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Relate function of the upper airway to its structure

Describe the anatomy of the upper airway and understand the differences encountered in the neonate, paediatric and adult populations

Upper Airway

• Nose

• Nasopharynx

• Larynx

Nose:

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• Vestibule:

o Anteroinferior part

o Has skin+sebaceous glands+hairs called vibrissae

o Medial wall-collumela

o Lateral wall- upperlateral cartiladge

• Nasal cavity: communicates to exterior through nares and nasopharynx through choanae

o Lateral wall:

▪ 3 turbinates-inferior, middle and superior

▪ 3 meatus – inferior, middle (receives opening of most sinuses)

▪ 1 sphenoethmoidal recess

o Medial wall: nasal septum

o Roof:

▪ Anteriorly: nasal bone

▪ Middle: cribriform plate of ethymoid bone

▪ Posterior: sphenoid bone

o Floor:

▪ Anterior ¾: maxillary bone

▪ Posterior ¼: palatine bone

• Lining membrane:

o Upper 1/3 : olfactory region – pale mucosa innervated by the olfactory n

o Lower 2/3 : respiratory region – highly vascular + erectile tissue, lined by the pseudostratified ciliated columnar epithelium with plenty of goblet cells. Submucosa with serous and mucus glands

• Nerve supply:

o Olfactory nerve

o Common sensations:

▪ Ant. Ethymoid n

▪ Branches of sphenopalatine ganglion

▪ Infraorbital n

o Autonomic

▪ Parasympathetic: via greater superficial petrosal n – causes vasodilatation and increased secretion

▪ Sympathetic: T1&T2 via greater superficial petrosal n causes vasoconstriction

• Functions of nose:

o Respiration - eddie currents ventilate sinuses

o Airconditioning

▪ Filtration (particles > 3µ)

▪ Temperature control

▪ Humidification (changes air to relative humidity ≥ 75%)

o Protection of lower airways:

▪ Muco-ciliary mechanism – 5-10mm/min movement of mucus belt to the oropharynx

▪ Sneezing

▪ PH ~ 7

▪ Lysozyme and immunoglobulins

▪ 600-700 ml of nasal secretions / 24 hrs

Nasopharynx:

• Roof: basisphenoid and basio-occiput

• Posterior wall – arch of atlas vertebra

• Floor – soft palate anteriorly, deficient posteriorly ( the nasopharyngeal isthmus

• Anterior – choanae+ turbinates + nasal septum

• Lateral – Eustachian tube opening, fossa of rusenmuller and salpingopharyngeal fold

• Adenoids- tonsils located at the junction of the roof and posterior wall

• Functions:

o Conduit

o Ventilation of middle ear and equalizes pressure

o Elevation of soft palate cuts off nasopharynx from oropharynx during swallowing

o Resonating chamber for voice

Larynx:

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Larynx extends from C3 to lower border of C6

• Cartilages:

o Paired (3) –

▪ Arytenoid (Hyaline) – pyramidal in shape. Base articulates with cricoids cartilage, lateral muscular process gives attachment to muscles, anterior vocal process gives attachment to VC and apex supports corniculate cartilage

▪ Corniculate (Fibroelastic)

▪ Cunieform (Fibroelastic)

o Unpaired (3) –

▪ Thyroid (Hyaline): largest. VC attach to middle of angle. Angle 90⁰ in male and 120⁰in female.

▪ Cricoid (Hyaline): only cartilage forming the complete ring.

▪ Epiglottis (Fibroelastic): leaf like yellow elastic cartilage. Attached to hyoid via hyoepiglottic ligament

• Joints: (synovial joints)

o Cricoarytenoid

o Cricothyroid

• Membranes:

o Extrinsic membranes:

▪ Thyrohyoid

▪ Cricohyoid

▪ Cricotracheal

o Intrinsic membranes:

▪ Cricovocal membranes

▪ Quadrangular membranes

• Muscles:

o Intrinsic:

▪ Acting on laryngeal inlet

• Opener – thyroepiglottic

• Closer – interarytenoid, aryepiglottic

▪ Acting on vocal cords

• Abductors: posterior cricoarytenoid

• Adductors: lateral cricoarytenoid, interarytenoid, thyroarytenoid

• Tensor: Cricothyroid vocalis

o Extrinsic: (connect larynx to neighboring structures)

▪ Elevators:

• Primary elevators – attached to thyroid cartilage and act directly – stylopharyngeus, salpingopharyngeus, palatopharyngeus and thyrohyoid

• Secondary elevators – attached to hyoid bone and act indirectly – mylohyoid, digastrics, stylohyoid, geniohyoid

▪ Depressors: - sternohyoid, sternothyroid, and omohyoid

• Cavity: starts at laryngeal inlet and ends at cricoid cartilage, divided by two pair of folds- vestibular and vocal into three parts – vestibule, ventricle and subglottic space

o Vestibule – extends laryngeal inlet to vestibular folds . Anterior part by epiglottis, lateral by aryepiglottic folds and posteriorly by arytenoids

o Ventricle – deep elliptical space between vestibular and vocal folds

o Subglottic space – extends from vocal cords to cricoid cartilage

o False vocal cords or vestibular folds – fold of mucous membrane extending anteroposteriorly- contains vestibular ligaments, few fibres of thyroarytenoideus muscle and mucous glands

o True vocal cords or vocal folds – two pearly white sharp bands extending from middle of thyroid angle to the vocal processes of arytenoids

o Glottis : elongated space between vocal cords anteriorly and vocal processes & bases of arytenoids posteriorly. Anteriorly 24 mm in men and 16 mm in women. Narrowest part of larynx.

• Mucosa:

o Epithelium: ciliated columnar epithelium except on VC & upper part of vestibule where it is squamous

o Mucus glands distributed all over max on posterior surface of epiglottis and aryepiglottic folds. None on VC

• Nerves

o Motor: All the muscles of VC (adductors, abductors and tensors) are supplied by the recurrent laryngeal nerve except the cricothyroid muscle which is supplied by the superior laryngeal nerve via the external laryngeal branch. Left recurrent laryngeal nerve arises in mediastenum at the level of arch of aorta and has a long course making it more prone to paralysis

o Sensory: above the VC, larynx is supplied by superior laryngeal nerve via internal laryngeal branch and below the VC larynx is supplied by the recurrent laryngeal nerve

• Functions

o Protection of lower airways – sphincteric closure of laryngeal opening, phonation, respiration and fixation of chest

o Phonation

o Respiration

o Fixation of chest

Pediatric larynx:

• Positioned high in the neck opposite C3 or C4 at rest and reaches C1 or C2 during swallowing.

