Author Archives: Ivan Rios

Unstable Bradycardia Resolves Following Atropine and Attempted Transcutaneous Pacing (TCP)

A  75 year old male experienced a syncopal episode. The event was witnessed by family members who contacted 9-1-1. On arrival of EMS personnel the patient appears acutely ill. He is pale, diaphoretic and cool to touch. He states that he is feeling lightheaded and weak.

Medical History

  • Hypertension
  • Hyperlipidemia
  • Gout
  • Bilateral knee replacement
  • Left bundle branch block

The family reports the patient is seeing a cardiologist and is scheduled for pacemaker implantation in 3 weeks due to previous episodes of symptomatic bradycardia.


  • Zocor (Simvastatin)
  • Lopressor (Metoprolol)
  • Aloprim (Allopurinol)
  • Multi-vitamins

Vital Signs

  • RR: 20
  • HR: 20
  • BP: 80/48 mm Hg
  • SpO2: 93% on room air
  • Capillary blood glucose: 118 mg/dL

Breath sounds are clear bilaterally.

The patient is placed on O2 via nasal cannula at 2 LPM with ETCO2 of 16 mmHg.

Cardiac monitoring is established and the following 12 lead ECG is obtained.

High degree AV block with heart rate less than 20.

When considering bradycardia management, 3 initial questions should be answered:

  • Is the patient bradycardic?
  • Is the patient symptomatic?
  • Is the patient symptomatic from the bradycardia?

If all of these have been answered with a YES, determine the patient’s hemodynamic status.

Signs of hemodynamically instability:

  • Altered mental status
  • Hypotension
  • Ischemic chest pain
  • Signs of hypoperfusion
  • Acute pulmonary edema

Based on these criteria this patient is clearly unstable.

Defibrillation pads are placed as a precaution, IV access is obtained, and 250 ml of normal saline is administered en route to the Emergency Department which is 4 minutes away from the scene.

Upon arrival blood samples are obtained and the following 12 lead ECG is obtained.

3rd Degree AV Block. The escape rhythm shows a wide QRS with bifascicular morphology (RBBB morphology with left axis deviation). It is likely a ventricular in origin.

The patient’s level of consciousness deteriorates and he responds only to painful stimuli.

0.5 mg atropine is administered rapid IV push followed by 10 ml saline flush.

After 1 minute transcutaneous pacing is initiated with no electrical capture up to 90 mA. Transcutaneous pacing is discontinued by the arriving cardiologist who requests vasopressors.

Prior to vasopressors being administered a change is noted on the cardiac monitor and another 12 lead ECG is obtained.

The heart rate is now 92. There is left bundle branch block which is consistent with the patient’s known medical history. At first glance this appears to be sinus rhythm although the last 3 cardiac cycles make the exact rhythm uncertain.

The patient now reports he is feeling better. His skin color improves and his blood pressure normalizes.

The patient was taken to cardiac cath lab for angiography and a permanent pacemaker. The procedure was successful and he was placed in the cardiac step-down unit for further observation.


Atropine is an anticholinergic drug – also known as a parasympatholytic – which means that it counteracts increased vagal tone by binding to cardiac muscarinic receptors, which can improve sinus, atrial, and AV-nodal conduction. However, it is not believed to have a direct affect on rhythms of ventricular origin.

The 2010 AHA ECC Guidelines caution:

“Avoid relying on atropine in type II second-degree or third-degree AV block or in patients with third-degree AV block with a new wide-QRS complex where the location of block is likely to be in non-nodal tissue (such as in the bundle of His or more distal conduction system). These bradyarrhythmias are not likely to be responsive to reversal of cholinergic effects by atropine and are preferably treated with TCP…”

There is a caveat regarding TCP:

“TCP is, at best, a temporizing measure. TCP is painful in conscious patients, and, whether effective or not (achieving inconsistent capture), the patient should be prepared for transvenous pacing and expert consultation should be obtained. It is reasonable for healthcare providers to initiate TCP in unstable patients who do not respond to atropine. Immediate pacing might be considered in unstable patients with high-degree AV block when IV access is not available. If the patient does not respond to drugs or TCP, transvenous pacing is probably indicated.”

In this case transcutaneous pacing was not successful but the milliamperes were not increased beyond 90 milliamperes. On the plus side, the clinicians who were caring for this patient realized that they had not achieved capture, which is not always the case!

