Pulseless Electrical Activity Cardiac Arrest Research Articles

Metformin-Associated Lactic Acidosis: A Case Report.

A 54-year-old woman with type 2 diabetes mellitus, hypertension, and peripheral vascular disease developed life-threatening lactic acidosis during treatment with metformin for type 2 diabetes. The woman received metformin at 1000 mg orally twice a day for type 2 diabetes. She presented to our emergency department with a 3-day history of severe watery diarrhea, nausea, and vomiting. Her grandson whom she cared for had gastroenteritis several days prior to the onset of her symptoms. She was confused and hypotensive with a blood pressure of 70/39 mmHg. Her initial laboratory findings were remarkable with an arterial blood gas pH 6.57, HCO _{3}^{ - } 2 mEq/L, anion gap 30 mmol/L, and lactate 16.3 mmol/L. She was diagnosed with severe lactic acidosis. Metformin was discontinued. Upon arrival in the emergency department, she became unresponsive and experienced a pulseless electrical activity cardiac arrest. After resuscitation, her severe acidemia persisted despite aggressive intervention with volume resuscitation and vasopressors, leading to the initiation of renal replacement therapy. After multiple dialysis treatments, her severe acidemia resolved. Serum metformin concentration from presentation ultimately returned to 42 mcg/mL (therapeutic concentration: 1–2 mcg/mL). She was discharged from the hospital on day 15 without any neurologic complications. A Naranjo assessment score of 8 was obtained, indicating a probable relationship between the patient’s lactic acidosis and her use of the suspect drug.

Bedside Identification of Massive Pulmonary Embolism with Point-of-Care Transesophageal Echocardiography

BackgroundPulmonary embolism can be difficult to diagnose, particularly in those who are hemodynamically unstable and cannot be imaged to confirm the diagnosis. Echocardiography can allow for rapid assessment of patients in shock, but requires adequate transthoracic windows to obtain clinically useful information. Emergency physician–performed transesophageal echocardiography (TEE) may be a useful tool when transthoracic echocardiography fails. Case ReportAn 86-year-old woman presented to the emergency department after a fall at home. She rapidly decompensated in the emergency department and sustained a pulseless electrical activity cardiac arrest. Attempts made during the resuscitation to obtain transthoracic echocardiographic views to elicit the cause of the patient's cardiac arrest were unsuccessful. An emergency physician, with previous focused training in TEE, performed emergent TEE. The TEE examination rapidly revealed a dilated right ventricle and an empty, hyperdynamic left ventricle, suggestive of an unsuspected massive acute pulmonary embolism. Why Should an Emergency Physician Be Aware of This?With continued growth and utility of point-of-care ultrasound in emergency medicine, TEE provides an attractive means to assess critically ill patients that may not otherwise be assessable.

A retrospective study of pulseless electrical activity, bedside ultrasound identifies interventions during resuscitation associated with improved survival to hospital admission. A REASON Study

ObjectiveOur objective was to determine whether organized or disorganized cardiac activity is associated with increased survival in patients who present in pulseless electrical activity (PEA) treated with either 1) standard advanced cardiac life support (ACLS) medications or 2) other interventions. MethodsThis was a secondary analysis of a prospective, multi-center observational study utilizing ultrasound in out-of-hospital or inemergency department PEA arrest. Bedside ultrasound was performed as ACLS protocol started and during pulse checks. Only cases with visible cardiac activity on ultrasound were included in the present analysis. Cardiac activity was categorized as disorganized (agonal twitching) or organized (contractions with changes in ventricular dimensions). Patients were categorized as receiving either standard bolus ACLS medications or alternative medications during the resuscitation (continuous adrenergic agents, thrombolytics, others). The primary outcome was survival to hospital admission. The secondary outcome was return of spontaneous circulation (ROSC). Multivariate modeling was performed to assess association between survival to hospital admission in patients with intravenous adrenergic agents and cardiac activity. ResultsIn our cohort of 225 patients in PEA cardiac arrest with cardiac activity on ultrasound, the overall survival rate was higher in patients with organized cardiac activity than with disorganized cardiac activity. PEA cardiac arrest patients with organized cardiac activity treated with standard ACLS interventions demonstrated improved survival to hospital admission compared to those with disorganized activity (37.7% (95%CI 24.8–50.2%) versus 17.9% (95%CI 10.9–28%). PEA cardiac arrest patients with organized cardiac activity who received continuous adrenergic agents during the resuscitation and prior to ROSC demonstrated higher survival to hospital admission 45.5% (95%CI 26.9–65.4%) and ROSC 90.9% (95%CI 71.0–98.7%) compared to those with disorganized cardiac activity who received continuous adrenergic agents during the resuscitation 0% (95%CI 0–23.0%) and 47.1% (95%CI 26–69%). Regression analysis demonstrates an association between increased survival in patients receiving intravenous adrenergic agents and organized cardiac activity. ConclusionSurvival in patients following PEA arrest is higher in patients with organized cardiac activity. The initiation of continuous adrenergic agents during PEA was associated with improved survival to hospital admission in patients with organized cardiac activity on bedside ultrasound, but this improvement was not seen in patients in PEA with disorganized cardiac activity. Bedside ultrasound may identify a subset of patients that respond differently to ACLS interventions.

