Posts tagged #ventilation

Crashing Patient on a Ventilator

Expert Commentary

Thank you for this succinct summary of an incredibly important topic. We as emergency physicians spend a lot of time thinking about peri-intubation physiology but the challenges do not end once the plastic is through the cords. The frequency with which our ventilated patients stay with us in the ED has been increasing for years and will likely continue to do so1. This means that managing both acute decompensation and refractory hypoxemia needs to be in our wheelhouse.

The crashing patient on the ventilator can be truly frightening and your post effectively outlines a classic cognitive forcing strategy for managing these emergencies. A truism in resuscitation is to always rule out the easily correctable causes immediately. In this case, it means removing the complexity of the ventilator and making things as idiot-proof as possible. Once you’ve ruled out the life threats like pneumothorax, tube displacement, and vent malfunction, you can try to bring their sats up by bagging. Just make sure that you have an appropriately adjusted PEEP valve attached to your BVM for your ARDS patients; the patient who was just requiring a PEEP of 15 isn’t going to improve with you bagging away with a PEEP of 5.

Once you’ve gotten the sats up and the patient back on the vent, your ventilator display can provide you with further data as to why your patient decompensated. Does the flow waveform fail to reach zero suggesting breath stacking and a need for a prolonged expiratory time? Is the measured respiratory rate much higher than your set rate with multiple breaths in a row indicating double-triggering? The measured tidal volume might fall short of your set tidal volume. This points towards a circuit leak, cuff leak, or broncho-pleural fistula. Maybe you’re seeing the pressure wave dip below zero mid-inspiration and the patient is telling you that they are in need of faster flow, a bigger breath, or deeper sedation. In these situations, your respiratory therapist is going to be your best friend in managing this patient-ventilator interactions2.

As your post alludes to, sometimes patients remain hypoxemic despite our usual efforts and refractory hypoxemia can be an intimidating beast when you’ve got a busy ED burning down around you. If your cursory efforts to maintain vent synchrony by playing with the ventilator dials have failed, there’s no shame in deepening sedation which will work to decrease oxygen consumption and prevent derecruitment. Once sedated, work with your RT to find appropriate PEEP and tidal volumes to meet your goals.

Most patients can be managed with usual lung-protective ventilation but some patients will require more support and you’ve correctly identified several salvage therapies. My general approach is to pursue prone positioning in any patient with a P:F ratio approaching 150 despite optimal vent settings as it has the only strong mortality benefit of the therapies outlined above. Proning in the ED is resource intensive and is probably better pursued as a department-wide protocol rather than you and your charge nurse trying to figure it out in the middle of the night3.

As you’ve pointed out, the neuromuscular blockade has more limited evidence and is not required for prone ventilation. Upstairs, we accomplish this with continuous infusions but in the ED you may be more comfortable using intermittent boluses of intubation dose rocuronium. Just make sure your patient is unarousable. I reach for this if I’m unable to achieve ventilator synchrony with sedation alone as it allows for very low tidal volumes and inverse ratio ventilation. I see inhaled pulmonary vasodilators in a similar light: there’s no data on patient-oriented outcomes but they can make your numbers look prettier while you wait for more definitive interventions such as transfer.

This finally brings me to VV ECMO for refractory hypoxemia. It’s worth considering that while there is some evidence for a mortality benefit for ECMO in ARDS, the evidence base is mixed. The CESAR trial did show a mortality benefit in patients transferred to an ECMO center but only 76% of patients actually received ECMO upon transfer4. The larger and more recent EOLIA trial failed to demonstrate this improvement in mortality5. The conclusion I take from this is that treatment at a high volume center matters and that a boarding patient with refractory hypoxemia warrants an early consideration for transfer to a tertiary center if high-quality ARDS care can’t be accomplished upstairs at your shop.

References

Mohr NM, Wessman BT, Bassin B, et al. Boarding of Critically Ill Patients in the Emergency Department. Crit Care Med. 2020;48(8):1180-1187. doi:10.1097/CCM.0000000000004385
Sottile PD, Albers D, Smith BJ, Moss MM. Ventilator dyssynchrony – Detection, pathophysiology, and clinical relevance: A Narrative review. Ann Thorac Med. 2020;15(4):190. doi:10.4103/atm.ATM_63_20
McGurk K, Riveros T, Johnson N, Dyer S. A primer on proning in the emergency department. J Am Coll Emerg Physicians Open. 2020;1(6):1703-1708. doi:10.1002/emp2.12175
Peek GJ, Mugford M, Tiruvoipati R, et al. Efficacy and economic assessment of conventional ventilatory support versus extracorporeal membrane oxygenation for severe adult respiratory failure (CESAR): a multicentre randomised controlled trial. Lancet Lond Engl. 2009;374(9698):1351-1363. doi:10.1016/S0140-6736(09)61069-2
Combes A, Hajage D, Capellier G, et al. Extracorporeal Membrane Oxygenation for Severe Acute Respiratory Distress Syndrome. N Engl J Med. Published online May 23, 2018. doi:10.1056/NEJMoa1800385

Matt McCauley, MD

How To Cite This Post:

[Peer-Reviewed, Web Publication] King, P. Akehtuamhen, A. (2022, Feb 28). Crashing Ventilator Patient. [NUEM Blog. Expert Commentary by McCauley, M]. Retrieved from http://www.nuemblog.com/blog/crashing -vent-patient.

Mechanical Ventilation Oversimplified

**Written by:** Shawn Luo, MD (NUEM ‘22) **Edited by:** Sam Stark, MD, MA (NUEM ‘20)
**Expert Commentary by**: Ruben Mylvaganam, MD

The ventilator: we’ve all learned about it - the lectures, the bed-side demonstrations on those mind-numbingly long ICU rounds. But we were also told, repeatedly, “Don’t touch it!” Unless you are an attending, fellow, or respiratory therapist (RT) of course. So for a lot of us, the ventilator is a black box, mythical and intimidating.

In this blog, I hope to demystify ventilators a little so when duty calls, you can set initial settings and make some basic adjustments.

