Emergency Transvenous Cardiac Pacing

This case was provided by one of our fine 5th year EM/IM residents, Rachael Krob MD. The description of the method for inserting a pacing wire is by one of our fine 3rd year EM residents, Mark Sandefur MD.

An elderly male was found on the floor with altered mental status. When EMS arrived, he was obtunded but occasionally able to answer yes/no questions. He was found to be bradycardic in the 20's-30’s. Glucose was normal.  

A prehospital 12-lead was recorded; unfortunately, only half of it made it into the chart:
There is a slow indeterminate rhythm with a right bundle branch block morphology.  

The medics report that there was complete heart block. They gave atropine with no response, so they initiated transcutaneous pacing. They believed they had capture by palpating pulses and his mental status improved somewhat, so they had to give midazolam.  

On arrival in the ED, he continued to have altered mental status and shock, and so was intubated using RSI.

A cardiac ultrasound was performed during transcutaneous pacing.:
You can see the atrium beating at a normal rate, but the ventricle is responding very slowly.
There is normal-appearing myocardial contractility, but that the transcutaneous pacing was not capturing.  

Pacer pad placement was optimized with good anterior and posterior placement, and the amperage was turned all the way up, without capture. Because he was hypotensive and in shock, and he continued to have a heart rate in the 20-40’s, he was given 0.25 mg of push dose epinephrine, with improvement in blood pressure and heart rate. 

The decision was made to place a transcutaneous pacing wire. While this was being placed, transcutaneous pacing was discontinued due to the failure of capture and quick response to low dose IV epinephrine. A 12-lead ECG was obtained:
There is sinus tachycardia with complete (3rd degree) AV block and ventricular rate of about 50.  Notice the QRS morphology is that of RBBB and Left Anterior Fascicular Block.  
This means that the source of the escape is in the posterior fascicle.  
This is merely an interesting, though not critical, observation!
This was interpreted as bradycardia with complete heart block. While the pacing wire was being inserted, the patient received push dose epinephrine every 3-5 minutes as his heart rate and blood pressure would drift down. During this period, continuous cardiac ultrasonography showed the pacing wire in the right atrium. There was some difficulty with advancing the wire through the tricuspid valve into the right ventricle, but eventually placement was successful and appropriate capture was achieved:
 You can see the wire in the RV (see still picture with arrow in explanation below)

He was then admitted to the MICU with plans to go to the cath lab for a screw-in pacer. Outcome was good.

Placement of an Emergency Transvenous Pacer.  Ultrasound is the preferred method.

Indications (1)

I. Used for unstable bradycardia when other measures fail:
--Medical treatment is inadequate (e.g.: atropine, treatment of hyperkalemia, reperfusion for ischemia, etc.)
--External (transcutaneous) pacing fails to achieve capture, even after optimal placement and high output, or when not tolerated by the patient
--Even if transcutaneous pacing succeeds, it is usually not a good solution for multiple hours and may not be persistently efficacious.
--Often utilized in the setting of high grade AV node block, Sick Sinus Syndrome, etc.

II. Also can be used for overdrive pacing for unstable tachydysrhythmias, especially Torsades de Pointes (polymorphic VT due to long QT).


Prosthetic tricuspid valve
Severe hypothermia
--Predisposes to VF
--Bradycardia is physiologic!


Studies generally show approx 70-80% success rate.2,3
Average time to successful placement was 18 minutes.2
--30% less than 5 minutes
A 1981 study4comparing flow directed balloon tipped catheters to standard semirigid electrode catheters revealed several important differences:
--Improved time: 6 min w/ balloon vs. 13 min w/ standard
--Fewer complications with balloon tipped catheters
Most studies assessing emergency transvenous cardiac pacing were preformed before the use of ultrasound.


There are a couple well-described methods for this procedure:
--Sensing method
--EKG monitoring method
The main benefit of these techniques was that a physician could determine when the catheter reached the heart during the procedure without needing radiographs.

