EMCrit Podcast 130 – Hemodynamic-Directed Dosing of Epinephrine for Cardiac Arrest

epi-pen

Today on the podcast, I address the last little bit from my SMACC lecture on the new management of the intra-arrest: hemodynamic, individualized dosing of epinephrine.

normanparadisadonehThe podcast is interspersed with clips from Professor Norman Paradis

Articles/Posts on Epinephrine by ACLS Guidelines

  • (15306666),
  • http://www.emdocs.net/epinephrine-cardiac-arrest/
  • http://www.jems.com/article/patient-care/new-resuscitative-protocol
  • (24846323)
  • (19934423)

Epinephrine Dosing Based on DBP

Three Swine Study

(Crit Care Med. 2013 Dec;41(12):2698-704)

(Resuscitation. 2013 May;84(5):696-701)

(24945902)
Here is the abstract from the latter study:

AIM: Advances in cardiopulmonary resuscitation (CPR) have focused on the generation and maintenance of adequate myocardial blood flow to optimize the return of spontaneous circulation and survival. Much of the morbidity associated with cardiac arrest survivors can be attributed to global brain hypoxic ischemic injury. The objective of this study was to compare cerebral physiological variables using a hemodynamic directed resuscitation strategy versus an absolute depth-guided approach in a porcine model of ventricular fibrillation (VF) cardiac arrest.

METHODS: Intracranial pressure and brain tissue oxygen tension probes were placed in the frontal cortex prior to induction of VF in 21 female 3month old swine. After 7minutes of VF, animalswere randomized to receive one of three resuscitation strategies: 1) Hemodynamic Directed Care (CPP-20): chest compressions (CCs) with depth titrated to a target systolic blood pressure of 100mmHg and titration of vasopressors to maintain coronary perfusion pressure (CPP)> 20mmHg; 2) Depth 33mm(D33): target CC depth of 33mm with standard American Heart Association (AHA) epinephrine dosing; or 3) Depth 51mm(D51): target CC depth of 51mm with standard AHA epinephrine dosing.

RESULTS: Cerebral perfusion pressures (CerePP )were significantly higher in the CPP-20 group compared to both D33 (p<0.01) and D51 (P=0.046), and higher in survivors compared to non-survivors irrespective of treatment group (P<0.01).Brain tissue oxygen tension was also higher in the CPP-20 group compared to both D33 (P<0.01) and D51 (P=0.013), and higher in survivors compared to non-survivors irrespective of treatment group (P<0.01).Subjects with a CPP>20mm Hg were 2.7 times more likely to have a CerePP>30mm Hg (P< 0.001).

CONCLUSIONS: Hemodynamic directed resuscitation strategy targeting coronary perfusion pressure>20mmHg following VF arrest was associated with higher cerebral perfusion pressures and brain tissue oxygen tensions during CPR. University of Pennsylvania IACUC protocol #803026.

Human Study by Dr. Paradis

Coronary Perfusion Pressure and the Return of Spontaneous Circulation in Human Cardiopulmonary Resuscitation

(10.1001/jama.1990.03440080084029)

Coronary perfusion pressure (CPP), the aortic-to-right atrial pressure gradient during the relaxation phase of cardiopulmonary resuscitation, was measured in 100 patients with cardiac arrest. Coronary perfusion pressure and other variables were compared in patients with and without return of spontaneous circulation (ROSC). Twenty-four patients had ROSC. Initial CPP (mean±SD) was 1.6 ± 8.5 mm Hg in patients without ROSC and 13.4 ± 8.5 mm Hg in those with ROSC. The maximal CPP measured was 8.4 ±10.0 mm Hg in those without ROSC and 25.6 ±7.7 mm Hg in those with ROSC. Differences were also found for the maximal aortic relaxation pressure, the compression-phase aortic-to— right atrial gradient, and the arterial Po2. No patient with an initial CPP less than 0 mm Hg had ROSC. Only patients with maximal CPPs of 15 mm Hg or more had ROSC, and the fraction of patients with ROSC increased as the maximal CPP increased. A CPP above 15 mm Hg did not guarantee ROSC, however, as 18 patients whose CPPs were 15 mm Hg or greater did not resuscitate. Of variables measured, maximal CPP was most predictive of ROSC, and all CPP measurements were more predictive than was aortic pressure alone. The study substantiates animal data that indicate the importance of CPP during cardiopulmonary resuscitation.

