DOCSLIB.ORG

Cardiac Arrest and Ventricular Fibrillation * a Method of Treatment by Electrical Shock

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Cardiac Arrest and Ventricular Fibrillation * a Method of Treatment by Electrical Shock Thorax: first published as 10.1136/thx.7.3.205 on 1 September 1952. Downloaded from Thorax (1952), 7, 205. CARDIAC ARREST AND VENTRICULAR FIBRILLATION * A METHOD OF TREATMENT BY ELECTRICAL SHOCK BY I. K. R. MCMILLANt F. B. COCKETT, AND P. STYLES Froml the Departnment of Cardiology, tile Professorial Surgical Unit, and tile Departalzent of Phlysical Medicine, St. Thomlas's Hospital, London (RECEIVED FOR PUBLICATION APRIL 30, 1952) Cardiac arrest during operation is a subject of VENTRICULAR FIBRILLATION importance to all surgeons. During intra-thoracic The treatment of ventricular fibrillation bv operations cardiac arrest and ventricular fibrilla- electrical shock therapy is not new and was first tion can be differentiated by direct observation of tried experimentally in 1899 (Prevost and Battelli). the heart. In recent years this method has been extensively Ventricular fibrillation is an incoordinated type investigated in the United States and France of contraction which produces no useful beats. (Kouwenhoven and Kay, 1951; Johnson and The typical rippling movements of the ventricular Kirby, 1951 ; Santy and Marion, 1950). muscle are unmistakable when seen or felt with The treatment of ventricular fibrillation by the hand directly on the heart. The treatment of zlectrical shock gives encouraging results in the copyright. a heart that has stopped is cardiac massage and experimental animal, and may be a useful adjunct adequate oxygenation. The treatment of ventri- in the operating theatre during cardiac and general cular fibrillation which we recommend is, first, surgery. Under these conditions shock therapy massage to maintain the oxygen supply to the can be rapidly applied. Provided that adequate heart through the coronary arteries, followed oxygenation is maintained and direct cardiac mas- http://thorax.bmj.com/ rapidly by electrical shocking to restore normal sage promptly initiated and maintained, shock rhythm therapy can be applied without undue haste. In abdominal operations, however, or during operations elsewhere in the body, once the pulse METHOD becomes undetectable most surgeons waste no time The principle of the method is to apply a powerful in performing a quick midline upper abdominal shock across the ventricles and produce complete incision and massaging the heart through the dia- arrest of the fibrillating heart. Once asystole occurs phragm. At the same time adrenaline is given a regular ventricular beat may start spontaneously or either intravenously, intramuscularly, or more cardiac massage may be needed to initiate it. on September 27, 2021 by guest. Protected usually directly into the ventricle. The latter is The apparatus comprises a double-wound trans- a most dangerous procedure, as it is now known former having a tapped secondary capable of supply- that one of the effects of adrenaline on a heart ing I ampere from any tapping. The primary circuit is supplied from 50 c/s mains via a foot-operated which is already anoxic may be the production of switch and a Londex motor-driven interrupter whose ventricular fibrillation. Until recent years ventri- contacts close every 1.5 seconds for 0.5 second. cular fibrillation was almost always fatal. The output voltage tappings are selected by means The purpose of this paper is twofold: (1) to of a rotary switch on the front panel. Available emphasize once again the dangerous effects of voltages are 85, 125, 185, 250. 270, and 300. A buzzer to describe the lead- operated from an auxiliary winding on the transformer adrenaline ; (2) experiments gives an audible warning that the electrodes are alive. ing up to the development of a satisfactory elec- Closure of the mains switch merely sets in motion the trical instrument for defibrillating the heart. interrupter. In order to administer a shock the foot * This work was assisted by a grant from the Endowment Fund of switch must be depressed. St. Thomas's Hospital. The consist t MacKenzie MacKinnon Research Fellow of the Royal College electrodes of two large curved plates of Physicians and the Royal College of Surgeons. which are shaped to fit the curve of the ventricles. 0 Thorax: first published as 10.1136/thx.7.3.205 on 1 September 1952. Downloaded from 206 1. K. R. McMILLAN, F. B. COCKETT, and P. STYLES FOOT SWITCH Another dog in which ven- tricular fibrillation occurred during a thoracic sympath- ectomy failed to revert to normal, probably because of inadequate oxygenation owing to of both -0 0 SELECTOR E.C.G.scollapsetaken after lungs.defibrilla- MAINS ° tion in one dog showed a regu- _ELECTRODES lar rhythm (Fig. 3). After electrical shocking sections of BUZERINDACTTOINICATOICATO ventricular muscle show some E______ superficial coagulation but no burning. Ventricular fibrilla- FIG. I .