AAU

Faculty of Medicine
School Anaesthesia
Subject → Airway and its maintenance

The Golden Rule in Anaesthesia is “ Perfect Airway Always” (the patients life depends on the patency of the
airway for which the anesthetist is responsible)

A Safety Rules in Anaesthesia includes

(a) Asses and prepare patient adequately

(b) Starve the patient
(c) Anaesthesize on a tipping table
(d) Check your drugs and equipment
(e) Keep a sucker instantly ready
(f) Keep his airway clear
(g) Be ready to control his respiration
(h) Have a vein open
(i) Monitor his pulse and BP continuously
(j) Always have some one in the room who can apply cricoid pressure effectively

Disasters to Airway management are usually preventable if you recognize them in time

The best anesthetic technique will be one with which you are most experienced and confident to maintain the
airway

Maintenance of airway

. Maintenance of a patient upper airway and intubation of the trachea (Trans laryngeal intubation) depends on the
knowledge of the anatomy of the airways and appropriate use of equipment and drugs.

Respiratory system is divided into

1. Upper respiratory tract – Nose, Mouth, Pharynx Larynx

2. Lower respiratory tract – trachea, bronchi, lungs

Functions and organs

1. Air distribution, and gas exchange, so that oxygen be supplied to and CO2 removed from the body cells
. First air must exchange gas with blood and blood must circulate and finally blood and blood cells must
exchange gases
. Tiny sacs or alveoli function as air distributors

Tiny passage ways (ducts) that open into them serve as gas exchangers

2. Filtering warming and Humidifying the inspired air

3. Sound production. Resonator in speech and acts as organ of olfaction
4. Control homeostasis of body PH
Upper respiratory tract

The Nose
(a) External
 (b) Internal

External - protrudes from the face

- consists bone and cartilages

- Skin with many sebaceous gland

Roof of Nose → formed by two nasal bones

→ surrounded by frontal bone

Laterally

Inferiorly the nose is surrounded by the maxilla

At its base

The flaring cartilllagous expansions forming and supporting the outer side of each oval nostril opening is called Ala:

NB→The fact that the skin of external nose contains many sebaceous glands which has great significance if these
glands become blocked it is possible for infectious material to enter and pass from facial veins near the nose to one
of the intracranial venous sinuses for this reason the triangular shaped zone surrounding the external nose is often
known as the Danger area of the face.

The internal Nose (Nasal Cavity)

. Lies the roof of the mouth

. Palatine bone forms the floor of the nose

. Hard palate – forms the roof of the nose

. Nasal cavity separated from mouth cavity by palatine bones

. Sometimes the palatine bone fails to unite completely condition called Cleft Palate in which the mouth partially
separated from the nasal cavity and difficulty in swallowing

. THE ROOF OF THE NOSE IS SEPARATED FROM THE CRANIAL CAVITY BY A PORTION OF
ETHIMOID BONE CALLED CRIBRIFORM PLATE. PERFORATED BY MANY SMALL OPENING
PERMITS BRANCHES OF OLFACTORY NERVE FOR SPECIAL SENSE OF SMELL TO REACH
CRANIAL CAVITY (BRAIN)

The Hallow Nasal cavity separated by middle portion of the septum into (Rt and Lf)

The septum made up of four structures

(a) Pre pendicular plate of ethimoid bone from above

(b) The vomer vomeronasal and septal cartilages from bellow

The nasal septum has a rich blood supply nose bleeds or epitasis often occur as a result of septal collusions caused
by direct blow to the nose.

The external opening into nasal cavities nostrils (anterior nares) they open into an area called vestibule located in
nasal cavity below the inferior meatus
COARSE HAIRS CALLED VIBRISSAE SEBACEOUS GLANDS AND NUMEROUS SWEAT GLANDS
ARE FOUND IN THE SKIN OF VESTIBULE

- Once air has passed over the skin of the vestibule it inters the respiratory portion of each nasal passage
this area extends from the inferior meatus to funnel shaped orifices of the posterior nares or choanae
the posterior nares (choanae) are openings that allow air to pass from an area of internal nasal cavity
above superior meatus called speneo ethmiod recess into the naso pharynx once air has passed through
the posterior nares it has left nasal cavity and enter the next major segment of upper respiratory tract.
(the pharynx).

PASSAGE SEQUENCE OF AIR THROUGH THE NOSE

ANTERIOR NARES (NOSTRILIS)

VESTIBULE

INFERIOR, MIDDLE AND SUPERIOR MEATI SIMULTANEOUSLY

POSTERIOR NARES (CHOANAE) AND SPHENO ETHIMIODAL RECESS SIMULTANEOUSLY

Nasal Mucosa

. Highly specialized respiratory mucosa

. Has got pseudo stratified ciliated columnar epithelium rich in goblet cells

. Contains many mucous glands

. Respiratory mucosa posses a rich blood supply especially over the inferior conchae and is bright pink or red in
color

. Near the roof of the nasal cavity and over the superior conchae and opposing portions of the septum the mucosa
turns pale and has a yellowish tint in this area it is referred to as the olfactory epithelium this specialized membrane
contains many olfactory nerve cells and has a rich lymphatic plexus.

. Ciliated mucosal membrane lies the rest of the respiratory tract down as far as the smaller bronchioles

Para Nasal sinuses

. Lined by respiratory mucosa

. Mucous secretion swept into the nose by ciliated surface of respiratory membrane

Four pairs of Para nasal sinuses

. Air containing spaces that open or drain in to the nasal cavity and take their names from the skull bones in which
they are located

(a) Frontal – Right and left located above corresponding orbit

(b) Maxillary – The largest of the sinuses extend into maxilla on either side of the Nose
(c) Ethmiod – collection of small air cells divided into anterior, middle and posterior groups that open
independently
 (d) Sphenoid – lies in the body of the sphenoid bone on either side of the mid line in a very close proximity to
the optic nerves and pituitary gland.

Drainage of para nasal Sinuses

. Into middle meatus (passage way below middle turbinate) frontal maxillary, anterior, and middle ethmiod sinuses

. Into superior meatus – posterior ethomiodal sinuses

. Into the space above the superior turbinates) sphenoethimiodal recess) sphenoid sinuses

Functions of the nose

1. Air passage (if obstructed problem) e.g. pediatrics

2. Filtering of impurities – by vibrissae or hairs in vestibulae
3. Warming moistening – turbinates or chonchae provide copious quantities of mucous and rich blood supply
specially over the inferior conchae rapidly moistening and warming the inspired air

. Mucous secretions provide final trap for removal or remaining particulate matter from air as it passes through
nasal mucosa

. Fluid from lacrimal duct and additional mucous product in the Para nasal sinuses help to trap and moisten the
particulate matter

4. The hallow sinuses act to lighten the bones of the skull and serve as resonating chamber for speech
5. Deflection of air by the middle and superior chonchae over the olfactory epithelium makes the special
sense of smell possible

The pharynx

. Wide muscular tube about 12.5 cm. (5 inches) long

. Forms common pathway for respiration and alimentary tract

. Extends from base of skull to the esophagus and lies anterior to cervical vertebrae

. Communicates anterior with the nasal cavity, the mouth and larynx

Three Anatomical divisions of pharynx

I. Naso pharynx – located behind extending from posterior nares to the level of soft palate
(communicates with oropharynx through) pharyngeal isthmus which becomes closed off during
swallowing naso pharyngeal tonsils (Adenoids) lies on the roof and posterior wall of the naso pharynx.
II. Or pharynx → located behind the mouth from the soft palate above to the level of Hyoid. Bone below
the mouth cavity leads into the oropharynx through the or pharyngeal Isthmus which is bounded by the
palatoglossal arches the soft palate and the dorsum of the tongue the oropharynx itself extends in the
height from the soft palate to the tip of epiglottis. Its important features are the tonsils (the palatine
tonsils)

III. Laryngo pharynx

Extends from hyoid bone to its termination in the esophagus

. Extends from the tip of epiglottis to the lower border of the cricoids at level of C6. Its anterior aspect
faces first the laryngeal inlet bounded by the aryepiglottic folds then below this the posterior aspect of
the arytenoids and finally the cricoids cartilages the larynx bulges back in to the center of laryngo
pharynx leaving arecess on either side termed the priform fossa. It is here that swallowed sharp
foreign bodies such as fish bone tend to impact.
 The palatine and pharyngeal tonsils together with lymph collections on the posterior part of the tongue
and in relation to the Eustachian tube form a more or less continuous ring of lymphoid tissue around
the pharyngeal entrance which is termed waldeyers ring.

Anaesthesia for oro and naso pharynx

. Obtained by LA spray to posterior or lateral wall of pharynx

Seven openings are found in the pharynx

(a) Right and left Auditory Opening in to Nasopharynx (Eustachian tubes)

(b) Two posterior nares into naso pharynx
(c) The opening from the mouth known as fauces into oropharynx
(d) The opening into the larynx from the laryngo pharynx
(e) The opening into the esophagus from the laryngo pharynx

The Adeniods or Pharyngeal Tonsils

. Location – Naso pharynx (behind posterior nares)

. If enlarged – fill space behind posterior nares

- Difficult for air to pass

- Patient keeps mouth open to breath “Adenoidy Appearance”

. Two pair of organs in oropharynx

(a) The faucial

Or Located behind and below pillars of fauces
. the palatine tonsils
(b) The lingual tonsils – Located at base of tongue

NB. The palatine tonsils are usually removed by tonsillectomy

Functions of pharynx

(a) Common passage for food and air

. Plays part in phonation (by changing its shape can the different vowel sound be formed)

Nerve supply to pharynx (three fold)

. glosso pharyngeal nerve – via pharyngeal plexus

. the posterior palatine branch of maxillary nerve
. twigs from the laryngeal branch of mandibular nerves for this reason in filtration of anesthesia of the tonsils is
more practicable than attempts at nerve blockade.

Ludwig’s Angina that means pain in throat

. Because of the facial coat inflammatory edema may spread down wards from infections with in the mouth or the
tonsils or from dental sepsis can produce edema of pharynx and larynx and may cause difficulty of swallowing and
then immediately progress to laryngeal obstructions.

Remedy → surgical drainage of deep pharyngeal tissues

Anesthesia → tracheostomy under LA (Advisable)
THE LARYNX

- Protective valve at the upper end of respiratory passages

- Triangular in shape
- Consists of large articulating cartilages
- Linked together by ligaments
- Moves in relation to each other by the action of laryngeal muscles
- Lined by ciliated mucous membrane
- The mucous membrane lining the larynx forms two pairs of folds that jut inward into its cavity and
divide in to three compartments or divisions

The upper pair → vestibular or false vocal folds (they play no part in vocalization)

The lower pair → true vocal cords

The slit like space between the true vocal cords →Rimaglottis or glottis (the narrowest part of larynx adults)

The Divisions or Compartment of Laryngeal Cavity

Laryngeal Cavity – Extends from the triangular inlet at epiglottis to circular out let at the lower border of cricoids
cartilage. Where it continuous with the lumen of trachea.

