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Sinus Tachycardia (sinus + tachycardia)

Distribution by Scientific Domains

Medical Sciences	100%

Kinds of Sinus Tachycardia

inappropriate sinus tachycardia

Selected Abstracts

Efficacy of Ivabradine in a Case of Inappropriate Sinus Tachycardia and Ventricular Dysfunction

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2010
ANTONELLA SETTE M.D.
Ivabradine in IST., We present a case of a 49-year-old man with inappropriate sinus tachycardia and ventricular dysfunction. The conventional treatment (ace-inhibitor and beta-blockers) was not well tolerated by the patient, so Ivabradine, a specific inhibitor of If current in the sinus node, was started. After 3 months of using this medication, we observed an improvement of ejection fraction and quality of life. (J Cardiovasc Electrophysiol, Vol. pp. 815-817, July 2010) [source]

Anatomy and Physiology of the Right Interganglionic Nerve: Implications for the Pathophysiology of Inappropriate Sinus Tachycardia

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 9 2008
JING ZHOU M.D.
Objective: To simulate inappropriate sinus tachycardia (IST) in experimental animals. Background: We recently found that epinephrine injected into the anterior right ganglionated plexi (ARGP) adjacent to the sinoatrial (SA) node induced an arrhythmia simulating IST. Methods: In 19 anesthetized dogs, via a right thoracotomy, the course of the interganglionic nerve (IGN) from the right stellate ganglion along the superior vena cava to the heart was delineated. High-frequency stimulation (HFS; 0.1 msec duration, 20 Hz, 4.5,9.3 V) was applied to IGN at the junction of innominate vein and SVC. Results: HFS of the IGN significantly increased the sinus rate (SR) (baseline: 156 ± 19 beats/minutes [bpm], 4.5 V: 191 ± 28 bpm*, 8.0 V: 207 ± 23 bpm*, 9.3 V: 216 ± 18 bpm*; *P < 0.01 compared to baseline) without significant changes in A-H interval or blood pressure. P-wave morphology, ice mapping, and noncontact mapping indicated that this tachycardia was sinus tachycardia. In 8 of 19 dogs, injecting hexamethonium (5 mg), a ganglionic blocker, into the ARGP attenuated the response elicited by IGN stimulation (baseline: 160 ± 21 bpm, 4.5 V: 172 ± 32 bpm, 8.0 V: 197 ± 32 bpm*, 9.3 V: 206 ± 26 bpm*; *P < 0.05 compared to baseline). In 19 of 19 animals, after formaldehyde injection into the ARGP, SR acceleration induced by IGN stimulation was markedly attenuated (baseline: 149 ± 17 bpm, 4.5 V: 151 ± 21 bpm, 8.0 V: 155 ± 23 bpm, 9.3 V: 167 ± 24 bpm*; *P < 0.05 compared to baseline). Conclusions: HFS of the IGN caused a selective and significant acceleration of the SR. A significant portion of IGN traverses the ARGP or synapses with the autonomic ganglia in the ARGP before en route to the SA node. Dysautonomia involving the IGN and/or ARGP may play an important role in IST. [source]

Treatment of Inappropriate Sinus Tachycardia with Ivabradine in a Patient with Postural Orthostatic Tachycardia Syndrome and a Dual Chamber Pacemaker

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2009
SITARA KHAN M.R.C.P.
We present the case of a 44-year-old woman with postural orthostatic tachycardia syndrome (POTS) and a dual chamber pacemaker. The patient suffered from inappropriate sinus tachycardia that had been resistant to treatment with traditional rate-slowing medications. Ivabradine,the specific sinus node If current inhibitor,was used to successfully lower the heart rate. The patient had no evidence of POTS on repeat autonomic function testing, and there was a corresponding symptomatic benefit. We propose that this class of drugs, the use of which is established as antianginals, should be considered in patients with resistant inappropriate sinus tachycardia. [source]

High Density Endocardial Mapping of Shifts in the Site of Earliest Depolarization During Sinus Rhythm and Sinus Tachycardia