Physiology

1. How Mechanical Ventilation affects Oxygenation: PEEP & FiO2

You can reference this nice ARDSnet table for FiO2/PEEP combinations.

FiO2 – its effect is immediate

PEEP – takes up to an hour to show full effect

Therefore, when weaning, wean FiO2 before weaning PEEP so that if the patient desaturates, you have room to go up on FiO2.

2. How Mechanical Ventilation affects Ventilation: Tidal Volume, Respiratory Rate, Inspiratory Pressure or Inspiratory Time

This should be titrated in response to the patient's CO2 levels. Patients in respiratory failure from profound metabolic acidosis will need you to set higher minute ventilation to attempt respiratory compensation.

3. Peak Pressure and Plateau Pressure

Peak pressure is the summation of both airway resistance (dynamic compliance) and plateau pressure (static compliance). Most modern ventilators will automatically report peak pressures without any special maneuvers required. When thinking about airway resistance, think of when you blow air through a straw – the narrower the tubing the higher the resistance and thus a lot of pressure is needed to generate that flow. To measure airway resistance, have the RT set the flow rate to 60 LPM, adjust the flow pattern to a square wave form, and ask them to perform an inspiratory hold.

Plateau pressure is related to lung compliance (higher plateau pressure = less compliant lung). It is the pressure “felt” by the alveoli, and keeping it less than 30 cm H2O helps to prevent barotrauma. It’s only measured after the air stops moving (via an inspiratory hold maneuver – ask RT how to do this on your ventilator) so that dynamic airway resistance is not a factor.

4. Breath-stacking / Auto-PEEP

This occurs when the patient does not have enough time to finish exhalation before the next breath is delivered. This results in progressive hyperinflation of the lung, high peak pressures, and eventually hemodynamic collapse if not identified and intervened upon. It is most common in obstructive airway diseases such as asthma and COPD. Be vigilant for the flow diagram below on the ventilator to detect it early.

Modes

Volume vs Pressure – WHAT TYPE of breath is targeted

Volume mode means the vent will deliver a set tidal volume of air and results in whatever pressure (i.e. stiffer lungs result in higher pressure)
Pressure mode in turn means the vent will deliver at a set inspiratory pressure, and results in whatever volume (i.e. stiffer lungs result in lower volume)

A/C (Assist/Control) vs Support – WHEN the breath is delivered

In A/C mode, the machine delivers breath at a pre-set frequency (control), but the patient can also trigger additional breaths (assist) to faster than the set frequency. A quick and dirty trick is that any mode that contains the word “Control” means there will be a minimal respiratory rate set by the clinician.
Support (or Spontaneous) mode, in turn, will only deliver a breath when the patient initiates it. It senses the negative pressure generated by the patient and delivers a breath. If the patient does not breathe, it will not deliver. Usually safety back-up is in place to prevent prolonged apnea.

Volume Control

Delivers set tidal volume at or above a set rate
You set: tidal volume (6-8mL/kg ideal body weight), respiratory rate (16-22 breaths per minute), flow rate (60-80 LPM), and PEEP & FiO2 as needed
Check: Plateau pressure <30 (inspiratory hold maneuver)
This is a good initial setting for most of the patients you just intubated

Pressure Control

Delivers set pressure at or above set rate
You set: inspiratory pressure (5-15 cm H2O), inspiratory time (“I-time”; 0.6-0.8), respiratory rate (16-22), PEEP & FiO2 as needed
Check: to make sure the patient is getting tidal volumes of 6-8 mL/kg
This can be a helpful setting in some patients that do not tolerate volume control. Adjust pressure support to achieve tidal volume of 6-8 mL/kg while ensuring total pressure is less than 30-35 cm H20.

Pressure Support

Delivers set pressure when the patient initiates a breath to help the patient move the air
You set: Pressure support (5-15 cm H2O), PEEP & FiO2 as needed
Check: to make sure the patient is getting tidal volumes of 6-8 mL/kg
Usually a weaning mode to check if the patient is likely to tolerate extubation

*The bottom line is, by adjusting the parameters, you can achieve the same result with different ventilation modes.

My step-wise approach to initiate mechanical ventilation on most patients:

Build initial settings around Volume Control (tidal volume 6-8mL/kg ideal body weight, respiratory rate 16-22, PEEP 5, FiO2 100%)
Tweak according to patient’s clinical scenario – e.g. higher respiratory rate for acidotic patients, higher initial PEEP for hypoxemic respiratory failure, longer expiratory time for asthmatics/COPD patients with auto-PEEP
Start mechanical ventilation, quickly wean FiO2 for a goal SpO2 of 94-98%
Adjust settings further based on clinical response and ABGs
When in doubt, disconnect and bag the patient.

References:

The 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;342:1301-1308.

Weingart, S. Managing Initial Mechanical Ventilation in the Emergency Department. Annals of Emergency Medicine, Volume 68, Issue 5, November 2016, Pg 614-617

Hyzy, R. Modes of Mechanical Ventilation. In: UpToDate, Parsons P. Finlay G (Ed), UpToDate, Waltham, MA. (Accessed on May 5, 2020.)

Expert Commentary

Thank you for the opportunity to review this very helpful and concise review on the basics of invasive mechanical ventilation. I hope to make this commentary brief, a contrast to our notoriously long ICU rounding habits. I would recommend any reader to view this editorial for a more in depth and nuanced understanding of mechanical ventilation. (1)

As you have described above, one way in which to think about mechanical ventilation is in the context of the most common scenarios in which we implement it, ie: hypoxemia and hypercapnia. Understanding that for hypoxemic patients, our tools to improve physiology are by manipulating the set FiO2 and PEEP to achieve specified targets for oxyhemoglobin saturation or P/F ratios (with regard to ARDS management). It is important to note that a few studies have demonstrated that an FiO2 greater than 50-60% can be toxic and may result in an increase in reactive oxygen species, increased airway damage (tracheobronchitis), and secondary infection from impaired bactericidal action of immune cells. (2,3) For our hypercapnic patients, knowing their prior baseline PCO2 is helpful in determining how to adjust the respiratory rate and tidal volume to appropriately improve their respiratory acidosis.

