Those Nursing Home Nurses Were Right about the Magic Nasal Cannua- Or Were They? HFNC, HFFM, Intensive Care JULY 2015

Some Nasal Background

For years, proponents of rapid sequence intubation have tried to identify the most reliable way to prevent desaturation. Pre-oxygenation is an important part of the RSI strategy, and avoidance of hypoxia in the head injured patient predicts an adverse outcome. RSI fundamentalists believe that NO positive pressure ventilation should take place during an RSI attempt. Positive pressure ventilation theoretically increases the risk for emesis and may cause gastric insufflation. Recently, the strategy\ of high flow oxygen via nasal cannula (HFNC) at flow rares in excess of 15 lpm has emerged as a feasible strategy for passive oxygenation. In patients undergoing RSI, the application of HFNC has been shown to increase "safe apnea time."

Dr. Rich Levitan, a nationally recognized (and emergency medicine trained) airway expert has published on the "NO-DESAT" protocol. This protocol advocates for HFNC in addition to the usual measures can prevent and perhaps maintain oxygen saturation during rapid sequence intubation.

Nice summary of "NO-DESAT" here:
http://www.epmonthly.com/archives/features/no-desat-/

THE PREOXYFLOW TRIAL
A recent study published in Intensive Care Medicine looks more specifically at the use of HFNC in hypoxic patients. The study randomized patients to either high flow oxygen via face mask or high flow (>60 lpm!) nasal cannula. The primary outcome of interest was the lowest saturation of oxygen measured by pulse oximetry.

The study randomized over 120 ***sick*** adult patients. These patients exhibited respiratory failure as evidenced by a high Fi02 requirement, tachypnea, or hypoxia. The study results did not establish the superiority of the HFNC technique, and both patient groups (HFFM and HFNC) experienced significant medical complications.

Does this study urge practitioners to back off the cannula?
Should HFNC be abandoned for patients exhibiting significant respiratory distress?

Before attempting to summarize this trial, we've got to remember that when talking about HFNC, we're still comparing oral airways to king LTs. That is to say, there's quite a lot of difference between the use of HFNC as an adjunct and the use of HFNC as a primary strategy for avoidance of hypoxia. Also, this study uses nasal cannulae specifically designed to accommodate high flow rates. Can the ordinary oxygen regulators supply flow rates in excess of 60 lpm? Probably not. Given peri-intubation hypoxia's association with adverse outcomes, it makes sense that airway practitioners should try to maximize a patients oxygen reserve. Sustaining normoxic values in distressed patients is always a challenging endeavor, and emergency medicine regularly encounters patients at risk for desaturation. Whether its poor respiratory mechanics, morbid obesity, acute blood loss, or baseline pulmonary disease, there are many threats to address in the pre-intubation phase of RSI. Furthermore, its pretty clear that a higher preintubation oximetry reading is linked to that precious "safe apnea" time... that wonderful interval prior to the obnoxious cascade of alarms that herald impending doom.

BOTTOM LINE:
-The PREOXYFLOW trial (HFNC vs HFFM) is NOT an indictment o the NO-DESAT protocol and does not mean that HFNC is bad for patients
-Hypoxia is, in general, something to avoid during RSI
-Use HFNC to complement preoxygenation efforts
-Severely hypoxemic patients may require more active measures to increase and maintain a satisfactory pre-oxygenation level
-In patients with respiratory failure, HFNC as a "stand alone" hypoxia prevention strategy may not represent best practice

Keep the high flow flowing!

The Agony of the Beta Agonists PART 1 of 2 JULY 2015

This was shared from a friend, provider, and colleague. Interesting case. Details changed to protect the innocent, respect privacy laws, comply with all appropriate regulations, and, well.. you get the picture.

SUBJECTIVE
HPI:
94 yo male requests 911 for shortness of breath. HPI  not obtainable due to patient presenting in extremis. The patient is alert, responsive to verbal stimuli, and is in obvious respiratory distress upon arrival. Providers appreciate audible wheezing. Family members relate that the patient is a "DNR" and was last seen acting "a little tired" 12 hours prior.
Meds: Unknown
PMH: COPD, CHF, HTN, HLD, DM

OBJECTIVE
Pt is slightly diaphoretic. BP: 134/92, R: 32, P: 90. ETC02 via NC is 20.
Supraclavicular and intercostal retractions are present as is mild JVD.

