea & cough for
last 2 days. In the past he had recurrent episodes
of cough & dysponea. O/E; RR = 50/min, marked
chest indrawing & bilateral expiratory wheeze:
What is the most
likely diagnosis?
Outline the steps of
management in this child?

43. SEQ-2
A three years old girl in emergency, has C/O cough &
breathlessness for last 6 hours. she had 2 similar
complaints & was admitted in hospital over last 3-
mons. O/E; she is in obvious respiratory distress &
has audible wheeze. Auscultation of chest reveals
bilateral rhonchi.
What is
your
differential
diagnosis
in order of
priority?
How will
you treat
her?

44. A 5 year old boy presented in ER with respiratory difficulty for 12 hours.
He was having low grade fever & mild cough for the last 3 days. There is
H/O recurrent similar episode since infancy. O/E; RR= 55/min with
subcostal & intercostal recessions. There are bilateral rhonchi & few
crepitations.
What is the
diagnosis?
Give steps of
emergency
treatment?

45. A 9 years old boy presents with cough,dyspnea, restlessness &
sweating. His PR = 105/min,RR =45/min , chest is hyperinflated with ↓
movements & hyperresonent percussion note. On auscultation: air
entry is bilaterally ↓ed & there are widespread expiratory ronchi.
What is the
diagnosis?
Write down 2
important
investigations in
this case?
Give 2 common
complications of
this condition?
Write down outline of management of this child?

46. SEQ-5
 A 10-year-old boy in respiratory distress arrives late in the evening to
ED; he has a 2-hour history of rapid breathing and a complaint that his
chest hurts. His mother gave him two nebulizer treatments without
improvement. She tells you that this is the fourth time in 3 months that
he has required ED visits for similar symptoms. O/E; an afebrile male
with RR = 60/min, HR = 120/min & BP = N. You note that his pulse varies
in amplitude with respiration but his capillary refill is somewhat sluggish
at 4 to 6 seconds. He is pale, appears drowsy, has mild perioral cyanosis,
and is using accessory chest muscles to breathe. You hear only faint
wheezing on chest auscultation.
A. What are the initial steps in evaluating this patient?
B. What is the most likely diagnosis?
C. What is the next step in evaluation?

47. KEY-5
• Initial steps:
– Treating this patient's respiratory distress is of immediate concern. The airway
is evaluated first, followed by an evaluation of breathing, and finally
assessment of the circulatory status (the "ABCs").
– Initial management includes administration of oxygen, an inhaled (β-agonist,
and a systemic dose of prednisone.
– Intravenous administration of fluids and medications is indicated for a patient
with this degree of distress.
– A stat blood gas determination and monitoring oxygen saturation levels will
aid further management.
• Most likely diagnosis:
– Asthma exacerbation.
• Next step in evaluation:
– After initial stabilization, past medical and family histories (medications,
triggers, frequency and severity of previous episodes, previous hospitalization
or intensive care unit admissions) and a review of systems are obtained.
– The physical examination, blood gas report, and response to initial treatments
will determine subsequent management.

48. SEQ-5
An 8 years old child presents with cough &
breathing difficulty.O/E; a thin afebrile child
with RR=60/min with intercostal & subcostal
retraction & bilateral reduced air entry with
few rhonchi.H/O 2 previous hospitalization
in last year with oral medication sparingly.
• What is the diagnosis?
• How would you manage?

49. MCQ-1
 A 12-year-old asthmatic girl presents to the ED with tachypnea,
intracostal retractions, perioral cyanosis, and minimal wheezing. You
administer oxygen, inhaled salbutamol, and intravenous prednisone.
Upon reassessment, wheezing increases in all fields, and the child's color
has improved. Which of the following is the appropriate explanation for
these findings?
A. The girl is not having an asthma attack.
B. The girl is not responding to the salbutamol, and her symptoms are
worsening.
C. The girl is responding to the salbutamol, and her symptoms are
improving.
D. The girl did not receive enough salbutamol.
E. The salbutamol was inadvertently left out of the inhalation treatment,
and the girl received only saline.

50. KEY-1
C.
 This child presented in severe respiratory distress. Her improved color
indicates reversible symptoms, confirming the diagnosis of asthma.
 Increased wheezing is auscultated after salbutamol treatment because
lung areas previously obstructed are now opening, allowing additional
airflow.
 Less-experienced examiners may misinterpret lack of air movement as
"clear" breath sounds, further delaying appropriate medical management.

