Ventricular Dysrhythmias Research Articles

Electrocardiographic changes with segmental akinesia after chloral hydrate overdose

We report a case of deliberate ingestion of 12.5 g chloral hydrate in a 25-year-old psychiatric patient. Coma and life-threatening ventricular dysrhythmias were observed soon after ingestion. Repeated electrocardiographic examination was consistent with ischemic changes appearing on day 3. They were associated with segmental abnormal left ventricular wall motion by echocardiography. A coronary angiogram was performed and was normal. Toxic metabolites of chloral hydrate, trichloroethanol and trichloroacetic acid were found in the urine until day 7. This case illustrates that with halogenated aliphatic hydrocarbons, sustained changes in cardiac contractility may occur in addition to early life-threatening ventricular dysrhythmias.

Droperidol Has Been Reported to Cause Serious Arrhythmias

University of Texas Southwestern Medical Center, Dallas, Texas. paul.white@utsouthwestern.eduThe interest of Dr. Sosis in our recent article1demonstrating the absence of a clinically significant effect of low-dose droperidol on the QT interval after a propofol induction is appreciated. As stated in my earlier editorial,2despite widespread clinical use in anesthesia for more than 30 yr, not a single case report describing a droperidol-induced arrhythmia has appeared in the peer-reviewed anesthesia literature despite the US Food and Drug Administration–imposed “black box” warning (excluding the questionable case report3mentioned by Dr. Sosis, which appeared in a Japanese journal in 2002). Even with extensive use of high-dose droperidol as part of a standard “neurolept” anesthetic technique, there have not been any reported cases of droperidol-induced dysrhythmias during anesthesia.In considering the facts of this particular case report,3Dr. Sosis neglected to mention that the administered dose of droperidol was more than 10 times the standard antiemetic dosage. Second, the alleged case of droperidol-induced multifocal ventricular dysrhythmias occurred in a woman with chronic renal failure who was receiving hemodialysis. Importantly, there was no mention of her electrolyte status at the time of the acute event. Third, she was given a 10-mg intravenous bolus dose of droperidol during general inhalation anesthesia with a combination of isoflurane and nitrous oxide. This combination of inhaled and intravenous drugs would hardly be described as classic neurolept anesthesia.I stand by my earlier published statements that there has not been a single documented case of a serious cardiac arrhythmia occurring in a patient receiving an antiemetic dose (e.g. , 0.625–1.25 mg) of droperidol or even a large dose of droperidol (e.g. , 10 mg) as part of a true neurolept anesthetic technique. Hopefully, the decision-makers at the Food and Drug Administration will come to their senses and remove the unwarranted black box warning on this highly cost-effective antiemetic drug.University of Texas Southwestern Medical Center, Dallas, Texas. paul.white@utsouthwestern.edu

Unbound Free Fatty Acids and Heart-Type Fatty Acid–Binding Protein: Diagnostic Assays and Clinical Applications

A biomarker that reliably detects myocardial ischemia in the absence of necrosis would be useful for initial identification of unstable angina patients and for differentiating patients with chest pain of an etiology other than coronary ischemia, and could provide clinical utility complementary to that of cardiac troponins, the established markers of necrosis. Unbound free fatty acids (FFA(u)) and their intracellular binding protein, heart-type fatty acid-binding protein (H-FABP), have been suggested to have clinical utility as indicators of cardiac ischemia and necrosis, respectively. We examined results of clinical assessments of FFA(u) and H-FABP as biomarkers of cardiac ischemia and necrosis. Data published on FFA(u) and H-FABP over the past 30 years were used as the basis for this review. Although little clinical work has been done on FFA(u) since the initial reports, recent studies documented an association between increased serum FFAs and ventricular dysrhythmias and death in patients with acute myocardial infarction (AMI). Recent data suggest that serum FFA(u) concentrations increase well before markers of cardiac necrosis and are sensitive indicators of ischemia in AMI. H-FABP is abundant in cardiac muscle and is presumed to be involved in myocardial lipid homeostasis. Similar to myoglobin, plasma H-FABP increases within 3 h after AMI and returns to reference values within 12-24 h. FFA(u) may have a potential role in identifying patients with cardiac ischemia. H-FABP is useful for detecting cardiac injury in acute coronary syndromes and predicting recurrent cardiac events in acute coronary syndromes and in congestive heart failure patients. Assays are available for both markers that could facilitate further clinical investigations to assess their possible roles as markers of cardiac ischemia and/or necrosis.