An important common 3 part methodology to better appreciate modes of mechanical ventilation is understanding the “trigger”, “target”, and “cycle” of each ventilator mode. In the simplest of terms, the “trigger” is what prompts the ventilator to deliver the breath (ie: an assisted breath when the ventilator senses a patient generated decrease in flow/pressure or a control breath when enough time has elapsed as mandated by the set respiratory rate). The “target” is what the ventilator aims to achieve with each breath (in the mode of AC-VC: a targeted flow rate [often ~60 L/min] or in the mode of AC-PC: a targeted inspiratory pressure [often ~15 cwp]). Finally, the “cycle” is a term that describes how the ventilator recognizes when it is time to terminate the breath that is delivered (in the mode of AC-VC: cycling off after the goal TV is reached [~600cc] or in the mode of AC-PC: cycling off after the set inspiratory time has occurred [~ 0.7 seconds]). See table below for a quick summary.

Finally, the best practical way to simplify mechanical ventilation is to request the changes by the respiratory therapist and see the effects. I encourage you to interpret all VBGs and ABGs, approach your respiratory therapist, pulmonary/CCM fellow, and suggest everything from initial ventilator settings, changes to both modes and individual parameter settings, and see the reflection of this work in your subsequent blood gases.

References

1. Walter JM, Corbridge TC, Singer BD. Invasive Mechanical Ventilation. South Med J. 2018 Dec;111(12):746-753. doi: 10.14423/SMJ.0000000000000905. PMID: 30512128; PMCID: PMC6284234.

2. Suttorp N, Simon LM. Decreased bactericidal function and impaired respiratory burst in lung macrophages after sustained in vitro hyperoxia. Am Rev Respir Dis. 1983 Sep;128(3):486-90. doi: 10.1164/arrd.1983.128.3.486. PMID: 6311064.

3. Griffith DE, Garcia JG, James HL, Callahan KS, Iriana S, Holiday D. Hyperoxic exposure in humans. Effects of 50 percent oxygen on alveolar macrophage leukotriene B4 synthesis. Chest. 1992 Feb;101(2):392-7. doi: 10.1378/chest.101.2.392. PMID: 1310457.

Ruben Mylvaganam, MD

Instructor of Medicine

Department of Pulmonology & Critical Care Medicine

Northwestern Memorial Hospital

How To Cite This Post:

[Peer-Reviewed, Web Publication] Luo, S. Stark, S. (2021, Nov 1). Mechanical Ventilation Oversimplified. [NUEM Blog. Expert Commentary by Mylvaganam, R]. Retrieved from http://www.nuemblog.com/blog/mechanical-ventilation-tips

Basic Capnography Interpretation

Written by: Shawn Luo, MD (NUEM ‘22) Edited by: Matt McCauley, MD (NUEM ‘21) Expert Commentary by: N. Seth Trueger, MD, MPH — **Written by:** Shawn Luo, MD (NUEM ‘22) **Edited by:** Matt McCauley, MD (NUEM ‘21) **Expert Commentary by**: N. Seth Trueger, MD, MPH

Continuous waveform capnography has increasingly become the gold standard of ETT placement confirmation. However, capnography can provide additional valuable information, especially when managing critically ill or mechanically ventilated patients.

Normal Capnography

Phase I (inspiratory baseline) reflects inspired air, which is normally devoid of CO2.
Phase II (expiratory upstroke) is the transition between dead space to alveolar gas.
Phase III is the alveolar plateau. Traditionally, PCO2 of the last alveolar gas sampled at the airway opening is called the EtCO2. (normally 35-45 mmHg)
Phase 0 is the inspiratory downstroke, the beginning of the next inspiration

EtCO2 is only one component of capnography. Measured at the end-peak of each waveform, it reflects alveolar CO2 content and is affected by alveolar ventilation, pulmonary perfusion, and CO2 production.

Figure 2. Factors affecting ETCO2 (EMSWorld)

EtCO2 - PaCO2 Correlation

Correlating EtCO2 and PaCO2 can be problematic, but in general, PaCO2 is almost always HIGHER than EtCO2. Normally the difference should be 2-5mmHg but the PaCO2-EtCO2 gradient is often increased due to increased alveolar dead space (high V/Q ratio), such as low cardiac output, cardiac arrest, pulmonary embolism, high PEEP ventilation.

Important Patterns

Let’s go through a few cases and learn some of the important capnography waveforms to recognize

Case 1: Capnography with Advanced Airway

An elderly gentleman with a history of COPD, CAD & CKD gets rushed into the trauma bay with respiratory distress and altered mental status. You gave him a trial of BiPAP for a few minutes without improvement.

You swiftly tubed the patient. It was not the easiest view, but you advance the ETT hoping for the best. Upon attaching the BVM to bag the patient, you saw this on capnography:

Oops, the ETT is in the esophagus, as evidenced by the low-level EtCO2 that quickly tapers off.

2. You remove the ETT, bag the patient up, and try again with a bougie. Afterward, you see…

Figure 4. Capnography with ETT in right main bronchus (EMSWorld)

This suggests a problem with ETT position, most often in the right main bronchus. Notice the irregular plateau--the initial right lung ventilation, followed by CO2 escaping from the left lung. Beware that capnography can sometimes still appear normal despite the right main bronchus placement.

3. You pull back the ETT a few cm and the CXR now confirms the tip is now above the carina. The patient’s capnography now looks like this:

Figure 5. Capnography showing obstruction or bronchospasm (SketchyMedicine)

Almost looks normal but notice the “shark fin” appearance, this is due to delayed exhalation, often seen in airway obstruction and bronchospasms such as COPD or asthma exacerbation.

4. You suction the patient and administer several bronchodilator nebs. The waveform now looks more normal:

Figure 6. Capnography showing normal waveform (SketchyMedicine)

5. However, just as you were about to get back to the workstation to call the ICU, the monitor alarms and you see this:

Figure 7. Sudden loss of capnography waveform (SketchyMedical)

Noticing the ETT still in place with good chest rise, you quickly check for a pulse. There is none.

