7 1 respiratory physiology - slcp · 2020-05-12 · sri lanka college of paediatricians 6...
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Respiratory Physiologypart 1
EDUCATION & TRAINING SRI LANKA COLLEGE OF PAEDIATRICIANS
SRI LANKA COLLEGE OF PAEDIATRICIANS 1
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Objectives
Differences between children and adults
Respiratory Physiology
Pathophysiology
Clinical signs of respiratory failure
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respiratory drive in small infants
Nasal congestion can lead to significant resp
distress until 2-6 months
Airway small<9 yrsLarge tongue, small
oropharynx (infants & small children) Relatively little
cartilaginous supportChest wall
extremely compliant (neonates)
Ribs relatively horizontal (early
infancy)
Respiratory muscles may fatigue rapidly
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SRI LANKA COLLEGE OF PAEDIATRICIANS 4
Features of paediatric respiratory system:
Airway is small and therefore small absolute changes in radius (due to oedema or secretions) result a large relative change in cross sectional area and hence resistance. Clinically significant up to age of 8-9 years
Younger children have relatively little cartilaginous support of the airways. Dynamic compression during high expiratory flow may occur.
Neonates chest wall extremely compliant – substantial recession, easily overinflated with mech vent, little opposition to deflating tendency of lungs leading to low FRC and rapid desaturation during apnoea (eg during intubation)
In early infancy ribs are relatively horizontal with the result that the respiratory system is very dependent on diaphragmatic function. In presence of hyperinflation or abdominal distension the diaphragmatic function may be restricted with severe respiratory embarrassment
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O2FiO2Alv MVV/Q DLO2
Alv MV
Alv MV = RR x (VT ‐ VDS)
CO2
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Respiratory Physiology
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SRI LANKA COLLEGE OF PAEDIATRICIANS 6
Respiratory Physiology: The major function of the lung is to get oxygen in and carbon dioxide outFiO2, the major determinant of PAO2: partial pressure of oxygen in the alveoli, Alveolar ventilation e.g. can climb Everest without oxygen only by extreme hyperventilationV/Q matching
DLO2 = Diffusing capacity: how well gas moves from alveoli to blood
Carbon dioxide removal is largely dependent on alveolar ventilation which, in turn, is dependent on the respiratory rate times the difference between tidal volume and dead space. The latter will vary, depending on ventilation perfusion matchingIt is an active process, there is nothing that we can augment to speed up the removal of carbon dioxide. Also it is not easy to detect ventilatory failure unless you very astute in clinical exam or with the help of a blood gas
CO2 closely related to work of breathing and respiratory reserve
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Respiration … the big picture
Ventilation & Gas Diffusion
Hb
Cardiac Output
Diffusion & Metabolic Demand
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This slide puts respiration into context –outlining that the purpose is cellular oxygenation. Effective cellular oxygenation relies on the pulmonary and cardiovascular system and briefly outline considerations when evaluating respiration.
Oxygen consumption in infants is 6-8mL/kg/min vs 3-4ml/kg/min adults
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Respiratory Drive
Considerations
•hypercarbia/hypocarbia•hypoxia•exhaustion/ sedation •reduced cerebral perfusion(low CO)•intact spinal cord
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Anatomy & Physiology
INCREASED AIRWAY RESISTANCE
COMPLIANT CHEST WALL
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Oxygenation & Carbon Dioxide
•GAS Exchange occurs at the alveoli•C02 diffuses readily but must be removed by adequate MV
•MV = RR x TV
•For 02 diffuses more slowly; critical that alveoli remain open
•Alveoli need a volume of gas to remain in them after expiration
•Alveolar Collapse • decreased oxygenation
• needs higher pressure to reopen (increased WOB_.Video of Alveoli https://www.bing.com/videos/search?q=alveolar+recruitment&&view=detail&mid=0A1A1BEDB98CFC3B24B90A1A1BEDB98CFC3B24B9&FORM=VRDGAR
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The alveolus is the essential component required for gas exchange, diffusion of 02 into the bloodstream and removal of C02. Infants are born with only 10% of their alveoli and continue to develop alveoli until they are 8 years of age. Not only are the number of alveoli reduce but the structure is immature. Young children have reduced pores of kohn and canals of lambert, reducing the communication between alveolar units. It is critical that the alveoli stay open for gas exchange to occur. Alveoli do not open and close but must remain open to ensure that all the blood passing can be oxygenated. If the alveolus collapses reduced oxygenation; a closed / small alveolus requires high pressures to reopen. An open alveolus requires minimal pressure to stay open. Avoiding opening and closing prevents damaging the delicate and fragile alveolar membranes and can prevent ALI.
Looking at the picture from an electron microscope we can see how delicate the alveolar structure is. It requires a pressure (distending pressure) to maintain the opening volume and support the open structure. During ventilation we use CPAP or PEEP to prevent the alveolus collapsing during expiration.
