A Case of Clinical Unstable Angina in the ED

A woman in late middle age with a history of a mild stenosis of the RCA seen on CT coronary angiogram 4 years prior presented 2 hours after the onset of nondescript substernal chest discomfort that radiated to both axillae.

Her daughter was worried and brought her to the ED.  This is her initial ECG:

There is a suggestion of inferior MI: the T-waves in II, III, and aVF are slightly large.  There is T-wave inversion in aVL, which is a soft sign of inferior MI.

She received nitroglycerin, and the discomfort was relieved, but she attributed the relief to the removal of a tight-fitting garment.

A repeat ECG was unchanged after pain relief.

I was worried about her, but with pain resolution and a non-diagnostic ECG, there was no indication for cath lab activation at night.

The first troponin was undetectable.

Nevertheless, I was still worried about her and gave her aspirin, ticagrelor, and heparin, and admitted her to the hospital.

After admission, serial troponin I later climbed, peaking at 1.6 ng/mL.

A formal Echo the next AM showed an inferior wall motion abnormality.  A repeat ECG in the morning was recorded:

This shows resolution of the enlarged T-waves, confirming that there had been inferior ischemia.

I was sure there would be a tight RCA lesion that would need stenting.

However, the angiogram showed a chronic total occlusion of the RCA, with the inferior wall supplied by collaterals.  No stent was deployed.

The angiographer explained it this way: "she could have had some small left to right collateral channels that closed off, and then she recruited more collaterals to reperfuse."  Perhaps as a result of nitroglycerin.

Nevertheless, until angiography was done, this was presumed ACS of the RCA (or possibly circumflex) until proven otherwise.

Learning Point

1.   Inferior hyperacute T-waves can be extremely subtle

2.   Even if they do not lead you to cath lab activation, such T-waves, along with lead aVL and the convincing history, may persuade you in spite of an undetectable troponin, to give maximal medical therapy (aspirin, ticagrelor, and heparin) for ACS.

3.  The territory of a chronic total occlusion which is supplied by collaterals is particularly vulnerable.

A Middle-Age Male with Chest Pain that Recurs in the ED

A middle aged male with some coronary risk factors presented to the ED after an episode of typical sounding chest pain that was resolved upon arrival.

He was in the ED for an hour when he developed chest pain again and had this ECG immediately recorded:

There is sinus rhythm at a rate of about 60.  There is ST elevation at the J-point that does not quite meet "STE criteria" of 2 mm for these 2 leads.   There is no convexity, ST depression, or Q-waves that would tell us that this ST elevation is clearly pathologic.  

So we can use the formula that differentiates STE from LAD occlusion from that due to early repolarization (normal variant).  The computerized QTc = 400, STE60V3 = 2.5, RV4 = 19; so the formula value = 20.39, and this is consistent with normal ST elevation. 

So the ECG is normal, right?

Some Background

What I neglected to tell you is that when the patient had arrived pain free, he had this ECG recorded:

Here there is subtle terminal T-wave inversion in V2, and a bit in V3, typical of early Pattern A Wellens' waves.

See this case for Wellens' original images of Pattern A and Pattern B Wellens' waves.

So the first ECG is not normal; it is "pseudonormal."

It triggered the recording of serial ECGs (sorry, not available) which showed increasing ST elevation diagnostic of LAD occlusion.

So this was Wellens' syndrome, a state of spontaneous reperfusion of the LAD, manifesting with "reperfusion T-waves" and R-wave preservation after an episode of closure of the LAD.  Thus, the patient presents pain free after an episode of angina.

The importance of Wellens' syndrome is that the artery can close off again at any moment, in which case the inverted T-waves will become upright again and look normal.  This is called "pseudonormalization".

The first ECG was recorded so soon after re-occlusion of the artery that this ECG shows no signs of occlusion other than pseudonormalization, which requires comparison with the previous.

See these other cases of less subtle pseudonormalization (there are 7 cases here, the best are the last two)

Syncope and a Possible Type 2 Brugada Morphology

A young man had 10 seconds of syncope without a prodrome.  He had had it once before.  Exam was normal.

This ECG was recorded:

There is rSr' in both V1 and V2, with a "saddleback" in lead V2, and the "beta" angle is wide.  It meets, or at least nearly meets, criteria for type 2 Brugada.

Having just written on this topic, I knew that this could be the result of lead placement that is too high.

V1 and V2 should be placed at the 4th intercostal space.  Placing them at the 3rd can result in false positives for Brugada.

I asked the tech if she was sure she had placed them correctly.

She returned saying that she had placed them one interspace too high, and handed me this ECG recorded at the right interspace:

The rSr' is gone and the saddle is gone as well.

Learning point:

Beware lead placement in the diagnosis of right ventricular conduction delay (rSr") and in the finding of Brugada pattern ECG.

One hour lecture on Subtle ECG findings of Acute LAD Occlusion (plus some inferior/lateral/posterior)

This is my most popular lecture, which Scott Joing of www.hqmeded.com just recorded for me in his amazing video recording studio.

When I give this lecture real-time, I usually do it in a workshop and have more time - enough time to stop and let people get a good look at the ECG and try to find the critical elements for themselves before going on to explain them.  That makes for a significantly longer lecture.

But if you want to have time to scrutinize any ECG, just pause the video to look at the ECG for a while before you play my explanation.

Cardiac arrest, defibrillated, diffuse ST depression and ST Elevation in aVR. Why?

A middle-aged male had a V Fib arrest.  He had not complained of any premonitory symptoms (which is very common).   He had a history of CAD with CABG.  Here was his initial ED ECG:

There is atrial fibrillation with a rapid ventricular response.  There is profound ST depression especially in I, II, V2-V6.

ST depression is common BOTH after resuscitation from cardiac arrest and during atrial fib with RVR.

The patient was cardioverted.  Here is the post cardioversion ECG:

ST depression, with ST elevation in aVR persists.

Does this patient have ACS?  Should he necessarily go to the cath lab?

Again, it is common to have an ECG that shows apparent subendocardial ischemia after resuscitation from cardiac arrest, after defibrillation, and after cardioversion.

One must wait a short time (perhaps 15 minutes?), and repeat the ECG, to see if the apparent ischemia persists.

This was done.  A third ECG was done about 25 minutes after the first:

This shows resolution of all apparent ischemia.

The patient thus did not need immediate angiography.

An echocardiogram showed:

Left ventricular hypertrophy concentric .
The estimated left ventricular ejection fraction is 58 %
Aortic stenosis, mild, 9.0 mmHg mean gradient. 1.50 cm^2 valve area.

Troponins were minimally elevated, consistent with type 2 MI from low flow state of cardiac arrest and high demand state of atrial fib with RVR.

The patient underwent angiography later (the next day) and there was no culprit lesion.  He did not have ACS.

He recovered and had an ICD implanted.

Learning Points:

1. Ventricular fibrillation is not only caused by acute coronary syndrome.   There are many other etiologies, including scarring from previous MI, medications, drugs, LVH, and channelopathies.  We found that 38% of out of hospital ventricular fibrillation was due to STEMI.  The remainder were due to other etiologies, (including NonSTEMI ACS).  But approximately 50% were due to non-ACS etiologies.

2. ST depression (with reciprocal ST elevation in lead aVR) is common shortly after BOTH resuscitation from ventricular fibrillation AND after cardioversion from atrial fibrillation.

3.  One should wait a short time (15 minutes?) to record another 12-lead ECG to ascertain whether there is ongoing ischemia and probable ACS, or whether the ST depression is transient only.

4. Not all patients with ventricular fibrillation necessarily need emergent angiography.  Much depends on the post resuscitation ECG and its evolution shortly after defibrillation.


Reference:

Scott NL. Mulder M. Bart B. Smith SW.  Correlation of STEMI in Resuscitated Non-traumatic out-of-hospital Cardiopulmonary Arrest patients with Initial Rhythm and Cardiac Catheterization Findings (Abstract 580). Academic Emergency Medicine 17(s1):S194; May 2010

Acute chest pain, bradycardia, and hypotension

A middle-aged male complained of acute onset of chest pain.  He was diaphoretic, weak, lightheaded, but alert.    Blood pressure was 60/palp with a pulse of 40.  was given aspirin and a 500 ml normal saline bolus.

Here is the prehospital 12-lead:

There is bradycardia and some kind of AV block.  P-waves are difficult to discern, so the exact nature of the block is unclear

There is obvious inferior STE.   Reciprocal ST depression in aVL confirms inferior STEMI, and ST depression in lead I is a good indicator that this is an RCA occlusion.

In inferior MI due to RCA occlusion, one should always look to lead V1 for ST elevation indicating right ventricular infarct also.

Here, there is ST depression in V1 and V2, but ST elevation in V3.  This is odd and one must suspect that leads V1 and V3 are reversed.

