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RESPIRATORY PHYSIOLOGY

Anaesthesiology Block 18 (GNK 586)

Prof Pierre Fourie

Outline

Ventilation Diffusion Perfusion Ventilation-Perfusion relationship Work of breathing Control of Ventilation

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Ventilation Function: Supply O2 to the alveoli and

remove CO2

Airways divided in conducting passages (dead space) and respiratory zone (gas exchange)

Respiratory zone – blood-gas interface ◦ Respiratory bronchiole ◦ Alveoli

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Figure 37-8 Respiratory passages.

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Blood-Gas interface

500 million alveoli Surface area of 50 – 100m2

Extremely thin 0.2 – 0.3 um Damaged by high capillary pressures

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Figure 39-7 Respiratory unit.

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Ventilation – Tidal Volume

Volume of air entering the lung with a normal breath = Tidal Volume (Vt)

Vt = 6 - 8 ml/Kg = 500 ml Vmin = Vt x RR = 500 x 12 = 6000 ml Vt = Alveolar volume (VA) + Physiological

dead space (VdPhys)

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Ventilation – Dead Space VdPhys = Anatomical dead space

(VdAnat) + Alveolar dead space (VdAlv) Vd/Vt = 1/3 2/3 of Tidal volume available for gas

exchange – Alveolar volume (330 ml) Anaesthesia - Apparatus dead space

(VdApp) Total Vd = VdApp + VdAnat + Vd Alv

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Ventilation – Dead Space

VdPhys = Vt(PaCO2 - PECO2) PaCO2 Bohr equation PaCO2 - PECO2 = 5 mm Hg

Dead space ventilation

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Figure 37-6 Diagram showing respiratory excursions during normal breathing and during maximal inspiration and maximal expiration.

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Ventilation – Alveolar Gas exchange depends on Alveolar

Ventilation (VA) VA = RR x Alveolar volume = 12 x 330 = 4000 ml Alveolar Ventilation Equation: VA = VCO2 / PaCO2 + K

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Oxygen cascade

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Ventilation

Function: Supply O2 to the alveoli and remove CO2

Alveolar gas equation

PAO2 = PiO2 – (PACO2/R) + K = FiO2(PB - PH2O) – (PACO2/R) + K

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Hypoventilation ↓ VA ↓ Vt ↑ Vd HYPERCAPNIA Headache, excitement, restlessness,

confusion Respiratory acidosis, sympathetic

stimulation – tachycardia, ↑ pulse pressure, sweating, cyanosis

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Functional Residual Capacity (FRC)

FRC = ERV + RV Amount of air that remains in the lungs,

end of normal expiration (+/- 2300 ml). Volume of air available for gas exchange –

diffusion of O2 to blood and of CO2 from blood to alveoli

↓ FRC – supine, ↑ age, respiratory disease, anaesthesia

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Figure 39-9 Ultrastructure of the alveolar respiratory membrane, shown in cross section.

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Diffusion – Fick’s Law

Rate of diffusion of a gas through a tissue slice is proportional to ◦ area of tissue ◦ Partial pressure difference ◦ Solubility of the gas in the tissue

Inversely proportional ◦ Thickness of the tissue ◦ Square root of the molecular weight of the

gas

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Oxygen uptake

Diffusion limited Perfusion limited ◦ RBC time spent in alveolar capillary = 0.75

sec ◦ PaO2 is reached within 0.25 sec ◦ Limited High cardiac output Very low mixed venous PO2

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Perfusion Cardiac output (Qt) = SV x HR Vmin = Vt x RR Pulmonary blood flow (Qp) = Qt Vmin = Qt then ventilation / perfusion

ratio = 1 Alveoli perfused but not ventilated =

shunt (Qs) Alveoli ventilated but not perfused = dead

space (Vd)

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Shunt equation

CcO2 – CaO2 CcO2 - CmvO2 CcO2 = O2 concentration in capillaries of

ventilated perfused alveoli (Alveolar gas equation)

CmvO2 = 40 mmHg or 70% saturated Qs / Qt = 2%

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Qs / Qt =

Ventilation Perfusion relationships

Ideal V/Q ratio = 1 If V = 0 V/Q = 0 = pure shunt If Q = 0 V/Q = infinity = pure dead

space ventilation V/Q ratio > 0 but < infinity = V/Q

mismatch High V/Q Hypercapnia Low V/Q Hypoxia

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V/Q mismatch and Anaesthesia

Loss of motor tone – compression atelectasis – low V/Q ratio

Vasodilatation and cardiac suppression - ↓ Qt – high V/Q ratio

V/Q mismatch ↑ open abdominal and thoracic procedures

Atelectasis ↑ with high O2 concentrations (Absorption atelectasis)

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Management of V/Q mismatch

Ventilatory support ◦ Rx atelectasis Avoid high O2 concentrations Apply PEEP

Circulatory support ◦ Rx low cardiac output Fluid management, correct hypovolemia Inotropes Vasopressors

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Work of breathing (WOB)

Energy and Work is required to expand the chest and move gas into the lungs and increase the lung volume = WOB

Pressure is required to overcome airway resistance and tissue elasticity

Volume change per unit of pressure change = Compliance

Normal Compliance = 200 ml / cm H20 transpulmonary pressure

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Work of breathing

↑ WOB ◦ Diseases that ↓ compliance = restrictive

lung disease (inspiration) ◦ Diseases that ↑ airflow resistance =

obstructive lung disease (expiration) ↑ WOB hypoventilation,

hypercapnia and hypoxia Respiratory failure

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Control of Breathing Central ◦ Respiratory centres in the brainstem control

spontaneous breathing by rhythmic neural activity ◦ Dorsal inspiratory and ventral expiratory

neurons in the medulla oblongata ◦ RR and rhythm fine-tuned by pontine centres

(apneustic and pneumotacic) which influence the dorsal neurons ◦ H+ sensitive chemoreceptors in the medulla is

stimulated by low CSF pH (↑ PCO2) stimulate breathing

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Figure 41-1 Organization of the respiratory center.

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Figure 41-2 Stimulation of the brain stem inspiratory area by signals from the chemosensitive area located bilaterally in the medulla, lying only a fraction of a millimeter beneath the ventral medullary surface. Note also that hydrogen ions stimulate the chemosensitive area, but carbon dioxide in the fluid gives rise to most of the hydrogen

ions.

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Control of Breathing

Peripheral Chemoreceptors in the Aortic arch and

Carotid body ◦ Sensitive to ↓ PaO2 - ↑ ventilation

Chemoreceptors in the Carotid body ◦ Sensitive to ↓ pH - ↑ ventilation

Juxta-capillary receptors Irritation receptors Stretch receptors

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Anaesthetic implications

Central respiratory centres ◦ Very sensitive to opioids - ↓ Vmin ◦ Insensitive by chronic hypercapnia (CSF

pH normalized by buffering with HCO3) stimulated by low PaO2 (hypoxic drive)

Peripheral centres ◦ Suppressed by Anaesthetic vapours ◦ ↓ benzodiasipines

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