RESPIRATORY physilogy anesthesia ventillation

repiratory physiology anesthesia

1. RESPIRATORY PHYSIOLOGY MODERATED BY PRESENTRD BY Dr Yogesh narwat dr raju gandham Md anaesthesia

2. RESPIRATORY CENTRES OF CNS and CONTROL OF BREATHING Primary portions that control ventilation -Medulla Oblongata & Pons Respiratory centers : Inspiratory centre (DORSAL RESPIRATORY GROUP) Expiratory centre (VENTRAL RESPIRATORY GROUP) Pneumotaxic centre (UPPER PONS) Sends continual inhibitory impulses to inspiratory center of the medulla oblongata, As impulse frequency rises, breathe faster and shallower Apneustic centre (LOWER PONS) Stimulation causes apneusis –deep, gasping inspiration Integrates inspiratory cut off information

3. CENTRAL AND PERIPHERAL CHEMORECEPTORS Central chemoreceptors are located in medulla oblangata of brain stem. They detect changes in arterial pCO2 ,pH (H+) when change is detected ,the receptors send impulses to the respiratory centres in brain stem that initiate changes in ventilation to restore normal pCO2 Detection of increased in pCO2 leads to an increased ventilation , more CO2 is exhaled co2 returns to normal Detection of a decrease in pCO2 leads in decrease in ventilation less CO2 is exhaled CO2 returns to normal The mechanism behind how central chemoreceptors detect changes in arterial pCO2 is complex and related to changes in pH of CSF

4. Peripheral chemoreceptors are located in both the carotid and the aortic body They detect changes in pO2,pH,pco2 as the arterial blood leaves the heart When low levels of oxygen is detected afferent impulses travel via the glossopharyngeal nerve and vagus nerve to medulla oblangata and the pons in brain stem , inducing number of responses The respiratory rate and tidal volume are increased to allow more oxygen to enter the lungs and diffuse o2 in to the blood Blood flow is directed towards kidney and brain Cardiac output is increased in order to maintain blood flow

5. PULMONARY REFLEXES Chemoreceptor Reflexes  monitor pco2,po2 , pH in blood(at aortic , carotid bodies) & CSF(medulla oblongata) Increased pco2 is more powerful stimulus to breath than decreased po2 Baroreceptor Reflexes  Monitor blood pressure (at aortic , carotid sinuses) Protective Reflexes coughing, sneezing Hering Bruer Reflex: Limits degree of inspiration , prevents over inflation of lung , Depends on stretch receptors in the walls of bronchi & bronchioles .An inhibitory influence on respiratory center , results in expiration(as expiration proceeds , stretch receptors are no longer stimulated)

6. OXYGEN CARRIAGE IN BLOOD Hb saturation - amount of O 2 bound by each molecule of Hb 1 molecule of Hb can carry 4 molecules of O 2 When O 2 binds to Hb, it forms OXYHAEMOGLOBIN Hb that is not bound to O 2 referred as DEOXYHAEMOGLOBIN Binding of O 2 to Hb depends on PO 2 in blood OXYGEN CONTENT IN BLOOD 97-98% in Combination With Hb 2-3% dissolved in Plasma CaO 2 = ( SaO 2 × Hb × O 2 combining capacity of Hb ) + ( O 2 solubility × PaO 2 ) where CaO2 (O2 content) is the milliliters of O2 per 100 Ml of blood, SaO2 is the fraction of hemoglobin (Hb) that is saturated with O2, O2-combining capacity of Hb is 1.34 mL ofO2 per gram of Hb, Hb is grams of Hb per 100 mL of blood,Pa o 2 is the O2 tension (i.e., dissolved O2), and solubility of O2 in plasma is 0.003 mL of O2 per 100 mL plasma for each mm Hg Pa o 2

7. OXYGEN FLUX EQUATION Global oxygen delivery describes the amount of oxygen delivered to the tissues in each minute and is a product of the cardiac output and arterial oxygen content DO 2 = CO x CaO2 DO2 = OXYGEN FLUX Normal value( O 2 flux) =1000 mI O 2 / min Normally ,250 ml O 2 /min is taken up in tissues

