Sunday, 22 November 2009

Miscellaneous conditions

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Myocarditis:

The ECG findings that are mostly seen in myocarditis are diffuse T wave inversions; saddle-shaped ST-segment elevations, these can also be seen in pericarditis.

Pericarditis

Types include:

  • Serous
  • Fibrinous
  • Purulent
  • Heamorrhagic
  • Caseous
Acute vs. chronic
Acute pericarditis is more common than chronic pericarditis, and can occur as a complication of infections, immunologic conditions, or heart attack.


Clinical presentation


Chest pain, radiating to the back and relieved by sitting up forward and worsened by lying down, is the classical presentation. Other symptoms of pericarditis may include dry cough, fever, fatigue, and anxiety. Pericarditis can be misdiagnosed as myocardial infarction (heart attack), and vice versa.

The classic sign of pericarditis is a friction rub. Other signs include diffuse ST-elevation and PR-depression on ECG in all leads except aVR and V1;

PRINZMETALS ANGINA

Specific ECG ST segment changes in Prinzmetals angina are elevation rather then depression


PULMONARY EMBOLISM


ECG changes can develop in a very proportion of patient's with a pulmonary embolism, changes strongly suggestive of a diagnosis of pulmonary embolism are: 

  • S1Q3T3 pattern: large S waves in Lead I, large Q waves in V3 and T wave inversion in lead III.
  • Abnormal right axis deviationbnormal rigright

  • T wave inversion in the right precordial leads 

But, the commoner findings are non-specific T wave changes and non-specific ST segment elevation or depression. 



WOLFF-PARKINSON-WHITE SYNDROME

Wolff-Parkinson-White syndrome (WPW) is a syndrome of pr-excitation of the ventricles of the heart, this is due to an accessory abnormal electrical conduction pathway known as the bundle of kent, and vast majority of individuals remain asymptomatic throughout their entire lives, but there is a risk of sudden death associated with this syndrome, this is in rare cases due to the fact of the accessory tachyarrhythmia's   in these individuals.


LOWN-GANONG-LEVINE SYNDROME


HYPERTHYROIDISM


HYPOTHYROIDISM


BRUGADA SYNDROME


EARLY REPOLARISATION


TAKO-TSUBO SYNDROME


SUBARACHNOID HAEMORRHAGE


PIGGYBACK HEART TRANSPLANT (HETEROTOPIC)


PERICARDIAL EFFUSION


COPD


RESTRICTIVE CARDIOMYOPATHY



DILATED CARDMYOPATHY


EBSTEIN's ANOMALY


TRICUSPID ATRESIA


TETRALOGY OF FALLOT


PULMONARY STENOSIS


ANEURYSM



















Cardiac arrest rhythms & protocols

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VENTRICULAR TACHYCARDIA















VENTRICULAR FIBRILLATION















Recognizing ventricular fibrillation: There will be large fibrillation waves as seen on the ECG strip above, this is called coarse ventricular fibrillation, this will eventually lead to small fibrillatory waves, then the rhythm is called fine ventricular fibrillation

  • Rhythm: Chaotic
  • Rate: Indiscernible
  • P wave: Absent
  • R wave interval:  Unmeasurable
  • QRS complex: Indiscernible
  • T wave: Indiscernible
  • QT interval: Indiscernible
  • Fibrillation waves: Present



ASYSTOLE

















BASIC/ADVANCED LIFE SUPPORT GUIDELINES







DISTINGUISHING VENTRICULAR FLUTTER FROM TORSADES DE POINTES

Pacemakers

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TERMINOLOGY


FAILURE TO CAPTURE OR PACE PROBLEMS


SENSING AND OVER SENSING


PACEMAKER-MEDIATED TACHYCARDIA


PACEMAKER CODES & MODES


TRANSCUTANEOUS PACEMAKERS


IMPLANTABLE CARDIOVERTER-DEFIBRILLOR



Hypertrophy chamber enlargement

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ATRIAL ABNORMALITY


LEFT ATRIAL ABNORMALITY (p mitrale)


