Out-of-hospital sudden cardiac arrest is a major public health problem with an overall survival of less than 5%. Upon cardiac arrest, cessation of coronary blood flow rapidly leads to intense myocardial ischemia and activation of the sarcolemmal Na+-H+ exchanger isoform-1 (NHE-1). NHE-1 activation drives Na+ into cardiomyocytes in exchange for H+ with its exchange rate intensified upon reperfusion during the resuscitation effort. Na+ accumulates in the cytosol driving Ca2+ entry through the Na+-Ca2+ exchanger, eventually causing cytosolic and mitochondrial Ca2+ overload and worsening myocardial injury by compromising mitochondrial bioenergetic function. We have reported clinically relevant myocardial effects elicited by NHE-1 inhibitors given during resuscitation in animal models of ventricular fibrillation (VF). These effects include: (a) preservation of left ventricular distensibility enabling hemodynamically more effective chest compressions, (b) return of cardiac activity with greater electrical stability reducing post-resuscitation episodes of VF, (c) less post-resuscitation myocardial dysfunction, and (d) attenuation of adverse myocardial effects of epinephrine; all contributing to improved survival in animal models. Mechanistically, NHE-1 inhibition reduces adverse effects stemming from Na+–driven cytosolic and mitochondrial Ca2+ overload. We believe the preclinical work herein discussed provides a persuasive rationale for examining the potential role of NHE-1 inhibitors for cardiac resuscitation in humans.

ABSTRACT Exsanguination leading to cardiac arrest is the terminal phase of uncontrolled hemorrhage. Resuscitative interventions have focused on preload and afterload support. Outcomes remain poor due to several factors but poor coronary perfusion undoubtedly plays a role. The aim of this study is to characterize the relationship between arterial pressure and flow during hemorrhage in an effort to better describe the terminal phases of exsanguination.Male swine weighing 60 kg to 80 kg underwent splenectomy and instrumentation followed by a logarithmic exsanguination until asystole. Changes in hemodynamic parameters over time were compared using one-way, repeated measures analysis of variance.Nine animals weighing 69 ± 15 kg were studied. Asystole occurred at 53 ± 13 min when 52 ± 11% of total blood volume has been shed. The greatest fall in mean hemodynamic indices were noted in the first 15 min: SBP (80-42 mm Hg, P = 0.02), left ventricular end-diastolic volume (94-52 mL, P = 0.04), cardiac output (4.8-2.4 L/min, P = 0.03), coronary perfusion pressure (57-30 mm Hg, P = 0.01), and stroke volume (60-25 mL, P = 0.02). This corresponds to the greatest rate of exsanguination. Organized cardiac activity was observed until asystole without arrythmias. Coronary flow was relatively preserved throughout the study, with a precipitous decline once mean arterial pressure was less than 20 mm Hg, leading to asystole.In this model, initial hemodynamic instability was due to preload failure, with asystole occurring relatively late, secondary to failure of coronary perfusion. Future resuscitative therapies need to directly address coronary perfusion failure if effective attempts are to be made to salvage these patients.

The rate of out-of-hospital cardiac arrest is increasing according to the changes in the proportion of ages in super-aged society. We developed a novel transcutaneous cannulation-type mechanical circulatory system for an alternative therapeutic approach to cardiac arrest using a small centrifugal blood pump. We proposed a transcutaneous mechanical circulatory support capable of rapid installation and quick start of circulatory support for recovery after cardiac arrest by left ventricular direct puncture using the Seldinger technique. The cannula consisted of three components as follows: a) a double-layered cylindrical blood pump housing, b) a centrifugal blood pump impeller primarily installed inside of the cannula, and c) an insertable actuator with magnet coupling. The special feature of the cannula inflow was a backflow resistive unit for adjusting backflow in the process of ventricular puncture. In this study, we performed an in vivo experiment to install the direct cannulation centrifugal blood pump on a goat after cardiac arrest induced by ventricular fibrillation as a proof of concept. As a primary result, the mechanical circulatory support could start in a short period by around one minute installation from the start of cannulation, which could be effective for the recovery after cardiac arrest under the assisted flow of 1.6 L/min at 13,000 rpm of the cannulation pump. Consequently, the novel approach may be useful for the prompt start of mechanical circulatory support.

