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Dr.Tipu SultanDr.Tipu Sultan

Dr.Shivali Pandey (M.D.)

Dr.Shivali Pandey (M.D.)

Respiratory function and importance to anesthesia

CELLULAR RESPIRATION

The principal function of the lungs is to allow gas exchange between blood and inspired air.

Types :

Aerobic Respiration

Anaerobic respiration

1) Aerobic respiration

Nearly all human cells derive energy aerobically (i.e. by using

O2).

Carbohydrates, fats and proteins are metabolized to two carbon

fragments (acetyl-CoA) that enter the citric acid cycle within

mitrochondria.

Acetycl-CoA is metabolized to CO2 energy is derived and stored

in nicotinamide adenine dinucleotide (NDA), flavin adenine

dinucleotide (FAD), and guanosine triphosphate (GTP).

Energy is subsequently transferred to adenosine triphosphate

(ATP) through a process called oxidative phosphorylation.

2) Anaerobic respiration

In the absence of O 2, ATP can be produced only from the

conversion of glucose to pyruvate to lactic acid.

When O2 tension is restored to normal, lactate is reconverted to

pyruvate and aerobic metabolism is resumed.

Effects of anesthesia on Cell metabolism

General anesthesia typically reduces both oxygen consumption

and CO2 production by about 15%.

The greater reductions are in cerebral and cardiac O2

consumption.

MUSCLES OF RESPIRATION

I) Inspiratory muscles

A) During normal breathing

1) Diaphragm

Contraction of diaphragm cause base of thoracic cavity to

descent 1.5 to 7 cm in deep inspiration.

Responsible for 75% of the change in intrathoracic volume

during quiet inspiration.

2) External intercostals muscles

B) During forced inspiration

Also other accessory muscles like sternocleidomastoid, scalene and

pectoralis major muscle play role.

II) Expiratory muscles

A) During normal breathing – Expiration is passive process occur

due to elastic recoil of lung.

B) During forced expiration - abdominal muscles and internal

intercostals muscle play role.

Mechanism of ventilation

The movement of lungs are determined by impedance of the respiratory system which can be divided into the –

1) Elastic resistance of tissue and gas liquid interface

It governs lung volume and the associated pressure under static condition.

2) Non elastic resistance to gas flow

It relates to frictional resistance to airflow and tissue deformation.

1) Elastic resistance

The lung and the chest wall are elastic structure. In between lung and chest wall, a thin layer of fluid is present by which lung slide easily on the chest wall but resist being pulled away from it.

Due to elastic recoil of the chest wall, chest wall has a tendency to expand outward and lungs has tendency to collapse due to elastic recoil of lung.

At the end of quiet expiration, the elastic recoil of the chest wall is just balanced by the elastic recoil of lung.

If the chest wall is opened, the lung collapse and if the lung lose their elasticity, the chest wall expands and become borrow shaped. The recoil property of chest wall due to structure component that resist deformation and probably include chest wall muscle tone. The elastic recoil of the lung is due to their high content of elastin fibre and the surface tension forces acting at the airfluid interface in alveoli.

Surface tension forces

Surface tension forces tend to reduce the area of interface and

favour alveolar collapse.

According to Laplace law

Pressure =2T

=2×surface tension

R Radius

So alveolar collapse is directly proportional to surface tension but

inversely proportional to alveolar size. Collapse is more likely

when surface tension increases or alveolar size decrease.

The surface tension of the alveoli is reduced by the surfactant which is secreted by type II pneumocyte .

Ability of surfactant to lower surface tension is directly proportional to its concentration with in alveolus.

In smaller alveoli Surfactant are more concentrate surface tension Prevent collapse

In larger alveoli Surfactant are less concentrated

Relative in surface tension

Prevent over-distens of alveoli

Compliance of respiratory system

Elastic recoil is usually measured in terms of compliance which is defined as the change in volume divided by change in transpulmonary pressure.

Compliance of lung =Change in lung volume

Change in transpulmonary pressure

Transpulmonary pressure – The pressure needed to keep the lung inflated at a certain volume, i.e pleural minus alveolar pressure ,is known as transpulmonary pressure.

