Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5573_Библиотеки_им_академика_М_И_Перельмана.pdf
Ap
proach toECG Interpretation inCritical Care
2
Fig. 2.9 Atrioventricular nodal reentrant tachycardia. Nathanson LA, McClennen S, Safran C,
Goldberger AL.ECG Wave-Maven: Self-Assessment Program for Students and Clinicians. http://
ecg.bidmc.harvard.edu
47
there is a 1:1 relationship between atrial (if present) and ventricular depolarization,
resulting in a P-QRS index of 1.
Atrioventricular Nodal Reentrant Tachycardia (AVNRT)
AVNRT is a supraventricular tachyarrhythmia characterized by reentrant conduction
within the AV node (Fig.2.9). In AVNRT, there is typically a narrow QRS complex
tachycardia with a regular rhythm and absent P waves or retrograde P waves occurring shortly after the QRS complex (RP interval< PR interval). Again, due to the
rapid and direct conduction from the AV node to the ventricles, there is typically a 1:1
relationship between atrial and ventricular depolarization, resulting in a P-QRS=1.
2.5.2.3 Prolonged P-QRS Ratio
Conversely, a prolonged P-QRS ratio (P-QRS>1) may indicate delayed conduction
through the AV node (see next section). This variability can provide additional diagnostic clues regarding the underlying rhythm disorder [20].
2.5.3 PR Interval
The PR interval on an ECG reects the time it takes for the electrical impulse to
travel from the atria through the AV node and into the ventricles. Variations in the
PR interval indicate abnormalities in AV conduction. We can schematically divide it
into the following [20].
48
M. H. Vicco et al.
2.5.3.1 Shortened PR Interval
A shortened PR interval (less than 120ms) is indicative of accelerated conduction
through the AV node, often seen in conditions such as Wolff-Parkinson-White syndrome (Fig.2.8).
2.5.3.2 Prolonged PR Interval
A prolonged PR interval (greater than 200ms) may suggest delayed conduction
through the AV node. Overall, delayed conduction of electrical impulses through
the AV node that creates a PR interval longer than 200ms is known as rst-degree
AV block. This delay may arise due to various factors, including degenerative
changes in the conduction system, medications affecting AV nodal conduction
(beta-blockers, calcium channel blockers, digoxin), electrolyte imbalances, vagal
stimulus, or myocardial ischemia.
2.5.3.3 Second-Degree AV Block
It represents a more advanced conduction abnormality. Second-degree AV block
can be further divided into.
Mobitz Type I(Wenckebach)
There is a progressive prolongation of the PR interval until a P wave is not conducted. This is usually followed by a shorter PR interval, and the cycle starts over. On
an ECG, there are a series of PR intervals that become progressively longer, while
the RR interval becomes shorter until a QRS complex is dropped. This can be usually
seen in normal hearts and does not necessarily imply a pathological nding [21].
Mobitz
Type II
It is characterized by intermittent non-conducted P waves without progressive prolongation of the PR interval. This presents as regular PR intervals with occasional
dropped QRS complexes (Fig.2.10). This nding is almost always pathologic and
deserves further investigation.
Advanced AV Block
This group encompasses the 2:1 AV block, where for every two P waves, only one
is conducted to the ventricles [13–17]. This results in a 2:1 ratio of P waves to QRS
complexes, and more extreme forms of AV block, where three or more P waves are
observed for each QRS (i.e., 3:1, 4:1, 5:1 AV block), also known as high-degree AV
Ap
2
proach toECG Interpretation inCritical Care
Fig. 2.10 Mobitz II second-degree AV block. Nathanson LA, McClennen S, Safran C, Goldberger
AL.ECG Wave-Maven: Self-Assessment Program for Students and Clinicians. http://ecg.bidmc.
harvard.edu
49
block. These types of blocks exhibit a great risk of progressing into a complete
heart block.
Third-Degree AV Block (Complete Heart Block)
In third-degree AV block, there is complete dissociation between atrial and ventricular activity, which means that the atria activity is not conducted to ventricles.
