Respiratory system

Respiratory system

1. RESPIRATORY SYSTEM
By- Dr. Armaan Singh

2. CONTENTS
Introduction
Developmental anatomy
Functions of Respiration
Regulation of Respiration
Applied aspects :
Periodontal disease and Respiratory infections
Medical emergencies

3. Cells use O2 for the metabolic reactions that
release energy from nutrient molecules and
produce ATP with the release of CO2.The two
systems that supply O2 and eliminate CO2 are
CVS and RS. Failure of either of the systems
leads to disruption of homeostasis and rapid
cell death from O2 starvation and buildup of
waste products.

4. RESPIRATION is “exchange of gases between
atmosphere, blood and cells” - GUYTON and HALL
The goals of respiration are to provide oxygen
to the tissues and to remove carbon dioxide.
To achieve these goals, respiration can be
divided into four major functions :
1. Pulmonary Ventilation
2. Diffusion of oxygen and carbon dioxide
between the alveoli and the blood

5. 3. Transport of oxygen and carbon dioxide
in the blood and body fluids to and from
the body’s tissue cells
4. Regulation of ventilation

6. Developmental anatomy of
respiratory system

8. At about 4 weeks of fetal developmental
respiratory system begins as an outgrowth of
endoderm of foregut just behind the pharynx called
as laryngotracheal bud.
Bud grows and elongates and differentiates into
future larynx.
Its proximal end maintains a slit like opening into
pharynx called glottis.
Middle portion of bud gives rise to trachea

9. Distal portion divides into lung buds which
grow into bronchi and lungs.
Lung buds develop, branch and rebranch
and gives rise to bronchial tubes.
After 6 months, closed terminal portions of
tubes dilate and become the alveoli of lungs.
Smooth muscles, cartilage and connective
tissue of the bronchial tubes and pleural sacs
are contributed by mesenchymal cells.

11. Respiratory System
Upper RS Lower RS
nose, pharynx larynx, trachea,
bronchi, lungs
Conducting portionRespiratory portion
nose,
pharynx,larynx,trach
ea,bronchi,terminal
bronchioles
respiratory
bronchioles,alveolar
ducts,alveoli
Anatomically
Functionally
Organs

13. Pulmonary ventilation

14. Mechanics

15. Compliance of the lungs
Pleural pressure is the pressure of the fluid in the thin
space between the lung pleura and the chest wall pleura.
Alveolar pressure is the pressure of air inside the lung
alveoli.
Transpulmonary/ Recoil pressure is the difference
between pleural pressure and alveolar pressure.

17. The extent to which the lungs will expand for each unit
increase in transpulmonary pressure is called the lung
compliance.
Fibrosis is associated with a decrease in pulmonary
compliance.
Emphysema/COPD may be associated with
an increase in pulmonary compliance due to the loss of
alveolar and elastic tissue.

18. Surfactant and surface tension
It is secreted by special surfactant secreting epithelial cells
called type II alveolar epithelial cells which constitute about
10% of surface area of alveoli.
Important components are dipalmitoylphosphatidylcholine,
surfactant apoproteins and calcium ions.

19. Also, surfactant does not normally begin to be secreted
in the alveoli until 6
th
and 7
th
months of gestation.
Therefore, many premature babies have little or no
surfactant and their lungs have extreme tendency to
collapse. This is called respiratory distress syndrome of
the newborn.

21. Pulmonary volumes
There are four pulmonary lung volumes
sum of which equals maximum volume to
which lungs can be expanded.
Tidal Volume 500 ml
Inspiratory Reserve Volume 3000 ml
Expiratory Reserve Volume 1100 ml
Residual Volume 1200 ml

22. Pulmonary capacities
Combination of one or more pulmonary volumes in a
pulmonary cycle is referred as pulmonary capacities.
Inspiratory capacity TV + IRV 3500 ml
Functional residual capacity ERV + RV 2300 ml
Vital capacity IRV + TV +
ERV
4600 ml
Total lung capacity VC + RV 5800 ml

24. Functions of respiratory passageways
Muscular wall of the bronchi and bronchioles and its
control
Resistance to airflow in the bronchial tree
Sympathetic dilation of bronchioles
Parasympathetic constriction of bronchioles
Mucuos lining respiratory passageways
Cough reflex
Sneeze reflex

25. Regulation of respiration

26. Respiratory center is composed of several groups of
neurons located bilaterally in the medulla oblangata and
pons of the brain stem.
It is divided into three major collection of neurons

29. At rest about 200ml of oxygen consumed /mt.
During exercise it rises to 30 fold. So a
mechanism must exist to match respiratory effort to
metabolic demand.
Basic rhythm of respiration controlled by portions
of the nervous system in the medulla and pons.
They normally adjusts the rate of alveolar
ventilation almost exactly to the body demands so
that pO2 and pCO2are hardly altered.

