1. The document discusses the anatomy and physiology of the respiratory system and acute respiratory failure. It describes the structures of the upper and lower respiratory tract including the nose, pharynx, larynx, trachea, bronchi, and lungs. 2. Details are provided on lung volumes, the mechanics of breathing, gas exchange, and the control of respiration. Factors that can cause respiratory failure by reducing lung compliance or increasing airway resistance are discussed. 3. Respiratory failure is defined as the inability of the lungs to provide sufficient oxygenation or remove carbon dioxide to meet metabolic demands.

1. ANATOMY AND PHYSIOLOGY OF
RESPIRATORY SYSTEM AND ACUTE
RESPIRATORY FAILURE
PRESENTED BY: DR. ABHISHEK SAINI

2. RESPIRATORY TRACT
The Upper Respiratory Tract
• Nose
• Nasal cavity
•
Sinuses
•
Pharynx
The Lower Respiratory Tract
• Larynx
•
Trachea
•
Bronchial Tree
•
Lungs

3. Tracheobronchial Tree
MODEL
• The most useful and
widely MODEL
accepted approach
remains that of
WEIBEL. He
numbered
successive
generations of air
passages from the
trachea(generation
0) down to the
alveolar
sacs(generation 23)

4. Contd…
TRACHEA
Rt. Main bronchus
Superior lobar
Bronchus(3)
• Apical
• Posterior
•Anterior
Middle
lobar
bronchus(2)
• Lateral
• Medial
Lt. Main bronchus
Inf. Lobar
Sup. Lobar
bronchus(5) bronchus(5)
• Superior
•Medial basal
• Ant. Basal
• Post basal
• Lateral basal
• Apical
•Posterior
• Anterior
•Superior lingular
•Inferior lingular
Inf. Lobar
bronchus(4)
•Apical
•Ant basal
•Lat basal
•Post basal

5. CONTD

6. GRAYS
ANATOMY

7. • There are about 300
million alveoli.
• Between 75-300 micron
in diameter.
• Most gas exchange takes
place at alveoli capillary
membrane.
• 85-90% alveoli are
covered by capillary
membrane.
• The cross sectional area is
approx. 70m square
LINING EPITHELIUM
Trachea
Terminal
bronchioles:
ciliated psuedo stratified
columnar epithelium
Respiratory bronchioles
alveolar ducts
alveoli:
non ciliated cuboidal
epithelium

8. GRAYS ANTOMY
STUCTURE
ARTERIAL SUPPLY
NERVE SUPPLY
VENOUS DRAINAGE
TRECHEA
INFERIOR THYROID
ARTERY(⅔ rd)
MIDDLE CERVICAL
PLEXUS(SYMPTH)
INFERIOR THYROID
VEIN
DIAPHRAGM
PHRENIC
ARTERY,INTERNAL
MAMARY
ARTERY,INTRECOSTAL
ARTERY
EXTERNAL
&INTERCOSTAL
MUSCLE
BRONCHI
TERMINAL
BRONCHIOLS
RESPIRATORY
BRONCHIOLS
ALVEOLI
INTERCOSTAL
ARTERIES
BRONCHIAL
ARTERY
PHRENIC NERVE
(C3-C5)
SUPERIOR AND
INFERIOR PHRENIC
VEIN
THORACIC NERVE
(T1-T11)
INTERCOSTAL VEINS
PULMONARY
PLEXUS(VAGUS AND
SYMPTH)
BRONCHIAL VEIN
PULMONARY ARTERY PULMONARY
PLEXUS(VAGUS AND
SYMPTH)
PULMONARY VEIN

9. CIRCULATION GANONG 23
RD
PULMONARY
CIRCULATION
BRONCHIAL
CIRCULATION
• LOW-PRESSURE,
HIGH-FLOW
CIRCULATION
HIGH-PRESSURE,
LOW-FLOW
CIRCULATION
CONTAIN 100%
CARDIAC OUTPUT
CONTAIN 1-3%
CARDIAC OUTPUT
SUPPLIES
RESPITARY
BRONCHIOLS TO
ALVEOLI
SUPPLIES
BRONCHI TO
TERMINAL
BRONCHIOLS
ARIES FROM HEART
ARIES FROM AROTA
EXCEPTION ARTERY
CARRY
DEOXYGENETED
BLOOD
SHUNT(COMMON)

10. RESPIRATORY PHYSIOLOGY GANONG23rd
• A) PULMONARY FUNCTION
• B) GAS TRANSPORT BETWEEN
LUNG AND TISSUES
• C) REGULATION OF
RESPIRATION

11. For pulmonary ventilation to occur there should be a
pressure gradient driving air in & out
1. The movement of air into & out of the lungs (ventilation)
occurs as a result of pressure difference between the alveoli &
environment.
2. The pressure differences in pulmonary system are induced by
changes in lung volumes occurring as a result of coordinated
movement of diaphragm & chest.
3. The lung volumes are affected by its physical properties;
compliance, elasticity & surface tension.

