Filed under: Bradyarrhythmia
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Patient: n/a
ECG discussion: The top strip starts with sinus rhythm at ca. 75 bpm. Note that this generates a mean arterial pressure (MAP) of only 18 mmHg. A marked horizontal ST depression is also seen, which correlates with the pleth signal showing SpO2 of 74%. After 8 beats, there is no visible sinus activity any longer. No junctional escape rhythm is initiated, which indicates that the atrioventricular junction is also poorly perfused and suffering. The following beats are wide and slow, at only 35 bpm. Even though they resemble a ventricular/Purkinje escape rhythm by their morphology and regularity, this electrical activity is not able to create myocardial contraction. In the second strip, MAP is 13 and flatlined. This is explained electrophysiologically as electromechanical dissociation (EMD), which is similar to the term pulseless electrical activity (PEA).
The final (bottom) strip shows how the electrical activity ceases. Although mechanical asystole probably has happened already (hard to say without echocardiography), electric asystole has now also occured. Note that at the end of the strip the pleth wave is also flat.
September 8, 2009
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Patient: Woman, 55 y/o, using metoprolol. Diabetes Mellitus II, angina pectoris, adipositas. Admitted with general weakness and fatigue, dehydration and dyspnea. Blood pressure is 100/55. No signs of infection.
ECG description:
- Sinus rhythm with sinus arrest
- Axis within the normal quadrant, at ca. 0 degrees
- Poor R wave progression
- Low amplitude in limb leads
- Baseline artefact from patient movement
- T wave flat/inverted in I, aVL
Discussion: After two sinus beats, a two second atrioventricular asystole occurs, which is then terminated by atrial escape. By comparing the escape P wave with the P waves of the three sinus cycles (the two first and the very last on the ecg), we can see that both P wave morphology, axis and PR interval varies slightly. The PR interval in the sinus cycles is 170 ms, while the escape PR interval is 150 ms. This could indicate that the escape pacemaker is atrial ectopic, but is located in the near vicinity of the sinoatrial node. The sinus pause is longer than, but not a multiple of the normal interval, so this is most likely no SA block. There are also no signs of blocked atrial impulses or reciprocating impulses causing the pause. These observations are important to make, as sinus arrest is often confused with SA block and other mechanisms.
July 1, 2009
The prehospital ECG obtained in the patient's home, the moment before cardiac arrest. Click image for full scale version (will open in a new window)
Patient: Male 90 y/o. Previous medical history unknown. Sudden onset of chest pain and severe dyspnea in his home. EMS responds quickly and this ECG is obtained in home. The ECG shows an AV junctional rhythm in the bradycardic range. The patient is awake but in severe pain. During transport to the hospital, the patient goes into full cardiac arrest. ACLS is started and is continued during transport to the ER. On arrival in the ER, ACLS continues. The patient is pulseless, with agonal respiration. After a total of one hour of ACLS without result, the resuscitation attempt is called off.
These strips are obtained in the ER from the defibrillator pads and show the progression from Pulseless Electrical Activity (PEA) into a flatline on the monitor. Note: PEA is also sometimes referred to as Electromechanical Dissociation (EMD), which is perhaps a more precise description of the electrophysiologic phenomenon that occurs. EMD is simply the term for when electrical activity occurs in the myocardium, but fails in depolarizing the cells and causing contraction of the heart muscle. This means that PEA/EMD is an agonal rhythm, and that PEA per definition is equal to asystole. However, when people say asystole, they usually refer to a flat line on the monitor/ECG. The next strips show the progression from PEA/EMD into a flat line.
First strip show chest compressions at a rate of ca. 140 bpm, followed by a rhythm check that displays an agonal rhythm/PEA. Compressions then start again. The next strips are recorded from the defibrillator during the next minutes and show the gradual morphologic progression from PEA into what is commonly referred to as flatline.
June 1, 2009
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This ECG is from a healthy, 29 year old caucasian male with no medical history.
