Article

Evaluation of Sino-atrial Node Function in Man by Overdrive Suppression

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Abstract

Sino-atrial node (SAN) function was evaluated in 46 patients, three of whom had the sick sinus syndrome. Patients were paced from the right atrium for 15 to 180 sec at rates of 90, 110, 130, and 150 beats/min. The rapid cessation of pacing was associated with suppression of the SAN at all paced rates and at all durations of pacing. The observed pause was terminated by a sinus beat in all instances. The duration of pacing had little influence on the duration of the observed pause. The pause increased as the pacing rate was increased until, at a rate of 150 beats/min, a marked decrease in the pause was noted. Atropine (1.5-3.0 mg iv) diminished but did not eliminate the SAN suppression. Subthreshold pacing did not suppress SAN function. Three patients with sick sinus syndrome had a greater degree of SAN suppression than normal patients (4732 ± 415 msec [SSS] M ± sem; 1041 ± 56 msec for normal patients). The determination of the duration of the pause following cessation of atrial pacing provides a technique for recognition of abnormalities of SAN function.

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... Normally, the SNRT is less than 1500 ms [28] while SNRT tends to be shorter with shorter baseline sinus cycle lengths [26], which is illustrated by the dashed line in Fig. 5B, where BCL denotes intrinsic sinus cycle length, and the maximum pause represents SNRT. ...
... The study in [26] shows an increase in the maximum pause of SAN as the pacing rate increases. We pace the model with the intrinsic cycle length of 786 ms. ...
... They explain that the drop may be the result of enhanced sympathetic discharge [26]. While d 4 in our model can represent the sympathetic control, we do not link the heart rates to this parameter. ...
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Objective: A flexible, efficient and verifiable pacemaker cell model is essential to the design of real-time virtual hearts that can be used for closed-loop validation of cardiac devices. A new parametric model of pacemaker action potential is developed to address this need. Methods: The action potential phases are modeled using hybrid automaton (HA) with one piecewise-linear continuous variable. The model can capture ratedependent dynamics, such as action potential duration (APD) restitution, conduction velocity (CV) restitution, and overdrive suppression by incorporating non-linear update functions. Simulated dynamics of the model compared well with previous models and clinical data. Conclusion: The results show that the parametric model can reproduce the electrophysiological dynamics of a variety of pacemaker cells, such as sinoatrial node (SAN), atrioventricular node (AVN) and the His-Purkinje system (HPS), under varying cardiac conditions. Significance: This is an important contribution toward closed-loop validation of cardiac devices using real-time heart models.
... The basal heart rate was measured first. The rats were then stimulated with a voltage of 1.5 V, pulse width of 10 ms, and frequency of 20%, 40% and 80% higher than the primitive sinus rate, with a stimulus duration of 30 s and a stimulus interval of 3 min [9]. (2) Sinoatrial conduction time (SACT): It was calculated using Narula's method [10]. ...
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The Sick Sinus Syndrome (SSS) is a serious life-threatening heart disease. It is important to establish a credible and stable sinus node damage model. In this study, we use two methods to construct an SSS damage model in rats. One is to inject sodium hydroxide to the SSS area through internal jugular vein. Another is to cause ischemia-reperfusion injury on the SSS area. 43 healthy SD rats were randomly divided into 4 groups, namely ischemia-reperfusion injury group (IRIG), inject sodium hydroxide group (ISHG), and propranolol group (PG) and the control group (CG). The achievement ratio of modeling was 67% in the IRIG and 83% in the ISHG. The HR significantly decreased after operation in the IRIG and ISHG compared with pre-operation (P<0.01). The HR was reduced by above 30% in these 2 groups after modeling, while the reduction was better maintained in IRIG. Additionally, the sinoatrial node recovery time (SNRT) and sinoatrial conduction time (SACT) were significantly prolonged compared with pre-modeling in 2 groups (P < 0.01). Morphology results showed blurry in structure and boundaries with pale cytoplasm. It is speculated that IRIG and ISHG modeling might influence the calcium concentration and damage the sinus node function by decrease the expression of HCN4 and SCN5A, which impaired the driving ability of sinus node and leading to apoptosis. Ischemia reperfusion injury and sodium hydroxide injury could construct stable SSS models which could represent clinic pathological damage. Thus, both methods could be used for further studies of the SSS mechanisms and drugs.
... ). Bei der Ermittlung der Sinusknotenerholzeit oder auch sinus node recovery time (SNRT) wird durch Überstimulation des Vorhofs mit einer Frequenz, die über der des Sinusknotens liegt, die intrinsische Aktivität des Sinusknotens supprimiert. Nach der Stimulationsserie ist der Sinusknoten unter physiologischen Bedingungen wiederum die erste Instanz der Erregungsbildung, welche durch Automatiemechanismen die Initiation des folgenden Herzschlages übernimmt(Lange, 1965;Mandel et al., 1971). Dieses Zeitintervall bis zum Einsetzen der ersten spontanen Vorhofdepolarisation (p-Welle) nach atrialer Überstimulation wird als Sinusknotenerholzeit bezeichnet. ...