6. You holler, push the code button and start ACLS with a team of clinicians. With CPR in progress, you notice this capnography:

Figure 8. Capnography during CPR (SketchyMedicine)

Initially, your patient’s EtCO2 was only 7, after coaching the compressor and improving CPR techniques, it increased to 14.

You are also aware that EtCO2 at 20min of CPR has prognostic values. EtCO2 <10 mmHg at 20 minutes suggests little chance of achieving ROSC and can be used as an adjunctive data point in the decision to terminate resuscitation.

7. Fortunate for your patient, during the 3rd round of ACLS, you notice the following:

Figure 9. ROSC on capnography (emDOCs.net)

This sudden jump in EtCO2 suggests ROSC. You stop the CPR and confirm that the patient indeed has a pulse.

8. As you are putting in orders for post-resuscitation care, you notice this:

Figure 10. Asynchronous breathing on capnography (SketchyMedical)

This curare cleft comes from the patient inhaling in between ventilator-delivered breaths and is usually a sign of asynchronous breathing. However, in the post-arrest scenario, it is a positive prognostic sign as your patient is breathing spontaneously. You excitedly call your mom, I meant MICU, about the incredible save.

Case 2: Capnography with Non-intubated Patient

You just hung up the phone with MICU when EMS brings you a young woman with a heroin overdose. She already received some intranasal Narcan from EMS but per EMS report patient is becoming sleepy again.

She mumbles a little as you shout her name, and as you put an end-tidal nasal cannula on her, you saw this:

Figure 11. Hypoventilation on capnography (emDOCs.net)

Noticing the low respiratory rate and high EtCO2 value, you recognize this is hypoventilation.

2. But very soon she becomes even less responsive and the waveform changed again:

Figure 12. Airway obstruction on capnography (emDOCs.net)

The inconsistent, interrupted breaths suggest airway obstruction, while the segments without waveform suggest apnea. You have to act fast.

3. By then your nurse has already secured an IV, so you pushed some Narcan. However, in the heat of the moment, you gave the whole syringe. The patient quickly woke up crying and shaking.

Figure 13. Hyperventilating on capnography (emDOCs.net)

She was quite upset and hyperventilating. The waveform reveals a high respiratory rate and relatively low EtCO2.

As much as you are a little embarrassed by putting the patient into florid withdrawal, you know it could have been a lot worse. Walking away from the shift, you think about how many times capnography has assisted you during those critical moments. “Hey, perhaps we should buy a capnography instead of a baby monitor,” you ask your wife at dinner.

Additional Resources

This website provides a tutorial and quiz on some of the basic capnography waveforms.

References

American Heart Association. 2019 American Heart Association Focused Update on Advanced Cardiovascular Life Support. Circulation. 2019; 140(24). https://doi.org/10.1161/CIR.0000000000000732
Brit Long. Interpreting Waveform Capnography: Pearls and Pitfalls. emDOCs.net. www.emdocs.net/interpreting-waveform-capnography-pearls-and-pitfalls/, accessed May 12, 2020
Capnography.com, accessed May 12, 2020
Kodali BS. Capnography outside the operating rooms. Anesthesiology. 2013 Jan;118(1):192-201. PMID: 23221867.
Long, Koyfman & Vivirito. Capnography in the Emergency Department: A Review of Uses, Waveforms, and Limitations. Clinical Reviews in Emergency Medicine. 2017; 53(6). https://doi.org/10.1016/j.jemermed.2017.08.026
Nassar & Schmidt, Capnography During Critical Illness. CHEST. 2016; 249(2). https://doi.org/10.1378/chest.15-1369
Sketchymedicine.com/2016/08/waveform-capnography, accessed May 13, 2020
Wampler, D. A. Capnography as a Clinical Tool. EMS World. www.emsworld.com/article/10287447/capnography-clinical-tool. June 28, 2011. Accessed May 13, 2020

Expert Commentary

This is a nice review of many of the intermediate and qualitative uses of ETCO2 in the ED. For novices, I recommend a few basic places to start:

Confirmation of intubation. Color change is good but it’s just litmus paper and gets easily defeated by vomit. Also, in low output states, it may not pick up. Further, colorimetric capnographs require persistent change over 6 breaths, not just a single change. Waveform capnography uses mass spec or IR spec to detect CO2 molecules. There are so many uses, it’s good to have, I don’t see why some are resistant to use this better plastic adapter connected to the monitor vs the other, worse, plastic adapter.

a. The mistake I have seen here is assuming a lack of waveform is due to low cardiac output, ie there’s no waveform because the patient is being coded, not because of esophageal intubation. There is always *some* CO2 coming out if there is effective CPR; if there isn’t, the tube is in the wrong place. If you really don’t believe it, check with good VL but a flatline = esophagus.

2. Procedural sedation. There’s lots of good work and some debate about absolute or relative CO2 changes or qualitative waveform changes that might predict impending apnea, but for me, the best use is that I can just glance at the monitor for a second or two and see yes, the patient is breathing. No more staring at the chest debating whether I see chest rise, etc. It’s like supervising a junior trainee during laryngoscopy with VL: it’s anxiolysis for me.

a. Using ketamine? Chest movement or other signs of respiratory effort without ETCO2 waveform means laryngospasm. Jaw thrust, bag, succinylcholine (stop when better).

3. Cardiac arrest.

a. Quality of CPR. Higher number means more output. Can mean the compressor needs to fix their technique, or more often, is tiring out and needs a swap.

b. ROSC. There can be a big jump (eg from 15 to 40) when ROSC occurs. Very helpful.

c. Ending a code. 20 mins into a code, if it’s <10 during good CPR, the patient is unlikely to survive. I try to view this as confirming what we know – it’s time to end the code. The mistake here is to not end a code that should otherwise end because the ETCO2 is above 10; it doesn’t work like that, it’s a 1-way test.

