Filed under: ST-depression
Click image for full scale version (will open in a new window)
Click image for larger version (will open in new window)
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
Click image for full scale version (will open in a new window)
Click image for full scale version (will open in a new window)
Patient: Woman, 82 y/o with permanent atrial fibrillation. Accidental digitalis intoxication. Serum digoxin level when arriving in the ER is 6.6 ng/ml. General fatigue, but no recent history of syncopal episodes.
ECG description:
- Irregular, narrow QRS bradycardia at approx. 35 bpm
- Atrial fibrillation with slow ventricular response
- Normal axis at ca. 60 degrees
- Prominent U waves, best seen in leads V2 -V3
- Cohn effect: ST segment depression and flattened T wave in leads V4-V6
- Poor R wave progression
- Low amplitude in limb leads
- Baseline noise artefact
Discussion: This 12 lead ECG displays atrial fibrillation with slow ventricular response. There is a high degree of AV block, resulting in a bradycardic rate at ca 35 bpm (50 mm/s). The axis is in the normal quadrant and at ca. 60 degrees. Limb leads show T wave flattening, and there is perhaps a slight ST segment depression visible in leads II and AVF. There is a quite prominent U wave. Normally, the U wave is best appreciated in the lateral precordial leads (V5-V6). Here however, it is seen in leads V2 and V3. The classic ST segment morphology induced by digitalis both at therapeutic and toxic serum levels, is the “coved” or “scooped”, or sometimes referred to as “bowl shaped” ST segment depression. It is sometimes described as if the ST segment has been dragged downwards from a point at the middle of the segment. Digitalis intoxications may however, manifest with or without the classic morphology even at high serum levels. The classic digitalis effect on the ST segment is sometimes called the Cohn Effect, named after Alfred E. Cohn, the American cardiologist, for his early 1900-century studies on the effect of digitalis on T wave morphology. It is generally recognized by ST segment depression together with T wave flattening in the same lead. Although this ECG lacks the coving ST segment, the Cohn effect is present in leads V4-V6.
Overall, digitalis has a positiv inotropic effect and a negative chronotropic effect. The negative chronotropy is due to both decreased automaticity of the SA node as well as prolongation of the refractory period of the AV nodal tissue, thus inducing higher degrees of AV block. It also increases AV nodal automaticity which often results in for instance accelerated junctional rhytm and junctional extrasystolia.
This ECG is in the low bradycardic range at around 35 bpm, which is due to the high serum levels of digoxin. Different AV ratios can occur, but 2:1 is rare. With second degree AV blocks, Wenckebach conduction is common. In this ECG it’s impossible to determine the AV ratio, due to atrial fibrillation, and one can only conclude that it is varying. Following is a continous rhythm strip (25 mm/s) of the patient that was obtained 10 minutes later, showing the development of higher degrees of AV block, resulting in long bradycardic cycles.
Click image for full scale version (will open in a new window)
Note the long, asystolic pauses. The first and third cycles are so long (>2 seconds) that ventricular escape occurs.
June 18, 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:
Click to see full scale version (will open in a new window)
Click to see full scale version (will open in a new window)
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.
Click to see full scale version (will open in a new window)
Click to see full scale version (will open in a new window)
Click to see full scale version (will open in a new window)
January 26, 2009
Click to see full scale version (will open in a new window)
Click to see full scale version (will open in a new window)
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.