-Circuit diagram. tion is a terminal event, and any procedure with a chance The voltage required varies with the size of the heart of success is worth attempting in spite of possible and its electrical resistance, and this latter factor is minor damage. Later experiments with large elec- also governed by the efficiency of the contact between trodes showed no coagulation or burning. electrodes and heart surface. Single shocks may be sufficient to stop ventricular fibrillation or, if they are insufficient, the voltage may be increased and further RESULTS IN MAN single shocks applied. If these are still inadequate Case 1.-Mrs. T., aged 65 years, who had been a series of about six shocks at 1.5-second intervals attending as an out-patient, had gross left ventricular may be given (Wiggers, 1940). enlargement, anginal attacks, and multiple ventricular extrasystoles. During a visit to the hospital she RESULTS IN DoGs collapsed while climbing a flight of stairs. She was All dogs were under nembutal anaesthesia. found to be pulseless and respiration had almost stopped. She was put on a couch, and within copyright. three Seven dogs were given ventricular fibrillation elec- minutes the upper abdomen was opened and sub- trically by means of an induction coil. Three dogs diaphragmatic cardiac massage started. The heart have been given ventricular fibrillation by the appli- then started to beat again, but weakly, and soon cation of aconitine (one drop 0.2% solution in faded away. She was intubated and oxygen given benzene) to the auricle, which causes auricular by means of controlled respiration from an anaes- fibrillation and later ventricular fibrillation. To thetic apparatus. Next the diaphragm was incised, defibrillate the heart of a 20-kg. dog 185 volts was the pericardium was entered, and direct cardiachttp://thorax.bmj.com/ sufficient when given in a series of five shocks. massage started. A few minutes later, as the strength Nine dogs have been successfully defibrillated at of the -beat was poor, adrenaline (1 fml. of 1/1,000) periods of up to five minutes after the onset of was given intracardially. This produced a strong beat ventricular fibrillation, but in all cases cardiac mas- temporarily, but was rapidly superseded by ventricu- sage has been continued through the intervening lar fibrillation. Procaine amide hydrochloride (" pro- period. Of the three dogs chemically stimulated, two nestyl ") was injected intravenously without effect. were defibrillated with a voltage of 300. The third, Cardiac was due to other procedures on the heart, was in very massage continued, and 10 minutes later poor condition and inadequately oxygenated. the defibrillator was used. The electrodes were Ventricular fibrillation was not arrested. on September 27, 2021 by guest. Protected _ _ ~~~~*. 11 ......... .............. P~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~.FIG. 2a.-The defibrillator. FIG. 2b.--The electrodes. Thorax: first published as 10.1136/thx.7.3.205 on 1 September 1952. Downloaded from CARDIAC ARREST AND VENTRICULAR FIBRILLATION "Z.07 by massage and showed no sign of returning to fibrillation. The strength of the beat, however, was poor and the heart would only beat spontaneously for about two minutes following massage. To-.ri 1-*--: i:i '--T'J---~ti;+1! ; qz;!1r After an hour the strength of the beat was getting progressively weaker and asystole followed the cessa- .f4 tion of massage. Further measures were considered ; .- }; t tz -- .*- X -- e 0 - 8 <-;4'* useless. She had not had a spontaneous respiration for half an hour and the heart was no longer filling following inspiration. LiI' .+,..o.-< .f_v= B The shock produced only slight localized muscle . _, .i. s contraction .; * outside - s -- *,, the .** e ++-^'t-' > heart. +>S_.e;i ri-.t tti V_ j _-+-1ia it-4 i tM i - i; Necropsy confirmed the above findings, and section 1*-J-.--.o ;+ of .1.,_._\X=>W99 the ventricles showed no evidence of damage due *As v>\¢ Svl. tw z.-.Fa zt-.--tet..4 to electrical shocks or burns. t/'**t...*.4* t*.._.tt Case 2.-A man of 62, suffering from polycythaemia vera, was taken to the theatre for the evacuation of a haematoma following a rib biopsy. After 60 mg. of pethidine he was given gas, oxygen, and a little cyclopropane. During this minor procedure respira- tion ceased, and at about the same time the pulse could not be felt. At once the patient was turned on to his back, a ;7'j:1 t ~- I midline upper abdominal incision was made, and the cessation of the heart beat confirmed. A transverse ._: t ....... slit in the diaphragm opposite the pericardial attach- ment was then made, four fingers thrust through this. and direct cardiac massage started. A regular but copyright. weak beat was started without difficulty. In order :^ 0 I r to strengthen this 25 at 1/1,000 adrenaline was given intracardially. Almost at once the rhythm changed from normal to ventricular fibrillation. Intracardiac & procaine " was then given without effect. Massage .|......................?....... was continued and the defibrillator was sent for. This http://thorax.bmj.com/ arrived, from another hospital, and was set up ready for use within 45 minutes of the start of cardiac massage.