Thesis
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... It suggests that the maximum sinus node recovery time (clinically about 1.5 s [8]) appears around %Kzero = 23. ...
... The maximum value obtained during atrial pacing at frequencies of 8.4, 10 Hz, and 11.6 Hz was chosen because of the pioneering work of Berul and colleagues (Berul et al. 1996). These investigators reported the maximum value from all three pacing drives in the calculations of SNRT because this approach is analogous to the methods used in human studies (Mandel et al. 1971). ...
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Chapter
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Chapter
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Chapter
Störungen der Sinusknotenfunktion beruhen auf einer gestörten Impulsbildung im Sinusknoten und/oder der sinuatrialen Überleitung. Da die elektrische Aktivität des Sinusknotens durch die konventionelle EKG-Schreibung nicht erfaßt werden kann, lassen sich Funktionsstörungen der Sinusknotenautomatie und/oder der sinuatrialen Überleitung nur auf indirektem Weg nachweisen. Elektro-kardiographische Hinweise sind das Auftreten einer Sinusbradykardie, sinuatrialer Blockbilder oder eines Sinusarrests. Auf die elektrokardiographischen Merkmale dieser Rhythmusstörungen wird weiter unten einzugehen sein. Oft wird sich nicht entscheiden lassen, ob eine oder beide Teilfunktionen (Automatie und sinuatriale Leitung) des Sinusknotens gestört sind (Steinbeck u. Lüderitz 1977). Das elektrokardiographische Erscheinungsbild wird nicht selten kompliziert durch das Auftreten von Ersatzrhythmen (atrial, junktional oder ventrikulär) mit physiologischer Interferenz oder mit einer Rhythmenverknüpfung (s. unter F).
Chapter
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Article
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Chapter
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Chapter
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Chapter
Störungen der Sinusknotenfunktion gewinnen zunehmend an klinischer Bedeutung. Aus einer 1979 zusammengestellten Weltübersicht geht hervor, daß derzeit etwa jede dritte Schrittmacherimplantation wegen eines Sinusknotensyndroms vorgenommen wird [10]. Da sich die elektrischen Potentiale des natürlichen Herzschrittmachers im Elektrokardiogramm nicht direkt darstellen, besteht jedoch eine erhebliche diagnostische Unsicherheit. Durch die Analyse der P-Welle im EKG ist nur eine summarische Beurteilung der Sinusknotentätigkeit am Patienten möglich, in die die Impulsbildung und die Leitung dieses Impulses über ein sowohl funktionell als auch anatomisch nicht homogenes sinuatriales Übergangsgewebe eingehen [25].
Chapter
Durch die zunehmende Verbreitung der technischen Einrichtungen zur Rhythmusüberwachung am Patienten (Langzeit-Monitorüberwachung, Telemetrie, Bandspeicher-EKG) wurde in den letzten Jahren immer mehr die Häufigkeit pathologischer Sinusbradykardien und ihre klinische Bedeutung erkannt. Die dabei auftretenden Rhythmusstörungen und ihre klinische Symptomatik werden unter dem Begriff des kranken Sinusknotens (Sick-Sinus-Syndrom) zusammengefaßt [4, 5, 13, 14, 15, 24]. Über die Therapiebedürftigkeit von pathologischen Sinusbradykardien besteht allgemeine Einmütigkeit, wobei hier die akute Intervention beim sog. Bradykardie-Hypotoniesyndrom im Rahmen eines akuten Myokardinfarktes nicht diskutiert werden soll [2, 6, 11, 12, 23].
Chapter
Electrophysiology studies (EPS) began in the late 1960s in the dog laboratory where recording of the His bundle electrogram was accomplished.1 The first recordings in the human heart occurred in a patient with atrial septal defect2; whereas in 1969, Scherlag et al3 were the first investigators to percutaneously, by right heart cardiac catheterization, record a His bundle in humans by safely placing an electrode catheter across the tricuspid valve.
