EKG: From Ion Channels to Rhythm Interpretation

The cardiac action potential, phase by phase

An ECG is a voltmeter taped to the chest. Everything it draws is the summed movement of ions across cardiac cell membranes. So we start there.

Resting membrane potential: why −90 mV

At rest, a ventricular myocyte sits at about −90 mV — the inside is negative relative to the outside. Two things create it:

1. The Na⁺/K⁺-ATPase pumps 3 Na⁺ out for every 2 K⁺ in, burning ATP. Net: one positive charge leaves per cycle, and steep gradients are built — potassium high inside, sodium high outside.
2. The membrane is far more permeable to K⁺ than to Na⁺ at rest (through inward-rectifier K⁺ channels, I_K1). Potassium leaks out down its gradient, leaving negative charge behind, until the electrical pull inward balances the chemical push outward — the potassium equilibrium potential, near −90 mV.

The five phases (ventricular myocyte)

Why the plateau exists, and why it matters

Skeletal muscle has no phase 2. Cardiac muscle does, because L-type calcium channels stay open for a few hundred milliseconds.

Two consequences, both clinically enormous:

1. Calcium enters and triggers contraction. That calcium binds ryanodine receptors on the sarcoplasmic reticulum, releasing a much larger calcium store — calcium-induced calcium release — which binds troponin C and permits crossbridge cycling.¹ The plateau is literally the electrical event that causes the mechanical one. It is also the phase every calcium channel blocker acts on.

2. The refractory period is enormously long. During phases 0–2 and much of 3 the cell cannot be re-excited, because the fast sodium channels are inactivated and require repolarization to reset. Cardiac muscle therefore cannot tetanize — it must relax and fill between beats. Skeletal muscle can; a heart that could would be fatal.

Mapping the ECG to the action potential

The surface ECG is not the action potential of one cell. It is the summed electrical activity of millions of cells, recorded from the body surface.

Nodal cells are different

SA and AV nodal cells have no fast sodium channels and no stable resting potential. They sit around −60 mV — too depolarized for sodium channels to reset — and depolarize on calcium instead.

Three clinical facts fall straight out of this:

• Calcium channel blockers and beta blockers slow the SA and AV nodes by acting on the currents nodal cells actually use. Sodium channel blockers barely touch them.
• Nodal conduction is slow — the phase 0 upstroke is gradual — which is exactly why the AV node introduces the delay that lets the atria empty before the ventricles fire.
• Sympathetic stimulation raises cAMP, which binds HCN channels directly and steepens phase 4, reaching threshold sooner. That is the whole mechanism of β-agonist tachycardia. Vagal stimulation and adenosine do the reverse.

Automaticity and the conduction system

The hierarchy of pacemakers

Every cell with phase-4 automaticity is a potential pacemaker. The fastest one wins, because it depolarizes the rest before they reach their own threshold — overdrive suppression.

This single table explains almost every escape rhythm you will see. A junctional escape at 45 in a patient whose sinus node failed is not a disease — it is a backup system doing exactly what it was designed to do. A ventricular escape at 25 is the last line of defense, and it is unreliable.

The route, and the timing

1. SA node — in the high right atrium near the superior vena cava. Depolarizes spontaneously.
2. Atrial myocardium — spreads cell to cell through gap junctions, with preferential internodal pathways. Produces the P wave (<0.12 s, <2.5 mm).
3. AV node — the only electrical connection between atria and ventricles in a normal heart. Deliberately slow (~0.04 m/s), producing the PR segment delay of roughly 100 ms so that atrial contraction completes before ventricular systole begins. Also acts as a rate filter, protecting the ventricles in atrial fibrillation and flutter.
4. Bundle of His → right and left bundle branches (the left dividing into anterior and posterior fascicles) → Purkinje fibers. Conduction here is fast (2–4 m/s), which is why a normal QRS is under 0.12 s: the entire ventricular mass is activated nearly simultaneously.