RIGHT ATRIAL ABNORMALITY (p pulmonale)


LEFT VENTRICULAR HYPERTROPHY (LVH)


RIGHT VENTRICULAR HYPERTROPHY (RVH)


BIVENTRICULAR ENLARGEMENT (p biatrial)


STRAIN PATTERNS

Conduction and bundle branch blocks

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INCOMPLETE LEFT BUNDLE BRANCH BLOCK


INCOMPLETE RIGHT BUNDLE BRANCH BLOCK


COMPLETE LEFT BUNDLE BRANCH BLOCK


COMPLETE RIGHT BUNDLE BRACH BLOCK


INTRAVENTRICULAR CONDUCTION DELAY


HEMIBLOCK, (LEFT ANTERIOR)


HEMIBLOCK, (LEFT POSTERIOR)


FASCICULAR BLOCKS


LEFT ANTERIOR FASCICULAR BLOCK (LAFB)


LEFT POSTERIOR FASCICULAR BLOCK (LPFB)


MULTIFASCICULAR BLOCK


TRIFASCICULAR BLOCK

Acute coronary syndrome (ACS) rhythms

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ISCHEMIA


INJURY


INFARCTION


LOCALIZING THE INFARCT


ESTIMATING THE EXTENT OF THE INFARCTION


ISCHEMIC HEART DISEASE


POSTERIOR WALL INFARCTION


ANTERIOR WALL


ANTEROLATERAL WALL


INFERIOR WALL


LATERAL WALL


RIGHT VENTRICULAR WALL


MYOCARDIAL ISCHEMIA (SUBENDOCARDIAL)


DIAGNOSIS OF INFARCTION IN SPECIAL CIRCUMSTANCES


WELLEN's SIGN


ST Segment Elevations in ECG

Toxic and systemic disorder effects on the ECG

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HYPERCALCAEMIA ECG EFFECTS


HYPOCALCEMIA ECG EFFECTS


HYPERKALEMIA ECG EFFECTS


HYPOKALEMIA ECG EFFECTS


drugs effects on ECG:


ANTIARRHYTHIC DRUGS
DIGOXIN
QUINIDINE
OTHER
QTc MEASUREMENTS
PROLONGED QT INTERVAL SYNDROME

Supraventricular rhythms

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SVT


ABERRANT VENTRICULAR CONDUCTION


AV NODAL RE-ENTRY TACHYCARDIA


AV NODAL RECIPROCATING TACHYCARDIA



































NON-PAROOXYSMAL TACHYCARDIA


ECTOPIC ATRIAL TACHYCARDIA


SINUS NODE RE-ENTRY TACHYCARDIA


PAROXYSMAL ATRIAL TACHCARDIA WITH BLOCK



Ventricular rhythms

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SUSTAINED VT


VENTRICULAR ESCAPE BEATS


DIFFERENTIAL DIAGNOSIS OF WIDE COMPLEX TACHYCARDIA's


DISTINGUISHING VT FROM SVT


IDIOVENTRICULAR RHYTHM


ACCELERATED IDIOVENTRICULAR RHYTHM


DISTINGUISHING ACCELERATED IDIOVENTRICULAR RHYTHM FROM JUNCTIONAL


POLYMORPHIC VT


TORSADES DE POINTES







Premature beats

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PREMATURE ATRIAL CONTRACTIONS


PREMATURE ATRIAL CONTRACTION (PAC) OR ATRIAL PREMATURE BEAT (APB)


PREMATURE JUNCTIONAL CONTRACTION (PJC) OR JUNCTIONAL PREMATURE BEAT (JPB)


PREMATURE VENTRICULAR CONTRACTION (PVC) OR VENTRICULAR PREMATURE BEAT (VPB)


