Tag Archives: airway

Can’t Intubate Can’t Ventilate

Originally published at Pediatric EM Morsels on May 20, 2016. Reposted with permission.

Follow Dr. Sean M. Fox on twitter @PedEMMorsels

transtracheal-ventilation-attachments

“Can’t Intubate Can’t Ventilate” is one of the frightening statements that causes massive surges of adrenaline in everyone. Unfortunately, most neural synapses don’t function well with that large surge of adrenaline, and it is, therefore, imperative to contemplate how to manage this scenario before it arises.  We have previously discussed Transtracheal Ventilation and have several videos to view, but let us review this important topic briefly once more. Can’t Intubate Can’t Ventilate: How Do I Oxygenate?

 

Can’t Intubate Can’t Ventilate: Anatomy Matters!

  • With larger children and adults, the can’t intubate can’t ventilate scenario often leads to the Cricothyrotomy.
  • In younger children and infants, the differences in anatomy make a traditional cricothyrotomy challenging.
  • In infants and young children:
    • Generous proportions of subcutaneous adipose tissue (chunky little babies are cute…) obscures landmarks.
    • The Hyoid bone is more prominent than the thyroid cartilage.
    • The Thyroid notch is often not palpable.
    • The Cricothyroid membrane is:
      • More horizontally positioned vs its typical vertical position
      • Small!
        • Around 8 years of age it is 1/2 the height and width of an adult’s
        • In neonates, the size is not sufficient enough to insert any commonly used rescue device. [Navsa, 2005]
  • The altered anatomy makes location of the cricothyroid membrane more difficult (if at all possible) and the small size may make it impossible to pass a large cric-tube through.

 

Can’t Intubate Can’t Ventilate: Go Transtracheal

  • This is THE MOST IMPORTANT PROCEDURE TO KNOW!
  • Transtracheal ventilation has been used successfully in children as well as adults. [Frerk, 2015; Cote, 2009]
  • It may not “secure” an airway, but it will provide the patient with oxygen while you sort out the problem (and change your pants).
  • It is also easier than placing an IV in a child!
    • Locate the trachea!
      • If you are able to locate the cricothyroid membrane and it is large enough you can use it
      • Potential to use this catheter later to convert to a guidewire-assisted percutaneous cricothyrotomy. [Boccio, 2015]
    • Load a large gauge needle/catheter (14 gauge), ideally one that is reinforced(as simple peripheral IV catheters are prone to kink and become obstructed) onto a fluid-filled syringe.
    • Aspirate as you enter the skin at a 30-45 degree angle aimed caudally.
    • When you aspirate bubbles, you are in the airway! Advance the catheter and retract the needle.
    • Boom… done. High-Fives all around! {oh wait… we need oxygen!}

 

Can’t Intubate Can’t Ventilate: The Hard Part

  • The most difficult aspect of the procedure is not waiting too long to do it and leading to hypoxic insult.
  • The next most difficult aspect is figuring out how to connect oxygen to the tiny catheter you just placed in the neck.
  • This is where contemplation of how to do this before you need to do it is important, because most of us are not going to successfully “MacGyver it” on the fly.
  • Oxygen Connection Options

    1. Commercial products
      • Have flow regulators that are easy to use. [Cote, 2009]
      • Connect easily via Lure-lock to the catheter.
      • Many have pressure regulators as well.
      • Con = Expensive.
    2. Oxygen Tubing and High Flow O2 from Wall 
      • Not as optimal as commercial products, but may be best you have available.
      • Turn flow up all of the way. [Bould, 2008]
      • Need to “MacGyver” a flow regulator and a connector
        • Flow Regulator
          • Cut large holes (several) in side of oxygen tubing.
          • Need large/multiple holes to allow air flow to egress easily and not add to PEEP. [Sasano, 2014]
          • May also use Y-connector to another oxygen tube.
        • Connector
          • 3-way stop cock can be used to fit into distal end of oxygen tubing and Lure-lock onto the catheter.
          • Need to ensure 3 way valve is open to flow!
    3. Self-Inflating Ventilation Bag [Sasano, 2014]
      • Not as optimal as commercial products, but may be best you have available.
      • 3.0 ETT bag connector
        • Remove from ETT
        • Insert distal end into catheter
      • 7.5 ETT bag connector
        • Remove from ETT
        • Insert into proximal end of 3 mL syringe (after removing the plunger).
        • Use Lure-lock on syringe to connect to catheter
      • Will need to disengage the bag’s pop-off valve.
  • Oxygenate!
    • Occluding the flow regulator will lead to airflow into the trachea (inspiration).
    • Uncovering the flow regulator will allow air flow from oxygen source and patient to escape (expiration).
    • Inspiration : Expiration = 1 second :  4 seconds
    • Use longer expiration phases for completely occluded upper airway (ex, 1:9)
      • Patient will tolerate hypercapnia better than barotrauma/pneumothorax.

 

Moral of the Morsel

  • Do not let the first time you think about transtracheal ventilation be when you realize you need to do it.
  • Know what equipment you have available.
    • If you have a commercial product, know how to use it and where it is.
    • If you don’t have a commercial product, make your MacGyver survival bag and keep it handy with the tools you need, so you don’t need to recall how to do it in the time of need.

 

References

Boccio E1, Gujral R2, Cassara M3, Amato T4, Wie B5, Ward MF6, D’Amore J7. Combining transtracheal catheter oxygenation and needle-based Seldinger cricothyrotomy into a single, sequential procedure. Am J Emerg Med. 2015 May;33(5):708-12. PMID: 25791154. [PubMed] [Read by QxMD]

Frerk C1, Mitchell VS2, McNarry AF3, Mendonca C4, Bhagrath R5, Patel A6, O’Sullivan EP7, Woodall NM8, Ahmad I9; Difficult Airway Society intubation guidelines working group. Difficult Airway Society 2015 guidelines for management of unanticipated difficult intubation in adults. Br J Anaesth. 2015 Dec;115(6):827-48. PMID: 26556848. [PubMed] [Read by QxMD]

Bould MD1, Bearfield P. Techniques for emergency ventilation through a needle cricothyroidotomy. Anaesthesia. 2008 May;63(5):535-9. PMID: 18412654. [PubMed][Read by QxMD]

Pearls for the management of GSW associated traumatic injury

Author: Joshua Bucher, MD (Assistant Professor, Department of EM, Rutgers – RWJMS; Assistant EMS Medical Director, RWJ-MHS) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician at SAUSHEC)

Case

A 27-year-old male is brought in by EMS after sustaining several gunshot wounds. On arrival, the patient withdraws from painful stimuli, does not open his eyes and makes incomprehensible noises. His heart rate is 130 bpm, blood pressure 84/42, RR 26, and Sp02 88%. While preparing to begin resuscitation, what are the first and most important steps?

Airway

As with all critical patients, the first step is airway management. Care should be taken and best practices should be followed to allow for first pass success including preoxygenation if possible to avoid desaturation. Resuscitation before intubation if possible is important. The appropriate induction agent is of vital importance. Ketamine is associated with the most neutral hemodynamic properties, and it is also the ideal agent for head injured patients.1,2 By maintaining hemodynamic stability and its dissociative properties, it is useful to blunt the response to laryngoscopy. Fentanyl is another option as well at doses 3-5 mcg/kg IV.3

Gunshot wounds may directly involve airway structures. In that case, surgical airway may be preferred, compared to endotracheal intubation. Team preparation is key for this step, and verbalizing the need for potential surgical airway is essential.

C-Spine

Along with airway management, unless there is a focal neurologic injury, it is not necessary to perform cervical spine immobilization of patients suffering from gunshot wounds. This is based on a strong retrospective study as well as supported by the NAEMSP/ACS-COT position paper on spinal immobilization.4 Cervical spine immobilization can directly interfere with airway management, obscure the mouth opening, require increased laryngoscopic force and can lead to worse patient outcomes in the setting of a failed airway.5-7

Breathing

Breathing can be significantly affected depending on where your patient has been shot. Any sign of a tension pneumothorax (decreased breath sounds on one side, tracheal deviation, or hemodynamic instability) needs to be immediately treated with needle decompression or finger thoracostomy followed by tube thoracostomy. A standard pneumothorax can be treated with tube thoracostomy, either during the primary survey or after. High flow NRB oxygen is indicated as well. A GSW to the abdomen may cause difficulty with ventilation due to pain or abdominal distention, and this needs to be monitored.

There have been some newer developments in the management of pneumo/hemothoraces. Inaba et al. described their experience using a smaller chest tube catheter for traumatic pneumo- or hemothoraces and found no difference in patient outcomes with 28-32 vs traditional 36-40 French chest tubes.8 Furthermore, Russo et al. studied a new method of using a pigtail catheter in a swine model vs traditional chest tube and found that both were able to drain the same amount of blood from a hemothorax.9 Although pigtail catheters have been used for pneumothoraces, this is a good step forward towards utilization of more patient oriented resources in the management of a hemothorax. The EAST guidelines currently recommend tube thoracostomy for all hemothoraces. They also suggest that occult pneumothoraces be treated with observation in a stable patient, even with positive pressure ventilation.10

Circulation

The next step of the primary survey is circulation. At this point, fluid resuscitation should begin with blood products in the critically injured patient. Permissive hypotension should be considered to target a systolic of 90 mm Hg or a MAP or 45 – 50 mm Hg, although further prospective studies are required.11  In addition, blood products should be transfused in a 1:1:1 ratio of 6 units of PRBCs:6 units FFP:1 pack of platelets, based on the results of the PROPPR trial.12 Furthermore, crystalloid fluids should be limited unless absolutely necessary to maintain perfusion.13 Fluids can theoretically prohibit clotting and dilute hemoglobin carrying capacity, and this recommendation is supported by the EAST guidelines.14

Thoracotomy

Emergency department thoracotomy is a life-saving procedure for patients with a very low survival. The EAST guidelines define signs of life as pupillary response, ventilation, vital signs, cardiac electrical activity, or extremity movement. They released the following evidence-based recommendations.

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Recently, there has been research looking at this issue. Inaba et al prospectively studied patients undergoing resuscitative thoracotomy in the ER and related it to the FAST exam. They found that if the FAST exam was negative for pericardial fluid or any cardiac activity, the sensitivity was 100% for predicting the patient would not survive.15  This can be added to the EAST guidelines to determine the efficacy and necessity of thoracotomy.

REBOA

Resuscitative endovascular balloon occlusion of the aorta (REBOA) is a last-ditch procedure that can stop hemorrhagic shock in patients with bleeding below the diaphragm. The instrument is comprised of a sheath and balloon, which is inserted into the femoral artery and inflated at one of three areas in order to stop blood flow. This can be especially useful for pelvic fractures with hemorrhage or other intra-abdominal hemorrhagic processes. There currently is limited data since it is a novel device, but it appears to be promising for specific situations. You can read more about REBOA at http://lifeinthefastlane.com/ccc/resuscitative-endovascular-balloon-occlusion-aorta-reboa/.