The ST depression in V2 shows extension to the posterior wall.

The cath lab was activated by the medics.

The patient arrived alert and conversant.   BP was in the 40's to 60's, with pulse in 30s to 40s.

An ECG was recorded 11 minutes after the first:

Now it is clearly 3rd degree AV block.
There is clearly ST elevation in V1 (and now also V2) confirming right ventricular involvement, and confirming that prehospital leads were reversed.  This is such a large RV infarct that the ST elevation extends all the way to V3, which is often called a "Pseudoanteroseptal MI" (See more cases of pseudoanteroseptal MI)

A right sided ECG was immediately recorded (limb leads are not changed):

3rd degree heart block.  There is ST elevation in V2R (identical to V1 on regular 12-lead) extending all the way out to V6R

A bedside echo was done:


There is bradycardia.  The RV is massively dilated due to RV failure from RV infarct.


He was given ticagrelor and heparin.  He was given 25 mg of ketamine and transcutaneous pacing was begun.  Capture was achieved at 114 mA at a rate of 70.  Systolic BP rose to 110.


Capture was verified by bedside echo:



He went for angiogram which showed occlusion of the proximal RCA, proximal to the right ventricular marginal branch to the RV.

It was opened and stented.

The patient did well.

Learning Points

1.  Occlusion of the proximal RCA may result in hemodynamically significant RV MI.
2.  These occlusions also frequently lead to complete AV block because of blood supply to the AV node from the RCA
3.  RV MI can lead to RV failure and dilatation
4.  Fluids are indicated, as cardiogenic shock due to RV failure responds to fluid loading and does NOT result in pulmonary edema
5.  Transcutaneous pacing can be verified with bedside ultrasound.
6.  Rapid reperfusion of RV MI results in a good outcome

Ventricular Fibrillation, Resuscitation, and Hyperacute T-waves: What does the Angiogram show?

An elderly person collapsed and was found to be pulseless.  He had immediate bystander CPR.  An AED was placed and one shock was given within 5 minutes of arrest.  He immediately awoke.  EMS arrived and recorded these ECGs:

Time = 0

Sinus rhythm. Inferior and lateral ST elevation, with hyperacute T-waves in V4-V6.

1 min later

No definite difference.

He was stable en route to the ED.  On arrival, he was awake and complained of only mild aching left chest pain.  He stated that prior to his collapse, he had been walking briskly and was feeling short of breath, but not having any chest pain. He does have a history of CAD with a stent, and takes clopidogrel, but he did not take it on this particular day.

He had this ED ECG recorded, 13 min after first

There is inferior ST elevation with reciprocal ST depression in aVL, diagnostic of inferior injury.  The hyperacute T-waves in V4-V6 are diminished and there is less ST elevation.

The cath lab was activated.  He was given aspirin and heparin.

Prior to transport, another ECG was recorded. This one is 25 min after first prehospital, and 12 min after the first ED ECG:

There is nearly complete resolution of all injury pattern

Angiogram showed no culprit, but did show severe 3 vessel disease, with 100% chronic LAD and RCA occlusions, and chronic 75% circumflex.  All territories were supplied by collaterals from the circumflex!

An immediate Echo showed distal inferior and distal septal, anterior, and apical wall motion abnormality, with EF of 55-60%.

The patient was prepared for CABG.

Here is an ECG 15 hours after first:

Some reperfusion T-wave inversion in V5 and V6.

Troponin I peaked at 0.59 ng/mL.


ECG recorded 24 hours after first

More pronounced reperfusion waves in V3-V6 (Lateral Wellens' waves)

The patient underwent successful CABG.

Here is an ECG recorded after CABG:

There was some inferior injury that occurred from bypass.  This is not unusual.

So what happened?

1. The patient had demand ischemia from walking with severely restricted coronary flow.
2. The ischemia resulted in ventricular fibrillation.
3. The extreme low flow state of arrest, along with extremely poor coronary flow after resuscitation, resulted in transmural ischemia (subepicardial ischemia) with ST elevation and hyperacute T-waves.

So this is Type 2 MI with ST elevation (we avoid the term "type 2 STEMI", as STEMI is a term associated with ACS)

Giant Inverted T waves in an Elderly Patient

This is another contribution from Victoria Stephen.  Victoria is a third year EM Registrar from at the University of the Witwatersrand in Johannesburg, South Africa, and a great asset to FOAMed.  Follow her on Twitter: @EMcardiac.

Here is her previous contribution: Pulseless ventricular tachycardia – why did the AED not advise a shock?  

Case

A 91 year old presented to the ED of a small hospital with a history of sudden onset syncope. A family member thought she was having a seizure. She reported no chest pain or dyspnoea when conscious. The patient had a history of hypertension which was poorly controlled.

She appeared alert and well-oriented. Her initial BP was 184/90, HR 41 BPM. An ECG was recorded in the ED:

There is second degree heart block with a HR of 41 BPM. The QRS complex is 144ms indicating an infranodal escape. There is an RBBB configuration with a LAFB, indicating it may be originate from the left posterior hemi-fascicle. The QTc is significantly prolonged at 535 ms. There are deep wide bizarre looking T waves seen in virtually all the leads, but most notably in the precordial leads.

She had a CT of the Brain which showed no intracranial bleed. Her renal function was normal and the electrolytes including calcium and magnesium were normal. Two troponin I were increased at 140 ng/L (0.14 ng/mL) and 70 ng/L (0.070 ng/mL) on consecutive days, (negative is less than 40 ng/L for this assay). 

Two days later she was referred to a regional hospital where she was admitted to the CCU with the following ECG:

Complete Heart block still present, HR 33 BPM, QTc prolonged, 503ms. T waves are now upright in leads I and AVL.

An informal bedside echo done by a cardiologist showed a normal ejection fraction with no regional wall motion abnormalities. In view of the positive troponins and the T wave inversions she was taken to the cath lab for angiography, as well as for a pacemaker. No obstructive coronary artery disease was present. She subsequently developed runs of VT while in the lab which were too transient to determine the specific type of VT. A transvenous pacing wire was inserted for temporary pacing and the decision was made to bring her back for a permanent pacemaker.

Here is the ECG post venous pacemaker:

Notice the T-wave inversion is present in spite of the ventricular pacing, which should result in discordant T-waves (opposite the QRS).  Concordant T-waves of this dimension indicate ischemia that cannot be hidden by pacing.

And here is the ECG post permanent pacemaker, recorded 7 days after the first ECG:

This is a single chamber pacemaker. HR 62 BPM. The T waves are upright in in the inferior leads and biphasic in the precordial leads.

Commentary

This patient suffered a Stokes-Adams attack, which is a sudden loss of consciousness due to a high grade atrioventricular block. Seizure like activity is commonly seen in this form of syncope. Two very different arrhythmogenic mechanisms have been shown to induce the abrupt loss of cardiac output causing the syncope. At the onset of complete heart block, asystole can occur for a brief period before a new pacemaker has kicked in. Either 1) the AV node may act as the new pacemaker, leading to a junctional or narrow escape on the ECG,  or 2) infranodal tissue will take over the pacemaker role.

The second arrhythmia which can abruptly occur during complete heart block (CHB) is Torsade de Pointes (TdP).  TdP is an example of a triggered dysrhythmia. Triggered dysrhythmias are heart rate dependent and are either triggered by a fast or slow heart rate. TdP is triggered by slow heart rates. (This is why overdrive pacing to a higher rate works in terminating TdP) In some patients, at the onset of complete heart block, there is an abrupt decrease in heart rate as well as prolongation of the QTc. The resulting pause plus a well-timed PVC then triggers the onset of TdP. Both asystole and TdP following CHB are often brief, allowing the patient to regain consciousness.

The giant inverted T waves are not common in CHB, but are commonly seen in CHB complicated by Stokes-Adams attacks. Their presence is not fully understood but has been associated with TdP and stress cardiomyopathy occurring after the onset of Complete Heart Block. Stress cardiomyopathy is a spectrum disorder characterized by transient left ventricular systolic dysfunction clinically, ST elevation or T wave inversions on the ECG, and regional wall motion abnormalities on echo which are induced by a catecholamine surge. Takotsubo cardiomyopathy is a specific form of stress cardiomyopathy. This paper demonstrates takotsubo cardiomyopathy developing in patients with complete heart block, preceding TdP:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2644362/ (Open access)

Stress cardiomyopathy has been seen frequently in a myriad of different critical illnesses, particularly in subarachnoid haemorrhage, which often is associated with giant inverted T waves on the ECG:

http://circ.ahajournals.org/content/118/4/397.full#F1 (Open access)

Troponins can be elevated in stress cardiomyopathy and demonstrate a rising and falling pattern like an acute myocardial infarction. It is very difficult to differentiate SCM from MI; it often produces a PseudoSTEMI pattern that is very difficult, and sometimes impossible, to distinguish based on the ECG, though there are some guidelines.   Even echo can be misleading: the takotsubo apical ballooning can also be seen in acute STEMI.

