When the heart gets the jitters

Tachyarrhythmia

There is wide variation in patient awareness of arrhythmias. Some cause few or no symptoms but are associated with an adverse prognosis while others, though symptomatic, are benign.

You get called to see a patient who has presented acutely with palpitations and when you get to the bedside, you find them on a cardiac monitor:

   beep … beep … beep …

You look at the rhythm on the monitor, and it reads a blur: there are narrow spikes recurring at more or less equal, if frequent, intervals and apart from that little else registers in your head than that the person in front of you is sitting up in bed and breathing, perhaps a little quickly, but looking otherwise fine.  beep … beep … beep …

But because of the nature of arrhythmias, your ears prick because you consider your options in this the haemodynamically stable patient:

1. You note the shape of the QRS complex.
2. You look at the regularity of the QRS, and note its rate.
3. You look for overt signs of ischaemia — at the ST-T segment and T-wave.
4. You then look at the P waves and their regularity (and rate)
5. Compare P-wave regularity to that of the QRS
6. Examine T-wave for evidence of a disturbed kalaemia (and other ionic disturbance)

Arrhythmias that cause haemodynamic upset are usually sustained bradycardias or tachycardias and may be life-threatening.

A ventricular rhythm is tricky because unlike atrial arrhythmias it can more readily track into a malign rhythm. A bradycardic ventricular rhythm (e.g. idioventricular rhythm, CHB) may well need pacing, while a ventricular tachycardia is a call for urgent chemical or electrical cardioversion to revert it to a more stable rhythm. In that case, frequent PVCs, for instance, can be an early warning of a VTac, especially in the context of ischaemia.

The first thought to enter your mind when confronted by a patient with an arrhythmia (i.e. where the mind instinctively first goes to) where the patient is sitting up and talking, is less to concern for the current arrhythmia itself than to anticipation for what may come next. For the patient sitting up, watching their (own) arrhythmia on a monitor, your thoughts are as much about anticipating and maybe preventing their next rhythm disturbance as it is about treating the present one: the patient may be haemodynamically stable now, but will they be in 5, 10 minutes or an hours’ time? The patient appear haemodynamically stable, but are stable electrophysiologically? Is there heart jittery so that they’re just the one beat away from a more significant arrhythmia.

By that I mean: what is the anatomy (and conductivity) of their cardiac conduction system; what is the physiology of their coronary circulation; what the electronegativity or excitability of their cardiomyocytes; what the stability of their cellular membranes … well apart even from the electrolyte concentrations of their blood plasma? What we in effect ask ourselves when confronted with such a patient is does this patient have a structural problem with their heart and the heart’s conducting system and is the evident aberrancy of conduction that led to the arrhythmia merely a transient and (immediately) reversible phenomena? And that thought in essence reduces down to whether the patient has structural heart disease or active myocardial ischaemia.

Is this patients coronary fractional reserve adequate and their electrical circuitry functioning adequately?

Because life-saving treatment should still, where possible, be optimized even in an emergency, we aim to infer from the little we glean from the monitor and from our examination of the patient the unseen electrophysiology that informs acute management. So it is the inferences that we make of the unseen from that which is seen that prompts treatment: things like; is the patient taking diuretics that would suggest they could have a hypokalaemia or other electrolyte disturbance; things like, is the patient (also) on digoxin which can promote an arrhythmia especially in the context of a hypokalaemia; things like, does the patient have diabetes where cardiac ischaemia can present atypically (even silently); things like the presence of atrial or ventricular ectopics. So furosemide, digoxin, diabetes, and ectopics can all be “signs” that the patient has an underlying electrolyte abnormality or an ischaemia; and these may be sign enough to inform immediate management — even before you see a print-out of the patient’s current plasma electrolyte concentrations.

The nature and severity of underlying heart disease is often of greater prognostic significance than the arrhythmia itself.

So what? If the patient has a new and rapid atrial fibrillation with some symptoms but otherwise fine and sitting up talking to you, you can wait for their electrolytes to come back. What if an SVT and they are breathless??

In the acute setting, where treatment is urgent, how to take these critical and as-yet unknown factors into account to help optimize immediate management? Do you take an educated guess? Do you draw inferences and extrapolate? Because you cannot wait in many cases to start treatment once results of the investigations are back.

Ostensibly, there is only you, the patient, a nurse, and a cardiac monitor (that may double as a defibrillator).

Once, then, you have made an expedient summative view of the clinical situation, best it is to consider in-toto what the options available to you are and by process of elimination consider which of these are most appropriate to the case in point. What are the possibilities and what the tools to draw upon to inform your possible intervention(s) in the first few minutes? What in the first half hour? And what in the first few hours, in which to respond?

Dizziness and syncope are common and may disqualify patients from driving or from certain occupations. These arrhythmias require urgent attention and, often, hospitalisation.

Momentarily, what we do is to conceptually test these options in our mind against the scenario in front of us and use that to hypothesize toward a next move. Quickly, we then review that intervention in our mind and where it rings true– where it sits well with us–move to it. Once acted upon, move then to the next; and then to the next. And so on. And, were time permits, look for the response to that first move, the second move, and so on.

