Sudden Cardiac Death While Running

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Illustration by Heikenwaelder Hugo, wikimedia commons

The Tell-Tale Heart

Examining your risk for sudden cardiac arrest while running

DAVID ROCHE FEBRUARY 2ND, 2017

My wife and I have only one rule when it comes to running through pain. If either of us ever feels any unusual sensation in our heart, we promise to stop and walk home.

Initially, that philosophy was motivated not by science, but by fear. We had read the news stories about cardiac arrest in otherwise healthy athletes, and the tragedies stuck with us. You may have read about Micah True—also known as “Caballo Blanco,” of Born to Run fame—who died of cardiac arrest on a trail run in 2012, and every so often a similar story crops up in the local or national press.

In reality, sudden cardiac arrest in runners is much rarer than the hype machine suggests, but it is a serious risk that is important to understand.

Most cases arise from a heart condition known as hypertrophic cardiomyopathy, or HCM. “Many runners think they’re in the clear from chronic diseases solely because they run,” says Emily Kraus, a sports-medicine doctor at Stanford University. “Although physical activity is an excellent cardio-protective practice, it can’t always shield from those underlying, non-modifiable risk factors.”

Here are five questions to help you understand your risk of sudden cardiac arrest from HCM.

What causes cardiac arrest in healthy athletes?

HCM is a genetic condition that causes progressive thickening of the heart tissue. According to the American College of Sports Medicine (ACSM), when the muscle gets large enough, during exercise it “can start to quiver in ventricular fibrillation, which is the cause of sudden death.”

“Imagine the heart as an inflatable bouncy castle,” says Robyn Reed, a pathologist at Children’s Hospitals and Clinics of Minnesota. “The kids ricocheting around inside are the blood. If you get the castle too pumped up, the doorway gets squeezed shut and the kids have trouble squeezing their way out. It can even get so pumped up that it cuts off its own air supply (or blood supply), leading to tissue damage.”

Reed adds that HCM can interfere with heart-muscle contraction and even result in the muscle cells no longer “correctly conducting the electrical signals that tell your heart how to beat. They’ll still try to contract, but they’ll do it in a disorganized way.”

How common is HCM?

According to the ACSM, about one in 500 people have HCM. The condition is more common in men and in families with a history of the diagnosis.

How often does HCM lead to sudden death?

A 2012 study in the New England Journal of Medicine found that one out of every 259,000 marathon and half-marathon participants died of sudden cardiac arrest. For cases where data was available, 23 of 31 were due to HCM.

To put that in perspective, your odds of being struck by lightning this year are 1 in 960,000. So even though both events seem unlikely, just as you wouldn’t venture outside with a metal umbrella during a thunderstorm, you shouldn’t expose yourself to unnecessary risk from HCM.

While no statistics are available for lifetime mortality risk, most people with HCM never know. It’s a time bomb with a fuse that may never be lit. But when it is, it often ends quickly and tragically.

What can I do to understand my risk?

You wouldn’t drive 50,000 miles without taking your car in for a checkup. The same goes for your body—the ACSM recommends regular physical exams to screen for things like HCM. People with HCM “may develop a heart murmur or arrhythmia,” according to the organization.

Not all people with HCM get a “check-engine-light” warning, but some do. Symptoms include “chest discomfort with exertion, unreasonable breathlessness (this is not the same as the breathlessness experienced from hill or sprint repeats—that’s normal), dizziness, fainting or blacking out,” says Kraus. If one of those lights pops on, see a doctor before continuing activity.

Kraus identifies additional heart-related risk factors as “a family history of a blood relative who had a heart attack before the age of 55 years (father or brother) or age 65 years (mother or sister), or an unexplained sudden death before age 50 (including drowning, unexplained car accident or sudden-infant-death syndrome).”

A sure diagnosis requires an electrocardiogram or echocardiogram. Some universities, like Rice, now require these tests before an athlete competes in intercollegiate athletics. Consider having your heart tested before embarking on a grueling training regimen.

 What should I do if I have HCM?

If you have HCM, it’s not the end of the world. The risk of death for people with HCM is 2 to 4 percent per year.

