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2 Approach toECG Interpretation inCritical Care
Prompt recognition of ST-segment deviations is crucial for timely intervention
and management to minimize myocardial damage.
It is imperative to meticulously identify deviations from the normal J point, as
they may be crucial indicators of underlying cardiac pathology or ischemic events.
Differential diagnoses should be considered based on the clinical context, accompanying symptoms, and additional ECG ndings to determine appropriate management strategies and interventions.
37
2.4.5 ST Segment
The ST segment reects the period between ventricular depolarization (end of the
QRS complex) and repolarization [3–5]. It extends from the J point to the onset of
the T wave. Understanding the normal characteristics and recognizing pathological
changes in the ST segment are essential for accurate interpretation and diagnosis in
clinical practice.
2.4.6 T Wave
T waves follow the QRS complex and reect the electrical recovery of the ventricles
as they prepare for the next cardiac cycle [3–5]. The T wave is typically a smooth,
rounded waveform with upward deection in most leads, though variations in morphology can occur. It corresponds to the phase of ventricular repolarization, during
which potassium ions exit the cardiac myocytes. This leads to cellular relaxation
and restoration of the electrical potential. Clinically, abnormalities in the T-wave
morphology or duration can indicate underlying cardiac pathology or electrolyte
imbalances.
The duration of the T wave is generally less than 0.2seconds (or 200ms), and its
voltage varies widely among individuals and leads. A typical T-wave voltage range
is 0.5–5 millivolts (mV), but higher voltages can be observed in certain pathological
conditions such as ventricular hypertrophy.
Abnormalities such as attening, inversion, or prominent peaked T waves may
indicate underlying cardiac pathology, for example:
T
-wave inversion: Inverted T waves can be indicative of myocardial ischemia,
•
injury, or infarction. They may also occur in the setting of electrolyte imbalances
(e.g., hypokalemia), left ventricular hypertrophy, or conduction abnormalities.
• Peaked T waves: Tall, peaked T waves may suggest ischemia or hyperkalemia,
especially in the setting of acute kidney injury or metabolic acidosis. Peaked T
waves are considered a medical emergency and require immediate attention to
prevent life-threatening arrhythmias.
• Flattened T waves: Flattened T waves may be nonspecic but can be associated
with myocardial ischemia, electrolyte disturbances, or early repolarization patterns.
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M. H. Vicco et al.
2.4.7 QT Interval
The QT interval on an ECG represents the duration of ventricular depolarization
and repolarization [3–5]. It begins at the onset of the QRS complex and ends at the
termination of the T wave, encompassing the total electrical activity of ventricular
contraction and relaxation. Thus, it corresponds to the period when the ventricles
contract (systole) and then relax (diastole) before the next cardiac cycle.
Normal QT intervals vary depending on age, sex, and heart rate. In adults, a nor-
mal QT interval is typically less than 450ms for men and less than 460 ms for
women, according to consensus when the heart rate (HR) is between 60 and 100
beats per minute. QT interval values outside this range may be considered abnormal
and warrant further evaluation. Given the dependence of QT interval duration on
heart rate, it is crucial to correct QT interval variations based on abnormal heart
rates using formulas such as Bazett’s, Fridericia’s, or other validated methods. QT
correction helps standardize QT interval interpretation across different heart rates.
Bazett’s correction formula is still utilized by many clinicians worldwide; how-
ever, the formula is most accurate between the heart rates of 60 and 100bpm. At
heart rates of less than 60bpm, the formula under-corrects the QTc value, while at
HR values over 100bpm, the formula overcorrects the QTc interval. Due to this
limitation, other formulas have been proposed:
•
•
•
•
s formula: QTc=QT/[√RR in seconds] [6].