What are the options available for managing a Tachyarrhythmia (in primary care)??

Pharmacologics

Drug doses for OFFICE BASED treatment of arrhythmias
Drug	Initial dose	For urgent rate control or when IV therapy is indicated
Atenolol	50 mg orally once per day; titrate to 100 mg as required	5 mg IV slowly, titrate to effect; repeat if needed (Maximum 10 mg)
Metoprolol	50 mg orally twice per day; titrate to 100 mg twice per day as required	1 mg IV slowly, titrate to effect (Maximum 10 mg)
Diltiazem	30 mg orally three times per day; increase to 60 mg three times per day	Not available in Australia
Verapamil		2.5–5.0 mg IV slowly; repeat in 15–30 minutes, as required (Maximum 20 mg)
Digoxin	1000 μg in 3–4 divided doses over 24 hours	No advantage over oral administration
Flecainide	50 mg orally twice per day (AF) 100 mg orally twice per day (VT)	Not applicable
Sotalol	80 mg twice per day
Amiodarone	5 mg/kg IV over 20–120 mins
Procainamide	Not applicable	17 mg/kg at maximum rate 50 mg/min; 100 mg every 5 minutes (Maximum 500 mg)

A supraventricular tachyarrhythmia can be managed with adenosine, atenolol, or verapamil. But first ensure there is no high-degree heart block hidden within the rhythm. And make sure the patient is not in cardiogenic shock. A wide complex regular rhythm can be treated with sotalol, or alternatively flecainide or amiodarone. In the acute setting, amiodarone is safe, but usually needs one or more (often two, and occasionally three) 150 mg loading doses. Amiodarone has more longer-term consequences.

Physiological maneuvers: Carotid sinus massage can be used as first-line treatment for a (haemodynamically stable) paroxysmal SVT. It may also help to clarify the type and origin of a narrow-complex tachycardia. Massage of the carotid sinus is contraindicated in patients who are at risk for stroke due to carotid artery disease. Because listening for a carotid bruit lacks negative predictive value for carotid atheroma, patients with a history of IHD or PAI should best undergo carotid examination by a POCUS before performing any carotid sinus massage. Massage of the carotid sinus is also contraindicated in those who have had a previous complicated carotid sinus massage, AMI within 3 months, or in those with a history of ventricular arrhythmia.

The Important Pharmacology

Tachycardia:

Adenosine: a class V antiarrhythmic, has first-line indication for narrow complex tachycardias, and is generally a safe drug to use. It slows conduction of the action potential through the A-V node and has mild vasodilating properties. It works instantly, often with profound flushing and bradycardic effect, and its effect is gone within 30 second. It should be avoided in sick sinus syndrome or third-degree heart block and used with caution in second-degree block. Give 6 mg (0.1 mg/kg) as a rapid IV push through a cubital line, and wait 1-2 minutes. If no change in rhythm, give 12 mg IVI push.

The ALS algorithm for tachycardia suggests that second-line after adenosine, a beta-receptor or calcium-channel blocker should be tried.

Beta-blocker: Sotalol is a non-selective beta-adrenergic receptor blocker, class II and III antiarrhythmic; C/I: HR < 50 bpm, long QT, sick sinus syndrome, cardiogenic shock. The only circumstance you would use sotalol to treat a tachyarrhythmia in a patient with coincident second (or third) degree heart block is if they have a pacemaker! Use Sotalol for a VT or a very symptomatic AF/Flutter. “Very” symptomatic because often patients in Flutter (and occasionally those in AF) have a second-degree heart block, and you could precipitate a bradycardia or third-degree block. Over 10% of oral sotalol users experience fatigue, dizziness, light-headedness, headache, weakness, nausea, shortness of breath, bradycardia (16%), a sensation of the heart beating too hard, fast, or irregularly, or chest pain. A patient with a narrow complex tachycardia is not then an automatic candidate for beta-blockade, despite what the ALS algorithm says. You have to scrutinise the rhythm. You have to contextualise the tachycardia within the clinical situation. Sotalol can cause VT/VF in those with an SVT. In a patient with a history of VT, sotalol should be used only in a hospital setting., as its use has been associated with a 1% risk for torsades de pointe. (That is, Sotalol also acts on potassium channels and causes a delay in relaxation of the ventricles. By blocking these potassium channels, sotalol inhibits efflux of K⁺ ions, which results in an increase in the time before another electrical signal can be generated in ventricular myocytes. Q on T).¹

Calcium-blocker: class IV antiarrhythmic, verapamil is indicated for treatment of SVT or for the prophylaxis against a paroxysmal supraventricular tachycardia (PSVT). Verapamil will cause a decrease in HR, cardiac contractility, and vasodilatation. It is c/i in CCF, heart block, and a wide complex tachycardia. Do not use together with a beta-blocker. Give 2.5-5 mg IV over 2 minutes, then 5-10 mg IVI 30 minutes later. Its effect can be reversed with the intravenous administration of calcium gluconate.

