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Respiratory physiology in awake and anaesthetized patients

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Respiratory physiology
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Respiratory physiology in awake and anaesthetized patients

  1. 1. Respiratory Physiology in awake and anaesthetized patients Moderator: Dr Ramesh Kumar Presented by: Dr Puneet Verma
  2. 2. Ventilation • Ventilation refers to movement of gas into and exhaled gas out of lungs. • Alveolar Ventilation: The portion of the minute ventilation that reaches the alveoli and respiratory bronchioles each minute and participates in gas exchange is called the alveolar ventilation , and it is approximately 5 L/min. • Dead space ventilation: The portion of minute ventilation that can not participate in gas exchange, it can either be anatomic dead space or physiologic dead space.
  3. 3. LUNG VOLUMES&CAPACITIES 1.PULMONARY VOLUMES: a)Tidal volume b)Inspiratory reserve volume c)Expiratory reserve volume d)Residual volume 2.PUMONARY CAPACITIES: a)Inspiratory capacity b)Functional residual capacity c)Vital capacity d)Total lung capacity
  4. 4. LUNG VOLUMES&CAPACITIES • Tidal volume : The volume of gas that moves in and out of the lungs during quiet breathing and is 6 to 8 mL/kg. Tidal volume falls with decreased lung compliance or when the patient has reduced ventilatory muscle strength. • Inspiratory reserve volume: The maximal amount of additional air that can be drawn into the lungs by determined effort after normal inspiration. • Expiratory reserve volume: The additional amount of air that can be expired from the lungs by determined effort after normal expiration. • Residual volume: The volume of air still remaining in the lungs after the most forcible expiration possible. • Inspiratory capacity: It is the largest volume of gas that can be inspired from the resting expiratory level and is frequently decreased in the presence of signiicant extrathoracic airway obstruction. • FUNCTIONAL RESIDUAL CAPACITY: FRC is defined as the volume of gas in the lung at the end of a normal expiration when there is no airflow. Under these conditions, expansive chest wall elastic forces are exactly balanced by retractive lung tissue elastic forces. • Vital capacity: Volume of air that can be forcibly exhaled after a full inspiration. • Total lung capacity: The volume of air contained in the lungs at the end of a maximal inspiration.
  5. 5. Transport of Respiratory Gases in Blood Oxygen • O2 is carried in blood in two forms: • 1 :Dissolved Oxygen: • The amount of O2 dissolved in blood can be derived from Henry's law i.e. concentration of any gas in solution is proportional to its partial pressure. • The solubility coefficient for O2 at normal body temperature is 0.003 mL/dL per mmHg • Even with a PaO2 of 100 mm Hg, the maximum amount of O2 dissolved in blood is very small (0.3 mL/dL) compared with that bound to hemoglobin. • 2: Associated with hemoglobin • Each gram of hemoglobin can theoretically carry up to 1.34 mL of O2. • Each hemoglobin molecule binds up to four O2 molecules • The complex interaction between the hemoglobin subunits results in nonlinear binding with O2 represented by Oxygen-Hb dissociation curve. • Oxygen content of blood can be denoted by equation – CaO2 =(SaO2 × Hb × O2 combining capacity of Hb) + (O2 solubility × PaO2)
  6. 6. Oxygen hemoglobin dissociation curve
  7. 7. Factors influencing oxygen-Hb dissociation curve • A rightward shift in the oxygen–hemoglobin dissociation curve lowers O2 affinity, displaces O2 from hemoglobin, and makes more O2 available to tissues; a leftward shift increases hemoglobin's affinity for O2, reducing its availability to tissues • The normal P50 in adults is 26.6 mm Hg (3.4 kPa) • Left-shifted oxy-Hb curve: Alkalosis (metabolic and respiratory—the Bohr effect), hypothermia, abnormal fetal Hb, carboxyhemoglobin, methemoglobin, and decreased RBC 2,3-diphosphoglycerate (2,3-DPG) content. • Decreased RBC 2,3-diphosphoglycerate (2,3-DPG) content may occur with the transfusion of blood stored in acid citrate-dextrose solution, reducing O2 delivery to tissues; storage of blood in citrate-phosphate-dextrose minimizes changes in 2,3-DPG with time. • Right-shifted oxy-Hb curve: Acidosis (metabolic and respiratory—the Bohr effect), hyperthermia, abnormal Hb, increased RBC 2,3-DPG content.