Bazett’
Fridericia’
Framingham’
Hodges’
s formula: QTc=QT/(RR 0.33) [6]
s formula: QTc=QT+0.154(1−RR) [6]
s formula: QTc=QT+1.75(HR−60) [6]
Prolongation of the QT interval can predispose individuals to life-threatening
arrhythmias such as polymorphic ventricular tachycardia and ventricular brillation, increasing the risk of sudden cardiac death [7, 8]. The causes of QT prolongation include congenital long QT syndrome, electrolyte imbalances (e.g., hypokalemia
and hypomagnesemia), certain medications (e.g., antiarrhythmics and psychotropic
drugs), and myocardial ischemia (Table2.2).
Table 2.2 Drugs associated with QTc prolongation and polymorphic ventricular tachycardia [7, 8]
Antiarrhythmics Antimicrobials Antidepressants Antipsychotics Others
Amiodarone Levooxacin Amitriptyline Haloperidol Cisapride
Sotalol Ciprooxacin Desipramine Droperidol Sumatriptan
Quinidine Gatioxacin Imipramine Quetiapine Zolmitriptan
Procainamide Moxioxacin Doxepin Thioridazine Arsenic
Dofetilide Clarithromycin Fluoxetine Ziprasidone Dolasetron
Ibutilide Erythromycin Sertraline Methadone
Ketoconazole Venlafaxine
Itraconazole
2 Approach toECG Interpretation inCritical Care
Conversely, shortening of the QT interval may occur in hypercalcemia, in hyper-
thyroidism, or following cardiac sympathectomy. The short QT syndrome is an
inherited cardiac channelopathy much less common than the long QT syndrome.
Regardless of its etiology, short QT syndrome is also associated with an increased
risk of arrhythmias and sudden cardiac death.
39
2.4.8 U Wave
The U wave is a small, often subtle deection, low in amplitude, seen following
the T wave. It is most prominent in leads V2–V4 but may be present in other
leads as well [3–5]. The precise physiological origin of the U wave is not fully
understood, but it is believed to reect the repolarization of the papillary muscles
and Purkinje bers of the ventricles. While the U wave is commonly observed in
normal ECGs, its clinical signicance is less well dened compared to other
ECG components.
2.4.9 RR Interval
The RR interval represents the interval between consecutive R waves, reecting the
duration of one complete cardiac cycle. Its duration varies based on heart rate;
shorter intervals correspond to faster heart rates, while longer intervals indicate
slower heart rates [3–5]. In adults with a normal sinus rhythm, the RR interval typically ranges from 1000 to 600ms (50–100 beats per minute).
2.5 Approach toECG Interpretation Using
the“Left- to-Right Approach”
Reading an ECG involves a systematic approach from left to right, examining various components to assess cardiac rhythm, conduction, and morphology [3–5].
The process begins by identifying the paper speed and calibration marks on the
ECG strip. The standard paper speed is 25mm/s horizontally and 10mm/mV vertically. The calibration marks indicate the standardization of voltage measurements.
Each small square typically represents 1mm or 0.1mV vertically, while each large
square represents 5mm or 0.5mV.
After checking the speed and calibration, the initial focus lies on assessing tech-
nical aspects such as lters, patient’s name, and lead placement. Then attention
starts by focusing on rhythm and frequency. The normal rhythm is sinus rhythm,
characterized by a regular RR interval and upright P waves preceding each QRS
complex. Normal HR falls within the range of 60–100 bpm, although it can be
40
M. H. Vicco et al.
higher in young children and lower in athletes or individuals with elevated vagal
tone. It is calculated by measuring the distance between R waves (RR interval) with
the formula:
• HR=60/RR interval (in seconds).
For example, if the RR interval is 0.8seconds, the HR would be calculated as:
• HR=60/0.8; HR=75bpm.
Various drugs can inhibit or impair sinus node and conduction system function
through various pharmacological mechanisms. Common drugs in critical care associated with bradyarrhythmia include opioid analgesics, anticonvulsants, antihistaminics, antipsychotics, benzodiazepines, steroids, and sedatives such as
dexmedetomidine.
The next step is to determine if the electrical activation follows a normal pattern,
which is done by assessing each of the elements that constitute the heart cycle. For
this, the left-to-right approach can be used.