• Laryngeal cartilages are soft and collapse easily

• Epiglottis is omega shaped

• Arytenoids relatively large

• Thyroid cartilage is flat

• Cricothyroid and thyrohyoid spaces are narrow and not easily discernible

• Larynx is small and conical. The diameter of cricoids cartilage is smaller than glottis unlike in adults making the subglottis narrowest portion of larynx

• Submucosal tissue is loose and easily undergo edematous change leading to obstruction

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To explain the structure of the chest wall and diaphragm and to relate these to respiratory mechanics

The diaphragm constitutes the great muscular septum between the thorax and the abdomen; it is one of the distinguishing features of mammalian anatomy.

Anatomical features

The diaphragm consists of peripheral muscle with a central trefoil-shaped tendon of strong interlacing bundles that blend above with the fibrous pericardium. The muscle takes a complex origin from the crura, the arcuate ligaments, the costal margin and the xiphoid.

The crura arise from the lumbar vertebral bodies; the left from the 1st and 2nd, the larger right from the 1st, 2nd and 3rd. The arcuate ligaments are the median, which is a fibrous arch joining the two crura, the medial, which is a thickening of the fascia over the psoas and

the lateral, which is a condensation of fascia over quadratus lumborum ending laterally near the tip of the 12th rib.

The costal origin is from the tips of the last six costal cartilages.

The xiphoid origin comprises two slips from the posterior aspect of the xiphoid.

The diaphragmatic foramina

The three major openings are for:

1 the inferior vena cava, at the level of the body of the 8th thoracic vertebra;

2 the oesophagus, together with the vagi and the oesophageal branches of the

left gastric vessels, at T10;

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3 the aorta, together with the thoracic duct and azygos vein, behind the median

arcuate ligament at T12.

In addition, the sympathetic trunk passes behind the medial arcuate ligament, the splanchnic nerves pierce the crura, the hemiazygos vein drains through the left crus, the superior epigastric vessels pass between the xiphoid and costal origins of the diaphragm into the posterior rectus sheath, the lower intercostals nerves and vessels enter the anterior abdominal wall between the interdigitations of diaphragm and transversus abdominis and lymphatics stream from the retroperitoneal tissues through the diaphragm to the mediastinum. The oesophageal hiatus is reinforced by a sling of muscle fibres from the right

crus, which probably plays a part in maintaining competence at the oesophagogastric

junction. Not uncommonly, the left crus supplies some of the fibres forming this sling which is occasionally derived solely from it.

Nerve supply

The phrenic nerve (C3–5; see p. 151 for a detailed description) provides the motor supply of the diaphragm, apart from an unimportant contribution to the crura from T11 and 12. Section of the phrenic nerve is followed by complete atrophy of the corresponding hemidiaphragm. The phrenic nerve also transmits proprioceptive fibres from the centre of the diaphragm, although the periphery of this muscle has its sensory supply from the lower thoracic nerves. The right phrenic nerve pierces the central tendon to the lateral side of the

inferior vena cava (some fibres may actually accompany the vein through its foramen). The left nerve pierces the muscle about 1 cm lateral to the attachment of the pericardium. The terminal fibres of each nerve supply the muscle on its abdominal aspect.

The diaphragm as a muscle of respiration

The apex of the dome of the diaphragm reaches the level of the 5th rib in the mid-clavicular line, i.e. it is level with a point about 2.5 cm below the nipple. The right hemidiaphragm is rather higher than the left, and both domes rise somewhat in the horizontal position. When the subject lies on his/her side, the upper cupola sinks to a lower level than its partner and its movements are relatively diminished. The level of the diaphragm is elevated in late pregnancy, gross ascites or obesity, in pneumoperitoneum and in patients with large abdominal tumours; such subjects all have some degree of respiratory limitation.

In inspiration, the diaphragm moves vertically downwards (the domes considerably

more than the central tendon) and this has a piston-like action in enlarging the thoracic cavity. A subsidiary effect is that the lower costal margin is raised and everted with consequent expansion of the base of the thorax. In expiration, the diaphragm relaxes; in forced expiration, it is actually pushed upwards by the increased intra-abdominal pressure effected by contraction of the muscles of the anterior abdominal wall.

It is estimated that the movement of the diaphragm accounts for some 60–75% of the total tidal volume of respiration; in some subjects during quiet breathing it may, indeed, be the only functioning muscle in inspiration. It is therefore interesting that bilateral phrenic interruption with complete diaphragmatic paralysis may cause little respiratory difficulty providing the lungs are relatively normal. In quiet respiration, the diaphragm has a range of movement of 1.5 cm. In deep breathing this increases to 7–13 cm.

In addition to its important role as a muscle of respiration, the diaphragm helps increase the intra-abdominal pressure in defecation, micturition, vomiting and parturition, as well as taking part in the mechanism of the ‘cardiac sphincter’

The diaphragm and the ‘cardiac sphincter’

At the cardio-oesophageal junction, there exists a rather extraordinary sphincter mechanism that allows food and liquids to pass readily into the stomach, which prevents free regurgitation into the oesophagus even when standing on one’s head or in forced inspiration (when there is a pressure difference of about 80 mmHg between the intragastric and intra-oesophageal pressures), but which can relax readily to allow vomiting or belching to occur.

In spite of extensive investigations, the exact nature of this sphincter is not understood. It is probably a complex affair made up of:

1 a physiological muscular sphincter at the lower end of the oesophagus;

2 a plug-like action of the mucosal folds at the cardia;

3 a valve-like effect of the obliquity of the oesophago-gastric angle;

4 a diaphragmatic sling which maintains the normal position of the cardia and

has a pinch-cock action on the lower oesophagus;

5 the positive intra-abdominal pressure which tends to squeeze the walls of the

intra-abdominal portion of the oesophagus together.

Although a true anatomical sphincter cannot be shown by dissection, a physiological sphincter can be deduced from the high-pressure zone demonstrated within the lower oesophagus, which disappears when the oesophageal muscle is divided, as in Heller’s operation for achalasia of the cardia. Reinforcing the sphincter are the mucosal folds of the cardia, which act as a plug wedged within the muscular ring.

The crural sling of the diaphragm around the lower oesophagus is important in maintaining the normal position of the cardio-oesophageal junction below the diaphragm. If the hiatus is enlarged and lax, the stomach can slide upwards into the chest (a ‘sliding hiatus hernia’) and the normal valve-like angle between oesophagus and cardia straightens out.

