Filed under: Supraventricular arrhythmias
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Patient: Woman, 51 y/o. Mitral valve replacement 21 years ago. Known paroxysmal atrial fibrillation. Presents in the ER with nausea, pale skin, mild diaphoresis, palpitations and diffuse chest pain.
Prehospital ECG:
- Supraventricular tachycardia
- Ventricular rate is ca. 120 bpm
- Normal axis at ca. 10°
- Atrial activity best visible in lead V1, showing P waves with a slightly varying and prolonged PR interval.
- Several P waves superimposed and partially hidden in T waves
- Pseudo R waves in lead V1
Interpretation: This faxed ECG shows a supraventricular tachycardia, but right precordial lead V1 shows clear atrial activity. The small, peaked P waves with a slightly changing and prolonged PR interval suggests atrial ectopy. Ectopic Atrial Tachycardia rarely occurs with 1:1 ratio, as the AV node usually blocks half or more of the impulses. A common AV block ratio is 2:1. With a ventricular rate of 120 bpm, a 2:1 AV block would indicate an atrial rate of 240 bpm. This would be a typical atrial rate for ectopic atrial tachycardia. Using a ruler or a caliper and measuring from one of the visible P waves here, we will see exactly that: P waves appear at a rate of 240 bpm. The most visible P waves are right after or superimposed on T waves, and the others are hidden in or appearing right after each QRS, creating what looks like a small S wave, a pseudo S wave.
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To confirm the diagnosis, carotid pressure is applied while a rhythm strip is recorded. Paper speed is set to 50 mm/s in order to discern P waves more easily. When pressure is applied, a larger AV block is induced and 3:1 periods occur intermittently. During these blocks, clearly discernable P waves are seen in the right precordial leads. The P waves show atrial ectopic activity at a rate of 240 bpm, just as we suspected from the previous ECG. By marching out the P waves with a caliper, we’ll see that every other P wave gets completely or partially hidden in the QRS complexes when the ratio changes back to 2:1.
May 17, 2009
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Patient: Woman, 70 y/o. Congestive Heart Failure. Using digitalis.
ECG description:
- Narrow complex tachycardia of supraventricular origin.
- Variable ventricular rate. Rate varies from 73-105 bpm.
- Right Axis Deviation. Cardiac axis is at approx. 150°
- Multiple P’ waves. Atrial rate is 210 bpm.
- Varying AV Block. P:QRS ratio ranging from 1:1 to 3:1.
- Ectopic P’ waves, inverted in inferior leads II, III, aVF. P waves superimposed on QRS complexes.
- Prominent Q waves in inferior leads, II, III aVF.
- T wave inversion in inferior leads, II, III, aVF
ECG comments: This EKG shows an Ectopic Atrial Tachycardia (EAT) with variable degree of AV Conduction, and was in the clinical setting mistaken for atrial flutter when the patient was presented in the ER. A common mistake to make, as atrial flutter is probably the arrhythmia that resembles EAT the most electrocardiographically. Atrial flutter is a common differential diagnosis with EAT, but making the wrong diagnosis here can however, be dangerous for the patient. The pitfall is that paradoxically, atrial flutter is treated with digitalis, which again induces EAT. Which means that if EAT is being mistakenly treated with digitalis, the arrhythmia will be sustained, as well as the degree of AV block could be increased. This will be like adding fuel to a fire. Untreated EAT with block can at some point compromise the patient’s cardiac output and result in hemodynamic unstability. The treatment for EAT is, of course to remove the digitalis intoxication.
Differentiating Ectopic Atrial Tachycardia and Atrial Flutter
The reason that EAT is often mistaken for atrial flutter, is because of the multiple P waves. Depending on their axis and morphology, they can for the untrained eye easily resemble flutter waves (F waves). Also, if one suspects an atypical flutter pattern, one might think that the P waves are due to flutter activity. However, the key is to understand the electrophysiology behind the two mechanisms and how they will appear on a surface EKG. If you understand the underlying electrophysiologic mechanisms of atrial flutter, differentiating it on a surface EKG is much easier. Also, by examining both the P waves and the baseline of the different leads, the correct diagnosis will be easily within reach in most cases.