2.5.1 P Wave
When assessing the P wave, it is useful to consider if P waves are present, if the P
wave originates from the sinus node, if there are multiple P wave morphologies, if
the P waves are regular, and the P wave rate [3–5].
As the normal atrial impulse originates from the sinus node (located in the upper
right part of the right atrium), the activation front will propagate downward and
from right to left. Therefore, the P wave is usually positive in lead II, which is the
best lead for assessing the presence of the P wave and its regularity on the ECG.If
P waves are not visible, then it could be because they are absent or hidden (blended
with other ECG waves).
Once the presence of P waves is determined, the wave should be analyzed to
see if its origin is the sinus node. A P wave originating from the sinus node typically has a smooth, rounded morphology with a duration of ≤0.12 seconds
(120 ms). Abnormalities in the left atrium, such as dilation, can sometimes be
detected by assessing the morphology of the P wave. Lead V1 is particularly informative in evaluating the condition of the left atrium. In this lead, the P wave often
exhibits a biphasic pattern, with the initial positive deection originating from the
right atrium.
The axis of the P wave (the direction of its electrical vector) can provide clues
about its origin. A P wave with a normal axis (upright in lead II, biphasic, or inverted
in lead aVR) is suggestive of a sinus node origin. Deviations from this axis may
indicate ectopic atrial depolarization. In addition, the P wave precedes the QRS
complex consistently. This reects the physiological sequence of atrial depolarization preceding ventricular depolarization. Any variation from this pattern may indicate an abnormal atrial depolarization site.
2
Approach toECG Interpretation inCritical Care
41
2.5.1.1 Atrial Arrhythmias
Atrial Fibrillation
Atrial brillation (AF) (Fig.2.4) is the most common sustained arrhythmia and can
manifest as paroxysmal or persistent [9, 10]. In paroxysmal AF, the onset and termination of episodes may be visible on an ECG or more commonly on a Holter monitor.
Within the atria, there is chaotic electrical activity, characterized by very rapid activations exceeding 300cycles per minute. These impulses irregularly reach the AV node,
which regulates their passage to the His-Purkinje system to safeguard ventricular
hemodynamics. Consequently, the ventricular response appears irregularly irregular.
While AF typically results in narrow QRS tachycardia, widened QRS complexes
may occur due to bundle branch block or the presence of an accessory pathway.
In the absence of an accessory pathway, the number of impulses conducted to the
ventricles depends on the “strictness” of the AV node, determined by its anatomical
characteristics and medications. Agents such as beta-blockers and calcium channel
blockers are primarily used to slow AV nodal conduction. Digoxin also affects AV
nodal conduction but is considered a weaker agent. This approach, termed rate control strategy, manages the heart rate. Alternatively, the rhythm control strategy aims
to restore and maintain sinus rhythm. Electrical cardioversion is the most effective
method for restoring sinus rhythm, especially in unstable patients. Pharmacological
agents (e.g., amiodarone, vernakalant, ecainide, or propafenone) may also be used,
particularly for recent-onset AF, in stable patients.
Furthermore, several drug classes are linked to AF development, including ino-
tropic agents (e.g., dobutamine, dopamine, and levosimendan), antiarrhythmics
(e.g., adenosine, amiodarone, atenolol, digoxin, diltiazem, and verapamil), as well
Fig. 2.4 Atrial brillation Nathanson LA, McClennen S, Safran C, Goldberger AL.ECG WaveMaven: Self-Assessment Program for Students and Clinicians. http://ecg.bidmc.harvard.edu
42
M. H. Vicco et al.
as medications frequently used in critical care medicine (e.g., aminophylline, theophylline, albuterol, aformoterol, corticosteroids, uticasone, ipratropium, pseudoephedrine, salmeterol, and atropine) [9, 10].
Returning to the ECG, while an irregularly irregular HR is typical of AF, other
rapid atrial arrhythmias may produce a similar ventricular response pattern, such as
atypical utter, atrial tachycardias, or typical utter in certain circumstances.
Adenosine administration or carotid sinus massage may aid in clarifying the ECG
by enhancing visualization of atrial activity and separating QRS complexes.