12. PRESSURES WITHIN THE THORACIC CAVITY
Boyle’sLaw
(P∞1/V)

13. Changes in lung volume, alveolar
pressure, pleural pressure, and
transpulmonary pressure during normal
breathing.
(TP = ALp - IPp)
Ventilation cycle. Lung volume changes due
to airflow into or out of the lung. Gas flow
depends on a gradient of pressure from the
mouth to the alveolus; alveolar pressure
change occurs in response to altered
intrapleural pressure.

15. MUSCLES OF RESPIRATION

16. Muscles of inspiration
Primary muscles
1. Diaphragm
• Increase AP-VERTICAL diameter,phrenic nerve(C3-C5
2.External intercostal muscles(inspiratory muscles)
• Run obliquely downward and forward from rib to rib.
• Innervated by segmental spinal nerves.
• Their contraction has 2 result.
• Bucket-handle effect-( increase in transverse diameter ).
• Water-pump-handle effect-( increase in AP diameter )

18. contd
DURING FORCED INSPIRATION
• The accessory (or secondary) muscles of inspiration also
come into play.
• 1.Scalene.( lift the first two ribs)
• 2.Sternocleidomastoids (lift the sternum outward)
• 3.Neck and back muscles.(increasing the transverse area)
MUSCLES OF EXPIRATION
• No primary muscles of expiration, passive process.
FORCED EXPIRATION
Expiratory(internal intercostals),abdominal muscles.

20. Lung volumes(adult) Ganong 23rd

21. CHILDREN VOLUMES
MEASUREMENT
VALUE(ML/KG)
TIDAL VOLUME
8-10
RESIDUAL VOLUME
18-20
FUNCTIONAL RESIDUAL CAPACITY
25-30
VITAL CAPACITY
35-40
TOTAL LUNG CAPACITY
55-70
ADULT
RESPIRATORY MINUTE VENTILLATION(RMV)
6L/MIN
ALVEOLAR VENTILLATION(AV)
4.2L /MIN
IN CHILDREN RMV & AV VARY WITH AGE

22. LungCompliance(CL)
(CL) is change in lung volume per unit change in airway pressure,
it reflects stretchability of lung and chest wall.
CL = ΔV / ΔP
compliance of both lungs = .2liter/ per centimeter of water
FACTORS : Elastic recoil elasticity of the pulmonary cells
the extracellular matrix(e.g. elastin and collagen)
surface tension
High CL EMPHYSEMA
Low CL Interstitial pulmonaryfibrosis,hydropneumothorax,
asthama ,pneumonia.

23. Pressure-volume (compliance) curve for a maximal breath. TLC, total lung capacity; FRC,
functional residual capacity; RV, residual volume.

24. SURFACE TENSION
.

25. Surfactant

26. The pulmonary surfactant present at the alveolar air-water interface
has three major effects:
1. Because surfactant reduces surface tension, it increases
compliance, making it far easier to inflate the lungs.
2. By reducing surface tension, surfactant minimizes fluid
accumulation in the alveolus.(20 mm hg)
3. Surfactant helps keep alveolar size relatively uniform during
the respiratory cycle.
Ganong 23rd

27. WORK OF BREATHING in quiet respiration is.3-.7 kgm/min.it can be calculated by pressure volume curve.
ELASTIC WORK(65%)
STRETCHING THE ELASTIC TISSUES OF THE
CHEST WALL &LUNGS
NONELASTIC WORK
a) VISCOUS RESISTANCE(7%)
MOVING IN ELASTIC TISSUE
b) AIRWAY RESISTANCE(28%)
MOVING AIR THROUGH RESPIRATORY
PASSAGES

28. GAS EXCHANGE IN LUNG
• Diffusion of gases oocur according
to pressure gradient.
• Equilibrium reach in .75 sec
• Diffusion Capacity of Lung: The
diffusing capacity is defined as the
volume of gas that diffuses
through the alveolar membranes
per second for a pressure
difference of 1 kPa.
• The diffusing capacity of the lung
for a given gas is directly
proportionate to the surface area of
the alveolocapillary membrane and
inversely proportionate to its
thickness.
• Sarcoidosis
increase.
,berylliosis
thickness

