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Presentation on theme: "Marian Williams RN BN CEN CCRN CFRN CTRN BASIC ECG INTERPRETATION Marian Williams RN."— Presentation transcript:


2 Heart Anatomy Layers Pericardium Myocardium Endocardium Four Chambers Atria Left Right Ventricles Left Right Marian Williams RN


4 Heart Valves Atrioventricular Bicuspid Tricuspid Semi-lunar Pulmonic Aortic Marian Williams RN


6 Major Vessels Superior Vena Cava Inferior Vena Cava Coronary Sinus Aorta Pulmonary Vein Pulmonary Artery Marian Williams RN

7 Heart Blood Flow Marian Williams RN

8 Cardiac Cycle Atrial Systole Atrial Kick Atrial Diastole Ventricular Systole Ventricular Diastole Marian Williams RN




12 Coronary Arteries Right Coronary Artery Posterior Descending SA Node (60%) Right Atrium Right Marginal Right Ventricle AV node (85%-90%) Proximal portion Bundle of His Part of Left Bundle Branch Marian Williams RN


14 Coronary Arteries Left Coronary Artery Left Anterior Descending Anterior – Left Ventricle Right Bundle Branch Part – Lateral Left Ventricle Most Interventricular Septum Left Bundle Branch Marian Williams RN

15 Coronary Arteries Circumflex Left Atrium Lateral – Left Ventricle Inferior–Left Ventricle (15%) Posterior-Left Ventricle SA Node (40%) AV Node (10%-15%) Marian Williams RN


17 Cardiac Muscle Syncytium Network of cells – Electrical impulses Atrial Ventricular Sarcolemma Membrane enclosing cardiac cell Marian Williams RN

18 Cardiac Muscle Sarcolemma Holes in Sarcolemma T-(transverse) tubules Go around muscle cells Conduct impulses Sarcoplasmic Reticulum Series of tubules Stores Calcium Calcium moved from sarcoplasm into sarcoplasmic reticulum by pumps Marian Williams RN

19 Cardiac Muscle Sarcomeres Made of thick and thin filaments Thin Troponin Thick Myosin Contraction Thin/thick filaments slide over each other Marian Williams RN

20 Cardiac Muscle Marian Williams RN

21 ION Concentrations Extracellular Sodium and Chloride Intracellular Potassium and Calcium

22 Cardiac Muscle Channels Openings (pores) in cell membrane Sodium – Na+ Potassium – K+ Calcium – Ca++ Magnesium – Mg++ Marian Williams RN

23 EFFECTS ON HEART RATE 1. Baroreceptors (Pressure) Internal Carotids Aortic Arches Detects changes in BP 2. Chemoreceptors Internal Carotids Aortic Arches Changes in pH (Hydrogen Ion, Oxygen, Carbon Dioxide) Marian Williams RN

24 Autonomic Nervous System Parasympathetic SA Node Atrial Muscle AV Node Vagus Nerve Acetycholine is released and binds to parasympathetic receptors Slows SA node rate Slows AV Conduction Decreases atrial contraction strength Marian Williams RN

25 Autonomic Nervous System Sympathetic Electrical system Atrium Ventricles Norepinephrine release Increased force of contraction Increased heart rate Increased BP Marian Williams RN

26 Autonomic Nervous System Sympathetic Receptor Sites Alpha Receptors Constriction of blood vessels Skin Cerebral Splanchnic Beta 1 Receptors Heart Beta 2 Receptors Lungs Skeletal Muscle Blood Cells Dopaminergic Receptors Coronary arteries Renal Blood Vessels Mesenteric Blood Vessels Visceral Blood Vessels Marian Williams RN

27 CARDIAC OUTPUT Stroke Volume x Heart Rate = CO (4-8 L/min) Stroke Volume approx. 70 ml/beat Increased by: Adrenal medulla Norepinephrine; Epinephrine Pancreas Insulin; Glucagon Medications Calcium; Digitalis; Dopamine; Dobutamine Marian Williams RN

28 CARDIAC OUTPUT Decrease in Force of Contraction Severe hypoxia Decreased pH Elevated carbon dioxide Medications – Calcium channel blockers, Beta Blockers Marian Williams RN

29 BLOOD PRESSURE Definition Force exerted by circulating blood on artery walls Equals: Cardiac output xs peripheral vascular resistance CO x PVR Marian Williams RN

