The ECG in Other Diseases and Different Situations


Chapter 23
The ECG in Other Diseases and Different Situations


This chapter will review the different ECG characteristics in non‐cardiac processes and other situations, which are sometimes striking.


Cerebrovascular accidents


Cerebrovascular accidents, and particularly subarachnoid hemorrhage, frequently show general repolarization abnormalities of the T wave, which can be highly negative or highly positive but are generally wide, and with long QT and mirror patterns in frontal plane leads (Figure 23.1). Even transient evident ST segment elevation with or without a negative T wave, very similar to an acute coronary syndrome, can be observed (Figure 23.2).


Endocrine diseases


Due to the presence of myocardial and infiltration in myxedema, the following ECG signs can be found: low QRS complex voltage, bradycardia, and flattening or even inversion of the T wave (Figure 23.3). In hyperthyroidism, in addition to sinus tachycardia, the presence of supraventricular arrhythmias, particularly atrial fibrillation, is frequent.


In the case of decompensated diabetes (ketoacidosis), repolarization abnormalities can often be observed, including even an ST segment elevation in the absence of a known clinical heart disease (Figure 23.4) (Chiariello et al. 1985). Furthermore, the ECG, if there is associated ischemic heart disease, shows more alterations in cases of type II diabetes than in non‐diabetic patients. It has been proven that diabetic patients have the same risk of cardiovascular complications as patients who have suffered a myocardial infarction. Consequently, risk factors (hypertension, high cholesterol levels, smoking, etc.) should be more intensively treated in these cases. (Hypertension in Diabetes Study (HDS): II 1993).


Respiratory diseases


Numerous lung diseases may cause involvement of the right chambers both: (i) in the acute setting, acute cor pulmonale due to pulmonary embolism (see Figures 10.15 and 10.16) or acute decompensation of chronic obstructive pulmonary disease (COPD) (see Figure 10.14); and (ii) in the chronic phase, emphysema and chronic cor pulmonale (see Figure 10.12). The usefulness of the ECG in the diagnosis and prognosis of acute and chronic cor pulmonale, and primary pulmonary hypertension (see Figure 22.13), has been discussed in Chapter 22.


With regard to lung diseases that do not directly involve the right chambers, the ECG can be altered in the presence of a pneumothorax, particularly if it occurs on the left side. The alterations observed are probably a result of the interpositioning of air and displacement of the heart, together with a sudden increase in intrathoracic pressure. In the case of a left pneumothorax, an ÂQRS deviated to the right is usually observed, as well as a reduction in the QRS complex voltage which, in some cases, causes morphologies with a decreasing reduction in the R wave voltage in the precordial leads, which may mimic an anterior infarction. Confusion with ischemic heart disease may also be caused by the occasional presence of symmetric negative T waves in the precordial leads. A PR interval elevation has also been described and, rarely, a sometimes striking ST segment elevation in leads II, III, and aVF, with a reciprocal descent in leads I, aVL, and aVR, which may mimic an acute coronary syndrome (Figure 23.5).


ST segment upward deviation is probably caused by hypoperfusion and/or coronary spasm, and is shown in leads II, III, and aVF because the cardiac inferior wall of the LV is in contact with the collapsed lung. PR segment elevation might be seen due to atrial injury (Strizik and Forman 1999; Monterrubio Villar et al. 2000). In general, all these alterations are temporary and disappear when the condition is resolved.

Schematic illustration of a 30-year-old patient with subarachnoid hemorrhage.

Figure 23.1 A 30‐year‐old patient with subarachnoid hemorrhage. The ECG shows quite significant repolarization changes, with a very long QT interval mainly at the expense of a very wide T wave, positive in some leads (precordial and inferior leads) and negative in others (I, aVL).

Schematic illustration of ECG from a 65-year-old patient with cerebrovascular accident that in its acute phase shows subepicardial injury morphology of the type observed in the acute phase of an acute coronary syndrome with ST segment elevation, or in some cases of perimyocarditis.