Cardioversion: DC cardioversion aims to restore sinus rhythm among patients in persistent arrhythmias. Cardiovert with 100J (narrow, regular) or 200J [4J/kg] (narrow irregular) tachycardia; 100J for a wide regular tachycardia. Give adenosine if narrow complex, beta-blocker or CCB. Sotalol can cause prolonged QT, as can Procainamide. Alternatively, amiodarone 150 mg over 10 minutes can be given. Often, a second dose is required. All patients should be anticoagulated for a minimum of 4 weeks post DC cardioversion.

1. Place Defibrillator pads on chest in a manner that ensures the current will pass across the heart:
2. Attach cardiac monitor / SpO2 — keep resusc trolley handy
3. Sedate patient: due to pain associated with DC cardioversion, patients must be sedated in all but the most urgent situations. Have the following drugs readily available at the bedside:
   • Midazolam: 0.2 mg per kg
   • Turn Defibrillator on to “Sync” (i.e. cardioversion setting)
   • Dial discharge energy and set to 150J
   • Everyone except Oxygen away
4. Charge defibrillator
   • Ensure everyone is clear
5. Apply the DC Shock

N.B. In some hospitals, cardioversion is done under transoesophageal echo (TOE) guidance to exclude any right atrial thrombus.

Is the arrhythmia primary or a secondary phenomena?

A cardiac arrhythmia calls for an immediate assessment of the situation, but many of the presenting features could be either cause or the effect of the arrhythmia, rendering disambiguation b/n cause and effect difficult: is the arrhythmia the primary problem (of an established abnormal conducting pathway, e.g. from prior infarct/scarred tissue, accessory pathway) or some transient phenomenon of another pathology: e.g. reversible ischaemia? All things being equal, an ischaemic heart may benefit acutely from beta-blockade where, prima facie, the case for beta blockers in, say, a patient with established first-degree HB is less clear.

If the first-degree HB is the phenomena of (acute) inferior myocardial ischaemia, judicious use of a beta blocker in the rapidly evolving scenario may yet be appropriate but not without risk, for it may yet complicate the clinical picture to cause further conduction blockade.

What do you do?

How to decide in the acute setting what to do? You also have to look at what might be considered “second-order” variables in the context of the presentation of arrhythmia with heart block: i.e. what is the clinical context? If the patient now bradycardic is perfusing poorly then on the face of it beta-blockade might best be avoided–they could still help if the originating problem is an underlying ischaemia, but the negative chronotropic effect of beta blockers here carries some risk.

Is there evidence of reduced organ perfusion?

• CNS:
  • presyncope: dizziness/ light-headedness
    • syncope: blackout
    • convulsions: shake
• Heart: chest pain (cause or effect?)
  • ask after symptoms and look for signs of any LVF, which incurs an increased risk of arrhythmia
    • orthopnoea
    • PND
    • ankle oedema
    • fatigue
• Lung: SOB

Symptomatic patients warrant more aggressive treatment.

Is there co-existent disease:

• IHD / CAD
• COPD
• CRF: K⁺, Ca²⁺ (Mg²⁺)

Look for (ask after) a Family History of:

• Dilated CM
• HOCM
• Brugada Sx

Approach to take at follow-up:

1. Establish probable cause that an arrhythmia exists
2. Determine whether there may be a risk of dying
3. Document the arrhythmia
4. Consider the anti-arrhythmic pharmacological options

Class	I			II	III	IV
Pharmacological effect	Na-channel blockade			b-receptor blockade	K+-channel blockade	Ca2+-channel blockade
agents	quinidine	lidocaine	flecainide	atenolol	amiodarone	verapamil
	procainamide	mexiletine	encainide	propranolol	sotalol	diltiazem
	disopyramide	tocainide	propafenone	metoprolol	bretylium tosylate
		ethmozin
		phenytoin
EPS effect	Ia	Ib	Ic
AH	↑ ↓	0	↑	(↑)	↑	↑
HV	↑	0	↑ ↑	0	↑	0
QRS	↑	0	↑ ↑	0	0	0
QT	↑	0	↑	0	↑ ↑	0
Accessory Pathway conduction	↑	↑ or 0	↑	0	↑	0
Atrial ERP	↑	0	↑ or 0	0	↑	0
Principal Clinical Indications	VA Narrow QRS tachycardia AF	VA	VA Narrow QRS tachycardia AF	VA AF	VA Narrow QRS tachycardia AF	Narrow QRS tachycardia

Conditions:

• Atrial Fibrillation or Flutter
• Atrial Premature Contractions (APCs)
• Atrial Tachycardia, paroxysmal (AT, PAT)
• Atrioventricular Nodal Re-entrant Tachycardia (AVNRT)
• Atrioventricular Re-entry (AVR)
• Long QT syndrome
• Multifocal Atrial Tachycardia (MAT)
• Sick Sinus Syndrome
• Supraventricular tachycardia (SVT)
• Syndrome of inappropriate sinus tachycardia
• Ventricular premature contractions (VPCs)
• Ventricular tachycardia

References