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British Heart Journal Sep 1970The incidence, natural history, prognosis, and electrocardiographic characteristics of idioventricular rhythm complicating acute myocardial infarction are described. It...
The incidence, natural history, prognosis, and electrocardiographic characteristics of idioventricular rhythm complicating acute myocardial infarction are described. It occurred as a transient arrhythmia nearly always within 24 hours of infarction in 61 (8%) of 737 patients, and was characterized by paroxysms of between 6 and 20 beats with widened bizarre QRS complexes at a rate of between 60 and 90 a minute. Most cases showed fusion beats and P waves dissociated from the QRS complexes, and in many cases idioventricular rhythm started during the slow phase of sinus arrhythmia. Though it usually occurred in patients with moderately severe transmural infarcts, the incidence of ventricular fibrillation and subsequent mortality was no greater than in patients with infarcts of equivalent severity who did not have idioventricular rhythm. It is concluded that this rhythm is a common and relatively benign arrhythmia complicating myocardial infarction, and that it should be distinguished from ventricular tachycardia.
Topics: Adult; Arrhythmia, Sinus; Arrhythmias, Cardiac; Electrocardiography; Heart Ventricles; Humans; Male; Myocardial Infarction; Tachycardia
PubMed: 5470042
DOI: 10.1136/hrt.32.5.617 -
Cureus Dec 2022Bradycardia, renal failure, atrioventricular (AV) nodal disease, shock, and hyperkalemia (BRASH) syndrome is a well-recognized constellation of distinct...
Bradycardia, renal failure, atrioventricular (AV) nodal disease, shock, and hyperkalemia (BRASH) syndrome is a well-recognized constellation of distinct clinicopathologic entities comprising bradycardia, renal failure, AV nodal disease, shock, and hyperkalemia. Our patient is an 89-year-old female with a past medical history significant for hypertension and diabetes, who was newly started on labetalol and had recent gastroenteritis; she presented to our Emergency Department with bradycardia and shock. Upon presentation, she showed physical signs of volume depletion, and her blood pressure was 50 mmHg systolic and heart rate was 25 beats per minute. The initial electrocardiogram showed an idioventricular rhythm. The laboratory workup revealed hyperkalemia. The patient was given repeated doses of atropine with no significant response. She was resuscitated with isotonic fluids. The patient improved clinically, her blood pressure stabilized, her potassium level, renal function, and heart rate were normalized, and normal sinus rhythm was restored with a narrow QRS complex. A diagnosis of BRASH syndrome was made retrospectively. Overall, the treatment of this syndrome is largely symptomatic. Hemodynamic support with fluid and treatment of hyperkalemia remains the goal of care. The overall prognosis is good if identified early and managed appropriately.
PubMed: 36620804
DOI: 10.7759/cureus.32217 -
Clinical Cardiology Apr 1996The aim of this review is the utmost simplification of the cellular electrophysiologic background of ischemia-related arrhythmias. In the acute and subacute phase of... (Review)
Review
The aim of this review is the utmost simplification of the cellular electrophysiologic background of ischemia-related arrhythmias. In the acute and subacute phase of myocardial infarction, arrhythmias can be caused by an abnormal impulse generation, abnormal automaticity or triggered activity caused by early or delayed afterdepolarizations (EAD and DAD), or by abnormalities of impulse conduction (i.e., reentry). This paper addresses therapeutic intervention aimed at preventing the depolarization of "pathologic" slow fibers, counteracting the inward calcium (Ca) influx that takes place through the L-type channels (Ca antagonists), or hyperpolarizing the diastolic membrane action potential, increasing potassium (K) efflux (K-channel openers) in arrhythmias generated by an abnormal automaticity (ectopic tachycardias or accelerated idioventricular rhythms). If the cause enhanced impulse generation is related to triggered activity, and since both EAD and DAD are dependent on calcium currents that can appear during a delayed repolarization, the therapeutic options are to shorten the repolarization phase through K-channel openers or Ca antagonists, or to suppress the inward currents directly responsible for the afterdepolarization with Ca blockers. Magnesium seems to represent a reasonable choice, as it is able to shorten the action potential duration and to function as a Ca antagonist. Abnormalities of impulse conduction (re-entry) account for the remainder of arrhythmias that occur in the acute and subacute phase of ischemia and for most dysrhythmias that develop during the chronic phase. Reentrant circuits due to ischemia are usually Na channel-dependent. Drug choice will depend on the length of the excitable gap: in case of a short gap (ventricular fibrillation, polymorphic ventricular tachycardia, etc.), the refractory period has been identified as the most vulnerable parameter, and therefore a correct therapeutic approach will be based on drugs able to prolong the effective refractory period (K-channel blockers, such as class III antiarrhythmic drugs); on the other hand, for those arrhythmias characterized by a long excitable gap (most of the monomorphic ventricular tachycardias), the most appropriate therapeutic intervention consists of depressing ventricular excit-ability and conduction by use of sodium-channel blockers such as mexiletine and lidocaine. Compared with other class I antiarrhythmic agents, these drugs minimally affect refractoriness and exhibit a use-dependent effect and a voltage dependent action (i.e., more pronounced on the ischemic tissue because of its partial depolarization).