Chapter
Since the end of the 19th century the proximity of the esophagus to the atrial wall has suggested the possibility of using this route to record electrical activity from the heart. In 1889 Waller was the first to record the electrical activity of the heart from the esophagus (55). In 1906 Cremer recorded a transesophageal (TE) electrogram through an electrode that a sword eater had swallowed under fluoroscopic control (10). In 1936 Brown extensively reviewed the method and introduced the TE electrocardiogram (ECG) in the clinical setting (7,8)- Brody further clarified the theory of TE recording in 1959 (5). Zoll (1952) first reported the experimental application of TE pacing in dogs (59). McNally et al. resorted to an esophageal catheterism for low energy defibrillation in 1966 (39), and in 1969 Burack and Furman performed TE emergency ventricular pacing (6). Barold (1972) refined TE recording technique achieving a stable and high voltage bipolar atrial electrogram (1), and in the same year Stopczyc and Zochowski resorted to TE pacing in sinus arrest (52). Montoyo reported on the possibility of cardioverting tachycardia by TE pacing (42) in 1973, and Santini assessed the sinus node recovery time by TE pacing (48) in 1979. The unfavorable anatomical relationship between the esophagus and the ventricles soon suggested the opportunity to restrict TE pacing to the atria. In subsequent years, a vast diffusion of TE recording and pacing was prevented by the general inadequacy of catheters and stimulators beside a certain degree of inexperience also caused by the absence of a suitable animal model with a humanlike anatomical relationship between the heart and esophagus (57).
Chapter
History records that in ancient Rome those afflicted with periodic loss of consciousness, whatever its cause, were often venerated as special individuals. One can easily understand such mysticism regarding this occurrence: a previously healthy individual suddenly became almost lifeless, as if dead, yet complete recovery occurred. Indeed, some of the older literature referred to death as “permanent syncope.”
Chapter
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Chapter
In this chapter we will review electrocardiological techniques which enhance clinical utility of the conventional ECG and are commonly used: VCG, exercise ECG, Holter ECG and intracavitary electrocardiography. We will be emphasizing more their clinical applications than their theoretic and methodological aspects. Other techniques less commonly employed in daily clinical practice (wave and signal amplification, spatial velocity, etc.) will be mentioned throughout the book in the instances in which their utility has been demonstrated.
Chapter
Until now the selective recording of sinus potentials in man is not yet possible. Therefore, information about the sinus node function can only be obtained by means of indirect methods. One of these methods is the measurement of the so-called sinus node recovery time (Mandel et al., 1971 and Mandel et al., 1972). This method is based upon the known electrophysiological phenomenon of postdrive or overdrive suppression.
Chapter
The electrophysiological evaluation of sinus node function is extensively reviewed in this symposium on the sinus node. In addition, several excellent studies review the effects of pharmacologic agents on sinus node function. In this presentation, we will not attempt to duplicate that which has been said already in this symposium. This manuscript instead will be somewhat philosophic in its tone, and deal with trying to evaluate the current place of electrophysiological evaluation of sinus node function.
Chapter
Although Eyster and Evans (1915) and Levine (1916) described second-degree sinoatrial block in ECG recordings many years ago they realized that other possible sinoatrial conduction disturbances eluded analysis, primarily because electrical activity in the sinus node cannot be directly recorded in vivo. In 1973, Strauss et al. proposed that the pre- mature atrial stimulation technique could be used to derive the sinoatrial conduction time. In the application of this technique a programmable stimulator is used to elicit variably coupled atrial premature depolarizations during spontaneous sinus rhythm. The last undisturbed spontaneous sinus cycle (A1A1), premature cycle (A1A2) and return cycle (A2A3) are analyzed and the normalized return cycles (A2 A3/A1 A1) are plotted as a function of the normalized premature cycles (A1A2/A1A1) (Figure 1). Late atrial premature cycles are followed by compensatory return cycles. Atrial premature depolarizations elicited earlier in atrial diastole are followed by less than compensatory return cycles. The duration of the less than compensatory A2A3 cycle is determined by the retro- grade conduction time from the atrium to the sinus node (A2SAN2), the sinus node return cycle (SAN2SAN3) and the antegrade sinoatrial conduction time (SAN3A3). The estimation of the sinoatrial conduction time is based on the assumption that the sinus node return cycle (SAN2SAN3) equals the spontaneous sinus node cycle (SAN1SAN1) or the corresponding spontaneous atrial cycle (A1A1) (Figure 1). Hence, the difference between the atrial return cycle (A2A3) and the spontaneous atrial cycle (A1A1) should equal the retrograde conduction time (A2SAN2) for A2 and the antegrade conduction time (SAN3A3) for the subsequent sinus node depolarization (SAN3). The difference between A2A3 and A1A1 computed for atrial premature depolarizations falling in the latest third of the reset zone (zone II) is used to derive a mean value for the estimated antegrade and retrograde sinoatrial conduction time (SACTA+R) (Strauss et al., 1976). It is also assumed that the sum of the A2SAN2 + SAN3A3 equals a value that is twice the normal antegrade sinoatrial conduction time (SAN1 A1). For this reason many investigators have divided SACTA+R by 2 to obtain a value that approximates the antegrade sinoatrial conduction (Dhingra et al., 1975; Breithardt et al., 1976; Jordan et al., 1977). Since antegrade and retrograde conduction times may not be equal, (Bonke et al., 1969; Klein et al., 1973; Miller and Strauss, 1974) we have chosen to express our sinoatrial conduction times as the total value, i.e. SACTA+R.