Load more

Recommended publications
  • Non Commercial Use Only
    Cardiogenetics 2017; volume 7:6304 Sudden death in a young patient with atrial fibrillation Case Report Correspondence: María Angeles Espinosa Castro, Inherited Cardiovascular Disease A 22-year-old man suffered a sudden Program, Cardiology Department, Gregorio María Tamargo, cardiac arrest without previous symptoms Marañón Hospital, Dr. Esquerdo, 46, 28007, María Ángeles Espinosa, while he was at rest, waiting for a subway Madrid, Spain. Víctor Gómez-Carrillo, Miriam Juárez, train. Cardiopulmonary resuscitation was Tel.: +34.91.586.82.90. immediately started using an Automated E-mail: [email protected] Francisco Fernández-Avilés, External Defibrillation that identified the Raquel Yotti Key words: KCNQ1; mutation; channelopa- presence of ventricular fibrillation and thy; sudden cardiac death; atrial fibrillation. Inherited Cardiovascular Disease delivered a shock. Return of spontaneous Program, Cardiology Department, circulation was achieved after three Contributions: MT, acquisition and interpreta- Gregorio Marañón Hospital, Madrid, attempts, being atrial fibrillation (AF) the tion of data for the work, ensuring that ques- Spain patient’s rhythm at this point (Figure 1). tions related to the accuracy or integrity of any He was admitted to our Cardiovascular part of the work is appropriately investigated Intensive Care Unit and therapeutic and resolved; MAE, conception of the work, hypothermia was performed over a period critical revision of the intellectual content, final approval of the version to be published, Abstract of 24 h. After completing hypothermia, ensuring that questions related to the accuracy rewarming, and another 24 h of controlled of any part of the work is appropriately inves- Sudden cardiac death (SCD) in young normothermia the patient awakened with no tigated and resolved; VG-C, acquisition and patients without structural heart disease is residual neurologic damage.
    [Show full text]
  • Atrial Arrhythmia Triggering Electromechanical Dissociation And
    EP CASE REPORT ....................................................................................................................................................... Atrial arrhythmia triggering electromechanical dissociation and ventricular fibrillation in a patient with atrial switch operation Nicolas Combes1,2,3*, Stefano Bartoletti1,2,Se´bastien Hascoet€ 3, Olivier Vahdat2, Franc¸ois Heitz2, and Victor Waldmann 4,5 1Electrophysiology Unit, Clinique Pasteur, Toulouse, France; 2Pediatric and Adult Congenital Heart Disease Department, Clinique Pasteur, 45, Avenue de Lombez, 31076 Toulouse, France; 3Pediatric and Adult Congenital Heart Disease Department, Hoˆpital Marie Lannelongue, Le Plessis-Robinson, France; 4Cardiology Department, Electrophysiology Unit, European Georges Pompidou Hospital, Paris, France; and 5Cardiology Department, Adult Congenital Heart Disease Unit, European Georges Pompidou Hospital, Paris, France * Corresponding author. Tel: 133 562213131; fax: 133 562211641. E-mail address: [email protected] A 26-year-old man with D- transposition of the great arteries (D-TGA) and pre- vious Mustard atrial switch surgery was referred for catheter ablation of a recur- rent symptomatic paroxys- mal atrial flutter. The arrhythmia was easily induci- ble (Figure 1A, cycle length 310 ms, rate 194 b.p.m.), with rapid conduction to the ventricles. While mapping flutter, simultaneous record- ing of endocardial signals and invasive blood pressure monitoring showed haemo- dynamic deterioration with intermittent electromechan- ical dissociation (Figure 1B) and then pulseless electrical activity (Figure 1C). After ini- tiation of cardiopulmonary resuscitation, several electric shocks failed to restore sinus rhythm and atrial flutter transitioned a few minutes later into ventricular tachy- cardia and then ventricular fibrillation (Figure 1D); this was ultimately terminated by defibrillation after an Figure 1 (A) Atrial flutter on 12-lead ECG induced by atrial bursts (240 ms), average ventricular response adrenaline bolus.
