Fig. 22.1
The figure shows the patient’s ECG when he arrived at the emergency room: it was characterized by type II sinoatrial block; biphasic T waves were present in V4, V5, and V6, and negative T waves in III and aVF
The patient was then transferred to our arrhythmology and cardiology clinic for further evaluation and treatment.
Medical History and Cardiovascular Risk Factors
1.
Cardiovascular risk factors: hypertension, dyslipidemia, overweight body, and family history of cardiovascular disease
2.
In 2011 the patient had a non-ST-elevation myocardial infarction treated with PCI + stenting of the first segment of the left anterior descending coronary. The angiography did not reveal significant stenoses of other coronaries. Since then, the patient underwent annual cardiology visit with EKG and echocardiography, the last of which dated back about 1 month before he entered the emergency room. No abnormalities were found during that visit. The echocardiogram reported the same alterations listed above. Moreover, he denied angina, dyspnea, or syncope before that day.
Medications
ASA 1 cp, ramipril 2.5 mg 1 cp bid, potassium canrenoate 100 mg 1 cp, bisoprolol 2.5 mg 1 cp, atorvastatin 80 mg 1 cp, pantoprazole 20 mg 1 cp, tamsulosin chlorhydrate 1 cp, and allopurinol 1 cp
Vital Signs
Temperature 36.5 °C, heart rate 35 bpm, arterial blood pressure 95/55 mmHg, respiratory rate 20 breaths/min, and oxygen saturation 98 %
Physical Examination
General appearance: alert and cooperative and slightly dyspneic
Lungs: clear to percussion and minimal rales on pulmonary bases
Cardiovascular system: normal S1 and S2. Murmur 2/6 at the apex. Bradycardic rhythm. No peripheral edema, cyanosis, or pallor. Warm and well-perfused extremities
Abdomen: positive bowel sounds. Soft and non-distended. No guarding or rebound. No masses
Routine Laboratory Test
Potassium 6.1 mEq/l, sodium 136 mEq/l, and creatinine 2 mg/dl. Normal in other blood tests
Instrumental Examination
A complete echocardiogram was performed and showed upper limits of normality for LVM index (LV diastolic volume/BSA 75 ml/m2) with a slightly reduced ejection fraction (EF 48 %) due to hypokinesia of interventricular septum and apical segments of the anterolateral wall. Normal dimensions and function of right cardiac chambers, a mild mitral regurgitation, a calcification of the aortic valve without regurgitation nor stenosis, a slightly enlarged tubular ascending aorta (38 mm), and a mild tricuspid regurgitation with 32 mmHg pulmonary artery systolic pressure were already shown by the echocardiogram that the patient underwent 1 month before.
A chest radiograph was done and disclosed normal cardiac and pulmonary findings.
Clinical Course and Therapeutic Management
These findings altogether were suggestive of symptomatic sinoatrial block. All possible removable causes of sinoatrial block were checked: a strict control of kalemia was performed, and the patient continued to be treated by hydration with glucose and insulin 10 IU and administration of furosemide and Kayexalate. Moreover, administration of bisoprolol, ramipril, and potassium canrenoate was interrupted. A continuous telemetric monitoring was placed and showed a restoration of sinus rhythm when the level of potassium reached values of 5.5 mEq/l. The protocol for hyperkalemia was continued until the values of potassium in the blood were normal. The patient became asymptomatic dyspnea, asthenia, and dizziness. During the hospitalization he underwent an ECG stress test that showed a normal chronotropic competence and no ischemia signs. On the 5th day, he was discharged with a diagnosis of “symptomatic sinoatrial block secondary to iatrogenic acute renal failure and hyperkalemia in patient with ischemic cardiomyopathy.” Since the ECG was unchanged from the previous, myocardial enzymes were normal, and there was no evidence of ischemia at the ECG stress test, it was then decided to not perform a coronarography. Before the discharge, a patch-type long-term external Holter recorder was applied to the patient.
A follow-up visit was performed 1 month later. The patient was completely asymptomatic. Physical examination was normal. The ECG showed a sinus rhythm (heart rate of 62 bpm). Holter monitoring did not record any arrhythmia. Laboratory blood tests were normal, including the values of potassium (4 mEq/l) and creatinine (1.4 mg/dl). Blood pressure level was 145/95 mmHg, so it was decided to resume administration of ramipril 2.5 mg ½ cp bid. It was also recommended to perform periodic checks of renal function and echocardiographic follow-up of the tubular ascending aortic dimensions.