There are a few different approaches to living with HCM. In general, says Kraus, “If a runner has been diagnosed with HCM, they should not run due to the risk of sudden cardiac death.” She adds that “depending on the severity of the diagnosis,” a doctor may prescribe low-to-moderate-intensity activity or install an implantable defibrillator. Treatment plans are highly personal and should be determined by a cardiologist.

David Roche is a two-time USATF trail national champion, the 2014 U.S. Sub-Ultra Trail Runner of the Year and a member of team Hoka One One and Team Clif Bar. He works with runners of all abilities through his coaching service, Some Work, All Play. Follow David’s daily training on Strava here, and follow him on Twitter here.

Why hypokalemia causes tachycardia

Principles of Critical Care, 4e >

Potassium is the most common cation in the body.Normal serum potassium ranges from 3.5 to 5.2 mmol/L. The molecular weight of potassium is 39.1, so a daily potassium intake of 80 mmol is roughly equivalent to 3.1 g of potassium.

The normal physiologic handling of potassium can be viewed as a three-step process: 

1. ingestion
2. cellular distribution
3. excretion

Irregularities at any of these steps can result in pathologic serum potassium concentrations.

Cell Uptake: Following absorption, potassium distributes among the intracellular and extracellular compartments. The intracellular compartment acts as the primary buffer to changes in serum potassium concentration.

The Na-K-ATPase pump, driven by a ubiquitous cell surface enzyme, moves potassium into cells while pumping sodium out of cells. The pump is stimulated by β2-adrenergic activity, while α-adrenergic activity results in potassium efflux.53 Insulin also stimulates the activity of this pump and is independent of its hypoglycemic activity.54

Extracellular pH can affect the cellular distribution of potassium. Various explanations have been proposed, including a direct effect of pH on the Na-K-ATPase, or an H+-K+exchange to maintain electroneutrality. The effect of pH on potassium distribution varies depending on the nature of the acid-base disturbance. Respiratory acidosis, alkalosis, and organic acidosis all have minimal effect on potassium distribution. Inorganic acidosis can increase serum potassium, while metabolic alkalosis can lower potassium. Inorganic acidosis  (ie, non-Anion Gap). Diabetic ketoacidosis (DKA) often presents with hyperkalemia that does not parallel the acidosis; in this case, hyperkalemia results from insulin deficiency and the effects of hyperosmolality. Lactic acidosis and other forms of organic acidosis generally do not present with a significant potassium shift.

Hypokalemia is defined as a serum potassium concentration below 3.5 mmol/L, and is found among 20% of the hospitalized population. However, this high frequency probably does not reflect total body potassium depletion. In a review of 70 hospitalized patients with a potassium less than 2.8 mmol/L, the potassium rose toward normal regardless if they were given potassium or not. The authors suggested that hospitalization for acute illness was associated with increased adrenergic stimulation, resulting in intracellular movement of potassium and transient hypokalemia.60

Hyperkalemia is defined as a serum potassium concentration above 5.2 mmol/L

Increased Potassium Intake is one cause; e.g., KCl salt substitute

Transfusion of red blood cells

Intracellular Redistribution of Potassium - The Na-K-ATPase is critical in preventing intracellular potassium from causing hyperkalemia. Any factor that decreases the activity of this enzyme will cause potassium to leak from cells. A lack of insulin slows the Na-K-ATPase. In diabetic ketoacidosis hyperkalemia is typical.  β-Blockers inhibit the Na-K-ATPase activity and are associated with a mild increase in serum potassium. Uremia reduces Na-K-ATPase activity so that renal failure patients are less able to use the intracellular compartment to buffer potassium loads. Digitalis is an Na-K-ATPase antagonist. Digitalis toxicity can cause severe hyperkalemia.

Inorganic acids increase serum potassium. Decreases in pH due to respiratory or organic acidosis (e.g., lactic acidosis) have minimal effect on serum potassium.

Clinical Sequelae: The potassium concentrations inside and outside of the cell are the primary determinants of the cellular resting membrane potential (Em). Changes in the extracellular concentration can have dramatic effects on the resting membrane potential and the cell’s ability to depolarize. As extracellular potassium rises, the normally negative Em increases toward zero; this allows easier depolarization (ie, increased excitability). However, this excitability is short-lived as chronic hyperkalemia ultimately inactivates the sodium channels critical to producing an action potential. Hyperkalemia shortens the refractory period following depolarization by facilitating faster potassium uptake.