The University of Minnesota Atlas of Human Cardiac Anatomy conduction system tutorial shows this pathway in reanimated human hearts, including the anatomy of the AV node and bundle branches that the ECG intervals correspond to.²

Why the QRS is wide when it is wide

A wide QRS means ventricular activation did not use the His–Purkinje highway.

• Bundle branch block — one branch is blocked, so that ventricle is activated late, cell-to-cell from the other side. Slow route, wide complex.
• Ventricular origin (PVC, VT, ventricular pacing) — the impulse starts in myocardium and spreads cell to cell throughout. Slowest, widest.
• Aberrancy — a supraventricular beat arriving while one bundle is still refractory, conducting down the other. Usually right-bundle morphology, because the right bundle has the longer refractory period.
• Hyperkalemia, sodium channel blocker toxicity — the tissue itself conducts slowly because sodium channel availability is reduced. This widens every complex, everywhere, and is a metabolic emergency rather than a conduction-system problem.

Blood supply, and why inferior MIs cause bradycardia

Coronary anatomy predicts which conduction structures fail with which infarct:

• SA node artery — from the RCA in about 60% of people, the left circumflex in about 40%.
• AV node artery — from the RCA in roughly 80–90% (right dominance).
• Bundle branches — largely from LAD septal perforators.

Therefore:

• Inferior MI (RCA) → sinus bradycardia and AV nodal block, typically transient, narrow-complex, atropine-responsive, and often accompanied by nausea and vomiting from vagal stimulation (the Bezold–Jarisch reflex). Frequently resolves with reperfusion.
• Anterior MI (LAD) → infranodal block, typically wide-complex, atropine-unresponsive, and ominous — it means a large septal infarct has destroyed the bundle branches themselves. These patients need pacing, and their mortality is high.

Escape, ectopy and reentry: three mechanisms

Enhanced automaticity — a focus fires faster than the sinus node. Causes: catecholamines, hypoxia, ischemia, hypokalemia, hypomagnesemia, stimulants, digoxin toxicity, stretch.

Triggered activity — afterdepolarizations riding on the preceding action potential.

• Early afterdepolarizations (EADs) occur during phase 2/3, are favored by prolonged repolarization, and cause torsades de pointes. This is why long QT is dangerous.
• Delayed afterdepolarizations (DADs) occur after repolarization is complete, are caused by calcium overload, and are the mechanism of digoxin-toxic and catecholamine-driven ectopy.

Reentry — the mechanism of most sustained tachyarrhythmias. It requires three ingredients: two pathways with different conduction velocities and refractory periods, a unidirectional block in one of them, and slow enough conduction in the other that the first pathway has recovered by the time the impulse comes back around. The impulse then circles indefinitely.

That description covers AVNRT (dual AV nodal pathways), AVRT/WPW (an accessory pathway), atrial flutter (a macro-reentrant circuit around the tricuspid annulus), and most monomorphic VT (a circuit around a scar). It also explains why the treatments work: adenosine and vagal maneuvers break AV-nodal reentry by transiently blocking one limb of the circuit; cardioversion depolarizes the entire circuit at once so it has nowhere to travel.

Vectors: why a lead sees what it sees

The one rule that makes leads make sense

That is the entire theory. Everything else — axis deviation, bundle branch morphology, reciprocal changes, lead placement errors — is that rule applied.

The twelve leads and where they look

Limb leads (frontal plane) — six leads looking at the heart from the front:

Precordial leads (horizontal plane) — six leads looking across the chest:

Normal R wave progression

Across V1 → V6, the R wave should grow and the S wave shrink, with the transition (R = S) at V3 or V4. That progression is the horizontal-plane vector rotating from rightward-anterior (septal depolarization, giving the small r in V1) to leftward-posterior (the LV free wall dominating).

• Poor R wave progression — anterior MI, LVH, LBBB, COPD, or lead misplacement.
• Early transition (tall R in V1–V2) — posterior MI (a mirror image), RVH, WPW type A, RBBB, or a normal variant.