If there is ST elevation, and the differential diagnosis is acute coronary occlusion vs. SCM, an angiogram is usually required.  

However, in this setting of Stokes Adams attack with CHB and bizarre T-wave inversion, emergent angiogram is not necessary.

Here is another blog case of Stokes Adams attack, this one with alternating left and right BBB.

Summary:

Complete Heat Block accompanied by giant inverted T waves is associated with Stokes-Adams attacks.

A prolonged QTc with CHB is at risk of torsades. Treat any associated electrolyte abnormalities that may be present.

Torsade de Pointes is triggered by bradycardia, a prolonged QTc and an abrupt change in heart rate, which creates a pause.

Inverted T waves are often seen in stress cardiomyopathy syndromes. Stress cardiomyopathy is a diagnosis of exclusion after formal echocardiography with or without angiography. 

Other references:

Mechanisms of syncope and Stokes-Adams attacks: 

http://www.bmj.com/rapid-response/2011/10/28/mechanisms-syncope-and-stokes-adams-attacks-bradyarrhythmia-asystole-and-t  (open access)

Giant T wave inversion: 

http://heart.bmj.com/content/28/6/768.full.pdf  (open access)

Cardiac and non-cardiac causes of T-wave inversion in the precordial leads:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4325305/ (open access) 

EM Crit Podcast: Part 2 Interview on "Who needs acute PCI?"

Scott Weingart Interviews me: 


Part 2 of Who needs acute PCI?

Pulseless ventricular tachycardia – why did the AED not advise a shock?

This case was submitted by my friend Dr. Victoria Stephens.  She is a third year Emergency Medicine Registrar from at the University of the Witwatersrand in Johannesburg, South Africa, and a great asset to FOAMed.  Follow her on Twitter: @EMcardiac.

Case

A 71 year old man was admitted to the ICU with neutropenic sepsis complicated by septic shock. He was intubated and ventilated and was started on an adrenaline infusion to maintain his blood pressure. The admission ECG was normal. Thirty-six hours into his ICU stay he went into a cardiac arrest. The monitor showed a wide complex tachycardia. CPR was commenced while the defibrillator was brought to the bedside. A doctor was called from the ED to assist. The pads were attached to the patient and the defib was placed in AED mode by the nurse. The following rhythm strip was recorded (on a separate monitor from the AED, of course):

A rhythm strip recorded from lead II. A wide complex tachycardia is present with a rate of approximately 170 BPM. The QRS duration is very wide.  It is regular and monomorphic and all but diagnostic of VT.

The code blue team recognized that the rhythm was ventricular tachycardia and that immediate defibrillation was required. They waited for the AED function on the defib to recommend a shock. Instead, it kept saying “…analysing…analysing”.  No shock was advised. The doctor could not remember how to operate the manual mode of the AED defibrillator (this was an defibrillator that has an AED mode; not all defibrillators have that).  Since the AED was not advising a shock, he assumed that the defibrillator was faulty, and called for another defibrillator to be fetched from the ED.  CPR was continued, adrenaline and amiodarone were given.  By the time the second defibrillator  arrived, return of spontaneous circulation (ROSC) had occurred. The patient converted into a normal sinus rhythm a short while later.

Comment

What happened? Why did the AED not recognize such an obvious case of VT? Was the defibrillator faulty?

No, the defibrillator was not faulty.  The technology is, rather, imperfect.

How does an AED work?

The automatic external defibrillator (AED) was initially designed to be used by laypeople or first responders with little or no experience in defibrillation, in order to improve survival from out-of-hospital cardiac arrest (OHCA) (1).  The AED uses a Rhythm Analysis Algorithm (RAA) which essentially is software that is programmed to discriminate between shockable and non-shockable rhythms.  The RAA then prompts the AED to advise or not advise a shock. The RAA uses up to 18 internal algorithms to determine if a rhythm is shockable or not; the most important of these are: 1) heart rate, 2) QRS width and 3) QRS amplitude. 

With regards to VT, the RAA is programmed to recognize VT as shockable only at certain heart rates.  For most AEDs, this heart rate is above 150 BPM (2).  The rationale for this is twofold; 1) to prevent lay people from potentially defibrillating a perfusing VT in a patient who may still have a pulse, and 2) that patients are more likely to arrest from VT at heart rates greater than 150.

How does the manual defib work?

There is no RAA. The healthcare provider decides if the rhythm is shockable and whether a shock is advised. The number of joules for each shock is also set by the operator.

When can the RAA in the AED fail?

Multiple studies have demonstrated the safety and efficacy of AEDs in Cardiac Arrest.(1)  They have demonstrated not only improved survival but also improved neurological outcomes. However, as with any device, error does occur. The RAA in the AED can in certain circumstances fail to recognize a shockable rhythm or incorrectly advise a non-shockable rhythm to be shocked. These circumstances are:

1) Interference from artifact   

a. Pacemaker spikes and internal cardioverter defibrillators can cause artifact, interfering with the RAA function. 

b. Motion artifacts caused by chest compressions, handling of the patient, movement during ambulance transportation, breathing and seizures may also interfere with the RAA. 

Below is an example where external artifacts occurred at the beginning of the AED analysis.(3)  The AED incorrectly advised no shock for this case of coarse VF. 

This is an image of coarse VF.   The AED incorrectly made a "no shock advised" decision.

[Image used with permission from: Calle PA et al.  Inaccurate treatment decisions of automated external defibrillators used by emergency medical services personnel: Incidence, cause and impact on outcome. Resuscitation 2015;88:68-74]

2) The type of shockable rhythm: they detect VF better than VT

Several studies have examined the accuracy of the RAA by downloading the ECG strips and responses advised from the AED memory module. (3-5) These studies showed that the AED is more accurate in correctly detecting VF than VT; the AED being 100% specific and 95% sensitive for coarse VF. AEDs have also demonstrated similar accuracy in correctly detecting non-shockable rhythms such as PEA, normal sinus rhythm, supraventricular arrhythmias and asystole. 

The AED is much less reliable however, in correctly detecting VT: the sensitivity for VT ranged from only 63% to 83% in these studies, indicating that in several instances no shock was advised when VT was actually present.

Inconsistent shock advisories have also been demonstrated for polymorphic VT, including the subtype Torsades de Pointes. One AED advised did not advise shock for any of the Torsades rhythms  it was subjected to(!)(2). 

Several authors have recommended that manufacturers improve their algorithms and that physicians should be aware of the potential pitfalls in their use.

3) The VT rate

As mentioned above, the RAA of several AEDs is set to recommend a shock if the VT rate is more than 150. Slower forms of VT will not get a shock advisory, even if the patient is in arrest and requires it.  Though higher VT heart rates are more likely to cause cardiac arrest, patients with poor systolic function may not tolerate a sustained VT of 130-150 BPM and may indeed be in arrest or near-arrest. (2).  Several AEDS were shown in a recent study to only advise a shock if the VT rate exceeded 180, and others only if higher than 250 (!).(6) 

In summary:

Multiple studies have shown that the AED is very accurate at detecting VF and tends to advise a shock nearly 100% of the time. AEDs have been shown to reduce mortality in cardiac arrest, especially in OHCA.

The AED similarly recognizes sinus rhythms, supraventricular rhythms and asystole reliably.

The AED is far less accurate at determining VT; with regards to both the monomorphic and polymorphic forms. If the AED fails to recognize the VT, the VT will eventually degrade to VF which subsequently the AED is more likely to recognize. However, this delay may result in significant harm to the patient’s outcome as time to defibrillation is crucial to survival. 

With VT arrests, the trained healthcare provider is superior to the AED.  For those staff who have a defibrillator with both manual and AED modes, they should know how to recognize VT, or probable VT, use the AED, and, if using the defibrillator in AED mode, know how to switch to manual mode.  

References: 

1. Part 6: Electrical therapies: automated external defibrillators, defibrillation, cardioversion and pacing. 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Link MS, Atkins DL, Passman RS, Halperin HR, Samson RA, White RD, Cudnik MT et al. Circulation 2010;122(suppl 3):s706-s719

2. Inconsistent shock advisories for monomorphic VT and Torsade de Pointes – a prospective experimental study on AEDs and defibrillators. Fitzgerald A, Johnson M, Hirsh J, Rich M-A, Fidler R. Resuscitation 2015 (Article in press)

3. Inaccurate treatment decisions of automated external defibrillators used by emergency medical services personnel: Incidence, cause and impact on outcome. Calle, PA, Mpotos N, Calle SP, Monsieurs KG. Resuscitation 2015;88:68-74

4. Performance and error analysis of automated external defibrillator use in the out-of-hospital setting. JL, Weinstein C. Ann Emerg Med 2001;38:262-267. 