30 STROKE VOLUME Stroke Volume determined by Preload Force exerted on ventricles walls at end of diastole Increased volume means increased preload Afterload Pressure or resistance against which the ventricles must pump to eject blood Marian Williams RN


32 STROKE VOLUME Afterload influenced by: Arterial BP Ability of arteries to stretch Arterial resistance Marian Williams RN

33 STROKE VOLUME Frank Starlings Law The greater the volume of blood in the heart during diastole, the more forceful the cardiac contraction, the more blood the ventricle will pump (to a point) Marian Williams RN

34 CARDIAC CELLS Two Types Myocardial Cells Mechanical Can be electrically stimulated Cannot generate electricity Pacemaker Cells Electrical cells Spontaneously generate electrical impulses Conduct electrical impulses Marian Williams RN

35 CARDIAC CELLS Current Electrical charge flow from one point to another Voltage Energy measurement between positive and negative points Measured in millivolts Marian Williams RN

36 CARDIAC CELLS Action Potential Five Phase cycle reflecting the difference in concentration of electrolytes (Na+, K+, Ca++, Cl-) which are charged particles across a cell membrane The imbalance of these charged particles make the cells excitable Marian Williams RN

37 Cardiac Cell Action Potential Phase 0 Depolarization Rapid Na+ entry into cell Phase 1 Early depolarization Ca++ slowly enters cell Phase 2 Plateau-continuation of repolarization Slow entry of Sodium and Calcium into cell

38 Cardiac Cell Action Potential Phase 3 Potassium is moved out of the cell Phase 4 Return to resting membrane potential


40 CARDIAC CELLS At rest K+ leaks out Protein & phosphates are negatively charged, large and remain inside cell Polarized Cell More negative inside than outside Membrane potential is difference in electrical charge (voltage) across cell membrane Marian Williams RN

41 CARDIAC CELLS Current (flow of energy) of electrolytes from one side of the cell membrane to the other requires energy (ATP) Expressed as volts Measured as ECG Marian Williams RN

42 CARDIAC CELLS Depolarization When interior of cell becomes more positive than negative Na+ and Ca+ move into cell and K+ and Cl- move out Electrical impulse begins (usually) in SA node through electrical cells and spreads through myocardial cells Marian Williams RN

43 CARDIAC CELLS Repolarization Inside of cell restored to negative charge Returning to resting stage starts from epicardium to endocardium Marian Williams RN

44 CARDIAC CELLS Action Potential Phase 0 – rapid depolarization Na+ into cell rapidly Ca++ into cell slowly K+ slowly leaks out Phase 1 – early rapid repolarization Na+ into cell slows Cl- enters cell K+ leaves Phase 2 – Plateau Ca++ slowly enters cell K+ still leaves Phase 3 – Final rapid repolarization K+ out of cell quickly Na+ & Ca++ stop entering VERY SENSITIVE TO ELECTRICAL STIMULATION Marian Williams RN

45 CARDIAC CELLS Phase 4 – Resting membrane potential Na+ excess outside K+ excess inside Ready to discharge Marian Williams RN

46 CARDIAC CELLS Properties 1. Automaticity 1. Cardiac pacemaker cells create an electrical impulse without being stimulated from another source 2. Excitability 1. Irritability 2. Ability of cardiac muscle to respond to an outside stimulus, Chemical, Mechanical, Electrical Marian Williams RN

47 CARDIAC CELLS 3.Conductivity Ability of cardiac cell to receive an electrical impulse and conduct it to an adjoining cardiac cell 4.Contractility Ability of myocardial cells to shorten in response to an impulse Marian Williams RN

48 CARDIAC CELLS Refractory Periods Period of recovery cell needs after being discharged before they are able to respond to a stimulus Absolute Refractory Relative Refractory Supernormal ERP – Effective refractory period Marian Williams RN

49 CARDIAC CELLS Absolute refractory Cell will not respond to further stimulation Relative refractory Vulnerable period Some cardiac cells have repolarized and can be stimulated to respond to a stronger than normal stimulus Marian Williams RN

50 CARDIAC CELLS Supernormal Period A weaker than normal stimulus can cause cardiac cells to depolarize during this period Marian Williams RN

