Basics of in GA Mechanical ventilation .pptx

Basics of mechanical ventilation in general anesthesia

1. BASICS OF MECHANICAL VENTILATION Moderator-Dr Sai Kumar Presenter-Dr Ashiq

2. Definition Mechanical ventilation can be defined as the technique through which gas is moved toward and from the lungs through an external device connected directly to the patient .

3. Mechanical ventilation is a useful modality for patients who are unable to sustain the level of ventilation necessary to maintain the gas exchange functions (oxygenation and carbon dioxide elimination). Regardless of the diagnosis or disease state, patients who require mechanical ventilation generally have developed ventilatory failure, oxygenation failure, or both.

4. Specifically, when a patient fails to ventilate or oxygenate adequately, the problem may be caused by one of six major pathophysiological factors: increased airway resistance (2) changes in lung compliance (3) hypoventilation (4) V/Q mismatch (5) intrapulmonary shunting (6) diffusion defect.

5. Airway resistance is defined as airflow obstruction in the airways. Resistance = Δ Pressure / Δ flow In mechanical ventilation, the degree of airway resistance is primarily affected by the length, size, and patency of the airway, endotracheal tube, and ventilator circuit.

6. The pressure change (DP) in the equation reflects the work of breathing imposed on the patient. Since airway resistance is directly related to pressure change (the work of breathing), an increase in airway resistance means the patient must exert more energy for ventilation

7. Factors Affecting Airway Resistance Airway resistance depends on (1) radii of the airways (total cross-sectional area), (2) length of airways, (3) flow rate (4) density and viscosity of gas.

8. Airflow Resistance The airflow resistance of a patient-ventilator system may be monitored using the pressure-volume (P-V) loop display on a ventilator waveform display. An increased bowing of the P-V loop suggests an overall increase in airflow resistance

9. Lung compliance Lung compliance is volume change (lung expansion) per unit pressure change. C = DV/DP C = compliance, DV = volume change, and DP = pressure change.

10. Low Compliance . Low compliance (high elastance) means that the volume change is small per unit pressure change. Under this condition, the lungs are stiff or noncompliant. In many clinical situations ( e.g.ARDS ), low lung compliance is associated with refractory hypoxemia.

11. Refractory hypoxemia : A persistent low level of oxygen in blood that is not responsive to medium to high concentration of inspired oxygen. It is usually caused by intrapulmonary shunting.

12. High Compliance High compliance means that the volume change is large per unit pressure change. In extreme high compliance situations, exhalation is often incomplete due to lack of elastic recoil by the lungs

13. Static and Dynamic Compliance Static Compliance. Static compliance is calculated by dividing the volume by the pressure (i.e., plateau pressure) measured when the flow is momentarily stopped. When airflow is absent, airway resistance becomes a non-factor. Static compliance reflects the elastic resistance of the lung and chest wall.

14. Dynamic Compliance . Dynamic Compliance . Dynamic compliance is calculated by dividing the volume by the pressure (i.e., peak inspiratory pressure) measured when airflow is present. Dynamic compliance reflects the airway resistance (nonelastic resistance) and the elastic properties of the lung and chest wall (elastic resistance).

15. Pressure-Volume Loop. the P-V loop is essentially a “compliance loop,” and it provides useful information on the characteristics of a patient’s compliance.

16. CLINICAL CONDITIONS LEADING TO MECHANCIAL VENTILATION Depressed Respiratory Drive Excessive Ventilatory Workload Failure of Ventilatory Pump

17. Depressed Respiratory Drive These patients may have normal pulmonary function but the respiratory muscles do not have adequate neuromuscular impulses to function properly.

18. Excessive Ventilatory Workload When it exceeds the patient’s ability to carry out the workload, ventilatory and oxygenation failure ensues and mechanical ventilation becomes necessary.

