respiratory physiology - wickupwickup.weebly.com/.../block_18_-_resp_physiology.pdf · respiratory...
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RESPIRATORY PHYSIOLOGY
Anaesthesiology Block 18 (GNK 586)
Prof Pierre Fourie
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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 =
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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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