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 4p1 2003
TIM R. BETTS
BETTS, T.R., et al.: High Density Endocardial Mapping of Shifts in the Site of Earliest Depolarization During Sinus Rhythm and Sinus Tachycardia.Previous mapping studies of sinus rhythm suggest faster rates arise from more cranial sites within the lateral right atrium. In the intact, beating heart, mapping has been limited to epicardial plaques or single endocardial catheters. The present study was designed to examine shifts in the site of the earliest endocardial depolarization during sinus rhythm and sinus tachycardia using high density activation mapping. Noncontact mapping of the right atrium during sinus rhythm was performed on ten anesthetized swine. Recordings were made during sinus rhythm, phenylephrine infusion, and isoproterenol infusion. The hearts were then excised and the histological sinus node identified. The mean minimum and maximum cycle lengths recorded were355 ± 43and717 ± 108 ms. A median of three (range two to five) sites of earliest endocardial depolarization were documented in each animal. With increasing heart rate the site of earliest endocardial depolarization remained stationary until a sudden shift in a cranial or caudal direction, often to sites beyond the histological sinoatrial node. The endocardial shift was unpredictable with considerable variation between animals; however, faster rates arose from more cranial sites(r = 0.46, P = 0.023). There was no difference in the mean cycle length of sinus rhythm originating from specific positions on the terminal crest(r = 0.44, P = 0.17). Cranial sites displayed a more diffuse pattern of early depolarization than caudal sites. In the porcine heart the relationship between heart rate and site of earliest endocardial depolarization shows considerable variation between individual animals. These findings may have implications for clinical mapping and ablation procedures. (PACE 2003; 26[Pt. I]:874,882) [source]

Cardiac monitoring of patients receiving arsenic trioxide therapy

BRITISH JOURNAL OF HAEMATOLOGY, Issue 5 2004
Dilip Unnikrishnan
Summary Arsenic trioxide (ATO) is approved for the treatment of acute promyelocytic leukaemia and is under investigation for other malignancies. We report the cardiac findings in 18 patients with haematologic malignancies treated with ATO and assess the role of cardiac factors in fluid retention syndrome observed during ATO therapy. Based on initial observations in 10 patients treated with ATO, cardiac functions in the subsequent eight patients were evaluated prospectively. Evaluation included pre- and during-treatment electrocardiograms, Holter monitoring, echocardiograms, multigated acquisition scan and cardiac stress tests if indicated. All eight patients developed fluid retention during ATO, evidenced by pulmonary congestion, oedema and pleural/pericardial effusions. No cardiac factors were identified that contributed to fluid retention. Six patients had prolonged corrected QT (QTc) compared with baseline, three developed ventricular tachycardia. Sinus tachycardia, ventricular premature contractions, and non-sustained ventricular/supraventricular tachycardia were seen during ATO treatment. Fluid retention and cardiac events did not correlate with the dose or total amount of ATO or prior anthracycline therapy. In summary, fluid overload during ATO therapy does not appear to be cardiac in origin but appears to be drug-related, and may reflect cytokine-induced capillary leak. QTc prolongation, transient arrhythmias and clinically significant arrhythmias were seen with therapeutic doses of ATO. [source]

Effect of an Electronic Control Device Exposure on a Methamphetamine-intoxicated Animal Model

ACADEMIC EMERGENCY MEDICINE, Issue 4 2010
Donald M. Dawes MD
Abstract Objectives:, Because of the prevalence of methamphetamine abuse worldwide, it is not uncommon for subjects in law enforcement encounters to be methamphetamine-intoxicated. Methamphetamine has been present in arrest-related death cases in which an electronic control device (ECD) was used. The primary purpose of this study was to determine the cardiac effects of an ECD in a methamphetamine intoxication model. Methods:, Sixteen anesthetized Dorset sheep (26,78 kg) received 0.0 mg/kg (control animals, n = 4), 0.5 mg/kg (n = 4), 1.0 mg/kg (n = 4), or 1.5 mg/kg (n = 4) of methamphetamine hydrochloride as a slow intravenous (IV) bolus during continuous cardiac monitoring. The animals received the following exposures in sequence from a TASER X26 ECD beginning at 30 minutes after the administration of the drug: 1) 5-second continuous exposure, 2) 15-second intermittent exposure, 3) 30-second intermittent exposure, and 4) 40-second intermittent exposure. Darts were inserted at the sternal notch and the cardiac apex, to a depth of 9 mm. Cardiac motion was determined by thoracotomy (smaller animals, , 32 kg) or echocardiography (larger animals, > 68 kg). Data were analyzed using descriptive statistics and chi-square tests. Results:, Animals given methamphetamine demonstrated signs of methamphetamine toxicity with tachycardia, hypertension, and atrial and ventricular ectopy in the 30-minute period immediately after administration of the drug. Smaller animals (n = 8, , 32 kg, mean = 29.4 kg) had supraventricular dysrhythmias immediately after the ECD exposures. Larger animals (n = 8, > 68 kg, mean = 72.4) had only sinus tachycardia after the exposures. One of the smaller animals had frequent episodes of ventricular ectopy after two exposures, including runs of delayed onset, nonsustained six- to eight-beat unifocal and multifocal ventricular tachycardia that spontaneously resolved. This animal had significant ectopy prior to the exposures as well. Thoracotomy performed on three smaller animals demonstrated cardiac capture during ECD exposure consistent with previous animal studies. In the larger animals, none of the methamphetamine-intoxicated animals demonstrated cardiac capture. Two control sheep showed evidence of capture similar to the smaller animals. No ventricular fibrillation occurred after the exposure in any animal. Conclusions:, In smaller animals (32 kg or less), ECD exposure exacerbated atrial and ventricular irritability induced by methamphetamine intoxication, but this effect was not seen in larger, adult-sized animals. There were no episodes of ventricular fibrillation after exposure associated with ECD exposure in methamphetamine-intoxicated sheep. ACADEMIC EMERGENCY MEDICINE 2010; 17:436,443 © 2010 by the Society for Academic Emergency Medicine [source]