Reciprocal changes: the mirror

Because leads look at the heart from opposite directions, injury current that elevates the ST in one region depresses it in the opposite one. Inferior leads (II, III, aVF) are reciprocal to lead aVL and lead I; anterior leads are reciprocal to the inferior leads.

Posterior and right-sided MI: the leads you have to add

The standard 12 leads do not look directly at the posterior wall or the right ventricle.

• Posterior MI appears as a mirror image in V1–V3: ST depression with tall R waves and upright T waves. Confirm with posterior leads V7–V9 (posterior axillary line, mid-scapular line, and left border of the spine, at the V6 level), where you look for 0.5 mm of ST elevation.
• Right ventricular MI complicates up to 40% of inferior MIs. Confirm with V4R — the right-sided mirror of V4. ST elevation there indicates RV infarct.

Axis: where the mean vector points

The mean QRS axis is the average direction of ventricular depolarization in the frontal plane. Normal is −30° to +90°.

The two-lead quick method, using leads I and aVF:

The systematic read

Interpretation errors are almost always errors of sequence — someone spots a dramatic finding and stops looking. The fix is a fixed order, every time.

The paper

Standard speed 25 mm/sec, standard gain 10 mm/mV.

• Small box = 1 mm = 0.04 sec horizontally, 0.1 mV vertically
• Large box = 5 mm = 0.20 sec horizontally, 0.5 mV vertically
• Five large boxes = 1 second. Thirty large boxes = 6 seconds.

Check the calibration mark on every tracing. Half standard gain (5 mm/mV) halves every amplitude and can hide LVH or make ST elevation look trivial; double standard does the reverse.

Rate

• Regular rhythm: 300 ÷ (number of large boxes between R waves). The sequence to memorize: 300, 150, 100, 75, 60, 50 for 1 through 6 large boxes.
• Irregular rhythm: count QRS complexes in a 6-second strip and multiply by 10. Never use the box method on an irregular rhythm.
• Count atrial and ventricular rates separately whenever they might differ — this is what reveals complete heart block, atrial flutter with variable conduction, and VT with AV dissociation.

The seven-step read

1. Rate. Atrial and ventricular, separately.

2. Rhythm. Regular, regularly irregular, or irregularly irregular?

3. P waves. Present? One per QRS? Same shape? Upright in II (they should be, since atrial depolarization moves toward lead II)? A P wave inverted in II means the atria were depolarized from below — a junctional or low atrial origin.

4. PR interval. Normal 0.12–0.20 sec (3–5 small boxes). Constant, lengthening, or variable?

• Short PR with a delta wave → pre-excitation (WPW)
• Long PR → first-degree AV block
• Lengthening → Wenckebach
• Variable and unrelated to QRS → complete heart block

5. QRS duration. Normal < 0.12 sec (< 3 small boxes). Wide means the ventricles were not activated through His–Purkinje.

6. QT interval. Measure from the start of the QRS to the end of the T wave, in the lead where it is longest (often II or V5–V6). Then correct for rate (see the QT section).

7. ST segments and T waves. In every lead. Compare with a prior ECG if one exists — the comparison is often more informative than the tracing itself.

Then: axis, hypertrophy, and Q waves.

Measuring properly

• Measure the interval in the lead where it appears longest — conduction abnormalities are not visible in every lead.
• Measure several complexes and take a representative value; in atrial fibrillation, average.
• For the QT, use the tangent method when the T wave has a gradual downslope: draw a line along the steepest part of the T wave's descent and take its intersection with the isoelectric baseline as the end. Exclude a U wave unless it merges with the T.
• Use the isoelectric TP segment as your baseline reference, not the PR segment, when they differ.

Documenting an interpretation

A useful strip note says what you measured and what changed:

"0430: Rate 132, irregularly irregular, no discernible P waves, QRS 0.08, new from sinus rhythm at 88 on the 0200 strip. BP 88/54 (was 118/70), patient reports palpitations and is diaphoretic. 12-lead obtained, Dr. — notified, at bedside."

That is a rhythm strip note that will still be useful to someone reading the chart three days later — and it is the observable form of the assessment-and-communication competency the exam is measuring.