We will not discuss these techniques.

Ultrasound Technique: This is the preferred method at Hennepin County Medical Center because it is technically simpler and there are fewer opportunities for error.  It utilizes another physician or sonographer for real time ultrasound guidance. 

Place a Sheath Introducer

Right internal jugular or left subclavian veins preferred.
A Touhy-Borst Adaptor tightens around the wire, preventing leakage of blood or entry of air.

Insert the Pacing Catheter:

Roughly measure distance that will be needed.
Place a Tuohy-Borst adaptor with Cathgard on the introducer.
Insert the temporary pacing catheter into the Cathgard/sheath.
--Curvature must be directed to the left so the catheter can enter the heart:

Insert with Ultrasound Guidance:

A second provider uses ultrasound to identify the catheter entering the RV.
--Subcostal view preferred

The heart is bradycardic

Now the pacer wire is in place (see still image with arrow below) and the heart is being paced and is beating much faster.

Here is a still of the second ultrasound image:
The arrow shows the pacer wire.

Pacing Module:

An assistant connects the pacing catheter to the pacing module/box.
--Use the V ports
--Ensure correct placement of positive and negative electrodes in the module
--When the catheter is seen in the heart, turn on the pacing module.
Hit the “Emergency, Async” button, which initiates predetermined automatic settings (may vary depending on equipment):
--Rate 80
--A output 20 milliAmps (mA) (not applicable for our purposes)
--V output 25 mA

Confirm capture: ultrasound, pulse check, EKG
Adjust the rate if needed.
Tighten the Tuohy-Borst adaptor to help prevent displacement and extend the sterile sleeve.

Final Details

Obtain a CXR to confirm placement.
The pacer wire is in the RV.  Difficult to see here.  The image below shows its exact placement.
Ideal placement is in the apex of the RV.  This is not ideal, but is working perfectly.

Further Management

Discuss need for more definitive treatment with cardiology (placement of a screw-in temporary catheter, permanent pacemaker, etc).  

Temporary Pacers should be immediately replaced by more permanent ones.  Without the fixation into the myocardium with a screw (as permanent ones have), the temporary pacers can come loose and this is very dangerous!

Admit the patient to the ICU with pads in place.

1. Roberts JR. Roberts and Hedges’ clinical procedures in emergency medicine, 6e. Philadelphis, PA: Saunders; 2014:278.
2. Rosenberg AS, Grossman JI, Escher DJW, et al.: Bedside transvenous cardiac pacing. Am Heart J. 1969;77:697.
3. Kimball JT, Killip T: A simple bedside method for transvenous intracardiac pacing. Am Heart J. 1965;70:35.
4. Lang R, David D, Herman HO, et al.: The use of the balloon-tipped floating catheter in temporary transvenous cardiac pacing. Pacing Clin Electrophysiol. 1981;4:491.

Palpitations in a Young Healthy Male

A previously completely healthy young man presented to the ED after an episode of palpitations, dizziness and weakness while at work today.   He experience a sensation of anxiety and then had sudden onset tightness in his chest, palpitations, dizziness, and weakness.  He tried to rest, but his symptoms became worse and he started to sweat profusely.  He began to hyperventilate and describes carpal spasm.  By the time he arrived in the ED, symptoms were largely resolved.  The etiology seemed to be a panic attack, but he had never had one before.

An ECG was recorded:  

Besides the RSR' (right ventricular conduction delay), what do you see?

There is a long QT (computer measured at 488 ms is correct).  There is also a large U-wave fused to the T-wave in V3.  Hypokalemia was suspected.

K returned at 2.6 mEq/L.

His K was replenished and he was admitted for monitoring.

Here is the ECG the next AM with a K of 4.4 mEq/L: 
Normal QT and normal U-waves.  RSR' persists.
Aside: you might be worrying about type 2 Brugada.  It is not type 2 Brugada as the beta angle is too narrow.  See this post on Type 2 Brugada Syndrome.
Mg was 1.6 mEq/L.  Etiology of hypokalemia would be evaluated as an outpatient.  He was discharged.


