To VT or not to VT- the Persistent Question Part 1/2

EMS responds to the report of an elderly female with palpitations. The patient's blood pressure is 100/76 and she has intact distal pulses. The patient reports mild retrosternal chest pain. There is no shortness of breath. The patient has a history of atrial fibrillation and called EMS when vagal maneuvers and an additional dose of metoprolol (prescribed) failed to correct the symptoms. 

What is your diagnosis ? 

What treatments would your crew consider? 

12 LEAD ECG

SVT or VT or SVT ***Abnormal ECG Unfonfirmed***

CASE PRESENTATION

A 50 yo male calls EMS for palpitations and chest discomfort. A 12 lead ECG (of course!) is obtained. The patient is short of breath and symptomatic. He remains awake, alert, oriented, and slightly diaphoretic. No obvious history.

12 LEAD ECG

12 LEAD ECG

ECG ANALYSIS AND INTERPRETATION

This ECG is particularly challenging, especially when the patient is symptomatic. Lifenet is raising all of the appropriate alerts, and you're faced with a couple of immediate treatment decisions. First, let's tackle therapy. 

1. In general, FIX THE RATE FIRST! Not only will fixing the rate provide relief from demand ischemia, but it may provide you with a diagnosis. This ECG is rapidly marching a long, and its very difficult in the heat of the moment to sort out p waves from QRS complexes from flutter waves. Demand ischemia occurs when the heart is unable to fill.

2. Unstable patient=SHOCK

3. Stable patient=consider drug therapy. In this case, adenosine **MAY** be an appropriate first line drug because the tachycardia is either some type of aberrant SVT or monomorphic VT

4. There are WIDESPREAD repolarization changes which I suspect are complicated by some lead placement issues. The narrow-looking complex in V2 doesn't fit with the rest of the ECG

5. The ECG is regular and FAST. VT usually occurs at a rate of 150; other differentials to consider in the setting of narrow complex tachycardia that is regular include SVT and A flutter. Intermittent and regularly occurring (small) positive deflections appear in this ECG to suggest an underlying atrial flutter rhythm

6. Examining lead one, the RIGHT rabbit ear is "taller." This favors SVT. Interestingly enough, RSR' complexes with a taller LEFT rabbit ear favor ventricular tachycardia. 

7. Other features that favor VT are absent, such as:
-AV dissociation
-Fusion beats
-Entirely positive or negative concordance in the chest (precordial) leads. This finding is best described as when the QRS complexes all point in the same (positive or negative) direction

8. With regard to the widespread ST segment elevation, it is never a bad idea to transport to a center capable of percutaneous coronary intervention. In this case, I suspect the widespread ECG changes (lots of ST segment depression) are due to repolarization  abnormalities or rate related ischemia. There doesn't appear to be a clear-cut anatomic distribution of the elevation. 

I shall offer my humble interpretation reminiscent of several recent radiology reads:
Regular, wide complex tachycardia suggesting either VT or an aberrantly conducted supraventricular rhythm. 2:1 atrial flutter is also in the differential. Correlate clinically. 

So the bottom line remains that I don't have a definitive interpretation here. Perhaps some of the other online ECG gurus could weigh in and provide some direction. What is clear, however, is that providers should keep some core principles in mind when confronted with a concerning and potentially confounding ECG:
1. Fix the rate first

2. Treat wide complex tachycardia as VT 

3. Always consider ischemia in your differential diagnosis

***Abnormal EKG Unconfirmed*** CONSIDER BRUGADA SYNDROME, Consider Ischemia

EMS crews respond to the report of a sick 70 year old male. An ECG is obtained. As your crew performs patient assessment and works on obtaining IV access, your astute EMT obtains a 12 lead ECG.

1) What's your interpretation ?
2) What is an emergency-focused differential that is consistent with this ECG?
3) Why NOT Brugada ?

12 LEAD ELECTROCARDIOGRAM

First, there is a wavy baseline that interferes with rhythm interpretation. The rhythm is obviously bradycardic and the rate is consistent with a ventricular etiology. The complexes are wide, bizarre, and irregular. There is evidence of ST segment elevation in (possibly) V1 and V2. ST elevation may also be present in Lead II. Diffuse ST segment depression is present in leads I, III, aVF, V5-V6. 

Interpretation

Ventricular rhythm, diffuse ST-T segment depression

Differential diagnosis

Ischemia
Hyperkalemia
Myocardial infarction

Therapy
As this ECG arrived in my inbox without any clinical context, it seems reasonable to consider calcium. In the late stages of hyperkalemia, the QRS can widen considerably and the p waves simply disappear. If the patient presented with a story concerning for ischemia, transport to a cath capable hospital would comprise an excellent treatment plan!

WHY NOT BRUGADA?
The ECG software seems a bit confused by the wandering baseline and the presence of atypical ST segment elevation. Brugada, however, is a curious interpretation because it is a clinically distinct entity that involves specific clinical and electrocardiographic findings. Brugada syndrome was first described in the 1990's. It is the result of an abnormality in the cardiac sodium channel gene. It iis associated with sudden cardiac death in certain patients. The Life in the Fast Lane blog has an excellent (and succint) review of this syndrome.

