Cardiovascular Shock Research Articles

Hémorragie digestive haute de l’adulte au Burundi : aspects épidémiologiques, étiologiques, thérapeutiques et évolutifs

To describe by a prospective study the epidemiological, etiological, therapeutic and evolutive aspects of the upper gastrointestinal bleedind in Burundi. Prospective study that included from January 2010 to February 2011 all patients hospitalized in three main public hospitals of Bujumbura for an upper gastrointestinal bleeding. During this period, we included 61 patients, 37 males (60.7%) and 24 females (39.3%). The middle age was: 49.2±8years. 52.5% of the upper gastrointestinal bleeding (32 patients) concerned patients aged between 30 and 60 years. Hematemesis associated to the melena was the main manifestation of bleeding in 50.8%. The use of gastro-toxic medicines was noted among 8 patients (13.1%). At the admission, the blood pressure was abnormal in 51patients (86,9%) among which 27 patients (44.3%) were in a state of cardiovascular shock. The upper endoscopy was performed in 39 patients (63.9%). The mains etiologies were the gastroduodenal ulcers (46.1%) and the esophageal varices (28.2%). The treatment was essentially medical. 39 patients (63.9%) were transfused. The evolution was favorable with the bleeding arrest in 47 patients (77.1%). Mortality rate was 22.9% (14 patients). Recurrent bleeding was recorded in 7 patients (14.7%). The upper gastrointestinal bleeding are severe with an elevated mortality in public hospitals in Burundi. The improvement of the technical equipment and the accessibility to medical cares remain major challenges to improve their prognosis in those public hospitals.

Mortality in free range rescued wild animals of Shivalik Hills in Himachal Pradesh, India

The present study was conducted on 143 free range wild animals of 12 different species rescued from different locations in Shivalik Hills since Jan 2004 to June 2011. Mortality was reported in 79.02% (113) of rescued wild animals. Mortality in Herbivores, Carnivores, Pheasants and Omnivores was 84.74% (50), 79.06% (34) 72.72% (24) and 62.50% (05) respectively. Post mortem was conducted at field level to determine causes of mortality in all the 113 died wild animals. Necropsy findings revealed musculoskeletal injuries 68.14% (77), more specifically fractures 37.16% (42) and fatal trauma 30.97% (35) as most common cause of mortality in all the animals. On the other hand Cardiovascular and haemorrhagic shock constituted 11.50% (13) while septicemia were noted in 8.84% (10) of all the recorded causes of mortality in rescued animals. Mortality with other causes noticed in 11.50% cases is attributable to diagnosed causes including froathy bloat, tympany, intussusceptions, senility with associated lesions and unknown causes like infectious diseases or toxicosis without a clear symptomatology. The highest mortality was found in male herbivores 28.31% (32) followed by female carnivores 16.81% (19) and male pheasants 13.27% (15). Only 39.82% (45) mortality was observed in adult animals compared to juveniles 51.32% (58). Mortality in winter season 52.21 % (59) was higher than summer 33.62% (38) and rainy season 14.15% (16).

Mortality in free range rescued wild animals of Shivalik Hills in Himachal Pradesh, India

The present study was conducted on 143 free range wild animals of 12 different species rescued from different locations in Shivalik Hills since Jan 2004 to June 2011. Mortality was reported in 79.02% (113) of rescued wild animals. Mortality in Herbivores, Carnivores, Pheasants and Omnivores was 84.74% (50), 79.06% (34) 72.72% (24) and 62.50% (05) respectively. Post mortem was conducted at field level to determine causes of mortality in all the 113 died wild animals. Necropsy findings revealed musculoskeletal injuries 68.14% (77), more specifically fractures 37.16% (42) and fatal trauma 30.97% (35) as most common cause of mortality in all the animals. On the other hand Cardiovascular and haemorrhagic shock constituted 11.50% (13) while septicemia were noted in 8.84% (10) of all the recorded causes of mortality in rescued animals. Mortality with other causes noticed in 11.50% cases is attributable to diagnosed causes including froathy bloat, tympany, intussusceptions, senility with associated lesions and unknown causes like infectious diseases or toxicosis without a clear symptomatology. The highest mortality was found in male herbivores 28.31% (32) followed by female carnivores 16.81% (19) and male pheasants 13.27% (15). Only 39.82% (45) mortality was observed in adult animals compared to juveniles 51.32% (58). Mortality in winter season 52.21 % (59) was higher than summer 33.62% (38) and rainy season 14.15% (16).