Extremity Hemorrhage

I want to briefly mention two specific interventions that are geared towards pre-hospital providers. The first intervention is the use of tourniquets for extremity trauma. We now have a large body of literature that supports the use of tourniquets as a life-saving device for extremity trauma with minimal risk of side effects.16 Likewise, the use of clotting agents, such as the commercially named QuickClot agent, are safe and effective to stop bleeding and are recommended by the Tactical Combat Casualty Care guidelines for hemorrhage not amenable to tourniquet placement.16 These two options are highly efficacious and warrant our attention.

Case resolution:

The patient is intubated appropriately. Bilateral chest tubes are placed, with immediate return of 2L from the left chest and a large rush of air from the right. Massive transfusion protocol is activated, and the patient is immediately transfused blood and plasma products. An E-FAST is performed, showing no pericardial fluid but large intraabdominal fluid. The patient is taken to the operating room by the trauma team with successful repair of his thoracic and abdominal injuries and makes a full recovery.

 

Take Home Points

  1. Utilize ketamine for airway management as it is the most hemodynamically neutral agent.
  2. Use traditional large chest tubes for hemothoraces and large pneumothoraces.
  3. Aggressively resuscitate with blood products for the exsanguinating trauma patient.

 

References / Further Reading

  1. Bucher J, Koyfman A. Intubation of the Neurologically Injured Patient. The Journal of emergency medicine. 2015;49(6):920-927.
  2. Cohen L, Athaide V, Wickham ME, Doyle-Waters MM, Rose NG, Hohl CM. The Effect of Ketamine on Intracranial and Cerebral Perfusion Pressure and Health Outcomes: A Systematic Review. Annals of emergency medicine. 2014.
  3. Pouraghaei M, Moharamzadeh P, Soleimanpour H, et al. Comparison between the effects of alfentanil, fentanyl and sufentanil on hemodynamic indices during rapid sequence intubation in the emergency department. Anesthesiology and pain medicine. 2014;4(1):e14618.
  4. White Iv CC, Domeier RM, Millin MG, Standards, Clinical Practice Committee NAoEMSP. EMS Spinal Precautions and the Use of the Long Backboard -Resource Document to the Position Statement of the National Association of EMS Physicians and the American College of Surgeons Committee on Trauma. Prehospital emergency care : official journal of the National Association of EMS Physicians and the National Association of State EMS Directors. 2014;18(2):306-314.
  5. Gruen RL, Jurkovich GJ, McIntyre LK, Foy HM, Maier RV. Patterns of errors contributing to trauma mortality: lessons learned from 2,594 deaths. Annals of surgery. 2006;244(3):371-380.
  6. Santoni BG, Hindman BJ, Puttlitz CM, et al. Manual in-line stabilization increases pressures applied by the laryngoscope blade during direct laryngoscopy and orotracheal intubation. Anesthesiology. 2009;110(1):24-31.
  7. Goutcher CM, Lochhead V. Reduction in mouth opening with semi-rigid cervical collars. British journal of anaesthesia. 2005;95(3):344-348.
  8. Inaba K, Lustenberger T, Recinos G, et al. Does size matter? A prospective analysis of 28-32 versus 36-40 French chest tube size in trauma. The journal of trauma and acute care surgery. 2012;72(2):422-427.
  9. Russo RM, Zakaluzny SA, Neff LP, et al. A pilot study of chest tube versus pigtail catheter drainage of acute hemothorax in swine. The journal of trauma and acute care surgery. 2015;79(6):1038-1043; discussion 1043.
  10. Mowery NT, Gunter OL, Collier BR, et al. Practice management guidelines for management of hemothorax and occult pneumothorax. The Journal of trauma. 2011;70(2):510-518.
  11. Dunser MW, Takala J, Brunauer A, Bakker J. Re-thinking resuscitation: leaving blood pressure cosmetics behind and moving forward to permissive hypotension and a tissue perfusion-based approach. Critical care. 2013;17(5):326.
  12. Holcomb JB, Tilley BC, Baraniuk S, et al. Transfusion of plasma, platelets, and red blood cells in a 1:1:1 vs a 1:1:2 ratio and mortality in patients with severe trauma: the PROPPR randomized clinical trial. JAMA : the journal of the American Medical Association. 2015;313(5):471-482.
  13. Chatrath V, Khetarpal R, Ahuja J. Fluid management in patients with trauma: Restrictive versus liberal approach. Journal of anaesthesiology, clinical pharmacology. 2015;31(3):308-316.
  14. Cotton BA, Jerome R, Collier BR, et al. Guidelines for prehospital fluid resuscitation in the injured patient. The Journal of trauma. 2009;67(2):389-402.
  15. Inaba K, Chouliaras K, Zakaluzny S, et al. FAST ultrasound examination as a predictor of outcomes after resuscitative thoracotomy: a prospective evaluation. Annals of surgery. 2015;262(3):512-518; discussion 516-518.
  16. Defense Do. Tactical Combat Casualty Care Guidelines for Medical Personnel 2015.

 

R.E.B.E.L. EM – Is Apneic Oxygenation Overhyped? with Scott Weingart

Originally published at R.E.B.E.L. EM on April 4, 2016. Reposted with permission.

Follow Dr. Salim R. Rezaie (@srrezaie) and Dr. Scott Weingart (@emcrit

Apneic-Oxygenation-765x583Welcome back to the April 2016 edition of REBELCast. For this episode I was lucky enough to get Scott Weingart on the show to talk to us about all things Apneic Oxygenation (ApOx). ApOx is a concept that has been around for some time in the operating room literature, but only recently been gaining acceptance in the ED, especially after the publication of this concept by Scott and Richard Levitan in the Annals of Emergency Medicine in 2011 [1]. Many nay sayers will argue that the OR studies were in controlled settings with elective surgical patients who were not in critical condition. The believers would argue that ApOx makes sense, its low cost,  and low complexity.  To date there has been no randomized controlled trials (RCTs) on ApOx in the ED.  There has been one ICU Trial (i.e. The FELLOW Trial) [2] and an even more recent observational trial in the ED [3] that have been published on the topic of ApOx. So the question remains: Is Apneic Oxygenation Overhyped?

What are Preoxygenation (PreOx), Apneic Oxygenation (ApOx), and Reoxygenation (ReOx)?

Preoxygenation (PreOx)

  • Should be broken up into 2 separate terms: Preoxygenation and Denitrogenation
  • Denitrogenation = Washing out as much nitrogen from the lungs so that you have a buffer/bag of oxygen when the patient isn’t breathing
  • Requires Time: 3 min of tidal volume breathing on a high FiO2 source
    • With a Non-rebreather (NRB) mask alone,  you are giving approximately 60% FiO2 which will make it impossible to accomplish denitrogenation
  • Preoxygenation (PreOx) = Getting the O2 saturation as close to 100% before pushing RSI meds to intubate

Apneic Oxygenation (ApOx)

  • This occurs during the time from pushing intubation medications, which is anywhere from 45 – 60 seconds, while the paralytic is taking effect, that the patient is burning through their oxygen stores
  • Apneic Oxygenation (ApOx) = Passive movement of oxygen to the alveoli without the patient having to breath and without you having to breath for them
  • Apneic CPAP = Little Brother of ApOx; In patients who have closed alveoli or flooded alveoli; Essentially used for maintenance of recruitment of alveoli during apneic period

Apneic CPAP

Reoxygenation (ReOx)

  • Reoxygenation (ReOx) = Attempts to increase O2 sats when a patient drops their sats during airway management
  • If patient has physiologic shunt physiology, standard BVM will not suffice to fix patients desaturation in between attempts at intubation

BOTTOM LINE: PreOx, ApOx, and ReOx are all attempts to avoid the deadly DeOx (Deoxygenation)

What are your thoughts on the The Fellow Trial? [2]

  • Summary of Trial:
    • Randomized Controlled Trial (RCT) of 150 Critically Ill Patients in a Single ICU
    • Randomized to Apneic Oxygenation vs Usual Care
    • Study Conclusion: Use of Apneic Oxygenation vs Usual Care Made no Difference in the Lowest Arterial Oxygen Saturation Between Induction and Two Minutes After Completion of Intubation
  • Issue with Usual Care in this Trial:
    • Majority of patients had BVM during apneic period
      • Most ED patients are not fasted and using BVM could potentially cause vomiting
    • Not maintaining an open pathway from the nares to the glottis for patients not being bagged
    • Combination of these 2 things hurt the take home message of the study

Does Apneic Oxygenation help in patients with pulmonary shunt physiology (i.e. pulmonary edema, multifocal pneumonia, etc…)?

  • ApOx will help if it is being given with Apneic CPAP
  • Without CPAP, ApOx will not work in patients with shunt physiology
  • Bagging with BVM alone will give O2 and PEEP but again we really want to avoid bagging our patients in the ED as this can cause vomiting
    • With this strategy ApOx may be superfluous
  • A better strategy might be NC at 15 LPM + BVM (without bagging) and with a PEEP Valve

What are your thoughts on the Observational ED Trial recently published by Sackles et al? [3]

  • Summary of Trial:
    • Observational trial in a single ED of 635 patients who received either ApOx or No ApOx
    • Study Conclusion: ApOx in Adult Patients Undergoing RSI had better 1st pass intubation without hypoxemia with a NNT of 7.6
  • The Fact that this Trial is Observational:
    • For People Who Believe in ApOx: Helpful trial that confirms their belief structure
    • For People Who Don’t Believe in ApOx: Does not change their minds, because this is still only observational data
  • Bottom Line:  We need an ED RCT on ApOx

Can you walk us through your exact approach to preoxygenation in a septic patient with pneumonia who is tachypneic, hypoxic, and hypotensive?

  • The Physiologically Difficult Airway (HOp Killers)
    • Hypotension
    • Oxygenation (i.e. Hypoxemia)
    • pH and Ventilation
  • How to Manage our Patient with Hypotension and Hypoxemia
    • Oxygenation (i.e. Hypoxemia)
      • Place patient on standard nasal cannula (NC) at 15L
      • BVM with PEEP valve with 2 hand mask seal for 3 minutes (NO NEED TO BAG) for  preoxygenation and denitrogenation
    •  Hypotension
      • RSI Meds (Great Explanation HERE)
        • Ketamine IV 0.5 mg/kg
        • Rocuronium IV 1.6 – 2.0 mg/kg
      • Start norepinephrine drip or push aliquots of push-dose epinephrine
        • Norepinephrine IV 0.01 – 1 mcg/kg/min
        • Push-Dose Epinephrine IV 5 – 20 mcg every 2 – 5 min

Push-Dose Pressor

Image Borrowed from emcrit.org

Is there a patient we should not use ApOx in?

