Cardiac Blog

The Obvious and the Hidden

10/4/2014

We recently responded to a call for chest pain for a 53 year old woman who was at home working out. We arrived on scene and evaluated a patient who was pale, nauseated, weak, and extremely diaphoretic. The patient denied any cardiac history. The resulting assessment and care is a great case study in things both obvious and hidden.

The Obvious
The patient’s initial blood pressure was 112/80, with a pulse of 50, respirations of 18 and a room air pulse oximetry reading of 98%. The patient’s pulse remained in the high 40’s-low 50’s range throughout treatment. There is a lot going on in the initial 12 lead. The obvious issue is the STEMI in the inferior leads: II, III, and AVF. This patient is definitely having an inferior MI. One very common characteristic of an inferior infarction is the reciprocal changes in leads I and AVL. The down-sloped ST depressions are seen in almost all inferior STEMI’s and are very obvious here. If you are unsure of an inferior diagnosis, look for the depressions in I and AVL.

This patient showed a textbook example of an inferior presentation. She was weak, pale, bradycardic, hypotensive and diaphoretic. Inferiors often have intranodal blocks associated with AV dysfunction. The same artery that supplies the inferior heart with oxygenated blood also supplies blood to the SA node, AV node and other critical parts of the heart’s electrical conduction system.

Careful analysis of the patient’s cardiac rhythm reveals extreme AV node dysfunction. Trace the occurrence of P waves across Leads I, AVR and V1 at the top of the strip. There is a very regular pattern of P waves every 20 mm representing a depolarization of the SA node at a rate of about 75. The QRS complexes are also fairly regular but are 30 mm apart, representing a ventricular depolarization rate of about 50. The atrial and ventricular complexes have different rates and are not synchronized. This patient was experiencing complete atrioventricular dissociation (third degree heart block). The dysrhythmia is not uncommon with in inferior MI because the same arterial occlusion that causes the inferior is responsible for hypoperfusion of the AV node. AV node dysfunction is demonstrated here by the completely refractory pathway from the atria to the ventricles.

The Hidden
Inferior STEMI’s are caused by an arterial occlusion of the right coronary artery (RCA). The standard 12 lead EKG is not really set up to see the areas of the heart served by the RCA very well. As a matter of fact, about the only finding indicative of RCA occlusion that can be seen on a standard 12 lead is an inferior MI. There are many areas of the heart served by the RCA that are endangered by this occlusion, but are practically invisible on the 12 lead. One of these areas is the posterior heart wall. About 85% of people get their posterior heart perfusion from the RCA (the other 15% use the circumflex artery). We cannot see the posterior heart directly but we can get a hint of problems with the posterior heart by looking for reciprocal changes in the septal leads: V1-V3. Notice the ST depressions in leads V1 and V2. If we were to flip those leads over 180 degrees we would be looking at the characteristic STEMI pattern of ST segment elevation.

The right ventricle is another area of the heart that depends on the RCA for blood supply. The electrical activity of the right ventricle is completely overwhelmed by the magnitude and vector of the left ventricle. The standard 12 lead EKG is not set up to examine the right ventricle. If we want to see the activity of the right ventricle, we have to go looking for it. We do this by running a right-sided 12 lead. This is usually done by moving V4, V5, and V6 from the left chest wall to mirror image positions on the right chest wall. The positions are called V4R, V5R and V6R. When the 12 lead is printed in this configuration, any ST elevation that show up in V4R, V5R, or V6R are indicative of a right ventricular myocardial infarction (RVMI)

The “Take-Home”
How often do these “hidden” infactions happen and how do we make sure that we never miss when they occur? It all comes back to recognizing that the RCA is involved. Whenever you see significant ST changes in the inferior leads (II, III, AVF), it is important to examine the posterior reciprocal leads (V1-V3) and to run another 12 lead with V4, V5, and V6 moved to the right side of the chest (V4R, V5R, V6R). This patient was having an inferior, posterior, and right ventricular infarction and that’s a real game-changer as far as treatment goes. Cardiac output from the right ventricle can be significantly diminished in cases of RVMI. It’s possible that this can cause deficits in left ventricular preload. This patient becomes very dependant on preload to maintain their systemic blood pressure. We want to avoid vasodilators like nitroglycerine and we want to establish an IV line for fluids to inflate venous preload.

If you suspect an inferior MI:
    ·         Check V1-V3 for reciprocal changes that may indicated posterior involvement
    ·         Check V4R-V6R for ST elevation (right ventricular involvement)

If you have evidence of right ventricular involvement:
    ·         Avoid vasodilators like nitroglycerine
    ·         Be prepared to fluid bolus the patient to maintain systemic pressure

3 Comments

Narrow, fast, and regular

9/1/2014

1 Comment

This EKG is a lesson for anyone who simply reads the printed diagnosis at the top of the page and then starts
treating the patient based on that print-out. It says "Extreme tachycardia with wide complex" and ">>>Very High Heart Rate<<<". It's even capitalized. Based on that diagnosis, we probably have a case of ventricular tachycardia and should start antiarrhythmics and applying the cardioversion pads.

That would be a mistake. The monitor couldn't find the real J point (end of the QRS complex) so it mistakenly lists the QRS width at 0.159 seconds. Looking closely at the precordial leads, especially V3, tells a different story. That QRS complex is about 0.08 seconds, well within normal limits. This is some sort of supraventricular tachycardia.

The rate is fast, around 150 beats a minute. The rhythm is highly regular, so its not atrial fibrillation. Your best picture of the supraventricular activity is seen in leads II, III, and AVF. This is atrial flutter with a 2:1 conduction ratio. The AV node is blocking every other flutter wave so the atrial rate of 300 is translated to a ventricular rate of 150. This 2:1 ratio is the most common form of atrial flutter. As a matter of fact, since flutter waves are often hard to see in some leads, you should do a 12 lead EKG on any regular rhythm tachycardia with a rate around 150 so you can look for the characteristic sawtooth baseline in leads II and III. If it's irregular, think atrial fib, however, many regular tachycardias that hold a steady rate near 150 are actually atrial flutter with a 2:1 AV block.

What causes this? It is often seen in conjuction with atrial enlargement. As the atria stretch to unusual size, they may set up a reentry impulse cycle that spins around the atrial, tracing the same electrical path over and over again at ferocious rates (like this one at 300!). If not for the protective blockade provided by the AV node, your patient would have a ventricular rate of 300 also. You wouldn't last long with a heart rate like that.

Remember that our treatment for atrial flutter and atrial fibrillation centers on maintaining an appropriate heart rate, not abolishing the dysrhythmia. Atrial flutter and atrial fibrillation present the danger of thromboemboli if disrupted abruptly. That's why, when you interview these patients, you'll find them taking at least two medications: something for rate control (digitalis, cardizem, verapamil, beta blockers) and something to reduce clotting (warfarin, coumadin).

1 Comment

Blocks and More Blocks

7/31/2014

1 Comment

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.

1 Comment

Bradycardia and electrolytes

7/31/2014

2 Comments

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.

2 Comments

Asystole: treat or terminate?

7/31/2014

1 Comment

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.

1 Comment

The Obvious and the Hidden

Narrow, fast, and regular

Blocks and More Blocks

Bradycardia and electrolytes

Asystole: treat or terminate?

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