8. VENOUS 02 CONTENT CvO 2 =(SvO 2 x Hb x 1.34) + (PvO 2 x 0.003) ‒ (normally-15ml/dl) mixed venous saturation (SvO 2 ) - pooled venous saturation from all organs Normally, SvO 2 is about 75% Oxygen Consumption (VO2) can be calculated using Fick principle VO2=Arterial Oxygen Transport – Venous Oxygen Transport VO2 = (CO x CaO2) – (CO x CvO2)

9. OXYGEN CASCADE The oxygen cascade describes the sequential reduction in po2 from atmosphere to cellular mitochondria STEPS Uptake in the lungs Transport in blood Global delivery to tissues Regional distribution of O 2 delivery Diffusion from capillary to individual cell Cellular utilization of O 2

10. PAO2 = PiO2 –PACO2/R

11. OXYGEN DISSOCIATION CURVE   curve  that plots the proportion of  hemoglobin  in its saturated ( oxygen -laden) form on the vertical axis against the prevailing  oxygen tension  on the horizontal axis Sigmoid Shaped Mathematically equates % saturation of Hb with PO 2 in blood Amount of O 2 carried by Hb rises rapidly up to PO 2 of 60mmHg but above that curve becomes flatter Cooperativity – binding of O 2 to one site on Hb molecule facilitates binding of O 2 at other sites

12. Plateau: ► haemoglobin highly saturated with O 2 -> favour the loading of O 2 in lung Steep slope: ► small drop of O 2 partial pressure leads to a rapid decrease in % saturation of haemoglobin ► favour the release of O 2 in tissue cells

13. STEEP PORTION OF CURVE Dissociation Portion Between 10 - 60 mm Hg Small increases in PO 2 yields large increases in SO 2 At tissue capillary, blood comes in contact with reduced tissue PO 2 , O 2 diffuses from capillary to tissue

14. FLAT PORTION OF CURVE Association Portion >60 mm Hg Large increases in PO 2 yields small increase in SO 2 At pulmonary capillary, blood comes in contact with increased alveolar PO 2 , O 2 diffuses from alveolus to the capillary As PO 2 rises, O 2 binds with hemoglobin (increasing SO 2 ) Very little rise in O 2 saturation above 100 mm Hg of PaO 2

15. P50 PO 2 in blood at which Hb is 50% saturated P50 is a conventional measure of Hb affinity for O 2 Normal P50 value - 26.8 mm Hg As P50 increases/decreases, we say “curve has shifted” – P50 < 26.7: left shift, P50 >26.7: right shift

16. BOHR EFFECT Christian Bohr in 1904 hemoglobin's lower affinity for oxygen secondary to increases in the partial pressure of carbon dioxide and/or decreased blood pH High PCO 2 or H + and low pH decrease affinity of Hb for O 2 (right-shift) Occurs at tissues , where a high level of PCO 2 and acidemia contribute to unloading of O 2

17. DOUBLE BOHR EFFECT Reciprocal changes in acid - base balance that occurs in maternal & fetal blood in transit through placenta FETAL BLOOD MATERNAL BLOOD loss of CO 2 gain of CO 2 raise in PH fall in PH left shift of ODC right shift of ODC Fetal hemoglobin has higher affinity to O 2 so as obtain O 2 from maternal blood in the placenta .

18. PHSYIOLOGY OF CO 2 TRANSPORT end-product of aerobic metabolism production averages 200 ml/min in resting adult during exercise , amount may increase 6 times Produced almost entirely in mitochondria T ransport of CO2 : CO 2 is transported in blood from tissues to the lungs in 3 ways - dissolved form -buffered with water as carbonic acid - bound to proteins, particularly Hb Approximately 75% of CO 2 transport by Hb

19. HALDANE EFFECT   oxygenation of blood in the lungs displaces carbon dioxide from hemoglobin, increasing the removal of carbon dioxide Quantitatively more important in promoting CO 2 transport than Bohr effect in promoting O 2 transport Most of H + combine with Hb because reduced Hb is less acidic so better proton acceptor In lungs oxygenation causes unloading of CO 2

20. VENTILATION Ventilation refers to movement of inspired gas into and exhales gas out of the lung ALVEOLAR VENTILATION DEAD SPACE VENTILATION

21. ALVEOLAR VENTILATION Fresh gas enters the lung by cyclic breathing at a rate and depth (TIDAL VOLUME , V T ) determined by metabolic demand , usually 7 to 8L /min. Some of the fresh gas (100 to 150 mL) remains in the airway and doesn’t participate in gas exchange called DEAD SPACE V D (constitutes one third of each V T ) Anatomic dead space V A is the fraction that remains in conducting airway Physiologic V D is any part of V T that doesn’t participates in gas exchange V T = V A + V D