22.2 Electrocardiographic Diagnosis of Sinoatrial Exit Block
The major electrocardiographic expressions of sinus node dysfunction (SND) are the presence of abnormal sinus bradycardia or the occurrence of “sinus pause.”
The term “sinus pause” is usually used to describe the occurrence on ECG of a sudden pause in the underlying sinus rhythm: one or more sinus beats fail to appear at the expected time and a pause occurs (long P-P interval). After the pause, the resumption of the basic sinus rhythm can be slower for some cycles (temporary rate suppression); some rescue rhythms (escape beats or rhythm) may also appear from ectopic subsidiary supraventricular sites (perisinus, atrial, or junctional).
The occurrence of a sinus pause can be due to the failure of a sinoatrial (SA) node to initiate (sinus arrest) or to conduct the impulse (sinus exit block). Some authors don’t distinguish the sinus pause from the sinus arrest, restricting the latter in case of prolonged sinus inactivity, even if no precise definition exists [1]. For practice purposes in this text, we refer to sinus pause in its broadest sense.
Electrocardiographically the sinus impulse is only recorded once it has left the sinus node and activated the atrium, thereby resulting in the P wave. The presence of delay or block in conduction at the SA junction can be detected by calculation of certain rhythmic sequences involving the pause and the P-P intervals [2].
In sinus arrest there is a failure of impulse formation within the sinus node, disappointing the timing of SA node discharge. In this case the underlying rhythm would not resume on time after the pause; the long cycle has no mathematical relation with the basic P-P interval but is random in duration, often interrupted by escape beats or rhythm.
In sinus exit block, an electrical impulse is initiated by the SA node but not conducted to the atria because it is blocked within the SA node or the sinoatrial junction. The dropped beats may occur sporadically or in regularly recurring patterns as fixed block. In the presence of a regular basic sinus rhythm, SA block can almost always be distinguished from sinus arrest because the sinus block generating pause is mathematically related to the baseline P-P interval (see later in the text).
Sinoatrial exit block can be divided into three types (first, second, and third degrees), analogous to those occurring at the atrioventricular (AV) node. Being characterized by a prolongation of the sinoatrial conduction time (SACT), the first SA exit block cannot be recognized on the surface ECG.
The second-degree exit block is further classified into type I (SA block with Wenckebach conduction) and type II (SA Mobitz II). Type I block is characterized by the decremental progressive lengthening of the conduction between the sinus node and the atria, until a sinus impulse is not conducted to the atria. The classical criteria for the diagnosis of SA Wenckebach conduction are: (1) The P-P interval following the dropped SA impulse is larger than the interval preceding it. This phenomenon is common to all Wenckebach forms, even in the most atypical, and it is due to the fact that the lengthening of SA conduction is present at the beginning of the sequence (the second beat in typical series) [3]. (2) The P-P interval including a blocked SA impulse is shorter than double (or multiple in case of more than one consecutively dropped beat) the distance of the P-P interval preceding it. (3) There is a progressive diminution of the P-P intervals until the pause. The pause generated in a Wenckebach series is twice the sinus cycle minus the sum of the increments of conduction delay at each cycle. However, the P-P interval doesn’t accurately reflect the sinus interval, as it has been modified by varying SA conduction times.
For this reason, the duration of presumed sinus cycle may be calculated on the basis of Wenckebach principle periodicity, by dividing the total duration of the period by the number of visible cycles + 1 (sinus impulses which are conducted after a long pause will probably have SA intervals of similar length, i.e., they are corresponding impulses. The isoconduction interval between these corresponding impulses will be the same at both sinus and atrial levels) [2].
Type II SA block shows a failed conduction of a sinus impulse without previous prolongation of SCAT. For this reason the pattern of type II block is characterized by the following: (1) a P-P interval following the dropped SA impulse is not significantly larger than the interval preceding it (this is the most important criterion for diagnosis) [3], (2) the P-P interval including a blocked SA impulse is an exact multiple of the P to P cycle length, and (3) the P-P intervals until the pause are constant.
In the presence of concomitant sinus arrhythmia causing beat to beat variations, it could be impossible to distinguish between sinus arrest and SA exit block because of the presence of the variable and unpredictable long intervals without mathematical relation to short P-P intervals (which are not constant). In this case the ECG panel may be categorized as a pathological or chaotic sinus arrhythmia usually associated with sinus bradycardia and representing another sign of underlying sinus node dysfunction [4].
