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

Hey, my heart just stopped- can you downgrade the ambulance?

The EMS community is all a-twitter with the results of the trial published in the latest issue of JAMA- Internal Medicine.

Sanghavi, et al (2014) published an observational study of over 32,000 cases of out of hospital cardiac arrest. The study examined relevant outcomes such as survival to hospital discharge and neurological outcome. Not surprisingly, patients treated by BLS crews experienced a higher rate of overall survival AND better neurologic functioning. Sanghavi's study affirms the results of the landmark Ontario Prehospital Advanced Life Support (OPALS) study in which the introduction of advanced life support services failed to demonstrate improvement in survival rates from out of hospital cardiac arrest.

So, what are the take home points of this study? Are we to heed calls to mothball ALS ambulances? Do paramedics make any difference at all? What's the value of ALS in cardiac arrest?

First of all, this study is consistent with decades of resuscitation research. Interventions associated with survival from cardiac arrest have remained relatively constant: high quality, minimally interrupted compressions, early defibrillation, hypothermia, and possibly percutaneous coronary intervention. The reflexive, historical practice of intubating every arrest simply to "secure" an airway has no basis in evidence. Its not that the presence of a paramedic is harmful. Rather, the routine addition of advanced life support interventions to a prehospital resuscitation event continually fails to confer additional benefit. The value of a paramedic rests with his/her ability to orchestrate resuscitative efforts and prioritize those things most likely to achieve ROSC. Survival has inched ever higher in the wake of high performance and bystander CPR initiatives- the EMS community should take notice and embrace a "BLS centric" approach to the problem of out of hospital cardiac arrest.

Practice patterns shouldn't change on the basis of one study- that's why we'll follow this discussion up  by highlighting recent articles focusing on the role of epinephrine and advanced airways in cardiac arrest management.

PubMed abstract

Outcomes After Out-of-Hospital Cardiac Arrest Treated by Basic vs Advanced Life Support.

Sanghavi P1, Jena AB2, Newhouse JP3, Zaslavsky AM4.

Author information

Abstract

IMPORTANCE:

Most out-of-hospital cardiac arrests receiving emergency medical services in the United States are treated by ambulance service providers trained in advanced life support (ALS), but supporting evidence for the use of ALS over basic life support (BLS) is limited.

OBJECTIVE:

To compare the effects of BLS and ALS on outcomes after out-of-hospital cardiac arrest.

DESIGN, SETTING, AND PARTICIPANTS:

Observational cohort study of a nationally representative sample of traditional Medicare beneficiaries from nonrural counties who experienced out-of-hospital cardiac arrest between January 1, 2009, and October 2, 2011, and for whom ALS or BLSambulance services were billed to Medicare (31 292 ALS cases and 1643 BLS cases). Propensity score methods were used to compare the effects of ALS and BLS on patient survival, neurological performance, and medical spending after cardiac arrest.

MAIN OUTCOMES AND MEASURES:

Survival to hospital discharge, to 30 days, and to 90 days; neurological performance; and incremental medical spending per additional survivor to 1 year.

RESULTS:

Survival to hospital discharge was greater among patients receiving BLS (13.1% vs 9.2% for ALS; 4.0 [95% CI, 2.3-5.7] percentage point difference), as was survival to 90 days (8.0% vs 5.4% for ALS; 2.6 [95% CI, 1.2-4.0] percentage point difference). Basic life support was associated with better neurological functioning among hospitalized patients (21.8% vs 44.8% with poor neurological functioning for ALS; 23.0 [95% CI, 18.6-27.4] percentage point difference). Incremental medical spending per additional survivor to 1 year for BLS relative to ALS was $154 333.

CONCLUSIONS AND RELEVANCE:

Patients with out-of-hospital cardiac arrest who received BLS had higher survival at hospital discharge and at 90 days compared with those who received ALS and were less likely to experience poor neurological functioning.

Beyond the Thin Red Amplitude Line

There's lots of dialogue on social media and twitter feeds indicating a broader interest that extends beyond prehospital ECGs. In addition to the usual STEMI related banter, I'd like to include relevant articles addressing relevant prehospital and emergency medicine contributions to the resuscitation literature. Hopefully there will be some sustained interest in a brief review of resus articles that you've got to know. I'd very much like to stimulate some informed discussion on resuscitation related topics. Next up: the eternal BLS vs ALS in cardiac arrest resuscitation debate. Thanks in advance for your comments and participation- keep sending in those ECGs!

Oh yeah- the blog would need a new title to reflect its expanded focus. Suggestions welcome-
1) Going beyond ROSC
2) Resuscitate, Intubate, Irradiate: Case Studies in Resuscitation Science

Simple STain on the Strain

Sometimes LVH isn't all that simple. The "strain" pattern has been discussed elsewhere on this and other blogs, but this is an example of an atypical, and concerning, ECG:

What's not (so) unusual: 
The ECG reveals a sinus rhythm. The downsloping ST segments and T wave inversions seen in the lateral leads and precordial leads may be expected in the setting of high left ventricular voltage. The pattern of LVH and ST/T wave changes is consistent with, "strain."

What's concerning: 
The ST segment elevation present in aVL and V1-V2 is NOT concave and almost horizontal. This type of ST segment change is consistent with ischemia. Furthermore, it appears in an anatomic distribution. ST segment changes in aVL and V1-V2 suggest anterior or anterior lateral ischemia. Though LifeNET measures the ST segment elevation at less than 2 mm, it is nevertheless cause for concern especially given a "typical" story or history consistent with an acute coronary syndrome.

Bottom line and interpretation:
Carefully evaluate ST segment deviation in all leads. Look for atypical elevation and an anatomic distribution of the ECG changes.
Sinus rhythm, ST segment depression and T wave inversion consistent with strain pattern. ST segment elevation in the anterior precordial leads and aVL suspicious for STEMI.