Oxygenate, Ventilate, Do No Harm

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Vent Basics for Emergency Physicians – Part 2 of 3

(Read Part 1 here)

Introduction

The emergency physician must know how to safely manage the ventilated patient. This includes interpretation of waveforms and alarms, proper sedation and implementation of vent bundles that can save lives. As discussed in Part One, your patients will benefit from a lower Vt (tidal volume) of 6-8 ml/kg IBW (ideal body weight), down titration of oxygen to safe levels and higher PEEP in ARDS.

DO NO HARM

Waveforms and Alarms

A working knowledge of the ventilator can help you improve patient mortality and provide the best care possible for your patients. While initially intimidating, ventilator waveforms provide simple, graphical representations of the patient’s pulmonary function. Let’s look at a few waveforms that every emergency physician should know how to measure. The ventilator pressures important to EPs include peak pressure, plateau pressure and end-expiratory pressure (2). Figure 1 is a normal waveform for volume control. In the figures below the top yellow is the pressure waveform, the green is the flow waveform and the bottom blue is volume waveform.

The peak pressure is primarily a reflection of large airway resistance but because it is the sum of plateau pressure and airway resistance, it will also increase as the plateau pressure increases. The gradient between the plateau and peak pressure represents airway resistance and is helpful in determining the cause of a high peak pressure. Patients with airway obstruction (increased airway resistance) will have elevated peak pressure but the plateau will be normal if the lung parenchyma is normal, such as an asthmatic with tight airways but normal alveoli, see Figure 2 (2).

Vents Part 2.fig 1 and 2An increase in peak pressure without an increase in plateau pressure is not itself concerning because unlike a high plateau pressure it should not cause alveolar damage (2). Other causes of high peak pressures but normal plateau pressures would include narrowed ET tube from secretions, tube kinking, small tube size, and bronchospasm (13).  A clinically relevant example is a patient with a new peak pressure alarm-knowing that the peak pressure is from high airway resistance can help the EP generate a quick differential of the immediate causes of the increased pressure.

In addition to mechanical obstructions, a faster flow rate can cause an increase in peak pressure because of airway resistance and turbulent flow. For example if you give 600 ml over 0.7 second instead of 1.0 second, you will have a higher peak pressure with the shorter inspiratory time. This is commonly seen when managing asthma and COPD patients and is a good illustration of how decreasing the inspiratory time can affect the peak pressures without changing the degree of bronchospasm or pressure the alveoli are exposed to. A few practical considerations in managing a patient with a high peak pressure are that you may have to increase the peak pressure limit on the ventilator so that the full tidal volume is given.  Also, if there is resistance to air going in, there is also resistance to air exhaling, meaning your patient is at risk for breath-stacking resulting in auto-PEEP.

If your patient is at risk for air trapping (a.k.a breath-stacking, dynamic hyperinflation etc.), an end expiratory hold and intrinsic PEEP (a.k.a auto-PEEP) should be measured, see Figure 3. When the end expiratory hold is performed, the ventilator measures the alveolar pressure at the end of expiration (total PEEP). Intrinsic PEEP is the difference between set PEEP and the total PEEP. Intrinsic PEEP develops from incomplete exhalation and dynamic hyperinflation (breath-stacking) of the lungs (13). If this intrinsic PEEP is elevated it should be aggressively treated by bronchodilators and maximizing expiratory time primarily by decreasing the respiratory rate or by disconnecting from the ventilator in extreme cases causing hemodynamic compromise.

Plateau pressure will increase with increasing tidal volumes, poor lung compliance and PEEP (both intrinsic and extrinsic/set.) The plateau pressure, measured as an end inspiratory pause at the end of a delivered tidal volume when flow in the circuit is zero, is an approximation of alveolar pressure. See Figure 4 (2).  The plateau pressure should be measured only in a heavily sedated or paralyzed passive patient because a cough or patient respiratory effort will cause a change in pressure and an erroneous measurement.

Vents Part 2.fig 3 and 4

The plateau pressure is both the PEEP (pressure maintained throughout the respiratory cycle) and the compliance (distensibility) of the lung.  The normal lung is maximally distended between 30-35 cm H2O of transpulmonary pressure, more pressure causes overdistension and potentially lung injury. The transpulmonary pressure is the difference between plateau pressure (in the alveoli) and pleural pressure (outside the alveoli) (2). Since we do not routinely measure pleural pressure in the ED, it is best to keep the plateau < 30 cm H2O. The concept of transpulmonary pressure can be relevant in those with stiff chest wall (obese patients) or in those with increased abdominal pressure (i.e. abdominal compartment syndrome). In these scenarios the plateau may be higher than 30 cm H2O but the pressure felt by the alveoli (transpulmonary pressure) is still safe (2). One extreme example is a musician playing the tuba. The airway pressures are very high, but the thorax and abdomen muscles are also contracting (high pressure outside the alveoli) so the transpulmonary pressure is not significantly elevated.