Chapter
Invasive electrophysiological testing has become the definitive investigation in the majority of arrhythmias, and clinical electrophysiology has grown from the ability to record electrical activity directly from the heart as a branch of cardiology. Earliest recordings identified local atrial and ventricular electrograms, but it was the subsequent recording of His bundle activity followed by the introduction of programmed stimulation that led the way towards a sophisticated investigation procedure having diagnostic, mechanistic, therapeutic and prognostic implications.
Chapter
The spectrum of human cardiac performance is amazingly broad with cardiac output varying 10–20-fold between that measured during the deepest of sleep to that seen at peak of exercise. In large part this tremendous cardiac reserve is modulated both by cardiac contractility as well as the heart rate itself. While many factors can affect contractility, heart rate as almost entirely regulated by the autonomic mediation of the sinoatrial (SA) node pacemaker. While uninhibited enhancement of sympathetic tone can result in normal sinus rates over 200/min in many young health individuals, uninhibited and un hindered parasympathetic (vagal) tone can completely suppress all SA nodal activity, even when there is no intrinsic abnormality of the node itself. Consequently, “SA node dysfunction,” manifested as symptomatic sinus pauses or SA nodal exit block, may not represent true intrinsic SA node disease, but instead, could merely result from dramatic neurogenic influences exerted by the autonomic nervous system (Figure 9-1). Therefore, one of the challenges facing the electrophysiologist in evaluating assumed abnormalities of the SA node is distinguishing between intrinsic SA node disease and functional (physiological) disturbances of SA node function related to extrinsic influences such as the autonomic nervous system.
Chapter
Störungen der Sinusknotenfunktion erlangen zunehmende klinische Bedeutung. Die dabei auftretenden Herzrhythmusstörungen sind in Tabelle 1 auf- gefuhrt (Ferrer 1968, Lown 1967).
Chapter
Die Indikationsstellung zur Behandlung bradykarder Rhythmusstörungen mit implantierbaren Herzschrittmachern hat sich in den letzten 10 Jahren geändert. 1973 lag bei 54% dieser Patienten eine höhergradige AV-Überleitungsstörung vor, bei 23% eine sinuatriale Blockierung und bei 22% eine Bradyarrhythmie (Büchner et al. 1973). Heute ist das Sinusknotensyndrom mit 38–39% die Hauptindikation, gefolgt vom höhergradigen AV-Block mit 30% und von der Bradyarrhythmie mit 15% (Scheuer-Leeser 1983). Sonstige Indikationen liegen bei 16–17% vor. Eine Hauptursache für diese Verschiebungen ist sicherlich die zunehmend breitere Anwendung aufwendiger arrhythmiediagnostischer Methoden, deren Wertigkeit im folgenden vergleichend beurteilt werden soll.
Chapter
The first year’s experience of a new London pacemaker clinic shows a high incidence of sick sinus syndrome- 17 or 33% of 51 new patients. The diagnosis was made in 15 patients by documenting sinoatrial block with delayed escape mechanism either on routine electrocardiography or on 24 hour Holter monitoring ( 1 ). 2 patients showed persistent sinus bradycardia at less than 60 beats per minute and abnormal sinus node behaviour with intravenous atropine and isoprenaline (1) and after rapid atrial pacing (2). Clinically 14 of these patients presented with syncope as the primary symptom and 3 with dyspnoea. Of the important additional symptoms of sick sinus syndrome 5 had paroxysmal tachycardias and 3 had angina pectoris. Ventricular pacing is generally the chosen mode of therapy in patients with sick sinus syndrome. It is noteworthy that in only 12 of 14 syncopal patients were the attacks abolished by ventricular pacing. Both of the other patients were subsequently converted to atrial pacing with abolition of the attacks, the patients confirming dependance on atrial systole. Its persistent lack in ventricular pacing appeared to be due to retrograde atrial activation via the atrio-ventricular node. 2 of 3 dyspnoeic patients were given relief by ventricular pacing. The other patient required digitalis and diuretics. In contrast paroxysmal tachycardias were not well suppressed by pacing alone and 4 of 5 required drug therapy also. Angina pectoris required drug therapy in all patients.
