Transcript EKG Criteria

CARDIAC
ARRYTHMIAS
Akmal Abbasi, M.D.
EKG Standard Leads
They are all bipolar (i.e., they detect a change in
electric potential between two points) and detect an
electrical potential change in the frontal plane.
Lead I is between the right arm and left arm electrodes,
the left arm being positive.
Lead II is between the right arm and left leg electrodes,
the left leg being positive.
Lead III is between the left arm and left leg electrodes,
the left leg again being positive.
Einthoven’s triangle
EKG Augmented Limb Leads
The same three leads that form the standard leads
also form the three unipolar leads known as the
augmented leads. These three leads are referred to
as aVR (right arm), aVL (left arm) and aVF (left leg)
and also record a change in electric potential in the
frontal plane.
EKG Precordial Leads
These six unipolar leads, each in a different position on the chest, record the
electric potential changes in the heart in a cross sectional plane. Each lead
records the electrical variations that occur directly under the electrode.
EKG paper is a grid where time is measured along the horizontal axis.
Each small square is 1 mm in length and represents 0.04 seconds.
Each larger square is 5 mm in length and represents 0.2 seconds.
Voltage is measured along the vertical axis.
10 mm is equal to 1mV in voltage.
The diagram below illustrates the configuration of EKG graph paper and
whereto measure the components of the EKG wave form
Heart rate can be easily calculated from the EKG strip:
When the rhythm is regular, the heart rate is 300 divided
by the number of large squares between the QRS complexes.
For example, if there are 4 large squares between regular
QRS complexes, the heart rate is 75 (300/4=75).
The second method can be used with an irregular rhythm to
estimate the rate.
Count the number of R waves in a 6 second strip and
multiply by 10.
For example, if there are 7 R waves in a 6 second strip,
the heart rate is 70 (7x10=70).
P wave
Indicates atrial depolarization, or contraction of the atrium.
Normal duration is not longer than 0.11 seconds (less than 3 small squares)
Amplitude (height) is no more than 3 mm
No notching or peaking
QRS complex
Indicates ventricular depolarization, or contraction of the ventricles.
Normally not longer than .10 seconds in duration
Amplitude is not less than 5 mm in lead II or 9 mm in V3 and V4
R waves are deflected positively and the Q and S waves are negative
T wave
Indicates ventricular repolarization
Not more that 5 mm in amplitude in
standard leads and 10 mm in precordia
leads
Rounded and asymmetrical
ST segment
Indicates early ventricular repolarization
Normally not depressed more than 0.5 mm
May be elevated slightly in some leads (no more than 1 mm)
PR interval
Indicates AV conduction time
Duration time is 0.12 to 0.20 seconds
QT interval
Indicates repolarization time
General rule: duration is less than half the preceding R-R interval
Normal Sinus Rhythm (NSR)
Description
This is the normal heart rhythm. It originates in the SA node and
follows the appropriate conduction pathways. The rate is normal, and
the rhythm is regular. Every beat has a P wave, and every P wave is
followed by a ventricular response.
EKG Criteria
Rate: 60-100 bpm.
Rhythm: Regular. A normal variant called Sinus Arrythmia changes
rhythm in response to respiration. This is seen most often in young
healthy people.
Pacemaker: Each beat originates in the SA node.
P wave: look the same, all originate from the same locus (SA node)
PRI: 120-200 msec
QRS: 80-120 msec, narrow unless effected by underlying anomoly
SINUS BRADYCARDIA
Description
Sinus bradycardia originates in the SA node. It has reduced rate
generally from a reduction in sympathetic input, or excessive vagal
(parasympathetic) tone. This rhythm may accompany inferior MI's,
hypoxia, hypothermia, or drug reactions. At moderately slow rates,
the patient may be asymptomatic. At slower rates, they may become
hypotensive and present with symptoms consistant with decreased
perfusion: dizziness, syncope, shock like signs and symptoms.
Treatment is aimed at increasing the heart rate. Therapies include
atropine, transcutaneous and transvenous pacing, epinephrine,
dopamine, isoproterenol.
EKG Criteria
Rate: <60 bpm.
Rhythm: Regular generally.