- Sinus bradycardia with varied ventricular rate
- Normal cardiac axis at approx 60 °
- Flattened T wave in aVL
- Voltage criteria (Sokolow-Lyon index) suggests Left Ventricular Hypertrophy
Sinus Bradycardia
Sinus bradycardia is normally considered clinically significant when then rate drops under 50 beats/min. However during sleep and in healthy, young individuals (especially athletes), heart rate may be as slow as 40 bpm without compromising cardiac output. Chou (2008: 329-330) states that a rate as slow as 35 bpm may be seen, but in healthy individuals the rate is usually > 40 bpm during waking hours. Increased vagal tone is often the cause of sinus slowing. In sinus bradycardia, the sinoatrial node fires slower than in normal sinus rhythm. The cell automaticity in the SA node is prolonged. When considering the action potential, this is equivalent with a longer phase 4 repolarization. This again manifests electrocardiographically as a prolonged TP segment.
Respiratory Sinus Arrhythmia
Variations in heart rate commonly occur in relation to the respiratory cycle. In respiratory sinus arrhythmia the heart rate increases with inspiration and decreases with expiration, due to changes in vagal tone during the respiratory cycle. Sinus arrhythmia occurs more frequently when the sinus rate is slow. This arrhythmia is considered benign and normal. Prevanlence is higher in infants and young individuals and tends to decrease with age.
May 17, 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
This is a case of an 84 y/o man who just had his VVI pacemaker replaced. The first night after changing the pacemaker, he woke up in the middle of the night with breathing problems. Paramedics reported on the way in to the emergency room that he was bradycardic and hypotensive with a low, but stable BP of 80/40. He is also reported to be respiratory stable. As they are not far away from the hospital and he seems stable in spite of his hypotension, he is not paced externally by the paramedics. He has a congestive heart failure and an EF (ejection fraction) of 45%. He also has a persistent/chronic atrial fibrillation. He was given his first VVI pacemaker 20 years ago because of a high-grade AV block.
He presents in the ER with a slow, but palpable radial pulse bilaterally. He is awake with GCS 15, no chest pain, dry and pale skin. No cyanosis. Initial blood pressure is 140/80, probably due to prehospital fluid resuscitation. He says he can feel that there is something wrong with his pacemaker.
First, a 12 lead ECG is obtained:
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ECG description:
- Narrow complex bradycardia with irregular rate from 30-50 bpm
- Axis approx. 0°
- No visible P waves
- Regular pacemaker spikes, best seen in precordial leads. All pacemaker spikes dissociated from QRS complexes.
- QRS is
- T-inversion in leads II, III, aVF and all precordial leads
- ST-depression 1-2 mm in leads V2-V5
With a VVI pacemaker, one would expect a wide QRS configuration and a regular ventricular rate. The narrow QRS complexes and the irregular rate shown here suggests that the pacemaker is not functioning properly. This is confirmed by the pacemaker spikes, which are best seen in the precordial leads. The spikes are regular, but in no relation to the QRS. When marching out the pacemaker spikes, the pacemaker lead seems to be dissociated from the ventricles. Either the sensor or the pacing lead is misplaced or has moved out of position. When comparing the rates, the pacemaker is emitting charges at at a rate of 59 bpm, while the ventricular rate here is much lower.
With these irregular and narrow-complexed QRS complexes, one can exclude a junctional escape rhythm. If this was junctional escape, the RR intervals would be regular. I would assume that these QRS-complexes are paced from the atria. Remember, this patient has atrial fibrillation, but since he also has a sick AV Node, only a small amount of impulses are conducted through to the ventricles. This patient has a high grade (also called ‘advanced’) AV Block, which explains why only an uneven and small amount of atrial impulses are conducted through the AV Node.
In this 12 lead tracing it seems that none of the pacemaker discharges succeed in depolarizing the ventricles, but still this is a potentially dangerous condition for the patient. If the pacemaker lead discharges to the ventricles while they are refractory, this could induce life-threatening tachyarrhythmias. As we can see from the rhythm strips below, which were recorded immediately after the 12 lead tracing, the pacemaker occasionally succeeds in depolarizing the ventricles. This also means that pacemaker discharge could be conducted to the ventricles during the refractory period.