Normal lung compliance is 0.2-0.3L/cm of H2O (2-3 L/k Pa)

Pressure volume relationships of lung It is typical of an elastic structure.

pleural pressure is lower in upper regions.

Regional transpulmonary pressure is thus higher for apical lung units than for basal ones in an upright subject.

The consequences will be that lower lung regions expand more for a given increase in transpulmonary pressure than the upper units do.

Thus ventilation goes preferably to the lower lung regions.

Compliance is critically dependent on the lung volume at which it is measured.

Change in pressure volume curve in different disease

Right shift

Fibrotic lung disease

Idiopathic fibrosis

Alveolar proteinosis

Granulomatous diseases like sarcoidosis

Interstitial and alveolar edema

Left shift

Emphysema (loss of elastic tissue)

Chronic bronchitis

Asthma

Examples of pressure volume curves of the lung in health and lung disease. The much flatter slope of the curve in fibrotic lung disease which reflects a considerable increase in pressure variation and respiratory work. Parallel shift in the pressure volume curve of an asthmatic and bronchitic patient, which shows that compliance need not change in these diseases, although lung volume may have increased. Finally note the sleep slope of the curve of an emphysematous patient. This indicates loss of elastic tissue and might even suggest reduced respiratory work.

Compliance of chest wall

Compliance of chest wall =Change in chest volume

Change in transthoracic pressure

* Transthoracic pressure equals atmospheric pressure minus intrapleural pressure.

Normal value 0.2 L/cm H2O

Compliance of chest wall reduce :-

Obesity

Condition causing generalized edema

Joint disorder like amkylosing spondylitis.

Lung volumes

These are important parameter in respiratory physiology and clinical practice. Lung capacities are clinically useful measurement that represent a combination of two or more volumes.

Measurement Definition Average adult value

Male Female

Tidal volume (V T) Volume of air that is expired and inspired during normal breath

500 ml 500ml

Inspiratory reserve volume (IRV) Maximum additional volume that can be inspired above tidal volume

3300ml 1900ml

Expiratory reserve volume (ERV) Maximum volume that can be expired below tidal volume

1000ml 700ml

Residual volume (RV) Volume remaining after maximal exhalation

1200ml 1100ml

Total lung capacity (TLC) RV+ERV+VT + IRV 6000ml 4200ml

Functional residual capacity (FRC)

RV+ERV 2200ml 1800ml

Diagram showing respiratory excursions during normal breathing and during maximal inspiration and maximal expiration

Functional residual capacity (ERV+RV)

FRC determined by the balance between the inward elastic recoil of the lungs, and the outward recoil of the thoracic cage.

FRC decreases with paralysis and anaesthesia.

Other factor effect the FRC:

o Body size (increases of about 32-51 ml/cm of height)

o Gender (10% less in women of same height)

o Posture (supine posture decreases FRC by 0.5-1.0 litre in an adult)

o Lung pathology.

Measuring FRC – 3 main approaches

1) Nitrogen washout

2) Helium wash-in

3) Body plethysmography

Closing volume (CV)

Small airway lacking cartilaginous support depend on radial

traction caused by the elastic recoil of surrounding tissue to

keep them open.

The volume above RV at which airways begin to close

during expiration is called closing volume.

Closing capacity (CC)

Sum of RV and closing volume is called closing capacity.

Airway closure is normal physiological phenomenon and is the

effect of increasing pleural pressure during expiration.

When pleural pressure became “positive”, it will exceed the

pressure inside the airway which is just or nearly atmospheric

at a low flow rate.

Higher pressure outside than inside will comprises the airway

and may close it.

There is a vertical pleural pressure gradient with a difference of approximately 7.5cm H 2O between the upper most and lowermost regions, Causes a transpulmonary pressure gradient with higher pressure inside the airway and alveolus in the upper part and higher pressure outside the alveolus and airway in the lower part, This results in closure of the airways in lower part.

In young subjects airway closure may not occurs until they have expired to RV.

With increasing age of 65 to 70 years, airway closure may occurs above FRC.