Fortunately, the patient spontaneously converted into a perfusing rhythm. The atropine may have contributed to the termination of this 3rd degree AV block, it may have been related to sympathetic stimulation from attempted transcutaneous pacing, or it could be a coincidence. These types of scenarios are susceptible to the “post hoc ergo propter hoc” fallacy (after this, therefore because of this).

A common error when treating patients with bradycardia is a rush to drug or electrical therapy prior to identifying reversible causes. Remember, Hs and Ts aren’t just for asystole and PEA!

Most importantly, hypoxemia should be rapidly identified and treated, but other conditions like hyperkalemia can also cause bradycardia. There is little to lose and much to gain from giving a patient calcium gluconate or calcium chloride prior to pacing. The quote Stephen Smith, M.D.: “The treatment [of hyperkalemia with calcium] is benign and cheap. How many life-threatening diseases can you treat benignly and cheaply?”

The definitive care for this patient was a permanent pacemaker.

Further reading: ACLS Bradycardia Algorithm


Neumar R, Otto C, Link M et al. Part 8: Adult Advanced Cardiovascular Life Support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(18_suppl_3):S729-S767. doi:10.1161/circulationaha.110.970988.

Abrich V, Le R, Friedman P, et al. Aggressive Management of Bradycardia is Associated With Improved Clinical Outcomes and Shorter Length of Stay: A Comparison of Two Academic Centers. Circulation. 2016;134:A20838

EMCrit Podcast 42: A phD in EKG with Steve Smith. EMCrit Podcast. 2011. Available at: Accessed November 26, 2017.


Everything You Should Know About Diltiazem (Cardizem)

A 50-year-old male with a history of hypertension (HTN) and atrial fibrillation (AF) presents to the Emergency Department with complaint of palpitations, which started while mowing the lawn.

He is alert and oriented with a Glasgow Coma Scale (GCS) of 15 and no signs of Hypoperfusion.

  • Heart Rate: 165/min, strong and irregular
  • Blood Pressure: 140/100 mmHg
  • Ventilatory Rate: 22/min
  • SpO2: 98% on room air

The patient is compliant with his medications and denies any allergies.

A 12 Lead ECG is recorded.

Atrial fibrillation with rapid ventricular response (RVR) and generalized ST-segment depression indicative of subendocardial ischemia.

The patient was treated with 20 mg of diltiazem (Cardizem) over 2 min, followed by 10 mg over 1 hr, and 0.25 mg digoxin (Lanoxin).

A rhythm change was noted on the monitor and another 12-lead ECG was recorded.

There is a sinus rhythm with left ventricular hypertrophy by limb lead voltage criteria and left atrial enlargement. There are no signs of subendocardial ischemia, suggesting the ST-segment depression was rate-related.

The patient was now asymptomatic and admitted for observation without further incident.

Understanding Diltiazem (Cardizem)


Diltiazem (Cardizem) is a Class IV antiarrhythmic and one of the most common pharmacological agents used for treatment of AF with RVR.

Class IV antiarrhythmics are Calcium Channel Blockers (CCBs), which inhibit intracellular calcium influx via calcium channel antagonism. These particular pharmacological agents can be further divided into subdivisions based on their molecular composition:

Dihydropyridines (DHPs)

  • These CCBs can be easily identified by the last four letters of the generic name ending with “pine”.
  • DHP CCBs are more selective to peripheral vasculature than cardiac cells, leading to arterial smooth muscle relaxation and decreased Systemic Vascular Resistance (SVR), thus, decreasing afterload and Myocardial Oxygen Demand (MVO2).
  • Because of this peripheral calcium channel selectivity, they are commonly used for treatment of Hypertension and angina.
  • Their hemodynamic effects can be associated with adverse effects such as hypotension and reflex tachycardia secondary to sympathetic stimulation as a compensatory mechanism for the decreased cardiac output.

Examples include:

  • Amlodipine (Norvasc)
  • Nicardipine (Cardene)
  • Nifedipine (Procardia)

Non-dihydropyridines (NDHPs)

  • These CCBs are those which generic name does not end with “pine”.
  • Can be further divided into benzothiazepines (not to be confused with benzodiazepines) and phenylalkylamines.
  • Non-dihydropyridine CCBs are more selective to L-Type Calcium Channels in cardiac cells, such as the Sino Atrial Node (SAN) and Atrio Ventricular Node (AVN), although all CCBs cause peripheral vasodilation.
  • This Calcium Channel antagonism leads to decreased SAN chronotropic effect and decreased AVN conduction, making it useful for treatment of atrial arrhythmias such as AF, Atrial Flutter and Supra-ventricular Tachycardias (SVTs).