    [Show full text]
  • Mitral Valve Prolapse, Arrhythmias, and Sudden Cardiac Death: the Role of Multimodality Imaging to Detect High-Risk Features
    diagnostics Review Mitral Valve Prolapse, Arrhythmias, and Sudden Cardiac Death: The Role of Multimodality Imaging to Detect High-Risk Features Anna Giulia Pavon 1,2,*, Pierre Monney 1,2,3 and Juerg Schwitter 1,2,3 1 Cardiac MR Center (CRMC), Lausanne University Hospital (CHUV), 1100 Lausanne, Switzerland; [email protected] (P.M.); [email protected] (J.S.) 2 Cardiovascular Department, Division of Cardiology, Lausanne University Hospital (CHUV), 1100 Lausanne, Switzerland 3 Faculty of Biology and Medicine, University of Lausanne (UniL), 1100 Lausanne, Switzerland * Correspondence: [email protected]; Tel.: +41-775-566-983 Abstract: Mitral valve prolapse (MVP) was first described in the 1960s, and it is usually a benign condition. However, a subtype of patients are known to have a higher incidence of ventricular arrhythmias and sudden cardiac death, the so called “arrhythmic MVP.” In recent years, several studies have been published to identify the most important clinical features to distinguish the benign form from the potentially lethal one in order to personalize patient’s treatment and follow-up. In this review, we specifically focused on red flags for increased arrhythmic risk to whom the cardiologist must be aware of while performing a cardiovascular imaging evaluation in patients with MVP. Keywords: mitral valve prolapse; arrhythmias; cardiovascular magnetic resonance Citation: Pavon, A.G.; Monney, P.; Schwitter, J. Mitral Valve Prolapse, Arrhythmias, and Sudden Cardiac Death: The Role of Multimodality 1. Mitral Valve and Arrhythmias: A Long Story Short Imaging to Detect High-Risk Features. In the recent years, the scientific community has begun to pay increasing attention Diagnostics 2021, 11, 683.
    [Show full text]
  • The Refractory VF Arrest Patient: a Review of the Current Treatment
    1/24/2018 The Refractory VF Arrest Patient: A Review of the Current Treatment Options Marc Conterato, MD, FACEP Office of the Medical Director North Memorial Health Ambulance Service DISCLOSURE STATEMENT • Board Member, MN Resuscitation Consortium - Images of any commercial devices or medications are for illustration purposes only. The inclusion of such images in this presentation does not imply endorsement of any specific device or company. 2 Objectives • Delineate Refractory Ventricular Fibrillation (RVF) • Recurrent VF versus Refractory VF • What is “Electrical Storm” • Current Pre-hospital treatments • Additional hospital treatments • Dual/Double Sequential Defibrillation • ECMO/ECLS-A New Hope? 3 1 1/24/2018 A Standard Scenario • 55 YOF collapses at stop light, and her car rolls into the car in front of her. Airbags do not deploy, and bystanders find her slumped over the steering wheel and pulseless. • First responder/bystanders start CPR, and deliver three AED shocks prior to EMS arrival. • On EMS arrival, a fourth shock is delivered, an IO and alternative airway placed. Automated CPR started. • Epinephrine 2 mg (total) and Amiodarone 300 mg given, and the patient remains in VF. • Patient downtime is now ~25 minutes, and repeat evaluation reveals persistent VF. 4 What are your options • Continue CPR for a total of 30 minutes with recurrent defibrillations, additional epinephrine, bicarbonate and Amiodarone? • “Load and Go” to the local hospital with CPR enroute and continuing the resuscitation? • “Load and Go” to the local CCL (Cardiac Cath Lab) hospital with CPR enroute and continuing the resuscitation, with possible PCI with ongoing CPR? • Call HEMS unit for transfer to CCL hospital, but can they continue effective CPR in the helicopter? • “Load and Go” to a ECMO/ECLS center with CPR enroute and continuing the resuscitation, on the basis they can accept the patient and continue resuscitation? 5 Defining the problem: What is recurrent versus refractory VF (RVF)? • Recurrent VF is a rhythm that terminates with cardioversion, but then recurs rapidly.
