J.S.S.G. de Jong, MD I.

Sinus Node Rhythms and Arrhythmias The sinus node (SA) is located in the roof of the right atrium. It is the fastest physiological pacemaker. When the sinus node generates an electrical impulse, the surrounding cells of the right atrium depolarize. Then the cells of the left atrium, the AV (atrioventricular)node, follow, and at last the ventricles are stimulated via the His bundle.

Criteria for normal sinus rhythm (see also Basics): A P wave morphology P wave (atrial contraction) precedes every QRS complex The rhythm is regular, but varies slightly during respirations The rate ranges between 60 and 100 beats per minute The P waves maximum height at 2.5 mm in II and/or III The P wave is positive in I and II, and biphasic in V1

Sinus arrhythmias
Some variants of sinus rhythm exist:

Asystole Sinustachycardia (>100 beats per minute) Sinusbradycardia (<60 beats per minute) Sinus arrest or pause Sino-atrial exit block Sick Sinus Syndrome Sinus Arrythmia

Arrhythmias are discussed in the Arrhythmias chapter. If the heart rate exceeds 100 bpm, the tachcyardia flow chart should be followed. II. Rate What is the heart rate? To answer this question, determine the time between two QRS complexes. Previously, the ECG was printed on a paper strip transported through an ECG writer at the speed of 25 mm/second. Now, digital ECGs are common; however, the method for determining the frequency remains the same. The ECG has a grid with thick lines 5 mm apart (= 0,20 second) and thin lines 1 mm (0,04 second). There are three simple methods to determine the heart rate (HR) The square counting method The square counting method is ideal for regular heart rates. Use the sequence 300-150-10075-60-50-43-37. Count from the first QRS complex, the first thick line is 300, the next thick line 150 etc. Stop the sequence at the next QRS complex. When the second QRS complex is

between two lines, take the mean of the two numbers from the sequence or use the finetuning method listed below. Use a calculator Count the small (1mm) squares between two QRS complexes. The ECG paper runs at 25 mm/sec through the ECG printer; therefore: This method works well in case of tachycardia (>100 beats/minute) The marker method Non-regular rhythms are best determined with the "3 second marker method". Count the number of QRS complexes that fit into 3 seconds (some ECG writers print this period on the ECG paper). Multiply this number by 20 to find the number of beats/minute.

What changes the frequency of the heart?

A number of factors change the heart frequency, including:

the (para) sympathic nervous system. o The sympathic system, e.g. epinephrine, (=adrenalin) increases atrioventricular conduction and contractility (the fight or flight reaction.) o The parasympathic system (nervus vagus,) e.g. acetycholine, decreases the frequency and atrioventricular conduction. The parasympathic system affects mainly the atria. Cardiac filling increases the frequency. arrhythmias influence heart rate.

III. Conduction

The PQ interval

The PQ duration depends on the conduction velocity in the atria, AV node, His bundle, bundle branches and Purkinje fibers The PQ interval starts at the beginning of the atrial contraction and ends at the beginning of the ventricular contraction. The PQ interval (sometimes referred to as the PR interval as a Q wave is not always present) indicates how fast the action potential is transmitted through the AV node (atrioventricular) from the atria to the ventricles. Measurement should start at the beginning of the P wave and end at the beginning of the QRS segment. The normal PQ interval is between 0.12 and 0.20 seconds. A prolonged PQ interval is a sign of a degradation of the conduction system or increased vagal tone (Bezold-Jarisch reflex), or it can be pharmacologically induced. This is called 1st, 2nd or 3rd degree AV block. A short PQ interval can be seen in the WPW syndrome in which faster-than-normal conduction exists between the atria and the ventricles.

The QRS duration

The QRS duration indicates how fast the ventricles depolarize. The normal QRS is < 0.10 seconds The ventricles depolarize normally within 0.10 seconds. When this is longer than 110 miliseconds[1], this is a conduction delay. Possible causes of a QRS duration > 110 miliseconds include:

Left bundle branch block Right bundle branch block Electrolyte Disorders Idioventricular rhythm and paced rhythm

For the diagnosis of LBBB or RBBB QRS duration must be >120 ms.