Examples include:

  • Benzothiazepines: Diltiazem
  • Phenylalkylamines: Verapamil

Vaughan-Williams Anti-arrhythmic Classification

There are four specific classes of antiarrhythmics with specific physiological functions divided into classes based on their mechanism of action. The rest of the pharmacological agents used as antiarrhythmics fall under the fifth class with different mechanisms of action from the previous classes.

One important aspect to understand is that although they are all antiarrhythmics, each class works under different mechanisms and therefore may have different effects on cardiac cells. Some target atrial, AV nodal or ventricular cells, while some have the capacity to address both atrial and ventricular arrhythmias.

Pharmacological Use

Diltiazem has a COR I, LOE-b classification, used for rate control of atrial arrhythmias, predominantly Atrial Fibrillation, and COR IIa, LOE-b for treatment of SVT with a reentry pathway mechanism.

2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2014;64(21):2246-2280. doi:10.1016/j.jacc.2014.03.021

2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2015 Sep 16. pii: S0735-1097(15)06203-8. doi: 10.1016/j.jacc.2015.09.019.

Mechanism Of Action

  • Negative Chronotropic, Inotropic and Dromotropic effect by blocking L-Type Calcium Channels in cardiac tissue
  • Decreased Calcium influx affects Phase 2 of cardiac depolarization, delaying atrial and AVN conduction
  • This ultimately leads to decreased ventricular rate, with or without conversion to sinus rhythm


  • Diltiazem should be avoided in the presence of pre-excited AF with RVR, that is, AF in the presence of accessory pathway, i.e. Wolff Parkinson White (WPW) syndrome, as AVN blockage can lead to increased conduction through the accessory pathway, leading to life-threatening rapid ventricular rates.
  • Procainamide and Ibutilide are the preferred treatment of pre-excited AF with RVR and hemodynamically stable patients.
  • Diltiazem can be used in patients with AF and Heart Failure (HF) but with caution in reduced Left Ventricular Ejection Fraction and hypotension.

Dose and Administration

Although dosages may vary based on physician orders, protocols and age, a standard initial dose is 0.25 mg/kg, ranging between 10-20 mg over 2 minutes, with a second dose of 0.35 mg/kg, ranging between 20-25 mg over 2 minutes, often followed by a 5-10 mg/hr infusion.

Treatment of hemodynamically unstable patients in narrow QRS complex AF with RVR requires synchronized cardioversion at 120-200 J initially, and should not be delayed for administration of an anti-arrhythmic agent.


  • Diltiazem is a Class IV, non-dihydropyridine CCB anti-arrhythmic, serving as the most common pharmacological agent used for the treatment of AF and SVTs, for patients that are hemodynamically stable.
  • Caution should be used with CCBs and HF with decreased EF and hypotension.
  • Electrical Cardioversion should not be delayed for treatment with an anti-arrhythmic agent in the presence of Hypoperfusion and hemodynamically unstable patients.

Wide Complex Tachycardia Treated With Amiodarone and Synchronized Cardioversion

A 55 year old male presents to EMS with complaint of intermittent shortness of breath.

Symptom onset occurred while he was taking his daily walk about 15 minutes prior to EMS arrival.

The patient has a Glasgow Coma Score of 15, with a patent airway, clear lung sounds, and mild respiratory distress. Strong and regular bilateral radial pulses are noted, with no obvious signs of hypoperfusion.

The following medical history is reported:

  • Hypertension
  • Coronary artery disease
  • 2 coronary stents of unknown location
  • Occasional smoking and alcohol consumption

Medications include metoprolol, nitroglycerin tablets, and daily supplements.

Vital signs are assessed.

  • RR: 25
  • HR: 62
  • NIBP: 141/91
  • SpO2: 99% on room air
  • BGL: 97 mg/dL

The patient is placed on the cardiac monitor.

Vital Signs

Normal sinus rhythm with flattened T waves. Otherwise, nothing alarming.

A few seconds later the patient complains of acute shortness of breath, while the initial 12 lead ECG is obtained.

Initial 12-Lead ECG

The following questions come to mind:

  • What is the rhythm?
  • Could this be the cause of the sudden onset of shortness of breath?
  • Is the patient stable or unstable?
  • What will your treatment consist of?

