Last updated 11/9/26
Below is an ECG Exercise focused on electrolyte and drug effects (part of the Self-Study Curriculum). ECGs are from Garcia, 12-Lead ECG: The Art of Interpretation, Chapter 16.
Hyperkalemia - The Spectrum and T Waves
What are the main ECG changes of hyperkalemia? - T wave abnormalities (especially tall, peaked T waves)
- IVCD (wide QRS that is not a typical LBBB or RBBB)
- Small or absent P waves
- ST changes that can mimic injury
- Any arrhythmia - including sine wave and asystole at any point
At what potassium levels do the changes appear? - ≥ 5.5 mEq/L: T wave changes (earliest sign)
- ≥ 6.5 mEq/L: intervals widen
- ≥ 7.0 mEq/L: PR lengthens, P waves shrink
- ≥ 8.8 mEq/L: P waves disappear
- The jump to sine wave / asystole can happen in seconds at any point along the spectrum
What do hyperkalemic T waves look like, and where do they show up first? - Classic tall, peaked, narrow T waves occur in only ~22% of cases
- Most are some mix of tall, peaked, narrow, or wide - but always symmetrical
- Changes often start in V2-V4 and may stay there - they do not need to be diffuse
- T waves more than 2/3 the height of their R wave are pathologic
ECG 1
[Insert image - Garcia ECG 16-1]
What are the rate, rhythm, and axis? - Rate: 84 bpm
- Rhythm: normal sinus rhythm
- Axis: normal
What is the most striking finding, and what does it suggest? - Huge tall, peaked, narrow T waves in V2-V4
- Classic hyperkalemia
Are the inferior T waves normal? - No - less dramatic, but still more than 2/3 the height of the R wave in III and aVF
- Also pathologic and also from hyperkalemia - don't let the obvious leads distract you from the subtle ones
What is the "string theory" of hyperkalemia? - Picture the complex as a string pulled up at the T wave peak while held before the P wave
- T wave peaks, then intervals widen and amplitudes shrink, P waves vanish, and finally sine wave and flat line
ECG 2
[Insert image - Garcia ECG 16-2]
What are the rate, rhythm, and axis? - Rate: 78 bpm
- Rhythm: normal sinus rhythm
- Axis: normal
Are the T waves consistent with hyperkalemia? In which leads? - Yes - not as dramatic as ECG 1, but very tall relative to their R waves and symmetrical
- Pathologic in I, II, III, aVF, and V2-V6 - a diffuse pattern
What should symmetrical T waves make you do? - Symmetrical T waves are usually pathologic
- Rule out life-threatening causes (hyperkalemia, ischemia) before calling them benign
What underlying disorder most commonly causes hyperkalemia? ECG 3
[Insert image - Garcia ECG 16-3]
What are the rate, rhythm, and axis? - Rate: low 100s
- Rhythm: sinus tachycardia
- Axis: normal to borderline left
Evaluate the T waves. What is your leading diagnosis? - Tall, narrow, peaked T waves in V2-V4, continuing into V5-V6
- Significant T wave changes in the inferior leads too
- Hyperkalemia
The QT is longer than the rest of the widening would explain. Why? - Renal failure causes both hyperkalemia and hypocalcemia
- Hypocalcemia prolongs the QT - the two effects add together
What other ECG finding is common in these renal failure patients? - Low voltage from pericardial effusion
ECG 4
[Insert image - Garcia ECG 16-4]
What are the rate, rhythm, and axis? - Rate: 102 bpm
- Rhythm: sinus tachycardia
- Axis: normal
Evaluate the T waves and QT. What is your diagnosis? - Very tall, peaked T waves ("painful to sit on")
- Markedly prolonged QT
- Hyperkalemia plus hypocalcemia - typical of end-stage renal disease
There is LVH by voltage. Why are these T waves not LVH with strain? - LVH: S in V1 + R in V5 > 35 mm
- Strain T waves are inverted and asymmetric; these are tall, peaked, and symmetrical = electrolyte effect
Should you correct the low calcium aggressively in a dialysis patient with mild hyperkalemia? - No - treat the potassium, not the calcium
- These patients run high phosphate; extra calcium can precipitate as calcium phosphate in soft tissues
