respiratory physiology and it's anaesthetic implications

Respiratory physiology

1. Respiratory mechanics: compliance of respiratory system: dynamic and static, Resistance of respiratory system Distribution of gas in lungs and perfusion and pathophysiology Moderator : Dr Nanish Sharma Presented by : Dr Abhinay Chauhan RESPIRATORY PHYSIOLOGY-2

2. One of the major role of the lungs is to facilitate gas exchange between the circulatory system and the external environment. Lungs are composed of branching airways that terminate in respiratory bronchioles and alveoli , which participates in gas exchange. Ventilation refers to the flow of air into and out of alveoli, while perfusion refers to flow of blood to alveolar capillaries.

3. The lungs can be expanded and contracted in two ways: By downward or upward movement of the diaphragm to lengthen or shorten the chest cavity; By elevation or depression of the ribs to increase or decrease the anteroposterior diameter of the chest cavity. Normal quiet breathing is accomplished almost entirely by movement of the diaphragm.

4. Normal Breathing Commences with active contraction of inspiratory muscles, which, Lowers intrathoracic and intra pleural pressures Enlarges the thorax Enlarges alveoli, bronchioles, bronchi Lowers alveolar pressure below atmospheric pressureInspiratory muscles provide the force necessary to overcome, Elastic recoil of the lungs and chest-wall Frictional resistance I) Tissue resistance: caused by deformation of lung tissue and thoracic cage. ii) Airway resistance: to airflow in the conducting airways.

5. Pleural pressure is the pressure of the fluid in the thin space between the lung pleura and chest wall pleura. The normal pleural pressure at the beginning of inspiration is about − 5 centimeters of water (cm H2O), which is the amount of suction required to hold the lungs open to their resting level. During normal inspiration, expansion of the chest cage pulls the lungs outward with greater force and creates more negative pressure to an average of about −7.5 cm H2O which increases the lung volume. During expiration, the events are essentially reversed. Pleural Pressure and Its Changes During Respiration.

6. Alveolar pressure at end inspiration and end expiration is equal to atmospheric pressure that is, 0 cm H2O. during normal inspiration, alveolar pressure decreases to about −1 cm H2O. This slight negative pressure is enough to pull 0.5 litre of air into the lungs in the 2 seconds required for normal quiet inspiration. During expiration, alveolar pressure rises to about +1 cm H2O, which forces the 0.5 litre of inspired air out of the lungs during the 2 to 3 seconds of expiration. Alveolar Pressure—Air Pressure Inside the Lung Alveoli.

7. The transpulmonary pressure is the pressure difference between that in the alveoli and that on the outer surfaces of the lungs (pleural pressure); it is a measure of the elastic forces in the lungs that tend to collapse the lungs at each instant of respiration, called the recoil pressure. Transpulmonary Pressure: (Distending pressure) P TP =P AW -P PL Lungs can be distended by positive pressure inside and negative pressure outside

8. Definition: The compliance of a lungs is defined as the change in volume that occurs per unit change in the transpulmonary pressure. It is the ability of the lungs to expand. C= ∆V/ ∆P C= Compliance ∆V= Change in Lung volume ∆P=change in transpulmonary pressure (Alveolar pressure- Pleural pressure) Compliance:-

9.  It represents pulmonary compliance at a given fixed volume when there is no airflow, and muscles are relaxed.  Reflects the elastic resistance of the lung and chest wall. It only measures the elastic resistance. Therapeutically, it serves to select the ideal level of positive end-expiratory pressure(PEEP), which is calculated based on the following formula: Cstat = V / ( Pplat – PEEP) It can be measured using manometer or electric transducers, but in concious individuals it is difficult to measure as muscle relaxation can not be achieved. Static Compliance:

10. Dynamic Compliance: It is the continuous measurement of pulmonary compliance calculated at each point representing schematic changes during rhythmic breathing. It monitors both elastic and airway resistance. CD= VT/(PI-PE) In normal lungs at low respiratory rates the dynamic and static compliances are more or less equal. Dynamic compliance

11. The volume change per unit pressure change is low. The lungs are stiff and are resistant to expansion. The patient has low lung volumes and low minute ventilation. Clinical conditions that decrease lung compliance: Low Compliance:

12. Volume change is large per unit pressure change. When the compliance is very high, Exhalation is incomplete due to lack of elastic recoil of the lungs. Usually seen in conditions that increase FRC of the patient like COPD, Emphysema, Obstructed airway, incomplete exhalation, and poor gas exchange. High Compliance:

13. P-V CURVE

14. RESISTANCE OF THE RIESPIRATORY SYSTEM Elastic resistance- 65%. Non-elastic resistance- 35% i ) Airflow – 80% ii) Viscous- 20% Resistance is overcome by (driving) pressure. In spontaneous breathing, driving pressure will be the Pleural pressure. In positive pressure ventilation, the driving pressure will be the difference between the pressures applied to the endotracheal tube and the alveolus. Resistance (R) is calculated as driving pressure (ΔP) divided by the resultant gas flow (F): R = ΔP/F

15. Factors Affecting Elastic Resistance 1.Elastic recoil forces of the lung tissue The elastin fibers forming the pulmonary interstitium resist stretching and exhibit the property of returning to its original length, when stretch. This accounts for approximately 1/3rd of the total elastic resistance of the lungs, and this is responsible for generating the recoil forces necessary to increase intra-alveolar pressure during expiration.

