1 Arrhythmias

Learning Objectives

  • Distinguish between different forms of common arrhythmias.
  • Describe the underlying pathophysiology of an arrhythmia.

This chapter will address the arrhythmias listed in the USMLE (United States Medical Licensing Exam) Step 1 content guide on a section-by-section basis. Learning the arrhythmias here will be substantially easier with a robust understanding of electrocardiogram (ECG) fundamentals and lead orientation, so going back to basics is likely to be very worthwhile.

Atrial Fibrillation

Figure shows lead one of a 12-lead electrocardiogram (ECG). There is an absence of distinct P-waves. Instead there are multiple smaller and irregular waves between normal QRS complexes.
Figure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.

Atrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1); the action potentials produced are low amplitude, and P-waves will not be seen.

 

The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node’s long refractory period. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be “lucky” and reach the AV node when it is not in a refractory period. When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).

Atrial fibrillation (afib) shows lack of P-waves; atrial fibrillation (aflutter) has regular QRS complexes and sawtooth patterns which resemble P-waves but there are too many of them; Multifocal atrial tachycardia (MAT): P-waves are present but they have different shapes reflecting their different origins in the atrial wall. Each of the P-waves is followed by a QRS complex.
Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right).

Atrial fibrillation summary
No visible P-waves
Irregularly irregular QRS complexes
High ventricular rate
Atrial fibrillatory waves possible

Table 1.1: Atrial fibrillation summary.

Atrial Flutter

Sawtooth pattern between QRS complexes.
Figure 1.3: Atrial flutter — “sawtooth” P-waves with lower frequency than the fibrillation waves of atrial fibrillation.

Atrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2).

 

As with atrial fibrillation, the AV node’s refractory period prevents most of the P-waves from progressing to the ventricle, but commonly the AV conduction will be 2-to-1, so with an atrial rate of 300 bpm the ventricular rate will be 150 bpm. Parasympathetic stimulation or changes in AV node refractoriness can modify how many P-waves pass into the ventricle, but the the resultant rhythm is “regularly irregular.” When the heart rate is elevated, then distinguishing flutter from fibrillation becomes challenging and slowing ventricular rate pharmaceutically (adenosine) helps the flutter waves reemerge for a definitive diagnosis to be made.

Atrial flutter summary
Sawtooth atrial pattern
Regularly irregular QRS complexes
High ventricular rate

Table 1.2: Atrial flutter summary.

Multifocal Atrial Tachycardia

Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. Thus, each QRS complex will be preceded by a P-wave; however, each P-wave will have a different morphology because they originate from different areas. By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.

At least three different shapes of P-waves are seen, some small, some broader and some taller. But each one is followed by a QRS complex.
Figure 1.4: Three distinct P-wave morphologies in a case of MAT.

MAT frequently occurs in the setting of severe lung disease and, more specifically, during an exacerbation of lung disease. This rhythm is benign, and once the underlying lung disease is treated, it should resolve.

MAT summary
P-waves followed by QRS complexes
P-waves have different morphology (at least three)
High ventricular rate (100 bpm)

Table 1.3: MAT summary.

Premature Atrial Contraction

A premature atrial contraction (PAC) is generated by a depolarization instigated outside of the SA node. This produces an extra P-wave, and consequently a shortening from previous P-P intervals is seen. The aberrant P-wave also has a different morphology from a sinus P-wave because of its different anatomical origin.

The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. This means that a PAC may cause a “compensatory pause” as the SA node restarts its pacemaker depolarization. Consequently the ECG can show “atrial bigeminy” where complexes appear to be in pairs with a normal complex followed by a complex driven by the atrial ectopic activity, then a pause while the SA node begins its depolarization again (see figure 1.5).

If a PAC occurs when the AV node has not yet recovered from its refractory period, the PAC will fail to conduct to the ventricles; meaning the PAC will not be followed by a QRS complex or the ectopic P-R interval will be prolonged. The ECG will show a premature, ectopic P-wave and then no QRS complex afterward. When this occurs along with bigeminy, the ECG can appear as if there is sinus bradycardia.

Normal QRS complex is rapidly followed by a premature atrial contraction which leads to another QRS complex. These two beats (bigemenie) are followed by a prolonged gap which is followed by another normal P-wave and QRS complex which again is followed by an abnormal premature atrial contraction (PAC) instigating another QRS complex. This process is repeated resulting in two QRS complexes clustered together all separated by prolonged gaps.
Figure 1.5: Atrial bigeminy in PAC with ECG complexes appearing in pairs.
PAC summary
Extra P-wave with abnormal morphology
Compensatory pause leading to atrial bigeminy

Table 1.4: PAC summary.

Sinus Bradycardia

Sinus bradycardia denotes a sinus rhythm below 60 bpm. Otherwise the ECG waveform is normal on an ECG with an upright P-wave in lead II preceding every QRS complex. There are many intrinsic causes associated with the heart itself, as well as extrinsic causes, some of which are listed table 1.5. Sinus bradycardia is usually asymptomatic as rates of 40–50 bpm can maintain hemodynamic stability. Rates below this can produce symptoms of fatigue, dizziness, and dyspnea on exertion.