  • We know ApOx Works in Patients Without Shunt Physiology
    • THRIVE Trial: Transnasal humidified Rapid-Insufflation Ventilatory Exchange [4]
      • 25 patients with difficult airways undergoing general anesthesia
      • Median Apnea was 14 minutes
      • No patient experienced O2 Sat <90%
  • Most Modalities we use for Pre-Oxygenation and Denitrogenation are NOT good enough on their own (i.e. Non-Rebreather Mask)
  • BOTTOM LINE: There is no reason at this time to not be using nasal cannula for ApOx with intubation

Take Home Messages:

  • PreOx is getting the O2 saturation as close to 100% before pushing RSI meds to intubate
  • ApOx is passive movement of oxygen to the alveoli without the patient having to breath and without you having to breath for them
  • In patients with pulmonary shunt physiology, a better strategy might be NC at 15LPM + BVM (Without Bagging) + a PEEP Valve because this will provide both O2 and CPAP for alveolar recruitment
  • The Physiologically Difficult Airway = HOp Killers
    • Hypotension
    • Oxygenation (i.e. Hypoxemia)
    • pH and Ventilation
  • There is no reason at this time to not be using nasal cannula for ApOx with intubation

BONUS Question:

Lets say for a moment that you are not Scott Weingart.  You are working as a faculty at a teaching institution and you have a resident approach you saying they had just listened to the EMCrit podcast. They want to try something because they heard it on the podcast.  How would you handle that situation?

  • Things discussed on the EMCrit podcast are things that are able to be done in the environment of an ED ICU with fellows, which is different than what most people have.
  • In general, as a resident you shouldn’t say you heard something on a podcast and want to do it:
    • Puts people in a tough situation
    • Its important to read the primary literature behind what is being said
  • As the attending who is hearing this, a good way to handle this is telling the resident:
    • Lets discuss this more after we get our patient stabilized
    • Lets do a journal club on this and see if this is something we can incorporate into our practice

For More on This Topic Checkout:

References:

  1. Weingart, Scott D, and Richard M Levitan. Preoxygenation and prevention of desaturation during emergency airway management. Ann Emerg Med 2011; 59 (3): 165 – 75. PMID: 22050948
  2. Semler MW et al. Randomized Trial of Apneic Oxygenation During Endotracheal Intubation of the Critically Ill. Am J Respir Crit Care Med 2015 [Epub ahead of print] PMID: 26426458
  3. Sackles JC et al. First Pass Success Without Hypoxemia is Increased with the Use of Apneic Oxygenation During RSI in the Emergency Department. Acad Emerg Med 2016. [epub ahead of print] PMID: 26836712
  4. Patel A et al. Transnasal Humidified Rapid-Insufflation Ventilatory Exchange (THRIVE): a physiological method of increasing apnoea time in patients with difficult airways. Anesthesia 2015; 70: 323 – 329. PMID: 25388828

Post Peer Reviewed By: Anand Swaminathan (Twitter: @EMSwami)

Bi-level Ventilation: Who Needs it and Who Doesn’t? Pearls and Pitfalls

Authors: Robert Goodnough, MD (EM Resident Physician, UCSF-ZSFG Emergency Medicine Residency Program), Karla Canseco, MD (EM Resident Physician, UCSF-ZSFG Emergency Medicine Program), and Marianne Juarez, MD (Assistant Clinical Professor of Emergency Medicine, UCSF-ZSFG Medical Center) // Edited by: Jennifer Robertson, MD, MSEd and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

Case:

A 65 year-old presents to the emergency department (ED) via emergency medical services (EMS) due to respiratory distress that awakened him from sleep. EMS reports that, upon their arrival, the patient had an oxygen saturation of 85% on room air. Continuous positive airway pressure (CPAP) was provided to the patient and his oxygen saturation improved to 94%. The CPAP also improved the patient’s work of breathing.

On examination in the ED, the patient is tachypneic. He also demonstrates rales, supraclavicular retractions, and is in atrial fibrillation with heart rate (HR) in the 110s. His blood pressure (BP) is 205/104 mmHg.  A nitroglycerin drip is ordered and respiratory therapy is called to place the patient on bi-level positive airway pressure (BiPAP). At this point, one of your seasoned colleagues mentions that he remembered a time when all heart failure patients were intubated.

You tuck your endotracheal (ET) tube into your back pocket and you wonder if your patient will eventually need this…

Introduction:

Noninvasive Positive Pressure Ventilation (NIPPV) is mechanical ventilation that is provided via nasal prongs, a full or oral-nasal facemask, or mouthpiece.  Different modes of mechanical ventilation are available, but the most commonly used methods are CPAP and BiPAP1.  The majority of evidence in NIPPV does not differentiate between CPAP and bi-level, or other modes of NIPPV, and the majority of outcomes and data are applied to NIPPV as a generalized intervention.

PIC1

(photo courtesy of Kai Romero, MD)

Why avoid endotracheal intubation?

Endotracheal intubation is a life-saving intervention when applied skillfully, but its attendant risks are well described.  Staving off intubation has been shown to decrease complications such as hypotension, arrhythmias, death, and nosocomial infections. Intubation also places patients at an increased need for sedation and invasive procedures2. Noninvasive ventilation has become commonplace in the ED to treat respiratory failure and prevent intubation1.

Some Definitions:

  • CPAP: applies constant pressure throughout the breathing cycle to increase functional residual capacity (FRC) by recruiting alveoli, decreasing work of breathing, and improving oxygenation. It is best given in hypoxemic patients 1,3.
  • PEEP/EPAP: Positive End Expiratory Pressure, which is the alveolar pressure before inspiratory flow begins. Adding PEEP helps decrease the amount of work required to initiate a breath. It also helps to decrease atelectasis1,4.
  • Bi-level: Cycled ventilation between Inspiratory Positive Airway Pressure (IPAP) and Expiratory Positive Airway Pressure/PEEP1BiPAP supports ventilation and increases oxygenation.
  • Pressure Support: The difference between EPAP and IPAP is referred to as pressure support. Pressure support makes it easier to draw larger tidal volumes1,4.

Applications for NPPV/Bi-level

1. Chronic Obstructive Pulmonary Disease (COPD)

In COPD, acute respiratory failure manifests as hypoxic, hypercapneic respiratory failure with collapse of small airways. Hyperinflation also occurs. Acute respiratory failure from COPD leads to increased work of breathing, acidosis, altered mental status, and ultimately coma, decompensation, and death5

Bi-level ventilation is a primary treatment option in COPD with good evidence for success5. When compared to usual medical care, bi-level ventilation decreases the risk of death (relative risk reduction 48%) and intubation rates (RRR 60%)5.

Number Needed to Treat (NNT) for mortality benefit = 10

NNT to prevent intubation = 4

Furthermore, when comparing patients with moderate and severe acidosis, bi-level ventilation decreased mortality, rates of intubation, and lengths of stay. It also improved work of breathing, acidosis, and PaC02 levels. Finally, regarding these outcomes, there were no significant differences between more and less acidotic patients at admission5,6.

Indications for NIPPV/bi-level ventilation6

1.      pH <7.35or PaC02 >45 mmHg

2.      Severe dyspnea with signs of increased work of breathing

3.      Caution: In severe respiratory acidosis (pH <7.25), failure rates of NIPPV may be as high as 50%1

Common Initial Settings:

  • IPAP 8-20 cm H2O (up to 30 cm H20)
  • EPAP 2-6 cm H2O to overcome intrinsic airway collapse3,5,7
  • Begin with either high IPAP and then titrate down, or low and titrate high. Both are reasonable, but require close monitoring to meet ventilation goals.7 Each patient is different.
  • Endpoints for physiologic improvement:  at 1 hour, reassessment should be made. Decisions regarding treatment failure, worsening clinical status of bi-level should be made early.5

2. Cardiogenic Pulmonary Edema (CPO)

Acute cardiogenic pulmonary edema is a common and potentially fatal cause of acute respiratory distress. CPO is related to a critical interaction between worsening left ventricular systolic function and an acute increase in systemic vascular resistance that results in rapid accumulation of fluid in the interstitium of the lung. This leads to decreased lung compliance, increased airway resistance, hypoxia, decreased diffusion capacity, and hypercarbia from muscle fatigue8.

Bi-level offers the advantage of improving both cardiac and pulmonary function by providing pressure support with IPAP and EPAP/PEEP. IPAP assists ventilation, which decreases the work of breathing and assures adequate ventilation. The EPAP/PEEP increases the FRC by recruiting collapsed alveoli, improving oxygenation, and helping to force interstitial fluid back into the pulmonary vasculature9,10.

Bi-level ventilation also increases intrathoracic pressure, which can lead to decreased left ventricular (LV) end diastolic volume. This results in decreased afterload and increased LV ejection fraction/stroke volume. Thus, the heart muscle is stretched less, and placed at a steeper part of the Starling curve. This results in stronger LV contractions, and reductions in BP and HR11.

PIC2

(Figure: in the failing heart, NIPPV both decreases preload and also shifts the Starling curve (decreases afterload) to augment cardiac performance)12,13

Common Initial Settings:

·         IPAP: 10 to 20 cm H20

·         EPAP: 5 to 10 cm H20

·         I:E ratio of IT to ET and is usually set at 1:3 or 1:4 (Inspiratory to Expiratory ratio)

Evidence for Bi-level ventilation in CPO:

Unfortunately, most of the evidence for NIPPV for CPO is centered on CPAP with few trials comparing the two modalities (CPAP and bi-level) head-to-head.

In a Cochrane review looking at NIPPV in CPO, CPAP alone has been proven to decrease intubation rates and to decrease in-hospital mortality, without the same benefit seen using bi-level ventilation14.

In the treatment of CPO, controversy regarding the safety of bi-level ventilation stems mainly from a single small study comparing the two NIPPV modalities. This study showed a more rapid improvement in vital signs, dyspnea and arterial blood gas (ABG) results with bi-level, but it also showed higher rates of myocardial infarction (MI) with bi-level ventilation15.  However, subsequent trials comparing CPAP and bi-level showed no difference in MI rates, but decreased intubation rates for those treated with bi-level, especially in patients presenting with hypercarbia16,17.

A trend that holds true is that bi-level leads to rapid improvement in physiological parameters such as respiratory rate, pH, PaCO2, PaO2, HR, work of breathing, afterload, preload, cardiac index, and ejection fraction. However,  more studies need to be performed to show a clear benefit in patient mortality and consistently decreased intubation rates18–21.

Indications for NIPPV in CPO:

1.      Increased work of breathing

2.      Hypercapnia and respiratory failure

3. Asthma

In asthma, NIPPV/bi-level ventilation might help to overcome intrinsic auto-PEEP, to decrease ventilation/perfusion (V/Q) mismatch by increased recruitment of alveoli, and to have a direct bronchodilatory effect in order to decrease work of breathing22.

In the mechanical ventilation of an asthmatic, one should carefully weigh the risk of critical error if the patient is not allowed a prolonged period of expiration in order to prevent “auto-PEEP”. Auto-PEEP is a condition where inhaled breaths are progressively delivered to lungs that have not returned to their FRC. This can subsequently lead to life-threatening hypotension and severe barotrauma, such as pneumothorax2.

