cardiac arrest

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CARDIAC ARREST AND RESUSCITATION :

CARDIAC ARREST AND RESUSCITATION Unit of Dr: Mona A.Alkareem Presented by: Dr: Salwa Sirelkhatim

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Introduction Cardiopulmonary arrest results in a rapid decline in oxygen delivery to the brain Permanent disability or death results if the period of cerebral hypoxia lasts longer than 3 minutes During cardiac arrest a victim loses consciousness, stops normal breathing and loses pulse and blood pressure Give cardiopulmonary resuscitation (CPR) to help keep the cardiac arrest victim alive until emergency help arrives

Sudden Cardiac Arrest (SCA):

Sudden Cardiac Arrest (SCA ) SCA claims an estimated 325,000 lives each year 1,000 lives every day, one life every two minutes SCA accounts for half of all cardiac-related deaths Over half of SCA victims have no prior symptoms Survival requires emergency medical intervention and defibrillation within the first minutes following arrest The survival rate is as high as 90 percent if treatment is initiated within the first minutes following arrest An estimated 95 percent of SCA victims die before they reach a hospital or other source of emergency help

Impact of Sudden Cardiac Arrest:

Impact of Sudden Cardiac Arrest More people die from Sudden Cardiac Arrest than from AIDS, Breast Cancer and Lung Cancer combined Heart Rhythm Society 2005; American Cancer Society 2005, CDC 2003 Est.

What is cardiac arrest?:

What is cardiac arrest? is the cessation of normal circulation of the blood due to failure of the ventricles of the heart to contract effectively during systole. The resulting lack of blood supply results in cell death from oxygen starvation. Cerebral hypoxia, or lack of oxygen supply to the brain, causes victims to lose consciousness and stop breathing.. The primary first-aid treatment for cardiac arrest is cardiopulmonary resuscitation

Pathophysiology of cardiac arrest:

Pathophysiology of cardiac arrest With cardiac arrest, blood flow ceases, preventing oxygen delivery to vital tissue and anaerobic (living without oxygen) metabolism begins Lactic acid is generated through anarobiosis. Lactic acidosis,decreased pH and bicarbonate concentration in the body fluids caused by accumulation of lactic acid due to tissue hypoxia Acidosis produces vasodilatation and depression of catecholamine action 7

Causes of cardiac arrest :

Causes of cardiac arrest Ventricular tachycardia Ventricular fibrillation Hypertrophic cardiomyopathy Inherited and acquired electrical diseases, e.g. Long QT syndromes Congenital anomalous coronary artery Reduced Ejection Fraction

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The most common underlying reason for patients to die suddenly from cardiac arrest is coronary heart disease Most cardiac arrests that lead to sudden death occur when the electrical impulses in the diseased heart become rapid (ventricular tachycardia ) or chaotic (ventricular fibrillation ) or both This irregular heart rhythm (arrhythmia) causes the heart to suddenly stop breathing Some cardiac arrests are due to extreme slowing of the heart. This is called bradycardia . 9

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Other factors besides heart disease and heart attack can cause cardiac arrest. They include: respiratory arrest, electrocution, drowning, choking and trauma, as well as other cardiac conditions suchas the cardiomyopathy Cardiac arrest can also occur without any known cause 10

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Myocardial ischemia with irritability in the ischemic region leading to VF. In ventricular fibrillation, the electrical signals that control the pumping of the heart suddenly become rapid and chaotic. As a result, the lower chambers of the heart, the ventricles, begin to quiver (fibrillate) instead of contract, and they can no longer pump blood from the heart to the rest of the body. If blood cannot flow to the brain, it becomes starved of oxygen,and the person loses consciousness in seconds. 11

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Unless an emergency shock is delivered to the heart to restore its regular rhythm, using a machine called a defibrillator, death can occur within minutes. It’s estimated that more than 70% of ventricular fibrillation victims die before reaching the hospital. VF can also result from worsening of electrolyte imbalances (especially K and Ca), haemolysis from fresh water near drowning, profound hypothermia (< 28° C [< 82.4° F]), and excessive sympathetic stimulation of ventricular myocardium sensitized by hypoxemia 12

Treatable causes:

Treatable causes The potentially treatable causes of cardiac arrest (4 Ts and 4 Hs) are: Cardiac tamponade Tension pneumothorax Toxins or drug overdoses Pulmonary thromboembolism (or other mechanical obstruction to cardiac outflow) 13

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Hypoxia (lack of oxygen) Electrolyte disturbances (such as hypokalemia, hyperkalemia,, and hypocalcaemia. Hypovolemia (decreased blood volume) due to haemorrhage or dehydration Hypothermia 14

Electrical dysfunction:

Electrical dysfunction Is the most common mechanism of sudden cardiac death, with ventricular fibrillation representing the major rhythm in prehospital cardiac arrest (70% of patients). 15

Risk Factors:

Risk Factors High-risk patient populations have been identified: Prior Sudden Cardiac Arrest Prior Myocardial Infarction Heart Failure (Class II to IV) Ejection Fraction less than 40% Family History of Sudden Cardiac Arrest

Risk Factors:

Risk Factors Additional risk factors include: Recurrent unexplained syncope Idiopathic cardiomyopathy with syncope or VT Hypertrophic cardiomyopathy with syncope or VT Right ventricular dysplasia Long-QT syndrome

Underlying diseases:

Underlying diseases Include coronary artery disease, cardiomyopathy, hypokalemia, and digitalis toxicit prolonged QT interval that occurs in patients receiving antiarrhythmic drugs, antidepressants, or phenothiazines or in patients with hypokalemia or hypomagnesemia 18

Symptoms and Signs of Cardiac Arrest:

Symptoms and Signs of Cardiac Arrest Major clinical findings in cardiac arrest include: loss of consciousness; rapid, shallow breathing leading rapidly to apnea; ineffective respiratory gasping profound arterial hypotension with nonpalpable pulses over major vessels; absent heart sounds.(Consciousness, pulse and BP are lost immediately) the pupils of the eyes dilating within 45 seconds seizures may or may not occur within several minutes, tissue hypoxemia results, leading to vital organ injury. 19

Heart Attack Warning Signs:

Heart Attack Warning Signs Here are signs that can mean a heart attack is happening: Chest discomfort. Most heart attacks involve discomfort in the center of the chest that lasts more than a few minutes, or that goes away and comes back. It can feel like uncomfortable pressure, squeezing,fullness or pain. Discomfort in other areas of the upper body. Symptoms can include pain or discomfort in one or both arms, the back, neck, jaw or stomach. Shortness of breath. May occur with or without chest discomfort. Other signs: These may include breaking out in a cold sweat, nausea 20

Cardiac arrest strikes immediately and without warning. Here are the signs::