Beta-Rezeptorenblocker bei Patienten mit obstruktiven Atemwegserkrankungen - Risiken und Alternativen

The use of beta-blockers should be avoided in the treatment of patients with asthma and COPD because of their broncho-constrictive effect if there are medical alternatives available. This is the case in arterial hypertension, glaucoma, supraventricular and ventricular dysrhythmia. The use of beta-I-selective drugs is indicated in the treatment of patients with coronary heart disease after myocardial infarction, since the benefit of reduction of morbidity and mortality through the coronary heart disease outweighs the potential risks if the patient is under close and careful observation and the initial dose of the beta-blocker is low. On principle patients suffering from asthma bronchiale should not be treated with beta-blockers because the risk of severe airway obstruction is higher than in patients with COPD.

The effect of amiodarone pretreatment on survival of mice with cocaine toxicity.

Cocaine is a common drug of abuse and use has been associated with ventricular dysrhythmias. Published guidelines suggest that amiodarone is the first line antidysrhythmic for ventricular tachycardia and fibrillation. However, the effects amiodarone in the setting of cocaine toxicity are unknown and unstudied. The purpose of this study was to evaluate the safety and efficacy of amiodarone pretreatment in a murine model of acute cocaine toxicity. This was a randomized, blinded, placebo controlled investigation using male CF-1 mice weighing 29-37 g. First, the safety of an intraperitoneal dose of amiodarone (40 mg/kg) was confirmed in 5 mice. Second, based on preliminary investigations, an approximate intraperitoneal LD50 dose of cocaine (110 mg/kg) was identified and used as the cocaine dose in this study. Animals were then randomized to 2 groups. The control group received 0.5 mL of intraperitoneal 0.9% saline 30 minutes before cocaine. The study group received 40 mg/kg of intraperitoneal amiodarone (40 mg/kg) 30 minutes before cocaine. A blinded observer monitored mice for 2 hours after cocaine administration. No mice in the amiodarone-only group developed any signs of toxicity or died. In the saline + cocaine group 31/32 (96.9%; 95% CI 83.8 to 99.9) mice seized with a median time to seizure of 2.5 minutes, and 23/32 (71.9%; 95% CI 52.3 to 86.3) died with a median time to death of 5.5 minutes. In the amiodarone + cocaine group 31/33 (93.9%; 95% CI 79.0 to 99.3) mice seized with a median time to seizure of 2.0 minutes, and 24/33 (72.7%; 95% CI 54.5 to 86.7) died with a median time to death of 6.0 minutes. All animals that died did so within 9 minutes. The difference in the proportion of animals dying in the amiodarone + cocaine group compared to the saline + cocaine group was 0.008 (-21 to 22%). In this study, pretreatment with amiodarone in cocaine poisoned mice resulted in no change in seizure incidenceor mortality. However, definite conclusions about the reason for these findings cannot be drawn from this model.

Lack of Utility of Telemetry Monitoring During Transport to Inpatient Beds for Identification of Dysrhythmias for Emergency Department Patients With Potential and Known Acute Coronary Syndromes

Patients admitted with acute and potential acute coronary syndromes (ACS) frequently required accompaniment by a registered nurse from the emergency department (ED) to inpatient telemetry beds. We tested the hypothesis that telemetry transport monitoring for patients with acute and potential ACS is of limited utility. We conducted a prospective cohort study of patients who were admitted from the ED with acute and potential ACS. Endpoints were life threatening ventricular dysrhythmias requiring intervention and duration of transport time. The setting was an urban tertiary-care emergency department with 55,000 annual visits, and the subjects were adult patients admitted from the ED to inpatient beds (intensive care unit or floor telemetry) with ACS and potential ("rule-out") ACS. Main outcome measures were the development of a life threatening ventricular dysrhythmias during transport, any intervention by the transporting nurse, and the total transport time. Of 315 total admissions involving 310 patients, there were no life threatening ventricular dysrhythmias and interventions during transport [0%; 95% confidence interval 0-0.95%]. The total nurse time out of the ED spent transporting was 13.6 minutes (SD 5.2, range 4-40). The routine use of nurses accompanying patients admitted with acute and potential acute coronary syndromes is of limited utility. Patient transportation without nurses may help alleviate ED overcrowding by saving almost 15 minutes of nursing time currently being used for transport without measurable benefit.