30. Breathing stops if spinal cord is transected
above the origin of phrenic nerve.
Spontaneous respiration are regulated by
alternations in arterial pO2,pCO2 and H+
concentration.

31. NEURAL CONTROL OF BREATHING
Control Systems
Size of thorax is affected by the action of the
respiratory muscles. These contract and relax as a
result of nerve impulses transmitted to them from
centers in the brain.
2 separate neural mechanisms
Voluntary control- in cerebral cortex via
corticospinal tract
Automatic control- in pons and medulla-
through white matter of spinal cord b/w lateral and
ventral corticospinal tracts.

32. n fibres mediating inspiration converge on
phrenic motor neurons and external intercostal
motor neurons.
n fibres mediating expiration converge on
internal intercostal motor neurons.
motor neurons to expiratory muscles are
inhibited when those supplying inspiratory
muscles are active, and viceversa. This is
RECIPROCAL INNERVATION.

33. MEDULLARY SYSTEMS
Rhythmic discharge of neurons in medulla and
pons produce automatic respiration.
Brain stem respiratory neurons are of 2 types.
I neurons – discharge during inspiration
E neurons – discharge during expiration.
Expiration is passive during quiet breathing,
and E neurons are quiet. Active only when
ventilation increased.

34. RESPIRATORY CENTER
Area in the medulla concerned with respiration is
called the respiratory center.
Consists of widely dispersed group of neurons.
Functionally divided into 3 areas
1,Medullary rhythmic area in the medulla
2.Pneumotaxic center in pons
3.Apneustic center in pons

36. MEDULLARY RHYTHMIC AREA
Function is to control the basic rhythm of respiration.
Normal resting – inspiration 2 sec.
-expiration 3 secs.
Within medullary rhythmicity area are
-inspiratory area (Dorsal Respiratory Group)
-inspiratory/expiratory area (Ventral Respiratory
Group)
-E neurons rostral
-I neurons mid
-E neurons caudal

37. Dorsal Respiratory Group of Neurons – Its Control
of Inspiration and of Respiratory Rhythm
Located within the nucleus of tractus solitarius
which is the sensory termination of vagal and
glossopharyngeal n. which transmit sensory signals
into respiratory center from
1.peripheral chemoreceptors
2.baroreceptors
3.receptors in lungs

38. Pneumotaxic Center
-It limits duration of inspiration and increases
the respiratory rate.
-Located in nucleus parabrachialis in upper
pons.
-Control the ‘switch off’ point of inspiratory ramp,
thus controlling the duration of filling phase and
starting elastic recoil of lungs.
-Thus secondary effect of rate of respiration.

39. Apneustic Center
Apneusis- prolonged inspiratory gasps abruptly
interrupted by very brief expirations.There is a
possibility of Apneustic center in lower pons. It
sends signals to DRG to prevent ‘switch off’ of
inspiratory ramp. So lungs become full with air, and
short expiratory gasps.

40. HERING-BREUER INFLATION REFLEX
Stretch receptors in bronchi & bronchioles
transmit signals through vagi into DRG when lungs
are overstretched.
When lungs overly inflated, stretch receptors
activate feed back response that ‘switches off’
inspiratory ramp and stops further inspiration. This
also increases rate of respiration.
It is a protective mechanism for preventing
excess lung inflation.

42. CHEMICAL CONTROL OF BREATHING
Goal of respiratory system is to maintain
proper levels of CO
2
and O
2
.
CO
2
is lipid soluble. It diffuses across plasma
membrane including BBB
CO
2
+ H
2
O H
2
CO
3
H
+
+ HCO
3
-
So increase in CO
2
and hence increase in
H
+
decrease in CO
2
decreases H
+

43. Chemosensitive area in RS
Within medulla, neurons sensitive to pH form
central chemosensitive area, located bilaterally
lying 1/5th mm beneath ventral surface of medulla.
In peripheral nervous system are peripheral
chemoreceptors sensitive to changes in H
+
, CO
2
,
and O
2
in blood.
Located within carotid bodies near the bifurcation
of CCA and in aortic bodies.
No direct effect by O
2
; but by peripheral through
carotid and aortic bodies.

