When the heart gets the jitters

Approaching tachyarrhythmia in primary care

Revised 17.09.2026. This post has been updated to correct dosing inaccuracies (previously stated midazolam and procainamide doses) and to tighten some of the clinical reasoning. The original version is available on request.

You get called to see a patient who has presented acutely with palpitations. 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 as a blur — narrow spikes recurring at more or less equal, if frequent, intervals. Apart from that, little else registers except that the person in front of you is sitting up in bed and breathing, perhaps a little quickly, but looking otherwise fine.

But because of the nature of arrhythmias, your ears prick up, and you run through your options in this haemodynamically stable patient.

A systematic first look at the ECG

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

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

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

Ventricular vs atrial: why the distinction matters

A ventricular rhythm is trickier than an atrial one because it can more readily degenerate into a malignant rhythm. A slow ventricular escape rhythm — such as occurs below complete heart block once the higher pacemakers fail — may need pacing; ventricular tachycardia, by contrast, calls for urgent chemical or electrical cardioversion back to a more stable rhythm. Frequent PVCs, particularly in the context of ischaemia, are associated with an increased risk of VT — though it’s worth remembering that suppressing PVCs pharmacologically doesn’t reduce that risk, and in some settings (per the CAST trial) has worsened outcomes. They’re a marker to heighten vigilance, not a target to treat in themselves.

The first thought that enters your mind when confronted by a patient with an arrhythmia who is sitting up and talking is less about the current arrhythmia itself than about what may come next. The patient may be haemodynamically stable now — but will they be in 5 minutes, 10 minutes, or an hour’s time? They may appear haemodynamically stable, but are they stable electrophysiologically? Is there “heart jitter,” such that they’re just 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 is the excitability of their cardiomyocytes and the stability of their cell membranes — quite apart from the electrolyte concentrations of their blood plasma? In effect, what we’re asking is whether this patient has a structural problem with their heart and conducting system, or whether the aberrant conduction that led to the arrhythmia is a transient, immediately reversible phenomenon. That question, in essence, reduces to two others: is there a fixed structural or electrical substrate — is their electrical circuitry sound? — or is this a transient, reversible disturbance, whether from ischaemia (is their coronary reserve adequate?) or from a metabolic or electrolyte derangement destabilising the myocyte membrane?

Because life-saving treatment should still, where possible, be optimised even in an emergency, we try to infer from the little we glean from the monitor and from examination the unseen electrophysiology that should inform acute management. It’s the inference of the unseen from what is seen that guides treatment: is the patient on diuretics, suggesting possible hypokalaemia or another electrolyte disturbance? Are they also on digoxin, which can promote arrhythmia especially with hypokalaemia? Do they have diabetes, where cardiac ischaemia can present atypically or even silently? Is there evidence of atrial or ventricular ectopy? Furosemide use raises the suspicion of hypokalaemia; digoxin raises the risk of arrhythmia, particularly if hypokalaemia is also present; diabetes raises the possibility of atypical or silent ischaemia; and ectopics point to underlying electrical instability. Each is a “sign” pointing toward a specific unseen risk — electrolyte disturbance, ischaemia, or electrical instability — and together they can inform immediate management, even before the plasma electrolytes come back.

From clues to action

None of those clues confirm anything on their own — what they do is shift your pre-test probability, so that when you act empirically, you’re acting on a reasoned guess rather than a coin flip. The next step is to let that weighting drive pre-emptive action, before bloods are back:

• Suspected hypokalaemia or hypomagnesaemia (diuretic use, ECG features such as flattened T-waves or U-waves): empirical IV magnesium — and potassium if the ECG supports it — is low-risk and can be arrhythmia-terminating in its own right, so there’s little reason to wait for confirmation.
• On digoxin: hold further dosing, look for toxicity clues (visual disturbance, GI symptoms, characteristic ECG changes), and avoid further AV-node– or QT-depressing agents until levels return.
• Diabetic: lower your threshold for troponin and serial ECGs even in the absence of classic chest pain.
• Prominent ectopy with a rhythm that hasn’t yet declared itself: escalate monitoring, keep the defibrillator and pads close, and hold off on any agent that could be proarrhythmic in an unclarified rhythm.

Throughout, secure IV access and continuous cardiac monitoring, and choose your antiarrhythmic in light of the suspected substrate rather than by rhythm alone — for instance, avoiding a class III agent if an electrolyte-driven QT problem is already in play.

Only once you’ve weighted the differential this way does the haemodynamic state become the deciding factor in tempo:

So what? If a patient has new, rapid atrial fibrillation with mild symptoms but is otherwise fine and sitting up talking to you, you can wait for the electrolytes. But what if it’s an SVT and they’re breathless?

