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!