Intrinsic causes Extrinsic causes
Chest trauma Hypothyroidism
Ischemic heart disease Carotid sinus sensitivity
Sick sinus syndrome Calcium channel blockers
Myocarditis Antiarrhythmic class I to IV
Familial disorder Intracranial hypertension
Radiation therapy Hypoglycemia
Lyme disease Sleep apnea

Table 1.5: Intrinsic and extrinsic causes associated with the heart.

Sinus bradycardia summary
60 bpm
Normal P-wave before every QRS complex

Table 1.6: Sinus bradycardia summary.

Premature Ventricular Contractions

Similar to a PAC, a premature ventricular contraction (PVC) occurs when a focus in the ventricle generates an action potential before the pacemaker cells in the SA node depolarize. This early depolarization is out of rhythm with the normal R-R interval, and because it starts outside of the normal conduction pathways, it has a very different shape from a normal, scheduled QRS complex (figure 1.6). The PVC is wider as it has to travel from myocyte to myocyte, so it is much slower than a normal SA node–driven depolarization that travels through the faster conduction network fibers. There is also a compensatory pause following the PVC as the unscheduled depolarization puts the ventricular myocardium into refractory state, forcing it to “skip a beat” (figure 1.6).

Two normal QRS complexes followed by a taller and wider QRS complex that is not preceded by a P-wave. ECG returns back to normal for 3 beats and then another taller, broader QRS complex, again, not preceded by a P-wave, occurs.
Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause.
PVC summary
Put of step with normal R-R interval
Wider complex
Followed by compensatory pause

Table 1.7: PVC summary.

Ventricular Tachycardia

Ventricular tachycardia (VT) is caused by reentry currents being established in the ventricular myocardium or groups of ventricular myocytes that have aberrant electrical behavior. As such, VT is usually caused by underlying cardiac disease.

Like a PVC, the aberrant depolarizations do not follow the normal conduction pathways so are wide (>120 msecs), but unlike a PVC, VT involves a ventricular rate >100 bpm. With disorganized contractility and reduced filling time, VT can lead to hemodynamic instability and severe hypotension—hence it is life threatening.

The QRS morphology in VT is highly variable between patients and depends on where the arrhythmia originates. Consequently there are several ways to classify VT based on duration, symptoms, QRS morphology, rate, and origin.

Sustained VT is any VT that lasts for more than 30 seconds or is symptomatic. Nonsustained VT lasts for less than 30 seconds and is asymptomatic.

Image shows large, broad complexes with no resemblance to a normal ECG. The complexes are uniform in shape each with a dome peak.
Figure 1.7: Monomorphic and polymorphic VT.

VT can be monomorphic or polymorphic (figure 1.7). The QRS complexes in monomorphic VT have the same shape and are symmetrical because they start in the same place in the myocardium. Polymorphic VT has a variable QRS shape because the depolarizations are instigated at multiple points. An electrophysiologist can describe the location(s) within the ventricles from where the VT originates using the shape(s) of the QRS complexes.

Torsades de pointes (twist of peaks) is a form of VT with multiple QRS morphologies. The twist references the undulating amplitude of the QRS complexes that twist around the isoelectric line, giving the ECG the appearance of a twisted ribbon (figure 1.8).

Large, broad, polymorphic waves with no discernable components of a normal ECG. The peaks alternate between being above and being below the isoelectric baseline.
Figure 1.8: Torsades de pointes.

Torsades de pointes is associated with a prolonged QT interval (>600 msecs) that helps distinguish it from other forms of polymorphous VT. The longer QT interval can be caused by ionic abnormalities that reduce the repolarizing current of Phase 3 of the cardiac action potential. This makes the myocardium susceptible to early after-depolarizations—the trigger for torsades de pointes. These after-depolarizations do not happen uniformly across the myocardium and are more common in endocardial tissue where the repolarization currents are slower. So torsades de pointes arises from the after-depolarizations causing reentry currents in neighboring tissue.

Both common garden variety VTs and torsades de pointes can progress to ventricular fibrillation.

VT summary
Ventricular rate >100 bpm
QRS complex not associated with P-wave
Wide QRS complex morphology

Table 1.8: VT summary.

Ventricular Fibrillation

Ventricular fibrillation (VF) occurs when the ventricular rate exceeds 400 bpm. The disorganized and uncoordinated contraction of the myocardium causes cardiac output to fall to catastrophic levels. Rates of survival for out-of-hospital VF are low.

There are a number of instigating events, but coronary artery disease and resultant myocardial ischemia or tissue scarring are the most common. The onset of VF may be preceded by other changes in the myocardial rhythmicity, such as PVCs, ST changes, VT, or QT prolongation. The tissue damage allows formation of reentry patterns that cause the chaotic ventricular depolarization. These reentry patterns break up into multiple smaller wavelets that cause high-frequency activation of the myocytes. The result is an ECG that is chaotic (figure 1.9) and consequently a heart that has little output.

ECG is highly irregular with broad waves that vary in amplitude and shape. The ECG contains none of the features of a normal ECG.
Figure 1.9: Example of VF with no recognizable P-waves or QRS complexes.
VF summary
Chaotic, irregular, and varying intervals
No P-waves, QRS complexes, or T-waves
High rate

Table 1.9: VF summary.

First-Degree Atrioventricular Block

A first-degree atrioventricular node block results from slow action potential conduction through the AV node conduction. The slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting the conductive tissue of the atria, AV node (most common), bundle of His or bundle branches, and Purkinje system. It takes longer for the action potential to reach the ventricles, so P and R appear further apart. The P-R interval is normally between 0.12 and 0.20 seconds, but in first-degree block it exceeds 0.20 seconds (>5 small boxes; figure 1.10).

