Periods Of Asystole Research Articles

Mitral valvuloplasty with left atrial appendage closure and pacemaker implantation in a dog with severe myxomatous mitral valve degeneration: a case report

BackgroundMitral valvuloplasty (MVP) has been widely recognized as a treatment option for myxomatous mitral valve disease (MMVD). However, postoperative complications such as thromboembolism, arrhythmia, and pancreatitis in some cases have resulted in death. We treated a dog with severe MMVD complicated by impaired sinus function with MVP and pacemaker implantation. Also, due to an intrinsic procoagulant state and severe arrhythmia after the MVP, left atrial appendage (LAA) closure was performed to reduce the postoperative risk of thrombosis.Case presentationAn 11-year-old castrated 7.5-kg male Miniature Schnauzer with a history of congestive heart failure was brought to Shiraishi Animal Hospital for MMVD surgical treatment. Echocardiography revealed an enlarged left atrium and ventricle secondary to MMVD. Sinus arrest with 2 to 3-second periods of asystole was identified by electrocardiogram. Mitral valvuloplasty was performed with cardiopulmonary bypass to treat the MMVD. After coronary reperfusion, there was no spontaneous electrical activity. Cardiac arrest continued. Based on this surgical outcome, a permanent pacemaker was implanted. In addition, LAA closure with an AtriClip was performed to prevent intra-atrial thrombus formation. Cardiac remodeling and congestion were ameliorated after surgery. Sinus rhythm was restored 5 days postoperatively; however, the patient continued pacemaker dependent. All cardiac drugs were discontinued 3 months after surgery. The owner reported no postoperative complications (i.e., thrombosis), and the patient was brought for a check-up 4 months after the operation in good health.ConclusionsFor surgical MMVD cases complicated with impaired sinus function, the chances of spontaneous sinus rhythm are low, requiring pacemaker implantation. LAA closure may be considered to protect against decreased atrial function after mitral valvuloplasty and prevent intra-atrial thrombus formation.

Regular heart rhythm restoration after a period of asystole: modeling in experimental cardiology

Abstract Funding Acknowledgements Type of funding sources: None. Regular heart rhythm restoration after a period of asystole: modeling in experimental cardiology Purpose To study the arterial hemodynamics during the regular heart rhythm restoration after a period of asystole using the original device for modeling of intra-arterial circulation. Materials and methods We used the device for modeling of intra-arterial circulation made by us (Document of invention № RU 202780 U1). The main part of the device is rotameter glass tube - a prototype of human arterial vessel. Electric pump with various modes of work was connected into the closed system with rotameter by flexible silicone tubes. Inside the closed system we introduced an aqueous solution of glycerin diluted to have the same viscosity as the human blood. As indicators for studying the intra-arterial hemodynamics we used intravascular piezoelectric crystal pressure sensor connected to an oscilloscope, 5 mm long silk thread alternately installed inside the tube, and a dye - clerical ink. Results With the electric pump work modes, we were able to imitate the regular heart rhythm (RR) restoration after a period of asystole inside the device for modeling of intra-arterial circulation. We observed the speed of fluid increased in comparison with the RR with the pendency: if longer pause of asystole was than more speed increased. We observed the appearance of reflected, stand waves on the walls of rotameter during the spread of the pulse wave after the long asystole pause. We alternatively put the plastic diaphragm inside the rotameter with internal lumen stenosis of 70% with symmetrical and asymmetrical hole. The speed with a RR was 3.24 m/s, after the pause of asystole 1 s speed was 4.08 m/s, after the pause 2 s speed was 7.36 m/s, after the pause 3 s speed was 9.22 m/s. The pressure measured by piezoelectrical probe increased proportionally to the speed. Conclusion Intense mechanical effect of the pressure waves after the long period of asystole can cause the additional trauma of intima of arterial vessels that can lead to non-stability of atherosclerotic plaques, stimulating of endothelial dysfunction and as a result of atherosclerosis progression with further complications. Changes in hemodynamics we characterized by proposed concept of "hydraulic shock".

