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Presentation on theme: "BASIC ECG INTERPRETATION"— Presentation transcript:

Marian Williams RN BN CEN CCRN CFRN CTRN Marian Williams RN

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

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

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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 Diastole Ventricular Systole
Atrial Kick Atrial Diastole Ventricular Systole Ventricular Diastole Marian Williams RN

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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

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

18 Cardiac Muscle Sarcolemma Sarcoplasmic Reticulum 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 Contraction Made of thick and thin filaments
Troponin Thick Myosin Contraction Thin/thick filaments slide over each other Marian Williams RN

20 Cardiac Muscle Marian Williams RN

21 ION Concentrations Extracellular Intracellular Sodium and Chloride
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) 2. Chemoreceptors
Internal Carotids Aortic Arches Detects changes in BP 2. Chemoreceptors 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 x’s peripheral vascular resistance CO x PVR Marian Williams RN

30 STROKE VOLUME Stroke Volume determined by Preload Afterload
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

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

33 STROKE VOLUME Frank Starling’s 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 Pacemaker 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 Voltage
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 3 – Final rapid repolarization
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 Automaticity Excitability
Cardiac pacemaker cells create an electrical impulse without being stimulated from another source Excitability Irritability Ability of cardiac muscle to respond to an outside stimulus, Chemical, Mechanical, Electrical Marian Williams RN

47 CARDIAC CELLS 3.Conductivity 4.Contractility
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 ERP – Effective refractory period 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 Relative 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
Bachmann’s Bundle Left atrium Wenckebach’s Bundle Thorel’s 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

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
Anterior portion left ventricle Posterior Fascicle Posterior portions of left ventricle Septal Fasicle Mid-spetum Marian Williams RN

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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

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

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

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

69 ECG PAPER Graph Paper Small boxes Horizontal axis 1mm wide; 1 mm high
Time in seconds 1 mm box represents 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

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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

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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

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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 Normal duration of QRS
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

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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

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

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

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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

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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

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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

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

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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

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

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

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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

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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 Medications Cardiac 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 H’s and T’s Hypoxia Toxins
Hypovolemia Tamponade, cardiac Hydrogen Ion (acidosis) Tension Pneumothorax Hypo-Hyperkalemia Thrombosis (coronary or pulmonary) Hypoglycemia Trauma (Increased ICP; hypovolemia) Hypothermia Marian Williams RN

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133 ECG Sinus Tachycardia SA node fires faster than 100-180/minute
Normal pathway of conduction and depolarization Regular rate Why? Coronary artery disease Fear; anger; exercise; Hypoxia Fever Treatment: Treat Cause Beta-Blockers Marian Williams RN

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137 ECG Sinus Arrhythmia The SA node fires Irregularly / Rate 60-100/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

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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

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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 MI Altered 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- Hypoxia Pulmonary embolism MI Chronic Lung disease Pneumonia 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 First Degree Block Treatment? Usually None
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? Ischemia Medications Hyperkalemia Inferior MI Increased 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 Treatment
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 Atropine Pacing 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 Important: Treatment Why
Ischemia LCA – Anterior MI Organic heart disease Important: Ventricular Rate QRS duration How many dropped QRS’s 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) Treatment
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 heart’s 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 PVC’s
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 PVC’s in a row); Triplets (3 PVC’s in a row)
Marian Williams RN

191 ECG Couplets also known as ‘Salvos’. Marian Williams RN

192 ECG Run of PVC’s Marian Williams RN

193 ECG Ventricular Tachycardia
Defined as Three or more PVC’s 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 D5W 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 OD’s; 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 Consider Magnesium Sulfate (Torsades)
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 1st or 2nd 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! H’s and T’s Hypoxia Toxins Hypovolemia Tamponade, cardiac Hydrogen Ion (acidosis) Tension Pneumothorax Hypo-Hyperkalemia Thrombosis (coronary or Hypoglycemia pulmonary) Hypothermia Trauma (Increased ICP, hypovolemia)

207 ECG Check Patient Always check rhythm in 2 leads
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 1st or 2nd 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! H’s and T’s Hypoxia Toxins Hypovolemia Tamponade, cardiac Hydrogen Ion (acidosis) Tension Pneumothorax Hypo-Hyperkalemia Thrombosis (coronary or Hypoglycemia pulmonary) Hypothermia Trauma (Increased ICP, hypovolemia) Marian Williams RN

210 ECG Check Patient What do we do? Always check rhythm in 2 leads
CPR for 5 cycles Epinephrine 1 mg of 1:10,000 IVP OR may give Vasopressin 40 Units IV for 1st or 2nd 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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