Suspected Anaphylactic Reaction Associated with Microemulsion Propofol during Anesthesia Induction

Although rare, intraoperative anaphylaxis can lead to significant morbidity and mortality. Aquafol® (Daewon Pharmaceutical Co. Ltd., Seoul, Korea), a microemulsion propofol, was developed to eliminate lipid solvent-related adverse events, and was used in clinical anesthesia since 2009 with little data about severe side effects such as anaphylaxis. A healthy 16-yr-old male patient who had past medical history with two previous operations of no complications developed cardiovascular shock with generalized erythema following administration of microemulsion propofol during anesthesia induction. Intravenous injection of epinephrine and steroid rescued him. He remained in a stable state without any problems postoperatively and was discharged. Clinicians should consider this rare but serious complication during induction of anesthesia with propofol.

Clinical Considerations of Heritable Factors in Common Heart Failure

Heart failure is a common condition responsible for at least 290 000 deaths each year in the United States alone.1 A small minority of heart failure cases are attributed to Mendelian or familial cardiomyopathies. The majority of systolic heart failure cases are not familial but represent the end result of 1 or many conditions that primarily injure the myocardium sufficiently to diminish cardiac output in the absence of compensatory mechanisms. Paradoxically, because they also injure the myocardium, it is the chronic actions of the compensatory mechanisms that in many instances contribute to the progression from simple cardiac injury to dilated cardiomyopathy and overt heart failure. Thus, the epidemiology of common heart failure appears to be just as sporadic as its major antecedent conditions (atherosclerosis, diabetes, hypertension, and viral myocarditis). Familial trends in preclinical cardiac remodeling2 and risk of developing heart failure3 reveal an important role for genetic modifiers in addition to clinical and environmental factors. Candidate gene studies performed over the past 10 years have identified a few polymorphic gene variants that modify risk or progression of common heart failure.4 Whole-genome sequencing will lead to the discovery of other genetic modifiers that were not candidates.5 The imminent availability of individual whole-genome sequences at a cost competitive with available genetic tests for familial cardiomyopathy will no doubt further expand the list of putative genetic heart failure modifiers. Heart failure risk alleles along with traditional clinical factors will need to be considered by clinical cardiologists in their design of optimal disease surveillance and prevention programs and in individually tailoring heart failure management. The use of individual genetic make-up is likely to have the earliest and greatest impact on managing patients with heart failure by tailoring available pharmacotherapeutics to optimize patient response and minimize adverse effects (ie, the …

Transient osteoporosis of the hip in pregnancy resulting in bilateral fracture of the neck of the femur

crosis scattered within the basal ganglia and around the third ventricle, and ischemic damage in all cerebellar nuclei examined. The placenta did not show amniotic embolus in the vessels of the chorionic plate. AFE is usually present in cases that combine maternal cardiovascular shock, neurological disorders, and hemorrhage with disseminated intravascular coagulopathy [1,2]. In the present case, the sudden onset of symptoms in the absence of other known causes immediately suggested AFE. Diagnosis can be made even if epithelial cells found in maternal blood cannot be proved to be fetal cells [1]. The increase in serum tryptase indicates mast cell degranulation, which is observed inconsistently in AFE [4]. Because the pregnancy proceeded without other notable events it seems likely that the ischemic fetal brain damage was caused by severe hypoxia during AFE. AFE can occur in the absence of labor during the second trimester of pregnancy and should be considered in the presence of sudden respiratory, neurological, or cardio-vascular distress. Fetal consequences can occur despite full maternal recovery.

