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BASIC LIFE SUPPORT GUIDELINES IN GIVING EMERGENCY CARE GETTING STARTED 1. Plan of Action Emergency plans should be established based on anticipated needs and available resources 2. Gathering of Needed Materials The emergency response begins with the preparation of equipment and a personnel before any emergency occurs. 3. Initial Response ‡ Ask for HELP. ‡ Intervene ‡ Do no further harm 4. Instruction to Helper/s Proper information and instruction to a helper/s would provide organized first aid care. EMERGENCY ACTION PRINCIPLES Activate Medical Assistance In some emergency, you will have enough time to call for specific medical advice before administering first aid. But in some situations, you will need to attend to the victim first. Call First and Care first adult victim = call first . infants and children = care first Do a Primary Survey In every emergency situation, you must first find out if there are conditions that are an immediate threat to the victim s life 1. Check for Consciousness 2. Check for Airway 3. Check for Breathing 4. Check for Circulation ‡ RESPIRATION - Respiration = 1 A. INTERVIEW THE VICTIM inhalation & 1 exhalation ‡ Victim s name ‡ SKIN APPEARANCE ‡ Address Temperature, color & capillary ‡ Phone number refill ‡ Ask what happen ‡ PUPILS - PERRLA ‡ S A M P L E history ‡ BLOOD PRESSURE ‡ Signs & symptoms C. PERFORM HEAD-TO-TOE EXAMINATION ‡ Allergies ‡ Deformities ‡ Medications ‡ Contusions ‡ Past medical history ‡ Abrasions ‡ Last oral intake ‡ Punctures/penetrations ‡ Events prior to the episode ‡ Burns B. CHECK VITAL SIGNS ‡ Tenderness ‡ PULSE - Rate, Strength & ‡ Lacerations Rhythm ‡ Swelling Basic Precautions and Practices ‡ Personal Hygiene ‡ Protective Equipment ‡ Equipment Cleaning & Disinfecting Review on breathing and circulation ‡ Air that enters the lungs contains about _____% oxygen and only a trace of carbon dioxide. ‡ Air that is exhaled from the lungs contains about ______% oxygen and ______% carbon dioxide. BASIC LIFE SUPPORT An emergency procedure that consists of recognizing respiratory or cardiac arrest or both and the proper application of CPR to maintain life until a victim recovers or advanced life support is available. Guidelines The American Heart Association s Guidelines for CPR and ECC provide science-based recommendations for treating cardiovascular emergencies, particularly sudden cardiac arrest in adults, children, infants and newborns. Every five years, hundreds of leading resuscitation experts from around the world review all new and existing research as part of an international consensus process. This is the basis for any revisions to the American Heart Association s Guidelines for CPR and ECC. History of CPR In 1960, researchers combined breaths and compressions to create CPR as we know it today. CPR training has been recommended for healthcare professionals and for the general public for more than 40 years. 2010 marks a change in the sequence of CPR from Airway-Breaths-Compressions (A-B-C) to Compressions-Airway-Breaths (C-A-B) sequence. Sudden Cardiac Arrest EMS treats nearly 300,000 victims of out-of-hospital cardiac arrest each year in the U.S. Less than eight percent of people who suffer cardiac arrest outside the hospital survive to make it home from the hospital. Sudden cardiac arrest can happen to anyone at any time. Many victims appear healthy with no known heart disease or other risk factors. Sudden cardiac arrest is not the same as a heart attack. Strengthening the Links in the Chain of Survival Immediate recognition of cardiac arrest and activation of the emergency response system Early CPR with an emphasis on chest compressions Rapid defibrillation Effective advanced life support Integrated post cardiac arrest care Respiratory Arrest - the condition in which the breathing stops or inadequate

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3. Other causes of Respiratory Arrest Electrocution Circulatory collapse Anatomical External strangulation Mechanical Chest compression (by physical forces) 2. Diseases Drowning Bronchitis Poisoning Pneumonia Suffocation COPD Rescue Breathing - a technique of breathing air into a person s lungs to supply him / her with the oxygen needed to survive Cardiopulmonary-cerebro Resuscitation (CPCR) Less than one-third of out-of-hospital sudden cardiac arrest victims receive bystander CPR. Effective bystander CPR, provided immediately after sudden cardiac arrest, can double or triple a victim s chance of survival. Chest compressions should be provided at a rate of at least 100 compressions per minute the same rhythm as the beat of the Bee Gee s song, Stayin Alive. Compressions of adequate rate and depth allowing complete chest recoil between compressions minimizing interruptions in compressions avoiding excessive ventilation Building Blocks of CPR Simplified Adult BLS Algorithm. Causes: 1. Obstruction

