The electrical impulses of atrium arise from the sinus node, subsequently pass through the right and left atrium, and finally arrive at the atrioventricular node. The P wave is the summation of the electrical current generated by depolarization due to its passage through the atrial conduction pathway. It provides many clinical clues that may be useful for diagnosis of atrial, ventricular, or valvular heart diseases. This review article briefly describes the clinical implications, mechanism of genesis, and normal and pathologic features of the P wave.
Atrioventricular Node ; Diagnosis ; Heart Atria ; Heart Valve Diseases ; Sinoatrial Node

The aim of present study is to investigate the effects of cGMP on hyperpolarization activated inward current (If), pacemaker current of the heart, in rabbit sino-atrial node cells using the whole-cell patch clamp technique. When sodium nitroprusside (SNP, 80 muM), which is known to activate guanylyl cyclase, was added, If amplitude was increased and its activation was accelerated. However, when If was prestimulated by isopreterenol (ISO, 1 muM), SNP reversed the effect of ISO. In the absence of ISO, SNP shifted activation curve rightward. On the contrary in the presence of ISO, SNP shifted activation curve in opposite direction. 8Br-cGMP (100 muM), more potent PKG activator and worse PDE activator than cGMP, also increased basal If but did not reverse stimulatory effect of ISO. It was probable that PKG activation seemed to be involved in SNP-induced basal If increase. The fact that SNP inhibited ISO-stimulated If suggested cGMP antagonize cAMP action via the activation of PDE. This possibility was supported by experiment using 3-isobutyl-1-methylxanthine (IBMX), non-specific PDE inhibitor. SNP did not affect If when If was stimulated by 20 muM IBMX. Therefore, cGMP reversed the stimulatory effect of cAMP via cAMP breakdown by activating cGMP-stimulated PDE. These results suggest that PKG and PDE are involved in the modulation of If by cGMP: PKG may facilitate If and cGMP-stimulated PDE can counteract the stimulatory action of cAMP.
1-Methyl-3-isobutylxanthine ; Guanylate Cyclase ; Heart ; Nitroprusside ; Sinoatrial Node*

Human heart rhythm is mainly regulated and controlled by the sinoatrial node. Fibrosis plays an important regulating role in adjusting the structural and functional integrity of the sinoatrial node pacemaker complex. In physiological state, the fibrosis degree of sinoatrial node is negatively correlated with heart rate, positively correlated with age and heart size, and can maintain a relatively stable heart rate. Pathological fibrosis of sinoatrial node can induce various types of arrhythmias which can result in sudden death. Determination of the mechanisms related to sinoatrial node pathological fibrosis could provide a target for clinical treatment of sinoatrial node fibrosis and diagnosis basis for forensic pathologists. This paper reviews the main mechanism of sinoatrial node pathological fibrosis, including abnormal activation of cardiac fibroblast cells in sinoatrial node, hyperplasia of epicardial adipose tissue, calcium clock disorder, artery stenosis, etc., introduces the test methods, diagnostic criteria as well as its role in sudden cardiac death and discusses the potential application, to provide reference for relevant research and application.
Arrhythmias, Cardiac ; Fibrosis ; Heart Rate ; Humans ; Sinoatrial Node

Nine patients of mean age 47.8 years, with suspected sinus node dysfunction, underwent extensive electrophysiological studies. Sinus bradycardia(6the electrophysiological study, AH and HV intervals were prolonged in 2/9 and 1/9 patients, respectively. Maximal sinus node recovery times were prolonged in 7/9 patients, ranging from 1,330 msec to 12,330msec. Sinoatrial conduction times measured by atrial premature stimulation technique were prolonged in 5/7 patients, ranging from 137msec to 310 msec. And sinoatrial conduction time measured by continuous pacing technique also revealed prolonged value in 4/6 patients ranging from 140 msec to 195 msec. The effective refractory periods, of atrium were prolonged in 6/8 patients (320 msec to 470 msec). The effective and functional refractory periods of AV node were prolonged in 3/8 patients (440 csec to 490 msec) and 4/8 patients (530 msec to 560 msec), respectively. Retrograde VA conduction could be observed in 3/7 patients and ventricular effective refractory periods were normal in 7/7 patients. Atrial flutter was induced in 1/9 patients by electric stimulation during electrophysiological study. Above data suggest that the electrophysiological study is very useful in assessing the sinus node function and other electrophysiological properties in sick sinus syndrome patients and also suggest that the data could be utilized in choosing the proper mode of artificial pacemaker for each patient.
Atrial Flutter ; Atrioventricular Node ; Electric Stimulation ; Humans ; Pacemaker, Artificial ; Sick Sinus Syndrome* ; Sinoatrial Node

