Introduction

“ECGs are the most useful tool that can provide the most information” [1].

Traditional ECG interpretation as taught in textbooks, study guides, and published algorithms may be based on detailed anatomy, electrical conduction patterns, and complex vector analysis. Common algorithmic treatment protocols for dysrhythmia are predicated on precise rhythm recognition and some clinical parameters [2-7]. These method scan prove challenging, particularly when a definite rhythm diagnosis is not immediately apparent. Rhythm interpretation is often the most difficult step in the process.  We propose a simplified approach to management of dysrhythmia that requires recognition of only a few simple factors: fast or slow, regular or irregular, wide or narrow complex, and present/absent P-waves. We also present a pharmacologic table of anti arrhythmic medications grouped by site of action and cardiac rate and/or rhythm-modifying characteristics.

Overview

The ECG is a static picture of the cardiac electrical conduction system. It is inexpensive, painless, and reproducible.  The conduction pathways can be affected by many different factors, therefore ECG interpretation must include clinical context. In the emergent setting, the exact rhythm diagnosis may not be as important as simply recognizing that the rate is slow or fast.

Along with a rhythm strip, the 12-lead ECG is crucial in identifying the heart rhythm.  It is important to remember a few rules when determining the origin of a rhythm. A “P” wave identifies organized atrial activation. The QRS represents ventricular activation. The QRS width (normal < 120 ms) and morphology describe the origin and pattern of ventricular activation. Recognizing P-QRS association, and QRS width and regularity differs in importance between bradycardia and tachycardia rhythms. This results in necessary decision point asymmetry between the “fast” and “slow” algorithms.

In tachycardia the priority is recognizing VT. P waves and their association to QRS complexes is likely to be too difficult at rapid ventricular rates; QRS width takes higher importance. P-QRS relationships can be very difficult to identify in all arrhythmias. In bradycardia P waves are more obvious yet their association to QRS complexes may be equally uncertain. When the P-QRS relationship is uncertain in slow rhythms, QRS regularity rather than width becomes a key decision point.

Treatment should be based primarily on patients’ overall clinical picture.  Using the simple flowcharts in Figures1 and 3, a practitioner can rapidly employ a safe and effective treatment strategy for every dysrhythmia regardless of precise diagnosis. Pharmacologic options may vary depending on local availability and expertise. Prompt electrical cardio version is indicated for any tachycardia patient with severe cardiac chest pain, hemodynamic compromise, or decreased mental status when the symptoms of instability are directly related to their rate or rhythm.

Ventricular fibrillation and Pulse less Electrical Activity (PEA) do not appear in our modified flowcharts. VF is easily recognized by the characteristic chaotic tracing and severely compromised patient. These patients require prompt defibrillation. A patient with PEA, will also present in extremis and should be treated immediately.  Littman, Bustin, and Haley describe the management of PEA based on the width of the QRS complex: narrow is a mechanical problem (Pseudo-PEA) and wide is a metabolic problem (True-PEA) [8]. This algorithm needs to be used while keeping in mind the “H’s and “T”s of PEA: Hypovolemia, Hypoxia, Hydrogen ions (acidosis), Hyper/Hypokalemia, Hypothermia, Toxins, Tamponade, Thrombosis of lungs or heart, Tension pneumothorax.

Pharmacology

Medication classes listed in flow diagrams are based on their rate and/or rhythm-controlling characteristics. We place less emphasis on the biochemical mode of action. Treatment is dictated as much by patient condition as by the arrhythmia mechanism. Frequently, a dysrhythmia is a bystander to concomitant illness. In this instance treatment should focus on the primary problem and not the dysrhythmia e.g. antibiotics and fluid resuscitation of sepsis, diuresis and preload reduction for heart failure, thrombolysis for pulmonary embolism, and angioplasty or thrombolysis for urgent acute coronary syndrome (ACS) [9-11].

When targeted treatment of the arrhythmia is appropriate, there are a number of medications available. The traditional system of classifying anti arrhythmic medications can be confusing and impractical for non-cardiologists [12-14]. We have organized these medications according to their most basic function: rate control or rhythm control. There is overlap in the functions of these agents and Table 1 lists common available drugs that would be used in the different clinical situations.

Chronotropes

Chronotropes increase heart rate. They are adrenergic stimulants that enhance all rhythm foci and circuits, and accelerate AV node conduction. Atropine is also a chronotrope but accelerates heart rate by inhibiting parasympathetic input to the sinus and AV nodes.

Rate controlling agents

The signs and symptoms of tachycardia are dictated mostly by the ventricular (pulse) rate rather than rhythm. Rate control refers to slowing of the ventricular rate. For supraventricular tachycardia, this is achieved by slowing conduction in the AV node. Calcium channel blockers (non-dihydropyridine class), beta blockers, and digoxin have this property.