YOUR ROLE IN A CODE BLUE PHASE I: Putting the code in motion NURSE 1 NURSE2 - LOC - Call for help - Check circulation - Initiate CPCR make sure the code has been called according to hospital procedure Obtain emergency equipment (Crash cart) Begin 2-responder CPCR with nurse 1

NURSE 3 / 4 Connect the patient to a monitor Set up AED or defibrillator, oxygen, and suction equipment Get intubation equipment ready Set up IV equipment

Phase II: Drugs and Defibrillation Initiate ACLS protocols and evaluation of the patient s response to therapy CODE TEAM Team Leader Usually a physician directs and coordinates the resuscitation effort, but a nurse who s trained in ACLS may direct the code until a physician arrives The team leader usually stands at the foot or head of the bed: she needs a clear view of the patient to ensure that procedures and patient assessments are performed rapidly and correctly Defibrillator Operator A physician or a specially prepared nurse actually delivers the shock Rapid defibrillation is the key to survival from ventricular fibrillation, so the team must be prepared to defibrillate immediately. -

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Recorder At the start of the code, one nurse should begin recording the events and interventions Document all events and interventions, including the type and time of arrest, respiratory management, procedures, medication administration, Iv fluids, VS, cardiac rythms, defibrillations, patient response to treatment, patient outcome, and termination of code. The role of a recorder is vital. She should nt be asked to participate in any other way that distracts her from this responsibility. An important duty of a recorder is to announce when a medication maybe due Identify which clock should be the official code clock and be precise about the timing on the resuscitation record. A physician (anaesthesiologist), respiratory therapist, nuse anesthetist, or other specially prepared nurse may do so. Prepare: Laryngoscope : endotracheal tube and a stylet : 10 ml syringe : Lubricating gel : Suction to remove oral secretions and improve visualization of anatomical landmarks : Stethoscope If patient can t be intubated within 30 seconds, stop and hyperventilate and hyperoxygenate Solutions typically used during resuscitation efforts include .9% sodium chloride and lactated ringers solution Familiarize self with the drugs used during codes As you prepare a drug, repeat the drug name and dosage order out loud, so no one s confused about what you re drawing up. Again, announce the drug and dosage prior to administration Throughout the entire code, the other patients in the unit must be cared for

Intubationist -

IV nurse

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Medication nurse

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Floor nurse

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Phase III: Winding down Typically begins after initial ACLS measures have been instituted and their effectiveness evaluated. In this phase, the team leader continues to coordinate all the medical therapies, vital signs, cardiac rhythm, and patient response must be assessed frequently throughout the code. Efforts are now aimed at one of the following: Maintaining the patient in stable condition until he can be transported to a critical care bed Attempting other strategies to restore cardiac function Deciding to terminate the code Key Challenges to Improve CPR Quality for Adults, Children, and Infants Recognition Failure to recognize gasping as sign of cardiac arrest Unreliable pulse detection Initiation of CPR Low bystander CPR response rates Incorrect dispatch instructions Compression rate Slow compression rate Compression depth Shallow compression depth Chest wall recoil Rescuer leaning on the chest Compression Interruptions Excessive interruptions for rhythm/pulse checks ventilations defibrillation intubation intravenous (IV) access other Ventilation Ineffective ventilations Prolonged interruptions in compressions to deliver breaths Excessive ventilation (especially with advanced airway) Defibrillation Prolonged time to defibrillator availability Prolonged interruptions in chest compressions pre- and post-shocks Team Performance Delayed rotation, leading to rescuer fatigue and decay in compression quality Poor communication among rescuers, leading to unnecessary interruptions in compressions Being prepared y Each code situation is unique. y Knowing that a code usually progresses through three phases will help you feel more confident when the actual event occurs. Tips to fine-tune your skills  Keep your CPCR skills up-to-date and review hospital policy on code procedures and documentation  Know current BLS guidelines  If rule permit, open your crash cart and medication box every 1 to 2 months and review where supplies and medications are located.  Review the drugs used most frequently during a code and their indications, usual dosages, dilutions, and administration times.  Know how to operate the cardiac monitor and AED in you unit.  Make sure you know how to change batteries in the laryngoscope handle and the lightbulb in the blade. Practice connecting the handle to the blade