4. Leak. One waveform shape I wanted to add that I find helpful: if the downstroke kinda dribbles down like a messy staircase, it’s a leak. Can be an incomplete connection (eg tubing to the vent) or the balloon is too empty or full.

Seth Trueger, MD, MPH

Assistant Professor of Emergency Medicine

Department of Emergency Medicine

Northwestern University

How To Cite This Post:

[Peer-Reviewed, Web Publication] Luo, S., McCauley M. (2021, Sept 9). Basic Capnography Interpretation. [NUEM Blog. Expert Commentary by Trueger N.S]. Retrieved from http://www.nuemblog.com/blog/capnography

Physiologically Difficult Intubations

Written by: Samantha Stark, MD (NUEM ‘20) Edited by: Steve Chukwulebe, MD (NUEM ‘19) Expert Commentary by: Seth Trueger, MD, MPH — **Written by:** Samantha Stark, MD (NUEM ‘20) **Edited by:** Steve Chukwulebe, MD (NUEM ‘19) **Expert Commentary by**: Seth Trueger, MD, MPH

It’s the first few minutes of your shift, and the paramedics roll by your workstation with your first patient, a young woman clutching an inhaler and breathing with every accessory muscle in her body. You direct them to your resuscitation room and they inform you that she has a history of asthma and is having an attack; she’s too exhausted from breathing to verify this, but it seems true. You quickly get her on BiPAP, which mildly improves her work of breathing, but as she becomes drowsy, you obtain a VBG showing a climbing CO2 of 45. You realize that it’s time to intubate this patient, and as you get set up, you collect your thoughts and quickly review everything you’ve heard about intubating asthmatics.

Obstructive Airway Disease

First, remember that asthma is an obstructive airway disease, meaning that there are two main processes to worry about during and after intubation:

Auto PEEP
Hypotension secondary to increased intrathoracic pressure from auto PEEP

*Note: auto PEEP is caused by breath stacking in a patient whose expiration is impaired (such as asthma or COPD) – the ventilator initiates a breath before there’s time for full exhalation, and this leads to progressively more volume retained in the lungs, increasing the risk of barotrauma. This can also lead to increased intrathoracic pressure, in turn decreasing preload to the heart and thus causing hypotension.

How to optimize the intubation:

As you already have this patient on BiPAP, try to preoxygenate as much as possible with this mode of positive pressure

Consider attempting delayed sequence intubation with ketamine
- It will maintain the patient’s respiratory drive and may help with BiPAP synchrony and anxiolysis
- It serves as a bronchodilator
Use rocuronium for paralysis
- It will last longer than succinylcholine, and initially help with vent synchrony
- *Note: remember to fully sedate the patient after intubation, as they won’t tell us that they’re not sedated during their prolonged paralysis
Decrease the dead space and resistance of your vent by using the largest endotracheal tube feasible
Frequently reassess the ventilator to ensure that breath stacking is not occurring:
- Low respiratory rate to allow for exhalation
- Higher tidal volumes of 6-8 cc/kg IBW
- Decreased I:E ratio (at least 1:3, may very well need to be longer)

You’ve successfully intubated this patient, and now the lab pages you to let you know that there is a patient in the waiting room with a bicarb of 9. When the patient is wheeled back, his marked tachypnea and work of breathing makes you think he may need to be intubated as well. But he’s so acidotic, and you’re sure you’ve hear something about intubating acidotic people…

Metabolic Acidosis

What you’ve heard is that if you intubate a severely acidotic patient, you’ve killed them. There are two reasons for this:

It’s very difficult to keep up with their minute ventilation
There is a transient increase in pCO2 with paralysis (this is normally inconsequential, but in the decompensating acidotic patient, can lead to cardiovascular collapse)

How to optimize the intubation:

Optimize cardiovascular status as much as possible beforehand
Bolus fluids
Consider starting pressors pre-intubation, or having push-dose phenylephrine or epinephrine on hand during intubation
Match the patient’s minute ventilation
Ensure adequate pre-oxygenation, using NIPPV
However, even if oxygenation is not an issue, BiPAP should be used to assess the minute ventilation the patient is maintaining on their own, to help determine what is needed post intubation
Using delayed sequence technique with ketamine as the induction agent and a short acting paralytic like succinylcholine could theoretically help to avoid apnea as much as possible
Once intubated, the patient’s pre-intubation minute ventilation (respiratory rate and tidal volume) MUST be matched on the ventilator
Don’t be surprised to see higher tidal volumes of 8 cc/kg IBW

As you’re sitting down to catch up on notes, a nurse gets your attention to let you know that there is an altered, febrile, tachycardic patient with a pressure of 65/40 tucked away in a bed at the back of the ED that you should probably see right away. As it turns out, this patient needs to be intubated as well.

Shock

As mentioned above, increased intrathoracic pressure from PPV results in decreased venous return to the heart, leading to decreased preload. This obviously has the potential to be quite detrimental to a patient with shock.

How to optimize the intubation:

Optimize cardiovascular status as much as possible beforehand
Fluid resuscitation and vasopressors started prior to intubation
Have push dose pressors available at the bedside should they be needed
Induction agents:
- Avoid propofol as it has a propensity to cause hypotension
- Use etomidate or ketamine
- Ketamine has been shown to be more hemodynamically stable than etomidate
- Also, the body should prioritize cerebrovascular blood flow in shock, therefore if etomidate is used, consider decreasing the dose to minimize hemodynamic effects

At this point, you’re too tired to write any notes, so you decide to sit down and, given how your shift has been going so far, do some reading about patients that are dangerous to intubate or difficult to manage on the vent. The first topic you come across is pulmonary hypertension.

Pulmonary Hypertension

Mechanical ventilation is dangerous in these patients due to their inability to tolerate decreased preload, increased afterload, or really any alteration in their tenuous hemodynamics. Unfortunately, in patients with pulmonary hypertension but also systemic hypotension, IV fluids can over-distend the right ventricle and make things worse. There’s not a super reliable way to tell if these patients will be fluid responsive or not; most would suggest a small fluid bolus challenge to see how they respond. There may or may not be time for this prior to intubation, but if there is time, it’s probably worth a try.