22. The product of V T (mL) times respiratory rate (per minutes ) is the minute ventilation V E V ˙ E = V ˙ A + f × V D The portion of the V E that reaches the alveoli and respiratory bronchioles each minute and participates in gas exchange is called the alveolar ventilation ( V A ) ( approx. 5L/min which is equal to cardiac out put 5l/min ) Hence the overall alveolar ventilation perfusion ratio is approx. 1

23. DEAD SPACE VENTILLATION   T he volume of air that is inhaled that does not take part in the gas exchange Anatomical dead space (100 to 150ml) Physiological dead space( 2mL/kg of body weight ) Alveolar dead space = difference between the physiologic dead space and the anatomic dead space Maintenance of Pa co 2 is a balance between CO2 production ( VCO2 , reflecting metabolic activity) and alveolar ventilation ( VA ). If VE is constant but VD is increased, VA will naturally be reduced, and the Pa co 2 will therefore rise. Therefore, if VD is increased, VE must also increase to prevent a rise in Pa co 2. Such elevations in VD occur when a mouthpiece or facemask is used, and in such cases, the additional VD is termed “apparatus deadspace” (which can be up to 300 mL; anatomic VD of the airways is 100-150 mL).

24. SHUNT shunt occurs in lung that is perfused but poorly ventilated The physiologic shunt (Q˙ SP) is that portion of the total cardiac output (Q˙T) that returns to the left heart and systemic circulation without receiving oxygen in the lung When pulmonary blood is not exposed to alveoli or when those alveoli are devoid of ventilation, the result is absolute or true shunt, in which V˙A/Q˙ = ∞ Shunt effect, or venous admixture, is the more common clinical phenomenon and occurs in areas where alveolar ventilation is deficient compared with the degree of perfusion

25. small percentage of venous blood normally bypasses the right ventricle and empties directly into the left atrium This anatomic, absolute, or true shunt arises from the venous return of the pleural, bronchiolar, and thebesian veins. This venous admixture accounts for 2% to 5% of total cardiac output and represents the small shunt that normally occurs. Anatomic shunts of greatest magnitude are usually associated with congenital heart diseases that cause right-to-left shunt Diseases that may cause absolute or true shunt include acute lobar atelectasis, extensive acute lung injury, advanced pulmonary edema, and consolidated pneumonia. Disease entities that tend to produce venous admixture include mild pulmonary edema, postoperative atelectasis, and COPD.

26. PERFUSION The pulmonary circulation differs from the systemic circulation as it operates at a five to tenfold lower pressure, and the vessels are shorter and wider. There are two important consequences of the particularly low vascular resistance. First, the downstream blood flow in the pulmonary capillaries is pulsatile, in contrast to the more constant systemic capillary flow. Second, the capillary and alveolar walls are protected from exposure to high hydrostatic pressures DISTRIBUTION OF LUNG BLOOD FLOW : Pulmonary blood flow depends on driving pressure and vascular resistance; these factors (and flow) are not homogenous throughout the lung.

27. DISTRIBUTION OF BLOOD FLOW IN THE LUNG AND THE EFFECT OF GRAVITY Blood has weight hence its been affected by gravity The height of an adult lung is approx. 25 cm When an adult is standing the hydrostatic pressure at the base is 25 cm of H2O (18 mm of Hg) and 12 mm of Hg at heart level Hence the pulmonary artery pressure at the apex approx. approaches to zero , so less blood flow occurs at the apex Based on gravitational distribution of pulmonary artery west and colleagues divided the lung zones based on the principle that perfusion depends to an alveolus depends on the pressure in pulmonary artery ,pulmonary vein and alveolus

28. Lung zones and distribution of blood flow in the lung

29. HYPOXIC PULMONARY VASOCONSTRICTION HPV is a compensatory mechanism that diverts blood flow away from hypoxic lung regions toward better oxygenated regions. The major stimulus for HPV is low alveolar oxygen tension (PAO2), whether caused by hypoventilation or by breathing gas with a low PO2, and is more potent when affecting a smaller lung region.