19. Spontaneous Breathing the diaphragm and other respiratory muscles create gas flow by lowering the pleural, alveolar, and airway pressures. When alveolar and airway pressures drop below atmospheric pressure, air flows into the lungs. Negative pressure ventilation uses this principle by creating a negative pressure on the chest wall. When negative pressure is used for ventilation, the pressures in the airways, alveoli, and pleura are decreased during inspiration

20. Positive pressure ventilation Mechanical ventilation in which the volume is delivered by a positive pressure gradient (i.e., airway pressure higher than alveolar pressure). Under normal conditions, the pressure gradient and tidal volume are directly related

21. However, there are some exceptions to this relationship

22. Airway Pressures peak inspiratory pressure (PIP) : Maximum pressure measured during one respiratory cycle, usually at end-inspiration. Pressure used to deliver tidal volume by overcoming non elastic (airways) and elastic (lung parenchyma) resistance offered by the airways Less than 40 cmH20 It is always greater than alveolar plateau pressure

23. Conditions which increases peak inspiratory pressure Bronchospasm Retained secretions Foreign body in bronchus Kinking of the tube

24. Plateau pressure: The pressure needed to maintain lung inflation in the absence of air flow Obtained by applying inspiratory hold 0.5-2 seconds or occluding exhalation port at end inspiration. The pressure equilibrates throughout the system Less than 30 cm of H₂0

25. Positive end-expiratory pressure (PEEP): PEEP is an airway pressure strategy in ventilation that increases the end-expiratory or baseline airway pressure to a value greater than atmospheric pressure. It is used to treat refractory hypoxemia caused by intrapulmonary shunting

26. Mean Airway Pressure This is the average pressure in the respiratory system over time (taking into account both inhalation and exhalation) Mean airway pressure can be understood as the area under the curve (the integral) of the pressure vs. time graph The pressure in inspiration multiplied by the relative amount of time spent in inspiration added to the pressure in expiration multiplied by the relative amount of time spent in expiration .

27. [PIP( insp time) + PEEP (exp time)]/ ( insp time+ exp time)

28. Positive pressure ventilation is an essential life support measure in the intensive care and extended care environments Some of the Physiological effects of PPV are beneficial while others may cause complications

29. PULMONARY CONSIDERATIONS Spontaneous breathing Diaphragm and other respiratory muscles create gas flow by lowering pleural, alveolar and airway pressures Alveolar and airway pressure < atmospheric pressure = air flows into the lung Negative pressure ventilation uses this principle

30. Positive Pressure Ventilation During positive pressure ventilation gas flow is delivered to the lungs under a positive pressure gradient (airway pressure > alveolar pressure) When positive pressure is used for ventilation, pressures in the airways, alveoli and pleura are increased during inspiration In pressure controlled ventilation --Tidal volume delivered to the lungs is directly related to positive pressure

31. Airway pressures Peak inspiratory pressure(PIP): Max pressure measured during one respiratory cycle usually at end inspiration During pressure controlled ventilation -PIP is PRESET according to estimated TV requirement of the patient When preset pressure is reached – inspiratory phase terminates In conditions of Low compliance and high airway resistance--preset pressure is reached prematurely—patient receives smaller volume

32. During volume controlled ventilation – the TV volume is preset Pressure used by the ventilator to deliver preset volume is variable PIP at end inspiration is HIGHER –condition of low compliance or high airway resistance and vice versa. In PPV –airway pressures incl PIP and mean airway pressure( mPaw ) are directly related to TV, airway resistance,peak inspiratory flow rate inversely related to compliance mPaw —average pressure within airway during one complete respiratory cycle

33. Compliance In lungs with normal compliance – 50% airway pressure is transmitted to thoracic cavity In non compliant/stiff lung( atelectasis,ARDS ) – pressure transmitted to thoracic cavity is less—higher levels of PIP or PEEP (positive end expiratory pressure)is required to ventilate or oxygenate the patient PEEP-airway pressure strategy in ventilation that increases end expiratory or baseline airway pressure to value greater than atm pressure.