- Exception: calcium is first-line for life-threatening hyperkalemia (arrhythmias or hemodynamic compromise)
ECG 5
[Insert image - Garcia ECG 16-5]
What are the rate, rhythm, and axis? - Rate: 96 bpm
- Rhythm: normal sinus rhythm
- Axis: normal
Evaluate the T waves. What is your leading diagnosis? - Subtle, but pathologic T waves in V2-V5 - tall for their QRS and symmetrical
- Hyperkalemia
What makes a T wave "hyperacute" (pathologically tall)? - T wave more than 2/3 the height (or depth) of the R or S wave pointing the same direction
Do subtle T wave changes buy you more time? - No - the T waves only need to be present to be dangerous
- A lethal arrhythmia or sine wave can come within seconds to minutes - treat now
IVCD and P Waves in Hyperkalemia
What is an IVCD, and what should it make you think of first? - QRS ≥ 0.12 s that meets criteria for neither LBBB nor RBBB
- Common pattern: V1 looks like LBBB (rS or QS), while I and V6 look like RBBB (wide slurred S)
- Hyperkalemia - the most life-threatening cause; don't wait 30-90 minutes for the lab K+ (a blood gas K+ is faster)
Why do P waves disappear in severe hyperkalemia, and why does it matter? - Atrial muscle stops depolarizing, but the SA node and atrial conduction pathways keep working
- Technically still a sinus rhythm ("P-less sinus") - but it can't be told apart from an idioventricular rhythm
- P waves return dramatically with treatment
What resuscitation drugs and devices fail in hyperkalemic arrest? - Antiarrhythmics, pressors, catecholamines (epinephrine), and pacemakers (may not capture)
- Give calcium and sodium bicarbonate first - before atropine or pacing
- Arrest patient with an AV graft = think hyperkalemia
ECG 6
[Insert image - Garcia ECG 16-6]
What are the rate, rhythm, and axis? - Rate: 80s
- Rhythm: sinus rhythm with first-degree AV block
- Axis: right axis
How long is the PR interval? - Markedly prolonged - the P wave sits on top of the preceding T wave
What is the conduction pattern? - IVCD
- V1 looks like LBBB (large monomorphic S)
- V6 is full of artifact, so use lead I - wide, slurred S like RBBB
What do the QT and T waves show? - QT very prolonged - more than 1/2 the R-R interval
- T waves wide, symmetrical, and more than 2/3 the R wave height in I, II, III, aVL, V3-V6
Estimate the potassium level. - Peaked T (≥ 5.5) + wide intervals (≥ 6.5) + long PR / small P (≥ 7.0)
- P waves still visible (lost at ≥ 8.8)
- Best guess: 7.0-8.8 mEq/L
ECG 7
[Insert image - Garcia ECG 16-7]
What are the rate and axis? Are there P waves? - Rate: 80-90 bpm
- Axis: left axis
- No consistent P waves - only a possible P before the third complex in V1
- Wide-complex rhythm with no visible P waves
- Looks idioventricular, but in severe hyperkalemia a "P-less" sinus rhythm looks identical - you can't tell them apart
What features point to hyperkalemia? - QRS wide with an IVCD pattern
- All intervals widened
- T waves wide and symmetrical, though not very peaked
- Absent P waves = severe hyperkalemia
What is the next-to-last complex? Is that possible without P waves? - A premature complex with a compensatory pause - PAC or PJC
- Yes - the atria still fire; the atrial muscle just doesn't produce a visible P wave
ECG 8
[Insert image - Garcia ECG 16-8]
What are the rate, rhythm, and axis? - Rate: 48 bpm
- Rhythm: wide-complex rhythm, likely idioventricular
- Axis: left axis
What feature raises suspicion that hyperkalemia is the cause? - Idioventricular rhythms almost always have an LBBB or RBBB morphology
- This is an IVCD - so work hard to disprove hyperkalemia
- Dialysis patient, K+ 10.4 mEq/L
- Reversed quickly with aggressive hyperkalemia treatment
ECG 9
[Insert image - Garcia ECG 16-9]
What are the rate, rhythm, and axis? - Rate: 60-66 bpm
- Rhythm: wide-complex rhythm, no discernible P waves (idioventricular vs P-less sinus)
- Axis: left axis
What features point to hyperkalemia? - IVCD
- All intervals widened
- Peaked T waves
- No visible P waves
- Your next question: "What is the potassium?"