The ECG contains the normal elements of a P-wave, QRS complex and T-wave. however the distance between the P-wave and the QRS is abnormally long with an extended flat-line (isoelectric period) between the end of the P-wave and start of the QRS.
Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds.

In first-degree block each P-wave is accompanied by a QRS complex (i.e., “they all get through”) (figure 1.10), which is not the case in second-degree and third-degree blocks (see below). Generally a first-degree block is asymptomatic and does not require any treatment, but long-term monitoring for worsening conduction is advisable.

First-degree block summary
Prolonged P-R interval (>0.2 sec)

Table 1.10: First-degree block summary.

Second-Degree Atrioventricular Block

A second-degree atrioventricular block also has changes in P-R interval, but it starts to show failure of the P-wave to propagate a QRS complex every time (i.e., intermittently the depolarization fails to reach the ventricles). The pattern of missed ventricular depolarizations, or blocked P-waves, is often very regular and described as a ratio of P-waves to QRS complex. The way in which the P-R interval changes in relation to the blocked P-waves produces subclassifications of second-degree blocks, Mobitz I and II.

Mobitz I (or Wenckebach)—The P-R interval progressively lengthens until a P-wave is missed and then goes back to its original length (figure 1.11). So P-R is longest before the dropped QRS complex and shortest immediately after it. This progressive difficulty in traversing the AV node is reflective of the node becoming increasingly refractory.

The image of an ECG shows four consecutive P-waves and QRS complexes and the P-R interval for each is shown in seconds. Each P-R interval is longer than the previous one. The first is 0.24 seconds, the next is 0.28 seconds, the next is 0.32 seconds and the fourth is 0.36 seconds. These four ECG complexes are then followed by a P-wave that does not have a following QRS complex. There is then a prolonged isoelectric period which is then ended with a normal P-wave, QRS sequence with a P-interval back at the original duration of 0.24 seconds.
Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds.

Mobitz II has blocked P-waves as well, but the P-R interval remains unchanged, and the P:QRS ratio appears in a fixed pattern (figure 1.12). This is a rarer and more serious condition and usually involves problems with the conduction system below the AV node, most commonly in the bundle branches. What can frequently been seen is a widening of the QRS complex that are generated.

ECG shows P-waves occurring regularly but some are not followed by QRS complexes. The example shows a normal P-wave, QRS complex, T-wave sequence followed by a P-wave without a subsequent QRS complex or T-wave. Then two normal P-QRS-T sequences which are followed by isolated normal looking P-waves without QRS complexes. The ECG then returns to normal structure.
Figure 1.12: Mobitz II (second-degree block) with arrows showing P-waves. The P-R interval is stable, and the ratio is 3:1.
Second-degree block summary
Prolonged P-R interval (>0.2 sec)
Intermittently blocked P-waves
Variable (Mobitz I) or stable (Mobitz II)

Table 1.11: Second-degree block summary.

Third-Degree Atrioventricular Block

A third-degree atrioventricular block is where no action potentials pass through the AV node, hence it is often called “complete heart block”. This is usually because of damage (e.g., ischemia) or disease (e.g., Lyme disease, sarcoidosis) affecting the AV node. In a third-degree atrioventricular block, no P-waves have associated QRS complexes. Without any descending control by the SA node pacemakers, the ventricular pacemaker cells are finally free to rule the ventricles (insert maniacal laughter). Consequently P-waves and QRS complexes are completely unrelated to each other, and this is termed “AV dissociation.” The ECG (figure 1.13) reflects this with P-waves occurring at an SA node rate (~75 bpm with parasympathetic tone) and the ventricles depolarizing at between thirty and fifty times per minute, depending on which ventricular tissue acts as pacemaker.

Normal P-waves occur at sinus rate. QRS complexes occur at a much slower rate and are completely independent of the P-waves. Arrows below the ECG point at the P-waves, arrows above the ECG point at the QRS complexes. More frequent arrows below the ECG than above emphasize the difference in atria and ventricular depolarization rates.
Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm.
Third-degree block summary
P-waves and QRS complexes dissociated

Table 1.12: Third-degree block summary.

 

 

 

 

Note:
Prior to reading the next sections, revisit the lead orientations of a 12-lead ECG, and it might be useful to have the normal ECG for comparison.

Left Bundle Branch Block

A left bundle branch block (LBBB) is generated when the conductivity of the His-Purkinje system in the left ventricle is compromised, either through damage or disease. The ECG changes, and criteria for LBBB relate to these changes in conductivity and the left-side location.

The image shows a 12-lead ECG print out depicting an example of left bundle branch block. Lead 1 tracing shows broadened QRS complexes and the R-wave appears to be notched with a peak followed by another peak. A similar double peaking is seen in the R-waves in the tracing from the AVR lead. As the R-wave is negative in this lead the double peaking makes a W like shape. The S-wave in leads V1 and V2 are negative and very large.
Figure 1.14: Example of LBBB with defining features labeled.