Good Review on Epinephrine

Epi Review

AHA Cardiopulmonary Resuscitation Quality Statement

by Meaney P. et al (Circulation 2013;128:417)

Metrics

  • CCF>80%
  • Rate 100-120
  • 5cm depth
  • Full Recoil
  • <12 BPM, Minimal Chest Rise

Monitoring/Feedback

  • Art/CVP CPP>20
  • Just Art Line DBP>25-30 (I disagree)
  • ETCO2>20 mm Hg

If DBP < 20 optimize compressions or vasopressors (Circulation 2011;123:e236)

CVP can be higher during the poor flow of the arrest state (3970745),(Am J Emerg Med. 1985 Jan;3(1):11-4.), and (3946853) and this one had a mean of 16 (10.1161/01.CIR.80.2.361)

so I would shoot for 35-40 mm Hg

Goal is to give less epineprhine

Hemodynamic-directed CPR Review

(24783998)

Now on to the Podcast…

Play

Bibliography

Podcast 129 – LAMW: The Neurocritical Care Intubation

head-explode

This is the another of the Laryngoscope as a Murder Weapon lectures; though in this case it is really more of an aggravated assault.

Who is this For?

Semi-elective intubations for patients with presumed or known elevated ICP

In TBI severity of brain injury doesn’t predict the lack of need for pharmacological blunting of increase in MAP or ICP (23511147)

The prototypical case requiring this treatment is a high-grade SAH prior to securing the aneurysm

This is the same way we would intubate an aortic dissection patient

Preoxygenation

Ap Ox and high-flow fiO2 for the full 3 minutes or longer

ETCO2

Put it on the BVM

Non-Pharmacologic Methods to Blunt Reflex Response

Limit time of laryngoscopy and atraumatic laryngoscopy

Leave the patient upright until the last possible moment, then intubate in 20 degrees head-up

No-touch intubation with video laryngoscopy by the best intubator

Pretreatment

Control the BP BEFORE the intubation

Lidocaine

While there is evidence that it blunts ICP rise and cough response, there is no good evidence that this has clinical results.(11696494) Literature is pretty good on endotracheal suctioning, but nothing on patient-important outcomes during intubation. Not hemodynamically active in this one study, but I have experienced radical drops in BP. (22633717)

Local is more effective than IV. (10861151)

Lidocaine References (11696494), (17358099), (23683444), (7772359),

Fentanyl

Dose 5 mcg/kg (6318605), (7032347)

All equipment meds must be prepared before administration. Someone must be watching the pt.

Remifentanil

Remifentanil can also be used, but I don’t have so I can’t speak about it

Esmolol

Dose 1.5-2 mg/kg ~ 3min beforehand

Combo of Esmolol and Fentanyl (1363221) (7788827) (9084524),(1672488)

Nicardipine

Dose 20 mcg/kg (average 1.4 mg)

(21696933) and (10553821) and Review Article (16978041)

Other Group’s Recs

At this stage, Emergency Airway Course only recommends Lidocaine and Fentanyl: they state prefasiculation is dead

Osmotic Therapy

Probably a good time to give a dose of hypertonic saline

Induction Agents

Etomidate, Propofol, or Propofol/Ketamine (75%/25%). If Thiopental was still available, it would be on the list as well.

Muscle Relaxants

Rocuronium or Succinylcholine at full dose

Post-Intubation Sedation

Propofol and Fentanyl

Post-Intubation Ventilation

Shoot for 95% saturation, use PEEP only if necessary; but if it is necessary it is safe to use

Increase Respiratory Rate until ETCO2 of 35 mm Hg; then send a blood gas

Other Situations

Basilar Stroke and Stuttering Stroke-lower bp=screwed

Review Article

Has anyone found a good one????

Rich Levitan’s Airway Course

Go here to get the scoop

Now on to the Podcast…

Play

Bibliography

Podcast 128 – Pulmonary Embolism Treatment Options and the PEAC Team with Oren Friedman

pe-show

OrenFriedmanWe now have way too many treatment options for sub-massive and massive pulmonary embolism (PE) patients who aren’t coding in front of you. How do you decide which one is right for your patient? To help answer this question, I am joined today by Oren Friedman, pulmonary critical care doc and one of the members of the Cornell PEAC team.

Cornell Pulmonary Embolism (PE) Advanced Care Team (PEAC), aka the CLOT Team

Oren Friedman MD, Pulm Crit Care; James Horowitz MD, Cardiology; Arash Salemi MD, Cardiac Surgery; Akhilesh Sista MD, Interventional Radiology

You can shoot the team an email: peadvancedcare at gmail dot com

Who Should We Treat?

