HPI:An 82-year-old male with a history of bradycardia, HTN and HLD arrives in the emergency department via EMS with altered mental status, pacer pads in place active pacing going. Patient is primarily Russian-speaking and his wife is assisting with translation. The patient is not able to correctly answer what his name is or his date of birth, the wife states that he is just mumbling and not making sense. EMS states that the patient was heard falling to the ground and was immediately found by his wife. EMS arrived 3 to 4 minutes after a syncopal episode. Was found to be bradycardic in the 20s. There are no rhythm strips available from EMS and there is a report of home medication of amlodipine. The rest of the history is limited due to the critical nature of the patient being unstable and altered mental status.
Pertinent Exam Findings:General Appearance: Patient is awake, he is unable to follow commands or answer questions, he is actively twitching secondary to being actively paced Respiratory: Lungs are clear to auscultation, on a non-rebreather Cardiovascular: External pacer pads are actively pacing with capture noted on EMS monitor, he is 90 mA with a heart rate paced at 90 but rate is actually about 60 Neurological: Somnolent and confused, limited exam due to emergent nature
Diagnostic Studies:Figure 1: 12 lead ECG showing third degree heart block
ED Course:Patient arrived without EKG actively being paced and there are reports of amlodipine. Because the patient was altered and hemodynamically unstable he was emergently intubated to protect his airway. While setting up for RSI, to address any potential reversible causes of bradycardia, the patient was givena, high dose insulin, D50, glucagon, calcium gluconate. The patient was emergently intubated using rocuronium and etomidate. After the patient was intubated an EKG obtained showed complete heart block. Cardiology was immediately consulted. The pacer machine had difficulty achieving capture requiring up to 140 mA with different positions of pacer pads tried, including both anterior/lateral and anterior/posterior. Best success with anterior posterior placement. At one point his blood pressure did drop to 60s systolic. At that point, push dose epi was given which transiently increased his heart rate and blood pressure. The emergency physician considered placing a transvenous pacer bedside for better capture however cardiology showed up bedside and the patient had stabilized enough for him to be taken to the cath lab for a temporary pacemaker to be placed.
Hospital Course:In the hospital he had a normal heart cath, EF on echo was 65%, a permanent pacemaker placed by cards. Per cardiology: “Complete Heart Block- causing loss of consciousness, was unknown cause. Perhaps progression of his bifascicular block. Electrolytes normal. No evidence of ischemia.” He was discharged with normal neurologic function and no evidence of hypoxemic brain injury.
Background:Third degree heart block occurs when no impulses are conducted from the atria to the ventricles and may be due to structural or physiological disruptions. While congenital causes of third degree heart block are typically irreversible, pathogenic or iatrogenic causes may be reversible and can present differently. As such, a detailed and accurate history is essential in proper diagnosis and determination of treatment course. Among the top iatrogenic causes of third degree heart block is the use of drugs including beta-blockers and calcium channel blockers. Cardiac procedures such as open heart surgery or catheter ablation are another common iatrogenic cause of complete heart block. Pathophysiologic changes such as fibrosis and sclerosis of the conducting system are often idiopathic and responsible for nearly half of AV blocks. Due to the idiopathic nature of pathophysiologic changes, these causes of third degree heart block are difficult to distinguish clinically. Regardless of underlying cause, patients will usually present with symptoms that may include fatigue, dyspnea, chest pain, syncope/presyncope, or sudden cardiac arrest. However, the severity of symptoms may vary, and in the case of very fast escape rhythms, patients may have little to no symptoms at all.
Diagnosis:A thorough patient history is the first step in diagnosis with particular attention being paid to medication use, past procedures, and family history. In areas known to have Lyme disease, history of tick exposure is important in considering Lyme carditis as a diagnosis. TSH and potassium should be checked as hypothyroid and hypokalemia may cause a complete heart block. The primary diagnostic method is the 12-lead ECG. Independent P-waves and QRS complexes are indicative of complete heart block. Location of the block can be identified by looking at QRS complex duration. A normal QRS length is most often associated with a block at the AV node and bundle of His. Bundle branch blocks are seen with longer QRS complexes. ST segment changes can occur when coronary heart disease is exacerbated by the third degree block. In rare cases the ECG may be nondiagnostic, and in these cases the next step would be invasive electrophysiological studies (EPS). Asymptomatic patients, partially reversible block, and inability to find the block site are also indications for EPS.
