2. Q What is breathing?
Breathing is entrance and exit of air into and out of lungs.
Mechanism of breathing:
Breathing called ventilation consists of two phases:-
Inspiration
Expiration
Inspiration: - is an active process. During inspiration the size
of thoracic cavity is increased by contraction of appropriate
muscles.
Expiration:- is a passive process. At the end of inspiration,
the muscle which contracts actively during inspiration relaxes
and the elastic recoil of thoracic wall and lungs cause passive
expiration
At rest an adult breathes at a respiratory rate of 12-
14 breaths per minute and the amount of air inspired or
expired per breath(i.e. tidal air) is approximately 500
ml.Thus,6-7 litres of air is breathed on or out of the lungs
per minute called pulmonary ventilation
3. Q what is the difference between breathing and
respiration?
Generally breathing and respiration are often
considered the same, however there is a big
difference in the meaning of the two.
Breathing is when you consistently breathing air
in and out. It is the process of taking in oxygen
and expelling carbon-dioxide.
Respiration is the process in which the C-H
bonds (carbon-hydrogen bonds) in food are
broken down by oxidation reduction reactions
and the energy is transformed in to ATP.
4. Breathing is under the control of the Autonomic
nervous system. This means it is involuntary
action.
An involuntary action is one which occurs without
the conscious choice of an organism.
We can control the rate and depth of breathing
voluntarily by;
Nervous system which includes:-
Chemoreceptor’s (sensitive to CO2 and H+
Respiratory centre of medulla oblongata
Stretch receptors in Alveoli
5. When the CO2 and subsequently H+ concentration in
the blood increases, the activity of Medulla Oblongata
is temporarily increases
(NOTE:- The medulla oblongata is the most vital part
of the brain because it is the control centre for
breathing, blood pressure and heart beat among
other involuntary body functions under all
unconscious control)
What happens to CO2 in the blood?
CO2 + H+-------------------H2CO3
Then,
H2CO3----------------------- H+ + HCO3
This is why CO2 level in the blood lead to an increase
in H+ level
6. Chemoreceptor’s located in the carotid arteries
and the aorta respond O2 level in the blood.
( A Chemoreceptor, also known as chemo
sensor, is a sensory receptor that produces a
chemical signal into an action potential.)
When O2 level in the blood are low, a nerve
impulse is stimulate the respiratory centre of
medulla oblongata.
7. The alveoli contain stretch receptors.
(Stretch receptors:-They are the
mechanoreceptors responsive to various
organs and muscles, and are neurologically
linked to the medulla in the brain via afferent
nerve fibers.)
When the alveoli are full, the stretch receptors
sent a signal to the respiratory centre.
This signal inhibits the respiratory centre
(negative feedback)
8. The muscles of respiration are also called the breathing
pump muscles they form a complex arrangement in the
form of semirigid bellows around the lungs.
All muscles which are attached to the human rib cage have
the inherent potential to cause a breathing action.
Muscles that help in expanding the thoracic cavity are
called the inspiratory muscles because they helps in
inhalation, while those that compress the thoracic cavity
are called expiratory muscles and they induce exhalation.
The specialities of these muscles are that they are
composed of fatigue resistant muscle fibres; they are
controlled by both voluntary and involuntary mechanisms
The primary inspiratory muscles are the diaphragm and
external intercostals
9. It is a double-domed sheet of internal skeletal muscle that
separates the thoracic cavity from the abdominal cavity
Origin:- xiphoid process (posterior surface), lower six ribs
and their coastal cartilage (inner surface) and upper three
vertebrae as right crus and upper two lumbar vertebrae as
left crus.
Insertion:- central tendon
Nerve supply:- Motor nerve supply by phrenic nerve(C3 C4
C5) and sensory supply by phrenic nerve to central tendon
and lower 6 or 7 intercostals nerve to peripheral parts.
Blood supply: - inferior phrenic arteries deliver the
majority of blood supply and the remaining supply is
delivered via superior phrenic, musculophrenic and
pericardiacophrenic arteries.
10. They are of three types
External intercostal muscles(most superficial
muscle)
Internal intercostal muscle.
Innermost intercostal muscle.
External intercostal muscle:-
Origin:-inferior border of rib above.
Insertion:-superior border of rib below
11. Internal intercostal muscle:-
Origin:- from the costal groove(lower part of
inner surface of rib near the inferior border) of the
rib above.