16. 2. Forces exerted by surface tension at the Air- Alveolar interface Therefore,Smaller alveoli have greater tendency to collapse.

17. Types of Flow patterns: 1.Laminar Flow Laminar Flow below critical flows, gas proceeds through a straight tube which slide one another. Fully developed flow has a velocity of zero at the cylinder wall and maximum velocity at the center of the advancing cone. Peripheral cylinders tend to be stationary and the central cylinder moves fastest. The advancing conical front means that some fresh gas reaches the end of the tube before the tube has been completely filled with fresh gas.

18. A clinical implication of laminar flow in the airways is that significant alveolar ventilation can occur even when the tidal volume is less that anatomic dead space. This is important in high-frequency ventilation. Laminar flow is given by Hagen–Poiseuille equation. Q = ΔPπr4 / 8ηl where Q is the volumetric flow rate, R and L are the tube radius and length, ΔP the pressure drop, and η is the fluid viscosity.

19. Turbulent flow usually presents with a square front so fresh gas will not reach the end of the tube until the amount of gas entering the tube is almost equal to the volume of the tube. Conditions that change the flow from laminar to turbulent: High gas flows Sharp angles within the tube Branching in the tube Change in the tube’s diameter. 2.Turbulent flow

20. Reynolds number

21. Distribution of inspired gases

22. Effect of position on ventilation The pleural pressure gradient is oriented according to gravity, the distribution of ventilation changes with body position. During inspiration, most gas goes to the basal units (dorsal, when supine; lower right lung when in the right lateral position). This distribution is because of the compliance properties of the lung and the effects of position on the distribution of the distending pleural pressure (i.e., the PPL gradient) Although the vertical height of the lung is the same in the prone and supine positions, the vertical gradient PPL is less when prone ,as the mediastinum compresses the dependent lung when supine but rests on the sternum when prone. A more even distribution of inspired gas—with improved oxygenation—in the prone position. 1,2,3 1.Bryan AC. Am Rev Respir Dis. 1974;110:143.45. 2. Mayo JR, et al. J Thorac Imaging. 1995;10:73.46. 3. Petersson J, et al. J Appl Physiol. 2004;96:1127

23. Density of normal lung is approx. 0.3 , PPL will become more positive by 0.3 cm H20 for each downward vertical cm. PPL gradient is affected by : Lung density Gravity Conformation of lung to the shape of thorax

24. Distribution of ventilation in upper vs lower lung in relation to flow. During low flow state ( at rest ) : Distribution is determined by difference in compliance During high flow state ( during exercise ) : Resistance is key determinant of distribution

25. Airway Closure Expiration causes the airway to narrow, deep expiration make them close. Closing volume -“ Volume remaining above residual volume where expiration below FRC closes some airways.” Closing capacity-Closing volume + Residual volume When PPL is more than PAW, the airway if collapsible will tend to close usually commences at the base

26. Three applications of closing capacity relevant to anaesthesia : 1) Airway closure depends upon age : In youth airway closure does not occur until expiration is at or near RV. In older age, it occurs earlier in expiration .This occurs because PPL is more positive. 2) In supine position FRC is less than when upright but CC is unchanged . 3) COPD increases lung volume at which closure occurs.

27. Equal pressure point (EPP) Point when the airway pressure is equal to the pleural pressure. The two ways of moving the EPP toward the mouth and to less collapsible airways is:- by raising alveolar recoil pressure ( Pst ) by an increase in lung volume. by lowering the expiratory flow rate so that the pressure drop along the airway tree is slowed down.

28. Diffusion of Gas Gas moves in large and medium sized airways by bulk flow (convection) Flow is through multiple generation of bronchi and net resistance falls with each division. Cross-sectional area expands massively ( trachea-2.5 cm2, 23 rd generation bronchi-0.8 m2,alveolar surface-140 m2) Velocity falls rapidly and become zero at alveolar memberane Therefore diffusion, not convection is important for transport in distal airways and alveoli.