Cardiac arrest following arteriovenous fistula manipulation: a cautionary note

Arteriovenous fistulas can lead to a number of different chronic complications. We describe a case where a patient developed a thrombosis within her brachiobasilic arteriovenous fistula, which was manually manipulated...

Systemic Mastocytosis as a Rare Cause of Pulseless Electrical Activity (PEA) Cardiac Arrest and Recurrent Syncope

Systemic Mastocytosis as a Rare Cause of Pulseless Electrical Activity (PEA) Cardiac Arrest and Recurrent Syncope

Induced Hypothermia: Implications for Free Flap Survival.

Plastic surgeons may not be aware that the new advanced cardiac life support (ACLS) guidelines released in 2010 include induced hypothermia as an adjuvant treatment to improve neurologic outcomes following cardiac arrest [1]. Induced hypothermia (IH) is thought to mitigate ischemic damage by lowering metabolic demand and preventing noxious byproducts of resuscitation. IH is recommended for patients who experience the return of spontaneous circulation after cardiac arrest, but remain unconscious [2]. The hypothermia protocol involves the reduction of body temperature to 32℃–34℃ for 12 to 24 hours, followed by slow rewarming [1,2]. However, the use of induced hypothermia in microvascular free tissue transfer has not been studied. We present the case of a patient who underwent IH following free-flap reconstruction of a head and neck cancer defect. A 69-year-old male with a history of coronary artery disease and three-vessel coronary artery bypass grafting presented with recurrent basal cell carcinoma of the left ear canal. He underwent total auriculectomy and lateral temporal bone resection, and the defect was reconstructed with a left vertical rectus abdominis myocutaneous free flap. On the second postoperative day, the patient was found unresponsive in pulseless electrical activity cardiac arrest. The ACLS protocol was initiated, including mechanical ventilation and vasopressors for hemodynamic support. The patient was successfully resuscitated but suffered a second cardiac arrest with ventricular fibrillations. He was resuscitated again but remained unresponsive. Hypothermia was induced, with the patient cooled to 32℃ for 48 hours (Fig. 1). The free flap remained well perfused with an audible Doppler signal during the cardiac arrests, vasopressor therapy, hypothermic cooling, and the remainder of his hospitalization (Fig. 2). Unfortunately, the patient had no meaningful neurologic recovery and magnetic resonance imaging showed diffuse hypoxic brain injury. Therefore, the family elected to withdraw care on postoperative day 10. Fig. 1 Temperature curve showing induced hypothermia to 32℃–34℃, from postoperative day three until postoperative day five. Fig. 2 A 69-year-old male underwent composite resection of the left auriculotemporal area and temporal bone for recurrent basal cell carcinoma, and the defect was reconstructed with a left vertical rectus abdominis myocutaneous free flap. The effects of systemic hypothermia on free tissue transfer are not fully understood. Limited animal and human studies have demonstrated conflicting results. Some data have suggested that hypothermia causes decreased perfusion, vasospasm, and thrombosis, while other animal experiments have shown a protective effect of mild hypothermia on free flaps [3,4,5]. Clotting enzymes, platelets, and leukocytes function less effectively in a hypothermic setting; however, no reports have been published on the effect of severe hypothermia (<34℃) on free flap survival in humans. This is the first reported case of induced hypothermia after free tissue transfer. Plastic surgeons should be aware of ongoing changes to the ACLS algorithm and its impact on perioperative care. In this case, a free tissue transfer remained viable despite induced hypothermia and vasopressors, which is a single data point suggesting that free flaps can tolerate such interventions. However, further research is needed to clarify the effects of hypothermia on free tissue transfer.