    [Show full text]
  • Basic Rhythm Recognition
    Electrocardiographic Interpretation Basic Rhythm Recognition William Brady, MD Department of Emergency Medicine Cardiac Rhythms Anatomy of a Rhythm Strip A Review of the Electrical System Intrinsic Pacemakers Cells These cells have property known as “Automaticity”— means they can spontaneously depolarize. Sinus Node Primary pacemaker Fires at a rate of 60-100 bpm AV Junction Fires at a rate of 40-60 bpm Ventricular (Purkinje Fibers) Less than 40 bpm What’s Normal P Wave Atrial Depolarization PR Interval (Normal 0.12-0.20) Beginning of the P to onset of QRS QRS Ventricular Depolarization QRS Interval (Normal <0.10) Period (or length of time) it takes for the ventricles to depolarize The Key to Success… …A systematic approach! Rate Rhythm P Waves PR Interval P and QRS Correlation QRS Rate Pacemaker A rather ill patient……… Very apparent inferolateral STEMI……with less apparent complete heart block RATE . Fast vs Slow . QRS Width Narrow QRS Wide QRS Narrow QRS Wide QRS Tachycardia Tachycardia Bradycardia Bradycardia Regular Irregular Regular Irregular Sinus Brady Idioventricular A-Fib / Flutter Bradycardia w/ BBB Sinus Tach A-Fib VT PVT Junctional 2 AVB / II PSVT A-Flutter SVT aberrant A-Fib 1 AVB 3 AVB A-Flutter MAT 2 AVB / I or II PAT PAT 3 AVB ST PAC / PVC Stability Hypotension / hypoperfusion Altered mental status Chest pain – Coronary ischemic Dyspnea – Pulmonary edema Sinus Rhythm Sinus Rhythm P Wave PR Interval QRS Rate Rhythm Pacemaker Comment . Before . Constant, . Rate 60-100 . Regular . SA Node Upright in each QRS regular . Interval =/< leads I, II, . Look . Interval .12- .10 & III alike .20 Conduction Image reference: Cardionetics/ http://www.cardionetics.com/docs/healthcr/ecg/arrhy/0100_bd.htm Sinus Pause A delay of activation within the atria for a period between 1.7 and 3 seconds A palpitation is likely to be felt by the patient as the sinus beat following the pause may be a heavy beat.
    [Show full text]
  • Pub 100-04 Medicare Claims Processing Centers for Medicare & Medicaid Services (CMS) Transmittal 3054 Date: August 29, 2014 Change Request 8803
    Department of Health & CMS Manual System Human Services (DHHS) Pub 100-04 Medicare Claims Processing Centers for Medicare & Medicaid Services (CMS) Transmittal 3054 Date: August 29, 2014 Change Request 8803 SUBJECT: Ventricular Assist Devices for Bridge-to-Transplant and Destination Therapy I. SUMMARY OF CHANGES: This Change Request (CR) is effective for claims with dates of service on and after October 30, 2013; contractors shall pay claims for Ventricular Assist Devices as destination therapy using the criteria in Pub. 100-03, part 1, section 20.9.1, and Pub. 100-04, Chapter 32, sec. 320. EFFECTIVE DATE: October 30, 2013 *Unless otherwise specified, the effective date is the date of service. IMPLEMENTATION DATE: September 30, 2014 Disclaimer for manual changes only: The revision date and transmittal number apply only to red italicized material. Any other material was previously published and remains unchanged. However, if this revision contains a table of contents, you will receive the new/revised information only, and not the entire table of contents. II. CHANGES IN MANUAL INSTRUCTIONS: (N/A if manual is not updated) R=REVISED, N=NEW, D=DELETED-Only One Per Row. R/N/D CHAPTER / SECTION / SUBSECTION / TITLE D 3/90.2.1/Artifiical Hearts and Related Devices R 32/Table of Contents N 32/320/Artificial Hearts and Related Devices N 32/320.1/Coding Requirements for Furnished Before May 1, 2008 N 32/320.2/Coding Requirements for Furnished After May 1, 2008 N 32/320.3/ Ventricular Assist Devices N 32/320.3.1/Postcardiotomy N 32/320.3.2/Bridge-To -Transplantation (BTT) N 32/320.3.3/Destination Therapy (DT) N 32/320.3.4/ Other N 32/320.4/ Replacement Accessories and Supplies for External Ventricular Assist Devices or Any Ventricular Assist Device (VAD) III.