Objectives of hemodynamic resuscitation

Cardiovascular failure or shock, of any etiology, is characterized by ineffective perfusion of body tissues, inducing derangements in the balance between oxygen delivery and consumption. Impairment in oxygen availability on the cellular level causes a shift to anaerobic metabolism, with an increase in lactate and hydrogen ion production that leads to lactic acidosis. The degree of hyperlactatemia and metabolic acidosis will be directly correlated to the development of organ failure and poor outcome of the individuals.The amount of oxygen available at the tissues will depend fundamentally on an adequate level of perfusion pressure and oxygen delivery. The optimization of these two physiologic parameters can re-establish the balance between oxygen delivery and consumption on the cellular level, thus, restoring the metabolism to its aerobic paths. Monitoring variables such as lactate and oxygen venous saturations (either central or mixed) during the initial resuscitation of shock will be helpful to determine whether tissue hypoxia is still present or not. Recently, some new technologies have been developed in order to evaluate local perfusion and microcirculation, such as gastric tonometry, near-infrared spectroscopy and videomicroscopy. Although monitoring these regional parameters has demonstrated its prognostic value, there is a lack of evidence regarding to its usefulness during the resuscitation process.In conclusion, hemodynamic resuscitation is still based on the rapid achievement of adequate levels of perfusion pressure, and then on the modification of oxygen delivery variables, in order to restore physiologic values of ScvO2/SvO2 and resolve lactic acidosis and/or hyperlactatemia.

Spontaneous aortic rupture during pregnancy

Aortic dissection is a rare entity. Half of the aortic dissection cases occur during pregnancy in women under the age of 40. The authors report a case of a multiparous woman at the third trimester of her sixth pregnancy, who died from a sudden and intractable cardiovascular shock. Autopsy revealed the dissection of the ascending aorta. The case is interesting, especially because in the pregnant woman's family it was not the first sudden death during pregnancy. Authors review the relevant literature regarding the symptoms and the genetic basis of this rare but potentially lethal complication of pregnancy.

Haemodynamic effects of the carboxylic ionophore monensin when administered before and during shock induced by E. coli endotoxin.

The haemodynamic effects of the carboxylic ionophore monensin have been examined in cats anaesthetized with sodium pentobarbitone. Marked increases in left ventricular dP/dtmax (and dP/dt at fixed isovolumic pressures) and slight increases in cardiac output and stroke volume occurred, indicating increased myocardial contractility. Heart rate was unchanged but systemic arterial pressure was substantially increased. Satisfactory increases in contractility and arterial pressure were obtained when monensin was infused intravenously in a total dose of 0.25 mg kg-1 over 10 min. Larger doses, especially if rapidly injected, resulted in very marked increases in myocardial contractility leading eventually to cardiac failure. The haemodynamic effects of monensin were markedly reduced during shock induced by E. coli endotoxin and there was unfortunately no evidence to suggest that this extremely potent compound might be potentially beneficial in this form of profound cardiovascular shock.

The Conservative Management of Severe Caustic Gastric Injuries

To determine the safety of a conservative approach to treating severe caustic injury in patients lacking clinical and biochemical signs of transmural necrosis. Esophagogastrectomy is thought to limit the progression of severe caustic injury in the upper gastrointestinal tract observed upon initial endoscopic examination. However, endoscopic evaluation of the depth and spread of necrosis is challenging and may lead to unnecessary gastrectomy. From January 2002 to December 2008, 70 patients were classified as having stage III gastric injury in an initial digestive tract endoscopic examination. When patients had no signs of peritonitis, their treatment was determined by 6 clinical and biochemical factors of severity (abdominal rebound tenderness, neuropsychiatric troubles, cardiovascular shock, metabolic acidosis, disseminated intravascular coagulation, and kidney failure) in addition to endoscopic staging. If one of these clinical and biochemical factors was present, the patient underwent emergency laparotomy. Patients with isolated stage III gastric injury were kept under close observation. Twenty-four of the 70 endoscopic stage III patients required emergency surgery. Conservative treatment was initiated in the remaining 46. There were 4 postoperative deaths (5.7%). Fifteen patients required subsequent surgery: distal gastrectomy with Billroth I anastomosis (n = 7) for distal stricture and esophagoplasty for nondilatable esophageal stricture (n = 8). At the end of the follow-up period, total or partial gastric conservation was achieved in all 46 patients (65.7%) and the esophagus was conserved in 38 patients (54.3%). In the absence of clinical and biological signs of severity, conservative management of stage III gastric injury is clinically feasible, precludes gastrectomy and has a low mortality rate.