Rhythm controlling agents

Rhythm controlling agents aim to terminate the underlying tachycardia mechanism. They act both in the atria and the ventricles and are classified by their site of action on the cardiac action potential. In accordance with the Vaughan Williams classification, Class 1 agents such asprocainamide, lignocaine (lidocaine), and flecainide block sodium channels. Class 3 agents like amiodarone and sotalol act primarily on the potassium channel. Both of these drugs have beta-blocking properties useful for rate as well as rhythm control.

It is important to note that in AV Node reentry Tachycardia (AVNRT) and AV reentry tachycardia (AVRT), so-called “rate control agents”(beta blockers and calcium channel blockers) will terminate the tachycardia mechanism. Adenosine which uniquely works at the adenosine type 1 receptor, also has this property [15]. Adenosine can be very effective at terminating node-dependent tachycardia, and is therefore a useful diagnostic tool in unmasking Atrial Flutter (AF) or Atrial Tachycardia (AT) when the tachycardia mechanism is unclear. In the setting of undifferentiated Broad Complex Tachycardia (BCT) that is not clearly Ventricular Tachycardia (VT), its short half-life allows safe administration even when the diagnosis is VT [16-20].

Magnesium is also included in this class. Unless contraindicated, specifically in severe renal impairment, it may have some efficacy at treating polymorphic VT and AF [21,22].

Treatment Algorithm: Bradycardia

Slow

The nature and urgency of treatment for bradycardia is determined by symptoms and rhythm. Prompt treatment is required if there is hemodynamic compromise, decreased mental status, or severe cardiac symptomology.  Marked sinus bradycardia is common in athletes, is typically asymptomatic, and rarely warrants treatment. Asymptomatic bradycardia in other clinical settings may signal clinical deterioration warranting prompt attention to the underlying cause, rather than to the heart rate or rhythm. Common scenarios include drug overdoses, hypoxia, hypothermia, hypothyroid, and acute coronary syndromes.  Other important clinical situations to consider are increased intracranial pressure as part of a Cushing reflex and hyperkalemia.

P Waves Present?

The presence of P waves represents atrial depolarization.  If P waves are connected to QRS complexes the rhythm is atrial in origin, either sinus or an alternative (ectopic) atrial focus. The absence of clear P waves may represent a rhythm originating at the level of the AV node (functional rhythm), or AF. Absence of P waves is the hallmark of AF, typically associated with an irregularly irregular QRS rate.

In bradycardia QRS regularity is more important than QRS width and is discussed in more details below. A wide QRS maybe one of four things: a ventricular rhythm, supraventricular rhythm with bundle branch aberrancy, ventricular pacing, or a supraventricular rhythm with pre-excitation (delta wave), but is seldom useful in determining the acute management of bradycardia. Aberrant conduction in the Purkinje system is commonly structural or metabolic as in electrolyte disturbance or digitalis toxicity. Lastly consider the reperfusion rhythm of accelerated idioventricular rhythm in the post thrombolytic patient [23].

Regularity and Relationship of P waves to the QRS complexes

The next step in determining the diagnosis and treatment depends on the association and frequency of the P wave to the QRS complex. The relationship of the P waves to the QRS describes the flow of the electrical impulse from the atria, through the junction and into the ventricles. If every QRS is consistently preceded by a P wave at the same rate then the bradycardia has a supraventricular origin like sinus bradycardia, sinus pause, or first degree AV block.

If every P wave is not followed by a QRS complex the rhythm is either not arising from the atrium, or it is an atrial rhythm with AV conduction disturbance. The AV node is exquisitely sensitive to autonomic modulation, and physiological AV block from excessive vagal stimulation is common. It typically occurs at night, can range from PR prolongation to AV dissociation, and almost never requires treatment. Pathological AV block is commonly due to atherosclerotic heart disease. First degree and Type 1 second degree AV block is disease limited to the AV node and is typically benign.

The priority in bradycardia is identifying complete (third degree) Atrio Ventricular (AV) block. A hallmark of complete AV block is the “regularity” of QRS complexes.

Group clustering of QRS complexes can identify second degree AV block. Type 1 block is characterized by progressive PR lengthening and RR shortening prior to non-conduction of a P wave; the resultant clustering of QRS complexes gives rise to the so-called “Wenckebach footprint.” (Figure 2) In Type 2 second degree block the PR interval is stable. The non-conducted P appears as a QRS “gap” with groups of conducted beats either side (Table 2).