    [Show full text]
  • Persistent Ventricular Fibrillation During Therapeutic Hypothermia and Prolonged High-Dose Vasopressor Therapy: Case Report
    ARTICLE IN PRESS The Journal of Emergency Medicine, Vol. xx, No. x, pp. xxx, 2009 Copyright © 2009 Elsevier Inc. Printed in the USA. All rights reserved 0736-4679/09 $–see front matter doi:10.1016/j.jemermed.2009.05.027 Clinical Communications: Adults PERSISTENT VENTRICULAR FIBRILLATION DURING THERAPEUTIC HYPOTHERMIA AND PROLONGED HIGH-DOSE VASOPRESSOR THERAPY: CASE REPORT Joshua C. Poles, BA* Tyler F. Vadeboncoeur, MD† and Bentley J. Bobrow, MD‡ *Kansas City University of Medicine and Biosciences, Kansas City, Missouri, †Department of Emergency Medicine, Mayo Clinic Florida, Jacksonville, Florida, and ‡Department of Emergency Medicine, Maricopa Medical Center, Phoenix, Arizona Reprint Address: [email protected] e Abstract—Background: Recent emphasis on high qual- survival rates remain low, many communities have real- ity prehospital cardiopulmonary resuscitation has resulted ized substantial improvements in meaningful survival in more out-of-hospital cardiac arrest victims surviving to the after OHCA. This has occurred primarily through emergency department. As such, standardized in-hospital emergency medical services (EMS) systems focusing post-cardiac arrest care is necessary to assure optimal neuro- logical recovery. Although therapeutic hypothermia has on delivering high quality cardiopulmonary resuscita- arisen as a key component in the post-cardiac arrest care tion (CPR) (1,2). paradigm, its interaction with other therapies remains Therapeutic hypothermia (TH) is currently an American poorly defined. Objective: The purpose of this communica- Heart Association (AHA) 2005 Guideline IIa therapy for tion is to demonstrate a potential interaction between thera- adult victims who remain unconscious after a ventricular peutic hypothermia and routinely administered resuscitation fibrillation (VF) arrest in the out-of-hospital setting (3).
    [Show full text]
  • Basic Cardiac Rhythms – Identification and Response Module 1 ANATOMY, PHYSIOLOGY, & ELECTRICAL CONDUCTION Objectives
    Basic Cardiac Rhythms – Identification and Response Module 1 ANATOMY, PHYSIOLOGY, & ELECTRICAL CONDUCTION Objectives ▪ Describe the normal cardiac anatomy and physiology and normal electrical conduction through the heart. ▪ Identify and relate waveforms to the cardiac cycle. Cardiac Anatomy ▪ 2 upper chambers ▪ Right and left atria ▪ 2 lower chambers ▪ Right and left ventricle ▪ 2 Atrioventricular valves (Mitral & Tricuspid) ▪ Open with ventricular diastole ▪ Close with ventricular systole ▪ 2 Semilunar Valves (Aortic & Pulmonic) ▪ Open with ventricular systole ▪ Open with ventricular diastole The Cardiovascular System ▪ Pulmonary Circulation ▪ Unoxygenated – right side of the heart ▪ Systemic Circulation ▪ Oxygenated – left side of the heart Anatomy Coronary Arteries How The Heart Works Anatomy Coronary Arteries ▪ 2 major vessels of the coronary circulation ▪ Left main coronary artery ▪ Left anterior descending and circumflex branches ▪ Right main coronary artery ▪ The left and right coronary arteries originate at the base of the aorta from openings called the coronary ostia behind the aortic valve leaflets. Physiology Blood Flow Unoxygenated blood flows from inferior and superior vena cava Right Atrium Tricuspid Valve Right Ventricle Pulmonic Valve Lungs Through Pulmonary system Physiology Blood Flow Oxygenated blood flows from the pulmonary veins Left Atrium Mitral Valve Left Ventricle Aortic Valve Systemic Circulation ▪ Blood Flow Through The Heart ▪ Cardiology Rap Physiology ▪ Cardiac cycle ▪ Represents the actual time sequence between