Insertion:-upper border of rib below
12. Innermost intercostal muscles:-
It is an incomplete muscle layer and crosses more
than one intercostal space. These muscles assist in
the function of external and internal intercostal
muscles.
Origin:- from the costal groove of the rib above
Insertion:- the superior border of rib below.
Nerve supply:-
All the intercostal muscles are supplied by their
respective intercostal nerves
Blood supply:-
All three muscles receive blood supply from anterior
and posterior intercostal arteries, in addition to
internal thoracic and musculophrenic arteries,
costocervical trunk for internal and innermost
intercostal muscles.
13. PFT tracings have:
Four Lung volumes: tidal volume, inspiratory
reserve volume, expiratory reserve volume, and
residual volume
Five capacities:, inspiratory capacity, expiratory
capacity, vital capacity, functional residual
capacity, and total lung capacity
14.
15. Tidal Volume (TV): volume of air inhaled or exhaled
with each breath during quiet breathing (6-8 ml/kg)
Inspiratory Reserve Volume (IRV): maximum volume
of air inhaled from the end-inspiratory tidal
position.(1900-3300ml)
Expiratory Reserve Volume (ERV): maximum volume
of air that can be exhaled from resting end-
expiratory tidal position.( 700-1000ml).
Residual Volume (RV): Volume of air remaining in
lungs after maximum exhalation (20-25 ml/kg)
(1700-2100ml)
Indirectly measured (FRC-ERV)
It cannot be measured by spirometry.
16. Total Lung Capacity (TLC): Sum of all volume compartments or
volume of air in lungs after maximum inspiration (4-6 L)
Vital Capacity (VC): TLC minus RV or maximum volume of air
exhaled from maximal inspiratory level. (60-70 ml/kg) (3100-
4800ml)
Inspiratory Capacity (IC): Sum of IRV and TV or the maximum
volume of air that can be inhaled from the end-expiratory tidal
position. (2400-3800ml).
Expiratory Capacity (EC): TV+ ERV
Functional Residual Capacity (FRC):
Sum of RV and ERV or the volume of air in the lungs at end-
expiratory tidal position. (30-35 ml/kg) (2300-3300ml).
Measured with multiple-breath closed-circuit helium dilution,
multiple-breath open-circuit nitrogen washout, or body
plethysmography.
It cannot be measured by spirometry
17. TIDAL VOLUME (TV):
VOLUME OF AIR INHALED/EXHALED IN EACH
BREATH DURING QUIET RESPIRATION.
N – 6-8 ml/kg.
TV FALLS WITH DECREASE IN COMPLIANCE,
DECREASED VENTILATORY MUSCLE STRENGTH.
INSPIRATORY RESERVE VOLUME (IRV):
MAX. VOL. OF AIR WHICH CAN BE INSPIRED AFTER
A NORMAL TIDAL INSPIRATION i.e. FROM END
INSPIRATION PT.
N- 1900 ml- 3300 ml.
18. EXPIRATORY RESERVE VOLUME (ERV):
MAX. VOLUME OF AIR WHICH CAN BE EXPIRED
AFTER A NORMAL TIDAL EXPIRATION i.e. FROM
END EXPIRATION PT.
N- 700 ml – 1000 ml
INSPIRATORY CAPACITY (IC) :
MAX. VOL. OF AIR WHICH CAN BE INSPIRED AFTER
A NORMAL TIDAL EXPIRATION.
IC = IRV + TV
N-2400 ml – 3800 ml.
19. VITAL CAPACITY: COINED BY JOHN HUTCHINSON.
MAX. VOL. OF AIR EXPIRED AFTER A MAX.
INSPIRATION.
MEASURED WITH VITALOGRAPH
VC= TV+ERV+IRV
N- 3.1-4.8L. OR 60-70 ml/kg
VC IS COSIDERED ABNORMAL IF ≤ 80% OF
PREDICTED VALUE
VC correlates with capability for deep breathing
and effective cough.
So in post operative period if VC falls below 3
times VC– artificial respiration is needed to
maintain airway clear of secretions.
20. TOTAL LUNG CAPACITY:
Maximum volume of air attained in lungs
after maximal inspiration.
N- 4-6 l or 80-100 ml/kg
TLC= VC + RV
RESIDUAL VOLUME (RV):
Volume of air remaining in the lungs after
maximal expiration.
