Pulmonary Pitfalls

Pitfalls in the Management of Mechanical Ventilation: ARDS and Hypermetabolic States

Brooks T. Kuhn, MD; Jimmy Nguyen, RRT; Nicholas J. Kenyon, MD, MAS; and Jason Y. Adams, MD, MS

Authors:
Brooks T. Kuhn, MD; Jimmy Nguyen, RRT; Nicholas J. Kenyon, MD, MAS; and Jason Y. Adams, MD, MS

Citation:
Kuhn BT, Nguyen J, Kenyon NJ, Adams JY. Pitfalls in the management of mechanical ventilation: ARDS and hypermetabolic states. Consultant. 2017;57(5):289-292,295.


 

Mechanical ventilation (MV) is a lifesaving intervention for patients with respiratory failure due to acute respiratory distress syndrome (ARDS) and septic shock. ARDS was first recognized in the late 1960s, approximately 20 to 30 years after the implementation of the first generation of mechanical ventilators.1,2 As stressed in the previously published first part of this review,3 understanding the underlying physiologic derangements leading to endotracheal intubation and MV is the most important aspect of managing mechanical ventilators. In this review, we provide pragmatic recommendations for the MV management of ARDS and hypermetabolic diseases such as sepsis that are commonly managed by nonintensivist providers.

Acute Respiratory Distress Syndrome

ARDS is a common syndrome resulting from myriad inflammatory insults and is characterized by diffuse bilateral alveolar and endothelial injury, edema, loss of surfactant, and subsequent regional atelectasis leading to hypoxemic respiratory failure (Figure 1). Early approaches to ARDS focused on improving oxygenation by using large tidal volumes (TVs) to combat atelectasis. While oxygenation does initially improve with higher TV (eg, 12 mL/kg of predicted body weight), repetitive opening and closing of alveoli (atelectrauma), alveolar rupture (barotrauma), and excessive alveolar distention (volutrauma) result in ventilator-induced lung injury,4 ultimately leading to increased mortality compared with a strategy of lung-protective MV that includes lower TVs (eg, 6 mL/kg of predicted body weight).5 The deleterious effects of volutrauma and atelectrauma have no immediate manifestations in terms of vital signs or patient discomfort but instead result in progressive worsening of lung injury that is difficult if not impossible to distinguish from worsening of the underlying disease process that caused ARDS initially. Table 1 describes common pitfalls in the management of patients with ARDS who require MV.

severe ARDS figure 1
A chest radiograph of a patient with severe ARDS. Note the bilateral patchy alveolar filling abnormalities.

managing patients with ARDS table 1

 

Despite the clear and reproducible benefit of a low-tidal-volume ventilation (LTVV) strategy and avoiding alveolar collapse through the use of positive end-expiratory pressure (PEEP), adoption in clinical practice has been slow.4-6 Santamaria and colleagues6 demonstrated a mere 13% adherence to LTVV over the 14-year period after publication of the ARDS Network trial.5 While the use of actual rather than predicted body weight when calculating the target TV may in part explain nonadherence to LTVV (predicted body weight, which determines lung size, is determined by height and sex and does not vary with actual body weight), underrecognition of ARDS by health care providers remains a serious but modifiable problem.6,7

Targeting low TVs presents challenges, including patient-ventilator asynchrony (PVA) and hypercapnia. LTVV results in relative hypoxemia and hypercarbia, which increase patient ventilatory drive and often make it difficult to maintain low TVs and synchronous patient-ventilator interactions. Even after optimizing the respiratory rate (by increasing it so that each new breath triggers immediately after the previous exhalation is complete), the increased physiologic dead space commonly seen in ARDS can contribute further to respiratory acidosis.8