The QT interval

The QT interval starts at the onset of the Q wave and ends where the tangent line for the steepest part of the T wave intersects with the baseline of the ECG.

The eyeballing method to estimate QT prolongation. If the QT interval ends before the imaginary boundary halfway two QRS complexes, the QTc is probably normal. If the QTc reaches beyond the halfway line, the QTc is probably prolonged. This method is only 'valid' in registrations with normal (60-100/min) heart rates. The normal QTc (corrected) interval The QT interval indicates how fast the ventricles are repolarized, becoming ready for a new cycle. The normal value for QTc is: below 450ms for men and below 460ms for women. [2] If QTc is < 340ms short QT syndrome can be considered. The QT interval comprises the QRS-complex, the ST-segment, and the T-wave. One difficultly of QT interpretation is that the QT interval gets shorter as the heart rate increases. This problem can be solved by correcting the QT time for heart rate using the Bazett formula:

Thus at a heart rate of 60 bpm, the RR interval is 1 second and the QTc equals QT/1. The QTc calculator can be used to easily calculate QTc from the QT and the heart rate or RR interval. On modern ECG machines, the QTc is given. However, the machines are not always capable of making the correct determination of the end of the T wave. Therefore, it is important to check the QT time manually.

Alternatives to the Bazzett correction formula are the Fridericia, Framingham and Hodges formulas. The latter two perform better at high heart rates (>100 /min). [3][4] Fridericia: QTc = QT{HR/60}1/3, Framingham: QTc = QT + 0.154{1 (60/HR)}, Hodges: QTc = QT + 1.75 (heart rate - 60).

Dr Surawicz, founder of the tangent method, still active in November 2006, at age 89. Although QT prolongation is potentially lethal, measurement of the QT interval by physicians is not standardized, since different definitions of the end of the T wave exist.[5] Most QT experts define the end of the T wave as the intersection of the steepest tangent line from the end of the T-wave with the base line of the ECG.[6] This leads to the following stepwise approach:

1. 2. 3. 4. 5.

Stepwise approach to correct measurement of the QT interval Use lead II. Use lead V5 alternatively if lead II cannot be read. Draw a line through the baseline (preferably the PR segment) Draw a tangent against the steepest part of the end of the T wave. If the T wave has two positive defle taller deflection should be chosen. If the T wave is biphasic, the end of the taller deflection should be The QT interval starts at the beginning of the QRS interval and ends where the tangent and baseline cr If the QRS duration exceeds 120ms the amount surpassing 120ms should be deducted from the QT int QT=QT-(QRS width-120ms) )

6. Calculate QTc according to Bazett:

. You can use the QTc calculator for this

In a pathological prolonged QT time, it takes longer than the normal amount of time for the myocardial cells to be ready for a new cycle. There is a possibility that some cells are not yet repolarized, but that a new cycle is already initiated. These cells are at risk for uncontrolled depolarization, induction of Torsade de Pointes and subsequent Ventricular Fibrillation.

Causes of QT prolongation The QT interval is prolonged in congenital long QT syndrome, but QT prolongation can also occur be acquire of:

Medication (anti-arrhythmics, tricyclic antidepressants, phenothiazedes, for a complete list see Torsad Electrolyte imbalances Ischemia.

QT prolongation is often treated with beta blockers. If the QT segment is abnormal, it can be difficult to define the end of the T wave. Below are a number of examples that suggest how QT should be measured in these patients.

