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

Marian Williams RN BN CEN CCRN CFRN CTRN

BASIC ECG INTERPRETATION

Marian Williams RN

Heart AnatomyLayers

PericardiumMyocardiumEndocardium

Four ChambersAtria

LeftRight

VentriclesLeftRight

Marian Williams RN

Marian Williams RN

Heart ValvesAtrioventricular

BicuspidTricuspid

Semi-lunarPulmonic

Aortic

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Marian Williams RN

Major Vessels

Superior Vena CavaInferior Vena CavaCoronary Sinus

AortaPulmonary VeinPulmonary Artery

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Heart Blood Flow

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Cardiac CycleAtrial Systole

Atrial Kick

Atrial Diastole

Ventricular Systole

Ventricular Diastole

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Marian Williams RN

Coronary ArteriesRight Coronary

Artery

Posterior DescendingSA Node (60%)Right Atrium

Right MarginalRight VentricleAV node (85%-90%)Proximal portion

Bundle of HisPart of Left Bundle

Branch

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Marian Williams RN

Coronary ArteriesLeft Coronary

Artery

Left Anterior DescendingAnterior – Left VentricleRight Bundle BranchPart – Lateral Left

VentricleMost Interventricular

SeptumLeft Bundle Branch

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Coronary ArteriesCircumflex

Left AtriumLateral – Left

VentricleInferior–Left

Ventricle (15%)Posterior-Left

VentricleSA Node (40%)AV Node (10%-15%)

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Cardiac MuscleSyncytium

Network of cells – Electrical impulses

Atrial

VentricularSarcolemma

Membrane enclosing cardiac cell

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Cardiac MuscleSarcolemma

Holes in SarcolemmaT-(transverse) tubulesGo around muscle

cellsConduct impulses

Sarcoplasmic Reticulum

Series of tubulesStores CalciumCalcium moved from

sarcoplasm into sarcoplasmic reticulum by pumps

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Cardiac MuscleSarcomeres

Made of thick and thin filaments

ThinTroponin

ThickMyosin

ContractionThin/thick

filaments slide over each other

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Cardiac Muscle

Marian Williams RN

ION ConcentrationsExtracellular

Sodium and Chloride

IntracellularPotassium and Calcium

Cardiac Muscle

ChannelsOpenings (pores)

in cell membraneSodium – Na+Potassium – K+Calcium – Ca++Magnesium – Mg+

+

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EFFECTS ON HEART RATE

1. Baroreceptors (Pressure)Internal CarotidsAortic Arches

Detects changes in BP

2. ChemoreceptorsInternal CarotidsAortic ArchesChanges in pH

(Hydrogen Ion, Oxygen, Carbon Dioxide)

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Autonomic Nervous System

ParasympatheticSA NodeAtrial MuscleAV NodeVagus NerveAcetycholine is

released and binds to parasympathetic receptors

Slows SA node rateSlows AV ConductionDecreases atrial

contraction strength

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Sympathetic Electrical systemAtriumVentriclesNorepinephrine

releaseIncreased force of

contractionIncreased heart

rateIncreased BP

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Sympathetic Receptor SitesAlpha Receptors

Constriction of blood vesselsSkinCerebralSplanchnic

Beta 1 ReceptorsHeart

Beta 2 ReceptorsLungsSkeletal Muscle

Blood Cells

Dopaminergic ReceptorsCoronary arteriesRenal Blood

VesselsMesenteric Blood

VesselsVisceral Blood

Vessels

Marian Williams RN

CARDIAC OUTPUTStroke Volume x

Heart Rate = CO (4-8 L/min)

Stroke Volume approx. 70 ml/beat

Increased by:Adrenal medulla

Norepinephrine; Epinephrine

PancreasInsulin; Glucagon

MedicationsCalcium; Digitalis;