Complications from intubation in a severe asthmatic can be severe, including cardiovascular collapse, pneumothorax, and prolonged intubation23.  However, a systematic review comparing NIPPV to medical care did not find a significant benefit to mortality or decreased rates of intubation, though these end points were likely limited by small numbers of patients studied in the intervention22.

Given the risks of intubation, and the purported physiologic benefits of bi-level ventilation to a severe asthmatic, NIPPV is a reasonable treatment strategy.  However, this should be done in tandem with medical management in carefully selected and monitored patients. Of note, NIPPV in asthma has not yet achieved the standard of care.

Indications for NIPPV in Asthma:

1.      As a carefully applied adjunct to medical management in refractory asthma

4. Acute Respiratory failure (no pre-existing chronic lung disease)

The benefits of NIPPV is not clear in undifferentiated acute respiratory failure and the evidence is often conflicting.  The use of NIPPV in undifferentiated acute respiratory failure (ARF) has shown similar mortality rates to conventional ventilation, but it has also demonstrated decreased intubation rates. On the other hand, decreased intubation rates may not apply to those with pneumonia or non-hypercapneic respiratory failure (PNA)24.

A recent multi-center trial showed no decrease in intubation rates for non-hypercapneic ARF (64% PNA) in those without chronic lung disease when compared to high flow or regular oxygen. Additionally, 90 day mortality was decreased in the high flow oxygen group compared to NIPPV. Also, delayed intubation via NIPPV did not show an association with increased mortality25.

Method of delivery and severity of illness likely affect mortality rates in patients with adult respiratory distress syndrome (ARDS) treated with NPPV, as a recent RCT showed decreased 90 day mortality in patients ventilated with helmeted NPPV compared to face mask NPPV26.

Indications:

1.      There are no clearly recommended indications and it should be on a case by case basis.

5. Blunt Thoracic Trauma

In a recent meta-analysis of 219 patients with thoracic trauma, NIPPV decreased intubation rates, improved oxygenation, decreased infection rates and showed mortality rates of 3% vs 22.9% in “standard management,” which was CPAP or face mask oxygen27.

6. Special Populations:

NIPPV decreases intubation rates and in-hospital mortality when applied to acute hypoxic respiratory failure in immunocompromised patients1,28.

It may also provide a benefit to patients with palliative care needs in whom endotracheal intubation is not within their goals of care, with some studies showing reversal of acute respiratory failure and return to home1,28,29.

The use of NPPV in the ARF of decompensation of neuromuscular disease is controversial, and may not be indicated in those with rapidly progressive disease29.

Pre-oxygenation For Intubation:

Much of the focus has been on avoiding intubation, but in critically ill patients, intubation and mechanical ventilation can be life-saving; to intubate an unstable patient is perilous, with desaturation, arrhythmia, cardiovascular collapse and cardiac arrest as well recognized entities30.

Pre-oxygenation prior to intubation is the standard of care to prevent life threatening complications during intubation.  Some patients display refractory hypoxia in the face of usual facemask pre-oxygenation, and failure to reach 93-95% Sp02 prior to intubation places the patient at risk for desaturation and apnea during the procedure31.

NIPPV has been shown to decrease desaturation rates in refractory hypoxia during pre-oxygenation for intubation and should be strongly considered for pre-oxygenation prior to intubation in refractory hypoxia30–32.

Pearls:

  1. Positive Pressure is not everything. Do not forget medical management
  2. Bi-level ventilation is an early “go-to” in moderate to severe COPD exacerbations
  3. Experienced respiratory therapists (RTs) and staff are critical to the success of non-invasive ventilation
  4. Once applied, reassess your patient frequently and be ready to adjust!
  5. Can be used to stave off intubation at the end of life
  6. Consider for pre-oxygenation prior to intubation

Pitfalls:

  1. Positive pressure can cause hypotension and decompensation if blindly applied
  2. Do not place a pressure mask on a damaged face or a fluid filled mouth
  3. Do not delay necessary intubation
  4. Do not let your patient Auto-PEEP
  5. Your severely acidotic patient is at high risk for failure: be ready to intubate.
  6. If your patient is not awake, then the patient should be intubated.

 Who Needs It?

  1. Patients with moderate to severe COPD exacerbations
  2. Those patients with cardiogenic pulmonary edema with increased work of breathing or hypercapnia
  3. Patients with isolated blunt thoracic trauma
  4. The immunocompromised patient with hypoxic respiratory failure
  5. Patients who require pre-oxygenation prior to intubation

Who Does Not?

  1. Altered Mental Status
  2. Facial Trauma/Can’t Handle their own secretions

Gray Zones?

  1. Asthma
  2. Neuromuscular Disease
  3. Undifferentiated Hypoxic Respiratory Failure

References / Further Reading

1. Aboussouan, L. S. & Ricaurte, B. Noninvasive positive pressure ventilation: Increasing use in acute care. Cleve. Clin. J. Med. 77, 307–316 (2010).

2. Leatherman, J. Mechanical ventilation for severe asthma. Chest 147, 1671–1680 (2015).

3. Bolton, R. & Bleetman, A. Non-invasive ventilation and continuous positive pressure ventilation in emergency departments: where are we now? Emerg. Med. J. EMJ 25, 190–194 (2008).

4. Appendini, L. et al. Physiologic effects of positive end-expiratory pressure and mask pressure support during exacerbations of chronic obstructive pulmonary disease. Am. J. Respir. Crit. Care Med. 149, 1069–1076 (1994).

5. Ram, F. S. F., Picot, J., Lightowler, J. & Wedzicha, J. A. Non-invasive positive pressure ventilation for treatment of respiratory failure due to exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst. Rev. CD004104 (2004). doi:10.1002/14651858.CD004104.pub2

6. Pauwels, R. A., Buist, A. S., Calverley, P. M. A., Jenkins, C. R. & Hurd, S. S. Global Strategy for the Diagnosis, Management, and  Prevention of Chronic Obstructive Pulmonary Disease. Am. J. Respir. Crit. Care Med. 163, 1256–1276 (2001).

7. Prinianakis, G., Delmastro, M., Carlucci, A., Ceriana, P. & Nava, S. Effect of varying the pressurisation rate during noninvasive pressure support ventilation. Eur. Respir. J. 23, 314–320 (2004).

8. Wiesen, J., Ornstein, M., Tonelli, A. R., Menon, V. & Ashton, R. W. State of the evidence: mechanical ventilation with PEEP in patients with cardiogenic shock. Heart Br. Card. Soc. 99, 1812–1817 (2013).

9. Cross, A. M. Review of the role of non-invasive ventilation in the emergency department. J. Accid. Emerg. Med. 17, 79–85 (2000).

10. Peter, J. V., Moran, J. L., Phillips-Hughes, J., Graham, P. & Bersten, A. D. Effect of non-invasive positive pressure ventilation (NIPPV) on mortality in patients with acute cardiogenic pulmonary oedema: a meta-analysis. Lancet Lond. Engl. 367, 1155–1163 (2006).

11. Sheldon, R. Congestive heart failure and noninvasive positive pressure ventilation. Emerg. Med. Serv. 34, 64–67 (2005).

12. Figueroa, M. S. & Peters, J. I. Congestive heart failure: Diagnosis, pathophysiology, therapy, and implications for respiratory care. Respir. Care 51, 403–412 (2006).

13. Shekerdemian, L. & Bohn, D. Cardiovascular effects of mechanical ventilation. Arch. Dis. Child. 80, 475–480 (1999).

14. Vital, F. M. R., Ladeira, M. T. & Atallah, A. N. Non-invasive positive pressure ventilation (CPAP or bilevel NPPV) for cardiogenic pulmonary oedema. Cochrane Database Syst. Rev. CD005351 (2013). doi:10.1002/14651858.CD005351.pub3

15. Mehta, S. et al. Randomized, prospective trial of bilevel versus continuous positive airway pressure in acute pulmonary edema. Crit. Care Med. 25, 620–628 (1997).

16. Nava, S. et al. Noninvasive ventilation in cardiogenic pulmonary edema: a multicenter randomized trial. Am. J. Respir. Crit. Care Med. 168, 1432–1437 (2003).

17. Gray, A. J. et al. A multicentre randomised controlled trial of the use of continuous positive airway pressure and non-invasive positive pressure ventilation in the early treatment of patients presenting to the emergency department with severe acute cardiogenic pulmonary oedema: the 3CPO trial. Health Technol. Assess. Winch. Engl. 13, 1–106 (2009).

18. Park, M. et al. Oxygen therapy, continuous positive airway pressure, or noninvasive bilevel positive pressure ventilation in the treatment of acute cardiogenic pulmonary edema. Arq. Bras. Cardiol. 76, 221–230 (2001).

19. Crane, S. D., Elliott, M. W., Gilligan, P., Richards, K. & Gray, A. J. Randomised controlled comparison of continuous positive airways pressure, bilevel non-invasive ventilation, and standard treatment in emergency department patients with acute cardiogenic pulmonary oedema. Emerg. Med. J. EMJ 21, 155–161 (2004).

20. Levitt, M. A. A prospective, randomized trial of BiPAP in severe acute congestive heart failure. J. Emerg. Med. 21, 363–369 (2001).

21. Pang, D., Keenan, S. P., Cook, D. J. & Sibbald, W. J. The effect of positive pressure airway support on mortality and the need for intubation in cardiogenic pulmonary edema: a systematic review. Chest 114, 1185–1192 (1998).

22. Ram, F. S. F., Wellington, S., Rowe, B. & Wedzicha, J. A. Non-invasive positive pressure ventilation for treatment of respiratory failure due to severe acute exacerbations of asthma. Cochrane Database Syst. Rev. CD004360 (2005). doi:10.1002/14651858.CD004360.pub3

23. Landry, A., Foran, M. & Koyfman, A. Does Noninvasive Positive-Pressure Ventilation Improve Outcomes in Severe Asthma Exacerbations? Ann. Emerg. Med. 62, 594–596

24. Honrubia, T. et al. Noninvasive vs conventional mechanical ventilation in acute respiratory failure : A multicenter, randomized controlled trial. Chest 128, 3916–3924 (2005).

25. Frat, J.P. et al. High-flow oxygen through nasal cannula in acute hypoxemic respiratory failure. N. Engl. J. Med. 372, 2185–2196 (2015).

26. Patel, B. K., Wolfe, K. S., Pohlman, A. S., Hall, J. B. & Kress, J. P. Effect of Noninvasive Ventilation Delivered by Helmet vs Face Mask on the Rate of Endotracheal Intubation in Patients With Acute Respiratory Distress Syndrome: A Randomized Clinical Trial. JAMA 315, 2435–2441 (2016).

27. Chiumello, D., Coppola, S., Froio, S., Gregoretti, C. & Consonni, D. Noninvasive ventilation in chest trauma: systematic review and meta-analysis. Intensive Care Med. 39, 1171–1180 (2013).

28. Hill, N. S., Brennan, J., Garpestad, E. & Nava, S. Noninvasive ventilation in acute respiratory failure. Crit. Care Med. 35, 2402–2407 (2007).

