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Cardiovascular Drugs during Pregnancy
Published in “Bert” Bertis Britt Little, Drugs and Pregnancy, 2022
Ventricular tachycardia is a life-threatening arrhythmia. It may lead to ventricular fibrillation, cardiac decompensation, and death. This arrhythmia type is encountered infrequently during pregnancy, and is especially infrequent in the absence of specific cardiac disease (e.g., myocardial infarction). Therapy is primarily electric cardioversion, especially if the patient has hemodynamic instability. Lidocaine (75–100 mg IV bolus followed by 1–4 mg/min infusion) should be given in conjunction with countershock and as initial therapy in the stable patient (Brown and Wendel, 1989). Lidocaine, procainamide, or bretylium may be used to prevent recurrence of tachycardia.
Circulation
Published in Kelvin Yan, Surgical and Anaesthetic Instruments for OSCEs, 2021
Defibrillation is the only effective treatment for ventricular fibrillation. An automated external defibrillator allows the restoration of sinus rhythm through breaking the cycle of uncoordinated ventricular depolarisations thereby allowing the sinus atrial node to re-establish the sinus rhythm through coordinated depolarisations. It is also used to treat pulseless ventricular tachycardia.
Obstetrics: Answers
Published in Euan Kevelighan, Jeremy Gasson, Makiya Ashraf, Get Through MRCOG Part 2: Short Answer Questions, 2020
Euan Kevelighan, Jeremy Gasson, Makiya Ashraf
Attach 2 adhesive pads and connect to machine.If shock advised make sure ‘all clear’.Ventricular tachycardia and ventricular fibrillation.
A critical review of fosphenytoin sodium injection for the treatment of status epilepticus in adults and children
Published in Expert Review of Neurotherapeutics, 2022
Jordan L. Clay, Nathan B. Fountain
IV infusion of PHT is also associated with cardiovascular adverse effects when infused at rates greater than 50 mg/min in previously healthy adults or greater than 25 mg/min in those with preexisting cardiovascular disease [34,39]. Possible effects include hypotension, cardiac conduction depression, and ventricular fibrillation. It has been suspected that the propylene glycol vehicle present in the parenteral formulation of PHT is in part responsible for these effects [34]. Overall rates of systemic adverse effects with IV fPHT vary across studies and have ranged from 0 to 20.9%, with paresthesia being the most frequently reported [46,51–53]. IV fPHT was associated with no clinically significant cardiac arrhythmias in early pharmacokinetic and safety studies in adults [27,37,38,46] or in the later Established Status Epilepticus Treatment Trial (ESETT) which included 125 children and adults in the IV fPHT treatment arm [51,52]. Clinically insignificant decreases in systolic and diastolic blood pressure were noted with IV fPHT in the earlier clinical safety and tolerability studies [38]; 3.5% of patients had life-threatening hypotension within 60 min of initiation of fPHT in the ESETT; however, this was not significantly different than VPA and LEV arms of the study [51,52].
Comparison of de novo versus upgrade cardiac resynchronisation therapy on clinical effect and long-term outcome
Published in Acta Cardiologica, 2021
Jan Stassen, Martijn Scherrenberg, Dagmara Dilling-Boer, Johan Vijgen, Pieter Koopman, Joris Schurmans, Lieven Herbots, Jan Verwerft, Matthew Schroyens, Philippe Timmermans
Evolution in NYHA functional class and echocardiographic response [difference in left ventricular ejection fraction (Δ LVEF) and left ventricular end diastolic diameter (Δ LVEDD)] were collected at 6 months. A clinical response was defined as an improvement of at least 1 NYHA functional class. Potential life-threatening ventricular arrhythmias were collected during long-term follow-up and were defined as the occurrence of sustained ventricular tachycardia (>30 s) not requiring therapy or appropriate therapy for ventricular tachycardia/ventricular fibrillation. Furthermore, 1-year and long-term mortality were collected and further categorised into cardiac death and non-cardiac death. Vital status was checked via the electronic health record that is linked to a national death registry (‘Belgian National Register Number’). The exact mode of death was retrieved from the patient’s individual EMR. For patients who died outside the hospital, mode of death was retrieved through information from the primary care physician if this was recorded in the individual EMR. In all other cases, mode of death was recorded as ‘unknown’. Sudden cardiac death (SCD) was defined as death due to electromechanical dissociation without a shockable rhythm or unexpected death during sleep. Tachyarrhythmic death was defined as death due to documented ventricular tachycardia or ventricular fibrillation.
Devices to enhance organ perfusion during cardiopulmonary resuscitation
Published in Expert Review of Medical Devices, 2021
Matthew A. Bridges, Julie B. Siegel, Joshua Kim, Kristen M. Quinn, Jennie H. Kwon, Brielle Gerry, Taufiek Konrad Rajab
Cardiac arrest is one of the leading causes of morbidity and mortality in the US. In 2019, more than 356,000 people experienced an out-of-hospital cardiac arrest (OHCA) with an overall survival rate of only 10% [1]. A contributing factor to these dismal outcomes is the poor perfusion of vital organs during cardiac arrest. Cardiopulmonary resuscitation (CPR) is the American Heart Association (AHA) recommended treatment for emergent cardiac arrest with the goal of providing circulatory support via chest compressions and ventilatory support via rescue breaths. Without CPR, the survival rate of witnessed cardiac arrest from ventricular fibrillation decreases by 7–10% per minute; however, when CPR is administered, the survival rate decreases by only 3–4% per minute from the time of collapse to defibrillation [2]. The increase in survival is due to perfusion of vital organs, most importantly the heart and the brain, as these tissues have the lowest tolerance to ischemia. In animal models, when the focus of CPR is on increasing coronary perfusion pressure (CPP) and cerebral perfusion pressure (CerePP), survival from cardiac arrest increases [3–5].