Cardiac arrest strikes immediately and without warning. Here are the signs: Sudden loss of responsiveness. No response to gentle shaking. No normal breathing. The victim does not take a normal breath when you check for several seconds. No signs of circulation. No movement or coughing. . 21

Diagnosis:

Diagnosis The state of cardiac arrest is diagnosed in an unconcious (unresponsive to vigorous stimulation) person who does not have apulse. An ECG clarifies the exact diagnosis and guides treatment. but treatment should begin without awaiting an ECG. The ECG may reveal: Asystole (known as a flatline) Pulseless electrical activity (formerly called electromechanical dissociation) 22

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Ventricular fibrillation Ventricular tachycardia Severe bradycardia Complete heart block with a slow ventricular escape rate 23

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Agonal rhythm: an idioventricular rhythm may be seen during the course of a cardiac arrest as the patient fails to respond to chemical stimulation. It can deteriorate into agonal rhythm or asystole. There is no P wave or P-R interval to monitor as atrial input into the cardiac contraction is extraneous. Because there is one site within the ventricle acting as pacemaker, each QRS complex will look the same. 24

Treatment of cardiac arrest:

Treatment of cardiac arrest Basic life support A: Airway B: Breathing C: Circulation D: defibrilation 25

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When the breathing stop the heart will soon stop beating within 0-4 minutes clinical death will occur. In 4-6 minutes brain damage is possible. In 6-10 minutes brain damage is likely. More than ten minutes irreversible brain damage (biological death). Basic life support and cardiopulmonary resuscitation are two important life saving techniques Basic life support is a method of marinating cardiac output following cardiac arrest. It maintains viability until full CPR can be commenced. 26

Can cardiac arrest be reversed?:

Can cardiac arrest be reversed? Brain death and permanent death start to occur in just 4 to 6minutes after someone experiences cardiac arrest Early CPR and rapid defibrillation combined with early advanced care can result in high long-term survival rates for witnessed cardiac arrest . 27

Cardiopulmonary resscitation:

Cardiopulmonary resscitation

Definition :

Definition Cardiopulmonary resuscitation (CPR) is the term used to describe the maintenance of adequate breathing and circulation in a patient who cannot do so for him- or herself The aim of CPR is to restore respiration and adequate cardiac output as soon as possible to prevent death or permanent disability 29

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Cardio Pulmonary Resuscitation

Indications of CPR:

Indications of CPR It is indicated in those who are Unresponsive with cardiac arres t and no breathing or only gasps 31

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About 40% of SCA victims have ventricular fibrillation (VF) Sudden cardiac arrest is a leading cause of death in Europe,USA and Canada (More than 700,000 individuals per annum) Early resuscitation is most successful if defibrillation is performed in about the first 5 minutes after collapse 32

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Early recognition  call for help Early CPR  Compression first, avoid interruption Early defibrilation  Single DC Post Rescucitation care 33

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Recognition of cardiac arrest & activation of EMS Early CPR with emphasis on compression Rapid defibrillation Effective advanced life support Integrated post-cardiac arrest care

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Main changes in adult basic life support:

Main changes in adult basic life support The decision to start CPR is made if a victim is unresponsive and not breathing normally place their hands on the centre of the chest , rather than to spend more time using the ‘rib margin’ method 36

Types of CPR:

Types of CPR Basic cardiovascular life support (BCLS) – no special equipment required Advanced cardiovascular life support (ACLS)- requires specialist skill and equipment In any type of resuscitation protocol, the following three areas must be assessed and supported in order of priority 37

Areas of priority in resuscitation:

Areas of priority in resuscitation Airway Breathing Circulation 38

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BASIC LIFE SUPPORT (BLS) refers to maintaining a irway patency and supporting b reathing and the c irculation , without the use of equipment other than a protective device.

PRIMARY SURVEY:

PRIMARY SURVEY Airway : Open the airway Breathing : Provide positive-pressure ventilation Circulation : Give chest compressions Defibrillation : Shock VF / pulse less VT Airway : Establish advanced airway control Perform endotracheal intubation Breathing : Assess the adequacy of ventilation via endotracheal tube Provide positive-pressure ventilations Circulation : Obtain iv access Continue CPR Provide rhythm cv tx Differential Diagnosis SECONDARY SURVEY 40

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Basic Steps PRIMARY ABCD SURVEY Airway Open the airway Breathing Provide positive-pressure ventilations Circulation Give chest compressions Defibrillation Shock VF / pulseless VT 41

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Basic Steps SECONDARY ABCD SURVEY Airway Provide advanced airway management (tracheal intubation, laryngeal mask airway, combitube ) Breathing Confirm proper tube placement by primary (physical exam) and secondary (exhaled CO 2 and esophageal detector device) methods, check for adequate oxygenation and ventilation Circulation Obtain IV access, determine rhythm, give medications appropriate for rhythm and vital signs Differential Diagnosis Search for, find, and treat reversible causes 42

Points to note:

Points to note Each rescue breath, is given by mouth-to-mouth inflation with the nose occluded and should deliver approximately 500mL of expired air into the lungs of the victim. The operator should watch the chest wall of the victim to ensure that it raises and falls with each breath. Each breath will take approximately 1-1.5 sec. It is important to allow the chest wall to fall back completely before taking the next breath . 43

Points to note:

Points to note Assessment of the carotid pulse should take no more than 10sec. If there is no pulse  chest compressions performed by placing the heel of the hand over the lower half of the sternum two fingerbreadths above the xiphoid process. Enough pressure should be applied to depress sternum 4-5cm and no more. The operator should be vertically above the victim’s chest, and the arms should be kept straight. The rate of compressions should be 100/min. After each compression the pressure should be released and the chest wall allowed to rise back up. 44

Principle of chest compressions:

Principle of chest compressions Chest compression increase intrathoracic pressure, which propels blood out of the thorax. The veins collapse, whereas the arteries remain patent. Therefore, flow is in a forward direction. 45

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Check the victim for a response ‘‘Are you all right?’’

‘‘Are you all right?’’:

If he responds • leave him in the position in which you find him provided there is no further danger • try to find out what is wrong with him and get help if needed • reassess him regularly ‘‘Are you all right?’’

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If he does not respond shout for help HELP !!! HELP !!!

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Turn the victim onto his back and then open the airway using head tilt and chin lift

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Place your hand on his forehead and gently tilt his head back keeping your thumb and index finger free to close his nose if rescue breathing is required

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Keeping the airway open, look , listen and feel for normal breathing FOR NO MORE THAN 10 SEC.