29. RESPIRATORY MEMBRANE: diffusion across alveolar-capillary membrane

30. Perfusion of lungs The lung has dual blood supply Pulmonary circulation: Low pressure, high flow circulation Supplies venous blood from all parts of body to alveolar capillaries where oxygen is added and CO2 is removed Supplies deoxygenated blood to lungs to become oxygenated. Starts at Rt atrium--- Rt ventricle----Pulmonary artery----Capillaries----Pulmonary veins-----Lt atrium

31. Pulmonary circulation differs from systemic circulation : It operates 5-10 folds lower pressure,vessels are short and wider. Flow in pulmonary capillaries is pulsatile Capillary and alveolar walls are protected from exposure to high hydrostatic pressure.

32. Bronchial circulation: High pressure,low flow circulation supplies systemic arterial blood to the trachea, the bronchial tree ( including terminal bronchioles), the supporting tissues of the lung, outer coats (adventitia) of the pulmonary arteries and veins. Supplies oxygenated blood to lung tissue. Starts from Aorta---Bronchial arteries---capillaries---Bronchial veins which drain either into pulmonary veins ( i.e. Lt atrium) or right atrium It is 1-2% of cardiac output

33. Distribution of lung blood flow Based on gravitational distribution of pulmonary artery pressure, West and colleagues divided lung into three zones. This system is based upon pressures in pulmonary artery( P PA ), pulmonary vein(P PV ) and alveolus (P ALV ). ZONE 1 : Apex P ALV > P PA > P PV Zone of no perfusion Constitute additional dead space (V D ) ZONE 2 : Below the apex P PA > P ALV > P PV Perfusion occurs intermittently during systole ZONE 3 : PPA > PPV > PALV Perfusion throughout systole and diastole Gravity increases both PPA and PPV

34. EFFECT OF POSITION ON DISTRIBUTION OF BLOOD FLOW

35. Lung height appeared to account for less than 10 % distribution of flow in either prone or supine position. Some studies have shown preponderance of perfusion to central lung (than peripheral) which can be reversed by application of positive end-expiratory pressure (PEEP).

36. Determinants of blood flow distribution Passive processes Cardiac output b) Lung volume 2)Active processes and pulmonary vascular tone Four major categories: a) Local tissue autocrine or paracrine products b) Alveolar gas concentrations (chiefly hypoxia) c) Neural influences d) Humoral effects

37. Hypoxic pulmonary vasoconstriction HPV is a compensatory mechanism that diverts blood flow away from hypoxic lung region towards better oxygenated regions. Major stimulus for HPV is low alvelolar oxygen tension (P A O 2 ),whether caused by hypoventilation or by breathing gas with a low PO 2 . Pulmonary hypertension , because of vascular remodeling owing to ongoing HPV, can develop in humans at high altitude or in the presence of chronic hypoxemic lung disease.

38. Exact mechanism of HPV is still under investigation. Current data supports a mechanism that smooth muscles mitochondrial electron transport chain act as HPV sensor. Reactive oxygen species are released from complex III of electron transport chain and serve as second messanger to increase calcium in pulmonary artery smooth muscles. Elevated PaCO2 has vasoconstrictor effect.

39. Clinical effects of HPV Life at high altitude or whole lung respiration of a low inspired concentration of O2 increases PPa . Increased PPa increases perfusion in apices of lung, which result in gas exchange in region of lung not normally used. High altitude pulmonary artery hypertension is an important component in development of mountain sickness subacutely (hours to days) and cor pulmonale chronically ( weeks to years).

40. 2) Hypoventilation,atelactasis causes diversion of blood flow away from hypoxic to nonhypoxic lung. 3) In patients with COPD,asthma,pneumonia administration of vasodilator drugs inhibits HPV and causes decrease in PaO2 and PVR.

41. Ventilation perfusion relationship Discrepancy between ventilation and blood flow in the lung will result in ventilation perfusion (V/Q) mismatch. If flow of blood to the lung unit is to match that of ventilation to the same unit then the ratio of ventilation to perfusion should be in a ratio of 1:1 If lung is being underventilated but perfused as normal ; V/Q <1 If lung is underperfused ; V/Q >1 V/Q ratio at the apices = 3.3 V/Q ratio at base = 0.6

42. Ventilation perfusion relationship

43. Shunt Shunt refers to V/Q = 0 Ventilation perfusion mismatch is also referred to as shunt. Physiological shunt refers to amount of venous admixture which is directly added to main circulatory blood without having passed through the oxygenating mechanism of the lung. Blood from bronchial veins draining the lung parenchyma and the the besian veins draining the cardiac muscle represent the physiological shunt.