Management in ED:As is often the case with emergency management, the patient’s stability and etiology determine the initial approach. The unstable patients will often require pharmacotherapy in addition to transvenous or transcutaneous pacing to improve cardiac output. Pacing is indicated for symptomatic bradycardia. The quickest approach is transcutaneous pacing. This can be accomplished with the anterior/posterior position or anterior/lateral position. Transcutaneous Pacing: 1. Pad Placement: Best capture is obtained with anterior/posterior, as shown below in figure b. The positive pad is placed posteriorly to the left of the spine, beneath the left scapula. The negative pad is placed anteriorly between the xiphoid process and the left nipple. A second option is to place both pads anteriorly with positive electrode to the right of the sternum and negative electrode at V6 position. Figure 2: Pacer pad placement shown in a.) Anterior/lateral and b.) Anterior/posterior positions 2. Select Mode: Select the pacemaker button on the box and choose the fixed mode (this means that the pacemaker will fire at your set rate). 3. Set rate and output: The initial pacing rate should be set to 80 bpm with the current set to 30 mA. The current can be increased by 10 mA at a time until capture is noted by a QRS complex and T wave following each pacemaker spike. A pulse can be appreciated when a perfusing rhythm is achieved. Adjust the current to 5-10 mA above capture threshold to ensure continued capture, this typically occurs somewhere between 50-100 mA. Transvenous Pacing: Please watch this excellent review of intravenous pacemaker placement by Dr. Jessica Mason with EMRAP here. Medications: Calcium-channel blockers (CCB) and beta blockers (BB) should always be considered in reversible causes of complete heart block. In 2015, the American Association of Poison Control Center database recorded 10,577 single-exposure cases of beta-blockers toxicity, making it fairly common. While BB overdose is more common, CCB is more lethal. Treatment with glucagon boluses start at 5 mg and should improve pulse and/or blood pressure within 15 minutes, and if not can be followed by an additional 5 mg. With improved pulse and blood pressure, the patient is then placed on a continuous infusion of 2-5 mg/hr aiming for mean arterial pressures of approximately 60 mmHg. If additional treatment is needed to achieve these therapeutic goals, IV calcium gluconate or chloride should be pushed slowly regardless of percent mixture with a limit of 3 grams total in adults. A more novel approach is high-dose insulin with euglycemia, start with a 1 unit/kg bolus followed by 0.5 units/kg/hr infusion until blood pressure stabilizes. Should have concomitant dextrose at 0.5 g/kg/hr, titrating to maintain glucose of 110 – 150 mg/dL. Atropine typically improves cardiac output by inhibiting the parasympathetics, however, in the setting of complete heart block this is rarely effective. Pressers should be considered, dopamine is useful in symptomatic bradycardia and dobutamine in cardiogenic shock while both can improve perfusion in the case of diminished cardiac output.
Prognosis:In patients exhibiting complete heart block, the outcome varies greatly depending on comorbidities, rate of escape rhythm, and etiology. While comorbidities such as amyloidosis will lead to chronic conduction abnormalities, acute conditions like injuries from block-related syncope can also worsen prognosis. Complete blocks without AV nodal involvement can be recognized by their slower rates and have better outcomes compared to those with AV node involvement who are more likely to progress to heart failure. Myocardial infarction can cause 3rd degree blocks that resolve within 48 hours, but the resulting sclerosis and damage to the heart can lead to future conduction abnormality. In addition, outcomes are worse in those patients experiencing an infarct-induced complete block. If the complete block is the result of an anterior wall MI then the outcomes are actually worse than if it had been the inferior wall.
Differential:Pathognomonic EKG findings often help eliminate other possibilities in the differential. Initial presentation may include syncope, palpitations, chest pain, or shortness of breath. With this presentation, it is necessary to rule out other cardiac etiologies. Several emergent possibilities include other cardiac blocks, infarct, angina, and iatrogenic injury. Additional systemic etiologies that can present with cardiac symptoms include Lyme disease, sarcoidosis, and thyrotoxicosis. Identifying the underlying cause of a third degree heart block can be difficult especially in cases of underlying pathophysiology. A detailed patient history and EKG are typically sufficient in narrowing down the differential.
- Various types of blocks; 1st degree vs 2nd degree (I & II), vs 3rd degree
- Myocardial infarction
- Lyme disease
- Iatrogenic presentation post catheterization/pacemaker placement/other cardiac surgery
- Cardiac sarcoidosis
- Toxicology (i.e. BB or CCB)
If the rhythm originates at or below the bundle of His, atropine is unlikely to be effective. The more distal conducting system is not likely to receive the increased rate from the SA node in the setting of block. On EKG, rhythms originating in the distal conducting system are noted by a wide QRS complex. Wide QRS complex=poor response to atropine.
Transcutaneous pacing is quick and most effective in the anterior/posterior position. It may require sedation and/or intubation.
Transvenous pacing is within the scope of practice of the ED physician and has many similarities to central line placement.
CCB/BB toxicity is most effectively managed with high dose insulin at 1unit/kg. This requires a concomitant glucose drip.
Hypoglycemia and hypokalemia are potential adverse events when using high dose insulin.
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Stolper K, Long B. Identifying Complete Heart Block and the use of Temporary Cardiac Pacing in the Emergency Department. emDOCs.net – Emergency Medicine Education. http://www.emdocs.net/identifying-complete-heart-block-and-the-use-of-temporary-cardiac-pacing-in-the-emergency-department/. Published April 22, 2017. Accessed January 14, 2020.
Aaron Wolfe, DO, FACEP
Joshua Bridge, MSII
Sarah Rokhlin, MSI