12 LEAD ECG:












Case related questions: 
1. What is your prehospital treatment?
2. What are some concerning ECG findings?
3. Is this patient treated as a STEMI alert?

April 2015: Sighting the Subtlety Down Below

CASE: 

A 63 y/o gentleman calls 911 for "chest pressure" and indigestion. The patient is nauseated but denies LOC, SOB, or dizzinesss. The pressure started approximately 1 hour prior to 911 arrival. The patient has a history of hypertension and takes an aspirin daily. He is hemodynamically stable. BP is 110/70, P: 82, R: 16. Sp02: 95% on RA.

12 LEAD ECG:

12 LEAD ECG DISCUSSION:

There is a sinus rhythm. PR depression is present in lead II. There is slight ST segment elevation present in II, III, and aVF. Elevation measures about 1 mm. There is no evidence of recriprocal change. A biphasic T wave is present in lead III and terminal T wave inversion is present in the lateral precordial leads. The QRS axis appears physiologic.

12 LEAD INTERPRETATION: 

Inferior wall STEMI

TREATMENT

The patient was transported to a hospital capable of percutasneous coronary intervention. A right sided ECG was not performed, and NTG was withheld due to the patient's marginal blood pressure or relative hypotension. 325 mg of ASA was administered. The patient's RCA was 75% occluded.

Thanks always to the Baltimore City Fire Department for its endless supply of pathologic 12 lead tracings.

Fix the Rate First ?

CASE PRESENTATION:
Providers respond to a 68 yo female with a sudden onset of paroxysmal nocturnal dyspnea. The patient reports slight dyspnea on exertion for the past few weeks and endorses a mild, non productive cough. The patient speaks in 2-3 word sentences and appears in severe respiratory distress. The patient denies chest discomfort, nausea, vomiting or fever. The patient is in severe respiratory distress and is profoundly diaphoretic. Another paramedic provider onscene diagnoses SVT and readies adenosine for administration.

EXAM:

BP:     220/120
P:        168
R:        40
Spo2:  88%


12 LEAD ECG:

12 LEAD ECG ANALYSIS:

There is a supraventricular tachycardia. P waves are difficult to discern but the QRS complexes are narrow and occur at regular intervals. Diffuse repolarization abnormalities in the form of biphasic T waves are present in the inferior leads. There is no obvious ST segment elevation.

TREATMENT:

High flow oxygen is administered and an intravenous line is inserted. The senior paramedic recommends against adenosine administration. A total of 1.2 mg of nitroglycerin is administered sublingually. 324 mg of aspirin is administered. As the patient is prepared for transportation, CPAP is started at 10 cm H20. The patient experiences rapid improvement and the hypoxia resolves. A repeat ECG shows sinus rhythm with some lateral ST segment depression. Vital signs following CPAP and NTG are as follows: BP: 180/100, P: 110, R: 22, Sp02: 100%. A chest xray shows cardiomegaly and bilateral opacities consistent with pulmonary edema are present.

DISCUSSION:

Though fixing a fast heart rate can reduce ischemia, it is important to consider the underlying cause of a dysrhythmia. Administration of adenosine could convert this ECG but the SVT is very likely due to the catecholamine surge that accompanies acute pulmonary edema. A reduction in cardiac output and afterload results in improved oxygenation, reduced work of breathing, and resolution of the supraventricular tachycardia. Following a hospitalization for acute heart failure, the patient was discharged to home on an aggressive medical regimen targeted at maintaining an acceptable blood pressure. The prehospital application of CPAP is consistently linked to a reduced endotracheal intubation and improved mortality.

Non Sustained VT: Making a Lasting Impression!

Putting on the Pressure

A 60 yo male presents to EMS with several hours of chest pressure and diaphoresis. A 12 lead ECG is obtained following a 10 beat run of non sustained ventricular tachycardia. Despite the EMT's excitement at "firing up the paddles," the paramedic administers 324 mg of aspirin and prepares for transport to the nearest facility capable of percutaneous coronary intervention. Your partner informs you that the monitor discerns the presence of a paced rhythm. The patient has no previous medical history.


