Management of Arrhythmic Patients in the Emergency Department: General Principles

Look for:

shock signs

Chest pain

Respiratory distress

Do:

Monitor the patient, IV line, blood samples

Ensure patent airway and ventilation and give oxygen (if needed)

Support perfusion pressure (use mean arterial pressure as a good index)

12-leads ECG; gather medical history

Treat reversible causes

Patient’s ECG, blood pressure, and O₂ saturation (sat O₂) should be immediately put under continuous monitoring and intravenous line with blood samples provided. Airways have to be kept patent, breathing assisted, and oxygen given if sat O₂ is below 94 %. A 12-lead ECG should be obtained as soon as possible for a correct diagnostic evaluation of the arrhythmia. Medical history must be gathered.

Should a cardiac arrest occure, advanced life support protocols have to be applied.

Hemodynamic instability, defined as an acute organ failure or a near-cardiac arrest situation, may be due to tachy- or bradyarrhythmia.

In the event of a tachyarrhythmia, an immediate defibrillation or synchronized cardioversion should be done regardless of the arrhythmia mechanism.

In addition, bradyarrhythmias may lead to a severe decrease in cardiac output, causing hemodynamic instability with hypotension, mental dizziness, decreased consciousness level, cyanosis, dyspnea, etc.

A treatment based on atropine, catecholamine, or an electrical stimulation may be helpful or even lifesaver [1, 2].

1.2.1 Tachyarrhythmia

By definition, tachycardia is a heart rate exceeding 100 beats per minute.

By far the most common tachycardia diagnosed in the emergency department is sinus tachycardia.

In the healthy patient, it is a physiological response to physical stress or anxiety. Sinus tachycardia is also a normal condition during the pregnancy. In most other cases, it is due to an underlying pathological condition (e.g., fever, dehydration, anemia and hypoxia, ACS, P.E., hyperthyroidism, high blood pressure, smoking, alcohol, beverages containing caffeine, medication side effects, abuse of recreational drugs, such as cocaine, or imbalance of electrolytes) [3].

“Appropriate” sinus tachycardia offsets an underlying condition, while “inappropriate” sinus tachycardia can be a consequence of deficit of vagal tonus or a hyperactivity of/excessive sensibility to the sympathetic nervous system. During sinus tachycardia heart rate is usually lower than 140–150 bpm, even if, in young people under extreme stimulation, it can exceed 220 bpm. Typically, in sinus tachycardia, the P wave is positive in inferior and lateral leads (as in sinus rhythm). As sympathetic activation increases AV conduction, PR interval is shorter than in sinus rhythm; therefore, with few exceptions, the coexistence of long PR and sinus tachycardia is unlikely, even in patients with I degree AV block during normal sinus rhythm, and usually suggests other mechanisms of tachycardia, as atrial tachycardia or atrial flutter, possibly with 2:1 conduction and a P wave hidden within the QRS complex.

In order to identify if the tachycardia is the main cause of the patient’s symptoms, a complete physical examination, blood draw to test metabolic and renal function, emogasanalysis (EGA), 12-lead ECG results and medical history should be performed and any potential reversible causes should be corrected.

Usually tachycardia may be considered as hemodynamically significant when they exceed 150 bpm.

However, it is important to remark that even frequencies lower than 150 bpm may cause hemodynamic compromise, mainly if it is sustained for a prolonged time and/or coexists with an underlying heart disease, leading to chest pain, altered mental status, pulmonary edema, or cardiogenic shock, requiring an emergency electrical cardioversion.

It is advised to perform an effective pre-procedural sedation if the patient is conscious, although hemodynamically unstable.

1.2.1.1 Procedural Sedation/Anesthesia During Cardioversion

Sedative or dissociative drugs, coupled with or analgesics, are used to relieve the patient from unpleasant procedures. Many of these drugs can lead to central nervous system and cardiac and/or respiratory depression. Given the potential risks, regulatory agencies are debating about the medical privileges needed to perform this procedure, particularly about the presence of an anesthesiologist during the procedure.

Recommendations for a safe employ consist of a proper setting (ECG, respiratory rate, sat O2, NIBP monitoring, advance life support trained personnel, devices for life support) and frequent reevaluations (prior to, during, and after procedure); trained staff should choose appropriate drugs and dosing depending on the distinctive features of each patient.

A growing literature highlights the safety of administration of ketamine, midazolam, fentanyl, propofol, and etomidate in the ED [4–6].