Pacemaker: SA node
P wave: Present, all originating from SA node, all look the same.
PRI: <200 msec, and constant.
SINUS TACHYCARDIA
Description
This arrythmia originates from the SA node. It is defined as a sinus
rhythm exceeding 100 bpm. Sinus tach is a normal rhythm which
occurs in response to increased oxygen demand. This occurs with
exercise, infection, hypovolemia, hypoxia, myocardial infarct, and in
response to stimulant drugs, The rate usually has a gradual onset
and elimination. Treatment is not usually needed, but is aimed at
treating the underlying condition.
EKG Criteria
Rate: >100 bpm.
Rhythm: Regular, generally.
Pacemaker: SA node.
P wave: Present and normal, may be buried in T waves in rapid
tracings.
PRI: 120-200 msec., generally closer to 120 msec.
PREMATURE ATRIAL
COMPLEXES(PAC)
Description
These complexes originate in the atria. They often originate from
ectopic pacemaker sites within the atria which results in an abnormal
P wave. The complex occurs before the normal beat is expected,
hence the prematurity. It is followed by a pause. There are many
causes including: increased sympathetic input, exogenous stimulants,
drug interactions, AMI, cardiac ischemia, idiopathic. These complexes
can indicate increased automaticity. They may lead to re-entry
rhythms.
EKG Criteria
Rate: Underlying rhythm.
Rhythm: Irregular with PACs.
Pacemaker: Ectopic atrial pacemaker outside SA node.
P wave: Ectopic P wave present, generally different than normal SA
ATRIAL FIBRILLATION
Description
This is the most common sustained cardiac arrhythmia. It is
characterized by an undulating baseline replacing P waves and an
irregularly irregular ventricular response. This arrhythmia occurs with
hypertension, ischemic, mitral, myocardial and pericardi al disease,
thyrotoxicosis, aging and sometimes occurs in normals. Treatment
includes anticoagulation, drugs to slow ventricular conduction and/or
cardioversion
EKG Criteria
Undulating baseline replaces P waves
ATRIAL FLUTTER
Description
Atrial flutter is characterized by "sawtooth" atrial activity and a
conduction ratio to the ventricles of 2:1 to 8:1. It is caused by a
reentrant circuit located in the right atrium. It may occur when the
atria are enlar ged in chronic obstructive lung disease, mitral or
tricuspid disease, pericarditis or post-operatively. Definitive treatment
is direct-current cardioversion, surgical or catheter ablation.
EKG Criteria
Rate: 250 - 350 bpm (atrium)
Rhythm: Atrial rate regular, ventricular conduction 2:1 to 8:1
Pacemaker: Reentrant circuit rhythm located in the right atrium
P wave: Saw-tooth or picket fence
PRI: Constant onset
SUPRAVENTRICULAR
TACHYCARDIA (SVT)
Description
There are several different types of SVT depending on the site of
reentry (accessory pathway, atrioventricular node or atrium). This
rapid rhythm starts and stops suddenly. Treatment includes vagal
maneuvers, antiarrhythmia medication, radio-frequency ablation or
surgical modification of site of reentry.
EKG Criteria
Rate: 140 - 220 bpm
Rhythm: Regular
Pacemaker: Reentry circuit
Accessory pathway: Normal or short (if down accessory pathway)
A-V nodal reentry: Hidden in or at end of QRS
PRI: Depends on location of circuit
PREMATURE JUNCTIONAL
COMPLEXES (PJC)
Description
These premature complexes originate in the atrioventricular junction.
Retrograde conduction through the atria may cause an inverted P
wave in Lead 2. Integrate conduction may be normal (<120 msec).
Common etiologies include ischemia, hypoxemia, valvular disease,
digitalis or normal variant.
EKG Criteria
Rate: Underlying rhythm
Rhythm: Irregular with PJC's
Pacemaker: Ectopic junctional pacemaker
P wave: If present, negative in Lead 2
PRI: 120 msec or less
QRS: 80-120 msec, unless prolonged by aberrant conduction
JUNCTIONAL RHYHTM
Description
An escape beat serves as a protective mechanism when higher
centers in the conducting system fail to fire. Junctional escapes are
recognized by their unchanged or only slightly changed QRS complex
ending a cardiac cycle longer than the dominant cycle. This rhythm
occurs with increased vagal tone to the sinoatrial node, hypoxemia,
and digitalis toxicity.