Atrial Flutter
- Is characterized by a rapid and regular atrial rhythm at rates from 250 to 400 bpm.
- Due to the macroreentry mechanism of atrial flutter, where an ectopic impulse travels counterclockwisely in a circular fashion usually within the right atria, flutter waves are created on the EKG. When the impulse has travelled a full circle, it reactivates the same focus again, creating a reentry loop mechanism. Thus, where one F-wave ends, the next one arises immediately. Several F waves together makes out the hallmark saw tooth baseline.
- Flutter waves (F waves) and the saw tooth pattern are best seen in the inferior leads, II, III and aVF. Sometimes, F waves are more clearly visible in lead V1.
- Seldom coexist with ectopic atrial tachycardia in the same patient
Ectopic Atrial Tachycardia with block
- Is characterized by a rapid and regular atrial rhythm at rates from 150 to 250 bpm
- Has abnormal P (or P’) waves whose morphology is different from that of the sinus P waves. P waves are often inverted in inferior leads (II, III, aVF) if the ectopic focus sits distally in the atria.
- Has isoelectric intervals between P waves in all leads.
- When atrial rates become fast, the AV Node usually blocks signals. EAT never occurs with First Degree AV Block. Always presents with Second Degree or Third Degree AV Blocks. Wenckebach conduction can also occur.
- P waves are often difficult to spot as they are often small and dysmorph, and often get buried in or superimposed on the QRS complex. Lead II is often difficult to use, while lead V1 is often a good lead for discerning P waves.
- Often occurs due to digitalis intoxication
Cherchez le P!
The above are the famous words by EKG master Henry J. L. Marriott, and is french for “Look for the P!”. What Marriott meant, was that finding and evaluating the P waves is the key to understanding and diagnosing arrhythmias. Marriott especially pointed out that one must look for P waves buried in T waves. In both premature contractions, like for instance a PAC, and in other conditions, P waves can get buried in both the preceding T wave, in the QRS and practically anywhere. And as we will see with this EKG, spotting P waves is what pinpoints the diagnosis.
The rhythm is obviously supraventricular, as QRS complexes are within the normal range (<120 ms). There are multiple, small P waves before many of the QRS complexes. The P:QRS ratio varies from 3:1 in the longest cycles to what seems like 1:1 in the shortest cycles. However, the latter is actually 2:1. When examining the QRS complexes, there are P waves buried in the QRS complex. The buried P waves appear at the end of the QRS, and are best seen in leads V2-V5, as they create a pseudo S wave at the end of each QRS. By marching out the P waves with a caliper, the buried P waves are easy to spot. With this in mind, and knowing that First Degree AV Block doesn’t occur with EAT, we will conclude that where AV block ratio seemed to be 1:1, the block is really 2:1. This means that in those cycles, there are actually two P waves for each QRS, but the second P wave is buried in the QRS itself. These are however, not sinus P waves. They are deflections from an ectopic atrial focus, and should therefore be referred to as P’ waves, which is the correct labelling for ectopic P waves.
By measuring the P’P’ interval, the atrial rate is constant and regular at 210 bpm. In the 2:1 block cycles, the ventricular rate is 105 bpm. The ventricular rate is half the atrial rate, which correlates with a 2:1 block. Now, remembering what Dr. Marriott preached, when examining the T waves, there are clearly P waves buried in their humps. This is best seen in lead V3, where T wave morphology changes throughout the lead. The extra peaks and bumps on the T waves are actually buried P’ waves. If these were not observed, this rhythm could be mistaken for an AV Nodal Reentry Tachycardia, as there would be no P waves preceding the QRS, with seemingly retrograd P waves shortly after ventricular depolarization. Also, you will note that:
- The baseline is perfectly isoelectric between each P’ wave, ruling out the macro reentry impulse rotation mechanism of atrial flutter.
- In inferior leads II, III and aVF, the P’ waves are inverted as the P wave axis is shifted superiorly. This indicates a low atrial focus and is a common sign of atrial ectopy. This again rules out atrial flutter, which would produce F-waves in the same leads.
- Unlike MAT (Multifocal Atrial Tachycardia), there are not multiple ectopic foci here. The P wave configuration is constant and unimorph throughout the leads.