12 LEAD ECG:

12 LEAD ECG Analysis:

A sinus rhythm is present and the rate is regular. Diffuse and concerning ST segment changes appear in this tracing. First, pathologic ST segment elevation occurs in leads V2, V3 and V4. Q waves also appear throughout the tracing. The monitor misinterprets the ischemic Q wave as a pacer spike. The QRS is narrow, so an interventricular conduction delay is less likely responsible for the "false pacer" call. Reciprocal changes appear in lead aVF. There is minimal J point depression in lead III and V6. The baseline is also irregular.


12 Lead ECG Interpretation: 

Sinus rhythm, anterior wall ST segment myocardial infarction.

Comments:

• It is difficult to discern the location of the anatomic lesion based upon this ECG. The large ST segment elevation in the precordial leads suggests involvement of the LAD. The findings of lateral wall ischemia could implicate the circumflex as well. 
• The run of VT was likely due to ventricular irritability. Remember that the most devastating complications of anterior wall ischemia are lethal dysrhythmia and cardiogenuc pulmonary edema 
• Pathologic Q waves generally follow a few rules: (1) larger than a third of the corresponding R wave or (2) measure in excess of 0.03 seconds. Q waves that accompany poor R wave progression are more likely to indicate ischemia. 

Casting a Wide Net for a Complex Tachycardia 2/2

Case conclusion to the ECG / scenario posted in September 2014:

Casting a Wide Net for Wide Complex Tachycardia 1/2

A 40 yo female is brought into the emergency department. The patient is unresponsive, hypotensive, and tachycardic. EMS providers are assisting ventilations with a bag valve masked and have attempted defibrillation without success. Paramedics state that the patient was somnolent prior to the arrest and has no cardiac history. A 12 lead ECG is obtained upon arrival at the emergency department.

BP:    80/50
P:      150
R:      12/assisted
Spo2: 100% via BVM

Initial 12 lead

This is a wide complex, regular tachycardia. The widespread concordance across the precordial leads (and regular rhythm) suggest a ventricular rhythm. This rhythm was correctly interpreted- and treated- by the responding paramedics. Unfortunately, this dysrhythmia was refractory to prompt defibrillation. Why ?

Lead aVR

In addition to the wide complex tachycardia and concurrent hypotension, there is a HUGE terminal R wave (positive deflection) in lead aVR. This is a well recognized feature of tricyclic anti-depressant toxicity. Sodium channel blockade results in prolongation of the QRS and is also responsible for the hypotension. The clinical progression of TCA toxicity also involves alpha receptor blockade. Hypotension and loss of consciousness are associated with mortality in the setting of TCA toxicity. 

So, what can EMS providers do? 

1. Early defibrillation

2. Empiric administration of bolus sodium bicarbonate 50-100 mEQ IV/IO

3. If TCA overdose is suspected, consider vasopressors. An alpha agonist such as levophed (norepinephrine) is more ideally suited for this scenario

4. Early airway protection

5. Be very cautious with charcoal as patients with TCA toxicity experience a precipitous decrease in LOC and are at risk for aspiration. Activated charcoal produces a very nasty chemical pneumonitis. 

Any other cutting edge therapies? 

The use of a lipid emulsion has been studied as a treatment for suspected TCA overdose. In addition to vasopressors and fluid boluses, the lipid emulsion is thought to reduce the drug's bioavailability. Essentially, administration of a lipid emulsion can "remove" active metabolites from the intravascular compartment. The usual initial dose of a lipid emulsion is: 1.5mL/kg of a 20% solution. The bolus dose is given over one minute and is usually followed by a 400 mL infusion over 30 minutes or less. 

Epinephrine needs some epinephrine, stat!

The Journal of the American College of Cardiology recently published a paper on the use of epinephrine for out of hospital cardiac arrest. The results are about as encouraging as the development of a wide-complex pulseless electrical rhythm!

Over 1500 patients were eligible for inclusion into this study. The study involved a European EMS system in which physicians staffed ambulances. Outcomes of interest included (1) survival to discharge and a (2) neurologically favorable outcome. Neurologically favorable outcomes were reported as Cerebral Performance Category (CPC) scores of 1 or 2. Not surprisingly, the administration of epinephrine was associated with a worsened neurological outcomes. The authors performed a multivariate logistic regression analysis in an attempt to control for patient and situation specific factors. Simply stated, the negative association of epinephrine persisted across various patient subgroups (older patients, patients with witnessed arrest, etc).