Broadening of the QRS with, Type 2 second degree or third degree AV block, signal involvement of the distal His-Purkinje conduction system and warrant consideration for a pacemaker [24,25] Third degree AV block or “complete heart block” is particularly important to recognize. The hallmark of third degree block is complete AV dissociation, where P waves are independent of QRS complexes, with a ventricular escape rhythm that can be slow and unreliable. In atrial fibrillation the only clue will be slow, regular QRS complexes. Acute transcutaneous pacing or chronotropic medication like isoproterenol can be effective. Adrenergic stimulants should be used with caution in ACS. Atropine, acting on the AV node, will not improve block due to disease in the distal His-Purkinje system. Cardiology referral is mandatory with Type 2 second degree AV block or third degree AV block

Treatment Algorithm: Tachycardia

Fast

Tachycardic rhythms are those > 100 BPM, however they are seldom symptomatic and rarely life-threatening at rates < 120 BPM. It is important to consider that most tachycardias are secondary to non-cardiac causes. Common secondary causes include life-threatening emergencies such as cardiac tamponade and tension pneumothorax, hypoxia, pulmonary embolus, acute coronary syndrome, hypovolemia or blood loss. Also consider fever and infections, anemia, sympathomimetic syndromes, phaeochromocytoma, andhyperthyroidism. More benign conditions such as pain and anxiety will be diagnoses of exclusion. In an unwell patient, tachycardia <150 BPM is unlikely to be the root cause of the instability; rate or rhythm control is unlikely to be helpful and may be harmful [9-11].

Is the QRS wide or narrow?

After determining clinical stability, the next priority is recognizing QRS width. Recognising ventricular tachycardia is of utmost importance. If the QRS is narrow the diagnosis is unlikely to be VT.

Is the QRS regularand are P waves present?

The next question is determining QRS regularity and the presence of P waves. This determines the origin of the cardiac impulse. A narrow, regular QRS is most likely to be SVT. Identification of P waves is of secondary importance; they can be difficult to see and seldom influence acute management.  Treatment with AV blockade such as vagal stimulation by carotid sinus massage or a valsalva manoeuvre may be effective. If this is unsuccessful rate-control medication is the next appropriate step. This may terminate node-dependent processes (AVNRT or AVRT), or halt QRS complexes long enough to uncover rapid P waves in the case of atrial tachycardia or flutter.

Irregular narrow complex tachycardia is likely to be multifocal AT or AF. The presence of P waves may differentiate AT from AF but the priority for both is using rate control agents. Rhythm control may carry thromboembolic risks in the non-anticoagulated patient and additional precautions may be required but is beyond the scope of this manuscript. Rhythm control is of secondary importance in this setting.

Broad Complex Tachycardias (BCT) may be ventricular or supraventricular. In supraventricular tachycardia (SVT) the cause of broad QRS complexes is bundle branch aberrancy, ventricular pacing, or pre-excitation. In a regular BCT, VT can be difficult to distinguish from SVT with aberrancy. There is a significant amount of literature that describes specific ECG criteria and clinical characteristics to differentiate these rhythms [26-32] Adenosine can be helpful in this setting, and is a notable inclusion in our “fast” algorithm. Adenosine will not perturb VT, but is likely to terminate node-dependent tachycardia, or reveal the underlying atrial oscillations of AT or AF. If the diagnosis of VT is strongly suspected or remains uncertain rhythm agents such as procainamide or amiodarone should be used [32-34] Calcium channel blockers should be avoided because of a risk of enhancing conduction in an accessory pathway (thereby exacerbating antidromic AVRT or pre-excited AF), or causing hypotension in VT [35,36].

An irregular BCT may be multifocal AT or AF with pre-excitation, bundle branch aberrancy or ventricular pacing, or polymorphic VT. If the diagnosis cannot be clarified amiodarone is reasonable. Examination of the baseline, non-tachycardic ECG for pre-existing bundle branch aberrancy, AF, ventricular pacing, or pre-excitation can provide valuable clues. Cardioversion of AF to sinus rhythm (with anti arrhythmics or electrical cardio version) may carry thromboembolic risks in the non-anticoagulated patient as mentioned previously.

Summary

Arrhythmia management in the acute setting is based on rate, rhythm and clinical stability. Textbooks and standard published algorithms rely on a physician’s ability to correctly identify a cardiac rhythm. “ECG 123” algorithms aim to identify key diagnostic groupings with shared treatment options. These new algorithms allow for safe and effective dysrhythmia treatment based upon easily identifiable ECG characteristics. The medication classifications of chronotropes, rate controlling agents, and rhythm controlling agents provide easy and usable classification categories

Figure 1: Slow Algorithm.

Figure 2: Wenckebach footprint and example of small P waves.

Figure 3: Fast Algorithm.

Table1: Drug Classifications (Vaughan Williams classification)
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