Click to see full scale version (will open in a new window)
Click to see full scale version (will open in a new window)
Click to see full scale version (will open in a new window)
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
Click to see full scale version (will open in a new window)
Click to see full scale version (will open in a new window)
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
Patient: Middle-aged man with no known cardiovascular diseases. Acute onset of pressing chest pain that he said developed gradually in intensity over three hours before he called 911. On their way in to the ER, the paramedics report that the patient suddenly becomes worse and more symptomatic, with severe dyspnoea, sinusbradycardia at around 40bpm and a much more intense chest pain, now radiating towards his back. On arrival in the ER, the patient is sitting upright in his bed, with tachypnea. His skin is cool, pale and diaphoretic. He is very restless and unable to lie flat. He sits up constantly, still hyperventilating. He scores 15 on Glasgow Coma Scale. His initial systolic blood pressure is 170 mmHg on the right arm and 140mmHg on the left arm. His radial pulse is palpable and strong bilaterally, and it is regular and normofrequent. A 12 ECG is acquired quickly:
Timeline: Zero hours. ECG taken immediately after arrival in ER
Click to see full scale version (will open in a new window)
Click to see full scale version (will open in a new window)
ECG description:
- Sinus rhythm at ca. 80 bpm
- ST elevation ½ mm in I, ½ – 1 mm in aVL.
- ST elevation 2 mm in V1, 3mm in V2, 1mm in V3.
- Minor ST depression in II and aVF
- Small Q waves (ca. 1.5 mm) in leads I and aVL
- R-progression is normal.
- Cardiac axis normal at around 30°
The ST elevation in this ECG suggests MI, but with these subtle st changes and also taking in consideration that the chest pain radiates towards his back and that he is very restless and can’t lie flat, aorta dissection is also considered at this point. The situation is still a bit unclear. The patient is given intravenous morphine and antiemetics.
A few minues goes by, and suddenly, almost in the middle of a sentence, he falls backwards in his bed. Monitors show a coarse ventricular fibrillation and the patient is pulseless. Cardiac arrest has occured. Chest compressions are started immediately while the defibrillator is attached. Airways are secured with only an airway/pharyngeal tube and a jaw grip, as he breathes good. After 20 seconds of compressions, the defibrillator is ready. Quick rhythm check shows VF and the patient is shocked at 250 Joule. Compressions continue and adrenalin is administered. He comes back with gasping breath and a what looked like a nodal arrhythmia at around 120 bpm. He is awake and conscious. Then after three or four minutes, cardiac arrest reoccurs, again with initial VF. More compressions, oxygen and another shock and voila.. back again. Then cardiac arrest occurs two more times and he is brought back each time with successful defibrillation. The cath lab team has been alerted and are getting ready for PCI. As we are waiting for them to get ready, a new ECG is done.
Timeline: 21 minutes
Click to see full scale version (will open in a new window)
Click to see full scale version (will open in a new window)
ECG description:
- Atrial fibrillation with rapid ventricular rate at around 125 bpm
- Large and convex ST segment elevation 10-15mm in V2-V6
- ST segment elevation >2 mm in leads I and aVL
- Reciprocal ST segment depression in leads III and aVF
- Small Q waves (ca. 1-2mm) in precordial leads
This correlates with stenosis of the LAD and possibly also RCA. This would indicate an acute anterolateral transmural infarction.
The patient is still hemodynamically and respiratory stable, with a GCS of 15. His pain is reliefed with morphine iv and 100% oxygen. His arterial blood pressure is around 125/80. Transcutaneous SpO₂ shows a saturation at around 84%. The cath lab is still not ready, and another ECG is acquired.
Timeline: 45 minutes
Click to see full scale version (will open in a new window)
Click to see full scale version (will open in a new window)
ECG description:
- Atrial fibrillation with rapid ventricular rate at around 120 bpm
- ST segment elevation lowered, but still present and severe
- Small Q waves (ca. 1-2mm) in precordial leads
- The elevation of the ST segments is now more horisontal, with tall and peaked T waves
- Reciprocal changes in III and aVF still present
Now the interventionists and the rest of the team at the cath lab are ready, and the patient is rushed over to the lab. When presented in the cath lab, he is fatigued and still in some pain. He is hypoxic, but respiratory and circulatory stable. Once he is lifted over to the operating table, sustained VT occurs, which then changes into VF and a new cardiac arrest. The patient is quickly defibrillated, and returns with with sinus rhythm. See next strip.