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These preparations will help you stay calm and focused during a code organized code.!! and may make the difference between chaos and a smooth-running, well-

CARDI AC ARREST DEFINITION y It is the cessation of effective pumping action of the heart wherein the electro-conduction of the heart suddenly stops due to cardiac related disorders. y When this happens, blood stops flowing into the brain and vitals organs which in turn will cause death to a person within minutes if untreated. y Irreversible brain damage can occur within ten minutes if arrest is not treated. y About 95% of people who experiences cardiac arrest die, most within minutes CAUSES ‡ ‡ Most cases of cardiac arrest are due to ventricular fibrillation and other electrical related problems of the heart such as CAD and MI. Other causes may include the following: ‡ Physical stress ‡ Inherited problems (LQTS) ‡ Structural changes in the heart (cardiomegaly)

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Physical Stress Certain types of physical stress can cause the heart's electrical system to fail. Examples include:  Intense physical activity. The hormone adrenaline is released during intense physical activity. This hormone can trigger CA in people who have other heart problems.  Very low blood levels of potassium or magnesium. (These minerals play an important role in your heart's electrical signaling).  Major blood loss. (surgical operations)  Severe lack of oxygen. Inherited Disorders LQTS (Long QT syndrome)  is a disorder of the heart's electrical activity due to problems with tiny pores on the surface of heart muscle cells. LQTS can cause sudden, uncontrollable, dangerous heart rhythms. Septal Defects  Patent ductus arteriosus  Atrial septal defect  Ventricular septal defect Many cases of CA in children are due to these problems. Non cardiac causes  35% of SCDs are related to non cardiac causes. The most common non cardiac causes were: trauma, non-trauma related bleeding (such as gastrointestinal bleeding, aortic rupture, and intracranial hemorrhage), overdose, drowning and pulmonary embolism. Non cardiac causes the H s  Non cardiac causes the T s  Hypovolemia - A lack of blood volume  Tablets or Toxins  Hypoxia - A lack of oxygen  Cardiac Tamponade - Fluid building around the heart  Hydrogen ions (Acidosis) - An abnormal pH in the body  Tension pneumothorax - A collapsed lung  Hyperkalemia or Hypokalemia - Both excess and inadequate  Thrombosis (CVA) - stroke potassium can be life-threatening.  Thromboembolism (Pulmonary embolism) - A blood clot in the lung  Hypothermia - A low core body temperature  Trauma  Hypoglycemia or Hyperglycemia - Low or high blood glucose Risk Factors ‡ Persons with heart problems  CAD  CHF  Hypertension ‡ Obesity ‡ Cigarette smoking ‡ Drug abusers and excessive alcohol intoxication ‡ Affects men twice as often as women and those aging 35-45 years old.  CA in children is rare unless they have inherited heart conditions. Signs and Symptoms ‡ Usually, the first sign of cardiac arrest is loss of consciousness (fainting). At the same time, no heartbeat (or pulse) can be felt. ‡ Some people may experience the following prior to loss of consciousness:  a racing heartbeat (tachycardia)  feeling dizzy or lightheadedness  chest pain  shortness of breath  nausea and vomiting. Diagnosis ‡ Cardiac arrest is rarely diagnosed before it can happen or as it is happening due to the fact that it can occur without warning. ‡ Instead it is diagnosed after the incident through series of laboratory exams and by ruling out other causes of a person s sudden collapse. Diagnostic Test  EKG  Painless procedure that records the electrical activity of the heart, used to detect and locate the source of several heart problems.  It also shows the rhythm and strength of the heart to pump blood.  Echocardiogram  is a painless test that uses sound waves to create pictures of the heart. It provides the doctor with information about the size and shape of the heart and how well the heart's chambers and valves are working.  The test also can find areas of heart muscle that aren't contracting normally due to poor blood flow or injury from a previous heart attack.  Cardiac magnetic resonance imaging (MRI)  is a safe procedure that uses radio waves and magnets to create detailed pictures of the heart. The test creates images of the heart as it is beating, producing both still and moving pictures of the heart and major blood vessels.  Cardiac catheterization o is a procedure used to diagnose and treat certain heart conditions. A long, thin, flexible tube (catheter) is put into a blood vessel in an arm, groin or neck and threaded to the heart. Through the catheter, the doctor can do diagnostic tests and treatments on the heart.  Sometimes a special dye is put into the catheter to make the inside of the heart and blood vessels show up on x rays. The dye can show whether plaque has narrowed or blocked any coronary artery.  In addition the patient may have blood tests to check the levels of potassium, magnesium, and other chemicals in the blood that play an important role in the heart's electrical signaling. o CBC o Troponin T/I Used to diagnose MI o CPK-MB

