Sinoatrial Block: Disturbance in the atrial activation that is caused by transient failure of impulse conduction from the SINOATRIAL NODE to the HEART ATRIA. It is characterized by a delayed in heartbeat and pauses between P waves in an ELECTROCARDIOGRAM.Adams-Stokes Syndrome: A condition of fainting spells caused by heart block, often an atrioventricular block, that leads to BRADYCARDIA and drop in CARDIAC OUTPUT. When the cardiac output becomes too low, the patient faints (SYNCOPE). In some cases, the syncope attacks are transient and in others cases repetitive and persistent.Sinoatrial Node: The small mass of modified cardiac muscle fibers located at the junction of the superior vena cava (VENA CAVA, SUPERIOR) and right atrium. Contraction impulses probably start in this node, spread over the atrium (HEART ATRIUM) and are then transmitted by the atrioventricular bundle (BUNDLE OF HIS) to the ventricle (HEART VENTRICLE).Heart Block: Impaired conduction of cardiac impulse that can occur anywhere along the conduction pathway, such as between the SINOATRIAL NODE and the right atrium (SA block) or between atria and ventricles (AV block). Heart blocks can be classified by the duration, frequency, or completeness of conduction block. Reversibility depends on the degree of structural or functional defects.Tachycardia, Sinoatrial Nodal Reentry: Abnormally rapid heartbeats caused by reentry circuit in or around the SINOATRIAL NODE. It is characterized by sudden onset and offset episodes of tachycardia with a HEART RATE of 100-150 beats per minute. The P wave is identical to the sinus P wave but with a longer PR interval.

*  Phenytoin (Injection Route) Precautions - Mayo Clinic

Heart block (eg, Adams-Stokes syndrome, AV block, or sinoatrial block) or ...

*  Verapamil Extended Release Capsules - FDA prescribing information, side effects and uses

... verapamil hydrochloride may interfere with sinus node impulse generation and may induce sinus arrest or sinoatrial block. ... Atrioventricular Block. The effect of verapamil on AV conduction and the SA node may lead to asymptomatic first-degree AV block ... Marked first-degree block or progressive development to second- or third-degree AV block requires a reduction in dosage or, in ... However, there have been reports of excess bradycardia and AV block, including complete heart block, when the combination has ...

*  Parenteral Dilantin┬« (Phenytoin Sodium Injection, USP)

... sino-atrial block, second and third degree A-V block, and patients with Adams-Stokes syndrome. ... Cardiac arrhythmias have included bradycardia, heart block, ventricular tachycardia, and ventricular fibrillation which have ...

*  STEPS: Ivabradine (Corlanor) for Heart Failure - American Family Physician

... sinoatrial block, second- or third-degree atrioventricular block (unless a functioning demand pacemaker is present), a resting ... It inhibits the so-called funny current within the sinoatrial node, reducing heart rate without lowering blood pressure.1 ... Conduction disturbances such as sinus arrest and heart block may also occur.2,3 ...

*  Biophysical Characterization of the Underappreciated and Important Relationship Between Heart Rate Variability and Heart...

... from the living animal all the way down to the fundamental building block of automaticity, the sinoatrial node cell. ... B, Data before and after 100 nmol/L isoprenaline in rabbit sinoatrial node cell (SANC). C, Data before and after 100 nmol/L ... In the sinoatrial node, the membrane depolarizes throughout diastole (the pacemaker potential). If the pacemaker potential is ... Mathematical models of action potentials in the periphery and center of the rabbit sinoatrial node. Am J Physiol Heart Circ ...

*  Oalib search

A Combination of Atrioventricular Block and Sinoatrial Block in a Horse A Rezakhani, M Godarzi, I Tabatabei Naeini Acta ... There was no electrical activity during this pause indicating a concomitant sinoatrial block (SAB). The underlying rhythm was ... Sinus arrhythmia, sinoartrial block, wandering pacemaker, first and second degree atrioventricular blocks are considered to be ... Following the first blocked P-wave, there was a long pause, which was slightly more than twice the previous P-P interval. ... Moazzami Godarzi&searchField=authors

*  Rx Scoops | Drugs Detail

Sinoatrial and Atrioventricular Nodal Block [see WARNINGS AND PRECAUTIONS]. *Atrial Fibrillation/Atrial Flutter [see WARNINGS ... Second-degree AV block. 1/1209 (0.1%). 9/618 (1%). AV conduction abnormalities (other than AV blocks). 1/1209 (0.1%). 0/618 (0 ... Sinoatrial And Atrioventricular Nodal Block. Adenosine receptor agonists, including Lexiscan, can depress the SA and AV nodes ... heart block (including third-degree block), asystole, marked hypertension, symptomatic hypotension in association with ...