N- 1570 – 2100 ml OR 20 – 25 ml/kg.
21. FUNCTIONAL RESIDUAL CAPACITY (FRC):
Volume of air remaining in the lungs after
normal tidal expiration, when there is no
airflow.
N- 2.3 -3.3 L OR 30-35 ml/kg.
FRC = RV + ERV
Decreases under anesthesia
with spontaneous Respiration – decreases by
20%
With paralysis – decreases by 16%
22. FACTORS AFFECTING FRC
FRC INCREASES WITH
Increased height
Erect position (30% more than in supine)
Decreased lung recoil (e.g. emphysema
23. FRC DECREASES WITH
Obesity
Muscle paralysis (especially in supine)
Supine position
Restrictive lung disease (e.g. fibrosis, Pregnancy)
Anesthesia
FRC does NOT change with age.
FUNCTIONS OF FRC
Oxygen store
Buffer for maintaining a steady arterial po2
Partial inflation helps prevent atelectasis
Minimized the work of breathing
Minimized pulmonary vascular resistance
Minimized v/q mismatch
- only if closing capacity is less than frc
Keep airway resistance low (but not minimal
24. Pulmonary function tests are a group of tests that measure how
well the lungs take in and release air and how well they move
oxygen into the blood(it is a non-invasive).
GOALS
To predict the presence of pulmonary dysfunction
To know the functional nature of disease (obstructive or
restrictive. )
To assess the severity of disease
To assess the progression of disease
To assess the response to treatment
To identify patients at increased risk of morbidity and
mortality, undergoing pulmonary resection.
To wean patient from ventilator in ICU.
Medico legal- to assess lung impairment as a result of
occupational hazard.
Epidemiological surveys- to assess the hazards to document
incidence of disease
To identify patients at perioperative risk of pulmonary
complications.
25. In a spirometry test, you breathe into a
mouth piece that is connected to an
instrument called a spirometer.The
spirometry records the amount and the rate
of air that you breathe in and out over a
period of time.
Spirometry is a medical test that measures
the volume of air an individual inhales or
exhales as a function of time.”
Measures VC, FVC, FEV1, PEFR.
CAN’T MEASURE – FRC, RV, TLC
26. INDICATIONS OF PFT IN PAC
TISI GUIDELINES FOR PREOPERATIVE SPIROMETRY
Age < 70 yrs.
Morbid obesity
Thoracic surgery
Upper abdominal surgery
Smoking history and cough
Any pulmonary disease
INDICATIONS FOR PREOPERATIVE SPIROMETRY
Lung resection
H/o smoking, dyspnoea
Cardiac surgery
Upper abdominal surgery
Lower abdominal surgery
Uncharacterized pulmonary disease(defined as history
of pulmonary Disease or symptoms and no PFT in last
60 days)
27. (I)PLETHSYMOGRAPH:-
The most accurate way is to sit in a sealed, clear box that looks
like telephone booth(body plethysmography) while breathing in
and out into a mouth piece. Changes in pressure inside the box
helps to determine the lung volume.
(ii) Lung volume by helium dilution:-
Patient breathes in and out of a spirometer filled with 10% helium
and 90% 02, till concentration in spirometer and lung becomes
same (equilibrium).
As no helium is lost; (as helium is insoluble in blood)
C1 × V1 = C2 ( V1 + V2)
V2 = V1 (C1 – C2)
C2
V1= VOL. OF SPIROMETER
V2= FRC
C1= Concentration of Helium in the spirometer before
equilibrium
C2 = Concentration of Helium in the spirometer after equilibrium
28. Patient inspires a diluted mixture of Co and hold the breath
for 10 seconds (contains 10% helium, 0.3% Co, 21% oxygen
and remaining nitrogen)
Carbon-monoxide is taken up is measured by infared
analysis
Normal range is 20-30 ml/min/mmhg
DLO2= DLCo × 1.23
DECREASED DLCo:-
Obstructive lung disease
Parenchyma disease
Pulmonary vascular disease
Anaemia
INCREASED DLCo:-
Asthama
Pulmonary haemorrhage
Polycythemia
Left or right shunt
29. 4. EXERCISE TEST:-
Incidence of exercise induced broncho-
constriction is observed in 70-80% of
patients with Asthama.
Before performing this test broncho-dilators
are with-held, spirometry is then performed
before and after 5, 15 & 30 minutes of post
exercise.