This means that in elderly subjects, dependent regions are intermittently closed during the breath, it is the major explanation of why arterial oxygenation decreases with age.

In supine position FRC is reduced where as CC is not affected by body position, so closure of airways may occur above FRC even in young subjects.

In 70 years old subjects, in supine position, the airways may be continuously closed if CC exceeds FRC plus VT.

Airway closure occurs at higher lung volumes in patients with –

i. Obstructive lung disease

ii. Secretions, edema of the airway wall

iii. Increase bronchial muscle tone.

Vital capacity (VC)

It is the maximal volume of air which can be expelled from lungs by forcefull effort following a maximal inspiration in addition to body habits.

VC is also dependent on respiratory muscle strength, and chest lung compliance.

Normal VC is ~60-70ml/kg.

II) Non elastic resistance

Normal total airway resistance is about 0.5-2cm H2O

Resistance is mainly contributed by medium sized bronchi.

Resistance in larger airway is low because of their larger diameter, whereas resistance is smaller airway is also low because of their large total cross sectional area.

The most important cause of increased airway resistance include bronchospasm, secretions and mucosal oedema as well as volume related and flow related airway collapse.

A) Volume related airway collapse

At low volume airway resistance become inversely proportional to lung volume.

Increasing lung volume upto normal with positive end expiratory pressure (PEEP) can reduce airway resistance.

B) Flow related airway collapse

During forced exhalation, reversal of normal transmural airway pressure can cause collapse of these airway (dynamic airway compression).

This is because of if generation of a positive pleual pressure and if large pressure drop across intrathoracic airway.

The point along the airway where dynamic compression occurs is called the equal pressure point. This equal pressure point move towards smaller airway as lung volume decreases. Emphysema and asthma predisposes patient to dynamic airway compression. Emphsema destroys the elastic tissues that normally support smller airway.

Forced vital capacity

Measuring vital capacity as an exhalation that is as hard and as rapid as possible provides important information about airway resistance.

The ratio of the forced expiratory volume is 1s (FEV1) to the

total forced vital capacity (FVC) is proportionate to the degree of airway obstruction.

Normally, FEV1/FVC >80%

Forced mid expiratory flow (FEV25-75%) is effort independent

and a more reliable measurement of obstruction.

Work of breathing

Component that make up the work of breathing during quiet

inspiration are :-

I) Non elastic work

a. Viscous resistance (7%)

b. Airway resistance (28%)

II) Elastic work (65%)

VENTILATION PERFUSION RELATIONSHIP

Ventilation

Ventilation is usually measured as the sum of all exhaled gas volumes in 1 min (minute ventilation, or V). if VT is constant.

Minute ventilation = respiratory rate × tidal volume

For the average adult at rest, minute ventilation is about 5L/min.

Some of the inspiratory gas remain in the airway and not take part in alveolar gas exchange,is known as Dead space,

Dead space may be –

Apparatus dead space

Anatomical dead space

Alveolar dead space

Anatomical dead space – related to the volume of conducing passage.

Alveolar dead space – related to alveoli that are well ventilated but poorly perfused.

Physiological dead space – sum of anatomical dead space and alveolar dead space

In upright position – dead space is normally about 150ml for most adult (~2ml/kg)

Dead space is approximately 30% of VT.

VD=

PACO2- PECO2= 0.3

VT PACO2

PACO2= alveolar CO2 tension.

PECO2= mixed expired CO2 tension.

Factors effecting dead space

Distribution of ventilation

Alveolar ventilation is unevently distributed in the lungs.

Right lung receives more ventilation than the left one (53% versus 47%), and lower (dependent) areas of both lungs tend to be better ventilated than do not the upper areas because of a gravitationally induced gradient in intrapleural pressure.

Pleural pressure increase by 0.3cmH2O/cm vertical distance.

Because of a higher transpulmonary pressure, alveoli in upper lung areas are near maximally inflated and relatively noncompliant, and they undergo little expansion during inspiration.

In contrast, the smaller alveoli in dependent areas have a lower transpulmonary pressure, are more compliant, and undergo greater expansion during inspiration.