  8. 8. Carbon dioxide 1. Dissolved Carbon Dioxide(7%) Carbon dioxide is more soluble in blood than O2, with a solubility coefficient of 0.03 mmol/L/mm Hg at 37°C. 2. Bicarbonate(80%) In plasma, although less than 1% of the dissolved CO2 undergoes this reaction, the presence of the enzyme carbonic anhydrase within erythrocytes and endothelium greatly accelerates the reaction. As a result, bicarbonate represents the largest fraction of the CO2 in blood 3. Carbamino Compounds(13%) At physiological pH, only a small amount of CO2 is carried in this form, mainly as carbamino-hemoglobin.
  9. 9. Bohr and Haldane Effects • Bohr Effect: – It describes the effect of PCO2 and [H+] ions on the oxy-Hb curve. – In the systemic capillaries, the Pco2 is higher than in the arterial blood (and the pH correspondingly lower) because of local CO2 production. These circumstances shift the Hb-O2 dissociation curve to the right, which increases the offloading of O2 to the tissues. – In the pulmonary capillaries; the Paco2 is lower (and the pH correspondingly higher) because of CO2 elimination, and the dissociation curve is shifted to the left to facilitate O2 binding to Hb. • Haldane Effect: – Increased Pao2 decreases the ability to form carbamino compounds reducing the amount of CO2 bound to Hb—thereby raising the amount of dissolved CO2 (i.e., elevated Pco2). – This effect is responsible for occasional hypercapnia induced by supplemental oxygen.
  10. 10. Distribution of pulmonary perfusion Perfusion Zone Characterestics Zone 1 PA>Ppa>Ppv •Vessels collapsed. •Dead space/wasted ventilation Zone 2 Ppa>PA>Ppv •Blood flow is determined by mean Ppa-PA Zone 3 Ppa>Ppv>PA •Vascular pressures exceed PA. •Blood flow is continuous. Zone 4 Ppa>PISF>Ppv>P A •Fluid can transduate into interstitial compartment in dependent parts at high Ppa values. •Blood flow is governed by arteriointerstitial difference Ppa-PISF. •Flow is lesser then in zone 3.
  11. 11. Lung Compliance Distribution of Ventilation • Compliance: It expresses how much distention occurs for a given level of transpulmonary pressure (PTP). • Gravity causes differences in vertical Pleural pressure (Ppl), which in turn causes differences in regional alveolar volume, compliance, and ventilation. • There is relatively more negative pressure at the top of the pleural space (where the lung pulls away from the chest wall) and relatively less negative pressure at the bottom of the lung (where the lung is compressed against the chest wall). • Dependent alveoli are relatively compliant (steep slope), and nondependent alveoli are relatively noncompliant (flat slope). Therefore, most of the tidal volume is preferentially distributed to dependent alveoli which expand more per unit pressure change than the nondependent alveoli.
  12. 12. Airway Closure • Expiration causes the airways to narrow, and deep expiration can cause them to close. • The volume remaining above RV where expiration below FRC closes some airways is termed closing volume (CV), and this volume added to the RV is termed the closing capacity (CC; i.e., the total capacity of the lung at which closing can occur).
  13. 13. The Ventilation Perfusion Ratio • Blood flow and ventilation increase linearly down the normal upright lung. • Blood flow increases from a very low value and more rapidly than ventilation does with distance down the lung. • The ventilation-perfusion ratio (VA/Q) decreases rapidly at first and then more slowly. • VA/Q best expresses the amount of ventilation relative to perfusion in any given lung region. It is less then 1 in overperfused regions and more then one in overventilated regions.