*  Bradycardias and Tachycardias - CARDIAC RHYTHM DISTURBANCES - Clinical Electrocardiography: A Simplified Approach, 7th Edition ...

Sinus bradycardia, including sinoatrial block. Atrioventricular (AV) junctional (nodal) escape rhythm. AV heart block (second ... including SA block), AV junctional escape rhythm, AV heart block (or AV dissociation), AF or atrial flutter with a very slow ... AV HEART BLOCK (SECOND OR THIRD DEGREE) OR AV DISSOCIATION. A slow ventricular rate of 60 beats/min or less (even as low as 20 ... SA block refers to situations in which impulses formed in the sinus node fail to depolarize the atria.. AV JUNCTIONAL (NODAL) ...

*  Intraventricular block - Wikipedia

An intraventricular block is a heart block of the ventricles of the heart. ... An example is a right bundle branch block.[1]. References[edit]. *^ "Lesson VI - ECG Conduction Abnormalities". Retrieved 2009- ... Sinoatrial arrest. Other / ungrouped. *hexaxial reference system *Right axis deviation. *Left axis deviation ... "Clinical significance of intraventricular block in acute myocardial infarction". Bull N Y Acad Med. 47 (8): 987-98. PMC ...

*  Bradycardia | Open Access articles | Open Access journals | Conference Proceedings | Editors | Authors | Reviewers | scientific...

The clinical relevance pertaining to AV blocks is greater than that of sinoatrial blocks.[9] ... Atrioventricular conduction disturbances (a.k.a.: AV block; 1o AV block, 2o type I AV block, 2o type II AV block, 3o AV block) ... "exit block"). Second-degree sinoatrial blocks can be detected only by use of a 12-lead EKG.[9] It is difficult and sometimes ... The third, Sick sinus syndrome, covers conditions that include severe sinus bradycardia, sinoatrial block, sinus arrest, and ...

(1/24) Conduction disturbances and increased atrial vulnerability in Connexin40-deficient mice analyzed by transesophageal stimulation.

BACKGROUND: Recently, it has been reported that connexin40 (Cx40) deficiency in targeted mouse mutants is associated with a prolongation of P-wave and QRS complex duration on surface electrograms. The specific effects of Cx40 deficiency on sinus node function, sinoatrial, and atrioventricular conduction properties as well as on atrial vulnerability have not yet been investigated systematically by electrophysiological analysis. METHODS AND RESULTS: Fifty-two mice (18 Cx40(+/+), 15 Cx40(+/-), and 19 Cx40(-/-) mice) were subjected to rapid atrial transesophageal stimulation after anesthesia with avertin. A significant prolongation of sinus node recovery time was noticed in Cx40(-/-) mice compared with Cx40(+/-) and Cx40(+/+) mice (287.8+/-109.0 vs 211.1+/-61.8 vs 204.4+/-60.9 ms; P<0.05). In addition, Wenckebach periodicity occurred at significantly longer atrial pacing cycle lengths in Cx40(-/-) mice than in Cx40(+/-) or Cx40(+/+) mice (93. 3+/-11.8 vs 83.9+/-9.7 vs 82.8+/-8.0 ms, P<0.05). Analysis of 27 Cx40(-/-) mice showed a significant increase in intra-atrial conduction time and atrioventricular conduction time compared with 52 Cx40(+/-) and 31 wild-type (Cx40(+/+)) mice. Furthermore, in Cx40(-/-) mice, atrial tachyarrhythmias could be induced frequently by atrial burst pacing, whereas no atrial arrhythmias were inducible in heterozygous or wild-type mice. CONCLUSIONS: This study demonstrates that Cx40 deficiency is associated with sinoatrial, intra-atrial, and atrioventricular conduction disturbances. In atrial myocardium of the mouse, Cx40 deficiency results in increased atrial vulnerability and might contribute to arrhythmogenesis.  (+info)

(2/24) Development of sinus node disease in patients with AV block: implications for single lead VDD pacing.

