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Blocks and More Blocks

7/31/2014

This EKG has lots of interesting stuff in it despite the fact that it is a non-STEMI, sinus rhythm. You will probably first notice the wide QRS complexes and the pathological left axis deviation. These are two distinct issues. One is caused by a bundle branch block, the other by a hemiblock.

Wide QRS Complex
Look at the QRS complex. These are considered wide when they measure greater than 0.10 (2.5 mm) seconds. At 0.12 seconds (3mm) they are pathological. According to the EKG printout, these QRS's are 0.177 seconds wide; they are definitely not normal. Now look at the orientation of the complex in Lead V1. It is mostly positive producing a large R wave. This is an unusual finding because it indicates an electrical vector flowing toward the right side of the heart. In a bundle branch block, the primary electrical flow is toward the blocked ventricle. These QRS complexes indicate a right bundle branch block (RBBB).

Unusual Axis
Now look at the axis. When Lead III is negatively deflected, you have a left axis deviation (LAD). In some cases, this may be a normal finding, a physiological LAD. The way to tell a normal LAD from an abnormal LAD is to check Lead II. If it is also mostly negative, you have a pathological LAD. This patient has inverted Lead II and III complexes, thus has a pathological LAD. Another way to determine pathological LAD is to refer to the hexaxial QRS measurement on the printout. Normal axis is 90 to 0 degrees. Physiological LAD is 0 to about -30 degrees. A pathological LAD is -30 to -90 degrees. This patient has a QRS axis of -59 degrees. The most common reason for a pathological LAD is a left anterior hemiblock. An anterior hemiblock causes a pathological LAD because it throws the ventricular electrical vectors both left and anterior. You can confirm anterior hemiblock with pathological left axis deviation by looking for small R waves in leads II and III.

What the point?
We all have three main conductive paths going down to our ventricles: the right bundle branch, and the two sections of the left bundle branch: anterior and posterior. If you have a block in your right bundle and a block in your left anterior branch, you are running your ventricles off the single, solitary left posterior hemifascicle. This can be a relatively benign and chronic condition or it can be very dangerous. If unsure, the patient should be evaluated for pacemaker placement. In any case, this patient is a single hemifascicle from a complete heart block with enough pathology present to have knocked out the other two paths already.

This is called a bifascicular block because two fascicles or branches are blocked. There are other bifascicular blocks: a RBBB with a posterior hemiblock is relatively rare, but very serious when observed. The other bifascicular block is a LBBB. All LBBB are bifasicular because the LBBB takes down both the anterior and posterior branches of the left bundle. This is why LBBB is clinically more significant than a RBBB.

Left ventricular hypertrophy is indicated because the height of the R waves in AVL is greater than 12 mm.

One more thing about this EKG. Zoom in on the P wave in Lead II. This P wave is 2.5 to 3.0 mm wide and it has a characteristic "M" shape due to the notching of the P wave. This is a mitral P wave or P-mitrale. mitral P waves are a sign of left atrial enlargement. Mitral stenosis is a common cause, thus the name.

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Bradycardia and electrolytes

7/31/2014

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This EKG displays a couple of significant pathologies. The EKG is from a female patient complaining of diffuse bilateral chest pain and hypoperfusion. It is notable that she presents at a local dialysis clinic.

The most obvious EKG characteristic is probably the slow rate. She presents with a bradycardia that the monitor software initially diagnosed as atrial fibrillation. A quick check on the R-to-R intervals reveals that every interval is precisely 45 mm. Since atrial fib is always chaotically irregular, it is unlikely that this is the right diagnosis. The QRS complexes are narrow, meaning that the pacemaker for this rhythm is supraventricular, but there are no discernable P waves present. We have excluded a ventricular-based rhythm with the narrow QRS complexes, we have excluded a sinus rhythm because of the absence of P waves, and we have excluded atrial fib because of the regularity. This is, by exclusion, a junctional rhythm.

We should also designate this as a junctional escape rhythm because of its slow rate. The slow junctional rate indicates that the junction has assumed the pacemaker function because the SA node is not firing at its faster, intrinsic rate. This patient is in sinus failure and that alone warrants a stat cardiology consult. Looking at the rhythm further may reveal clues as to why the patient is in this state.