Dopamine; Dobutamine

Marian Williams RN

CARDIAC OUTPUTDecrease in Force

of ContractionSevere hypoxiaDecreased pHElevated carbon

dioxideMedications –

Calcium channel blockers, Beta Blockers

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BLOOD PRESSURE

DefinitionForce exerted by

circulating blood on artery walls

Equals: Cardiac output x’s peripheral vascular resistanceCO x PVR

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STROKE VOLUMEStroke Volume

determined by Preload

Force exerted on ventricles walls at end of diastole Increased volume

means increased preload

AfterloadPressure or resistance

against which the ventricles must pump to eject blood

Marian Williams RN

Marian Williams RN

STROKE VOLUME

Afterload influenced by:Arterial BPAbility of arteries

to stretchArterial resistance

Marian Williams RN

STROKE VOLUME

Frank Starling’s LawThe 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 CELLSTwo Types

Myocardial CellsMechanicalCan be electrically

stimulatedCannot generate

electricity

Pacemaker CellsElectrical cellsSpontaneously generate

electrical impulsesConduct electrical

impulses

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CARDIAC CELLSCurrent

Electrical charge flow from one point to another

VoltageEnergy

measurement between positive and negative points

Measured in millivolts

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CARDIAC CELLSAction 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

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Cardiac Cell Action Potential

Phase 0Depolarization Rapid Na+ entry into

cellPhase 1

Early depolarizationCa++ slowly enters

cellPhase 2

Plateau-continuation of repolarization

Slow entry of Sodium and Calcium into cell

Cardiac Cell Action Potential

Phase 3Potassium is

moved out of the cell

Phase 4Return to resting

membrane potential

CARDIAC CELLSAt rest

K+ leaks out Protein & phosphates

are negatively charged, large and remain inside cell

Polarized CellMore negative inside

than outsideMembrane 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 voltsMeasured as ECG

Marian Williams RN

CARDIAC CELLSDepolarization

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

RepolarizationInside of cell

restored to negative charge

Returning to resting stage starts from epicardium to endocardium

Marian Williams RN

CARDIAC CELLSAction Potential

Phase 0 – rapid depolarizationNa+ into cell rapidlyCa++ into cell slowlyK+ slowly leaks out

Phase 1 – early rapid repolarizationNa+ into cell slowsCl- enters cellK+ 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

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CARDIAC CELLSPhase 4 – Resting

membrane potential

Na+ excess outsideK+ excess insideReady to discharge

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CARDIAC CELLSProperties

1. Automaticity1. Cardiac pacemaker

cells create an electrical impulse without being stimulated from another source

2. Excitability1. Irritability2. Ability of cardiac

muscle to respond to an outside stimulus, Chemical, Mechanical, Electrical

Marian Williams RN

CARDIAC CELLS3.Conductivity

Ability of cardiac cell to receive an electrical impulse and conduct it to an adjoining cardiac cell

4.ContractilityAbility of

myocardial cells to shorten in response to an impulse

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CARDIAC CELLSRefractory Periods

Period of recovery cell needs after being discharged before they are able to respond to a stimulusAbsolute

RefractoryRelative

RefractorySupernormal

ERP – Effective refractory period

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CARDIAC CELLSAbsolute refractory

Cell will not respond to further stimulation

Relative refractoryVulnerable periodSome cardiac cells

have repolarized and can be stimulated to respond to a stronger than normal stimulus

Marian Williams RN

CARDIAC CELLS

Supernormal PeriodA weaker than

normal stimulus can cause cardiac cells to depolarize during this period

Marian Williams RN

CONDUCTION SYSTEM

Sinoatrial Node (SA)Primary pacemakerIntrinsic rate 60-

100/minLocated in Rt.

AtriumSupplied by

sympathetic and para-sympathetic nerve fibers

Blood from RCA-60% of people

Marian Williams RN

CONDUCTION SYSTEM

Three internodal pathways

Anterior tractBachmann’s BundleLeft atrium

Wenckebach’s Bundle

Thorel’s Pathway

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CONDUCTION SYSTEM

Atrioventricular JunctionInternodal

pathways mergeAV NodeNon-branching

portion of the Bundle of His

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CONDUCTION SYSTEM

AV NodeSupplied by RCA

– 85%-90% of peopleLeft circumflex

artery in rest of people

Delay in conduction due to smaller fivers

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CONDUCTION SYSTEM

Bundle of HisLocated in upper

portion of interventricular septum

Intrinsic rate 40-60/min

Blood from LAD and Posterior DescendingLess vulnerable to

ischemia

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CONDUCTION SYSTEM

Right & Left Bundle Branches

RBB Right Ventricle

Marian Williams RN

CONDUCTION SYSTEM

LBB – Left Bundle BranchAnterior Fasicle

o Anterior portion left ventricle

Posterior FasciclePosterior portions

of left ventricle

Septal FasicleMid-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 FibersIntrinsic