This implies that on the ECG, P waves occur at their own regular rate. Alternatively,
QRS complexes (ventricular activity) occur at a slower rate, often regular but independent of atrial activity. Ventricular beats originate in the AV node (supra- or intraHisian), which causes the QRS to be narro
w (Fig.2.11), or below the AV node,
which makes the QRS wide (the most frequent presentation in adults).
2.5.4 PR Segment
The PR segment, situated between the end of the P wave and the onset of the QRS
complex on the ECG tracing, serves as a crucial interval for assessing AV conduction. Alterations in the PR segment, such as depression or elevation, can indicate
underlying cardiac pathology.
2.5.4.1 PR-Segment Elevation
It is rare to observe in daily practice, but it can occur in the context of junctional
rhythms or exceptional cases of atrial infarction. In acute pericarditis or Takotsubo
syndrome, the PR segment can be elevated in aVR.
50
Fig. 2.11 Third-degree AV block with narrow QRS (supra-Hisian escape beats) 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.
2.5.4.2 PR-Segment Depression
This refers to a downward displacement of the baseline following the P wave, typically observed in leads where the P wave is upright. Causes of PR segment depression include the following.
Acute Pericarditis
PR-segment depression is a characteristic of ECG ndings in acute pericarditis, often
described as a “saddleback” appearance. It results from inammation and irritation
of the pericardium, affecting atrial repolarization (Fig.2.12). In addition, a widespread ST-segment elevation can be observed, typically seen in multiple leads and
with a characteristic concave “upwards”: morphology. This is due to inammationinduced alteration in the transmural electrical gradient across the myocardium.
Digitalis
Toxicity
Digitalis toxicity can manifest with various ECG changes, including PR-segment
depression, due to its effects on atrial conduction and refraction.
Acute Myocardial Ischemia
gment depression may occur in the setting of acute myocardial ischemia,
PR-se
reecting impaired atrial repolarization due to inadequate blood supply to the
myocardium.
2 Approach toECG Interpretation inCritical Care
Fig. 2.12 Acute pericarditis. Nathanson LA, McClennen S, Safran C, Goldberger AL.ECG WaveMaven: Self-Assessment Program for Students and Clinicians. http://ecg.bidmc.harvard.edu
51
2.5.5 Q Waves
While physiological Q waves are typically small and insignicant, pathological Q
waves can signify myocardial damage or infarction [3–5]. Pathological Q waves are
characterized by increased duration (>0.04 seconds), depth (>30% of the subsequent R-wave amplitude), and presence in specic leads indicative of myocardial
territory (Fig.2.13).
2.5.6 QRS Complex
A normal QRS complex typically lasts between 0.06 and 0.10seconds (60–100ms)
[3–5]. A QRS complex is considered wide if its duration exceeds 0.12 seconds
(120ms). This can be indicative of various pathological conditions such as bundle
branch blocks, ventricular hypertrophy, myocardial infarction, or electrolyte
imbalances.
Bundle branch blocks (BBBs) are characterized by delayed or blocked conduction through one of the bundle branches (left or right). This delay results in widened
QRS complexes. There are two main types:
1. Left Bundle Branch Block (LBBB) (Fig.2.14): The QRS complex is widened
due to delayed activation of the left ventricle. It typically presents as a broad, S
wave in leads V1–V3 and a broad notched R wave in lateral leads.
2. Right Bundle Branch Block (RBBB): The QRS complex is widened due to
delayed activation of the right ventricle. It typically presents as a broad S wave
followed by a slurred R wave in leads V1 and V2, often described as an “rsR”
pattern.
52
Fig. 2.13 Abnormal Q waves in the inferior lead a manifestation of an old myocardial infarction.
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.
Fig. 2.14 Left bundle branch block (LBBB) Nathanson LA, McClennen S, Safran C, Goldberger
AL.ECG Wave-Maven: Self-Assessment Program for Students and Clinicians. http://ecg.bidmc.
harvard.edu
2.5.6.1 Heart Rate
The heart rate can be calculated based on the frequency of QRS complexes [3–5].