Whether the hypokalemia was the etiology of the symptoms, by causing an unrecorded cardiac dysrhythmia, is uncertain.  But severe hypokalemia (K less than 3.0 mEq/L), especially when manifesting on the ECG as ST depression, long QT, or prominent U-waves, is a known cause of cardiac dysrhythmias, including malignant ventricular dysrhythmia.

A low serum K is representative of a VERY low total body K.  It cannot be replaced with a single dose of K replacement, as that will immediately redistribute to the intracellular space and hypokalemia will quickly recur.  Therefore, severe HypoK requires inpatient replacement with cardiac monitoring.

This ECG shows one of the reasons why it is important to obtain an ECG for syncope or palpitations.

How can you detect severe hypokalemia on the ECG?

Here are several examples.    Here are several more interesting cases of hypokalemia.

There is little literature on recognition of hypoK on the ECG.  Obvious large U-waves are very specific with a high Positive Predictive Value, but that is not sensitive.  

Below is an abstract we wrote back in 2010 in which we identify 3 important variables for diagnosing HypoK.  Unfortunately, one is a subjective critierion.

Abstract 400 (ACEP Research Forum): Derivation of a Rule for Diagnosis of Hypokalemia on the Electrocardiogram     Get rights and content

Annals of Emergency Medicine, 2010-09-01, Volume 56, Issue 3, Pages S129-S130, Copyright © 2010 American College of Emergency Physicians

Study Objectives

There is little data on the electrocardiographic (ECG) diagnosis of hypokalemia (HypoK). We hypothesized the ECG to be an accurate predictor of significant HypoK (K ≤ 2.9 mEq/L) or normoK (K ≥ 3.5 mEq/L) (NormoK).


Retrospective study. We searched the electronic medical record for consecutive emergency department diagnoses of HypoK, then hand searched for those in which there was an ECG recorded before administration of potassium (K), and the K was ≤ 2.9 mEq/L. For controls, we searched for consecutive ECGs in patients with K ≥ 3.5 mEq/L. Abnormal QRS (bundle branch block or intraventricular conduction delay) or extreme tachycardia (HR > 130) were excluded, as were redundant patients. One expert reader (ExR) and two resident readers (RRs) who underwent a short tutorial interpreted the randomly sorted ECGs while blinded to the K level and the Bazett-corrected QT interval (QTc-B). ECGs were analyzed for computerized QTc-B, presence of U-waves [None (NUW), subtle (SUW), or prominent (PUW)], T-Wave flattening (TF), and ST segment depression (STD). Resident readers combined, and the expert reader, noted subjective interpretations (SI, either ExR-SI or RR-SI) [definite HypoK (SI+), or not]. Analysis was by descriptive statistics, by Student's t-test and by Chi-square (CS).


There were 100 cases of HypoK with an ECG; 13 were excluded, leaving 87. There were 58 controls. QTc-B was the single best differentiator, with accuracy (Acc) of 74%. Expert reader Acc was 72%, and Resident reader was 63% (p=.10 by CS). Mean QTc-B for HypoK was 475 ± 8.2 milliseconds (ms); for NormoK is was 429 ± 5.5 ms (p<0 .0001="" 100="" 3="" 78="" 79="" 80="" 83="" 86="" 89="" 92="" 98="" a="" acc.="" acc="" added="" and="" best="" by="" combination="" criteria="" diagnosis="" exr="" font="" had="" if="" none="" objective="" of="" or="" prolonged="" prominent="" qtc-b="" results="" rrs="" s="" sens="" spec="" student="" subjective="" t-test="" the="" these="" to="" two="" u-wave="" versus="" was="" were="" with="">


QTc is longer in HypoK than NormoK. Significant HypoK in the ED can be recognized on the ECG with high accuracy using QTc-B and presence of prominent U-waves. HypoK can be recognized with very high Sens, Spec, and Acc, using subjective interpretation of either the expert reader or the residents, plus QTc-B and presence or absence of prominent U-waves.