Topics: Animals; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Electrophysiology; Heart Ventricles; Humans; Ion Transport; Myocardial Ischemia; Tachycardia, Ventricular; Ventricular Function
PubMed: 8706374
DOI: 10.1002/clc.4960190409 -
BMC Cardiovascular Disorders Mar 2023Accelerated idioventricular rhythm (AIVR) is a slow ventricular arrhythmia, commonly due to myocardial ischemia in coronary artery disease. It is a transitory rhythm...
BACKGROUND
Accelerated idioventricular rhythm (AIVR) is a slow ventricular arrhythmia, commonly due to myocardial ischemia in coronary artery disease. It is a transitory rhythm that rarely causes hemodynamic instability or necessitates any specific therapy. Besides, the common predisposing factors for ventricular arrhythmias after open-heart surgery are hemodynamic instability, electrolyte imbalances, hypoxia, hypovolemia, myocardial ischemia and infarction, acute graft closure, reperfusion injury, and administration of inotropes and antiarrhythmic drugs. Here we report a case of AIVR after cardiac surgery, mostly due to hypothermia that to our knowledge, it is the first report.
CASE PRESENTATION
We describe a 76-year-old man presenting with typical chest pain. Following routine investigations, the patient underwent coronary artery bypass grafting. Postoperatively, he was transferred to the intensive care unit with good hemodynamic status. However, about 3 h later, he developed rhythm disturbances, leading to hemodynamic instability without response to volume replacement or inotropic support. His rhythm was AIVR, although, at first glance, it resembled the left bundle branch block. Given his unstable hemodynamic status, he was emergently transferred to the operating room. Cardiopulmonary bypass (CPB) was resumed for hemodynamic support. After the patient was rewarmed to about 35 ºC, AIVR returned to normal. He was weaned from CPB successfully and with an uneventful hospital course.
CONCLUSIONS
Hypothermia is a potential cause of rhythm disturbance. Preventing the causes of arrhythmias, including hypothermia, is the best strategy.
Topics: Male; Humans; Aged; Accelerated Idioventricular Rhythm; Hypothermia; Electrocardiography; Arrhythmias, Cardiac; Cardiac Surgical Procedures; Myocardial Ischemia
PubMed: 36941559
DOI: 10.1186/s12872-023-03178-y -
Anesthesia Progress Dec 2021Some anesthetic agents or adjunct medications administered during general anesthesia can cause an accelerated idioventricular rhythm (AIVR), which is associated with...
Some anesthetic agents or adjunct medications administered during general anesthesia can cause an accelerated idioventricular rhythm (AIVR), which is associated with higher vagal tone and lower sympathetic activity. We encountered AIVR induced by vagal response to injection-related pain following local anesthetic infiltration into the oral mucosa during general anesthesia. A 48-year-old woman underwent extraction of a residual tooth root from the left maxillary sinus under general anesthesia. Routine preoperative electrocardiogram (ECG) was otherwise normal. Eight milliliters of 1% lidocaine (80 mg) with 1:100,000 epinephrine (80 μg) was infiltrated around the left maxillary molars over 20 seconds using a 23-gauge needle and firm pressure. Widened QRS complexes consistent with AIVR were observed for ∼60 seconds, followed by an atrioventricular junctional rhythm and the return of normal sinus rhythm. A cardiology consultation and 12-lead ECG in the operating room produced no additional concerns, so the operation continued with no complications. AIVR was presumably caused by activation of the trigeminocardiac reflex triggered by intense pain following rapid local anesthetic infiltration with a large gauge needle and firm pressure. Administration of local anesthetic should be performed cautiously when using a large gauge needle and avoid excessive pressure.