IV. QRS axis

When you average all electrical signals from the heart, you can indicate the direction of the average electrical depolarization with an arrow (vector). This is the heart axis. A change of the heart axis or an extreme deviation can be an indication of pathology. To determine the heart axis you look at the extremity leads only (not V1-V6). If you focus especially on leads I, II, and AVF you can make a good estimate of the heart axis. An important concept in determining the heart axis is the fact that electricity going towards a lead yields a positive deflection in the electric recording of that lead. Imagine the leads as cameras looking at the heart. Lead I looks horizontally from the left side. Lead II looks from the left leg. Lead III from the right leg and lead AVF from below towards the heart. A positive deflection here is defined as the QRS having a larger 'area under the curve' above the baseline than below the baseline. With these basics in mind, one can easily estimate the heart axis by looking at leads I and AVF:

Positive (the average of the QRS surface above the baseline) QRS deflection in lead I: the electrical activity is directed to the left (of the patient) Positive QRS deflection in lead AVF: the electrical activity is directed down.

This indicates a normal heart axis. Usually, these two leads are enough to diagnose a normal heart axis! A normal heart axis is between -30 and +90 degrees.

A left heart axis is present when the QRS in lead I is positive and negative in II and AVF. (between -30 and -90 degrees) A right heart axis is present when lead I is negative and AVF positive. (between +90 and +180) An extreme heart axis is present when both I and AVF are negative. (axis between +180 and -90 degrees). This is a rare finding.

The largest vector in the heart is from the AV-node in the direction of ventricular depolarization. Under normal circumstances, this is directed left and down.(towards leads I and AVF). The position of the QRS vector is given in degrees. See the figure. A horizontal line towards the left arm is defined as 0 degrees. An iso-electric lead can help estimate the heart axis more precisely: Iso-electric When the depolarization is perpendicular on the lead, this is called iso-electric. The QRS is neither positive nor negative. Undetermined axis When all extremity leads are biphasic, the axis is directed to the front or back, in a transverse plane. The axis is than undetermined.

Left axis deviation

Left heart axis

Left anterior hemiblock Causes of left axis deviation include:

Normal variation (physiologic, often with age) Mechanical shifts, such as expiration, high diaphragm (pregnancy, ascites, abdominal tumor) Left ventricular hypertrophy Left bundle branch block left anterior fascicular block Congenital heart disease (e.g. atrial septal defect) Emphysema Hyperkalemia Ventricular ectopic rhythms Preexcitation syndromes Inferior myocardial infarction Pacemaker rhythm

Right axis deviation

Right heartaxis Causes of right axis deviation include:

Normal variation (vertical heart with an axis of 90) Mechanical shifts, such as inspiration and emphysema Right ventricular hypertrophy Right bundle branch block Left posterior fascicular block Dextrocardia Ventricular ectopic rhythms Preexcitation syndromes Lateral wall myocardial infarction Right ventricular load, for example Pulmonary Embolism or Cor Pulmonale (as in COPD)

V. P Wave Morphology The Normal P wave The P wave morphology can reveal right or left atrial hypertrophy or atrial arrhythmias and is best determined in leads II and V1 during sinus rhythm. Characteristics of a normal p wave:[1]

The maximal height of the P wave is 2.5 mm in leads II and / or III The p wave is positive in II and AVF, and biphasic in V1 The p wave duration is shorter than 0.12 seconds

The Abnormal P wave

Elevation or depression of the PTa segment (the part between the p wave and the beginning of the QRS complex) can result from atrial infarction or pericarditis. If the p-wave is enlarged, the atria are enlarged. If the P wave is inverted, it is most likely an ectopic atrial rhythm not originating from the sinus node.

Altered P wave morphology is seen in left or The PTa segment can be used to diagnose

right atrial enlargement. VI. QRS Morphology

pericarditis or atrial infarction.

The basic questions in judging QRS morphology are:

Are there any pathological Q waves as a sign of previous myocardial infarction? Are there signs of left or right ventricular hypertrophy? Does the QRS complex show microvoltage (roughly QRS < 5mm)? Is the conduction normal or prolonged (QRS-interval > 0,12s)? Is the R wave propagation normal? Normally R waves become larger from V1-V5. At V5 it should be maximal. If the R wave in V2 is larger than in V3, this could be a sign of a (previous) posterior myocardial infarction. Other causes are noted in the chapter Clockwise and Counterclockwise rotation.