Efficacy of Ivabradine in a Case of Inappropriate Sinus Tachycardia and Ventricular Dysfunction

Anatomy and Physiology of the Right Interganglionic Nerve: Implications for the Pathophysiology of Inappropriate Sinus Tachycardia

Fatal Inappropriate ICD Shock

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 3 2007
CHRISTIAN VELTMANN M.D.
Introduction: Inappropriate implantable cardioverter defibrillator (ICD) therapy carries a low but relevant risk of ventricular proarrhythmia. In the present case, the extremely rare event of a fatal arrhythmia caused by inappropriate therapy is reported. Dislodgement of the ventricular lead to the level of the tricuspid annulus led to additional sensing of the atrial signal during sinus tachycardia. Spuriously, ventricular fibrillation was sensed and induced inappropriate ICD shocks. The fourth inappropriate shock caused ventricular fibrillation, which was subsequently undersensed by the dislodged lead due to low ventricular amplitudes. The ICD started antibradycardic pacing during ventricular fibrillation. After initial successful resuscitation, the patient died 1 week later due to severe hypoxic brain damage. Although not preventable in the present case, it underlines the necessity of immediate interrogation of the ICD after ICD therapy and deactivation of the ICD in the setting of a dislodged endocardial lead and intensive care monitoring of the patient until revision. [source]

Incidence and Clinical Significance of Inducible Atrial Tachycardia in Patients with Atrioventricular Nodal Reentrant Tachycardia

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2001
CHRISTIAN STICHERLING M.D.
Significance of Atrial Tachycardia.Introduction: The purpose of this prospective study was to determine the prevalence and clinical significance of inducible atrial tachycardia in patients undergoing slow pathway ablation for AV nodal reentrant tachycardia who did not have clinically documented episodes of atrial tachycardia. Methods and Results: Twenty-seven (15%) of 176 consecutive patients who underwent slow pathway ablation for AV nodal reentrant tachycardia were found to have inducible atrial tachycardia with a mean cycle length of 351 ± 95 msec. The atrial tachycardia was sustained in 7 (26%) of 27 patients and was isoproterenol dependent in 20 patients (74%). The atrial tachycardia was not ablated or treated with medications, and the patients were followed for 9.7 ± 5.8 months. Six (22%) of the 27 patients experienced recurrent palpitations during follow-up. In one patient each, the palpitations were found to be due to sustained atrial tachycardia, nonsustained atrial tachycardia, recurrence of AV nodal reentrant tachycardia, paroxysmal atrial fibrillation, sinus tachycardia, and frequent atrial premature depolarizations. Thus, only 2 (7%) of 27 patients with inducible atrial tachycardia later developed symptoms attributable to atrial tachycardia. Conclusion: Atrial tachycardia may be induced by atrial pacing in 15% of patients with AV nodal reentrant tachycardia. Because the vast majority of patients do not experience symptomatic atrial tachycardia during follow-up, treatment for atrial tachycardia should be deferred and limited to the occasional patient who later develops symptomatic atrial tachycardia. [source]

Assessment of an ECG event recorder in healthy dogs in a hospital environment

JOURNAL OF SMALL ANIMAL PRACTICE, Issue 4 2003
J. M. Eastwood
Ambulatory electrocardiography techniques are superior to standard electrocardiography in evaluating rhythm disturbances in dogs with episodic weakness or collapse. Disadvantages include cumbersome equipment, short recording periods and an inherent delay in trace analysis. A small programmable cardiac event recorder with combined automatic and owner-triggered recording capability was evaluated in 13 healthy dogs in a hospital environment. The unit was well tolerated and produced diagnostic recordings directly to a personal computer, with useful information about continuous heart rate. It detects premature complexes, pauses and bradycardias according to programmed detection thresholds. These events were counted frequently but trace review revealed concerns regarding specificity. Recordings were often triggered by sinus arrhythmia, sinus tachycardia and unclassifiable rate changes rather than by clinically significant arrhythmias. Correct detection of ventricular ectopic complexes, a single supraventricular premature complex, sinus arrest and second-degree atrioventricular block occurred in individual dogs. Visual review of all automatically recorded events was essential and significantly increased the time required for event recording analysis. Manual recordings might be more useful and the overall results suggest that further studies are warranted to evaluate the system in clinical cases in the home environment. [source]