Treatment

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Emergency Treatment includes the following: o Use of defibrilator (AED)  AEDs unlike the conventional defibrilator, are programmed devices with command features that tells the rescuer what to do, thereby reducing the risk of giving too much electric shock. o CPR- cardio pulmonary rescusitation o Emergency drugs e.g. epinephrine Treatment in the hospital depends on the cause of cardiac arrest but generally will include the following: o Cardiac drugs- beta blockers o Sympathomimetic drugs- dobutamine o Catecholamines- dopamine o The latter two drugs are used to control hypertension and may be given as adjuncts via continuous intravenous drip. Prevention is better than CURE o Lifestyle changes  Daily regular exercise  Avoidance of foods high in sodium, trans fat, & sugar  Stay within your caloric levels and increase intake of fruits and vegetables.  Maintain appropriate weight by balancing intake and activity levels  Quit smoking and excessive alcohol consumption.  

MYOCARDIAL INFARCTION Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as a heart attack, is the interruption of blood supply to a part of the heart, causing heart cells to die. This is most commonly due to occlusion (blockage) of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, which is an unstable collection of lipids (fatty acids) and white blood cells (especially macrophages) in the wall of an artery. The resulting ischemia (restriction in blood supply) and oxygen shortage, if left untreated for a sufficient period of time, can cause damage or death (infarction) of heart muscle tissue (myocardium).

TYPES OF MI ‡ A transmural MI is characterized by ischemic necrosis of the full thickness of the affected muscle segment(s), extending from the endocardium through the myocardium to the epicardium. ‡ A nontransmural MI is defined as an area of ischemic necrosis that does not extend through the full thickness of myocardial wall segment(s). In a nontransmural MI, the area of ischemic necrosis is limited to the endocardium or to the endocardium and myocardium. ‡ It is the endocardial and subendocardial zones of the myocardial wall segment that are the least perfused regions of the heart and the most vulnerable to conditions of ischemia ‡ 1. Q wave infarction, which is diagnosed by the presence of pathological Q waves and is also called transmural infarction. However, transmural infarction is not always present; hence, the term Q-wave infarction may be preferable for ECG description ‡ 2. Non-Q wave infarction, which is diagnosed in the presence of ST depression and T wave abnormalities. Symptoms of acute myocardial infarction ‡ sudden chest pain (typically radiating to the left arm or left side of the neck) ‡ shortness of breath ‡ nausea& vomiting ‡ Palpitations ‡ sweating ‡ anxiety (often described as a sense of impending doom) ‡ Women may experience fewer typical symptoms than men, most commonly shortness of breath, weakness, a feeling of indigestion, and fatigue. ‡ Approximately one quarter of all myocardial infarctions are "silent", without chest pain or other symptoms. Diagnostic tests ‡ electrocardiogram (ECG) ‡ Echocardiography ‡ blood tests The most often used markers are the creatine kinase-MB (CK-MB) fraction and the troponin levels. Treatment ‡ Immediate treatment is to give oxygen, aspirin, and sublingual nitroglycerin. ‡ Most cases of STEMI (ST elevation MI) are treated with thrombolysis or percutaneous coronary intervention (PCI). NSTEMI (non-ST elevation MI) should be managed with medication, although PCI is often performed during hospital admission. In people who have multiple blockages and who are relatively stable, or in a few emergency cases, bypass surgery may be an option. ‡ *Nitroglycerin 3 tabs 5 mins apart ELECTROCARDIOGRAM ‡ a diagnostic tool that measures and records the electrical activity of the heart in exquisite detail. Interpretation of these details allows diagnosis of a wide range of heart conditions. These conditions can vary from minor to life threatening. ‡ The term electrocardiogram was introduced by Willem Einthoven in 1893 at a meeting of the Dutch Medical Society. In 1924, Einthoven received the Nobel Prize for his life's work in developing the ECG. ‡ The 12- lead ECG that is used throughout the world was introduced in 1942. ‡ Reasons to Have an ECG Heart problems can produce a wide array of symptoms. ‡ Without the benefit of an ECG, it may be impossible to tell whether these symptoms are being caused by a heart problem or just mimicking one. Common symptoms that frequently require an ECG include the following: ‡ Chest pain or discomfort ‡ Shortness of breath ‡ Nausea ‡ Weakness ‡ Palpitations (rapid or pounding heartbeats or increased awareness of heart beating) ‡ Anxiety