Because the normal route through conductive tissue is impaired or blocked, the depolarization has to travel through myocytes, which takes more time. Consequently, the QRS complex is wider (figure 1.14) (i.e., has a duration >120 msecs, with 80–100 msecs being normal). The slower conduction through the left ventricle means the right ventricle depolarizes first and the left last. This means the depolarization has a prominent right-then-left direction and will be moving away from lead V1, causing that lead to have a deep downward S-wave (figure 1.14).

The lateral leads (I, V5, and V6) normally show a downward deflecting Q-wave as normal septal deflection initially occurs left-to-right (i.e., away from the lateral leads). In LBBB the change in direction to right-to-left, plus the longer duration, eliminates the Q-wave from the lateral leads, and Q-waves will be small in aVL.

The image shows an ECG from lead V6 with a positive R-wave that is broader than normal and has two distinct peaks, similar to an uppercase letter M.
Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave.

The R-wave in the lateral leads may also change morphology when there is a distinct separation of right and then left ventricular depolarization. This manifests as an M-shaped R-wave (figure 1.15) or a notched R-wave in the lateral leads (figure 1.14).

Conversely a W-shaped R-wave may occur in leads facing the opposite direction (e.g., aVR) (figure 1.14).

LBBB summary (also see figure 1.14)
QRS complex >120 msecs
Dominant S-wave in V1
Absence of Q-waves in lateral leads

Table 1.13: LBBB summary.

Right Bundle Branch Block

The figure is comprised of two panels, one showing the ECG of lead V1. The other shows the ECG from lead I. The V1 ECG includes a broader wave that has a notched appearance with a peak, followed by another peak. The first peak has been labelled R and the second has been labelled R prime. The lead I ECG shows a slurred S-wave which has a shallower downward slope than a normal S-wave and so the S-wave has a longer duration.
Figure 1.16: Typical RSR’ pattern (upper) and slurred S-wave pattern (lower) of RBBB.

The causes and manifestations of a right bundle branch block (RBBB) bear some similarities to those described for LBBB, but of course this time its depolarization of the right ventricle is delayed. Causes of RBBB include ischemic heart disease again as well as other myocardial diseases, but pulmonary issues such as pulmonary embolism and cor pulmonale can be added to the list.

 

Again the QRS complex becomes broad (>120 msecs) because of the slower conduction through ventricular myocytes. However, the delayed activation of the right ventricle causes a secondary R-wave (RSR’) to occur in the right precordial leads (V1–V3) and a slurred S-wave in the lateral leads (I, aVL, and frequently V5 and V6) (figure 1.16).

 

RBBB summary
QRS complex >120 msecs
RSR’ pattern in V1–V3
Slurred S-wave in lateral leads

Table 1.14: RBBB summary.

Wolff-Parkinson-White Syndrome

Normally the only electrical connection between the atria and the ventricles is the AV node. Otherwise the fibrous skeleton of the heart electrically insulates the atria from the ventricles. In Wolff-Parkinson-White (WPW) syndrome, that insulation is incomplete, and an “accessory pathway” connects the electrical system of the atria directly to the ventricles. If you think of the AV node as a bridge over the fibrous wall with regulated access, the accessory pathway is like a pathological tunnel under it with no regulation.

The accessory pathway provides a second route (figure 1.17) for normal sinus rhythm to pass from atrium to ventricle much more quickly (there is no AV node delay), thus the P-R interval is shortened. Because of this “preexcitation” through the accessory pathway, the ECG shows a slurring of the onset of the QRS complex, referred to as a delta wave because of its triangular shape (figure 1.18).

Two diagrams of the conductive pathways of the heart are shown. The first is normal, with an arrow showing normal transition of the action potential through the AV node into and around the ventricular myocardium. The second heart diagram shows two arrows from the AV node - one taking the normal conductive pathway into the ventricles, the other travelling across the atrium and passing through the atrial-ventricular septum through an aberrant pathway into the ventricles. This aberrant pathway causes the WPW syndrome. ECGs below each heart diagram show a normal ECG associated with the normal conductive pathway, but with the WPW pathway the associated ECG shows a delta wave which is seen as a slower rise to the QRS complex compared to the sharp depolarization seen in the normal ECG.
Figure 1.17: Schematics of normal WPW syndrome conductivity pathways.
The figure shows an ECG with an abnormal R-wave. The R-wave has a broad base and then narrows as it ascends into a more normal, narrow width. The board base means the gap between the P-wave and R-wave is very short and gives the appearance of an extra wave starting after the P-wave and merging with the R-wave. The extra wave has been labelled the delta wave.
Figure 1.18: Delta wave of WPW syndrome.

WPW syndrome is often asymptomatic, and patients do not require immediate treatment. However, if atrial fibrillation occurs in a WPW patient, the accessory pathway can allow the atrial fibrillation waves through to the ventricle (with no AV nodal refractory period to prevent them). Consequently a high ventricular rate is seen, and the risk of ventricular fibrillation being established means immediate clinical attention is required.

WPW syndrome summary
Short P-R interval (120 msecs)
Delta wave slurring the onset of QRS complexes
Broad QRS complexes (>100 msecs)

Figure 1.18: Delta wave of WPW syndrome.

Hyper- and Hypocalcemia

Moderate rises in extracellular levels of Ca++ (3.0–3.4 mmol/L, normal = 2.1–2.6 mmol/L) block the movement of sodium through voltage-gated sodium channels. This results in a reduced depolarization of myocytes, and consequently repolarization time is less. Raised extracellular Ca++ also changes the closing kinetics of the L-type Ca++ channels such that the plateau phase of the cardiac action potential is shortened and repolarization occurs earlier. These two effects manifest as the most common ECG finding of short QT intervals, mainly through shortening of the ST segment (figure 1.19).