51 CONDUCTION SYSTEM Sinoatrial Node (SA) Primary pacemaker Intrinsic rate /min Located in Rt. Atrium Supplied by sympathetic and para- sympathetic nerve fibers Blood from RCA-60% of people Marian Williams RN

52 CONDUCTION SYSTEM Three internodal pathways Anterior tract Bachmanns Bundle Left atrium Wenckebachs Bundle Thorels Pathway Marian Williams RN

53 CONDUCTION SYSTEM Atrioventricular Junction Internodal pathways merge AV Node Non-branching portion of the Bundle of His Marian Williams RN

54 CONDUCTION SYSTEM AV Node Supplied by RCA – 85%-90% of people Left circumflex artery in rest of people Delay in conduction due to smaller fivers Marian Williams RN

55 CONDUCTION SYSTEM Bundle of His Located in upper portion of interventricular septum Intrinsic rate /min Blood from LAD and Posterior Descending Less vulnerable to ischemia Marian Williams RN

56 CONDUCTION SYSTEM Right & Left Bundle Branches RBB Right Ventricle Marian Williams RN

57 CONDUCTION SYSTEM LBB – Left Bundle Branch Anterior Fasicle oAnterior portion left ventricle Posterior Fascicle Posterior portions of left ventricle Septal Fasicle Mid-spetum Marian Williams RN


59 CONDUCTION SYSTEM Spread from interventricular septum to papillary muscles Continue downward to apex of heart- approx 1/3 of way Fibers then continuous with muscle cells of Rt and Lt ventricles Marian Williams RN

60 CONDUCTION SYSTEM Purkinje Fibers Intrinsic pacemaker rate 20-40/min Impulse spreads from endocardium to epicardium Marian Williams RN

61 ECG Records electrical voltage of heart cells Orientation of heart Conduction disturbances Electrical effects of medications and electrolytes Cardiac muscle mass Ischemia / Infarction Marian Williams RN

62 ECG Leads Tracing of electrical activity between 2 electrodes Records the Average current flow at any specific time in any specific portion of time Marian Williams RN

63 ECG Types of leads Limb Lead (I, II, III) Augmented (magnified) Limb Leads (aVR, aVL, aVF) Chest (Precordial) Leads (V1,V2,V3,V4,V5,V6) Each lead has Positive electrode Marian Williams RN

64 ECG Each lead sees heart as determined by 2 factors 1. Dominance of left ventricle 2. Position of Positive electrode on body Marian Williams RN


66 ECG Lead I Negative electrode Right arm Positive electrode Left arm Marian Williams RN

67 ECG Lead II Negative Electrode Right Arm Positive Electrode Left Leg Marian Williams RN

68 ECG Lead III Negative Lead Left Arm Positive Lead Left Leg Marian Williams RN

69 ECG PAPER Graph Paper Small boxes 1mm wide; 1 mm high Horizontal axis Time in seconds 1 mm box represents 0.04 seconds ECG paper speed is 25 mm/second One large box is 5 (1 mm boxes or 0.04 sec)=.20 seconds Marian Williams RN


71 ECG PAPER Vertical Axis Voltage or amplitude Measured in millivolts 1mm box high is 0.1 mV 1 large box is (5 x 0.1=0.5 mV) However, in practice the vertical axis is described in millimeters. Marian Williams RN

72 ECG PAPER Waveforms Movement from baseline Positive (upward) Negative (downward) Isoelectric –along baseline Biphasic - Both upward and downward Marian Williams RN


74 ECG P Wave First waveform Impulse begins in SA Node in Right Atrium Downslope of P wave – is stimulation of left atrium 2.5 mm in height (max) O.11 sec. duration (max) Positive in Lead II Marian Williams RN






80 ECG QRS Complex Electrical impulse through ventricules Larger than P wave due to larger muscle mass of ventricles Follows P wave Made up of a Q wave R wave S wave Marian Williams RN

81 ECG Q wave First negative deflection following P wave Represents depolarization of the interventricular septum activated from left to right Marian Williams RN

82 ECG R wave First upright waveform following the P wave Represents depolarization of ventricles Marian Williams RN

83 ECG S wave Negative waveform following the R wave Normal duration of QRS 0.06 mm – 0.10 mm Not all QRS Complexes have a Q, R and S Marian Williams RN





88 ECG T wave Represents ventricular repolarization Absolute refractory period present during beginning of T wave Relative refractory period at peak Usually 0.5 mm or more in height Slightly rounded Marian Williams RN