High-dose insulin therapy in beta-blocker and calcium channel-blocker poisoning

Introduction. High-dose insulin therapy, along with glucose supplementation, has emerged as an effective treatment for severe beta-blocker and calcium channel-blocker poisoning. We review the experimental data and clinical experience that suggests high-dose insulin is superior to conventional therapies for these poisonings.Presentation and general management. Hypotension, bradycardia, decreased systemic vascular resistance (SVR), and cardiogenic shock are characteristic features of beta-blocker and calcium-channel blocker poisoning. Initial treatment is primarily supportive and includes saline fluid resuscitation which is essential to correct vasodilation and low cardiac filling pressures. Conventional therapies such as atropine, glucagon and calcium often fail to improve hemodynamic status in severely poisoned patients. Catecholamines can increase blood pressure and heart rate, but they also increase SVR which may result in decreases in cardiac output and perfusion of vascular beds. The increased myocardial oxygen demand that results from catecholamines and vasopressors may be deleterious in the setting of hypotension and decreased coronary perfusion.Methods. The Medline, Embase, Toxnet, and Google Scholar databases were searched for the years 1975–2010 using the terms: high-dose insulin, hyperinsulinemia–euglycemia, beta-blocker, calcium-channel blocker, toxicology, poisoning, antidote, toxin-induced cardiovascular shock, and overdose. In addition, a manual search of the s of the North American Congress of Clinical Toxicology and the Congress of the European Association of Poisons Centres and Clinical Toxicologists published in Clinical Toxicology for the years 1996–2010 was undertaken. These searches identified 485 articles of which 72 were considered relevant.Mechanisms of high-dose insulin benefit. There are three main mechanisms of benefit: increased inotropy, increased intracellular glucose transport, and vascular dilatation.Efficacy of high-dose insulin. Animal models have shown high-dose insulin to be superior to calcium salts, glucagon, epinephrine, and vasopressin in terms of survival. Currently, there are no published controlled clinical trials in humans, but a review of case reports and case series supports the use of high-dose insulin as an initial therapy.High-dose insulin treatment protocols. When first introduced, insulin doses were cautiously initiated at 0.5 U/kg bolus followed by a 0.5–1 U/kg/h continuous infusion due to concern for hypoglycemia and electrolyte imbalances. With increasing clinical experience and the publication of animal studies, high-dose insulin dosing recommendations have been increased to 1 U/kg insulin bolus followed by a 1–10 U/kg/h continuous infusion. Although the optimal regimen is still to be determined, bolus doses up to 10 U/kg and continuous infusions as high as 22 U/kg/h have been administered with good outcomes and minimal adverse events.Adverse effects of high-dose insulin. The major anticipated adverse events associated with high-dose insulin are hypoglycemia and hypokalemia. Glucose concentrations must be monitored regularly and supplementation of glucose will likely be required throughout therapy and for up to 24 h after discontinuation of high-dose insulin. The change in serum potassium concentrations reflects a shifting of potassium from the extracellular to intracellular space rather than a decrease in total body stores.Conclusions. While more clinical data are needed, animal studies and human case reports demonstrate that high-dose insulin (1–10 U/kg/hour) is a superior treatment in terms of safety and survival in both beta-blocker and calcium-channel blocker poisoning. High-dose insulin should be considered initial therapy in these poisonings.

Objetivos de la reanimación hemodinámica

Cardiovascular failure or shock, of any etiology, is characterized by ineffective perfusion of body tissues, inducing derangements in the balance between oxygen delivery and consumption. Impairment in oxygen availability on the cellular level causes a shift to anaerobic metabolism, with an increase in lactate and hydrogen ion production that leads to lactic acidosis. The degree of hyperlactatemia and metabolic acidosis will be directly correlated to the development of organ failure and poor outcome of the individuals. The amount of oxygen available at the tissues will depend fundamentally on an adequate level of perfusion pressure and oxygen delivery. The optimization of these two physiologic parameters can re-establish the balance between oxygen delivery and consumption on the cellular level, thus, restoring the metabolism to its aerobic paths. Monitoring variables such as lactate and oxygen venous saturations (either central or mixed) during the initial resuscitation of shock will be helpful to determine whether tissue hypoxia is still present or not. Recently, some new technologies have been developed in order to evaluate local perfusion and microcirculation, such as gastric tonometry, near-infrared spectroscopy and videomicroscopy. Although monitoring these regional parameters has demonstrated its prognostic value, there is a lack of evidence regarding to its usefulness during the resuscitation process. In conclusion, hemodynamic resuscitation is still based on the rapid achievement of adequate levels of perfusion pressure, and then on the modification of oxygen delivery variables, in order to restore physiologic values of ScvO 2/SvO 2 and resolve lactic acidosis and/or hyperlactatemia.