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

In the acute setting, where treatment is urgent, there often isn’t time to wait for investigations. Ostensibly, there is only you, the patient, a nurse, and a cardiac monitor that may double as a defibrillator. Once you’ve formed an expedient, summative view of the clinical situation, it’s best to consider — in toto — the options available and, by elimination, which is most appropriate to the case in front of you. What’s available in the first few minutes? The first half hour? The first few hours? We conceptually test these options against the scenario in front of us, hypothesise toward a next move, review it quickly in our mind, and — where it sits well with us — act. Then move to the next step, and the next, checking the response to each as time allows.

Is the arrhythmia primary or secondary?

An arrhythmia demands immediate assessment, but many of the presenting features could be either cause or effect, making that distinction difficult. Is this the primary problem — an established abnormal conducting pathway from prior infarct, scarred tissue, or an accessory pathway — or a transient phenomenon of another pathology, such as reversible ischaemia?

All things being equal, an ischaemic heart may acutely benefit from beta-blockade, whereas the case for beta-blockers is much less clear in, say, a patient with established first-degree heart block. If that first-degree block is instead a manifestation of acute inferior myocardial ischaemia, judicious beta-blockade may still be appropriate in the rapidly evolving picture — but not without risk, since it may worsen the conduction blockade.

Second-order questions to ask: – What is the clinical context? A now-bradycardic patient who is perfusing poorly is generally not a candidate for beta-blockade — even though beta-blockade might otherwise help if the underlying problem is ischaemia — because of the added negative chronotropic risk. – Is there evidence of reduced organ perfusion? – CNS: presyncope (dizziness/light-headedness), syncope, convulsions – Heart: chest pain (cause or effect?) – Ask after symptoms and signs of LVF (which itself raises arrhythmia risk): orthopnoea, PND, ankle oedema, fatigue – Lung: shortness of breath – Is there co-existing disease: IHD/CAD, COPD, chronic renal failure (deranged K⁺, Ca²⁺, Mg²⁺)? – Is there a family history of dilated cardiomyopathy, HOCM, or Brugada syndrome?

Symptomatic patients warrant more aggressive treatment.

Management options for tachyarrhythmia in primary care

Pharmacological options

Drug	Initial oral dose	For urgent rate control / IV therapy
Atenolol	50 mg once daily; titrate to 100 mg as required	5 mg IV slowly, titrate to effect; repeat if needed (max 10 mg)
Metoprolol	50 mg twice daily; titrate to 100 mg twice daily as required	2.5–5 mg IV slowly, repeated every 5 min, titrate to effect (max ~15 mg)
Diltiazem	30 mg three times daily; increase to 60 mg three times daily	Not available IV in Australia
Verapamil	—	2.5–5.0 mg IV slowly; repeat in 15–30 min as required (max 20 mg)
Digoxin	—	1000 μg in 3–4 divided doses over 24 hours; no advantage to IV over oral
Flecainide	50 mg twice daily (AF only — avoid in structural or ischaemic heart disease)	Not applicable
Sotalol	80 mg twice daily	—
Amiodarone	—	5 mg/kg IV over 20–120 min
Procainamide	—	17 mg/kg at max rate 50 mg/min, given as 100 mg every 5 min until arrhythmia suppressed, hypotension, QRS widens >50%, or total 17 mg/kg reached

Always weigh side-effect profile and contraindications for each agent. A supraventricular tachyarrhythmia can be managed with adenosine, a beta-blocker, or verapamil — but first exclude a high-degree heart block hidden within the rhythm, and make sure the patient isn’t in cardiogenic shock. A wide-complex regular rhythm can be treated with sotalol or, alternatively, amiodarone. In the acute setting amiodarone is comparatively safe but usually needs one or more (often two, occasionally three) 150 mg loading doses; it carries more longer-term consequences.

Physiological manoeuvres

Carotid sinus massage can be used as first-line treatment for a haemodynamically stable paroxysmal SVT, and may help clarify the type and origin of a narrow-complex tachycardia. It is contraindicated in patients at risk of stroke from carotid artery disease. Because listening for a carotid bruit lacks negative predictive value for carotid atheroma, patients with a history of IHD or peripheral arterial disease should ideally have carotid assessment (e.g. by POCUS) before the manoeuvre. It is also contraindicated in those with a history of a complicated carotid sinus massage, AMI within the last 3 months, or a history of ventricular arrhythmia.

