COMPLICATIONS OF Mechanical ventilations

Historically, structures were ventilated using natural means, such as opening a window or door to let fresh air into a space. However, with greater air-sealing methodologies on the rise, this method is insufficient. Enter mechanical ventilation, which offers several options for moving stale indoor air out and fresh outdoor air inside. The different types include exhaust, supply, balanced and energy recovery.

In this brief white paper, we’ll take a look at each mechanical ventilation option, and discuss how they work, their benefits and any concerns that exist. We’ll get to the “how and what” of ventilation, but let’s start with the “why.” Why do we even need ventilation in the first place? The answer is to support the health and wellbeing of indoor occupants by improving the quality of the air they brea

1. COMPLICATIONS OF MECHANICAL VENTILATION MODERATOR-DR.ANITHA MAM (ASSOCIATE PROFFESSOR) PRESENTER-DR.J.VAISHNAVI (2 ND YR PG)

2. OUTLINE 1)DEFINITION & INDICATIONS OF MECHANICAL VENTILATION 2)PULMONARY COMPLICATIONS 3)CARDIOVASCULAR COMPLICATIONS 4)RENAL COMPLICATIONS 5)GIT COMPLICATIONS 6)NEUROLOGICAL COMPLICATIONS

3. INDICATIONS OF MECHANICAL VENTILATION

4. PULMONARY EFFECTS 1)BAROTRAUMA 2)VENTILATOR ASSOCIATED LUNG INJURY 3)ASPIRATION AND VENTILATOR-ASSOCIATED PNEUMONIA 4)ENDOTRACHEAL TUBE COMPLICATIONS 5)RESPIRATORY MUSCLE WEAKNESS 6)REDUCED MUCOCILIARY MOTILITY

5. NON PULMONARY EFFECTS 1)CARDIOVASCULAR: Hypotension Falsely elevated hemodynamic measurements Venous thromboembolism 2)GASTROINSTESTINAL: Stress ulceration Hypomotility 3)ACUTE KIDNEY INJURY

6. 4)NEUROLOGIC : Peripheral neuromuscular weakness Increased intracranial pressure Disordered sleep 5)NUTRITIONAL COMPLICATIONS:

7. PULMONARY COMPLICATIONS 1)VENTILATOR ASSOCIATED LUNG INJURY 2)BAROTRAUMA 3)ASPIRATION AND VENTILATOR-ASSOCIATED PNEUMONIA 4)ENDOTRACHEAL TUBE COMPLICATIONS 5)RESPIRATORY MUSCLE WEAKNESS 6)REDUCED MUCOCILIARY MOTILITY

8. VENTILATOR ASSOCIATED LUNG INJURY Refers to alveolar injury caused by mechanical ventilation. This is distinct from barotrauma (which is alveolar rupture caused by high pressures). High distending pressure > 30 cm H2o Pulmonary edema Mainly due to: 1) Increased filtration due to a)increased Pulmonary capillary permeability b)decreased Lung interstitial pressure 2) Alteration in capillary permeability

9. ROLE OF INFLAMMATORY MEDIATORS: High tidal volume with zero end expiratory pressure results in release of 1)TNF ALPHA 2)INTERLEUKIN 1 BETA 3)INTERLEUKIN 6 4)MACROPHAGE INFLAMMATORY PROTEIN 2(MIP-2)

10. VALI is associated with alveolar edema and increased permeability caused by large tidal volumes irrespective of airway pressures. High risk- 1)receiving large tidal volumes, 2) with underlying restrictive lung diseases, 3)with ALI/ARDS and 4)who have received blood transfusions.

11. Even physiologic or low tidal volumes can lead to VALI in some patients. In patients with atelectasis, air tends to flow  towards more compliant alveoli (i.e. the ones that are already open)  may overdistend them. Furthermore those portions of the lung which are atelectatic but are being opened with each breath (cyclic atelectasis) are also prone to lung injury due to shear forces associated with this.

12. PREVENTION STRATEGIES 1)P revent alveolar overdistension by employing low tidal volume ventilation. The general recommendation is to use tidal volumes of 8ml/kg of ideal BW  to gradually keep lowering this by 1 ml/kg / lbw to get to the lowest tidal volume which the patient tolerates whilst providing acceptable oxygenation and ventilation. Mild acidosis and hypercapnia should be tolerated. 2)T o prevent collapse of alveoli during expiration and hence preventing cyclic atelectasis. 3) PRONE POSITION :Due to homogeneous distribution of tidal volume because of downward displacement of diaphragm.