29. Mas, A. & Masip, J. Noninvasive ventilation in acute respiratory failure. Int. J. Chron. Obstruct. Pulmon. Dis. 9, 837–852 (2014).

30. Mosier, J. M. et al. The Physiologically Difficult Airway. West. J. Emerg. Med. 16, 1109–1117 (2015).

31. Weingart, S. D. & Levitan, R. M. Preoxygenation and prevention of desaturation during emergency airway management. Ann. Emerg. Med. 59, 165–175.e1 (2012).

32. Baillard, C. et al. Noninvasive ventilation improves preoxygenation before intubation of hypoxic patients. Am. J. Respir. Crit. Care Med. 174, 171–177 (2006).

 

Unstable Sepsis: Airway First? Not Always

Author: Jennifer Robertson, MD, MSEd // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

 Case

A 50 year-old male presents to the emergency department (ED) with a five day history of worsening abdominal pain. He states this has never occurred before, but he thinks he has a known ventral hernia.  He really has no other complaints other than the pain. Upon arrival, he appears diaphoretic and a little confused but is otherwise answering questions appropriately.  The patient’s brother states that his brother is “always” sweaty and that the diaphoresis is nothing unusual. The patient denies any significant past medical history, including no history of diabetes, immunosuppression or chronic steroid use.

Initial vital signs (VS):

Heart rate (HR) 100 beats per minute (bpm), normal temperature, normal blood pressure, an oxygen saturation (SpO2) of 99% on room air (RA) and a respiratory rate of 24 breaths per minute.

Initial examination:

The patient is an obese male who appears ill and diaphoretic. He is somewhat tachypneic but is able to answer questions in full sentences. He has clear breath sounds and remains slightly tachycardic. His abdominal exam appears grossly abnormal, including marked distention and firmness. There is focal enlargement of his abdomen in the right lower quadrant and he has overlying erythema and warmth of this site. His genitourinary exam is normal.

Initial interventions:

An initial concern was for an incarcerated hernia, possibly bowel necrosis. Two large bore peripheral intravenous (IV) lines were placed and an initial crystalloid bolus was administered. Broad spectrum antibiotics were given immediately due to concern for early sepsis. Labs were ordered and pending.  An electrocardiogram (ECG) was obtained showing sinus tachycardia without any acute abnormalities. The patient was deemed hemodynamically stable enough to go to computed tomography (CT) scan for imaging.

Sepsis: General Review

Extensive research, peer reviewed articles and online sites have studied, reviewed and evaluated sepsis and its dangers. The current article is not intended to cover sepsis or its definitions, however the following excellent articles can be reviewed on emdocs.net for an extensive review:

http://www.emdocs.net/sepsis-care-whats-new-the-cms-guidelines-for-severe-sepsis-and-septic-shock-have-arrived/

http://www.emdocs.net/fluid-choice-does-it-matter/

http://www.emdocs.net/utility-obtaining-lactate-measurement-ed/

http://www.emdocs.net/8362-2/

http://www.emdocs.net/early-sepsis-why-do-we-miss-it-and-how-do-we-improve/

http://epmonthly.com/article/sepsis-mimics/

http://www.emdocs.net/the-dangers-of-over-resuscitation-in-sepsis/

http://www.emdocs.net/septic-shock-who-should-be-treated-with-early-pressors/

http://www.emdocs.net/blood-cultures-when-does-obtaining-them-make-a-meaningful-impact-on-clinical-care/

In general, sepsis can be a continuum from a very mild infection to fulminant septic shock. As a medical student and resident, one may have been taught that the airway always takes priority in any unstable patient, especially in altered patients who cannot protect their airways and those with primary airway or pulmonary diseases. However, immediately intubating a patient with sepsis may not be the right thing to do, especially if he or she is hemodynamically unstable. It should be mentioned that with the exception of the need for pre-oxygenation (see #2 below), this review is not about the patient who requires immediate intubation. Importantly, one should never wait until a patient’s physiologic reserve is completely gone and thus, if any planned resuscitation fails, then intubation should not be delayed (1).

Case Continuation

The patient returns from the CT scanner and the read is pending. The nurse taking care of the patient notifies you that the cardiac monitor demonstrates an irregularly irregular rhythm at 180 beats per minute.

 Repeat examination:

HR 180 (irregular)

Blood pressure 90/50 mmHg

RR 40 breaths per minute

Patient more confused, remains diaphoretic

Repeat ECG: atrial fibrillation with rapid ventricular response (RVR), rate 180

The nurse asks what to do next…

Issues to Consider Prior to Intubation

There are two main issues to consider prior to intubating an unstable patient who requires an urgent but not immediate airway. These issues include (1) hemodynamic instability such as severe tachycardia, bradycardia and hypotension and (2) hypoxia that does not respond to standard oxygen therapy.

(1) Hemodynamic instability

Studies have shown that tracheal intubation is not a benign event. The simple act of intubating can cause hemodynamic changes that can affect post-intubation outcomes (2). In addition, the process of intubation typically requires induction agents and positive pressure ventilation, which can also significantly contribute to the hemodynamic changes seen during and after intubation (2, 3, 4, 5). In addition, repeat laryngoscopy attempts also can be detrimental (6).  Not only can hemodynamic instability occur with intubation in normal, healthy patients, but it most definitely occurs in the critically ill emergency department (ED) patient and usually to a greater extent (2). The hemodynamic changes that result from laryngoscopy and tracheal intubation are complicated and multifactorial (8). However, research has demonstrated airway manipulation is a potent stimulator of the sympathetic and parasympathetic nervous systems, with initial increases in heart rate and blood pressure due to transient catecholamine release (3). Endogenous epinephrine has a very short half-life, however, and post-intubation hypotension (typically described as ≤ 90 mm Hg systolic) is thought to be due to rapid attenuation of this sympathetic tone (2). In addition, the addition of positive end expiratory pressure (PEEP) can further decrease cardiac preload by decreasing venous return (2). This is especially a problem in those patients who have diminished cardiac reserve, are hypovolemic, or septic (2).  Extreme bradycardia and hypotension can also occur due to repetitive laryngoscopy and can also be worsened in those patients who have concomitant hypoxemia (2, 6).

While the hemodynamic changes during intubation can be considered “normal” physiologically, it is not a benign process (8). In fact, post-intubation hypotension (and really any hypotension in the ED) is associated with increased morbidity, prolonged patient stays, cardiac arrest and death (8-14). In addition, other studies have demonstrated that lower blood pressures and elevated shock indices (such as seen in sepsis) prior to intubation are associated with post-intubation hypotension and poorer outcomes (8, 10, 15, 16). Thus, hemodynamic resuscitation prior to intubation should be considered in the unstable (but not crash airway) patient (1, 12).

Case Continued

Upon re-examination, the patient remains diaphoretic and altered. Laboratory tests started to return and demonstrated a leukocytosis and a lactate level of 4.0. Surprisingly, the serum bicarbonate level was only mildly decreased. The CT read was still pending. Clinically, the patient was septic and likely from an intra-abdominal pathology. The decision was made to intubate and start a central line, however, given the new onset atrial fibrillation with RVR and low blood pressures, it was decided to first attempt synchronized cardioversion to see if conversion to sinus rhythm would allow for increased cardiac output and blood pressure prior to intubation. Using a small dose of ketamine for comfort and pain relief, the patient was cardioverted twice without success.  He was finishing his second liter of crystalloid, remained hypotensive and tachycardic, and the nurse started to look concerned…

Solutions

A few strategies to avoid hypotension and maximize cardiac preload and afterload prior, during and after intubating an urgent airway (1, 2, 17):

(a) Maximize fluid status

(b) Consider using push dose vasopressors such as phenylephrine or epinephrine. The dose of push dose phenylephrine is 50-200 micrograms (mcg) every two to five minutes. The dose of push dose epinephrine is 5-20 mcg every two to five minutes.  A good review of dosing can be seen at http://emcrit.org/wp-content/uploads/push-dose-pressors.pdf (18).

(c) Cardiovert any unstable rhythms

(d) Consider using induction and sedative agents that work best for each patient’s hemodynamic status. This article is not intended to be a review of pharmacologic agents. A nice medication review can be seen at http://www.emdocs.net/8751-2/ (19).

(e) Avoid too much PEEP after intubating if possible

Case Resolution

After a failed cardioversion, the patient’s blood pressure continued to decline. Three doses of push dose phenylephrine were given while the patient was prepared for intubation. His blood pressure rose and his heart rate declined with the phenylephrine, but he did remain in atrial fibrillation. The patient was given an induction dose of ketamine and intubated on the first pass without any complications. The patient’s CT read finally returned, demonstrating a ruptured bowel with pneumoperitoneum. A central line was placed and the patient was transferred to a higher level of care and he was extubated by day ten of hospitalization.

(2) Hypoxia

While the patient did not sustain hypoxia and had a normal PO2 on his initial and subsequent arterial blood gas (ABG) measurements, many patients do. On occasion, patients with an urgent, but not crash, need for an airway may not be able to sustain oxygen saturations above 90% on high levels of supplemental oxygen. In this case, ED providers may be eager to intubate the patient to “increase oxygen levels”. However, it is not the intubation that helps this but likely the positive pressure that is provided after intubation and during the patient’s therapy on the ventilator (17).

The goal of pre-oxygenation is to get the oxygen saturation as high as possible in order to allow for enough time for intubation and prevent severe hypoxemia during the procedure (17). If patients are intubated prior to adequate pre-oxygenation, they are at risk for a rapid decline in oxygen levels. This is even more pronounced in the obese and critically ill patients (20, 21). The oxygen-hemoglobin dissociation curve demonstrates this physiology.

PIC FOR POST

Severe hypoxemia is a risk factor for cardiac arrest and thus, it is imperative that patients, even those whose oxygen saturations do not reach above 90% on supplemental oxygen, receive adequate pre-oxygenation prior to intubation (7, 17, 22). Patients with poor alveolar oxygenation whose oxygen saturations do not rise with simple supplemental oxygen may be undergoing a number of possible pathologies such as dead space where there is normal ventilation but no perfusion, a shunt, and a low venous oxygen saturation (17).  Examples include a septal cardiac defect (anatomic shunt), pneumonia or pulmonary edema (physiologic shunt), a pulmonary embolism (dead space), and shock states (poor venous oxygen saturation) (17).

In order to properly pre-oxygenate the above types of patients, it may be necessary to incorporate other techniques prior to intubation. It is imperative that emergency physicians understand this need to take the time to properly pre-oxygenate and not to “jump to intubation” when a patient does not respond to simple supplemental oxygen therapy and a standard bag valve mask.  Techniques to consider include: (1) Non-invasive positive pressure ventilation (NIPPV) and the use of PEEP valves, (2) Apneic oxygenation and (3) Delayed sequence intubation (17, 21, 22).