Brugada syndrome presents commonly following a syncopal episode. The patient may not complain of any chest pain or shortness of breath. The syncope is usually caused by a transient ventricular dysrhythmia. It is most commonly diagnosed in younger aged Asian males.

EKG Findings in The Brugada Syndrome
Atypical ST segment elevation is the hallmark of Brugada syndrome. Typically, there is a "coved" type of ST segment elevation present in leads V1-V3 .Another type of ST segment abnormality seen in the syndrome include a "saddle-back" deformity:

Treatment
Treatment is directed at correction of the underlying defect. Because these patients are at increased risk for death, they will usually benefit from a cardiology referral and consideration of AICD insertion.

Key Brugada points for the EMS provider:

• Brugada syndrome is a clinical entity consisting of distinct ECG and clinical characteristics
• Perform an ECG in ALL patients following a syncopal episode
• Scrutinize the ECG for atypical, "coved" or "saddle back" ST segment abnormalities, especially in the precordial leads

Way Too Overdue: Subtle STEMIs, Stubborn Platelets. Part 2/2

EMS is attending to a patient with chest discomfort. A 48 yo female presents to EMS with hypertension, right sided chest pain, and the following EKG.

12 lead EKG interpretation:

There is a baseline sinus rhythm. There is minimal, but significant, ST segment elevation in leads III and aVF. Reciprocal change in the form of ST segment depression is seen in the anterior/high lateral leads. The precordial leads do not exhibit ST segment depression which makes the diagnosis of posterior wall extension less likely. This ECG is consistent with a (subtle) inferior wall ST elevation myocardial infarction.

Case discussion:

Female patients, diabetic patients, elderly patients, and patients with a history of cocaine use are at increased risk for atypical presentations of acute coronary syndromes. Cocaine causes platelet aggregation and accelerates the development of coronary plaque. Cocaine is directly toxic to myocytes and can also induce vasospasm. Providers should remain vigilant for atypical presentations and treat accordingly.

EMS transports this patient to a STEMI center and administers NTG and ASA in accordance with established protocol. The patient does not experience any hypotension and remains hemodynamically stable. Chest pain resolves upon arrival to the ED. The patient undergoes emergent coronary angiography and has a 100% occlusion of the RCA. The lesion is ballooned. Initial troponins are positive. The patient is rapidly transitioned to a cardiac step down unit and has an uneventful recovery.

Way Too Overdue: Subtle STEMIs and Stubborn Platelets March 2016 PART 1/2

SUBJECTIVE:
EMS responds to the report of a 48 yo female with chest pain. Upon arrival, the patient is in mild distress and reports sharp, intermittent, right sided chest discomfort lasting for approximately 30 minutes. The patient reports nausea, some slight diaphoresis, and denies vomiting. The patient reports recent intake of cocaine and has a history of substance abuse. The patient has no allergies.

PMHX:
HIV
HTN

OBJECTIVE: 
The patient is awake, alert, oriented, and seated in a chair. BP: 160/100, P: 80, R: 72. Sp02: 97% on RA. Lungs are clear to auscultation bilaterally. Heart sounds are regular. The abdomen is soft and the remainder of the physical assessment is unremarkable. Peripheral pulses are strong and equal.

A 12 lead ECG is obtained:

What's your interpretation and treatment plan? 
An intravenous line is started.

The Agony of the Beta Agonists PART 2 AUGUST 2015

We left off with a rather critically ill patient. EMS responded to a patient in respiratory failure:

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.

The patient's ECG was similarly concerning:

Let's review this case: 

PREHOSPITAL TREATMENT 

Prehospital treatment should be directed at symptom relief and mitigation of the underlying cause. Audible wheezing does not always indicate COPD, and this patient may be suffering from CHF, cardiac asthma, pneumonia, or a combination of entities! Fortunately, CPAP therapies have utility with respect to reducing the work of breathing and reducing preload. Of course, the concurrent rise in intrathoracic pressure may precipitate hypotension. However, this patient is alert enough to probably warrant a trial of non invasive positive pressure ventilation. Beta agonists may have utility if there is evidence of bronchospasm. However, B1 receptor stimulation may cause an increase of cardiac contractility and irritability. Nitroglycerin

wouldn't be unreasonable, but its probably safe to consider initiating IV access. The take home point in this case is that elderly patients are often highly comorbid. Physical assessment and end tidal C02 readings are often confounded by the critical presentation! Is the patient's end tidal reading low due to tachypnea alone? Is there an underlying metabolic disturbance? Is the wheezing due to bronchospasm or does it represent sequelae of pulmonary edema? Often times, more information is needed in the form of xray and bloodwork to determine the underlying diagnosis- or diagnoses. CPAP and other respiratory treatments represent reasonable therapies, and there is no all inclusive, correct answer. There is really no role for the emergent, prehospital administration of furosemide for suspected acute cardiogenic pulmonary edema. If the patient can follow the occasional verbal commands and swallow without difficulty, 325 mg of chewable aspirin is indicated. 