How to optimize the intubation:

Can consider pre-medication with fentanyl:
- Thought to blunt the hypertensive response to laryngoscopy, similar to head-injured patients
- In theory, this prevents increased afterload in the pulmonary vasculature
Induction agent:
- Consider etomidate
- Theoretically should have less of an effect on preload than propofol
- Additionally, less of an effect on afterload than ketamine
Ventilator settings:
- Closely monitor plateau pressures to keep them less than 30 cm H2O, to avoid drops in preload due to increased intrathoracic pressure
- Consider placing an arterial line for frequent ABG checks
- Both hypercapnia and hypoxia can cause vasoconstriction (increasing afterload in the pulmonary vasculature)

Two days later, while you’re following up on some of your prior patients, you note that the patient in septic shock that you intubated a couple of days ago now has ARDS, and it seems that the inpatient team is having some difficulty managing her on the vent.

ARDS

While this is an area of active research and there are different strategies and methods for helping to improve these patients’ oxygenation, the main thing to remember from the perspective of managing the ventilator is the lung protective strategy:

Tidal volume 6 cc/kg IBW
Plateau pressure less than 30 cm H2O
Minimum PEEP of 5 cm H2O (and remember that these patients may often need significantly higher PEEP)

Expert Commentary

Thank you for this review of intubating sick patients - intubating complex physiology is arguably one of the most dangerous things we can do, but there are some straightforward, concrete steps we can take to do it as safely as possible.

For me, the first step is to consider every ED intubation potentially dangerous. Maximize resuscitation (IV fluids; pressors if needed, always ready) and optimize preoxygenation to provide the biggest possible safety net. It’s much more CBA than ABC.

Every patient we intubate in the ED has potential to crump: the sympatholysis from sedation will reduce endogenous catecholamines, and the switch to positive pressure ventilation impairs preload.

Every intubated patient needs post-intubation sedation. I generally default to a fentanyl drip and modify from there (eg add propofol if BP tolerates; add ketamine if not). Do not remove sedation for hypotension; do not use pain as a pressor. That is torture and it is bad. Sedate the patient adequately and if that means more resuscitation (fluid, blood, pressors, etc) then do that too. Do not torture patients to maintain BP.

The easiest tactic to ensure post-intubation sedation is to think of RSI as 3 medications: NMBA, induction agent, and post-intubation sedative. I should not be surprised that I will need post-intubation sedation shortly after intubation.

Perhaps the biggest lesson in ARDS management and prevention in recent years is that nearly everyone potentially benefits from lung protective ventilation, i.e. 6 ml/kg *ideal* body weight. I’ve changed my default tidal volume to 400-450ml (it was 550-600 when I was in med school). Otherwise, ventilation (minute ventilation, or CO2 management) is all about adjusting respiratory rate (my default is 16-18, not 12) as the patient’s height usually does not change in the ED.

Special situations: asthma patients don’t have a big enough tube to exhale properly. Pay special attention, make sure they have sufficient time to exhale (and they may the one group that may benefit from *not* being on 6 ml/kg IBW. Perhaps even more importantly, unlike many other situations, intubation does not fix asthma; it makes it even harder to manage, as even the largest ET tubes are, by definition, smaller than the patient’s natural airway. Maximize NIV and other management options (eg epinephrine) if at all possible.

Acidosis is tough and the key is maximizing ventilation before and after intubation. These patients may need absurd-seeming respiratory rates and regardless of how hypercarbic they are, acidosis does not make patients taller so there is no reason to adjust tidal volume.

Pulmonary hypertension is complex and scary. Prepare beforehand, and work with your intensivists and other relevant specialists.

The most important part of airway management is preparation – not just in the ED, but learning as much as I can beforehand.

Seth Trueger, MD, MPH

Assistant Professor of Emergency Medicine

Department of Emergency Medicine

Northwestern University expert commentator

How To Cite This Post:

[Peer-Reviewed, Web Publication] Stark, S. Chukwulebe, S. (2020, Oct 5). Physiologically Difficult Intubations. [NUEM Blog. Expert Commentary by Trueger, S]. Retrieved from http://www.nuemblog.com/blog/physiologically-difficult-intubations

References

Ebert TJ, Muzi M, Berens R. Sympathetic responses to induction of anesthesia in humans with propofol or etomidate. Anesthesiology. 1992;76:725-33.
Van Berkel MA, Exline MC, Cape KM, et al. Increased incidence of clinical hypotension with etomidate compared to ketamine for intubation in septic patients: a propensity matched analysis. Journal of Critical Care. 2017;38:209-214.
Dalabih M, Rischard F, Mosier JM. What’s new: the management of acute right ventricular decompensation of chronic pulmonary hypertension. Intensive Care Med. 2014;40(12):1930-3.
Hemmingsen C, Nielson PC, Odorico J. Ketamine in the treatment of bronchospasm during mechanical ventilation. Am J emerg Med. July 1994;12(4):417-420.
Eames WO, Rooke GA, Wu RS, Bishop MJ. Comparison of the effects of etomidate, propofol, and thiopental on respiratory resistance after tracheal intubation. Anesthesiology. June 1996;84(6):1307-11.
Gragossian A, Asp A, Hamilton R. High Risk Post Intubation Patients. www.emdocs.net/ high-risk-post-intubation-patients/ June 2017
The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes fo acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342:1301-1308.
NIH NHLBI ARDS Clinical Network. Mechanical Ventilation Protocol Summary. www.ardsnet.org/files/ventilator_protocol_2008-07.pdf
Marino, Paul L. 2009. The Little ICU Book. Wolters Kluwer Health. Philadelphia, PA.
Arbo, John E. 2015. Decision Making in Emergency Critical Care: An Evidence-Based Handbook. Wolters Kluwer Health. Philadelphia, PA.

Posted on October 5, 2020 by NUEM Blog and filed under Airway and tagged intubation ventilation post-intubation rapid sequence intubation shock.

