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Amy Gutman MD ~ EMS Medical Director
prehospitalmd@gmail.com / www.TEAEMS.com
Part I: Cardiac Anatomy Review
Part II: The Cardiac Cycle
Part III: From One Beat to Many
Part IV: Rhythm Analysis
What is an EKG really looking at?
German “Elektrokardiogramm”
Record of the heart’s electrical depolarizations & repolarizations over time Arrhythmias, ischemia, & conduction abnormalities Electrolyte disturbances Non-cardiac diseases (i.e. hypothermia, PE)
3 lead “overview” image of heart I (lateral) II (inferior) III (inferior)
Useful for checking arrhythmias
Not great for looking for ischemic changes
Leads I, II & III are “limb leads”
Leads aVR, aVL, & aVF are “augmented” limb leads
V1 - 4th ICS to right of sternumV2 - 4th ICS to left of sternum
V3 - Between V2 & V4
V4 - 5th ICS at MCLV5 - Horizontally with V4 at AAL
V6 - Horizontally with V4 & V5 at MAL
Lead II Continuous Strip
I AvR V1 V3
II AvL V2 V4
III AvF V3 V5
I AvR V1 V4
Lateral Septal Anterior
II AvL V2 V5Inferior Lateral Septal Lateral
III AvF V3 V6Inferior Inferior Anterior Lateral
Right Coronary Artery (RCA) perfuses right ventricle / inferior heart Inferior heart
Left Main Artery (LMA) divides into: Left Anterior Descending
Artery (LAD) perfuses anterior left ventricle
Left Circumflex Artery (LCX) perfuses lateral left ventricle
Each coronary artery = one part of the EKG
You must see changes in >two “contiguous” leads to diagnose ischemia
Contiguous leads = heart “territories”: Inferior, Anterior, Lateral, Septal
Right ventricle positioned downward & inferior
Innervated by vagus nerve Same nerve as stomach IMIs often present with
N/V not “chest pain”
IIInferior
III AvF Inferior Inferior
Two vessels cover large area
V2 overlaps septal & anterior areas
Septal MI is best seen in V1 & V2
V1Septal
V2Septal
Septum & anterior left ventricle are the “precordial” leads
V1 & V2 directly over cardiac septum
V2 (septal overlap), V3, V4 look at anterior heart
V3Anterior
V4Anterior
Winds around lateral heart & left ventricle
LMA “Widow Maker”: Divides into LAD & LCX,
perfuses left ventricle LMA occlusion causes
massive antero-lateral MI
I Lateral
AvL V5 Lateral Lateral
V6 Lateral
I AvR V1 V4
Lateral Septal Anterior
LMA, LCX RCA, LAD LAD
II AvL V2 V5
Inferior Lateral Septal Lateral
RCA LMA, LCX RCA, LAD LMA, LCX
III AvF V3 V6
Inferior Inferior Anterior Lateral
RCA RCA LAD LMA, LCX
Contiguous Leads
I, AvL, V5, V6
II, III, AvF
V1, V2
(V2, V3)
V3, V4
The heart is nothing more than a mechanical pump running on electricity
The heart is a mechanical pump running on electrical energy
Electrical energy pathways determine how well the heart functions
Changes in electricity = changes in heart function
Sinoatrial Node Atrioventricular NodeLeft Atrium
Right Atrium
Right Ventricle Left Ventricle
Bundle of His
1. SA Node
2. AV Node
3. Bundle of His
4. Right & Left Ventricles
Electrical Electrical PathwayPathway
SA Node
AV Node
HisBundle
RightVentricle
Left Ventricle
One complex = one cardiac cycle
Recognizing normal means understanding abnormal
Atrial DepolarizationVentricular DepolarizationVentricular Repolarization
Width = time
Height & depth = voltage
Upward deflection = positive
Downward delection = negative
SA to AV node path causes atrial contraction
Upright in II, III, & aVF
Inverted in aVR
Variable P wave shapes suggests ectopic pacemaker
120 - 200 ms (3 to 5 small boxes) Long = 1st degree heart block Short = pre-excitation syndrome (WPW) Variable = other heart blocks
PR depression = atrial injury or pericarditis
Short PR interval <120 ms, <3 small boxes
Slurred QRS upstroke = “delta wave”
Young, healthy person with CP & palpitations
Consider with “shackalitis”
Atrial impulses conducted to ventricles via accessory pathway causing reentry
Ventricular contraction coordinated by Bundle of His & Purkinje fibers
0.06 to 0.10 sec
Duration, height & shape diagnose arrhythmias, conduction abnormalities, hypertrophy, infarction, electrolyte derangements
Short: <0.08 secs Seen in SVT
Long: >0.12 secs Often related to a
bundle branch block
Normal (physiologic) or abnormal (pathologic)
Normal: Septal depolarization Best seen in lateral leads I, aVL, V5 & V6