EKG Criteria
Rate: 40 - 60 bpm
Rhythm: Regular
Pacemaker: Atrioventricular junction
P wave: If present, negative in lead 2
PRI: 120 msec or less
QRS: 80 -120 msec, unless prolonged by aberrant conduction
FIRST DEGREE AV BLOCK
Description
Conduction disturbances are characterized as first degree, second
degree Mobitz 1, second degree Mobitz II and complete heart block.
The normal P-R interval is 120 - 200 msec. First degree AV block is a
constant and prolonged PR interval. Possible etiologies include insult
to AV node, hypoxemia, myocardial infarction, digitalis toxicity,
ischemia of the conduction system and increased vagal tone but is
also seen in normals.
EKG Criteria
Rhythm: Regular
PRI: >200 msec
SECOND DEGREE AV BLOCK
MOBITZ I (WENKEBACH)
Description
Wenkebach is characterized by progressive delay at the AV node until
the impulse is completely blocked. Etiologies are the same as cause
first degree AV block and is also seen in normals. This conduction
abnormality does usually not progress to higher degree heart blocks.
EKG Criteria
Rhythm: Irregular
PRI: Progressive lengthening of PRI until dropped beat. A clue to
Wenckebach is that the QRS's appear to occur in groups.
SECOND DEGREE AV BLOCK
MOBITZ II
Description
This is a higher degree of conduction block then Mobitz I and may
progress to complete AV block. AV conduction appears normal until
suddenly there is no AV conduction following one P wave. This may
occur in a pattern (every 2nd, 3rd or 4th complex) or may occur
randomly. This is intermittent block at the AV node and may progress
to complete heart block.
EKG Criteria
PRI: Constant on conducted complexes until a sudden block of AV
conduction. That is, a P wave is abruptly not followed by a QRS
THIRD DEGREE AV BLOCK
Description
Third degree AV block is total lack of conduction through the AV
node. The rate and the interval between the QRS depend upon the
origin of the escape mechanism. This conduction defect is dangerous
and may progress to ventricular standstill. Treatment is an artificial
ventricular pacemaker.
EKG Criteria
P wave: Independent P waves and QRS's with no relationship with
the two (AV dissociation)
QRS: The QRS is normal in duration and slow (40-60 msec) with
junctional escape rhythm. The QRS is wide (>120 msec) and slower
(30-40 bpm) with ventricular escape rhythm.
PREMATURE VENTRICULAR CONTRACTIONS (PVC)
Description
A PVC is a depolarization that arises in either ventricle before the next
expected sinus beat. The normal sequence of depolarization is altered
because the impulse originates in the ventricle. The two ventricules
depolarize sequentially instead of simultaneously. Conduction moves more
slowely than through the specialized conduction pathways, this results in a
widened QRS complex (greater than 0.12 sec). PVCs may occur as isolated
complexes or may occur in pairs, triplets, or in a repeating sequence with
normal QRS complexes. Three or more PVCs in a row is considered a run of
Ventricular Tachycardia. If it lasts for more than 30 seconds it is designated
sustained VT. Treatment: Rarely treated unless symptomatic. PVCs may
indicate acute mycardial ischemia requiring rapid intervention including
oxygen, NTG, morphine, thrombolytic. Treating with lidocaine will cease the
PVC, but won't address the ischemic cause.
EKG Criteria
Rhythm: Irregular
QRS: Is not normal looking. Broadened, greater than 0.12 seconds. P waves
BIGEMINY PVCs
Description
PVC's may occur in patterns. When each normal complex is
followed by a PVC forming groups of 2, the term "ventricular
bigeminy" is used.
EKG Criteria
QRS: Normal QRS complex followed by premature wide
bizarre complex (PVC) in patterns of 2
VENTRICULAR TACHYCARDIA
Description
Ventricular Tachycardia (VT) is defined as three or more beats of
ventricular origin in succession at a rate greater than 100 beats per
minute. There are no normal (narrow) looking QRS complexes.