Figure 23.2 ECG from a 65‐year‐old patient with cerebrovascular accident that in its acute phase shows subepicardial injury morphology of the type observed in the acute phase of an acute coronary syndrome with ST segment elevation, or in some cases of perimyocarditis. Enzymes were negative, the patient never complained of chest pain, and the ECG returned to normal (B) on the following day, coinciding with the improvement of the clinical picture.

Schematic illustration of ECG from a 60-year-old patient with myxedema presenting with the typical abnormalities found in this process: slow baseline rhythm, generalized low voltage, and diffuse repolarization changes.

Figure 23.3 ECG from a 60‐year‐old patient with myxedema presenting with the typical abnormalities found in this process: slow baseline rhythm, generalized low voltage, and diffuse repolarization changes.

Schematic illustration of a 24-year-old patient with decompensated diabetes and asymptomatic ketoacidosis with an ECG tracing showing an ST segment elevation, particularly visible in precordial leads and II, III, aVF.

Figure 23.4 A 24‐year‐old patient with decompensated diabetes and asymptomatic ketoacidosis with an ECG tracing showing an ST segment elevation, particularly visible in precordial leads and II, III, aVF. This pattern disappeared when the decompensation was resolved a few days later.


Other diseases (see Chapter 22)


There are many other pathological processes in which the ECG shows alterations that may go from slight repolarization changes to patterns of evident chamber enlargement, bundle branch block, or even patterns suggesting myocardial ischemia or necrosis, as well as different active or passive arrhythmias. A description of the most characteristic findings occasionally observed during some of these conditions is discussed in the following paragraphs (see references p. XI).

Schematic illustration of striking elevation of the ST segment in leads II, III, and aVF with a mirror image in I, aVL, and aVR, and low voltage in the precordial leads in a patient with a left pneumothorax.

Figure 23.5 Striking elevation of the ST segment in leads II, III, and aVF with a mirror image in I, aVL, and aVR, and low voltage in the precordial leads in a patient with a left pneumothorax. Following evacuation of the pneumothorax, the ECG was almost normalized.


Infectious diseases


It has already been mentioned, when discussing myocarditis (Chapter 22), that infectious diseases of viral origin or having other etiologies may occasionally cause alterations in the ECG, in particular in repolarization, which are generally not very evident, and transient, and of no clinical significance. In the presence of septic shock, the alterations can be much more striking and may even cause malignant ventricular arrhythmias.


Hepatic cirrhosis


Often, a generalized low voltage with sometimes flat or slightly negative T waves is found in association with hepatic cirrhosis.


Anemia


In anemia, there is often sinus tachycardia and occasional repolarization changes, usually slight and in the form of a flat or somewhat negative T wave, as well as a usually slight ST segment depression (see Chapter 20).


Pheochromocytoma


Hypertensive crises, may be frequent, but not occur in more than 50% of cases of pheochromocytoma. Patients frequently exhibit symptoms such as headaches, palpitations, sweating, etc., but at least 10% of the crises are completely asymptomatic. The ECG is abnormal in almost 75% of the cases. Different active arrhythmias may appear as a result of the increase in the concentration of catecholamines, ranging from sinus tachycardia to supraventricular and ventricular tachyarrhythmias, and sometimes also a shortening of the PR interval. Also, left ventricular enlargement can be observed, as well as left bundle branch block, repolarization abnormalities, and Q waves compatible with necrosis, particularly in cases with myocarditis or dilated cardiomyopathy. Some of these findings are reversible, at least partially, once the process is resolved.


Systemic diseases (especially amyloidosis, sarcoidosis, and hemochromatosis)


All of these systemic diseases may cause a more or less significant ventricular myocardial involvement, which can result in a cardiomyopathy and/or involvement of the specific conduction system. As a result, the ECG may show pattern of: (i) atrial and/or ventricular enlargement; (ii) different types of atrioventricular (AV) or bundle branch block, (iii) alterations of repolarization and (iv) necrosis Q waves. These patients may also sometimes exhibit serious ventricular arrhythmias (sustained ventricular tachycardia) (see Chapter 22, restrictive CM).