One aspect of LTVV known as “permissive hypercapnia” tolerates hemodynamically acceptable levels of acidemia (typically a pH > 7.2) in order to achieve lung-protective TVs, but the effects of low pH and high arterial carbon dioxide on ventilatory drive paradoxically may result in increased difficulty maintaining low TV in pressure-limited modes of MV and substantially more PVA in both pressure and volume-limited modes. As a result, deep sedation is often required in early ARDS to decrease respiratory drive. Emerging evidence from animal models suggests that permissive hypercapnia and the resulting acidosis may have direct lung-protective effects in ARDS, but no clinical trials have been performed in humans.9

PVA, colloquially referred to as “bucking the vent,” occurs when a patient’s ventilatory demands are not matched by assistance from the mechanical ventilator. PVA occurs frequently with MV, identified in 10% to 63.5% of patients.10 PVA is a general term for a number of stereotypical patient-ventilator interactions, including ineffective patient triggering of ventilator-delivered breaths (the patient attempts to breathe but does not receive a breath from the ventilator), double triggering (2 breaths delivered in rapid sequence without exhalation in between), delayed breath termination (the patient attempts to exhale before the ventilator will allow exhalation), and flow asynchrony (the patient attempts to inhale rapidly, but flow is delivered slowly by the ventilator) (Figure 2).11,12

double triggers figure 2
Double-trigger asynchrony occurs when a patient wants a longer breath than the ventilator is programmed to give (neural inspiratory time [Ti] > ventilator Ti), such that a second breath is immediately triggered before any meaningful exhalation, functionally doubling the inspired tidal volume. Delayed termination occurs when the patient begins exhalation while the ventilator is still providing inspiratory support. The ventilator does not allow expiratory flow at this time, and pressure increases as the patient attempts to exhale against a closed expiratory valve (neural Ti < ventilator Ti). Ineffective or “failed” triggers occur when the patient attempts a breath but cannot meet the predetermined pressure or flow threshold for the ventilator to trigger a breath.11,12

 

Discussion >> 

PVA is associated with prolonged time on MV, subjective dyspnea, increased work of breathing, and increased use of sedative medications.13,14 PVA may result in significant patient discomfort and agitation. While sedation may need to be increased for patients with refractory discomfort or agitation, the first intervention should always involve bedside assessment for PVA and appropriate adjustment of ventilator settings (Table 2). Adjusting settings, such as changing the set inspiratory time or changing the MV mode, has been shown to be more effective than increasing sedation for some types of PVA.14

ventilator settings for patients with ARDS table 2

Because the primary outward manifestation of ARDS is hypoxemia, there is often a temptation to use high doses of inhaled oxygen. While it is appropriate immediately after intubation, rapid de-escalation to the minimal fraction of inspired oxygen (Fio2) required is recommended, since high doses of oxygen (typically > 0.50) carry a risk of lung injury due to the formation of oxygen free radicals.15

Recently, Panwar and colleagues16 showed no harm in targeting lower oxygen saturation goals of 88% to 92% compared with a target of greater than 96%. In addition to avoiding oxygen toxicity, targeting an oxygen saturation between 88% and 96% improves the diagnostic utility of pulse oximetry to detect worsening gas exchange. An unnecessarily high Fio2 that results in an oxygen saturation (Sao2) of 100% can mask physiologic worsening until the point where the arterial partial pressure of oxygen (Pao2) finally falls to a value close to the inflection point of the oxygen-hemoglobin dissociation curve, potentially delaying clinical attention. Titrating Fio2 to target a saturation of 88% to 96% allows immediate recognition of clinical deterioration, which should then prompt an evaluation for potential causes of worsening lung function. Due to the negligible effect of dissolved oxygen on the oxygen-carrying capacity of blood, there is very little difference in tissue oxygen delivery when targeting Sao2 in the lower 90s compared with higher targets.