Wood 2002 PE Mortality Curve

Wood 2002 PE Mortality Curve

30% normotensive patients have RVD; 10% progressed to shock; 5% in hospital mortality(10859287)

The Better Risk Categories for Pulmonary Embolism

  • Well and Stable Sub-Massive
  • High-Risk Sub-Massive
  • Massive

PEITHO Trial

NEJM 2014;370(15):1402

Full dose tenecteplase with concurrent heparin

  • Death or hemodynamic decompensation occurred in 2.6% of the tenecteplase group as compared with 5.6% of the placebo group
  • Extracranial bleeding occurred in 32 patients (6.3%) in the tenecteplase group and 6 patients (1.2%) in the placebo group (P<0.001)
  • Intracranial Bleed 10 patients (2%) in the tenecteplase group and 1 patient (0.2%) in the placebo group (P=0.003)

Also see my bud, Salim Rezaie’s post on PEITHO and Konstantinides’ prior study (12374874)

Ryan Radecki made some great observations in his post on PEITHO

  • The criteria for myocardial injury was a troponin I >0.06 ?g/L or troponin T >0.01 ?g/L.  These may be relatively inclusive thresholds.
  • Not all placebo patients developing hemodynamic collapse received subsequent thrombolysis; likewise, almost half of those who received open-label thrombolysis had no hemodynamic collapse.
  • Half the deaths in the placebo arm were “sudden unexplained” or “other”, compared with bleeding or stroke complications in the thromboysis arm.

TOPCOAT Trial

Jeff Kline’s trial was stopped midway through due to an institution change. Complicated primary endpoint with promising, but unusable results (24484241)

For the scoop on this one see the Bottom Line Review post on TOPCOAT

MOPETT Trial

Half-dose alteplase led to a marked reduction in pulmonary hypertension without sig. complications

Sharifi M et al. Moderate pulmonary embolism treated with thrombolysis (from the “MOPETT trial). (J Cardiol 2013; 111: 273)

See this prior EMCrit Wee as well on MOPPETT

Update: This meta-analysis states that the half-dose may be appropriate, effective, and safe (24412030)

Meta-Analysis

Chatterjee et al. have the most current meta-analysis on this topic (JAMA. 2014;311(23):2414-2421)

See the Bottom Line Review post on this study

Nakamura just published another MA this week; see Rory Spiegel’s take on the two here

Is it just in the Oldies?

Markedly lower risk in <75 y/o in PEITHO and <65 in the Meta-Analysis

The Treatment Options

Heparin Alone

tried and true. but even if some degree of resolution of presenting severe symptoms, there is the question of long-term consequences of leaving a large clot burden–namely, loss of exercise tolerance due to chronic pulmonary hypertension

Systemic Thrombolysis

With either full or half-dose alteplase or full-dose tenecteplase

Catheter-Based Intra-Arterial Thombolytic Infusion

Angiography guided placement of pulmonary artery catheters allowing a 24-hour infusion of low dose tPA. (19875060)

A newer therapy is the EKOS catheter. This uses ultrasound to continuously break up the clot during the IA Thrombolysis. Many of us wonder if this is any better than standard catheter-based therapy. (24226805), (23601295) See the PulmCCM Post on the Circulation RCT of EKOS

Interventional Mechanical Clot Disruption

Angiojet

Angiojet

AngioJet-a catheter that breaks up the clot with a high speed jet of saline, heparin, or tPA that then sucks up clot using Bernoulli physics. Very little systemic drug is delivered. Oren’s center doesn’t like the device; other centers use it. This letter is by an adovcate.

Angiovac-Vortex

Angiovac-Vortex

AngioVac-This device uses an ECMO-like system to suck up clot and then return the declotted blood to the venous circulation. It requires huge introducer sheaths. Oren alluded to its main benefit being intra-cavitary or vena cavae clots. Some are billing this as a replacement for embolectomy in many cases.

Surgical Embolectomy

Requires the patient to go on cardiopulmonary bypass and have a sternotomy. Recent experience with surgical embolectomy has had much
better results , much lower mortality than historical, (15867775)

Temporary VA ECMO as a bridge to one of these other therapies

See the EDECMO site for more on this therapy

Oren’s Algorithm

Oren's PE Algorithm

Oren’s PE Algorithm

Oren’s Slide Set

We discussed this topic with Jeff Kline a few years ago in Podcast 51

Fibrinolysis in PE with Jeff Kline

Want to know what to do for the rest of resuscitation for these patients?

We’ll have a podcast soon regarding the management of right ventricular failure, until then see this excellent post by Josh Farkas.

If they go into arrest, give tPA (10.1371/journal.pone.0008323)

As to what dose, who knows? Here is a great post on it. I would give tenecteplase.

expert-commentExpert Commentary on the Podcast

Provocative topic. Like it or not, these [PE Treatment Teams] are here to stay. I managed to get one going at Methodist. How? Well, maybe a little by perseverance, knowing the evidence, showing up for meetings, building alliances. Yeah, sure. But what sold it was when I found out for sure that the main competitor hospital, St. Vincents’ Hospital, was setting up the same program and had treated 18 patients with CDT [catheter-directed therapy] the month before. Then, suddenly attitudes changed. So what will be the main driver? The old ‘reducing practice variability’ line will be the party line. The real driver will be market share.