In the myocardium, inactivated sodium channels slow conduction velocity, and high serum potassium speeds repolarization. On ECG, hyperkalemia causes widened QRS complexes (slowed conduction velocity) and shortened ST intervals with tented T waves (rapid repolarization). The slowed conduction associated with rapid repolarization predisposes the myocardium to ventricular fibrillation.

During Phase 4 there is also a slow decline in the outward movement of K⁺ as the K⁺ channels responsible for Phase 3 continue to close. This fall in K⁺ conductance (gK⁺) contributes to the depolarizing pacemaker potential.

Hypokalemia increases the rate of phase 4 depolarization and causes tachycardia.  It apparently does this by decreasing gK during phase 4.

E_m = g'_K E_K  + ..................

The effects of hyperkalemia and hypokalemia on heart rate are explained by changes in membrane conductance rather than by changes in the potassium Nernst potential.  The increase in K conductance that occurs in hyperkalemia causes the maximum diastolic potential (MDP) to shift closer to EK. Accordingly, even though EK becomes more positive in hyperkalemia, the MDP becomes more negative.  This negative shift in MDP acts to slow heart rate by increasing the potential difference between MDP and the threshold for activation of the L-type calcium current.  In addition, the increased K conductance that occurs in hyperkalemia makes it more difficult for the funny sodium current to drive phase 4 depolarization.  Heart rate is also slowed by a decrease in the rate of phase 4 depolarization.   Just the opposite effects are produced by the decreased K conductance associated with hypokalemia.  The decreased conductance causes MDP to become more positive even though EK becomes more negative.  In addition, the decreased K conductance allows the funny sodium current to be more effective at driving phase 4 depolarization which results in a faster phase 4 depolarization.

Why the patient's murmur can be heard at other listening posts

Pathophysiology of Heart Disease by Leonard S. Lilly 

ECG Changes in Right and Left Bundle Branch Blocks

In right bundle branch block (RBBB), normal depolarization of the right ventricle is interrupted. In this case, initial depolarization of the ventricular septum (which is stimulated by a branch of the left bundle) is unaffected so that the normal small R wave in lead V1 and small Q wave in lead V6 are recorded. As the wave of depolarization spreads down the septum and into the left ventricular free wall, the sequence of depolarization is indistinguishable from normal, because left ventricular forces normally outweigh those of the right. However, by the time the left ventricle has almost fully depolarized, slow cell-to-cell spread has finally reached the “blocked” right ventricle and depolarization of that chamber begins, unopposed by left ventricular activity (because that chamber has nearly fully depolarized). This prolonged depolarization process widens the QRS complex and produces a late depolarization current in the direction of the anteriorly situated right ventricle. Since the terminal portion of the QRS complex in RBBB represents these right ventricular forces acting alone, the ECG records an abnormal terminal upward deflection (known as an R′ wave) over the right ventricle in lead V1 and a downward deflection (S wave) in V6 on the opposite side of the heart. The appearance of the QRS complex in lead V1 in RBBB (upward R, downward S, then upward R′) is often described as having the appearance of “rabbit ears.” 

Left bundle branch block (LBBB) produces even more prominent QRS abnormalities. In this situation, normal initial depolarization of the left septum does not occur; rather, the right side of the ventricular septum is first to depolarize, through branches of the right bundle. Thus, the initial forces of depolarization are directed toward the left ventricle instead of the right (see Fig. 4-19B; see also Fig. 4-30). Therefore, an initial downward deflection is recorded in V1, and the normal small Q wave in V6 is absent. Only after depolarization of the right ventricle does slow cell-to-cell spread reach the left ventricular myocytes. These slowly conducted forces inscribe a widened QRS complex with abnormal terminally upward deflections in the leads overlying the left ventricle (e.g., V5 and V6),

Lung Cancer Image

Lung Cancer, CT scan with 3D reconstruction, presents dry cough and left chest pain.