FUSION & PSEUDO-FUSION BEATS


DISTINGUISHING NON-CONDUCTED PAC'S FROM SINOATRIAL BLOCK 


DISTINGUISHING INTERMITTENT VENTRICULAR PACING FROM PVC's


BIGEMINY


TRIGEMINY


QUADGEMINY


MUTIFOCAL PVC's


COUPLETS


SALVO's


R-ON-T PHENOMENON







Junctional rhythm

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JUNCTIONAL ESCAPE BEATS


JUNCTIONAL RHYTHM


JUNCTIONAL TACHYCARDIA


PREMATURE JUNCTIONAL CONTRACTION (PJC)


ACCELERATED JUNCTIONAL RHYTHM

Atrial rhythms

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ATRIAL FIBRILLATION


ATRIAL FLUTTER


ATRIAL ESCAPE


ATRIAL BIGEMINY


SINUS ARREST


SINUS EXIT BLOCKS


WONDERING ATRIAL PACEMAKER


DISTINGUISHING WAP FROM PAC'S


SICK SINUS SYNDROME OR SINUS NODE DYSFUNCTION


MUTIFOCAL ATRIAL TACHYCARDIA


DISTINGUISHING MAT FROM AF


PARAOXYSMAL ATRIAL TACHYCARDIA


ATRIAL TACHYCARDIA WITH BLOCK


DISTINGUISHING ATRIAL FLUTTER FROM ATRIAL FIBRILLATION


DISTINGUISHING ATRIAL FIBRILLATION FROM JUNCTIONAL RHYTHM







Sinoatrial blocks

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TYPE-1


FIRST-DEGREE ATRIOVENTRICULAR BLOCK


TYPE-2


SECOND-DEGREE (TYPE I) ATRIOVENTRICULAR BLOCK


SECOND DEGREE (TYPE II) ATRIOVENTRICULAR BLOCK


TYPE III


THIRD-DEGREE ATRIOVENTRICULAR BLOCK


ATRIOVENTRICULAR DISSOCIATION



Sinus node arrhythmias

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NORMAL SINUS RHYTHM


SINUS ARRHYTHMIA


SINUS BRADYCARDIA


SINUS TACHYCARDIA


TACHYARRHYTHMIAS


BRADYARRHYTHMIAS


INTRINSIC CAUSES


EXTRINSIC CAUSES


BRADYCARDIA-TACHYCARDIA SYNDROME


ESCAPE RHYTHMS 


PARASYSTOLE


ASHMAN'S PHENOMENON


CATURE BEATS


FUSION BEATS







12-lead ECG interpretation

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NORMAL ECG FINDINGS


LOCATING MYOCARDIAL DAMAGE
































THE RIGHT SIDED LEADS

Introduction to the 12-lead ECG

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THE 12-LEAD ELECTRICAL AXIS


12-LEAD ELECTRODE POSITIONING/PLACEMENTS


WILSON'S (PRECORDIAL LEADS)


NEHB'S SPECIAL LEADS


HOW TO PERFORM A 12-LEAD ECG



Basic rhythm interpretation (arrhythmias)

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DEFINITIONS


MECHANISM


ALTERED IMPULSE FORMATION


ALTERED IMPULSE CONDUCTION


CLASSIFICATION OF ARRHYTHMIAS


CAUSES OF ARRHYTHMIAS

Technical problems (troubleshooting)

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ARTIFACTS ON THE ECG


SIGNAL-AVERAGED ECG


PAPER SPEED


CALIBRATION


ELECTROBE MISPLACEMENT


TROUBLESHOOTING CARDIAC MONITORS


DEXTROCARDIA

Cardiac axis, leads and planes

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LEADS I,II,III





In both the 5- and 12-lead configuration, leads I, II and III are called limb leads. The electrodes that form these signals are located on the limbs—one on each arm and one on the left leg. The limb leads form the points of what is known as Einthoven's triangle.
  • Lead I is the voltage between the (positive) left arm (LA) electrode and right arm (RA) electrode.
  • Lead II is the voltage between the (positive) left leg (LL) electrode and the right arm (RA) electrode.
  • Lead III is the voltage between the (positive) left leg (LL) electrode and the left arm (LA) electrode. 



