Widowmaker!

Widowmaker

 

We recently ran an early morning 911 call for chest pain. Upon arrival we encountered a 69 year-old male who stated that he had intense pressure-like pain rated 10 of 10 that began after minor exertion. His wife administered 325 mg of aspirin and called 911 as soon as the symptoms were reported. The patient reported no significant medical history.

The initial 12 lead EKG is seen here. There are ST elevations noted in V1, V2, V3, AVL, and Lead I. Notable ST depressions are seen in all the inferior leads (II, III, AVF) as well as the precordial lateral leads (V5 and V6).

This evidence indicates an acute infarction with widespread consequences. The involvement of V1-V3 indicates anteroseptal damage. The addition of AVL and Lead I indicate damage that extends to the lateral left ventricle. Anteroseptal STEMI’s are caused by an occlusion of the artery that supplies this part of the heart with perfusion, namely the left anterior descending artery (LAD). Lateral STEMI’s are caused by an occlusion of the circumflex artery that wraps around the left lateral wall of the left ventricle.

Since this patient shows evidence of simultaneous occlusion of two different arteries, the LAD and circumflex, we have to decide whether this is a poorly timed coincidence or if the two arteries are linked in some way. Looking at the anatomy of the cardiac arteries, you can see that the arteries are linked in that they both stem from the main stem of the left coronary artery (LCA).

Occlusions of the proximal LAD that interrupt blood flow to the intraventricular septal wall, anterior left ventricle and lateral left ventricle are devastating events. This type of MI is often called the widowmaker. Aside from the fact that the occlusion deprives a huge part of the myocardium from perfusion you have the complications associated with damage to the intraventricular septum.

If you get a chance one day to raise your hand and pick your heart attack, don’t pick the septal one. Within the wall of the ventricular septum lies the AV node, the Bundle of His and the proximal origins of both the right and left bundle branches. This is the core processing unit for your ventricles’ electrical stimulation center. Damage to these structures can cause profound and deadly disruptions to electrical stimulation of the ventricles.

With any MI involving the septum (V1, V2), closely monitor your patient’s EKG for dire signs such as sudden axis shift, widening of the QRS, or new onset of bundle branch blocks. Seeing these events in the context of a septal MI is seeing the patient electrical conduction system coming apart right before your eyes. These patients are statistically more likely to present with sudden cardiac arrest with their MI event.  As a matter of fact, the first cardiac symptom for some patients with septal infarction is death!

Definitive treatment for anteroseptal, anterolateral, or combination infarctions includes recognition with assessment, 12 lead confirmation, labs to evaluate electrolyte levels and cardiac biomarkers and early involvement with cardiology consultation. The arterial occlusion is best addressed in the cardiac catheterization suite. Supportive therapy and early intervention should include consideration of aspirin, oxygen, nitrates, and morphine, but none of these treatments should delay access to percutaneous cardiac intervention (PCI).

This patient benefitted from the outstanding cardiac care between the local EMS and hospital organizations and received immediate access to the PCI lab where they opened his occlusion with 4 stents. The patient rolled to recovery laughing and joking with the PCI staff.

Asystole: treat or terminate?

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.

Blocks and More Blocks

More evidence to support the Mediterranean-style diet

This new study pulled from Medscape indicates the value of a Mediterranean-style diet to improve chances to avoid pathologies like cardiovascular disease, stroke, diabetes, and impaired cognition.
Are you using this diet? What do you think?

More below:

Middle-aged women following a healthy Mediterranean-type diet — with an emphasis on fruits, vegetables, whole grains and fish, moderate amounts of alcohol, and little red meat — have much greater odds of healthy aging later on, a new study reports.

"In this study, women with healthier dietary patterns at midlife were 40% more likely to survive to age 70 or over free of major chronic diseases and with no impairment in physical function, cognition or mental health," said lead study author, Cécilia Samieri, PhD, Institut pour la Santé Publique et le Developpement, Université Bordeaux, France.

This new study adds to growing research on the health benefits of the Mediterranean diet recently reported. Various studies have shown that this diet may contribute to reduced fasting glucose concentrations and lipid levels in those at risk for diabetes, may lower the risk for cardiovascular events and stroke, and improve cognition.

The new study was published in the November 5 issue of Annals of Internal Medicine.

The analysis included 10,670 participants in the Nurses' Health Study, which began in 1976 when female nurses aged 30 to 55 years completed a mail-in survey. Since then, study participants have been closely followed on a regular basis.