Pulmonary perfusion

Approximately 5L/min of blood flowing through the lungs, only about 70-100mL at any one time is within the pulmonary capillaries undergoing gas exchange.

Small increases in pulmonary blood volume normally occur during cardiac systole and with each normal (spontaneous) inspiration.

A shift in posture from supine to erect decreases pulmonary blood volume (upto 27%).

Changes in systemic capacitance also influence pulmonary blood volume: systemic venoconstriction shift blood from the systemic to the pulmonary circulation, whereas vasodilation causes a pulmonary to systemic redistribution.

Hypoxia is a powerful stimulus for pulmonary vasoconstriction.

Distribution of pulmonary perfusion

Pulmonary pressure increases down the lung by 1cm H2O/cm

distance.

This cause pressure difference between apex to base of 11 to 15mmHg.

Vertical distribution of blood flow in the lungZone I :Alveolar pressur > vascular pressure No perfusionZone II :Pulmonary arterial pressure >alveolar pressure whcih in trun exceeds venous pressure.Increase blood flowZone III:Both arterial and venous pressure exceed alveolar pressure, so perfusion pressure is arterial minus venous pressure.Zone IV: In the bottom of lung decrease in blood flow because of increase in interstitial pressure comprising extraalveolar vessels..

Blood flow

Distance

Causes of Hypoxemia and Hypercapnia

Hypoventilation

Shunting of deoxygenated blood past the lung

Ventilation/perfusion mismatched.

Diffusion impairment (grossly abnormal lungs)

Hypoventilation

Defined as ventilation that results in a PaCO2 above 45mmHg.

Present when minute ventilation is high if the metabolic demand or dead space increases.

Ventilation/perfusion mismatched

At rest, both ventilation and perfusion increase down the lung.

Perfusion increases more than ventilation.

The difference between upper most and lowermost 5cm segment being 3 times for ventilation and 10 times for perfusion.

V/Q ratio :

At apex = 5.0

At middle = 1.0

At bottom = 0.5

Shunts

Shunting denotes the process whereby desaturated, mixed venous

blood from the right heart returns to the left heart without being

resaturated with O2 in the lungs.

The overall effect of shunting decrease (dilute) arterial O2

content ; this type of shunt is referred to as right to left.

Intrapumonary shunts are often classified as absolute or relative.

Absolute shunt refers to anatomic shunts and lung units where

V/Q is zero. A relative shunt is an area of the lung with a low but

finite V/Q ratio.

In normal person, the amount of shunt is 2-3% (due to venous blood flow from bronchi entering the pulmonary vein, as well as coronary venous blood entering the left ventricle via thebesian vein).

Pathological shunt –

o Obstructive lung disease

o Vascular disorders

o Atelectasis

o Consodilation

TRANSPORT OF GASES

I)Oxygen transport

Most oxygen is carried in the blood as oxyhemoglobins.

Hb carrying about 1.39ml of O2 per gram of Hb.

The normal adult hemoglobin –oxygen dissociation curve

Right shift

Increase CO2 concentriction

Increase temperature

Increase 2-3 DPG (diphosphoglycerate) concentration

Increase pH (acidosis)

Decrease PO2

Anaemia

Left shift

Fetal blood

Decrease pH (alkalosis)

Decrease temperature

Decrease 2-3 DPG

II) CO2 Transport

This is carried in three forms :-

Dissolved

As bicarbonate

As carbamino compounds, especially carbamino haemoglobin

Respiratory function during anaesthesia

Lung volume and respiratory mechanics during anesthesia

Lung volume

FRC is reduced by 0.8 to 1.01 by changing body position from upright to supine, and there is another 0.4-0.5L decrease when anesthesia has been induced.

End expiratory lung volume is thus reduced from approximately 3.5 to 2L, the latter being close or equal to RV.

Anesthesia per se causes a fall in FRC despite maintenance of spontaneous breathing.

Compliance and resistance of the respiratory system

Resistance of the total respiratory system and the lungs during anesthesia increase during both spontaneous breathing and mechanical ventilation.