As Vic Tapson said in ATS two months ago “The practice is racing ahead of the evidence.” While I study lytics, and am a proponent of using them in massive and severe submassive, as your speaker advocates, I have to think like a contrarian for a minute. Funny thing is by reducing variability, we may all be doing the wrong thing instead of just some of us.

The standard lines  from most pulmonologists is “All my submassive PE patients do fine with heparin and warfarin. You guys are putting them at risk because there is no mortality benefit.”

Then the JAMA SR [the Chatterjee one mentioned above] came out 3 weeks ago showing mortality benefit and a huge NNH:NNT ratio for age<65 for survival. A huge shift. Now they say “It still increases bleeding risk…and there is no improvement in quality of life.” So I show them TOPCOAT, and they don’t read it except to see that part of the outcome was a survey, and conclude that they don’t believe in surveys (despite similar surveys being the endpoint for many other lung treatments they use; besides, the SF36 was by far the minority driver of the composite endpoint in TOPCOAT). This is going to be like stroke: a substantial number of physicians with ambiguity intolerance syndrome will say the devil you know is better than the devil you don’t. They see the clot in the lungs as better than the bleed that might happen. There are outspoken emergency physicians who still think lytics are dead wrong for stroke, monkey-fisted that position,  and in some sense have marginalized themselves from the mainstream. I suspect as we go forward, about 40% of the pulmonology community will be shaking their heads saying “what are you guys doing.” But, even if the evidence is mixed, market competition will drive this forward.

At this point, I agree with the speaker, who I believe is a pulmonologist. We should be giving systemic lytics to patients<70 years (more or less) with no contraindications, when the RV that is smashing the LV. Whether we should use catheter-directed therapy (CDT), is to me, the real question at this point. CDT offers the advantage of lower lytic dose, and Ekos  just got FDA clearance to market, and has an army of cardiologists behind them. Curiously, IR guys think Ekos is bogus and prefer CDT. But no trial has compared Ekos or general CDT to systemic lytics, and I doubt any CDT advocates will try such an RCT.

Jeffrey Kline [aka the Man]

comments in brackets are EMCrit’s

Update: Great Post on All of the Above from PulmCrit

Now on to the Podcast…

Play

Bibliography

Podcast 127 – The Oxylator with Jim DuCanto

oxylator

from inter-rescue.de

james-ducantoToday on the show, I talk with my friend Jim DuCanto, MD about the oxylator. Jim is an anesthesiologist extraordinaire with a constant drive to perfect new airway techniques and document them on video along the way.

What is the Oxylator?

A mainly plastic device about the size of your fist with a incredibly quick magnetic valve

It runs on pressurized wall or tank oxygen

Only two main controls, a pressure setting knob and a manual inhalation/automatic mode button

Manual Resuscitator Mode

Press the button and the device will give 30 lpm of inhalation until you let go or it hits the pressure limit you set

Automatic Ventilator Mode

Press in the button and give it a turn and the device switches to automatic ventilation mode. Think of it as a flow-controlled, pressure cycled ventilator in your hand

It gives 30 lpm fixed flow (slow, safe flow) until it hits the user-selectable pressure limit, it then cycles to passive exhalation until it reaches 2-4 cm H20 PEEP and then it begins a new breath

On a patient who is not spontaneously breathing, you can titrate that pressure setting to an inhalation time of 1-2 seconds; this will deliver 500-1000 mls per breath

At those settings, the minute volume will be 10-12 liters/minute

oxylator with mask

from inter-rescue.de

Feedback

The device indicates when you are obstructing by clicking and tells you when there is a mask seal leak by not cycling to the next breath

It Solves the 5 Problems of the BVM

  1. We give too many breaths
  2. Those breaths are at too high a pressure
  3. The breaths are given too rapidly
  4. We get no feedback on whether the breath went in or it was given against an obstructed airway
  5. In a spontaneously breathing patient, the BVM will give variable FiO2s depending on the exhalation port

How we use it

We both use an inline hepa filter, ETCO2 port, and sometimes extension tubing. If you want to use it on a spontaneously breathing patient, OR mask straps are a great addition.

Two models

EMX (25-45 cm H20) and HD (15-30). There are also specialty models for chemical/explosive situations.

Here is Jim’s Overview on the Device

And here are the Slides from a lecture Jim gave at SAM

Here is an example of the use of the Oxylator for an OR Induction

 

Nasal CPAP in Unconscious Patient is More Effective than Full-Face Masks

Crit Care. 2013 Dec 23;17(6):R300.

Oxylator Product Page

This is the EMX Model

Disclaimer and COI

Neither Jim nor I take any money, kickbacks, or incentives from the manufacturer. Both Jim and I have been provided with Oxylators to test and research.