Research efficiency of hypothermia prfusion of donor visceral cavities with circulatory arrest to prolong myocardium vital capacity of donor heart in experiment

Introduction. In transplantology, there has always been a problem of organ donor shortage, especially hearts. One of the possible ways to increase the pool of donor hearts is to use donors with circulatory arrest, however irreversible changes in the myocardium after circulatory arrest progress rapidly, which significantly complicates the use of a heart removed from an asystolic donor for transplantation. Objective. To evaluate the effectiveness of hypothermic perfusion of visceral cavities (HPVC) as a method of prolonging the viability of the myocardium of the donor heart during asystole. Materials and methods. The experiments were performed on male rats weighing 200–250 g. The animals were divided into 5 groups, deepening on the duration of HPVC, carried out after a 10-minute period of normothermal asystole: control – 0 min. HPVC and groups with HPVC lasting 30, 60, 90 and 120 min. After complete of perfusion of the heart cavities, they were connected to a Langendorff apparatus to evaluate functional parameters and then determine the volume of necrosis. Results. By the tenth minute of the asystole, the core temperature of the rats’ body was 37.2 ± 0.3 °C. The size of necrosis in the control group was 4.1± 0.6 %. In the groups with a duration of HPVC of 30, 60, and 90 minutes, the size of necrosis was significantly higher than in the control (p<0.05), and was 13.4±3.6 %, 10.3±4.4 % and 14.1±3.4 %, respectively, but there were no difference between these groups. There was a significant increase of the necrosis size in the group with HPVC lasting 120 min compared with the HPVC lasting 90 minutes (24.2±7.1 %, p><0.05). Conclusions. Cold perfusion of the visceral cavities of an asystolic donor, initiated 10 minutes after circulatory arrest, can significantly slow the progression of irreversible myocardial damage in up to 90 minutes, which can expand the potential for the use of hearts from asystolic donors.>< 0.05), and was 13.4±3.6 %, 10.3±4.4 % and 14.1±3.4 %, respectively, but there were no difference between these groups. There was a significant increase of the necrosis size in the group with HPVC lasting 120 min compared with the HPVC lasting 90 minutes (24.2±7.1 %, p< 0.05). Conclusions. Cold perfusion of the visceral cavities of an asystolic donor, initiated 10 minutes after circulatory arrest, can significantly slow the progression of irreversible myocardial damage in up to 90 minutes, which can expand the potential for the use of hearts from asystolic donors.

Transient Asystole Linked to Dexmedetomidine Infusion

This is a case series of five adult patients obtained from the medical intensive care unit in a community teaching hospital between May 2019 through August 2020. These patients were each receiving dexmedetomidine infusion while on invasive mechanical ventilation leading to periods of asystole that resolved after stopping dexmedetomidine infusion in all five patients.

Regulations and Procurement Surgery in DCD Liver Transplantation: The Custodial Role of Professional Societies in the DCD and Liver Perfusion Revolution

We thank Dr Choubey and Dr Ortiz for their interest in and insightful commentary regarding our International Liver Transplantation Society (ILTS) consensus guidelines on regulations and procurement surgery in controlled donation after circulatory death (cDCD) liver transplantation.1,2 Based on logistical and technical as well as ethical complexities associated with cDCD, we agree it is essential to have clear, consistent language describing the cDCD process and organ recovery. This is important to achieving our goals as transplant professionals of not only optimizing graft utilization rates and outcomes but also maintaining a high degree of confidence in our work among the remainder of the medical community and population at large. In their letter, Choubey and Ortiz highlight the importance of limiting donor warm ischemia in recovering organs for transplantation and achieving adequate posttransplantation outcomes. In this regard, we refer the authors to the thorough work performed by our colleagues from the ILTS Working Group on definitions and evaluation of donor warm ischemia times in cDCD.3 With respect to providing more explicit guidance on the minimum no-touch period of electrical or mechanical asystole required for declaring death, we necessarily defer to the directives of our colleagues in anesthesia and critical care. As transplant professionals, our role is to be at the ready but not to influence let alone manage decisions or care at the end of a patient’s life. Coinciding with the focus of the 2020 ILTS Consensus Conference on DCD, Liver Preservation, and Machine Perfusion, Choubey and Ortiz also describe in their letter the fact that greater use of DCD organs will be accompanied by increased use of perfusion technologies. These include not only ex situ modalities hypothermic and normothermic machine perfusion but also in situ normothermic regional perfusion (NRP). While at present, ex situ machine perfusion treats a single organ after a variable length of cold ischemia, NRP restores oxygenated blood flow to the kidneys, liver, and pancreas (abdominal NRP) or all aforementioned organs plus the heart and lungs (thoracoabdominal NRP) immediately following donor cardiac arrest and declaration of death. As such, it effectively converts the period of donor hypoperfusion and arrests into one of ischemic preconditioning, restoring energy substrates, removing metabolic waste products, and increasing levels of endogenous antioxidants before cold preservation and recovery. For the liver, these benefits have translated into the successful transplantation of cDCD livers from older donors or with prolonged donor warm ischemia times, with graft and patient survival rates comparable with those seen with donation after brain death livers and minimal to no ischemic biliary injury observed in published multicenter experiences.4,5 Given current trends, clinical application of cDCD liver transplantation will continue to expand in the coming years. We, as professionals and societies, have an important role as custodians in this process, and we must continue to provide experience-, evidence-, and value-based directives to help guide the DCD and liver perfusion revolution.

