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? 

Deadly 12 Lead ECG Diagnosis: Pulmonary Embolism

Its well known that there are things other than STEMI that stand ready to confound, perturb, and otherwise confuse your clinical impression. Pulmonary embolism (PE)  is one of those things. Massive PE has been linked to all sorts of ECG changes. A recent article printed in the American Journal of Emergency Medicine highlighted some of the ECG features associated with cardiogenic shock:

• The S1 Q3 T3 sign
• qR in lead V1
• T wave inversions in V2-V4
• STE in lead V1
• STE in lead aVR

These problematic ECG signs come as no surprise to fellow ECG enthusiasts. The incomplete right bundle branch pattern + T wave inversion indicate "heart strain" that accompanies large pulmonary emboli, 

Here's a recent prehospital 12 lead concerning for pulmonary embolism: 

Bottom line:

The ECG represents a valuable screening tool. Though its not particularly sensitive or specific for pulmonary embolism, there are definitely patterns that should alert the clinician to an adverse outcomes. In the setting of suspected pulmonary embolism, for example, watch out for:

• Right bundle branch block
• Anterior T wave inversions
• STE in aVR or V1

Pointy ST Segments and Abnormal Labs

Your crew responds to a local skilled nursing facility for a patient with "abnormal labs." The nurse tells you that the patient's "K was elevated." The patient reports a near syncopal episode approximately 40 minutes prior to arrival. The patient feels weak and dizzy. No chest pain, shortness of breath, or vomiting is endorsed. The patient is ill appearing but awake, alert, and oriented.

Vital signs:
BP: 82/40
P: 49
R: 16
Sp02: 86% on room air

A 12 lead ECG is obtained:

12 Lead ECG Discussion

The rhythm is sinus bradycardia. Unless this 80 year old is a marathon runner, the rate is abnormal. Furthermore, the bradycardia occurs in association with (1) near syncope and (2) abnormal vital signs. ST segment elevation is seen in leads II, III, and aVF. Reciprocal change in the form of ST segment depression is seen in lead aVL. STE is also observed in the lateral precordial leads. The R waves are tall in V2 and V3 but there is no concurrent ST segment depression to suggest involvement of the heart's posterior wall. Q waves, though not pathologic, appear in leads II, III, and aVF, and favor the diagnosis of ischemia.

12 Lead ECG Interpretation 

Sinus bradycardia, Inferior-lateral ST segment myocardial infarction. 

Case Discussion

This case presents more than a few dilemmas and teaching points. First, it emphasizes the association between dizziness, weakness, and acute coronary syndromes. Elderly patients may not present with the classic "chest pain" or "chest pressure." Dyspnea, dizziness, and weakness are well known anginal equivalents and should be aggressively investigated, especially in the setting of abnormal vital signs. The presence of peaked T waves might suggest underlying hyperkalemia. The changes associated with hyperkalemia are usually diffuse. The STE in this ECG follows an anatomic (inferior-lateral) pattern. If there is concern for "abormal labs," then the administration of calcium is probably warranted. Calcium should always be considered first line in the management of hyperkalemic emergencies.

What About the Rate? 

This patient also presents with symptomatic bradycardia. A well accepted axiom in EMS and emergency medicine is, "fix the rate FIRST." EMS protocols would probably advocate for a healthy dose of atropine. Ischemia of the SA node (caused by RCA occlusion) can certainly result in a symptomatic bradycardia, heart blocks, and other types of badness. However, be cautious when administering atropine to a patient suffering from an active MI. Atropine will increase myocardial demand and have the potential to exacerbate ischemic symptoms. A gentle fluid bolus may suffice to mitigate hypotension, and opening of an occluded RCA will make everything right as rain...

KEY POINTS:

• Fix the rate first (WITH CAUTION in cases of active ischemia!) 
• Calcium is first line in the treatment of suspected hyperkalemia and ECG changes
• Weakness, dizziness, and syncope should be regarded as anginal equivalents- especially in the elderly 
• Inferior wall myocardial infarction can produce bradycardia, heart blocks, and syncope

Special thanks to JoElyn for providing these ridiculously complex ECGs! (And best wishes as a newly minted registry medic...) 

STill a STEMI? PART 2/2

The 80 year old male patient feels better following the administration of aspirin and NTG. The ECG is unchanged (since you're one of those providers with an incredible attention to detail, you've already recorded 2 or 3 ECGs).  Chest pain is currently 2/10, and the shortness of breath is resolved.The patient is stable and loaded into the back of your ambulance for transport to:

1) The closest facility?
2) The closest cath capable facility?

You pour over the ECG and make the call.

LEAD V1

• Lead V1 shows approximately 1 mm of elevation at the J point. The baseline is a bit wavy, however the elevation is measured at one small box.

LEAD V2

• Again, there is a slight amount of ST elevation present in leads V2-V3. Elevation is approximately 1.5mm-2mm. 

LEADS aVL and aVF

• You screen the ECG for evidence of reciprocal change, but there is no evidence of ST segment depression in the (1) inferior leads or (2) lateral leads. Again, the wavy baseline interferes with the finer details. Reciprocal change, if present, can solidify your impression of STEMI. 

