anesthesisa and airway physiology anesthesia

anestheic implications of respiratory physiology

1. Respiratory physiology Presenter: Dr. MEDHA MODERATOR: DR. SANTOSH MAM

2. MECHANICS OF BREATHING DISTRIBUTION OF VENTILATION & PERFUSION IN LUNG WEST ZONES HYPOXIA SHUNTS What is This Lecture About?

3. Mechanism of breathing Inspiration (active process ) Air moves in. occurs when the alveolar pressure < atmospheric pressure Gases move from an area of high pressure to low pressure Expiration (passive process) Breathing out occurs when the alveolar pressure > atmospheric pressure Air moves out because pressure inside is HIGHER than OUTSIDE atmosphere

4. Sternocleidomastoid Scalenes group (anterior and middle) Pectoralis minor Serratus anterior Abdominal recti External oblique Internal oblique Transversus abdominis Internal intercostal Muscles of inspiration Muscle of expiration ACCESSORY MUSCLES ACCESSORY MUSCLES Diaphragm (75%) External intercostal muscle(25%) Passive process

5. Movement of diaphragm During inspiration diaphragm contracts (75 %) Thoracic cavity descends 1.5 to 7 cm. Intra-thoracic volume increases thus intra thoracic pressure decreases (BOYLE’S LAW)

6. Relaxation of the diaphragm causes expiration due to the elastic recoil. Elastic work done during inspiration stored as potential energy is used for expiration. Thus expiration is normally a passive process.

7. Mechanics of rib cage during inspiration Accessory muscles of inspiration also increase chest volume by their action on the ribs . Pump handle motion at rib cage : S ternum moves upward and forward thus increases anterior-posterior dimensions of rib cage. (2-6 th rib ).

8. Buckle handle motion: Increases lateral dimension of rib cage (7-10 th rib)

9. Respiratory pressures Intra-alveolar pressure : at end of inspiration and expiration= atmospheric pressure=760mmHg (considered zero) Intra-pleural pressure : at end expiration , intrapleural pressure normally averages about -5cm of H2O during inspiration chest expands and intrapleural pressure decreases from -5cm of H2O to -8 to -9 cm of H2O Trans–pulmonary pressure : alveolar pressure- intrapleural pressure

10. inspiration Normal Breathing Commences with active contraction of inspiratory muscles, which, a. enlarges the thorax b. lowers intrathoracic and intrapleural pressures c. enlarges alveoli, bronchioles, bronchi d. lowers the alveolar pressure below atmospheric pressure Air flows from mouth and nose to alveoli

11. INSPIRATION 760 mm Hg 754 mmHg Lungs Intrapleural pressure Airways Atmosphere Pleural Sac Thoracic Wall 759mm Hg Intra-pleural pressure= 754- 760= -6mmHg Intra- alveolar pressure = 759 -760= -1mmHg Trans-pulmonary pressure = 759-754 = +5 mmHg

12. expiration Return of ribs to rest position causes diminishing of lung volume Return of diaphragm to rest position also causes diminishing of lung volume Diminishing of lung volume causes pressure in lung to raise to a higher value than atmospheric pressure Air flows out of the lung s

13. EXPIRATION 760 mm Hg 758 mmHg Lungs Intrapleural pressure Airways Atmosphere Pleural Sac Thoracic Wall 761 mm Hg Intra-pleural pressure =758-760= -2mmHg Intra- alveolar pressure = 761-760= +1mm Hg Trans – pulmonary pressure = 761-758= +3mmHg

14. Pressure change during quiet breathing

15. VENTILATION/PERFUSION RATIO : It is the ratio of alveolar ventilation and the amount of blood that perfuse the alveoli. Normal lung perfusion (i.e., CO) = 5L/min Normal alveolar ventilation= 4.2L/min Thus , V/Q= 0.84 At apex V/Q = 3 At base V/Q = 0.6

16. The V/Q ratio <1 near the base of the lung due to the relatively high perfusion in this area compared to ventilation .(increased shunt fraction) The V/Q ratio >1 near at the apex of the lung due to the relatively low perfusion in this area compared to ventilation. (increased dead space) An increase in dead space ,Q=0, e.g. in a pulmonary embolus, results in a V/Q ratio of infinity . If V=0 i.e. shunted blood e.g., atelectasis , V/Q ratio is zero .