Topics: Accelerated Idioventricular Rhythm; Anesthesia, General; Anesthesia, Local; Anesthetics, Local; Arrhythmias, Cardiac; Electrocardiography; Female; Humans; Lidocaine; Middle Aged
PubMed: 34911065
DOI: 10.2344/anpr-68-03-09 -
Heart International 2020: Myocarditis is a rare presentation of drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome, traditionally associated with poor clinical outcomes.... (Review)
Review
Prolonged Extracorporeal Membrane Oxygenation Support In a Patient with Drug Reaction with Eosinophilia and Systemic Symptoms Syndrome-associated Fulminant Myocarditis - A Case Report and Literature Review.
: Myocarditis is a rare presentation of drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome, traditionally associated with poor clinical outcomes. Prompt recognition and treatment are crucial. : A 16-year-old patient presented with acute chest pain, hypotension, and pulmonary oedema 2 months after being diagnosed with trimethoprim/sulfamethoxazole-induced DRESS syndrome. Typical DRESS features were absent at onset of these symptoms. Echocardiography demonstrated biventricular systolic dysfunction, and electrocardiography (ECG) showed complete right bundle branch block and diffuse ST-segment elevation. The patient was admitted for high-dose inotropic support; however, his condition deteriorated. Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) and intra-aortic balloon pump were initiated on the third day of admission. Endomyocardial biopsy suggested the diagnosis of DRESS-associated myocarditis and a high-dose corticosteroid was commenced. While he was ECMO-dependent, the patient suffered multiple episodes of ventricular tachycardia on a background of cardioversion-resistant accelerated idioventricular rhythm. After 24 days of ECMO support, the ventricular function improved, and ECG reverted to sinus rhythm. His recovery allowed corticosteroid discontinuation 15 months after hospital discharge. : Typical DRESS syndrome features may not accompany the onset of DRESS-associated myocarditis. Mechanical circulatory support and adequate immunosuppression could save patients with malignant arrhythmias and delayed myocardial recovery.
PubMed: 36276511
DOI: 10.17925/HI.2020.14.2.112 -
American Heart Journal Nov 1986Accelerated idioventricular rhythm has been used as a marker for coronary reperfusion. The incidence of accelerated idioventricular rhythm and ventricular tachycardia... (Clinical Trial)
Clinical Trial Randomized Controlled Trial
Accelerated idioventricular rhythm has been used as a marker for coronary reperfusion. The incidence of accelerated idioventricular rhythm and ventricular tachycardia was evaluated in 52 consecutive patients undergoing thrombolysis with intracoronary streptokinase during acute myocardial infarction. Complete 12-hour Holter recordings during and after intracoronary streptokinase were obtained in 39 patients. Reperfusion was documented in 17 patients (44%), no reperfusion in 14 (36%), and subtotal occlusion in eight (20%). Accelerated idioventricular rhythm occurred in 83%, 57%, and 63% of patients by group, respectively (p greater than 0.05). Ventricular tachycardia occurred in 100%, 71%, and 100% of patients by group, respectively (p less than 0.05). These data demonstrate that accelerated idioventricular rhythm is not specific for reperfusion and cannot be used as a marker for this event, and that ventricular tachycardia is more common with reperfusion and subtotal occlusion.
Topics: Cardiac Catheterization; Coronary Circulation; Humans; Myocardial Infarction; Streptokinase; Tachycardia
PubMed: 3776819
DOI: 10.1016/0002-8703(86)90302-9 -
The Western Journal of Medicine Feb 1987While patients who present with a pulseless idioventricular rhythm have a dismal prognosis, such a rhythm following electrical defibrillation from ventricular...
While patients who present with a pulseless idioventricular rhythm have a dismal prognosis, such a rhythm following electrical defibrillation from ventricular fibrillation (VF) may have an entirely different clinical significance. By reviewing the cases of 100 consecutive patients with prehospital ventricular fibrillation, we found the following: Subsequent development of field pulses, survival to hospital admission and hospital discharge in 49 patients who initially had pulseless idioventricular rhythm following defibrillation were statistically significantly worse (P<.05) than for 20 patients successfully defibrillated into any other organized rhythm. They were statistically significantly better, however, than for 25 patients who failed to achieve any organized rhythm in the field. Outcomes were statistically no different in 40 patients who received standard advanced cardiac life support drug therapy for pulseless idioventricular rhythm after defibrillation than in 9 patients who spontaneously progressed to another rhythm before drug therapy could be given. These findings suggest that pulseless idioventricular rhythm may be a transient recovery rhythm following defibrillation from prehospital VF, that it can in this circumstance be associated with a good outcome in a reasonable number of patients and that a short trial of cardiopulmonary resuscitation only, without immediate drug therapy, may be appropriate in these patients.
