Respiratory failure and VQ matching for moodle 2022-23.pptx

Respiratory Failure : VQ mismatching and more - the basics and regulation Respiratory Disease 20 credits Learning Objectives • Describe alveolar-blood gas diffusion and partial pressures for O2 and CO2 exchange (in mmHg and/or kPa). • Describe factors that influence gas exchange in health (includi...

Respiratory Failure : VQ mismatching and more - the basics and regulation Respiratory Disease 20 credits Learning Objectives • Describe alveolar-blood gas diffusion and partial pressures for O2 and CO2 exchange (in mmHg and/or kPa). • Describe factors that influence gas exchange in health (including exercise) and in disease states – Influential factors (Fick’s principle) – Ventilation-perfusion VQ matching • Explain the effect of gravity on Ventilation and Perfusion and the VQ ratios from lung apex to base – Comparison of pulmonary and systemic circulation characteristics • Explain how VQ is controlled and the effect of increased and decreased VQ matching on partial pressures • Define Respiratory Failure, describe main causes and explain clinical examples arising from these causes Gas diffusion and Partial pressures of O2 and CO2 Normal arterial values PaO2 (11-15 kPa; ~90-113 mmHg) Hypoxia is low PaO2 PaCO2 (4.6-6.4 kPa, ~33-46 mmHg) Hypercapnia is high PaCO2 Outside these ranges are abnormal and may indicate respiratory failure Respiratory Failure Definition: A failure to maintain adequate gas exchange and is characterised by abnormalities in arterial blood gas partial pressures • Type 1: hypoxaemia (< 8 kPa) with a normal or low CO2 • Type 2: hypoxaemia with a high CO2 (>6 KPa) • Normally breathing rate cannot keep up • They can co-exist. Respiratory Failure: Pathophysiological causes 4 main causes a) alveolar hypoventilation • reduction in minute ventilation characteristically shows an increase in PaCO2 b) diffusion deficit c) shunts d) ventilation – perfusion (VQ) mismatch a) Hypoventilation • CO2 retention – a reduction in minute ventilation – an increase in proportion of dead space ventilation – Causes Type II – E.g. respiratory muscle fatigue – Correctable with oxygen (careful) b) Diffusion deficit Fick’s Law describes the rate of diffusion across the alveoli into the blood A = surface area T = tissue thickness D = diffusion coefficient of gas P1-P2 = partial pressure gradient Diffusion rate ∞ gas solubility gradient √gas mol. weight x alveolar surface area x air-blood barrier thickness Measured how?? pressure Examples Partial pressure gradient Increased metabolism or 100% O2 increases rate. Altitude decreases rate of diffusion. Notes 100% O2 increases the gradient about 5 x so speeds up the delivery of O2 and so helps relieve breathing demand Gas physical properties Heavier gas or less soluble decreases rate Although heavier, CO2 is 20x more soluble than O2 and diffuses faster! Alveolar-capillary membrane Pathological - pulmonary fibrosis (chronic RF), oedema (acute RF), asbestosis, pneumonia Lung compliance also reduces (i.e. stiff lungs) Reduced gas exchange area Emphysema (permanent loss) Pneumonia (inflammatory consolidation) c) Shunts • venous blood mixing with arterial blood – extra-pulmonary shunt • Mainly paediatric cardiac causes e.g. ductus arteriosus. This usually reverses. – intra-pulmonary shunt • blood is transported through the lungs without taking part in gas exchange. • Commonest causes are alveolar filling (pus, oedema, blood or tumour) and atelectasis • oxygen does ‘not’ correct pure shunt hypoxia d) Ventilation-Perfusion VQ matching • Gas exchange needs good ventilation (V) and perfusion (Q) of alveolar capillaries V – V = 5L air/min; Q = 6 L blood/min – Whole lung VQ ratio is ~0.8 and 1 alveolus Q To tissues PaO2 • Correlating alveolar ventilation (about 5 L/min) and perfusion (about 5 L/min) maximises gas exchange and efficiency. Ideally it should be a 1: 1 (i.e. 1.0). Regulation is needed to maximise gas exchange and maintains normal blood gas partial pressures • Mismatching is the most common cause of hypoxia in respiratory diseases and of major significance in respiratory failure • VQ mismatch increases the area that is not used for gas exchange (alveolar dead space) – i.e. physiological ‘dead space’. Normal lung Emphysema • PaO2 falls and the PA-PaO2 gradient increases – Breathing rate may increase • Range of causes : – Lack of inspired oxygen – Lack of circulation/ blood flow (shunts) – Respiratory dysfunctions Consequence of VQ mismatch • Blood leaving the relatively healthy alveoli will have an oxygen saturation of about 97% (normal) because of the flat upper portion of the oxyhaemoglobin dissociation curve • Blood leaving alveoli that do not have optimum V/Q ratios will have a much lower oxygen saturation and overall causes hypoxaemia when they mix in the circulation. Common respiratory dysfunctions causing VQ mismatch and reduced PaO2 • • • • • • • • • Adult respiratory distress syndrome Pneumonia Asthma Pulmonary oedema Chronic obstructive lung disease Interstitial fibrosis Pneumothorax Pulmonary embolism Pulmonary hypertension Type 1 respiratory failure occurs before Type 2 • • • •• •• • •• • •• •• •• Rarer Common Acute asthma Lung collapse/atelectasis (tumour, foreign body, infection) Exacerbation COPD Interstitial lung disease/ pulmonary fibrosis Pneumonia Pulmonary haemorrhage Pulmonary oedemaweakness (Gullian-Barre syndrome, myasthenia gravis, Acute respiratory Pulmonary embolism polio) Pleural effusionobstruction (foreign body, tumour, epiglottis) Upper airway Pneumothorax Fat embolism ARDS/ALI Chest trauma Respiratory depression anaphylaxis Drugs e.g. opiates How