Rhythms

Sinus rhythms

Normal sinus — rate 60–100, upright P before every QRS in lead II, PR 0.12–0.20, regular.

Sinus bradycardia (<60) — normal in athletes and during sleep. Pathologic causes: increased vagal tone, inferior MI, hypothyroidism, hypothermia, raised intracranial pressure, hypoxia (a late and ominous sign), and drugs (beta blockers, calcium channel blockers, digoxin, dexmedetomidine, amiodarone). Treat the patient, not the number — the question is whether perfusion is adequate.

Sinus tachycardia (>100) — almost always a response, not a primary problem. Fever, pain, anxiety, hypovolemia, anemia, hypoxia, hypoglycemia, sepsis, pulmonary embolism, withdrawal, thyrotoxicosis, drugs. Find the cause; rate-slowing a compensatory tachycardia can be harmful.

Sinus arrhythmia — rate varies with respiration (faster on inspiration). A normal vagal phenomenon, especially in the young.

Atrial rhythms

Premature atrial contractions (PACs) — early, abnormally shaped P wave, usually narrow QRS. Usually benign; frequent PACs can precede atrial fibrillation.

Atrial fibrillation — irregularly irregular with no discernible P waves and a fibrillatory baseline. The most common sustained arrhythmia in the ICU.

• Loses the atrial kick — which can drop cardiac output substantially in a stiff (HFpEF) or hypertrophied ventricle.
• Stasis in the left atrial appendage causes thrombus and stroke; anticoagulation decisions use CHA₂DS₂-VASc.
• Rate control versus rhythm control, and the unstable patient gets synchronized cardioversion.
• ICU causes are usually reversible: sepsis, hypovolemia, hypoxia, electrolyte derangement (K⁺, Mg²⁺), catecholamines, pain, post-cardiac-surgery inflammation, pulmonary embolism.

Atrial flutter — sawtooth flutter waves, atrial rate about 250–350 (classically ~300), with conduction ratios producing regular ventricular rates: 2:1 → 150, 3:1 → 100, 4:1 → 75.

Multifocal atrial tachycardia (MAT) — irregularly irregular with three or more distinct P wave morphologies. Classically in severe COPD; treat the lung disease, not the rhythm.

Junctional rhythms

Absent, inverted (in II), or retrograde P waves with a narrow QRS. Junctional escape 40–60; accelerated junctional 60–100; junctional tachycardia >100. Accelerated junctional rhythm is a classic digoxin toxicity finding.

Ventricular rhythms

PVCs — wide, bizarre, early, usually with a full compensatory pause. Patterns: bigeminy, trigeminy, couplets, and multiform (different morphologies = different foci). Investigate electrolytes (K⁺, Mg²⁺), ischemia, hypoxia, catecholamines, and central line or PA catheter irritation.

Ventricular tachycardia — three or more consecutive ventricular beats at >100.

• Monomorphic — uniform complexes; usually reentry around scar.
• Polymorphic — varying morphology. With a long baseline QT, this is torsades de pointes.
• Non-sustained (<30 sec) versus sustained.

Ventricular fibrillation — chaotic, no organized complexes, no pulse. Immediate defibrillation and high-quality CPR.⁵

Idioventricular / accelerated idioventricular rhythm (AIVR) — wide complexes at 20–40 (idioventricular) or 50–110 (accelerated). AIVR is a classic reperfusion rhythm after successful PCI or thrombolysis; usually transient and usually left alone if perfusing.

Pulseless electrical activity and asystole

PEA — organized electrical activity without a pulse. The rhythm is not the problem; the cause is. Work the Hs and Ts: Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypo/Hyperkalemia, Hypothermia; Tension pneumothorax, Tamponade, Toxins, Thrombosis (pulmonary and coronary). Point-of-care ultrasound identifies several of these in seconds.

Asystole — confirm in two leads and check that leads are connected before calling it; fine VF can masquerade as asystole in a single lead.