29. Alveocapillary membrane

30. VENTILLATION/PERFUSION RATIO at rest .8(4.2L/min
ventillation divided by 5.5L/min blood flow)

31. Functions of the lung

33. B)GAS TRANSPORT
OXYGEN TRANSPORT GANONG 23
RD
• FACTORS
a)lung ventillatoin
b)gas exchange
c)blood flow(cardiac output)
d)capacity-blood-carry 0₂
amount of hemoglobin
affinity of hemoglobin
• Affinity of hemoglobin
Ph(H˖)
Temp
CO₂
2,3BPG(biphosphoglycerete)
HbO₂+2,3BPG↔Hb-2,3BPG+O₂

34. O2 Dissociation Curve

35. CO2 TRANSPORT

37. EFFECTS
• BOHR EFFECT
deoxygenated hemoglobin
(deoxyhemoglobin) binds H+
more actively than does
oxygenated
hemoglobin
(oxyhemoglobin).
• HALDANE EFFECT
binding of O2 to hemoglobin
reduces its affinity for CO2.
• FLOW DOWNHILL

38. C)REGULATION OF RESPIRATION GANONG 23RD
A) NEURAL CONTROL
①VOLUNTARY CONTROL
② AUTONOMIC CONTROL
①VOLUNTARY CONTROL
Mediated by a pathway originating from cerebral
cortex, bypass the medullary respiratory centres to
project directly on the spinal respiratory neurons.
EXAMPLES : Voluntary breathing practisedTalking, Singing, Swimming
Breath holding spell(50-60 sec)
Voluntary hyperventillation
.

39. ②AUTONOMIC (RECIPROCAL INNERVATION)
Medulla
MOTOR NEURON
THORACIC
CORD(T1-T11)
EXTERNAL
INTERCOSTAL
INTERNAL
INTERCOSTAL
MOTOR NEURON
CERVICAL
CORD(C3-C5)
DIAPHRAGM
(PHRENIC)

40. MEDULLARY CENTER GANONG 23RD
• DRG : “INSPIRATORY RAMP”
NORMAL BREATHING
• VRG : BOTH “INSPIRATORY
& EXPIRATORY” FORCED
• APNEUSTIC CENTER(PONS)
PREVENT SWITCH OFF
INSPIRATORY RAMP
INHIBIT BY
VAGUS&PNEUMOTAXIC CENTER
• PNEUMOTAXIC
CENTER(PONS)
SWITCHING IN BETWEEN
INSPIRATION & EXPIRATION
• VAGUS NERVE
INHIBIT RESPIRATION

41. • Pre-Bötzinger complex (preBÖTC) PACEMAKER
• Between nucleus ambiguus
and the lateral reticular
nucleus( dorsal medulla)
•
TRANSECTIONS & SPIROMETER TRACINGS

42. B)NON NEURAL CONTROL
• a) CHEMICAL CONTROL
PERIPHERAL RECEPTOR
AROTIC & CAROTID BODIES
CENTRAL MEDULLARY RECEPTOR
• b) NON-CHEMICAL CONTROL
DIFFERENT MECHANISMS

43. PERIPHERAL RECEPTOR

44. CONTROL
CAUSE(H+,CO₂,
O₂,OTHERS)
RECEPTOR(CEN
TRAL &
PERIPHERAL)
CENTERS=EFFEC
T(VOLUNTARY)

45. b)NON CHEMICAL
RECEPTOR IN LUNG&AIRWAY GANONG 23
RD

46. CONTD
• MYELINATED (slowely adapting)
Hering–Breuer inflation reflex
Hering Breuer deflation reflex
• MYELINATED (rapidly adapting /irritant)
Stimulated by histamine,prostaglandins
causes coughing, bronchoconstriction, and mucus secretion
• UNMYELINATED/C FIBERS/J RECEPTOR(PATHOLOGICAL)
Pulmonary congestion , embolization, pneumonia
Exogenous and endogenous substances (eg, capsaicin,
bradykinin, serotonin)
Response that is produced is apnea followed by rapid breathing,
bradycardia, and hypotension (pulmonary chemoreflex)