OBJECTIVE: To investigate the incidence of sinus node disease after pacemaker implantation for exclusive atrioventricular (AV) block. DESIGN: 441 patients were followed after VDD (n = 219) or DDD pacemaker (n = 222) implantation for AV block over a mean period of 37 months. Sinus node disease and atrial arrhythmias had been excluded by Holter monitoring and treadmill exercise preoperatively in 286 patients (group A). In 155 patients with complete AV block, a sinus rate above 70 beats/min was required for inclusion in the study (group B). Holter monitoring and treadmill exercise were performed two weeks, three months, and every six months after implantation. Sinus bradycardia below 40 beats/min, sinoatrial block, sinus arrest, or subnormal increase of heart rate during treadmill exercise were defined as sinus node dysfunction. RESULTS: Cumulative incidence of sinus node disease was 0.65% per year without differences between groups. Clinical indicators of sinus node dysfunction were sinus bradycardia below 40 beats/min in six patients (1.4%), intermittent sinoatrial block in two (0.5%), and chronotropic incompetence in five patients (1.1%). Only one of these patients (0.2%) was symptomatic. Cumulative incidence of atrial fibrillation was 2.0% per year, independent of the method used for the assessment of sinus node function and of the implanted device. CONCLUSIONS: In patients undergoing pacemaker implantation for isolated AV block, sinus node syndrome rarely occurs during follow up. Thus single lead VDD pacing can safely be performed in these patients.  (+info)

(3/24) Atrio-sinus interaction demonstrated by blockade of the rapid delayed rectifier current.

BACKGROUND: Proper pacemaking of the heart requires a specific organization of the sinoatrial (SA) node. The SA node drives the surrounding atrium but needs to be protected from its hyperpolarizing influence, which tends to suppress pacemaker activity. It has been suggested that the hyperpolarizing atrial influence is minimal at the site of the central nodal area. METHODS AND RESULTS: Atrio-sinus interaction was assessed by specific depolarization of the SA node by blocking the HERG-encoded rapid delayed rectifier current (I(K,r)) with the drug E-4031. In the SA node, E-4031 (1 micromol/L) changed action potential configuration drastically but never resulted in pacemaker arrest. In the atrium, E-4031 did not affect the membrane resting potential, thereby leaving the normal hyperpolarizing load on the SA node intact. When the SA node was sectioned into strips and subsequently separated from the atrium, spontaneous electrical activity of the strip containing the primary pacemaker ceased on I(K,r) blockade. When not separated from the atrium, I(K,r) blockade never resulted in pacemaker arrest. A similar effective atrio-sinus interaction was demonstrated in computer simulations. CONCLUSIONS: Our results demonstrate that the atrium provides an effective hyperpolarizing load on the central SA nodal area and is at least one of the controlling mechanisms for normal pacemaking function. The present study can be of help in understanding why patients with long-QT2 syndrome secondary to a mutation in HERG do not show sinus arrest.  (+info)

(4/24) Comparative study of sinoatrial conduction time and sinus node recovery time.

Atrial stimulation were performed in 5 normal patients (group A) and 4 patients with electrocardiographic evidence of sinoatrial disease (group B). The technique of premature atrial stimulation was used to calculate sinoatrial conduction time. Rapid atrial pacing was applied to measure maximum sinus node recovery time. In 4 cases both stimulation methods were repeated after intravenous administration of atropine Group A had a sinoatrial conduction time of 56 ms +/- 11 (SD) and a maximum sinus node recovery time of 1122 ms +/- 158. In 3 out of 4 patients with sinus node dysfunction a prolongation of sinoatrial conduction time could be demonstrated (145, 105, and 150 ms). In addition, one showed probable sinus node exit block after premature atrial stimulation. Sinus node recovery time was excessively prolonged in 2 (3880 and 3215 ms) and normal in the other 2 patients with sinoatrial disease (1330 and 1275 ms). Atropine leads to a decrease of sinoatrial conduction time. Results indicate that sinus node recovery time may not be a reliable indicator of sinus node automaticity if sinoatrial conduction is disturbed. The premature atrial stimulation technique makes it possible to study the pattern of sinoatrial conduction and to evaluate its reaction to therapeutic drugs.  (+info)

(5/24) Sinus node dysfunction in acute myocardial infarction.