There also appears to be a definite pinch-cock mechanism on the oesophagus when the diaphragm contracts in full inspiration; a phase at which intrathoracic pressure is lowest, intra-abdominal pressure highest and conditions most favourable for fluids to be forced at high pressure upwards through the cardiac orifice. The diaphragm is an important but not essential part of the cardiac sphincter mechanism, since a sliding hiatus hernia is not necessarily accompanied by regurgitation providing the physiological sphincter is competent. Similarly, free regurgitation occurs in some subjects with an apparently normal oesophageal hiatus, presumably because of some defect in the function of the physiological sphincter.

Anatomy relevant to the insertion of an intercostal catheter

Preffered intercostals space: Mid-axillary line 5th ICS

Location of site: 2nd rib detected using its attachment at the level of angle of Louis. Ribs are then counted downwards to 5th rib, traced down to MAL. 5th ICS lies beneath the 5th rib.

‘Triangle of safety’: lateral border of the pectoralis major anteriorly, the anterior border of the latissimus dorsi posteriorly and the upper border of the sixth rib below

The intercostal spaces

Superficial to deep: skin, superficial fascia with varying thickness of fat, intercostals muscles and parietal pleura.

Intercostal muscles: 3 layers – external intercostals, internal intercostals and innermost layer which is poorly developed and in MAL it blends with internal intercostals except at the lower border of the upper rib where they are separated by the neurovascular bundle.

Neurovascular bundle: Runs in the subcostal groove near the lower border of upper rib. Comprising, from above downwards, the posterior intercostal vein, artery and nerve. Artery becomes tortuous in coarctation of aorta. Hence dissection should be near upper border of lower rib.

Deep structures

The apex of the dome of the diaphragm reaches the level of the fifth rib in the midclavicular line – the right rather higher than the left because of liver.

Alterations in diaphragm level: elevated in late pregnancy, gross obesity, severe ascites, a large intraabdominal tumour or when there is a considerable pneumoperitoneum. In inspiration, the diaphragm moves vertically downwards by its muscular contraction. In expiration, the diaphragm relaxes passively, while in forced expiration it is pushed upwards by contraction of the muscles of the anterior abdominal wall. Beneath the diaphragm lies the liver on the right and the stomach and spleen on the left.

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Tracheal and bronchial anatomy and structure

The airways consist of a series of branching tubes, which become narrower, shorter, and more numerous as they penetrate deeper into the lung

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There is no alveoli up to terminal bronchioles and hence this region is known as conducting zone. The volume of gas occupying this region does not participate in gas exchange and is approx 150ml i.e. anatomical dead space. The portion of lung distal to terminal bronchioles forms anatomical unit called ‘acinus’. The distance from the terminal bronchiole to the most distal alveolus is only a few millimeters, but the respiratory zone makes up most of the lung, its volume being about 2.5 to 3 liters during rest.

Adult trachea:

• Length: 9-15 cm

• Extra-thoracic length ~ 5 cm

• Internal diameter: 12-18 mm

• Outer diameter: 21-27 mm

• 18-22 cartilaginous rings

• Becomes intrathoracic at 6th cartilaginous ring

• Average cross-sectional area is 2.8 cm2

• Diameter 13mm - 27mm

Right main bronchus:

• 2cm long, I.D. 10-16mm

• Branches:

o Right upper lobe

▪ Apical

▪ Anterior

▪ Posterior

o Bronchus intermedius

▪ Middle lobe

• Medial

• Lateral

▪ Lower lobe

• Superior

• Medial basal

• Anterior basal

• Lateral basal

• Posterior basal

Left main bronchus:

• 4-5cm long

• I.D. 8-14mm

• Branches

o Left upper lobe

▪ Apicoposterior

▪ Anterior

o Lingular

▪ Superior

▪ Inferior

o Left lower lobe

▪ Superior

▪ Anterior basal

▪ Lateral basal

▪ Posterior basal

Outline the vascular anatomy and structure of the pulmonary and bronchial circulations

The pulmonary artery provides a capillary plexus in intimate relationship to

the alveoli and is concerned solely with alveolar gas exchange. The blood supply

to the lung itself, to its lymph nodes, to the bronchi and to the visceral pleura

is entirely provided by the bronchial arteries. Venous drainage from the walls

of the larger bronchi is carried out by the bronchial veins; the drainage of the

smaller bronchi, together with that of the alveolar capillaries, is a function of

the pulmonary veins. Thus, although there is no communication between the

bronchial and pulmonary arteries, a good deal of blood brought to the lung by

the bronchial arteries is drained by the pulmonary veins.

The pulmonary artery and its subdivisions closely follow the ramifications

of the bronchial tree, so that each air sac has its own minute twig, which then

breaks up into capillaries that form the richest vascular network in the body.

The pulmonary vein tributaries are derived partly from the capillaries of the

pulmonary artery and partly from those of the bronchial artery. Unlike the

branches of the pulmonary artery, which run in close relation to the bronchial

tree, the venous tributaries lie between the lung segments, thus providing a

valuable landmark to the surgeon in the performance of segmental resections.

At the apex of each bronchopulmonary segment, the pulmonary vein draining

that segment meets the segmental artery and passes alongside it to the hilum.

There are two main pulmonary veins on each side, which drain separately

into the left atrium. On the left side, the upper and lower lobe each have their

own main pulmonary vein; on the right side, the upper and middle lobes share

the upper pulmonary vein, the lower lobe drains via the lower vein.

The bronchial arteries are to the lungs what the hepatic artery is to the liver:

they supply the actual pulmonary stromaathe bronchi, lung tissue, visceral pleura

and pulmonary nodes.

The arteries are variable in both number and origin; there are usually three,

one for the right lung and two for the left. The left bronchial arteries usually

arise from the anterior aspect of the descending thoracic aorta. The right artery

is more variable; it may arise from the aorta, the 1st intercostal artery, the 3rd

intercostal artery (which is the first intercostal branch of the aorta), the internal

thoracic artery or the right subclavian artery. Occasionally, all three arteries arise

from a common trunk derived from the aorta. The arteries lie against the posterior walls of their respective bronchi. They

follow and supply the bifurcating bronchial tree as far as the small bronchioles

but disappear as soon as alveoli appear in the walls of the ducts; all available

respiratory epithelium is thus supplied from the pulmonary arterial tree.

The bronchial veins are usually two in number on each side; the right drain

into the azygos vein, the left into the superior hemiazygos or the left superior intercostal vein. They only drain blood from the first two or three bifurcations

of the bronchial tree; more distally the bronchial arterial blood drains into the

radicles of the pulmonary veins.