pacemaker rate 20-40/min

Impulse spreads from endocardium to epicardium

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ECGRecords electrical

voltage of heart cellsOrientation of heartConduction

disturbancesElectrical effects of

medications and electrolytes

Cardiac muscle mass

Ischemia / Infarction

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ECGLeads

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

ECGTypes 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

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ECG

Each lead ‘sees’ heart as determined by 2 factors1. Dominance of

left ventricle2. Position of

Positive electrode on body

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Marian Williams RN

ECGLead I

Negative electrodeRight arm

Positive electrodeLeft arm

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ECGLead II

Negative ElectrodeRight Arm

Positive ElectrodeLeft Leg

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ECGLead III

Negative LeadLeft Arm

Positive LeadLeft Leg

Marian Williams RN

ECG PAPERGraph Paper

Small boxes1mm wide; 1 mm

highHorizontal axis

Time in seconds1 mm box

represents 0.04 secondsECG paper speed

is 25 mm/secondOne large box is 5 (1

mm boxes or 0.04 sec)=.20 seconds

Marian Williams RN

Marian Williams RN

ECG PAPERVertical Axis

Voltage or amplitudeMeasured in

millivolts1mm box high is 0.1

mV1 large box is (5 x

0.1=0.5 mV)However, in practice

the vertical axis is described in millimeters.

Marian Williams RN

ECG PAPERWaveforms

Movement from baseline

Positive (upward) Negative

(downward)

Isoelectric –along baseline

Biphasic - Both upward and downward

Marian Williams RN

Marian Williams RN

ECGP Wave

First waveformImpulse 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

ECGQRS Complex

Electrical impulse through ventricules

Larger than P wave due to larger muscle mass of ventricles

Follows P waveMade up of a

Q waveR waveS wave

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ECG

Q waveFirst negative

deflection following P wave

Represents depolarization of the interventricular septum activated from left to right

Marian Williams RN

ECG

R waveFirst upright

waveform following the P wave

Represents depolarization of ventricles

Marian Williams RN

ECGS 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

Marian Williams RN

ECGT 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

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Marian Williams RN

ECG

U waveSmall waveformFollows T waveLess than 1.5

mm in amplitude

Marian Williams RN

Marian Williams RN

ECG

J PointPoint where the

QRS complex and ST-segment meet

Marian Williams RN

Marian Williams RN

ECGPR Interval

Measurement where P wave leaves baseline to beginning of QRS complex

Activation AV NodeBundle of HisBundle BranchesPurkinje FibersAtrial repolarization

0.12 - .20 sec.

Marian Williams RN

Marian Williams RN

ECGQT interval

Begins at isoelectric line from end of S wave to the beginning of the T wave - 0.44 sec.

Represents total ventricular activity

Measured from beginning of QRS complex to end of T wave

Marian Williams RN

Marian Williams RN

ECGArtifact

Distortion of electrical activity

Noncardiac in origin

Caused byLoose electrodesBroken cables/wiresMuscle tremorPatient movement60 cycle

interferenceChest compressions

Marian Williams RN

Marian Williams RN

ECGAnalysis

RateSix Second Method

Two – 3 second markers

Count complexes and multiply x 10

Marian Williams RN

Marian Williams RN

ECGAnalysis

RegularityAtrial Rate

Measure distance between P waves

Ventricular RateMeasure distance

between R-R intervals

0.04 mm ‘off’ is considered regular

Marian Williams RN

Marian Williams RN

ECGAnalysis

Measure P wave length

Measure PR Interval

Measure QRS wave duration

Measure QT interval

Marian Williams RN

Marian Williams RN

ECGAnalysis

ST segmentElevated?Depressed?