VII. ST Morphology The ST segment represents ventricular repolarization. Repolarization follows upon contraction and depolarization. During repolarization the cardiomyocytes elongate and prepare for the next heartbeat. This process takes much more time than the depolarization. The elongation that takes place during repolarization is not passive; it is an active process during which energy is consumed. On the ECG, the repolarization phase starts at the junction, or j point, and continues until the T wave. The ST segment is normally at or near the baseline. Minor STT changes are not necessarily associated with cardiac ischemia[1]. The T wave is usually concordant with the QRS complex. Thus if the QRS complex is positive in a certain lead (the area under the curve above the baseline is greater than the area under the curve below the baseline) than the T wave usually is positive too in that lead. Accordingly the T wave is normally upright or positive in leads I, II, AVL, AVF and V3-V6. The T wave is negative in V1 and AVR. The T wave flips around V2, but there is likely some genetic influence in this as in Blacks the T wave usually flips around V3. The T wave angle is the result of small differences in the duration of the repolarization between the endocardial and epicardial layers of the left ventricle. The endocardial myocytes need a little more time to repolarize (about 22 msec). This difference causes an electrical current from the endocardium to the epicardium, which reads as a positive signal on the ECG.[2]

ST changes occur when the action potential in the ischemic area changes, resulting in an electric injury current from the healthy cardiomyocytes towards the ischemic area during the repolarization fase.

ST elevation

ST elevatie is measured at the junctional or j-point.[3]

common causes of ST shift

Examples of normal ST elevation. Adapted from [4]

Examples of pathologic ST elevation. LVH, LBBB, Pericarditis, Hyperkalemia, Anterior AMI. Adapted from [4] The most important cause of ST segment elevation is acute Ischemia. Other causes are [4][5]:

Early repolarization Acute pericarditis: ST elevation in all leads except aVR Pulmonary embolism: ST elevation in V1 and aVR Hypothermia: ST elevation in V3-V6, II, III and aVF Hypertrophic cardiomyopathy: V3-V5 (sometimes V6) High potassium (hyperkalemia): V1-V2 (V3) During acute neurologic events: all leads, primarily V1-V6 Acute sympathic stress: all leads, especially V1-V6 Brugada syndrome. Cardiac aneurysm. Cardiac contusion Left ventricular hypertrophy Idioventricular rhythm including paced rhythm

In a study by Otto et al., among 123 patients with chest pain and ST segment elevation of >1mm, 63 patients did not have a myocardial infarction. Diagnoses in patients who did not have a myocardial infarction were LVH (33%) and LBBB (21%). [6] In daily practice this means that in these patients the diagnosis of myocardial infarction has to depend on other diagnostic means, such as laboratory tests, echocardiography and coronary angiography. An important clue for the diagnosis of ischemia is the presence of reciprocal ST segment depression.

Characteristics of early repolarization Early repolarization is a term used for ST segment elevation without underlying disease. It probably has nothing to do with actual early repolarization. It is commonly seen in young men. It is important to discern early repolarization from ST segment elevation from other causes such as ischemia. Characteristics of early repolarization are:[7]

an upward concave elevation of the RS-T segment with distinct or "embryonic" J waves slurred downstroke of R waves or distinct J points or both RS-T segment elevation commonly encountered in the precordial leads and more distinct in these leads rapid QRS transition in the precordial leads with counterclockwise rotation persistence of these characteristics for many years absence of reciprocal ST depression large symmetrical T waves

Early repolarization in inferior leads (II, III en AVF) has recently been found to be associated with an increased risk of cardiac death (1 mm of ST elevation carried an OR of 1.3 and 2 mm

an OR of 3.0 )[8]

ST depression
The most important cause of ST segment depression is Ischemia. Other causes of ST segment depression are:

Reciprocal ST segment depression. If one lead shows ST segment elevation then usually the lead 'on the other side' shows ST segment depression. (This is usually seen in ischemia as well. Left ventricular hypertophy with "strain" or depolarization abnormality Digoxin effect Low potassium / low magnesium Heart rate-induced changes (post tachycardia) During acute neurologic events.