The bronchial blood flow, together with that in the venae cordis minimae

(Thebesian veins) of the heart, constitutes a physiological shunt whereby venous

blood is mixed with arterial blood in the heart. An increase in bronchial blood

flow may occur during acute pulmonary infections and bronchiectasis and will

inevitably increase the shunt effect. Normally, this shunt of venous blood to the

left side of the heart constitutes less than 1–2% of the cardiac output; this is the

so-called ‘physiological shunt’. In the normal individual, this shunt is increased

by minimal ventilation/perfusion mismatching in the lung and may then total

5% of the cardiac output.

The fine arrangement of the blood vessels within the bronchial wall is of

some practical interest. The arterial plexus derived from the bronchial artery

lies external to the bronchial muscle; vessels pierce the muscle coat to form a

capillary plexus in the submucosa. The venous radicles, in turn, pierce the

muscle layer in order to drain into the venous plexus in the areolar tissue outside

the muscle. Blood must therefore traverse the bronchial muscle both to reach

and to leave the submucous capillary plexus. Oedema of the bronchial wall will

occlude the low-pressure veins before the high-pressure arteries; the resultant

venous obstruction produces further mucosal swelling and thus accentuates the

bronchial obstruction.

describe the anatomy relevant to the performance of a surgical airway or tracheostomy

The anterior relations of the cervical portion of the trachea are naturally of prime importance in performing a tracheostomy

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The trachea lies exactly in the midline in the cervical part of its course. In the neck, it is covered anteriorly by the skin and by the superficial and deep fascia, through which the rings are easily felt. The 2nd to the 4th rings are covered by the isthmus of the thyroid where, along the upper border, branches of the superior thyroid artery join from either side. In the lower part of the neck, the edges of the sternohyoid and sternothyroid muscles overlap the trachea, which is here also covered by the inferior thyroid veins (as they stream downwards to the brachiocephalic veins), by the cross-communication between the anterior jugular veins and, when present, by the thyroidea ima artery, which ascends from the arch of the aorta or from the brachiocephalic artery. It is because of this close relationship with the brachiocephalic artery that erosion of the tracheal wall by a tracheostomy tube may cause sudden profuse haemorrhage. It is less common for the carotid artery to be involved in this way. On either side are the lateral lobes of the thyroid gland, which intervene between the trachea and the carotid sheath and its contents (the common carotid artery, the internal jugular vein and the vagus nerve). Posteriorly, the trachea rests on the oesophagus, with the recurrent laryngeal nerves lying on either side in a groove between the two.

The close relationship of the unsupported posterior tracheal wall and the oesophagus is revealed during oesophagoscopy. When a tracheal tube with an inflated cuff is in the trachea, the anterior wall of the oesophagus is compressed. For this reason, patients with inflated tracheostomy tubes (especially highpressure cuffs) may have difficulty in swallowing. During oesophagoscopy with a rigid oesophagoscope, an over-inflated tracheal tube cuff may be mistaken for an oesophageal obstruction. Because the trachea is a superficial structure in the neck, it is possible to feel the bulge caused by the rapid injection of 5 ml of air into the cuff of an accurately placed tracheal tube. This is detected by placing two fingers over the trachea

above the suprasternal notch.

Describe the medullary and pontine respiratory control centers and explain how the ventilatory pattern is generated and controlled

Inspite of widely differing demands for O2 uptake and CO2 output made by body, the arterial PO2 and PCO2 are normally kept within close limits – because of ‘respiratory control system’

Respiratory control system: 3 elements

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Central controller:

• Impulses for automatic process of breathing originate from brainstem centers

• Cortical centers can override these centers in case of voluntary control. PCO2 can be halved by voluntary hyperventilation, however it may cause carpo-pedal spasms owing to alkalosis. Voluntary hypoventilation is more difficult due to several limiting factors including PO2 and PCO2

• Brain stem centres in medulla and pons

• Other parts of brain: limbic system and hypothalamic can alter pattern of breathing eg emotional states

Brain stem centers:

• Medulla: Medullary respiratory center located beneath floor of 4th ventricle

o Dorsal respiratory group: Associated with inspiration. Spontaneous repetitive burst of AP increasing in crescendo over few seconds – transmitted to inspiratory muscles ( activity becomes stronger in a aramp like pattern( inspiratory action potential cease ( inspiratory muscle tone falls.

o Ventral respiratory group: Associated with expiration. Remains quiescent during normal breathing as expiration is passive. Active during forced expiration eg during exercise

• Pons:

o Apneustic centre in lower pons: (role not clear) – sends excitatory impulses to inspiratory centre ( prolonging the ramp action potential

o Pneumotaxic centre in upper pons: “switches off” inspiration, hence regulate inspiratory volume and rate

describe the chemical control of breathing via central and peripheral chemoreceptors, and indicate how this is altered in abnormal clinical states

Central Chemoreceptors

• Located near the ventral surface of the medulla in the vicinity of the exit of the 9th and 10th nerves.

• Involved in the minute-by-minute control of ventilation

• An increase in H+ conc. in surrounding ECF stimulates ventilation, whereas a decrease inhibits it. ECF composition altered by CSF (most imp), blood flow and local metabolism

• BBB is impermeable to H+ and HCO-3 ions, although molecular CO2 diffuses across into ECF & CSF. When PCO2 ↑, cerebral vasodilatation and more CO2 diffuses into CSF ( ↓PH and ↑ protons ( stimulates ventilation to wash out excess CO2

• The normal pH of the CSF is 7.32, because of lower buffering capacity in lack of proteins. Hence ΔpH in CSF > blood.

• Over a prolonged period, a compensatory change in HCO-3 occurs as a result of transport across the blood-brain barrier bringing CSF pH close to normal inspite of high blood pCO2 levels.

Peripheral receptors

• Peripheral Chemoreceptors

• Lung receptors

o Pulmonary Stretch Receptors

o Irritant Receptors

o J Receptors

o Bronchial C Fibers

• Other receptors

o Nose and Upper Airway Receptors

o Joint and Muscle Receptors

o Gamma System

o Arterial Baroreceptors

o Pain and Temperature

Peripheral Chemoreceptors

• Located in the carotid bodies (most important) at the bifurcation of the common carotid arteries, and in the aortic bodies above and below the aortic arch

• glomus cells:

o ? sites of chemoreception and that modulation of neurotransmitter release from the glomus cells affects the discharge rate of the carotid body afferent fibers

o Two types of glomus cells:

▪ Type I cells- large content of dopamine. close apposition to endings of the afferent carotid sinus nerve

▪ Type II cells with a rich supply of capillaries.