  14. 14. Nongravitational determinants of blood flow distribution • 1. Passive Processes A: Cardiac output Pulmonary vascular bed is a high flow- low pressure system. Pulmonary vascular pressures increase minimally with increase in flow. Increase in flow distend open vessels and recruit previously closed vessels, which decreases PVR. Decrease in flow decrease pressure and radii of pulmonary vessels and PVR consequently increases. B: Lung Volume PVR is minimal at FRC. At volumes above FRC, PVR increases due to alveolar compression of small intra alveolar vessels. At volumes below FRC, PVR increases due to mechanical effect in large vessels and due to hypoxic pulmonary vasoconstriction.
  15. 15. Hypoxic Pulmonary Vasoconstriction • It 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). • The HPV response occurs primarily in pulmonary arterioles of about 200 μm internal diameter (ID) in humans. • HPV probably results from a direct action of alveolar hypoxia on pulmonary smooth muscle cells, sensed by the mitochondrial electron transport chain, with reactive O2 species (probably H2O2 or superoxide) serving as second messengers to increase calcium and smooth muscle vasoconstriction. • Elevated PaCO2 has a pulmonary vasoconstrictor effect. Both respiratory acidosis and metabolic acidosis augment HPV, whereas respiratory and metabolic alkalosis cause pulmonary vasodilation and serve to reduce HPV. • Mitral stenosis, volume overload, thromboembolism, hypothermia, vasoactive drugs can decrease HPV by increasing pulmonary artery pressure. • Direct vasodilating drugs (e.g., isoproterenol, nitroglycerin, sodium nitroprusside), inhaled anesthetics and hypocapnia can directly decrease HPV.
  16. 16. • 2. Active Processes and Pulmonary vascular tone – TISSUE (ENDOTHELIAL- AND SMOOTH MUSCLE–DERIVED) PRODUCTS • Vasodilatation: Nitric oxide, Prostaglandin PGI2, Endothelin(ETB receptor on endothelium) • Vasoconstriction: Prostaglandin PGF2a, Thromboxane A2, Leucotrine, Endothelin(ETA receptor on smooth muscle). – ALVEOLAR GASES • Hypoxia induced vasoconstriction in pulmonary arterioles. • Elevated Paco2 also has pulmonary vasoconstrictor effect. – NEURAL INFLUENCES ON PULMONARY VASCULAR TONE • Sympathetic fibers cause pulmonary vasoconstriction through α1-receptors. • Parasympathetic (cholinergic) nerve fibers originate from the vagus nerve and cause pulmonary vasodilation through an NO-dependent process. • NANC nerves cause pulmonary vasodilation through NO-mediated systems by using vasoactive intestinal peptide as the neurotransmitter. – HUMORAL INFLUENCES ON PULMONARY VASCULAR TONE • Vasodilatation: Histamine, Substance P, Bradykinin, Vasopressin. • Vasoconstriction: Epinephrine, Norepinephrine, Serotonin, Neurokinin A, Angiotensin. Nongravitational determinants of blood flow distribution
  17. 17. Nongravitational determinants of blood flow distribution • 3. Alternative (Nonalveolar) Pathways of Blood Flow Through the Lung (right to left shunt) – Bronchial and Pleural circulation : 1 to 3% of cardiac output normally and upto 10% of CO in chronic bronchitis and 5% in pleuritis. – Intrapulmonary arteriovenous malformations. – Patent foramen ovale.
  18. 18. Lung volume and respiratory mechanics during anesthesia • Resting lung volume or FRC is reduced by 0.6 to 1 L by changing body position from upright to supine and there is another 0.4 to 0.5 L decrease when anaesthesia is induced. • End expiratory lung volume is thus reduced from approx 3.5 to 2 L almost being close to RV.