The Final (non satisfying) Answer

The ECG reveals a sinus rhythm. There is a slight amount of ST segment elevation present in the precordial leads. The ECG does not meet the strict definition of STEMI. In male patients, recall that STE of greater than 2 mm / 2 small boxes must be present in the precordial leads. Specifically, AHA/ACC guidelines state that STEMI is diagnosed if > 2 mm of elevation is present in leads V2 or V3. Elevation of one small box in 2 contiguous limb leads also satisfies diagnostic criteria. There is also the absence of dynamic change when serial ECGs are examined. There is also no evidence of reciprocal change. The ST segment elevation appears physiologic and accentuated by a wavy baseline. That said, I'd probably transport the patient to a cath capable facility. When ECG findings are equivocal, it is important to look at the PATIENT. In an 80 yo male with a significant past medical history and concerning presentation, it is best to err on the side of caution. Myocardial infarction should probably be at the top of everyone's list, and a certain amount of overtriage to regional STEMI centers is acceptable. Though this ECG does not meet strict criteria for the diagnosis of STEMI, the patient's (1) advanced age and (2) concerning presentation probably warrant a trip to a cath capable facility. Sometimes, it is impossible to achieve diagnostic certainty. If patient stability and local protocols permit, a trip to a cath-capable facility is probably a good idea. Optimizing the quality of your tracing is a wonderful strategy; patient movement should be kept to a minimum when obtaining the tracing. Tachypnea, diaphoresis, and cellular phones have all been implicated as causes of interference with the ECG tracing. Finally, the presence of absence of relief following administration of NTG is unreliable for the diagnosis of acute myocardial ischemia. 

INTERPRETATION

Sinus rhythm with ST segment elevation in the septal precordial leads. Agree with LifeNET.  :-/  Acute septal MI was indeed considered. 

PREHOSPITAL TREATMENT

Serial 12 lead ECGs. Aspirin and nitroglycerin as needed for pain. Transport to a cardiac interventional center. Oxygen only if hypoxic or severe respiratory distress.

CASE RESOLUTION

The patient was admitted to the medicine floor for further observation. Serial ECGs were unchanged, and troponin measurements were normal. The patient had a bedside echocardiogram which did not show any acute wall motion abnormalities suggestive of acute infarction. The patient was scheduled for an inpatient nuclear medicine stress test.  

RESOURCES

There's a great discussion, complete with visual examples, of septal STE patterns at the Life in the Fastlane blog.  Check it out! 

Abnormal ECG **Unconfirmed** but I'm worried about ***MEETING ST ELEVATION MI CRITERIA!*** PART 1/2

Family members call 911 for an 80 yo male experiencing chest discomfort. The patient has a history of HTN, dementia. The patient reports chest discomfort that began "a few hours" prior to EMS arrival. The patient reports some mild shortness of breath. The patient is otherwise alert and in mild distress.

PHYSICAL ASSESSMENT
BP: 136/78
P: 60
R: 22
Sp02: 95% on RA
Lung sounds are clear.
Heart tones present, no murmur.
No leg edema.

12 LEAD ECG
















12 LEAD ECG INTERPRETATION
It appears that LifeNet has done the job for you. There are three stars on either side of the ***MEETS ST ELEVATION MI CRITERIA***. Guess there's nothing more to say.

What say you? To cath or not to cath? Treatment? Additional questions?

Ruh Roh: Interpretation vs Clinical Correlation. PART 1

EMS responds to the report of a 50 year old patient suffering from weakness, altered mental status, and generalized "body pain." The patient is minimally alert. There are no signs of apparent trauma. History is significant for DM and kidney disease. After loading the patient onto the stretcher, vital signs reveal:
BP: 80/P
P: 60
R: 20/min
Blood glucose: 40 mg/dL

Providers administer 25g of IV dextrose and initiate fluid therapy. A 12 lead ECG is obtained: 

12 LEAD ECG


12 LEAD ECG FINDINGS
The rhythm reveals a bizarre and wide QRS complex. The rhythm is slightly irregular and no P waves are discernable. The rhythm appears to be ventricular in origin.

EMS TREATMENT AND TRANSPORT RELATED QUESTIONS
1. What is the most appropriate destination for this patient? Should this patient be transported to a cath capable facility? Should the patient's instability necessitate transport to the closest hospital?
2. What are your treatment priorities?
3. What is the most probable cause of the ECG findings?

Prehospital ECGs Featured on Amal Mattu's ECG Case of the Week!

What happens when the computer calls, "Pericarditis?" Do you defer to LifeNet when encountering cases such as, "Abnormal ECG- Unconfirmed?" Watch this video to learn more about PR depression and how to differentiate pericarditis (not so bad) from STEMI (a bit more terrible). Watch, listen, save a life- and transmit those 12 leads!


Dr Mattu's ECG Case of the Week: Pericarditis?