If unable to decrease the Fio2 to less than 0.50, higher PEEP should be considered in accordance with an “open lung” approach. The ideal amount of PEEP varies based on factors such as lung compliance, distribution of lung injury, and hemodynamic stability.17 The National Heart, Lung, and Blood Institute’s ARDS Network provides a free online ventilator protocol card with PEEP titration tables18 to guide the management of PEEP and Fio2 in patients with ARDS, with a target Pao2 range from 55 to 80 mm Hg.5,19 While controversy still exists about the use of lower vs higher PEEP titration strategies, Briel and colleagues19 found a modest mortality benefit in the subgroup of ARDS patients with moderate to severe disease with the use of the higher PEEP strategy. Whether using the lower or higher PEEP strategy, further increases in PEEP should always come with a consideration of the potential hemodynamic effects (increasing intrathoracic pressure decreases preload and increases pulmonary vascular resistance, often leading to hypotension), potential overdistention of alveoli causing paradoxical worsening of oxygenation and ventilation, and a potential increase in the risk of pneumothorax from barotrauma.17,20

The risk of ventilator-induced lung injury in patients with ARDS has clearly been reduced with LTVV. More recent studies have also suggested benefit from LTVV in mechanically ventilated patients without ARDS, including patients requiring perioperative MV.20-22 These studies suggest that broader application of lung-protective ventilation may become part of the standard management of all patients requiring MV in the future. While definitive studies are lacking at this time, we feel it is reasonable to attempt to prevent volutrauma through the application of LTVV (6-8 mL/kg of predicted body weight) in all mechanically ventilated patients unless clear indications for higher TV exist. As stated above, LTVV may be difficult to apply without significant sedation and the availability of team members who are capable of making frequent adjustments to the ventilator; therefore, decisions weighing the potential risks and benefits of LTVV should be made on an individual basis.

 

Septic Shock >>

Sepsis and Septic Shock

Sepsis is associated with substantial respiratory morbidity and mortality, including a high incidence of ARDS. ARDS occurs in 18% to 38% of patients with severe sepsis/septic shock and portends worse outcomes for both diseases: higher disease severity scores, more prolonged recovery from ARDS with less-successful extubation, and higher mortality compared with nonsepsis ARDS.23

The Society of Critical Care Medicine’s Surviving Sepsis Campaign24 recognizes the intimate relationship between sepsis and respiratory failure requiring MV and makes recommendations about the management of patients on MV, including regular spontaneous breathing trials (after hemodynamic stability has been achieved without use of vasopressors), measures to prevent ventilator-associated pneumonia (head of bed elevation, oral hygiene, etc), and LTVV for all patients with sepsis, not just those with ARDS. While a fluid-restrictive strategy is recommended for patients with sepsis and ARDS, this does not apply to patients with persistent shock.20,25

Aside from patients with concurrent ARDS, the management of sepsis may require MV due to pulmonary edema from large volume fluid resuscitation, for airway protection due to a depressed level of consciousness, or for respiratory muscle fatigue resulting from the high minute ventilation required to compensate for lactic acidosis. In the immediate postintubation period, failure to set an adequate minute ventilation on the ventilator can lead to worsening acidosis and shock, especially when LTVV is instituted. While healthy adults require approximately 4 to 6 L/min (or approximately 1 L/min/10 kg of predicted body weight), patients with profound metabolic acidosis (as in sepsis or diabetic ketoacidosis) can require minute ventilations twice their normal predicted rate.

Pulmonary edema is a frequent concern during fluid resuscitation for septic shock. The Surviving Sepsis Campaign recommends that a fluid challenge technique be applied in which fluid administration is continued as long as there is hemodynamic improvement.24 Careful quantitative fluid resuscitation with well-defined clinical end points is critical to ensuring adequate end-organ perfusion while avoiding excessive fluid administration.

In sepsis, pulmonary edema does not develop from elevated pulmonary venous hydrostatic pressure alone; rather, it is influenced strongly by capillary leak and inflammation such that MV may be unavoidable when acute lung injury is the mechanism for edema formation.26 In the Early Goal-Directed Therapy trial,27 the intervention group received almost 1500 mL more fluid in the first 6 hours than the control group but had no difference in the need for MV. At 72 hours, the 2 groups had no difference in volume received, but patients in the intervention group had a 15% relative risk reduction in MV. Therefore, pulmonary edema and the potential need for MV should be monitored carefully during resuscitation, but concern for pulmonary edema should not deter from fluid administration in patients in whom indexes of end-organ perfusion are clearly improving with ongoing fluid resuscitation.