Topics: Arrhythmias, Cardiac; Electric Countershock; Emergencies; Heart Arrest; Humans; Prognosis; Ventricular Fibrillation
PubMed: 3825117
DOI: No ID Found -
Animals : An Open Access Journal From... Jun 2023This study aimed at describing the change in echocardiographic variables after high-dose medetomidine and the reversal with atipamezole in six cats undergoing sedation...
This study aimed at describing the change in echocardiographic variables after high-dose medetomidine and the reversal with atipamezole in six cats undergoing sedation for semen collection. Further cardiac Troponin I (cTnI) concentration and the effect of repeated sedation were assessed. Echocardiography was performed before and 20 min after sedation with 0.1 mg/kg medetomidine intramuscularly (IM) for urethral catheterisation. Prior to epididymectomy, S-ketamine was administered intravenously. Twenty minutes after reversal with 0.5 mg/kg atipamezole IM, the third echocardiography was performed. Sedation with medetomidine and reversal with atipamezole was repeated on day 7, 14, 21 and 28. Heart rate (HR) and rhythm were monitored throughout all sedations. On day 0 and 28 cTnI concentrations were measured before and after the procedure. After normality testing, the values were compared over time. The administration of medetomidine led to a marked reduction in HR, cardiac output and ventricular systolic function and a significant increase in left ventricular dimensions. Rhythm abnormalities, such as ventricular premature complexes and idioventricular rhythm, could be observed. The administration of atipamezole completely reversed sedation and the changes in haemodynamic variables. No significant increase in cTnI concentrations could be detected, although two out of six cats showed values above the reference range.
PubMed: 37370419
DOI: 10.3390/ani13121909 -
Indian Heart Journal 2016Accelerated idioventricular rhythm (AIVR) is a common arrhythmia observed in patients with ST segment elevation myocardial infarction (MI). It is not clear how much... (Observational Study)
Observational Study
BACKGROUND
Accelerated idioventricular rhythm (AIVR) is a common arrhythmia observed in patients with ST segment elevation myocardial infarction (MI). It is not clear how much value AIVR has in predicting successful reperfusion, since there have been conflicting data regarding this in the past. Streptokinase (STK) even today is the commonest thrombolytic agent used in the public health care set-up in India.(1) Most data for the use of STK are from the 1990s, which had showed that at best it is effective in only 50% of patients in restoring adequate flow.(2) It is probable that with the current dual-antiplatelet loading dose regimen and other newer medications, this figure could be higher. Also, rescue angioplasty for failed thrombolysis is the standard of care now, unlike before. Hence, we need reliable non-invasive markers to judge successful reperfusion in the present era. While ST segment resolution is the standard marker for reperfusion used in thrombolytic trials, in several instances it is not definitive. An additional marker would thus be very useful, especially in such cases.
METHODS
This was a prospective observational study carried out at a public teaching hospital. 200 consecutive patients with a diagnosis of acute MI who were given STK within 12h of index pain were included. The STK dose was 1.5 million units, infused over 30min; the ECG was again recorded after 90min of completion of the infusion. Continuous ECG monitoring for the first 24h of ICCU stay was performed and AIVRs during this period were documented. Early AIVR was defined as that occurring within 2h of completing the STK infusion. Echocardiography was performed 24h after presentation. The time course of AIVR was studied vis-a-vis the outcome of thrombolysis.
RESULTS
AIVR was seen in 41% of the patients. Though AIVR was found to have low sensitivity (45%) and specificity (64%) as a predictor of successful thrombolysis, early AIVR was a reliable sign of successful thrombolysis (p<0.05). The sensitivity (45%) of early AIVR was low; however, the specificity (94%) and positive predictive value (94%) were very good.
CONCLUSION
AIVR is a common arrhythmia in the setting of STEMI receiving thrombolytic therapy. Early AIVR is more common with successful thrombolysis, with an excellent positive predictive value. Thus, early AIVR can be used as an additive criterion to ST segment resolution as a non-invasive marker of successful thrombolysis with STK.
Topics: Accelerated Idioventricular Rhythm; Dose-Response Relationship, Drug; Electrocardiography; Fibrinolytic Agents; Follow-Up Studies; Humans; Incidence; India; Myocardial Reperfusion; Prospective Studies; ST Elevation Myocardial Infarction; Streptokinase; Thrombolytic Therapy
PubMed: 27316481
DOI: 10.1016/j.ihj.2015.09.023