A positive test is diagnosed when FEV1 and
FVC is reduced by 15% after exerciser as
compared to before exercise
30. (a) Breath holding time:-
It is very simple and useful bed side test.
Normal is more than 25 seconds
Breath holding time 15-20 sec is border line cases
Breath holding time less than 15 sec indicates severe
pulmonary dysfunction
(b) Match blow test:-
Patient is asked to below off math stick from a distance
of 15 cms. A person with normal pulmonary reserve
will blow off this match stick from this distance.
(c) Tracheal auscultation:-
If breath sounds are audible for more than 6 sec. It
denotes significant airway obstruction
(d) Able to blow a balloon
31. DEAD SPACE:-
Dead space is the amount of air in respiratory
passage which does not take part in gas exchange.
It is of two types
Anatomical dead space
Physiological dead space
32. Anatomical dead space: - is the volume of air
present in conducting zone of respiratory
passage i.e. from nose and mouth up to
terminal bronchioles where exchange of
gases does not takes place
Normal value:-150 ml or 2ml/kg or 30% of
tidal volume. (Approx equal to body weight in
pounds)
33. Physiological dead space:- includes anatomical
dead space plus volume of air in the alveoli which
does not take part in exchange of gases(i.e. wasted
alveolar ventilation)
For example,
Volume of inspired air which ventilates alveoli but
receives no pulmonary capillary blood flow.
Some of the alveoli may be over ventilated, i.e.
volume of inspired air which ventilates alveoli in
excess of that volume which is required to
equilibrate with blood.
Clinically anatomical dead and physiological dead
spaces are same in healthy subjects.
34. Alveolar dead space:- constituted by alveoli which
are only ventilate but not perfused.it is 60-80 ml in
standing position and Zero in lying position(in lying
position perfusion is equal in all parts of the body)
It is increased by lung pathologies, general
anaesthesia, IPPV, PEEP, and hypotension
ANAESTHESIA AND DEAD SPACE:-
All anaesthesia circuits, masks, humidifiers
increases dead space.
ET tubes, tracheotomy tubes decreases the
anatomical dead space by bypassing the upper
airways.
All inhalational agents increase both anatomical
dead space and alveolar dead space. Anatomical
dead space is increased because all these agents are
bronchodilators and alveolar dead space is
increased because of hypotension produced by
these agents (V/Q mismatch).
35. The pleural cavity also known as the pleural space is
the thin fluid-filled space between the two pulmonary
pleurae (known as visceral and parietal) of each lung.
The space is filled with (approximately 2ml) of serious
lubricating fluid called pleural fluid. This fluid keeps
the two pleurae together. Therefore when one moves
the other follows. That is why the lungs slide easily on
the chest wall but resist by being pulled away from it in
the same way that two moist pieces of glass slide on
each other but resist separation.
The lungs are enveloped by pleura which has
two layers
Parietal pleura
Visceral pleura
36. PARIETAL PLEURA:- is adherent to the parieties, i.e.
inner side of the chest wall and the thoracic side of
the diaphragm. Therefore, when these structures
move, the parietal pleura has to move
VISCERAL PLEURA:- is adherent to the underlying
viscus i.e. the lungs. Therefore when the viscus
(lungs) moves, it has to follow the viscus
37. Intrapleural pressure also called intrathoracic
pressure refers to the pressure within the pleural
cavity. Normally, the pressure within the pleural
cavity is slightly less than the atmospheric pressure
(known as negative pressure).
When the pleural cavity is damaged/ruptured and
the intrapleural pressure becomes equal to or
exceeds the atmospheric pressure, pneumothorax
may ensure.
Intrapleural pressure depends on the ventilation
phase, atmospheric pressure and the volume of
intrapleural cavity
At rest we have a negative intrapleural pressure
38. Factors affecting are:-
Physiological effects:-
Muller’s manoeuvre(forced inspiration against a
closed glottis results in negative pressure)
Deep inspiration
Pathological effects:-
Emphysema
Pneumothorax condition
39. This condition occurs when air leaks into the
space between the lungs and chest
wall(pleural space). A blunt or penetrating
chest injury, certain medical procedures or
lung disease can cause a pneumothorax.