In addition to narrow, slow QRS complexes, this EKG diplays unusual T wave morphology. T waves are not typically as tall as their corresponding QRS complexes as they are here in at least half the leads. They aren’t usually this pointed either. Tall, pointy T waves can indicate hyperkalemia. This T wave abnormality, along with the inclusion of dialysis in the history paints a very strong case for hyperkalemia.

Hyperkalemia can be classified into three stages, each with their own characteristic EKG changes.

Early EKG changes of hyperkalemia, typically seen at a serum potassium level of 5.5-6.5 mEq/L, include the following:

Tall, peaked T waves with a narrow base, best seen in precordial leads
Shortened QT interval
ST-segment depression

At a serum potassium level of 6.5-8.0 mEq/L, the EKG typically shows the following:

Peaked T waves
Prolonged PR interval
Decreased or disappearing P wave
Widening of the QRS
Amplified R wave

At a serum potassium level higher than 8.0 mEq/L, the EKG shows the following:

Absence of P wave
Progressive QRS widening
Intraventricular/fascicular/bundle branch blocks

As the potassium level approaches 6.5-8.0 it is common to see sinus arrest like that seen in the example EKG. If the potassium goes much farther beyond that you begin to see ventricular dysfunction with wide QRS complexes, “sine wave” V tach, and rapid progression to cardiac arrest. The patient with hyperkalemia is not playing around. This is a deadly electrolyte imbalance. When the penal system executes death row inmates, it uses potassium to do the job. This patient’s initial K was 8.0 mEq/L.

Your first clue for hyperkalemia is probably going to be history. If you do not have access to lab values, you will have to pick up on clues like the tall, peaked T waves, the prolongation of PR intervals, and the vanishing P wave to gauge the severity of problem. Field treatment can include administration of calcium to correct cardiotoxicity, bicarbonate to correct metabolic acidosis, and a beta-agonist like albuterol to stimulate increase intracellular potassium uptake. ED treatment may also include the administration of glucose and insulin or administration of emergency dialysis. In the meantime, if the patient is symptomatic of the dysrhythmias, i.e. bradycardia, it may be necessary to treat for that problem as well.

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Asystole: treat or terminate?

7/31/2014

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Asystole or cardiac flatline indicates the absence of electrical activity. When asystole is the presenting rhythm in cardiac arrest, resuscitation rates are dismally low. Several mitigating factors can make a real difference. Patient age, concurrent pathology, known treatable causes, and length of arrest are all variables that can influence resuscitation rates.

Asystole is best treated with immediate high quality CPR and a search for an underlying cause. A key component of the medical history includes determination of the patient's possible Do-Not-Resuscitate status, known patient wishes, and family wishes. Each patient should be treated with all reasonable resuscitation efforts when applicable, but it must be understood that asystole is often a sign that the patient has died....permanently.

Part of our difficulty lies in deciding what constitutes a reasonable resuscitation effort. Each case is unique and the determination of "reasonable" depends on the situation, the patient, and the response to initial therapies.

Consider two extremes. In one case your asystolic patient is 89 years old and has an extensive medical history including prior cardiac disease, diabetes, debilitating arthritis, and neurological consequences from a stroke. The second case is a six-year old child just pulled from a cold swimming pool in a witnessed immersion event with asystole on the monitor. These two cases are clearly going to produce two very different resuscitation events. The child's event will involve prolonged attempts using every available therapy to restore a perfusing rhythm. Children have been resuscitated more than an hour after arrest in this circumstance. The adult's resuscitation, though just as important, will be maintained for a much shorter duration and terminated much earlier if therapies do not produce noticable effects. Elderly adults simply do not respond well to therapies after prolonged periods of ventricular asystole.

The decision to continue or terminate in both instances should be made by the most experienced and knowlegable parties involved. Many factors need to be considered. It is common practice to consult with the entire resuscitation team before making the termination decision. A quick survey of the team with the question, "Does anyone have any ideas or any additional information that we should consider before we terminate our efforts?" will tap into the combined experience and expertise of all members of the team.

What do you do when asystole is the presenting arrest rhythm? Respond with immediate high quality CPR, American Heart Association treatment protocols, a diligent search for an underlying treatable cause and be prepared to terminate the event if a response to therapy is not seen after a reasonable effort.

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Blocks and More Blocks

Bradycardia and electrolytes

Asystole: treat or terminate?

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