44. Carotid bodies located in space b/w origin of ICA
and ECA. Sensory n fibers from carotid body joins
carotid sinus to form carotid sinus n, pass through
Hering’s nerve, joins glossopharyngeal n to DRG.
Aortic bodies near arch of aorta. Sensory fibers
join vagus n to DRG.
Excess CO
2
or H
+
act directly on respiratory
center.

45. Normal pCO
2
in arterial blood is 40mmHg
Increase is HYPERCAPNIA
Central chemosensitive area stimulated by
increased H
+
H
+
and CO
2
conc. Fluctuate more readily in CSF
because of few CSF buffers.
Peripheral receptors stimulated by increased pCO
2

and increased H
+
Input from central chemosensitive area and
peripheral chemoreceptors causes inspiratory area to
become highly active, rate and depth of breathing
increases.

46. Rapid and deep breathing is
HYPERVENTILATION. It allows exhalation of
more CO2 until pCO2 and H+ decreased.
Arterial pCO2 <40 mmHg is HYPOCAPNIA
Central chemosensitive area and peripheral
chemoreceptors not stimulated. So no impulse to
inspiratory area.
Area sets its own moderate pace until pCO2
accumulated and pCO2 rises to 40 mmHg.
Slow and shallow breathing is
HYPOVENTILATION

47. Peripheral chemoreceptors sensitive only to
large decrease in pO
2
.
If arterial pO
2
falls from 105mmHg to 50mmHg,
peripheral chemoreceptors stimulated. So
impulses to inspiratory area. So respiration
increases.
If pO
2
<50mmHg, cells of inspiratory area suffer
O
2
starvation (hypoxia) and do not respond to
chemical changes. They send fewer impulses to
medullary inspiratory area. As respiration
decreases, pO
2
falls lower and lower, thus positive
feed back cycle is established.

50. Effect of low arterial pO
2
to stimulate alveolar
ventilation when arterial CO
2
and H
+
conc. remain
normal
No effect as long as arterial pO
2
remains>100mmHg
At pressures <100mmHg, ventilation increases and
may become 5 fold if pressure <60mmHg.
Effects of heights and Depths on the body
Effects of high altitude on body
Mountain climbers- Acute mountain sickness due to
hypoxic hypoxia and resultant hypocapnia induced
alkalosis.
Symptoms- fatigue, nausea, loss of appetite, labored
breathing, rapid heart rate, n dysfunction
characterized by poor judgment, dizziness and
incoordination

51. Effects of deep sea diving on the body
Greater atmospheric pr. under water Air provided by scuba equipment at
high pr.
1. Amount of gas in soln. proportional to partial pr. of gas
2.Air is composed of 79% N
2

under water at high atmos. pr. more of N
2
in blood causes nitrogen
narcosis or rapture of the deep. Reduction in excitability of neurons due
to N
2
in lipid membrane. Euphoria and drowsy, weak and clumsy,
unconsciousness. O
2
toxicity results from high pO
2
under water.
Decompression sickness- during ascent due to N
2
coming out of the tissues.
Patient bends with pain- so ‘the bends’. Prevented by slow ascent to
surface or by decompression in a decompression tank.

52. ACCLIMATIZATION
Chronic breathing of low O
2
stimulates respiration
more.
Reason: Within 2-3 days respiratory center in
brainstem loses 4/5
th
of its sensitivity to changes in
arterial pCO
2
and H
+
. Therefore excess ventilatory blow
off of CO
2
that normally would inhibit an increase in
respiration now fail to do so, and the low O
2
can drive
the resp. system to a much higher level of alveolar
ventilation than under acute low O
2
conditions.
Instead of a 70% increase in ventilation that might
occur on acute exposure to low O
2
, alveolar ventilation
often increases 400-500% after 2-3 days of low O
2
.

53. Ventilatory responses to change in Acid-Base
balance
Respiratory acidosis
-Acidosis caused by an increase in pCO
2
>45mmHg.
- excess H
+
in tubular fluid due to rise in ECF pCO
2
,
which stimulates H
+
secretion.
-Any factor that decreases rate of pulmonary ventilation
increases pCO
2
of ECF. This causes increase in H
2
CO
3

and H
+
leading to acidosis.
Causes
-Pathological conditions that damage resp. centers or
that decrease the ability of lungs to eliminate CO
2
.
-Emphysema, pulmonary edema, airway obstruction or
disorders of muscles involved in breathing.