The figure shows three ECGs. The ECGs are typical of hypocalcemia, hypercalcemia, and a normal ECG for comparison. The hypercalcemia ECG shows a shortened Q-T interval whereas the hypocalcemia ECG shows a prolonged Q-T interval compared to the normal.
Figure 1.19: Changes in QT interval in moderate hypercalcemia and hypocalcemia.
The figure shows ECGs from three leads, (V3, V4, and V5). In each lead a J-wave appears and arrows point to the J-wave in leads V3 and V4. The J-wave consists of an extra, small positive inflection after the R-wave then slopes back to the isoelectric state before the onset of a normal looking T-wave.
Figure 1.20: J-waves arise during hypothermia but can also be caused by hypercalcemia.

If hypercalcemia becomes severe (>3.4 mmol/L) then Osborne waves (or J-waves) may be seen—an extra wave seen at the J-point of the ECG (the R-ST junction). The pathophysiology of the J-wave (figure 1.20) is poorly understood, but it is likely caused by an early repolarization of the epicardium—think of it as a chunk of early T-wave. (The other common cause of J-waves is hypothermia.) During hypocalcemia (<2.2 mmol/L) the opposite changes are seen in the ECG—the QT interval is prolonged, primarily due to a lengthened ST segment (figure 1.19).

Hypercalcemia summary Hypocalcemia Summary
Reduced ST and QT intervals Prolonged ST and QT intervals
J-waves in severe hypercalcemia

Table 1.16: Hyper- and hypocalcemia summary.

Hyper- and Hypokalemia

The pathophysiology is not as simple as changes in extracellular K+ changing the electrochemical gradient for K+. Because of potassium’s role in maintaining the resting membrane potential, shifts in extracellular potassium can also influence the activity of Na+ and Ca++ channels.

The figure shows lead V4 of an ECG associated with hypokalemia. The R-wave looks normal, but the T-wave is inverted with a negative deflection (an arrow points to the inverted T-wave). Leading from the T-wave the signal transitions to a positive hump (labelled with an arrow titled U-wave). The humped U-wave declines toward the isoelectric state and then the subsequent P-wave of the next myocardial depolarization occurs. The next complex also shows the inverted T-wave and the U-wave.
Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia.

 

Your intuition may lead you to think that hypokalemia (<2.7 mmol/L) would increase K+ conductances because there is a greater gradient from inside to outside the cell, but that is not the case. Instead hypokalemia suppresses K+ channel conductances by destabilizing K+ channels. With low K+ conductance, the ECG changes reflect problems with repolarization. The T-wave is flattened and can be inverted, and a prominent U-wave may be seen in the precordial leads (figure 1.21). ST depression may also be apparent.

 

As hypokalemia also inhibits Na+-K+ ATPase, Na+ accumulates inside the cell. This in turn leads to an accumulation of Ca++ because of a subsequent failure of the Na+-Ca++ exchanger. Extended presence of these two positive ions inside the myocyte prolongs the action potential and may manifest as an increased width and amplitude of the P-wave.

The figure shows the X- and Y-axis of the graph. The X-axis is time with seconds as units and the Y-axis is membrane potential with millivolts as units. A gray line shows a normal myocyte action potential with a positive inflection from a resting membrane potential of about -80 mv to above 0 mv. The depolarization then declines as repolarization begins slowly, then there is a rapid return to the same resting membrane potential of -80 mv. The duration of this depolarization is 0.2 s. On the same graph there is a red line overlaid. This shows the membrane potential of a myocyte exposed to mild hypokalemia. The red line differs from the normal (gray) depolarization with a lower resting membrane potential of -100 mv and a longer duration of 0.3 seconds, otherwise the shape is about the same. A brown line is also overlaid to show the impact of worsening hypokalemia, this also shows a resting membrane potential of -100 mv and the action potential again involves a depolarization to above 0 mV, the repolarization however involves early afterdepolarization - the line begins to descend as normal but then at about -25 mv it rises up again to form a hump before descending back to resting membrane potential of -100 mV. The hump is labelled as an EAD (early after-depolarization) and extends the period of depolarization so it lasts about 0.8 s. A fourth, black line is also shown with a lower resting membrane potential at -100 mv again and a depolarization to above 0 mv. The repolarization phase is represented by the black line beginning to descend but during this descent two EADs occur and are seen as two humps, one after the other. The EADs are followed by a full repolarization to -100 mv, but they have extended the depolarization time to about 1 s.
Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia.

 

As hypokalemia worsens, the problems with K+ conductance and repolarization increase, and the myocardium becomes susceptible to early after-depolarization (EAD) arrhythmias.

 

As K+ is retained in the myocyte (due to the poor K+ conductance) and elevated intracellular Na+ and Ca++ results in the myocyte being more capable of depolarizing again.  Because these after-depolarizations (figure 1.22) may not be uniform across the whole myocardium, an arrhythmia can be established. Potential arrhythmias include life-threatening forms, such as VT, VF, or torsades de pointes.