By counting the number of QRS complexes present in 10seconds and multiplying
by six, the number per minute can be calculated—because 10seconds times six
equals 60seconds or 1minute. One alternative method is based on identifying two
consecutive R waves and counting the number of large squares between them. By
dividing this number into 300 (remember, this number represents 1minute), we can
2 Approach toECG Interpretation inCritical Care
53
calculate a person’s heart rate. Rate=300/number of large squares between consecutive R waves.
When the rate exceeds 100bpm, it indicates tachycardia. Furthermore, tachycardia can be categorized based on the duration of the QRS complex into narrow or
wide QRS arrhythmias.
Causes ofNarrow QRS Complex Tachycardia
Regular
– The possible diagnoses are sinus tachycardia, atrial tachycardia, atrioventricular
nodal reentry tachycardia (AVNRT), orthodromic AV reentrant tachycardia
(AVRT) via accessory pathway, and atrial utter. Certain types of ventricular
tachycardias may have a borderline narrow QRS complex (fascicular ventricular
tachycardia).
Irregular
– The possible diagnoses are atrial brillation, multifocal atrial tachycardia (MAT),
atrial utter with variable AV conduction, and atrial tachycardia.
It is noteworthy that certain medications, including antiarrhythmics, beta-blockers,
and calcium channel blockers, can inuence AV nodal conduction, leading to
irregular narrow QRS complexes. Additionally, abnormal levels of electrolytes,
particularly potassium and magnesium, can disrupt atrial and AV nodal function,
resulting in irregularities and narrow QRS complexes.
Causes ofWide QRS Complex Tachycardia
Regular
– Supraventricular tachycardia in the context of a bundle branch block or ventricu-
lar preexcitation syndromes.
– V
entricular tachycardia (VT): VT is a rapid rhythm originating from the ventricles. It can occur in the setting of structural heart disease (such as myocardial
infarction or cardiomyopathy) or as an idiopathic condition. VT typically presents with wide QRS complexes (>0.12 seconds) with a regular or irregular
rhythm (Fig.2.15).
– Hyperkalemia:
Elevated levels of potassium in the blood can affect myocardial
conduction, leading to widened QRS complexes. Hyperkalemia can result from
various causes, including renal failure, certain medications, and metabolic
disorders.
– Ventricular preexcitation syndromes: These syndromes involve abnormal acces-
sory pathways between the atria and ventricles, leading to early activation of
ventricular tissue. Conditions such as Wolff-Parkinson-White (WPW) syndrome
can result in widened QRS complexes during sinus rhythm or supraventricular
tachycardia.
54
Fig. 2.15 Monomorphic ventricular tachycardia. 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.
– Myocardial infarction: Acute myocardial infarction can disrupt normal myocar-
dial conduction pathways, resulting in widened QRS complexes, particularly if
the infarction involves the bundle branches or signicant portions of the ventricular myocardium.
– Medications: Some medications, such as sodium channel blockers (e.g., e-
cainide, propafenone) or calcium channel blockers (e.g., verapamil, diltiazem),
can delay ventricular conduction and widen QRS complexes, especially in overdose or in patients with underlying heart disease [22].
– Hypothermia: Severe hypothermia can affect cardiac conduction and lead to
widened QRS complexes.
Irregular
– V
entricular brillation (VF): VF is a life-threatening arrhythmia characterized by
chaotic and irregular ventricular electrical activity. It results in disorganized ventricular depolarization and wide irregular QRS complexes on the ECG. VF
requires immediate debrillation to restore normal cardiac rhythm.
– Polymorphic
ventricular tachycardia (VT) (Fig. 2.16): Polymorphic VT, also
known as torsades de pointes, is a type of VT characterized by a changing QRS
morphology on the ECG.It often occurs in the setting of prolonged QT interval,
electrolyte imbalances (such as hypokalemia or hypomagnesemia), or certain
medications.
– Atrial brillation with aberranc
y: In cases of atrial brillation (AF) with aberrancy or rate-dependent bundle branch block, irregular electrical impulses from
the atria can lead to irregular and wide QRS complexes on the ECG.