47. NON CHEMICAL CONTD GANONG 23
RD
RECEPTOR
LOCATION
EFFECT
PROPIORECEPTOR
JOINT,MUSCLE & TENDON
EXCERCISE(↑ RATE & DEPTH
OF RESPIRATION)
HIGHER CENTERS
LIMBIC SYSTEM &
HYPOTHALAMUS( PAIN &
EMOTIONAL STIMULI)
↑ RATE & DEPTH OF
RESPIRATION
BARORECEPTOR
CAROTID SINUSES, AORTIC
ARCH, ATRIA, AND
VENTRICLES
↓RATE & DEPTH OF
RESPIRATION(LITTLE EFFECT)
CHEST WALL STRETCH
RECEPTORS
MUSCLE SPINDLES
(INTERCOSTALS MUSCLES)
COORDINATE BREATHING
DURING CHANGE IN
POSTURE OR DURING
SPEECH.
THERMORECEPTOR
SKIN,HYPOTHALAMUS
↑ RATE & DEPTH OF
RESPIRATION

49. ADULT v/s CHILDREN
MEHARBAN SINGH 5TH MEDICAL EMERGENCIES
CHARECTER
ADULT
CHILDREN
BUCKET HANDLE EFFECT
MORE EFEICIENT
RIBS-OBLIQUE,STERNUMHARD,INTERCOSTAL
MUSCLES-DEVELOPED
LESS EFEICIENT RIBSHORIZANTAL,STERNUMSOFT, INTERCOSTAL
MUSCLES-LESS DEVELOPED
DIAPHRAGM CURVATURE
MORE( LESSWORK )
LESS(MORE WORK)
CORDINATION MOVEMENTS
(RIBCAGE-ABDOMINAL
WALL)
CORDINATED
POORLY CORDINATD
LUNG VOLUMES
MORE
(50 ml/500ml=10%)
LESS
(50 ml/100ml=50%) 10 kg

50. ADULT v/s CHILDREN CONTD
CHARECTER
SMALL AIRWAYS(≤2mm diameter)
AIRWAY RESISTANCE(A∞⅟r)
TENDENCY TO COLLAPSE
(Laplace`law P=2T/r)
ADULT
CHILDREN
20%
50 %
LESS(13cm-water/l/sec)
LESS
more(18cm-water/l/sec)
MORE

51. APPLIED PHYSIOLOGY nelson 19th ,ganong 23rd
•
Neuromuscular disease such as Guillain-Barre syndrome Causes respiratory muscle weakness
•
Pneumothorax
•
Pulmonary fibrosis/lung edema
•
Pulmonary emphysema
•
Atelectasis
•
RDS of the newborn
•
Pleural effusion
Deficiency of surfactant molecules
alveolar collapse due
to increased surface tension
Deficiency of surfactant and is associated with prematurity
and with infants of diabetic mothers
Increased fluid in pleural space resists lung expansion
•
Thoracic musculoskeletal pain
Patient avoids deep inspiration due to pain
•
Rib fracture
•
Morbid obesity
There is reflex spasm of intercostal muscles to produce rigid
chest wall
Especially in supine position, weight of tissue on the chest
wall and abdomen resists thoracic expansion
•
Increased abdominal pressure(e.g. ascites, bowel
obstruction)
Obstructive lung disease(asthma/emphysema/ chronic
bronchitis)
Restrictive lung disease
•
•
If the chest wall is punctured, air will flow into the pleural
space until PIP equals atmospheric pressure; the lung will then
collapse and the chest wall will spring outward
Reduced lung compliance and therefore, have increased work
of breathing, which is sensed as dyspnea
Increased lung compliance
Airway obstruction on expiration
Pressure from below resists descent of the diaphragm during
inspiration
Obstruction to air flow
Reduces lung volume

52. DEFINITION NELSON19TH
RESPIRATORY FAILURE
• Respiratory failure is defined as inability of the
lungs to provide sufficient oxygen (hypoxic
respiratory failure) or remove carbon dioxide
(ventilatory failure) to meet metabolic demands.
RESPIRATORY FAILURE MEHARBAN SINGH 5
TH
MEDICAL EMERGENCIES)
RESPIRATORY DISTRESS+CYANOSIS WITH CNS* and/or
CADIOVASCULAR* SIGNS OF HYPOXEMIA
CNS(RESTLESNESS,ALTERED SENSORIUM,SEIZURE,COMA)
CVS(TACHYCARDIA,BRADYCARDIA,HYPOTENSION,CARDIAC ARREST)
ABG (PCO₂>50mmHg and/or PO₂<60mmHg,40% O₂)