Blocks and bundles

AV blocks

First degree — PR > 0.20 sec, every P conducts. Not really a "block"; a delay. Usually benign, but watch it as a trend, especially with rate-slowing drugs.

Second degree, Mobitz I (Wenckebach) — the PR interval progressively lengthens until a P wave fails to conduct, then the cycle resets. The R-R intervals actually shorten before the dropped beat, and the grouped beating gives a characteristic "regularly irregular" pattern. The block is in the AV node, it is usually benign and often drug- or vagally-mediated, and it rarely progresses.

Second degree, Mobitz II — constant PR intervals with sudden, unpredictable dropped beats. The block is infranodal (His–Purkinje), often with a wide QRS. This one is dangerous: it progresses to complete heart block without warning, does not reliably respond to atropine, and typically requires pacing.

2:1 AV block — every other P conducts. You cannot classify it as I or II from the strip alone, because you never see two consecutive conducted PRs to compare. Clues: a narrow QRS favors nodal (type I); a wide QRS favors infranodal (type II). A longer rhythm strip, exercise, or atropine can distinguish (nodal block improves with atropine; infranodal often worsens).

Third degree (complete heart block) — no relationship between P waves and QRS complexes. The atria march at their rate, the ventricles at the escape rate, each regular but dissociated. Measure the P-P and R-R intervals separately — both are regular; that is the tell.

• Narrow escape (40–60) — junctional; higher, more reliable, often from an inferior MI or drugs; may respond to atropine.
• Wide escape (20–40) — ventricular; unreliable and slow; from an anterior MI or infranodal disease; needs pacing.

Bundle branch blocks

Both require QRS ≥ 0.12 sec with a supraventricular rhythm.

Right bundle branch block (RBBB)

• RSR′ ("rabbit ears") in V1–V2
• Wide slurred S wave in I, aVL, V5–V6
• Right ventricle is depolarized late, cell-to-cell from the left — so the terminal vector points rightward and anteriorly, toward V1.
• Often benign; can occur in normal hearts. New RBBB may accompany pulmonary embolism or an anterior MI.

Left bundle branch block (LBBB)

• Broad, monophasic, often notched R wave in I, aVL, V5–V6
• Deep QS or rS in V1–V2
• Terminal vector points leftward and posteriorly.
• Almost always indicates structural heart disease.
• Also reverses the normal direction of septal depolarization, which is why LBBB produces secondary ST-T changes.

Fascicular blocks (hemiblocks) — the left bundle has two fascicles.

• Left anterior fascicular block: left axis deviation (−45° to −90°), qR in I and aVL, rS in II/III/aVF, normal or slightly widened QRS.
• Left posterior fascicular block: right axis deviation, rS in I and aVL, qR in II/III/aVF. Rarer, because the posterior fascicle is thicker and has a dual blood supply.
• Bifascicular block: RBBB plus a fascicular block. Trifascicular implies bifascicular plus first-degree AV block — a term that is imprecise but still used, and it flags a patient at risk of complete heart block.

The discordance rule, and reading ischemia through a block

In LBBB and in ventricular paced rhythms, depolarization is abnormal, so repolarization is abnormal too. The expected pattern is appropriate discordance: the ST segment and T wave point opposite to the main QRS deflection.

• Deep S wave in V1–V3 → expect ST elevation with an upright T there.
• Tall R wave in V5–V6, I, aVL → expect ST depression with an inverted T there.

That expected discordance is why LBBB was traditionally said to obscure MI. But it does not obscure it entirely — it just requires different criteria.

Ischemia, injury and the OMI paradigm

The three stages, and their mechanisms

Ischemia — T wave changes. Reduced perfusion prolongs and alters repolarization in the affected region. Classically: symmetric T wave inversion, or hyperacute T waves — broad-based, tall, and fat relative to the QRS — which are often the earliest change and appear before any ST elevation.

Injury — ST segment shift. Injured, still-viable cells cannot maintain the phase-2 plateau. A voltage gradient exists between injured and healthy tissue during the ST segment, and the electrode records a current of injury. Transmural injury elevates the ST in the leads facing it; subendocardial injury depresses it.