Pylorogastric intussusception in a Chihuahua puppy. A case report

A three-month-old Chihuahua dog was presented with acute abdominal pain, vomiting and cardiovascular shock. Abdominal ultrasound (US) and iodated contrast gastrogram revealed suspected pylorogastric intussusception. Because of the poor prognosis the dog was euthanatized. Diagnosis of pylorogastric intussusception was confirmed at necropsy. Parasitological, virological, serological and histological examinations were also performed. This report documents the sixth case of pylorogastric (i.e. duodenogastric, gastrogastric) intussusception in the veterinary medical literature and it is the first report on a puppy dog in which US and radiographic diagnosis were confirmed post mortem.

Fatal cold agglutinin-induced haemolytic anaemia: a case report

IntroductionCold agglutinin disease usually develops as a result of the production of a specific immunoglobulin M auto-antibody directed against the I/i and H antigens, precursors of the ABH and Lewis blood group substances, on red blood cells. Autoimmune and lymphoproliferative disorders, Mycoplasma pneumoniae and other infections can be associated with the production of cold agglutinins. In its classic presentation with haemolytic anaemia and Raynaud's syndrome, cold agglutinin disease is usually idiopathic. Several factors play a role in determining the ability of a cold agglutinin to induce a haemolytic anaemia such as antibody concentration and temperature range, in particular the highest temperature at which antibodies interact with red blood cells.Case presentationA 48-year-old Caucasian man presented to our hospital with symptoms of extreme asthenia caused by severe anaemia. The transfusion of red blood cells (O Rh-positive), started as prescribed by the emergency guidelines in force without pre-transfusion tests, induced fatal haemolysis because of the presence of high levels of anti-H antibodies in his blood, that reacted with the large amount of H antigen in universal (0) red blood cells.ConclusionEmergency transfusion of universal red blood cells (0 Rh-positive or negative) is usually accepted by the international guidelines in force in emergency departments. In this report we describe a rare complication caused by the very high concentration in the recipient of cold agglutinins and the activation of the complement system, responsible for red blood cell lysis and consequent fatal cardiovascular shock. We conclude that emergency transfusion of universal red blood cells (0 Rh-positive or negative) may be dangerous and its risk should be assessed against the risk of delaying transfusion until the pre-transfusion tests are completed.

Combat-Associated Drowning

The purpose of this article is to describe the clinical course and outcome of drowning cases related to current US military combat operations. This retrospective case series spans December 2002 to January 2009 of survivors transferred to an echelon IV military trauma center in Europe serving as the primary evacuation hub for ongoing combat operations. Patient demographics and the situational and clinical findings at the initial drowning scene were reviewed. A comprehensive analysis of care as each patient transitioned through the combat theater to the echelon IV trauma center in Europe was performed. Overall, mortality was 37.5% mortality rate (3 of 8 patients). Advanced modes of respiratory support such as high-frequency ventilation, airway pressure release ventilation, and extracorporeal membrane oxygenation were required in a majority of the cohort (6 of 8 patients). Limited-duration vasopressor infusions (7 of 8 patients) were also required to ensure adequate end-organ perfusion. Glasgow Coma Scale (GCS) scores and the need for cardiopulmonary resuscitation (CPR) at the scene of injury were associated with eventual patient mortality (100% mortality for an initial GCS score of 3 and 75% mortality for on-scene CPR). Survivor long-term morbidity was often related to the sequelae of acute respiratory distress syndrome and hypoxic encephalopathy. Drowning associated with combat operations was associated with severe acute respiratory distress syndrome and cardiovascular shock. GCS score and the need for CPR at the scene of injury were associated with eventual mortality because of anoxic brain injury in all cases.

Cutting-edge Discussions of Management, Policy, and Program Issues in Emergency Care

Cutting-edge Discussions of Management, Policy, and Program Issues in Emergency Care

Acute carbamazepine poisoning treated with resin hemoperfusion successfully

Carbamazepine (CBZ) poisoning has been occurring more frequently. We describe the use of synthesized resin–absorbed hemoperfusion in the therapy of a 48-year-old man who developed carotic, cardiovascular shock and multiorgan dysfunction due to a CBZ overdose (the highest concentration of drug >20 mg/L; therapeutic range, 8-12 mg/L). The treatment was very successful; and the patient eventually was discharged with a full recovery and no complications, although his diagnosis and treatment had been delayed for 56 hours. Hemoperfusion has a steady clearance of this drug without subsequent rebound or potential hazards. Resin hemoperfusion should be first considered for acute CBZ intoxication, especially when drug-induced gastrointestinal hypomotility prevents elimination via the gut and patient is under life-threatening condition.