Now on to the Podcast…

Play

Podcast 126 – TTM Trial Right from Niklas Nielsen’s Mouth

coldie

niklas-nielsenIn this episode, I speak with Niklas Nielsen on his thoughts on the TTM trial.

Coverage of the TTM Trial

Kee Polderman’s Editorial

 

Play

Podcast 125 – The New Intra-Arrest from SMACCgold

05intra

Here’s my first lecture from SMACCgold: The New Intra-Arrest. It generated a bit of controversy amongst my critical care friends, so we’ll be discussing various parts in more detail in the coming weeks.

Pitches

 Links and References

VSE Stuff

JAMA 2013;310(3):270

1 mg Epi and 20 IU Vasopressin Q3 minutes for 5 cycles, plus 40mg methylprednisolone for the 1st cycle. Hydrocortisone if in persistent shock

Journal Club Crit Care 2014;18:308

Why Epi and not Phenylephrine

From MH Weil’s Article Above:
Adrenergic agents with predominant a2 effect have been shown to be more effective as vasoconstrictor drugs, presumably because extrajunctional a2-receptors are more accessible to circulating catecholamines than postjunctional a1-receptors. This may explain why adrenergic amines that have predominant a1 actions such as methoxamine (Vasoxyl) and phenylephrine (Neo-Synephrine) are less effective than epinephrine after prolonged cardiac arrest.

Mechanical CPR

LUCAS seems equivalent to excellent manual compressions (from ResusMe)

Cardiac Arrest: To the cath lab with ongoing chest compressions?

Steve Smith has a great post on the topic with a ton of evidence

Consider Dual-Shock for Non-Converting VF/VT

Charles Bruen has a great post with the evidence

Abstract on Esmolol presented at Social Media and Critical Care 2014, Gold Coast, Australia

Emergency Department Use of Esmolol in Refractory Ventricular Fibrillation

Brian Driver David Plummer Stephen W Smith
OBJECTIVE
We describe the outcomes for patients receiving esmolol during refractory ventricular fibrillation (RVF) in the emergency department (ED).
METHODS
A structured chart review in an urban academic ED of patients between January 2011 and March 2013 who received esmolol with an ED diagnosis of cardiac arrest (CA), ventricular fibrillation, or pulseless ventricular tachycardia, excluding patients who received esmolol before CA or after sustained return of spontaneous circulation (ROSC).  Cardiac rhythms, CA management, timing of ROSC, and patient outcomes were recorded.
RESULTS
Six male patients met inclusion criteria; one was excluded because esmolol was administered after sustained ROSC.  Four of five patients had out-of-hospital CA; all had automatic mechanical chest compressions delivered by a LUCAS™ device.  All patients received repeated doses of epinephrine, amiodarone, lidocaine, sodium bicarbonate, as well as other adjunctive medications. Defibrillation was attempted many times for each patient prior to esmolol administration (median = 6.5, range 4-10). Some had temporary ROSC, but no patient had sustained ROSC after administration of these medications and defibrillation. All patients had a rhythm of VF at the time of esmolol administration. An esmolol loading dose and infusion of 500 mcg/kg and 50-100 mcg/kg/min, respectively, was subsequently administered to all patients.  One patient with incessant VF achieved temporary ROSC and three others attained sustained ROSC after the administration of esmolol with repeat defibrillation; two survived to discharge with excellent neurologic outcomes.
CONCLUSION
Beta-blockade should be considered in all patients with RVF in the ED prior to cessation of resuscitative efforts.

The Slides

Now on to the Podcast…

 

 

Podcast 124 – The Logistics of Proning for ARDS

proning

joseph-tonnaProning is one of the only evidence-based techniques to affect the mortality of ARDS patients. I’ve been wanting to do an episode on proning for a while. Serendipitously, Joseph Tonna recently published a piece on the topic in the ACEP Critical Care Section Newsletter. Dr. Tonna is a fellow in Anesthesia Critical Care at the University of Washington. He recently did a rotation on a refractory ARDs unit (read about all of his experiences below) and learned the way they prone. We discuss it on the podcast today.

Article on the Physiology of Proning

Eur Resp J 2002;20(4):1017

Meta-Analysis of RCTs on Proning

Crit Care Med 2014;42(5):1252

LITFL’s CCC Entry on Proning

Lots of good stuff here

Video on Proning from the Guerin Study

Here is the Dr. Tonna’s Original Piece:

Prone Positioning: An experience of actually doing it

by Joseph E. Tonna, MD, Associate Newsletter Editor. This piece was originally published in the ACEP Critical Care Section Newsletter

 

