RCSI Ventilation/Perfusion Relationships PDF

RCSI Royal College of Surgeons in Ireland Coláiste Ríoga na Máinleá in Éirinn Ventilation/perfusion relationships Respiratory module Dr. Marc Sturrock – [email protected] Presented by Dr Ebrahim Rajab – [email protected] 4-May-2023 LEARNING OUTCOMES • • • • • • Describe alveolar and blood gas p...

RCSI Royal College of Surgeons in Ireland Coláiste Ríoga na Máinleá in Éirinn Ventilation/perfusion relationships Respiratory module Dr. Marc Sturrock – [email protected] Presented by Dr Ebrahim Rajab – [email protected] 4-May-2023 LEARNING OUTCOMES • • • • • • Describe alveolar and blood gas partial pressures Describe alveolocapillary membrane function Describe what diffusing capacity is Describe the alveolar-arterial PO2 gradient Explain the ventilation/perfusion relationship Explain the mechanism of hypoxic pulmonary vasoconstriction 80 160 LO: Describe alveolar and blood gas partial pressures • These % values (in the previous slide) are for dry gas but air is 100% saturated with water vapour in conducting airways • water exerts a saturated water vapour pressure of 47 mmHg • so the partial pressure is calculated as (PB47) X % gas • PB = 760 mmHg LO: Describe alveolar and blood gas partial pressures PB x %gas = 760 mmHg x 0.21 = 160 mmHg (PB - 47) x %gas = (760 mmHg - 47 mmHg) x 0.21 = 150 mmHg LO: Describe alveolar and blood gas partial pressures • Arterial blood gas (ABG) partial pressures are measured using arterial blood samples and a blood gas analyser • Alveolar PCO2 values are measured approximately by measuring end-tidal values LO: Describe alveolar and blood gas partial pressures ‘Capnography’ is the continuous analysis and recording of the CO2 concentration in respiratory gas LO: Describe alveolar and blood gas partial pressures www.derangedphysiology.com CO 2 Alveolar epithelium Alveolar lining fluid 0.5 microns Capillary endothelium RBC O2 LO: Describe alveolocapillary membrane function Plasma The alveolar-capillary membrane is normally very thin (0.5 µm) and so there is rapid, complete equilibration of O2 and CO2 between the alveolar gas and the blood (perfusion rather than diffusion limited) LO: Describe alveolocapillary membrane function (gas) exchange across the alveolocapillary membrane is by simple diffusion which is directly proportional to pressure difference and surface area and inversely proportional to distance (this is Fick’s law of diffusion; but these variables are not measurable directly) exchange is reduced in emphysema (reduced surface area) and in lung fibrosis (increased distance for diffusion) LO: Describe alveolocapillary membrane function DIFFUSING CAPACITY (USA) OR TRANSFER FACTOR (EU) Various definitions of Diffusing Capacity • “the extent to which a gas (e.g. oxygen or CO2) passes from the air sacs of the lungs into the blood” • “the volume of gas that will diffuse through the membrane each minute for a partial pressure difference of 1mmHg” • Diffusing capacity = Rate of transfer of gas from lung to blood Partial pressure difference • It is therefore a distillation of all the factors which influence the diffusion of respiratory gases into one numerical representation. • This property is usually referred to as DL or DL, the SI units are mmol/min/kPa, and the traditional units are ml/min/mmHg LO: Describe what diffusing capacity is MEASURING DIFFUSING CAPACITY • This can be done non-invasively using small non-lethal amounts of carbon monoxide • Carbon monoxide (CO) is used because the binding to haemoglobin is so strong and the PCO in the blood is zero so the partial pressure difference is the alveolar PCO • DL= Rate of transfer of gas from lung to blood PACO – PaCO • Technique: subject inhales a CO mixture, holds their breath for 10 s, exhales and the alveolar air analysed • CO consumption (difference in partial pressure between inhaled and exhaled CO) and alveolar PCO are measured and diffusing capacity is calculated LO: Describe what diffusing capacity is DIFFUSING CAPACITY (DL) OR TRANSFER FACTOR (TL) • DLCO unit is ml/min/kPa - diffusing capacity • TLCO unit is mmol/min/kPa • Expected value depends on haemoglobin, age, sex • Reduced in lung fibrosis, pneumonia, oedema, emphysema Severity and classification of DLCO reduction [not examinable]: •Normal DLCO: >75% of predicted, up to 140% •Mild: 60% to LLN (lower limit of normal) •Moderate: 40% to 60% •Severe: <40% LO: Describe what diffusing capacity is ALVEOLAR –ARTERIAL PO2 GRADIENT • normally, arterial (a) blood PO2 is slightly less (95 mmHg) than alveolar (A) PO2 (A-a PO2 gradient) because of venous admixture which is caused by: – anatomical shunt (bronchial and thebesian veins) – ventilation/perfusion mismatch LO: Describe the alveolar-arterial PO2 gradient ANATOMICAL SHUNT Lower PO2 than expected LO: Describe the alveolar-arterial PO2 gradient