ECG Advance

Ashman’s Phenomenon

aberrant ventricular conduction (RBBB morphology)

LONG-SHORT RULE: long beat then a short beat = a PAC will aberrant conduction.

Setting of sinus have non-compensatory pause

Common in AF settings.

RBBB diagnosis:

QRS > 12 seconds

Strain in V1 and V2

Slurring S in I, V6

Upright Fat R in V1 ***

RAD

LBBB diagnosis

QRS > 0.12s

S in V1 and V2

R in I, V5, V6

which has longer refractory period LBBB or RBBB?

RBBB

How is wave depolarization sent in BBB setting?

from the unaffected side to afefcted side via cell to cell transmission (sequential)

How is QT measured in the setting of BBB

Bogossian Method

QTm = QTBBB - 50%duration of BBB QRS

RVH diagnosis:

R > 7 mm w/o strain

Strain in V2 to V4

RAE/RAD may be present

R/S > 1 with skinny QRS

absent of RBBB

can mimic LAPFB

LVH diagnosis

voltage + non-voltage criteria

S wave in V1 and V2 > 30 mm

R wave in V1 and V2 > 30 mm

limb leads > 20 mm (straight 3)

ST depression; strain (3 points)

LAE in V1 (3 points)

LAD (2 points)

Probable (4 points) / Definite (5 points)

BVH diagnosis:

Katz-Watchel Phenomennon;

Large biphasic QRS V2 to V5

R+S in v3/v4 > 500

common in pediatrics with VSDs

Adults with amyloidosis

RAE diagnosis:

peaked p wave > 2.5mm in II // >1,5 mm in V1

LAE diagnosis:

p > 0.11second in II // negative portion in v1 > 1mm deep

Pulmonary Embolism

clot in the artery in the lungs blocked.

Type of chest pain that almost always occurs with deep vein thrombosis

PE ECG Signs:

1.Tachycardia at rest**

2. S1Q3T3 pattern*

3. T wave inversion inferior/V1-V4*

3. Right sided changes; RAD/R with strain/RBBB (due to RV overload)

4. Hypotension

Cor-Pulmonale:

causes right sided HF associated with RV dilation

Other diagnostic tools for PE

1. D-dimer test (protein leftover after clot breaks down) High levels present with PE

2. X-Ray

3. Troponin Test (Elevated)

4. Echo/ CT scan (RV dilation/Dsyfunction)

Differentials for PE:

1. Pericarditis

2. Fever

3. Ischemia

4. Anxiety

Chest Pain Differentials:

Cardiac: Infarct, Angina (Wellens), Aortic Dissection, Pericarditis

Stomach: GERD

Musculoskeletal

Respiratory: PE, Pulmonary HTN

Miscellaneous: Anxiety, Shingles

Aortic Dissection

tear int eh inner aorta that causes blood to flow between the layers of the aorta.

Severe chest pain/upper back pain

Weak pulse

Negative cardiac biomarkers

ST elevation stages:

Hyperacute: ST elevation only

Acute: significant Q and STE

Old: Sig Q with T wave changes

Sig Q: 1/3 of R wave and 1 mm wide (transmural death)

What 2 causes Chest Pain at rest?

Unstable Angina and Wellen’s Syndrome

Wellen’s Syndrome

Chest pain at rest typically due to proximal LAD stenosis > anterior MI (need PCI/CABG!)

DO NOT DO GXT.

ECG Wellen’s

T wave changes**

History of Angina**

Minimal Elevation < 1mm

Type A: V2-V3 Biphasic negative QRS (±/-)

DO NOT CONFUSE TYPE A WITH HYPOKALEMIA (-/+)

Type B: symmetrical inverted T waves

Pericarditis

inflammation of the pericardium

Sharp CP during respiration

Pericarditis Cardiac Tamponade/Constrictive

Constrictive: scarring

Cardiac Tamponade: fluid build up which compresses the heart.