93 ECG U wave Small waveform Follows T wave Less than 1.5 mm in amplitude Marian Williams RN


95 ECG J Point Point where the QRS complex and ST-segment meet Marian Williams RN



98 ECG PR Interval Measurement where P wave leaves baseline to beginning of QRS complex Activation AV Node Bundle of His Bundle Branches Purkinje Fibers Atrial repolarization sec. Marian Williams RN



101 ECG QT interval Begins at isoelectric line from end of S wave to the beginning of the T wave sec. Represents total ventricular activity Measured from beginning of QRS complex to end of T wave Marian Williams RN



104 ECG Artifact Distortion of electrical activity Noncardiac in origin Caused by Loose electrodes Broken cables/wires Muscle tremor Patient movement 60 cycle interference Chest compressions Marian Williams RN




108 ECG Analysis Rate Six Second Method Two – 3 second markers Count complexes and multiply x 10 Marian Williams RN




112 ECG Analysis Regularity Atrial Rate Measure distance between P waves Ventricular Rate Measure distance between R-R intervals 0.04 mm off is considered regular Marian Williams RN




116 ECG Analysis Measure P wave length Measure PR Interval Measure QRS wave duration Measure QT interval Marian Williams RN




120 ECG Analysis ST segment Elevated? Depressed? T wave Normal height Upright? Marian Williams RN



123 ECG Normal Sinus Rhythm Electrical activity activity starts in SA node AV Junction Bundle Branches Ventricles Depolarization of atria and ventricles Rate: /Regular PR interval / QRS duration normal Marian Williams RN





128 ECG Sinus Bradycardia Sinus Node fires at a rate slower than normal Conduction occurs through atria, AV junction, Bundle Branches and Ventricles Depolarization of atria and ventricles occurs In adults – rate is slower than 60 / minute Rate is regular Why? Athletes;Vagal Stimulation MedicationsCardiac disease Treatment : TCP; Atropine 0.5 mg IVP if symptomatic (maybe); Epinephrine or Dopamine 2-10 mcg/kg/min infusion Marian Williams RN

129 ECG Sinus Bradycardia Causes Hs and Ts HypoxiaToxins HypovolemiaTamponade, cardiac Hydrogen Ion (acidosis) Tension Pneumothorax Hypo-HyperkalemiaThrombosis (coronary or pulmonary) Hypoglycemia Trauma (Increased ICP; hypovolemia) Hypothermia Marian Williams RN




133 ECG Sinus Tachycardia SA node fires faster than /minute Normal pathway of conduction and depolarization Regular rate Why? Coronary artery diseaseFear; anger; exercise; HypoxiaFever Treatment: Treat Cause Beta-Blockers Marian Williams RN




137 ECG Sinus Arrhythmia The SA node fires Irregularly / Rate /min. Normal pathway of electrical conduction and depolarization PR and QRS durations are normal Why? Respiratory- Increases with inspiration; decreases with expiration Often in children; Inferior Wall MI; Increased ICP; Medications: Digoxin; Morphine Treatment: Often None Marian Williams RN




141 ECG Sinus Arrest SA node fails to initiate electrical impulse for one or more beats May see no beats on monitor or other pacemaker cells in the heart may take over Rate: Variable ; Rhythm: Irregular Why? Hypoxia; Coronary artery disease; Hyperkalemia Beta-Blockers; CA channel blockers; Increased vagal tone Treatment Pacemaker; Atropine; Epinephrine or Dopamine Marian Williams RN




145 ECG Premature Atrial Complexes An electrical cell within the atria fires before the SA node fires Rate: Usually closer to 100; Irregular rhythm P wave usually looks abnormal and complex occurs before it should Why? Emotional stress; CHF; Acute coronary syndromes Stimulants; Digitalis Toxicity; etc. Treatment Reduce stress; Reduce stimulants; Treat CHF; Beta-blockers Marian Williams RN

146 ECG Marian Williams RN

147 ECG Marian Williams RN

148 ECG Marian Williams RN

149 ECG Supraventricular Tachycardiac (SVT) Fast rhythms generated Above the Ventricles Paroxysmal SVT (starts or ends suddenly) Rate – usually Why?Stimulants; Infection; Electrolyte Imbalance MIAltered atrial pathway (WPW)-Kent S & S Lightheadedness; Palpitations; SOB; Anxiety; Weakness Dizziness; Chest Discomfort; Shock Treatment Vagal maneuvers;Adenosine 6 mg fast IVP; Repeat with 12 mg Adenosine; Cardioversion Marian Williams RN