• Respond to

o ↓ PO2 and pH

o ↑ PCO2

• Sensitivity to changes in arterial PO2

o begins around 500 mm Hg

o relatively little response occurs until the arterial PO2 is reduced below 100 mm Hg, but then the rate rapidly increases

o peripheral chemoreceptors are responsible for all the increase of ventilation that occurs in humans in response to arterial hypoxemia. Complete loss of hypoxic ventilatory drive has been shown in patients with bilateral carotid body resection

• Sensitivity to changes in arterial PCO2 & pH

o response is more rapid, and they may be useful in matching ventilation to abrupt changes in PCO2

o carotid but not the aortic bodies respond to a fall in arterial pH

o Increases in chemoreceptor activity in response to decreases in arterial PO2 are potentiated by increases in PCO2 and, in the carotid bodies, by decreases in pH.

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Lung Receptors

1. Pulmonary Stretch Receptors

o Slowly adapting receptors within airway smooth muscle.

o Afferent nerve - vagus nerve.

o Discharge in response to distension of the lung, and their activity is sustained with lung inflation( slowing of respiratory frequency due to an increase in expiratory time. This is known as the Hering-Breuer inflation reflex. The opposite response is also seen; that is, deflation of the lungs tends to initiate inspiratory activity (deflation reflex).

o Reflexes are largely inactive in adult humans unless the tidal volume exceeds 1 liter, as in exercise.

2. Irritant Receptors

o Lie between airway epithelial cells

o Afferent nerve – vagus nerve

o Stimulated by noxious gases, cigarette smoke, inhaled dusts, and cold air ( bronchoconstriction & hypernea

3. J Receptors

o Lie in the alveolar walls, close to the capillaries.

o Afferent nerve – vagus nerve

o Respond very quickly to (i) noxius chemicals injected into the pulmonary circulation, (ii) engorgement of pulmonary capillaries, (iii) increases in the interstitial fluid volume of the alveolar wall ( rapid, shallow breathing. Intense stimulation causes apnea.

4. Bronchial C Fibers

o Lie close to capillaries in bronchial circulation

o Respond quickly to chemicals injected into the bronchial circulation ( rapid shallow breathing, bronchoconstriction, and mucous secretion.

Other Receptors

1. Nose and Upper Airway Receptors: Irritant receptors ( sneezing, coughing, and bronchoconstriction. Laryngeal spasm may occur.

2. Joint and Muscle Receptors: believed to be part of the stimulus to ventilation during exercise, especially in the early stages.

3. Gamma System: intercostal muscles and diaphragm, contain muscle spindles that sense elongation of the muscle ( reflexly control the strength of contraction. involved in the sensation of dyspnea

4. Arterial Baroreceptors: An increase in BP can cause reflex hypoventilation or apnea & vice versa

5. Pain and Temperature: Pain often causes a period of apnea followed by hyperventilation. Heating of the skin may result in hyperventilation.

Describe the reflex control of ventilation

(After outlining the central and peripheral components of respiratory control system, describe the integrated responses below)

Response to Carbon Dioxide

• Most important factor in the control of ventilation under normal conditions is the PCO2 of the arterial blood.

• Highly sensitive (arterial PCO2 is probably held to within 3 mm Hg) and rapid

• Main stimulus to increase ventilation when the arterial PCO2 rises comes from the central chemoreceptors, which respond to the increased H+ concentration of the brain extracellular fluid. An additional stimulus comes from the peripheral chemoreceptors, because of both the rise in arterial PCO2 and the fall in pH.

• Methods to measure ventilator response to CO2:

o Inhalation of CO2 mixtures or rebreathing from a bag so that the inspired PCO2 gradually rises. In one technique, the subject rebreathes from a bag that is prefilled with 7% CO2 and 93% O2.

o Recording the inspiratory pressure during a brief period of airway occlusion. The pressure generated during the first 0.1 second of attempted inspiration (known as P0.1) against closed shutter is taken as a measure of respiratory center output.

• With a normal PO2 the ventilation increases by about 2 to 3 liters/min for each 1 mm Hg rise in PCO2.

• Lowering the PO2 produces two effects: ventilation for a given PCO2 is higher, and the slope of the line becomes steeper.

• A reduction in arterial PCO2 reduces the stimulus to ventilation.

• Causes of reduced ventilator response:

o Sleep

o Increasing age

o Genetic, racial, and personality factors

o Athletes and divers

o Drugs which depress respiratory centre morphine and barbiturates.

o Increased work of breathing

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Response to Oxygen

• hypoxemia reflexly stimulates ventilation by its action on the carotid and aortic body chemoreceptors

• When the alveolar PCO2 is kept at about 36 mm Hg (by altering the inspired mixture), the alveolar PO2 can be reduced to the vicinity of 50 mm Hg before any appreciable increase in ventilation occurs.

• Raising the PCO2 increases the ventilation at any PO2 . The combined effects of both stimuli exceed the sum of each stimulus given separately

• On ascent to high altitude, a large increase in ventilation occurs in response to the hypoxia

• In some patients with severe lung disease (COPD), the hypoxic drive to ventilation becomes very important. If such a patient is given a high O2 mixture to breathe to relieve the hypoxemia, ventilation may become grossly depressed.

• no action on the central chemo-receptors; indeed, in the absence of peripheral chemoreceptors, hypoxemia depresses respiration. However, prolonged hypoxemia can cause mild cerebral acidosis, which, in turn, can stimulate ventilation.

[pic]

Response to pH

↓ PH stimulates ventilation.

Stimulus from pH and PCO2 are independent

Chief site of action of a reduced arterial pH is the peripheral chemoreceptors.

Response to Exercise

On exercise, ventilation increases promptly and during strenuous exertion may reach very high levels.

Fit young people who attain a maximum O2 consumption of 4 liters/min may have a total ventilation of 120 liters/min

It is remarkable that the cause of the increased ventilation on exercise remains largely unknown. The arterial PCO2 does not increase during exercise; indeed, during severe exercise it typically falls slightly. The arterial PO2 usually increases slightly, although it may fall at very high work levels. The arterial pH remains nearly constant for moderate exercise, although during heavy exercise it falls because of the liberation of lactic acid through anaerobic glycolysis. It is clear, therefore, that none of the conventional mechanisms can account for the large increase in ventilation observed during light to moderate exercise.

Other stimuli have been suggested –

• Passive movement of the limbs stimulates ventilation. This is a reflex with receptors presumably located in joints or muscles.

• Oscillations in arterial PO2 and PCO2 may stimulate the peripheral chemoreceptors, even though the mean level remains unaltered.

• Central chemo-receptors increase ventilation to hold the arterial PCO2 constant by some kind of servomechanism

• Ventilation is linked in some way to the additional CO2 load presented to the lungs in the mixed venous blood during exercise. No suitable receptor has been found though.

• Increase in body temperature during exercise, which stimulates ventilation, and impulses from the motor cortex.