Atrial Flutter
Atrial utter (AFL) (Fig.2.5) is a supraventricular tachyarrhythmia characterized
by regular atrial depolarizations at rates typically between 240 and 340bpm [11].
AFL shares similarities with AF but differs in its distinct pattern of atrial activation.
The underlying mechanism of AFL involves reentry circuits within the atria, most
commonly revolving around the tricuspid annulus. Macro-reentry loops perpetuate
rapid and organized atrial depolarizations, leading to the characteristic sawtooth
pattern on ECG.Unlike the brillation waves in AF, utter waves in atrial utter
have a more organized appearance.
Atrial Tachycardia
Atrial tachycardia (AT) is a common cardiac arrhythmia characterized by rapid, abnormal electrical activity originating from the atria, leading to an increased heart rate [12].
It poses signicant clinical implications due to its association with symptoms such as
Fig. 2.5 Atrial utter Nathanson LA, McClennen S, Safran C, Goldberger AL.ECG Wave-Maven:
Self-Assessment Program for Students and Clinicians. http://ecg.bidmc.harvard.edu
2
proach toECG Interpretation inCritical Care
Ap
43
palpitations, dyspnea, and potential hemodynamic compromise. Early and accurate
diagnosis is essential for appropriate management and prevention of complications.
AT typically arises from abnormal automaticity or triggered activity within the atrial
myocardium. AT may also result from reentry circuits involving anatomical or functional abnormalities. Mechanisms underlying AT include enhanced automaticity of
atrial cells, focal ectopic beats originating from specic sites, or micro-reentrant circuits within the atria. Factors such as sympathetic stimulation, electrolyte imbalances,
structural heart disease, and ischemia can predispose individuals to AT.
The ECG serves as the foundation for diagnosing AT. Specic ECG criteria aid
in distinguishing AT from other supraventricular arrhythmias. The following features are the characteristics of AT [3–5]:
• P-wave morphology: In AT, P waves may exhibit abnormal shapes, durations,
and morphologies compared to sinus rhythm. Sometimes, P waves may blend
into the preceding or following T waves, making them difcult to distinguish.
• Atrial rate: AT typically presents with a regular atrial rate ranging from 100 to
250bpm.
• P-wave morphology in different leads: Variability in P-wave morphology across
different leads indicates multifocal or chaotic atrial activity, characteristic of AT.
Multifocal Atrial Tachycardia
Multifocal atrial tachycardia (MAT) (Fig.2.6) is a distinct form of supraventricular
tachyarrhythmia characterized by irregular atrial activity originating from multiple
ectopic foci within the atria [12]. Its diagnosis poses challenges due to its variable
presentation and similarity to other atrial arrhythmias. The pathogenesis of MAT
involves enhanced automaticity and triggered activity in atrial cells, often
Fig. 2.6 Multifocal atrial tachycardia Nathanson LA, McClennen S, Safran C, Goldberger
AL.ECG Wave-Maven: Self-Assessment Program for Students and Clinicians. http://ecg.bidmc.
harvard.edu
44
M. H. Vicco et al.
exacerbated by underlying pulmonary or systemic disorders. Factors such as
hypoxia, acid-base imbalances, sympathetic stimulation, and electrolyte disturbances contribute to the development of ectopic foci within the atria. These foci
generate rapid and irregular atrial impulses.
The following electrocardiographic criteria aid in the identication of MAT:
• Irregular RR intervals: MAT is characterized by irregularity in the ventricular
response due to the variable atrial depolarizations originating from multiple
ectopic foci.
• Variable P-wave morphology: P waves in MAT exhibit diverse morphologies,
amplitudes, and durations, reecting the asynchronous atrial activity originating
from different sites within the atria.
2.5.1.2 Interatrial Blocks
Interatrial block (IAB) is a distinct electrocardiographic pattern describing the conduction delay between the right and left atria, through Bachmann’s bundle [13–17].
Because of the above, the ECG shows a P wave of ≥120ms in leads II, III, and aVF
(P wave must be measured from the earliest detection of the P wave in any lead
[onset] to the last one [offset]).