5. Machine and operator performance analysis of automated external defibrillator utilization. Ko PC1, Lin CH, Lu TC, Ma MH, Chen WJ, Lin FY J Formos Med Assoc. 2005 Jul;104(7):476-81

6. What is ventricular tachycardia for automated external defibrillators? Kette F, Bozzola M, Locatelli A, Zoli A. J Clin Exp Cardiolog 2014;5:285 doi:10,4172/2155-9880.1000285

Emergency Department Syncope Workup: After H and P, ECG is the Only Test Required for Every Patient.....

Summary of ED Approach to Syncope 

Please excuse the formatting problems, which I have not been able to fix!

I have used this to educate our residents, and I think they find it useful.  It is NOT a structured review or meta-analysis.  

Approach to Syncope

Syncope definition: Brief loss of consciousness with loss of postural tone and complete spontaneous recovery without medical intervention.

First: Are you sure it was syncope, and not SEIZURE?  
Conversely, frequently syncope has a short episode of tonic-clonic activity that mimics seizure.

Look for Vascular Etiology -- think of these while doing H and P:

--Bleeding: ruptured AAA, GI bleed, ruptured ectopic pregnancy, other spontaneous bleed such as mesenteric aneurysms. Check: [vitals, Abd/Pelvic Ultrasound, Aortic ultrasound, orthostatics, heme test, hemoglobin, UPT]

--Stroke (very uncommon cause of syncope, must be TIA, as syncope implies reversibility: Subarachnoid hemorrhage (severe headache at moment of syncope), TIA (must be either vertebrobasilar or hemispheric in patient with previous stroke of other hemisphere)  Check: [History, neurological exam]
--Obstructive: Pulmonary Embolism (Dyspnea?), Aortic Dissection, Valvular (especially Aortic Stenosis), Tamponade.  Check: [vitals, SOB, Chest Pain, Ultrasound]


If the patient has Abdominal Pain, Chest Pain, Dyspnea or Hypoxemia, Headache, Hypotension, then these should be considered the primary chief complaint (not syncope).   Most physicians will automatically be worried about these symptoms.  If the patient has Abnormal Vital Signs (fever, hypotension, tachycardia, or tachypnea, or hypoxemia), then these are the primary issue to address, as there is ongoing pathology which must be identified.

Also consider non-hemorrhagic volume depletion, dehydration: orthostatic vitals may uncover this [see Mendu et al. (3)].

True Syncope: If, on the other hand,  the patient is well, had no other serious symptoms, has a normal sinus rhythm, and normal physical exam, then you need to be certain the syncope was not due to a dangerous brady- or tachydysrhythmia that could recur.  

See this website for the best online scoring system for the Canadian rule: www.teamvenk.com/csrs

Cardiac Syncope ("True Syncope")

Independent Predictors of Adverse Outcomes 
condensed from multiple studies

1.   Abnormal ECG – looks for cardiac syncope. 

a.   Abnormal Electrocardiogram (ECG): Defined (San Fran syncope rule) as any new changes when compared to the last ECG or presence of non-sinus rhythm. If no previous ECG was available, ECG was classified as abnormal if any abnormality was present.  This San Fran definition, however, is too non-specific, so I list more specific ECG abnormalities below:

b.    In particular, pay attention to findings indicating these pathologies:

            Long QT (at least 480-500ms), Brugada morphology, RV dysplasia, WPW, HOCM
c.   And these findings come from OESIL, EGSYS, and Sarasin studies:
            i:      Non-sinus rhythm
            ii:     SVT or VT (obviously, and this makes for an abnormal vital sign anyway)
            iii.    2nd or 3rd degree AV blocks or sinus pause of at least 2 seconds
            iv.    Right bundle branch block (BBB) with hemiblock (bifascicular block)
            v.     Left BBB
            vi.    Evidence of acute ischemia (may be subtle)
            vii.   Pathologic Q-waves
            viii.  LVH or RV
d. Abnormal but less worrisome:
             i. Frequent or repetitive PACs
             ii. Isolated Right BBB or intraventricular conduction delay
             iii.  PVCs

Not generally considered abnormal ECG findings: Isolated PAC, First Degree AV Block, Sinus bradycardia at a rate of 35-45, and Nonspecific ST-T abnormalities (even if different from a previous ECG).

2.  Age greater than 65 (Sarasin and STePS)

3.   History of Cardiovascular disease (all studies):
            Especially any history of heart failure or structural cardiac disease, including valvular
4.   Syncope without a prodrome, no precipitating factors (EGSYS)
5.   Hemoglobin less than 10 (SF rule)
6.   Syncope with Exertion (EGSYS)
7.   Syncope while supine (EGSYS)
8.   Palpitations preceding syncope (highest value on EGSYS score)
9.   Negative predictors of adverse outcome:
            Pacemaker
            Pre-syncope or "near-syncope," but there is still some small risk (5, 18)
These last two are identified in studies, but I consider them dangerous signs and symptoms in their own right, as above:
10. Hypotension (obviously)
11. SOB or Hypoxemia (obviously)

Vasovagal (Neurocardiogenic syncope or Reflex Syncope) is the most common cause of cardiac syncope, even in patients with cardiac disease: In this entity, there is BOTH a bradycardic and/or a vasodepressor response.  Thus, if there is documented sinus bradycardia, and no suspicion of high grade AV block, at the time of the syncope, this is very useful.  Premonitory symptoms (Nausea, pallor, diaphoresis, flushing), or triggers (Valsalva, Pain, Emotion, Prolonged Standing, Dehydration) are very useful in making the diagnosis.   Vasovagal syncope is generally benign.  

These premonitory symptoms were negative predictors of adverse outcomes in EGSYS.

Finally, much of this correlates well with The new Canadian Syncope Arrhythmia Risk Score, published in 2016, results of which are given below in the Annotated Bibliography.

See this website for the best online scoring system for the Canadian rule: www.teamvenk.com/csrs

Summary: 
In patients who truly have syncope as the chief complaint (It's not seizure, and it's not abdominal pain, chest pain, hypotension, dyspnea, headache, and VS and rhythm are normal in the ED), and after ruling out the bleeding, stroke, and obstructive problems, we’re left with these worrisome predictors:

—Abnormal ECG – looks for cardiac syncope.

—QRS longer than 130 ms, non-sinus rhythm, ischemia

—QT longer than 480 ms, HOCM, WPW, RV dysplasia, Type 1 Brugada

—Q-waves diagnostic of old MI

—Age greater than 65-90 (not so good a predictor)

—History of cardiovascular disease (valve dz, CHF, MI)

—(or high BNP or elevated troponin)

—Syncope without a prodrome, or with exertion, or supine, or with palpitations preceding

—Hemoglobin less than 10.0 g/dL

—Hypotension (obviously!)

—SOB or hypoxemia (obviously!)

—(oxygen saturation less than 94%??)

—Family history of sudden death at age less than 40

—Negative predictors:

—pacemaker, pre- or near- syncope only

Workup (Smith opinion from literature)

Always evaluate with:

1.       Good History and Physical exam, including 
    a. orthostatic vitals
    b. heart auscultation (aortic stenosis); 
    c. FHx of sudden death.

2.       ECG

Consider in some patients:

Ultrasound of aorta, of heart

Abd free fluid (FAST exam)

Hgb
Urine Pregnancy Test in women of child bearing age

BNP

Troponin

d dimer

Admit and/or Further Workup:

--Serious symptoms often mandate admission and/or further workup: chest pain, SOB, Abdominal Pain, Severe Headache, or Hypotension

--Admit for observation patients with worrisome physical findings suggesting a serious etiology

--Admit for observation patients with presence of 1-2 or more high risk factor (in case of pre-syncope or near syncope, which is much lower risk than full syncope, more than one high risk factor is usually required)
--Ideally, all of these predictors would be studied with multivariate analysis to find if any are covariate.  Until then, I consider any of these to be independent adverse risk factors.

--Finally, a dedicated syncope unit may improve evaluation and outcome (17).


Annotated Bibliography

For an excellent overview of ED Syncope management, see this article by Kessler C et al. in 2010 EM Clinics of North America (full text link)

For an Exhaustive Review of Syncope and its full management outside the ED environment, go to the 2009 European Society of Cardiology Guidelines (full text pdf).

The most recent and probably best study is this:

Canadian Syncope Arrhythmia Risk Score.

Thiruganasambandamoorthy, V., Stiell, I., Sivilotti, M., Rowe, B., Mukarram, M., Arcot, K., . . . Baumann, B. (2017). Predicting Short-term Risk of Arrhythmia among Patients With Syncope: The Canadian Syncope Arrhythmia Risk Score. Academic Emergency Medicine., 24(11), 1315-1326.