17. Pulmonary venous blood from areas with low v/q ratios has a low o2 tension and high co2 tension. Point 1 :  PERFUSION>VENTILATION Oxygen levels fall as a consequence of reduced delivery due to low ventilation. Carbon dioxide increases as perfusion is not affected, and continues to deliver CO 2  to the lungs. Point 3 : VENTILATION=PERFUSION In this situation, ventilation and perfusion are fairly evenly matched Point 5 : VENTILATION>PERFUSION Oxygen levels are high as ventilation is in excess. However, CO 2  levels fall as it is not being delivered back to the lung due to poor perfusion. .

18. Ventilation/perfusion ratio less than one The P A O 2  gradually falls and the P A CO 2  rises. Thus, PaO2 also falls . When ventilation is completely abolished , the P A O 2  and P A CO 2  and end-capillary blood are the same as in mixed venous blood . ( ABSOLUTE SHUNT) At this point V/Q ratio=0 .

19. Problems with lung ventilation, resulting in low V/Qratio . This is the most common cause of hypoxaemia . CAUSES OF LOW V/Q: upper airway obstruction foreign body aspiration Pneumonia Pneumothorax Atelectasis ARDS Emphysema one-lung ventilation normal ageing increased CC associated with obesity.

20. Ventilation/perfusion greater than one When there is no perfusion , PO 2  and PCO 2  are the same as in the inspired air , as no gas transfer is taking place . (DEAD SPACE) At this point the ratio is infinity (∞).

21. Problems with lung perfusion, resulting in high V/Q ratio. CAUSES OF HIGH V/Q: Pulmonary embolism reduced Right ventricular stroke volume (SV) due to hypovolaemia , right ventricular infarction ,pericardial tamponade .

22. WEST ZONES OF LUNG Zone 1: Ventilation(V) >>> Perfusion(Q) V/Q= 3.4 (high) Zone 2 : Ventilation(V) = Perfusion(Q) V/Q= 0.8 (average) Zone 3: Perfusion(Q) >>> Ventilation(V) V/Q=0.63(low)

23. 25-04-2012 27 Zone 1  A lveolar pressure exceeds systolic pulmonary artery pressure, so capillary is compressed- no blood flow , no gas exchange, hence wasted ventilation-alveolar dead space . Under normal conditions little or no zone 1 exists. Can exist in : hypovolemic shock (low Pa) large tidal volume ventilation or high PEEP ventilation during IPPV (high P A )

24. 25-04-2012 28 In zone 2  alveolar pressure exceeds venous pressure causing compression of the venous end of pulmonary capillary (from apex to hilum ). Capillary blood flow is dependant on the arterial-alveolar pressure difference . Blood only flows through the pulmonary capillary only during systole, intermittent flow .

25. WATERFALL EFFECT- The height of the upstream river before reaching the dam is the Pa & the height of the dam is the PA. So the rate of water flow over the dam is equivalent to the diff between the height of the upstream river & the height of the dam(Pa-PA). It does not matter how far below the dam the height of the downstream river bed is- Pv . Also known as STARLING resistor, WEIR / SLUICE effect.

26. 25-04-2012 30 In zone 3  both arterial and venous pressure exceeds alveolar pressure. The capillary systems are thus permanently open and blood flow is continuous. (below hilum ) In this region, blood flow is governed by the pulmonary arteriovenous pressure difference ( P pa - P pv )

27. For accurate measurement of pulmonary capillary wedge pressure , the pulmonary artery catheter must wedge in a pulmonary artery within WEST ZONE 3, it is essential that the PAC is in communication with an uninterrupted static column of blood between the pulmonary artery and left atrium.