Neuromuscular diseases


The ECG in neuromuscular diseases is often pathological and presents with P wave, QRS complex, and/or ST/T changes, as well as a series of different arrhythmias. In Duchenne’s progressive muscular dystrophy, the ECG is almost always abnormal. The occurrence of patterns suggesting ventricular enlargement, particularly right ventricular enlargement, and/or a usually partial right bundle branch block (RBBB), is frequent (Figure 23.6). In Steinert’s disease (myotonic muscular dystrophy), the most frequently found changes are signs of chamber enlargement, repolarization abnormalities, conduction disorders, pathologic Q waves, and arrhythmias, especially atrial fibrillation (Figure 23.7). In Friedreich’s ataxia, there are usually necrosis Q waves and diffuse negative T waves.


Rheumatic diseases


Most rheumatic diseases with systemic involvement, particularly rheumatoid arthritis, sclerodermia and lupus erythematosus, present ECG pattern related to coronary heart disease, pericardial and/or myocardial involvement, as well as different types of arrhythmias, more frequently than in a healthy population.


Kidney diseases


The most striking ECG alterations in kidney disease are a consequence of the hypertension that usually affects these patients. In addition, due to chronic renal failure, other ECG anomalies can be observed, usually as a result of associated ionic abnormalities (hyperkalemia) (see below).

Schematic illustration of a 15-year-old patient with Duchenne disease.

Figure 23.6 A 15‐year‐old patient with Duchenne disease. Note the SI, SII, SIII morphology, Rs in V1 with negative T wave, and RS morphology in V6 with positive T wave. All of this is the result of myocardial involvement with an ECG morphology showing mainly right ventricular enlargement.

Schematic illustration of a 27-year-old patient with Steinert disease.

Figure 23.7 A 27‐year‐old patient with Steinert disease. This ECG displays pathological characteristics and evident signs of significant left ventricular enlargement (R in aVL ≥ 25 mm), diffuse left intraventricular conduction disorder (QRS ≥ 0.12 sec), but with an evident involvement of the superoanterior division area (ÂQRS −50°) and QS morphology in left precordial leads.


Psychiatric diseases


Various psychiatric diseases, including anorexia nervosa (Vázquez et al., 2003), are accompanied by ECG alterations either related or not to ionic alterations. These include sinus bradycardia, a long QT interval, arrhythmias, and even sudden death.


Athletes (Figures 23.8–23.11) (Corrado et al. 2010); Uberoi et al. 2011)


We have already remarked (Chapters 7 and 9) the QRS–ST–T changes that may be found in athletes, and especially how to perform the differential diagnosis of ECG pattern with rSr′ and/or ST elevation in V1–V2 found relatively often in athletes, with variants of normality such as thoracic malformation, especially pectus excavatum, and with Brugada pattern, especially type II (see Figure 7.16).


Now, we will comment on the global ECG changes that may be found in athletes in surface ECG, divided into:



  1. frequent ECG findings that may be training related and
  2. uncommon ECG findings that are not training related.

Surface ECG morphology changes


Training‐related ECG findings


The morphology of ECG in athletes very frequently shows findings that may be training related and require no additional evaluation, such as:



  • sinus bradycardia;
  • first‐degree AV block, or even Wenckebach‐type second‐degree AV block during rest (see below);
  • partial RBBB pattern (see Figures 7.14 and 23.9);
  • high voltage of R wave in precordial leads in the absence of other criteria for left ventricular hypertrophy;
  • isolated premature ventricular complexes (PVCs) (see below);
  • early repolarization (ER) pattern. In this case, we have to remember that this pattern has been recently associated with sudden death (Haïssaguerre et al. 2008) although this is exceptional in the benign type of ER usually found in athletes (see Chapter 24, Early repolarization pattern). A crista supraventricularis pattern is also common (Martinez‐Sellés et al. 2020).