34. CARDIOVASCULAR CONSIDERATION HIGHER mPaw –LOWER Cardiac output PPV---Increases mPaw and decreases CO. mPaw –is a function of Inspiratory time Respratory rate PIP PEEP These parameters should be kept minimum to keep mPaw at lowest level

35. Decrease in cardiac output and oxygen delivery

36. Blood pressure changes During spontaneous breathing there is transient decrease of arterial BP Pulsus paradoxus: In cardiac tamponade/acute asthma exacerbation this transient decrease in systolic BP becomes exaggerated(>10 mmhg decrease ) During PPV: Reverse Pulsus paradoxus is observed—arterial BP is higher than the measured during spontaneous breathing Mechanism– reduction in left ventricular afterload Significant reverse pulsus paradox (increase in SBP>15 mmHg) during PPV—sensitive indicator of Hypovolemia In Patients with Cardiopulmonary d/s or compromised cardiovascular reserve –PPV and PEEP—further lower venous return

37. Pulmonary Blood flow and thoracic pump mechanism Thoracic pump mechanism During inspiratory phase of PPV—pulmonary blood vessels are compressed—blood flow from RV LV Decreased During expiratory phase of PPV – Pulmonary vessels are no longer under high pressure and large TV-- blood flow from RV LV Increased During PPV—Intra thoracic pressure changes—affect pulmonary blood flow entering and leaving ventricles In Hypotensive pts—increase in TV causes decrease in pulmonary venous return to left ventricle In hypertensive pts—increase in TV causes increase in venous return to left ventricle—because compression of pulmonary vessels is minimal in hypertensive pts

38. HEMODYNAMIC CONSIDERATIONS Major Hemodynamic changes affected by PPV are CVP and PAP Central venous pressure(CVP)—Pressure measured in the vena cava or right atrium. It reflects status of blood volume in systemic circulation—Right ventricular preload. Pulmonary artery pressure(PAP)—Pressure measured in the pulmonary artery. It reflects the volume status of the pulmonary artery and functions of the ventricles—Right ventricular afterload.

39. RENAL CONSIDERATION PPV—Decrease in blood flow—Renal perfusion is decreased—urine output decreased If hypoperfusion of kidneys persists—renal failure

40. HEPATIC CONSIDERATION PPV alone does not alter the blood flow to the liver PEEP is added to mechanical ventilation hepatic blood flow is noticeably reduced PEEP—Decrease in cardiac output—decrease in hepatic blood flow

41. ABDOMINAL CONSIDERATION Elevated Intra abdominal pressure transmits excessive pressure across diaphragm to the heart and great vessels — decreased cardiac output and renal perfusion Use of PEEP > 15 CM H2O in the presence of high IAP >20 mmHg—cardiovascular, renal and pulmonary dysfunction

42. GASTROINTESTINAL CONSIDERATION PPV—decreased of perfusion to the GI tract causes Erosive esophagitis Stress related mucosal damage Diarrhea Decreased bowel sounds constipation

43. NUTRITIONAL CONSIDERATION Malnutrition in critically ill pts—create muscle fatigue, ventilatory insufficiency, ventilatory failure—lead to need for mechanical ventilation Muscle fatigue—work of breathing can be affected by mechanical abberations such as changes in airway resistance and chest wall compliance Diaphragmatic Dysfunction—Prolonged mechanical ventilation—muscle proteolysis and decrease in myofiber content

44. NEUROLOGICAL CONSIDERATION During mechanical ventilation—intentional hyperventilation—constrict these blood vessels—minimise intracranial pressure Sustained hyperventilation >24 hours causes respiratory alkalosis, reducing cerebral blood flow and intracranial pressure If hyperventilation is prolonged cerebral tissue hypoxia may result due to leftward shift of the oxyhaemoglobin curve.

45. Reference Clinical application of Mechanical ventilation-David W.Chang

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