BASIC ECG INTERPRETATION

BASIC ECG INTERPRETATION
Marian Williams RN BN CEN CCRN CFRN CTRN Marian Williams RN

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

Marian Williams RN

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

Marian Williams RN

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

Heart Blood Flow Marian Williams RN

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

Marian Williams RN

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

Marian Williams RN

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

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

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

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

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

Cardiac Muscle Marian Williams RN

ION Concentrations Extracellular Intracellular Sodium and Chloride
Potassium and Calcium

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

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

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

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

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

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

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

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

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

Marian Williams RN

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

CONDUCTION SYSTEM Three internodal pathways Anterior tract
Bachmann’s Bundle Left atrium Wenckebach’s Bundle Thorel’s Pathway Marian Williams RN

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

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

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

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

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

Marian Williams RN

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

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

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

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

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

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

Marian Williams RN

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

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

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

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

Marian Williams RN

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

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

Marian Williams RN

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

Marian Williams RN

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

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

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

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

Marian Williams RN

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

Marian Williams RN

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

Marian Williams RN

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

Marian Williams RN

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

Marian Williams RN

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

Marian Williams RN

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

Marian Williams RN

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

Marian Williams RN

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

Marian Williams RN

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

Marian Williams RN

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

Marian Williams RN

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

Marian Williams RN

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

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

Marian Williams RN

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

Marian Williams RN

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

Marian Williams RN

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

Marian Williams RN

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

ECG Marian Williams RN

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

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

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

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

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

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

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

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

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

ECG May be from Different sites (Foci) and are called Multifocal PVC’s
Marian Williams RN

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

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

ECG R on T PVC Marian Williams RN

ECG Couplets (2 PVC’s in a row); Triplets (3 PVC’s in a row)
Marian Williams RN

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

ECG Run of PVC’s Marian Williams RN

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

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

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

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

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)

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

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

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

BASIC ECG INTERPRETATION

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BASIC ECG INTERPRETATION

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