There are several causes of a high plateau pressure that the EP should know. A high plateau pressure can be seen with right mainstem intubation or pneumothorax. In these cases you are putting all the tidal volume into one lung. Forcing this tidal volume into only half of the lung units leads to overdistension and a high pressure. As seen in Figure 4, a high plateau pressure could be from “stiff lungs” with low compliance such as ARDS, pneumonia, pulmonary edema and pulmonary fibrosis. In ARDS there is alveolar derecruitment and less healthy, functional lung tissue receiving the tidal volume, this can be thought of as “baby lung” (7). In this case PEEP should be increased to maintain alveolar recruitment (see PEEP table) and the tidal volume incrementally decreased by 1 ml/kg to as little as 4 ml/kg to keep the plateau pressure < 30 cm H2O. To maintain the minute ventilation and PCO2, respiratory rate may need to be increased as the Vt is decreased. Patients with ARDS will generally tolerate RR up to 30-35 without air trapping (7).

Sedation of the intubated patient

Matching the patient’s desired breathing pattern to the ventilator is a dynamic process that can be challenging. Assist-control modes of ventilation provide a set volume over a set time at a set flow rate. Contrast this to normal breathing, where the brain responds to stimuli to breathe (i.e. pH, PaCO2, PaO2) and sends a signal to the diaphragm via the phrenic nerve. The diaphragm contracts and initiates a breath. The duration, frequency, intensity and inspiratory flow of this contraction is highly variable, and failure to meet this expected pattern can produce dyspnea and ultimately lead to vent dyssynchrony (14).

Selection of the appropriate ventilator mode and sedation strategy comes down to one fundamental question: does the ventilator need to be adjusted to accommodate the patient or does the patient need to be sedated to accommodate the ventilator?  Placing a patient in a pressure support mode when spontaneously breathing can allow the patient to determine their breathing pattern and is often more comfortable for patients rather than a mandatory breathing pattern set by a ventilator.

In patients where a mandatory ventilatory pattern is being used for lung protection, as with strict volume control ventilation in ARDS, attempts can be made to increase patient-vent synchrony through adjusting the inspiratory flow pattern (i.e. decelerating flow), as well as increasing patient sedation. Some patients will continue to exhibit vent dyssynchrony despite adjusted flow patterns and heavy sedation, in these patients neuromuscular blockade can ensure vent synchrony and lung protective ventilation.

For sedation we prefer a combination of analgesia and anxiolysis. The recommended approach is to control pain first, as pain can be a major source of agitation and vent dyssynchrony. Deep sedation is associated with worse outcomes so try to target a lighter sedation such as a RASS (Richmond Agitation-Sedation Score) of -2 (awakens and makes eye contact to voice) to 0 (awake, alert and calm) (15,16).

Propofol and fentanyl (or other opiates) infusions work well for most patients. Dexmedetomidine (Precedex™) is an alpha-2 agonist that exhibits sedative, analgesic and anxiolytic effects without respiratory depression that is increasingly being used for sedation and analgesia in vented patients. The most common side effect is bradycardia. Dexmedetomidine is as effective, and possibly reduces ICU length of stay and time on the ventilator as compared to traditional sedatives (17).  Although benzodiazepines may have a favorable hemodynamic profile, we try to avoid benzodiazepine drips as they have shown worse ICU outcomes, with prolonged sedation, higher mortality and increased delirium (16,18).

Vent Bundle

We recommend implementing a vent bundle in every intubated patient in the emergency department. Routine measurement of patient height to determine appropriate tidal volume for ventilation, head of bed (HOB) elevation to at least 30°, orogastric tube placement for gastric decompression, oral care with a chlorhexidine solution every two hours, and stress ulcer prophylaxis with an H2 blocker can help ensure appropriate ventilation and decrease the rate of ventilator associated pneumonias (1,19).

We also recommend scheduled reassessment of intubated patients after initial neuromuscular blockade has worn off to assess adequacy of sedation, decrease the FiO2 quickly to avoid hyperoxia, and adjust ventilatory strategy to meet your patient’s needs. Depending on the wait time for ICU beds at your institution, the implementation of venous thromboembolism prophylaxis as well as daily sedation holidays and spontaneous breathing trials should be considered as part of standard ventilator bundles in those patients expected to be housed in the emergency department for ≥ 24 hours.

CONCLUSION: What to do for your next intubated patient

Emergency physicians must be ready to manage initial mechanical ventilation in various disease processes. Parts One and Two discussed the basics of ventilator management, Part Three will discuss management of challenging patient populations. For most patients with hypoxemia, higher PEEP and lower tidal volumes improve mortality.