Terminal QRS Distortion: Diagnostic of LAD Occlusion. Or is it Pericarditis?

A middle-aged woman presented with what is described as a burning feeling in her chest which the physician said was "very atypical."  It did occur during exercise and radiated to both wrists.

Here is the first ECG:
Sinus rhythm.  
Computerized QTc is 437.  
There is some ST Elevation in II and aVF but without reciprocal ST depression in aVL.  
Precordial leads also have ST Elevation:  Is this normal variant or is it Ischemic ST Elevation?  There is upward concavity in all leads, suggesting normality. But upward concavity is seen in all of leads V2-V6 in almost 50% of LAD occlusion.  There is no ST depression, Q-waves, or T-wave inversion.
The first impression of the clinicians was "pericarditis" because of the diffuse ST elevation.

The computer algorithm might say: "Diffuse ST elevation, consider pericarditis, early repolarization, or myocardial infarction." I don't know what it actually said.

Early repol vs. LAD occlusion

Should we use the LAD-Early Repol calculator?
If you did, and it was negative, it would likely be a false negative.  Why?
There is Terminal QRS distortion in V3, which is not a finding of normal variant ST elevation.
What is Terminal QRS distortion?
Terminal QRS distortion is the absence of both an S-wave or a J-wave in either V2 or V3.  It is not seen in early repolarization, or is very rare.  In the right clinical context, and in the presence of non-diagnostic ST elevation, it is highly suspicious for coronary occlusion.

They did apply the formula, using these measurements: 1.5 mm for STE at 60 ms after the J-point in lead V3, QTc of 437, and R-wave amplitude in V4 of 13.  (I would have used 2, 437, 14)

Their numbers resulted in 23.34 (very close to 23.4, but technically negative.  I recommend that anything above 22.0 be investigated further)

My measurements would have resulted in 23.6, also very close but positive.

Pericarditis vs. LAD occlusion

I always say "You diagnose pericarditis at your (and your patient's) peril." 

Why is this not pericarditis:
1. ST vector: The ST vector in pericarditis should be lateral and inferior and only slightly anterior.  The vector here is towards V3.
2. Large T-waves: in pericarditis, the ST elevation is much more pronounced than the T-wave.  Here the T-wave is more pronounced, hyperactute.
3. No diagnostic PR depression.
4. Notice there is a Spodick's sign in V3-V5. But this is a worthless sign (see this recent post).

They recorded 2 more ECGs at unknown intervals:

Perhaps some increase in STE

There is slightly increasing ST Elevation

Fortunately, the troponin came back slightly elevated, and fortunately they did not not attribute that elevation to myocarditis.

The patient was taken to angiography and found to have a 99% thrombotic LAD occlusion.

A 30 year old African American with Chest pain and T-wave Inversion

A 30 yo African American Male presented agitated and with active chest pain, thought to be on a stimulant.  This ECG was recorded:
There is T-wave inversion in II, III, aVF and V4-V6.  What is it?

The patient was sedated and this was recorded 2.75 hours later:
Now there is sinus bradycardia.  The T-wave inversion is now seen in V2 and V3 in addition to V4-V6.  Inferior T-waves are no longer inverted.
Does this change your mind about the first? 

I was shown these ECGs without that information and asked if the patient was African American.  That is because they are classic "Benign T-wave Inversion (BTWI)."

What is particularly interesting here is the 2nd one: there is an apparently long QT interval, large U-waves in V2 and V3, and the development of T-wave inversion in V2 and V3 when it was not there on the previous.

The worry here was that it was Wellens' syndrome.  BTWI has a comparatively short QT.  My hand-measured, Bazett-corrected QTc in both of them is 415 ms.  The apparent increase on the 2nd is because the raw QT is longer, but is limited by the correction.  Wellens' is generally (but not always!) longer.