It's complicated, but they derived a score based on these variables:

1. Vasovagal predisposition (warm crowded place, prolonged standing, fear, emotion, pain: (-1)
2. h/o heart disease (+1)
3. Any ED systolic blood pressure less than 90 or greater than 180 mm Hg (+1)
4. Troponin greater than 99th percentile (+1)
5. QRS duration greater than 130 msec (+2)
6. QTc interval greater than 480 msec (+1) 
7. ED diagnosis of vasovagal syncope (-1)
8. ED diagnosis of cardiac syncope (+2)

*ED diagnosis by ED physicians according to the guidelines of the European Society of Cardiology, which are well represented by the ideas presented here.

Other studies

1)     EGSYS score (full text link).  Del Rosso A, et al. Clinical predictors of cardiac syncope at

initial evaluation in patients referred urgently to general hospital: the EGSYS

score. Heart 2008;94(12):1620–6.

Score interpretation: At 2 years, patients with a score of greater than or equal to 3 had mortality of 17% and 21% in the derivation and validation groups, vs. 3% and 2% for those with a score less than 3.

2)    Boston syncope rule: J Emerg Med. 2007 Oct; 33(3): 233–239.   (full text link)  
Presence of any one of these 8 criteria had 97% sensitivity and specificity of 62% for adverse outcomes: 1) Signs of Acute Coronary Syndrome (ACS), 2) conduction disease, 3) worrisome cardiac history, (eg. Dysrhythmia, pacer), 4) valvular heart disease, 5) FHx sudden death, 6) volume depletion, 7) persistent abnormal vitals, 8) primary CNS event

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3)   Mendu ML et al.  Yield of Diagnostic Tests in Evaluating Syncopal Episodes in Older Patients
Arch Intern Med 2009 Jul 27; 169:1299-1305.   
Commentary by Heidenreich PA. Arch Intern Med 2009 Jul 27; 169:1262.  
Another commentary by Quinn JV. Arch Intern Med 2009 Jul 27; 169:1305. (starts at end of article on p. 1305)

a. Orthostatic hypotension important

Background: Syncopal episodes are common among older adults; etiologies range from benign to life-threatening. We determined the frequency, yield, and costs of tests obtained to evaluate older persons with syncope. We also calculated the cost per test yield and determined whether the San Francisco Syncope Rule (SFSR) improved test yield.
Methods: Review of 2,106 consecutive patients 65 years and older admitted following a syncopal episode.
Results: Electrocardiograms (99%), telemetry (95%), cardiac enzymes (95%), and head computed tomography (CT) (63%) were the most frequently obtained tests. Cardiac enzymes, CTs, echocardiograms, carotid ultrasounds, and electroencephalography all affected diagnosis or management in <5 2="" and="" b="" cases="" determine="" etiology="" helped="" of="" syncope="" the="" time.=""> Postural blood pressure, performed in only 38% of episodes, had the highest yield with respect to affecting diagnosis (18-26%) or management (25-30%) and determining etiology of the syncopal episode (15-21%).

The cost per test affecting diagnosis or management was highest for electroencephalography ($32,973), CT ($24,881), and cardiac enzymes ($22,397) and lowest for postural blood pressure ($17-$20). The yields and costs for cardiac tests were better among patients meeting, than not meeting, SFSR. For example, the cost per cardiac enzymes affecting diagnosis or management was $10,331 in those meeting, versus $111,518 in those not meeting, the SFSR.Conclusions: Many unnecessary tests are obtained to evaluate syncope. Selecting tests based on history and examination and prioritizing less expensive and higher yield tests would ensure a more informed and cost-effective approach to evaluating older patients with syncope.

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4)    Reed MJ.  The ROSE (Risk Stratification of syncope in the emergency department) Study.  J Am Coll Cardiol, 2010; 55:713-721, doi:10.1016/j.jacc.2009.09.049

  Objectives: The aim of this study was to develop and validate a clinical decision rule (CDR) to predict 1-month serious outcome and all-cause death in patients presenting with syncope to the emergency department. 

Background: Syncope is a common, potentially serious condition accounting for many hospital admissions.   Methods: This was a single center, prospective, observational study of adults presenting to the emergency department with syncope. A CDR was devised from 550 patients in a derivation cohort and tested in a validation cohort of a further 550 patients.  Results: One-month serious outcome or all-cause death occurred in 40 (7.3%) patients in the derivation cohort. Independent predictors were brain natriuretic peptide concentration greater than 300 pg/ml (odds ratio [OR]: 7.3), positive fecal occult blood (OR: 13.2), hemoglobin less than 90 g/l (OR: 6.7), oxygen saturation less than 94% (OR: 3.0), and Q-wave on the presenting electrocardiogram (OR: 2.8). One-month serious outcome or all-cause death occurred in 39 (7.1%) patients in the validation cohort. The ROSE (Risk stratification Of Syncope in the Emergency department) rule had a sensitivity and specificity of 87.2% and 65.5%, respectively, and a negative predictive value of 98.5%. An elevated B-type natriuretic peptide (BNP) concentration alone was a major predictor of serious cardiovascular outcomes (8 of 22 events, 36%) and all-cause deaths (8 of 9 deaths, 89%).  Conclusions: The ROSE rule has excellent sensitivity and negative predictive value in the identification of high-risk patients with syncope. As a component, BNP seems to be a major predictor of serious cardiovascular outcomes and all-cause death. The ROSE rule and BNP measurement might be valuable risk stratification tools in patients with emergency presentations of syncope and should now be subjected to external validation.

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5)   Sun BC et al. Predictors of 30-day serious events in older patients with syncope. Ann Emerg Med 2009 Dec; 54:769. 

Study objective: We identify predictors of 30-day serious events after syncope in older adults.  Methods: We reviewed the medical records of older adults (age ≥60 years) who presented with syncope or near syncope to one of 3 emergency departments (EDs) between 2002 and 2005. Our primary outcome was occurrence of a predefined serious event within 30 days after ED evaluation. We used multivariable logistic regression to identify predictors of 30-day serious events.  Results: Of 3,727 potentially eligible patients, 2,871 (77%) met all eligibility criteria. We excluded an additional 287 patients who received a diagnosis of a serious clinical condition while in the ED. In the final study cohort (n=2,584), we identified 173 (7%) patients who experienced a 30-day serious event. High-risk predictors included age greater than 90 years, male sex, history of an arrhythmia, triage systolic blood pressure greater than 160 mm Hg, abnormal ECG result, and abnormal troponin I level. A low-risk predictor was a complaint of near syncope rather than syncope. A risk score, generated by summing high-risk predictors and subtracting the low-risk predictor, can stratify patients into low- (event rate 2.5%; 95% confidence interval [CI] 1.4% to 3.6%), intermediate- (event rate 6.3%; 95% CI 5.1% to 7.5%), and high-risk (event rate 20%; 95% CI 15% to 25%) groups.  Conclusion: We identified predictors of 30-day serious events after syncope in adults aged 60 years and greater. A simple score was able to stratify these patients into distinct risk groups and, if externally validated, might have the potential to aid ED decision making.

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6)    Gabayan GZ et al.  Predictors of Short-Term (Seven-Day) Cardiac Outcomes After Emergency Department Visit for Syncope.  Am J Cardiol 2010;105:82–86

Syncope is a common reason for emergency department (ED) visits, and patients are often admitted to exclude syncope of cardiovascular origin. Population-based data on patterns and predictors of cardiac outcomes may improve decision-making. Our objective was to identify patterns and predictors of short-term cardiac outcomes in ED patients with syncope. Administrative data from an integrated health system of 11 Southern California EDs were used to identify cardiac outcomes after ED presentation for syncope from January 1, 2002, to December 31, 2005. Syncope and cause of death were identified by codes from the International Classification of Disease, Ninth Revision. Cardiac outcomes included cardiac death and hospitalization or procedure consistent with ischemic heart disease, valvular disease, or arrhythmia. Predictors of cardiac outcomes were identified through multivariate logistic regression. There were 35,330 adult subjects who accounted for 39,943 ED visits for syncope. Risk of cardiac outcome sharply decreased following the 7 days after syncope. A 7-day cardiac outcome occurred in 893 cases (3%). Positive predictors of 7-day cardiac outcomes included age greater than 60 years, male gender, congestive heart failure, ischemic heart disease, cardiac arrhythmia, and valvular heart disease. Negative predictors included dementia, pacemaker, coronary revascularization, and cerebrovascular disease. There was an age-dependent relation between 7-day cardiac outcomes and arrhythmia and valvular disease, with younger patients ( less than 60 years of age) having greater risk of an event compared to their same-age counterparts. In conclusion, ED decision-making should focus on risk of cardiac event in the first 7 days after syncope and special attention should be given to younger patients with cardiac co-morbidities.

7)   Soteriades ES et al. “Incidence and Prognosis of Syncope” NEJM 347(12):878-885, Sept. 19, 2002. 