Comparison of the Bain system and Uniflow universal anaesthetic breathing systems in spontaneously breathing young pigs

ObjectiveTo compare minimum fresh gas flow (Vmin) requirements and respiratory resistance in the Uniflow and Bain anaesthetic breathing systems used in the Mapleson D mode. AnimalsSeven pigs, aged 8–12 weeks, anaesthetized for ophthalmic surgery. Materials and methodsAnaesthesia was maintained with halothane delivered in oxygen using a (Mapleson D) Bain breathing system. The Vmin that prevented re-breathing was found, and peak inspiratory (PIP) and peak expiratory (PEP) pressures measured. The fresh gas flow (Vf) was then increased to Vmin + 50%, then Vmin + 100%, and respiratory pressures re-measured. A heat and moisture exchanger (HME) was inserted at the endotracheal tube and the procedure repeated. The breathing system was then exchanged for a Uniflow and the protocol repeated. After final disconnection from the breathing system, the animals’ peak inspiratory and expiratory flows, tidal, and minute volumes (Vm) were measured over five respiratory cycles. ResultsThe Vmin (L minute−1; mL kg−1 minute−1) required to prevent rebreathing in the Uniflow system [8.1(mean) ±1.7 (SD); 332 ± 94] was significantly greater than the Bain system (6.5 ± 1.1; 256 ± 64). At Vmin, PEP with the Uniflow (3.5 ± 0.1 cmH2O) was significantly higher than the Bain system (2 ± 0.7 cmH2O), but PIP values did not differ (Uniflow −0.6 ± 2.1 cmH2O; Bain system −0.2 ± 0.6 cmH2O). With both systems, PEP increased significantly (p < 0.001) with each increase in Vf: Uniflow system 4.2 ± 0.4 (Vmin + 50%) and 5.5 ± 0.5 cmH2O (Vmin + 100%); Bain system 2.8 ± 0.7 (Vmin + 50%) and 3.5 ± 0.7 cmH2O (Vmin + 100%). Insertion of the HME did not alter pressures. The mean tidal volume was 6.4 ± 1.6 mL kg−1; mean Vm was 184.9 ± 69.8 mL kg−1 and mean respiratory rate was 28 ± 5 breaths minute−1. In one pig breathing with the Uniflow system PEP rose sharply; respiratory and heart rates increased, and ventricular dysrhythmias occurred. When the system was changed and Vf reduced, physiological variables became normal. ConclusionThe study discredited the hypothesis that the two breathing systems behave similarly. Values for Vmin and PEP were higher with the Uniflow system. Increasing Vf increased PEP with both systems. Insertion of an HME did not affect respiratory pressures. Clinical relevanceThe Uniflow used in Mapleson D mode is not suitable for anaesthesia in young spontaneously breathing pigs.

Transplantation of Autologous Bone Marrow-Derived Cells into the Myocardium of Patients Undergoing Coronary Bypass

Animal studies suggest that cell transplantation, including bone marrow-derived cells, can ameliorate left ventricular remodeling following myocardial ischemia. Clinical evaluation of the potential benefits of this approach is limited by the lack of safety and feasibility studies. We have assessed the safety and feasibility of intramyocardial transplantation of autologous bone marrow-derived cells in patients undergoing coronary artery bypass graft (CABG) surgery. Between December 2001 and May 2002 7 patients, scheduled for CABG, consented to the trial. All had CABG using hypothermic cardiopulmonary bypass (CPB) and cold cardioplegic arrest. An average of 21 10(6) (8.6 10(6) to 35.1 10(6)) nucleated cells, and 4.2 10(4) (2.5 10(4) to 8.1 10(4)) CD34+ cells were injected into the anterior-lateral wall of the left ventricle, after discontinuation of cardiopulmonary bypass. The end points to assess safety included death, massive bleeding, electrocardiographic or biochemical evidence of myocardial infarction, ventricular dysrhythmia, myocardial perfusion, ventricular function, and the patients' functional status. All patients recovered well without ventricular arrhythmia, bleeding, or other major peri-operative complications. The average intensive care unit (ICU) and hospital stay was 1 and 7 days, respectively. Repeat Technetium-99m myocardial perfusion stress imaging and echocardiography 6 weeks after surgery showed improvement in tissue perfusion, and an average improvement of left ventricular function of 13.5% +/- 11.54% (the mean pre- and post-operative left ventricular EF were 32.5% +/- 15.46% and 46% +/- 18.55%, respectively). Twenty-four hours Holter monitoring showed no significant arrhythmia, 3 months post-operatively. All patients with narrow QRS complex showed no evidence of late potential, on signal-averaged electrocardiogram. At 4 to 9 months after surgery patients were in NYHA functional class "I". This early clinical experience shows that autologous bone marrow-derived cell transplantation into myocardium is feasible and relatively safe. Further clinical trials to assess the role of cell transplantation for myocardial repair are required.

