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Approach toECG Interpretation inCritical Care
2
57
– Myocardial ischemia: It typically manifests as a horizontal or downward-sloping
ST-segment depression. It is usually seen during exercise or periods of increased
myocardial demand and may be transient.
– Hypokalemia: This causes diffuse ST-segment depression, often with a charac-
teristic “sagging” appearance, T-wave attening, or inversion.
– Hypoxia: Decreased oxygen supply to the myocardium, as seen in respiratory
failure or severe anemia.
– Digitalis toxicity: Digitalis toxicity can cause down-sloping ST-segment depres-
sion, typically with associated T-wave attening or inversion. It may also manifest as a “scooped” appearance of the ST segment.
2.5.8.2 ST-Segment Elevation
This is diagnosed when the ST segment is observed to be elevated above the baseline (isoelectric line) by at least 0.5mm (or 0.05mV) in leads with predominantly
positive QRS complexes or 1mm (or 0.1mV) in leads with predominantly negative
QRS complexes [3–5]. Examples of causes of ST-segment elevation are the
following:
– Acute myocardial infarction (STEMI): STEMI (Fig. 2.17) is characterized by
persistent ST-segment elevation (usually >1mm in two contiguous leads) along
with pathological Q waves (indicating myocardial necrosis) and T-wave changes
(often inversion or hyperacute T waves).
– Pericarditis: Pericarditis (Fig.2.12) typically presents with diffuse ST-segment
elevation across multiple leads, often with concave upward morphology. The
elevation is usually widespread and does not localize to specic coronary artery
distributions.
Fig. 2.17 Acute inferior STEMI Nathanson LA, McClennen S, Safran C, Goldberger AL.ECG
Wave-Maven: Self-Assessment Program for Students and Clinicians. http://ecg.bidmc.harvard.edu
58
Fig. 2.18 Hypercalcemia, showing an ST-segment elevation with a scooped appearance.
Nathanson LA, McClennen S, Safran C, Goldberger AL.ECG Wave-Maven: Self-Assessment
Program for Students and Clinicians. http://ecg.bidmc.harvard.edu
M. H. Vicco et al.
– Myocarditis: Myocarditis can present with ST-segment elevation, like acute
myocardial infarction. However, the elevation may be more diffuse and less pronounced compared to STEMI.ST-segment elevation may not meet the criteria
for STEMI (>1mm in two contiguous leads) but can still be present, along with
T-wave changes and sometimes pathological Q waves.
– Prinzmetal’s variant angina: Prinzmetal’s angina is characterized by transient
episodes of ST-segment elevation during angina attacks, typically occurring at
rest and unrelated to exertion.
– Hypercalcemia: It can produce a wide range of ECG abnormalities, with shorten-
ing the c interval being the most common nding. However, a normal QTc interval is relatively common in mild-to-moderate hypercalcemia. ST-segment
elevation mimicking acute myocardial infarction has been well described:
gment elevation has a scooped appearance and is usually followed by indis-
ST- se
tinct or absent T waves (Fig.2.18). This false-positive ECG nding should be
included in the differential diagnosis of myocardial ischemia, although it is not
the most common manifestation of hypercalcemia. Additionally, sick sinus syndrome and bradycardia have been reported in hypercalcemia.
2.5.9 T Waves
Normal T waves are typically asymmetric, with a gradual upslope and a more rapid
downslope, resulting in a slightly rounded or dome-like appearance [3–5]. Normally,
the duration ranges between 0.08 and 0.10seconds, and its amplitude varies but
generally does not exceed 5mm in limb leads or 10 mm in precordial leads. The
2
proach toECG Interpretation inCritical Care
Ap
59
polarity of the T wave is positive in most leads but may be negative in leads where
the electrical vector is directed away from the electrode, such as in the aVR lead.
Pathological T waves are often categorized based on their morphology and can be
broadly classied as peaked, attened, biphasic, or inverted. Peaked T waves may
indicate hyperkalemia or acute myocardial infarction, while attened or inverted T
waves may suggest myocardial ischemia, electrolyte disturbances, myocardial
injury, or ventricular hypertrophy. Moreover, T-wave abnormalities can be transient
or persistent, requiring careful evaluation to determine their clinical signicance.
2.5.9.1 Inverted T Wave
– Left ventricular hypertrophy: Inverted T waves may be seen in leads with pre-
dominantly negative QRS complexes (e.g., V1–V3). The presence of LVH criteria, such as increased voltage in the QRS complexes or repolarization
abnormalities, supports the diagnosis.
– Hypertrophic cardiomyopathy: Inverted T waves, often deep and asymmetric,
may be present in leads facing the hypertrophied septum (e.g., V1–V3).