BIPOLAR & UNIPOLAR LEADS




There are two types of leads: unipolar and bipolar. Bipolar leads have one positive and one negative pole. In a 12-lead ECG, the limb leads (I, II and III) are bipolar leads. Unipolar leads also have two poles, as a voltage is measured; however, the negative pole is a composite pole (Wilson's central terminal) made up of signals from lots of other electrodes. In a 12-lead ECG, all leads besides the limb leads are unipolar (aVR, aVL, aVF, V1, V2, V3, V4, V5, and V6).
Wilson's central terminal is produced by connecting the electrodes, RA; LA; and LL, together, via a simple resistive network, to give an average potential across the body, which approximates the potential at infinity (i.e., zero).



LEADS avr, avl and avf



Leads aVR, aVL, and aVF are augmented limb leads. They are derived from the same three electrodes as leads I, II, and III. However, they view the heart from different angles (or vectors) because the negative electrode for these leads is a modification of Wilson's central terminal. This zeroes out the negative electrode and allows the positive electrode to become the "exploring electrode" or a unipolar lead. This is possible because Einthoven's Law states that I + (−II) + III = 0. The equation can also be written I + III = II. It is written this way (instead of I − II + III = 0) because Einthoven reversed the polarity of lead II in Einthoven's triangle, possibly because he liked to view upright QRS complexes. Wilson's central terminal paved the way for the development of the augmented limb leads aVR, aVL, aVF and the precordial leads V1, V2, V3, V4, V5, and V6.
  • Lead augmented vector right (aVR) has the positive electrode (white) on the right arm. The negative electrode is a combination of the left arm (black) electrode and the left leg (red) electrode, which "augments" the signal strength of the positive electrode on the right arm.
  • Lead augmented vector left (aVL) has the positive (black) electrode on the left arm. The negative electrode is a combination of the right arm (white) electrode and the left leg (red) electrode, which "augments" the signal strength of the positive electrode on the left arm.
  • Lead augmented vector foot (aVF) has the positive (red) electrode on the left leg. The negative electrode is a combination of the right arm (white) electrode and the left arm (black) electrode, which "augments" the signal of the positive electrode on the left leg.
The augmented limb leads aVR, aVL, and aVF are amplified in this way because the signal is too small to be useful when the negative electrode is Wilson's central terminal. Together with leads I, II, and III, augmented limb leads aVR, aVL, and aVF form the basis of the hexaxial reference system, which is used to calculate the heart's electrical axis in the frontal plane.



Einthoven's triangle


GOLDBERGERS AUGMENTED LEADS


GRAPH PAPER MEASUREMENTS


LEAD ELECTROBE POSITIONING


LEFT AXIS DEVIATION (LAD)






Left axis deviation occurs when additional electrical forces move to the left (hypertrophy), or when the time required for the electrical activity to move over the ventricle is prolonged (LBBB, left ventricular dilation).
Causes of left axis deviation include hypertension, aortic stenosis or regurgitation, subaortic stenosis, mitral regurgitation, and left ventricular conduction defects.
The QRS axis may shift during the respiratory cycle if elevation of the diaphragm changes the physical position of the heart. Beat-to-beat variation in QRS axis (an every-other-beat change in QRS shape) is called “electrical alternans.” This is thought to be caused by the heart physically swinging back and forth in a pericardial effusion.



RIGHT AXIS DEVIATION (RAD)






Right axis deviation is seen on the ECG when more electrical forces are moving to the right than normal. This is usually due to hypertrophy of the right ventricle (RVH). Causes of right axis deviation include COPD, pulmonary emboli, valvular disease, septal defects, and pulmonary hypertension.
An axis of +90 is common in persons with emphysema. This so-called “vertical heart” reflects both the rotation of the heart downward as the diaphragm position drops due to air trapping, and some degree of hypertrophy of the right ventricle.



EXTREME AXIS DEVIATION


RIGHT SUPERIOR AXIS DEVIATION (RARE CASES)


ROTATION OF THE CARDIAC AXIS





Axis Deviation:


The QRS axis is the “average” direction of electrical activity during ventricular depolarization. The QRS axis may shift due to physical change in the position of the heart, chamber hypertrophy, or conduction block.