Most intensivists have read Guérin’s 2013 NEJM study on the mortality benefit of prone positioning. Previous studies [1,2] have established that dorsal consolidations improve when the patient is placed prone. Taken together, the practice of prone positioning in select patients makes sense. Despite this, I haven’t found that it is done as often as one might infer from the robustness of its benefit in this study or others. In my experience, while we are likely to notice the profound dorsal pulmonary consolidations on our patient’s CT scans, we don’t take the next step and actually prone the patient until we have already progressed further down the path towards worsening hypoxemia—often only when the pO2/FiO2 ratio is well below 150 on upwards of 70% FiO2. At this stage, we begin to consider the patient “refractory” and allow ourselves to begin the intellectual path of discussing the evidence for and risk/benefit or cost/benefit of therapies like inhaled nitric oxide (iNO), epoprostenol, prone positioning, high frequency ventilation, paralysis or extracorporeal membrane oxygenation (ECMO). The evidence for many of these therapies is thin at best, and given how infrequently we reach these states of worsening refractory hypoxemia, and gain personal experience with implementing them, many newly trained intensivists will finish training having managed no more than a handful of patients on these therapies. As we all know, increased volume leads to increased comfort and competence; so as part of my fellowship training, I wanted to know what it looked like to routinely implement these therapies. Did they work? What did this process actually look like?

Prior to turning a patient prone, the medical team places pillows on the chest, the thighs, and the feet. Sheets are used to wrap the patient in preparation for proning.

Prior to turning a patient prone, the medical team places pillows on the chest, the thighs, and the feet. Sheets are used to wrap the patient in preparation for proning.

I had the opportunity recently to train at Legacy Emanuel Medical Center in Portland, OR at the Randall & Emanuel Severe Cardiopulmonary Failure and ECMO (RESCUE) Center under two talented surgical intensivists, Drs. Andrew Michaels and Sandra Wanek. Patients brought to this unit have already failed conventional therapies for hypoxemic respiratory failure, and often already have a P/F of <100 on 80-100% FiO2. These patients have not only failed excellent critical care, but most have failed alternative therapies such as airway pressure release ventilation (APRV), iNO, or paralysis. Among the therapies implemented the RESCUE center for this subset of patients, prone positioning is routine.

Who to Prone?

Given the practical risks of proning, I wanted to find out exactly when, why, and how it was done. I watched the process, participated in it and talked extensively with one of its champions at Legacy Emmanuel, Christine Lasich, RN. Proning was done in a very simple and sensical way. It was initiated if the patient had hypoxemia with a P/F of roughly <150 and the thoracic CT scan showed significant dorsal consolidation. Without dorsal predominant consolidation, even with refractory hypoxemia, the prone position was not felt to be beneficial.

How to Prone

The way in which the patient was proned was also simple yet effective. All proning at the RESCUE center was done manually. The patient would have telemetry leads disconnected and have stacked pillows placed on their chest, lower pelvis and shins in a way to elevate the head, allow the abdomen to hang free and protect the knees and feet. The patient was then covered in a top sheet above the pillows and bundled tightly. The flip would involve 3 people per side, with highly experienced people at the chest and pelvis. Two respiratory therapists would be at the head, one managing the head, airway and pillow, and another managing the tubing and providing backup. One nurse would manage the IV lines if they absolutely couldn’t be disconnected, though they most often were after appropriate medication doses (By disconnecting the central lines, the proning movements could be more brisk and complete without the risk of traumatic removal.) The arterial lines were almost always unhooked. Most patients were also on ECMO and would have a dedicated nurse at each cannula. The specialist at the foot of the bed would oversee the whole process and monitor the bypass circuit. The pulse oximeter would be left until the last minute to monitor saturation and heart rate. The process was announced overhead prior to flipping so that assistants could begin to free themselves. One RT would ensure the ETT was taped and secured without hard plastic holders or bite blocks to avoid oral trauma while the bedside nurse would disconnect the leads, bolus analgesia, sedation and often paralytics, and ready the patient so that the assistants could step in, participate in the “time out” and then help flip. As such, additional help was only needed for no more than 5 minutes but during this time, the room had no fewer than 8-9 people plus anyone needed for the ECMO circuitry. It felt very safe and controlled.

Post-Proning Care

Once prone, meticulous care was given positioning the patient’s face, eyes and endotracheal tube such that pressure points were protected, oral trauma to the lips and gums was avoided, and the eyes were lubricated and closed. Frequent assessments and adjustments were made of all these parts to avoid pressure wounds. Given the aforementioned internal jugular ECMO cannulas, patients were positioned face down in the bed rather than “head to side,” and so these frequent assessments were of utmost importance. The RT or nurse would ensure that at any given time s/he could pass the endotracheal suction catheter without resistance. It was common in this face down position to have significant facial and lingual edema, and on speaking with experienced providers and nurses, in most patients without such cervical limitations, there are distinct advantages to a “head to side” position, including easier oral care and less edema. Feeding was continued while prone as long as the patient’s feeding tube was post pyloric. If not, feeds were held but the total daily goals were achieved by doubling the feeding rate while supine. I found this ensured the patients continued to receive adequate nutrition.