Qs > 1/3 R wave height, or >0.04 sec length abnormal May show infarction
0.08 - 0.12 sec
J point to beginning of T wave
Flat or depressed ST: Ischemia
ST elevation: Infarction
J Point
Ventricular repolarization
T wave usually upright Inverted: ischemia, hypertrophy, CVA Tall: hyperkalemia Flat: ischemia, hypokalemia
Beginning of QRS to end of T wave Ventricular depolarization to “resetting” the
conduction system
Normal ~ 0.40 secs Interval varies based on HR & must
be adjusted (Corrected QT / QTc)
• The heart takes too long to repolarize leaving it vulnerable to aberrant electrical impulses
• Torsades de pointes, VT, VF
Prolonged QT interval Alcohol abuse Hypomagnesemia, hypokalemia
May have a pulse, but are never “stable”
RX: magnesium bolus
Not always seen, typically small, follows T wave
Purkinje fiber repolarization
Hypokalemia, hypercalcemia, hypothermia, CVA, or thyroid disease
Inverted U wave: ischemia, volume overload
Putting it together…
1 small block = 1 mm² = 0.04 s = 40 ms
5 small blocks = 1 large block = 0.20 s = 200 ms
5 large blocks = 1 second
Each large black line = 300 150 100 75 60 50
If there is an P wave before each QRS & both are upright, then the rhythm is “sinus” From sino-atrial / SA node
P wave round, not peaked & unidirectional except in V1 & V2 (often biphasic)
Normal axis leads I & AVF are positive (upright)
When heart enlarges / hypertrophies or normal pathways are re-routed, the “axis” changes
Anything more beyond the scope of this lecture
Right Ventricular Hypertrophy R wave >S in V1, becomes
progressively smaller S wave in V5,V6 RAD with wide QRS
Left Ventricular Hypertrophy S in V1 + R in V5 (in mm) = 35mm LA with wide QRS
Why is this important for prehospital providers?
Anywhere in conduction system
Ectopic beats generated from foci other than usual sites of electrical activity Some ectopic beats in a healthy persons normal Persistent ectopic beats become “blocks” / conduction dz
Conduction disorders manifest as slowed conduction (1st degree), intermittent conduction failure (2nd degree), or complete conduction failure (3rd degree)
Slowed electrical signal not travelling through atrial tissue at normal speed resulting in long P-R PR > 0.20 sec Always a P waves before QRS P-R interval consistent
May be due to ischemia or infarct
Progressive delay AV conduction, until impulse completely blocked Occurs because impulse arrives during absolute refractory
period, so no conduction no QRS P-P intervals shorten until pause occurs Next P wave occurs & the cycle begins again
P-P interval following pause greater than P-P interval before pause
Block usually located in AV node, so QRS narrow
Multiple constant PR intervals before blocked P wave
Ventricular rate always les than atrial rate, depends on number of impulses conducted through AV node Atrial & ventricular rates irregular P waves present in 2, 3 or 4:1 conduction with QRS PR interval constant for each P wave prior to QRS
Type II AV block is almost always located in bundle branches so QRS is wide
Atria & ventricles controlled by separate pacemakers
Narrow QRS suggests AV block with junctional escape
Wide QRS suggests AV node or bundle branch block block with ventricular escape (“idioventricular”)
•40 – 60 BPM
•“Junction” between atria & ventricles
•P wave “flipped” as beat originates below SA node
LBBBLBBB• RBBB
• QRS >0.12
• “M” shaped QRS in V1 or V2
• R = 1st peak
• Ischemia, infarction, electrolyte abnormalities, meds, CNS disease
LBBB QRS >0.1-0.12s• Wide & “Peaked” QRS in V6• R Prime = 2nd peak
Stage I: Ischemia
Stage 2: Injury
Stage 3: Infarction
Stage 4: Resolution
Look in all leads for:Q waves
Inverted T wavesST segment elevation or depression
• Normal T wave upright when QRS upright
• If T wave inverted, then = ischemia
• Try and compare with old EKG to determine if inversion is new or old
• ST elevation + Q waves = acute infarction
• “Non-Q” MI = infarct without Q waves
• ST often returns to baseline in time
6 hours from lumen blocked by clot to start of tissue death appears as ST elevation
6 hour period is when must start TPA (“clot busters”) to salvage heart tissue
“Time is Muscle!”