is V/Q regulated locally? Regulation •Airflow and blood flow are governed by the same principles of flow, pressure and resistance (Poiseulle’s Law). Resistance to flow is inversely proportional to the radius 4 Bronchioles provide most resistance to airflow V Q Arterioles provide most resistance to perfusion VQ matching – continuous local changes • Altering respiratory bronchiolar and pulmonary arteriolar radius changes resistance and hence flow V Q • Bronchioles dilate in response to raised PaCO2 (hypercapnia) to improve airflow • Pulmonary arterioles constrict to low PaO2 (hypoxia) to reduce flow and redirect blood to better perfused areas • Opposite to systemic circulation • Diff Note the Different Effects of O2 Ventilation and Perfusion is not uniform throughout the lungs due to gravity so VQ is not uniform VA Q V A/ Q 0.4L/min 3.0 Top 1.2L/min Middle 1.8L/min 2.0L/min 0.9 Bottom 2.1L/min 3.4L/min 0.6 ~ 2 x larger ~ 5 x larger Imagine…. • Perfusion but no ventilation • Called a ‘shunt’ • V/Q = 0 • Ventilation but no perfusion • Called ‘ dead space’. • V/Q is infinity Effect of gravity on VQ ratio Both blood flow and ventilation vary from bottom to top of the lung The result is that the average arterial and alveolar partial pressures of O2 are not exactly the same. Normally this effect is not significant but it can be in disease. Changed body position? Why the VQ difference from base to apex? Pulmonary ventilation increases from apex to base due to gravity AND COMPLIANCE • The intrapleural pressure becomes more negative towards the base. • The alveoli here are highly compliant so can accommodate more air Pulmonary blood flow depends on pressure changes in the surrounding areas Zone II The normal pressure gradient from arteries to veins can be disrupted by intermittent high alveolar pressures. Pulmonary arterial pressure is low. The flow is independent of the eventual venous pressure and depends only on the difference between pulmonary arterial pressure and alveolar pressure. Pa > Palv > Pv Zone III Normal pressure gradient from arteries to veins. Pulmonary artery pressure is greater than venous pressure and alveolar pressure ensuring perfusion. Pa > Pv > Palv Little/no flow Flow only if Pulmonary Arterial pressure > Alveolar pressure Normal a-v Pressure gradient Determines flow Lung Base Increased perfusion Zone I The Alveolar pressure is greater than BOTH local pulmonary arterial and venous pressures. Irrespective of the normal pressure gradient from arteries to veins, the Vessels are compressed by the high alveolar pressure and there is only intermittent flow if Pa increases during the breathing cycle. Palv > Pa > Pv Lung Apex Summary • Normal diffusion pressures • VQ ratio – what is means and how it affects blood gas partial pressures • Factors that alter the VQ (gravity and pathologies) • VQ control • Differences between pulmonary and systemic circulations Reading and help… Interested in the cellular mechanism for hypoxic pulmonary vasoconstriction? • Hypoxic pulmonary vasoconstriction: physiology and anaesthetic implications: Lumb AB and Slinger P (2015). Anesthesiology.122:932-46. • http://anesthesiology.pubs.asahq.org/article.aspx?articleid=2205943 Need help with the gravitational effects on pulmonary perfusion? • https://www.youtube.com/watch?v=IAlmdoc4bqI Need help with distribution of blood flow in the lungs? • Hickin, S, Renshaw J & Williams R (2015) Crash Course in Respiratory Syste. 4th ed. Elsevier. • Rhoades RA, Bell DR (2019) . Medical Physiology: Principles for Clinical Medicine. 4th ed. Lippincott Williams and Wilkins. E-book • https://meded.lwwhealthlibrary.com/book.aspx?bookid=2188 Zones are established as a result of gravitational effects. The three zones are established in an upright person and are dependent on the relationship between pulmonary arterial pressure (Pa), pulmonary venous pressure (Pv), and alveolar pressure (Pa). A zone 1 is established when alveolar pressure exceeds arterial pressure and there is no blood flow. Zone 1 occurs toward the apex of the lung and occurs only in abnormal conditions in which alveolar pressure is increased (e.g., positive pressure ventilation) or when arterial pressure is decreased below normal (e.g., the gravitational pull while standing at attention or during the launching of a spacecraft). A zone 2 is established when arterial pressure exceeds alveolar pressure, and blood flow depends on the difference between arterial and alveolar pressures. Blood flow is greater at the bottom than at the top of this zone. In zone 3, both arterial and venous pressures exceed alveolar pressure, and blood flow depends on the normal arterial– venous pressure difference. Note that arterial pressure increases down each zone, vessel transmural pressure also becomes greater, capillaries become more distended, and pulmonary vascular resistance falls. Area in which blood flow (perfusion) is greater than airflow (ventilation) Helps balance Large blood flow Causes? Effect on VQ Helps balance Small airflow CO2 in area O2 in area Relaxation of local-airway smooth muscle Contraction of local pulmonary arteriolar smooth muscle Dilation of local airways Constriction of local blood vessels Airway resistance Airflow Vascular resistance Blood flow Causes? Effect on VQ Area in which airflow (ventilation) is greater than blood flow (perfusion) Helps balance Helps balance Large airflow Small blood flow CO2 in area Contraction of local-airway smooth muscle Constriction of local airways Airway resistance Airflow O2 in area Relaxation of local pulmonary arteriolar smooth muscle Dilation of local blood vessels Vascular resistance Blood flow