Infarct — Q waves. Dead tissue is electrically silent. The electrode over it records the depolarization vector of the opposite wall moving away, producing a Q wave. Pathologic: >0.04 sec wide or >25% of the R wave height.

Localizing by lead group

Contiguous leads matter: two or more leads in the same anatomic group make a territory.

The OMI paradigm

This is the most significant conceptual shift in acute-ECG interpretation in decades, and it is worth understanding rather than just naming.

The claim. The clinically important distinction is not whether the ECG meets millimeter criteria for ST elevation — it is whether a coronary artery is acutely occluded and the myocardium behind it is dying. The proposed replacement for STEMI/NSTEMI is OMI (occlusion MI) versus NOMI (non-occlusion MI).⁸

The evidence. Meyers and colleagues compared expert interpretation using OMI findings against formal STEMI criteria in patients with angiographically confirmed acute coronary occlusion. STEMI criteria had a sensitivity of roughly 43%, while OMI-oriented interpretation reached roughly 86% at comparable specificity.⁹ In other words, millimeter criteria miss a large share of acute occlusions — patients who have an occluded artery, are labeled "NSTEMI," and wait.

The patterns that identify occlusion without meeting STEMI criteria:

• Hyperacute T waves — broad, symmetric, disproportionately large relative to the QRS. Often the first change of an LAD occlusion.
• de Winter T waves — upsloping ST depression at the J point in the precordial leads with tall, symmetric T waves, and often slight ST elevation in aVR. Described in 2008 as a static pattern indicating proximal LAD occlusion; it does not evolve into ST elevation and is easy to dismiss as "just depression."¹⁰
• Posterior MI — ST depression with tall R waves in V1–V3, which is elevation viewed from behind. Confirm with V7–V9.
• Subtle ST elevation with reciprocal change — elevation below threshold in one territory with reciprocal depression elsewhere is far more meaningful than the millimeters alone suggest.
• Terminal QRS distortion — loss of the S wave and J wave in V2 or V3.
• Proportionality — ST deviation judged relative to QRS amplitude, the same principle as the modified Sgarbossa rule.
• Aslanger's pattern — inferior MI in the presence of multivessel disease, with ST elevation only in III and ST depression in V4–V6.

Wellens' syndrome is the related "warning" pattern: deeply inverted (type B) or biphasic (type A) T waves in V2–V3 in a patient who is now pain-free after an episode of chest pain, with preserved R waves and no Q waves. It signifies a critical proximal LAD stenosis with spontaneous reperfusion.¹¹ These patients look well and their ECG looks unimpressive — and they have a high rate of anterior infarction in the following days. They should not receive a stress test; they need catheterization.

The mimics

Not everything with ST elevation is an occlusion:

The QT interval and torsades

What the QT represents

The QT interval spans the whole of ventricular depolarization and repolarization — phases 0 through 3. Its duration is set mostly by how long the repolarizing potassium currents take to bring the cell back to baseline, and specifically by I_Kr, the rapid delayed rectifier potassium current carried by the hERG channel.

Measuring and correcting

Measure from the start of the QRS to the end of the T wave, in the lead where it is longest (commonly II, V5 or V6). Use the tangent method on a gradually sloping T wave: draw a tangent along its steepest descent and take the intersection with the isoelectric baseline.

Because the QT shortens as heart rate rises, it must be corrected.

Bazett: QTc = QT ÷ √RR (RR in seconds). The most widely used and the one implemented on most monitors. It over-corrects at high heart rates and under-corrects at low ones — a tachycardic patient's Bazett QTc is often falsely alarming.

Fridericia: QTc = QT ÷ ∛RR. More accurate at rate extremes, and increasingly preferred in drug-safety work.

Torsades de pointes

Polymorphic VT with a long baseline QT — the QRS complexes appear to twist around the isoelectric line ("twisting of the points"). It typically starts after a pause, in the classic short–long–short sequence: a PVC, a compensatory pause (which further lengthens repolarization), then a second PVC landing on the prolonged T wave.