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If he is breathing normally turn him into the recovery position send or go for help/call for an ambulance check for continued breathing

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If he is NOT breathing normally send someone for help or, if you are on your own, leave the victim and alert the ambulance service; return and start CHEST COMPRESSION

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Place the heel of one hand in the centre of the victim’s chest

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Place the heel of your other hand on top of the first hand

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Interlock the fingers of your hands and ensure that pressure is not applied over the victim’s ribs . Do not apply any pressure over the upper abdomen or the bottom end of the bony sternum

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Position yourself vertically above the victim’s chest and, with your arms straight, press down on the sternum 4—5 cm

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After each compression, release all the pressure on the chest without losing contact between your hands and the sternum; repeat at a rate of about 100/min Compression and release should take equal amounts of time

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THEORY OF CHEST COMPRESSION HEART PUMP THEORY : squeezing the heart between the bony sternum & vertebral column results in forward flow of blood. THORACIC PUMP THEORY : proposes that chest compression increases intrathoracic pressure that propels blood out of arteries into veins.

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After 30 compressions open the airway again using head tilt and chin lift

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Continue with chest compressions and rescue breaths in a ratio of 30:2. 30 2

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Continue resuscitation until • qualified help arrives and takes over • the victim starts breathing normally • you become exhausted

Airway ventilation and protection:

Airway ventilation and protection During these cycles of CPR Adequate ventilation must be established The airway must be protected by an operator who remains at the patient’s head The optimal method of protecting the airway is by insertion of a cuffed endotracheal tube. This device minimizes the risk of aspiration of the gastric contents and allows effective ventilation to be carried out. Endotracheal intubation can be a hazardous procedure and laryngeal mask airway is alternative . 66

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I V access:

I V access Via large peripheral vein or preferablyvia a central vein. 68

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Recovery Position stable near a true lateral position head dependent no pressure on the chest to impair breathing.

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Head tilt Right angles Right angles If the victim has to be kept in the recovery position for more than 30 min turn him to the opposite side to relieve the pressure on the lower arm.

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No Movement or response Call for help / or call emergency number Get AED Or send second rescuer (if available) to do this Open AIRWAYS, check BREATHING If not breathing give 2 BREATH that make chest rise ( A ssess responsiveness) ( A ctivate E M S) (Airways, A ssess breathing) (rescue B reathing) 74 EMS: Emergency medical system AED: Automated external defibrillator

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If no response, check pulse : Do you DEFINITELY feel Pulse within 10 seconds ? Give 1 breath every 5-6 seconds Recheck pulse every 2 minutes 30 COMPRESSION and 2 BREATHS Until AED/defibrillator arrives, ALS providers take over Or victim starts to move Push hard and fast (100x/min) and release completely Minimize interruption in compression AED / defibrillator ARRIVES Definite pulse No pulse (Check Pulse) (Chest Compression) (Defibrillation) 75

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Check Rhythm Shockable rhythm ? Give 1 shock Resume CPR immediately For 5 cycles Resume CPR immediately For 5 cycles Check rhythm every 5 cycles Continue until ALS providers take over Or victim starts to move Not shockable Shockable 76

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CPR 30:2 Until defibrillator / monitor attached Assess Rhythm Shockable (VF/ Pulsless VT) Non-shockable (PEA / Asystole ) 1 Shock 150-360 J biphasic lub 360 J monophasic Immediately resume : CPR 30:2 For 2 min Call Resuscitation Team During CPR: Correct reversible causses Check electrode position and contact Attempt / verify: IV access Airway and oxygen Give uninterrupted compressions when airway secure Give adreanline every 3-5 mins Consider: amiodarone, atropine, magnesium * Reversible causes Hipoxia Tension pneumothorax Hipovolaemia Tamponade cardiac Hipo/Hiperkalaemia / Metabolic Toxins Hipothermia Thromb osis ( coronary or pulmonary ) Immediately resume: CPR 30:2 For 2 min Open Airway Look for signs of life Unresponsive ?

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During CPR: Correct reversible causses Check electrode position and contact Attempt / verify: IV access Airway and oxygen Give uninterrupted compressions when airway secure Give adreanline every 3-5 mins Consider: amiodarone, atropine, magnesium

Post Resuscitation Care:

Post Resuscitation Care The goal: Normal cerebral function Stable cardiac rhythm Adequate organ perfusion

Cardiac Arrest:

Cardiac Arrest Arrest arrhythmias are divided into non-shockable and shockable. Ventricular fibrillation and pulseless ventricular tachycardia are both treatable by defibrillation In other arrhythmias such as asystole and Pulseless Electrical Activity (PEA) defibrillation is not indicated, rather the underlying cause must be treated.

Shockable arrhythmias:

Shockable arrhythmias Ventricular Fibrillation Pulseless Ventricular Tachycardia What is happening to these individual’s hearts?

Non-shockable Arrhythmias:

Non-shockable Arrhythmias Asystole Pulseless Electrical Activity What is happening to these individual’s hearts?

Ventricular Fibrillation (VF):

Ventricular Fibrillation (VF) Characteristics Chaotic, irregular, ventricular rhythm Wide, variable, bizarre complexes Fast rate of activity Multiple ventricular foci No cardiac output Terminal rhythm if not corrected quickly Most common rhythm causing sudden cardiac death in adults

Asystole:

Asystole Is the absence of electrical activity on ECG, with absent perfusion, BP, and pulse. Causes include severe generalized myocardial ischemia, ventricular rupture, and hyperpolarization of cardiac cell membranes in severe hyperkalemia (serum K+ > 7 mEq/L) or hypermagnesemia 84

Asystole:

Asystole Characteristics The ultimate unstable bradycardia A terminal rhythm poor prognosis for resuscitation best hope if ID & treat cause No significant positive or negative deflections

Asystole:

Asystole Possible Causes Hypoxia: ventilate Preexisting metabolic acidosis: Bicarbonate 1 mEq/kg Hyperkalemia: Bicarbonate 1 mEq/kg, Calcium 1 g IV Hypokalemia: 10mEq KCl over 30 minutes Hypothermia: rewarm body core

Asystole:

Asystole Possible Causes Drug overdose Tricyclics: Bicarbonate Digitalis: Digibind (Digitalis antibodies) Beta-blockers: Glucagon Ca-channel blockers: Calcium

Electromechanical dissociation (EMD)- Pulseless electrical activity:

Electromechanical dissociation (EMD)- Pulseless electrical activity Refers to organized electrical depolarization without mechanical contractions, (persistence of electrical activity in the heart but there is ineffective cardiac contraction) The primary mechanisms are cardiac rupture, acute tamponade, global ischemia, acute MI, obstructing by intracardiac tumor or thrombus, and chronic heart failure, hypovolemia, hypothermia, significant acidosis, medication overdose (tricyclic agents, digitalis, betblockers, calcium channel blockers). 88

PEA:

PEA Possibilities Massive pulmonary embolus Massive myocardial infarction Overdose: Tricyclics - Bicarbonate Digitalis - Digibind Beta-blockers - Glucagon Ca-channel blockers - Calcium

PEA:

PEA Identify, correct underlying cause if possible Possibilities: Hypovolemia: volume Hypoxia: ventilate Tension pneumo: decompress Tamponade: pericardiocentesis Acute MI: vasopressor Hyperkalemia: Bicarbonate 1mEq/kg Preexisting metabolic acidosis: Bicarbonate 1mEq/kg Hypothermia: rewarm core

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CPR 30:2 Until defibrillator / monitor attached Assess rhythm Call Resuscitation Team Precordial thump The interventions that contribute to improved survival after CA: Early defibryllation (VT/VF) Prompt and effective bystander basic life support (BLS) Advanced airway intervention and the delivery of drugs – have not been shown to increase survival after cardiac arrest (CA) During ALS – attention must be focused on early defibrillation and high-quality, uninterrupted BLS Confirm Cardiac Arrest

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Shochable rhythms (ventricular fibryllation / pulsless ventricular tachycardia)

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Shockable (VF/ pulsless VT) 1 Shock 150-360 J (biphasic) or 360 J (monophasic) Immediately resume : CPR 30:2 for 2 min Assess rhythm If shockable rhythm is confirmed: Charge the defibrillator Give one shock (biphasic or monophasic energy) Resume CPR immediately after shock without reassessing the rhythm for 2 min(CV ratio 30:2) Check the monitor If there is still VF/VT give next shock Resume CPR immediately - 2min Check the monitor If there is still VF/VT give adrenaline followed immediately by a third shock Resumption of CPR SEQUENCE DRUG – shock – CPR – rhythm check Minimise the delay between stopping chest Compressions and delivery of shock

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Adrenaline – give immediately before the shock 1 mg every 3-5min (start followed the third shock) Amiodarone – if VT/VF persists after third shock 300 mg iv bolus during rhythm analysis before delivery of the fourth shock Drug – shock – CPR – rhythm check SEQUENCE

STOP of the algorithm:

STOP of the algorithm If signs of life return during CPR – movement, normal breathing or coughing Check the monitor: Organised rhythm present Check for a pulse Pulse palpable ROSC (return of spontaneous circulation) Continue post-resuscitation care (PRC) Pulse not present Continue CPR

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Assess rhythm Non-shockable (PEA / asystole ) Immediately resume : CPR 30:2 for 2 min Non-shockable rhythms (PEA and asystole)

Asystole:

Asystol e Start CPR (CV ratio 30:2) Check that the leads are attached correctly Give adrenaline – as soon iv access is achieved 1 mg every 3 - 5 min s Atropin a 3 mg i.v . – will provide max. vagal blokade Secure the airway After 2 min CPR No change in ECG appearance – resume CPR Organised rhythm is present – check the pulse Pulse is present – begin PRC Pulse is not present – resume CPR

Pulseless electrical activity (PEA):

Pulseless electrical activity (PEA) Start CPR (CV ratio 30:2) Check that the leads are attached correctly Give adrenaline Atropin e 3 mg i.v . – rhythm rate < 60/min Secure the airway Check potentially reversible causes (4 Hs, 4Ts) After 2 min CPR No change in ECG appearance – resume CPR Organised rhythm is present – check the pulse Pulse is present – begin PRC Pulse is not present – resume CPR

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Potentially reversible causes : Hypo xia Hypo volaemia Hypo / hyperkal a emia , metabolic disorders Hypot hermia Tension pneumothorax Cardiac tamponade To xins Throm bosis (coronary or pulmonary)

Hypothermia-Initial Therapy:

Hypothermia-Initial Therapy Remove wet garments Protect against heat loss & wind chill Maintain horizontal position Avoid rough movement and excess activity

Hypothermia – No Pulse:

Hypothermia – No Pulse CPR Defibrillate X 3 if VF/VT ETT with warm, humidified O2 IV access with warm fluids Temp >30C/86F: Continue as usual with longer intervals Repeat defibrillation as temp rises Temp <30C/86F Continue CPR Withhold medications and further defibrillation Transport for core warming

Summary:

Summary In patients in VF/ pulseless VT attempt defibrillation without delay In patients in refractory VF or with a non-VF/VT rhythm identify and treat any reversible cause

Treatment of cardiac arrest:

Treatment of cardiac arrest Advanced life support: treats cardiac arrest definitively with drugs, fluids, DC countershock or artificial pacemaker when appropriate Continous of effective Basic Life Support remains important to maintain vital organ perfusion assure circulation of lifesaving drugs 103

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Administration of drugs through a peripheral IV, endotracheal tube, or intracardial injection. Peripheral IV should be established as soon as possible by a team member who is not operforming CPR. 104

DRUGS for cardiac arrest:

DRUGS for cardiac arrest

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There are 3 groups of drugs relevant to the management of cardiac arrest : Vasopressors Anti-arrhytmics Other drugs Drugs should be considered only after initial shocks have been delivered and chest compressions and ventilation have been started .

Adrenaline (epinephrine) primery agent for the management of cardiac arrest:

Adrenaline ( epinephrine ) primery agent for the management of cardiac arrest Its primary efficacy is due to effects :  - adrenergic – arterial vasoconstriction  systemic vascular resistance  coronary and cerebral perfusion pressures  - adrenergic –  coronary blood flow  force of contraction  myocardial O 2 consumption (may increase ischaemia )

Adrenaline:

Adrenaline Indications: The first drug used in cardiac arrest of any ethiology Second-line treatment for cardiogenic shock Preferred in the s pecial circumstances: anaphylaxis

Adrenaline:

Adrenaline Dose: 1 mg intravenous (1 ml sol. 1:1,000) every 3-5 min of CPR 2-3 mg diluted to 10ml with sterile water via tracheal tube 2–10 mcg / min continous infusion for atropine resistant bradycardia , hypotensive patients 0.5ml 1:1,000 i.m ., 3-5 ml (sol. 1:10,000 ) i.v . - in anaphylaxis, depending on severity

Vasopressin:

Vasopressin Naturally occuring antidiuretic hormone High doses – powerful vasoconstricor that acts by stimulation of smooth muscle V1 receptors AHA – recommended vasopressin as an alternative to adrenaline for the treatment of adult shock-refractory VF Dose – 40 U (comp. 1mg adrenaline) Currently – insufficient evidence of improvement in survival to discharge

Other drugs:

Other drugs OXYGEN – high concentration should be given to all patients in cardiac arrest

Atropine:

Atropine A ntagonises the action of the parasympthatetic neurotransmitter acetylcholine at muscarinic receptors : b locks effects of the vagus nerve on SA and AV nodes i ncreases sinus node automaticity i ncreases atrioventricular conduction

Atropine:

Atropine Indications: Asystole PEA (rate < 60 beats / min) Sinus, atrial or node bradycardia – unstable haemodynamic condition

Atropine:

Atropine Dose: Asystole / PEA (rate < 60 beats / min) 3 mg i.v ., single bolus 6 mg via tracheal tube Bradycardia 0.5 mg i.v ., repeated as necessary, maximum 3 mg

Theophylline:

Theophylline Phosphodiesterase inhibitor that: Increases tissue concentrations of cAMP and releases adrenaline from adrenal medulla Has chronotropic and inotropic action

Theophylline:

Theophylline Indications: Asatolic cardiac arrest Peri-arrest bradycardia refractory to atropine Doses: Recommended for adults: 250 – 500mg (5mg/kg) (narrow therapeutic window, optimal plasma concentration 10 – 20mg/l) Side effects: arrhythmias, convulsions

Sodium Bicarbonate (Buffer):

Sodium Bicarbonate ( Buffer ) Indications: Severe metabolic acidosis (pH < 7.1) Hyperkalaemia Special circumstance Tricyclic antidepressant poisoning

Sodium Bicarbonate (Buffer):

Sodium Bicarbonate ( Buffer ) Agent used in treatment of acidaemia in cardiac arrest b ut generate carbon dioxide , which diffuses rapidly into cells : exacerbates intracellular acidosis produces a negative inotropic effect on ischaemic myocardium cause s hypernatraemia Compromises circulation and brain interact with adrenaline

Sodium Bicarbonate:

Sodium Bicarbonate Dose: 50 mmol (50 ml of 8.4% solution) i.v .

Calcium:

Calcium Constituent e ssential for normal cardiac contraction , but: high plasma concentrations are harmful to the ischaemic myocardium and impair cerebral recovery e xcess may lead to arrhythmias

Calcium:

Calcium Indications: Pulseless electrical activity caused by: severe hyperkalaemia severe hypocalcaemia overdose of calcium channel blocking drugs Dose 10 ml 10% calcium chloride (6.8 mmol ) May be repeated (D o not give immediately before or after sodium bicarbonate )

Naloxone:

Naloxone Indications: Opioid overdose Respiratory depression secondary to opioid administration

Naloxone:

Naloxone Actions: Opioid receptor antagonist Reverses all opioid effects, particularly respiratory and cerebral May cause severe agitation in opioid dependence

Naloxone:

Naloxone Dose: 0.2 - 2.0 mg i.v . May need to be repeated up to a maximum of 10 mg May need an infusion

Route alternative routes for drug delivery:

Route alternative routes for drug delivery If a peripheral cannula is in place and working, use it initially Central veins are the route of choice if expertise is available The tracheal route can be used with appropriate adjustment of dose Intraosseous route – drugs will achieve adequate plasma concentrations , safe and effective , may be used for children and adults

Tracheal administration of drugs:

Tracheal administration of drugs Drugs that can be given via the trachea: Adrenaline Lidocaine Atropine Naloxone Drugs that cannot be given via the trachea Amiodarone Sodium bicarbonate Calcium

DEFIBRILLATORS :

DEFIBRILLATORS

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NEED FOR A DEFIBRILLATOR Ventricular fibrillation is a serious cardiac emergency resulting from asynchronous contraction of the heart muscles. Due to ventricular fibrillation, there is an irregular or rapid heart rhythm . Fig. Ventricular fibrillation Fig. Normal heart beat

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Ventricular fibrillation can be converted into a more efficient rhythm by applying a high energy shock to the heart. This sudden surge across the heart causes all muscle fibres to contract simultaneously. The instrument for administering the shock is called a DEFIBRILLATOR . Possibly , the fibres may then respond to normal physiological pacemaking pulses. NEED FOR A DEFIBRILLATOR

Mechanism of defibrillation:

Mechanism of defibrillation Defibrillation is the passage of an electrical current of sufficient magnitude across the myocardium to depolarize acritical mass of cardiac muscle simultaneously,enabling the natural pacemaker tissue to resume control.

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All defibrillators have three features: 1-a power sourse 2-a capacitor 3- two electrodes

Placement of defibrillator paddle:

Placement of defibrillator paddle The right paddle should be placed below the clavicle in the midclavicular line The left paddle should be placed on the lower rib cage on the anterior axillary line. 132

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134

TYPES OF DEFIBRILLATORS:

135 TYPES OF DEFIBRILLATORS Internal External

TYPES OF DEFIBRILLATORS:

TYPES OF DEFIBRILLATORS Internal defibrillator Electrodes placed directly to the heart Eg.-Pacemaker External defibrillator Electrodes placed directly on the heart Eg.-AED

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DEFIBRILLATOR ELECTRODES Types of Defibrillator electrodes:- Spoon shaped electrode Applied directly to the heart. Paddle type electrode Applied against the chest wall Pad type electrode Applied directly on chest wall

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DEFIBRILLATOR ELECTRODES

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Fig.- Pad electrode DEFIBRILLATOR ELECTRODES

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PRINCIPLE OF DEFIBRILLATION Energy storage capacitor is charged at relatively slow rate from AC line. Energy stored in capacitor is then delivered at a relatively rapid rate to chest of the patient. Simple arrangement involve the discharge of capacitor energy through the patient’s own resistance.

Classes of discharge waveform :

Classes of discharge waveform Monophasic pulse or waveform Bi-phasic pulse or waveform

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Classes of discharge waveform There are two general classes of waveforms: mono- phasic waveform Energy delivered in one direction through the patient’s heart Biphasic waveform Energy delivered in both direction throuth the patient’s heart

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Classes of discharge waveform Fig:- Generation of bi-phasic waveform

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Classes of discharge waveform The biphasic waveform is preferred over monophasic waveform to defibrillate .why????? A monophasic type, give a high-energy shock, up to 360 to 400 joules due to which increased cardiac injury and in burns the chest around the shock pad sites. A biphasic type, give two sequential lower-energy shocks of 120 - 200 joules, with each shock moving in an opposite polarity between the pads.

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AUTOMATIC EXTERNAL DEFIBRILLATOR

AED:

AED

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AEDs require self-adhesive electrodes instead of hand held paddles. AED is a type of external defibrillation process. AUTOMATIC EXTERNAL DEFIBRILLATOR AED is a portable electronic device that automatically diagnoses the ventricular fibrillation in a patient. Automatic refers to the ability to autonomously analyse the patient's condition. The AED uses voice prompts, lights and text messages to tell the rescuer what steps have to take next.

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ELECTRODE PLACEMENT OF AED Anterior electrode pad Apex electrode pad Fig. anterior –apex scheme of electrode placement

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WORKING OF AED turned on or opened AED. AED will instruct the user to:- Connect the electrodes (pads) to the patient. Avoid touching the patient to avoid false readings by the unit. The AED examine the electrical output from the heart and determine the patient is in a shockable rhythm or not.

Sequence of actions when using an automated external defibrillator:

Sequence of actions when using an automated external defibrillator As soon as the AED arrives :  If more than one rescuer is present, continue CPR while the AED is switched on. If you are alone, stop CPR and switch on the AED.  Follow the voice / visual prompts.  Attach the electrode pads to the patient’s bare chest.  Ensure that nobody touches the victim while the AED is analysing the rhythm. 3A. If a shock is indicated:  Ensure that nobody touches the victim.  Push the shock button as directed (fully-automatic AEDs will deliver the shock automatically).  Continue as directed by the voice / visual prompts.  Minimise, as far as possible, interruptions in chest compression.