In septic shock, the hemodynamic effects of PEEP must be weighed against the potential benefits with regard to ensuring adequate oxygenation and prevention of ventilator-induced lung injury (atelectrauma), especially when ARDS is also present. PEEP can adversely affect hemodynamics by increasing intrathoracic pressure, reducing preload, and increasing right ventricular afterload.28 In patients with septic shock, PEEP can lead to lower blood pressure, especially in those who have not been adequately fluid resuscitated. The benefits of PEEP in the management of acute respiratory failure need to be balanced with its potentially deleterious hemodynamic effects. The lowest tolerable PEEP should be used to achieve oxygenation targets, and patients should be assessed frequently with regard to the need for additional fluid administration vs the use of vasoactive medications to ensure that resuscitation end points are maintained during PEEP titration.

Save Lives and Do No Harm

MV is an invaluable, lifesaving therapy for patients with acute respiratory failure, but it must be individualized for each specific underlying physiologic derangement to maximize benefits and minimize harms. Early optimization of ventilator settings should be aimed at counteracting respiratory and cardiac pathophysiology, fully supporting the work of breathing, preventing ventilator-induced lung injury, and minimizing PVA.

Improper MV management in the first few hours can be dangerous. It is not a “set it and forget it” intervention but instead requires frequent and careful attention to patient-ventilator interactions and close collaboration with the entire intensive care unit team, including bedside nurses and respiratory therapists, to ensure that ventilator settings are continually adjusted to meet patient needs. 

Non–critical care-trained clinicians can use their comprehensive understanding of pathophysiology in combination with a practical understanding of MV in commonly encountered diseases to successfully manage acute respiratory failure in patients requiring MV.

Brooks T. Kuhn, MD, is an assistant professor of medicine in the Department of Internal Medicine, Division of Pulmonary, Critical Care, and Sleep Medicine at UC Davis Medical Center in Sacramento, California.

Jimmy Nguyen, RRT, is registered respiratory therapist in the Department of Respiratory Care at UC Davis Medical Center.

Nicholas J. Kenyon, MD, MAS, is a professor of medicine and chief of the Division of Pulmonary, Critical Care, and Sleep Medicine at UC Davis Medical Center.

Jason Y. Adams, MD, MS, is an assistant professor of medicine in the Department of Internal Medicine, Division of Pulmonary, Critical Care, and Sleep Medicine at UC Davis Medical Center.

REFERENCES:

  1. Ashbaugh DG, Bigelow DB, Petty TL, Levine BE. Acute respiratory distress in adults. Lancet. 1967;290(7511):319-323.
  2. Kacmarek RM. The mechanical ventilator: past, present, and future. Respir Care. 2011;56(8):1170-1180.
  3. Kuhn BT, Nguyen J, Kenyon NJ, Adams JY. Pitfalls in the initial management of mechanical ventilation: COPD and asthma. Consultant. 2017;57(2):​94-98.
  4. Slutsky AS, Ranieri VM. Ventilator-induced lung injury. N Engl J Med. 2013;​369(22):2126-2136.
  5. Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342(18):1301-1308.
  6. Santamaria JD, Tobin AE, Reid DA. Do we practise low tidal-volume ventilation in the intensive care unit? A 14-year audit. Crit Care Resusc. 2015;​17(2):108-112.
  7. Fröhlich S, Murphy N, Doolan A, Ryan O, Boylan J. Acute respiratory distress syndrome: underrecognition by clinicians. J Crit Care. 2013;28(5):663-668.
  8. Nuckton TJ, Alonso JA, Kallet RH, et al. Pulmonary dead-space fraction as a risk factor for death in the acute respiratory distress syndrome. N Engl J Med. 2002;346(17):1281-1286.
  9. Dewhirst E, Corridore M, Klamar J, et al. Accuracy of the CNAP monitor, a noninvasive continuous blood pressure device, in providing beat-to-beat blood pressure readings in the prone position. J Clin Anesth. 2013;25(4):​309-313.
  10. Gutierrez G, Ballarino GJ, Turkan H, et al. Automatic detection of patient-ventilator asynchrony by spectral analysis of airway flow. Crit Care. 2011;15(4):R167.
  11. Gilstrap D, MacIntyre N. Patient–ventilator interactions: implications for clinical management. Am J Respir Crit Care Med. 2013;188(9):1058-1068.
  12. Mellott KG, Grap MJ, Munro CL, et al. Patient ventilator asynchrony in critically ill adults: frequency and types. Heart Lung. 2014;43(3):231-243.
  13. Piquilloud L, Vignaux L, Bialais E, et al. Neurally adjusted ventilatory assist improves patient-ventilator interaction. Intensive Care Med. 2011;37(2):263-271.
  14. Chanques G, Kress JP, Pohlman A, et al. Impact of ventilator adjustment and sedation–analgesia practices on severe asynchrony in patients ventilated in assist-control mode. Crit Care Med. 2013;41(9):2177-2187.
  15. Jackson RM. Pulmonary oxygen toxicity. Chest. 1985;88(6):900-905.
  16. Panwar R, Hardie M, Bellomo R, et al; CLOSE Study Investigators; ANZICS Clinical Trials Group. Conservative versus liberal oxygenation targets for mechanically ventilated patients. A pilot multicenter randomized controlled trial. Am J Respir Crit Care Med. 2016;193(1):43-51.
  17. Mercat A, Richard J-CM, Vielle B, et al; Expiratory Pressure (Express) Study Group. Positive end-expiratory pressure setting in adults with acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA. 2008;299(6):646-655.
  18. NIH NHLBI ARDS Clinical Network mechanical ventilation protocol summary. http://www.ardsnet.org/files/ventilator_protocol_2008-07.pdf. Accessed April 12, 2017.
  19. Briel M, Meade M, Mercat A, et al. Higher vs lower positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome: systematic review and meta-analysis. JAMA. 2010;303(9):865-873.
  20. Wilson JG, Matthay MA. Mechanical ventilation in acute hypoxemic respiratory failure: a review of new strategies for the practicing hospitalist. J Hosp Med. 2014;9(7):469-475.
  21. Serpa Neto A, Simonis FD, Barbas CSV, et al. Association between tidal volume size, duration of ventilation, and sedation needs in patients without acute respiratory distress syndrome: an individual patient data meta-analysis. Intensive Care Med. 2014;40(7):950-957.
  22. Serpa Neto A, Cardoso SO, Manetta JA, et al. Association between use of lung-protective ventilation with lower tidal volumes and clinical outcomes among patients without acute respiratory distress syndrome: a meta-analysis. JAMA. 2012;308(16):1651-1659.
  23. Sheu C-C, Gong MN, Zhai R, et al. Clinical characteristics and outcomes of sepsis-related vs non-sepsis-related ARDS. Chest. 2010;138(3):559-567.
  24. Society of Critical Care Medicine. Surviving Sepsis Campaign. http://www.survivingsepsis.org. Accessed April 12, 2017.
  25. Bernard GR. Acute respiratory distress syndrome: a historical perspective. Am J Respir Crit Care Med. 2005;172(7):798-806.
  26. Marik P, Bellomo R. A rational approach to fluid therapy in sepsis. Br J Anaesth. 2016;116(3):339-349.
  27. Rivers E, Nguyen B, Havstad S, et al; Early Goal-Directed Therapy Collaborative Group. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345(19):1368-1377.
  28. Luecke T, Pelosi P. Clinical review: positive end-expiratory pressure and cardiac output. Crit Care. 2005;9(6):607-621.