54. Compensatory Mechanism: Increased excretion of
H
+
and increased reabsorption of HCO
3
-
by
1. buffers of body fluids
2.kidneys (require several days to compensate)
Treatment
IV bicarbonate, or sod. lactate or sod. gluconate or
oral sod. bicarbonate
Ventilation
Respiratory Alkalosis
Alkalosis caused by decrease in pCO
2
<35mmHg.
Caused by overventilation of the lungs, stimulation
of resp. center.

55. Conditions:
O
2
def. due to high altitude, Pulmonary
disease, CVA, severe anxiety, aspirin
overdose.
Compensatory mechanism
decreased excretion of H
+
increased reabsorption of HCO
3
-
Treatment
Increase the level of CO
2 in the body
Rebreath from paper bag
Ammonium chloride orally or IV or IV lysine
monohydrochloride

56. Responses in patients with Heart – Lung
transplants
Recipients right atrium and ascending arch of
aorta sutured to donor heart, and donor heart does
not reinnervate
Donor trachea sutured to recipients, just above to
carina, and afferent fibers from lungs do not regrow
Cough response normal to stimulation of trachea
because trachea remains innervate, but to
stimulation of smaller airways absent. Bronchi tend
to be dilated more.
Normal no. of yawns and sighs. So these do not
depend on innervation of lungs.
Lack H-B reflex

57. Respiratory components of Visceral Reflexes
During vomiting, swallowing and gagging, there is
inhibition of respiration and closure of glottis. This
prevents aspiration of food and vomittus into
trachea.
In vomiting, chest fixed – so contraction of
abdominal muscles increases intra abdominal
pressure
Similar glottic closure and inhibition of respiration
occur during voluntary and involuntary straining
Hiccup spasmodic contraction of diaphragm that
produces an inspiration during which glottis
suddenly closes. Glottic closure responsible for
characteristic sensation and sound.

58. Yawning Underventilated alveoli tend to
collapse. Deep inspiration and stretching open
them and prevent atelectasis.
Yawning increases venous return to heart

59. PERIODIC BREATHING
Person breathes deeply for a short interval and then
breathes slightly or not at all for an additional interval.
Cycle repeats.
Chyne – Stokes Breathing is slow waxing and waning
respiration, occurring over and over again about 40-60
sec.

60. Mechanism
When person overbreathes, increases pulmonary O2and
decreased CO2. Takes few secs. To transport to brain and
inhibit respiration. Center responds and inhibit ventilation.
Opposite cycle begins. ie. CO2 increases and O2 decreases.
Takes few secs. To respond. Cycle repeats.

62. PERIODONTAL DISEASE
AND RESPIRATORY
INFECTION

63. Pathogenesis and Risk factors for
Lung Infection
Sterility of lower airways in normal individuals is
maintained by
 Intact cough reflexes
Action of tracheo bronchial secretions
Mucociliary transport of inhaled microorganisms and
particulate matter from the lower respiratory tract to the
oropharynx
Defense factors like surfactant, fibronectin, complement
and immunoglobulins

64. Microorganisms can contaminate lower airways by four
possible routes
Aspiration of oropharyngeal contents
Inhalation of infectious aerosols
Spread of infection from contiguous sites
Hematogenous spread from extrapulmonary sites of
infection

65. DENTAL
CONSIDERATIONS

66. Oral bacteria as etiological agents
of respiratory infection
Severe anaerobic lung infection can occur following
aspiration of salivary secretions especially in patients
with periodontal disease.
A variety of oral anaerobes and facultative species have
been cultured from infected lung fluids including P.
gingivalis, Bacteroids gracilus, Bacteroids oralis,
Bacteroids buccae, Eikenella corrodens, Fusobacterium
nucleatum, Fusobacterium necrophorum etc.

67. Oral bacteria may also have a role in the exacerbations
of COPD. Anaerobic bacteria were cultured from 17% of
transtracheal aspirates from patients with COPD.
Streptococcus was found to be cause of pneumonia in
4% of COPD patients.
P. gingivalis can cause marked inflammation when
instilled into lungs of laboratory animals.