February 3, 2009
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Patient: n/a
ECG description:
- Sinus arrhythmia / sinus rhythm with varied rate. V-rate varies from 45-110 bpm.
- Left Axis Deviation (LAD). Cardiac axis approx. – 40°
- Left Anterior Fascicle Block
- Premature Atrial Contractions (PAC) in bigeminal pattern
- Widespread T wave abnormalities. T flat/negative in leads II, III, aVF, V5, V6
- Deep Q-wave in lead V1
Detection of Atrial Bigeminy
The 12 lead ECG displays multiple supraventricular extrasystoles. Each sinus beat is followed by a supraventricular extrasystole with a fixed coupling interval throughout the recording. Since the coupling interval is fixed and the P’ waves are morphologially similar, the term unimorph is used. Unimorph complexes signal that all the premature beats arise from the same automaticity focus, insinuating ectopic unifocality. Though, there is always a possibility that unimorph complexes can originate in different foci. Therefore, the term unimorph is used instead of unifocal.
Determining from the P wave axis and morphology, the ectopic focus is not sinoatrial. The narrow QRS suggests that the ectopic impulse is being conducted normally through the His-Purkinje fibers, ruling out a ventricular ectopy. The PR interval measures 120 ms, which lets us conclude that the irritable focus is atrial, not junctional. The inverted P waves suggests that the ectopic impulse is spreading retrogradely and inferiorly from its focus.
Each premature complex is followed by a postextrasystolic pause, slowing down the rhythm. By measuring the pause, the coupling interval and the normal sinus interval, the pause can be labeled compensatory or noncompensatory, with the latter being the normal finding with premature atrial contractions. As premature atrial impulses normally depolarize the whole atrium and thereby resets the SA Node, sinus pacing is usually interrupted, causing a pause after the extrasystole. This pause is a result of the sinoatrial slowing and is longer than, but not a multiple of the normal interval. With noncompensatory pauses, the coupling interval + the postextrasystolic pause is less than twice the normal interval. With compensatory pauses, the sum of the coupling interval and the postextrasystolic pause is exactly twice the normal interval length. Because of the bigeminal pattern here, there is no “normal” sinus cycle, making it difficult to establish whether the pauses are compensatory or non-compensatory.
January 31, 2009
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Patient: n/a
ECG description:
- Sinus rhythm with varied rate: 75-130 bpm
- Premature Atrial Contractions (PAC) presenting in couplets
- Left Axis Deviation (LAD). Cardiac Axis is deviated leftwards and superiorly at approx. 90°
- Left Anterior Fascicular Block (LAFB) due to LAD, deep S in III, no sign of LVH or MI
- Low Voltage in Limb Leads
- Poor R Wave Progression (PRWP)
Atrial Couplets, PACs and P waves
After one sinus cycle, the rhythm is interrupted by a PAC (complex no. 3 from the left). The change in P wave axis and morhpology of this complex suggests ectopy. The P’ wave is inverted in leads II, III and aVF, suggesting that the ectopic impulse originates in the left atria, spreading in a retrograde fashion. Determining by the PR interval, which is 100 ms, the ectopic pacemaker is atrial and not junctional, and sits closer to the AV Node than the SA Node.
The PAC is immediately followed by a new PAC, creating an atrial couplet. This second PAC seems to originate from another focus, as there is a change in P’ wave axis and configuration. The PR interval of this PAC is 110ms, and the P’ waves are upright in the inferior leads, suggesting that it spreads inferiorly and towards the left. The second PAC is followed by two sinus cycles, which is then followed by another PAC couplet. The PACs in this couplet seem to originate from the same ectopic foci as in the first couplet, although there is a variation in coupling interval length.
Atrial couplets can be benign, but are less common in healthy hearts, and should increase suspicion towards onset of atrial fibrillation. Ultimately, one would prefer to print a longer rhythm strip at this point, to see the phenomenon over a longer time interval. Unfortunately this is not available for this particular case.