CPC Score Description: 

Some other interesting observations:

• Favorable neurologic outcome became less likely with an increased duration of arrest
• The delay in epinephrine administration was "linearly" associated with worsened outcomes
• Worsened neurological outcomes occurred in patients receiving "state of the art" in hospital care such as hypothermia and PCI

So, is the use of epinephrine beyond resuscitation? 

Not quite. As the authors state, it is difficult to establish a cause and effect relationship in the absence of a randomized controlled trial. Even then, out of hospital cardiac arrest does not always lend itself to an orderly collection of data. The timing of epinephrine is something that is not completely understood- epinephrine probably has no role during the "metabolic" phase of cardiac arrest. During this phase, which occurs very late into the event, epinephrine may only potentiate an already acidotic and cytotoxic environment. On the other hand, should epi be routinely administered to patients in the "electrical" phase of the arrest? In the first few minutes following collapse, defibrillation should probably take priority over IV/IO access and catecholamine administration. Perhaps epinephrine administration needs to be tailored to the individual patient presentation as opposed to routinely given every 3-5 minutes. There's actually quite a bit of conversation around a "goal directed" protocol. Epinephrine should be titrated to achieve a minimum diastolic blood pressure.

Prehospital bottom line:

• Timing of epinephrine administration may be important (the earlier, the better) 
• Continue to focus on time-tested interventions linked to improved neurologic survival
• Minimally interrupted, high performance CPR is key to maintaining adequate coronary perfusion
• Epinephrine may be linked to an increased incidence of prehospital ROSC but does not appear to confer longer term survival or neurologic benefits following out of hospital cardiac arrest

Article abstract in PubMed

J Am Coll Cardiol. 2014 Dec 9;64(22):2360-7. doi: 10.1016/j.jacc.2014.09.036. Epub 2014 Dec 1.

Is epinephrine during cardiac arrest associated with worse outcomes in resuscitated patients?

Dumas F1, Bougouin W2, Geri G2, Lamhaut L3, Bougle A4, Daviaud F4, Morichau-Beauchant T4, Rosencher J5, Marijon E6, Carli P7, Jouven X6, Rea TD8,Cariou A2.

Author information

Abstract

BACKGROUND:

Although epinephrine is essential for successful return of spontaneous circulation (ROSC), the influence of this drug on recovery during the post-cardiac arrest phase is debatable.

OBJECTIVES:

This study sought to investigate the relationship between pre-hospital use of epinephrine and functional survival among patients without-of-hospital cardiac arrest (OHCA) who achieved successful ROSC.

METHODS:

We included all patients with OHCA who achieved successful ROSC admitted to a cardiac arrest center from January 2000 to August 2012. Use of epinephrine was coded as yes/no and by dose (none, 1 mg, 2 to 5 mg, >5 mg). A favorable discharge outcome was coded using a Cerebral Performance Category 1 or 2. Analyses incorporated multivariable logistic regression, propensity scoring, and matching methods.

RESULTS:

Of the 1,556 eligible patients, 1,134 (73%) received epinephrine; 194 (17%) of these patients had a good outcome versus 255 of 422 patients (63%) in the nontreated group (p < 0.001). This adverse association of epinephrine was observed regardless of length of resuscitation or in-hospital interventions performed. Compared with patients who did not receive epinephrine, the adjusted odds ratio of intact survival was 0.48 (95% confidence interval [CI]: 0.27 to 0.84) for 1 mg of epinephrine, 0.30 (95% CI: 0.20 to 0.47) for 2 to 5 mg of epinephrine, and 0.23 (95% CI: 0.14 to 0.37) for >5 mg of epinephrine. Delayed administration of epinephrine was associated with worse outcome.

CONCLUSIONS:

In this large cohort of patients who achieved ROSC, pre-hospital use of epinephrine was consistently associated with a lower chance of survival, an association that showed a dose effect and persisted despite post-resuscitation interventions. These findings suggest that additional studies to determine if and how epinephrine may provide long-term functional survival benefit are needed.

Copyright © 2014 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

KEYWORDS:

cardiac arrest; hypothermia; percutaneous coronary intervention