Additional ndings may include left atrial enlargement, left ventricular outow
tract obstruction, or dynamic left ventricular hypertrophy.
– Myocardial ischemia: Inverted T waves may appear in leads facing the ischemic
region. Additionally, ST-segment changes (depression or elevation) and Q waves
may be present, depending on the severity and chronicity of the ischemia or
infarction (Fig.2.19).
– Digitalis toxicity: Inverted T waves, often associated with ST-segment depres-
sion and a “scooped” appearance of the ST segment, may be present. Additional
Fig. 2.19 T-wave inversion and ST-segment depression in precordial leads in the context of acute
anterior ischemia. Nathanson LA, McClennen S, Safran C, Goldberger AL.ECG Wave-Maven:
Self-Assessment Program for Students and Clinicians. http://ecg.bidmc.harvard.edu
60
Fig. 2.20 Pulmonary embolism. Nathanson LA, McClennen S, Safran C, Goldberger AL.ECG
Wave-Maven: Self-Assessment Program for Students and Clinicians. http://ecg.bidmc.harvard.edu
M. H. Vicco et al.
features of digitalis toxicity include bradyarrhythmias, AV block, or enhanced
automaticity.
– Cerebrovascular events: Inverted T waves may occur as a secondary manifesta-
tion of neurogenic cardiac effects such as acute stroke or transient ischemic
attack affecting the brain’s autonomic control centers. Diagnosis involves correlating ECG ndings with neurological symptoms and imaging studies to conrm
the cerebrovascular event.
– Acute pulmonary embolism: Inverted T waves (Fig.2.20) in leads reecting right
ventricular involvement (e.g., V1–V4) may be observed. Additional ECG ndings
may include right-axis deviation, S1Q3T3 pattern, or signs of right heart strain
(e.g., T-wave inversion in leads V1–V3 with simultaneous ST elevation in lead III).
2.5.9.2 Flattened T Wave
– Hypokalemia: Flattened T waves are observed, and additional ndings that may
be accompanying are ST-segment depression and prominent U waves (Fig.2.21).
The diagnosis is conrmed by correlating ECG ndings with serum potassium levels.
– Hypocalcemia (Fig.2.22): Flattened T waves may be present on the ECG, often
accompanied by prolonged QT intervals.
– Hypothermia: Flattened T waves may be seen on the ECG, along with other signs
of hypothermia such as bradycardia and Osborn (J) waves.
– Acute myocardial ischemia/infarction: Flattened T waves may be observed in
leads facing the ischemic region, along with other signs of ischemia such as STsegment changes and chest pain.
Approach toECG Interpretation inCritical Care
2
Fig. 2.21 Hypokalemia. Nathanson LA, McClennen S, Safran C, Goldberger AL. ECG WaveMaven: Self-Assessment Program for Students and Clinicians. http://ecg.bidmc.harvard.edu
61
Fig. 2.22 Hypocalcemia. Nathanson LA, McClennen S, Safran C, Goldberger AL.ECG WaveMaven: Self-Assessment Program for Students and Clinicians. http://ecg.bidmc.harvard.edu
2.5.9.3 Peaked T Wave
– Hyperkalemia (Fig.2.23): Peaked T waves may be observed on the ECG, typi-
cally with a narrow base and tall amplitude. Associated ndings may include
widened QRS complexes, prolonged PR intervals, and attened P waves.
– Early repolarization: Peaked T waves with a characteristic “tombstone” appear-
ance may be present on the ECG, particularly in precordial leads (V2–V5).
– Acute myocardial ischemia/infarction: Peaked T waves may be observed in leads
facing the ischemic region, typically in the early stages of myocardial ischemia.
Associated ndings may include ST-segment elevation and chest pain.
62
Fig. 2.23 Hyperkalemia, peaked T waves. Nathanson LA, McClennen S, Safran C, Goldberger
AL.ECG Wave-Maven: Self-Assessment Program for Students and Clinicians. http://ecg.bidmc.
harvard.edu
M. H. Vicco et al.
– Hyperacute phase of myocardial infarction: Peaked T waves may be present on
the ECG, often with concomitant ST-segment elevation. The T waves may initially appear tall and narrow before progressing to broader and symmetrically peaked.
– BBB: Peaked T waves may occur as secondary repolarization changes due to
altered ventricular activation.
– Acute intracranial events: diagnosis: Peaked T waves may occur as a secondary
manifestation of neurogenic cardiac effects.