Chapter
In a premier essay on ventricular fibrillation published in 1887, the famous physiologist John Mc.William (1) wrote: “It may, in any case, be safely affirmed that the spontaneous contraction in the mammalian heart arises in the terminal (or ostial) portions of the great veins either exactly at their junction with the auricles, or in the walls of the veins at some little distance from the actual junction.” In 1907 Keith and Flack (2), a medical student at that time, identified an aggregate of cells at the sino-atrial location exactly where Mc.William had predicted that the master pacemaker of the heart resided. They called it “the Primum mobile,” the sino-atrial node (SAN) or pacemaker of the heart located at the antero-lateral junction of the superior vena cava with the base of the right atrial appendage.
Chapter
Die Zusammenfassung der Diskussion erfolgte nach ausführlicher Erörterung aller Probleme. Sie gibt die Meinung aller Beteiligten wieder.
Chapter
Die programmierte Vorhofstimulation hat in der Diagnostik von Sinusknotenfunktionsstörungen weite klinische Verbreitung erfahren. Mit Hilfe dieser invasiven Untersuchungsmethode lassen sich elektrophysiologische Daten gewinnen, die eine genauere Beurteilung von Sinusknotenautomatie und sinuatrialer Leitung erlauben. So gibt die Sinusknotenerholungszeit (Skez) nach schneller atrialer Stimulation Aufschluß über die Sinusknotengeneratorfunktion [8, 12, 13], die Kalkulation der sinuatrialen Leitungszeit (Salz) mittels atrialer Einzelstimulation [15, 16, 20] ermöglicht eine qualitative und quantitative Beurteilung der Erregungsleitung über das sinuatriale Grenzgebiet. Die praktische Bedeutung dieser elektrophysiologischen Befunde für die Indikationsstellung zur Schrittmacherimplantation ist nicht ausreichend geklärt. 70 konsekutive Patienten mit klinischen und elektrokardiographischen Zeichen eines Sinusknotensyndroms wurden unterteilt in eine Gruppe A, die konservativ behandelt wurde, und in eine Gruppe B, die einer Schrittmachertherapie zugeführt werden mußte. Alle Patienten wurden einer diagnostischen Vorhofstimulation unterzogen, so daß eine Korrelation zwischen Ausmaß der Sinusknotenerkrankung und elektrophysiologischen Parametern möglich wurde.
Chapter
Zur Prüfung der atrio-ventrikulären Erregungsleitung und deren Beeinflußung durch Pharmaka untersucht man neuerdings die frequenzabhängige Änderung der PQ-Zeit bei der Vorhofstimulation [8], die Änderung des A- H -Intervalls bei der Ableitung von HIS-Bündelelektrogrammen [1, 4, 5, 12, 17] oder mißt die funktionelle Refraktärzeit des AV-Erregungsleitungssystems [6, 10, 19] mit der Einzelstimulusmethode oder der kontinuierlichen Vorhofstimulation. Qualitativ reagieren beide Methoden gleich : Je kürzer die Cycluslänge zweier hintereinander folgender Vorhofserregungen ist, desto stärker wird die Erregung im AV-Leitungssystem zeitlich verzögert, im EKG erkennbar als PQ-Zeitverlängerung. Quantitativ bestehen deutliche Unterschiede, z. B. wurden verschieden lange Refraktärperioden bei gleicher Herzcycluslänge gemessen [10, 19]. Wir haben mit der Einzelimpulsmethode und bei kontinuierlicher Vorhofstimulation unterschiedliche AV-Lei- tungsverzögerungen gefunden. Bei gleichen Herzcycluslängen waren die PQ- Zeiten (von uns SiQ-Zeiten genannt, „Si“ ist die Abkürzung von tftimulations- impuls) der kontinuierlichen Vorhofstimulation stets länger. Die anhaltende schnelle Vorhofstimulation belastet den AV-Knoten stärker. Dieser benötigt eine Einstell- oder Ermüdungszeit, bis er maximal belastet und die frequenzabhängige längste SiQ-Zeit erreicht ist. Über diese Ermüdungszeit liegen unseres Wissens bisher noch keine Veröffentlichungen vor1. In der Literatur finden sich Hinweise, daß man den Vorhof mindestens 1 min [14] bzw. 2 bis 5 min [15] stimulierte, bevor elektrophysiologische Messungen vorgenommen wurden.