T waveNormal heightUpright?

Marian Williams RN

Marian Williams RN

ECGNormal Sinus

RhythmElectrical activity

activity starts in SA node AV Junction Bundle BranchesVentriclesDepolarization of

atria and ventriclesRate: 60-100

/RegularPR interval / QRS

duration normal

Marian Williams RN

Marian Williams RN

ECGSinus Bradycardia

Sinus Node fires at a rate slower than normalConduction occurs through atria, AV

junction, Bundle Branches and VentriclesDepolarization of atria and ventricles occursIn adults – rate is slower than 60 / minuteRate is regularWhy?

Athletes; Vagal StimulationMedications Cardiac disease

Treatment: TCP; Atropine 0.5 mg IVP if symptomatic (maybe); Epinephrine or Dopamine 2-10 mcg/kg/min infusion

Marian Williams RN

ECGSinus Bradycardia

CausesH’s and T’s

Hypoxia ToxinsHypovolemia Tamponade, cardiacHydrogen Ion (acidosis) Tension PneumothoraxHypo-Hyperkalemia Thrombosis (coronary

or

pulmonary)Hypoglycemia Trauma (Increased ICP;

hypovolemia) Hypothermia

Marian Williams RN

Marian Williams RN

ECGSinus Tachycardia

SA node fires faster than 100-180/minuteNormal pathway of conduction and

depolarizationRegular rateWhy?

Coronary artery disease Fear; anger; exercise;

Hypoxia FeverTreatment:

Treat CauseBeta-Blockers

Marian Williams RN

Marian Williams RN

ECGSinus Arrhythmia

The SA node fires Irregularly / Rate 60-100/min.

Normal pathway of electrical conduction and depolarization

PR and QRS durations are normalWhy?

Respiratory- Increases with inspiration; decreases with expiration

Often in children; Inferior Wall MI; Increased ICP;

Medications: Digoxin; MorphineTreatment: Often None

Marian Williams RN

Marian Williams RN

ECGSinus 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: IrregularWhy?

Hypoxia; Coronary artery disease; Hyperkalemia

Beta-Blockers; CA channel blockers; Increased vagal tone

TreatmentPacemaker; Atropine; Epinephrine or Dopamine

Marian Williams RN

Marian Williams RN

ECGPremature 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 syndromesStimulants; Digitalis Toxicity; etc.

TreatmentReduce stress; Reduce stimulants; Treat CHF;

Beta-blockers

Marian Williams RN

ECG

Marian Williams RN

ECGSupraventricular Tachycardiac (SVT)

Fast rhythms generated ‘Above the Ventricles’Paroxysmal SVT (starts or ends suddenly)Rate – usually 130-250Why? Stimulants; Infection; Electrolyte

ImbalanceMI Altered atrial pathway (WPW)-Kent

S & SLightheadedness; Palpitations; SOB; Anxiety;

WeaknessDizziness; Chest Discomfort; Shock

TreatmentVagal maneuvers; Adenosine 6 mg fast IVP; Repeat

with 12 mg Adenosine; Cardioversion

Marian Williams RN

ECG

Marian Williams RN

ECGAtrial Flutter

Irritable focus within the atrium typically fires at a rate of about 300 bpm

Waveforms resemble teeth of a sawAV node cannot conduct faster than about 180

beats/minuteAtrial vs ventricular rate expressed as a ratioWhy: Re-entry- Hypoxia Pulmonary embolism

MI Chronic Lung diseasePneumonia etc.S & S: SOB; Weakness; Dizziness; Fatigue; Chest

discomfortTreatment: Ca Channel Blocker; Beta Blockers;

Amiodarone; Cardioversion – anticoagulants; Corvert

Marian Williams RN

ECG

Marian Williams RN

ECGAtrial Fibrillation Irritable sites in atria fire at a rate of

400-600/minuteMuscles of atria quiver rather than contract

(fibrillate)No P waves – only an undulating lineOnly a few electrical impulses get through to the

ventricles – may be a lot of impulses or a fewA 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