44. Shunt equation : Also known as Berggren equation .

45. Dead Space ventilation Dead space and alveolar ventilation in normal and diseased lungs. Either cessation of blood flow or excessive alveolar ventilation relative to perfusion will cause an increase in dead space (VD). If VD is increased, a large compensatory increase in minute ventilation is required to preserve ˙VA.VD/VT, dead space to tidal volume ratio; ˙VA , alveolar ventilation; ˙VE, minute ventilation. ˙VE =˙VA + f × VD. Double arrows indicate normal CO2 exchange

46. Isoshunt curves showing effect of varying amount of shunt on PaO2

47. RESPIRATORY MECHANICS DURING ANESTHESIA LUNG VOLUME :- FRC is maintained by a balance of the forces inward (lung recoil) versus forces out-ward (chest wall recoil, chest wall muscles, diaphragm) Resting lung volume (i.e., FRC) is reduced by almost 1 L by moving from upright to supine position; induction of anesthesia further decreases the FRC by approximately 0.5 L.This reduces the FRC from approximately 3.5 to 2 L, a value close to RV. General anesthesia causes a fall in FRC (approximately 20%) COMPLIANCE AND RESISTANCE :- Static compliance of the total respiratory system (lungs and chest wall) is reduced on average from 95 to 60 mL/cmH2O during anesthesia. Anesthesia increases respiratory reisitance , especially during mechanical ventilation.

48. ATELECTASIS DURING ANESTHESIA “atelectasis” as a cause of impaired oxygenation and reduced respiratory compliance during anesthesia Atelectasis develops in approximately 90% of patients who are anesthetized. 15% to 20% of the lung is atelectatic during uneventful anesthesia. Degree of atelectasis is larger After thoracic surgery Cardiopulmonary bypass Abdominal surgery (adds little to the atelectasis, but after such surgery, it can persist for several days) Increased body mass index (BMI) Directly proportional to inspired oxygen concentration

49. Anesthetized patient with atelectasis in the dependent regions of both lungs

50. Atelectasis and distribution of ventilation and blood flow

51. PREVENTION OF ATELECTASIS DURING ANESTHEISA Positive End-Expiratory pressure(PEEP):- PEEP of 7 cm H2O in normal-weight patients (BMI < 25 kg/m2) will recruit most of the lung. NOTE:-SaO2 may decrease during the application of increased PEEP for two reasons. First, the negative circulatory effect of high PEEP and presence of an intrapulmonary shunt. Second, increased PEEP can cause redistribution of blood flow away from the aerated, expanded regions(distended by PEEP) toward atelectatic areas. 2. Recruitment Maneuvers :- A large VT, has been suggested for reversing atelectasis. Paw of 30 cm H2O is required for initial opening, and 40 cm H2O for more complete reversal

52. 3. Minimizing Gas Resorption An alternative approach may be application of CPAP 10 cm H2O permitted the use of 100% inspired O2 without formation of significant degrees of atelectasis The use of 30% versus 100% O2 during induction was demonstrated in a clinical study to eliminate the formation of atelectasis 4. Maintenance of Muscle Tone Intravenous ketamine does not impair muscle tone and is the only individual anesthetic that does not cause atelectasis restoration of respiratory muscle tone by diaphragm pacing. This approach is achieved with phrenic nerve stimulation

53. Computed tomographic scans and ˙VA/˙Q distributions in the lung of a healthy, awake subject during anesthesia (zero positive end- expiratorypressure [ZEEP]) and during anesthesia (10 cm H2O positive end-expiratory pressure [PEEP]). In the awake state, there is no atelectasis and the corre-sponding minor low ˙VA/˙Q distribution (left side of plot) may reflect intermittent airway closure. During anesthesia with ZEEP, atelectasis is apparent inthe lung bases (and the diaphragm has been pushed cranially). The low ˙VA/˙Q has been replaced by atelectasis and large shunt; in addition, a small “ high”˙VA /˙Q mode (right side of plot) may reflect alveolar dead space in upper lung regions. With the addition of PEEP during anesthesia, the collapsed lungtissue has been recruited and the shunt has been reduced considerably. Moreover, the “high” ˙VA/˙Q mode (right side of plot) has significantly increased;this may reflect additional inflation of nonperfused upper lung.

54. V/Q relationship in anaesthtized,open chest and paralysed patient in LDP

55. One lung vs. two lung ventilation physiology

56. 72.5% of the perfusion is directed to the dependent lung during one-lung ventilation, the matching of ventilation in this lung is important for adequate gas exchange. The dependent lung is no longer on the steep (compliant) portion of the volume–pressure curve because of reduced lung volume and FRC. There are several reasons for the reduction in FRC; general anesthesia, paralysis, pressure from abdominal contents, compression by the weight of mediastinal structures, suboptimal positioning on the operating table.

57. Other considerations that impair optimal ventilation to the dependent lung; absorption atelectasis, accumulation of secretions, formation of a fluid transudate in the dependent lung.

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