Article
Full-text available
1. Action potentials from sinus venosus and auricle fibers of spontaneously beating frog hearts have been recorded with intracellular electrodes. 2. Sinus fibers show a slow depolarization, the pacemaker potential, during diastole. The amplitude of this potential varies in different parts of the sinus. In some fibers the membrane potential falls by 11 to 15 mv. during diastole and the transition to the upstroke of the action potential is comparatively gradual. In other regions the depolarization develops more slowly and the action potential takes off more abruptly from a higher membrane potential. It is proposed that the fibers showing the largest fall in membrane potential during diastole are the pacemaker fibers of the heart, and that the rest of the preparation is excited by conduction. In auricle fibers the membrane potential is constant during diastole. 3. The maximum diastolic membrane potential and the overshoot of the action potential vary inversely with the amplitude of the pacemaker potential. The highest values were measured in auricle fibers. 4. Stimulation of vagi suppresses the pacemaker potentials. While the heart is arrested the membrane potential of the sinus fibers rises to a level above the maximum diastolic value reached in previous beats. In 28 experiments vagal stimulation increased the membrane potential from an average maximal diastolic value of 55 mv. to a "resting" level of 65.4 mv. The biggest vagal polarization was 23 mv. 5. In contrast to the sinus fibers vagal inhibition does not change the diastolic membrane potential of frog auricle fibers. 6. Vagal stimulation greatly accelerates the repolarization of the action potential and reduces its amplitude. These changes were seen both in the sinus and in auricle fibers stimulated by direct shocks during vagal arrest. 7. The conduction velocity in the sinus venosus of the tortoise is reduced by vagal stimulation. Block of conduction often occurs. 8. In the frog sinus venosus sympathetic stimulation increases the rate of rise of the pacemaker potential, accelerating the beat. The threshold remains unchanged. The rate of rise of the upstroke and the amplitude of the overshoot are increased. 9. The analogies between the vagal inhibition of the heart and the nervous inhibition of other preparations are discussed.
Article
Blockade of cardiac autonomic nervous activity by an intravenous injection of 0.2 mg/kg propranolol and 0.04 mg/kg atropine was used with cardiac catheterization to study intrinsic cardiac function in 47 patients with normal hearts and known graded myocardial disease. After blockade, significant hemodynamic abnormalities became apparent at rest in the majority of patients with known disease, many of whom had normal control findings. This occurred partly through a reduction in the normal range of cardiac function at rest, and partly through changes in the abnormalities associated with disease: after blockade, diseased hearts had normal stroke volumes, but beat more slowly, and had higher left ventricular filling pressures. The heart rate after blockade was fixed; this was defined as the intrinsic heart rate (IHR); it ranged from 57 to 126 beats/min in different patients. Both the IHR and left ventricular end-diastolic pressure after blockade were sensitively and quantitatively related to the severity of myocardial disease. When, after blockade, arterial pressure was raised by angiotensin, the IHR was unchanged; normal hearts maintained their stroke volume and increased stroke work; diseased hearts maintained stroke volume less well and stroke work was unchanged or fell. Abnormal ventricular responses corresponded well with abnormal ventricular function at rest. In different patients the IHR was significantly related to each available index of left ventricular function. Other studies in animals have shown that the IHR is closely related to intrinsic myocardial contractility in certain forms of experimental heart failure. An analogous relationship existing between the IHR and myocardial function in patients with heart disease is suggested as the explanation for the IHR/ventricular function relationship in this study. If so, the IHR may prove valuable as an index of myocardial function in man, since it can be measured simply and safely in clinical practice.
Article
Simultaneous recording of action potentials from cells in different parts of sinoatrial preparations from cat and rabbit hearts confirms the suggestion by Meek and Eyster that the dominant pacemaker site shifts during treatment with high [K+]. The direction of the shift can be either upward or downward depending upon the location of the original dominant pacemaker site. In the majority of cases, the original dominant site is located in the upper part of the preparation, consequently the shift is from above downward. In environments with high [K+], both true and latent pacemaker cell action potentials show a decrease in both maximal diastolic potential and the slope of the prepotential but these changes seem to be more marked in the true pacemaker cell. It is suggested that the shift of dominant pacemaker site in response to high [K+] is due to the difference in sensitivity to K+ between these two types of pacemaker cells.
Article
Myocardial electrolyte balance and lactate metabolism were studied in 30 patients before, during, and after a period of atrial pacing utilizing a continuous automated sampling technic with simultaneous electrocardiographic and hemodynamic observations. Eight patients with coronary artery disease who had no symptoms during pacing and four normal subjects demonstrated myocardial potassium loss but no abnormalities in lactate metabolism, the electrocardiogram, and hemodynamics during pacing. Myocardial potassium loss was correlated with increments in heart rate and was followed by potassium uptake during the post-pacing period. Eighteen subjects developed angina during pacing associated with hemodynamic and electrocardiographic abnormalities. This ischemic group showed significantly greater myocardial potassium loss during pacing than the non-ischemic group, and this was closely associated with myocardial lactate production at a ratio of 1 mEq of potassium being lost for each 2 millimoles of lactate produced. Increased acidity of coronary sinus blood also accompanied potassium loss during ischemia. No significant changes were seen in sodium balance in either group during the study.
Article
This report describes a patient with recurrent and refractory ventricular tachycardia occurring in the presence of normal atrioventricular conduction. The rhythm was unresponsive to the usual antiarrhythmic drugs, and control was finally achieved by permanent implantation of an epicardial atrial pacing electrode coupled to a subcutaneously buried pulse generator.
