2 Februari 2018 EKG

Download as docx, pdf, or txt
Download as docx, pdf, or txt
You are on page 1of 24

PETA KONSEP

BASICS OF EKG
INTERPRETATION 1

Rate 2 QRS breakdown 2

Axis 2 Review of the


conduction system 2

Rhythm 2

Sistem Konduksi Jantung3 Gambaran EKG Normal4

SA Node - Internodal track - -Komplek QRS -Gel


AV Node - Berkas His - - Interval QT -Gel
Serabut Purkinje -Interval PR -Gel

Lead EKG5

The standard EKG has 12 leads:


-3 Standard Limb Leads (Lead I, II, III)
-3 Augmented Limb Leads (aVL, aVR, aVF)
-6 Precordial Leads (V1, V2, V3, V4, V5, V6)
*The axis of a particular lead represents the viewpoint from which
it looks at the heart.

Anatomy Grup (Summary)10

Rate 11

-Rule of 300
Take the number of “big boxes” between neighboring QRS
complexes, and divide this into 300. The result will be
approximately equal to the rate. Although fast, this method only
works for regular rhythms.12
* 300 dibagi jumlah kotak besar antara kompleks QRS = Rate

-10 second rule


As most EKGs record 10 seconds of rhythm per page, one
can simply count the number of beats present on the EKG and
multiply by 6 to get the number of beats per 60 seconds. This
method works well for irregular rhythms.17
*Hitung denyut dalam 10 detik (10 dtk = 50 kotak besar) dikali 6
= ratenya, biasanya klo ireguler pake ini.

The QRS Axis 19

By near-consensus, the normal


QRS axis is defined as ranging
from -30° to +90°.

-30° to -90° is referred to as a left


axis deviation (LAD)

+90° to +180° is referred to as a


right axis deviation (RAD)

Determining the Axis20


Predominan Predominan Equiphasic21
Positif21 negatif21

-The Quadrant Approach


Examine the QRS complex in leads I and aVF to determine
if they are predominantly positive or predominantly negative.
The combination should place the axis into one of the 4
quadrants below.22
In the event that LAD is present, examine lead II to
determine if this deviation is pathologic. If the QRS in II is
predominantly positive, the LAD is non-pathologic (in other
words, the axis is normal). If it is predominantly negative, it is
pathologic.23
*LAD (Lead I +, aVF -)
-LAD Patologis
(Lead I +, aVF -, Lead II -)
-LAD Patologis
(Lead I +, aVF -, Lead II +)
*RAD (Lead I -, aVF +)

-The Equiphasic Approach


Determine which lead contains
the most equiphasic QRS complex.
The fact that the QRS complex in this
lead is equally positive and negative
indicates that the net electrical vector
(i.e. overall QRS axis) is
perpendicular to the axis of this
particular lead.26
Examine the QRS complex in whichever lead lies 90° away
from the lead identified in step 1. If the QRS complex in this
second lead is predominantly positive, than the axis of this lead is
approximately the same as the net QRS axis. If the QRS
complex is predominantly negative, than the net QRS axis lies
180° from the axis of this lead.26
*Equiphasic in aVF->Predominantly positive in I-> QRS axis=0°

*Equiphasic in II ->Predominantly negative in aVL ->


QRS axis = +150°

Systematic Approach30
-Rate (pake 2 cara tadi rule of 300 atau 10 second rule)
-Rhythm
-Sinus
-Atrial
-Junctional
-Ventricular
-Axis
-Wave Morphology
-P, T, and U waves and QRS complex
-Intervals
-PR, QRS, QT
-ST Segment
Sinus Rhythms: Criteria/Types32
-P waves upright in I, II, aVF
-Constant P-P/R-R interval
-Rate
-Narrow QRS complex
-P:QRS ratio 1:1
-P-R interval is normal and constant

Sinus Arrhythmias: Criteria/Types33


-Normal Sinus Rhythm (rate 60-100)34

-Sinus Bradycardia

*Can be normal variant, Can result from medication, Look for


underlying cause35
-Sinus Tachycardia

*May be caused by exercise, fever, hyperthyroidism, Look for


underlying cause, slow the rate.36
-Sinus Arrhythmia

*Seen in young patients, Secondary to breathing, Heart beats


faster 37
Atrial Arrhythmias: Criteria/Types38-39
-P waves inverted in I, II and aVF
-Abnormal shape
-Notched
-Flattened
-Diphasic
-Narrow QRS complex
-Type
-Premature Atrial Contractions