Treatment:^5,14

1. IV magnesium sulfate — 1–2 g, effective even when the serum magnesium is normal. First-line.
2. Correct potassium to the high-normal range (often 4.5–5.0) and correct calcium.
3. Stop every offending drug — check the full list, including recently given one-time doses.
4. Increase the heart rate to shorten repolarization and eliminate the pauses: overdrive pacing at 90–110, or isoproterenol if pacing is not immediately available. Slowing the rate is exactly wrong.
5. Unstable or pulseless → defibrillate (unsynchronized, since polymorphic VT often cannot be reliably synchronized).

Risk factors worth screening for

• Drugs. Antiarrhythmics (sotalol, amiodarone, procainamide, ibutilide), antipsychotics (haloperidol — particularly IV, quetiapine, ziprasidone), antibiotics (macrolides, fluoroquinolones), antifungals, methadone, ondansetron, droperidol. The free CredibleMeds/QTdrugs list is the standard reference and is worth bookmarking.¹⁵
• Electrolytes. Hypokalemia, hypomagnesemia, hypocalcemia — all three lengthen repolarization, and all three are common in the ICU.
• Bradycardia and pauses, complete heart block.
• Congenital long QT syndromes (LQT1–3 and others), often with a family history of syncope or sudden death.
• Hypothyroidism, hypothermia, starvation, anorexia nervosa.
• Female sex, and structural heart disease.

Short QT

A QTc under about 340 ms is abnormal. Causes: hypercalcemia, digoxin (with its characteristic "scooped" ST segment), hyperkalemia, hyperthermia, and congenital short QT syndrome — which also carries a risk of sudden death.

Electrolytes, drugs and mimics

This section is where the action potential pays you back. Every finding below is derivable from what happens to a channel or a gradient — you should not have to memorize any of it.

Potassium

Recall the rule from the first section: resting membrane potential tracks the potassium gradient.

Hyperkalemia — a progression, in order

Hypokalemia

Lower extracellular K⁺ hyperpolarizes the cell and slows repolarization (paradoxically, because of how I_Kr behaves with low extracellular potassium):

• ST depression
• Flattened or inverted T waves
• Prominent U waves — the classic finding, best seen in V2–V3
• Apparent QT prolongation (often really a fused QU interval)
• Increased ectopy, and increased digoxin toxicity risk (potassium and digoxin compete for the Na⁺/K⁺-ATPase binding site)

Calcium

Calcium sets the duration of the plateau (phase 2), and the plateau is most of the ST segment.

• Hypocalcemia → prolonged plateau → long ST segment → long QT, with a normal-looking T wave. Causes: citrate from massive transfusion, pancreatitis, renal failure, post-parathyroidectomy, rhabdomyolysis.
• Hypercalcemia → shortened plateau → short ST → short QT. Severe cases show an Osborn-like wave.

Magnesium

• Hypomagnesemia — prolonged QT, torsades risk, refractory hypokalemia, increased ectopy.
• Hypermagnesemia — prolonged PR and QRS, bradycardia, and at high levels AV block and arrest. Seen with magnesium infusions in eclampsia and in renal failure.

Drug effects

Other conditions with ECG signatures

• Hypothermia — Osborn (J) waves, a positive deflection at the J point; bradycardia; prolonged intervals; shivering artifact; and a high risk of VF with handling.
• Pulmonary embolism — sinus tachycardia is the most common finding. The classic S1Q3T3 is neither sensitive nor specific. Also: new RBBB, right axis deviation, T inversion in V1–V4 (right heart strain).
• Raised intracranial pressure / subarachnoid hemorrhage — deep, widely splayed inverted T waves ("cerebral T waves"), long QT, U waves, and bradycardia with hypertension (Cushing response).
• Pericardial effusion / tamponade — low voltage and electrical alternans (beat-to-beat QRS amplitude variation as the heart swings in the fluid).
• Wolff–Parkinson–White — short PR, delta wave, wide QRS. Critical: in atrial fibrillation with WPW, AV-nodal blocking agents (adenosine, diltiazem, verapamil, digoxin, and beta blockers) can preferentially conduct down the accessory pathway and precipitate VF. These patients need procainamide or cardioversion.