https://app.figure1.com/images/56b67fefbb09089d1f2310d4

Licorice

Stewart et al.4 have proposed that licorice acts by inhibiting Cortisol oxidase, a component of the widely distributed 11β-hydroxysteroid dehydrogenase system that converts Cortisol to cortisone, producing a state of apparent mineralocorticoid excess similar to that in children with 11/3-hydroxysteroid dehydrogenase deficiency5 (Fig. 1FIGURE 1Overview of Cortisol Metabolism.). In vitro, cortisol has the same binding affinity for mineralocorticoid receptors as aldosterone,6whereas that of cortisone is much less. Licorice, by inhibiting 11β-hydroxysteroid dehydrogenase in aldosterone-responsive tissues such as the kidney, where it is found in high concentrations,7 , 8 produces high renal levels of cortisol, which then binds to and activates mineralocorticoid receptors.4 The degree to which licorice inhibits 11β-hydroxysteroid dehydrogenase activity can be measured by examining the ratio of the metabolites of cortisone to those of cortisol in urine.

Heart Failure - Bowditch Phenomenon

Cardiovasc J Afr. 2009 Feb; 20(1): 37–38.

From Bowditch to beta-blockers: evolution of the understanding of the importance of heart rate and myocardial energetics in cardiomyopathy

James Ker, MB ChB, MMed, MRCP, PhD, FESC, FACC, L Akad SA

Author information ► Article notes ► Copyright and License information ►

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Summary

Summary

During the past three decades, every aspect of cardiomyopathy has undergone dramatic change. When examining the literature on the physiological aspects of the failing heart, one immediately recognises that South Africa has made a contribution: Brink, Bester and Lochner evaluated the possible therapeutic aspects of the Bowditch phenomenon and myocardial energetics in cardiomyopathy almost four decades ago, at a time when the condition even had another name, myocardiopathy.

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Summary

All aspects of cardiomyopathy – from our knowledge on ultra-structural and physiological alterations, to pharmacological approaches to therapy, surgical treatment modalities and later device-based therapies – have undergone dramatic changes during the last three decades. Even the terminology has changed. If one scrutinises articles from the 1950s to the 1970s one will find that the preferred term then was ‘myocardiopathy’.

When analysing the progression of knowledge on the physiology of the failing heart that has made an impact on therapeutic advances over the past 30 years, I am proud to state that South Africa has made a contribution. In 1972, the following article by Brink, Bester and Lochner appeared:1 A comparison of stimulation frequency and electro-augmentation on myocardial function, extensibility, coronary flow rate, oxygen consumption and glucose metabolism.

Thirty years later, we would see dramatic paradigm shifts regarding the importance of heart rate in cardiomyopathy. Today we understand the importance of heart rate variability and heart rate turbulence as prognostic markers in various cardiovascular disorders and we have conclusive evidence from clinical trials that reducing heart rate in cardiomyopathy confers a survival advantage.

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The Bowditch phenomenon

When cardiac myocytes are stimulated at faster rates, they increase their force of contraction.2 This ability of the vertebrate heart is central to survival and is known as the Bowditch phenomenon. 2,3 It is also known as the ‘treppe’ or staircase phenomenon.

Henry Pickering Bowditch, famed physiologist (nephew of the well-known Boston physician Henry Ingersoll Bowditch) and later dean of Harvard Medical School,4 published his classic article in 1871, describing the positive inotropic response of the heart when the heart rate increases. The next 100 years would see many articles examining the response of the myocardium to various stimulation frequencies, effected by electrical devices external to the heart.2

It would be many years after Bowditch’s article before it became apparent that the failing heart behaves very differently to an increase in heart rate. The failing heart does not exhibit a Bowditch phenomenon – there is no increase in the inotropic response to an increase in heart rate,5-7 with some failing hearts even exhibiting a reverse Bowditch response. It was during this era that the article by Brink et al.1 raised the issue that it was doubtful whether the phenomenon of increasing heart rate could be used for therapeutic purposes in the failing heart. Today we have ample clinical and laboratory evidence that reducing the heart rate improves the prognosis of patients with heart failure.

In 1967, Brink et al.8 published an article on the work performance of the isolated, perfused, beating heart in Syrian hereditary cardiomyopathic hamsters. In 2007, exactly 40 years later, work on similar Syrian cardiomyopathic hamsters clearly demonstrated that the chronic administration of carvedilol (a beta-blocker) improved cardiac function.9 This was in striking contrast to the line of thought in 1972, when the Bowditch staircase phenomenon was being explored as a possible therapeutic modality in heart failure. Already in 1972, work by Brink et al.1 had raised the question that this would not be a viable therapeutic option, thus paving the way for a major paradigm shift and the current therapeutic knowledge to use beta-blockers in heart failure patients.