Background Little is known about the epidemiology and prognosis of syncope in the general population.   Methods We evaluated the incidence, specific causes, and prognosis of syncope among women and men participating in the Framingham Heart Study from 1971 to 1998.   Results Of 7814 study participants followed for an average of 17 years, 822 reported syncope. The incidence of a first report of syncope was 6.2 per 1000 person-years. The most frequently identified causes were vasovagal (21.2 percent), cardiac (9.5 percent), and orthostatic (9.4 percent); for 36.6 percent the cause was unknown. The multivariable-adjusted hazard ratios among participants with syncope from any cause, as compared with those who did not have syncope, were 1.31 (95 percent confidence interval, 1.14 to 1.51) for death from any cause, 1.27 (95 percent confidence interval, 0.99 to 1.64) for myocardial infarction or death from coronary heart disease, and 1.06 (95 percent confidence interval, 0.77 to 1.45) for fatal or nonfatal stroke. The corresponding hazard ratios among participants with cardiac syncope were 2.01 (95 percent confidence interval, 1.48 to 2.73), 2.66 (95 percent confidence interval, 1.69 to 4.19), and 2.01 (95 percent confidence interval, 1.06 to 3.80). Participants with syncope of unknown cause and those with neurologic syncope had increased risks of death from any cause, with multivariable-adjusted hazard ratios of 1.32 (95 percent confidence interval, 1.09 to 1.60) and 1.54 (95 percent confidence interval, 1.12 to 2.12), respectively. There was no increased risk of cardiovascular morbidity or mortality associated with vasovagal (including orthostatic and medication-related) syncope.   Conclusions Persons with cardiac syncope are at increased risk for death from any cause and cardiovascular events, and persons with syncope of unknown cause are at increased risk for death from any cause. Vasovagal syncope appears to have a benign prognosis.

8)     Sarasin FP. Louis-Simonet M. Carballo D. Slama S. Rajeswaran A. Metzger JT. Lovis C. Unger PF. Junod AF.  Prospective evaluation of patients with syncope: a population-based study.  American Journal of Medicine. 111(3):177-84, 2001 Aug 15.

Abstract PURPOSE: To determine the diagnostic yield of a standardized sequential evaluation of patients with syncope in a primary care teaching hospital. PATIENTS AND METHODS: All consecutive patients who presented to the emergency department with syncope as a chief complaint were enrolled. Their evaluation included initial and routine clinical examination, including carotid sinus massage, as well as electrocardiography and basic laboratory testing. Targeted tests, such as echocardiography, were used when a specific entity was suspected clinically. Other cardiovascular tests (24-hour Holter monitoring, ambulatory loop recorder ECG, upright tilt test, and signal-averaged electrocardiography) were performed in patients with unexplained syncope after the initial steps. Electrophysiologic studies were performed in selected patients only as clinically appropriate. Follow-up information on recurrence and mortality were obtained every 6 months for as long as 18 months for 94% (n = 611) of the patients. RESULTS: After the initial clinical evaluation, a suspected cause of syncope was found in 69% (n = 446) of the 650 patients, including neurocardiogenic syncope (n = 234, 36%), orthostatic hypotension (n = 156, 24%), arrhythmia (n = 24, 4%), and other diseases (n = 32, 5%). Of the 67 patients who underwent targeted tests, suspected diagnoses were confirmed in 49 (73%) patients: aortic stenosis (n = 8, 1%), pulmonary embolism (n = 8, 1%), seizures/stroke (n = 30, 5%), and other diseases (n = 3). Extensive cardiovascular workups, which were performed in 122 of the 155 patients in whom syncope remained unexplained after clinical assessment, provided a suspected cause of syncope in only 30 (25%) patients, including arrhythmias in 18 (60%), all of whom had abnormal baseline ECGs. The 18-month mortality was 9% (n = 55, including 8 patients with sudden death); syncope recurred in 15% (n = 95) of the patients. CONCLUSION: The diagnostic yield of a standardized clinical evaluation of syncope was 76%, greater than reported previously in unselected patients. Electrocardiogram-based risk stratification was useful in guiding the use of specialized cardiovascular tests.

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9)   François P. Sarasin, “A Risk Score to Predict Arrhythmias in Patients with Unexplained Syncope”.  Academic Emergency Medicine, 2003 Volume 10, Number 5 539-540.

Objectives: To develop and validate a risk score predicting arrhythmias for patients with syncope remaining unexplained after emergency department (ED) noninvasive evaluation. Methods: One cohort of 175 patients with unexplained syncope (Geneva, Switzerland) was used to develop and cross-validate the risk score; a second cohort of 269 similar patients (Pittsburgh, PA) was used to validate the system. Arrhythmias as a cause of syncope were diagnosed by cardiac monitoring or electrophysiologic testing. Data from the patient's history and 12-lead emergency electrocardiography (ECG) were used to identify predictors of arrhythmias. Logistic regression was used to identify predictors for the risk-score system. Risk-score performance was measured by comparing the proportions of patients with arrhythmias at various levels of the score and receiver operating characteristic (ROC) curves. Results: The prevalence of arrhythmic syncope was 17% in the derivation cohort and 18% in the validation cohort. Predictors of arrhythmias were abnormal ECG (odds ratio [OR]: 8.1, 95% confidence interval [CI] = 3.0 to 22.7), a history of congestive heart failure (OR: 5.3, 95% CI = 1.9 to 15.0), and age older than 65 (OR: 5.4, 95% CI = 1.1 to 26.0). In the derivation cohort, the risk of arrhythmias ranged from 0% (95% CI = 0 to 6) in patients with no risk factors to 6% (95% CI = 1 to 15) for patients with one risk factor, 41% (95% CI = 26 to 57) for patients with two risk factors, and 60% (95% CI = 32 to 84) for those with three risk factors. In the validation cohort, these proportions varied from 2% (95% CI = 0 to 7) with no risk factors to 17% (95% CI = 10 to 27) with one risk factor, 35% (95% CI = 24 to 46) with two risk factors, and 27% (95% CI = 6 to 61) with three risk factors. Areas under the ROC curves ranged from 0.88 (95% CI = 0.84 to 0.91) for the derivation cohort to 0.84 (95% CI = 0.77 to 0.91) after cross-validation within the same cohort and 0.75 (95% CI = 0.68 to 0.81) for the external validation cohort. Conclusions: In patients with unexplained syncope, a risk score based on clinical and ECG factors available in the ED identifies patients at risk for arrhythmias.   Key words: unexplained syncope; arrhythmia; risk factor; scoring system

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10)  Ammirati F. Colivicchi F. Santini M.  Diagnosing syncope in clinical practice. Implementation of a simplified diagnostic algorithm in a multicentre prospective trial - the OESIL 2 study (Osservatorio Epidemiologico della Sincope nel Lazio). European Heart Journal. 21(11):935-40, 2000 Jun.

Abstract 
BACKGROUND: In some patients with syncope health care is inappropriate and ineffective. In a recent observational investigation in community hospitals of the Lazio region of Italy (the OESIL study) 54.4% of patients admitted with syncope from the emergency room were discharged without a conclusive diagnosis. AIM OF THE STUDY: A simplified two-step diagnostic algorithm was developed and prospectively implemented in nine community hospitals of the Lazio region of Italy in order to improve the diagnostic performance of clinicians, thereby reducing the number of undiagnosed patients. STUDY POPULATION: The study population included 195 consecutive patients (85 males and 110 females, mean age 62.5 years, range 13-95 years) presenting with a syncopal spell at the emergency room of one of the nine participating hospitals in a 2-month period. RESULTS: The systematic implementation of the proposed diagnostic algorithm resulted in a striking reduction of undiagnosed cases. The percentage of patients discharged without a conclusive diagnosis decreased from 54.4% to 17.5%. Neurally mediated syncope was diagnosed in 35.2% of cases, cardiac syncope in 20.9% and neurological syncope in 13.8%. CONCLUSIONS: The use of specific, simplified diagnostic guidelines and algorithms results in an improvement of overall clinical performance. However, the development of such decision-making aids should carefully consider the local circumstances of daily clinical practice. Copyright 2000 The European Society of Cardiology.