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‡ Abdominal pain ‡ Fainting (syncope) The Heart ‡ The heart itself is made up of 4 chambers, 2 atria and 2 ventricles. De-oxygenated blood returns to the right side of the heart via the venous circulation. It is pumped into the right ventricle and then to the lungs where carbon dioxide is released and oxygen is absorbed. The oxygenated blood then travels back to the left side of the heart into the left atria, then into the left ventricle from where it is pumped into the aorta and arterial circulation. ‡ Systolic blood pressure: ‡ Is the pressure created in the arteries when the ventricles contract ‡ Diastolic blood pressure: ‡ When the ventricles starts to refill, the pressure from the arteries falls simultaneously the atriums contract creating pressure known as the diastolic pressure. Role of the ECG Machine y The ECG machine is designed to recognise and record any electrical activity within the heart. It prints out this information on ECG paper made up of small squares 1mm squared.

Each electrical stimulus takes the form of a wave and so patterns emerge made up of a number of connected waves. A standard ECG is printed at 25mm per second or 25 small squares per second (see above). In this way it is possible to calculate the duration of individual waves. ‡ 10 small squares vertically is equal to 1 millivolt. So it is possible to calculate the amount of voltage being released within the heart. If the line is flat at any time in the duration of a series of waves, it indicates no electrical activity at that particular moment. ‡ The direction in which the waves point indicates whether electricity is moving towards or away from a particular lead. Sinus Rhythm ‡ Sinus rhythm is the name given to the normal rhythm of the heart where electrical stimuli are initiated in the SA node, and are then conducted through the AV node and bundle of His, bundle branches and Purkinje fibres. ‡ Depolarisation and repolarisation of the atria and ventricles show up as 3 distinct waves on ECG. A unique labelling system is used to identify each wave. ‡ Less muscle means less cells which means less voltage. ‡

The QRS Complex ‡ ‡ After the first wave there follows a short period where the line is flat. This is the point at which the stimulus is delayed in the bundle of His to allow the atria enough time to pump all the blood into the ventricles. As the ventricles fill, the growing pressure causes the valves between the atria and ventricles to close. At this point the electrical stimulus passes from the bundle of His into the bundle branches and Purkinje fibres. The amount of electrical energy generated is recorded as a complex of 3 waves known collectively as the QRS complex. Measuring the waves vertically shows voltage. More voltage is required to cause ventricular contraction and therefore the wave is much bigger. Q wave and represents depolarisation in the septum.

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The R Wave ‡ R wave represents the ventricular depolarisation

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The S Wave ‡ S wave represents depolarisation of the Purkinje fibres.

The T Wave ‡ T wave represents ventricular repolarisation.

The ST Segment ‡ There is a brief period between the end of the QRS complex and the beginning of the T wave where there is no conduction and the line is flat. This is known as the ST segment and it is a key indicator for both myocardial ischemia and necrosis if it goes up or down.

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V1: 4 intercostal space right sternal border th V2: 4 intercostal space left sternal border V3: halfway between V2 and V4 th V4: left 5 intercostal space,mid-clavicular line V5: horizontal to V4, anterior axillary line V6: horizontal to V5, mid-axillary line

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Points To Remember: ‡ Ask the patient to remove all metalic objects including watches, rings, neclaces, pocketed coins and phones etc