    [Show full text]
  • Update on the Diagnosis and Management of Familial Long QT Syndrome
    Heart, Lung and Circulation (2016) 25, 769–776 POSITION STATEMENT 1443-9506/04/$36.00 http://dx.doi.org/10.1016/j.hlc.2016.01.020 Update on the Diagnosis and Management of Familial Long QT Syndrome Kathryn E Waddell-Smith, FRACP a,b, Jonathan R Skinner, FRACP, FCSANZ, FHRS, MD a,b*, members of the CSANZ Genetics Council Writing Group aGreen Lane Paediatric and Congenital Cardiac Services, Starship Children’s Hospital, Auckland New Zealand bDepartment[5_TD$IF] of Paediatrics,[6_TD$IF] Child[7_TD$IF] and[8_TD$IF] Youth[9_TD$IF] Health,[10_TD$IF] University of Auckland, Auckland, New Zealand Received 17 December 2015; accepted 20 January 2016; online published-ahead-of-print 5 March 2016 This update was reviewed by the CSANZ Continuing Education and Recertification Committee and ratified by the CSANZ board in August 2015. Since the CSANZ 2011 guidelines, adjunctive clinical tests have proven useful in the diagnosis of LQTS and are discussed in this update. Understanding of the diagnostic and risk stratifying role of LQTS genetics is also discussed. At least 14 LQTS genes are now thought to be responsible for the disease. High-risk individuals may have multiple mutations, large gene rearrangements, C-loop mutations in KCNQ1, transmembrane mutations in KCNH2, or have certain gene modifiers present, particularly NOS1AP polymorphisms. In regards to treatment, nadolol is preferred, particularly for long QT type 2, and short acting metoprolol should not be used. Thoracoscopic left cardiac sympathectomy is valuable in those who cannot adhere to beta blocker therapy, particularly in long QT type 1. Indications for ICD therapies have been refined; and a primary indication for ICD in post-pubertal females with long QT type 2 and a very long QT interval is emerging.
    [Show full text]
  • Pulseless Ventricular Tachycardia Legend EMR Universal Patient Care SMO EMT Cardiac Arrest SMO Intermediate Paramedic Medical Control
    Ventricular Fibrillation/ Pulseless Ventricular Tachycardia Legend EMR Universal Patient Care SMO EMT Cardiac Arrest SMO Intermediate Paramedic Medical Control Not applicable. Emergency Medical Responders and Emergency Medical Technicians are not equipped EMT EMR with ACLS medications and shall treat the patient in accordance with current AHA guidelines and the EMR EMT system Cardiac Arrest SMO. (HPCPR) 1. Continue EMR/EMT care. 2. Evaluate rhythm after 2 minutes CPR. If VF/pulseless VT continue chest compressions while charging and then defibrillate per manufacturer’s recommendations for biphasic monitors or 200J (or 360J for monophasic defibrillators). 3. Immediately resume CPR for 2 minutes and re‐evaluate the patient/rhythm. 4. While performing CPR initiate IV/IO Normal Saline TKO. I 5. Epinephrine (1:10,000) 1 mg IV/IO. I 6. Evaluate rhythm after 2 minutes CPR. If VF/pulseless VT continue chest compressions while charging and then defibrillate per manufacturer’s recommendations for biphasic monitors or 300J (or 360J for monophasic defibrillators). 7. Check rhythm, if still VF/pulseless VT continue, otherwise go to appropriate SMO. CPR for 2 minutes. 8. Evaluate rhythm after 2 minutes CPR. If VF/pulseless VT continue chest compressions while charging and then defibrillate per manufacturer’s recommendations for biphasic monitors or 360J (or 360J for monophasic defibrillators). P 9. Intubate ONLY if it can be accomplished without interruptions to compressions and monitor with ETCO2. Confirm and maintain blind insertion airway device (BIAD) if already inserted. P 10. Epinephrine, 1 mg 1:10,000 IV/IO. Repeat Epinephrine every 3‐5 minutes. 11. CPR for 2 minutes.