Ischaemic heart disease in the dog: a review of 65 cases

JOURNAL OF SMALL ANIMAL PRACTICE, Issue 3 2000
T. Falk
Sixty-five dogs are reviewed with histopathologically confirmed intramural arteriosclerosis. Clinical data (clinical signs, electrocardiographic findings and ultrasound parameters) on these animals were collected from nine small animal clinics in Sweden: 16 dogs had died suddenly, with few or no previous clinical signs; 13 dogs died or were euthanased during or shortly after general anaesthesia or sedation; 30 dogs developed acute (14) or chronic (16) congestive heart failure; and six dogs died or were euthanased for causes unrelated to cardiac disease. Electrocardiography of 23 of the dogs revealed several types of arrhythmias, with atrial fibrillation and sinus tachycardia being most commonly detected. Ultrasonographic examinations of 24 dogs found a relatively high number (19) with decreased indices of contractility. Dogs that had died suddenly and in relation to general anaesthesia or sedation had a higher incidence (25 of 29) of purely arteriosclerotic changes in the myocardial vessels, whereas just over half the dogs with congestive heart failure (16 of 30) had other concomitant heart lesions (in most cases endocardiosis). The incidence of myocardial infarcts was high (51 of 65 cases). It is postulated that arteriosclerosis in the dog may be an important reason for sudden death and death during general anaesthesia. Coronary arterial disease should also be a consideration in the clinical evaluation of dilated cardiomyopathy and may contribute to the decreased myocardial contractility when it is present in dogs with mitral regurgitation. [source]

SOMA (carisoprodol) toxicity in a dog

JOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 1 2005
Stephen G. Lane DVM
Abstract Objective: To describe a case of SOMA intoxication in a dog. Case summary: A 13-year-old, 25 kg, female spayed Australian shepherd presented to the emergency service after ingestion of ten to fifteen 350 mg tablets of SOMA (carisoprodol), a muscle relaxant used for back pain in humans. Toxic effects of the drug in this dog included mild sinus tachycardia, respiratory depression, seizures, and ataxia. The dog's mentation progressively deteriorated from depressed to comatose within 1 hour after admission. Treatment on initial presentation consisted of induction of emesis while the dog still had a gag reflex, administration of activated charcoal, oxygen therapy, and supportive care. The dog was discharged to the owner prior to full recovery (4 days later). New or unique information provided: This is the first known report of carisoprodol intoxication in the dog. [source]

Treatment of Inappropriate Sinus Tachycardia with Ivabradine in a Patient with Postural Orthostatic Tachycardia Syndrome and a Dual Chamber Pacemaker

High Density Endocardial Mapping of Shifts in the Site of Earliest Depolarization During Sinus Rhythm and Sinus Tachycardia

The Diagnostic Dilemma of "Pseudopacemaker Spikes"

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2 2000
ANDREW J.M. BROADLEY
In a patient who sustained sudden collapse, later attributed to pulmonary embolization, an ECG during her evaluation demonstrated sinus tachycardia and stimulus artefacts at a rate of 250 per minute which did not capture the heart. Implanted pacemaker malfunction was considered the cause until a chest X ray showed a transcutaneous electrical nerve stimulation (TENS) device, which was the source of the artefacts. In instances of rapid stimulus artefacts on the ECG that do not capture the heart, the presence of a TENS device should be considered. [source]

Thyroid storm prior to induction of anaesthesia

ANAESTHESIA, Issue 10 2004
E. A. Hirvonen
Summary A 53- year-old woman without a previous history of thyroid disease was scheduled for mastectomy. On arrival in the operating theatre unpremedicated she appeared restless and tachycardic. Midazolam and fentanyl was administered intravenously. Concomitantly, sinus tachycardia developed and a flush reaction was observed in the skin of the thoracic region and neck. The blood pressure increased to 265/160 mmHg and the patient lost consciousness and became apnoeic. Unconsciousness and apnoea lasted for approximately 25 min and the operation was postponed. Further investigations revealed an elevated serum free thyroxine level and suppressed serum thyrotropin diagnostic of hyperthyroidism. The serum TSH receptor antibody concentration was elevated, indicating that the patient was suffering from Graves' disease. We present a case of a previously unknown hyperthyroid patient, with breast cancer, presenting as a thyroid crisis on induction of anaesthesia. Although being quite a rare occurrence, unsuspected thyroid disease should be borne in mind when an agitated patient enters the operating theatre. [source]