*QRS complex narrow, RR interval shorter than sinus QRS


complexes, P wave shows different morphology than sinus P
wave.40
-Ectopic Atrial Rhythm

*Narrow QRS complex, P wave inverted 41


-Wandering Atrial Pacemaker

*3 different P wave morphologies possible with ventricular rate <


100 bpm 42
-Multifocal Atrial Tachycardia

*3 different P wave morphologies with ventricular rate>100


bpm43
-Atrial Flutter

*Regular ventricular rate 150 bpm, Varying ratios of F waves to


QRS, complexes, most common is 4:1,Tracing shows 2:1
conduction 44

*Tracing shows 6:1 conduction 45


-Atrial Fibrillation

*racing shows irregularly irregular rhythm with no P waves,


Ventricular rate usually > 100 bpm 46

*Tracing shows irregularly irregular rhythm with no P waves,


Ventricular rate is 40. 47
-Atrial Tachycardia

*Tracing shows regular ventricular rate with P waves that are


different from sinus P waves, Ventricular rate is usually 150 to
250 bpm 48
Junctional Arrhythmias: Criteria 49-50
-P wave
-May be absent
-Buried in QRS
-If present
-inverted in leads I, II, and aVF
-Inverted after QRS
-PR interval < 0.12 secs
-Rate: Varies
-Narrow QRS complex

Junctional Arrhythmias: Types 51


-Premature Junctional Contractions

*R-R interval is shorter, Beat is early, narrow QRS complex,


Inverted P wave, P wave can be buried in QRS complex. 52
-Junctional Escape Rhythm

*Junctional origin, Rate is 40 to 60. 53


-Accelerated Junctional Tachycardia

*Junctional origin, Rate is 60 to 100. 54


-Junctional Tachycardia

*Junctional origin, Rate is > 100. 55


-AV Nodal Reentrant Tachycardia (AVNRT)

*Secondary to bypass tract within AV node, Premature Atrial


Contraction (PAC) depolarizes. 56

Rate Summary 57
-Sinus Tachycardia (100-160 BPM)
-Atrial Tachycardia (150-250 BPM)
-Atrial Flutter (150-250 BPM)
-Junctional Tachycardia (100-180 BPM)

AV Nodal Blocks 58
-Delay conduction of impulses from sinus node
-If AV node does not let impulse through, no QRS complex is
seen
-AV nodal block classes: 1st, 2nd, 3rd degree
-1st Degree AV Block

*PR interval constant, >.2 sec, All impulses conducted. 59


-2nd Degree AV Block
-Type 1

*AV node conducted each impulse slower and finally no impulse


is conducted, Longer PR interval, finally no QRS complex. 60
-Type 2

*Constant PR interval, AV node intermittently conducts no


impulse. 61
-3rd Degree AV Block

*AV node conducts no impulse, Atria and ventricles beat at


intrinsic rate (80 and 40 respectively),No association between P
waves and QRS complexes. 62

Another Consideration:
-Wolfe-Parkinson-White (WPW)
*Caused by bypass tract, AV node is
bypassed, delay, EKG shows short PR
interval <.11 sec, Upsloping to QRS
complex (delta wave). 63

*Delta wave, short PR interval. 64

Ventricular Arrhythmias:65
-Criteria
-Wide QRS complex
-Rate : variable
-No P waves
-Types
-Premature Ventricular Contractions

*Occurs earlier than sinus beat, Wide, no P wave. 66


-Idioventricular Rhythm

*Escape rhythm, Rate is 20 to 40 bpm. 67


-Accelerated IVR

*Rate is 40 to 100 bpm. 68


-Ventricular Tachycardia

*Rate is > than 100 bpm. 69


-Torsades de Pointes

*Occurs secondary to prolonged QT interval70


-Ventricular Fibrillation

Chamber Enlargements
-Left Ventricular Hypertrophy (LVH)
-Differential Diagnosis 74
A)Hypertension (HTN)
B)Aortis Stenosis (AS)
C)Aortic Insufficiency (AI)
D)Hypertrophic Cardiomyopathy (HCM)
E)Mitral Regurgitation (MR)
F)Coarctation of the Aorta (COA)
G)Physiologic
-False positivem75
A)Thin chest wall
B)Status post mastectomy
C)Race, Sex, Age
D)Left Bundle Branch Block (LBBB)
E)Acute MI
F)Left Anterior Fascicular Block
G)Incorrect standardization

EKG Criteria: Diagnosis of LVH 76-77

-S V1, V2 + R V5,V6 > 35 42.5 95%


(Sokolow-Lyon)
-R V5 orV6 > 27 25% 98%
-R V5 or V6 > 25 Framingham 14% 86%
-R plus S > 45 any lead 45% 93%