Qs represent progression of injury to infarction
Pathologic Qs = QRS (-) deflection after PR interval & >1/3 size of QRS
If ST elevations & Qs at same time, STEMI evolving from injury to necrosis
Development of scar tissue in infarcted area occurs roughly 2 weeks after necrosis
Affected part of heart may show EKG changes forever
Be careful – flipped T waves can also mean pt having new ischemia!
Persistent ST depression may indicate “Non-Q” MI
Pacemakers Atrial or ventricular
or both
Looks like “spikes” on the ECG
Be wary of the patient with a pacer who has no spikes
Some EKG lead groups are electrical “mirrors”
ST elevations in one group appear as depressions in the other group in two specific areas: Inferior and Lateral Septal & Posterior
Elevations always come first If there are ST elevations on EKG, ST depressions on the
same EKG might be reciprocal instead of ischemic
There are no true posterior leads on a standard EKG
Septal leads look at anterior & posterior heart & “mirror” an infero-posterior infarction
Remember the RCA perfuses inferior & posterior areas: ST elevations in II, III,
aVF? ST depressed in V1, V2?
II
III
V1
V2
Most prominent feature are peaked-T waves
“Sine waves” also seen
Changes seen across ALL leads, not in a single coronary artery pattern Common with all
electrolyte / metabolic abnormalities
Anatomy plus electricity equals rhythm
SA node origin
Rate 60 – 100 beats/ minute > 100 = sinus tachycardia < 60 = sinus bradycardia
If irregular, rate determined by both a “ventricular” & “atrial” rate
Normal variant
Irregular rhythm varies with respiration
All P waves look identical
Intrinsic rate for SA node: 60 - 100bpm
Causes: Inferior MI (RCA lesion) Sedation
Rhythm originates in the SA node P wave for every QRS Rate > 100 / minute
Increased cardiac stress from systemic process: Hypovolemia / Hypotension Hypoxia Anxiety Drugs (i.e. cocaine) Exercise
Rate 60 – 90 bpm
Occasional “escape” ectopic beats
Also known as “PACs”
Atrial reentry from a circular conductive pathway
Single ectopic pacemakerMay have inverted P-waves
Two or more asynchronous cardiac pacemakers
The hallmark of this form of SVT is multiple P-wave morphologies (one from each pacemaker)
Absence of p-waves before each QRS
Irregularly irregular from ectopic foci with re-entry
Rate ~ 200-300bpm
No True P Waves
Multiple sawtooth edged P waves before each QRS
Many ectopic pacemakers Unstable rhythm May progress to atrial fibrillation
• No P waves or atrial activity
• Normal QRS • Ventricles generating slow escape rate (20-40 BPM)
“Accelerated” IVR faster than expected rate (>60) Ventricular pacemakers speed up & capture as pacers
are faster than the underlying rhythm
SVT: Generated above
ventricle P waves present Narrow
VT: Generated in
ventricles No P waves Wide
Generated above ventricles so narrow complex with P waves
May be normal in bursts in young, healthy individuals
Often difficult to differentiate from VT
•Wide QRS (>140 ms) without atrial activity / P waves
•ANY wide tachycardia is VT until proven otherwise
•Often caused by ischemic / infarcted conductive ventricular tissue causing a reentry tachycardia
SVT
Rhythm - Regular Rate - 140-220 BPM QRS Duration - normal P Wave - Buried in preceding
T wave P-R Interval - Depends on site
of supraventricular pacemaker
Impulses stimulating heart are not generated by sinus node, instead from a collection of tissue around the AV node
VT
Rhythm - Regular Rate - 180-190 BPM QRS Duration - Prolonged P Wave - Not seen Abnormal ventricular
tissues generating a rapid & irregular heart rhythm & poor cardiac output is
Wide and slow No P waves as rhythm starts below atria
<6 in a minute = Normal >6 in a row= Ventricular Tachycardia
Multiple ventricular areas contract without coordination
Quivering results in loss of cardiac output & death
Cure for VF is electrical defibrillation
Alan Lindsey ECG Learning Center in Cyberspace
Dubin’s Guide to ECGs London Ambulance Sercice Unoffical
ECG Guide Brady’s, Mosby’s, Caroline’s
Prehospital Provider Textbooks www.TheMDSite.com Wikipedia, Google The ECG Guide (Iphone App)
“Almost” everything you need to know: Part I: Cardiac Anatomy Review Part II: The Cardiac Cycle Part III: From One Beat to Many Part IV: Basic Rhythm Analysis
Is this everything you truly need to know?
Look at every strip, ECG & rhythm you can…you need to know “normal” before you can know “abnormal”
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