51. MCQ-2
 A 15-year-old adolescent male uses his salbutamol inhaler shortly after
he mows the lawn because of a mild feeling of chest "tightness." He later
returns home early from dinner at a friend's house when he has the
sudden onset of wheezing, cough, and chest pain. Which of the following
is the most likely explanation for these circumstances?
A. He likely aspirated a piece of grass.
B. His salbutamol inhaler must be empty.
C. His salbutamol inhaler must be outdated.
D. He is having a late-phase reaction.
E. He has been exposed to a new allergen that is more irritating than grass.

52. KEY-2
D.
A late-phase reaction typically occurs 2 to 4
hours after an initial wheezing episode. It is
caused by accumulation of inflammatory cells
in the airway.

53. MCQ-3
 A 5-year-old boy with a history of recurrent chest infections
has been admitted to hospital with increasing shortness of
breath, night-time cough and wheeze. Select the most likely
diagnosis.
A. Upper respiratory tract infection
B. Asthma
C. Inhaled foreign body
D. Bronchiolitis
E. Pertussis

54. KEY-3
B. Asthma
 Asthma is a condition of chronic airway inflammation, airway
hyperactivity and reversible airway obstruction.
 It affects 10-15% of the school-age population, and is the
cause of 10-20% of all acute hospital admissions.
 It can present subtly with a night-time cough, or with a full-
blown exacerbation.
 In the early stages it can often be misdiagnosed as recurrent
chest infections.
 There is usually a family history of atopic illnesses.

55. MCQ-4
 All of the following are triggers for asthma in a susceptible
child except:
A. Dust mite
B. Air pollution
C. Cigarette smoke
D. Gastro-oesophageal reflux
E. Exercise.

56. KEY-4
D
Gastro-oesophageal reflux does not lead to
bronchospasm, although in babies it may
cause crying, posseting and rarely apnoea.
The others in the list are all common triggers
for asthma in a susceptible child.

57. MCQ-5
 Which of the following is the accepted definition of
asthma?
A. Cough or wheeze in a child who has tested positive for
allergens on skin prick testing
B. Cough or wheeze in a child with a strong family history of
asthma
C. Recurrent cough or wheeze that responds to bronchodilator
therapy
D. Persistent cough or wheeze in a child exposed to passive
smoking in the home
E. All of the above.

58. KEY-5
C
 A family history of asthma is common in children with asthma
but
 the correct definition is recurrent cough or wheeze that
responds to bronchodilator therapy, (confirming that the
bronchospasm is reversible).
 Skin prick testing may be helpful in the identification of
allergens but is not a diagnostic feature.
 Passive smoking is a trigger for asthma but is also not a
defining feature.

59. MCQ-6
 It is important to use an appropriate device for
administering asthma treatment. An MDI (metered dose
inhaler) with a spacer device is appropriate for what age
child?
A. An infant
B. A preschool child
C. A school age child with severe asthma
D. All of the above.
E. None of the above.

60. KEY-6
D
 MDIs with a spacer device have been shown to be as
effective as nebulizers for administering
bronchodilators and inhaled steroids.
 A mask, rather than a mouth-piece, is attached to
the spacer device for babies.
 The use of a spacer device with an MDI can be
effective in older children who have difficulty
coordinating their breathing during a severe attack.

61. MCQ-7
 Which one of the following signs is not likely to
occur when asthma is life threatening?
A. Confusion
B. Hyperactivity
C. A silent chest
D. Hypotension
E. Being too breathless to talk.

62. KEY-7
B
 Confusion and drowsiness can occur as a result of hypoxia,
but hyperactivity is unlikely.
 Hypotension and severe breathlessness are common in very
severe asthma.
 The chest may appear to be silent as air entry is so poor, and
this may mislead an inexperienced doctor to believe that
there is no bronchospasm present.

63. MCQ-8
 A child with poor control of their asthma is likely to have any
of the following symptoms or signs except:
A. Clubbing
B. Poor growth
C. Chronic chest deformity
D. Frequent acute exacerbations
E. Persistent cough at night.

64. KEY-8
A
• Clubbing is not a sign of asthma and if present
suggests cystic fibrosis, bronchiectasis or
congenital heart disease.

65. MCQ-9
 A school girl is a known asthmatic for last five
years. She has been taking steroids and β₂
stimulant regularly. Which of the following is
indicator of her disease severity?
A. Platelet count
B. IgE level
C. IgM level
D. Absolute neutrophil count
E. CT scan chest.