Evaluation of the suitability of a donor heart for transplantation after various asystole periods in experiment

The lack of donor hearts for transplantation in patients with end-stage chronic heart failure makes us look for new ways to increase the pool of donors. One of the possible ways to increase the donor base may be the use of asystolic donors, i. e. patients with in-hospital cardiac arrest or patients with cardiac arrest after brain death. The aim of the study was to examine the morphofunctional state of the heart after various periods of normothermic asystole in an experiment on rats. Materials and methods . Experiments were performed on female Wistar rats. After cervical dislocation and registration of respiratory arrest, the body temperature of the rat was maintained above at 36.5±0.5 °C for 10, 15 and 20 minutes, depending on the group. After asystole period, the heart was connected to the Langendorff apparatus to provide perfusion for 90 minutes. During perfusion of the heart, the pulse pressure inside the left ventricle (LVPP) and the volumetric flow rate of coronary perfusion (CP) were recorded every 15 minutes. After the end of the experiment, the volume of necrosis was calculated. Results . In the group with 20-minute ischemia, there was no recovery of ventricular contractions, the volume of necrosis was 34,9±11,7 %. In the group with 15-minute ischemia, the volume of necrosis was 19,5±7,6 %. In the group with 10-minute normothermic ischemia, the volume of necrosis was 13,1±5,1 %. Conclusions . 15 minutes of normothermic cardiac arrest in situ causes irreversible damage to the heart of the animal, which does not allow us to consider it as a potential donor heart. However, this volume of damage to the myocardium and microvasculature, together with the restoration of the contractile activity of the heart, makes this group the main one for the continuation of such experiments using various methods of heart reconditioning.

Ictal Bradyarrhythmia in a 2-Year-Old Male with Brainstem Embryonal Tumor

AbstractIctal bradyarrhythmia can be challenging to diagnose when motor features of seizures are absent. Associated bradycardia can involve periods of asystole requiring cardiac pacemaker placement. Here, we report a 2-year-old male with a brainstem embryonal tumor with more than 30 seizures per day manifesting as bradycardia, loss of tone, and decreased responsiveness, followed by vomiting. Associated electrographic changes were localized to the right temporal head region, where the patient's tumor exerted mass effect. The patient was treated with lacosamide at higher doses than previously reported (24 mg/kg/d) and became seizure-free on a combination of this medication with clobazam. Oral albuterol was also used to augment his heart rate as the patient was not a candidate for cardiac pacemaker insertion.

The yield of long-term electrocardiographic recordings in refractory focal epilepsy.