Key pharmacology for tachycardia

Adenosine — a class V antiarrhythmic and first-line agent for narrow-complex tachycardias; generally safe. It slows conduction through the AV node and has mild vasodilating effects. It works within seconds, often with profound flushing and a transient bradycardic effect, wearing off within about 30 seconds. Avoid in sick sinus syndrome or third-degree heart block, and use with caution in second-degree block. Give 6 mg (0.1 mg/kg) as a rapid IV push through a large-bore cannula, and wait 1–2 minutes; if there is no change in rhythm, give 12 mg as a rapid IV push. The ALS tachycardia algorithm suggests a beta-blocker or calcium-channel blocker as second-line after adenosine.

Beta-blockers — sotalol is a non-selective beta-blocker with class II and III antiarrhythmic properties. Contraindicated in HR < 50 bpm, long QT, sick sinus syndrome, and cardiogenic shock. The only setting in which you’d use sotalol for a tachyarrhythmia in a patient with coincident second- or third-degree heart block is if they already have a pacemaker. Reserve sotalol for VT or a very symptomatic AF/flutter — “very,” because patients in flutter (and occasionally AF) often have an underlying second-degree block, and beta-blockade could precipitate bradycardia or complete block. Over 10% of oral sotalol users experience fatigue, dizziness, light-headedness, headache, weakness, nausea, shortness of breath, bradycardia (~16%), palpitations, or chest pain. A narrow-complex tachycardia is not an automatic candidate for beta-blockade despite what the ALS algorithm implies — you have to scrutinise the rhythm and contextualise it clinically. Sotalol can precipitate VT/VF in a patient whose rhythm is actually an SVT, and carries roughly a 1% risk of torsades de pointes; in a patient with a history of VT it should be used only in a hospital setting. (Mechanistically, sotalol also blocks potassium channels, delaying ventricular repolarisation — prolonging the QT interval.)

Calcium-channel blockers — verapamil (class IV) is indicated for SVT, or for prophylaxis against paroxysmal SVT. It reduces heart rate and contractility and causes vasodilation. Contraindicated in CCF, heart block, and wide-complex tachycardia; do not combine with a beta-blocker. Give 2.5–5 mg IV over 2 minutes, then 5–10 mg 30 minutes later if needed. Its effect can be reversed with IV calcium gluconate.

DC cardioversion

DC cardioversion aims to restore sinus rhythm in persistent arrhythmias. Energies below are indicative (monophasic-era figures) — confirm against your device and local protocol, as many modern biphasic defibrillators use lower or differently staged starting energies.

• Narrow, regular tachycardia: 100 J
• Narrow, irregular tachycardia: 200 J (or 4 J/kg)
• Wide, regular tachycardia: 100 J

For a narrow-complex rhythm, try adenosine, a beta-blocker, or a calcium-channel blocker first. Sotalol and procainamide can both prolong the QT interval. Alternatively, amiodarone 150 mg over 10 minutes can be given, often requiring a second dose. All patients should be anticoagulated for a minimum of 4 weeks post-cardioversion.

Procedure: 1. Place defibrillator pads to ensure current passes across the heart. 2. Attach the cardiac monitor and SpO₂; keep the resuscitation trolley close. 3. Sedate the patient — DC cardioversion is painful, and sedation is required in all but the most urgent situations. Have midazolam available at the bedside (titrated IV, typically ~0.02–0.05 mg/kg). 4. Set the defibrillator to “Sync” (cardioversion mode) and dial in the discharge energy (e.g. 150 J). 5. Clear everyone except oxygen, charge the defibrillator, confirm the area is clear, and deliver the shock.

Some hospitals perform cardioversion under transoesophageal echo (TOE) guidance to exclude a left atrial appendage thrombus.

Classifying antiarrhythmics: Vaughan Williams

Class	I	II	III	IV
Mechanism	Na⁺-channel blockade	β-receptor blockade	K⁺-channel blockade	Ca²⁺-channel blockade
Example agents	Quinidine, procainamide, disopyramide (Ia); lidocaine, mexiletine, tocainide (Ib); flecainide, encainide, propafenone (Ic)	Atenolol, propranolol, metoprolol	Amiodarone, sotalol, bretylium	Verapamil, diltiazem
Principal indications	Narrow-QRS tachycardia, AF, VA	Narrow-QRS tachycardia, AF, VA	AF, VA	Narrow-QRS tachycardia

Conditions to keep in mind

• Atrial fibrillation or flutter
• Atrial premature contractions (APCs)
• Paroxysmal atrial tachycardia (PAT)
• AV nodal re-entrant tachycardia (AVNRT)
• AV re-entry (AVR)
• Long QT syndrome
• Multifocal atrial tachycardia (MAT)
• Sick sinus syndrome
• Supraventricular tachycardia (SVT)
• Inappropriate sinus tachycardia
• Ventricular premature contractions (VPCs)
• Ventricular tachycardia

Approach at follow-up

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