This patient arrests. Will epinephrine, dopamine, or pacing work? - Unlikely - catecholamines, pressors, and pacemakers don't work well in hyperkalemic arrest
- Treat the potassium first (calcium, bicarbonate)
ECG 10
[Insert image - Garcia ECG 16-10]
What are the rate and axis? What is the conduction pattern? - Rate: 72 bpm
- Axis: left axis
- IVCD - rabbit ears with a slurred S in V6, but a monomorphic R in lead I
What is the underlying rhythm? - P waves of different morphologies with varying PR intervals
- Irregularly irregular
- Wandering atrial pacemaker
What do the QT and T waves show? - Very prolonged QT
- T waves peaked and wide
There is ST elevation in the septal leads. Is this a septal AMI? - No - hyperkalemia can (rarely) mimic the ST elevation of AMI
- ST segments normalize when the potassium does
- Always correlate with the patient
ECG 11
[Insert image - Garcia ECG 16-11]
What are the rate, rhythm, and axis? - Rate: 96 bpm
- Rhythm: sinus rhythm with first-degree AV block and IVCD
- Axis: left axis
What abnormalities do you see, and what do they suggest? - Peaked, wide T waves
- IVCD
- QT prolongation
- PR prolongation
- Hyperkalemia
The patient came in short of breath with no history of renal disease. Does that lower your concern? - No - the ECG makes the diagnosis; no renal history doesn't rule it out
- The diagnosis was missed and the patient waited - shortly after, the monitor pattern changed (see ECG 12)
ECG 12
[Insert image - Garcia ECG 16-12]
This is the same patient as ECG 11 a short time later. What are the rate, rhythm, and axis? - Rate: 110-120 bpm
- Rhythm: regular wide-complex tachycardia - looks like VT
- Axis: extreme axis deviation
What pattern is this, and what is the cause? - Sine wave pattern - individual complexes still visible but starting to merge
- Severe hyperkalemia
The patient is asymptomatic. How should you treat? - If a known hyperkalemic patient progresses to this: treat the hyperkalemia immediately
- If a patient arrives in this pattern: it is reasonable to treat for VT and hyperkalemia at the same time
What happened to this patient? - Treated with lidocaine for presumed stable VT
- Arrested as the ECG leads were coming off
- K+ came back at 9.4 mEq/L
ECG 13
[Insert image - Garcia ECG 16-13A]
[Insert image - Garcia ECG 16-13B]
What does ECG 13A (4:20 PM) show? - Classic hyperkalemic peaked T waves with narrow QRS complexes
What does ECG 13B (4:28 PM) show? - Deterioration to a wide-complex bradyarrhythmia
How much time passed between them, and what is the lesson? - 8 minutes
- A narrow-complex hyperkalemic ECG is not a stable one - treat immediately, don't wait for it to get worse
ECG 14
[Insert image - Garcia ECG 16-14]
Same patient as ECG 13. What pattern is this? - Sine wave pattern - QRS and T waves merging into a smooth undulating wave
- A pre-arrest rhythm requiring immediate treatment
How long did this patient take to go from peaked T waves to a sine wave? - Less than 13 minutes (ECG 13A to ECG 14)
- "You only have seconds"
Hypokalemia, Calcium, and the Prolonged QT
What are the ECG findings of hypokalemia? What is the differential for U waves? - Most common: prominent U wave (normally under 1/10 the T wave height)
- Nonspecific: mild ST depression, flattened T waves, slight QRS prolongation
- Real danger: hypokalemia + digoxin
- U wave differential:
- Hypokalemia
- Bradycardia
- LVH
- CNS events
- Drugs: digoxin, Class I antiarrhythmics, phenothiazines
How do calcium levels change the QT? - Hypercalcemia: short ST segment, short QTc
- Hypocalcemia: long ST segment, long QTc (T wave itself fairly normal)
- Quick test: QT more than 1/2 the preceding R-R interval = prolonged
What is the differential for a prolonged QT, and what is the danger? - AMI and ischemia
- Hypocalcemia
- Drugs: Class Ia antiarrhythmics, amiodarone, phenothiazines, TCAs
- CNS events
- Hypothermia
- Hypothyroidism
- Congenital: Romano-Ward, Jervell-Lange-Nielsen, sporadic
- Danger: torsades de pointes and sudden death
ECG 15
[Insert image - Garcia ECG 16-15]
What are the rate, rhythm, and axis? - Rate: 90 bpm
- Rhythm: normal sinus rhythm
- Axis: normal, a little vertical (borderline right)
Is there atrial enlargement or LVH? - RAE - large P-pulmonale in lead II
- LVH - meets voltage criteria (S in V1/V2 + R in V5/V6 ≥ 35 mm)
Look at V2. What is the second hump after the T wave? - It does not line up with the P waves in V1 and V3, so it isn't a P wave
- Not part of the T wave either - it sits between the T and the next P
- A U wave - here it is taller than the T wave; smaller versions are in most other leads
What do the giant U waves and ST-T changes suggest? - Severe hypokalemia - flattened T waves, prominent U waves, nonspecific ST-T changes