ObjectiveTo determine the incidence of clinically relevant arrhythmias in refractory focal epilepsy and to assess the potential of postictal arrhythmias as risk markers for sudden unexpected death in epilepsy (SUDEP).MethodsWe recruited people with refractory focal epilepsy without signs of ictal asystole and who had at least one focal seizure per month and implanted a loop recorder with 2‐year follow‐up. The devices automatically record arrhythmias. Subjects and caregivers were instructed to make additional peri‐ictal recordings. Clinically relevant arrhythmias were defined as asystole ≥ 6 seconds; atrial fibrillation < 55 beats per minute (bpm), or > 200 bpm and duration > 30 seconds; persistent sinus bradycardia < 40 bpm while awake; and second‐ or third‐degree atrioventricular block and ventricular tachycardia/fibrillation. We performed 12‐lead electrocardiography (ECG) and tilt table testing to identify non–seizure‐related causes of asystole.ResultsWe included 49 people and accumulated 1060 months of monitoring. A total of 16 474 seizures were reported, of which 4679 were captured on ECG. No clinically relevant arrhythmias were identified. Three people had a total of 18 short‐lasting (<6 seconds) periods of asystole, resulting in an incidence of 2.91 events per 1000 patient‐months. None of these coincided with a reported seizure; one was explained by micturition syncope. Other non–clinically relevant arrhythmias included paroxysmal atrial fibrillation (n = 2), supraventricular tachycardia (n = 1), and sinus tachycardia with a right bundle branch block configuration (n = 1).SignificanceWe found no clinically relevant arrhythmias in people with refractory focal epilepsy during long‐term follow‐up. The absence of postictal arrhythmias does not support the use of loop recorders in people at high SUDEP risk.

LIGHTNING STRIKE: RECOGNITION AND MANAGEMENT

SESSION TITLE: Tuesday Fellows Case Report Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: 10/22/2019 01:00 PM - 02:00 PM INTRODUCTION: While lightning strike injuries are uncommon in clinical practice, these cause approximately 100 deaths and 300 injuries a year. Though 66% of the fatalities occur in the first hour due to arrhythmia or respiratory failure, substantial organ dysfunction can occur afterward. These include severe burn complications, deep tissue injury, rhabdomyolysis, seizures, cognitive impairment, otic abnormalities and ophthalmologic injury. Furthermore, 74% of survivors from strikes have permanent disabilities with a wide range of manifestations (1). CASE PRESENTATION: A 21-year-old man working on water hoses near a fire station had a witnessed collapse with prompt initiation of resuscitative efforts. En route to the emergency room and subsequently to the ICU, four tonic-clonic seizures were witnessed. Initial physical examination showed elevated temperature and blood pressure with a normal heart rate, an erythematous serpiginous rash from left head to the opposite foot where it ended in a caustic open wound, unilateral tympanic membrane rupture and pre-retinal macular hemorrhage. Labs demonstrated a leukocytosis, elevated liver enzymes, creatinine, creatinine kinase, and troponin. Electrocardiogram showed sinus arrhythmia without ischemia. Given the constellation of findings, a diagnosis of lightning strike was made. The patient was treated with fluid resuscitation, targeted temperature management and anti-seizure medications. He had numerous early sub-specialty consultations including trauma surgery, neurology, ophthalmology, otolaryngology, and dermatology. He was extubated on hospital day 9 and discharged on hospital day 18 neurologically intact. DISCUSSION: Cardiopulmonary stability is critical to prevent early mortality. The electrical impulse causes synchronous myocardial contraction followed by a variable period of asystole, causing ischemia and arrhythmias. Respiratory arrest is presumed to be a consequence of inhibition of the medullary respiratory center (2). Patients can have extensive, high degree burns that require specialist care. Interventions include aggressive fluid hydration, debridement and topical wound care. Muscle necrosis can lead to compartment syndrome, rhabdomyolysis and kidney injury. The central nervous system effects include autonomic instability, impaired consciousness, amnesia, seizures, tympanic membrane rupture, and ocular hemorrhage. Lasting ocular effects are common as 6% develop cataracts in the first year and a smaller population developing them within 3 years (3). CONCLUSIONS: The chances of a lightning strike are 1 in 500,000, conferring significant morbidity and mortality (1). Most practitioners have minimal experience with these injuries, affecting diagnosis and management. The effect of a lightning strike can damage numerous organ systems making it imperative to recognize different types of dysfunction for treatment of immediate injuries and long-term sequelae. Reference #1: “Lightning | CDC.” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, www.cdc.gov/disasters/lightning/index.html. Reference #2: Hiestand D, Colice GL. Lightning-strike injury. Journal of Intensive Care Medicine. 1988 Nov;3(6):303-14. Reference #3: Wesner ML, Hickie J. Long-term sequelae of electrical injury. Canadian family physician. 2013 Sep 1;59(9):935-9. DISCLOSURES: No relevant relationships by James Bardwell, source=Web Response No relevant relationships by Bhupinder Natt, source=Web Response No relevant relationships by Alan Nyquist, source=Web Response

Blood clotting behavior is innately modulated in Ursus americanus during early and late denning relative to summer months.