The frequency, clinical course, and prognosis of sinus node dysfunction in 431 patients with acute myocardial infarction admitted to the coronary care unit were studied. Sinus node dysfunction occurred in 20 patients. In 13, the principal manifestation consisted of severe sinus bradycardia. In the remaining 7, periods of bradycardia alternating with episodes of supraventricular tachycardia were noted. Though several of the patients with sinus bradycardia required intravenous atropine or temporary pacing, normal sinus rhythm returned in virtually all during follow-up. The clinical course of patients with both bradycardia and tachycardia was less benign, during the acute phase and during follow-up; 5 of the 6 survivors required continued antiarrhythmic therapy or permanent pacing. The differences in the clinical course between these two groups of patients may reflect distinct underlying pathological changes. The findings in this study suggest that in contrast to sinus bradycardia, the occurrence of bradycardia-tachycardia syndrome during the acute phase of myocardial infarction may have important prognostic implications.  (+info)

(6/24) Sinoatrial block complicating legionnaire's disease.

A 59 year old woman presented with acute onset of fever, chills, diaphoresis, vague chest discomfort, and was found to be hypotensive and tachypnoeic. An electrocardiogram demonstrated sinoatrial block with a junctional rhythm between 50 and 80 beats/min. All cultures were negative and imaging studies unrevealing. Her urine tested positive for Legionella pneumophila antigen serotype 1 and she improved with antibiotic therapy.  (+info)

(7/24) Sinoatrial node dysfunction and early unexpected death of mice with a defect of klotho gene expression.

BACKGROUND: Homozygous mutant mice with a defect of klotho gene expression (kl/kl) show multiple age-related disorders and premature death from unknown causes. METHODS AND RESULTS: The kl/kl mice subjected to 20-hour restraint stress showed a high rate (20/30) of sudden death, which was associated with sinoatrial node dysfunction (conduction block or arrest). Heart rate and plasma norepinephrine of kl/kl mice, unlike those of wild-type (WT) mice, failed to increase during the stress. Intrinsic heart rate after pharmacological blockade of autonomic nerves in kl/kl mice was significantly lower than that in WT mice (380+/-33 versus 470+/-44 bpm; n=7). The sinus node recovery time after an overdrive pacing (600 bpm, 30 seconds) in kl/kl mice was significantly longer than in WT mice (392+/-37 versus 233+/-24 ms; n=6). In isolated sinoatrial node preparations, the positive chronotropic effect of isoproterenol was significantly less, whereas the negative chronotropic effect of acetylcholine was significantly greater in kl/kl than in WT mice. There was no degenerative structural change in the sinoatrial node of kl/kl mice. The precise localization of klotho was analyzed in newly prepared klotho-null mice with a reporter gene system (kl(-geo)). Homozygous kl(-geo) mice showed characteristic age-associated phenotypes that were almost identical to those of kl/kl mice. In the kl(-geo) mice, klotho expression was recognized exclusively in the sinoatrial node region in the heart in addition to parathyroid, kidney, and choroid plexus. CONCLUSIONS: In the heart, klotho is expressed solely at the sinoatrial node. klotho gene expression is essential for the sinoatrial node to function as a dependable pacemaker under conditions of stress.  (+info)

(8/24) Quinine-induced arrhythmia in a patient with severe malaria.