– Ventricular premature complexes (VPCs) in bigeminy or trigeminy: Irregular
occurrences of premature ventricular contractions (PVCs) in a pattern of bigeminy (every other beat) or trigeminy (every third beat) can result in irregular wide
2 Approach toECG Interpretation inCritical Care
Fig. 2.16 Polymorphic ventricular tachycardia (TdP) Nathanson LA, McClennen S, Safran C,
Goldberger AL.ECG Wave-Maven: Self-Assessment Program for Students and Clinicians. http://
ecg.bidmc.harvard.edu
55
QRS complexes on the ECG. VPCs can occur in the setting of various cardiac
conditions or as isolated events.
– Medication effects: Certain medications, such as antiarrhythmics, psychotropic
drugs, or medications that prolong the QT interval, can lead to irregular wide
QRS complexes as a side effect.
– Electrolyte imbalances: Severe electrolyte imbalances, particularly hypokalemia
or hypomagnesemia, can disrupt normal ventricular conduction pathways and
result in irregular wide QRS complexes on the ECG.
– BBB with variable conduction: Incomplete or intermittent BBB can lead to irreg-
ular wide QRS complexes on the ECG.These irregularities in conduction may be
exacerbated by factors such as ischemia, electrolyte imbalances, or medication
effects.
2.5.7 QT Interval
The following elements, the QT interval, ST segment, and T wave, are part of the
“repolarization” assessment [3–5]. These elements should be considered highly as
they are the most affected by factors inuencing myocardial tissue repolarization.
There are several causes of repolarization abnormalities, such as acute myocardial
infarction, pericarditis, myocarditis, septic shock, and pulmonary embolism, among
others, that will be commented on below.
Regarding the QT interval, its duration varies according to age, gender, and heart
rate. In adults, a normal QT interval typically falls <450ms for men and <460ms
for women, according to the AHA/ACC/HRS consensus, when the heart rate is
56
M. H. Vicco et al.
between 60 and 100 beats per minute. QT interval values that deviate from this
range may indicate abnormalities and require additional assessment. Since the duration of the QT interval is inuenced by heart rate, it is important to adjust for heart
rate variability using formulas like Bazett’s formula, Fridericia’s formula, or other
established methods. As part of the QT prolongation, the T wave may appear taller,
wider, and aberrant. It may exhibit a notch, bid appearance, or alternate morphology, which reects increased electrical instability during repolarization.
An acquired long QTc interval, observed in various clinical settings including
the ICU, is associated with sudden cardiac death due to malignant ventricular
arrhythmias. Predisposing factors include heart diseases, prolonged QTc interval,
acute neurological events, ionic and metabolic imbalances, septic shock, female
sex, advanced age, hypothermia, and intoxications. Numerous drugs are associated
with QT prolongation and potential arrhythmogenic risk, including certain antiarrhythmics type I and III, macrolide antibiotics, uoroquinolones, antidepressants,
antipsychotics, and antihistamines.
Drew etal. recommend considering QTc values exceeding the 99th percentile as
abnormally prolonged. This value is 470ms for males and 480ms for females in
healthy postpubertal individuals. Values over 500ms pose a high risk of developing
arrhythmic events.
Prolongation of the QT interval on an electrocardiogram (ECG) can predispose
individuals to a potentially life-threatening arrhythmia known as torsades de pointes
(TdP). TdP is a type of polymorphic ventricular tachycardia characterized by a
twisting or “twisting of the points” appearance on the ECG.It can degenerate into
ventricular brillation and result in sudden cardiac death. Twisting QRS complexes
are recognized by their unique morphology, where the QRS complexes appear to
transition the QRS’ axis around the baseline.
2.5.8 ST Segment
When the ST segment on an ECG appears depressed or elevated, it signies an
abnormality in myocardial repolarization [3–5]. As mentioned previously, the ST
segment represents the interval between ventricular depolarization and repolarization. Normally, the ST segment is isoelectric.
2.5.8.1 ST-Segment Depression
This is diagnosed when the ST segment is observed to be below 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. Examples of causes of ST-segment depression are the following: