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First-degree AV block

Wide QRS Complex With First-degree AV Block

Fri, 06/07/2019 - 14:48 -- Dawn

The Patient:  This ECG was taken from a 73-year-old man with a history of heart failure with preserved ejection fraction, severe left ventricular hypertrophy, Type II diabetes, and stage 4 chronic kidney disease.  He also suffered deep vein thrombosis and is on anticoagulation.  He has a recent diagnosis of IgA myeloma.  He presented with a complaint of nausea and vomiting and was found to have a worsening of acute kidney infection.  There was suspicion of renal and cardiac amyloidosis, but the patient refused biopsy to confirm this.  He was started on chemotherapy for multiple myeloma and will be followed as an outpatient.

The ECG:  The rhythm is sinus at around 60 bpm, although the rate varies a little at the beginning of the strip.  The QRS complex is wide at .12 seconds, or 120 ms., representing interventricular conduction delay (IVCD).  The PR interval is .32 seconds, or 320 ms. This constitutes first-degree AV block.  There is left axis deviation in the frontal plane and poor R wave progression in the horizontal plane.

Instructors' Collection ECG: Wide QRS Complex With First-degree AV Block

Fri, 06/07/2019 - 13:40 -- Dawn

The Patient:  This ECG was taken from a 73-year-old man with a history of heart failure with preserved ejection fraction, severe left ventricular hypertrophy, Type II diabetes, and stage 4 chronic kidney disease.  He also suffered deep vein thrombosis and is on anticoagulation.  He has a recent diagnosis of IgA myeloma.

Right Bundle Branch Block With Probable Previous M.I.

Sat, 09/08/2018 - 14:35 -- Dawn

This ECG was obtained from an 87-year-old man with chest discomfort.  We have no other clinical information.

ECG Interpretation   The rhythm is regular and fast, with P waves, at 95 beats per minute. So, it is normal sinus rhythm, but the rate is probably not “normal” for this patient.  The P waves are small, and difficult to see.  We suggest Lead I to best view the P waves in this example. This is a good opportunity to teach the value of evaluating rhythm strips in more than one simultaneous lead, as subtle features may not show up well in all leads.  There is a first-degree AV block, with a PR interval of 232 ms.

We see the right bundle branch block (RBBB) pattern: rSR’ in the right precordial leads (with a tiny q wave in V1, which is not typical of  RBBB).  The QRS is wide at 148 ms (.148 seconds).  The R prime (R’) represents the right ventricle depolarizing slightly after the left ventricle.  This terminal delay widens the QRS without affecting the depolarization or contraction of the left ventricle.  This delay can be seen in every lead, but is especially easy to see in Leads I and V6, where there is a wide little s wave.  It is normal for the T waves to be in a direction opposite that of the terminal wave (inverted in Leads V1 and III, for example.)

There is left axis deviation.  The causes of LAD are many.  It is not unusual for people with RBBB to also have a left anterior hemiblock (LAH), also called left anterior fascicular block.  The left anterior fascicle has the same blood supply as the right bundle branch.   LAH causes a frontal plane axis shift – instead of Lead II having the tallest QRS of the limb leads, Leads I and aVL will be the tallest upright QRS complexes of the six limb leads.  Lead II will be very small, or flat, or negative. However, the probability of pathological Q waves in the inferior leads offers a more likely explanation for the leftward axis shift.  The M.I. that would have caused these Q waves is old, as there are no acute ST changes.  It would, of course, help to know this patient’s history.

Right bundle branch block can make evaluating for ST segment elevation a bit tricky.  Occasionally, the terminal delay – especially in Leads III and aVF – can be mistaken for ST elevation.  The J points in this ECG all appear to be at the baseline, with no overt STEMI.

 

Hyperkalemia

Sun, 08/23/2015 - 14:06 -- Dawn

This ECG was obtained from a patient who had a serum potassium level of 7.4 mEq/L.  It shows some of the earliest ECG signs of hyperkalemia.  There are tall, sharply-peaked T waves in many leads.  The P waves have not yet widened and lost amplitude, but they will soon flatten out and disappear.  At this level of hyperkalemia, we can expect to see conduction disturbances (first-degree AV block in this case) and bradycardia (not yet). It is a bit surprising that the QRS complexes have not yet widened at this serum K level.    Caution:  hyperkalemia can progress and become life-threatening very quickly.

Potassium is primarily an intracellular electrolyte.  It is necessary for proper electrical functioning of the heart.  Extracellular  serum potassium can rise due to renal failure, or taking potassium supplements, potassium-sparing diuretics, or ACE inhibitors.  Occasionally, serum K levels may be artificially elevated by drawing the blood with too much syringe pressure, or using too small a needle, as the red blood cells can be damaged and release intracellular K into the serum.

ECG signs may vary among people with hyperkalemia, but in general:

Serum K levels of 5.5 mEq/L or greater can cause repolarization abnormalities like tall, peaked T waves.

Left Ventricular Hypertrophy With Strain

Thu, 12/12/2013 - 10:38 -- Dawn

This ECG is from a man with left ventricular hypertrophy.  LVH causes taller-than-normal QRS complexes in leads oriented toward the left side of the heart, such as Leads I, II, aVL, V4, V5, and V6.  Leads on the opposite side, such as V1, V2, and V3, will have deeper-than-normal S waves.  A commonly-used criteria for determination of LVH is the  Sokolow-Lyon index:     S in V1 + R in V5 or V6 (whichever is larger) ≥ 35 mm (≥ 7 large squares);  and  R in aVL ≥ 11 mm.  There is no perfect ECG criteria for determining LVH. The most accurate way to evaluate the size and thickness of the chambers of the heart is echocardiogram (ultrasound).  Frequently, there is left axis deviation, especially if the hypertrophy is confined to the left ventricle.

The left ventricle can be enlarged for many reasons, some worse than others.  Athletes naturally enlarge the heart, as they work the muscle.  Pathological causes for LVH can include anything that strains the heart as it pushes against increased afterload, such as hypertension and aortic stenosis, and diseases of the myocardium, such as cardiac myopathies.

ECG BASICS: Sinus Bradycardia With First-degree AV Block

Sun, 04/21/2013 - 09:40 -- Dawn

TODAY, we are starting a new feature on the ECG GURU.  ECG BASICS will provide rhythm strips and 12-leads for your beginner or refresher students.  It can be discouraging to the entry-level student to see only intermediate or advanced material and not understand it.  We must remember to start at the most elementary concepts, and then build on them, just as we do with any other subject.  Even more advanced students sometimes benefit from a return to the "basics".  In this weekly feature, you will find downloadable content that is, like all ECG Guru content, FREE for use in an educational context.  Please let us know in the "Comments" section below what ECGs, rhythm strips, or illustrations you would like to see featured in this new area.

 

Today's strip:  Sinus bradycardia with first-degree AV block.  The rate is in the 30's and slowing, and the PR interval is .26 seconds.

Sinus Bradycardia With First-Degree AV Block and Left Anterior Fascicular Block

Sun, 03/10/2013 - 01:13 -- Dawn

This is a good ECG for demonstrating sinus brady and first-degree AV block. It shows the sinus node in the process of slowing down. For your more advanced students, there is left axis deviation due to left anterior fascicular block (left anterior hemiblock). The ST segments are flat, suggesting coronary artery disease. The fourth (bottom) channel is a good rhythm strip. Just crop the image. Please refer to Dr. Grauer's interesting post on teaching hemiblocks on our Ask The Expert page.

Inferior Wall M.I. With Sinus Bradycardia and First-degree AV Block

Mon, 08/13/2012 - 10:51 -- Dawn

Inferior wall MI: ST elevation in II, III, and aVF. Reciprocal ST depressions. Sinus bradycardia and first-degree AV block suggests sinus node and AV node ischemia. This is a good "classic" inferior wall M.I. It is good for teaching inferior-posterior injury, and the effects of RCA occlusion on the sinus and AV nodes. The low voltage in the limb leads may also be due to acute M.I., but in this case, we do not know the patient's body size.

 

jer5150's picture

Jason’s blog: ECG Challenge of the Week for June 24 – July 1, 2012. Pinpoint the primary disturbance.

This patient was seen by his primary care provider (PCP) on an outpatient basis.  The PCP decided to send her patient over to me to perform a routine ECG and establish a baseline, hince the computer's statement below of "No previous ECGs available".  I printed out the above 12-lead ECG and became slightly concerned with the rhythm I was seeing.  Consequently, I also recorded six full pages of continuous rhythm (not shown here).  I don’t ordinarily resort to doing this

Inferior - Posterior M.I.

Tue, 02/14/2012 - 21:39 -- Dawn

This ECG shows a classic inferior - posterior STEMI.  This M.I. was due to complete occlusion of the right coronary artery.  ST elevation apparent in Leads II, III, and aVF show the acute injury in the inferior wall, while ST depressions in V1 and V2 are reciprocal of the ST elevations in the posterior wall.  The tall R waves in Leads V1 - V3 most likely are reciprocal to pathological Q waves in the posterior wall.  Tall R waves in the right precordial leads can be caused by other cardiac conditions, such as right ventricular enlargement.  RV hypertrophy can probably be ruled out in this case because there is no right axis deviation or P pulmonale.  Because inferior wall M.I.s often extend into the posterior wall, it is the most likely cause of the tall R waves.

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