 

Hyperkalaemia produces different changes in myocardial excitability depending on the degree of excess potassium. Again the changes in excitability do not necessarily follow an intuitive logic of the change in the electrochemical gradient of K+. Mild hyperkalemia (5.5–6.5 mEq/L) causes peaked T-waves (figure 1.23)—the first sign of raised extracellular potassium. The excess potassium allosterically interferes with K+ channels and, inverse to hypokalemia, causes an increase in K+ conductance (despite the lower transmembrane gradient).

The ECG of mild hyperkalemia shows a relatively normal ECG in lead V5 except for very high T-waves that are peaked and exceed the height of the proceeding R-wave.
Figure 1.23: Peaked T-waves with mild hyperkalemia.

Moderate hyperkalemia (5.5–6.5 mEq/L) raises the membrane potential closer to the threshold of voltage-gated Na+ channels (-70 mV) and voltage-gated Ca++channels. Consequently these channels are more likely to fire and cause depolarization, hence the myocardium is initially more excitable. However, this persistent depolarization leaves the slow deactivation (h) gates on Na+ channels closed for longer, and the ECG manifestations soon reflect a decreased excitability. The P-wave is longer but has low amplitude (and may eventually disappear), the QT interval is prolonged, and there is a decreased R-wave amplitude (figure 1.24). In simpler terms, the overstimulation of Na+ channels causes them to “lock up.”

A 12-lead ECG associated with moderate hyperkalemia shows low, long P-waves and diminished R-waves. Conversely the T-waves are very pronounced and they tower over the smaller R-waves in leads V1-3.
Figure 1.24: Big T, and little p and r of moderate hyperkalemia.
The ECG associated with severe hyperkalemia has leads 1-3 shown. The QRS is very broad and almost sine-wave like with a slow descending negative component that rises up to become a slow ascending wave before returning to baseline.
Figure 1.25: Preterminal ECG of severe hyperkalemia.

Severe hyperkalemia (>7.0 mEq/L) sees a worsening of the unresponsiveness of the myocardium, and the SA node rhythm is slowed, producing sinus bradycardia until there is no P-wave. Conductive issues arise, and a high-grade atrioventricular block is likely, allowing ventricular pacemakers to take over, but the ventricular myocardium is also unresponsive, so the QRS complex becomes broad and sine wave–like on the ECG (figure 1.25); this is a preterminal rhythm. At this point cardiovascular collapse and death are imminent, often through a VF finale.

Hypokalemia summary Hyperkalemia summary
Flattened or inverted T-wave Mild: Peaked T-waves
Increased P-wave amplitude Moderate: Long P-wave, prolonged QT interval, decreased amplitude R-wave
Induced arrhythmias in severe hypokalemia Severe: Loss of P-wave, ventricular sine wave action potential

Table 1.17: Hypo- and hyperkalemia summary.

References, resources, and further reading

Text

Burns, Ed, and Robert Buttner. Hypercalcaemia. Lift in the Fast Lane, 2021. https://litfl.com/hypercalcaemia-ecg-library/, CC BY 4.0.

Burns, Ed, and Robert Buttner. Hypocalcaemia. Life in the Fast Lane, 2021. https://litfl.com/hypocalcaemia-ecg-library/, CC BY 4.0.

Buttner, Robert, and Ed Burns. Hyperkalaemia. Life in the Fast Lane. https://litfl.com/hyperkalaemia-ecg-library/, CC BY 4.0.

Buttner, Robert, and Ed Burns. Hypokalaemia. Life in the Fast Lane, 2021. https://litfl.com/hypokalaemia-ecg-library/, CC BY 4.0.

Chhabra, Lovely, Amandeep Goyal, and Michael D. Benham. Wolff Parkinson White Syndrome. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK554437/, CC BY 4.0.

Custer, Adam M., Varun S. Yelamanchili, and Sarah L. Lappin. Multifocal Atrial Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459152/, CC BY 4.0.

Farzam, Khashayar, and John R. Richards. Premature Ventricular Contraction. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532991/, CC BY 4.0.

Foth, Christopher, Manesh Kumar Gangwani, and Heidi Alvey. Ventricular Tachycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK532954/, CC BY 4.0.

Hafeez, Yamama, and Shamai A. Grossman. Sinus Bradycardia. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK493201/, CC BY 4.0.

Harkness, Weston T., and Mary Hicks. Right Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK507872/, CC BY 4.0.

Heaton, Joseph, and Srikanth Yandrapalli. Premature Atrial Contractions. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK559204/, CC BY 4.0.

Kashou, Anthony H., Amandeep Goyal, Tran Nguyen, and Lovely Chhabra. Atrioventricular Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK459147/, CC BY 4.0.

“Learn the Heart.” Healio. https://www.healio.com/cardiology/learn-the-heart.

Ludhwani, Dipesh, Amandeep Goyal, and Mandar Jagtap. Ventricular Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK537120/, CC BY 4.0.

Nesheiwat, Zeid, Amandeep Goyal, and Mandar Jagtap. Atrial Fibrillation. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK526072/, CC BY 4.0.

Pipilas, Daniel C., Bruce A. Koplan, and Leonard S. Lilly. “The Electrocardiogram.” In Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty, 5e edited by Leonard S. Lilly, Chapter 4. Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer Business, 2010.

Rodriguez Ziccardi, Mary, Amandeep Goyal, and Christopher V. Maani. Atrial Flutter. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK540985/, CC BY 4.0.