It was reported that there was a case of severe malaria patient with jaundice who presented with arrhythmia (premature ventricular contraction) while getting quinine infusion was reported. A man, 25 years old, was admitted to hospital with high fever, chill, vomiting, jaundice. The patient was fully conscious, blood pressure 120/80 mmHg, pulse rate 100 x/minute, regular. On admission, laboratory examination showed Plasmodium falciparum (++++), total bilirubin 8.25 mg/dL, conjugated bilirubin 4.36 mg/dL, unconjugated bilirubin 3.89 mg/dL, potassium 3.52 meq/L Patient was diagnosed as severe malaria with jaundice and got quinine infusion in dextrose 5% 500 mg/8 hour. On the second day the patient had vomitus, diarrhea, tinnitus, loss of hearing. After 30 hours of quinine infusion the patient felt palpitation and electrocardiography (ECG) recording showed premature ventricular contraction (PVC) > 5 x/minute, trigemini, constant type--sinoatrial block, positive U wave. He was treated with lidocaine 50 mg intravenously followed by infusion 1500 mg in dextrose 5%/24 hour and potassium aspartate tablet. Quinine infusion was discontinued and changed with sulfate quinine tablets. Three hours later the patient felt better, the frequency of PVC reduced to 4 - 5 x/minute and on the third day ECG was normal, potassium level was 3.34 meq/L. He was discharged on 7th day in good condition. Quinine, like quinidine, is a chincona alkaloid that has anti-arrhythmic property, although it also pro-arrhythmic that can cause various arrhythmias, including severe arrhythmia such as multiple PVC. Administration of parenteral quinine must be done carefully and with good observation because of its pro-arrhythmic effect, especially in older patients who have heart diseases or patients with electrolyte disorder (hypokalemia) which frequently occurs due to vomiting and or diarrhea in malaria cases.  (+info)


  • Atrioventricular block can occur in patients without preexisting conduction defects. (
  • Ivabradine is contraindicated in patients with severe hepatic impairment, sick sinus syndrome, sinoatrial block, second- or third-degree atrioventricular block (unless a functioning demand pacemaker is present), a resting heart rate less than 60 beats per minute (bpm), or pacemaker dependence. (
  • 19 Studies in patients with complete atrioventricular (AV) block and stable junctional escape rhythms have been limited, and interpretation of the results must take into account the heterogeneity of underlying pathology and the demonstrated variability in location of pacemaker activity. (

sinus arrest

  • However in patients with sick sinus syndrome, verapamil hydrochloride may interfere with sinus node impulse generation and may induce sinus arrest or sinoatrial block. (
  • Conduction disturbances such as sinus arrest and heart block may also occur. (


  • It inhibits the so-called funny current within the sinoatrial node, reducing heart rate without lowering blood pressure. (
  • the P wave is negative in lead aV R and positive in lead II, indicating that the sinoatrial (SA) node is the pacemaker. (
  • Sinus bradycardia may be related to a decreased firing rate of the sinus node pacemaker cells or to actual SA block. (
  • SA block refers to situations in which impulses formed in the sinus node fail to depolarize the atria. (
  • [4] This dysrhythmia also may occur when the electrical impulses from the SA node fail to reach the AV node because of SA or AV block. (
  • [7] [8] In a third-degree heart block, approximately 61% take place at the bundle branch-Purkinje system, 21% at the AV node, and 15% at the bundle of His. (
  • Sick sinus syndrome (SSS) is a type of bradycardia in which the sinoatrial (SA), or sinus node is not working as it should. (
  • Sinoatrial block is a type of SSS in which the electrical signals move too slowly through the sinus node. (


  • In addition, patients with second-degree AV block (either Mobitz type I [Wenckebach] or Mobitz type II) sometimes have a bradycardia because of the dropped beats (see Fig. 17-3 and Table 17-1). (


  • Most of these subjects received Lexiscan in two clinical studies that enrolled patients who had no history of bronchospastic lung disease as well as no history of a cardiac conduction block of greater than first-degree AV block, except for patients with functioning artificial pacemakers. (


  • A split S1 sound is common in the setting of a right bundle branch block or ventricular tachycardia/premature ventricular contractions, or PVCs, with a right bundle branch block morphology. (


  • An intraventricular block is a heart block of the ventricles of the heart. (
  • These problems are commonly called heart block. (
  • By blocking the making of angiotensin, these drugs help the blood vessels relax and widen, which lowers blood pressure, increases blood flow to the heart and reduces the heart's workload. (
  • Acute coronary syndrome is an umbrella term for when blood supplied to the heart muscle is decreased or blocked, leading to a heart attack . (


  • An example is a right bundle branch block . (
  • A left bundle branch block has the opposite effect on S1. (