Echocardiography integrated ACLS protocol versus conventional cardiopulmonary resuscitation in patients with pulseless electrical activity cardiac arrest

Objective:To examine the utility of bedside echocardiography in detecting the reversible causes of pulseless electrical activity (PEA) cardiac arrest and predicting the resuscitation outcomes. Methods:In this prospective interventional study, patients presenting with PEA cardiac arrest were randomized into two groups. In Group A, ultrasound trained emergency physicians performed echocardiography evaluating cardiac activity, right ventricle dilation, left ventricle function, peri-cardial effusion/tamponade and IVC size along with the advanced cardiac life support (ACLS) protocol. Patients in Group B solely underwent ACLS protocol without applying echocardiography. The presence or absence of mechanical ventricular activity (MVA) and evidences of PEA reversible causes were recorded. The return of spontaneous circulation (ROSC) and death were evaluated in both groups. Results:One hundred patients with the mean age of (58±6.1) years were enrolled in this study. Fifty patients(Group A) had echocardiography detected in parallel with cardiopulmonary resuscitation (CPR). Among them, 7 patients (14%) had pericardial effusion, 11 (22%) had hypovolemia, and 39 (78%) were revealed the presence of MVA. In the pseudo PEA subgroup (presence of MVA), 43% had ROSC (positive predictive value) and in the true PEA subgroup with cardiac standstill (absence of MVA), there was no recorded ROSC (negative predictive value). Among patients in Group B, no reversible etiology was detected. There was no significant difference in resuscitation results between Groups A and B observed (P=0.52). Conclusion:Bedside echocardiography can identify some reversible causes of PEA. However, there are no significant changes in survival outcome between the echo group and those with traditional CPR.

Lidocaine-Induced Cardiac Arrest in the Emergency Department: Effectiveness of Lipid Therapy

BackgroundLocal anesthetics are commonly used in the emergency department (ED). Overdoses can lead to disastrous complications including cardiac toxicity and arrest. Recognition of local anesthetic systemic toxicity (LAST) is important; however, prevention is even more critical. Knowledge of proper lidocaine dosage can prevent LAST. LAST may be effectively treated with lipid emulsion therapy. Although the mechanism is not well understood, its use may have a profound impact on morbidity and mortality. Case ReportFifty milliliters of 2% lidocaine was infiltrated for local anesthesia in a 35-year-old woman during the incision and drainage of a labial abscess. Following the procedure, the patient complained of vomiting, with rapid progression to an altered mental state and seizure requiring endotracheal intubation for airway protection. Suspecting lidocaine toxicity, intralipids were ordered. While waiting for the intralipids, the patient decompensated and suffered pulseless electrical activity (PEA) cardiac arrest. A 100-mL bolus of 20% intralipids was administered 3 minutes into the resuscitation, after which return of spontaneous circulation occurred. The intralipid bolus was then followed by a continuous infusion of 0.25 mL/kg/minute, for an infusion dose of 930 mL. Despite a complicated hospital course, the patient was discharged home neurologically intact. Why Should an Emergency Physician Be Aware of This?We believe this patient's cardiovascular collapse was secondary to an iatrogenic overdose of lidocaine. This is one of the first cases to support the efficacy of intravenous lipids in the treatment of LAST in humans in the ED.

Pulseless electrical activity cardiac arrest: time to amend the mnemonic "4H&4T"?