  19. 19. ATELECTASIS AND AIRWAY CLOSURE DURING ANESTHESIA • Atelectasis is a complete or partial collapse of a lung or lobe of a lung — develops when the alveoli within the lung become deflated. • Atelectasis develops in approximately 90% of patients who are anesthetized. • In addition to shunt, atelectasis may form a focus of infection and can certainly contribute to pulmonary complications.
  20. 20. PREVENTION OF ATELECTASIS DURING ANESTHESIA • Positive End-Expiratory Pressure: – Application of PEEP (10 cm H2O) has been repeatedly demonstrated to reexpand atelectasis partially. – Higher levels of PEEP impairs venous return and reduce cardiac output specially in presence of hypovolemia. – It can also cause redistribution of blood flow to less aerated regions. • Recruitment Maneuvers: – A sigh maneuver or a large tidal volume is given at an airway pressure 40cm H2O for 7 to 8 seconds. – Such inflation is equivalent to a Vital Capacity and can therefore be called a VC maneuver. • Minimizing Gas Resorption: – 100% oxygen is avoided as it can be absorbed completely leading to recurrance of atelectasis. – VC maneuver followed by ventilation with a gas mixture containing 60%N2 (40% O2) reduced the propensity for reaccumulation of atelectasis with only 20% reappearing 40 minutes after recruitment. • Maintenance of Muscle Tone: – loss of muscle tone in the diaphragm or chest wall appears to increase the risk of atelectasis, techniques that preserve muscle tone may have advantages. – Ketamine does not impair muscle tone and is the only individual anesthetic that does not cause atelectasis. – An experimental approach is restoration of respiratory muscle tone by diaphragm pacing.
  21. 21. Decrease in FRC • Induction of general anesthesia decreases FRC 15 – 20 % • MAX decrease is within the first few minutes • FRC decrease in awake patients is very slight, during spontaneous ventilation • FRC decrease continues into the post operative period • Application of PEEP may restore FRC to normal
  22. 22. Causes of reduced FRC 1. Supine position: FRC is reduced 0.5-1 litres because diaphragm is displaced 4 cm cephalad and pulmonary vascular congestion happens. Changing position every hour is beneficial. 2. Induction of GA: Thoracic cage muscle tone change: loss of inspiratory tone & increase in end expiratory tone (abdominal) increases intra abdominal pressure, displaces diaphragm more cephalad and decreases FRC.
  23. 23. Effect of Surgical position 1. Supine : decrease FRC 2. Trendelenburg: decrease FRC 3. Steep trendelenburg: decrease FRC 4. Lateral decubitus : FRC decrease in dependent lung and increase FRC in un dependent lung (overall FRC increases ) 5. Lithotomy : FRC decrease more than supine 6. Prone : FRC increases
  24. 24. PREEXISTING LUNG DISEASE • ANESTHESIA AND OBSTRUCTIVE PULMONARY DISEASE: – They are at increased risk for reflex bronchoconstriction during laryngoscopy and intubation – aggressive bronchodilator therapy should be used preoperatively. – Increased risk of hypercapnia- Preoperative FEV1 reduction correlates with the Paco2 increase during anesthesia. • ANESTHESIA AND RESTRICTIVE PULMONARY DISEASE: – FRC is reduced, so lower oxygen stores are available during apneic periods. – Increased risk of barotrauma as higher peak airway pressures are required to expand lungs.
  25. 25. Anesthetic Depth and Respiratory Pattern • When the depth of anesthesia is inadequate (less than MAC), the respiratory pattern may vary from excessive hyperventilation and vocalization to breath-holding. • When anesthetic depth approaches MAC (light anesthesia), irregular respiration progresses to a more regular pattern that is associated with a larger than normal tidal volume. • As anesthesia deepens to moderate levels, respiration becomes faster and more regular but shallower. • The respiratory rate is generally slower and the VT larger with nitrous oxide– narcotic anesthesia than with anesthesia involving halogenated drugs. • In the case of very deep anesthesia with all inhaled drugs, respirations often become jerky or gasping in character and irregular in pattern.
  26. 26. Thanks !Thanks !

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