The Master Female Athlete

The Master Female Athlete

You (Still) Can’t Disprove the Existence of Dragons

You (Still) Can’t Disprove the Existence of Dragons

Left ventricular pseudoaneurysm causing myocardial infarction and cerebrovascular accident

Although post-infarction mortality is most often due to ventricular dysrhythmias, the non-dysrhythmic causes of post-myocardial infarction death present a potential dilemma to the clinician. Non-dysrhythmic hemodynamic complications include cardiogenic shock, left ventricular free wall rupture, rupture of the interventricular septum, papillary muscle rupture, left ventricular pseudoaneurysm, and acute stroke. We present a rare case of a left ventricular pseudoaneurysm presenting with altered mental status, ultimately suspected to have caused the thromboembolic complications of acute myocardial infarction and cerebrovascular accident.

A Case of Carbon Monoxide Poisoning with Thrombus in the Heart: A Case Report

Carbon monoxide is a nonirritant, odorless, colorless gas, and is lighter than air. It is an end product of the incomplete combustion of hydrocarbons. Its effects are most prominent in organs sensitive to oxygen deprivation, such as the heart, brain, and kidney. Carbon monoxide poisoning becomes more abundant in winter and at cold places. In Turkey, every year we see several deaths due to poisonous gas leaks from coal or wood stoves. Deaths particularly due to hypoxia-related central nervous system damage and ventricular dysrhythmias are observed. On the other hand, an association between thromboembolic accidents and carbon monoxide poisoning has been shown in literature. Thromboembolic accidents in the mesenteric, central nervous system, and extremities are reported. However, no atrial thrombus has been mentioned. In this study, a case of an atrial thrombus associated with carbon monoxide poisoning following a diagnosis of carbon monoxide poisoning and treatment in the emergency room is reported and the literature is revisited.

Obesity and heart failure prognosis: paradox or reverse epidemiology?

This editorial refers to ‘Effect of obesity and being overweight on long-term mortality in congestive heart failure: influence of left ventricular systolic function’† by F. Gustafsson et al. , on page 58 Obesity is a problem reaching epidemic proportions in westernized society and is a major cause of preventable death.1 Obesity has many adverse effects on coronary artery disease (CAD) risk factors and is probably an independent risk factor for CAD events. Epidemiological studies have clearly shown a strong relationship between obesity and increased risk of cardiovascular disease and mortality in the general population,1,2 although in some of these studies a ‘J-shaped’ or ‘U-shaped’ curve has been present, meaning that those individuals with low body mass index (BMI) also have increased mortality. Obesity is also known to exert numerous adverse effects on cardiac function. In early obesity, an expanded intravascular volume results in an increase in cardiopulmonary volume or increased pre-load.1,3 Over time these changes lead to an increased prevalence of eccentric left ventricular hypertrophy and the propensity for more complex ventricular dysrhythmias; we and others have noted these early abnormalities as well as improvements in both diastolic and systolic ventricular function following marked, purposeful weight reduction.1 Finding the relationship between obesity and heart failure (HF), however, has been complex. A recent epidemiological study from the Framingham Heart Study clearly indicates that obesity and being overweight are potent predictors of subsequent clinical HF.4 Although obesity causes abnormalities in diastolic and systolic function and predisposes to clinical HF, obese patients with … *Corresponding author. Tel: +1 504 842 5874; fax: +1 504 842 5875. E-mail address : clavie{at}ochsner.org