Article
Rapid drive of isolated pacemaker tissues from cats resulted in a post-drive depression followed by a late acceleration to supernormal rates of pacemaker activity. These effects were similar to those occurring after drive of the pacemaker in situ. Lower SA nodal pacemakers discharged more slowly and irregularly than did upper SA nodal pacemaker cells. They were more readily depressed by rapid imposed drive. The balance between depression and acceleration varied in different preparations. Drive at only slightly above the intrinsic rate resulted frequently in acceleration not preceded by depression. Within limits, the greater the frequency and duration of drive, the greater the intensity and duration of both the depression and the late acceleration. Prostigmin augmented and atropine reduced post-drive depression. Cocaine potentiated the late acceleration. Excess potassium reduced post-drive depression and, in concentrations used, caused some acceleration. Pacemaker cells could be driven less rapidly than could other SA nodal cells. Drive generally shifted pacemaker action to a distant site; the first post-drive propagated responses originated from other pacemaker cells and dominance by the original unit was reestablished slowly. Rapid drive reduced amplitudes of action potentials and prepotentials. It also raised threshold potentials and during the post-drive period the durations of pacemaker cell action potentials were temporarily prolonged. In some preparations membrane potentials remained at a subnormal value after drive. Subthreshold potentials occurred at a somewhat subnormal rhythm but gradually developed an effective amplitude. Conduction block was observed in isolated SA nodal tissue. This was augmented during the post-drive period of depression. This work lends support to the hypothesis¹ that dominating action by pacemaker cells influences the pacemaker activity in other potential pacemaker tissues.
Article
The interactions between pacemakers, and the effects on pacemakers, of terminating imposed driving were studied in the in situ heart of anesthetized dogs. Following atrial fibrillation or termination of a fast drive imposed through an artificial pacemaker, pacemaker action in intrinsic pacemakers is suppressed. Pacemakers tend to accelerate and compete with imposed drives which exceed control rates by only a small percentage (10 to 15%). Arrhythmias may result if imposed drive is slower than or identical with intrinsic pacemaker rate. Post-drive depression of pacemakers and the resulting deceleration of the heart is followed normally by an overshoot or supranormal acceleration. The magnitudes and durations of depression and late acceleration are proportional, within limits, to the rate and duration of drive. Atrioventricular and ectopic atrial pacemakers are much more readily depressed than is the sinoatrial pacemaker. Furthermore, beats of ectopic origin are much more likely to occur while subsidiary pacemakers are recovering from post-drive depression. Augmentation of depression by Prostigmin, its diminution by atropine, and the potentiation of late acceleration by cocaine and its absence after reserpine or guanethidine pretreatment, indicate that acetylcholine and catecholamines are liberated by driving stimuli. Placement of the pacemaker over the sinoatrial node, or near to regions where nerve terminals are concentrated, results in the greatest post-drive effects. The fact that propagated action potentials cause depressions and accelerations subject to drug block or potentiation indicates that mediators are also released in the course of propagated activity. Since atropine does not completely block post-drive depression, it is thought that a potassium ion shift may be involved.
Article
The effects of changes in the extracellular concentrations of Ca, K and Mg on the transmembrane resting and action potentials of single fibers of the auricle, ventricle and specialized conducting system of the dog heart have been studied by means of intracellular microelectrodes. With respect to Ca, the three tissues exhibit quite different sensitivities. Changes in concentration of this ion alter the time course of the action potential recorded from auricle and ventricle but have little effect on the action potential configuration of the Purkinje fiber. In the latter tissue, on the other hand, pacemaker activity is most strongly enhanced by Ca depletion and excitability is lost at Ca concentrations permitting normal propagation in papillary muscle. The effect of K on the resting transmembrane potential is dependent on the simultaneous Ca concentration. The interrelationship is such that the depolarizing effect of high K is decreased by elevated Ca and the depolarization produced by low K is diminished by low levels of Ca. Changes in the concentration of Mg have little effect on the transmembrane potentials of cardiac muscle unless the level of Ca is low. Under this condition a simultaneous decrease in Mg gives rise to a marked prolongation of the action potential duration of both auricle and ventricle. Some evidence for the basic similarity of the processes underlying repolarization in these three tissues is presented and it is thought the normally encountered differences in their action potentials may be related to the sensitivity of each tissue to extracellular Ca.
Article
Potentials recorded at various sites in the atrioventricular (A-V) conduction system indicate that conduction is continuously electrical in nature and involves no synapse-like (i.e., chemical) conduction. The region between atrium and atrioventricular node has the slowest conduction velocity (.05 M./sec.) and lowest safety factor. Conduction through the A-V node is at about .12 M./sec. Results demonstrate shapes of potentials recorded extracellularly at various sites within the A-V node, first degree and complete block during rapid atrial stimulation, and echo-like phenomena.