Isolation of the right subclavian artery in interrupted aortic arch

A 15-day-old newborn presented with cardiovascular shock. Upon clinical suspicion of congenital heart disease (CHD), medical treatment was initiated. Echocardiography showed a left-sided interrupted aortic arch Type B and a large ventricular septal defect (VSD). Magnetic resonance imaging (MRI) was requested for preoperative exact anatomical delineation of the interrupted aortic arch and of its branches. Additionally, MR angiography depicted an isolated right subclavian …

Inadequate Antibiotic Therapy in Solid Organ Transplant Recipients Is Associated with a Higher Mortality Rate

Inadequate antibiotic therapy and failure to administer antibiotics in a timely fashion have been associated with substantial mortality rates in patients in the intensive care unit (ICU). We analyzed the infection pattern in solid organ transplant recipients as well as the impact of antibiotic resistance and inadequate antibiotic treatment on mortality rates and morbidity outcomes. Charts of adult solid organ transplant recipients in 2006 from a single institution were reviewed. Data on patients with bacterial and fungal infections acquired within one year after transplantation were compared with the primary outcome of death within 28 days. Statistical analysis included nonparametric tests (Wilcoxon rank sum, Fisher exact, and chi-square) and multivariable logistic regression with p < 0.05 considered significant. Of the 366 patients, 114 (31%) had a total of 208 bacterial or fungal infections, and 44 of them (39%) were admitted to the ICU. Our primary endpoint, the 28-day mortality rate, was 8% overall, whereas the six-month mortality rate was 11%. Patients treated inadequately with antibiotics had a significantly higher mortality rate. The leading causes of infection were multiple organisms, coagulase-negative Staphylococcus, and E. coli, of which 76% were resistant to antibiotics. Antibiotic-resistant infections were associated with longer hospital stays (p = 0.04), intravenous antibiotic use prior to infection (p = 0.04), nucleotide synthesis inhibitor use (p = 0.02), ICU admission (p < 0.01), and respiratory failure (p = 0.03). Most infections were treated inadequately initially (69%) but treated adequately at 24 h (56%). Inadequate antibiotic treatment was significantly associated with younger age (p = 0.04), prior intravenous antibiotic use (p = 0.04), longer stay prior to infection (p = 0.05), and cardiovascular shock (p = 0.014). Inadequate antibiotic therapy at 24 h was associated with a higher mortality rate (14% vs. 2%; p = 0.03) and a trend toward longer ICU and in-hospital stays. Most bacterial and fungal infections were resistant to antibiotics and were treated inadequately initially. Prior intravenous antibiotic use and longer stay prior to infection were associated with antibiotic resistance and inadequate antibiotic therapy. Failure to provide adequate antibiotic treatment within 24 h had a significant impact on the 28-day mortality rate and was associated with other detrimental clinical outcomes.

Levosimendan as Treatment Option in Severe Verapamil Intoxication: A Case Report and Review of the Literature

Cardiovascular shock due to verapamil intoxication is often refractory to standard resuscitation methods. Recommended therapy includes prevention of further absorption of the drug, inotropic therapy, calcium gluconate, and hyperinsulinemia/euglycemia therapy. Often further measures are needed such as ventricular pacing or mechanical circulatory support. Still, mortality remains high. Levosimendan, an inotropic agent, that enhances myofilament response to calcium, increases myocardial contraction and could therefore be beneficial in verapamil intoxication. Here, we report the case of a 60-year-old patient with clinically severe verapamil poisoning who presented with shock, bradycardia, and sopor. Standard therapy including high-dose inotropes failed to ameliorate the signs of intoxication. But additional therapy with levosimendan led to rapid improvement. Based on this observation, the literature is reviewed focusing on utilization of levosimendan in the treatment of calcium channel blocker overdose. We suggest to consider levosimendan as additional treatment option in patients with cardiovascular shock due to verapamil intoxication that are refractory to standard management.