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‡ Let the patient relax before the procedure starts and ask them to lay still for a minute during the procedure. ‡ Explain the procedure and reassure them that no pain will be felt during the procedure. Emergency DRUGS y Nsg considerations Epinephrine y May cause tachycardia and other arhythmias, BP y Indication fluctuations, nausea and hypokalemia y VF, pulseless VT, or asystole y Monitor heart closely; increases in heart heart y 1 mg I.V push every 3-5 min rate more than 10% may induce or exacerbate y Intermediate dosing: 2-5 mg IV push over 3Myocardial Ischemia 5 min Dopamine y Escalating dosing: 1mg, 3mg, 5 mg IV push 3 y Hypotension with symptomatic bradycardia, heart failure or min apart after spontaneous return of circulation y High dosing: ,1 mg/kg IV push every 3 5 y Initially, 1-5 mcg/kg/min; max is 20 mcg/kg/min min y Enhances renal blood flow 1-2 mcg/kg/min y Symptomatic Bradycardia: continous infusion at 2-10 y Nsg consideration mcg/min; titrate to hemodynamic response y May induce tachycardia, - dose y Nsg. consideration reduction/withdrawal y Each dose is followed by 20 mL iv fluid flush. y Extravasation may cause severe tissue necrosis y Can be given via ET tube 2-2.5 x the IV dose, followed y Norepinephrine should be added is more than with 10 mL Flush PNSS max dose is needed to maintain BP y IC when no other route is available y Use slowest infusion first y It increases systemic vascular resistance, BP, Cardiac y Can exacerbate pulmonary congestion and elec. Activity, strenth of contraction, automaticity, and compromise cardiac output myocardial O2 requirement y Eliminate hypovolemia as a cause of hypotension Lidocaine before treating y Indication Magnesium y VF or Pulseless VT: Initially 1-1.5 mg/kg IV push: every 3-5 y VF/VT with hypomagnesemia mins, max of 3mg/kg y 1-2 grams diluted in 10 mL D5W given IV push y Stable VT or Stable wide-complex tachycardia: repeat doses over 1-2 min half the original dose. y Torsades de pointes: 5-10 grams iv y If lidocaine succesfully converts the VF/VT: begin continous y Torsades de pointes, or simply torsades is a infusion at 2-4 mg/min French term that literally means "twisting of the y Nsg consideration y Toxicity( Slurred speech, altertered LOC, Muscle twitching, points". It was first described by Dessertenne in and seizures), stop the drug/reduce dose 1966 and refers to a specific, rare variety of y Via ET: 2-2.5 times the iv dose, flush with 10 ml PNSS ventricular tachycardia that exhibits distinct characteristics on the electrocardiogram (ECG). y Don t give if PVC occurs with bradycardia or escape rhythm. y No longer recommended for VT/VF prophylaxis in acute MI y Characteristics Atropine y Rotation of the heart's electrical axis y Symptomatic Bradycardia by at least 180º y .5-1 mg iv push q 3-5 min, not to exceed .04 y Prolonged QT interval (LQTS) mg/kg y Preceded by long and short RRy Asystole intervals y 1 mg iv push q 3-5 min, not to exceed a total dose y Triggered by an early premature of .04mg/kg ventricular contraction y Nsg consideration y Don t give less than .5 mg dose may further y Acute MI with hypomagnesemia slow heart rate y Intermitent of continous infusions y Via ET: dilute 1-2 mg in 10 mL sterile water of y Nsg consideration PNSS, flush with 10 mL PNSS Adenosine y Flushing, sweating, mild bradycardia, and hypotension y wide-complex tachycardia: may develop from rapid administration in non arrest y Initially 6 mg rapid iv push; if no response in 1-2 situations min, give 12 mg iv push; may be followed by a Procainamide third 12 mg dose given in 1-2 min. y Nsg consideration y PVCs or recurrent VT with pulse y Given rapidly over 1-3 sec y Initially, 20 mg/min until y Follow dose with a 20 ml PNSS flush y Hypotension occurs y If methylxanthines, dipyridamole and y QRS complex carbamazepine are present higher dose may be y PR interval needed y QT interval is widened by 50 % y A brief period of Asystole is common after y Total of 17mg/kg of the drug was administration administered Bretylium y Maintenance infusion 1-4 mg/min y VF/ pulseless VT unresponsive to defibrilation, epi and lido y Nsg consideration y 5mg/kg iv push; if arhythmia persists, increase to y Monitor BP closely during administration; may cause 10 mg/kg q 5-10 min, to a max dose of 35 mg/kg precipitous hypotension, infuse cautiously in patients y Stable VT or Stable wide-complex tachycardia: with acute MI y 5-10 mg/kg over 8-10 min, to max 35 mg/kg over y Contraindicated in patients with preexisting long QT 24 hrs, if loading dose converts arhythmia start intervals and torsades de pointes infusion of 2 mg/min. Dobutamine y Heart Failure y 2-20 mcg/kg/min

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