Attention to waveforms and plateau pressures will alert you to high pressures causing overdistension or obstructive physiology causing auto-PEEP, and allow you to adjust your ventilator accordingly. In those who are intubated for airway protection adjust the ventilator for comfort to modes such as pressure support once the RSI medications have worn off. All of your patients will benefit from normoxia, HOB up to 30o, plateau pressure <30 cm H2O and Vt ≤8 ml/kg by ideal body weight.

Things to do for all your intubated patients
●     Tidal volume  ≤ 8 ml/kg IBW (measure your patient’s height) for everyone, 6 ml/kg IBW for those with or at risk for ARDS
●     Plateau < 30 cm H2O for most patients
●     PEEP higher in hypoxemic and obese patients — start at 8 cm H2O and titrate with a PEEP table
●     Wean FiO2 quickly to saturation of 94-96%
●     Consider pressure support for comfort in your spontaneously breathing patient intubated only for airway protection (i.e. GI bleed)
●     Implement a vent bundle for intubated patients in your ED

 

References

1.Fuller, Brian et al. Lung-Protective Ventilation Initiated in the Emergency Department (LOV-ED): A Quasi-Experimental, Before-After Trial. Ann Emerg Med. 2017; 70:406-418

2. Tobin, Martin. Advances in Mechanical Ventilation. N Engl J Med 2001; 344: 1986-1996

3.    Massimo Girardis et al. Effect of Conservative vs Conventional Oxygen Therapy on Mortality Among Patients in an Intensive Care Unit: The Oxygen-ICU Randomized Clinical Trial. JAMA. 2016; 316(15):1583-1589

4. Page et al. Emergency Department Hyperoxia Is Associated with an Increased Mortality in Mechanically Ventilated Patients: A Cohort Study. Critical Care (2018) 22:9

5. Chu, DK et al. Mortality and morbidity in acutely ill adults treated with liberal versus conservative oxygen therapy (IOTA): a systematic review and meta-analysis. Lancet 2018:391; 1693–1705

6. James K. Stoller, Nicholas S. Hill. Respiratory Monitoring in Critical Care. Goldman-Cecil Medicine, 103, 652-655.e2.

7. Weingart, S. Managing Initial Mechanical Ventilation in the Emergency Department. Ann Emerg Med. 2016; 68:614-617.

8. Kraut, JA et al. Lactic Acidosis: Current Treatments and Future Directions. Am J Kidney Dis. 2016; 68(3):473-482

9. Pham, T et al. Mechanical Ventilation: State of the Art. Mayo Clin Proc. 2017; 92(9):1382-1400

10. The ARDS 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; 342:1301-8.

11. Serpa Neto 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

12. Tobin, Martin. Mechanical Ventilation. N Engl J Med 1994; 330:1056-1061

13. Wood, S et al. Care of the intubated emergency department patient. The Journal of Emergency Medicine 2011; 40:419-427

14. Manning, Harold et al. Pathophysiology of Dyspnea. N Engl J Med 1995; 333:1547-1553

15. Stephens et al. Analgosedation Practices and the Impact of Sedation Depth on Clinical Outcomes Among Patients Requiring Mechanical Ventilation in the ED A Cohort Study. CHEST 2017; 152(5):963-971

16. Barr, Juliana et al. Clinical Practice Guidelines for the Management of Pain, Agitation, and Delirium in Adult Patients in the Intensive Care Unit. Critical Care Medicine 2013; 41:263–306

17. Chen K, Lu Z, Xin YC, Cai Y, Chen Y, Pan SM. Alpha-2 agonists for long-term sedation during mechanical ventilation in critically ill patients. Cochrane Database of Systematic Reviews 2015, Issue 1. Art. No.: CD010269. DOI: 10.1002/14651858.CD010269.pub2.

18. Lonardo NW, Mone MC, Nirula R, Kimball EJ, Ludwig K, Zhou X, Sauer BC, Nechodom K, Teng C, Barton RG. Propofol is associated with favorable outcomes compared with benzodiazepines in ventilated intensive care unit patients. Am J Respir Crit Care Med. 2014 Jun 1; 189(11):1383-94.

19. DeLuca LA et al.  Impact and feasibility of an emergency department–based ventilator-associated pneumonia bundle for patients intubated in an academic emergency department.  Am J Infect Control. 2017:45(2):151-157. doi.org/10.1016/j.ajic.2016.05.037.

ABOUT THE AUTHORS

Skyler Lentz, MD is the Assistant Professor of Surgery and Medicine in the Divisions of Emergency Medicine and Pulmonary Critical Care at the University of Vermont Medical Center.

Matthew Roginski, MD, MPH, is an Assistant Professor of Medicine in the Sections of Emergency and Critical Care Medicine and the DHART Assistant Medical Director at Dartmouth-Hitchcock Medical Center.

Patricia Ruth Atchinson, DO, is a Critical Care Fellow at Dartmouth-Hitchcock Medical Center and an Emergency Medicine physician.

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