Normal QRS axis is from around -30 to +90 degrees. More negative than -30 is called left axis deviation. More positive than +90 is called right axis deviation.The average direction of electrical activity is the "QRS axis."
See the diagram: if the axis is in the direction labeled "II" the axis is +60 degrees.
vector.gif (2152 bytes)


Determining QRS axis by inspection:



The “inspection” method of determining axis requires that you check QRS orientation in specific leads. It is usually much faster than the vector method, and provides the same clinical information.QRS Axis by Inspection Method
lead I positive, lead III positive = normal axis
lead I negative (+/- R positive) = RIGHT axis
lead III negative, lead II negative = LEFT axis

First check lead I. If the QRS is “positive” overall (comparing negative deflections to positive deflections), right axis deviation is ruled out.
If the QRS in lead I is negative, right axis deviation is mild. Now check lead R. If the QRS is overall positive, right axis deviation is definite.
Now check for left axis deviation by inspecting lead III. If the QRS is overall positive, left axis is ruled out.
If the QRS is negative in III, check lead II. If lead II also shows an overall negative QRS, left axis deviation is diagnosed.

In this ECG, lead I is positive. Next we look at lead III and note it’s negative. We check lead II. Because lead III and lead II are both negative, we diagnose left axis deviation by the “inspection method.”
Vector method for QRS axis:
Determining QRS axis by vector method is most easily done using lead F and lead I. These leads are convenient because they are at right angles to each other.
First determine lead I’s QRS size and orientation by subtracting the S wave height from the R wave height. Then determine lead F’s size in the same way.



Plot out the overall QRS size on the line representing lead I. Positive is to your right, negative to your left. Plot out the QRS size on the line representing lead F. If F’s QRS is positive, draw downward. If negative, draw up.
Draw lines perpendicular to the end points of your lines, to form a rectangle. Draw a line from the centerpoint to the corner of your box. This is the electrical vector. Its orientation represents the electrical axis
Remember that lead I is pointing to zero degrees, directly to your right (the patient’s left). Clockwise from lead I is positive, counterclockwise is negative. In the diagram on the previous page, we would estimate the axis at minus 40 degrees.
Equiphasic lead method for QRS axis:
Another alternative for estimating QRS axis is the “equiphasic lead” method. Locate a lead that has the smallest total QRS complex and/or is equiphasic. The QRS axis should be at 90 degrees to this lead.
Now look at the lead that (on the vector diagram) is 90 degrees from the equiphasic lead. If this lead’s QRS complex is positive, the QRS axis is in the direction of that lead. If negative, the QRS axis is 180 degrees opposite.




In this ECG, lead III is most nearly equiphasic. The QRS axis will therefore be at 90 degrees to it. We would estimate the axis at around plus 30 degrees.


ECG Waves & Segments components

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P wave


The P wave represents right by left atrial depolarization and is low amplitude positive deflection preceding the QRS complex. Atrial repolarization occurs simultaneously with depolarization of the ventricular myocardium and is hidden by the QRS complex.

Assessment of the P wave allows an idea of where the atrial depolarization begins and whether or not the atrial are enlarged

  • The best leads to look for P waves in are leads II and V1.
  • Right Atrial Enlargement (RAE) tends to present as peaked P wave >2.5mm in lead II.
  • Left Atrial Enlargement (LAE) is seen as a biphasic P wave in V1 with a 1 small box deep and 1 small box deep negative deflecton.
  • Inverted P waves in leads II, III and aVF imply a negative axis of the P wave or retrograde conduction in the atrial due to a low atrial or junctional pacemaker.



PR interval


The PR interval is measured from the beginning of the P wave to the first part of the QRS complex. It includes time for atrial depolarization, conduction through the AV node, and conduction through the His-Purkinje system. Disruption at any point can prolong the PR interval. The length of the PR interval changes with heart rate, but is normally 0.12-0.20 seconds.