The Power of the 12th Lead

EMS responds to the home of a 70 yo female patient. She reports severe, left-sided chest pain and mild shortness of breath.  Her skin is warm and dry.  Her abdomen is soft and non-tender.  She denies any medical history.

Vital signs:
BP: 142/76
P: 75
R: 18

Sp02: 98%

12 Lead ECG:

12 Lead ECG Interpretation and Discussion:

There is a baseline sinus rhythm. The rate is approximately 75 beats per minute.

The ECG also reveals left anterior fascicle block as noted by the rS pattern in leads II, III, aVF, and Rs pattern in leads I and aVL.

There is left axis deviation as demonstrated by the predominantly positive QRS complex in lead I, and predominantly negative QRS complex in lead aVF.

There is ST segment elevation in leads aVR and V1. In addition, ST segment changes (flat, depressed, or T wave inversion) are present in essentially every other lead (reciprocal changes).  Simultaneous ST segment elevation in leads aVR and V1 may predict left main coronary artery, or left anterior descending artery occlusion, and is considered to be a STEMI equivalent.  Patients who present with ST segment elevation in leads aVR and V1 should be transported to a facility capable of performing cardiac angioplasty.

Take-Home Points
Simultaneous ST segment elevation in leads aVR and V1 predicts LMCA or LAD occlusion
Patients should be transported to a cardiac intervention center and treated the same as STEMI

Well, I didn't see anything in the rhythm strip...

Case Description


Medics respond to the report of a 66 yo male with nausea, chest pain, and chest pressure radiating to the left arm. The patient appears well. Chest discomfort started 2 hours prior to EMS arrival. The patient's vital signs are as follows: BP: 168/100, P: 72, R: 60/regular. Sp02: 96% on RA. Physical examination is unremarkable. The patient is loaded for transport, and the paramedics consider aspirin and nitrates. A 12 lead ECG is obtained


12 lead ECG

12 Lead ECG Interpretation and Discussion 

The rhytm is sinus in origin, and there does not appear to be any ectopic beats. ST segments are upright with the exception of expected T wave inversion in lead aVR. Careful scrutiny of the inferior leads reveals subtle ST segment elevation of approximately 1 mm. ST segments should be measured at the "J" point, and there is just about 1 mm / 1 box of elevation in the inferior leads. Further substantiating the findings of ischemia are the ST segment elevations present in leads V2-V5. The ST segments takes on an almost horizontal appearance in V5 and the R wave progression is preserved. Reciprocal change in the form of ST segment flattening and depression appears in leads I and aVL. When deciding if any one ECG represents ischemic patterns look for (1 ) anatomic distribution of abnormal findings and (2) reciprocal changes. This ECG features both of these findings. This patient was transported for urgent PCI; I do not have angiographic findings available. The ST elevation in the limb leads is not all that impressive. It is easy to imagine that placing this particular patient "on the monitor" would interfere with the recognition of concerning ST-T changes in the precordial leads. 

Closer look at ST segment ugliness

12 Lead Interpretation

Sinus rhythm, rate of 60, widespread ST segment elevation in the inferior and anterior-lateral leads concerning for acute ischemia.

Pearls

• If there is ANY suspicion for coronary ischemia or cardiac-related chest pain, perform a complete 12 lead
• The presence of recipocal change makes the diagnosis of ischemia more likely
• Territorial ST-T changes (anterior, lateral, inferior) are similarly concerning for ischemia

Thoughts on another acute process that might produce widespread, diffuse STE? 

From the venerable and informative blog, "EMS12LEAD.com"

Here's an interesting case that addresses the concepts of (1) typical ST elevation / ST morphology and (2) infarct territory. The case is an excellent reminder about how EMS providers and emergency clinicians must never let their guard down and pay attention to the history of present illness! This particular "44 yo male [with] chest tightness" had me at, "hello." Check out the case- and the EMS12LEAD blog- here:

Snapshot case: 44 yo male- chest tightness

There's STE in V1 !

EMS responds to the report of a 77 year old male with chest pain. The patient is hypertensive, alert, and hemodynamically stable. Aspirin and nitroglycerin are administered per treatment protocol. A 12 lead ECG is obtained, and the paramedic asks about transport to the closest hospital versus a facility capable of percutaneous coronary intervention...


12 lead ECG



12 lead ECG Discussion

There is a baseline sinus rhythm. The rhythm is regular. Close scrutiny of lead II and V1 reveals the presence of p waves. The ST segments are upright in most leads with the exception of aVR. The QRS duration is slightly prolonged consistent with an interventricular conduction delay. The (1) positively deflected QRS in lead V1 and the (2) lengthened QRS duration suggests the presence of a RIGHT bundle branch block. There is a subtle slurred l S wave in V6 which further corroborates the diagnosis of a right bundle branch block.

The Slurred S Wave

12 lead ECG Interpretation

Sinus rhythm, right bundle branch block, rate of approx 80 beats/min.

Case resolution

The patient was transported to a local facility. Serial ECGs remained unchanged and cardiac enzymes were normal. The patient was discharged to home following an overnight hospital stay and a cardiac stress test.