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3B. If no shock is indicated:  Resume CPR immediately using a ratio of 30 compressions to 2 rescue breaths.  Continue as directed by the voice / visual prompts. 4. Continue to follow the AED prompts until:  qualified help arrives and takes over OR  the victim starts to show signs of regaining consciousness, such as coughing, opening his eyes, speaking, or moving purposefully AND starts to breathe normally OR  you become exhausted

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PRECAUTIONS IN DEFIBRILLATION PROCESS The paddles used in the procedure should not be placed:- on a woman's breasts over an internal pacemaker patients. Before the paddle is used, a gel must be applied to the patient's skin

Implantable cardioverter-defibrillator (ICD:

Implantable cardioverter-defibrillator (ICD Prevent sudden cardiac death in patients experienced life-threatening ventricular arrhythmias such as sustained ventricular tachyarrhythmia (VT) or ventricular fibrillation (VF) Capable of treating bradycardia, VT, VF, and atrial tachycardia

ICD:

ICD Also known as automatic internal cardiac defibrillator (AICD). These devices are implants, similar to pacemakers (and many can also perform the pacemaking function). They constantly monitor the patient's heart rhythm, and automatically administer shocks for various life threatening arrhythmias, according to the device's programming. ICD using paddles applied directly across the ventricles requires less energy than external defibrillation

ICD Therapy:

ICD Therapy First-line therapy for ventricular tachycardia (VT)/ ventricular fibrillation (VF) patients Transvenous, single incision Local anesthesia; conscious sedation Short hospital stay Perioperative mortality < 1% Programmable therapy options Single- or dual-chamber therapy Battery longevity up to 7 years More than 100,000 implants/year

ICD:

ICD

Contraindications of ICD:

Contraindications of ICD Reversible triggering factor for VT/VF CAD patients without inducible or spontaneous VT undergoing bypass surgery NYHA class IV drug refractory congestive heart failure, not candidates for transplant Life expectancy not exceeds 6 months Significant behavioral disorders or psychiatric disorders

Peri-arrest arrhythmias :

Peri-arrest arrhythmias

Introduction:

Introduction Cardiac arrhythmias are relatively common in the peri-arrest period. They are common in the setting of acute myocardial infarction and may precipitate ventricular fibrillation (VF) or follow successful defibrillation.

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Cardiac arrhythmias - well rocognised complications of myocardial infarction The treatment of all arrhythmias poses two basic questions How is the patient? What is the arrhythmia? The presence or absence of certaine adverse signs or symptoms will dictate the appropriate treatment

Adverse signs of peri-arrest arrhythmias:

Adverse signs of peri-arrest arrhythmias Clinical evidence of low cardiac output – pallor, sweating, cold, clammy extremities, impaired consciousness, hypotension Excessive tachycardia – very high rates (>150 beats/min) reduce coronary flow resulting in myocardial ischeamia Excessive bradycardia – may not be tolerated by patients with poor cardiac reserve (<60 beats/min) Heart failure – arrhythmias reduce the efficiency of the heart as a pump (pulmonary oedema)

Sequence of actions:

Sequence of actions Assess the patient using the ABCDE approach. In all cases, give oxygen and insert an intravenous cannula and assess the patient for adverse features. Whenever possible, record a 12-lead ECG; this will help determine the precise rhythm, either before treatment or retrospectively, if necessary with the help of an expert. Correct any electrolyte abnormalities (e.g. K+, Mg++, Ca++).

Treatment options:

Treatment options Depending on the nature of the underlying arrhythmia and clinical status of the patient (in particular the presence or absence of adverse features) immediate treatments can be categorised under four headings: 1. Electrical (cardioversion for tachyarrhythmia or pacing for bradyarrhythmia) 2. Simple clinical intervention (e.g., vagal manoeuvres, fist pacing) 3. Pharmacological (drug treatment) 4. No treatment needed

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Most drugs act more slowly and less reliably than electrical treatments, so electrical treatment is usually the preferred treatment for an unstable patient with adverse features. If a patient develops an arrhythmia during, or as a complication of some other condition (e.g. infection, acute myocardial infarction, heart failure), make sure that the underlying condition is assessed and treated appropriately

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Emergency situations do not solely concern cardiac arrests. Patients with life threatening arrhythmias are said to be in a peri-arrest period. Peri-arrest rhythms include Bradycardia Broad complex tachycardia Narrow complex tachycardia Atrial Fibrillation

Tachycardias:

Tachycardias

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If the patient is unstable If the patient is unstable and deteriorating (i.e., has adverse features caused by the tachycardia) synchronised cardioversion is the treatment of choice.. If cardioversion fails to restore sinus rhythm, and the patient remains unstable, give amiodarone 300 mg IV over 10 - 20 min and re-attempt electrical cardioversion. The loading dose of amiodarone can be followed by an infusion of 900 mg over 24 h.

Synchronised cardioversion:

Synchronised cardioversion Carry out cardioversion under general anaesthesia or conscious sedation, Ensure that the defibrillator is set to synchronised mode. . For a broad-complex tachycardia or atrial fibrillation, start with 120-150 J biphasic shock (200 J monophasic) and increase if this fails. Atrial flutter and regular narrow-complex tachycardia will often be terminated by lower energies: start with 70-120 J biphasic (100 J monophasic). If

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If the patient is stable If there are no adverse features consider using drug treatment in the first instance (if any treatment is required). Assess the ECG and determine the QRS duration. If the QRS duration is greater than 0.12 s (3 small squares on standard ECG paper speed of 25 mm s-1), this is a broad-complex tachycardia. If the QRS duration is less than 0.12 s, it is a narrow-complex tachycardia.

Narrow Complex Tachycardia:

Narrow Complex Tachycardia Adverse sins: Systolic blood pressure < 90 mmHg Chest pain Heart failure Impaired consciousness Heart rate > 200 beats/min Treatment: Antiarrhythmic drugs – esmolol, amidarone DC shock

Narrow-complex tachycardia :

Narrow-complex tachycardia Examine the ECG to determine if the rhythm is regular or irregular. Regular narrow-complex tachycardias include :  sinus tachycardia ;  AV nodal re-entry tachycardia (AVNRT) – the commonest type of regular narrow-complex tachyarrhythmia;  AV re-entry tachycardia (AVRT) – due to WPW syndrome;  atrial flutter with regular AV conduction (usually 2:1). An irregular narrow-complex tachycardia is most likely to be AF or sometimes atrial flutter with variable AV conduction (‘variable block’).

