This EKG comes courtesy of Dr. Yousseff.
A 25 year old male presented to participate in an elective research study. He had no complaints. A screening EKG was performed.
Vital Signs: Pulse – 50, R -16, BP 120.70.
The rhythm is 3rd degree AV block. In this patient it turned out to be congenital.
This patient is asymptomatic. In asymptomatic congenital complete AV block, no specific treatment is needed.
The EKG demonstrates a bradycardia with dropped P waves, regular R-R intervals and irregular P-R intervals. This is consistent with 3rd degree AV block.
In congenital 3rd degree AV block, treatment depends on whether or not the patient has structural cardiac abnormalities. If the echocardiogram demonstrates structural abnormalities of the heart, treatment includes placement of a permanent pacemaker. If there are no structural abnormalities and the patient is asymptomatic, pacemaker placement can be delayed.
In this patient, he remembered being told as a child that he had “some kind of block in his heart”. He in fact had congenital 3rd degree AV block. His echo was normal. So, placement of a pacemaker was delayed. Ultimately most of these patients become symptomatic at some point in their life and they then require pacemaker placement.
The algorithm below is helpful for diagnosing bradyarrhythmias.
A 46 year old male presented to the emergency department complaining of headache and vomiting. He had no chest pain or shortness of breath. He was noted to be lethargic in the emergency department and was intubated.
Vital signs: Pulse 60, Respirations 8 and irregular, BP 190/100.
2. In this patient, what is the likely cause of these findings?
3. What is the next step?
The EKG shows diffuse T wave inversions in leads V3-V6, I, II, III and aVF.
The most likely cause is intracranial hemorrhage.
The next step is Stat head CT.
The EKG shows a sinus rhythm at rate of 60 with diffuse T wave inversions in leads V3-V6, I, II, III and aVF. This can be a sign of inferolateral cardiac ischemia. However, in the context of this patient’s symptoms, it most likely is a sign of intracranial hemorrhage. The patient had a head CT which showed an extensive intraventricular hemorrhage. A ventriculostomy was placed and the patient was admitted to the ICU.
T wave inversions can be caused by increased intracranial pressure. This can occur in intracranial hemorrhage or ischemic stroke. The finding is classically described as widening and inversion of the T waves in the lateral leads. These are sometimes called cerebral T waves. You can also see a prolonged QT interval (not present on this EKG) and bradyarrhythmias (Marriott’s Practical Electrocardiography, 10th ed, Ch 11, p.219). The mechanism for this is unclear. These findings are usually transient.
Our patient had a ventriculostomy placed and ultimately did well.
An 82 year old female presents for light-headedness. She states she feels weak and feels like she will pass out. No chest pain, no SOB.
Vital signs: Pulse – 45, BP 100/70, Respirations – 16.
The EKG shows 3rd degree AV block.
Pacing pads should be placed on the patient’s chest. Causes of the AV block should be sought and corrected.
The EKG shows a bradycardia, with the presence of P waves and some dropped P waves (i.e. P waves without a QRS following it).
This can be caused by 2nd degree or 3rd degree AV block. Differentiating these can sometimes be difficult. First, measure the R-R intervals. If they are irregular, you are likely dealing with a 2nd degree AV block (likely type I). If the R-R intervals are regular, you should then measure the P-R intervals. If the R-R intervals are regular and the P-R intervals are also regular, you are again dealing with a 2nd degree AV block (likely type II). If the R-R intervals are regular and the P-R intervals are irregular, that is consistent with 3rd degree AV block.
This is consistent with 3rd degree AV block.
The management of 3rd degree AV block depends on the patient’s stability and symptoms.
First look for correctable causes such as medication toxicity (beta blockers, calcium channel blockers, digoxin), or electrolyte abnormalities (hyperkalemia). If none of these exist and the patient is unstable they should have an emergent pacemaker placed. If the patient is stable, pacing pads should be placed on the chest in case the patient deteriorates and you need to start pacing them quickly. Otherwise they can then be observed until a permanent pacemaker can be placed.