I. The cavity above the false or vestibular vocal folds is called the vestibule
II. The very short middle portion of the cavity between the false and true vocal cords is the
ventricular division or ventricle
III. The lower compartment extending from the true vocal cords to the out let is referred to as the in
fraglottic larynx

N.B . EDEMA OF THE MUCOSA COVERING THE VOCAL CORDS IS A POTENTIALLY LETHAL
CONDITION

CARTILAGES OF LARYNX
THE PRINCIPAL CARTILAGES OF THE LARYNX ARE THE FOLLOWING

The three largest and unpaired

a. thyroid
b. cricoid
c. epiglottis

The three paired

a. arytenoids
b. corninulate
c. Cuneiform

1. The Thyroid Cartilage (Adams apple)

. largest cartilage of larynx
 . gives characteristic triangular shape to the anterior wall

2. The epiglottis

. Small roof shaped cartilage that projects up ward behind the tongue and hyoid bone

. Attached to the thyroid from below

. Free superior border (move up and down during swallowing and prevents liquids and food from entering the
trachea

3. The Cricoid or signeting Cartilages

. The most inferiorly placed of the nine cartilages
. Signet ring shaped
. The side of the line bears two articulate facets one for the inferior horn of the thyroid cartilages
and the other near its upper extremity for the arytenoids cartilages

4. Arytenoids Cartilages

. Pyramidal shaped

. Base of which articulate with superior border of the cricoids cartilage

. Anterior angle serve as points of attachment for the vocal cords

5. Corniculate Cartilage
- Small and conical in shape
- Rest on apex of each arytenoids cartilage
6. Cuneiform Cartilages

. Rod shaped

. Located near base of epiglottis

. Closely related to arytenoids cartilage

Muscles of the Larynx

Division – Intrinsic → moves cartilages of larynx one against the other

- Extrinsic → attach the larynx to its neighbors

The Laryngeal Ligaments

Division → Extrinsic →

Intrinsic Linked together by ligaments

The Extrinsic ligaments

A. Thyrohyiod Membrane
. Stretches between upper boarder of thyroid cartilage and hyoid
. Strengthened by median thyrohyiod ligament pierced by the internal branch of the superior
laryngeal nerve and superior laryngeal vessels
 B. The crico tracheal ligament – links cricoids to 1st ring of the trachea
C. The crico thyroid ligament – lies between cricoids and thyroid cartilage
- easily identified gap in the anterior surface of the skeleton. Through which intratracheal injections
may be administered
- Recommended site for emergency laryngotomy in case of laryngeal obstructions
D. The hyoepiglottic ligament connects the epiglottis to the back of the body of the hyoid

Muscles of Larynx

Intrinsic group

. they have both origin and insertion on the larynx

. they control vocal cord length and tension

. they regulate the shape of laryngeal inlet

(A) They open the cords during inspiration

They close the cords and laryngeal ligaments during deglutition
They alter the tension of the cords during speech

Abductors of the cord

. Posterior cricoaryteniods

Adductors of the cord

. Lateral cricoaryteniods, interaryteniods

. Sphincters to vestibule
- Aryepiglottis, thyroepiglottis

Regulators of cord tension

. Cricothyroids (tensors)

. vocalis → fine adjustment

. thyroaryteniods – relaxers

Extrinsic group (e.g. sternothyroid, thyrohyoid,

- Attach laynx to its neighbors

- Insert on the larynx but have their origin in some other structure e.g. Hyoid bone
- Contraction of the extrinsic muscles actually moves or displaces the larynx as a whole
Role of both group
. In respiration
. Vocalization
. Swallowing

Functions of Larynx
. Respiration – part of vital airway to the lungs
. Warming, humidification of air, and removal of waste particles being lined with ciliated mucous membrane
. Protective valve against entrance of foreign body into the airway
. Serves as the organ of voice production (the voice box air being expired through the glottis narrowed by partial
adduction of the vocal cords causes them to vibrate)
NB. Several other structures besides the larynx acts as boards or resonating chambers
e.g. Nose, pharynx, mouth sinuses etc (for quality of voice)

Blood Supply of Larynx

. Superior Laryngeal Artery → branch of superior thyroid artery – the 1st branch of external carotid artery
. Inferior Laryngeal Artery → branch of inferior thyroid artery arises from 1st part of subclavian artery accompanies
recurrent laryngeal nerve into larynx

Innervation of larynx (Nerve Supply of Larynx)

The nerve supply of larynx is from vagus via

(a) Superior
(b) Recurrent Laryngeal branches

(A) Superior Laryngeal Nerve

. Passes deep into both internal external carotid arteries there divides into small external branch and supplies

- Cricothyroid muscle
- Thyroid membrane

Sensory branch to – vocal cords

Motor fiber to –interaryteniod muscle

Internal Laryngeal nerve → runs beneath mucosa of piriform fossa

- Can easily be blocked by 4% Lignocaine topical spray to give anaesthesia for bronchoscopy and
laryngeal procedures
(B) The Recurrent Laryngeal Nerve

. Right side leaves vague → crosses right

Subclavian artery → loops under artery ascends to larynx in the groove between esophagus and trachea

. Left side → nerve originates from vagus

- Crosses Aortic arch – passes under the arch to reach the groove between esophagus and trachea (both
Right and Left same position at neck)
They provide
They provide

. Motor supply to intrinsic muscles of larynx apart from cricothyroid

. Sensory supply to laryngeal mucosa inferior to the vocal cords

Injuries of Laryngeal Nerves

. Damage to external branch of superior laryngeal nerve (during securing bleeding of thyroid artery and vein)
- As this nerve supplies the cricothyroid muscle (sole tensor muscle of vocal cord (Tuning fork of
Larynx) its damage will be followed by Hoarseness temporary

. Hoaresness temporary

. Compensated by over action of opposite cricothyroid

. Damage to the recurrent laryngeal nerve

. Expressed about its vulnerability to injury by wade (1955) as

a) It may be tethered to the goiter by branches of the inferior thyroid artery and be pulled forward when the
gland is retracted anteriorly during operation
b) It may be bound to the gland by thickened facia or
c) It may tunnel through the enlarged thyroid lobe which may if large produce gross distortion of the nerve

Recurrent laryngeal nerve paralysis may occur due to

1. As a result of injury at thyroidectomy

2. Involvement of the nerve by malignant or benign
3. Enlargement of the lymph nodes by cervical trauma
4. The left recurrent laryngeal nerve will be involved by thoracic, esophageal aortic arc or in mitral stenos is,
by compression between the left pulmonary artery left recurrent laryngeal affected twice as often as right
5. 25% of all nerve palsies are idiopathic or probably from peripheral neuritis

Damage to the recurrent laryngeal nerve results in

A. Paralysis of corresponding cord which lies motion less near the mid line and at lower level than the
opposite side the last being due to the down ward drag of the paralyzed muscles
B. Unilateral paralysis produces a slight hoarseness which usually disappears as a result of compensatory over
adduction of the opposite normal cord
C. Bilateral paralysis however results in complete loss of vocal power more over the two paralyzed cords flap
together producing a valve like obstruction, especially during inspiration with in capacitating dyspnoea and
marked respiratory stridor
D. If both recurrent and superior laryngeal nerve damage the cord remains in cadaveric position

NB. After thyroidectomy

. Respiratory obstruction could result from

(a) Direct trauma to tracheal cartilages causing tracheo malacia (if carcinoma more exaggerated)
(b) Bleeding may compress the tracheal and compromise the airway by both tracheal compression and
laryngeal edema

Laryngoscopic Anatomy

. To view the larynx at direct laryngoscopy and there to pass an ETT depends on getting the mouth. Or pharynx and
larynx in to one plane flexion of the neck brings the axis of the oro pharynx and the larynx in line but the axis of the
mouth still remains at right angels to the others their alignment is achieved by full extension of the head at the
atlanto occipital joint. This is the position with nose craning forwards and upwards that the Anaesthetist Assumes in
sniffing the fresh air after a long day in the operating theater.

. At laryngoscopy the anesthetist first views the base of the tongue the valleculi and the anterior surface of epiglottis

. The laryngeal aditus then comes into view bounded in front by posterior aspect of epiglottis with its prominent
epiglottis tubercle the aryepiglottic folds are seen on either side running posterio medially from the lateral aspects of
the epiglottis they are thin in front but become thicker as they pass back wards where they contain the cuneiform and
corniculate cartilages the vocal cords appear as a pale glistening ribbons which extend from the angle of the thyroid
cartilage back wards to the vocal process of the arytenoids between the cords is the triangular (apex forward)
opening of the rima glottides through which can be seen the upper two or three rings of the trachea.

Part II. Airway and Anesthesia

. Anatomic airway – lies between lips and nostrils and alveoli of the lungs

. During Anesthesia – lies between source of oxygen supply and the alveoli

The airway can be obstructed with in the patient or between the patient sources of oxygen

Airway Assessment

(a) History
(b) Physical Examination

(1) Anatomic characteristics that make air way difficult

(2) Difficulty to move the head
(3) Measurement of distance between lower border of mandible and thyroid notch with neck full extended
(three finger breadths or 6.5 cm. or above)
(4) Dental examination – protruded incisors or dentures

II. Malampathy grading

Class I – The soft palate facial pillars uvula visible

Class II – The soft palate and facial pillars are visible but the uvula is obscured by the base of the tongue

Class III – only soft palate visible

IV. Cormack Lehane’s Grading

Grade I – most of the glottis is seen no difficulty

Grade II – only the posterior part of glottis is visible pressure on the laynx may improve the view slight difficulty

Grade III – the epiglottis is visible but none of the glottis can be seen abougie may be used there may be severe
difficulty

Grade IV – not even the epiglottis is visible the situation usually arises with obvious pathology intubation may be
impossible without special techniques

III – Direct Laryngoscopy

Airway Equipments

. Must be available for every anaesthetic regardless of the anaesthetic technique employed (Local, Regional,
General)

. Masks – clear (evidence of exhalation, fogging condensation

. Airways – nasal and oral (prevents biting of tube, falling back of the tongue

. Laryngoscopes → with straight, curve blades

ETT = (age in yrs.) + 4 in pediatrics

→ Length → (age/2) + 12 for oral Pediatrics

(age/2 + 15 for nasal

→Length in Adult = 23 cm. (male) (21 cm. female)

 Size in Adult 8 – 10 cm. for (male ) (7-8.5 female)

. Most ETT → Made of clear non toxic plastic materials

→ Anode or Armored tube to minimize kicking

→ Double lumen tube → for Isolation selective ventilation

ETT Cuffs → Prevents aspiration facilitates PPV of the lungs

→ Uncuffed tubes for < 10 yrs. of age or tube size <6mm

→ When cuff tube used select 1 mm < size (tracheal Ischemia)

Ancillary Equipments → suction, stylete, tooth protector

. Airway Obstructions

. Upper airway obstructions during induction of anesthesia when there is relaxation of the mandible and tongue so
that the base of the tongue falls back against the posterior pharynx to relieve upper airway obstruction

(a) Extend patients head and elevate the mandible (head tilt Jaw thrust)
(b) Positive airway pressure to distend soft tissues and insertion of oroplanyngeal or naso pharyngeal airway

Effects of Obstruction of Airway

- Asphyxia
- Cardiac arrest if asypyxia > 2-3 minutes
- Drowning of fluid (wet lung)

Sites of Airway Obstruction

(1) In the apparatus

. Kicking compression and blockage of catheter mount, which is attached to the ETT

. Empty O2 cylinder leading to Anoxia

. Expiratory valve which does not open fully accumulates CO2

(2) In the patient

1) The commonest site of obstruction in any an intubated patient is

- The jaw sags as consciousness is lost
- The tongue falls back against the posterior pharyngeal wall if the patient is lying on his back