The face is padded with a cut-out for the endotracheal tube so that patients can maintain the face-down position to optimize the function of internal jugular ECMO cannulae.

The face is padded with a cut-out for the endotracheal tube so that patients can maintain the face-down position to optimize the function of internal jugular ECMO cannulae.

How Much Proning?

Proning was carried out in units of between 4 and 16 hours, with ABGs obtained prior to, 30 minutes after, and then at 4 hour intervals along the way to assess for trending improvement or zenith. ABGs were then repeated 30 minutes or so after supination and with these data points, trends could be drawn to see each patient’s optimal duration of prone position. Some patients with dorsal consolidation didn’t show any improvement in their PaO2 after proning. I had been used to the 16h prone/8h supine approach, without adjustment for changes in PaO2 during the day, and I was surprised to see that while some patients achieved peak PaO2 late while prone, or peaked early and maintained elevated PaO2 while prone, others peaked and started to fall by 4 to 6 hours, only to then have a rise in their PaO2 upon supination.

Patients at the RESCUE Center also had initiation of proning whenever or continued as long as the patient demonstrated the ‘inclusion’ criteria already mentioned, sometimes two weeks into their disease course. While many might critique this tailored approach to dynamic PaO2 changes as akin to the “better PaO2, but higher mortality” of the control arm of the ARDSNet study, it also harkens to a policy of “intervention, assessment, repeat” that defines not only good critical care but good medicine. While the Guérin study showed that 16h of prone positioning early in the course was beneficial, it is not known if intermittent prone positioning (IPP, as it is known) is better or worse. In the face of empiric data suggesting a benefit and no data to suggest harm, the providers at the RESCUE center argue that this is simply practical and attentive critical care [3]. While individual interventions are difficult to isolate among bundled care, the incredible outcomes support them.

Conclusion

Over my month I was able to participate in the care of multiple patients transferred for refractory hypoxemia, who through aggressive yet thoughtful interventions were able to be rescued from critical condition to a neurologically intact survival. Utilization of prone positioning aggressively and often was a key component of this care. It made physiologic sense, and had been practiced so often that the process was regimented and efficient among the staff. The number of staff required for the actual flip was far more than I had otherwise seen, but the process was also more regimented and, I thought, safer. I saw daily the benefit of prone positioning and came to ask myself why it wasn’t done earlier and more often, before patients reached “refractory” states of hypoxemia. While many would argue that without refractory hypoxemia, the risks of prone positioning, especially among unfamiliar providers exceeds any benefit. It’s hard to dispute that it may not be safe to have unpracticed providers proning patients, I think it’s also easy to believe that alveolar recruitment with improved oxygenation and ventilation leads to lower FiO2s, lower ventilatory pressures, and less atelectrauma, and fewer invocation of less proven, higher risk therapies. Like all new or unfamiliar practices, there are risks, yet the marked improvement in oxygenation and ventilation I saw with routine early prone positioning suggested to me that this was a skill worth learning so that I too could implement it safely and effectively to the benefit of my patients.

REFERENCES:

1. Gattinoni L, Pelosi P, Vitale G, et al. Body position changes redistribute lung computed-tomographic density in patients with acute respiratory failure. Anesthesiology. 1991;74(1):15–23.

2. Protti A, Chiumello D, Cressoni M, et al. Relationship between gas exchange response to prone position and lung recruitability during acute respiratory failure. Intensive Care Med. 2009;35(6):1011–7.

3. Michaels AJ, Wanek SM, Dreifuss BA, et al. A protocolized approach to pulmonary failure and the role of intermittent prone positioning. J Trauma Acute Care Surg. 2002;52(6):1037–47.

Now on to the Podcast…

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Podcast 123 – Selective Aortic Arch Perfusion (SAAP) with Jim Manning

A few weeks ago, we discussed REBOA, a cutting edge procedure to control hemorrhage. Let’s go beyond cutting edge to the future of trauma and medical arrest care using a similar aortic catheter. This one allows you to administer blood and drugs to the proximal aorta.

manningjamesJim Manning, MD has been working on these issues for over two decades in his lab in North Carolina. This may very well be the future of CPR for medical and traumatic arrests.

Here are Dr. Manning’s Disclosures: Inventor on patents for the Selective Aortic Arch Perfusion technology that are assigned to the University of North Carolina at Chapel Hill; Co-Founder of Resusitech, Inc., a medical device company developing invasive resuscitation technologies.

Selective Aortic Arch Perfusion

 

SAAP Catheter Prototype

SAAP Catheter Prototype

The following slide shows where SAAP may fit in with the other therapies for cardiac arrest:

AHR

And this one shows a possible progression during arrest:

med arrest progression

Update: Want More?