Identication of IAB is important as different studies have demonstrated its asso-
ciation with the development of AF, stroke, cognitive impairment, and mortality. Of
note, the association between IAB and SVT, particularly AF, has been named Bayes’
syndrome. According to the duration and morphology of the P wave, it is classied
into three groups:
P
artial Interatrial Block (P-IAB)
This is also called rst-degree IAB and manifests as a P-wave duration ≥120ms
without a negative terminal component in the inferior leads.
Intermittent Interatrial Block (I-IAB)
It is also kno
wn as second-degree IAB and represents an intermediate phase of IAB
with variable transitions between normal and partial or advanced IAB.P-wave morphology changes may appear after a premature beat-induced pause (known as atrial
aberrancy), suggesting a rate-dependent manifestation of IAB.
Advanced Interatrial Block (A-IAB)
This is also termed third-degree IAB and occurs because the sinus impulse is completely blocked in Bachmann’s bundle, and therefore, the left atrium is depolarized
retrogradely via muscular bundles located close to the AV junction. Therefore, P
2 Approach toECG Interpretation inCritical Care
Fig. 2.7 Advanced interatrial block P-wave duration <120ms with biphasic P wave in leads II, III,
and aVF.Personal archive
45
wave is longer than 120ms, and its morphology exhibits a biphasic conguration in
the inferior leads (Fig.2.7).
There are atypical patterns of A-IAB such as P-wave duration that is slightly
shorter than 120ms or P-wave morphology without the typical biphasic pattern in
all inferior leads. Accordingly, it can be classied as follows:
2.5.2 P-QRS Ratio
After assessing the P waves, the next step is to determine the P-QRS ratio [18]. The
P-QRS ratio provides valuable information about the conduction time between the
atria and the ventricles in the heart. Normally, there is a consistent relationship
between the duration of the P wave (atrial depolarization) and the duration of the
QRS complex (ventricular depolarization), P-QRS=1.
Abnormalities in the P-QRS ratio may indicate certain cardiac conditions or conduction disturbances:
2.5.2.1
A shortened P-QRS ratio (P-QRS
electrical impulse originates from the ventricles and the QRS complex is often widened and prolonged [3–5]. As a result, the P-QRS index is less than 1, indicating a
higher frequency of ventricular impulses compared to atrial impulses.
Shortened P-QRS Ratio
<1) may suggest ventricular rhythms because the
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M. H. Vicco et al.
2.5.2.2 P-QRS Ratio=1
Although P-QRS=1 is a characteristic of the normal sinus rhythm; it can also be
present in pathological conditions [18]. A special situation arises when a P-QRS
ratio=1 is accompanied by a shortened PR interval.
Wolff-Parkinson-White Syndrome (WPW)
WPW is an infrequent but clinically signicant cardiac condition characterized by
an abnormal accessory pathway, known as the bundle of Kent, which bypasses the
normal AV conduction system [3–5, 19]. This aberrant pathway allows for rapid
conduction of electrical impulses between the atria and ventricles, predisposing
individuals to various arrhythmias, including supraventricular tachycardia and atrial
brillation. The characteristics of ECG ndings include a shortened PR interval, a
widened QRS complex with a slurred initial upstroke called a delta wave, and a relatively short RR interval during tachyarrhythmias (Fig.2.8).
Junctional Rhythm
In junctional rhythm, the electrical impulse originates from the AV junction (around
the AV node or the bundle of His), bypassing the SA node. This leads to atrial depolarization and subsequent P wave being absent, or if present, it may appear retrograde (inverted) or buried within the QRS complex. The junctional impulse then
directly activates the ventricles, resulting in ventricular depolarization (QRS complex). Again, due to the direct conduction from the AV junction to the ventricles,
Fig. 2.8 Wolff-Parkinson-White. Nathanson LA, McClennen S, Safran C, Goldberger AL.ECG
Wave-Maven: Self-Assessment Program for Students and Clinicians. http://ecg.bidmc.harvard.edu