2.6 ECG Patterns Related toDrugs
In the critical care unit, certain ECG patterns may be due to drugs and inuenced by
various factors including comorbidities, critical illness, pharmacological interactions, and drug toxicity [22]. Pharmacists play a crucial role in understanding potential drug effects, thereby contributing to improving clinical outcomes and mitigating
adverse events [23–25].
The most important ECG patterns with clinical relevance for pharmacists are
discussed below.
2.6.1 Patterns Associated withSpecic Drugs or Toxics
• Tricyclic antidepressants: These drugs can block fast sodium channels, pro-
longing QRS duration and delaying conduction. They can produce sinus tachycardia due to anticholinergic and alpha-1 antagonism and interfere with
2
Approach toECG Interpretation inCritical Care
63
ventricular repolarization, leading to QT prolongation. A characteristic ECG
nding is an R wave in aVR.
• Antipsychotics: These medications may induce bradycardia, sinus tachycardia,
ventricular arrhythmias, or prolongation of QRS and QTc intervals.
• Digoxin: Arrhythmogenic effects of digoxin include triggered activity, automa-
tism enhancement, and vagal tone augmentation, manifesting as PR interval prolongation, “reverse tick” or “Salvador Dali sagging” ST-segment depression, and
shortened T-wave amplitude. Toxicity may be suspected with ventricular automatism, junctional tachycardia, atrial brillation, atrial tachycardia, AV block,
ventricular brillation, and other arrhythmias.
• Ethanol: Ethanol toxicity increases sympathetic tone, impairs repolarization,
and affects QTc duration, leading to sinus tachycardia, atrial tachycardia, atrial
brillation, ventricular tachycardia, and prolongation of PR, QRS, and QTc
intervals [22].
• Cocaine: Cocaine affects sodium, calcium, and potassium channels and exerts
adrenergic agonism [22]. This can potentially cause sinus tachycardia, ventricular tachycardia, QTc prolongation, TdP, idioventricular rhythms, and asystole.
• Organophosphates: Toxicity is associated with sinus tachycardia/bradycardia,
intraventricular conduction delays, variable AV blocks, and prolongation of PR,
QRS, and QTc intervals.
2.6.2 Specic Wave or Interval Impairments
• P wave: Prolongation may result from sodium and potassium channel blockade.
• PR interval: Prolongation may occur due to vagal stimulation, beta-blockers,
calcium channel antagonists, adenosine, and acetylcholinesterase inhibitors.
• QRS complex: Prolongation can be induced by sodium channel blockers.
QT
•
interval: Digoxin may shorten QT duration, while acetylcholinesterase
inhibitors and several other drugs can prolong it.
References
1. Jackevicius C. Pharmacist participation in CPR needs resuscitation. Can J Hosp Pharm.
2015;68(4):275–6.
2. Kronick SL, Kurz MC, Lin S, etal. Part 4: Systems of care and continuous quality improvement:
2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and
Emergency Cardiovascular Care. Circulation. 2015;132(18 Suppl 2):S397–413.
3. Bayés de Luna A, Fiol-Sala M, Bayés-Genís A, Baranchuk A.Clinical electrocardiography: a
textbook. 5th ed. Wiley-Blackwell; 2021. ISBN: 1119536456.
4. Bayés de Luna A, Baranchuk A. Clinical arrhythmology. 2nd ed. Wiley-Blackwell; 2017.
ISBN: 1119212758.
5. Baranchuk A. Atlas of advanced electrocardiogram interpretation. London: REMEDICA;
2013. www.ECGAtlas.com.
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6. Kotsialou Z, Makris N, Gall S. Fundamentals of the electrocardiogram and common cardiac
arrhythmias. Anaesth. Intensive Care Med. 2024;25:219–22.
7. Rautaharju PM, Surawicz B, Gettes LS, et al. AHA/ACCF/HRS recommendations for the
standardization and interpretation of the electrocardiogram: part IV: the ST segment, T and
U waves, and the QT interval: a scientic statement from the American Heart Association
Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the
American College of Cardiology Foundation; and the Heart Rhythm Society: endorsed by the
International Society for Computerized Electrocardiology. Circulation. 2009;119(10):e241–50.
8.
El-Sherif N,
Pacing Clin Electrophysiol. 2018;41(4):414–21.
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Xing L
implantable loop recorder: insights from the LOOP Study. Europace. 2023;25(5):euad014.
10.
Kaak
2012;72(12):1617–30.
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Johner N, Namdar M, Shah DC.
Electrophysiol. 2025.
12. Liwanag M, Willoughby C. Atrial Tachycardia. 2023 Jun 26. In: StatPearls [Internet]. Treasure
Island (FL): StatPearls Publishing; 2025.
wer DA, etal. Cardiovascular complications of interatrial conduction block: JACC state-of-
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Escalante Perez S, et
común del síndrome de Bayés. Arch Cardiol Mex. 2022;92(4):553–5.