The Postextrasystolic Pause
With supraventricular premature impulses, the dominant automaticity focus (normally the SA Node, as in this case) is usually reset by the premature impulse. The supraventricular impulse usually activates the whole atria and thereby also the SA Node. The early activation of the SA Node interrupts the pacing function of the node, and causes a delay in impulse generation. The next impulse will then be slightly delayed, causing the following RR interval to be prolonged. This is called a noncompensatory pause. If the SA Node is not reset, then its pacing function will not be disturbed, and the following RR interval will be an exact multiple of the normal interval, resulting in a compensatory pause.
PACs usually present with non-compensatory pauses, as ectopic atrial impulses will usually activate the whole atria, including the SA Node, and thereby interrupting the sinus pacing activity. In this EKG, the pause after the first PAC is interrupted early by another ectopic impulse, so this pause cannot be determined. The second PAC however (complex no. 4 from the left) is followed by a postextrasystolic pause that is prolonged, but still not an exact multiple of the normal sinus cycle length. This is a non-compensatory pause, which tells us that the SA Node has been reset. This helps to establish and diagnose an atrial origin for the ectopic beats.
January 30, 2009
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Patient: Male, 60 y/o. Medical history unknown.
ECG description:
- Sinusbradycardia at 46 bpm
- Normal cardiac axis. Approx. 30°
- AV Junctional Escape Complex
- Left Bundle Branch Block. Q
- T inversion in lead III and biphasic T wave in lead aVF.
ECG comments:
Supraventricular escape complexes are usually precipitated by long pauses, such as sinus arrest, intermittent SA block or long postextrasystolic pauses. Slow phases in sinus bradycardia however is also a common cause of such escape beats. The last QRS complex in this ECG is preceded by an inverted P wave in the inferior leads. The PR interval is also shorter. These morphologic clues tell us that the atria is depolarized retrogradely. The depolarization wave spreads away from leads II, III and aVF, making the P wave inverted. The shortened PR interval indicates an ectopic focus located closer to the AV node.
January 29, 2009
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Patient: Woman, 84 y/o with no known cardiac history. Lives in a nursing home and has reportedly been struggling with fatigue, dizzyness and general weakening the last two weeks. No syncopal episodes. She has recently been treated for a pneumonia. When presented in the ER, she is hemodynamically stable, but hypotensive with an initial BP of 80/40. Her SAT is 90 % with oxygen administered at two litres/min. She has a slow, palpable and irregular pulse in radialis, bilaterally. When palpated, the pulse is counted to around 35 bpm. Skin is normal and dry, but shows signs of dehydration. No cyanosis or diaphoresis. She is awake and conscious with a GCS of 15.
At first, a 12 lead ECG is obtained (above). This shows:
- Regular, narrow-complexed bradycardia of supraventricular origin
- Sinus bradycardia at 48 bpm
- Normal cardiac axis, at approx. 30°
- Minimal ST-depression laterally
- Prolonged QT interval, probably rate related. QTc is 470 ms
ECG comments: This ECG shows sinus bradycardia, but as the next strips will show, this is in fact a 2:1 SA Block. Persistent 2:1 SA Exit Block cannot be distinguished from marked sinus bradycardia, since the RR intervals are regular. The rhythm is so slow here, that this ECG only shows three cycles. A slow pulse at around 35 was palpated when she arrived, and considering her history of fatigue and dizzyness, a type of heart block should be suspected. In such cases, a longer rhythm strip must be obtained.
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These strips reveal the true problem: Long and frequent sinus pauses, resulting in a mean ventricular rate of approximately 35 bpm. This patient was hypotensive, which could be due to low cardiac output as a result of fewer ventricular contractions. Although, she was also clinically dehydrated. There are P waves preceding every QRS complex, with a normal and regular PR interval. The QRS complexes are sinus paced and does not represent any ectopy or escape. By using a caliper, a mathematical relationship between the normal cycles and the pauses is quickly established. Each long cycle is a multiple of the normal cycles. In fact, each pause is twice as long as the normal cycles. Every now and then, a P wave “falls out” without disturbing the underlying rhythm. Sinoatrial block may be due to failing SA Node automaticity or blocked conduction out of the node. These two mechanisms cannot be distinguished from a surface ECG.