    [Show full text]
  • Ventricular Fibrillation Recurrences in Successfully Shocked Out-Of-Hospital Cardiac Arrests
    medicina Article Ventricular Fibrillation Recurrences in Successfully Shocked Out-of-Hospital Cardiac Arrests Daniela Aschieri 1 , Federico Guerra 2,* , Valentina Pelizzoni 3, Enrico Paolini 4, Giulia Stronati 2, Luca Moderato 3 , Giulia Losi 1, Paolo Compagnucci 2 , Michela Coccia 1 , Michela Casella 5, Antonio Dello Russo 2, Gust H. Bardy 6 and Alessandro Capucci 2 1 Cardiology Department, Civil Hospital, 29015 Castel San Giovanni, Italy; [email protected] (D.A.); [email protected] (G.L.); [email protected] (M.C.) 2 Department of Biomedical Science and Public Health, Cardiology and Arrhythmology Clinic, University Hospital “Ospedali Riuniti Umberto I-Lancisi-Salesi”, Marche Polytechnic University, 60020 Ancona, Italy; [email protected] (G.S.); [email protected] (P.C.); [email protected] (A.D.R.); [email protected] (A.C.) 3 Cardiology Department, “Guglielmo da Saliceto” Hospital, 29121 Piacenza, Italy; [email protected] (V.P.); [email protected] (L.M.) 4 Cardiology Department, “Ospedali Riuniti Marche Nord”, 61121 Pesaro, Italy; [email protected] 5 Department of Clinical, Special and Dental Sciences, Cardiology and Arrhythmology Clinic, University Hospital “Ospedali Riuniti Umberto I-Lancisi-Salesi”, Marche Polytechnic University, 60020 Ancona, Italy; [email protected] 6 Seattle Institute for Cardiac Research, Seattle, WA 98195, USA; [email protected] * Correspondence: [email protected] Abstract: Background and Objectives: The prognostic impact of ventricular fibrillation (VF) recurrences Citation: Aschieri, D.; Guerra, F.; after a successful shock in out-of-hospital cardiac arrest (OOHCA) is still poorly understood, and Pelizzoni, V.; Paolini, E.; Stronati, G.; some evidence suggests a potential pro-arrhythmic effect of chest compressions in this setting.
    [Show full text]
  • Mitral Valve Surgery Under Perfused Ventricular Fibrillation with Moderate Hypothermia
    Circ J 2002; 66: 450–452 Mitral Valve Surgery Under Perfused Ventricular Fibrillation With Moderate Hypothermia Kazuhito Imanaka, MD; Shunei Kyo, MD; Masanori Ogiwara, MD; Hiroaki Tanabe, MD; Hiroshi Ohuchi, MD; Haruhiko Asano, MD; Yuji Yokote, MD; Satoshi Gojo, MD; Masaaki Kato, MD The safety and myocardial protective effect of perfused ventricular fibrillation (VF) under moderate hypothermia were investigated. Through a midline sternotomy and opening the left atrium from the right side, isolated mitral valve surgery was performed under aortic cross-clamping (ACC) and cardioplegic arrest using Bretschneider HTK solution in 96 patients, and under perfused VF in 20 patients (VF Group). Patient characteristics, clinical outcomes, and perioperative variables were compared. A satisfactory surgical view was obtained in all VF Group patients. Patient characteristics in the 2 groups were similar, and both groups had comparable results for mortality and morbidity, operation time, cardiopulmonary bypass time, peak levels of creatine kinase (CK) and its myocardial fraction, hours of mechanical ventilation, intensive care unit stay, and postoperative left ventricu- lar ejection fraction. Even in VF Group patients with preoperative critical hemodynamic compromise, inotropes could be discontinued within 3 days. Thus, no detrimental effect of perfused VF was observed. On the other hand, in patients who underwent ACC and cardioplegic arrest of 120min or longer, peak levels of CK and its myocardial fraction were significantly higher than those of the rest of C group patients and VF Group patients. Perfused VF under moderate hypothermia can be a good alternative myocardial protection strategy during mitral valve surgery, particularly in patients in whom ACC is unsuitable or the duration of ACC is expected to be long.
    [Show full text]