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Carbon Dioxide out
Largely dependent on alveolar ventilation
Alveolar Ventilation = Resp Rate x (Vtidal‐ VD)
Vtidal = tidal volume (6‐10ml/kg)
VD = dead space volume (3ml/kg)
Anatomical dead space constant
Physiological dead space variable Increases in sick patients
Equipment dead space
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Carbon dioxide removal is largely dependent on alveolar ventilation which, in turn, is dependent on the respiratory rate times the difference between tidal volume and dead space. The latter will vary, depending on ventilation perfusion matching
It is an active process, there is nothing that we can augment to speed up the removal of carbon dioxide. Also it is not easy to detect ventilatory failure unless you very astute in clinical exam or with the help of a blood gas
CO2 closely related to work of breathing and respiratory reserve
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V/Q MismatchVentilation /Perfusion
Alveolar collapse, consolidation or obstruction larger volume of poorly oxygenated blood returning from the lungs Sa02
Over distention of ventilated alveolar units can reduce blood flow not contributing to oxygenation.
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For effective oxygenation at the lungs good matching of ventilation and perfusion is required.Ideally all areas of the lung would be like the example in the middle – good ventilation of alveolus and good perfusion so that deoxygenated blood from the RV travels past the alveolus and picks up oxygen returning to the RA with 100% Sa02.
Some airways are collapsed or blocked not ventilated, the blood that passed by these will not pick up oxygen then mixes with the oxygenated blood reducing the overall Sa02.
Some areas of the lung may good ventilation but no blood flow (eg airways), however in sick lungs where ventilation may not be evenly distributed, IPPV can result in the volume going to compliant alveoli overstretching and restricting blood flow. This can be a problem as it may shunt blood to poorly ventilated alveoli.
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Lung Volumes
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Dead space
Anatomical Dead Space
Equipment Dead Space
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However not all the volume is involved in gas exchange. Some of the gas goes to alveoli that are not perfused. Because there is blood flow to these alveoli they do not take part in gas exchange. These alveoli take up part of what is known as dead space. The remainder of the dead space is made up by the pharynx, trachea and bronchial tree
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Lung Volumes
Closing CapacityVolume at which alveoli in dependent areas of the lung
start to collapse/close.
Functional Residual Capacity Volume remaining after expiration.
IMPORTANT FOR OXYENATION Normally ~30mL/kg
FRC is smaller in proportion to lung volume in children.
Infants & young children FRC drops below the closing capacity when they are supine alveolar collapse
Respiratory disease FRC alveolar collapse
Tidal VolumeVolume of gas with each breath.
IMPORTANT FOR C02 REMOVAL
To keep alveoli open need FRC > CC
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When thinking about breathing it is important to understand lung volumes. Tidal volume – ~ 7mL/kg . Tidal volume & minute ventilation are important for ventilation (C02 removal) . Discuss FRC and the relationship between FRC & CC and how CPAP/PEEP can support this. FRC is important for oxygenation.
FRC = ERV (expired residual vol ) + residual vol RVFRC decreased by about 30% in spine vs erect FRC falls during disease, loss of surfactant etc when lungs are more prone to collapsePaeds have poor chest wall compliance relatively lower FRCInfants & children FRC is about the same as CC risk of collapse and increase wobOther factors which drop FRC = anesthetic drugs, sedation, no spontaneous breathing rapid desaturation during intubation etc
C02 diffuses more readily than 02
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How to Support our Baby?MANAGE VENTILATION (C02)
Goal = improve minute volume
MV = RR x TV
RR – 80bpm
TV – air entry, chest wall movement
Options:
*decrease resistance (CPAP)
*support inspiration (NIV or IPPV)
MANAGE OXYGENATION (02)Goal = improve FRC
FRC = volume in lungs at expiration
Crackles, Sp02 grunting
Options:
*keep alvoli open (CPAP, PEEP)
*re‐open alveoli (mean airway pressure)
*Fi02 (symptomatic only)
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Remember that the aim of therapy is to restore oxygen delivery to tissues and that saturation notPO2 is a major determinant of oxygen delivery. Oxygen delivery is the product of the cardiacoutput, the oxygen content of blood and a correction factor. The oxygen content of blood is mainlydependent on the oxygen saturation and the haemoglobin saturation, with the a very smallcontribution from dissolved oxygen. As a result it is the saturation which is important indetermining oxygen delivery rather than the PaO2
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Oxygen Delivery to the Cells
222
2 2
PaO0.0031.37Hbsaturation O content O
10contentOoutput CardiacdeliveryO
HB 140
COPoor perfusion
Cap RefillBP, HR
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SRI LANKA COLLEGE OF PAEDIATRICIANS 23
Remember that the aim of therapy is to restore oxygen delivery to tissues and that saturationnot PO2 is a major determinant of oxygen delivery. Oxygen delivery is the product of thecardiac output, the oxygen content of blood and a correction factor. The oxygen content ofblood is mainly dependent on the oxygen saturation and the haemoglobin saturation, with thea very small contribution from dissolved oxygen. As a result it is the saturation which isimportant in determining oxygen delivery rather than the PaO2