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The failing heart as ‘an engine out of fuel’

Another important concept realised today in ‘modern’ cardiology is that the failing heart, as opposed to the normal heart, can be viewed as ‘an engine out of fuel’.10 In 1939, Herrmann and Decherd11 published an article on the chemical nature of heart failure. However, interest waned over the next few decades, only to be revived in the 2000s with Taegtmeyer12 elegantly summarising the situation as: ‘Metabolism – the lost child of cardiology’.

The human heart displays an enormous energy requirement – 6 kg of ATP every day.10 If this requirement is not met, it will result in the reduction of mechanical energy delivered to the actin–myosin interaction process and a drop in the contractile ability of the myocardium. However, we still do not possess an accurate method for determining the levels of ATP and phosphocreatine near the sarcoplasmic reticulum in the intact, in vivo human heart – they are extrapolated from global measurements using 18F-FDG PET imaging.10

Already in their 1972 article, Brink, Bester and Lochner1 had realised the importance of ‘myocardial energetics’,10 and glucose uptake and lactate production were analysed when evaluating the Bowditch phenomenon in the isolated, perfused rat heart. Unfortunately, in this case scenario, more than 30 years later we still do not possess the ideal, reliable way to measure myocardial energetics where we need to – in the peri-myofibrillar space, near the sarcoplasmic reticulum and sarcolemmal ion pumps.10

Therefore, I conclude that this historical article by Prof AJ Brink et al.1 was one of the bricks that paved the way to the current understanding and use of beta-blockers in patients with heart failure and, furthermore, that it should also be an inspiration to find new and better methods for measuring ‘myocardial energetics’ – cardiology’s lost child, in order to find a whole new therapeutic armamentarium to treat the ‘engine out of fuel’.

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References

1. Brink AJ, Bester AJ, Lochner A. A comparison of stimulation frequency and electro-augmentation on myocardial function, extensibility, coronary flow rate, oxygen consumption and glucose metabolism. Eur J Clin Invest. 1972;2(4):250–258. [PubMed]

2. Lakatta EG. Beyond Bowditch: the convergence of cardiac chronotropy and inotropy. Cell Calcium.2004;35:629–642. [PubMed]

3. Piot C, Lemaire S, Albat B, Seguin J, Nargeot J, Richard S. High frequency-induced upregulation of human cardiac calcium currents. Circulation. 1996;93(1):120–128. [PubMed]

4. Putnam JJ, Henry P. Bowditch dead. The Harvard Crimson. 1911 Mar 14;

5. Hajdu S, Posner CJ. Absence of Bowditch phenomenon in the ventricular muscle of hamsters with hereditary cardiomyopathy. Am Heart J. 1971;81(6):781–789. [PubMed]

6. Mulieri LA, Hasenfuss G, Leavitt B, Allen PD, Alpert NR. Altered myocardial force-frequency relation in human heart failure. Circulation. 1992;85:1743–1750. [PubMed]

7. Feldman MD, Alderman JD, Aroesty JM, Royal HD, Ferguson JJ, Owen RM. et al. Depression of systolic and diastolic myocardial reserve during atrial pacing tachycardia in patients with dilated cardiomyopathy. J Clin Invest. 1988;82:1661–1669. [PMC free article] [PubMed]

8. Brink AJ, Lochner A. Work performance of the isolated perfused beating heart in the hereditary myocardiopathy of the Syrian hamster. Circulation Res. 1967;XXI:391–401. [PubMed]

9. Cruz N, Arocho L, Rosario L, Crespo MJ. Chronic administration of carvedilol improves cardiac function in 6-month-old Syrian cardiomyopathic hamsters. Pharmacology. 2007;80:144–150. [PubMed]

10. Neubauer S. The failing heart – an engine out of fuel. New Engl J Med. 2007;356(11):1140–1151.[PubMed]

11. Herrmann G, Decherd GM. The chemical nature of heart failure. Ann Int Med. 1939;12:1233–1244.

12. Taegtmeyer H. Metabolism – the lost child of cardiology. J Am Coll Cardiol. 2000;36:1386–1388.[PubMed]

Cardiovascular in the News

Fit Young Woman Having Strokes -Why

Adrenergic effects with normal baroreceptor reflex

Notice:  norepinephrine causes an increase on heart rate and blood pressure and PVR as a direct effect on the heart and vessels.  BUT, the increase in pressure triggers the barorecptor reflex leading to a decreased heart rate.