(1) NIPPV – In a patient whose oxygen saturation does not improve with standard pre-oxygenation techniques, such as a patient with shunting, may require positive pressure ventilation. In this case, positive pressure ventilation has been shown to improve the efficiency of gas exchange, recruit more alveoli, increase lung volumes and increase the amount of time it takes for desaturation to occur (17, 21). In order to achieve this, a standard continuous positive airway pressure (CPAP) machine can be utilized, maintaining a PEEP of 5 to 15 cm H20 (17). Another strategy is to use the ventilator for this and the 2010 article by Dr. Weingart can be reviewed for the proper ventilator settings for pre-oxygenation (17). If a patient cannot tolerate the positive pressure mask, then a technique called delayed sequence intubation can be used as mentioned below (17, 23).

Another noteworthy topic is the use of the BVM. Standard BVMs do not provide any PEEP. Therefore, if there is a shunt and the patient’s oxygenation is not improving with the BVM, a tool called a PEEP valve can also be used (17). It is imperative that the mask seal is tight, otherwise the PEEP valve will not be useful (17).

(2) Apneic Oxygenation – The very act of rapid sequence intubation does entail a period of apnea while the tube is being placed. It is thought that placing supplemental oxygen via nasal cannula may be helpful to supply additional oxygen while the patient is apneic. It has been demonstrated that alveoli continue to take up some oxygen, even without active breathing (22). While carbon dioxide does increase during this time, the patient still may be oxygenated during the apneic period with the idea of “apneic oxygenation” (17, 22). Of note, once the patient is paralyzed, it is important to make sure that the tongue and posterior pharynx is not occluding the airway and a head tilt with chin lift is adequate for most patients. A nasal or oral airway may be required as well (22).

(3) Delayed sequence intubation – For the difficult patient who requires pre-oxygenation, a simple facemask may not work, as it may be pulled off due to agitation or confusion. In addition, the added hypoxia and hypercapnia may add to any agitation, causing patients to become even more uncooperative (17). One proposed way to get around this agitation is with a concept called “delayed sequence intubation” (DSI). Several articles have been written by Dr. Weingart and his articles are listed below for review. However, in short, DSI consists of administering a sedative agent that does not cause spontaneous respirations to decline, such as ketamine at a dose of 1-1.5 mg/kg slow intravenous push (17). After giving the medication, the patient becomes calmer, allowing proper preoxygenation to occur (17, 23). After the patient is adequately preoxygenated, then standard rapid sequence intubation can occur. This procedure was recently researched by Dr. Weingart in 2015 with promising results (23). The same concepts of needing PPV may be required in those patients who demonstrate shunt physiology.

Conclusions: Tracheal intubation is more complicated than a simple airway tube, especially in the critically ill and septic patients. While some patients require an immediate airway, many patients should be critically assessed prior to intubation. Proper pre-oxygenation should always occur and hemodynamic resuscitation should be considered in order to avoid post-intubation hypotension and increased morbidity and mortality.

References / Further Reading

  1. Manthous CA. Avoiding circulatory complications during endotracheal intubation and initiation of positive pressure ventilation. J Emerg Med 2010; 38 (5): 622-31.
  2. Mort TC. Complications of emergency tracheal intubation: hemodynamic alterations-Part I. J Intensive Care Med 2007; 22 (3): 157-65.
  3. Shribman AJ, Smith JG, Achola KJ. Cardiovascular and catecholamine responses to laryngoscopy with and without tracheal intubation. Br J Anaesth 1987; 59 (3): 295-99.
  4. Bucx MJL, Van Geel RTM, Scheck PAE, et al. Cardiovascular effects of forces applied during laryngoscopy.Anaesthesia 1992; 47 (12): 1029-33.
  5. Schwab TM, Greaves TH. Cardiac arrest as a possible sequela of critical airway management and intubation. Am J Emerg Med 1998; 16 (6): 609-12.
  6. Mort TC. Emergency tracheal intubation: complications associated with repeated laryngoscopic attempts. Anesth Analg 2004; 99 (2): 607-13.
  7. Mort TC. The incidence and risk factors for cardiac arrest during emergency tracheal intubation: a justification for incorporating the ASA Guidelines in the remote location. J Clin Anesth 2005; 16 (7): 508-16.
  8. Heffner AC, Swords DS, Nussbaum ML, et al. Predictors of the complication of post-intubation hypotension during emergency airway management. J Crit Care 2012; 27 (6): 587-93.
  9. Heffner AC, Swords DS, Kline JA. The frequency and significant of post-intubation hypotension during emergency airway management. J Crit Care 2012; 27 (4): 417-e9.
  10. Schwartz DE, Matthay MA, Cohen NH. Death and other complications of emergency airway management in critically ill adults. A prospective investigation of 297 tracheal intubations. Anesthesiology 1995; 82 (2): 367-76.
  11. Heffner AC, Swords DS, Neale MN, et al. Incidence and factors associated with cardiac arrest complicating emergency airway management. Resuscitation 2013; 84 (11): 1500-04.
  12. Kim WY, Kwak MK, Ko BS, et al. Factors associated with the occurrence of cardiac arrest after emergency tracheal intubation in the emergency department. PLOS One 2014; 9 (11): e112779.
  13. Jones AE, Yiannibas V, Johnson C, et al. Emergency department hypotension predicts sudden unexpected in-hospital mortality: a prospective cohort study.”CHEST 2006; 130 (4): 941-46.
  14. Merz TM, Etter R, Mende L, et al. Risk assessment in the first fifteen minutes: a prospective cohort study of a simple physiological scoring system in the emergency department. Crit Care 2011; 15 (1): 1.
  15. Green RS, Edwards J, Sabri E, et al. Evaluation of the incidence, risk factors and impact on patient outcomes of post-intubation hemodynamic instability. CJEM 2012; 14 (2): 74-82.
  16. Lin CC, Chen KF, Shih CP, et al. The prognostic factors of hypotension after rapid sequence intubation. Am J Emerg Med 2008; 26 (8): 845-51.
  17. Weingart SD. Preoxygenation, reoxygenation, and delayed sequence intubation in the emergency department. J Emerg Med 2011; 40 (6): 661-67.
  18. http://emcrit.org/wp-content/uploads/push-dose-pressors.pdf.
  19. http://www.emdocs.net/8751-2/
  20. Dargin J, Medzon R. Emergency department management of the airway in obese adults. Ann Emerg Med 2010; 56 (2): 95-104.
  21. Baillard C, Fosse JP, Sebbane M, et al. Noninvasive ventilation improves preoxygenation before intubation of hypoxic patients. Am J Respir CritCareMed 2006; 174 (2): 171-77.
  22. Weingart SD, Levitan RM. Preoxygenation and prevention of desaturation during emergency airway management. Ann Emerg Med 2012; 59 (3): 165-75.
  23. Weingart SD, Trueger S, Wong N, et al. Delayed sequence intubation: a prospective observational study. Ann Emerg Med 2015; 65 (4): 349-55.

PEM Playbook – Multisystem Trauma in Children Part I: Airway, Chest Tubes, and Resuscitative Thoracotomy

Originally published at Pediatric Emergency Playbook on February 1,
2016 – Visit to listen to accompanying podcast. Reposted with permission.

Follow Dr. Tim Horeczko on twitter @EMTogether

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Traumatized children need your full attention.

Protocols work well for adults, but trauma in children requires that we exercise our clinical muscles just a bit more.

Two main reasons:

  1.  Children have specific injury patterns.

  2.  Their physiologic response to trauma is unique.

Crash course in pediatric anatomy and physiology in trauma

When you think of trauma in children, think of Charlie Brown. Large head, no neck, his chest and abdomen form an underdeveloped, amorphous shape.

Alternatively, think of children as apples – they are rounder than they are tall, with a large increased surface area. Apples don’t have a hard shell or thick rind to protect them. If you drop them, you may not see any evidence of damage to the outside, but there can be considerable bruising just under the surface.

  • A child has thin skin, less subcutaneous deposits than an adult, and a non-calcified, pliable thorax that deforms more than it protects or shields.
  • The child’s abdominal muscles are not yet developed. There is less peritoneal fat to cushion a blow, and so traumatic forces transmit readily into internal organs, often without external bruising.
  • The child’s large surface area also causes him to dissipate heat more quickly. He may be wet from urine or blood, and in a major trauma, this faster cool-down predisposes him to coagulopathy.

Case

A 5-year-old boy who was playing with his older brother in front of their home when the ball rolled into the street. He ran after it, and was struck by a sedan going approximately 30 mph.

This is the so-called Wadell’s triad  that occurs in a collision of auto versus pedestrian or auto versus bicycle. The initial impact is the greatest, and will vary depending on the child’s height and what part of his body reaches up to the bumper of the car. Depending on the height of the child and the height of the car, the initial impact will cause a femur fracture, a pelvic fracture, or direct abdominal trauma. The second impact happens as the child is flung onto the grill or the hood of the car, causing usually thoracic trauma. The third impact can be the coup de grâce – to add insult to major injury, the child is then propelled forward, worsening the two previous impacts’ injuries and adding a third – severe blunt head trauma.

Intubation Pearl #1:

If your patient has any subtle change in mental status, intubate early. In pediatric trauma, we need to beproactive. Hypoxia is our enemy.

Intubation Pearl #2:

Thankfully cervical spine injuries in children are uncommon, and when they do occur, they typically occur at the child’s fulcrum, which is at C2. Compare this with an adult’s injury pattern with our fulcrum at C7. Be careful and minimize manipulation of the cervical spine, but do what you must to visualize the chords and place the tube. Keep the neck midline, and realize that the child’s usual decrease respiratory reserve is even more affected by trauma. Preoxygenate and pass that tube quickly.

Chest Tube Pearl #1:

Chest tube sizing in pediatrics is straightforward if we remember that the traditional chest tube size is 4 x the ETT size.

Chest Tube Pearl #2:

Try using a pigtail catheter.

Safety Triangle

  • Lateral edge of the pectoral muscle
  • Lateral edge of the latisimus dorsi
  • Line along the fifth intercostal space at the level of the nipple.

It’s roughly where you would put on a generous dose of deodorant. Insertion here minimizes the risk of damage to nerves, vessels and organs.

Resuscitative Thoracotomy in Children

In a 40-year review of ED thoracotomy, Moore et al. analyzed 1,691 patients who received ED thoracotomy. Overall all-cause adult survival was 6.1%. In children ? 15 years of age, overall all-cause survival was considerably less, at 3.4%.

In a large case series and review of the literature for pediatric ED thoracotomy, Allen et al. found a survival rate in penetrating trauma of 10.2%, with a much lower survival rate in blunt pediatric arrest, at 1.6%. Adolescents had more penetrating injuries, and younger children had more blunt trauma.

To synthesize, the rarity of ED thoracotomy in children is due to the fact that:

  1. Traumatic full arrest in children is uncommon.
  2. It is most often blunt trauma.
  3. Blunt traumatic arrest in children is mostly non-survivable.

REBOA

If you have access to resuscitative endovascular balloon occlusion of the aorta or REBOA, this may be an option to temporize the child to get him to the relative control of the operating room. REBOA involves accessing the common femoral artery, passing a vascular sheath, floating a balloon catheter to the appropriate section of the aorta, and inflating the balloon to occlude blood flow.