13. PHARMACOLOGIC INTERVENTION : 1) NF-KBETA Inhibited by Dexamethasone 2)Interleukin 1 receptor antagonists 3)Anti- TNF ALPHA antibody

14. BAROTRAUMA Barotrauma is described as lung tissue injury or rupture that results from the shearing force of alveolar over distention. End inspiratory plateau pressure -only variable correlated with occurrence of barotrauma. Risk of barotrauma is high when: PIP> 50 cm H2O, Plateau pressure >35 cm H2O, Mean airway pressures > 30 cm H2O, and PEEP > 10 cm H2O COPD patients are more susceptible to barotrauma presumably due to air trapping and weakened parenchymal areas (e.g., lung blebs and bullae).

15. POSSIBLE MECHANISMS FOR BAROTRAUMA IN MV PATIENTS Airway disruption/Alveolar rupture prior to intiation of MV Airway laceration Trauma Attempted central line placement Direct laceration of visceral pleura Complication of VAP Inadvertent alveolar distension Related to ventilator management ( TV,PEEP,Recruitment maneuvers )

16. MECHANISM OF ALVEOLAR RUPTURE

17. Other lung injuries that may occur as a result of positive pressure ventilation include pulmonary interstitial emphysema, pneumomediastinum, pneumoperitoneum, pneumothorax, tension pneumothorax, and subcutaneous emphysema.

18. Suggestive of barotrauma In a mechanically ventilated patient Sudden desaturation Tachypnoea Tachycardia Hypotension Rise in peak airway pressures Reduced breath sounds on one side/tracheal deviation Chest x ray should be done

19. MANAGEMENT Pneumothorax ,Systemic air embolism-require immediate treatment. Ventilator adjustments include: 1)Reducing PEEP 2)Reducing TIDAL VOLUME 3)Reducing MINUTE VENTILATION To the lowest compatible values with acceptable patient support &consideration of lung protection ventilation and permissive hypercapnia.

20. ATELECTRAUMA Injuries to the lungs that occur because of repeated opening and closing of lung units at lower lung volumes. It can occur in the management of ARDS when low VTs are used and inadequate levels of PEEP are applied . Alveoli tend to open on inspiration and close on expiration. This occurs most often in the dependent areas of the lung. The repeated opening and closing of lung units in ARDS produces three primary types of lung injury: shear stress, alteration and washout of surfactant , and microvascular injury .

21. VENTILATOR ASSOCIATED PNEUMONIA D efined as pneumonia which occurs after 48-hours hours of intubation and mechanical ventilation. E arly recognition and prompt treatment are important. The risk rises with duration of ventilation. Oropharyngeal secretions and leakage of secretions around the cuff are the primary routes of infection. Stomach and the sinuses may also act as reservoirs. Hematogenous spread or infections from aerosolized medications is rare. New onset of fever, purulent sputum, leucocytosis , and desaturation should prompt further investigation. Demonstration of an infiltrate on radiography consistent with a consolidation together with fever, leukocytosis and purulent sputum (two of the latter three) is enough to initiate empiric treatment.

22. CLINICAL PULMONARY INFECTION SCORE

23. PREVENTION: Efforts should be made to minimize the risk of aspiration. Elevating the head of the bed to 30°, minimizing sedation or paralysis, frequent suctioning of subglottic secretions and maintaining the cuff pressure at least 20cm H 2 O are measures which may limit aspiration. In addition, there is evidence that decontaminating the oral cavity with chlorhexidine swabs has reduced incidence of VAP. Prophylactic antibiotics too can reduce incidence of VAP but are not routinely recommended because of the risk of developing resistant pathogens.

24. AUTOPEEP It refers to hyperinflation of the lungs due to air trapping . It is caused by initiation of inspiration before expiration is complete. It can be caused by 1)large tidal volumes, 2)high respiratory rate (insufficient time for expiration), 3)obstructive air disease or 4)narrow endotracheal tube.

25. Unchecked AutoPEEP can lead to barotrauma as well as worsening of the hemodynamic effects of positive pressure ventilation (PPV). Increased intrathoracic pressure  decreased venous return  decreased cardiac output and hypotension.. AutoPEEP can also worsen ventilation-perfusion (V/Q) mismatch by compressing capillaries in the healthy part of the lung and diverting blood to the diseased lung. Work of breathing may also be increased because in pressure cycled settings it makes it harder to trigger a breath.

26. AutoPEEP should be suspected when ventilator/patient dyssynchrony is seen. Breaths may not be triggered despite visible inspiratory effort. AutoPEEP can also present as sudden hypotension or desaturation. AutoPEEP can be seen by looking at the flow versus time graph. If inspiratory flow begins before expiratory flow has stopped, then AutoPEEP will develop. Treatment : 1) address the underlying cause. 2)lowering the tidal volume, respiratory rate or 3) Increasing the inspiratory flow rate may also help by allowing more time for expiration.