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interatrial block. Eur Cardiol. 2015;10(1):54.
avone C, Pelargonio G. Reversible causes of atrioventricular block. Cardiol Clin.
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Electrocardiology and the International Society for Holter and Noninvasive Electrocardiology.
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Gupta S, Khakh P
tive reasoning: two cornerstones of electrocardiogram teaching. Can J Cardiol. 2024.
S0828-282X(24)00300-3.
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isdale JE, Chung MK, Campbell KB, etal. Drug-induced arrhythmias: a scientic statement
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Pozzolini
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Y, et al. Electrocardiographic markers of subclinical atrial brillation detected by
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al. Bloqueo interauricular avanzado atípico: una presentación poco
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A. Electrocardiography in practice: what to do? Queens
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Further Reading
Zipes DP, Calkins H, Daubert JP, et al. ACC/AHA/HRS advanced training statement on clinical
cardiac electrophysiology (a revision of the ACC/AHA 2006 update of the clinical competence
statement on invasive electrophysiology studies, catheter ablation, and cardioversion) Heart
Rhythm. 2015;2016;13(1):e3–e37.
Chapter 3
The Role of Chest Radiography
in the Critical Care Unit
FabioMacori
3.1 Introduction
Physical examination of patients can be challenging in the intensive care unit (ICU)
due to the complexity of medical conditions and the devices often used to support
life, and this is even more difcult when the patient is intubated. Portable chest
X-rays are often used as an adjunct to the physical examination (Fig.3.1a). Although
it has some limitations in technical diagnostic capabilities, CXR is readily available
and inexpensive and plays an important role in the daily evaluation of critically ill
patients. Effective communication between radiologists and clinicians is essential to
improve interpretation and ensure that quality care is provided to these patients.
It is recommended by the American College of Radiology (ACR) guidelines that
portable chest radiography should be used for patients who have cardiopulmonary
symptoms following cardiac or thoracic surgery, those who suffer from trauma,
patients on monitoring and life support devices, and critically ill patients [1]. There
are no strict guidelines dictating the frequency of chest radiography for ICU patients.
However, several studies assessing the benet of daily chest radiography in the ICU
have been performed with varied ndings. Patients who have acute cardiopulmonary problems are recommended to undergo daily chest radiography by the
ACR.Chest radiographs should also be obtained immediately after the placement of
endotracheal tubes, nasogastric tubes, vascular catheters, and chest tubes. Follow-up
is necessary when the tube or catheter position is suspected to have changed or
when otherwise clinically indicated. In the ICU, there are inherent challenges in
chest radiography, which limit diagnostic accuracy. Many patients are unable to
F. Macori (*)
Ospedale Santo Spirito Rome, Rome, RM, Italy
e-mail: fabio@macori.eu
Switzerland AG 2025
Y. Alzaidi, M. A. Gebily (eds.), The Pharmacist’s Expanded Role in Critical
Care Medicine, https://doi.org/10.1007/978-3-031-77335-8_3
65© The Author(s), under exclusive license to Springer Nature
66
F. Macori
a b
Fig. 3.1 Normal AP chest (a) and PA (b) for comparison
cooperate with the examination, which makes it difcult to obtain optimal upright
(posterior–anterior) positioning (Fig.3.1b). Radiographs are usually obtained in a
semi-upright or supine anteroposterior (AP) position, and a lateral radiograph is
often impractical. External monitoring devices, overlying tubes, and electrocardiographic leads may obscure underlying disease, mimic radiographic pathology, and
create ambiguity regarding the positioning of other support equipment.
It is important to understand that the chest examination can vary depending on
whether the patient is lying down or standing up. When a patient is lying down for
an AP lm, the cardiovascular structures may appear larger than they are, leading to
a misdiagnosis of vascular cephalization. The vascular pedicle may also appear
more prominent, which could be mistaken for congestive heart failure [2].
When interpreting chest radiographs of patients in intensive care units (ICUs), it
is crucial to follow a systematic approach [3, 4]:
– Ev
aluate the position of all catheters and support devices.
– Check the patient’
s cardiovascular status.
– Search for abnormally increased lung opacication areas, which may indicate
pneumonia or atelectasis.
– Assess the lm for the amount and distrib
– Observ
e for any abnormal air collections, including pneumothorax, subcutane-
ution of pleural uid.
ous emphysema, pneumomediastinum, or pneumopericardium.
This systematic approach can help ensure accurate interpretation of chest radiographs in ICU patients.