30. LUNG VOLUME AND CAPACITIES TI D AL V O L UM E (T V ): Tidal volume is the volume of gas that moves in and out of the lungs during quiet breathing and is about 500mL INSPIRATORY RESERVE VOLUME (IRV ): Maximum volume that can be inspired over the inspiration of a tidal volume/normal breath. Used during exercise/exertion.= Male 3100 ml/ Female 1900 ml EXPIRATRY RESERVE VOLUME (ERV) : Maximal volume that can be expired after the expiration of a tidal volume/normal breath. = Male 1200 ml/ Female 700 ml RESIDUAL VOLUME (RV): Following maximum expiratory effort, some air is left in the lung and constitutes the RV (ABOUT 2L)

31. INSPIRATORY CAPACITY is the largest volume of gas that can be inspired from the resting expiratory level (4500ML) VITAL CAPACITY The maximum volume that can be inhaled and then exhaled is the vital capacity (4 TO 6L ). TOTAL LUNG CAPACITY The gas volume in the lung after a maximum inspiration is called the total lung capacity (USUALLY 6L ).

32. LUNG VOLUMES AND CAPACITIES

33. FUNCTIONAL RESIDUAL CAPACITY is the volume of gas held in the lungs at a normal relaxed end expiratory point Significance: Allows continuous exchange of gases Preoxygenation – fills FRC with O 2 ,prior to intubation Prevent early desaturation during apnoea Load on Rt. Ventricle is reduced as collapsed lung increases PVR Factors affecting FRC: FRC Increased in- PEEP, CPAP, Emphysema , Asthma , Erect/propped up position FRC Decreased in – Obesity, Supine & Trendelenburg position , Pregnancy , Sedation, M. Gravis, Poliomyelitis ,Restrictive lung disease , Pneumothorax

34. CLOSING CAPACITY : Volume of lung at which small airways in the dependent parts of the lung begin to collapse during expiration Mathematically – sum of closing volume & the residual volume Normally, it is less than FRC Unlike FRC it is unaffected by posture , It gradually raises with age

35. DYNAMIC TESTS FOR VENTILLATION MAXIMUM BREATHING CAPACITY (MBC): designed to measure the speed and efficacy of filling and emptying the lung during increased effort and it defined as the maximum volume of air that can be breathed per minute.(ranges from 100 to 200 L/min) FORCED EXPIRATORY VOLUME (FEV): the patient makes a maximal inspiration and expires forcefully into spirometer and the total amount of air expelled out in a given times is measured in intervals of 0.5, 1 , 2 , 3seconds.usually FEV1 is measured expressed in percentage in young adults its about 83% of vital capacity PEAK EXPIRATORY FLOW RATE(PEFR) after maximal inspiration patient expires as forcefully as he can and the maximum flow rate of air is measured .indicates ventilation adequacy and obstructive airway

36. THE WORK OF BREATHING The energy required to ventilate the lungs to overcome certain forces which tend to prevent lungs being inflated is work of breathing There are 3 essential components in this opposition 1.The forces needed to overcome the elastic resistance of the lung 2.the forces to move non-elastic tissues of lung (structural resistance ) 3. the force to overcome resistance to the flow of air through trachea bronchial tree

37. COMPLIANCE Compliance — Change in lung volume (lung expansion ) per unit pressure change C = Δ V/ Δ P Lesser the distending pressure required , more compliant it is it is usually 0.2 to 0.3 L/cm H2O Lung compliance depends on the lung volume; it is lowest at an extremely low or high FRC In lung diseases characterized by reduced compliance (e.g., ARDS, pulmonary fibrosis, or edema), the pressure-volume (PV) curve is flatter and shifted to the right

38. P-V curve of lungs Slope of the curve indicates compliance ( Δ V/ Δ P ) High compliance around FRC(normal tidal respiration operates in this region),hence small changes in transpulmonary pressure causes large distension of lungs Curve flattens out near TLC as stretch ability of the elastin fibers near their maximum

39. TYPES OF COMPLIANCE Static Compliance measured when there is no airflow , reflects elastic resistance of lung & chest wall measures from 40-60 ml/cm H 2 O in critically ill patients Static Compliance ( ) = Plateau pressure is the pressure needed to maintain lung inflation in absence of air flow. Dynamic compliance measured when airflow is present Reflects condition of airway resistance & elastic properties of lung & chest wall Measures from 30-40 ml/cm H2O in critically ill patients Dynamic Compliance ( ) = PIP is pressure used to deliver tidal volume by overcoming non elastic (airway) and elastic (lung parenchyma) resistance.  