A 72 y/o female with history of a-fib, MI, complains of chest pressure, onset at rest, non-radiating, associated with SOB. The pain was worsened by taking a deep breath. There was no tearing sensation and no back pain. She had no recent travel, immobilization or surgery.
2. What is the differential diagnosis for this EKG pattern?
3. How would you work up this patient?
The EKG shows a-fib with 2 PVC’s and T wave inversions most pronounced in leads V2-V4.
This EKG pattern of T wave inversions in the anteroseptal leads can be seen in anterior wall ischemia, pulmonary embolism, aortic dissection, and intracranial hemorrhage.
Our patient received cardiac enzymes and a D-dimer. Tn was 0.06. D-dimer was 1173. CT showed Right main pulmonary artery embolism extending to right-sided segmental and subsegmental branches.
T wave inversions in the anteroseptal leads is abnormal and can be seen in several disease processes. Putting this finding in the context of the patient’s symptoms is very important. For example, if this is seen in a patient with head trauma, it is likely due to intracranial hemorrhage.
Our patient presented with chest pain. She had a previous MI. However, she said this pain was exacerbated by breathing. When asked, she also said this pain was different then her previous MI pain. That prompted the concern for pulmonary embolism which was confirmed by CT.
This patient actually had a chest CT two weeks prior which was negative for PE.
Several EKG patterns have been described in pulmonary embolism including sinus tachycardia, S1Q3T3, S1S2S3, incomplete or complete right bundle branch block, and T wave inversions V1-V4.
Remember to consider a broad differential in patients with chest pain and in patients with anteroseptal T wave inversions.
This EKG comes courtesy of Dr. Lukasz Cygan.
A 43 year old male with no past medical history presented with lightheadedness. He thought the symptoms were worsened by a sour patch candy. He had no chest pain or palpitations.
His vital signs were normal. His EKG is below.
2. What is the management of this condition?
The EKG shows high take off ST elevations in leads V1 and V2 with a gradually descending ST segment. This is consistent with Brugada type II.
Brugada syndrome is managed with ICD placement. There is no direct treatment for Brugada syndrome.
The EKG shows high take off ST elevations in leads V1 and V2 with a gradually descending ST segment. This is sometimes referred to as a “saddle back configuration”. This is consistent with Brugada type II.
Brugada syndrome is a genetic (autosomal dominant) sodium channel defect. It predominantly affects males (90%). Patients with Brugada syndrome are at risk for polymorphic V-tach. Patients who had a syncopal or near-syncopal episode who have an EKG pattern consistent with Brugada syndrome must be suspected of having had an episode of V-tach.
Brugada type I presents with downsloping, or “coved”, ST elevations in leads V1 and V2 leading into inverted T waves. There is no isoelectric separation between the QRS complex and the T wave.
There is no specific treatment for Brugada syndrome. So, these patients require placement of an ICD to manage their ventricular arrhythmias.
Our patient went to the EP lab and the diagnosis of Brugada was confirmed. He had an ICD placed and is doing well. The sour patch candy was likely a red herring.
This EKG comes courtesy of Dr. Kong.
A 60 y/o male with hx of HTN, presented for palpitations.
V/S: P - 140, BP 180/90, R - 18.
Two EKG's are below. EKG a was the first EKG.
EKG b was taken after the patient was given diltiazem.
1. What rhythm is demonstrated in EKG a?
2. What other pattern is demonstrated in EKG a?
3. What happened to the QRS complexes between EKG a and EKG b?
The rhythm is atrial fibrillation with a rapid ventricular response.
The bundle branch block went away. This is known as a rate related bundle branch block.
The first EKG shows rapid a-fib with a left bundle branch block. The patient was treated with diltiazem with resultant control of the heart rate. When that happened the bundle branch block disappeared and the QRS narrowed. This is known as a rate related bundle branch block.
As the heart rate increases, the cardiac cycle shortens. Eventually the next beat arrives when one bundle is still refractory. So it conducts down the other bundle and then across the heart, the same as in a regular bundle branch block. However, when the heart rate slows, the cardiac cycle lengthens and the bundle recovers. When the bundle recovers the bundle branch block disappears.
No specific treatment is needed for a rate-related bundle branch block.