Remedy → Hold the Jaw forward and insert airway

2) Swelling in the mouth will cause obstruction in that area

3) In the Larynx – Laryngeal spasm (see remedy)
4) Tumors → Complete airway obstruction if cord relaxed under GA
5) Stenos is →
6) Profuse secretions or sputum or inhaled vomit may obstruct trachea or bronchi
7) In the bronchus → Broncho spasm (see remedy)
8) Foreign bodies → if in carina
9) Pulmonary edema → as in heart failure leads to impaired diffusion across alveoli

(3) In the endo tracheal tube

 (Lumen of tube may be obstructed by)

a) Blockage by foreign matter → all tubes be checked for patency

b) Kicking in the pharynx → select tube depending on the position of operation
. Biting of tube by patient → insert airway
. Cuff collapsing the tube or Herniation (test before and never over in flat)
. Bevel may be pressed against tracheal wall (Common in infant rotate tube)

N.B. – In small children use un cuffed tube

- (Apply pack) with magil forceps, laryngoscope (wet) → to avoid sore throat and
Dryness
- Don’t forget to remove pack (special marking)

Signs of Airway Obstruction

. Strider (snoring)
. Flaring of nostrils
. Tracheal retractions
. Thoracic retractions (abdominal flaring rocking boat respiration)
. Failure to detect exhaled air against palm or hand used to extend head
. Decrease or absent breath sounds
. Absence of CO2 in exhaled gases

Signs of Airway Obstruction with Controlled Ventilation

. Increase in pressure required to inflate the lungs

. Diminished or absent chest movement on inflation

Signs of asphyxia

. Cyanosis (absent if HB < 5 gm %)

. Increase depth and rate of breathing
. Rapid pulse 1st then slow and bounding and finally weakness and fails
. BP rises 1st and falls at end
. Sweating due to CO2 retention
. Dilated pupils (in acute anoxia) if chronic CO2 retention pin pointed pupils)

Prevention of Respiratory Obstruction

Before induction
. Careful examination
. Never put patient to sleep unless you are sure that you can maintain the airway

During induction
. Support jaw from moment patient losses consciousness
. As soon as relaxed insert airway
. Occasionally tongue falls back before jaw relaxes (insert nasopharyngeal airway)
. If obstruction not corrected open the jaw with mouth gag and pull tongue forward with mayos forceps and
insert airway

During Maintenance

. Constant vigilance
. Watch bag movement constantly; be sure it does not diminish
. For spontaneously breathing patients check for
- Paradoxical chest movement – (instead of out on inspiration)
 . Chin tug → down ward movement of the chin on inspiration
. Check for depth of anesthesia
. Check for signs of obstruction

- Jerky bag movement

. Noisy breathing
. Silent breathing

. During PPV
- Check for amount of pressure required to inflate lungs (if marked sign of obstruction)
. If slight increase → need for further dose of relaxant
. Make sure for adequate movement of the chest and for any leak between connections

Check color of the patient continuously

. By observing the color of blood in the wound

. In the intubated patient look inside the mouth with laryngoscope
. Shine laryngoscope light through the tip of finger under the towels

NB – If failed to recognize it in time it may end up in unnecessary death

After operation

. Turn all patients to the side without pillow

. In children with copious vomit in or blood coming out through mouth increase head down tilt by placing
pillow under shoulders (head resting on bed but not suspended in air)
. In patients under traction place folded pillow under the shoulders (suck out pharynx)

Inhalation of vomit

. Greatest hazard of anaesthesia

. The only safe guard, (empty stomach) but no way to proof

Mechanism → Active vomiting (during induction) e.g. thiopentone

→ passive regurgitation → (Deep Anesthesia Muscle Relaxant)

Remedy → tilt down head of or table and clear pharynx by suction

→ cuffed ETT (best remedy)
→ plain tube with sufficient pack is also effective

Signs of inhalation of Vomit

. Obstruction in chest wall movement

. Wheezing breath sounds
. Cyanosis
. Change in vital signs

Factors contributing to vomiting or regurgitation

. High intragastric pressure (e.g. full stomach)

. High intrabdominal pressure (e.g. distended abdomen ascites, tumors
. Obstruction of airway for one breath
. Intrabdominal manipulations by the surgeon
. Anoxia

Factors that delay gastric emptying

. Food or fluid intake with in 4 hrs.
. Pain (accident)
. Pathologic conditions e.g. (Obstructions)
. Pharmacologic – drugs
. Physiologic conditions e.g. Pregnancy

Prevention of Aspiration

. NGT = suck it out before induction

. Aspiration prophylaxis e.g. drugs H2 receptor antagonists, antacids, gastro kinetic drugs
. Induce in head down or to the side position
. Crush (Rapid sequence induction) with cricoids pressure

NB. – Passive regurgitation (after relaxant in head down position more common so head up tilt (450)
. If active vomiting → head down tilt is important)

Rapid Sequence Induction (Crush Induction)

. Keep patient flat

. Insert canula
. NGT and Deflate stomach
. Aspiration prophylaxis
. Stand being the patients head, with intubation instruments at hand
. Pre oxygenate patient
. Turn on sucker
. Support jaw before injecting drugs it must never be allowed to sag
. Have some one to apply cricoids
. Inject drugs as soon as patient losses consciousness apply cricoids pressure
. With the inflating syringe attached to the side of the tube intubate the trachea
. In flate and check position of tube
. Attach to source of oxygen

During Intra Operative period if patient vomits

. Cuffed ETT is best safe guard

. (Warning signs swallowing and breath holding)
If under light anesthesia)

Immediately do as follows

. Tilt table head down

. Turn head of patient to side
. Suck and clear pharynx (airway)
. Stop anaesthesia
. Administer 100% oxygen
. Check and ascultate the lungs
. If signs of aspiration detected
(Continue management for aspiration)

See attached

Post Operative Airway Obstruction

CAUSES → FALL OF TONGUE

→ SOLID OBJECTS OBSTRUCTING THE AIRWAY

→ TRACHEAL COMPRESSION AFTER THYROIDECTOMY

 Remedy → Chin lift head tilt jaw thrust position

 → Insert oral airway
 → Release stitch and evacuate hematoma
 → 100 % O2 and assist ventilation
 → Search for the cause further

LARYNGOSPASM

Definition → reflex closure of vocal cords

Cause → irritation by secretions, anesthetic agents
→ painful stimulus
Types → (a) partial → characterized by high pitched phonation (crowning)
b) Total → Absence of sound as there is no air movement

Management →Apply head tilt Jaw Thrust maneuver

→ Apply positive airway pressure by mask – 100% O2
. If complete laryngeal spasm give
. SCCH 0.2 – 0.4 mg/kg IV
. Inflate lungs with 100% O2
(fill bag with oxygen and apply gentle pressure with mask firmly applied to face)

Bronchospasm (Solid chest)

Cause . Aspiration of vomit

. Left ventricular failure
. Asthmatic patient
. Foreign body
. Coughing under light anesthesia
. Kinked or herniated, or over distended cuff

Treatment

. Make sure his ETT is patent

. Give 100% oxygen
. Bronchodilators (Aminopyline 4 mg/kg IV over 5 minutes)
. Isoproternol is the best
. Subcutaneous adrenaline (if ether anesthesia if Halothane don’t)
. Deepen anesthesia
. If aspiration suspected (Start Management)

If Aspirated
- Turn patient to the side . intubate patient
 - Suck out vomitus . suck through ETT
- Antibiotics . corticosteroids
. 100% O2 therapy
For Asthmatic Patients

. Ask history of allergic to drugs

. Operate and anesthetize when he is at his best
. Continue with usual drugs
. Premeditate to relieve anxiety
. Regional or LA preferable
. If GA give prophylaxis of corticosteroids or aminopyline

ENDOTRACHEAL INTUBATIONS

. Using an Endotracheal tube to secure patients airway is still the Gold standard most routine oro
tracheal or nasotracheal intubations are performed with the help of the laryngoscope that has a curved
or straight blade other adjuncts such as external laryngeal pressure a bougie astylet or a pair of
Magill’s forceps may also be used.

Advantages of tracheal intubation

1. Patency of airway is reasonable assured also not guaranteed

2. Anatomic dead space is reduced by half
3. Control of respiration is facilitated
4. Secretion may be removed with relative ease from the tracheobronchal tree
5. Positive pressure can be applied to the airway without inflation of the stomach
6. The patient can be placed in any position for operation with less chance of
Compromising the airway
7. The operating position other than supine the anesthetist can be situated at some distance from the
patients head and yet maintain control of respiration

Indications for Intubations

1. Operation site nearer or involving the upper airway

2. Operating position other than supine
3. If airway maintenance by mask difficult (e.g. morbidly obese patient)
4. Disease involving the upper airway
5. Preterm infants, neonates with congenital anomalies e.g. (Diaphragmatic hernia)
6. If neuromuscular blocker’s are used
7. In all emergency operations ( e.g. maxillofacial trauma)
8. In all operations to facilitate positive pressure ventilations

Confirmations of endo tracheal intubations

(a) Measuring end tidal CO2 ET CO2 in exhaled gases (capnography) (ET CO2 > 30 mm Hg)
(b) Presence of bilateral and equal breath sounds on auscultation
(c) Absence of sounds over the epigastraim
(d) Seeing tube passing through the glottis
(e) Bilateral chest expansion
(f) Pulse oximetry (other devices)
Complications (pit falls) (during)

Endotracheal intubation

(1) Aspiration
(2) Dental damage
(3) Esophageal intubation
(4) Endobronchial intubation
(5) Laceration of lips or gum or tracheal mucosa
(6) Laryngeal injury
(7) Activation of S.N.S
(8) Bronchospasm or laryngospasm

Complications after Extubation

1. Aspiration
2. Laryngospasm
3. Transient vocal cord incompetence
4. Glottic or subglottic edema
5. Pharyngitis or tracheatis
6. Distraction of vocal cord and tracheal stenosis

N.B. - 70% subglottic edema in children

- Sore throat mainly in female

The Difficult Airway

The anesthetist must be familiar with the major decision making components of the difficult Airway
Algorithm. These are as follows.

. Recognition of difficult Airway

. Positioning patient for airway manipulation

. Awake intubation techniques

. Techniques for anesthetized patients with difficult airway

. Techniques for patients who cannot be intubated or ventilated

. Confirming position of ETT

. Extubation or tube change for patients with known difficult airway

N.B. You have to be ready with an alternative approach to secure the airway if intubation is difficult.