40. Specific compliance measures intrinsic elastic property of lung tissue similar value in both sexes & all ages Normally measures 0.05/cm H 2 O Specific Compliance =  

41. Factors affecting compliance Lung elastic recoil - surface tension Lung volume Gravity Diseased states Variations in compliance High compliance emphysema, asthma, ageing Exhalation is often inadequate due to lack of elastic recoil of lung Low static compliance fibrosis , ARDS, tension pneumothorax , atelectasis, obesity, retained secretion Work of breathing is high as lungs are stiff Low dynamic compliance Bronchospasm, airway obstruction

42. Compliance Curve

43. Resistance R esistance is the change in transpulmonary pressure needed to produce a unit flow of gas through the airways of the lung Resistance impedes airflow into (and out of) the lung. The major component of resistance is the resistance exerted by the airways (large and small), and a minor component is the sliding of lung and the chest wall tissue elements during inspiration (and expiration) Resistance is overcome by (driving) pressure. Resistance (R) is calculated as driving pressure ( Δ P) divided by the resultant gas flow (F): R = Δ P/F

44. Elastic resistance— the force tending to return lung to its original size after stretching Structural resistance —composed of thoracic wall, diaphragm & abdominal contents. related to the speed of air flow Air resistance —dependent on length & size of lumen of bronchial tree. Extra air resistance added on when endotracheal tube inserted DEPENDING ON THE LAMINAR OR TURBULENT FLOW PRESSURE REQUIRED CHANGES Airway resistance is constant where flow is laminar Airway resistance increases exponentially with increasing flow where flow is turbulent Under most normal conditions the airflow in human airways is mainly laminar because the flow rates ar relatively low With increasing flow, flow in the airways may transition from laminar to turbulent flow

45. Factors which affect airway resistance Effects of bronchial smooth muscle tone: Increased smooth muscle tone Bronchospasm Irritants, eg. histamine Parasympathetic nervous system agonists Decreased smooth muscle tone Bronchodilators Sympathetic nervous system agonists Decreased internal cross section Oedema Mucosal or smooth muscle hypertrophy Encrusted secretions Mechanical obstruction or compression Extrinsic, eg. by tumour Dynamic compression, eg. due to gas trapping or forceful expiratory effort Artificial airways and their complications, eg. endotracheal tube becoming kinked 

46. ANAESTHESIA IMPLICATIONS ON RESPIRATORY PHYSIOLOGY Effect on upper airway- GA causes relaxation of jaw and pharyngeal muscles and leads to posterior displacement of tongue Effect on volumes Anesthesia causes respiratory impairment by mismatch in alveolar ventilation ( Va ) and perfusion (Q). Effects on functional residual capacity Anesthesia leads to fall in FRC despite maintaining spontaneous breathing and irrespective of anesthetic used Effects of pre-oxygenation The higher oxygen concentration, used during pre-oxygenation, leads to faster gas adsorption and consequently collapse of alveoli and atelectasis.  Effect on dead space The distribution of pulmonary blood flow is altered during anesthesia due to increased mismatch of ventilation to perfusion ratios ( Va /Q ratio) Effect on ventilatory response Anesthesia depresses movements of intercostal muscles, alters the shape and motion of chest wall and diminish rib cage excursion affecting lung mechanics and consequent decrease in FRC and ventilatory response to CO

47. Effect on hypoxic pulmonary vaso constriction volatile anaesthetic agents suppress HPV in a dose-dependent manner Effect of position In the supine position, the contribution of the chest wall is reduced from 30% to 10% and diaphragmatic movements close to most dependent portions of lung are significantly restricted Effect of mechanical ventilation Mechanical ventilation with high VT may directly damage lung parenchyma by shearing stress in alveoli, which results in interstitial oedema, decreased lung compliance and gas transfer EFFECTS OF REGIONAL ANAESTHESIA During high spinal anaesthesia , owing to paralysis of abdominal muscles, there is a decrease in expiratory reserve volume and consequently the vital capacity, which may impair forced exhalation and ability to cough EFFECTS OF DRUGS USED DURING ANAESTHESIA Barbiturates , prpophol , ketamine , Inhalational agents ,

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