Little Lungs, Little Differences: Initiating Emergency Department Mechanical Ventilation in the Pediatric Patient

Written by: Matt McCauley MD (PGY-3) Edited by: Jacob Stelter, MD (NUEM ‘19) Expert commentary by: Katie Wolfe, MD

Airway management of pediatric patients is a reasonable source of anxiety for the emergency physician. Children are intubated three to six times less often than adult emergency department patients [1]. Hence, it stands to reason that EP experience with mechanically ventilated children can be scarce [2] . Additionally, evidence driven practice in pediatric mechanical ventilation is limited and practice patterns vary between institutions and providers. These unknowns can make the prospect of managing these patients even more intimidating [3]. However, pediatric ventilator management is largely driven by data extrapolated from adults, which should come as a relief to the EP [4]. By keeping in mind small differences in pediatric physiology and keeping the consulting intensivist (and Broselow Tape) close at hand, an EP can effectively initiate mechanical ventilation in the smallest and most anxiety-provoking patients.

Getting Help

Like the Fat Man said in House of God: “[Disposition] comes first.” The intubated child is bound for a pediatric ICU and hopefully the accepting pediatric intensivist is already aware of any intubated patient and can be a great deal of help and support as you work together to make your patient safe for transfer upstairs or across town. Although the use of a Broselow tape and other height based methods of estimating body weight for drug dosing is fraught with error 5, the Broselow’s color coding allows for quick estimation of ideal body weight (IBW) that is required to calculate ideal tidal volumes.

Choosing a Mode

As mentioned, practice patterns related to pediatric ventilator management vary greatly [3]. The most commonly used modes for emergency pediatric ventilation include pressure assist control ventilation (PCV), volume control ventilation (VCV), and pressure regulated volume control ventilation (PRVC) [2]. PCV is typically favored in neonates and infants while volume modes are preferred in larger children [2]. When utilizing PCV, the provider sets the, inspiratory rate, inspiratory time, and inspiratory pressure meaning that the delivered tidal volume is dependent on the lung compliance of the patient [6]. This means that worsening compliance results in low tidal volumes. (Table 1)

Vt = Compliance x Delta Pressure

In contrast, VCV ventilation requires that the physician set the inspiratory rate, inspiratory flow rate, tidal volume, and PEEP. The ventilator delivers a fixed flow of air until the desired tidal volume is reached. This means that worsening compliance results in higher airway pressures (Table 1) [1]. The final commonly used mode for ventilating pediatric lungs is PRVC which, rather than requiring a set inspiratory flow rate like most volume controlled modes, utilizes a set inspiratory time, a targeted tidal volume, and a range of allowed pressures. With each breath the ventilator delivers a decelerating breath over the set time at an inspiratory pressure within the allowed range. If the resulting tidal volume is too high, the next breath is delivered with less pressure, if the volume falls short of the targeted tidal volume, the next breath is delivered with more pressure (Table 1) [6].

Finally, synchronized intermittent mandatory ventilation (SIMV) is often added to the above modes in pediatric ventilation. In SIMV, any time the patient initiates breaths within the set respiratory rate, a pressure supported breath (usually at 5-10 mmHg) is given rather than the full volume or pressure controlled breath. Pediatric patients are more likely than their adult counterparts to over-breathe the set respiratory rate, putting them at risk of breath stacking from large volume breaths. SIMV can help to mitigate this risk [2]. Despite all this complexity, there is a paucity of good evidence for or against any particular mode for ventilation the critically ill child [4]. This should reassure the EP to choose their most familiar ventilator mode in conjunction with their intensivist.

Screen Shot 2020-02-03 at 10.30.04 AM.png

Choosing Age-Appropriate settings

Since pediatric respiratory rates vary wildly from adults, one should take the patient’s age into account when initiating mechanical ventilation (table 2) . With the exception of children with obstructive pathophysiology, the physician should attempt to match the patient’s pre-intubation minute ventilation [2]. Tidal volume goals for pediatric patients do not vary much from adults with most data being extrapolated from adult studies [4] and large trials have been unable to establish as safe threshold for tidal volume [8]. The Pediatric Acute Lung Injury Consensus Conference (PALICC) recommends targeting 5-8cc/kg of ideal body weight (IBW) for most children either by setting a tidal volume in VCV or altering driving pressures for pressure controlled modes to target tidal volumes in this range for most patients [9]. Just as in adult patients, the intubating physician can set initial FiO2 at 100% to overcome hypoxia caused by peri-intubation apnea and then quickly down titrate targeting a SpO2 of 92-97% [9] .

Screen Shot 2020-02-03 at 10.30.24 AM.png

If ventilating pediatric patients with pressure controlled ventilation, initially inspiratory times can be found on the Broselow or in a PALS manual 10 (table 3). If a volume controlled mode of ventilation is desired, inspiratory flow can be titrated to achieve a inspiratory to expiratory time ratio of 1:2 [2]. After initial setup, arterial blood gas analysis, continuous end-tidal CO2 measurement, and a chest X ray to evaluate tube positioning are just as critical here as they are in the adult patient.

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Ventilating the Child with Refractory Hypoxemia

While most pediatric patients will be relatively straightforward to ventilate, the patient intubated for infectious pathologies like pneumonia or bronchiolitis is at risk for ARDS and should be approached with lung-protective ventilation strategies in mind. Victims of drowning are similarly at risk and fall under the category of patients requiring lung-protective settings [11]. There is no pediatric equivalent for the ARDSnet trial [12] so adult data has been extrapolated to be applied to pediatric patients [3] making this familiar territory for the adult emergency physician.

While most children will tolerate levels of PEEP between 3-5cmH204, PALICC recommends that children at risk of ARDS receive moderately elevated levels of PEEP between 10-15cmH2O with an SPO2 goal between 88-92% for kids requiring PEEP more than 10mmH2O [9]. In order to assess the extent of lung injury, an inspiratory hold maneuver can be used to determine lung compliance which is typically 1.5-3.0/cmH2O/kg for an infant [2]. If the EP notes decreased compliance, tidal volumes closer to 3-6cc/kg should be targeted [9]. If these measures fail to improve oxygenation, inspiratory time can be increased in order to target an inspiratory to expiratory ratio closer to 1:2. With the exception of children with elevated intracranial pressure (ICP), congenital heart disease, or pulmonary hypertension, permissive hypercapnea is acceptable as long as the pH remains > 7.2 [4].