Atelectasis and airway closure during anesthesia

Atelectasis

Atelectasis appears in approximately 90% of all patients, who are anesthetized. It is seen during spontaneous breathing and after muscle paralysis and whether intravenous or inhaled anesthetics are used.

15-20% of the lung is regularly collapsed at the base of the lung during uneventful anesthesia.

After thoracic surgery and cardiopulmonary bypass, more than 50% of the lung can be collapsed even several hours after surgery.

The amount of atelectasis decreases toward the apex, which is mostly spared.

There is a weak correlation between the size of the atelectasis and body weight or body mass index (BMI).

Obese patients showing larger atelectasis areas than lean ones do.

The atelectasis is independent of age, with children and young people showing as much atelectasis as elderly patients.

Patients with COPD showed less or even no atelectasis during the 45 minutes of anesthesia.

The mechanism that prevents the lung from collapse is not clear but may be airway closure occurring before alveolar collapse takes place, or it may be an altered balance between the chest wall and the lung that counters a decrease in lung dimensions.

Cranial shift of the diaphragm and a decrease in transverse diameter of the thorax contribute to lowered functional residual capacity (FRC) during anesthesia.

Decreased ventilated volume (atelectasis and airway closure) is a possible cause of reduced lung compliance.

Decreased airway dimensions by the lowered FRC should contribute to increased airway resistance (Raw).

Prevention of atelectasis during anesthesia

Several interventions can help prevent atelectasis or even reopen collapsed tissue.

The application of 10cm H2O PEEP has been tested in several

studies and will consistently reopen collapsed lung tissue.

The persistence of shunt may be explained by a redistribution of blood flow toward more dependent parts of the lungs when intrathoracic pressure is increased by PEEP.

Under such circumstances, any persisting aatelectasis in the bottom of the lung receives a larger share of the pulmonary blood flow than without PEEP.

Increased intrathoracic pressure will impede venous return and decrease cardiac output. This results in a lower venous oxygen tension for a given oxygen uptake and reduces arterial oxygen tension.

Second the lung recollapses rapidly after discontinuation of PEEP. Within 1 minute after cessation of PEEP the collapse is as large as it was before the application of PEEP.

Maintenance of muscle tone

Use of an anesthetic that allows maintenance of respiratory muscle tone will prevent atelectasis from forming.

Ketamine does not impair muscle tone and does not cause collapse.

Another technique used in an attempt to restore respiratory muscle tone in pacing of the diaphragm by applying phrenic nerve stimulation, which did reduce the atelectatic area.

Recruitment maneuvers

The use of sigh maneuver or a double VT has been advocated to

reopen any collapsed lung tissue.

For complete reopening of all collapsed lung tissue,an inflation pressure of 40cm H2o is required.such a large inflation corresponds to a maximum spontaneous inspiration, called VC maneuver

Minimizing gas resorption

Ventilation of the lungs with pure oxygen after a VC maneuver that had reopened previously collapsed lung tissue resulted in rapid reappearance of the atelectasis.

If one the other hand, 40% O2 in nitrogen is used for ventilation

of the lungs, atelectasis reappears slowly and 40 minutes after the VC maneuver only 20% of the initial atelectasis had reappeared.

Breathing of 100% O2 just for a few minutes before and during

commencement of anesthesia, increases the safety margin in the event of difficult intubation of the airway with prolonged apnea. However there turned out to be a price for it.

Breathing of 100% O2 just for a few minutes before

and during commencement of anesthesia, increases the safety margin in the event of difficult intubation of the airway with prolonged apnea.

Avoidance of the preoxygenation procedure (ventilation with 30% O2) eliminated atelectasis formation during induction and

subsequent anesthesia.

Preoxygenation can also be provided without producing atelectasis if undertaken with continuously increased airway pressure, as with continuous positive airway pressure (CPAP).

Postanesthetic oxygenation (100% O2) 10 minutes before

termination of anesthesia together with a VC maneuver at the end of anesthesia.

This is most likely the effect of first reopening collapsed tissue and then under the influence of 100% O2 derecruiting previously

opened lung tissue.

A VC maneuver followed a lower O2 concentration, 40% kept the

lung open after recruitment until the end of anesthesia.