Genetic Disruption of Kir6.2, the Pore-Forming Subunit of ATP-Sensitive K+ Channel, Predisposes to Catecholamine-Induced Ventricular Dysrhythmia

Metabolic-sensing ATP-sensitive K+ channels (KATP channels) adjust membrane excitability to match cellular energetic demand. In the heart, KATP channel activity has been linked to homeostatic shortening of the action potential under stress, yet the requirement of channel function in securing cardiac electrical stability is only partially understood. Here, upon catecholamine challenge, disruption of KATP channels, by genetic deletion of the pore-forming Kir6.2 subunit, produced defective cardiac action potential shortening, predisposing the myocardium to early afterdepolarizations. This deficit in repolarization reserve, demonstrated in Kir6.2-knockout hearts, translated into a high risk for induction of triggered activity and ventricular dysrhythmia. Thus, intact KATP channel function is mandatory for adequate repolarization under sympathetic stress providing electrical tolerance against triggered arrhythmia.

Prophylactic magnesium sulphate vs. lidocaine during off-pump coronary artery bypass grafting

Prophylactic magnesium sulphate vs. lidocaine during off-pump coronary artery bypass grafting

The incidence and risk factors for cardiac arrest during emergency tracheal intubation: A justification for incorporating the ASA Guidelines in the remote location

Study objective To determine the incidence and etiology of cardiopulmonary arrest during emergency intubation in the remote location by comparing two periods (1990–1995 vs. 1995–2002) at the same institution to assess whether immediate access to advanced airway devices and endotracheal tube-verifying devices altered the incidence of hypoxemia-driven cardiac arrest. Design Retrospective review of a quality improvement (QI) database for emergency intubation outside the operating room (OR). Setting 765-bed tertiary care, level 1 trauma center. Patients 3035 critically ill patients suffering from cardiopulmonary, traumatic, septic, metabolic, or neurological-based deterioration and requiring emergency airway management. Measurements Rate of cardiac arrest, as defined as asystole, bradycardia, or ventricular dysrhythmia with non-measurable blood pressure during or within 5 minutes of intubation, requiring cardiopulmonary resuscitation (CPR), were measured. Main results 60 cardiac arrests were documented (2%, or one per 50 cases), 83% of which were associated with profound hypoxemia (oxygen saturation <70%) during the airway procedure. Esophageal intubation was a frequent complication (n = 38; 63%), often leading to hypoxemia (97%) and regurgitation (67%). The overall rate of cardiac arrest was reduced 50% between the two time periods (2.8%: 1990–1995 period and 1.4%: 1995–2002 period). The relative risk estimate for complications in a match cohort contributing to the etiology of cardiac arrest included hypoxemia (4X), regurgitation (28X), aspiration (22X), bradycardia (23X) (all P < 0.003), and esophageal intubation (7X), P < 0.04). A total of 34% patients survived less than 24 hours and 31% survived to be discharged. Conclusion Cardiac arrest during emergency tracheal intubation outside the OR is relatively common compared with the OR environment. Airway-related complications played a prominent role, either singly or in combination with the patient's underlying physiological state. Immediate access to advanced airway devices and endotracheal tube-verifying devices appear to have a significant impact on the incidence of hypoxemia-driven cardiac arrest.

Cardiac transplantation after the Fontan or Glenn procedure

The purpose of this study was to review the clinical course and outcome of cardiac transplantation after a failed Glenn or Fontan procedure. Late complications of the Glenn or Fontan procedure, including ventricular failure, cyanosis, protein-losing enteropathy, thromboembolism, and dysrhythmias often lead to significant morbidity and mortality. If other therapies are ineffective, cardiac transplantation is the only therapeutic recourse. Transplantation in this unique population presents significant challenges in the operative and perioperative periods. The anatomic diagnoses, previous operations, clinical status, and indications for transplantation were characterized in patients transplanted after a Glenn or Fontan procedure. Outcomes after transplantation, including postoperative complications and mortality, were reviewed. Comparisons were made between survivors and nonsurvivors. Primary orthotopic cardiac transplantation was performed in 35 patients (mean age 15.7 +/- 8.5 years) with a mean follow-up of 54 +/- 46 months. A total of 11 patients had undergone a Glenn shunt and 24 patients a Fontan procedure. Indications for transplantation were a combination of causes including ventricular dysfunction, failed Fontan physiology, and/or cyanosis. Ten patients died <or=2 months after transplantation; nine of the deaths occurred in the Fontan patients. Overall, one-year survival was 71.5%, and five-year survival was 67.5%. Survival was not significantly different between patients transplanted after a Glenn or Fontan procedure and patients transplanted for other etiologies. Cardiac transplantation can be performed successfully in patients with end-stage congenital heart disease after a Glenn or Fontan procedure, with outcomes similar to transplantation for end-stage heart failure secondary to other etiologies.