Remarkably, American black bears (Ursus americanus) are capable of varying their heart rates to coincide with their breathing, creating pauses of 30 s or more, yet they do not appear to suffer from embolic events. We evaluated some features of the clotting cascade of black bears, providing novel insights into the underlying mechanisms they evoke for embolic protection during hibernation. We measured activated clotting time, prothrombin time and activated partial thromboplastin time during early denning (December), late denning (March) and summer (August). Activated clotting time during early hibernation was ∼3times longer than that observed among non-hibernating animals. Clotting time was reduced later in hibernation, when bears were within ∼1 month of emerging from dens. Prothrombin time was similar for each seasonal time point, whereas activated partial thromboplastin time was highest during early denning and decreased during late denning and summer. We also examined D-dimer concentration to assess whether the bears were likely to have experienced embolic events. None of the non-parturient bears exceeded a D-dimer concentration of 250 ng ml-1 (considered the clinical threshold for embolism in mammals). Our findings suggest there is unique expression of the clotting cascade in American black bears during hibernation, in which extrinsic pathways are maintained but intrinsic pathways are suppressed. This was evaluated by a significant difference between the activated clotting time and activated partial thromboplastin time during the denning and non-denning periods. These changes are likely adaptive, to avoid clotting events during states of immobilization and/or periods of asystole. However, an intact extrinsic pathway allows for healing of external injuries and/or foreign body responses.

Lipid emulsion pretreatment has different effects on mepivacaine and bupivacaine cardiac toxicity in an isolated rat heart model

The use of lipid emulsions to reduce cardiac toxicity of local anaesthetics (LAs) has shown success in experimental studies and some clinical cases, and thus has been implemented in clinical practice. However, lipid treatment is usually given after the occurrence of neurological or cardiovascular symptoms of systemic intoxication. The aim of this study was to determine if pretreatment with lipid emulsion reduces cardiac toxicity produced by bupivacaine or mepivacaine. Isolated rat hearts were perfused with or without lipid emulsion (0.25 ml kg(-1) min(-1)) before administration of equipotent doses of bupivacaine (250 µM) or mepivacaine (1000 µM). Haemodynamic parameters and times from start of perfusion LA to a 1 min period of asystole and recovery were determined. Pretreatment with lipid emulsion extended the time until occurrence of asystole and decreased times to recovery in bupivacaine-induced cardiac toxicity but not in mepivacaine-induced cardiac toxicity compared with control. Lipid pretreatment impaired rate-pressure product recovery in mepivacaine-intoxicated hearts. This study confirms that pretreatment with a lipid emulsion reduces cardiac toxicity of LAs. The efficacy of pretreatment with lipid emulsion was LA-dependent, so pharmacokinetic properties, such as lipophilicity, might influence the effects of lipid emulsion pretreatment.

Sinus Arrest and Asystole Caused by a Peripherally Inserted Central Catheter

Transient bradycardia in the critical care setting is frequently caused by hypoxemia or oropharyngeal manipulation. Central lines have been associated with a variety of cardiac arrhythmias, but sinus arrest and asystole have not been previously reported. A 38-year-old woman with multisystem organ failure had several episodes of prolonged sinus arrest, slow junctional escape rhythm, and periods of asystole lasting over 6 seconds. The cause of the repetitive bradyarrhythmia was evaluated by clinical observation including the response to parasympatholytic agents, by detailed analysis of rhythm strips, and review of cardiac imaging studies. The episodes of bradycardia did not coincide with orotracheal manipulation, were not prevented by escalating doses of glycopyrrolate, and were not accompanied by AV conduction disturbance as is frequently seen during a transient increase in vagal tone. Review of the patient's chest X-ray and chest CT revealed that the tip of a peripherally inserted central catheter migrated to the vicinity of the sinoatrial node. Removal of the catheter resulted in prompt resolution of the episodes of sinus arrest. This case demonstrates that migration of a peripherally inserted central catheter to the sinoatrial node can provoke prolonged sinus bradycardia, sinus arrest and asystole.