Scherbak, Dmitriy, and Gregory J. Hicks. Left Bundle Branch Block. Treasure Island, FL: StatPearls Publishing, 2022. https://www.ncbi.nlm.nih.gov/books/NBK482167/, CC BY 4.0.

Figures

Figure 1.1: Atrial fibrillation. Grey, Kindred. 2022. CC BY-NC-SA 4.0. Added Burns, Ed, and Robert Buttner. Example 2 (image cropped), Atrial Fibrillation. Life in the Fast Lane, 2021. https://litfl.com/atrial-fibrillation-ecg-library/, CC BY-NC-SA 4.0https://archive.org/details/1.1_20220113

Figure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation, atrial flutter, and multifocal atrial tachycardia (MAT). Grey, Kindred. 2022. CC BY-NC-SA 4.0. Added Burns, Ed, and Robert Buttner. Example 1 (image cropped), Multifocal Atrial Tachycardia (MAT). Life in the Fast Lane, 2021. https://litfl.com/multifocal-atrial-tachycardia-mat-ecg-library, CC BY-NC-SA 4.0. Added Burns, Ed, and Robert Buttner. Example 4 (image cropped), Atrial Fibrillation (image cropped). Life in the Fast Lane, 2021. https://litfl.com/atrial-fibrillation-ecg-library/, CC BY-NC-SA 4.0. Added Buttner, Robert, and Ed Burns. Example 3 (image cropped), Atrial Flutter. Life in the Fast Lane, 2021. https://litfl.com/atrial-flutter-ecg-library/, CC BY-NC-SA 4.0https://archive.org/details/1.2_20220113

Figure 1.3: Atrial flutter. Burns, Ed, and Robert Buttner. Example 5 (image cropped), Atrial Flutter. Life in the Fast Lane, 2021. https://litfl.com/atrial-flutter-ecg-library/, CC BY-NC-SA 4.0.

Figure 1.4: Three distinct P-wave morphologies in a case of MAT. Burns, Ed, and Robert Buttner. Example 1 (image cropped), Atrial Flutter. Life in the Fast Lane, 2021. https://litfl.com/atrial-flutter-ecg-library/, CC BY-NC-SA 4.0.

Figure 1.5: Atrial bigeminy in PAC. Dawn. “ECG Basics: Sinus Rhythm with Atrial Bigeminy” (image cropped). ECG Guru, 2012. https://www.ecgguru.com/ecg/ecg-basics-sinus-rhythm-atrial-bigeminyCC BY-NC-SA 4.0.

Figure 1.6: PVCs have a wider complex and are followed by a compensatory pause. Burns, Ed, and Robert Buttner. Multifocal PVCs Example (image cropped, scale and arrows removed, and new arrows added), Premature Ventricular Complex (PVC). Life in the Fast Lane, 2021. https://litfl.com/premature-ventricular-complex-pvc-ecg-library, CC BY-NC-SA 4.0.

Figure 1.7: Monomorphic and polymorphic VT. Grey, Kindred. 2022. CC BY-NC-SA 4.0. Added Buttner, Robert, and Ed Burns. Monomorphic VT Figure, Ventricular Tachycardia—Monomorphic VT. Life in the Fast Lane, 2021. https://litfl.com/ventricular-tachycardia-monomorphic-ecg-library, CC BY-NC-SA 4.0. Added Smith, Stephen W. Polymorphic VT Figure (second image, cropped), “Polymorphic Ventricular Tachycardia.” Dr. Smith’s ECG Blog, October 12, 2013. http://hqmeded-ecg.blogspot.com/2013/10/polymorphic-ventricular-tachycardia.html, CC BY-NC-SA 4.0. https://archive.org/details/1.7_20220113

Figure 1.8: Torsades de Pointes. Grey, Kindred. 2022. CC BY-NC-SA 4.0. Added Burns, Ed, and Robert Buttner. Torsades de Pointes Figure (image superimposed), Polymorphic VT and Torsades de Pointes (TdP). Life in the Fast Lane, 2021. https://litfl.com/polymorphic-vt-and-torsades-de-pointes-tdpCC BY-NC-SA 4.0https://archive.org/details/1.8_20220113

Figure 1.9: Example of ventricular fibrillation with no recognizable P-waves or QRS complexes. Burns, Ed, and Robert Buttner. Example 2, Ventricular Fibrillation (VF). Life in the Fast Lane, 2021. https://litfl.com/ventricular-fibrillation-vf-ecg-library, CC BY-NC-SA 4.0.

Figure 1.10: Example of first-degree block with P-R interval >0.2 seconds. Larkin, John, and Robert Buttner. First Degree Heart Block Figure, First Degree Heart Block. Life in the Fast Lane, 2021. https://litfl.com/first-degree-heart-block-ecg-library, CC BY-NC-SA 4.0.