Since the long cycles are twice as long as the normal cycles, we can establish the diagnosis of SA Block Type II. Same as with Second Degree AV Block, Type II, the giveaway here is the dropped complexes. Here, the P waves are dropped, not the QRS complexes as in an AV Block. In these strips, the block is intermittent, which is also why we can see it. If this 2:1 block was persistent, the rhythm would present as a marked sinus bradycardia and could not be seen on the ECG.
January 24, 2009
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Patient: Woman, 69 y/o with no significant medical history. Presented in the ER with grave sepsis due to unknown focus of infection. Rectal temperature is 40.5°C, BP 170/100, pulse irregular at ca. 150 bpm, SAT 93 % w/O2 3 l/min, RF >50/min, peripher cyanosis, lip cyanosis, marmorated skin over the abdomen and thorax, serum glucosis 8.7. Arterial blood gas analysis showed a minor electrolyte imbalance and a respiratory alcalosis.
ECG interpretation: Multifocal / Chaotic Atrial Tachycardia with Variable Degree of AV Block, incomplete RBBB and Left Ventricular Hypertrophy
ECG description:
- Supraventricular Tachycardia / Narrow Complex Tachycardia
- Atrial ectopic rhythm with highly irregular rate
- Incomplete Right Bundle Branch Block (QRS 120ms)
- Varying P wave morphology and axis. Three or more morphologically distinct P’ waves in the same lead.
- Variable AV Block. P:QRS ratio ranges from 1:1 to 2:1. Several P’ waves buried in QRS complexes.
- Probable Left Ventricular Hypertrophy from Sokolow’s Criteria (RV5 + SV2 >35mm)
Note that there is a:
- Highly varying PP interval, which is due to a varying atrial rate. Mean A-rate is around 135 bpm
- Highly varying RR interval, which is due to a varying ventricular rate. Mean V-rate is around 150 bpm
- Highly varying PR interval, which is due to varying ectopic atrial foci.
- Isoelectric baseline between every ectopic P’ wave.
- No obvious dominant atrial pacemaker, ruling out sinus rhythm with multiple PACs.
Further observations:
- Cardiac axis pointing downwards at approx 90°
- Probable Left Ventricular Hypertrophy according to Sokolow-Lyon Index
- T wave inversion in leads V1-V3
Measured intervals, counting from the first (leftmost) P wave:
- PP (millimetres): 18, 22, 24, 19, 26, 12, 28, 18.5, 17.5, 22, 18
- PR (milliseconds): 80, 100, 80, 65, 100, 60, 70, 115, 120, 115, 80, 65
- RR (millimetres): 19. 21.5, 23.5, 20, 24, 18, 28, 19, 19.5, 19, 18
- All intervals are irregularly irregular.
Multifocal Atrial Tachycardia (MAT)
Term: MAT is also known as chaotic atrial tachycardia, and describes rapid firing of several ectopic atrial foci at a rate faster than 100 bpm.
Occurrence: MAT is often associated with COPD or CHF , but can also occur in the presence of hypokalemia, hypomagnesemia, hypoxia, acute myocardial infarction and mitral stenosis.The condition usually occurs in seriously ill patients, mostly elderly people.
Mechanism: Characterized by P waves of varying morphology, assuming that distinct P waves originate from ectopic atrial foci. The ectopic P waves may be called P’ (P Prime). Due to different automaticity foci, both P wave morphology and axis will vary. The PR interval will also vary, depending on the proximity of each atrial focus to the AV node and the prematurity of each ectopic impulse. Some P waves may be nonconducted, and some may be aberrantly conducted if they get conducted into the ventricles while they are still partially refractory. MAT is often preceded or followed by frequent PACs, sinus tachycardia, AF, A-flutter, ectopic AT or PAT. Compared to WAP (Wandering Atrial Pacemaker), the ecg findings and rhythm characteristics are the same, but in MAT the atrial rate is higher.
ECG characteristics: 1) Three or more morphologically distinct P waves in the same lead. 2) The absence of one dominant atrial pacemaker, in disctinction to sinus rhythm with multiple premature atrial complexes. 3) An isoelectric baseline. 4) Varying PP, PR and RR intervals. Ventricular rate is usually 100 to 150 bpm.