In 1980, participants completed a food-frequency questionnaire (FFQ) that asked how often on average they consumed standard portions of various foods. This questionnaire was repeated in 1984 and 1986 and then every 4 years.

To assess dietary quality at midlife, researchers averaged information from the 1984 and 1986 FFQs. They calculated scores on 2 diet indexes:

• Alternative Healthy Eating Index-2010 (AHEI-2010): This index considers greater intake of vegetables, fruits, whole grains, nuts, legumes, and polyunsaturated fatty acids (PUFAs); lower intake of sugar-sweetened beverages, red or processed meats, trans fats, and sodium; and moderate intake of alcoholic beverages. Total AHEI-2010 scores range from 0 (nonadherence) to 110 (perfect adherence).
• Alternate Mediterranean diet (A-MeDi): Developed to assess adherence to the traditional Mediterranean diet, this index includes 9 components that are similar to those in the AHEI-2010. Total A-MeDi scores range from 0 (nonadherence) to 9 (perfect adherence).

In 1992, 1996, and 2000, participants completed the Medical Outcomes Short-Form 36 Health Survey, a questionnaire that evaluates 8 health concepts, including mental health and physical functioning. Scores from the Telephone Interview for Cognitive Status, an adaptation of the Mini-Mental State Examination, were used to evaluate cognitive health. From 1995 to 2001, a cognitive study was administered to participants aged 70 years or older.

Investigators separated "healthy" from "usual" aging on the basis of 4 health domains. Overall, 11.0% of the participants were considered healthy (and so were free of chronic diseases, such as cancers, myocardial infarction, and diabetes, and with no limitation in cognitive function, mental health, and physical function), and the remaining participants were considered usual agers.

Several health domains were typically impaired among the "usual" agers, said Dr. Samieri. "For example, 33% had both chronic diseases and limitations in cognitive, physical, or mental health; 64% had only limitations in cognitive, physical, or mental health; and 3.4% had only 1 or more chronic diseases."

The analysis revealed that greater adherence at midlife to AHEI-2010 and A-MeDi was strongly associated with greater odds of healthy aging (P for trend < .001 for AHEI-2010; P for trend = .002 for A-Medi).

For example, compared with women in the worst quintile of diet scores, women in the highest quintile of the AHEI-2010 and A-MeDi scores had 34% (95% confidence interval [CI], 9% - 66%) and 46% (95% CI, 17% - 83%) greater odds of healthy aging, respectively.

Individual Components

When they analyzed individual dietary components, researchers found statistically significant associations of greater intake of fruits (odds ratio [OR] for upper versus lower quintiles, 1.46) and alcohol (OR, 1.28), and lower intakes of sweetened beverages (OR, 1.28) and PUFAs (OR, 1.38) with healthy aging (P for trend ≤ .04).

The authors noted that they could not exclude participants with impaired cognition, mental health, and physical function in midlife, and although probably few women had severe impairments at baseline, reverse causation in these participants may still be possible. Because they didn't follow participants through to death or onset of a condition that would classify them as no longer healthy, researchers couldn't prospectively estimate risks for transitioning from healthy to usual aging. As well, measurement errors may have occurred in the assessment of dietary patterns.

Other possible limitations were that the study was observational and, because it included mostly white women, its results may not be generalizable to other populations.

Middle age is probably the most relevant period of exposure for preventing chronic conditions of aging that develop over many years.

"It's largely accepted that cumulative exposures to environmental risk factors over the lifespan are probably more important than late-life exposures to determine health in older ages," said Dr. Samieri. "Several mechanisms of age-related chronic diseases, for example, atherosclerosis in cardiac diseases, brain lesions in dementia, start in midlife."

Various researchers have reported on other newly documented health benefits of the Mediterranean diet, including the following:

• Reduced fasting glucose concentrations and lipid levels in patients who are genetically at increased risk for type 2 diabetes as well as reduced risk for stroke.
• Lowered risk for type 2 diabetes by about 20% when the diet also included foods with low glycemic load.
• Slowed progression of carotid plaque.
• Improved cognitive function.
• Cardiovascular events reduced

  
  

   by 30% in people at high risk vs those receiving a low-fat diet.

Blogging vs Teaching

I love Sarah Andersen's perspective. She nails it here. See more of her at http://sarahseeandersen.tumblr.com/

Narrow, Fast, and Regular

 

 

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). 

 

Doug Morris

No Stress Training

www.nostresstraining.com

Electrolytes and Bradycardia

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.

Doug Morris

No Stress Training

nostresstraining@outlook.com