Consequences of VT depend on accompanying myocardial
dysfunction. It may be well tolerated or associated with lifethreatening hemodynamic compromise. Treatment: If patient is
stable, they are initially treated with lidocaine, procainamide, or
bretylium tosylate. Hemodynamically unstable VT (with a pulse) is
cardioverted at 200J, 300J, 360J as needed. VT without a pulse is
treated like VF and defibrillated.
EKG Criteria No normal looking QRS complexes, often bizzare with
notching. Width of QRS>0.12 sec. ST segment and T wave are
opposite polarity to the QRS. Sinus node may be depolarizing
normally. There is usually complete AV dissociation. P waves are
VENTRICULAR FIBRILLATION
Description
Ventricular Fibrillation is a rhythm in which multiple areas within the
ventricles display marked variation in depolarization and
repolarization. There is no organized depolarization, therefore the
ventricles do not contract as a unit. The myocardium is quivering
when visualized grossly. There is no cardiac output. This is the most
common arrythmia seen in cardiac arrest from ischemia or infarction.
The rhythm is described as coarse or fine VF. Coarse VF indicates
recent onset of VF. Prolonged delay without defibrillation results in
fine VF and eventually asysyole. Resuscitation becomes more difficult
as VF becomes finer. Treatment is always immediate unsynchronized
defibrillation at 200J, 300J, 360J for adult patients.
EKG Criteria
Rate: Very rapid, too disorganized to count.
Rhythm: Irregular, waveform varies in size and shape
No normal QRS complexes.
ASYSTOLE
Description
Asystole represents the total absence of ventricular electrical activity. Since
depolarization does not occur, there is no ventricular contraction. This may
occur as a primary event in cardiac arrest, or it may follow VF or pulseless
electrical activity (PEA). Ventricular asystole can occur also in patients with
complete heart block in whom there is no excape pacemaker. VF may
masquerade as asystole; it is best always to check two leads perpendicular
to each other to make sure that asystole is not VF. Treatment for each
arrythmia is very different. Fine VF which may mimic asystole should be
treated with defibrillation. But defibrillating asystole is potentially harmful.
Treatment: Epinephrine and Atropine are administered. Consider causes:
pulmonary embolism, acidosis, tension pneumothorax, cardiac tamponade,
hyperkalemia, hypokalemia, hypoxia, hypothermia, overdose, myocardial
infarction. (Pneumonic: PATCH(4)-O-MIne.
EKG Criteria
Complete absence of ventricular electrical activity. Occasional P waves or
erratic ventricular beats may be seen. These patients will be pulseless.
MYOCARDIAL INFARCTION
Description
Pathologic Q waves indicate myocardial death. Infarction locations are
determined by the presence of Q wave; Anterior: Q waves in leads V1, V4, I
and AVL. Inferior: Q waves in leads II, III, AVF, Lateral: Q waves in leads V5V6, I and AVL. Posterior: Tall R waves in leads V1-V2.
ST segment elevation may be present in an acute MI but also with Prinzmetal's
angina, LV aneurysm, pericarditis or a normal variant. With MI, ST segment
elevation resolves within days but pathologic Q waves may remain.
EKG Criteria
Pathologic Q waves are >30 msec wide or 1/3 length of the QRS complex.
ST segment elevation is >1mm above the isoelectric line. Leads involved will
localize the area of the myocardium involved.
Right Bundle Branch Block
•
•
•
wide QRS, more than 120 ms (3 small squares)
secondary R wave in lead V1
other features include slurred S wave in lateral leads and T wave
changes in the septal leads
Left Bundle Branch Block
•
•
•
•
•
•
•
•
•
•
left anterior hemiblock
QRS axis more left than -30 degrees
initial R wave in the inferior leads (II, III and aVF)
left ventricular hypertrophy
long PR interval (also called first degree heart block)
PR interval longer than 0.2 seconds
left atrial hypertrophy
M shaped P wave in lead II
P wave duration > 0.11 seconds
terminal negative component to the P wave in lead V1
Wolf-Parkinson-White syndrome
•
•
•
•
short PR interval, less than 3 small squares (120 ms)
slurred upstroke to the QRS indicating pre-excitation (delta wave)
broad QRS
secondary ST and T wave changes