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11)   Colivicchi F et al.  Development and prospective validation of a risk stratification system for patients with syncope in the emergency department: The OESIL risk score.  Eur Heart J 2003 May; 24:811-19.   http://eurheartj.oxfordjournals.org/content/24/9/811.full.pdf+html (full text link)

AIMS: Aim of the present study was the development and the subsequent validation of a simple risk classification system for patients presenting with syncope to the emergency departments. METHODS AND RESULTS: A group of 270 consecutive patients (145 females, mean age 59.5 years) presenting with syncope to the emergency departments of six community hospitals of the Lazio region of Italy was used as a derivation cohort for the development of the risk classification system. Data from the baseline clinical history, physical examination and electrocardiogram were used to identify independent predictors of total mortality within the first 12 months after the initial evaluation. Multivariate analysis allowed the recognition of the following predictors of mortality: (1) age greater than 65 years; (2) cardiovascular disease in clinical history; (3) syncope without prodromes; and (4) abnormal electrocardiogram. The OESIL (Osservatorio Epidemiologico sulla Sincope nel Lazio) score was calculated by the simple arithmetic sum of the number of predictors present in every single patient. Mortality increased significantly as the score increased in the derivation cohort (0% for a score of 0, 0.8% for 1 point; 19.6% for 2 points; 34.7% for 3 points; 57.1% for 4 points; p less than 0,0001 for trend). A similar pattern of increasing mortality with increasing score was prospectively confirmed in a second validation cohort of 328 consecutive patients (178 females; mean age, 57.5 years). CONCLUSIONS: Clinical and electrocardiographic data available at presentation to the emergency department can be used for the risk stratification of patients with syncope. The OESIL risk score may represent a simple prognostication tool that could be usefully employed for the triage and management of patients with syncope in emergency departments.

Electrocardiographic recordings were evaluated by the emergency physician and subsequently reviewed by a cardiologist, only in case of a specific request. The tracings were considered abnormal in the following cases: 
1. Rhythm abnormalities (atrial fibrillation or flutter, supraventricular tachycardia, multifocal atrial tachycardia, frequent or repetitive premature supraventricular or ventricular complexes, sustained or non-sustained ventricular tachycardia, paced rhythms),
2. Atrioventricular or intraventricular conduction disorders (complete atrioventricular block, Mobitz I or Mobitz II atrioventricular block, bundle branch block or intraventricular conduction delay),
3. Left or right ventricular hypertrophy,
4. Left axis deviation,
5. Old myocardial infarction,
6. ST segment and T wave abnormalities consistent with or possibly related to myocardial ischemia.

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12)   Derivation of San Francisco rule, Quinn JV, Stiell IG.  Ann Emerg Med 43(2):224; February 2004

San Francisco rule: patients greater than age 75, an abnormal  (ECG),  hematocrit less than or equal to 30, a complaint of SOB, BP less than 90, or a history of CHF, was 96% sensitive (95% CI 92-100) and 62% specific (95% CI 58-62).

Objective: The causes of syncope are usually benign, but are occasionally associated with significant morbidity and mortality. This study compares a clinical decision rule and physician judgment when predicting serious outcomes in patients with syncope. Methods: In a prospective cohort study, attending emergency physicians evaluated patients presenting to a university teaching hospital with syncope or near syncope. When possible a second physician also evaluated patients. As part of their evaluation, physicians were asked to predict the chance (0–100%) of the patient developing a predefined serious outcome. All patients were followed to determine whether they had suffered a serious outcome within seven days of their ED visit. Analyses included sensitivity and specificity for a low risk judgment threshold, and comparison of areas under the receiver operating characteristic curve (ROC) with 95% confidence intervals. Kappa coefficients were used to measure observer agreement. Results: During the 20-month study there were 684 visits for syncope, 79 resulting in serious outcomes. Of the patients to whom the physicians assigned a probability of serious outcome of 2% or less, 5 went on to develop serious outcomes. The sensitivity of this low risk 2% threshold was 94% (95%CI 86%–98%), with a specificity of 41% (95%CI 40%–42%). Agreement for this determination of risk was only fair, kappa = 0.44 (95%CI 0.34–0.54). The SFSR predicted the 5 patients with serious outcomes classified as low risk by physician judgment and had good overall sensitivity 96% (95%CI 92%–100%) and specificity 62% (95%CI 58%–66%). The area under the ROC was 0.90 (95%CI 0.86–0.94) for the SFSR and was significantly better (p = 0.01) than physician judgment 0.82 (95%CI 0.77–0.88). Conclusions: The SFSR performed better than physician judgment when predicting which patients with syncope will develop serious outcomes. This suggests great potential for the rule to help with physician decision making.

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Prospective Validation of the San Francisco Syncope Rule to Predict Patients With Serious Outcomes.  Quinn et al.  Annals of EM 2006:47(5):448; May 2006

Study objective: We prospectively validate the San Francisco Syncope Rule (history of congestive heart failure, Hematocrit less than 30%, abnormal ECG result [new changes or non–sinus rhythm], complaint of shortness of breath, and systolic blood pressure less than 90 mm Hg during triage). 

Methods: In a prospective cohort study, consecutive patients with syncope or near syncope presenting to an emergency department (ED) of a teaching hospital were identified and enrolled from July 15, 2002, to August 31, 2004. Patients with trauma, alcohol, or drug-associated loss of consciousness and definite seizures were excluded. Physicians prospectively applied the San Francisco Syncope Rule after their evaluation, and patients were followed up to determine whether they had had a predefined serious outcome within 30 days of their ED visit. 

Results: Seven hundred ninety-one consecutive visits were evaluated for syncope, representing 1.2% of all ED visits. The average age was 61 years, 54% of patients were women, and 59% of patients were admitted. Fifty-three visits (6.7%) resulted in patients having serious outcomes that were undeclared during their ED visit. The rule was 98% sensitive (95% confidence interval [CI] 89% to 100%) and 56% specific (95% CI 52% to 60%) to predict these events. In this cohort, the San Francisco Syncope Rule classified 52% of the patients as high risk, potentially decreasing overall admissions by 7%. If the rule had been applied only to the 453 patients admitted, it might have decreased admissions by 24%. 

Conclusion: The San Francisco Syncope Rule performed with high sensitivity and specificity in this validation cohort and is a valuable tool to help risk stratify patients. It may help with physician decisionmaking and improve the use of hospital admission for syncope. [Ann Emerg Med. 2006;47: 448-454.]

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14)   External Validation of the San Francisco Syncope Rule in the Canadian Setting. [Ann Emerg Med. 2010;55:464-472. 
External Validation much less sensitive and specific: 90% and 33%

Study objective: Syncope is a common disposition challenge for emergency physicians. Among the risk stratification.  instruments available, only the San Francisco Syncope Rule is rigorously developed. We evaluate its performance in Canadian emergency department (ED) syncope patients. Methods: This  retrospective review included patients aged 16 years or older who fulfilled the definition of syncope (transient loss of consciousness with complete recovery) and presented to a tertiary care ED during an 18-month period. We excluded patients with ongoing altered mental status, alcohol/illicit drug use, seizure, and head and severe trauma. Patient characteristics, 5 predictors for the rule (history of congestive heart failure, hematocrit level less than 30%, abnormal ECG characteristics, shortness of breath, and triage systolic blood pressure less than 90 mm Hg), and outcomes (as per the original study) were extracted. Results: Of 915 visits screened, 505 were included. Forty-nine (9.7%) visits were associated with serious outcomes. The rule performed with a sensitivity of 90% (44/49 outcomes; 95% confidence interval [CI] 79% to 96%) and a specificity of 33% (95% CI 32% to 34%). Including monitor abnormalities in the ECG variable would improve sensitivity to 96% (47/49 outcomes; 95% CI 87% to 99%). Although physicians failed to predict 2 deaths, the rule would have predicted all 3 deaths that occurred after ED discharge. Implementing th e rule in our setting would increase the admission rate from 12.3% to 69.5%. Conclusion: In this retrospective Canadian study, the San Francisco Syncope Rule performed with comparable sensitivity but significantly poorer specificity than previously reported. Implementing the rule would significantly increase admission rates. Further studies to either refine the San Francisco Syncope Rule or develop a new rule are needed. [Ann Emerg Med. 2010;55:464-472.]

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15)   STePS: (J Am Coll Cardiol 2008;51:276–83) ©

a. Short term risks: EKG, trauma, no prodrome, male. 

b. Long-term severe outcomes were 9.3% (40 deaths, 6.0%; 22 major therapeutic procedures, 3.3%), and their occurrence was correlated with an age _65 years, history of neoplasms, cerebrovascular diseases, structural heart diseases, and ventricular arrhythmias.

16)   Linzer M. Yang EH. Estes NA 3rd. Wang P. Vorperian VR. Kapoor WN.

Diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiography. Clinical Efficacy Assessment Project of the American College of Physicians. [Review] [34 refs].  Annals of Internal Medicine. 126(12):989-96, 1997 Jun 15.