Pulseless electrical activity (PEA) cardiac arrest is characterised by a residual organised electrical activity. PEA is frequently induced by reversible conditions. The mnemonic "4H&4T" was proposed as a reminder to assess for Hypoxia, Hypovolaemia, Hypo/Hyperkalaemia, Hypothermia, Thrombosis, cardiac Tamponade, Toxins, and Tension pneumothorax. Other potential aetiologies have been identified, but their respective probability and frequencies are unclear. The aim of this study was to analyse the aetiologies of PEA out-of-hospital cardiac arrests and to evaluate their relative frequencies. This was a retrospective study based on data routinely and prospectively collected. All adult patients with PEA as the first recorded rhythm and admitted between 2002 and 2012 to the emergency department (ED) after return of spontaneous circulation or under resuscitation were included. A total of 1,866 out-of-hospital cardiac arrests were included. PEA was the first recorded rhythm in 232 adult patients (12.4%) and 144 of these were admitted to the ED. The mean age was 63.8 ± 20.0 years, 58.3% were men. The survival rate at 48 hours was 29%. Hypoxia (23.6%), acute coronary syndrome (12.5%) and trauma (12.5%) were the most frequent causes. We were unable to identify a specific cause in 17.4%. Pulmonary embolism, hypovolaemia, intoxication and hypo/hyperkalaemia occurred in fewer than 10% of the cases. Nonischaemic cardiac disorders and intracranial haemorrhage occurred in 8.3% and 6.9%, respectively. Intracranial haemorrhage and nonischaemic cardiac disorders represent significant causes of PEA, with a prevalence equalling or exceeding the frequency of classical 4H&4T aetiologies. These conditions are potentially accessible to simple diagnostic procedures (computed tomography or echocardiography).

Return of spontaneous circulation confirmed by two dimensional ultrasound following pulseless electrical activity arrest

SummaryWe report a case of Pulseless Electrical Activity (PEA) cardiac arrest following induction of anaesthesia where, in the absence of central pulses, the return of spontaneous circulation was confirmed by two‐dimensional ultrasound (2D US) and colour flow Doppler of the femoral artery. When cardiac arrest occurs in hospital confirmation of palpable pulses forms part of the assessment of the return of spontaneous circulation and is a guide to subsequent therapeutic decisions. However difficulties in identifying central pulses during cardiopulmonary resuscitation are well documented. With the increasing availability and familiarity of 2D US, this modality may provide an option for assessment of quality of cardiopulmonary resuscitation and the return of spontaneous circulation.

Reduction in carotid blood flow after epinephrine during CPR in a porcine model of cardiac arrest is probably related to an increased vascular bed resistance

Introduction: We have previously reported the detrimental effect of epinephrine (epi) during CPR on carotid blood flow (CBF) in an animal model. We now sought to investigate the epi-altered CBF profile in a porcine model of post-shock pulseless electrical activity (PEA) cardiac arrest.

Two lessons from the empiric management of a combined overdose of liraglutide and amitriptyline.

We report the case of a 52-year-old man with a combined liraglutide and amitriptyline overdose who presented with a seizure and then pulseless electrical activity cardiac arrest. This is the largest reported overdose of liraglutide (36 mg), a novel glucagon-like peptide-1 analog recommended for certain patients with type 2 diabetes mellitus. The subsequent biochemical effects included severe electrolyte disturbances associated with polyuria. Regarding the amitriptyline, treatment with lipid emulsion correlated with resolution of electrocardiographic changes and successful resuscitation. The treatment of amitriptyline overdose with lipid emulsion is briefly discussed.

An Atypical Presentation and Management of Acute Necrotic Esophagus and Esophageal Perforation