TYPES:-
Traumatic pneumothorax
Non-traumatic pneumothorax
40. Traumatic pneumothorax:- occurs after some
type of trauma or injury has happened to the
chest or lung wall. It can be minor or
significant injury. The trauma can damage
chest structures and cause air to leak into the
pleural space e.g. broken ribs, trauma to
chest from a motor vehicle accident, medical
procedures such as center line placement,
ventilator use,CPR etc
41. Non-traumatic pneumothorax:-this type of
pneumothorax doesn’t occur due to injury,
instead it happens spontaneously, which is why
it’s also referred to as spontaneous
pneumothorax.
There are two types of spontaneous
pneumothorax
Primary spontaneous pneumothorax (PSP):-
occurs in people who have no known lung
disease, often affecting young males who are tall
and thin.
Secondary spontaneous pneumothorax (SSP):-
occurs in older people with known lung disease
e.g. COPD, Tuberculosis, lung cancer, asthma
42. Spontaneous hemopneumothorax (SHP) is a rare
sub type of spontaneous pneumothorax. It
occurs when both blood and air fill the pleural
cavity without any recent trauma or history of
lung disease
SYMPTOMS:
Sudden chest pain
Shortness of breath(dyspnea)
Turning blue or cyanosis
Severe tachycardia
Breaking out in a cold sweat
43. Chest injury: - any blunt or penetrating injury to
chest can cause lung injury e.g. Car crashes.
Lung disease:-damaged lung tissue is more likely
to collapse. Lung damage can be caused by many
types of underlying disease such as
COPD,Pneumonia and cystic fibrosis
Ruptured air blister:-small air blister can develop
on the top of the lungs. These blisters sometimes
burst allowing air to leak into the space that
surrounds the lungs.
Mechanical ventilation:-ventilator can create an
imbalance of air pressure within the chest, the
lung may collapse completely
44. Smoking
Genetics
Lung disease
Mechanical ventilation
Previous pneumothorax
TREATMENT
Treatment for a pneumothorax usually involves
inserting a needle or chest tube between the
ribs to remove the excess air.
A small pneumothorax may heal on its own.
45. Work of breathing (WOB) is the energy expended to inhale
and exhale a breathing gas. It is defined as, work=
pressure×volume, measured in joules.
It is usually expressed as work per unit volume, e.g.
joules/litre, or as work rate (power) such as joules/minute.
It is not particularly useful without a reference to volume or
time.
It can be calculated in terms of the pulmonary pressure
multiplied by the changes in pulmonary volume or in terms
of the oxygen consumption attributable to breathing.
In a normal resting state the work of breathing constitutes
about 5% of the total body oxygen consumption.
It can increase considerably due to illness, ambient
pressure or breathing gas consumption
46. Work of breathing is divided into
Elastic work: - refers to the work of intercostal
muscles, chest wall and diaphragm. Increases
the respiration rate, increases the flow resistive
work of the airways and decreases the elastic
work of the muscles. Decreasing the respiratory
rate reverses the type of work required.
It is about 65% of total work, and is stored as
elastic potential energy. Energy required
overcoming elastic forces:
Lung elastic recoil
Surface tension of alveoli
Resistive work:-about 35% of total work, and
refers to the work of alveoli and tissues in the
lungs
47. Airway resistance is the opposition to flow caused by
the force of friction. It is defined as the ratio of driving
pressure to the rate of air flow. Resistance to flow in
the airways depends on whether the flow is laminar or
turbulent, on the dimensions of the airway, and on the
viscosity of the gas.
Airway resistance decreases as lung volume increases
because the airways distend as the lungs inflate, and
wider airways have lower resistance.
Single small airway provides more resistance than a
single large airway, resistance to air flow depends on
the number of parallel pathways present, for this
reason, the large and particularly the medium-sized
airways actually provide greater resistance to flow than
do the more numerous small airways.
48. Lung compliance is a measure of lungs ability
to stretch and expand.
In clinical practice it is separated into two
different measurements:-
Static lung compliance:- is the change in
volume for any given applied pressure.
49. Dynamic lung compliance:- is the compliance of the
lung at any given time during actual movement of air.
Low compliance indicates a stiff lung (one with high
elastic recoil) and can be thought of as a thick balloon,
this is the case often seen in fibrosis.
High compliance indicates a pliable lung( one with low
elastic recoil) and can be thought of as a grocery bag,
this is the case seen in emphysema.
Compliance is highest at moderate lung volumes, and
much lower at volumes which are very low are very
high.