Ladder diagram for lead V1 (click to view larger)
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Ladder diagram description: The ladder diagram shows ectopic atrial foci firing at varying rate and with varying proximity to the AV Node, resulting in varying PR intervals and varying ventricular rate (RR intervals).
January 5, 2009
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Patient: Male, 80 years of age, with severe COPD (Chronic Obstructive Pulmonary Disease) and CHF (Congestive Heart Failure) class IV (NYHA Classification). He has had one inferior MI previously.
Anamnesis: Sudden onset of palpitations, followed by dyspnea/tachypnea. When presented in the ER, his respiratory rate is >40/min. Transcutaneous SpO₂ is 69% with two O₂ administered at 2 litres/min. Initial blood pressure is 85/60.
ECG description:
- Narrow-complexed/supraventricular tachycardia at 150 bpm
- F-waves (flutter waves), best seen in lead II, III and aVF
- Pathological Q-waves in lead II, III and aVF
- ST depression ca. 2mm in leads V3-V6
- One Ventricular Premature Beat
- Axis is shifted rightwards and pointing downwards at approx. 90°, but still within the normal range of -30° to 90°
ECG comments:
As atrial flutter most often occurs with atrial rates of 300 beats per minute, and because the atrioventricular node usually blocks half of the impulses, a ventricular rate of 150 bpm is the most common. Because of this, the diagnosis of atrial flutter with 2:1 AV conduction should be suspected if there are no indications that suggest otherwise. Also, with 2:1 conduction, F waves (flutter waves) can be hard to identify because of the short RR intervals. F-waves may sometimes appear more clearly like individual P waves in lead V1, but in this ECG, V1 hardly shows P waves at all. Discerning P waves is a common problem in atrial flutter with rapid ventricular rates.
Still, the very regular RR intervals and the ventricular rate of 150 bpm, together with the sawtooth/f-wave baseline, highly suggests atrial flutter. Here, the P waves can be seen best during the repolarization phase of the VPB, in leads V4-V6 at the very beginning of the ECG tracing. Though it’s difficult to calculate the PP rate here, as most P waves are hidden.
ECG interpretation: Type I Atrial Flutter. The conduction ratio is likely to be 2:1, due to ventricular rate of 150 bpm.
Atrial Flutter mechanism
The arrythmia mechanism behind atrial flutter is based on a large macro-re-entry conduction path in the right atria, where electrical impulses rotate in a counterclockwise direction at very high rates. With atrial flutter, normal P waves are replaced by flutter waves, also called F waves. They are often just also just called P waves, as they represent depolarization of the atria. All together the flutter waves creates a flutter baseline. The flutter waves appear like saw tooth looking waves, and are often just called saw tooth waves or saw tooth line. A flutter baseline is characterized by that where one flutter wave ends, the next begins.
Atrial flutter most often occurs with atrial rates of 300 beats per minute, and because the AV node usually blocks half of the impulses to protect the ventricles from dangerous override, a ventricular rate of 150 bpm is the most common. Because of this, the diagnosis of atrial flutter with 2:1 AV conduction should be suspected if there are no indications that suggest otherwise.
Common causes of Atrial Flutter: Congestive Heart Failure, MI and myocardial ischemia are well known and often seen causes of atrial flutter.
AV conduction during atrial flutter
The most common finding in non-treated patients, is a constant AV conduction ratio of 2:1, where every second flutter impulse from the atria is allowed through to the ventricles. This ratio often makes it difficult to discern the P waves / flutter waves, since they are hidden in QRS complexes and T waves. With a higher ratio, i.e. 3:1 or 4:1, they often appear.
Atrial Flutter is divided into two types, the first type with two subtypes:
Type 1 Atrial Flutter
Typical Type 1
- F wave (flutter wave) frequency of 200 to 340/min
- The usual form of re-entry with counterclockwise impulse rotation.
- …which makes saw-tooth flutter waves with negative/downwards oriented F waves in leads II, III and aVF
Atypical Type 1
- The more rare form of clockwise impulse rotation
- …which makes a flutter baseline with rounded, positive/upwards oriented F waves in leads II, III and aVF
Type 2 Atrial Flutter
- Quite rare
- Most often characterized by a very high F wave frequency at 340 to 400/min.
December 8, 2008