Abnormal Patterns of Breathing

• Subjects with severe hypoxemia often exhibit a striking pattern of periodic breathing known as Cheyne-Stokes respiration. This is characterized by periods of apnea of 10 to 20 seconds, separated by approximately equal periods of hyperventilation when the tidal volume gradually waxes and then wanes. This pattern is frequently seen at high altitude, especially at night during sleep. It is also found in some patients with severe heart disease or brain damage.

To describe the inspiratory and expiratory process involving the chest wall, diaphragm, pleura and lung parenchyma

Respiratory muscles:

Inspiratory muscles:

1. Diaphragm:

a. most imp inspiratory muscle supplied by phrenic nerve C3,4,5

b. Contraction causes:

i. Abdominal viscera to be forced downwards and forwards

ii. Chest cavity transverse and vertical diameter increase

iii. Ribs move upward and outward

c. Diaphragmatic excursion is ~1cm during quiet breathing and upto 10 cm in forced inspiration n expiration

d. Diaphragmatic paralysis causes paradoxical movement ( detected on fluoroscopy as in sniff test

2. External intercostals

a. Connect adjascent ribs. Fibres run forward and downward

b. Contraction causes upward and forward movement of ribs( ↑AP & lateral diameter of thorax ( bucket handle movement

c. Supplied by intercostals nerves arising from spinal cord at same level

d. Paralysis – no major impact

3. Accessory muscles of respiration

a. Scalene – elevate 1st 2 ribs

b. Sternomastoids – raise the sternum

c. Minor role by ala nasi

Expiratory muscles:

1. Passive during quiet breathing due to elasticity of lung

2. Most imp mucles of expiration are abdominal mucles – rectus, internal and external oblique and transverse abdominis.

3. Internal intercostals assist active expiration

[pic]

The dotted line in intrapleural pressure is the pressure tracing that would exist when there is no airway resistance. The shaded portion is the pressure created by airway resistance

Define compliance (static, dynamic and specific), its measurement and relate this to the elastic properties of the lung

Compliance – volume change per unit pressure change or slope of PV curve is known as compliance. Normal compliance of lung is ~ 200ml/cmH2O. compliance of chest wall is ~ 200ml/cmH2O. Lung and chest wall compliances are in series so the total compliance of respiratory system would be = 1/200 + 1/200 i.e. 100ml/cmH2O

Compliance = ΔV/ΔP

Static compliance – Volume change per unit pressure change the flow of gas having ceased.

Dynamic compliance – Volume change per unit pressure during normal breathing.

Specific compliance – compliance divided by FRC. Since compliance is dependent on lung size, concept of specific compliance is used to remove confounding factor of size. This allows comparison between different age groups and subjects. Typical value in an adult is 0.05 cmH2O. Specific compliance in neonate = specific compliance in adult

2 major contributors of compliance are – elasticity of lung tissue + surface tension

Measurement of compliance:

Measured as a slope of lung’s PV curve

Obtaining a PV curve:

A co-operative subject inspires and then expires in a series of steps of a given volume measured using a spirometer. At each step the subject holds the given lung volume while keeping glottis open. The intrapleural pressure is measured using oesophageal balloon. The volume is plotted on y axis either as absolute values above RV or as % of VC. The pressure is plotted on X axis as pressure gradient across lung i.e. transpulmonary pressure.

Transpulmonary pressure = alveolar pressure – intrapleural pressure

Since pressure is recorded with glottis open and state of no flow, the alveolar pressure is equal to mouth pressure i.e. atmospheric pressure. The PV curve obtained is as follows:

[pic]

Hysteresis: The PV trace during inspiration is different from that during expiration. This hysteresis Is due to surface tension reducing properties of surfactant. Since curve is not a straight line the compliance is reported by convention eg as the slope of expiratory curve between FRC and 1L above FRC

Typical values of transpulmonary pressures:

At RV:

Volume = RV = 0% of VC = 20% of TLC

Alveolar pressure = 0

Intrapleural pressure = -3 cmH20

Transpulmonary pressure = 0-(-3) = 3 cm H2O

At FRC

Volume = FRC = 45% TLC

Alveolar pressure = 0

Intrapleural pressure = -5 cmH20

Transpulmonary pressure = 0-(-5) = 5 cm H2O

At TLC

Volume = RV = 0% of VC = 20% of TLC

Alveolar pressure = 0

Intrapleural pressure = -30 cmH20

Transpulmonary pressure = 0-(-30) = 30 cm H2O

Explain the concepts of time constants and relate these to "fast" and "slow" alveoli

• Time constant (τ) is used to describe the rate of change of exponential process and is the time at which the process would have been complete had the initial rate of change continued.

• The process is 95% complete after 3 τ , 63% after 2 τ, 37% after 1 τ.

• Flow of air into lung unit is also an exponential process

• For lung unit time constant is given by

o τ = compliance * resistance

• Normal resistance is 2 cmH20/Liter/sec

• Normal compliance is 100 ml/cmH20 or 0.1 Liter/cmH2O

• Therefore τ = 0.2 sec

• Hence for normal lung tissue filling will be 95% complete within 0.6 Sec

• It is obvious from equation that;

o Units with high resistance will have higher time constants and will fill slowly & vice –versa

o Units with low compliance will have shorter time constant and will fill quickly & vice –versa

• Implications:

o The presence of lung units with varying time constants means that there can still be flow of gas within the lung between units at the end of expiration and inspiration and that regional ventilation will depend on frequency of ventilation

o Frequency dependant compliance – presence of lung units with differing time constants means that the measured dynamic compliance will decrease as respiratory rate increases

Describe the elastic properties of the chest wall and to plot pressure and flow-volume relationships of the lung, chest wall and the total respiratory system

Chest wall elasticity / compliance is assessed using pressure volume curve

Pressure volume curve for chest volume requires measurement of recoil pressure

Recoil pressure = intrapleural pressure – atmospheric pressure

Hence, Recoil pressure = intrapleural pressure

Measurment of recoil pressures requires:

• Chest muscles be fully relaxed i.e. glottis is fully closed

• Lung volume held constant

Intrapleural pressure is measured using esophageal balloon.

Typically recoil pressure is negative at all values upto lung volume of 75% of TLC. This suggests chest wall tends to spring outwards to reach its resting state which is near 75% of TLC. At FRC the outward recoil pressure of chest and inward recoil pressure of lung are equal and cancel each other.