Purpose: Acute necrotic esophagus is an extremely rare condition characterized by circumferential ischemia of the esophagus. Full thickness necrosis only occurs in 7% of cases. Management often includes proton pump inhibitors, sucralfate, and in severe cases, an esophagectomy. Case Description: A 58-yearold man with history of diabetes presented to the emergency room having been found unconscious at home. He went into pulseless electrical activity cardiac arrest with return of spontaneous circulation after 10 minutes of cardiopulmonary resuscitation. He was intubated and started on norepinephrine. He was found to be in diabetic ketoacidosis with an anion gap of 25 and glucose over 1000. He developed positive troponins with ST elevations in V1-V5 on electrocardiogram. He was transferred to a tertiary medical center for cardiac catheterization. Upon transfer, the patient was found to be in severe septic rather than cardiogenic shock requiring epinephrine, norepinephrine, vasopressin, and phenylephrine. He was also in acute respiratory distress syndrome and anuric renal failure. He had minimal neurologic function secondary to large watershed ischemic strokes. Bilateral thoracenteses revealed 4L of cola-colored fluid. Pleural fluid analysis was exudative with a pH of 8.2 and amylase of 756. Serum amylase was 522. Gastric lavage returned similar cola-colored fluid. Computed Tomography demonstrated pneumomediastinum and a collection around the esophagus with air-fluid levels. Esophagogastroduodenoscopy revealed friable, grey/black esophageal mucosa extending from the cricopharyngeus to the gastroduodenal junction and was most concentrated in watershed regions. There were multiple areas of perforation. Bilateral chest tubes were placed for continued drainage of fluid. Vancomycin, piperacillin/tazobactam, and fluconazole were initiated. Given the extent of necrosis and critical nature of the patient, neither esophageal stenting nor esophagectomy could be performed. Once weaned off pressor support, the patient underwent a tracheostomy, esophagostomy drainage of distal esophagus, exclusion of esophagogastric junction with stapler, draining gastric tube, and feeding jejunal tube placement. Discussion: This case demonstrates a rare condition of acute esophageal necrosis complicated by esophageal perforation secondary to cardiac arrest in the background of severe diabetic vasculopathy and ketoacidosis. Given the critical nature of the patient, traditional esophagectomy could not be performed. A combination of esophagostomy creation and drainage placements allowed the patient to stabilize and eventually be discharged to a vent facility.

Epinephrine reduces carotid blood flow during cardiopulmonary resuscitation in a porcine model of cardiac arrest

Introduction: Epinephrine (epi) administered during CPR improves return of spontaneous circulation. However, its effect on long term outcome is still controversial. Moreover, decreases in cerebral microcirculation after epinephrine have been earlier reported in a model of ventricular fibrillation (VF) cardiac arrest. We sought to investigate the effects of epi on carotid blood flow (CBF) during CPR in a porcine model of post shock pulseless electrical activity (PEA) cardiac arrest.

Randomised trial comparing the recording ability of a novel, electronic emergency documentation system with the AHA paper cardiac arrest record

ObjectiveTo evaluate the ability of an electronic system created at the University of Washington to accurately document prerecorded VF and pulseless electrical activity (PEA) cardiac arrest scenarios compared with the...

Severe Cardiotoxicity Associated with Ixabepilone use in Metastatic Breast Cancer

To report a case of cardiogenic shock and fulminant heart failure associated with a single dose of ixabepilone. A 32-year-old woman presented to the emergency department (ED) with abdominal pain and difficulty breathing within 1 hour after receiving a partial dose of ixabepilone (26 mg/m(2)) at an oncologist's office. She had breast cancer, with metastases to the bone and liver and evidence of early liver failure. While in the ED, she developed acute respiratory failure requiring intubation. Bedside ultrasound imaging showed free abdominal fluid. Computed tomography (CT) scans showed evidence of right-sided heart failure and abdominal fluid consistent with ascites but no evidence of pulmonary embolism. After the CT scan, the patient experienced pulseless electrical activity cardiac arrest. All attempts at resuscitation were unsuccessful. Ixabepilone is a novel drug for treatment of advanced breast cancer. The most commonly reported adverse effects are peripheral neuropathies and hematologic issues such as neutropenia. To our knowledge, this is the first detailed report of a severe adverse cardiac event associated with ixabepilone use. Many other chemotherapeutic agents have cardiotoxic effects. An objective causality assessment, using the Naranjo probability scale, revealed that an adverse drug event was probable. Clinicians should maintain broad differential diagnoses that include adverse reactions to drugs relatively new to the market. Ixabepilone may have cardiotoxic effects that necessitate further study, particularly when the drug is administered after cardiotoxic chemotherapy.