Anatomic characteristics associated with difficult exposure of glottis opening

. Short muscular neck . Inability to visualize uvula

. Receding mandible . Limited temporomandibular Joint Mobility

. Protruding maxillary incisor . Limited cervical spine mobility

. Maxillo facial injuries . Neck trauma

. Craniofacial abnormalities
Difficult Airway Algorithm

Difficult Airway

Anticipated Unanticipated

Proper preparation Proper preparation

Awake intubation choices Induced GA

Fail Succeed Failed to intubate

Tracheotomy Call for help

Cricotyrotomy

Mask ventilation One attempt at

Adequate No conventional intubation

Yes

Intubation Choices Fail – transtracheal

Jet ventilation

Fail and fail after multiple attempts

Awake Succeed

Awaken ventilate with mask Intubation

Choices

Cricothyrotomy

Tracheostomy

Confirm with ETC O2

Sa O2 test

Protocol for failed Rapid

Sequence intubation
. Maintain cricoids
. Call for help
. Suction airway if required
. Administer 100% O2 by PPV (mask)
. Maintain oral or jaw thrust
. Tilt operating room table head down
. Wake patient up if possible
. Consider attempt at reintubtion if possible
. Consider cricothyrotomy or tracheostomy

Emergency Cricothyrotomy

Definition → placement of 14 G. canula through cricothyroid membrane

Aim 1. To provide temporary oxygenation until more steps are taken

2. To reverse total upper airway obstruction

Equipments
. 14 G. IV cannula
. 3 ml syringe without plunger
. 15 mm ETT adapter
→ attach oxygen delivery source
→ attach jet injection device directly to iv cannula

Failure of tracheal intubation in Anaesthesized Patient

. Every practitioner will encounter airway difficulty

. Clear plan of action (rather than panic) can be pursued

When an initial attempts at intubation fails

(a) Mask ventilation

(b) Reassess the patients situation
(c) If risk of full stomach maintain cricoids
(d) Examine head position
(e) Examine laryngoscopic techniques (curved or straight blades)
(f) If repeatedly failed by experienced practitioner
- Allow to awaken patient
- Post pone case if non emergent
(g) If case can not be canceled
- Give anticholinergics (to obtund secretions
- Reattempt by using different laryngoscopic blades
- Use light wand sylets
→ finish case with mask anesthesia
→ fiber optic bronchoscopy
→ blind naso tracheal intubations
→ awake intubations
→ retrograde intuations
If patient who can neither be manually ventilated by mask nor intubated

. It is life threatening situation

(a) If patient pre oxygenated
(b) If short acting barbiturates with SCCH employed
- Spontaneous ventilation should return before life threatening hypoxia supervenes.
If ventilation not possible at all

. Surgical procedures

- Crico thyrodotomy (Laryngectomy)

- Tracheostomy

Summary

Can’t ventilate can’t intubate?

. If patient difficult to intubate stop trying and return to bag and mask ventilation

. If you are able to ventilate the patient then consider any adjuncts or procedures that may help you

. If you are unable to ventilate the patient inspite of the adjuncts mentioned previously “call for help! Wake the
patient up if appropriate or prepare for emergency cricothy rodotomy.

Cricothyrodotomy

14 G. cannula inserted through cricothyroid membrane and O2 under pressure administered this is called
transtracheal jet ventilation (TTJV)

Problem – Baro trauma (due to ↑ pressure

Remedy → Adjust driving pressure carefully and make sure that there is not obstruction to air flow on exhalation

During Oxygenation

. Amall tidal volume

. High respiratory rate (20 – 40or if you use the jet ventilation the rate can be increased-/minute)

. Longer I:E ratio (1:4)

Naso tracheal intubation (using direct laryngoscopy)

1. LA spray to nasal passage (4% cocaine maximum 1.5 mg/kg)

(Advantage vaso constrictor effect)
Or Lignocaine 2-10% (maximum 3 mg/kg.)

2. . Vasoconstrictor drugs → phenylephrine or pseudoephedrine nasal spray

3. Soften ETT by immersing it in a lubricant or (in warm clean water)
4. Insert ETT at angle perpendicular to the face and exert gentle pressure until the tube is visualized at the
back of oropharynx. Guide the tube using magills forceps into larynx rotate the bevel of ETT so that it
faces posteriorly and allows smoother passage of the tip across laryngeal in let

Awake Intubation

Indications

. Upper airway obstructions

. A known or suspected difficult intubation

. patient with an unstable cervical spine fracture where any traction on the neck should be avoided

. Full stomach (only in U.S.A)

. Respiratory failure in extremis where anesthetic induction may bring about the patients immediate Demise

Procedure → with minimal topical anesthesia with or without sedation

. Explain to the patient and surgeon

. IV access

. Pre oxygenation

. Monitoring devices fixed and in place

. Atropine 400 – 600 mcg or glycol pylorrate 200 – 400 mcg

. Sedative (midazolam 0.5 to 2 mg.) + fentanyl 50 mcg or droperidol (fear of respiratory depression)

. Local anesthesia of upper airways

(Spray, catheter or cotton swab)(Lignocaine spray 2 – 4%) maximum 3 mg/kg. applied to tongue mouth pharynx
nasal passages (Larynx)

. Tran laryngeal injection through cricothyroid membrane (2 – 4 ml. of lignocaine 4%) high concentration
penetrates mucosa easily

. As soon as injection performed patient will cough

. Have equipment ready for chosen technique e.g. Fiber optic bronchoscope or retrograde intubations

. Plan for the procedure and have a rescue plan in case it fails

Laryngeal mask and intubating LMA

. Important invention recently

. Used as a conduit by a passing a boogie, fiber optic bronchoscope or small ETT through it (ILMA left insitu until
end of anesthesia)

Augustine Guide

This device

. Consists of an anatomically – shaped disposable plastic channeled guide with special stylete

. Combined features of pharyngeal airway stylet boogie, esophageal detector device, the tube is loaded over the
guide, and the Hollow stylet is used to find the trachea, the stylet position is confirmed by injecting air with syringe
and Auscaltating the stomach (esophageal detector device) the tube is then guided over it.

. Inorder to use it mouth opening must be normal

. It is more traumatic than normal laryngoscopy though cervical spine mobility during the procedure is minimal

Retrograde Intubation

. first Described by D.J. Walters in 1963.

Technique

1. Passing a retrograde guide through cricothyroid membrane then taken out through the mouth or nose and
ETT guided over it
 . You can use, epidural catheter, a vascular guide wire, (J tip wire less traumatic in airways)
. Make cricothyroid puncture → by IV cannula (some advocate cricotracheal space than cricothyroid
space) → less vascular ↑ depth of insertion prevents tube dislodge
. Pass the guide wire through the cannula

2. Antero grade guide such as a 14 – 16 FG suction catheter passed over retrograde wire. So that ETT has a
better guide when railroaded rather than the thin and easily flexible retrograde wire
3. The procedure can be performed awake or LA, to airway, sedation or small dose of induction agent.

Contraindications

- Infection
- Tumor in the area
- Clotting disorders

LIGHTED STYLETS OR LIGHT WANDS

. Involves using a malleable stylet with a light at its tip that is placed inside, the ETT the stylet is bent to L.shape
and the patient positioned, with head fully extended the light wand is passed in the middle layer over the tongue.

. Abrupt Tran illumination occurs when the lighted tip passes the epiglottis enters the larynx the stylet is then
removed.

BLIND TECHNIQUES

. Performed without a direct or indirect view to glottis

. The techniques are blind nasal and tactile oral

Blind Nasal intubation

Indications

. When neck movement is prohibited

. When mouth opening is limited

. When nasal ETT is required

. When anaesthesia or paralysis is taught to be risky

Procedure

. LA to airway

. Induced patient breathing spontaneously

. Head positioned as direct laryngoscopes

. Lubricate ETT (softened ETT)

. Use small size (6.5, 7.5 mm for Adults)

. Pass ETT through nostrils until reaching to pharynx

. Then chin lifted forward and other nostril occluded

(if patient awake ask him to close his mouth and breathe deeply)

. If anaesthesized patient advanced tube deeply and slowly while listening for breath sounds at end of tube

. Use capnography which is best monitor

TACTILE ORAL (BLIND OROTRACHEAL)

. Reported in 1880 by William MaCEwen

. Performed by palpating the larynx, while guiding the tube in to it

THE CARE OF THE PATIENT UNDER GENERAL

The attention of Anaesthetist

. Maintenance of a perfect airway

. Adequate ventilation of the lungs and oxygenation of blood

. Maintenance of circulation

. Prevention of fire and explosion hazards

. Prevention of nerve palsies from incorrect position of the patient

. Prevention of damage to the eyes

. Preventon of burn’s from hot bottles, electric pads or incorrect use of diathermy

. Prevention of air embolism during intravenous infusion

CRITERIAS TO DISCHARGE PATIENT TO RECOVERY ROOM

. His respiration is normal

. His color is well maintained when breathing air

. Conscious able to speak and respond to commands

. His pulse and blood pressure are satisfactory

REGULATION OF RESPIRATION

. If center is severed the heart and smooth muscles continue to function but not the Respiratory Muscles.

For Respiration

Double Control Mechanism

(1) Voluntary System

. Center forebrain cerebral cortex
. Sends impulse through corticoid spinal tract (Located in Dorsal part of spinalcord)
 (2) Automatic System (Located in Brain Stem) (pons and medulla)

. The motor out flow of which is into the ventrolateral column of the spinal cord

The final integration between conscious and in voluntary breathing occurs at the spinal cord.
The main levels of respiratory center has been localized in Brainstem

(a) The highest in the Rostral Pons (pneumotaxic center)

(b) Next the appeustic center (part of the pontine reticular formation located near medullary boarder
(c) Finally the medullary center

MEDULLARY RESPIRATORY CENTER

. The basic rhythm generator

. Modified by its central and peripheral connections

- Central connections

Pons, hypothalamus, RAS, cortex central chemo receptors

Peripheral Connections

- Vagus, glosso pharyngeal nerves

- Brings informations from peripheral chemo receptor to the lungs and chest wall
- Two dense bilateral aggregation of neurons

1st aggregation 2nd aggregation

Dorsal Respiratory group Ventral Respiratory group

(Nucleus ambiguous and Retro ambiguous)

(1) . Contains primarily inspire atory cells 1) Contains inspiratory and expiratory cells
. I Alpha inspiratory Neuron
(Inhibited by lung in flation

. I Beta. Insp. Neuron 2) Insp. Neurons → project to controlateral phrenic

(Excited by lung in flation) intercostals and accessory muscles of Respiration

(2) Communicates with controlateral

Phrenic motor neuron

. Responsible for rhythmic contraction . Exp. Neurons → project to contro lateral internal
Of diaphragm intercostals and abdominal muscles (major function
of ventral group)

(3) G.P.N and vague casts informations from

Peripheral and stretch receptors

The Pontine Respiratory Center

. For smooth transition from inspiration to expiration without any interruptions.

The Pneumotaxic Respiratory Center

. To fine tune the respiratory pattern, by modulating the response of the respiratory system to various
Stimuli (e.g. Hypoxia hypercarbia lung inflation) its destruction leads to slowing of respiration.

The Apneustic Center

. Localization of the normal inspiratory cut off switch

. General phenomenon involving a sustained discharge of medullary inspiratory neurons which is
modified by vagal afferents

SPINAL INTEGRATION AND CORTICAL INFLUENCES

. Voluntary act → e.g. speaking → alter rhythmic respiratory activity etc…

. Voluntary N. fibers → from cortex → travel through reticular formation → to the dorso lateral part of
the spinal cord
. Involuntary Fibers → from pons and medulla lie in the ventrolateral part of the cord
Voluntary + involuntary + spinal reflexes → finally integrated at spinal cord centers.

At this level

(a) Descending neurons with inspiratory activity

1. Excite External Inhibit internal
Interiostal motor neuron intercostals motor neuron
By exciting spinal
Inhibitory inter Neurons

NB → Importance of the above reflex is that it prevents contraction of antagonist muscles when
agonist muscles are intact

NB → Lesions in CNS, in tumors compressing medulla bulbar poliomyelitis narcotic over dosage
e.g. (fentanyl citrate) patients will be apneic and insensitive to CO2 (but will breath on
command) (ondiness curse).

Lesions in CNS → can affect voluntary act without altering involuntary breathing

. Lesions in nuclei at brain stem → can affect respiratory rhythm without any impairment of
voluntary respiratory acts

. Patients with high bilateral antero cervical cordiotomy for relief of pain can have interruptions
of the descending involuntary respiratory tracts liable to stop breathing when asleep but because
of the presency of intact lateral corticospinal tracts can breath voluntarily when asked to do so
(On dines Curse).