[pic]

To describe the properties, production and regulation of surfactant and relate these to its role in influencing respiratory mechanics

Surfactant is a surface active agent produced by alveolar type II cells which serves the purpose of reducing surface tension of alveolar lining fluid

Properties:

• 80% of surfactant is phospholipid, 8% neutal lipids like cholesterol and 12 % protien

• Main lipid content is dipalmitoyl phosphatidylcholine (DPPC) with significant amounts of phosphatidyl glycerol

• Surfactant molecules align at the surface of alveolar lining fluid. They are amphipathic. They have a hydrophilic head (choline) which dips into the alveolar lining fluid and hydrophobic fatty acid tail (palmitoyl) which is oriented in the alveolar gas. Intermolecular repulsive forces between the hydrophobic ends of surfactant molecules account for surface tension reducing effect of surfactant

• 4 surfactant proteins (SPs): SPA, SP-B, SP-C and SP-D. Out of these, SP-A and SP-D have a role in the host defence of the lung. , While, SP-B and SP-C confer surface tension-lowering properties and are important for the adsorption and spreading of the surfactant

Production and regulation

• Produced in type II alveolar cells (10% of alveolar surface area)

• Stored in cytoplasmic lamellar bodies

[pic]

• Regulation: Surfactant secretion is regulated locally in the lung by changes in ventilation rate, possibly mediated by distension and altered intracellular pH. Secretion is also stimulated by various agents, including agonists for beta-adrenergic, purinoceptors, and vasopressin receptors and is associated with increased cytosolic Ca2+, cellular adenosine 3',5'-cyclic monophosphate, and activation of protein kinases.

Influence on respiratory mechanics

Surface tension and effect on alveoli:

Surface tension develops at the air water interface due to intermolecular attractive forces between water molecules > water gas molecules. Because of surface tension surface area tends to contract as much as possible. Inside a bubble surface tension leads to generation of pressure given by ‘laplace law’

P=2 surface tension/radius

Hence smaller bubbles will have more pressure within them as compared to larger bubbles. Alveoli are like bubbles as well and are governed by the same laws. The smaller alveoli would have larger pressure and would tend to empty into larger alveoli progressively and hence make the the system unstable. However this does not happen because of surface tension reducing action of surfactant. As shown in the experiment in the figure, with surfactant the surface tension gets paradoxically lowered as the surface area reduces – this is because of crowding of surfactant molecules and progressively large repulsive forces between the hydrophobic ends of surfactant molecules.

[pic]

Physiological advantages of surfactant:

• Low surface tension in the alveoli increases the compliance of the lung and reduces the work of expanding it with each breath.

• Stability of the alveoli is promoted. The 500 million alveoli appear to be inherently unstable because areas of atelectasis (collapse) often form in the presence of disease. This is explained above using laplace law on bubbles. However, Figure shows that when lung washings are present, a small surface area is associated with a small surface tension. Thus, the tendency for small alveoli to empty into large alveoli is apparently reduced.

• Keep the alveoli dry. Just as the surface tension forces tend to collapse alveoli, they also tend to suck fluid into the alveolar spaces from the capillaries. In effect, the surface tension of the curved alveolar surface reduces the hydrostatic pressure in the tissue outside the capillaries. By reducing these surface forces, surfactant prevents the transudation of fluid.

Explain the significance of the vertical gradient of pleural pressure and the effect of positioning

As compared to the basal alveoli the apical alveoli are :

Larger at end expiration

Lower ventilation

Loer perfusion

Higher VQ ratio (3.3 vs 0.63)

Higher PO2 (132 mmHg vs 89 mmHg)

Lower PCO2 (28mmHg vs 42 mmHg)

Higher respiratory exchange ratio at the apex (2 vs 0.67)

Causes of increased perfusion at the bases: hydroststaic pressure of the blood. The difference in hydrostatic pressure between top and bottom is 30mmHg

Causes of difference in ventilation:

1. Intrapleural pressure – The weight of lung causes the intrapleural pressure at the base beight less –ve (~2.5) as compared to the apex (~10). Intrapleural pressure is –ve because of outward pull on parietal pleura due to chest wall and inward pull on the visceral pleura due to lung elasticity

2. gradient of alveolar size: Apical alveoli are more distended because more negative intra pleural pressure

3. ventilation gradient: the basal alveoli are smaller in size and hence operate on lower part of PV, are more compliant and hence ventilated better. The apical alveoli being more larger operate on higher part of the PV curve are less compliant and hence ventilated lesser. There is reversal of this phenomenon at low lung volumes as shown in figure

[pic][pic]

At low volumes, intra-pleural pressures are less negative because the lung is not so well expanded and the elastic recoil forces are smaller. However, the differences between apex and base are still present because of the weight of the lung. So the intra-pleural pressure at the base can now actually exceed airway (atmospheric) pressure. Under these conditions, the lung at the base is not being expanded but compressed, and ventilation is impossible until the local intra-pleural pressure falls below atmospheric pressure. By contrast, the apex of the lung is on a favourable part of the pressure-volume curve and ventilates well. Thus, the normal distribution of ventilation is inverted, the upper regions ventilating better than the lower zones.

Explain the physics of gas flow and the significance of the relationship between resistance and flow in the respiratory tract

If air flows through a tube (Figure 7-12), a difference of pressure exists between the ends. The pressure difference depends on the rate and pattern of flow. At low flow rates, the stream lines are parallel to the sides of the tube (A). This is known as laminar flow. As the flow rate is increased, unsteadiness develops, especially at branches. Here, separation of the stream lines from the wall may occur, with the formation of local eddies (B). At still higher flow rates, complete disorganization of the stream lines is seen; this is turbulence

[pic]

The pressure-flow characteristics for laminar flow were first described by the French physician Poiseuille. In straight circular tubes, the volume flow rate is given by

[pic]

P = pressure

R = radius

n = viscosity

l = length

Because flow resistance R is driving pressure divided by flow

[pic]

Critical importance of tube radius

Turbulent flow has different properties.

• P = K[flow]2 rather than flow alone

• Viscosity of the gas becomes relatively unimportant, but an increase in gas density increases the pressure drop for a given flow.

• Turbulent flow does not have the high axial flow velocity that is characteristic of laminar flow

Reynolds number gives ratio of inertial to viscous forces

[pic]

d - density

v - average velocity

r – radius

n – viscosity

Turbulence is probable when the Reynolds number exceeds 2000.

Hence turbulence is most likely to occur when:

• High velocity

• Large diameter tube

• Higher density gas

In practice, for laminar flow to occur, the entrance conditions of the tube are critical. If eddy formation occurs upstream at a branch point, this disturbance is carried downstream some distance before it disappears. Thus, in a rapidly branching system such as the lung, fully developed laminar flow probably only occurs in the very small airways where the Reynolds numbers are very low (approximately 1 in terminal bronchioles). In most of the bronchial tree, flow is transitional (B), whereas true turbulence may occur in the trachea, especially on exercise when flow velocities are high. In general, driving pressure is determined by both the flow rate and its square: P = K1[flow] + K2[flow]2.