Abstract 71: A Novel Animal Model of Pulseless Electrical Activity Cardiac Arrest: Adrenergic Blockade and Coronary Occlusion

Introduction: The incidence of VF as the first documented rhythm in out-of-hospital cardiac arrest (OOHCA) has been declining, while the incidence of pulseless electrical activity (PEA) has been increasing. The increasing proportion of PEA as the initial rhythm for OOHCA has paralleled the increasing use of adrenergic antagonist therapy in the population most at risk for cardiac arrest. We hypothesized that PEA cardiac arrest can result from acute coronary occlusion in the setting of pre-arrest adrenergic blockade. Methods: Twenty-six anesthetized and instrumented immature male swine (mean weight 36 kg) were pre-treated with an infusion of labetalol, a β-1 and α-1 adrenergic blocker (mean dose 6 ± 3 mg/kg). Adequacy of adrenergic blockade was determined using an intravenous challenge of epinephrine 0.1 mg IV. After challenge and return to baseline, balloon occlusion of the left anterior descending (LAD) or proximal right coronary artery (RCA) was performed and the rhythm and hemodynamic response observed during sustained occlusion. Results: Occlusion of the RCA was followed by PEA or pseudo-PEA (defined as an organized rhythm with systolic arterial pressure &lt;50 mm Hg) in 10/13 animals (77%). During RCA occlusion, cooling of the vagus nerve (reversible thermal vagotomy) did not prevent the hypotensive hemodynamic response. LAD occlusion was followed by PEA in 6/13 animals (46%). Brief occlusion of the RCA followed by occlusion of the LAD was followed by PEA in 5/7 animals (71%). Conclusions: Adrenergic blockade followed by coronary occlusion may be followed by PEA. This combination may play a role in the declining incidence of VF as the initial cardiac arrest rhythm in out-of-hospital cardiac arrest.

Periportal edema after cardiac arrest due to calcium channel blocker overdose

A 41-year-old man with a history of diabetes mellitus and hypertension presented to our emergency department with changes in consciousness. The patient’s vital signs included a heart rate of 22 beats/min with presence of weak carotid pulses, respiration of 8 breaths/min, and a core temperature 33.8 C. On examination, the patient had a Glasgow coma score of 3, and was cold and clammy. Initial resuscitation included tracheal intubation, supplementary oxygen, 1 mg intravenous atropine, and starting a dopamine infusion. Pulseless electrical activity cardiac arrest occurred soon after arrival. Circulation was restored after 2 minutes of cardiopulmonary resuscitation and one bolus dose of 1 mg intravenous adrenaline. A 12-lead electrocardiogram revealed sinus rhythm. Cardiac enzyme analysis result was within normal limits. The patient’s blood pressure remained low, requiring aggressive fluid resuscitation and high-dose inotropes. Fifteen minutes after return of spontaneous circulation, abdominal computed tomography was ordered to evaluate the possibility of intra-abdominal sepsis, which demonstrated hypodense areas around portal veins of both lobes of the liver, compatible with periportal edema (Fig. 1), dilated inferior vena cava, minimal ascites, and

Sodium nitroprusside-enhanced cardiopulmonary resuscitation improves resuscitation rates after prolonged untreated cardiac arrest in two porcine models*