ECG FINDINGS AND STEMI ALERT? 
The underlying rhythm appears sinus in origin and there is evidence of a left bundle branch block (LBBB). LBBB is a common finding in elderly patients and may simply represent advanced disease. LBBB accompanies a relatively rare number of acute myocardial infarctions and is a maker of illness severity when present. A complete LBBB results from interruption of the anterior and posterior fascicles. Therefore, new onset LBBB in the setting of a critically ill patient should motivate EMS personnel to transport to a facility capable of percutaneous coronary intervention. LBBB often confounds the diagnosis of STEMI but recent literature and AHA guidelines recommend against activating the cath lab for an LBBB of unknown duration. In this setting, however, where providers are confronted with a patient in acute pulmonary edema, it may be wise to choose a cath capable hospital. 

SUBTLE SGARBOSSA

Criteria exist for the prediction of ischemia in the presence of LBBB. The Sgarbossa crtieria function to distinguish ischemia (terrible) from pre-existing conduction delay and established coronary artery disease (less terrible). In this ECG,  specifically in Lead V3, there is evidence of an "excessively discordant ST segment." In previous studies, the presence of discordant ST elevation (in leads with a negatively deflected QRS) was associated with myocardial infarction. This criteria alone is not sufficient to establish the diagnosis of STEMI but may bolster the provider's decision to transport to the cath lab. An excellent discussion of the original Sgarbossa criteria can be found on the Life in the Fast Lane Blog.

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

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. 

Where is the culprit lesion? ST segment morphology

CASE STUDY:

Medics respond to the report of someone with chest pain and shortness of breath. Vital signs are stable. Given concern for acute coronary syndrome, a 12 lead ECG is obtained.

12 LEAD ECG

12 LEAD ECG Discussion

There is a sinus rhythm. ST segment changes are widespread. The inferior leads reveal some ST segment straightening but no frank elevation. Profound ST segment elevation in present in leads V2, V3, and V4. Reciprocal change in the form of ST segment depression is present in lead aVL. ST segment morphology is linked to adverse outcomes. The ST segments in this particular case display a concerning, "straight" shape especially prominent in lead V3.

12 LEAD ECG Interpretation

Sinus rhythm, anterior wall ST elevation myocardial infarction. 

Resolution

The patient was delivered emergently to the cardiac catheterization lab. A bare metal stent was placed in the proximal left anterior descending artery. The patient was discharged without complication on hospital day 2. 

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


What are your thoughts on the 12 lead?

What is your next course of action?

August 2014: Right behind you with a STEMI!

A 60 yo male patient reports a sudden onset of chest pain and shortness of breath. The patient rates the pain at an 8/10 and is slightly nauseated. The patient has a history of "borderline" diabetes.

VS:
BP: 140/90, P: 62, R: 16, Sp02: 99%

EXAM:
The patient is slightly diaphoretic and appears uncomfortable. A 12 lead ECG is obtained.

ACTIONS:Do you activate the cath lab?
Do you administer NTG?

12 LEAD ECG: 

12 LEAD ECG CASE DISCUSSION:

The ECG shows a first degree heart block. ST segment elevations are apparent in Leads II, III, and aVF. Reciprocal changes are present in Leads I and aVL. ST segment changes are present in the septal leads of V3 to V4. The diagnosis of a posterior wall myocardial infarction is less likely given (1) the absence of tall R waves and (2) The absence of ST depression in leads V1-V3. However, anytime anterior precordial ST depression appears concurrently with an inferior wall MI, you should consider the diagnosis of a posterior wall infarction. Recall that the posterior descending coronary artery comes from the right coronary artery. It is wise to be cautious with nitroglycerin since this infarction may involve portions of the right ventricle. Have IV access established and consider right sided chest leads if there is concern for a right ventricular infarction. This patient went emergently to the cardiac catheterization lab and was found to have a completely (100%) occluded right coronary artery.  Finally, conduction delays and heart blocks are consistent with ischemia of the sinoatrial node and the conduction system.

12 LEAD ECG INTERPRETATION:
Inferior wall ST elevation myocardial infarction.

Purple Pacer People: Does the 12 Lead ECG Show the Whole Story? 1/2

CASE PRESENTATION 

CC:          SOB
HPI:         80 yo male with sudden onset SOB during walk. Pt recalls feeling sick and then experienced syncopal eposide. Pt denies CP. Denies recent illness.
EXAM:    Pale, anxious, diaphoretic. VS: BP: 107/70, P: 107, R: 20. Sp02: 89%. Pt retracting; clear lung sounds.
ASESS:  Severe respiratory distress
PLAN:     Vitals, 12 lead, high flow oxygen, fluid bolus, 324 mg ASA


12 LEAD ECG

12 LEAD ECG RHYTHM STRIP

EMS and ED COURSE

The providers package the patient for transport. The patient becomes progressively more short of breath. Truncal cyanosis appears and is refractory to high flow oxygen. The patient has seizure-like activity upon arrival to the ED. Compressions are started and the patient expires following thirty minutes of failed reususcitation. 

What clues are provided by the patient's history or 12 lead ECG?