A simplified method of the cardiac conduction system (CCS) is evaluated by the study of 73 forensic cases. The sinoatrial node were observed in all cases (100.0%), atrioventricular node in 70 cases (95.9%) and penetrating bundle (His bundle) in 70 cases (95.9%). We divided the cases into three groups as the group of cardiac death (25 cases), non-cardiac death (24cases) and sudden unexpected death but undeterminable cause of death (24 cases) diagnosed after routine autopsy including routine cardiac examination and toxicological analysis and compared the type and incidence of CCS lesions in each groups. Narrowing of the sinoatrial (SA) or atrioventricular (AV) artery by fibromuscular hyperplasia (FMH) and fatty infiltration in SA or AV node were identified in all groups, lymphocytic infiltration in SA or AN node in cardiac and non-cardiac death group, hemorrhage and fibrosis of SA or AV node were identified in cardiac death group. FMH of the artery of SA or AN node occured more commonly in undeterminable cause of death group (45.1%) than in cardiac (16.0%) and non-cardiac group (20.8%) and severe narrowing (> or =75%) of the artery of SA or AV node was only present in undeterminable cause of death group (29.2%). The results led to the conclusion that this simple technique is very useful in detection of major abnor-malities of CCS with minimal effort and examination of the CCS in death which the routine autopsy and drug screen fail to provide a cause of death can yield a cause of death in a significant percentage of cases.
Arteries ; Atrioventricular Node ; Autopsy ; Cause of Death ; Death ; Death, Sudden* ; Fibrosis ; Hemorrhage ; Hyperplasia ; Incidence ; Sinoatrial Node

Paroxysmal atrial fibrillation may be induced by coronary spasm presenting with typical angina-like pain and palpitations. It is typically treated using rate or rhythm control strategies, although sustained coronary spasm can induce sinus bradycardia with dizziness and syncope. In the present case, we reached a diagnosis of paroxysmal atrial fibrillation and sinus bradycardia due to coronary artery spasm using the methyl-ergonovine provocation test during angiography. While the treatment of coronary spasm can resolve paroxysmal atrial fibrillation, sinus bradycardia, and variant angina, the mechanism remains unclear, although it may be associated with sinus node ischemia. Similar symptoms, particularly chest discomfort, should be carefully considered in cases of paroxysmal atrial fibrillation.
Angiography ; Atrial Fibrillation* ; Bradycardia* ; Coronary Vasospasm ; Coronary Vessels* ; Diagnosis ; Dizziness ; Ischemia ; Sinoatrial Node ; Spasm* ; Syncope ; Thorax

BACKGROUND: It is very important to evalute the function of the atrioventricular conduction system in selecting appropriate pacemaker, pacing and sensing mode in sick sinus syndrome. It has been reported that atrioventricular conduction abnormalities were commonly accompanied with sinus node dysfunction (SND). However, there were several long term follow-up studies indicating that incidence of AV conduction abnormalities was as low as below 1% a year in patients with SND implanted pacemaker. This study was performed to evaluate the properties of the AV conduction system in patients with SND. SUBJECT AND METHODS: Patients subjected to this study were fifty-eight who underwent electrophysiologic study on suspicion of SND. Sinus node recovery time (SNRT) was defined as the longest time among the times that sinus rhythm reappeared after rapid atrial pacing for 45 seconds with several cycle lengths, and corrected SNRT (cSNRT) was worked out by subtracting sinus cycle length (SCL) from SNRT. Criteria for sinus node dysfunction were 1550 msec or more on SNRT, 550 msec or more on cSNRT and group A (23 cases, 58+/-13 yrs) was defined as SND not retrieved to normal after intravenous administration of atropine 1-2 mg, group B (21 cases, 52+/-14 yrs) was retrieved to normal and group C (14 cases, 54+/-13 yrs) was normal control group. Abnormalities of the AV conduction system were defined as 150 msec or more on AH interval, 500 msec or more on AVblock cycle length (AV-BCL), 450 msec or more on AV nodeeffective refractory period (AVN-ERP). RESULTS: SCL in group A, B, C was 1197+/-340 msec, 1215+/-273 msec, and 898+/-129 msec, respectively at baseline and 886+/-218 msec, 798+/-106 msec, and 722+/-110 msec respectively after atropine administration, showing a significant prolongation of SCL in group A and B at baseline (p<0.001) and group A after atropine administration (p<0.05). SNRT in group A, B, C was 3520+/-1817 msec, 3180+/-2390 msec, and 1282+/-116, respectively at baseline and 4155+/-4281 msec, 1237+/-210 msec, 1020+/-245 msec, respectively after atropine administration, showing a significant prolongation of SNRT in group A and B at baseline (p<0.001) and group A after atropine administration (p<0.05). AH intervals at baseline and after atropine administration were 107+/-27 msec and 100+/-20 msec in group A, 101+/-21 and 91+/-14 in group B, and 118+/-32 and 83+/-23 in group C, showing no significant difference between 3 groups. AV-BCLs at baseline and after atropine administration were 428+/-151 msec and 453+/-301 msec in group A, 525+/-140 and 370+/-53 in group B, and 461+/-120 361+/-94 in group C, showing no significant difference between 3 groups. AVN-ERP was 315+/-57 msec in group A, 343+/-132 msec in group B, 347+/-132 in group C, showing no significant difference between 3 groups. There was no significant difference in the incidences of cases with abnormal AH interval, AV-BCL, AVN-ERP, HV interval between 3 groups. AV block greater than second degree was observed in one patient of group A but none of group B and C. CONCLUSIONS: Atrioventricular conduction abnormalities in patients with sinus node dysfunction were not more common than control subjects. Therefore, atrial pacing rather than ventricular or dual chamber pacing may be safely selected as a permanent pacing mode for sick sinus syndrome with no combined significant AV block.
Administration, Intravenous ; Atrioventricular Block ; Atropine ; Humans ; Incidence ; Sick Sinus Syndrome* ; Sinoatrial Node*