Sodium nitroprusside-enhanced cardiopulmonary resuscitation consists of active compression-decompression, an impedance threshold device, abdominal binding, and large intravenous doses of sodium nitroprusside. We hypothesize that sodium nitroprusside-enhanced cardiopulmonary resuscitation will significantly increase carotid blood flow and return of spontaneous circulation compared to standard cardiopulmonary resuscitation after prolonged ventricular fibrillation and pulseless electrical activity cardiac arrest. Prospective randomized animal study. Hennepin County Medical Center Animal Laboratory. Forty Yorkshire female farm-bred pigs weighing 32 ± 2 kg. In protocol A, 24 isoflurane-anesthetized pigs underwent 15 mins of untreated ventricular fibrillation and were subsequently randomized to receive standard cardiopulmonary resuscitation (n = 6), active compression-decompression cardiopulmonary resuscitation + impedance threshold device (n = 6), or sodium nitroprusside-enhanced cardiopulmonary resuscitation (n = 12) for up to 15 mins. First defibrillation was attempted at minute 6 of cardiopulmonary resuscitation. In protocol B, a separate group of 16 pigs underwent 10 mins of untreated ventricular fibrillation followed by 3 mins of chest compression only cardiopulmonary resuscitation followed by countershock-induced pulseless electrical activity, after which animals were randomized to standard cardiopulmonary resuscitation (n = 8) or sodium nitroprusside-enhanced cardiopulmonary resuscitation (n = 8). The primary end point was carotid blood flow during cardiopulmonary resuscitation and return of spontaneous circulation. Secondary end points included end-tidal CO2 as well as coronary and cerebral perfusion pressure. After prolonged untreated ventricular fibrillation, sodium nitroprusside-enhanced cardiopulmonary resuscitation demonstrated superior rates of return of spontaneous circulation when compared to standard cardiopulmonary resuscitation and active compression-decompression cardiopulmonary resuscitation + impedance threshold device (12 of 12, 0 of 6, and 0 of 6 respectively, p < .01). In animals with pulseless electrical activity, sodium nitroprusside-enhanced cardiopulmonary resuscitation increased return of spontaneous circulation rates when compared to standard cardiopulmonary resuscitation. In both groups, carotid blood flow, coronary perfusion pressure, cerebral perfusion pressure, and end-tidal CO2 were increased with sodium nitroprusside-enhanced cardiopulmonary resuscitation. In pigs, sodium nitroprusside-enhanced cardiopulmonary resuscitation significantly increased return of spontaneous circulation rates, as well as carotid blood flow and end-tidal CO2, when compared to standard cardiopulmonary resuscitation or active compression-decompression cardiopulmonary resuscitation + impedance threshold device.

High-dose insulin: A consecutive case series in toxin-induced cardiogenic shock

Context. Cardiovascular medication overdoses can be difficult to treat. Various treatment modalities are currently recommended. Objective. To describe patient outcomes and adverse events of high-dose insulin therapy in consecutive overdose patients in cardiogenic shock after implementation of a high-dose insulin protocol (1–10 U/kg/h, while avoiding or tapering off vasopressors). Methods. This is an observational consecutive case series of patients identified from a registry. Data were collected by retrospective chart review of patients treated by our toxicology service with this protocol from February 2007 until March 2010. Results. Twelve patients were treated with high-dose insulin. The mean age was 36.5 years (SD 11.7). Seven patients had pre-existing vasopressor therapy, and all were tapered off vasopressors while on insulin. Two patients experienced pulseless electrical activity cardiac arrest prior to high-dose insulin therapy. Intravenous fat emulsion was given to two patients. The mean maximum insulin infusion rate was 8.35 U/kg/h (mean = 8.35, SD 6.34). The mean duration of insulin infusion was 23.5 h (SD 19.7). The mean duration of glucose infusion post-insulin was 25.2 h (SD 17.7). The primary toxins were β-blocker in five, calcium channel blocker in two, combined β-blocker/calcium channel blocker in two, tricyclic antidepressant in one, and polydrug in 2. Clinical outcomes. Eleven of 12 patients survived. One patient expired 9 h into insulin therapy from cardiac arrest shortly after the insulin was stopped and a vasopressor re-initiated (protocol deviation). Adverse events. Six patients experienced a total of 19 hypoglycemic events. Hypokalemia (defined as < 3.0 mEq/L) developed in eight patients. Adverse sequelae. Necrotic digits occurred in one patient with known clotting disorder after receiving high-dose norepinephrine and INR reversal with fresh frozen plasma prior to insulin therapy. One patient was discharged with mild anoxic injury thought due to pulseless electrical activity arrest prior to insulin therapy. Three of these 12 patients have been previously described in published case reports. Conclusion. High-dose insulin therapy based on a 1–10 U/kg/h dosing guideline and recommending avoidance of vasopressors appears to be effective in the treatment of toxin-induced cardiogenic shock. Hypoglycemia was the most frequent adverse event, followed by hypokalemia. Adverse events did not lead to adverse sequelae.