CENTRAL CHEMO RECEPTORS

. Respond to changes in the chemistry of blood or fluid around it

 . Sensitive to CO2 and changes in PH of the C.S.F

Location → Ventrolateral surface of medulla near the exit of G.P.N and vague nerve.

Sensitivity → High CO2 and H+ stimulates breathing within seconds low CO2 and H+ depress ventilation.
. Increased ↑ Pa CO2 → CO2 → diffuses readily to C.S.F and liberates H+ ion (Acidification)
. This stimulates the chemo receptors and the subject hyper ventilates by that reduces blood CO2
and C.S.F PH with in 60 seconds
. The reason for relatively rapid change in H+ ion concentration in C.S.F with hyper or
hypocapnia is that C.S.f. lucks the buffering capacity of HB
(The threshold for central ventilator effect of PCO2 is about 30 to 40 mmHg)

. In chronic Acidosis the PH of C.S.F is maintained normal because the B.B.B adjusts C.S.F
Bicarbonate concentration to bring its PH near its normal value of 7:32 the difference in the
HCO3 concentration between blood and C.S.F is maintained by an Ion pump at B.B.B.

Peripheral Chemo Receptors

Location → Carotid bodies → bifurication of common carotid arteries respond to ↓ PH ↑ PCO2↓

PO2
→ Aortic Bodies → found at ascending part of Aorta (they respond to changes in blood
gases but not to changes in PH)

. The glom us cell – found in carotid bodies which has high content of catecholamine such as
Dopamine and 5 – hydroxyl tryptamine.

Peripheral chemo receptors → the response to changes in the arterial PO2 and PCO2 and PH is very rapidly
relayed to the medullary centers but central chemo receptors relay the information after time lag.

The hypoxic drive for ventilation from the peripheral chemo receptors is very strong. Which is important
in Emphythematons patients with CO2 retension because of the chronic nature of the disease with
Associated Adjustment of C.S.F. PH the central chemo receptors are depressed.

The only stimulus to respiration in this patients is initiated by the effect of hypoxia on the peripheral chemo
receptors so administration of high concerntration of oxygen might lead to respiratory arrest in this patients
such concentration should be adjusted carefully and slowly. So that the hypoxia is mildly relieved but the
respiratory drive still continues.

Pulmonary Receptors

(1) (a) Stretch receptors inflation → inflation causes ↓ respiratory effort

→ Deflation causes ↑ respiratory effort
(Herring Bruer, inflation reflex modulated in medulla)
(b) Irritant receptors→ Stimulated by noxious gases (broncho constriction)
(c) Juxta capillary receptors respond to chemicals injected into pulmonary circulation
(activated by bradykinin, Histamine some prostagl and in)

(2) Arterial Baro Receptors → increased BP can cause reflex hypoventilation or apnea through
stimulation of Aortic or Carotid.

Baroreceptors conversely↓BP may cause hyperventilation during shock hyperventilation is caused by effect
of acidosis and hypoxia on the chemo receptors.

3. Other Reflexes

(a) Sneezing reflex → due to mechanical or chemical stimulation (nasal receptors (absent during
 sleep or anesthesia)
(b) Coughing reflex – starts under closed glottis by contraction of expiratory muscles and a linear
Velocity of 600 MPH expels the content to pharynx
- Due to mechanical or chemical stimulation of the larynx (via superior laryngeal nerve) or trachea
bronchi via vagus nerve leads to cough.

(c) Hiccup → sudden spasmodic contraction of the diaphragm during which the glottis closes suddenly
(involves central mechanism, largely independent of rhythmic respiratory system)

PAIN AND TEMPERATURE RECEPTORS

. Pain often causes a period of apnea followed by hyperventilation.

PARADOXICAL REFLEX OF HEAD

. Inflation of lung – produces paradoxic effect of further inspiration ( may help during sighing)
(can be abolished by cutting vagus)
- Opposite to Herring Bruer reflex
. (inflation of lung induces expiration

Ventilatory Response to Carbon Dioxide

. Normal, well oxygenated young → minute ventilation increases by 2 to 5 liters/ minute (mean 2.5 liters/
minute for every MM Hg. Rise in alveolar PCO2) at alveolar PCO2 40 to 70 mm Hg. (5 to 10% inspired)
. Higher levels of CO2 concentration produce direct respiratory depression so dyspnea severe headache
from cerebral vasodilatation, restlessness, faintness eventually at alveoli PCO2 of above 100 mmHg. (15%
inspired) loss of consciousness.

→ The ventilatory sensitivity ↓ with age (the curve shifts to Rt)

→ Narcotics and anesthetics depress the response to CO2 and elevate the end tidal CO2 in a dose related
fashion
→ When ventilation is stimulated by combination of hypoxia and hypercarbia, the ↑ in ventilation is greater
than the sum of the increments produced by each separately (this mechanism is probably due to the effects
of hypoxia in stimulating the chemo receptor mechanisms).

Sleep and ventilation

During REM sleep the breathing → pattern is very irregular → poor response to CO2 but responds to
hypoxia → ventilation is controlled by cortical mechanism at this point.

During NREM Sleep → the response to hypercarbic and hypoxia is only slight less than awake state
→ Resp. controlled by peripheral mechanism

Patients with O.S.A → episodes of apnea no air flow for more than 10 seconds.
→ poor response to hypoxia and hypercarbia
→ apneutic episodes is allocated with U.A.O

Premature neonates (symptoms occur during REM. Sleep have paradoxical response to Hypoxia
(exaggerated during stress full situation e.g. resp. infection post anesthesia.
Effect of anesthetics on Ventilation

Inhalational agents – depress the CO2 response curve

Cause ventilator depression- Ether → least effect on ventilation
Halogenated agents → Strong depressants of ventilation
With ↑ depth of anesthesia alveolar ventilation diminish because of ↓TV and
↑in RR

Enflourane → the most profound depressant effect on respiration less with Isoflurane and Halothane

Halothane → ↑RR→ surgical stimulation antagonize the resp. depression and PaCO2
N2O+ Halogenated agents → PaCO2 is lower than that of patient anesthesized with Haloginated
hydrocarbons.

Anesthetic Agents → raise the apneic threshold i.e. the minimum PaCO2 that initiates ventilation
→ under NI circumstances it is usually 4.5 mm Hg. Lower than the PCO2
produced by spontaneously ventilation
→ Most spontaneous breathing patients maintain PaCO2 of 50 mm Hg.
Assisting ventilation can achieve only a drop in PaCO2 of 5 mm Hg. From
then on resp. will stop and controlled ventilation may be required to achieve
normocapnia or hypocapnia.

Anesthetic agents =Depress the peripheral chemo receptor → at 0.1Mac → ventilator response attenuated
at 1 mac → it disappears important to monitor patients in recovery room where the usual residual
anesthetics will prevent the response to hypoxia

Narcotics → reduce the responsiveness of the respiratory centers to stimulation by CO2

→ they also depress hypnotic dive

↓RR Effect exaggerated in

TV patients who fall
Asleep

Ketamine Slow administration Doesn’t cause significant

Respiratory Depression

Resp. to CO2
Is maintained

Rapid administration diminision lasts

Resp. depression of PaCO2 5-10 minutes

CARDIO PULMONARY ARREST

Definition:- C.P. arrest Not expected to die at that particular time

What are classifications of Death these are

1. Clinical death
2. Biological death
3. Brain death

Causes of C.P.A
1. Resp.
2. Cardiac
3. Cardio circulatory

Cardio Pulmonary Arrest

- Def. of Death → analysis – critically ill patient

- Brain death clinical death biological death

Cause – Respiratory, cardiac or cardio circulatory

E.R.C.G.A.B.L.S - If under anaesthesia the management is different?

1. Ensure safety of rescuer and victim

2. Check the victim and see whether he responds (are you all right)

3. A. If responds by answering or moving

- Leave him in the position is which you find him (provided he is not in further danger)

(check his condition and get help if needed) Reassess him regularly

B. If he does not respond

. Shout for help

. Open his airway How?

(try to avoid head tilt there is trauma to the neck)

4. Keeping the airway open look, listen, and fell for breathing (10 seconds) before deciding that
he or she is not Breathing (10 seconds) before deciding that he or she is not breathing more
than an occasional gas P.)

5. A. If he is breathing (other than an occasional gas P.)

------- turn him into the recovery position check for continued breathing)

B. If he is not breathing
- quickly do as follows

1. Clear the airway

- Helminch maneuver ---
2. Breathe for the patient (2 effective rescuer breathes) (Mouth to Mouth or Mouth to
Nose.)

6. Asses the victim for signs of circulation (10 seconds)

7. A. If you are confident that you can detect for signs of a circulation with in 10 seconds
- Continue rescue breathing
- If patient starts spontaneous breathing and is un conscious turn him to recovery
Position

B. If there are no signs of circulation

- Start chest compressions
15!2 (1!5)
8. Continue Resuscitation until
- Qualified help arrives
- the victim shows signs of life
- you become exhausted

If no improvement

9. Start the Algorithm for ALS

Cardiac arrest

BLS Algorithm
If appropriate

Precordial Thump
If appropriate

Attach life scope

Defibrillator

Asses Rhythm

Asses Rhythm

Check Pulse

VFVT Non VF/VT

Defibrillate x 3
As necessary

CPR/ min During CPR 3 min

CPR 1 min if immediately
After defibrillation

Correct reversible causes

(i) hypoxia
(ii) hypovolemia
(iii) hypo/hyperkalemia
(iv) hypothermia
(v) tension pnumothorax
(vi) tamponade
(vii) toxic or therapeutic disorder
(viii) thrombo – embolic and mechanical obstruction

If not already

-Check electrode paddle

Attempt position and contact verify airway O2 (intubate and ventilate) iv access
 - give adrenaline/every 3 minutes
- consider antirrhyth mics
- pacing buffers

DC Shock 200 – 360 J

-intubation or LMA – ventilate with 100% O2
FiO2 – 1.0
TV - 500 – 600
-the administration of hypercarbic producing buffers e.g. NaHCO3 should be
Present – in closed chest compression the rate should be 100/minute
-iv line – peripheral or central
20 ml. of 0.9% N/S to expedite entry to circulation
-drugs → given by tracheal route adrenaline lidocaine, atropine doses 2 – 3 x standard iv dose diluted
up to total volume of 10 ml. of 0.9% saline
After administration. Five ventilation to facilitate dispersion to the distal bronchial tree for absorption

SPECIFIC DRUG THERAPY

a. Vaso pressers
i. Adrenaline/ epinephrine
For non VF/VT rhythms each drop of the algorithm lasts 3 minutes and there for
adrenaline/ epinephrine is given with every loop

b. Ant arrhythmic Agents

i. Lidocaine
ii. Bretylium
iii. Atropine – 3 mg.iv)

c. Buffer agents

Based on blood gas analysis

PH<7:1 BE < -10, hyper kalmia or following tricyclic antidepressant over dose

NaHCO3→ 50 ml. of 8.4 →

Post Resuscitation Care

- The most vulnerable organ for damage is brain 1/3 (motor or cognitive defects)
- (1 - 2% do not exist independently)

- Treat multi Foci arrhythmias

When to terminate Resuscitation?after multiple attempts and continous resuscitation for one hour if
there is no sign of life on ECG with certain limitations death can be announced .

