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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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Downloaded from: StudentConsult (on 24 May 2013 07:29 AM) © 2005 Elsevier

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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.

Downloaded from: StudentConsult (on 22 May 2013 07:53 PM) © 2005 Elsevier

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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.


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.


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.


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.


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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