68. Dental plaque as reservoir of
respiratory pathogens
Dental plaque provides a reservoir for colonization of
respiratory pathogens that can be shed into saliva.
Respiratory pathogens that establishes in dental plaque
may be difficult to eradicate.
Bacteria in biofilms are more resistant to antibiotics than
planktonic bacteria.

69. The amount of dental plaque on the teeth of inpatients
increased in three month period as did the proportion of
respiratory pathogens in their dental plaque [Fourrier
F.1998 Crit care Med]

70. Mechanism of Action
Several mechanisms can be envisioned to explain how
bacteria can participate in the pathogenesis of
respiratory infection.
Oral pathogens may be aspirated into lung to cause
infection
Periodontal disease associated enzymes in saliva may
modify mucosal surfaces to promote adhesion and
colonization by respiratory pathogens

71. Periodontal disease associated enzymes may destroy
salivary pellicles on pathogenic bacteria
Cytokines originating from periodontal tissues may alter
respiratory epithelium to promote infection by
respiratory pathogens

73. Prevention of oral colonization by
potential respiratory pathogens
SDD (Selective digestive decontamination) uses
antibiotics topically applied to the surface of git
(including oral cavity) to reduce carriage of pathogenic
bacteria and thus to prevent respiratory infection
Use of lozenges containing Polymyxin B, tobramycin and
amphotericin B have been shown to diminish oral
colonization by gram negative bacteria

74. Maintenance of good oral hygiene may itself reduce
oropharyngeal colonization by respiratory pathogens
Interestingly, chlorhexidine gluconate has been shown to
reduce transfer of group B Streptococci from mother to
infant during parturition.

75. It also appears to inhibit production of proteases by
subgingival bacteria. It diminishes the potential of these
enzymes to process oral surfaces to expose “crytitopes”
that may act as receptors for bacterial adhesins.

76. MEDICAL EMERGENCIES
IN DENTAL PRACTICE

77. Table 1 lists the most common emergencies found in a survey of 4309
dentists practicing in North America

78. Three causes of respiratory distress in dental
environment includes :
Foreign Body Airway Obstruction
Asthma
Hyperventilation

80. Foreign body airway obstruction
Instruments and techniques used to prevent aspiration and
swallowing of objects:
Rubber dam
Oral packing
Chair position
Dental assistant
Suction
Magill intubation forceps
Ligature ( Dental Floss)

81. Management of aspirated foreign
bodies
Place patient in left lateral decubitus position
Encourage patient to cough
If foreign body is retrieved, initiate medical consultation
before discharge
If foreign body is not retrieved, consult with radiologist
or emergency department. Obtain appropriate
radiographs to determine location of foreign body.

82. Perform bronchoscopy to visualize and retrieve foreign
body.
Non invasive procedures
Back blows
Manual thrust
Heimlich maneuver
Chest thrust

83. Invasive procedures
tracheostomy
cricothyrotomy

84. Hyperventilation
It is defined as ventilation in excess to that of required
to maintain normal blood arterial oxygen tension and
arterial carbon dioxide tension.
It is produced by increased frequency or depth of
respiration or both.

85. Clinical manifestations
Cardiovascular
Palpitations
Tachycardia
Neurologic
Dizziness
Light headedness
Disturbance of vision
Numbness and tingling of extremities

86. Respiratory
Shortness of breath
Chest pain
Dryness of mouth
Gastrointestinal
Globus hystericus
Epigastric pain

87. Musculoskeletal
Muscle pain
Tremor
Stiffness
Psychological
Tension
Anxiety

88. Management
Correction of respiratory alkalosis
3 to 5 mg midazolam is DOC

89. Asthma
It is defined as a chronic inflammatory disorders
characterised by reversible obstruction of airways.
Types : extrinsic
intrinsic
Causative factors include allergy, respiratory infection,
physical exertion, occupational stimuli and psychological
factors

90. Commonly prescribed drugs
1. Bronchodilators
Salbutamol , Terbutaline, Theophylline, Ipratropium bromide
2. Leukotriene antagonists
Montelukast, Zafirlukast
3. Mast cell stabilizers
Sodium cromoglycate, Ketotifen
4. Corticosteroids
Systemic (hydrocortisone, prednisolone)

91. Inhalational (beclomethasone dipropionate,budesonide)
Anti – IgE antibody
Omalizumab

92. Clinical manifestations
Chest congestion
Cough
Wheezing
Dyspnoea
Rise in blood pressure
Agitation
Somnolence
Confusion

93. Management
Administer oxygen
Administer bronchodilator