The giveaways are the tall R-waves in the affected leads, with minimal S-waves, and the presence of J-waves, especially in V3-V6 on the second ECG.  U-waves are a common feature of early repolarization, which is closely related to BTWI.

The really worrisome part is the change.  All I can say is that even normal "baseline" ECGs change from situation to situation.  Early repol is not stable over time.

The patient did indeed rule out for MI.

Here is much more on BTWI.

See especially this post.

Diffuse ST Elevation. Diagnosis confirmed with Bedside Echo.

A male in 40's with left sided chest pain since last night with associated shortness of breath. The pain worsens with turning on left side and is best when sitting forward.   He has some cough with sputum.  There was no pericardial friction rub.

Here is the initial ECG:
Diffuse ST elevation, without reciprocal ST depression, mostly in inferior limb leads and lateral precordial leads. This is very typical for pericarditis.

Some ECG factors to consider in diagnosing pericarditis:

1. Diffuse STE, fulfills
2. STE vector towards leads II and V5, fulfills
3. Absence of reciprocal ST depression, fulfills
4. Presence of PR segment depression, fulfills
                 [but is not diagnostic (only about 0.5 mm, which can be normal)]
5. T-waves not prominent, especially ST/T ratio in V6 greater than 0.25, fulfills
6. ST depression in aVR and V1, fulfills
7. Spodick's sign: downsloping TP segment.  This is now known to be neither sensitive nor specific for pericarditis (personal communication on research done by Amal Mattu).  It is absent here.

All these signs are discussed in this recent post.

Clinical factors:

1. Definitely positional
2. Friction rub, not present
3. Pericardial effusion (good specificity, poor sensitivity)

Case progression: 

A bedside echo was done:

Notice the small effusion, seen close to the transducer as a 5 mm echo free stripe.  Furthermore, there was no wall motion abnormality.

Effusion very much increases the probability of pericarditis (though beware hemopericardium in cases of MI with rupture or aortic dissection).

The chest X-ray was negative.

The patient was admitted and ruled out for MI.

Another ECG was recorded 24 hours later:
T-waves are slightly more prominent in affected leads

This is then a classic presentation for pericarditis.  He was treated with NSAIDs and Colchicine.

Lateral Hyperacute T-waves in V5 and V6

A middle aged male with no significant past medical history complained of several hours of chest pain.

Here is his initial ED ECG:
The computer read: left anterior fascicular block and old anterior MI.  No other comment.
What do you think?

--There is a large pathologic QR-wave in I and aVL, and small ones in V3-V6.  (Leads V2 and V3 must be reversed, as the QR progression is interrupted and only makes sense if one interprets them as switched).  These are diagnostic of MI of unknown age.
--The STE in aVL, with minimal reciprocal ST depression in inferior leads, in the setting of well-formed Q-waves, is also of unknown age, but very likely to represent old lateral MI with persistent ST elevation.
--There is less than 1 mm of STE in I, aVL, V5 and V6, but these leads are notoriously insensitive for coronary occlusion.  Only about 50% of occlusion of arteries supplying this area of myocardium have ST elevation that meets "criteria" of 1mm or more.
--However, the T-waves in V5 and V6 make this diagnostic of coronary occlusion.  They are far too tall and fat to be normal.  They are hyperacute.

An ED bedside ultrasound confirmed anterior wall motion abnormality.

The cath lab was activated.  At cath, a nearly occluded (TIMI-1 flow) first diagonal was found and stented.  Peak troponin I was 41.84 ng/mL.

Echo showed mid-anterior and anterolateral akinesis, with an EF of 58%.

Here was the post PCI ECG:
Now the T-waves are much more normal.  Q-waves are more well developed in V5 and V6.  The STE in aVL is still present and may well have been due to old MI (which is also, again, strongly suggested by the well-formed, deep and wide Q-waves).

Hyperacute T-waves in V5 and V6 are occasionally the only indication of coronary occlusion.

See V5 and V6 in this case, which is even more interesting. 

Also this case