Equipment and supplies: oxygen, suction, reversal agents, advanced life support medications and equipment, defibrillator, and CO₂ capnography. An IV line should be set; reversal agents should be available whenever opioids and benzodiazepines are administered.
Personnel: during the procedure, personnel dedicated to patient monitoring should focus only to the sedation and not to other tasks.
Training: the physician should know drug’s pharmacology of the agents used and their antagonists. Personnel with experience in Advanced Cardiac Life Support should be present.
Drugs. Electrical cardioversion is a brief but painful procedure. Light sedation is inadequate for a pain-free relaxed patient. Therefore, a moderate to deep sedation and analgesia or general anesthesia is required. In most US and Europe hospitals, emergency physicians are not allowed to provide general anesthesia, so sedation can be the only option if an anesthesiologist is not present. Drugs: midazolam and fentanyl are commonly used, but their long-lasting effects make them not handy or straight dangerous. Instead, for a brief and titratable deep sedation, it makes more sense to employ propofol, etomidate, or methohexital combined with fentanyl. There are contradictory statements from the American Society of Anesthesiologists (ASA) guidelines about authorization for propofol use by emergency physicians. Evidence is accumulating that non-anesthesiologist-administered propofol sedation has a safety and efficacy profile comparable or superior to that provided by benzodiazepines with or without opioids. Medications should be administered gradually, allowing sufficient time between dose and effect assessment. Concurrent administration of sedative and analgesic drugs requires evaluation on dose reduction.
Recovery: observation should be prolonged until there are no more risks for cardiorespiratory depression. Medical institution should set up appropriate discharge criteria [4–6].

1.2.1.2 Cardioversion/Defibrillation

If cardioversion is chosen, set the defibrillator into the synchronized mode. This to avoid shock delivery during ventricular “electric vulnerability” period (apex and descending branch of T wave), a potential trigger of ventricular fibrillation. Defibrillation, used for interruption of pulseless VT, VF, and torsade de pointes synchronization, should be avoided, as QRS complexes may not be identified.

Emergency physician should be trained to recognize the presence of the P wave and distinguish between narrow-complex (supraventricular) tachycardia and wide complex tachycardia, which in condition of urgency should be considered and treated as ventricular tachycardia.

The different types of tachycardia can be treated with different energies:

As recommended by international guidelines for regular narrow-complex tachycardia, the initial energy cardioversion should be 50–100 J with biphasic defibrillators and 200 J if monophasic (Class IIa, LOE B).
For irregular narrow-complex tachycardia, the recommended initial biphasic energy is 120–200 J (Class IIa; LOE A).
Regular wide complex tachycardia may resolve after discharge at 100 J by both biphasic and monophasic defibrillators (Class IIb, LOE C).

Anyway, if the first shock is inadequate to resolve the arrhythmia, increase energy “in a stepwise fashion.”

When using monophasic defibrillators, initial energy should be set to 200 J, proceeding in a stepwise fashion in the event of failure.

The irregular wide complex tachycardia should be treated with high-energy unsynchronized shock (i.e., defibrillation), because of the difficulty of the machine to distinguish between the QRS complex and T wave.

Even if there were doubts whether the tachycardia is monomorphic or polymorphic, the shock should not be delayed and a high-energy unsynchronized shock must be delivered.

In the unstable patient (if not hypotensive) presenting with a regular narrow QRS complex tachycardia, adenosine is safe to be used while cardiac electrical cardioversion is being set up both for therapeutic (in case of tachycardia involving the AV node as a part of the reentry circuit) and diagnostic (in case of atrial arrhythmias, unmasking atrial activity slowing AV conduction (Class IIb (LOE C)).

If the patient with tachycardia is stable, the emergency physician will have more time for a correct diagnosis and to choose the most appropriate therapy, with the help of a cardiologist if necessary.

After obtaining a complete medical history and a careful physical examination, QRS complex evaluation is needed. QRS duration should be measured in at least two orthogonal derivations: narrow-complex tachycardia (QRS duration <120 ms) should be always considered, by definition, as supraventricular: examples are sinus tachycardia, atrial fibrillation (AF), atrial flutter, AV nodal reentrant tachyarrhythmia (AVNRT), tachyarrhythmia mediated by accessory pathways, atrial tachycardia, multifocal atrial tachycardia (MAT), and junctional tachycardia (rare in adults) .

Based on ECG findings, the regularity of RR intervals and the relationship between P waves and QRS complexes along with the timing of onset of tachycardia may help to differentiate among the various kinds of supraventricular tachyarrhythmia.

If the anamnesis highlights sudden onset of palpitations and its rapid resolution, it is likely to be atrial fibrillation, atrial flutter, AVNRT, atrioventricular reciprocating tachycardia, and atrial tachycardia. Instead, sinus tachycardia, permanent atrial fibrillation, and permanent flutter, together with MAT and premature atrial contractions, show symptoms that arise and resolved more gradually [7].

P waves immediately preceding the QRS complexes address the ED physician’s diagnosis to sinus tachycardia, atrial tachycardia, multifocal atrial tachycardia or multiple atrial premature contractions.

P waves following QRS complexes suggest atrioventricular nodal reentrant tachycardia, atrioventricular reciprocating tachycardia, or atrial tachycardia. However, heart rate can be high enough to have T waves overlapping the P waves.