Article
Pharmacological evidence is presented supporting the theory that the increase in contractile strength of isolated cardiac muscle under suprathreshold stimulation is due to the release of an adrenergic mediator (norepinephrine). However, release of this material does not account for changes in contractile strength associated with changes in frequency of stimulation at threshold levels.
Article
In dogs poisoned with ouabain, potassium chloride was infused intravenously to study its antiarrhythmic properties. The ouabain-enhanced idioventricular automaticity, which leads to ventricular tachycardia, was progressively depressed by administration of potassium. Initially the polymorphic complexes caused by ouabain were replaced by a uniform ventricular tachycardia. As the rate of the idioventricular rhythm decreased, sinus rhythm reappeared intermingled with ventricular beats. When only the sinus rhythm was present, stimulation of the vagus, which provoked sinus arrest or atrioventricular block, could reveal a fast idioventricular rhythm. Later during infusion of potassium, when the P waves were still present on the electrocardiogram, the rate of idioventricular escape fell below control values. Thus, one of the ways potassium counteracts digitalis arrhythmias is the progressive depression of idioventricular automaticity. The possible mechanisms by which potassium depresses idioventricular automaticity are discussed. No data have been collected on the suppression by potassium of "re-entry" type beats. At an advanced stage of administration of potassium, the large diphasic ventricular complexes have been shown to result from disturbed intraventricular conduction of impulses originating from a supraventricular pacemaker; stimulation of the vagus consistently led to their inhibition. When cardiac arrest eventually ensued, direct stimulation of the ventricles elicited electric and mechanical responses. Therefore, cardiac arrest appears to be due either to the cessation of the activity of a supraventricular pacemaker or to failure of conduction, rather than to a depolarization or inexcitability of the ventricular muscle fibers.
Article
Transmembrane potentials were recorded from mammalian Purkinje fibers. Adding saccharose to the bathing solution slowed the spontaneous rate, probably as a result of cell shrinkage and an increase in the intracellular K concentration. An opposite result was found with hypotonic medium. In solutions containing 5.4 mm K the fibers were quiescent. Lowering K to 2.7 mm left the membrane resting potential unchanged but decreased the membrane conductance to half. There was only a minor effect of extracellular K on membrane conductance during the plateau of the action potential. Spontaneous firing regularly started when extracellular K was reduced to or below 2.7 mm. This was preceded by subthreshold oscillations which increased in amplitude. A low K conductance associated with a sizeable difference between membrane potential and potassium equilibrium potential seem to be essential for spontaneous activity to occur in cardiac tissue.
Release of autonomic mediators in cardiac tissue by direct subthreshold electrical stimulation Effect of several cations on transmembrane potentials of cardiac muscle
  • West Ff Vincenzi
  • Hoffman Bf
VINCENzi FF, WEST TC: Release of autonomic mediators in cardiac tissue by direct subthreshold electrical stimulation. J Pharmacol Exp Ther 141: 185, 1963 Circulation, Volume XLIV, July 1971 5. HOFFMAN BF, SUCKLING EE: Effect of several cations on transmembrane potentials of cardiac muscle. Amer J Physiol 186: 317, 1956
Electrophysiology of single car-diac cells Compara-tive study of reactions in sinoatrial and Purkinje pacemaker tissue. Fourth Internation-al Congress
  • Brooks Mcc
  • H-H Lu
HOFFMAN BF: Electrophysiology of single car-diac cells. Bull NY Acad Med 35: 689, 1959 20. BROOKS C McC, Lu H-H, LANGE G: Compara-tive study of reactions in sinoatrial and Purkinje pacemaker tissue. Fourth Internation-al Congress of Pharmacology (Basel), 1969, p 255
Release of autonomic mediators in cardiac tissue by suprathreshold stimulation JOSE AN: Effect of combined sympathetic and parasympathetic blockade on heart rate and cardiac function in man
  • Degubareff Rf T Furchgorr
FURCHGOrr RF, DEGUBAREFF T, GROSSMAN A: Release of autonomic mediators in cardiac tissue by suprathreshold stimulation. Science 129: 328, 1959 25. JOSE AN: Effect of combined sympathetic and parasympathetic blockade on heart rate and cardiac function in man. Amer J Cardiol 18: 476, 1966
Intranodal shifts of pacemaker action
  • H-H Lu
Lu H-H, BROOKS C MCC: Intranodal shifts of pacemaker action. Circulation 40 (suppl III): III-136, 1969 Circulation, Volume XLIV, July 1971 dol by guest on July 11, 2011 http://circ.ahajournals.org/ Downloaded from