Transport of O2 and CO2 by the blood

Gases in the lung flow down hill – diffuse from areas of higher partial pressure to areas of lower
partial pressure
 O2 Diffuses from alveoli to blood CO2 diffuses from blood to alveoli the transfer of these gases across
the alveoli capillary membrane occurs by simple diffusion with out the involvement of any enzymes.
It is influenced by physical factors. (directly proportional)

(a) The difference in the tension between two sides of the memberane
(b) Solubility of the gas in the blood inversely proportional to

The square root of the molecular wt. of the gas (little impact)

Because CO2 is 24 x more soluble than oxygen CO2 diffuses 20 x faster across the alveolar capillary
membrane

Oxygen transport → carried in blood in two forms

(a) in physical solution – at 100 mm Hg – in 100 ml. of plasma (0.3 ml dissolved poor solubility)
(b) In combination with HB

→ If 100% O2 Inspired → 2 ml. dissolved →

→ 12.5 liters of cout → to satisfy O2 demands of the tissues (250 ml/minute)

→ to guard such a high load on cout – efficient method to transfer O2 from lungs to tissues

→ a vital protein → Hemoglobin

→ Hemoglobin → a protein – MW = 64,400 → four sub units

Made up of heme group → enfolded with in a polypeptide unit

Made of two alpha two beta chains

141 chains

Amino acids

Heme molecule → gives blood its red colour – It is made of aring of four pyrrole groups (porphyrin) with
an, atom of iron at its center. Iron atom is bound to each of the pyrole groups and to one of the four
polypeptide chains

→ The sixth binding site on the ferrous iron is available to bind with oxygen. The Iron atom

must maintain in the ferrous or reduced form to preserve this reversible binding pattern.

Each Iron atom of the HB molecule reacts with one molecule of O2 thus four molecules of oxygen react
with one mole of HB which is the equivalence of 1:39 ml. of O2 to each gram of Hb. The uptake of O2 by
H.B → oxygenation (not oxidation).

Oxy hemoglobin Dissociation Curve

The combination of HB with O2 is achieved in four stages. (each involving different iron atom)

HB4 + O2 HB4 O2

HB4 O2 + O2 HB4 O4
 HB4O4+O2 HB4O6

HB4O6 + O2 HB4 O8

Each of these reactions has a different equilibration rate (constant) and the 1st reaction facilitates the
subsequent reactions thus giving the characteristics sigmoid shape to the oxyhemoglobin dissociation
curves.

- The curve rises gently at first. Then more steeply and finally flattens out as it approaches the
myoglobin curve.

- The shape signifies that O2 free molecule of HB do not readily take-up the 1st O2 molecule but their
appetite for O2 grows with oxygenation such that the Fourth site binds 200 x more easily than does the
1st.

- S. shaped → formation of a different type of a crystal by deoxyhemoglobin every time it takes up O 2.

CLINICAL IMPLICATIONS OF OX HEMOGLOBIN DISSOCIATION CURVE

1. Each gram of HB combines with 1.39 ml. of O2.

2. Small amount of HB is in the form of met hemoglobin and is combined with carbon monoxide for
this reason the human capacity of HB is considered to be 1:34 ml. O2 per gram of HB

O2 caring capacity of HB value of 15 gram

15 x 1:34 = 20.1 ml/ O2/dl/blood

Hemoglobin saturation percent = Blood O2 content (dissolved O2) x 100

Oxygen capacity of HB (dissolved O2)

Blood O2 content (dissolved O2) x 100

O2 Capacity of HB ( dissolved O2)

Several important physiologic properties of the blood depends on the S. shape of oxygen dissociation
curve.

1. At the lung the alveolar O2 tension is 100 mm Hg. Thus HB becomes 97.5% saturated. Assuming the
HB content of the individual is 15gm/dl. The HB in each 100 ml. blood would contain.

15/1.34 x 97.5 = 19.6 ml of O2 compared

100
With this volume the amount of O2 dissolved in blood in minimal = 0.3 ml/dl plasma

2. Increasing the PO2 in the lung to more than 100 mm Hg. Increases the O2 content only slightly. The
most it can do is increase the O2 dissolved in plasma to its maximum i.e. 2 ml. of O2 per 100 ml/of
blood.
ie. 1/10 of the volume than can be carried by HB

3. At the upper flat or Horizontal part of the curve drooping the PO2 from 100 to 70 mm Hg. Has very
little effect on the O2 content of blood ( of 5%) this is why a person can live at reasonably high
altitudes without much diminution in O2 carrying capacity.
4. Venous blood has a PO2 level of about 40 mm Hg. A 60 mm Hg. Drop in PO2 at the tissue brings the
O2 saturation to 75% allowing 5 vol. of O2 per 100 ml. of blood to be liberated and leaving the
remained 15 ml/dl. As reserve.

5. It is assumed that if O2 tension falls below 20 mm Hg. At the end capillary level then diffusion is
impaired at this critical partial pressure of O2 HB is 30% saturated therefore 7ml./dl of O2 is still
available to maintain a sufficient diffusion gradient of O2 from capillaries to tissues.

Factors affecting the shape of Oxyhemoglobin Dissociation Curve

Shift to right – desirable → O2 is unloaded more readily from HB at the tissues

Shift to left – HB is detracted from unloading oxygen P50 → 50% of HB saturated with O2 (50% released).

In the normal adult with a PH of 7.4 and temp. of 370 C P 50 is 27 mm Hg. With a shift to the right P50 is
increased whereas with a shift to the left it is diminished

Temperature shift to Rt affinity of HB for O2 is ↓ more O2 is delivered to the tissues at an equivalent partial
pressure.

PH → the effect of carbondioxide tension and (H+) concentration on HB dissociation curve is called the
“Bohr” is effect the changes produced by CO2 on the dissociation curve are secondary to changes in H+ ion
concentration with in RBC ↑ acidity ↓ PH like arise intemp. Shifts the curve to the Rt. The opposite occurs
with alkalosis.

The “Bohr” effect facilitates oxygen unloading at the tissues the dropping PH caused by CO2 production
lowers O2 affinity and enhances the release of O2. In contrast at the pulmonary level the rise in PH from the
efflux of CO2 increases O2 affinity and uptake.

2.3 Diphospogly cerides → the red blood cell is metabolically different from other tissues in
two respects its derives metabolic energy exclusively from an aerobic glycolysis and it has an un usually
high concentration of (2-3 DPG) the number of HB molecule is approximately equal to the number 2-3
DPG molecules.

The preferential binding of 2.3 DPG to Deoxyhemoglobin rather than oxyhemoglobin facilitates

the unloading of O2 from the HB molecule.

Therefore an ↑2-3 DPG → release of O2 from HB

↓2-3 DPG → oxygen retension

2-3 DPG level affect the O2 affinity of HB by altering the configuration of its molecule as the HB molecule
changes from a relaxed to the tight form the gap between the two beta chains becomes wider on the lining
of this opening is a string of amino acids carrying positively charges the 2.3 DPG occupies this space and
the negative charges on its surface neutralizes the positive changes of the HB. The formation of these
additional bonds stabilizes the HB molecule in the tight position.

Several factors affect 2-3 DPG con. Of RBC

1. Acidosis in hibits red cell glycolysis by the activity of phosphofructo kinase resulting in a diminution
of 2-3 DPG levels. Thus the beneficial effect of tissue acidosis in enhancing the release of O2 from HB
molecules lasts only a few hours the decrease in 2-3 DPG level soon will shift the curve to the left.
2. Chronic hypoxemic states such as those resulting from living in a high altitudes or in patients with
chronic lung disease congenital heart diseases with right to left shift are associated with high 2-3 DPG
(↑P50) levels in these patients the chronic desaturation of the HB induces an↑ in the level of 2-3 DPGs
(and P50) in an effort to help the unloading of) oxygen at the tissues.

3. Most anemias are associated with an increase in 2-3 DPGs.

4. Hormones such as thyroid hormone, growth hormone androgens ↑ the Erythrocyte 2-3 DPG levels.

5. The affinity of young erythrocytes for O2 is lower than that of the older red cells. This is due to
progressive diminution of 2-3 DPG production, presumably from the reduction of glycolysis process.

6. With storage of blood there occurs a progressive ↓ in red cell 2-3 DPG levels. Blood stored at 40C in
Acid Citrate Dextrose (ACD) solution will lose half of its 2-3 DPG content in four days and most of it
in seven days and blood stored in citrate phosphate dextrose (CPD) will lose 2-3 DPG but at about ½
this rate after transfusion the half recovery time from 2-3 DPG is 4 hrs. and it takes several days to
reach its Nl. Level.

7. Prolonged intravenous feeding can produce phosphate deficiency if adequate supplements are not
given these patients will have ↓ 2-3 DPG.

Oxygen Stores of the body

- The total body stores of O2 is equal to 1500 ml.

- Basal metabolic requirement of O2 250 ml. 1 minute so total stores cannot supply adequate tissue
oxygen tension for more than 4 minutes
- Most of the oxygen stores are in the arterial blood (1 liter)
- The lung stores of O2 – with room air are minimal i.e. If FRC 2000 ml. → the amount of O2 in the
lung is 400 ml.
→ Tissue function starts deteriorating at an arterial O2 tension of approximately, 40 mm Hg.
This store in the lung can sustain life only about 1 minute
→ If 100% is breathed the pulmonary storage capacity for oxygen can be ↑ by about 10 fold but
the O2 carrying capacity of blood can↑ very little
→ 100% O2 ↑ HB saturation from 97% to 100% and the dissolved amount from 0.3 to 2
ml/100ml. of plasma
Large amount of O2 bound to myoglobin this is only available insitu the hyperbolic curve of
myoglobin “locks in” O2 until the partial pressure drops to extremely low values. Back diffusion of O2
from myoglobin into blood is very unlike to occur

→ In contrast to oxygen stores the CO2 stores are very large whole body.

Can yield → 120 liters of CO2 → 80% in the bones of this 30% in the HCO3 form and 70% in carbonate
form

In an apneic individual → if oxygenation is maintained by prior ventilation with 100% O2 and the airway is
connected to a fresh gas O2 supply (apneic oxygenation) to replace the O2 absorbed from the lungs
satisfactory arterial O2 tension can be maintained for at least 20 minutes. However with this technique the
arterial PCO2 rises rapidly in the first minute (6 to 13 mm Hg per minute depending on the previous state of
ventilation) and then slows down 3 to 4 mm Hg per minute).
The initial rapid rise is from equilibration of the arterial CO2 in the lung with the mixed venous CO2. While
the slow rise is from the metabolic production of CO2 ↓ distributing itself between the lung and the body
stores.

Fetus Adult

HBF→ high affinity of or O2 Adult HBA → at 28 mm Hg. 50% saturate

↓ Affinity for 2-3 DPG
→ PO2 28 mm Hg. 80% saturated
→ Fetal HB → 17 gm %
O2 carrying capacity
(23 ml/dl)
→ ↑ Cout in fetus 200 ml/kg 1 minute
(tissue exposed for more blood)
Maternal HB con. = 12 gm %
Maternal O2 carrying capacity (16 gm/dl)
O2 dissociative Curve shifted to Rt. Owing to
↑ 2.3 DPG
↑ release of O2 to inter villious
space – more O2 fetus

→ Head and neck receive blood with
High O2
→ The fetus and new born resistant
To hypoxia
→ Fetal PCO2 also↓ to 38 mm Hg.
(due to maternal hyperventilation)
- This effect over rides the shift of the
curve to left due to slight hyperventilation
- Near term maternal arterial PCO2 drops to
33 mm Hg. (because of hyperventilation)

Myoglobin → Heme protein present in the muscles made of only one polypeptide chain and one home
molecule (therefore it combines with one mol. of O2) instead of if 4 HB. The advantageous in its
action as a reservoir of O2 allowing greater margin of safety between capillary and tissue O2 tension at
low partial pressure of O2 it contain larger amount of oxygen also the very steep slope at low O2
tension allows the myoglobin to off load rapidly as the O2 tension in the cell falls rapidly.