ALVEOLAR GAS EQUATION • a greater than normal A-a PO2 gradient suggests a problem with gas exchange, i.e., anatomical shunting or with V/Q mismatch. • The alveolar gas equation is used to calculate alveolar oxygen partial pressure as it is not possible to collect gases directly from the alveoli. • Carbon dioxide is a very important variable in the equation. The PO2 in alveoli can change significantly with variations in blood and alveolar carbon dioxide levels. If the rise in CO2 is significant, it can displace oxygen molecules which will cause hypoxemia • The arterial PO2 can be determined by obtaining an arterial blood gas. LO: Describe the alveolar-arterial PO2 gradient ALVEOLAR GAS EQUATION • At sea level, the alveolar PAO2 is: PaO2 = 0.21(760 - 47) - 40/0.8 = 99.7 mm Hg. • RER is the respiratory exchange ratio (depends on diet) = CO2 production = 200 ml/min = 0.8 O2 consumption 250 ml/min • Estimating A-a gradient: Normal A-a gradient = (Age + 10) / 4 A-a gradient increases 5 to 7 for every 10% increase in FiO2. LO: Describe the alveolar-arterial PO2 gradient VENTILATION/PERFUSION (V/Q) RATIO • Ventilation/perfusion (V/Q) matching is essential for normal gas exchange in the lungs. • For normal gas exchange, alveoli must be in close proximity to pulmonary capillaries • V/Q ratio expresses the matching of ventilation (V in L/min) to perfusion (Q in L/min). • For the entire lung, the average normal value of V/Q is 0.8 (ventilation is 80% of perfusion) • This average results in PaO2 of 100 mmHg and PaCO2 of 40 mmHg • However V/Q is not uniformly 0.8 throughout the entire lung… LO: Explain the ventilation/perfusion relationship VENTILATION/PERFUSION (V/Q) RATIO • normally, there is only a slight mismatch of ventilation to perfusion . Q VA/ Q . VA Base LO: Explain the ventilation/perfusion relationship Apex VENTILATION/PERFUSION (V/Q) RATIO • normally, there is only a slight mismatch of ventilation to perfusion PPL (pleural pressure) is more negative at the apex therefore alveoli are more expanded and therefore less compliant than at the base therefore more air goes to the base during inspiration (larger pressure gradient) because the apex has higher V/Q ratio, TB is more likely in the apex where there is a higher PO2 LO: Explain the ventilation/perfusion relationship VENTILATION/PERFUSION (V/Q) RATIO AND RESPIRATORY DISEASE • in respiratory disease, the V/Q ratio may be increased (overventilation/underperfusion) or decreased (underventilation/overperfusion) • an increased V/Q ratio means an increase in alveolar VD (= alveolar dead space) and “wasted ventilation” • a decreased V/Q ratio means “shunting” where deoxygenated venous blood bypasses the exchange area and enters the left heart causing arterial hypoxaemia; this is a common cause of hypoxaemia LO: Explain the ventilation/perfusion relationship LO: Explain the ventilation/perfusion relationship Obstruction (COPD, asthma, bronchitis) v Q = SMALL venous blood with low PO 2 —SHUNT“ LO: Explain the ventilation/perfusion relationship LO: Explain the ventilation/perfusion relationship LO: Explain the ventilation/perfusion relationship • a “true shunt” is where blood flows through a region with zero ventilation • examples would be abnormal right-left shunts in the heart, atelectasis*, consolidation** • oxygen therapy will improve PaO2 with a low V/Q ratio but not with “true shunt” *Atelectasis is the collapse of part or, much less commonly, all of a lung due to partial or complete, reversible collapse of the small airways **consolidation when the air in the small airways of the lungs is replaced with a fluid, solid, or other material such as pus, blood, etc. LO: Explain the ventilation/perfusion relationship HYPOXIC PULMONARY VASOCONSTRICTION Relative overventilation/underperfusion increases alveolar PO2 and decreases PCO2 LO: Explain the mechanism of hypoxic pulmonary vasoconstriction HYPOXIC PULMONARY VASOCONSTRICTION ­ relative underventilation/overperfusion decreases alveolar PO2 and increases PCO2 causing relaxation of airway smooth muscle but contraction of pulmonary arterioles (This response is the opposite of that in other organs, where hypoxia causes vasodilation) LO: Explain the mechanism of hypoxic pulmonary vasoconstriction HYPOXIC PULMONARY VASOCONSTRICTION • Hypoxic vasoconstriction is a protective mechanism in the lungs. It diverts blood flow away from unventilated (hypoxic) regions where blood flow would be wasted because gas exchange cannot occur, and directs it toward regions that are ventilated and where gas exchange can occur. • However, generalised alveolar hypoxia (altitude, some respiratory diseases) will cause pulmonary hypertension LO: Explain the mechanism of hypoxic pulmonary vasoconstriction V/Q RELATIONSHIPS Reading Sherwood – Human Physiology, 7th ed. – Chapter 13 Berne & Levy 7th Ed ‘Physiology’ – Chapter 22