ventricular fibrillation (VF, or V-fib) can lead to death within minutes. When a heart goes into V-fib, effective pumping of the blood stops. V-fib is considered Arrhythmias, also known as cardiac arrhythmias, are irregularities in the heartbeat, including when it is too fast or too slow. Essentially, this is anything but normal sinus rhythm. A resting heart rate that is too fast – above 100 beats per minute in adults – is called tachycardia, and a resting heart rate that is too slow – below 60 beats per minute – is called bradycardia. Some types of arrhyt Atrial fibrillation affects the upper chambers of the heart, known as the atria. Atrial fibrillation may be due to serious underlying medical conditions and should be evaluated by a physician. It is not typically a medical emergency. Ventricular fibrillation occurs in the ventricles (lower chambers) of the heart; it is always a medical emergency. If left untreated, ventricular fibrillation (VF, or V-fib) can lead to death within minutes. When a heart goes into V-fib, effective pumping of the blood stops. V-fib is considered a form of cardiac arrest. An affected individual will not survive unless cardiopulmonary resuscitation (CPR) and defibrillation are provided immediately. CPR can prolong the survival of the brain in the lack of a normal pulse, but defibrillation is the only intervention that can restore a healthy heart rhythm. Defibrillation is performed by applying an electric shock to the heart, which resets the cells, permitting a normal beat to re-establish itself.

Abstract Sudden Cardiac Arrest (SCA) is a case that made the heart stop pumping the blood. Ventricular fibrillation (VF) and ventricular tachycardia (VT) are the major causes that lead to cardiac arrest. To treat SCA, a defibrillator device is used to return the heart to its normal sinus rhythm. The main generation of the defibrillator is the manual type which has many limitations involved., It requires the physician’s instruction to determine the patient state and the amount of joule required; therefore, it is preferable to design an auto defibrillator. The aim of this paper is to design a hardware implementation system of auto dc-shock utilized in the emergency case for diagnosing patient case and recovering the normal state of the heart. This prototype consists of five main parts, including the diagnosing system, high voltage section, charging unit, discharging unit, and safety unit. The output of diagnosing system is followed by charging and discharging period in order to get a suitable amount of joule according to patient situation of 50, 100, 120, and 150 joule discharged on the patient body by using a biphasic system provided by safety mode circuit so that the discharge process automatically happens in the case of not discharged on the patient body. The proposed diagnosing system in hardware design was tested on several patients in Ibn al-Nafis hospital and healthy patients at home and the accuracy was achieved of 97.03%, specificity is 97.8%, and the detection error r

Abstract Sudden cardiac arrest is a situation in which the heart stop pumping the blood. Ventricular fibrillation and ventricular tachycardia are the major causes that lead to cardiac arrest. To treat sudden cardiac, a defibrillator device is used to return the heart to its normal sinus rhythm. There are several types of defibrillator, such as the manual type, which has many disadvantages since it requires the physician‘s instruction to determine the patient state and the amount of joule required; therefore, it is preferable to use auto defibrillator. In this paper propose to design a flyback converter which is the basic part of the defibrillator with a controller in feedback which can make a comparison between normal and abnormal ECG signals and give appropriate decision to defibrillator, simultaneously, the source of ECG signals will be taken from Physio bank database, then processed in Matlab for removing different types of noise and get a peak of signal, heart rate, in order to determine the patient state and required level of the shock. This design has accuracy 95 % with an error detection rate 5%.