Ventilating the Child with Obstructive Physiology

Endotracheal intubation of the asthmatic child is thankfully a rare event but one that portends to a high mortality [13]. At baseline, children exhibit higher airway resistance than their adult counterparts [2] and the even higher airway resistance in asthmatic patients creates high levels of intrinsic PEEP while increases the risk of breath stacking and pneumothorax [14]. If the patient’s respiratory rate is too high, lungs will remain progressively inflated at end expiration. This increases intra-thoracic pressure thereby decreasing preload and precipitating cardiovascular collapse. The level of this intrinsic PEEP can be assessed with an expiratory hold maneuver (Figure 1). To do this, the ventilator occludes the expiratory port at the end of exhalation allowing the alveolar and airway pressures to equilibrate. The total pressure at this moment minus the set PEEP on the ventilator represents the intrinsic PEEP [7]. More simply, a flow/time curve that fails to return to baseline prior to the onset of inspiration may signal to the EP that there may be high levels of intrinsic PEEP 2. (Figure 2)

Screen Shot 2020-02-03 at 10.32.23 AM.png

Screen Shot 2020-02-03 at 10.32.37 AM.png

To counteract this, asthmatics and other patients with obstructive physiology will need respiratory rates far below median age values. In one series of asthmatic children aged as young as nine months, rates as low as 8-12 breaths per minute were used [15]. In order to further facilitate full expiration, the I:E ratio should be increased to target values as low as 1:4-5 [15]. High levels of PEEP are typically not required in these patients and use of low to zero PEEP has been documented [14]. Hypercapnea should be expected and is allowable in these patients [14].

Prolonged mechanical ventilation of the pediatric patient exhibits far more complexities than this blog post covers and is beyond the scope of most emergency medicine practice. However, by relying on evidence driven practice for adult intubated patients with close guidance from a pediatric intensivist and pediatric resuscitation reference, the initial steps and safe monitoring of the intubated child are well within the abilities of the emergency physician.

Screen Shot 2020-02-03 at 10.31.15 AM.png

Expert Commentary

Thank you for this concise summary of mechanical ventilation in children. As noted, while this is an infrequent occurrence, the initial management of a ventilated child is incredibly important.

In choosing initial ventilator settings, the key is decision and reassessment. Most modes of ventilation will work in most children. However, careful attention to what support you’re providing your patient with and what the results of that support are, is vital. Personally, I like using PRVC mode because it adjusts support in children with changing lung compliance without a lot of manipulation required by the physician. But, in any mode of ventilation you can make adjustments as you note changes in compliance. In pressure mode, watch your tidal volumes and in volume control or PRVC, monitor your peak pressures (along with your saturations and end tidal) to see if you’re achieving your goals. Use of SIMV versus AC modes of ventilation are important in the weaning phase of ventilation but less important as you’re initiating mechanical ventilation as the patient is typically neuromuscularly blocked. I also want to emphasize the importance of weaning supplemental oxygen as soon as possible in order to understand the adequacy of your support from an oxygenation and ventilation standpoint. Hypoxemia is bad but so is hyperoxia and masking hypoventilation.

While the research in pediatric ARDS is not as robust as in adults, there is a growing body of literature describing epidemiology and current practice.[1] Current management strategies continue to be extrapolated from adult data- including lung protective strategies of permissive hypoxemia and hypercarbia (tidal volumes 3-6 cc/kg, saturations >92% in mild pARDS and >88% in severe pARDS, pH > 7.2 with exceptions for specific populations including those with pulmonary hypertension).[2] Restrictive fluid strategies (after initial resuscitation) and adequate sedation are recommended. There is ongoing research regarding the use of HFOV and prone positioning in pARDS but this is outside the scope of emergency department care.

The intubated asthmatic remains a source of anxiety among many pediatric intensivists. Key takeaways are low respiratory rate to allow for full exhalation and prevent air trapping and matching intrinsic PEEP. Permissive hypercapnia is appropriate in these patients and their CO2 should be measured by blood gas; recognizing that there is a significant amount of dead space and end tidal may be falsely reassuring/low. When intubating patient with obstructive physiology, it’s also important to ensure adequate preload and have a high suspicion for pneumothorax if they decompensate. Utilizing ketamine for sedation can be useful in these patients and has the advantages of bronchodilation and not significantly suppressing their respiratory drive, allowing them to participate in setting their inspiratory/expiratory times.

Final thought: don’t hesitate to ask for help- from the pediatric intensivists in house or over the phone- we are happy to collaborate!

References:

Khemani RG, Smith L, Lopez-Fernandez YM, et al. Paediatric acute respiratory distress syndrome incidence and epidemiology (PARDIE): an international, observational study. Lancet Respir Med. 2019 Feb;7(2):115-128. doi: 10.1016/S2213-2600(18)30344-8. Epub 2018 Oct 22.
Orloff KE, Turner DA, Rehder KJ. The Current State of Pediatric Acute Respiratory Distress Syndrome. Pediatr Allergy Immunol Pulmonol. 2019 Jun 1; 32(2): 35–44. doi: 10.1089/ped.2019.0999. Epub 2019 Jun 17.

Dr. Katie Wolfe, MD

Attending Physician

Pediatric Critical Care

Ann & Robert H. Lurie Children's Hospital of Chicago

Instructor of Pediatrics (Critical Care)

Northwestern University Feinberg School of Medicine

How To Cite This Post

[Peer-Reviewed, Web Publication] McCauley, M. Stelter, J. (2020, Feb 3). Initiating Emergency Department Mechanical Ventilation in the Pediatric Patient. [NUEM Blog. Expert Commentary by Wolfe, K]. Retrieved from http://www.nuemblog.com/blog/ped-mech-vent.

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