28. 25-04-2012 32 In zone 4  Pa > P ISF > Pv > PA In pulmonary edema or is possibly at a very low lung volume. B lood flow is governed by the arteriointerstitial pressure difference ( P a - PISF), which is less than P a - P v difference, and therefore zone 4 blood flow is less than zone 3. This produces positive interstitial pressure, which causes compression of extra-alveolar vessels, increased extra alveolar vascular resistance, and decreased regional blood flow.

29. Hypoxic pulmonary vasoconstriction, directs blood away from poorly ventilated alveoli. Blood is instead redirected to well-ventilated regions normalising V/Q ratio. OTHER THEORIES FOR V/Q RATIO VARIATION IN LUNG Embryonic development- structural similarities btw pulmonary arteries and bronchioles

30. Shunts : Shunt refers to blood that enters the arterial circulation without passing through ventilated lung. In a normal lung there is a small amount of blood shunted which reduces arterial PO 2  (P a O 2 ). (Physiological shunt) THREE-COMPARTMENT MODEL OF GAS EXCHANGE

31. Venous admixture: Venous admixture is defined as the calculated amount of mixed venous blood which would be required to mix with the blood draining ideal alveoli to produce the observed difference between the ideal alveolar and arterial PO2. Normal venous admixture is primarily due to communication between deep bronchial veins and pulmonary veins, the thebesian circulation in the heart, and areas of low but finite V/Q in the lungs. The venous admixture in normal individuals (physiological shunt) is typically less than 5%.

32. 25-04-2012 45 Interpretation of shunt percent (%) Physiological shunt Interpretation < 10% Normal 10% - 20% Mild Shunt 20%-30% Significant Shunt 30% Critical and severe Shunt Intrapulmonary shunts are often classified as absolute or relative. Absolute shunt refers to anatomic shunts and lung units where VA/Q is zero. A relative shunt is an area of the lung with a low but finite VA/Q ratio.

33. 25-04-2012 46 Classification of causes of shunt. PHYSIOLOGICAL SHUNT (NORMAL SHUNT) PATHOLOGICAL SHUNT (ABNORMAL SHUNT) EXTRA-PULMONARY Thebesian veins Bronchial vein Congenital disease of heart or great vessels with RIGHT TO LEFT SHUNT. INTRA-PULMONARY Areas of lung with V/Q>0 and <1 Atelectasis Pulmonary edema, Pulmonary contusions, Pulmonary hemorrhage Pulmonary infections (pneumonia, consolidation) Pulmonary arteriovenous shunts, Pulmonary neoplasms including haemangioma .

34. The degree of shunt can be calculated using the shunt equation When there is a shunt, the arterial oxygen content(CaO 2 ), is the sum of the oxygen content in the shunted blood and the end-capillary blood(CcO 2 ), The oxygen content in the shunted blood is the same as the mixed venous content (CvO 2 ) as it does not pass through a ventilated lung . DO2 (ml/min) = Q x CaO2 Therefore :                                                                               

35. Shunt fraction of the total cardiac output, i.e., Qs/Q T calculated clinically by obtaining mixed venous (from pulmonary artery catheter) and ABG measurements. We assume the end capillary O2 tension to be equal to the P A O 2. The alveolar gas equation is used to derive P A O2 PAO2 = {FiO2 x ( P atm –PH2O)} – (PaCO2/ Resp Q) P A O 2 = {0.21 x (760 –47)} – (PaCO 2 /0.8) CO2 (ml/dL) = ( S p O2 x Hb x 1.34 ml/dl blood ) + (PO2 x0.003 ml O2/dl blood/mmHg )

36. S hunt causes a decrease in PaO2 but unlike hypoventilation, shunt  does not  cause an increase in P a CO 2 . This is because any increase in CO 2  in the shunted blood is detected by chemoreceptors and causes ventilation to increase . Relative shunt can usually be partially corrected by increasing the inspired O 2 conc. by increasing the dissolved O2 conc. i n blood whereas hypoxemia caused by an absolute shunt cannot.

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