Regular narrow-complex tachycardia :

Regular narrow-complex tachycardia 1-Sinus tachycardia Sinus tachycardia is not an arrhythmia. This is a common physiological response to stimuli such as exercise or anxiety. In a sick patient it may occur in response to many conditions including pain, infection, anaemia, blood loss, and heart failure. Treatment is directed at the underlying cause; trying to slow sinus tachycardia that has occurred in response to most of these conditions will make the situation worse. Do not attempt to treat sinus tachycardia with cardioversion or anti-arrhythmic drugs.

2-AVNRT and AVRT (paroxysmal supraventricular tachycardia:

2-AVNRT and AVRT (paroxysmal supraventricular tachycardia AV nodal re-entry tachycardia is the commonest type of paroxysmal supraventricular tachycardia (SVT), often seen in people without any other form of heart disease. It is relatively uncommon in the peri-arrest setting. It causes a regular, narrow-complex tachycardia, often with no clearly visible atrial activity on the ECG. The heart rate is commonly well above the typical range of sinus rhythm at rest (60-100 min-1).

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AV re-entry tachycardia occurs in patients with the WPW syndrome, and is also usually benign, unless there is additional structural heart disease. The common type of AVRT is a regular narrow-complex tachycardia, usually having no visible atrial activity on the ECG

Atrial flutter with regular AV conduction (often 2:1 block) :

Atrial flutter with regular AV conduction (often 2:1 block) This produces a regular narrow-complex tachycardia. Typical atrial flutter has an atrial rate of about 300 min-1, so atrial flutter with 2:1 conduction produces a tachycardia of about 150 min-1. Much faster rates (160 min-1 or more) are unlikely to be caused by atrial flutter with 2:1 conduction. Regular tachycardia with slower rates (e.g. 125-150) may be due to atrial flutter with 2:1 conduction, usually when the rate of the atrial flutter has been slowed by drug therapy.

Broad Complex Tachycardia:

Broad Complex Tachycardia Adverse signs: Rate > 150/min Chest pain Heart failure Systolic blood pressure < 90 mmHg Treatment: Amidarone, lidocaine DC shock

Broad-complex tachycardia:

Broad-complex tachycardia Broad-complex tachycardias (QRS ≥ 0.12 s) are usually ventricular in origin. Broadcomplex tachycardias may be also caused by supraventricular rhythms with aberrant conduction (bundle branch block).

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Regular broad-complex tachycardia A regular broad-complex tachycardia is likely to be VT or a supraventricular rhythm with bundle branch block . Irregular broad-complex tachycardia This is most likely to be atrial fibrillation (AF) with bundle branch block Other possible causes are AF with ventricular pre-excitation (in patients with Wolff-Parkinson-White (WPW) syndrome), or polymorphic VT (e.g. torsade de pointes),

Atrial fibrillation:

Atrial fibrillation Adeverse signs: Rate > 150/min Ongoing chest pain Critical perfusion Breathlessness Treatment: Anticoagulation, beta-blockers, digoxin, amiodarone Synchronised DC shock

Treatment of regular narrow-complex tachycardia:

Treatment of regular narrow-complex tachycardia If the patient is unstable , with adverse features caused by the arrhythmia, attempt synchronised electrical cardioversion. It is reasonable to give adenosine to an unstable patient with a regular narrow-complex tachycardia while preparations are being madefor synchronised cardioversion. However, do not delay electrical cardioversion if adenosine fails to restore sinus rhythm.

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In the absence of adverse features:  Start with vagal manoeuvres . Carotid sinus massage or the Valsalva manoeuvre will terminate up to a quarter of episodes of paroxysmal SVT. Record an ECG (preferably multi-lead) during each manoeuvre . If the arrhythmia persists and is not atrial flutter, give adenosine 6 mg as a rapid intravenous bolus. Use a relatively large cannula and large ( e.g.,antecubital ) vein.

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. Record an ECG (preferably multi-lead) during the injection. If the ventricular rate slows transiently, but then speeds up again, look for atrial activity, such as atrial flutter or other atrial tachycardia, and treat accordingly. If there is no response to adenosine 6 mg, give a 12 mg bolus. If there is no response give one further 12 mg bolus. Apparent lack of response to adenosine will occur if the bolus is given too slowly or into a peripheral vein.

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Vagal manoeuvres or adenosine will terminate almost all AVNRT or AVRT within seconds. Failure to terminate a regular narrow-complex tachycardia with adenosine suggests an atrial tachycardia such as atrial flutter (unless the adenosine has been injected too slowly or into a small peripheral vein).  If adenosine is contra-indicated, or fails to terminate a regular narrow complex tachycardia without demonstrating that it is atrial flutter, consider giving a calcium-channel blocker, for example verapamil 2.5 - 5 mg intravenously over 2 min.

Treatment of Irregular narrow-complex tachycardia:

Treatment of Irregular narrow-complex tachycardia If there are no adverse features, treatment options include:  rate control by drug therapy;  rhythm control using drugs to encourage chemical cardioversion;  rhythm control by electrical cardioversion;  treatment to prevent complications (e.g. anticoagulation ).

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To control heart rate, the usual drug of choice is a beta-blocker. Diltiazem or verapamil Digoxin may be used in patients with heart failure. Amiodarone may be used to assist with rate control but is most useful in maintaining rhythm control

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In general, patients who have been in AF for more than 48 should not be treated by cardioversion (electrical or chemical) until they have been fully anticoagulated for at least three weeks, give either: 1-regular low-molecular-weight heparin in therapeutic dose or 2-an intravenous bolus injection of unfractionated heparin followed by a continuous infusion

Treatment of Regular broad-complex tachycardia:

Treatment of Regular broad-complex tachycardia If the broad complex tachycardia is thought to be VT, treat with amiodarone 300 m intravenously over 20-60 min, followed by an infusion of 900 mg over 24 h. If a regular broad-complex tachycardia is known to be a supraventricular arrhythmia with bundle branch block, and the patient is stable, use the strategy indicated for narrow-complex tachycardia .