Sinoatrial 2:1 block is a pattern that may be suspected in the presence of severe sinus bradycardia on ECG (usually <40 bpm). This pattern of SA exit block resembles a severe sinus bradycardia but may be distinguishable from it because in SA 2:1 block, the acceleration and deceleration of the sinus rhythm do not occur progressively. For diagnostic purposes, it is useful to have a more prolonged ECG recording to follow the onset/termination of the bradycardia or the observation of a sudden heart rate doubling during atropine test.
High-degree type II sinoatrial block – occasionally more than one sinus impulse in succession fails to reach the atrium, and two or three successive P waves are dropped, giving a 3:1 or 4:1 exit block and a long pause. The diagnosis is possible only in the presence of pause exactly multiple of an underlying regular sinus cycle. Usually it is difficult because this long pause is interrupted by the intervention of escaped beats/rhythm.
The third-degree (or complete) SA exit block is a term used to describe a complete absence of P waves because no SA node impulse is conducted to the atria. ECG shows an escape rhythm from a lower pacemaker site after a sinus pause, and so it is not distinguishable from a sinus arrest.
The occurrence of a sinus pause (or a long P-P interval) on ECG may result also from mechanisms that should be differentiated: marked sinus arrhythmia, sinus suppression after ectopic premature (often atrial) impulses even blocked or conducted, overdrive suppression after ectopic tachycardia, and single reciprocating “echo” P waves.
Respiratory sinus arrhythmia can be easily recognized because the cyclic lengthening of P-P interval is usually gradual and phasic; on the other hand, non-respiratory sinus arrhythmia presents variable and unpredictable long P-P intervals with different durations and no mathematical relationship with short P-P intervals.
Clinical Presentation: The Sick Sinus Syndrome
SA exit block may be chronic but often occurs as intermittent episodes, so patients may have normal sinus rhythm for several days or weeks between episodes. Furthermore, patients with SA block usually have additional rhythm disturbance because this arrhythmia is included in a broader clinical scenario, the so-called sinus node dysfunction or sick sinus syndrome.
Sick sinus syndrome (SSS) is a term used to describe the clinical manifestations associated with a collection of cardiac rhythm disturbances marked by sinus node inability (sinus node dysfunction) to generate an atrial rate matching the body’s physiologic requirements [5]. When SND is associated with symptoms or prolonged asystole, it is referred as SSS. Sick sinus syndrome is not a disease with a single etiology and pathogenesis.
Abnormalities encompassed in this syndrome include various bradyarrhythmias such as sinus bradycardia, sinus arrest with or without escape rhythm, or sinus exit block, associated or not with supraventricular tachyarrhythmias.
When complicating supraventricular arrhythmias are present, the condition is termed “the syndrome of alternating bradycardia and tachycardia” or simply the “bradycardia-tachycardia syndrome” (BTS) [6]. This syndrome is more common in older patients with advanced sick sinus syndrome. The most common tachyarrhythmias are atrial fibrillation and atrial flutter [7, 8]. It is argued that different electrophysiological mechanisms may be responsible for BTS: bradycardia associated with SND may favor reentrant beats and related tachycardias, while many evidences suggest that atrial fibrillation and atrial flutter can lead to atrial remodeling and subsequent SND [9, 10].
Clinically, SSS may produce a variety of ECG manifestations consisting in inappropriate sinus bradycardia, SA exit block or sinus arrest, prolonged sinus arrest with failing ectopic pacemaker, persistent atrial or atrioventricular escape rhythm, episodes of alternating supraventricular tachyarrhythmias with bradyarrhythmias, and long pause following cardioversion of atrial tachyarrhythmia.
Chronotropic incompetence (CI) is another manifestation of SSS. It is defined as a failure to achieve 85 % of the maximum predicted heart rate during exercise testing.
Prevalence of Sinus Node Dysfunction and SSS
Bradycardia is frequently seen in healthy individuals, especially in trained subjects, with a waking hour rate usually >40 bpm [11]. In highly trained athletes, a slower heart rate (30–35 bpm) may be seen, so that only profound sinus bradycardia and/or marked sinus arrhythmia (heart rate less than 30 bpm and/or pauses ≥3 s during wake hours) needs to be distinguished from sinus node disease [12].
Heart rate between 30 and 35 bpm, asymptomatic sinus pauses lasting between 2 and 3 s, escape junctional beats or rhythms (with functional AV dissociation), and first- and second-degree atrioventricular nodal block are normal variants during sleep [11].
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