Limb leads
-R in L + S in V3 >25 in men,
and >20 in women. 16% 97%
(Cornell Voltage)
-R in I + S in III > 25 10.6% 100%
-R in L > 11 man, 9 wom 10.6% 100%
-R in avF > 20 1.3% 99.5%
-S in avR > 14
LVH with Strain78

Right Ventricular Hypertrophy 79


-Reversal of precordial pattern
-R waves prominent in V1 and V2
-S waves smaller in V1 and V2
-S waves become prominent in V5 and V6

-Causes 81
-Chronic Obstructive Pulmonary Disease
-Pulmonary HTN (Primary)
-Pulmonary Embolus
-Mitral Stenosis
-Mitral Regurgitation
-Chronic LV failure
-Tricuspid Regurgitation
-Atrial Septal Defect
-Pulmonary Stenosis
-Tetralogy of Fallot
-Ventricular Septal Defect

Left Atrial Enlargement:83-84


-Causes
-Mitral Stenosis
-Mitral Regurgitation
-Left ventricular hypertrophy
-Hypertension
-Aortic Stenosis
-Aortic Insufficiency
-Hypertrophic Cardiomyopathy
-Criteria
-P wave
-Notch in P wave
-Any lead
-Peaks > 0.04 secs
-V1
-Terminal portion of P wave > 1mm deep and >
0.04 sec wide

P Wave: Left Atrial Enlargement86


- Lead II 85

- Lead V1 87

Right Atrial Enlargement:


-Causes 88
-CHD
-Tricuspid Stenosis
-Pulmonary Stenosis
-COPD
-Pulmonary HTN
-Pulmonary Embolus
-Mitral Regurgitation
-Mitral Stenosis
-Criteria 89
-Tall, peaked P wave > 2.5 mm in any lead
-Most prominent P waves in leads I, II and aVF

Bundle Branch Blocks 92


-Left
-Complete
-Incomplete

-Right
-Complete
-Incomplete
*Complete (QRS > .12 secs) , Incomplete (QRS .10 - .12 secs)

Left Bundle Branch Block 93-94


-Causes
-Normal variant
-Idiopathic degeneration of the conduction system
-Cardiomyopathy
-Ischemic heart disease
-Aortic Stenosis
-Hyperkalemia
-Left Ventricular Hypertrophy
-Criteria
-Bizarre QRS Morphology
-High voltage S wave in V1, V2 & V3
-Tall R wave in leads I, aVL and V5-6
-Often LAD
-QRS Interval
-ST depression in leads I, aVL, & V5-V6
-T wave inversion in I, aVL, & V5-V6

Right Bundle Branch Block:96-97


-Causes
-Idiopathic degeneration of the conduction
system
-Ischemic heart disease
-Cardiomyopathy
-Massive Pulmonary Embolus
-Ventricular Hypertrophy
-Normal Variant
-Criteria
-QRS morphology
-Wide S wave in leads I and V4-V6
-RSR’ pattern in leads V1, V2 and V3
-QRS duration
-ST depression in leads V1 and V2
-T wave inversion in leads V1 and V2
Ischemia and Infarction

-Ischemia104

*T wave inversion, ST segment depression, Acute injury: ST


segment elevation, Dead tissue: Q wave
EKG Changes: Ischemia → Acute Injury→ Infarction 108

Evolution of Transmural Infarction 109


Evolution of a Subendocardial Infarction 111

Hyperacute T waves 113


Q Waves114
-Non Pathological Q waves
(Q waves of less than 2mm
are normal)
-Pathological Q waves
(Q waves of more than
2mm indicate full
thickness myocardial damage
from an infarct, Late
sign of MI (evolved))

Look for Grouped Patterns (Footprints)115


-ST Depressions = Ischemia
-ST Elevations = injury
-Q Waves & T Wave Inversion = Infarction

Anterior Septal (Left Anterior Descending) 116

Anterior Lateral (Left Circumflex)117


Inferior (Right Coronary Artery) 118

ST-T Wave Changes


-Strain in Hypertrophy 126 -Strain in LVH 127

-Strain in RVH 128


-Strain vs Infarction 129

-Pericarditis130

-Digoxin Changes 131


-Ventricular Aneurysm 132

- T Waves 133

#Summary134
-Basic physiology of the conduction system
-Origin of a normal EKG
-Systematic approach to reading an EKG
-Major abnormalities when reading an EKG

You might also like