Brenner et al. described a case series of 6 patients from two Level I trauma centers. They used REBOA for refractory hemorrhagic shock due to either blunt or penetrating injury. After balloon occlusion, blood pressure improved sufficiently to take the patient either to interventional radiology or to the OR. Four patients lived, two died. The AORTA trial is underway to investigate its use in trauma.

Summary:

  1. Children are like Charlie Brown – large head, no neck, amorphous, underdeveloped and unprotected thorax and abdomen. Or, if you like, they’re like, apples – they have a large surface area and are easily internally bruised, often without overt signs of external bruising.
  2. Chest tubes for children are very similar to the adult procedure – the traditional chest tube size is 4 x the child’s ETT size. Try to use smaller pigtail catheters, available in commercial kits, whenever possible. They’re easy, safe, and effective.
  3. Resuscitative thoracotomy is for penetrating trauma with signs of life wthin 10-15 minutes of arrival. Find the correctable surgical cause of the arrest. Resuscitative thoracotomy for blunt trauma has a dismal prognosis in children.

Selected References

Allen CJ, Valle EJ, Thorson CM, Hogan AR, Perez EA, Namias N, Zakrison TL, Neville HL, Sola JE. Pediatric emergency department thoracotomy: a large case series and systematic review. J Pediatr Surg. 2015 Jan;50(1):177-81.

American College of Surgeons Committee on Trauma; American College of Emergency Physicians Pediatric Emergency Medicine Committee; National Association of Ems Physicians; American Academy of Pediatrics Committee on Pediatric Emergency Medicine, Fallat ME. Withholding or termination of resuscitation in pediatric out-of-hospital traumatic cardiopulmonary arrest. Pediatrics. 2014 Apr;133(4):e1104-16.

Holscher CM, Faulk LW, Moore EE, Cothren Burlew C, Moore HB, Stewart CL, Pieracci FM, Barnett CC, Bensard DD. Chest computed tomography imaging for blunt pediatric trauma: not worth the radiation risk. J Surg Res. 2013 Sep;184(1):352-7.

Moore HB, Moore EE, Bensard DD. Pediatric emergency department thoracotomy: A 40-year review. J Pediatr Surg. 2015 Oct 19.

Scaife ER, Rollins MD, Barnhart DC, Downey EC, Black RE, Meyers RL, Stevens MH, Gordon S, Prince JS, Battaglia D, Fenton SJ, Plumb J, Metzger RR. The role of focused abdominal sonography for trauma (FAST) in pediatric trauma evaluation. J Pediatr Surg. 2013 Jun;48(6):1377-83.

Stannard A, Eliason JL, Rasmussen TE. Resuscitative endovascular balloon occlusion of the aorta (REBOA) as an adjunct for hemorrhagic shock. J Trauma. 2011 Dec;71(6):1869-72.


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Pediatric Trauma on WikEM

 

This post and podcast are dedicated to Dr Al Sacchetti, MD, FACEP. Thank you for promoting the emergency care of children and for spreading the message that you don’t need subspecialty training to take good care of acutely ill and injured children.

Powered by #FOAMed — Tim Horeczko, MD, MSCR, FACEP, FAAP

 

Interpreting Waveform Capnography: Pearls and Pitfalls

Author: Brit Long, MD (@long_brit – EM Chief Resident at SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK – EM Attending Physician, UTSW / Parkland Memorial Hospital) and Manpreet Singh, MD (@MPrizzleER – Clinical Instructor & Ultrasound/Med-Ed Fellow / Harbor-UCLA Medical Center)

It’s been a busy day in the ED, full of sick patients requiring resuscitation. You just intubated a patient in respiratory distress with COPD who failed a trial of noninvasive positive pressure ventilation. The intubation went well, and you are now securing your ETT and connecting end-tidal waveform capnography to evaluate the tracing. The chest X-ray shows optimal position of the ETT, you have the post-procedural analgesia and sedative agents on board, and you’re feeling good as you exit the resuscitation bay.

The next patient is an 8 year-old male with a fall and forearm deformity. X-ray reveals an angulated, mid-shaft radial fracture that will need reduction. You evaluate the patient for the necessary procedural sedation, gather your equipment and airway supplies, and prepare for the sedation. You plan on using ketamine. Before you push the ketamine, you have the patient on monitors, including waveform capnography.

Background

Capnography has shown great potential in several conditions and procedures in emergency medicine. Literature exists for its use in cardiopulmonary resuscitation, intubation for confirmation of ETT placement, resuscitation of critically ill patients with sepsis, monitoring response to treatment in patients with respiratory distress (specifically COPD, CHF, and asthma), pulmonary embolism, and procedural sedation. For more details, go HERE.

However, how do you interpret quantitative capnography waveforms? We own the resuscitation of critically ill patients, and with boarding increasing in EDs, we need to know how to interpret waveforms. This instrument can provide a great deal of important information if properly understood.

The normal capnography waveform

The main determinants of ETCO2 include alveolar ventilation, pulmonary perfusion, and CO2 production. A normal waveform has four different phases:

  1. Phase I is the inspiratory baseline, which is due to inspired gas with low levels of CO2.
  2. Phase II is the beginning of expiration which occurs when the anatomic dead space and alveolar gas from the alveoli/bronchioles transition.
    a. The transition from phase II to III is the alpha angle.
    b. The alpha angle can be used to assess the ventilation/perfusion of the lung. V/Q mismatches will have an alpha angle greater than 90 degrees.
  3. Phase III is the alveolar plateau, where the last of the alveolar gas is sampled. This is normally the PETCO2.
    a. The transition from phase III to 0 is the beta angle.
    b. The beta angle can be used to assess rebreathing. If rebreathing occurs, the angle is greater than 90 degrees.
  4. This is actually phase 0, reflecting the inspiratory downstroke and the beginning of inspiration.

Of note, an additional phase IV is often seen in pregnancy, which is a quick upstroke before phase 0 begins.

Image 2

Image One
Picture from http://what-when-how.com/wp-content/uploads/2012/04/tmp2A92_thumb221.jpg

How do you analyze the waveform?

Just like you evaluate an ECG or chest Xray, I recommend using an algorithm or systematic process for analysis. This can be divided into several steps:

  1. Look for presence of exhaled CO2 (Is a waveform present?)
  2. Inspiratory baseline (Is there rebreathing?)
  3. Expiratory upstroke (What is the shape i.e. steep, sloping, or prolonged?)
  4. Expiratory/alveolar plateau (Is it sloping, steep, or prolonged?)
  5. Inspiratory downstroke (Is it sloping, steep, or prolonged)

Ensure you evaluate the height, frequency, rhythm, baseline, and shape. With these thoughts in mind, let’s discuss some clinical scenarios.

Cases…

Before you can reassess your other two patients, you receive an EMS radio call. They were called to the scene of a patient in PEA, and they have started compressions and will be at your doorstep in 3 minutes. The patient arrives, with the crew doing high quality CPR. The patient continues with no pulse, leads and ETCO2 are connected, one amp of epinephrine is given, and US shows a heart rate of 40 bpm. Your waveform capnography shows 10 mm Hg, and the person completing CPR is tiring. As the team leader, you ask another team member to take over.

Image 3
Picture from http://www.slideshare.net/larryide/capnography?next_slideshow=1

This waveform with a dip shows the time to transition to a different provider, with improved perfusion with the new provider doing compressions, as the CO2 has increased indicating better tissue perfusion.

After another minute of CPR, the ETCO2 jumps to 40. A sudden increase in ETCO2 is seen in ROSC during arrest or correction of an ETT obstruction.

Image 4
Picture from http://www.slideshare.net/larryide/capnography?next_slideshow=1

You now have return of pulses and are preparing to intubate the patient. Unfortunately, the resident completing it is not confident in his view and is unsure of tube placement. Your waveform shows the following:

Image 5

This waveform shows a tapering of the ETCO2, suggestive of esophageal intubation. You ask the resident to remove the ETT. He obtains an improved view with videoscope and passes the ETT without difficulty. The waveform looks normal, and the patient is now stable.

Finally you have time to go reassess your COPD patient. Just as you enter the resuscitation bay, he has a desaturation to 88% while on FiO2 of 100%, and your waveform is flat.

Image 6
Picture from http://www.slideshare.net/larryide/capnography?next_slideshow=1

You are now pretty tired of these flat waveforms, and you immediately curb your sphincter response while running to the bedside. Your mind quickly goes through the DOPES mnemonic (displacement, obstruction, PTX, equipment failure, breath stacking) and you see that while moving the patient, the ETT became disconnected from the circuit. You reconnect, with increase in saturation and good waveform.

What are other causes of a sudden flat EtCO2 tracing?

Extubation, capnography not connected to circuit, cardiorespiratory arrest, apnea test in brain dead patient, obstruction of capnography, ventilator disconnection, and esophageal intubation.

After caring for an ankle sprain and beginning the workup of a patient with chest pain, you again reassess the patient with COPD. You notice a steadily increasing EtCO2 baseline in your COPD patient. The waveform looks like this…

Image 7
Picture from http://www.slideshare.net/larryide/capnography?next_slideshow=1

The waveform reflects an elevation of baseline, as well as the plateau, indicating incomplete exhalation. The CO2 is not being appropriately removed. This is often due to insufficient expiratory time, inadequate inspiratory flow, or faulty expiratory valve.

Rebreathing can also appear with the following waveform with baseline elevation, which is due to inadequate exchange of CO2.

Image 8
Picture from http://www.paramedicine.com/pmc/End_Tidal_CO2.html.

Increased EtCO2 can be due to four components:

  1. Increased CO2 production (fever, NaHCO3 administration, tourniquet release, and overfeeding syndrome).
  2. Pulmonary perfusion increase (increased cardiac output, increased blood pressure).
  3. Alveolar ventilation decrease (hypoventilation, bronchial intubation (remember that victory shove?), partial airway obstruction, rebreathing).
  4. Equipment malfunction (exhausted CO2 absorber, inadequate fresh gas flow, ventilator tubing leak, ventilator malfunction).

Once you slow down his respiratory rate and increase the flow rate, his saturations and waveform improve. Suddenly, the alarm alerts you to high pressures in the circuit, and his waveform shows:

Image 9
Picture from http://www.paramedicine.com/pmc/End_Tidal_CO2.html

This waveform is due to obstruction of the ETT, either through ETT kink, foreign body in airway, bronchospasm, or mucous plug. You see high peak pressures and suction the tube, while ordering an in-line duoneb. Five minutes later the patient again improves. You wipe the sweat from your brow, as this patient is keeping you busy.

After all this excitement, you prepare for the sedation of the 8 year-old male with forearm fracture requiring reduction. The sedation and reduction go smoothly with ketamine. He is starting to wake from his dissociative state, and you see this:

Image 10
Picture from http://www.slideshare.net/larryide/capnography?next_slideshow=1

This waveform demonstrates hyperventilation. Notice the baseline is unchanged. This waveform shows steadily decreasing plateau, reflecting tachypnea, increase in tidal volume, decreased metabolic rate, or fall in body temperature.