<h4>Aims</h4>Long-term arrhythmic risk after myocarditis remains uncertain, and optimal management is debated. We aimed to assess the incidence and predictors of major arrhythmic events (MAEs) after myocarditis.<h4>Methods and results</h4>We conducted a systematic literature review and meta-analysis including 19 observational studies on myocarditis and MAEs during follow-up. Major arrhythmic events were defined as a composite of sudden cardiac death (SCD), ventricular fibrillation (VF), aborted cardiac arrest (ACA), sustained ventricular tachycardia (sVT), and appropriate implantable cardioverter defibrillator (ICD) or wearable-cardioverter defibrillator (WCD) intervention. The primary outcome was the incidence of MAEs after discharge; secondary outcomes included occurrence of each component of MAEs and the composite of all-cause mortality or heart transplantation (HTx). Three thousand nine hundred and fifty-four patients (71% male, 67% acute, 88% complicated myocarditis) were included. At presentation, 15% had high-grade atrioventricular block (AVB), 31% heart failure, 38% MAEs. At a median follow-up of 24 months (interquartile range 19-57), 28% suffered MAEs, with a median time of presentation of 12 months. The incidence of sVT, ACA/VF, appropriate ICD/WCD intervention, and SCD were 22%, 6%, 20%, and 1%, respectively. The combined rate of all-cause mortality/HTx was 11%. At meta-regression analysis, high-grade AVB, MAEs at presentation, and fulminant myocarditis were associated with higher risk of MAEs during follow-up, while male gender resulted as a protective factor.<h4>Conclusion</h4>The incidence of MAEs after a complicated acute myocarditis can be high over time. Further prospective studies are needed to better stratify high-risk patients, identify those with an underlying arrhythmogenic cardiomyopathy, and guide antiarrhythmic strategies.

<h4>Rationale</h4>Aconitine, a highly toxic alkaloid derived from Aconitum plants, exhibits a narrow therapeutic window, with a poisonous dose as low as 0.2 mg and lethal dose of 2 to 5 mg. Currently, no specific antidote exists for aconitine poisoning, which frequently triggers refractory electrical storms and cardiopulmonary arrest, culminating in high mortality. Elderly patients face particularly dire prognoses due to diminished physiological reserves. This study evaluated the efficacy of extended cardiopulmonary resuscitation (CPR) combined with hemoperfusion (HP) as a rescue strategy for aconitine-induced cardiac arrest.<h4>Patient concerns</h4>A 90-year-old female presented to the emergency department with a 2-hour history of dizziness, palpitations, and generalized numbness, followed by impaired consciousness after accidental ingestion of aconitine-containing medicinal wine. On admission, the patient exhibited respiratory failure, circulatory collapse, and malignant arrhythmias, including sustained ventricular tachycardia and fibrillation, which rapidly progressed to cardiac arrest.<h4>Diagnoses</h4>The patient was diagnosed with acute severe aconitine poisoning complicated by cardiopulmonary arrest based on a history of exposure, characteristic clinical manifestations, and electrocardiographic findings.<h4>Interventions</h4>A multidisciplinary rescue protocol was immediately implemented: endotracheal intubation and mechanical ventilation were performed, followed by continuous high-quality CPR using a Lund University Cardiopulmonary Assist System mechanical resuscitation device for a cumulative duration exceeding 200 minutes. Once CPR has established effective circulatory support, HP therapy should be initiated immediately to remove toxins from patient circulation. Combination of pharmacotherapy with antiarrhythmic agents (amiodarone and lidocaine) and vasoactive support (norepinephrine) to stabilize rhythm and perfusion.<h4>Outcomes</h4>After prolonged resuscitation and multimodal detoxification, the patient's electrical storm resolved, with restoration of sinus rhythm. She regained consciousness on hospital day 3, was successfully extubated on day 4, and was discharged after 16 days without significant neurological deficits. A 3-month follow-up confirmed sustained recovery of cardiopulmonary and cerebral function.<h4>Lessons</h4>This case demonstrates that extended high-quality CPR combined with HP is a feasible and effective intervention for aconitine poisoning-related cardiac arrest, particularly when conventional antiarrhythmic and electrical therapies fail. Success depends on early recognition, persistent resuscitation, and integrated toxin removal strategies.