27. OXYGEN TOXICITY Oxygen toxicity, two factors are primarily responsible for oxygen toxicity in the lungs: l) High O2 tension in inspired air, 2)Prolonged exposure to high inspired 0 2 tension. Patients may be at risk of developing 0 2 toxicity if they are given inspired air containing 50% or greater 0 2 concentration for prolonged time. As a general rule, just enough 0 2 concentration in the inspired air should be given to maintain a safe and adequate level of oxygen tension in the arterial blood for a given patient.

28. Pulmonary changes associated with oxygen toxicity DECREASED: 1)Tracheal mucus flow 2)Macrophage activity 3)Surfactant production 4)Compliance 5)Diffusing capacity 6)Pulmonary capillary blood volume

29. CONTINUED OTHER CHANGES 1)Capillary injury 2)Platelet aggregation in the pulmonary vasculature 3)Endothelial cell damage 4)Increased P(A-a)O2

30. ENDOTRACHEAL TUBE COMPLICATIONS ET COMPLICATIONS Damage to the Nasal Passages, Lips, or Eyes • During insertion: Facial trauma, damage to the nasal structures, lips, or eyes • While in place: Lip ulceration, pressure necrosis to the soft tissues, erosion of nasal septum, increased airway resistance from a small lumen tube • During and after extubation : Nasal stricture Damage to the Oropharynx • During insertion: Traumatic damage to the oropharyngeal soft tissues, dental accidents, retropharyngeal or hypopharyngeal perforation • While in place: Grooving of the hard palate from chronic pressure, dental deformities from constant pressure.

31. Damage to the Larynx and Trachea During insertion: Soft tissue damage (bleeding and swelling), laryngeal trauma, laryngospasm While in place: Laryngeal injury (ulceration, edema , bleeding), laryngeal muscle dysfunction, subglottic edema , necrosis over the arytenoid cartilages and the vocal cords, trauma to mucosa covering the cricoid cartilage in infants, necrosis of tissue leading to the innominate artery and uncontrolled bleeding, tracheal injury (ulceration, edema , bleeding, tracheomalacia, cartilage and mucosal necrosis), laryngotracheal web formation, laryngotracheal granuloma, tracheal dilation, irritation of the carina, tracheoesophageal fistula, spontaneous dislocation of the tube (into the right mainstem, too high in trachea, extubation ),

32. During and after extubation : Laryngospasm, Laryngeal edema , glottic injury, laryngotracheal granuloma, Laryngeal stenosis (glottic, subglottic), laryngeal motor dysfunction (vocal cord paralysis), Cricoarytenoid ankylosis, tracheomalacia, tracheal dilation, tracheal stenosis, perichondritis, laryngeal chondritis, laryngotracheal web.

33. Mechanical Problems With Tubes : Disconnection, kinking, obstruction from secretions, patient biting on the tube, displacement of the tube tip into the tracheal endothelial layer or against the side of the trachea or carina Mechanical Problems Associated With the Cuff : Compression of the tube by the cuff, excessive pressure (>25 mm Hg) from overinflation leading to tracheal necrosis, leaking or rupturing of the cuff causing inadequate ventilation, laceration of the cuff during insertion, leaking around the cuff preventing adequate ventilation, damage to the pilot balloon or connection preventing cuff inflation.

34. HEMODYNAMIC EFFECTS Positive pressure ventilation causes decreased cardiac output by decreasing venous return (worsened with high PEEP). PPV also compresses the pulmonary vasculature leading to reduced right ventricular output  to reduced left cardiac output. Applied PEEP also artificially elevates central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP) measurements. In general, fluid resuscitation seems to correct hypotension caused by PPV. However, be aware of flash pulmonary edema after extubation (because sudden removal of PEEP leads to a large venous return). Hence, T piece trial before extubation may be useful in patient who had been mechanically ventilated on a high applied PEEP.

35. 3)GASTROINTESTINAL COMPLICATIONS 1)Acute gastrointestinal bleeding, 2)Acute gastric dilation, ileus, and 3)Chronic aspiration during assisted ventilation.

36. 3)RENAL CHANGES 1. Renal responses to hemodynamic changes resulting from high intrathoracic pressures 2. Humoral responses, including antidiuretic hormone (ADH), atrial natriuretic factor (ANF), and renin-angiotensin aldosterone changes occurring with positive pressure ventilation 3. Abnormal pH, PaCO2, and PaO2 affecting the kidney

37. 1)RENAL RESPONSE TO HEMODYNAMIC CHANGES Initiation of positive pressure ventilation may cause decreased cardiac output  decrease in renal blood flow and glomerular filtration rates and ultimately a decrease in urine output. However, decreases in urine production seen during positive pressure ventilation may not be caused entirely by a decrease in cardiac output because returning cardiac output to adequate levels is not accompanied by a proportional increase in urinary output. Also, because the arterial BP is usually compensated when positive pressure ventilation is used, decreased BP is probably not a significant factor leading to decreased urinary output during mechanical ventilation. Redistribution of blood inside the kidney may actually be an important factor that is responsible for changes in kidney function. Flow to the outer cortex decreases, whereas flow to the inner cortex .