To describe the factors affecting airway resistance, and how airway resistance may be measured

Pulmonary resistance = airway resistance + tissue resistance

Tissue resistance is due to viscous forces and account for ~20% in young healthy adult

Resistance = pressure (cmH20)/ Flow (L per Sec)

Driving pressure is the pressure difference between the mouth (Pmouth) and the alveoli (PA)

[pic]

Both turbulent and laminar flow cause resistance to air moving in the airways.

The major site of airway resistance is the medium bronchi (lobar and segmental) and bronchi down to about the seventh generation

[pic]

Inspite of smaller diameter ( Pulmonary arterial pressure (Pa) > Pulmonary venous pressure (Pv). Occurs in appical part of lung. Hence there is no blood flow. Zone 1 is usually small or nonexistent in healthy people because the pulsatile pulmonary arterial pressure is sufficient to keep the capillaries partially open at the apex. However, when zone 1 does occur, alveolar dead space is increased in the lungs. Zone 1 may be created by conditions that elevate alveolar pressure or decrease pulmonary arterial pressure. For example, on positive pressures ventilation, Hemorrhage or low blood pressure etc.

o Zone 2: Pa > PA > Pv. In normal upright lung, this zone extends from apex down to 10cm above level of heart. Hence blood flow is determined not by the arterial-venous pressure difference, but by the difference between arterial pressure and alveolar pressure.

o Zone 3: Pa > Pv > PA. In normal upright lung this zone extends from 10 cm above the level of heart to the bases. Blood flow is affected only by arterio – venous gradient. The increase in blood flow down this region is primarily a result of capillary distention.

Explain the shunt equation and the alveolar gas equation

Shunt Equation:

[pic]

Where:

Qs is shunt blood flow

Qt is cardiac output

QS/Qt is the 'shunt fraction'

Cc'O2 is oxygen content of end pulmonary capillary blood

CaO2 is oxygen content of arterial blood

CvO2 is oxygen content of mixed venous blood

• Gives a measure of the amount of mixed venous blood that if added to end-capillary blood would produce the observed depression in arterial pO2

• This is a 'virtual' or 'as if' shunt. True shunt cannot be measured by this equation.

• The shunt equation is based on the assumption that the shunted blood has the same composition as mixed venous blood.

• The actual blood shunted may have a composition different from that of mixed venous blood so the value obtained by the use of this equation will not be accurate in these situations. In the normal situation, the shunts present are the bronchial circulation and the thebesian venous blood draining into the left ventricle and both these have a composition different from mixed venous blood.

Derivation of shunt equation:

[pic]

Alveolar gas equation:

Alveolar PO2= PIO2 – CO2/R + F

PIO2 = partial pressure of inspired oxygen = FIO2 (barometric pressure – water vapor pressure)

R = respiratory quotient = 0.8

F = correction factor = PACO2 * FIO2 [(1-R)/R], value is very small and hence ignored. Significant when breathing 100% O2

Explain normal ventilation-perfusion matching, including the mechanisms for these as well as the normal values

• Apex:

o Due to vertical gradient of intrapleural pressure - Alveoli at the apex are more distended owing to lower intrapleural pressure – therefore operate higher in PV curve, hence lower compliance and lower ventilation (

Ventilation (V) ~ 0.24 L/min

o Due to vertical hydrostatic pressure of blood column – Perfusion is lower ( Perfusion (Q)~ 0.07 L/min

o Hence V/Q at apex = 3.3

• Base:

o Due to vertical gradient of intrapleural pressure - Alveoli at the base are less distended owing to higher intrapleural pressure – therefore operate lower in PV curve, hence higher compliance and higher ventilation (

Ventilation (V) ~ 0.82 L/min

o Due to vertical hydrostatic pressure of blood column – Perfusion is greater ( Perfusion (Q)~ 1.29 L/min

o Hence V/Q at base = 0.63

• Therefore though both ventilation and perfusion increase from top to bottom but since change in perfusion is far greater than change in ventilation, the V/Q ratio decrease from top to bottom

Describe and explain regional ventilation-perfusion inequalities, their clinical importance, and changes with posture

OR

Explain the effect of ventilation-perfusion inequality on oxygen transfer and carbon dioxide elimination

As discussed above the V/Q ratio decreases from top to bottom, 3.3 ( 0.63, with ideal VQ ratio of 1 occurring in the middle zone some where at the level of 3-4th rib.

Normal Alveolar PO2 ~ 100mmHg, and mixed venous PO2 ~ 40mmHg, whereas normal alveolar PCO2 is ~ 40mmHg, and mixed venous PCO2 ~ 45mmHg. Since the gradient of PO2 is more than CO2 , alveolar PO2 is more sensitive to changes in VQ ratio than alveolar PCO2

The changes in alveolar gas composition with change in V/Q ratio can be explained by the V/Q ratio equation:

[pic]

Hence, Increasing V/Q ratio as would occur by decreasing perfusion increases PO2 and decreases PCO2 in the alveoli and vice versa

[pic]

In a normal lung the VQ ratio decreases from top to bottom, hence:

• Alveolar PO2 at the apex ~ 132 and at base ~ 89

• Alveolar PCO2 at the apex~ 28 and at base ~ 42

Effect of mismatch of V/Q ratio over the upright lung on gas exchange:

• Effect on arterial PO2:

o ↓ arterial PO2 below that of mixed alveolar PO2

o For oxygen transfer, the effect of high V/Q ratio area at the apex cannot compensate for the low PO2 alveoli at the lung bases. This is because most of the pulmonary blood flow passes through the bases at the lower alveolar PO2 and the apical alveoli with high VQ ratio cannot add significantly more oxygen to the hemoglobin of blood perfusing them as the oxygen-hemoglobin dissociation curve is flat at the upper end

• Effect on arterial PCO2

o Less affected

o Because areas of high ventilation perfusion ratio can compensate more effectively, because the CO2 blood dissociation curve is linear in the physiological range. In addition any rise in the PCO2 of arterial blood reflexly stimulate ventilation. Hence the arterial PCO2 is normally not increased by VQ mismatch. If the VQ mismatch increases the pco2 may decrease rather because of hypoxia driven increased ventilation.

Outline the methods used to measure ventilation-perfusion inequalities

Explain venous admixture and its relationship to shunt and ventilation-perfusion (V/Q) mismatch

• Definition of Shunt: refers to blood which enters the arterial system without passing through ventilated areas of the lung. Also called 'true' shunt.

o Normally, true shunt = Bronchial venous blood (from the bronchial circulation) ( ................
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