The incidence of intraoperative arrhythmia is extremely high, and some arrhythmias require clinical attention. Therefore, it is essential for the anesthesiologist to evaluate risk factors for arrhythmia and understand their etiology, electrophysiology, diagnosis, and treatment. Anesthetic agents reportedly affect normal cardiac electrical activity. In the normal cardiac cycle, the sinoatrial node initiates cardiac electrical activity through intrinsic autonomous pacemaker activity. Sequential atrial and ventricular contractions result in an effective cardiac pumping mechanism. Arrhythmia occurs due to various causes, and the cardiac pumping mechanism may be affected. A severe case may result in hemodynamic instability. In this situation, the anesthesiologist should eliminate the possible causes of arrhythmia and manage the condition, creating hemodynamic stability under proper electrocardiographic monitoring.
Anesthesia ; Anesthetics ; Arrhythmias, Cardiac* ; Diagnosis ; Electrocardiography ; Electrophysiology ; Hemodynamics ; Incidence ; Risk Factors ; Sinoatrial Node

Surface ECG findings in 29 patients with left isomerism were reviewed. Among the total 46 wave axis distributions, 25(54%) were abnormal axis, not originated from sinus node. Congenital atrioventricular block was found in 2 children. 6 patients showed the bradycardia and junctional escape rhythm intermittently or persistently. 4 of them, not related with heart surgery, were much older than 2 patients who showed these ECG findings after heart surgery. These ECG findings suggested the possibility of occurrence of sinus node or subsidiary pacemaker dysfunction in the patients with left isomerism, especially in the older patients. So we thought that electrophysiologic evaluation is necessary in some patients with left isomerism.
Atrioventricular Block ; Axis, Cervical Vertebra ; Bradycardia ; Child ; Electrocardiography* ; Humans ; Isomerism* ; Sinoatrial Node ; Thoracic Surgery ; United Nations

BACKGROUND: The arterial baroreflex is a key mechanism for maintaining blood pressure homeostasis. Low-dose atropine (LDA) causes bradycardia, either by acting on the sinoatrial node or due to its effect on central muscarinic receptors, which increases vagal activity. We evaluated the effect of LDA on baroreflex sensitivity (BRS) in healthy awake subjects. METHODS: We assessed changes in RR interval (RRI) and systolic blood pressure (SBP), power spectral densities of heart rate variability (HRV) and systolic blood pressure variability (SBPV), and spontaneous BRS by using transfer function analysis before and after LDA (2microgram/kg) in 17 healthy volunteers. RESULTS: LDA induced not only bradycardia but also increased of the high-frequency (HF) component of HRV, RMSSD (root mean squared successive difference interval), and pNN50 (percentage of sinus cycles differing from the preceding cycle by > 50 ms). The HF and LF components of SBPV remained unchanged. Spontaneous BRS determined by transfer function analysis increased significantly (P < 0.05), and changes in BRS were significantly associated with changes in the HF component of HRV (P < 0.05). CONCLUSIONS: LDA increased vagal cardiac function and arterial baroreflex in awake subjects. This result suggests that increased vagal cardiac function by LDA application is related to baroreflex increase.
Atropine* ; Baroreflex* ; Blood Pressure ; Bradycardia ; Healthy Volunteers ; Heart Rate ; Homeostasis ; Receptors, Muscarinic ; Sinoatrial Node