QRS complex


The QRS complex consists of the time needed for ventricular depolarization.

The first positive deflection of the QRS (R wave) is very steep, reflecting the quick distribution of electrical impulses through the His-Purkinje system. This represents depolarization of the left ventricular myocardium. The negative deflection following the R wave is the S wave which represents terminal depolarization of the high lateral wall. The lowercase letters are used for relatively small amplitude waves of less then 0.5mV or 5 mm (one large box).

A lengthened QRS complex can result from 3 possibilities:

  • Impairment of the conduction system exists so that the wave of depolarization coming down from the atria does not or cannot travel the normal conduction system (bundle branch block, abberrant ventricular conduction, or Wolff-Parkinson-White syndrome).
  • A beat initiated in the ventricle (PVC, Ventricular Tachycardia, or idioventricular).
In a normal ECG the R waves of the QRS complex begin small in V1-V2 and get larger as we progress through the precordial leads laterally. The R wave will be the dominant deflection in the QRS by V3-V4.

Early large R waves in V1-V2, as large as those in following leads, can reflect posterior wall infarction, lateral infarction, right ventricular hypertrophy or septal hypertrophy.

Poor R wave progression is when the R waves do not begin to dominate the QRS until V5 or V6. This may represent infarction or injury of the anterior left ventricle and carries almost as much significance as Q waves.

The size of the QRS can be determined by: the size of the patient (larger patients have smaller complexes), the left ventricular muscle mass, and the age of the patient (older patients tend to have smaller complexes).



ST segment


The ST segment occurs after ventricular depolarization has ended and before repolarization has begun. The ST segment is usually isoelectric and has a slight upward concavity. It is of particular interest in diseased states where it may have other configurations.

ST segments are measured for elevation or depression against the TP segment, not the PR interval. The TP segment is the true isoelectric line. The ST segment is always measure from the J point, where the QRS and ST segments meet. Many J points are an approximation with no clear transition from the QRS to the ST segment.

In young people, J-point elevation is seen as concave up-sloping ST segments that take off a bit above the isoelectric line and this is common. It does not indicate pathology.




T wave


The T wave represents the period of ventricular repolarization. Since repolarization is slower than depolarization, the T wave is broad and has a slow upstroke.

  • Flattened T waves may indicate ischemia.
  • T waves are normally upright in I, II, V3-V6 and inverted in lead aVR.
  • T waves can be observed for indications of ischemia or electrolyte disturbances.



QT interval


The QT interval consists of the QRS complex (representing only a brief part of the interval), along with the ST segment and T wave, which constitutes the majority of the duration. The QT interval is used primary as a measure of membrane repolarization. Since the QT interval varies with heart rate, the QT is "corrected" (QTc) to make comparisons between ECG's. The corrected QT interval equals the QT when the ventricular rate is 60 bpm (the RR=1).

Causes of prolonged QT intervals include:

  • Electrolyte abnormalities
  • hypothermia
  • Idiopathic long QT syndrome
  • Tricyclic antidepressants
  • Phenothiazines
  • Antiarrhytmics (quinine and procainamide)



U wave


The U wave may be seen in some leads, especially the right precordial leads: V2-V4. U waves are associated  with metabolic disturbances, typically hypokalemia and hypomagnesemia. Additionally, it may be seen following the T wave and can make interpretation of the QT interval especially difficult.


Determining heart rate



Standard ECG paper is standardized at 25mm/sec. The vertical lines on the ecg graph paper can be used to measure varying time intervals. There is a 0.20 sec between two of the large lines.

To count the number of heart beats (QRS complexes) in a regular rhythm, between 30 large boxes (6 seconds) you just multiply by 10, and this will give you a estimate of how many beats per minute. ECG paper also has additional markings every 3 seconds so you don't have to count 30 large boxes.

Other way that is quicker and easier to estimate the heart rate is to remember the table below:


Rhythm

Basic Eletrocardiology

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COMING SOON

ECG RULER

CALIPERS

MODERN ECG MACHINES


Abbreviations

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