1 2 3 4

CO2 → produced → diffuses out of the → to capillary

By the cell cell membrane lumen as dissolved CO2

8 7 6 5
In the lung 100 ml. pumped by heart CO2 diffuses easily the difference
Of blood un loads from blood to lungs out of cell because between pp of CO2
4 ml. of CO2 of high coefficient at tissues and capillary
Of diffusion and lumen is 1 to 2 mmHg.
Solubility

CO2 carried in three forms

Dissolved Carbamino 20 % HCO3 80 %

Form 5 % compound

CA
PCO2 – 46 – vein small 21 % combines H2O + CO2 H2CO3 HCO3 + H
 PCO2 – 40 artery amount with amino groups CA → absent in plasma
with plasma carbamino compounds in RBC renal contains CA,
proteins (carbonate)

reaction → HBNH2 + CO2

Hb NHCOOH
Rapid non enzymatic

HCO3 → if in the cell diffuses out in to to keep electro neutrally

Plasma in side the RBC

Thus the chloride ion content of Cl- ion diffuses into

RBC in the venous blood becomes
Higher than it is in the arterial blood
the cell chloride shift
This ↑ of the osmotically active ions of
HCO3 and Cl- in RBC of venous blood
Leads to more H2O retension by the cell
And ↑ in size

↑ in the Hct of venous blood by

3 % in the arterial blood

HB → affects CO2 transport by (forming carbamino compounds (21 by accepting H+ ion reduced HB is

aweaker acid than oxyhemoglobin

HB → when O2 is released at the tissues a tight (T) structure of HB is formed and protons (H +) are

absorbed and maintained by a small number of electrostatic bonds between protinated Histadine

and arginine residues.

These proteins are released at the lung during oxygenation of HB because of the formation of the relaxed form (R)
an extra base is then available to neutralize the acidity produced at the tissues (Haldane effect). It is estimated that
complete deoxygenation of 1 mmol of oxygen can neutralize 0.7 mmol of hydrogen ions without any change in PH.
The net result of the 200 ml. of CO2 liberated at the tissues every minute at rest is a rise in CO2 content of the blood
by 4 ml. per 100 ml of blood of this about 5 to 10% stays in a solution 20% transported as car amino compound and
the remaining is added to the HCO3 ion pool resulting in a drop of pH from 7:4 to 7:36. However the distribution
pattern of CO2 does not hold true for the total amount of CO2 present in the blood in the arterial blood the dissolved
CO2 and car amino compounds each represent less than 5 % of total CO2 while the remaining 90 % is in the form of
HCO3 of this HCO3 pool 2/3 is present in plasma and 1/3 in RBC.

Oxygen transport at high altitudes

Inspired oxygen tension diminishes as the Barometer pressure decreases.

Insp. O2 tension can be drived from the following equation

Insp. O2 tension (mmHg.) = 0.21 x (atmosphere pressure – H2O vapor)

Where 0.21 is the O2 con. Of air at sea level the atmospheric pressure is 760 mmHg and H2O vapor pressure is 47
mmHg. Hence the inspired tension is 150 mmHg. To calculate the alveolar O2 tension the CO2 tension in the
alveolar air is subtracted (with a correction factor) from the O2 tension e.g. altitude of 500 meters above sea level the
barometer pressure falls to about 400 mm Hg which becomes equivalent to inspired O2 tension of 73 mm Hg and
alveolar O2 tension of 43 mmHg the diminution of alveolar hypoxemia is partially compensated by hyperventilation
mediated through the chemo receptors. However the patient will show symptoms of mental irritability unless he
breathes high inspired concentration of O2 at about 16,000 meters the atmospheric pressure becomes so low that the
O2 in the alveoli drops to less than 40 mm Hg. And consciousness is lost unless the patient breathes O2 with high
pressure system.

The immediate compensatory reaction from moving to high altitudes are hyperventilation and ↑ cout. These changes
↑ the rate of O2 transfer from the lung to the capillaries further the ↑ cout, HPV constriction S.N.S stimulation of the
large pulmonary vessels result in a mean ↑ pulmonary artery pressure when will abolish preexisting zone I the
recruitment of under perfused alveoli and consequently improve oxygenation simultaneously.

Persons moving to high altitude

Compensatory Mechanisms (acclimatization)

(a) ↑ 2.3 DPGS – in HB – as compensation for the left shift of oxy. HB dissociation curve availability of O2 to
the tissue is ↑
(b) Arterial desaturation leads to ↑ erythropoietin production resulting in polycythemia Resp. alkalosis persists
for 3 to 4 wks.

Kidneys compensate by ↑ base excretion tissue compensation for the low O2 tension is by arteriolar dilation
↑ the site of oxidative reactions – manifested by ↑ in number of mitochondria. Myoglobin Con. of O2 ↑ – facilitating
the movement of O2 in to the muscles.

Clinical effect of hypoxemia

Nl. Man – MV = by 2.5 liters/ minute for q. mmHg in alveoli PCO2.

PCO2 = 40 to 70 mmHg.

(5 to 10% inspired)

PCO2 of alveolar above 100 mm Hg. Higher PCO2

15% inspired loss of consciousness direct resp. depression cerebral

Vasodilatation restless faintness

When ventilation is stimulated by combination of hypoxia and hypercapnia the increase in ventilation is > than the
sum of increments produced by each separately (due to effect of hypoxia stimulating the chemo receptors).

Assessment and treatment of patient with hypoxemia

Hypoxemia → reduction in the oxygen content of blood. Arterial O2 tension is determined by the inspired oxygen
tension, by the level of alveolar ventilation by distribution of ventilation and perfusion in the lung.

Monitoring Oxygenation
Clinical signs/ symptoms

(a) CNS – PaO2 55 mmHg → short term memory is altered (cognitive motor function is altered)
PaO2 30 mmHg → loss of consciousness and seizures occurs
→ dilated and fixed pupil

NB – GA abate all the signs of hypoxemia except seizure

(b) CVS – Immediate response initiated by carotid body chemo receptors (tachy cardiac stroke
volume little or no change in B/P and ST sequent and T-wave unchanged
When hypoxemia worsens (Brady Cardiac and Hypotension cardiac arrest)

(c) Respiratory → ↑ ventilator drive TV, RR and latter chynestokes breathing and apnea GA –
abolishes hyperpnoea response to hypoxemia

(d) Cyanosis the appearance of cyanosis merely reflects a critical amount of reduced HB the appearance of
cyanosis is highly variable at moderate levels of hypoxemia. Cyanosis is not specific for hypoxemia in
anesthetized patients.

Although lacking insensitivity and in specificity the appearance of cyanosis may be the only indicator of profound
hypoxemia during anesthesia.

B) Measurement of oxygenation clinical or physiologic signs have limited value during GA

Transcutaneous PO2 monitoring - Mass spectrometry

Ear oximetry - Continuous SV – O2 monitoring
Pulse oximetry - Arterial blood gas analysis

III – Pre Operative Evaluation

(a) Pre existing pulmonary disease – prospective and retrospective studies suggest evaluation did treatment of
patients with pulmonary disease (smoking, infection, bronchospasm
(b) Premeditation → vagolytics → have little effect on PaO2
→ ↑ anatomic dead space, and compliance
→ ↓ airway resistance diffusing capacity and thoracic blood volume
- Narcotics
- BZD
- Barbiturates → they ↓ PaO2

IV.Intraoperative Hypoxemia

A – Mechanism of Hypoxemia
1. Change in position → Supine tredelnburg lateral decubitus ↓ FRC
2. Induction of anesthesia → Smooth transition from consciousness to unconsciousness hypoxemia is our
goal – FRC 0.4 liters. During periods of apnea PaO2 will fall. (so preoxygenation with high FlO2 prior to
intubations)
3. Equipment malfunction → ETT obstruction (failure in O2 delivery)
4. Hypoventilation – may result from depth of anesthesia airway resistance ↓ lung compliance and
↓ lung volume
5. Hyperventilation → ↓ in PacO2 by cout VO2, shifting of oxy. HB dissociation curve, HPV airway resistance
and ↓ compliance
6. Decrease in FRC Induction of GA ↓ FRC 25% and ↓ in total lung compliance (10% - 50%)
 - FRC ↓ starts immediately up to post operation.
7. ↓ Mucociliary Flow – poor systemic hydration, low inspired humidity high inspired O2 concentration,
ETT cuff, and Halothane
8. High inspired oxygen concentration → absorption atlectasis, ↓ muco ciliary’s flow and inhibition of HPV

Pathophysiology → PaO2 is determined by FiO2

→ level of alveolar ventilation
→ distribution of ventilation and perfusion in the lungs

Two causes
(a) Diminished alveolar O2 tension (PAO2)
(b) Increased alveolar arterial O2 tension difference P (A – a) O2
1) Pulmonary Causes of Hypoxemia
(a) Hypoventilation → (low PIO2):- clinical conditions where hypoxemia may result from in adequate
ventilation include Obesity CNS disease or as a result of drug administration Diminished PIO 2 usually
results from mechanical problems with the oxygen delivery system.
(b) Abnormal Diffusion – usually a minor contribution to hypoxemia diffusion abnormalities are associated
with clinical conditions such as idiopathic pulmonary Fibrosis, sarcoidosis, and asbestosis.
(c) Ventilation – perfusion mismatch:- the most common cause of arterial hypoxemia in patients with chronic
pulmonary disease, assuming alveolar ventilation of 5 1/min and pulmonary blood flow of 6 L/min the over
all V/Q ratio would be 0.08 the more alveoli with higher or lower values than this the greater the P (A – a)
O2. V/Q. Mismatching is commonly associated with interstitial Fibrosis and asthma.
(d) Physiologic Shunt:- Common during and after anesthesia and operation it is attributable to mixed venous
blood that perfuses non-ventilated lung regions. Associated clinical conditions include pneumonia ARDS
and pulmonary hypertension.

2) Non Pulmonary Causes of Hypoxemia

(a) Decreased mixed venous PO2 – Conditions that return mixed venous blood with a lower than normal
PO2 can cause hypoxemia clinical examples include.
- decreased cardiac out put
- increase oxygen consumption
- anemia

SHIFT OF OXYHEMOGLOBIN DISSOCIATION CURVE

- Alteration in the factors defining the curve can also affect mixed venous PO2 and thereby causes
arterial hypoxemia. Determination of the position of the oxyhemoglobin dissociation curve include
PH and / or CO2 effect, temp and 2-3 DPG levels.

Post Operative Hypoxemia

A. Early Postoperative Period

1. Central/ peripheral ventilator depression – may result in alveolar hypoventilation. It may be caused by
CNS disease premed cant drugs anesthetic agent or neuromuscular blocking agents Alveolar
 hypoventilation could also result from mechanical impairment to breathing or increase respiratory dead
space

2. Diffusion Hypoxia (low PIO2) :- N2O is about 30 x more soluble than N2 when patient is switched from
breathing N2O/ O2 mix to breathing room air N2O is rapidly excited in to the alveoli thus there is a dilution
of inspired gas with the excess volume of N2O so PAO2 decreases. High inspired oxygen concentration
following ceasation of N2O use can avoid the problem also failure of the O2 delivery system can result in
hypoxemia.