150 ECG Marian Williams RN

151 ECG Marian Williams RN

152 ECG Marian Williams RN

153 ECG Marian Williams RN

154 ECG Atrial Flutter Irritable focus within the atrium typically fires at a rate of about 300 bpm Waveforms resemble teeth of a saw AV node cannot conduct faster than about 180 beats/minute Atrial vs ventricular rate expressed as a ratio Why:Re-entry- HypoxiaPulmonary embolism MIChronic Lung diseasePneumonia etc. S & S: SOB; Weakness; Dizziness; Fatigue; Chest discomfort Treatment: Ca Channel Blocker; Beta Blockers; Amiodarone; Cardioversion – anticoagulants; Corvert Marian Williams RN

155 ECG Marian Williams RN

156 ECG Marian Williams RN

157 ECG Marian Williams RN

158 ECG Atrial Fibrillation Irritable sites in atria fire at a rate of /minute Muscles of atria quiver rather than contract (fibrillate) No P waves – only an undulating line Only a few electrical impulses get through to the ventricles – may be a lot of impulses or a few A lot of impulses (ventricular rate high- then called atrial fibrillation with rapid ventricular response) A few impulses (ventricular rate slow – then called atrial fibrillation with slow ventricular response) Marian Williams RN

159 ECG Marian Williams RN

160 ECG Marian Williams RN

161 ECG Marian Williams RN

162 ECG Marian Williams RN

163 ECG Marian Williams RN

164 ECG Marian Williams RN

165 ECG AV Block Delay or interruption in impulse conduction Classified accordi8ng to degree of block and/or to site of block First Degree Block Impulses from SA node to the ventricles is DELAYED but not blocked Why?IschemiaMedicationsHyperkalemia oInferior MIIncreased Vagal Tone Treatment?Usually None Marian Williams RN

166 ECG Marian Williams RN

167 ECG Marian Williams RN

168 ECG Marian Williams RN

169 ECG Marian Williams RN

170 ECG Second Degree Block Type I - Wenckebach Lengthening of the PR interval and then QRS wave is dropped Why? Usually RCA occlusion (90% of population) Ischemia Increase in parasympathetic tome Medications Treatment If slow ventricular rate oAtropine oPacing Marian Williams RN

171 ECG Marian Williams RN

172 ECG Marian Williams RN

173 ECG Marian Williams RN

174 ECG Second Degree AV Block – Mobitz Type II Why Ischemia LCA – Anterior MI Organic heart disease Important: Ventricular Rate QRS duration How many dropped QRSs in relation to P waves? What is the ratio? Treatment Atropine Pacing Marian Williams RN

175 ECG Marian Williams RN

176 ECG Marian Williams RN

177 ECG Marian Williams RN

178 ECG Third Degree AV Block (Complete Block) No P waves are conducted to the ventricles The atrial pacemakers and ventricle pacemakers are firing independently Why? Inferior MI; Anterior MI Serious Treatment Atropine 0.5 mg IV Epinephrine 2-10 mcg/kg or Dopamine 2-10 mcg/kg/min Pacing Marian Williams RN

179 ECG Marian Williams RN

180 ECG Marian Williams RN

181 ECG Marian Williams RN

182 ECG Marian Williams RN

183 ECG Ventricular Rhythms Are the hearts least efficient pacemakers Generate impulses at 20-40/min Assume pacemaking if: SA nodes fail, very slow (below 20-40) or are blocked Ventricles site(s) is irritable Irritable due to ischemia Depolarization route is abnormal and longer, therefore QRS looks different and is wider. T wave is opposite in direction to QRS Marian Williams RN

184 ECG Premature Ventricular Contractions May be from One Site and all look the same Called Unifocal (from one focus or foci) Marian Williams RN