38. 2)ENDOCRINE EFFECTS These include 1)ADH, 2)ANF, and the 3)Renin-angiotensin-aldosterone cascade BP changes during positive pressure ventilation may precipitate ADH release Oliguria.

39. PPV and PEEP can reduce atrial filling pressure by 1)causing mechanical compression of the atria or 2)decreasing right atrial stretch from low venous return  decreased secretion of ANF. Reduced ANF levels contribute to water and sodium retention during positive pressure ventilation. Increased sympathetic tone is associated with increases in plasma renin activity (PRA). This appears to be another major factor in sodium and water retention during positive pressure ventilation and PEEP. The increased PRA activates the renin-angiotensin-aldosterone cascade and results in retention of sodium ( antinatriuresis ) and water (antidiuresis).

40. 3)ARTERIAL BLOOD GASES Changes in PaO2 and PaCO2 contribute to the effects of mechanical ventilation on renal function. Decreasing PaO2 values in patients with respiratory failure have been shown to cause a reduction in renal function and a decrease in urine flow. In fact, PaO2 levels below 40 mm Hg (severe hypoxemia) can dramatically interfere with normal renal function. Similarly, acute hypercapnia (i.e., PaCO2 greater than 65 mm Hg) can also severely impair renal function

41. IMPLICATIONS OF IMPAIRED RENAL EFFECTS Administering positive pressure increases water and sodium retention, resulting in weight gain and in some cases pulmonary edema. To compound this problem, reduced renal function in these patients can complicate fluid and electrolyte management. Additionally, many drugs (e.g., sedatives and neuromuscular blocking agents) and their metabolites are excreted by the kidney. Altered renal function can prolong the effects of these drugs and affect patient care

42. NUTRITIONAL COMPLICATIONS

43. CONTINUED

44. 4)NEUROLOGIC COMPLICATIONS 1) Positive pressure ventilation (with or without PEEP) can decrease cardiac output and MABP, it is reasonable to assume that CPP would also decrease during positive pressure ventilation. 2)Positive pressure ventilation can also reduce CPP by increasing the CVP. In this situation, CPP is reduced because of a reduction in venous return from the head increases ICP. 20-25% of PEEP is transmitted to central venous pressure in normal compliant lung >20% is transmitted to ICP compartment in pts with decreased lung compliance. Reduces stage 4 sleep.

45. MULTIPLE ORGAN DYSFUNCTION SYNDROME Chemical mediators produced in the lung can leak into the pulmonary blood vessels. The circulation then carries these substances to other areas of the body and sets up an inflammatory reaction in other organs, such as the kidneys, gut, and liver. The release of mediators may therefore lead to multiple organ failure, also called multisystem organ failure and multiple organ dysfunction syndrome

46. VENTILATORY INDUCED DIAPHRAGM DYSFUNCTION Delivering high airway pressures and volumes during mechanical ventilation can lead to damage to the lung parenchyma. Recent studies have shown that mechanical ventilation may also cause damage to the respiratory muscles. Specifically, imposing too little stress on the diaphragm during mechanical ventilation by lowering the demands on a patient’s respiratory muscles can induce respiratory muscle weakness.

47. VENTILATOR STRATEGY: The time spent in CMV must be curtailed to the extent possible, especially in older individuals, because the effects of aging and CMV are additive. Although CMV induced similar losses (24%) in diaphragmatic isometric tension in both young and old , the combined effects of aging and CMV resulted in a 34% decrement in diaphragmatic isometric tension as compared to young . Partial support modes should be used.

48. Assisted modes or even noninvasive ventilation in hypercapnic patients with chronic obstructive pulmonary disease is an alternative to the use of CMV in weaning failure patients —a strategy based on the premise that respiratory muscle fatigue (requiring rest to recover) is the cause of weaning failure.

49. VENTILATOR MECHANICAL AND OPERATIONAL HAZARDS

50. REFERENCES 1)PRINCIPLES AND PRACTICE OF MECHANICAL VENTILATION MARTIN J.TOBIN 3 RD EDITION 2)PILBEAMS MECHANICAL VENTILATION 7 TH EDITION 3)CHANG CLINICAL APPLICATION OF MECHANICAL VENTILATION 4 TH EDITION

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