Cardiac asystole following cannabis (marijuana) usage – Additional mechanism for sudden death?

A 21 year old university student previously operated during infancy for an unobstructed total anomalous pulmonary venous drainage with an excellent result, was noted on a routine follow up 24h Holter monitor to have multiple pauses related to cardiac asystole, the longest lasting 5.8s and temporally related to marijuana inhalation. A repeat Holter was normal following a two week cessation of marijuana usage and again when carried out 3 months later. The documented periods of asystole may be a precursor of sudden death seen in addicts even without evidence of ischaemic heart disease.

Video Microscopy Detection of Oyster Spat Heart Rate (HR): Acclimation temperature alters HR response to acute temperature change

We developed a non‐invasive method to measure oyster spat heart rate (HR) during a cooling/warming protocol. Triploid spat (1.1–1.8mm; 3–4 months) were acclimated to 10°C (“cool”; n=5) or 22°C (“hatchery”; n=5), and exposed to a temperature ramp protocol (22°C to 10°C to 22°C; 2°C intervals, 10 minutes per set‐point). Hearts were visualized using video acquisition/image analysis, and HR identified by commercially‐available software. HR was directly related to temperature in both groups. HR at each set‐point did not vary between cooling/warming; however, “hatchery” spat displayed consistently elevated HR vs. “cool” spat. Heart rate variability (HRV) was inversely related to temperature in both groups. “Cool” spat consistently displayed elevated HRV vs. “hatchery” spat, and displayed greater HRV during cooling vs. warming. Spat also displayed periods of asystole of varying lengths, which were more prevalent and prolonged at low temperatures, (“hatchery”: 5/5 asystolic at set‐point 10°C, vs. “cool”: 1/5 asystolic at set‐point 10°C). Our method provides a robust means of assessing HR in a simple, invertebrate model. Our data suggest that the HR phenotype of commercial oyster spat is altered by different acclimation temperatures, which may be useful in understanding spat thermal adaptation and growth in ocean aquaculture environments.

The Importance of Cardiac Monitoring in the Epilepsy Monitoring Unit: A Case Presentation of Ictal Asystole

ABSTRACT.Ictal asystole may be a potent marker for epilepsy patients at high risk for sudden unexpected death in epilepsy (SUDEP). The use of inpatient long-term video-electroencephalographic (VEEG) monitoring coupled with simultaneous continuous cardiac telemetry is an important tool to detect ictal asystole as well as other significant ictal cardiac arrhythmias. In this paper a case of ictal asystole detected during VEEG is presented. Routine 12-lead EKG was normal upon admission. After antiepileptic medication was tapered, the patient had a typical complex partial seizure with oral automatisms at onset followed by secondary generalization. Ictal onset was noted in left temporal lobe with subsequent spread to the right temporal region. A 20 second period of asystole began just prior to the secondary generalization. During this admission the patient underwent a potentially life-saving pacemaker implantation. The use of cardiac telemetry and baseline EKG are suggested for patients admitted into epilepsy monitoring units as part of the standard epilepsy monitoring protocol.

Asystole Following Complex Partial Seizures

A case is presented of a patient with a long history of epilepsy who presents with recurrent seizures and develops a period of asystole. The case highlights the need to consider the potential arrhythmic complications of seizures and the clinical characteristics that may be present in those with epilepsy that may warrant evaluation for arrhythmias.