Beck’s Triad for CT: 1.Hypotension 2. Muffle Heart Sounds 3. Jugular Vein distended

Pulse Paradox for CT: > 10mmHg drop during inspiration

CT need to do pericardiocentesis

Pericarditis ECG

Sinus tachycardia at rest**

PR depression**

Electric Alternans**

Low Voltage** (QRS limb < 5mm | QRS in precordial < 10 mm)

Spodick Sign: V1 downwards TP segment

Widespread STE** ½ weeks > T wave flattening 3 weeks> T wave inversion beyond 3 week > Normal ECG

what are non-specific ST changes?

when there is no clinical data to correlate with ECG changes

Secondary ST change

due to ventricular depolarization BBB, WPW, PVCs, LVH

Primary ST changes:

ischemia, drugs, electrolytes

Normal variant of ST changes

Early repolarization, symmetrical T wave (usually in young pts)

J point notching may be seen

Persistent coving ST elevation after a ACUTE MI (after a couple of weeks)

Ventricular Aneurysm

What can help alleviate MI

CCB, Nitroglycerin

early STD in aVL could indicate

impending inferior MI

Occlusion MI

isolated STE/STD in a single lead with prominent hyperacute T waves

RVMI

RVMI leads to reduce preload which can lead to hypotension

STE III > II**

STE V1 and STD V2**

STE V1 > V2

Posterior MI

Tall R waves in V1 to V3 and Horizontal STD in V1 to V3

Posterior Lead only need 0.5 mm STE to confirm (usually lower voltage)

If a person has RVMI what do you not give them?

Nitroglycerin or vasodilators as it decreases venous return and lead to dangerously low hypotension which can lead to shock.

Pitfalls of WCT

reliance on II

AF with rapid ventricular response can turn into rate related BBB (confused with VT) do not want to give lidocaine

Why do we not give lidocaine to AF?

increases conduction through AVN = increase AF

WTC 3 diagnosis

VT

SVT with aberrancy(due to BBB)

SVT aberrancy due to WPW

What is given for SVT?

What is given orally to prevent reoccurrence

adeosine

CCB, BB, Digitalis

VT criteria (7)

eRAD | all inferior lead pointed down | Upright V1 (99% specific)

or RAD with V1 negative (90%)

If V1 positive: Mariott signs (L>R) / STeeple sign/ Fireman Hat

All leads down or up Concordance

Josephson sign; Notch of S wave

Brugada sign: onset of QRS S > 100ms

Capture or fusion beats

Difference between RBBB and VT V1

L> R in VT

R>L in RBBB

Other prominent VT signs outside ECG

patient age > 35 years

Previous MI

Structural Heart Diease

Family history of SCA

SVT with aberrancy criteria:

Previous ECG shows BBB or WPW

Pt history has terminated with adenosine or VM

Triphasic RSR’

Pt is young

Really wide WTC

> 200 msec thick toxicity or metabolic

AVOID SODIUMC HANNEL BLOCKERS GIVE BICARBS OR CALCIUM

most common cause of hyperkalemia

renal failure

Normal Hyperkalemia AND Abnormal

3.5-5 mmol/l

>5.5 Peak T wave

>6.5 PRI prolongs, P goes.

>7 Bizarre QRS sinus wave

>9 VF, Cardiac Arrest. PEA

Hypokalemia

decrease in potassium, increases hyperexcitability which can lead to re-entrant arrhythmias

Usually caused by diuretics

Biphasic T waves (-/+) / STD / U waves

Normal Calcium and Magenisum

2.2 - 2.7 mmol/L

0.65 - 1.05 mmol/L

Hypercalcemia

Shortening of QT

Osborne waves (J wave; common in hypothermia)

Hypocalcemia

QT prolongations > 450 ms can lead to TDP

Hypomagnesium

often occurs with hypokalemia.

QT prolongation

Hypermageniusm

similar to hyperkalemia

uncommon due to kidneys eliminate Mg alot.