Ventricular Dysrhythmias in Heart Failure

Left-ventricular systolic dysfunction, or heart failure (HF), is a chronic, progressive condition with a poor prognosis. Approximately 50% of deaths, especially in mild to moderate cases, are sudden. Most sudden deaths are thought to be due to ventricular tachycardia; however, premature ventricular contractions and couplets parallel severity of HF and have been associated with increased mortality risk as opposed to dysrhythmic death. Ventricular arrhythmogenesis results from many mechanisms (afterdepolarizations, reentry, and enhanced automaticity) and preconditions (electrophysiologic abnormalities, neuroendocrine activation, electrolyte imbalances, scar from an ischemic event in ischemic cardiomyopathy, fibrosis in dilated cardiomyopathy, hemodynamic abnormalities, and HF medical management). Nurses are key caregivers in optimally managing HF, either by direct actions or by using advocacy, communication, and collaboration skills to promote positive outcomes. Ventricular dysrhythmia management consists of facilitating core HF pharmacologic and nonpharmacologic medical therapies, using amiodarone to improve symptoms, as needed, and utilizing implantable cardioverter-defibrillator therapy to reduce the risk of sudden cardiac death.

Use of intravenous flecainide in horses with naturally‐occurring atrial fibrillation

It has been reported that i.v. flecainide has a high efficacy for the treatment of experimentally-induced acute atrial fibrillation (AF) in horses and that its use is associated with minimal toxic side effects. The objectives were to study the efficacy of i.v. flecainide as a treatment for atrial fibrillation in horses with naturally-occurring AF. Ten horses with naturally-occurring AF were treated with 2 mg/kg bwt flecainide i.v. at a rate of 0.2 mg/kg bwt/min. In 3 horses, the infusion was continued at 0.05-0.10 mg/kg bwt/min until a total dose of 3.0 mg/kg bwt had been administered. Heart rate, QRS duration and average interval between fibrillation waves were measured before, during and following flecainide infusion. If conversion to normal sinus rhythm was not achieved, horses were treated with quinidine sulphate per os at a dose of 22 mg/kg bwt given every 2 h. None of the horses with chronic AF (n = 9) converted to sinus rhythm with flecainide i.v. The only horse treated successfully had acute AF of 12 days' duration. The QRS duration and fibrillation cycle length increased significantly (P = 0.006 and 0.002, respectively) during and following flecainide infusion. Heart rate did not increase significantly over time however, 3 horses developed heart rates in excess of 100 beats/min. Two horses developed a potentially dangerous ventricular dysrhythmia during the first 15 mins of treatment. Quinidine sulphate given per os restored sinus rhythm in 8 out of 9 horses, with minimal adverse effects. Although flecainide might be efficacious in cases of acute AF, it was not possible to restore sinus rhythm in horses with naturally-occurring chronic AF at the dosages used in this study. In 2 horses, 2.0 mg/kg bwt flecainide was associated with potentially dangerous dysrhythmias. Intravenous administration of 2 mg/kg bwt flecainide is unlikely to convert chronic AF in horses and could induce dangerous dysrhythmias.

Ventricular Dysrhythmias

Cardiovascular nurses contribute significantly to health outcomes and frequently assume responsibility for the clinical and organizational processes to ensure positive outcomes for patients and families. In ventricular dysrhythmia populations, nurses have provided evidence for practices that influence outcomes and have studied patient outcomes related to mortality, morbidity, quality of life, psychological and physical functioning, symptoms, and family responses. Additionally, nurses have contributed to understanding organizational outcomes, such as costs and resource use related to patients with dysrhythmias. Most ventricular dysrhythmia outcome studies are descriptive. More intervention research is needed to develop a cohesive and comprehensive body of evidence upon which to base dysrhythmia nursing care to improve patient outcomes.