- K+ was 1.6 mEq/L; changes resolved with correction
- Don't mistake the U wave for a very long QT
What else causes prominent U waves? - Hypokalemia
- Bradycardia
- LVH
- CNS events
- Drugs: digoxin, Class I antiarrhythmics, phenothiazines
ECG 16
[Insert image - Garcia ECG 16-16]
What are the rate, rhythm, and axis? - Rate: 96-102 bpm
- Rhythm: sinus
- Axis: normal
What is the most striking abnormality? - A markedly prolonged QT - about as long as it gets
What is the differential for a prolonged QT? - AMI and ischemia
- Hypocalcemia
- Drugs: Class Ia antiarrhythmics, amiodarone, phenothiazines, TCAs
- CNS events
- Hypothermia
- Hypothyroidism
- Congenital: Romano-Ward, Jervell-Lange-Nielsen, sporadic
She has fainted without warning since young adulthood and was labeled psychiatric. What is the diagnosis? - Syncope from torsades de pointes due to congenital long QT - Romano-Ward syndrome
- On the monitor she went into torsades, then woke up about a minute later on her own
- Her antidepressants and antipsychotics likely made the QT worse
ECG 17
[Insert image - Garcia ECG 16-17]
What are the rate, rhythm, and axis? - Rate: 96-102 bpm
- Rhythm: sinus
- Axis: normal
Is the QT prolonged? Which part of the interval is long? - Yes - more than 1/2 the R-R interval
- The ST segment is markedly prolonged while the T wave looks fairly normal
- Classic for hypocalcemia
- In ischemia/AMI (the most common cause of a long QT), the ST segment and T wave are usually equally prolonged
What else is on this ECG? - LVH by voltage (S in V1/V2 + R in V5/V6 ≥ 35 mm)
- Inverted, asymmetric lateral T waves - possible LVH with strain
- ST depression in the inferior leads - could be ischemia; needs clinical correlation
ECG 18
[Insert image - Garcia ECG 16-18]
This patient has a prolonged QTc. What happens on this tracing? - Frequent aberrant ventricular beats in a bigeminal pattern
- Then degenerates into polymorphic VT - torsades de pointes
When does torsades usually develop? - When the QTc is prolonged by a precipitating factor - e.g., AMI or drug overdose
- Every time you see a long QTc, ask why it's there and treat that cause
What are the mainstays of treatment for torsades? - Magnesium and overdrive pacing
- Correct the underlying cause
Digoxin and Other Drug Effects
What are the ECG effects of digoxin? - Scooped ("ladle") ST segments
- Smaller, sometimes biphasic T waves
- Shorter QT
- More prominent U waves
- Hypokalemia increases toxicity - any dig level can be toxic when K+ is low
Which arrhythmias does digoxin toxicity cause? What is PAT with block? - Any arrhythmia
- Classic: PAT with block - complete heart block with an underlying atrial rate of 150-200 bpm and a junctional or ventricular escape
- Suggestive of, but not pathognomonic for, dig toxicity - check a level
ECG 19
[Insert image - Garcia ECG 16-19]
What are the rate, rhythm, and axis? - Rate: 114-120 bpm
- Rhythm: sinus tachycardia
- Axis: normal
Describe the ST segments and T waves. What do they suggest? - Scooped-out ST segments in many leads (ladle shape)
- T waves smaller than expected
- Digoxin effect - this shows the drug is on board, not that it is toxic
What other findings are present, and how do they fit? - A PAC
- Biatrial enlargement
- Atrial enlargement predisposes to AFib - a common reason a patient is on digoxin
ECG 20
[Insert image - Garcia ECG 16-20]
What is the atrial rate? What is the ventricular rate? - Atrial: about 150 bpm
- Ventricular: about 60 bpm, junctional escape
- P waves and QRS complexes are unrelated = complete heart block
- With the fast atrial rate = PAT with block
What drug should you suspect, and how do you treat it? - Digoxin toxicity - this patient's level was 3.5 ng/mL
- PAT with block can occur from other causes or spontaneously, but always check a dig level
- Serious toxicity: digoxin-specific antibodies
ECG 21
[Insert image - Garcia ECG 16-21]
What are the rate, rhythm, axis, and intervals? - Rate: 96 bpm
- Rhythm: sinus
- Axis: left axis deviation
- PR prolonged, QRS wide, QTc prolonged
The QRS is wide. Is it LBBB, RBBB, or neither? - Neither - IVCD
- First thought with any IVCD: hyperkalemia (no evidence of it here, but you have to think of it)
This patient is altered after a possible overdose. What should you suspect? - Tricyclic antidepressant (sodium channel blocker) toxicity - IVCD in an overdose patient = TCA until proven otherwise
- Supporting: terminal R in aVR > 3 mm and R:S in aVR > 0.7
- Nothing on this ECG is unique to TCAs - the history makes the diagnosis
What is the treatment, and why is monitoring critical? - Sodium bicarbonate to overcome sodium channel blockade and narrow the QRS
- These patients often develop life-threatening arrhythmias - monitor closely
- This patient died despite aggressive therapy