Non‐training related ECG findings (Figures 23.9 and 23.10)


In contrast, uncommon and non‐training related ECG findings that may indicate further evaluation are:



  • negative T waves ≥ two adjacent leads;
  • ST segment depression;
  • pathologic Q waves;
  • important atrial abnormalities;
  • short or long QT interval;
  • advanced bundle branch block or hemiblocks;
  • evident criteria of right or left ventricular hypertrophy;
  • abnormalities of QRS–ST in V1 suggestive of Brugada pattern (see Figure 7.16 and Chapter 21);
  • the presence of some arrhythmias (runs or sustained ventricular tachycardia, vagal atrial fibrillation, advanced second‐ or third‐degree AV block) (see below).

Figure 23.8 shows the most frequent repolarization abnormalities found in well‐trained athletes (Plas 1976), which make it necessary to rule out hypertrophic cardiomyopathy and other possible causes.

Schematic illustration of the different types of repolarization abnormalities found in athletes (A to D).

Figure 23.8 Different types of repolarization abnormalities found in athletes (A to D). These are usually benign, but it is compulsory to perform an echocardiogram to rule out hypertrophic cardiomyopathy


(Based on Serra‐Grima et al. 2000).


Arrhythmias


The most frequent arrhythmias found in athletes are the following:



  • PVCs: These are not infrequent in healthy athletes, although they usually disappear with exercise. More than one PVC in a surface ECG must be referred for a further evaluation. Runs of ventricular tachycardia (VT) and especially sustained VT have to be considered definitively pathologic and need to be carefully studied.
  • Atrial fibrillation (AF): Whereas paroxysmal AF is rarely seen in young athletes, the incidence of AF paroxysmal or chronic in adult athletes or ex‐athletes is more frequent than in the normal population (Mont et al. 2009).
  • Some benign bradyarrhythmias, such as sinus bradycardia often with junctional escapes and/or first‐ and even second‐degree Wenckebach‐type AV block may be found, occurring especially at night (Figures 23.10 and 23.11).
  • Advanced AV block: This should not be assumed to be training‐related and requires further evaluation.
  • Sudden death: Although the incidence of sudden death among athletes is low, it constitutes a serious social problem, and extremely intense sports might increase the risk of sudden death (Martínez‐Sellés and Lucia 2019). In young competitive athletes, the incidence of sudden death is approximately 1/100 000 people/year (Maron et al. 1980, 1995). In athletes over 35 years of age, the most frequent cause is ischemic heart disease (Vicent et al. 2018), whereas in younger athletes, the conditions most frequently associated with sudden death are hypertrophic cardiomyopathy, coronary anomalies, arrhythmogenic right ventricular dysplasia (ARVD), Brugada syndrome, myocarditis, coronary artery anomalies, and many others (Maron et al. 1980) (Figure 23.12). It has been recently demonstrated that the use of doping agents (androgenic anabolic steroids) may cause a significant shortening of the QT interval (≈ 350 ms), albeit without reaching the values of short QT syndrome. This is related to the increase in Ito and Ik currents, resulting in a shortened repolarization (Bigi et al. 2009).

Table 23.1 shows cardiac abnormalities found in 161 elite athletes with arrhythmias considered pathologic after arrhythmologic study (Bayés de Luna et al. 2000). More than 40% had underlying heart abnormalities, four (2.5%) had documented recovered cardiac arrest, and three presented with sudden death.

Schematic illustration of athlete with normal ECG with sinus tachycardia and rSr′ pattern of benign characteristics in V1.

Figure 23.9 Athlete with normal ECG with sinus tachycardia and rSr′ pattern of benign characteristics in V1.

Schematic illustration of very important sinus bradycardia during the night (28 bpm).

Figure 23.10 Very important sinus bradycardia during the night (28 bpm).

Schematic illustration of another athlete with sinus bradycardia and Wenckebach AV block 3 × 2 during the night.

Figure 23.11

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  2. Other ECG Patterns of Risk
  3. The ECG Recording: Leads, Devices, and Techniques
  4. The ECG in Different Clinical Set of Ischemic Heart Disease

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Oct 9, 2021 | Posted by in CARDIOLOGY | Comments Off on The ECG in Other Diseases and Different Situations

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