Marian Williams RN

ECGAV 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? Ischemia Medications

Hyperkalemiao Inferior MI Increased Vagal Tone

Treatment? Usually None

Marian Williams RN

ECG

Marian Williams RN

ECGSecond 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 tomeMedications

Treatment If slow ventricular rate

o Atropineo Pacing

Marian Williams RN

ECG

Marian Williams RN

ECGSecond Degree AV Block – Mobitz Type

II Why

Ischemia LCA – Anterior MIOrganic heart disease

Important:Ventricular RateQRS durationHow many dropped QRS’s in relation to P waves?

What is the ratio?Treatment

AtropinePacing

Marian Williams RN

ECG

Marian Williams RN

ECGThird 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 MISerious

Treatment Atropine 0.5 mg IVEpinephrine 2-10 mcg/kg or Dopamine 2-10

mcg/kg/minPacing

Marian Williams RN

ECG

Marian Williams RN

ECGVentricular 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

ECGPremature Ventricular ContractionsMay be from One Site and all look the same

Called Unifocal (from one focus or foci)

Marian Williams RN

ECGMay be from Different sites (Foci) and are

called Multifocal PVC’s

Marian Williams RN

ECGMay occur every other beat – Ventricular

Bigeminy

Marian Williams RN

ECGMay occur every third beat – Ventricular

Trigeminy

Marian Williams RN

ECGR on T PVC

Marian Williams RN

ECG

Marian Williams RN

ECGCouplets (2 PVC’s in a row); Triplets (3

PVC’s in a row)

Marian Williams RN

ECGCouplets also known as ‘Salvos’.

Marian Williams RN

ECG Run of PVC’s

Marian Williams RN

ECGVentricular 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; CongenitalUsually 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

Marian Williams RN

ECGTorsades 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

Marian Williams RN

ECGVentricular Fibrillation

Chaotic rhythm of the ventricles Lethal if not treated Causes: MI; Electrolyte Imbalance; Drug OD’s;

TraumaHeart Failure; Vagal Stimulation; Increased SNSElectrocutions etc.

Treatment: Defibrillation and CPR; AICDDefibrillation: 360 Joules (monophasic

defibrillators) 150 Joules (biphasic

defibrillators)

Marian Williams RN

ECG

Marian Williams RN

ECGCPR 5 cycles (interrupt if defibrillator is there)DefibrillateContinue 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

CPRShockCPR Amiodarone 300 mg IV or Lidocaine 1 mg/kg

IV

CHECK PT/MonitorConsider Magnesium Sulfate (Torsades)

Marian Williams RN

ECG

Marian Williams RN

ECGPulseless Electrical Activity – PEA

Rhythm on monitor but no corresponding pulseWhy? Look for Cause!H’s and T’s

Hypoxia ToxinsHypovolemia Tamponade, cardiacHydrogen Ion (acidosis) Tension

PneumothoraxHypo-Hyperkalemia Thrombosis (coronary orHypoglycemia

pulmonary)Hypothermia Trauma

(Increased ICP, hypovolemia)

ECGPulseless Electrical Activity – PEA

What do we do?CPR for 5 cyclesEpinephrine 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 CPRAlways check rhythm in 2 leads

Check Patient

ECG

Marian Williams RN

ECGAsystole

No electrical activity on monitorNo pulseWhy? Look for Cause!H’s and T’s

Hypoxia ToxinsHypovolemia Tamponade, cardiacHydrogen Ion (acidosis) Tension

PneumothoraxHypo-Hyperkalemia Thrombosis

(coronary orHypoglycemia

pulmonary)Hypothermia Trauma

(Increased ICP, hypovolemia)

Marian Williams RN

ECGWhat do we do?

CPR for 5 cyclesEpinephrine 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 CPRAlways check rhythm in 2 leads

Check PatientMarian Williams RN

ECG

Marian Williams RN

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

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Transcript of Marian Williams RN BN CEN CCRN CFRN CTRN BASIC ECG INTERPRETATION Marian Williams RN.