POST‐EXERCISE HYPERPNEA AND CARDIAC ASYSTOLE

We have recently reported that, in resting conditions, spontaneous eupneic respiration is maintained following a cardiac arrest (CA) in humans and in an animal model of ventricular fibrillation. This response deprived from any relevant role in arterial blood gas homeostasis, as circulation is abolished, still results in the production of a low level of rhythmic arterial blood pressure and in a reduction in alveolar PCO2. We are reporting here that, in a sheep model, the ventilatory control system retains during a CA the fundamental property of maintaining breathing, for 70± 41 seconds, in proportion to the level of metabolism preceding the period of asystole. As a result, ventilation persists during CA following muscle contractions but at a much higher level than at rest, despite the lack of pulmonary blood flow and cardiac output. We discuss the view that this response could be the expression of a yet unrecognised rudimentary defence mechanism aimed at limiting the consequences of an acute failure of the cardiac pump in mammals. Moreover, this “protective” response is not predictable from the traditional respiratory control feedback systems thought to be involved during exercise or its recovery.

Protocols for uncontrolled donation after circulatory death

Organ shortages have led some countries, including Spain, France, and the USA, to start programmes of uncontrolled donation after circulatory death. 1 Wall SP Kaufman BJ Gilbert AJ et al. Derivation of the uncontrolled donation after circulatory determination of death protocol for New York City. Am J Transplant. 2011; 11: 1417-1426 Crossref PubMed Scopus (58) Google Scholar In these protocols, donors are people who have had unexpected out-of-hospital cardiac arrest. After ordinary life support attempts (30 min of advanced cardiopulmonary resuscitation [CPR]) by an emergency medical service are judged futile, patients are transported to the hospital with continuing mechanical chest compression and other interventions to preserve the organs, and declared dead at the hospital after a no-touch period of asystole (usually 5 min). Then, normothermic extracorporeal membrane oxygenation (ECMO) or in-situ cooling is started to preserve the organs until authorisation for donation is given by the family. 1 Wall SP Kaufman BJ Gilbert AJ et al. Derivation of the uncontrolled donation after circulatory determination of death protocol for New York City. Am J Transplant. 2011; 11: 1417-1426 Crossref PubMed Scopus (58) Google Scholar

Breathing during cardiac arrest following exercise: A new function of the respiratory system?

We have found in four sheep that, following a muscular exercise, minute ventilation is maintained for 34–131s during a cardiac arrest (CA), at a magnitude (from 28.2 and 54.7lmin−1) similar to the level of ventilation (and thus proportional to the metabolic rate) preceding the period of asystole. Breathing was maintained despite the lack of pulmonary blood flow and the cessation of the muscle contractions, leading to a dramatic reduction in alveolar FCO2 (1.9±1%). Secondly, swings in arterial blood pressure (ABP) were observed (pulse pressure of 31±3Torr) in phase with breathing movements in place of the cardiac activity. This “protective” response, deprived from any role in blood gas homeostasis, as circulation is virtually abolished, is not predictable from the traditional respiratory control feedback systems thought to be involved in exercise. We are presenting the view that this response, dissociated from the pulmonary gas exchanges, is the expression of a rudimentary defense mechanism aimed at limiting the consequences of an acute failure of the cardiac pump by the thoraco-abdominal pump.

Wolff-Parkinson-White Syndrome and myocardial infarction in ventricular fibrillation arrest: a case of two one-eyed tigers

A 42-year-old man was carrying a set of goalposts at his son's football match when he slumped against a fence and collapsed. Two off-duty nurses commenced cardiopulmonary resuscitation (CPR) and called an ambulance. When the crew arrived, ventricular fibrillation (VF) was identified and the patient was defibrillated (Figure 1). After a short period of asystole, he reverted into sinus rhythm. He was admitted to the hospital for further assessment. Figure 1. Electrocardiogram showing ventricular fibrillation, defibrillation and asystole. The patient made a rapid neurological recovery and was conscious on arrival. He had felt unwell and experienced palpitation only for a few seconds prior to collapse, but had no chest pain or other cardiovascular or neurological symptoms. He described intermittent and self-resolving palpitation when he was in his teens, which was not investigated. He had previously undergone treatment for Helicobacter pylori and gastroesophageal reflux disease, and had had three minor head injuries in the previous month. He took no medications, and had no significant family history. He was an ex-smoker, having stopped 8 years before. He normally drank ∼16 U of alcohol per week, although on the evening prior to admission he had consumed six cans of lager (∼16 …