Figure 1.11: Mobitz I (second-degree block) with P-R intervals shown in seconds. Grey, Kindred. 2022. CC BY-NC-SA 4.0. Added Burns, Ed, and Robert Buttner. AV Block: 2nd Degree, Mobitz Type I Figure (image superimposed), AV Block: 2nd Degree, Mobitz I (Wenckebach Phenomenon). Life in the Fast Lane, 2021. https://litfl.com/av-block-2nd-degree-mobitz-i-wenckebach-phenomenon, CC BY-NC-SA 4.0. https://archive.org/details/1.11_20220113

Figure 1.12: Mobitz II (second degree block) with arrows showing P waves. P-R interval is stable and ratio is 3:1. Grey, Kindred. 2022. CC BY-NC-SA 4.0. Added Burns, Ed, and Robert Buttner. Mobitz Type II Rhythm Strip Figure (image superimposed), AV Block: 2nd Degree, Mobitz II (Hay Block). Life in the Fast Lane, 2021. https://litfl.com/av-block-2nd-degree-mobitz-ii-hay-block, CC BY-NC-SA 4.0https://archive.org/details/1.12_20220113

Figure 1.13: Third-degree block with P-waves (black arrows) having an SA node rate of 100 bpm and the ventricles depolarizing (blue arrows) at 33 bpm. Larkin, John, and Robert Buttner. Complete Heart Block Figure, AV Block: 3rd Degree (Complete Heart Block). Life in the Fast Lane, 2021. https://litfl.com/av-block-3rd-degree-complete-heart-block, CC BY-NC-SA 4.0.

Figure 1.14: Example of LBBB with defining features labeled. Grey, Kindred. 2022. CC BY-NC-SA 4.0. Added Buttner, Robert, and Ed Burns. Example 1 (image superimposed), Left Bundle Branch Block (LBBB). Life in the Fast Lane, 2021. https://litfl.com/left-bundle-branch-block-lbbb-ecg-library, CC BY-NC-SA 4.0https://archive.org/details/1.14_20220113

Figure 1.15: Changes in R-wave morphology as differences in left and right depolarization produce an M-shaped wave. Buttner, Robert, and Ed Burns. LBBB Figure (image cropped), Left Bundle Branch Block (LBBB). Life in the Fast Lane, 2021. https://litfl.com/left-bundle-branch-block-lbbb-ecg-library, CC BY-NC-SA 4.0.

Figure 1.16: Typical RSR’ pattern (upper) and slurred S (lower) of RBBB. Grey, Kindred. 2022. CC BY-NC-SA 4.0. Added Typical RSR’ Pattern (‘M’-Shaped) QRS in V1 Figure (image superimposed), Right Bundle Branch Block (RBBB). Life in the Fast Lane, 2021. https://litfl.com/right-bundle-branch-block-rbbb-ecg-library, CC BY-NC-SA 4.0. Added Wide Slurred S Wave in Lead I Figure (image superimposed), Right Bundle Branch Block (RBBB). Life in the Fast Lane, 2021. https://litfl.com/right-bundle-branch-block-rbbb-ecg-library, CC BY-NC-SA 4.0https://archive.org/details/1.16_20220113

Figure 1.17: Schematics of normal WPW syndrome conductivity pathways. Grey, Kindred. 2022. CC BY 4.0. https://archive.org/details/1.17_20220113

Figure 1.18: Delta wave of WPW syndrome. Grey, Kindred. 2022. CC BY-NC-SA 4.0. Added Cadogan, Mike, and Robert Buttner. ECG Delta Wave 3 Figure (image superimposed), Delta Wave. Life in the Fast Lane, 2022. https://litfl.com/delta-wave-ecg-library, CC BY-NC-SA 4.0. https://archive.org/details/1.18_20220113

Figure 1.19: Changes in Q-T interval in moderate hypercalemia and hypocalcemia. Grey, Kindred. 2022. CC BY 4.0. https://archive.org/details/1.19_20220113

Figure 1.20: J-waves arising at the J-point during hypothermia but can also be caused by hypercalcemia. Grey, Kindred. 2022. CC BY-NC-SA 4.0. Added Example 3 (image superimposed), Osborn Wave (J Wave). Life in the Fast Lane, 2022. https://litfl.com/osborn-wave-j-wave-ecg-library, CC BY-NC-SA 4.0https://archive.org/details/1.20_20220113

Figure 1.21: A prominent U-wave and inverted T-wave associated with hypokalemia. Buttner, Robert, and Ed Burns. Hypokalaemia Figure (image letters edited), Hypokalaemia. Life in the Fast Lane, 2021. https://litfl.com/hypokalaemia-ecg-library, CC BY-NC-SA 4.0.

Figure 1.22: Early after-depolarizations occurring in a cardiac action potential due to poor K+ conductance in hypokalemia. Grey, Kindred. 2022. CC BY 4.0. https://archive.org/details/1.22_20220113

Figure 1.23: Peaked T-waves with mild hyperkalemia. Grey, Kindred. 2022. CC BY-NC-SA 4.0. Added Buttner, Robert, and Ed Burns. Example 2 (image superimposed), Hyperkalaemia. Life in the Fast Lane, 2021. https://litfl.com/hyperkalaemia-ecg-library, CC BY-NC-SA 4.0. https://archive.org/details/1.23_20220113

Figure 1.24: Big T, little p and r of moderate hyperkalemia. Cadogan, Mike. Figure 4, Hyperkalaemia Clinical Case. Life in the Fast Lane, 2020. https://litfl.com/hyperkalaemia-clinical-case, CC BY-NC-SA 4.0.

Figure 1.25: Preterminal ECG of severe hyperkalemia. Buttner, Robert, and Ed burns. Figure 6 (image cropped), Hyperkalaemia. Life in the Fast Lane, 2021. https://litfl.com/hyperkalaemia-ecg-library, CC BY-NC-SA 4.0.