Airway Closure

Intermittent closure of airways can be expected to reduce the ventilation of dependent lung regions.

Such lung regions may then become “low VA/Q” units if

perfusion is maintained or not reduced to the same extent as ventilation.

Because anesthesia causes a reduction in FRC of 0.4-0.5L, it may be anticipated that airway closure will become more prominent in an anesthetized subjects.

A simple three compartment lung model can be constructed to explain the impaired oxygenation during anesthesia.

Three compartment model of the lung in an anesthetized subject.Upper part of the lung, the alveoli and airways are open (Zone A).

Middle and lower parts of the lung, the airways are intermittently closed and impede ventilation (Zone B).

The bottom of lung, the alveoli have collapsed (atelectasis, Zone C).

Distribution of ventilation and blood flow during anesthesia

Distribution of ventilation

Ventilation was shown to be distributed mainly to the upper lung regions, and there was a successive decrease down the lower half of the lung.

PEEP increases dependent lung ventilation in anesthetized subjects in the lateral position.

More even distribution between the upper and lower lung regions have also been made in supine anesthetized humans after previous inflation if the lungs, similar to PEEP.

Thus, restrotation of overall FRC toward or beyond the awake level returns gas distribution toward the awake pattern.

Distribution of lung blood flow

PEEP causes a redistribution of blood flow toward dependent lung regions.

Forcing blood volume downward to the dorsal side of the lungs may increase fractional blood flow an atelectatic region.

Ventilation perfusion matching during anesthesia

Dead space, shunt, and ventilation perfusion relationships

Both CO2 elimination and oxygenation of blood are impaired in

patients during anesthesia.

The impended CO2 elimination can be attributed to increased

dead space ventilation.

Anatomic dead space is unchanged, indicating that the “alveolar” dead space must have increased during anesthesia.

The impaired CO2 elimination is most easily corrected by

increasing the ventilation.

The impairment is arterial oxygenation during anesthesia is generally considered to be more severe at higher ages, obesity worsens the oxygenation of blood and smokers show more impairment in gas exchange than nonsmokers do.

Effects of anesthetics on respiratory drive

Spontaneous ventilation is frequently reduced during anesthesia. Thus inhaled anesthetics, as well as barbiturates for intravenous use, reduce sensitivity to CO2.

Anesthesia also reduces the response to hypoxia. Attenuation of the hypoxic response may be attributed to an effect on the carotid body chemoreceptors.

Factors that influence respiratory function during anesthesia

Spontaneous breathing

During spontaneous breathing, the lower, dependent portion of the diaphragm moved the most, whereas with muscle paralysis, the upper, nondependent part showed the largest displacement.

Increased oxygen fraction

When FIO2 was increased to 0.5 an increase in shunt of 3% to

4% was noticed.

Thus a certain dependence on FIO2 appears to exist, explained

by attenuation of the HPV response with increasing FIO2 or

further development of atelectasis and shunt in lung units with low VA/Q ratios.

Body position

Because FRC is dramatically reduced by the combined effect of the supine position and anesthesia, it might be advantageous to choose a more upright position in an anesthetized subject to preserve FRC.

Age

Arterial oxygenation is further impeded with increasing age of the patient.

There appears to be increasing VA/Q mismatch with age, with

enhanced perfusion of low VA/Q regions both in awake subjects

and when they are subsequently anesthetized.

Major cause of impaired gas exchange during anesthesia at ages younger than 50 years is shunt, whereas at higher ages mismatch becomes increasingly important.

Obesity

Obesity worsens the oxygenation of blood.

A major explanation appears to be a markedly reduced FRC, which promotes airway closure to a greater extent than in a normal subject.

Pre-existing lung disease

Smokers and patients with lung disease have more severe impairment of gas exchange in the awake state than healthy subjects do and this difference also persists during anesthesia.

Regional anesthesia

Ventilatory effects of regional anesthesia depend on the type and extension of motor blockade.

With extensive blocks that include all the thoracic and lumbar segments, inspiratory capacity is reduced by 20% and expiratory reserve volume approaches zero. Diaphragmatic function however, is often spared.