3. Increased shunt fraction:- (V/Q mismatch) ↑ in trapulmonary shunt is the most common cause of post
operative hypoxemia. Atlectiasis is the most common etiology. Certainly obstruction of the airway. ETT
pneumothorax, aspiration and pulmonary edema (carcinogenic or A.R.D.S) can all lead to arterial
hypoxemia in the post operative period. The efficacy of supplementary O2 post operatively suggests there
is an↑ volume of lung at a low distribution of ventilation to perfusion compared with normal. There is
evidence that resting lung volume remains increased in the early post operative period. Especially in the
elderly which results in an unfavorable redistribution of ventilation with resulting venous admixture.

4. Post Hyperventilation Hypoxemia :- following an anaesthetic technique employing hyper ventilation the
body stores of CO2 are refilled from endogenous production of CO2and ventilation an PAO2 reduced
accordingly.

5. Decreased PVO2 → ↑ O2 consumption, reduced cout. Anemia or left shift of the oxyhemoglobin
dissociation curve may result in a decreased PVO2 causing an increased in P (A – a) O2 and resultant
hypoxemia.

B. Late post operative period

1. Incidence :- varies markedly with the extent and type of surgery. Reported incidence depends on the
diagnostic criteria used.

2. Changes in lung volume:- there is a post operative ↓ in FRC, ERV, IRV, VC and expiratory flow rates
even when atlectases is not clinically or roentogenographically detectable.

3. Lack of inflation :- the basic mechanism of at lactases in the post operative patient the lack of inflation
is due to a change in breathing pattern, supine position, ↑abdominal pressure and diaphragmatic
dysfunction, atlectasis is the principal post operative pulmonary complication associated with
hypoxemia.

4. Clinical risk factors:- include type and duration of surgery age, general physical status, nutritional
states, smoking history heart disease and lung disease.

VI. Treatment of Hypoxemia

A. Increased Fio2 :- most causes of hypoxemia are responsive to supplemental oxygen. Therefore,
since PaO2 is rarely measured post op. it has been advocated that all patients receive supplemental
O2 after GA until they are fully awake and vital signs stable supply mental O2 should be continued
there after only in patients following cardiothoracic surgery or those with significant cardio
pulmonary disease ↑ Fio2 in patient with a significant shunt fraction has little effect on PaO2.
B. Increasing alveolar ventilation :- an increase in alveolar ventilation has limited effect on PaO2
compared with increasing Fio2 or decreasing shunt units and areas with low V/O ratos however in
 patients breathing room air an increase in alveolar ventilation may make a significant difference in
oxygenation.
C. Prevention/ Reversal of Atlectasis :- Numerous techniques have been described to prevent post op.
airway collapse and atlectases which are the predominant causes of hypoxemia these mechanical
aids to lung expansion include I.P.P.B incentive sypitometery. PEEP/CPAP and chest
physiotherapy. A “Stir up” regimen is the basis for all post op. care i.e. turning, coughing, and
ambulation any patient with hypoxemia un responsive to high in spired. Concentrations of
supplemental oxygen should be considered a candidate for positive airway pressure therapy.
Since O2 has little effect on PaO2 in patients with large shunt fraction the positive airway pressure
(mechanical ventilation with PEEP or Mask CPAP) will increase FRC and improve arterial
oxygenation it will allow reduction in Fio2 without compromising PaO2.

VII. SUMMARY→ anesthesia and surgery result in an increased in efficiency of gas exchange abnormal
oxygenation and CO2 elimination arterial hypoxemia may result from hypoventilation or low PIO2 abnormal
diffusion. V/Q mismatching, intrapulmonary shunt decreased PVO2 and/ or changes in oxyhemoglobin
dissociation curve clearly the development of hypoxemia in the preoperative period requires prompt recognition
an intervention. Therapy should be directed at the underlying patho physiologic process by increasing Fio2,
improving alveolar ventilation and preventing or reversing atlectasis.

HPV → enhanced by extra cellular acidosis as well as hypercapnia

→ vasoconstriction subsequent to alveolar hypoxia – opposite to systemic where you have

vasodilatation

When Alveolar PO2 ↓ (markedly) → (markedly) → vascular smooth muscles vasoconstrictor diverting a blood to
better ventilated lung hence regional ventilation perfusion ratios are favourably adjusted and arterial O2 tension is
reversed. This response occurs in isolated enervated lungs as well as in intact lungs.

Vasoconstriction occurs when alveolar oxygen tension ↓ 70 mm Hg.

Exact mechanism not known most probably by the release of a vasoconstrictor substance by the peri arterial mast
cell acting on the alpha receptors of the small pulmonary arteries. Histane, serotonin, catecholamines and
prostlyglands – suggested as mediator substances. One of the mechanisms in people with C.P.O.D to develop
pulmonary hypertension. Can be blocked by pulmonary vasodilators e.g. nitroglycerine isoproternol Na +
nitroprosside or Ca++ channel blockers.

In a patient breathing air

PaCO2 + PO2 = to approximately 140 mmHg. (when breathing atmospheric air) (because body neither consume nor
manufacture N2 PP of N2 is constant in trachea bronchi and alveoli)

Occupies most of the atmospheric pressure the remaining space is available for water vapor and the
respiratory gases.

As the water vapor pressure is almost constant ant it follows that in the alveoli the sum of the respiratory gases must
occupy the remaining space. Whether this same sum appears in the arterial blood depends upon the accuracy of the
analysis and the performance of the lung. (When breathing atmospheric the sum of respiratory gases in the alveoli is
150 mm Hg. (if small sum → lungs are failing to transfer adequate O2 if greater sum – indicates error.

A. When moving to high altitudes the immediate compensatory response is by hyperventilation and
increasing cardiac out put these changes ↑ the rate of O2 transfer from lung pulmonary capillaries further
cout and HPV and sympthatetic stimulation of pulmonary vessels leads to pulmonary hypertension.
B. The rise in mean pulmonary artery pressure will abolish pre existing zone I by recurrent of under perfused
alveoli and improve oxygenation
C. When moving to high altitudes compensating mechanism appears with in few days acclimatization) the
first response is an ↑ in 2-3 DPG level in the HB. (O2 delivery (1) arterial desaturation lead to an in
Erythopoietin pectin production

Polycethemia respiratory alkalosis persists for about 3 to 4 weeks and eventually kidneys compensate by ↑ excretion
of base, the tissue compensate for the low O2 tension by arteriolar dilation site of oxidative reactions as manifested
by ↑ in number of mitochondria in the myoglobin concentration of tissues increased by facilitating transfer of O 2 in
to muscles.

Oxygen transport at high altitudes

At high altitudes the inspired O2 tension diminishes as the barometric pressure decreases the inspired
oxygen tension can be derived from the following formula. Inspired oxygen tension (mmHg) = 0.21 (atmospheric
pressure – water vapor pressure) where 0.21 is the oxygen concentration of air at sea level the atmospheric pressure
is 760 mmHg and water vapor pressure is 47 mmHg. Hence the inspired tension is 150 mmHg. To calculate the
alveolar O2 tension the CO2 tension in the alveolar air is subtracted (with a correction factor from the oxygen
tension).

Mixed Alveolar PO2 PCO2 PN2

101 mmHg 39 572

Mixed arterial 97 mmHg 40 575

A – a diff 4 1 3

Summary on Hypoxia

→ For O2 to be transferred from capillaries to tissues a certain pressure gradient is required below this

critical capillary oxygen tension diffusion is impaired.

→ Minimal end capillary O2 tension is 20 tension is 20 mmHg → at Nl. PH, Temp, this critical O2 tension

represents an O2 saturation of about 25% below this level cell metabolism becomes an aerobic and

break down of glucose steps at the stage of lactic acid formation. If this inadequate oxygenation

persists, metabolic derangements finally lead to the death of the cell in this respect the brain is the

most sensitive organ its oxygen up take diministhes when the venous oxygen tension falls into 20 to 25

mmHg range.
→ Kidneys → can tolerate moderate amounts of hypoxia if O2 supply falls to more than 2/3 of Nl. Na+

and urea handling becomes impaired in severe hypoxia tubular cell necrosis, with excretory failure.

→ Splanchnic hypoxia →impairment of liver function especially as measured by those tests than indicate

release of intracellular enzymes lactic dehydrogenate (LOH) and Glutamic oxalic transminase (SGOT)

→ Dysoxia abnormalities that underline all O2 related disease either as a result of diminished supply or

because of impaired utilization by the organelle

→ Hypoxic Hypoxia → if diminution of O2 supply is associated with decreased arterial O2 tension if it is

due to diminution of the number functioning RBC

→ Anemic anoxia → Can result from absolute decrease in HB or

Or can be due to diminution of functional HB as in CO. Poisoning or met hemo globinemia

→ O2 content of blood is diminished O2 carrying capacity of blood is decrease

→ An anemic patient is usually a symptomatic at rest. Exercise tolerance will be diminished. Basal

cardiac out put is altered little the HB is below 2/3 of normal the blood volume being unchanged

because the increase in plasma volume a dimnution inviscosity content will facilitate blood flow in the

vessels

The diminution in Hemoglobin Content will decrease the buffering capacity of the blood and thus the blood will be
more acidic at the venous side which in itself facilitates the un loading of oxygen at the tissue level (shift to the rt.)
the red cells increase their capacity to unload oxygen by increasing their 2.3 DPG levels.

→ A cause of acute functional anemia is carbon monoxide poisoning CO + O2 → carboxyhemoglobin

→which has no O2 carrying capacity

→ Shifts curve of remaining HB to left decrease O2 release to the tissue

→ CO → 210 x more affinity for HB

→ Histotoxic Anoxia → ↓ mitochondria O2 consumption this is due to poisoning of oxidative enzymes at the tissue
levels the blood perfectly saturated reaches the tissues but they are unable to utilize the oxygen. Because the
cyanide ion combines with cyto chrome oxidize disturbing the electron transport chain and reducing or even
completely abolishing mitochondria O2 consumption.

Na+ nitroprusside → potent vasodilator

Broken down by Hemoglobin → to cyanide → detoxified by liver and kidney to thio cyan ate if large amount taken
some amount of cyanide remain free and cause cyanide poisoning.

Cyanosis → Reduced HB has a dark colour in contrast to ox hemoglobin which has bright red colour cyanosis can
be noticed when the concentration of reduced HB in the capillary blood is above 5 gm/dl this an anemic patient with
HB con of less 5 gm/dl of blood cannot become cyanotic conversely patients with poly cythemia are more liable to
show cyanosis. Cyanosis is mostly evident as a bluish discoloration of the mucous membrane nail beds and in the
areas of the body in which the skin is thin such as ear lobes lips and fingers cyanosis can occur in the absence of
Generalized by Hypoxemia when the capillary circulation becomes extremely slow. More O2 is extracted from the
blood in the capillaries. This is typically seen in exposure to moderate cold and is sometimes termed peripheral
cyanosis in contrast to that associated with hypoxemia, which is termed central cyanosis. Although cyanotic patient
should administer a high con. Of O2 unless he can establish that the cause of cyanosis is peripheral.

Prepared by = Leulayehu Akalu

References

Clinical anesthesia Barash

Miller anesthesia

Gyton Physiology

Physiology for anesthesiologists (Agop karman )

Introduction to anesthesia (Dripps )

Anatomy for anesthetists