66. KEY-9

67. OSPE-1

68. Case Study: A wheezy child
An 18-month-old child presents with his first episode of
wheeze. He is pyrexial and has shortness of breath with
some subcostal recession. Wheeze is heard all over his
chest.
• Asthma;
• Inhaled foreign body;
• Bronchiolitis
• Croup
• Whooping cough.
(a) Which of the following diagnoses are most likely?

69. (b) If you were considering asthma as a likely
diagnosis, what family history may be relevant?
 Asthma and bronchiolitis are both possible.
 A child of this age is at risk of inhaling a foreign body as they
are inquisitive & put small objects in their mouth. A foreign
body will either cause airway obstruction leading to choking,
stridor and cyanosis, or if inhaled into one main bronchus may
cause unilateral wheeze. Fever is less likely.
 Croup causes a characteristic cough & stridor but no wheeze.
 Whooping cough presents with coughing & sometimes
vomiting but not wheeze.
 Bronchiolitis due to RSV infection is very common in the first
2 years of life. There may be a fever.
 Asthma does not cause fever, but may be triggered by a viral
upper respiratory tract infection.

70. (c) If you were considering bronchiolitis as a likely
diagnosis, what diagnostic test would you perform?
• if there is a family history of atopy—asthma, hay
fever or eczema in siblings or parents suggest this.
• Does anybody smoke in the house?
• Are there any pets in the home?
You should establish

71. (d) What treatment is likely
to have been given?
A nasopharyngeal aspirate or
swab for RSV
immunofluorescence, which can
identify the presence of RSV or
other respiratory viruses.
A chest radiograph may be
helpful if there is diagnostic
uncertainty or if the child is very
ill.
The child is admitted to the
ward.
Over the next few hours the
shortness of breath settles
with treatment.
The wheeze remains
intermittently present; worse
prior to each treatment.

72. (e) What would you prescribe and what would you tell
his parents about administering it?
 The response to treatment followed by recurrence suggests
reactive airways disease (asthma) which is responding to
bronchodilators such as short-acting beta-agonists (e.g.
salbutamol). These may be administered by inhaler (using a
spacer device) or by nebulizer.
 The next day the child is better and is discharged home.
 He is reviewed in the outpatient department 6 weeks later,
during which time he has had two further episodes of
shortness of breath. He coughs most nights.
 You decide to prescribe treatment.

73. • The child probably needs an inhaled beta-agonist such as salbutamol. It is
important that this is given via a spacer device as this child is too young to
use a metered dose inhaler directly. As he is coughing most nights the
bronchodilator should be given regularly at bedtime.
• On further review 3 months later he is well, but still coughing at night
several nights a week. He has been unable to attend nursery on a few
occasions.
• (f) What further treatment would you consider?

74. • He responds to the short-acting
bronchodilators but is having regular
symptoms despite these. Low-dose inhaled
corticosteroids should be given regularly for a
trial period to reduce airway inflammation
and gain symptom control.

76. Age Breaths/min
Preterm 40-60
Term 30-40
5 yrs 25
10 yrs 20
15 yrs 16
adult 12

77. Pattern Features
Obstructive
Mild ↓ rate
↑ TV
Slightly prolonged exp phase
moderate ↑ rate
↑ use of accessory muscles
Prolonged expiratory phase
Restrictive Rapid rate
↓tidal volume(TV)

78. Pattern features
Kussmaul respiration ↑ rate
↑tidal volume(TV)
Regular deep resp
Metabolic acidosis OR
DKA
Cheyne-stokes respiration Cyclic pattern of waxing & waning of breathing
interposed by central apneas/hypopneas
CNS injury
Depressant drugs
Heart failure
Uremia
Biot respiration Ataxic OR periodic breathing with a resp effort
fol by apnea
Brain stem injury
Posterior fossa mass
Gasping Slow rate
Variable TV
 Hypoxia
 Shock
 Sepsis
 Asphyxia

79. • Amount of air expired with each relaxed breath.
Tidal volume (TV)
• Volume of gas retained in the lung at the end of a relaxed exhalation.
• This gas volume maintains exchange of O₂ during exhalation.
Functional residual capacity (FRC)
• Volume of gas in the lungs at the end of maximal inhalation
Total lung capacity (TLC).
• Volume of gas left in the lungs at the end of a maximal exahalation.
Residual volume (RV)
• Maximal amount of air that can be expelled from the lungs
• TLC-RV.
Vital capacity (VC)