T wave changes

Different forms of T wave morphology The T wave is quite 'labile' and long lists of possible causes of T wave changes exist. A changing T wave can be a sign that 'something' is abnormal, but it doesn't say much about the severity. T waves can be peaked, normal, flat, or negative. Flat and negative T waves are defined as: flat T wave < 0.5 mm negative or positive T wave in leads I, II, V3, V4, V5 or V6 negative (or inverted) T wave > 0.5 mm negative T wave in leads I, II, V3, V4, V5 or V6 A concise list of possible causes of T wave changes:

Ischemia and myocardial infarction Pericarditis Myocarditis

Cardiac contusion Acute neurologic events, such as a subarachnoid bleed. Mitral valve prolapse Digoxin effect Right and left ventricular hypertrophy with strain

VIII Compare the Old and New ECG An abnormal ECG does not prove acute cardiac disease. And a normal ECG does not exclude cardiac disease. It is necessary therefore to compare new ECG with ECG's made in the past. Hallmarks are:

Is there a change in rhythm? Is there a change in frequency? Is there a change in conduction time? Is there a change in heart axis? Are there new pathological Q's? Is there a change in R wave size? Is there a change in ST? Is there a change in T wave?

So, one has to check for changes in all 7 steps.

Change in rhythm
Example: New atrial fibrillation. Atrial fibrillation occurs in ten percent of elderly people (>70 year) without clinical symptoms. Therefore atrial fibrillation in acute dyspneic patients does not prove atrial fibrillation-induced cardiac decompensation. Also other causes (e.g. cardiac ischemia, pneumonia) should be considered. Previous ECGs could provide additional information.

Frequency
Example: Bradycardia. New sinus bradycardia of 50 beats per minute (bpm) may cause dizziness; however, long-existing bradycardias are often without symptoms. Therefore it is important to know the patient's normal frequency.

Conduction time
An increase in PQ time may be seen in elderly patients, but may also be caused by the use of medication or by ischemia. Broadening of the QRS complex may also be caused by medication or ischemia. An increase in QTc time may be caused by medication, but may also be hereditary. Comparison of a previous ECG with new ECG may provide the clue.

Heart axis

Ischemia may cause a change in the heart axis; on the other hand, a deviated heart axis caused by left anterior fascicular block may have already been present for years at the time the ECG was made (and would remain for life). Again, a previous ECG differentiates between old and new changes.

Pathological Q's
Hallmark of the comparison between old and new ECG are pathological Q's. New pathological Q's provide evidence for the occurrence of a myocardial infarction.

Increase R wave
Decrease of the R wave may be a sign of an infarction. Tamponade, cardiomyopathy and increased body size also decrease the R wave. Increase of the R wave indicates hypertrophy of the left ventricle (leads V5-V6), or a posterior infarction (V2-V3) or a loss of body weight.

the ST segment
New elevation of the ST segment indicates an acute myocardial infarction. Chronic elevation of the ST segment may be caused by cardiac aneurysms or long-standing (several weeks) pericarditis.

T wave
T wave inversion can be caused by ischemia, disturbances in electrolytes or stress. Often no distinction can be made between these causes. T wave inversion indicates that something is possibly wrong and further investigation is needed. IX. Normal Tracing Characteristics of a normal ECG

Rhythm: sinus Rate: 60-100 bpm Conduction: o PQ interval 120-200ms o QRS width 60-100ms o QTc interval 390-450ms (use the QTc calculator for this) Heart axis: between -30 and +90 degrees P wave morphology: o The maximal height of the P wave is 2.5 mm in leads II and / or III o The p wave is positive in II and AVF, and biphasic in V1 o The p wave duration is usually shorter than 0.12 seconds QRS morphology: o No pathological Q waves o No left or right ventricular hypertrophy

No microvoltage Normal R wave propagation. (R waves increase in amplitude from V1-V5) ST morphology o No ST elevation or depression o T waves should be concordant with the QRS complex The ECG should not have changed from the previous ECG

o o