Timeline: 60 minutes. Successful defibrillation of VF during PCI. VF is converted into sinus rhythm at 280 Joule
Click to view the complete strip (will open in a new window)
ECG strip from the defibrillator:
- Ventricular fibrillation changing from fine fibrillation to coarse fibrillation, then being terminated by DC Shock and converted into sinus tachycardia.
After defibrillation, PCI continues and the patient is somnolent, but awake, with relatively good circulation and respiration. Then another cardiac arrest occurs. The patient is defibrillated once again, now for the sixth time. This time he returns with sinus rhythm again. He breathes on an oxygen mask, and his airways are still just secured with an oral tube and a jaw grip. The interventionists find an occluded LAD and RCA. The arteries are stented and reperfused successfully. The patient remains in sinus rhythm and gets transported to the ICU.
Timeline: Five hours after hospital arrival. Three hours after PCI.
Click to see full scale version (will open in a new window)
Click to see full scale version (will open in a new window)
Additional information:
Here is the report following the procedure from the cath lab. Note that the patient has both his RCA and LAD occluded.
Click image for full scale version (will open in a new window)
Click image for full scale version (will open in a new window)
Click image for full scale version (will open in a new window)
December 4, 2008
Click image for full scale version (opens in a new window)
Click image for full scale version (opens in a new window)
Patient: Elderly woman, around 80 years. Unfortunately, I don´t have any clinical information on this patient. All i know is that she was rapidly admitted to a cath lab where the perfusionists did a successful revascularization. AV block is secondary to infarction, hence it is intermittent.
ECG description:
- ST elevation > 4 mm in leads I , II, aVF and > 1 mm in leads V5, V6
- Reciprocal ST segment depression in leads I, aVL
- Complete atrioventricular dissociation. No relation between P waves and QRS complexes. Regular PP interval, regular RR interval. PR interval is variable, hence there is no apparent relationship between P waves and QRS complexes.
- Junctional escape rhythm at 50 bpm.
ECG diagnosis: Inferior wall STEMI. Third degree atrioventricular block with complete AV dissociation that probably has appeared because of damage to the AV node during the infarction. Because of the complete AV dissociation, an accessory pacemaker has taken over the pacing. Based on the rate and the normally configured QRS complexes here, the escape rhythm is junctional/nodal.
The patient was then transferred to the cath lab, where the perfusionists did a successful revascularization. She was transferred to an ICU. This next ecg was recorded 25 hours later since the initial ecg showing the acute STEMI.
Click image for full scale version (opens in a new window)
Click image for full scale version (opens in a new window)
ECG description:
- Normofrequent sinus rhythm at ca. 90 bpm
- PR interval is at 200 ms, so there is a borderline first degree AV block present.
- ST elevation ca. 2mm in II, III, aVF, and 1mm in V5 and V6
- Reciprocal changes still in I, aVL
ECG diagnosis: ST elevation and reciprocal ST depression due to inferior wall infarction. Third degree AV block has disappeared and the patient is in normal sinus rhythm. The AV block was transitory due to the infarction, and the AV node has recovered. The PR interval is 200 ms and signals a borderline first degree AV block which is may due to damage of the AV node.
Comments:
Now this is an interesting case, but also a classic display of heart block etiology. Coronary ischemia is the most common cause of third degree AV block. It is a known fact that acute inferior wall myocard infarction can sometimes cause damage to the AV node, causing third degree heart block. In such cases, the damage is often transitory and the AV node may be recovered if the perfusion is restored. This is the case here, where the patient was quickly admitted to a cath lab where revascularization was done successfully, and the AV node was then restored to a functioning state. The the heart block was terminated and reset into normal sinus rhythm. During the complete heart block, an accessory pacemaker takes over pacing control. The escape rhythm here probably originates in the AV junction, providing a narrow complex escape rhythm, aka a nodal or junctional escape rhythm.
Further reading on the web:
E-medicine: Third degree heart block
American Heart Association: Third degree heart block
The Merck Manuals: Atrioventricular blocks
E-medicine: Atrioventricular disassociation
Wikipedia: Third degree AV block
November 15, 2008