We should note that there is a regular Wide Complex Tachycardia (WCT) which should be presumed to be Ventricular Tachycardia (VT) until proven otherwise. You may or may not have time to fully scrutinize the ECG depending on the patient status.

A regular WCT should be presumed as VT until proven otherwise!

One important reason this should be our train of thought is that VT is less likely to be tolerated by a patient with a cardiac history or structural heart disease compared to a younger individual without these mitigating factors.

Three main possible causes of WCT should be considered:

  1. VT
  2. SVT with aberrancy (i.e. reentry tachycardia with a Bundle Branch Block)
  3. Antidromic AVRT (requires an accessory pathway)

There are multiple criteria to differentiate VT from SVT with aberrancy. The two conditions can be difficult to distinguish and in some cases, impossible.

Findings considered supportive of VT:

  • Structural heart disease or previous myocardial infarction
  • An extremely wide QRS complex > 160 ms (0.16s)
  • The presence of AV dissociation
  • The presence of fusion and captured beats
  • QRS concordance in the precordial leads (i.e., all negative or all positive)
  • Extreme Right Axis Deviation (ERAD)
  • However, the absence of ERAD does not rule out VT
  • Wellens, Brugada, or Verekei’s Criteria (outside the scope of this case study)

Let’s take a look at the same ECG again with some highlighted points.

ECG with highlighted points

  • There is a very broad QRS of at least 180 ms (0.18s)
  • Extreme right axis deviation is noted at -176 degrees
  • Ventricular complexes outnumber atrial complexes by a 2:1 ratio (marked with red circles)
  • There is a monophasic R wave in lead V1

All of these findings support the diagnosis of ventricular tachycardia, but again, VT should be your default diagnosis!

Oxygen was given via nasal cannula @ 3 LPM, IV access was established, defibrillation pads were placed, and 150 mg amiodarone drip was started.

A few seconds after starting the amiodarone drip the patient reported relief of shortness of breath and the following 12-lead ECG was recorded.

12-Lead 4 ECG

Normal sinus rhythm with left anterior fascicular block and right atrial enlargement.

Approximately 4 minutes later the shortness of breath returned along with substernal chest pressure.

12-Lead 7 ECG

The patient is back in ventricular tachycardia but with a slower rate due to the amiodarone.

The presence of one or more of the following qualifies a patient as unstable.

  • Hypotension
  • Ischemic chest pain
  • Dyspnea
  • Pulmonary edema
  • Altered mental status

The patient was given 2 mg of midazolam and synchronized cardioversion was performed @ 100 J which converted the patient back to sinus rhythm. The amiodarone drip was completed and the patient’s symptoms were completely resolved by arrival in the emergency department.


Consider this recommendation from the 2010 AHA ECC Guidelines (unchanged in 2015):

“For patients who are stable with likely VT, IV antiarrhythmic drugs or elective cardioversion is the preferred treatment strategy. If IV antiarrhythmics are administered, procainamide (Class IIa, LOE B), amiodarone (Class IIb, LOE B), or sotalol (Class IIb, LOE B) can be considered. Procainamide and sotalol should be avoided in patients with prolonged QT. If one of these antiarrhythmic agents is given, a second agent should not be given without expert consultation (Class III, LOE B). If antiarrhythmic therapy is unsuccessful, cardioversion or expert consultation should be considered (Class IIa, LOE C).”​

Although procainamide, lidocaine and sotalol are proven to be effective and even preferred by some clinicians, amiodarone (Class III antiarrhythmic with potassium, calcium, and sodium channel blocking properties) remains the primary antiarrhythmic agent in the prehospital setting for wide complex tachycardia.

Adenosine can be used initially for stable regular wide complex tachycardia. This is because a WCT caused by SVT with aberrancy (and right ventricular outflow tract ventricular tachycardia) are responsive to adenosine.

Synchronized Cardioversion is the preferred treatment for unstable WCT.


  • Wide complex tachycardia should be treated as ventricular tachycardia until proven otherwise
  • Stable WCT can be addressed with antiarrhythmic agents or synchronized cardioversion
  • Administration of multiple antiarrhythmic agents should be avoided without expert consultation
  • Treatment of unstable WCT should be synchronized cardioversion
  • Synchronized cardioversion is acceptable and avoids some of the pitfalls of antiarrhythmic infusion

Neumar R, Otto C, Link M et al. Part 8: Adult Advanced Cardiovascular Life Support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(18_suppl_3):S729-S767. doi:10.1161/circulationaha.110.970988.