Jim gave a lecture for GSA HEMS that is fantastic!

What do you think? Comment Below.

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Podcast 122 – Cardiac Arrest after the Toxicology of Smoke Inhalation with Lewis Nelson

fire-truck

We had a case a few months ago at Janus General–very sad and very scary. The patient came in after a house fire. He had some burns, but not enough to be the cause of his arrest. Instead, it had to be the asphyxia and possible toxicology of the smoke inhalation. I wanted to get a better idea of ideal care for these patients; for that I needed a toxicologist.

Lewis NelsonFew tox folks are smarter than Lewis Nelson, MD of the NYC Poison Center.

Note: In this episode we don’t deal with the thermal injury of smoke inhalation

Cyanide Toxicity

  • Empiric administration of  Hydroxocobalamin 5 g rapid IV drip x 1
  • Even better if this can be given at the scene as soon as the patient arrests or is profoundly hypotensive
  • Messes with labs that use colorimetric probes (cooximetry, lactate, LFTs, etc.) Get blood for cooximetry before giving the med if at all possible
  • Dr. Nelson doesn’t recommend giving sodium thiosulfate in addition to the Hydroxocobalamin
  • An IM version is in the pipeline–this will be easier for EMS/emergency use
Hydroxocobalamin

Hydroxocobalamin

You'll need 200 ml of Saline

You’ll need 200 ml of Saline

Carbon Monoxide

  • Put the patient on 100% fiO2
  • Not much to do beyond that until the patient stabilizes
  • See LITFL for more on CO

Methemoglobinemia

  • Caused by Hb oxidation from the heat of the fire
  • Administer Methylene Blue 2 mg/kg x 1 IVP
  • May be worthwhile to start a drip if patient has resistant hypotension, but this is an unproven therapy

Now on to the Podcast…

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EMCrit Podcast 121 – REBOA

reboa

Today, I got to interview one of the superstars at Shock Trauma on REBOA (resuscitative endovascular balloon occlusion of the aorta).

Balloon occlusion of the aorta was first described in 1954 (Surgery 1954;36(1):65). Other older articles include (Ann Emerg Med 1986;15(12):1466, J Endovasc Ther 2000;7(1):1, Endovasc Ther 2005;12(5):556).

The Shock Trauma Center (STC) Approach to REBOA

Gain Access to the Common Femoral Artery with Femoral A-line Kit

  • Just like normal, except make sure you are hitting common femoral and not superficial femoral artery

Float the Wire

  • STC uses Boston Scientific Amplatz superstiff wires (0.035in/260 cm/straight tip)
  • Measure externally from the catheter to the umblicus and then up to the level of the 2nd rib–mark this level on the wire
  • Advance the wire floppy-end first to the marked depth
  • Confirm location with either radiograph or fluoro before proceeding

Place the Sheath

  • At STC, they use a Check-Flo Performer Introducer (12 fr, 30cm)
  • Remove the femoral artery catheter
  • Measure the introducer externally from groin to just below the umbilicus
  • Dilate the vessel to accept the introducer
  • Place the introducer to the previously marked level

Place the Coda Catheter/Balloon

  • Grab a CODA balloon catheter (32 mm-balloon)
  • Measure externally; Zone 1 is measured to the xiphoid, Zone 3 is measured to just above the umbilicus
zones-of-aorta

from J Trauma. 2011 Dec;71(6):1869-72

 

  • Remove all air from the balloon using saline syringe
  • Insert the CODA catheter
  • The wire stays stationary throughout

Inflate the Balloon

  • Use a 30 ml syringe, ideally filled with 20 ml of NS and 10 ml of omnipaque (lohexol); use just saline if contrast not available
  • Inflate until resistance goes to moderate (would love to know what luminal pressure this corresponds to). In general, this corresponds to 12-22 mls depending on the size of the aorta–but this must be individualized to the patient.

Secure Everything for Transport

  • Here’s how they do it at STC

reboa-securing

  • Mark the levels of everything so you can verify there has been no migration

Get an Xray when time allows

Balloon in Zone-3

Balloon in Zone-3

Balloon in Zone-1

Balloon in Zone-1

Go to Definitive Management

  • The introducer sheath will need to be removed under direct observation after cutdown, with arterial repair (at least until smaller catheters are developed)

Shock Trauma Center Protocol

stc-reboa-prot

REBOA Articles

REBOA review article (J Trauma. 2011 Dec;71(6):1869-72)

Case series: Martinelli T et al. J Trauma 2010 Apr;68(4):942-8

Case Series: Brenner M et al. J Trauma Acute Care Surg. 2013 Sep;75(3):506

Update: Dr. Brenner’s new article on training with a REBOA simulator (10.1097/TA.0000000000000310) and the ESTARs Course Curriculum

Now on to the Podcast…

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Bibliography