185 ECG May be from Different sites (Foci) and are called Multifocal PVCs Marian Williams RN

186 ECG May occur every other beat – Ventricular Bigeminy Marian Williams RN

187 ECG May occur every third beat – Ventricular Trigeminy Marian Williams RN

188 ECG R on T PVC Marian Williams RN

189 ECG Marian Williams RN

190 ECG Couplets (2 PVCs in a row); Triplets (3 PVCs in a row) Marian Williams RN

191 ECG Couplets also known as Salvos. Marian Williams RN

192 ECG Run of PVCs Marian Williams RN

193 ECG Ventricular Tachycardia Defined as Three or more PVCs occurring in a row at a rate > 100/min Wide QRS No P waves No T waves Why? Ischemia; Infarction; Congenital Usually lethal S & S: Weakness, Dizziness, Shock, Chest Pain; Syncope Treatment: Lidocaine or Amiodarone; Cardioversion –if pulse; Defibrillation – if no pulse (see Ventricular Fibrillation) Marian Williams RN

194 ECG Marian Williams RN

195 ECG Marian Williams RN

196 ECG Marian Williams RN

197 ECG Torsades de Pointes (Twisting of the Points) Ventricular Tachycardia in which the QRS changes in shape, amplitude and width Causes: Hypomagnesium; Hypokalemia; Quinidine therapy S & S: Altered mental status; shock; Chest pain; SOB; Hypotension Treatment: Magnesium Sulfate 2 Grams diluted in 20 cc D 5 W and given IV Marian Williams RN

198 ECG Marian Williams RN

199 ECG Marian Williams RN

200 ECG Ventricular Fibrillation Chaotic rhythm of the ventricles Lethal if not treated Causes: MI; Electrolyte Imbalance; Drug ODs; Trauma Heart Failure; Vagal Stimulation; Increased SNS Electrocutions etc. Treatment: Defibrillation and CPR ; AICD Defibrillation: 360 Joules (monophasic defibrillators) 150 Joules (biphasic defibrillators) Marian Williams RN

201 ECG Marian Williams RN

202 ECG Marian Williams RN

203 ECG CPR 5 cycles (interrupt if defibrillator is there) Defibrillate Continue CPR for 5 cycles (2 minutes) Epinephrine 1 mg of 1:10,000 IVP OR Vasopressin 40 Units IV for 1 st or 2 nd dose of Epinephrine. Repeated every 3-5 minutes CHECK PT/Monitor CPR Shock CPR Amiodarone 300 mg IV or Lidocaine 1 mg/kg IV CHECK PT/Monitor Consider Magnesium Sulfate (Torsades) Marian Williams RN

204 ECG Marian Williams RN

205 ECG Marian Williams RN

206 ECG Pulseless Electrical Activity – PEA Rhythm on monitor but no corresponding pulse Why? Look for Cause! Hs and Ts HypoxiaToxins HypovolemiaTamponade, cardiac Hydrogen Ion (acidosis) Tension Pneumothorax Hypo-Hyperkalemia Thrombosis (coronary or Hypoglycemia pulmonary) Hypothermia Trauma (Increased ICP, hypovolemia)

207 ECG Pulseless Electrical Activity – PEA What do we do? CPR for 5 cycles Epinephrine 1 mg of 1:10,000 IVP OR may give Vasopressin 40 Units IV for 1 st or 2 nd dose of Epinephrine Give Epinephrine 1 mg of 1:10,000 IVP every 3-5 minutes If Rate is below 60/min. on monitor may give Atropine 1 mg IV up to 3 doses Always give a bolus of Normal Saline (1000 cc) Continue CPR Always check rhythm in 2 leads Check Patient

208 ECG Marian Williams RN

209 ECG Asystole No electrical activity on monitor No pulse Why? Look for Cause! Hs and Ts HypoxiaToxins HypovolemiaTamponade, cardiac Hydrogen Ion (acidosis) Tension Pneumothorax Hypo-Hyperkalemia Thrombosis (coronary or Hypoglycemia pulmonary) Hypothermia Trauma (Increased ICP, hypovolemia) Marian Williams RN

210 ECG What do we do? CPR for 5 cycles Epinephrine 1 mg of 1:10,000 IVP OR may give Vasopressin 40 Units IV for 1 st or 2 nd dose of Epinephrine Give Epinephrine 1 mg of 1:10,000 IVP every 3-5 minutes If Rate is below 60/min. on monitor may give Atropine 1 mg IV up to 3 doses Always give a bolus of Normal Saline (1000 cc) Continue CPR Always check rhythm in 2 leads Check Patient Marian Williams RN

211 ECG Marian Williams RN

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