A decreasing EtCO2 has several etiologies:

  1. Decreased CO2 production (hypothermia)
  2. Pulmonary perfusion decrease (reduced cardiac output, hypotension, pulmonary embolism, cardiac arrest)
  3. Alveolar ventilation increase (hyperventilation, apnea, total airway obstruction, extubation)
  4. Apparatus malfunction (circuit disconnection, leak in sampling, ventilator malfunction)
Capno
Recap of Factors Affecting EtCO2 – Table from EMSWorld

What if his respiratory rate had started to decrease?

The alveolar plateau will begin to steadily increase, which is due to decrease in respiratory rate, decreased tidal volume, increased metabolic rate, and hyperthermia. Notice the baseline is still close to 0, so CO2 is appropriately exchanged.

Image 11
Picture from http://www.paramedicine.com/pmc/End_Tidal_CO2.html

Just before you send the COPD patient to the ICU, the nurse grabs you, as the waveform has now changed.

Image 12
Picture from http://www.paramedicine.com/pmc/End_Tidal_CO2.html

This small dip in the alveolar plateau is known as a “curare cleft.” This waveform appears when the paralytic begins to subside and the patient tries to breathe during partial paralysis. You increase the analgesic drip, and the patient is transferred to the ICU.

Summary

Use an algorithm for waveform capnography analysis.

  1. Look for presence of exhaled CO2 (Is a waveform present?)
  2. Inspiratory baseline (Is there rebreathing?)
  3. Expiratory upstroke (What is the shape i.e. steep, sloping, or prolonged?)
  4. Expiratory/alveolar plateau (Is it sloping, steep, or prolonged?)
  5. Inspiratory downstroke (Is it sloping, steep, or prolonged)

Ensure you evaluate the height, frequency, rhythm, baseline, and shape.

Understanding waveforms and how to interpret them can provide a great deal of information. We are the masters of resuscitation, and this is a vital component of caring for critical patients.

Pocketguide
Pocket Guide: Left – Intubated Patient, Right – Non-intubated Patient Available at: http://www.emsworld.com/article/10287447/capnography-as-a-clinical-tool

References/Further Reading

-Kodali BS. Capnography outside the operating rooms. Anesthesiology. 2013 Jan;118(1):192-201.
-Thompson JE, Jaffe MB. Capnographic waveforms in the mechanically ventilated patient. Respir Care. 2005 Jan;50(1):100-8; discussion 108-9.
-Blanch L, Romero PV, Lucangelo U. Volumetric capnography in the mechanically ventilated patient. Minerva Anestesiol. 2006 Jun;72(6):577-85.

Online Resources

10 Procedural Sedation Errors in the Emergency Department

Authors: Nicole Vetter, MD (EM Resident Physician, University of Connecticut Emergency Medicine Residency) and Jesse Sturm, MD (Pediatric Emergency Medicine Attending, Connecticut Children’s Medical Center) // Edited by: Jennifer Robertson, MD, MSEd and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

Case: You are in the middle of a ketamine sedation on a 7-year-old child whose forearm fracture is being reduced by the orthopedist. You notice the patient is becoming more agitated so you push another 1mg/kg dose of ketamine. Shortly after, you notice a diminished respiratory rate and capnography waveform. Soon after, the patient’s oxygen saturations drop. What are the next steps?

Procedural sedation and analgesia (PSA) is a core skill set of the emergency physician (EP). It improves patient satisfaction by providing amnesia, anxiolysis and analgesia. Sedation also makes our consultants happier as it facilitates an easier and faster procedure.

However, studies show that EPs inadequately treat pain in the emergency department (ED) for multiple reasons (1):

  • Fear of over-sedation
  • Fear of adverse events
  • Inadequate knowledge
  • Inadequate dosing
  • Insufficient time
  • Insufficient resources

10 Common PSA Errors

Error #1: Delaying deep sedation until fasting times are met

  • The American Society of Anesthesiologists (ASA) states that the current fasting guidelines are based on insufficient evidence but still “strongly recommend” the following (2):
    • 2 hours for clear liquids, 6 hours for a solid light meal and 8 hours for a fatty or fried meal
    • ASA guidelines are often extrapolated to procedural sedation in the ED
  • However, literature for procedural sedation in the ED states that fasting makes no difference on the risk of emesis or aspiration (3).
    • Harms of delaying the procedure include increased pain, progression of lesion, and a more difficult procedure
    • The American College of Emergency Physicians (ACEP) Clinical Policy 2013 guidelines state that procedural sedation should not be delayed in the ED based on fasting time (4)
    • Always ensure, however, that your decisions on nil per os (NPO) status in sedation reflect your hospital’s applicable policies

Error #2: Believing PSA carries less risk than endotracheal intubation

  • Do not be any less vigilant during PSA than you would for a critical patient requiring emergent intubation
  • The risks of undergoing PSA may be less given that sedation in the ED generally involves healthy patients. However, PSA carries greater risk to those performing the sedation
  • When PSA goes wrong, it is usually attributed to the sedation (as opposed to the emergently intubated patient who is very high risk to begin with)

Error #3: Minimizing risk of airway and breathing complications while using ketamine

  • While it is true that ketamine has an excellent safety profile, airway/breathing events do occur by a variety of mechanisms
    • Central apnea
    • Airway malpositioning
    • Laryngospasm
    • Hypersalivation
  • Over sedation with ketamine can be corrected with early recognition and appropriately-sized equipment at the bedside

Error #4: Not having full intubation setup nearby

  • PSA = ‘Prepared to Solve Apnea’
  • Hypoventilation/apnea is a predictable and acceptable consequence of PSA if that amount of sedation is required to facilitate the procedure
  • Therefore, be prepared to manage airway obstruction and apnea using a stepwise approach (see below)

Error #5: Responding to hypoventilation or apnea with early and/or aggressive use of the bag-valve mask (BVM)

  • In a comparison of intubated versus PSA patients:
    • Oxygenation is more likely the predominant issue in intubated patients due to paralysis and thus, are more likely to benefit from early use of BVM
    • In the PSA patient, hypoventilation is most likely due to airway or breathing issues
      • Other steps should first be taken first to correct airway/breathing before using BVM
      • Also, the risk of vomiting with BVM is greater as PSA patients are not paralyzed
    • Use the BVM as only a PART of a stepwise approach to hypoventilation in PSA patients:
      • Detection of the condition
      • Stop any drug (s) and stop the ongoing procedure
      • Position the patient – chin lift, bring head up, towel roll under shoulders
      • Jaw thrust
      • Suction if needed
      • If laryngospasm: apply pressure to laryngospasm notch (medial to earlobe between mastoid & condyle of jaw) (5) Pic1
      • Use the BVM slowly and gently, ensuring a good seal and chest rise
      • If unable to correct complications with high quality BVM, prepare to intubate

Error #6: If the oxygen saturation is ok, then the patient is breathing ok

  • Focus on ventilation during PSA (not oxygenation)
    • Capnometry alerts clinician to hypoventilation earlier than clinical assessment or pulse oximetry
  • Use End Tidal CO2 (ETCO2) for all PSA – Level B recommendation by ACEP Clinical Policy (4)
    • The numeric value of ETCO2 is sometimes less important than the presence or absence of a waveform
  • Do not correct apnea and hypoventilation with passive oxygen delivery alone (i.e. nasal cannula, facemask). Refer to stepwise approach above

Bradypnea (slow breathing/tidal volumes preserved –> ETCO2 rises):

Pic1

Hypopnea (shallow breathing/low TV –> ETCO2 falls):

Pic2

Apnea (breathing stops):

Pic3

Error #7: Withholding ketamine sedation on adults

  • Ketamine provides excellent sedation and analgesia, and it can be safely used in adults
  • An emergence reaction only occurs in 10-20% of adults and can be reduced with pre-induction comfort and coaching (6)
    • How the patient feels entering a ketamine “trip” directly affects how they will emerge from the “trip”
    • Give midazolam in 2mg doses (up to 4mg) if emergence reaction is of concern
  • Concern for tachycardia and hypertension (HTN)
    • A transient increase in heart rate (HR) or blood pressure (BP) for 15 minutes or so is almost always irrelevant (except in patients with severe coronary artery disease)
    • If there is excessive HTN, give 10-20mg of propofol

Error #8: Adding an opioid with ketamine for sedation

  • “Intravenous Subdissociative-Dose Ketamine versus Morphine for Analgesia in the Emergency Department” (7)
    • Pain relief with ketamine (0.3mg/kg) and morphine (0.1mg/kg) are statistically similar
    • Adding an opiate to a ketamine sedation will subject the patient to the adverse effects of opiates without any added benefit

Error #9: Using the same dosing strategy for propofol sedations as with fentanyl/midazolam

  • Propofol is much shorter acting and does not accumulate in tissues like fentanyl/midazolam
  • Will need to rebolus propofol to stay on top of the sedation
  • Example propofol dosing strategy:
    • Give a generous bolus up front (1-2mg/kg) over 20 seconds
    • Anticipate a brief period of hypoventilation or apnea
    • Rebolus 0.5mg/kg every 5-10 minutes as needed

Error #10: Using the same PSA dosing strategy for the elderly

  • Elderly patients are highly sensitive to opiates, benzodiazepines, and propofol
  • They will have longer periods of hypoventilation and hypotension
  • Start low, go slow

*Adapted from Reuben Strayer’s PSA screencast at emupdates.com (8)

References / Further Reading

  1. Grant PS. Analgesia delivery in the Emergency Department. Am J Emerg Med, 2006;24(7):806–809.
  2. Apfelbaum et al. American Society of Anesthesiologists Committee. Practice guidelines for preoperative fasting and the use of pharmacologic agents to reduce the risk of pulmonary aspiration: application to healthy patients undergoing elective procedures: an updated report by the American Society of Anesthesiologists Committee on Standards and Practice Parameters. Anesthesiology. 2011;114(3):495-511.
  3. Thorpe RJ, Benger J. Preprocedural fasting in emergency sedation. Emerg Med J 2010; 27:254–261.
  4. Godwin SA, et al. Clinical policy: procedural sedation and analgesia in the emergency department. Ann Emerg Med. 2014;63(2)247-258.
  5. Larson CP Jr. Laryngospasm–the best treatment. Anesthesiology. 1998;89(5):1293-4.
  6. Strayer RJ, et al. Adverse events associated with ketamine for procedural sedation in adults. Am J Emerg Med. 2008 Nov;26(9):985-1028.
  7. Motov S, et al. Intravenous Subdissociative-dose Ketamine Versus Morphine for Analgesia in the Emergency Department: A Randomized Controlled Trial. Ann Emerg Med. 2015; 66(3):222-229.
  8. Strayer, Reuben. “The Procedural Sedation Screencast Trilogy.” Emergency Medicine Updates. 28 Nov 2013. Web. 18 Mar 2016.