Thus cause: renal failure

Digoxin Toxicity

hypokalemia adds to the effect

Scooped STD

Tricyclic Overdose ECG

R’ in avR

R > 3mm avR

Sinus tachycardia

WIDE WIDE QRS

sodium channel blockade****

Toxic Drug Effects: CAUSE LONG QT

Anti-arrhythmias I

Amiodarone

Phenothiazines

AAI: increase QT, blocks SA node and cause AV blocks

Amiodarone: slows conductions everywhere

Phenothiazines: widens QRS

AVNRT criteria

micro-circuit

short RP < 70 ms**

140-240 bpm

Pseudo R’ (retrograde P in V1)**

Pseudo S (rounded) in I and inferior leads; retrograde P waves)

AVRT

macro-circuit involving accessory pathways triggered by premature beats.

ECG: 200-300 bpm

Retrograde p waves in inferior leads

RP > 70ms***

Antidromic AVRT

Fat QRS Antegrade AP retrograde AVN

often confused with VT but VT < 180

Treatment: Vagal Man or amiodarone / Procainamide

Unstable: Cardioversion

Orthodromic AVRT

most common

antegrade AVN, retrograde AP

Thin QRS

often confused with junctional tachycardia

Treatment: Vagal Man. / Adenosine / CCB

unstable: cardioversion

WPW

Involves the Bundle of Kent ***

PRI < 120ms

Delta wave

QRS prolongations

ST-T discordance

Type A: V1 positive

Type B: V1 negative

some pt have concealed pathways where retrograde only AP conductions so no feature in sinus rhythm,

Long-Ganong Syndrome

short PRI no dealt wave

Bundle of James

Short RP (after QRS)

retrograde through fast pathway (retrograde P)

AVNRT

Orthodromic AVRT

junctional tachycardia with inverted P after QRS

Long RP (before QRS)

retrograde through slow pathway (Antegrade P)

Sinus tachycardia

Antidromic AVRT

Atrial Tachycardia

Junctional tachycardia with inverted P before QRS

Atrial Tachycardia

originate within the atrai outside SA and AVN node

Long RP

inverted P waves in inferior leads

Narrow complex above > 160 bpm treats as

SVT

Atrial Flutter

re-entry circuit around the TV

AF 1:1 300 bpm

AF 2:1 150 bpm (always be sus of A flutt at 150 bpm exact)

Counterclockwise inverted Flutter waves most common

What can help unmask flutter waves

adenosine

IV adenosine no change in rate:

VT or inadequate dose

adenosine causes gradual slowing:

sinus tachycardia

Atrial tachycardia

Junctional Tachycardia

adenosine causes termination:

AVRT or AVNRT

adenosine causes persistent atrial tachycardia with intermittent AV block:

atrial flutter

Adenosine works on

slowing conduction at the AVN

Sgarbossa Criteria

Concordance STE > 1mm in positive QRS

Concordance STD > 1mm in v1 to V3

Discordant STE > 5mm or STE 25% of S wave in negatvie QRS

Once determine LBBB cannot have

LVH

Once determine RBBB cannot have

RVH

Once determine RVH cannot have

LPFB

If determine LVH can still have

LAFB

Old lateral MI can cause

LAD

Old inferior MI can mimic

LAFB

Regular Atrial Fibrillation can mean

CHB with underlying AF.

Once determine WPW cannot have

LAFB

Hypertrophic Cardiomyopathy

dagger Q waves in lateral leads

LVH with strain may be present

Diastolic DSYFUNCTION

seen in young men/athletes

Arrhythmogenic Right Ventricular Cardiomyopathy (ARVD)

Autosomal dominant causes fat tissues to take over RV wall lead to ventricular arrhythmias and SCA.

Epsilon wave****

T wave inversion w/o RBBB

Prolong S upstroke and Localized QRS widening V1toV3

Fontan Leads for ARVD

RA: Manubrium

LA: Xiphoid

LL: V4

Intracardial Hemorrhage

Giant T wave inversion & QT prolongation