If tachycardia has a narrow QRS complex, vagal maneuvers and, if ineffective, the administration of adenosine at doses of 6–12 mg, (always under cardiac monitoring) may have a dual purpose:

Diagnostic, since the increase of degree of AV block can unmask the nature of the underlying rhythm; a transient slowing of ventricular rate may highlight atrial fibrillation, atrial flutter, and sinus tachycardia, while there might not be any effect on multifocal atrial tachycardia or frequent atrial premature contractions.
Therapeutic, because the increase in parasympathetic tone may slow electrical conduction through the AV node interrupting reentrant arrhythmias involving tissues sensitive to vagal stimulation (AV nodal reentrant tachycardia, AV reciprocating tachycardia, and sometimes atrial tachycardia).

If vagal maneuvers and adenosine are unsuccessful in converting to sinus rhythm or atrial fibrillation and atrial flutter are diagnosed, it is recommended to administer:

Diltiazem (15–20 mg or 0.25 mg/kg IV over 2 min); if needed, after 15 min an additional IV dose of 20–25 mg (0.35 mg/kg) can be administered; the infusion dose is 5–15 mg/h, titrated according to heart rate.
Verapamil (2.5–5 mg IV bolus over 2 min); if no response and non-drug-induced adverse events occur, it is possible to repeat doses of 5–10 mg every 15–30 min up to a total dose of 20 mg.
Beta–blockers (metoprolol, atenolol, propranolol, esmolol, and labetalol).

These drugs are able to convert the reentrant tachycardia by acting on the nodal tissue or slowing the ventricular response in case of other supraventricular arrhythmias [1].

In patients with atrial fibrillation/flutter/tachycardia lasting more than 48 h (or if the onset of the arrhythmia is unknown), electrical or pharmacological cardioversion should not be attempted in absence of adequate anticoagulation in the preceding 3 weeks. Otherwise, when prompt restoring of sinus rhythm is needed or preferred, cardioversion can be done after excluding the presence of thrombi in the left atrium by transesophageal echocardiography (Class IIa, LOE B) [8].

In most cases the patient with narrow QRS tachycardia is treated in ED, restoring the RS or starting a therapy aimed to control the heart rate, and resigned to be entrusted to the outpatient cardiologist, who will complete the diagnostic process and improve, if necessary, the treatment started in the emergency department.

Handling of wide-QRS complex tachycardia (>120 ms) is different. These tachycardias cannot be treated in PS only but require both an initial cardiac evaluation in the emergency department, including a careful analysis of the ECG and echocardiography, and hospitalization in the specialist department.

1.2.1.3 When should the Cardiology Consultant be called?

Cardiologist called in ED for a patient with a wide-QRS complex tachycardia has a daunting task. In fact, a mistaken diagnostic may lead to disastrous effects in terms of prognosis.

A wide-complex tachycardia can be:
Ventricular tachycardia.
Supraventricular tachycardia in a patient with preexisting bundle branch block.
Tachycardia-dependent bundle branch block (aberrancy).
Tachycardia caused by drug that have a widening effect on QRS.
Atrial arrhythmias in the presence of ventricular pre-excitation.

In the diagnostic path of a wide-QRS complex tachycardia, attention must be paid to the clinical examination (variability of the first tone and amplitude variable radial pulse lay for the presence of AV dissociation) and the careful analysis of the ECG [9].

Here is a summary of some general criteria that can help the cardiologist identify the origin of tachycardia (for detailed discussion of the ECG, see Chap. 6):

Search if the electrical activity of the atria is present; P waves, independent of QRS, are separated by constant intervals, paying more attention in derivation II and V1, where these waves can be easier to find.

If some ventricular impulses are not conducted to the atria and the QRS/P ratio is greater than 1, a diagnosis of ventricular tachycardia can be made.

Small deflections, fitting in a rhythmic manner inside the QRS complexes, suggest the presence of underlying sinus P waves when their rate is lower than the ventricular rate. Hence, a diagnosis of ventriculoatrial dissociation and therefore of ventricular tachycardia can be made. If there is a mathematical relationship between ventricular and atrial electrical activity, a retrograde ventricular-atrial conduction is likely, as it can be found in about 50 % of cases..

In presence of a clear QRS/P ratio = 1, the diagnosis may be more difficult; it may be expression of atrial tachycardia, sinus rhythm with aberrant conduction, nodal reentrant tachycardia, automatic junctional tachycardia, reciprocating orthodromic tachycardia with aberrant conduction, or ventricular tachycardia with 1:1 retrograde conduction.

Search for “concordance” aspect of QRS in the precordial leads. The presence of concordance suggests that the tachycardia has a ventricular origin. Common definitions are “positive concordance” if the QRS complex is “R wavelike” from V1 to V6 and “negative concordance” in the presence of a “QS-like” morphology from V1 to V6.

Cardiologists must remember that although a negative concordance is absolutely specific for VT, the positive could, in rare cases, be expression of a pre-excited tachycardia due to a left posterior Kent bundle (pre-excited tachycardia with conduction through ancillary pathway).

As stated by Brugada et al., in the diagnostic algorithm of regular wide-QRS complex tachycardia, the presence of RS complexes (R waves followed by S wave) in precordial leads suggests a diagnosis of VT when the interval between the beginning of the R wave and nadir of the S wave is >100 ms [10].

Only gold members can continue reading. Log In or Register to continue