Abstract PURPOSE: To review the literature on diagnostic testing in syncope and provide recommendations for a comprehensive, cost-effective approach to establishing its cause. DATA SOURCES: Studies were identified through a MEDLINE search (1980 to present) and a manual review of bibliographies of identified articles. STUDY SELECTION: Papers were eligible if they addressed diagnostic testing in syncope or near syncope and reported results for at least 10 patients. DATA EXTRACTION: The usefulness of tests was assessed by calculating diagnostic yield: the number of patients with diagnostically positive test results divided by the number of patients tested or, in the case of monitoring studies, the sum of true-positive and true-negative test results divided by the number of patients tested. DATA SYNTHESIS: Despite the absence of a diagnostic gold standard and the paucity of data from randomized trials, several points emerge. First, history, physical examination, and electrocardiography are the core of the syncope workup (combined diagnostic yield, 50%). Second, neurologic testing is rarely helpful unless additional neurologic signs or symptoms are present (diagnostic yield of electroencephalography, computed tomography, and Doppler ultrasonography, 2% to 6%). Third, patients in whom heart disease is known or suspected or those with exertional syncope are at higher risk for adverse outcomes and should have cardiac testing, including echocardiography, stress testing. Holter monitoring, or intracardiac electrophysiologic studies, alone or in combination (diagnostic yields, 5% to 35%). Fourth, syncope in the elderly often results from polypharmacy and abnormal physiologic responses to daily events. Fifth, long-term loop electrocardiography (diagnostic yield, 25% to 35%) and tilt testing (diagnostic yield less than or greater than 60%) are most useful in patients with recurrent syncope in whom heart disease is not suspected. Sixth, psychiatric evaluation can detect mental disorders associated with syncope in up to 25% of cases. Seventh, hospitalization may be indicated for patients at high risk for cardiac syncope (those with an abnormal electrocardiogram, organic heart disease, chest pain, history of arrhythmia, age > 70 years) or with acute neurologic signs. CONCLUSIONS: Many tests for syncope have a low diagnostic yield. A careful history, physical examination, and electrocardiography will provide a diagnosis or determine whether diagnostic testing is necessary in most patients. [References: 34]

17) Shen WK et al.  Syncope Evaluation in the Emergency Department Study (SEEDS);  A Multidisciplinary Approach to Syncope Management.  Circulation. 2004;110:3636-3645.

Background—The primary aim and central hypothesis of the study are that a designated syncope unit in the emergency department improves diagnostic yield and reduces hospital admission for patients with syncope who are at intermediate risk for an adverse cardiovascular outcome.  Methods and Results—In this prospective, randomized, single-center study, patients were randomly allocated to 2 treatment arms: syncope unit evaluation and standard care. The 2 groups were compared with 2 test for independence of categorical variables. Wilcoxon rank sum test was used for continuous variables. Survival was estimated with the Kaplan-Meier method. One hundred three consecutive patients (53 women; mean age 64 17 years) entered the study.  Fifty-one patients were randomized to the syncope unit. For the syncope unit and standard care patients, the presumptive diagnosis was established in 34 (67%) and 5 (10%) patients (P less than 0.001), respectively, hospital admission was required for 22 (43%) and 51 (98%) patients (P less than 0.001), and total patient-hospital days were reduced from 140 to 64. Actuarial survival was 97% and 90% (P = 0.30), and survival free from recurrent syncope was 88% and 89% (P = 0.72) at 2 years for the syncope unit and standard care groups, respectively. Conclusions—The novel syncope unit designed for this study significantly improved diagnostic yield in the emergency department and reduced hospital admission and total length of hospital stay without affecting recurrent syncope andvall-cause mortality among intermediate-risk patients. Observations from the present study provide benchmark data for improving patient care and effectively utilizing healthcare resources.

18) Venkatesh Thiruganasambandamoorthy et al.  Outcomes in Presyncope Patients: A Prospective Cohort Study.  Annals of Emergency Medicine March 2015; Volume 65, Issue 3, Pages 268–276.e6
http://www.henryfordem.com/ground/ul/2166_20150430142556_ho.pdf

By 30 days, 2 of 881 patients had died, but it was not know if these were from cardiovascular causes.  This is substantially less that the mortality rate for syncope.  5% had "serious outcomes," but because of poor definitions, this article greatly exaggerates the danger.

This study did not exclude patients whose etiology of symptoms was found in the ED.  And when you see the list of patients who had adverse events, 26 of 39 were identified in the ED.  They are not mysteries:   If you actually look at those patients (all listed in the Appendix), they all have serious problems while in the ED: atrial fib, atrial flutter, SOB, Chest pain, generalized weakness, SVT diagnosed by medics, upper GI bleeding 2 days prior, profound bradycardia in the ED, and more.  There are only 13 patients who appeared well in the ED and had an 'adverse event."  

By 30 days, 2 of 881 patients had died, but it was not know if these were from cardiovascular causes.  This is substantially less that the mortality rate for syncope.  5% had "serious outcomes," but because of poor definitions, this article greatly exaggerates the danger: being admitted within 30 days was an "adverse event."  

Abstract

Study objective: 

Presyncope is the sudden onset of a sense of impending loss of consciousness without losing consciousness (which differentiates it from syncope). Our goals are to determine the frequency of emergency department (ED) presyncope visits, management, 30-day outcomes, and emergency physicians’ outcome prediction.  Methods: Our prospective study at 2 academic EDs included adults with presyncope and excluded patients with syncope, mental status changes, seizure, and significant trauma. We collected patient characteristics, ED management, cause (vasovagal, orthostatic, cardiac, or unknown) at the end of the ED visit, and 30-day outcomes. Serious outcomes included death, arrhythmia, myocardial infarction, structural heart disease, pulmonary embolism, and hemorrhage. We also collected physicians’ confidence in assigning the cause and their prediction probability for 30-day serious outcomes. Results: Presyncope constituted 0.5% of ED visits. We enrolled 881 patients: mean age 55.5 years, 55.9% women, and 4.7% hospitalized. Among 780 patients with 30-day follow-up, 40 (5.1%) experienced serious outcomes: death 0.3%, cardiovascular 3.1%, and noncardiac 1.8%. Of the 840 patients discharged home, 740 had follow-up data and 14 patients (1.9%) experienced serious outcomes after ED disposition. The area under the receiver operating characteristic curve for physician prediction probability was 0.58 (95% confidence interval 0.38 to 0.78). The incidence of serious outcomes was similar, whereas physician diagnostic confidence and prediction probability varied among the 4 causal groups.  Conclusion: Presyncope can be caused by serious underlying conditions. Emergency physicians had difficulty predicting patients at risk for serious outcomes after ED discharge. Future studies are needed to identify risk factors for serious outcomes after ED disposition.

Not yet validated or incorporated into this post, but interesting abstract from 2015 SAEM:

107 The Canadian Syncope Risk Score to Identify Patients at Risk for Serious Adverse Events after Emergency Department Disposition

Venkatesh Thiruganasambandamoorthy1,2,

Kenneth Kwong1, Monica Taljaard1,2, Marco

L.A. Sivilotti3, Brian H. Rowe4, Robert

Sheldon5, George A. Wells1, and Ian G. Stiell1,2

1University of Ottawa, Ottawa, ON, Canada;

2Ottawa Hospital Research Institute, Ottawa, ON,

Canada; 3Queen’s University, Kingston, ON,

Canada; 4University of Alberta, Edmonton, AB,

Canada; 5University of Calgary, Calgary, AB,

Canada

Background: Considerable variations in ED management of

syncope exist with patients suffering serious adverse events (SAE)

outside the hospital.

Objectives: We sought to develop a risk scoring system to identify

ED syncope patients at risk for SAE after ED disposition.

Methods: This was a prospective cohort study at 6 large Canadian

EDs that enrolled adult syncope patients. We collected standardized

variables from history, clinical examination, results of investigations

including ECG, and patients’ disposition at index presentation.

Adjudicated SAEs included death, MI, arrhythmia, structural heart

disease, pulmonary embolism, significant or subarachnoid

hemorrhage, other syncope-related serious conditions or procedures

within 30-days of ED disposition. Multiple imputation for missing data,

multivariable logistic regression and bootstrap internal validation were

performed.

Results: Of the 4,611 patients enrolled (mean age 53.7 years, 55.0%

females, and 13.0% hospitalized), 285 (6.2%) suffered SAE during the

index visit and 292 (6.3%) were lost to follow-up, leaving 4,034

patients with 147 (3.6%) suffering SAE after ED disposition. Nine

variables were independently associated with SAE after ED

disposition: precipitating factors for vasovagal syncope, history of

heart disease, troponin (>99%ile), ED diagnosis of cardiac, or of

vasovagal syncope, any ED systolic blood pressure <90 or >180

mmHg, QRS duration >130msec, abnormal QRS axis and QTc interval

>480msec (Table 107). We developed the Canadian Syncope Risk Score

incorporating these variables with the risk ranging from 0.4% for a

score of -3 to 41.7% for a score of ≥7. Threshold scores of -2 and -1

had a sensitivity of 99.2% and 97.7% and a specificity of 25.6% and

47% for SAE respectively.

Conclusion: An important number of ED syncope patients suffer

SAE after ED disposition. Once validated, the Canadian Syncope Risk

Score has the potential to standardize ED management, and to improve

risk-stratification and disposition decisions.