Nursing actions and monitoring

Getting a clean tracing

Artifact causes real harm — unnecessary cardioversions, missed ischemia, and alarm fatigue. Most of it is preventable:

• Skin preparation is the single biggest factor. Clip (do not shave) hair, clean with soap and water or an alcohol wipe and let it dry, and gently abrade the stratum corneum with the tab on the electrode or a dry gauze. Impedance is what electrodes are fighting.
• Fresh electrodes, changed daily and whenever the gel dries. Dried gel raises impedance and produces baseline wander.
• Mark and standardize placement. Serial ECGs are only comparable if the electrodes are in the same place — this is the difference between "new anterior T wave inversion" and "someone put V2 in the third interspace."
• Provide strain relief on the lead wires so patient movement does not translate directly to the electrode.
• Know your filters. Monitoring mode uses aggressive filtering that distorts the ST segment; diagnostic mode (0.05–150 Hz) is required for ST-segment monitoring and interpretation.³

What to monitor, and why it is not everyone

The AHA practice standards define which patients warrant which monitoring — arrhythmia, ischemia, and QT monitoring are separate indications with separate patient populations. More monitoring is not better: unnecessary monitoring generates alarms, and alarm fatigue is a documented patient-safety hazard.³

Alarm management, concretely:

• Customize limits to the individual patient at the start of every shift, rather than accepting unit defaults.
• Set the amplitude high enough that the monitor counts QRS complexes rather than tall T waves (double-counting produces false tachycardia alarms).
• Fix the cause of the artifact instead of widening the limit or turning the alarm off.
• Change electrodes daily — this alone measurably reduces false alarms.
• Choose the right lead for the patient: V1 or MCL1 is best for distinguishing wide-complex rhythms and bundle branch morphology; lead II is best for P waves.
• Re-evaluate the need for monitoring daily and discontinue it when the indication has passed.

The nursing sequence for a rhythm change

1. Look at the patient before the monitor. Are they awake, talking, perfusing? Is there a pulse?
2. Check the leads. Artifact, a disconnected electrode, and movement account for a large share of "arrhythmias."
3. Get a 12-lead for anything you would act on.
4. Vital signs, including a blood pressure and an assessment of perfusion.
5. Review the reversible causes: potassium, magnesium, calcium; oxygenation; pH; new drugs and drugs held; volume status; pain; central line or PA catheter position; ischemia.
6. Escalate with specifics, not adjectives: rate, regularity, QRS width, what it changed from, what the blood pressure is, and what the patient reports.
7. Anticipate the intervention. If it is unstable VT, the defibrillator, pads, sedation and the code cart should be at the bedside before the physician asks.

Equipment readiness

• Defibrillator checked each shift; pads available and the patient's chest ready to receive them.
• Know your device: synchronized cardioversion requires pressing sync and confirming the marker is on the R waves — and remember that sync must be re-enabled after each shock on most devices.
• Transcutaneous pacing: know where the pads go, how to set rate and output, and how to confirm electrical capture (a pacing spike followed by a wide QRS) versus mechanical capture (a palpable pulse or an arterial waveform matching the paced rate). Electrical capture without mechanical capture is not capture. Expect the patient to need analgesia and sedation; transcutaneous pacing hurts.
• Transvenous and epicardial pacing wires: know the settings (rate, output, sensitivity) and how to recognize failure to capture (spike, no complex), failure to sense (spikes falling inappropriately, with R-on-T risk), and oversensing (inappropriate inhibition, so pacing does not occur when needed).

Documentation

Mount or save a strip at the change and at each intervention, with the time, rate, rhythm interpretation, the patient's response, the intervention, and to whom it was reported. That record is what lets the next shift and the next clinician see the trajectory — and, on the exam, it is the "evaluating the response to an intervention" competency in written form.