The compliance of the lungs demonstrates lung
hysteresis; that is, the compliance is different on
inspiration and expiration for identical volumes.
Lung compliance is an important measurement in
respiratory physiology.
Fibrosis is associated with a decrease in pulmonary
compliance.
Emphysema/COPD may be associated with an increase
in pulmonary compliance due to loss of alveolar and
elastic tissue
50. Compliance decreases in the following cases:-
Supine position
Laparoscopic surgical interventions
Severe restrictive pathologies
Pneumothorax
Acute asthma attacks
Hydrothorax
Compliance increases with increasing age
51. Anaesthesia causes impairment in pulmonary function, whether
the patient is breathing spontaneously or is ventilated
mechanically after muscle paralysis.
Impaired oxygenation of blood occurs in most subjects who are
anaesthetized.
It has therefore become routine to add oxygen to the inspired gas
so that the inspired oxygen fraction (fio2) is maintained at around
0.3-0.4.
Despite these measures, mild to moderate hypoxemia, defined as
an arterial oxygen saturation of between 85% and 90% may occur
in approximately half of all patients undergoing elective surgery,
and the hypoxemia can last from few seconds up to 30 minutes.
About 20% of patients may suffer from severe hypoxemia, or
oxygen saturation below 81% for up to 5 minutes.
Lung function remains impaired postoperatively, and clinically
significant pulmonary complications can be seen in 1% to 2% after
minor surgery in up to 20% after upper abdominal and thoracic
surgery
52. The first phenomenon that might be seen with anaesthesia
is loss of muscle tone with a subsequent change in the
balance between outward forces(i.e. respiratory muscles)
and inward forces (i.e. elastic tissue in the lung) leading to
fall in FRC.
The decrease in FRC affects the patency of lung tissue with
the formation of atelectasis (made worse with the use of
high concentrations of inspired oxygen) and airway closure.
This alters the distribution of ventilation, matching of
ventilation, blood flow, impedes oxygenation of blood and
removal of carbon-dioxide.
FRC is reduced by 0.8-1.0 litre by changing body position
from upright to spine, and there is another 0.4-0.5 litre
decrease when anaesthesia has been induced.
End-expiratory lung volume is thus reduced from
approximately 3.5 -2 litres, the later being close or equal to
Residual volume.
Static compliance of the total respiratory system ( lungs &
chest wall) is reduced on average from 95-60ml/cm H2O
during anaesthesia
53. There is decrease in compliance during anaesthesia when
compared to awake states.
There are also studies on resistance of the total respiratory
system and the lungs during anaesthesia; most of them
show a considerable increase during both spontaneous
breathing and mechanical ventilation.
Atelectasis appears in approximately 90% of all patients
who are anaesthetized; it is seen during spontaneous
breathing and after muscle paralysis and whether
intravenous or inhaled anaesthetics are used. Thus 15%-
20% of the lung is regularly collapsed at the base of the
lung during uneventful anaesthesia, before any surgery has
even been done.
Although this was expected, it came as a surprise that the
atelectasis is independent of age, with children and young
people showing as much atelectasis as elderly patients.
The mechanism that prevents the lung from collapse is not
clear but may be airway closure occurring before alveolar
collapse takes place, or it may be altered balance between
the chest wall and the lung that counters a decrease in lung
dimensions.
54. This is downward movement of trachea
during deep inspiration.
It is seen in:-
Deep anaesthesia (by inhalation agents).
Partially curarized patient.
Upper airway obstruction (this is the main
reason of tracheal tug at the end of
anaesthesia as airway is obstructed by
secreations).
55. During deep anaesthesia and partially
curarized patient diaphragm is not supported
by costal margins. Also larynx is not
supported by neck muscles so strong
contraction of central part of diaphragm pulls
the trachea downwards.
SIGN:-
It is deep inspiratory hold.
56. HICCUP:-
Intermittent clonic spasm of diaphragm of reflex
origin.
CAUSES:-
Light anaesthesia
Gastric and bowel distension.
Diaphragm irritation by touching diaphragm in upper
abdominal surgeries.
Uremia.
TREATMENT:-
Increase the depth of anaesthesia.
Muscle relaxants.
Pharyngeal stimulation by nasal catheters, Valsalva`s
maneuver, CO2 inhalation.
Drugs
Ether
For intractable hiccups, phrenic nerve block may be
required.