53. CLASSIFICATION
• GAS EXCHANGE ORGAN LUNG
ATMOSPHERE
ALVEOLAR VENTILATION
PULMONARY CAPILLARY
PERFUSION
ALVEOLAR CAPILLARY
MEMBRANE
• PUMP : CHEST WALL,
RESPIRATORY
MUSCLES,
BRAIN,
TRACTS AND NERVES
• TYPES
• TYPE I/HYPOXIC/
(V/Q)MISMATCH
FAILURE
• TYPE II/VENTILLATORY/
PUMP/HYPERCAPNIC

54. NELSON 19TH

55. LUNG
PUMP

56. CONTD IAP

57. NON PULMONARY CAUSES NELSON 23RD

58. asssesment
•
•
•
•
•
•
•
•
•
•
STABILIZE A B C
HISTORY & PHYSICAL EXAMINATION
GENERAL CONDITION
COLOUR
CHEST DEFORMITY/FACIAL DEFORMITY/AIRWAY
PROBLEMS
TACHYPNEA,BRADYPNEA OR APNEA
AUDIBLE WHEEZE/STIDOR
BREATH SOUNDS
ACESSORY MUSCLE
COUGH

59. LOCALIZING SIGN NELSON 19TH
RESPIRATORY
RATE
SITE OF PATHOLOGY
RETRACTIONS
AUDIBLE SOUNDS
EXTRATHORACIC AIRWAY ↑
↑↑↑↑
STRIDOR
INTRATHORACIC EXTRA↑
PULMONARY
↑↑
WHEEZING
INTRATHORACIC
INTRAPULMONARY
↑↑
WHEEZING
↑↑↑
GRUNTING
↑↑
ALVEOLAR INTERSTITIAL ↑↑↑
CENTRAL CAUSES
↑↑↑
↔
NONE

60. NELSON 19TH

61. BASIC INVESTIGATIONS
•
•
•
•
•
•
•
Pulse oxymeter
Complete blood count & blood culture
Renal profile
Arterial blood gas(ABG) analysis
X RAY
ECG
SPECIAL(Bronchoscopy,CT SCAN)

62. DIAGNOSTIC APROACH RESPIRATORY DISTRESS
IAP TEXT BOOK OF PAEDIATRICS
2013.

63. Treatment
•
•
•
•
(outline of principle) IAP 2013
Etiology Management
Keep airway open
Oxygen therapy
Ensure adequate alveolar ventilation, correct CO2 retenti
 Mechanical Ventilation
• General supportive care





Transfer to ICU for critical care and treatment
Infection control
Management of electrolyte and acid-base disturbance
Management of multi-organ dysfunction syndrome(MODS).
Nutrition support
63

64. TREATMENT
ETIOLOGY MANAGEMENT
KEEP AIRWAYOPEN
• Any underlying diseases :
• Bronchodilators(bronchosp
upper airway obstruction,
asm)
severe pneumothorax,
 β2-adrenoreceptor agonist,
massive pleural effusions
anticholinergic,
• Eliminate any factors that
glucocorticoid
cause respiratory failure
 Mode of administration :
secondary to infection or
parenteral first and then
shock
inhale
• Any factors leading to acute
 Airway humidify & nebulize
deterioration of chronic
respiratory failure：
• Establishing artificial airway
infection, malnutrition,
 Endotracheal intubation
inappropriate medication
 Tracheostomy
usage

65. TREATMENT
Indications of oxygen
therapy :
• Pump failure:
improve ventilation
• Pneumonia,
Pulmonary embolism,
acute attack of
asthma
• Severe pulmonary
edema, ARDS
• Acute deterioration or
worsening of COPD
• INon-invasive positive
pressure ventilation,
NIPPV
• INDICATION
 Conscious and
cooperative
 Stable circulation
 Be able to protect airway
 No facial trauma, injury
and deformity
 Be endurable to mask

66. Different kind of masks
66

67. Treatment
Mechanical ventilation
Goals of Mechanical Ventilation:
 improve alveolar ventilation, decrease PaCO2;
 improve pulmonary gas exchange;
 Decrease work of breathing, reverse respiratory muscle
fatigue.
 Indications for mechanical ventilation :




Deteriorating respiratory status despite oxygen and nebulization therapy.
Apnea
severe hypoxemia(Pao2<55 mm hg),hypercapnia(PaCO2>60mmhg)
progressive patient fatigue,anxious,sweaty child with deteriorating mental
status despite appropriate treatment.
 Adjust modes and settings for mechanical ventilation according to
blood gas analysis and clinical judgment
67

68. APPROACH TO A CASE OF RESPIRATORY FAILURE MANAGEMENT
IAP TEXT BOOK OF PAEDIATRICS
2013.

69. 69