SO, you always need to know whether you are considering the direct effect versus the response in the presence of reflex controls.  😎

Dromotropy

cvpharmacology.com

Regulation of Conduction

The conduction of electrical impulses throughout the heart, and particularly in the specialized conduction system, is influenced by autonomic nerve activity. This autonomic control is most apparent at the AV node. Sympathetic activation increases conduction velocity in the AV node by increasing the rate of depolarization (increasing slope of phase 0) of the action potentials. This leads to more rapid depolarization of adjacent cells, which leads to a more rapid conduction of action potentials (positive dromotropy). Sympathetic activation of the AV node reduces the normal delay of conduction through the AV node, thereby reducing the time between atrial and ventricular contraction. The increase in AV nodal conduction velocity can be seen as a decrease in the P-R interval of the electrocardiogram.

Sympathetic nerves exert their actions on the AV node by releasing the neurotransmitter norepinephrine that binds to beta-adrenoceptors, leading to an increase in intracellular cAMP. Therefore, drugs that block beta-adrenoceptors (beta-blockers) decrease conduction velocity and can produce AV block.

Parasympathetic (vagal) activation decreases conduction velocity (negative dromotropy) at the AV node by decreasing the slope of phase 0 of the nodal action potentials. This leads to slower depolarization of adjacent cells, and reduced velocity of conduction. Acetylcholine, released by the vagus nerve, binds to cardiac muscarinic receptors, which decreases intracellular cAMP. Excessive vagal activation can produce AV block. Drugs such as digitalis, which increase vagal activity to the heart, are sometimes used to reduce AV nodal conduction in patients that have atrial flutter or fibrillation. These atrial arrhythmias lead to excessive ventricular rate (tachycardia) that can be suppressed by partially blocking impulses being conducted through the AV node.

Phase 0 of action potentials at the AV node is not dependent on fast sodium channels as in non-nodal tissue, but instead is generated by the entry of calcium into the cell through slow-inward, L-type calcium channels. Blocking these channels with a calcium-channel blocker such as verapamil or diltiazem reduces the conduction velocity of impulses through the AV node and can produce AV block.

Because conduction velocity depends on the rate of tissue depolarization, which is related to the slope of phase 0 of the action potential, conditions (or drugs) that alter phase 0 will affect conduction velocity.  For example, conduction can be altered by changes in membrane potential, which can occur during myocardial ischemia and hypoxia. In non-nodal cardiac tissue, cellular hypoxia leads to membrane depolarization, inhibition of fast Na⁺ channels, a decrease in the slope of phase 0, and a decrease in action potential amplitude. These membrane changes result in a decrease in speed by which action potentials are conducted within the heart. This can have a number of consequences. First, activation of the heart will be delayed, and in some cases, the sequence of activation will be altered. This can seriously impair ventricular pressure development. Second, damage to the conducting system can precipitate tachyarrhythmias by reentry mechanisms. Click here to learn more about altered impulse conduction. 

Antiarrhythmic drugs such as quinidine (a Class IA antiarrhythmic) that block fast sodium channels cause a decrease in conduction velocity in non-nodal tissue.

baroreceptors & chemoreceptors innervation

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Cardiac Cycle Tutorial

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Evidence Based Medicine

Evidence Based Medicine

How to Write Learning Objectives, USMLE Step 1 MCQs, and Confidence Based Practice Questions

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How to Write Learning Objectives, USMLE Step 1 MCQs, and Confidence Based Practice Questions

2016/17

Steve Wood, PhD

How to Study in Medical School

How to Study in Medical School

What worked in undergraduate school (did well on the exam but forgot the material quickly) which was OK because you didn't need to use it again: Cram

What you need to do in medical school (do well on the exam AND remember the material for other modules and for Step1): study and re-study!


No pain, No gain (applies to learning too)

Use all the learning styles (even if they are not your preferred style)

Respiratory Failure

Respiratory Failure

Memory Tool:  Type 2 = CO2