The paced complex is at the end of the second strip below. Atrial fibrillatory waves are also seen here. They are best seen in leads I, II and aVR.
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January 26, 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: 84 y/o woman with no cardiac history. No syncopal episodes. Generally fatigued and “feeling a bit dizzy” the last week. Has not noticed any tick bites or had any symptoms of borreliosis. Comes walking into the ER and complains about tiredness. Initial BP is 180/80. SAT 96% w/o oxygen, RF 16/min. No pain/nausea.
ECG description:
- Narrow Complex Bradycardia
- More P waves than QRS complexes
- No association between P waves and QRS complexes
- Atrial rate 82 bpm
- Ventricular rate 39 bpm
- Axis at approx. 30°
- T wave inversion in leads V1-V3, III, aVF
ECG interpretation: Third Degree / Complete Atrioventricular Block with Junctional Escape Rhythm.
ECG comments: All P waves are blocked from leaving the AV Node. There is regular and normofrequent atrial activity, probably sinus, but none of the atrial impulses gets propagated further down the conduction system. The atrias and ventricles are acting independently. This is AV dissociation and produces a complete heart block. As the atria and the ventricles are now oblivious of each other, they run at different speeds. This is because they are independently paced. The ventricles are being paced from an ectopic focus, resulting in a rate of 39 bpm. Considering this rate and the narrow configuration (80ms) of the QRS complexes, the ectopic focus is most likely junctional. Usually, ectopic rhythms originating around the AV Node will pace from ca. 40-60 bpm.
Treatment: Isoprenaline and permanent pacemaker
CLICK TO SEE LARGER: Ladder diagram for lead V2, showing atrial impulses being blocked in the AV Node, and a nodal ectopic impulse generating an escape rhythm.
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January 4, 2009
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Patient: Male, 84 y/o. No cardiac history. Acute onset of severe, pressing chest pain. No relief from large doses of intravenous morhpine.
ECG description:
- Broad complex bradycardia with third degree atrioventricular block (3AVB) and AV dissociation
- Ectopic pacemaker firing at 48 bpm.
- Atrial rate 52 bpm
- Axis at approx. 60°
- ST elevation > in leads II, III and aVF
- Reciprocal ST depression in leads I and aVL
ECG comments: This is 3AVB. If you march out the P waves here, you will see that there is regular and normofrequent atrial activity, but none of the atrial impulses gets propagated further down the conduction system. The atrias and ventricles are acting independently. This is called AV dissociation, and is a criteria for 3AVB, also referred to as complete heart block. Third degree heart block is caused by a conduction block most commonly in the bundle branch/Purkinje system. According to American Journal of Critical Care, the block most commonly occurs in the bundle branch/purkinje system (61%), at the level of the AV node(21%) or the His bundle (15%). When a block occurs, an automaticity focus below the block will assume pacemaking activity at its inherent rate. An escape rhythm above the His bundle normally would produce a heart rate at 40-60 bpm and narrow QRS complex. When the ectopic focus sits lower in the ventricles, the heart will be paced a slower rhythms at around 20-40 bpm, and the QRS will become broad.
In this ECG, the heart rate suggests that the ectopic pacemaker is junctional. But the QRS configuration is wide, so the block is probably below the AV junction after all. Yet, it is pacing faster than expected. This can be referred to as an accelerated idioventricular escape rhythm.
ECG interpretation: Acute Inferior STEMI with reciprocal change, Third Degree Atrioventricular Block and Accelerated Idioventricular Escape Rhythm.
Note: This patient was transferred to a cath lab, where he was revascularized. I will soon update the post with more info on the culprit vessel, a post pci ecg and more.
December 26, 2008
ECG limb leads tracings from a middle-aged man with who went into cardiac arrest in his home. The patient was resuscitatated and transported to the hospital, but cardiac arrest occured during catheterization. Angiography showed 100 % occlusion of the distal LMCA and proximal LAD. Despite PCI and several hours of ACLS, success was not achieved.
These tracings show EMD/PEA, as the patient was pulseless at the time. Notice how the PEA slowes down, evolving more and more into a flatline ECG.
December 8, 2008
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