Treatment of Irregular broad-complex tachycardia:

Treatment of Irregular broad-complex tachycardia Treat torsade de pointes VT immediately by stopping all drugs known to prolong the QT interval. Correct electrolyte abnormalities, especially hypokalaemia. Give magnesium sulphate 2 g IV over 10 min If adverse features develop, immediate synchronised cardioversion. If the patient become pulseless, attempt defibrillation immediately

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Amiodarone:

Amiodarone - membrane-stabilising drug that increases : duration of the action potential refractory period in atrial and vetricular myocardium m ild negative inotrop ic action - may cause hypotension appers to improve the response to defibryllation

Amiodarone:

Amiodarone Indications: Refractory VF / Pulseless VT Haemodynamically stable VT Other resistant tachyarrhythmias

Amiodarone:

Amiodarone Dose: Refractory VF / Pulseless VT 300 mg diluted in 5% dextrose to a volume of 20ml , Stable tachyarrhythmias 150 mg in 5% dextrose over 10 min Repeat 150 mg if necessary 300 mg in 100 ml 5% dextrose over 1 hour

Adenosine:

Adenosine Naturally occuring purine nucleotide : Slows conduction across the AV node , Has little effect other myocardial cells Has short duration of action May reveal the underlying atrial rhythms by slowing the ventricular response Should be used in a monitored environment only

Adenosine:

Adenosine Indications: Undiagnosed narrow complex tachycardia Paroxysmal supraventricular tachycardia

Adenosine:

Adenosine Dose: 6 mg intravenously, by rapid injection to achieve adequate and effective blood levels If necessary, three further doses each of 12 mg can be given every 1–2 min

Magnesium sulphate:

Magnesium sulphate Constituent involved in ATP generation in muscle , neurochemical transmission : decreases acetylcholine release reduces the sensivity of the motor endplate improves the contractile response limits infarct size a cts as a physiological calcium blocker Hypomagnesaemia contribute to arrhythmias and cardiac arrest !!!

Magnesium sulphate:

Magnesium sulphate Indications: Shock refractory VF ( in the presence of possible hypomagnesaemia) Ventricular tachyarrhythmias ( in the presence of possible hypomagnesaemia) Digoxin toxicity ( hypomagnesaemia increases myocardial digoxin uptake )

Magnesium sulphate:

Magnesium sulphate Dose: Shock Refractory VF Initial dose – 2 g ( 4 ml (8 mmol ) ) of 50% magnesium sulphate i.v . over 1 – 2 min It may be repeated after 10-15 min

Bradycardia :

Bradycardia

Bradycardia is defined as a heart rate of < 60 min-1. :

Bradycardia is defined as a heart rate of < 60 min-1 . It may be:  physiological (e.g., in athletes);  cardiac in origin (e.g., atrioventricular block or sinus node disease);  non-cardiac in origin (e.g., vasovagal, hypothermia, hypothyroidism, hyperkalaemia);  drug-induced (e.g., beta blockade, diltiazem, digoxin, amiodarone).

Bradycardia – heart rate < 60/min:

Bradycardia – heart rate < 60/min Adverse signs: Systolic blood pressure < 90 mmHg Heart rate < 40/min Ventricular arrhytmias requiring suppresion Heart failure Treatment: Atropine Cardiac pacing – presence the risk os asystole Möbitz Type II Block

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If bradycardia with adverse signs persist despite atropine, consider cardiac pacing. If pacing cannot be achieved promptly consider the use of second-line drugs. In some clinical settings second-line drugs may be appropriate before the use of cardiac pacing. For example consider giving intravenous glucagon if a beta-blocker or calcium channel blocker is a likely cause ofthe bradycardia. Consider using digoxin-specific antibody fragments for bradycardia due to digoxin toxicity. Consider using theophylline (100-200 mg by slow intravenous injection) for bradycardia complicating acute inferior wall myocardial infarction, spinal cord injury or cardiac transplantation

Pacing Transcutaneous pacing:

Pacing Transcutaneous pacing ( also called external pacing) is a temporary means of pacing a patient's heart during a medical emergency. It is accomplished by delivering pulses of electric current through the patient's chest, which stimulates the heart to contract. The most common indication for transcutaneous pacing is an abnormally slow heart rate . By, a heart rate of less than 60 beats per minute in the adult patient is called bradycardia Initiate transcutaneous pacing immediately if there is no response to atropine, or if atropine is unlikely to be effective

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During transcutaneous pacing, pads are placed on the patient's chest, either in the anterior/lateral position or the anterior/posterior position. The anterior/posterior position is preferred as it minimizes transthoracic electrical impedance by "sandwiching" the heart between the two pads. The pads are then attached to a monitor/defibrillator, a heart rate is selected, and current (measured in milliamps) is increased until electrical capture (characterized by a wide QRS complex with tall, broad T wave on the ECG ) is obtained, with a corresponding pulse.

Pacing :

Pacing . Transcutaneous pacing can be painful and may fail to achieve effective electrical capture (i.e. a QRS complex after the pacing stimulus) or fail to achieve a mechanical response (i.e. palpable pulse). Verify electrical capture on the monitor or ECG and check that it is producing a pulse. Reassess the patient’s condition (ABCDE). Use analgesia and sedation as necessary to control pain; sedation may compromise respiratory effort so continue to reassess the patient at frequent intervals .

Fist pacing :

Fist pacing If atropine is ineffective atranscutaneous pacing is not immediately available, fist pacing can be attempted while waiting for pacing equipment. Give serial rhythmic blows with the closed fist over the left lower edge of the sternum to stimulate the heart at a rate of 50-70 min-1.

Tran venous pacing :

Tran venous pacing also called endocardial pacing , is a potentially life saving intervention used primarily to correct profound bradycardia. It can be used to treat symptomatic bradycardias that do not respond to transcutaneous pacing or to drug therapy. Transvenous pacing is achieved by threading a pacing electrode through a vein into the right atrium, right ventricle, or both.

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Temporary transvenous pacing should be considered if there is documented recent asystole (ventricular standstill of more than 3 s), Mobitz type II AV block; complete (third-degree) AV block (especially with broad QRS or initial heart rate <40 beats min-1).

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the procedure is done at the bedside with a local anesthetic alone or in conjunction with conscious sedation . The pacing electrode is advanced through the vein under flouroscopic and electrocardiographic guidance. An x-ray after the procedure is always obtained to confirm placement of the pacing electrode .

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Castle LW, Cook S: Pacemaker radiography. In Ellenbogen KA, Kay GN, Wilkoff BL [eds]: Clinical Cardiac Pacing. Philadelphia, WB Saunders, 1995, p 538.

The Pacemaker System:

The Pacemaker System Patient Lead Pacemaker Programmer Lead Pacemaker

Acute Complications of Pacemaker Implantation:

Acute Complications of Pacemaker Implantation Venous access Pneumothorax, hemothorax Air embolism Perforation of central vein Inadvertent arterial entry Lead placement Brady – tachyarrhythmia Perforation of heart, vein Damage to heart valve Generator Pocket hematoma Improper or inadequate connection of lead

Delayed Complications of Pacemaker Therapy:

Delayed Complications of Pacemaker Therapy Lead-related Thrombosis/embolization SVC obstruction Lead dislodgement Infection Lead failure Perforation, pericarditis Generator-related Pain Erosion, infection Migration Damage from radiation, electric shock

Pacemaker Follow-up:

Pacemaker Follow-up GOAL OF FOLLOW-UP Verify appropriate pacemaker operation Optimize pacemaker functions Document findings, changes and final settings in order to provide appropriate patient management

O2:

O 2 Please help me reach the brain within 3 min.!!! THANKYOU

THANKS……:

THANKS ……