3 EVALUATION AND TREATMENT OF CARDIAC DYSRHYTHMIAS
Alden H. Harken M.D.

1. Are cardiac dysrhythmias and cardiac arrhythmias the same?

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Yes. Some purists will tell you that an arrhythmia can be only the absence of a cardiac rhythm. But these are the same purists who use the word iatrogenic to mean “caused by a physician,” when, of course, the only thing that can truly be “iatrogenic” is a physician’s parents.

2. Are all cardiac dysrhythmias clinically important?

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Most are not. Many of us have isolated premature ventricular contractions (PVCs) or premature ventricular depolarizations (PVDs) all the time. Superbly conditioned athletes frequently exhibit resting heart rates in the 30s. A clinically important cardiac dysrhythmia is a rhythm that bothers the patient. As a rule, if the patient’s ventricular rate is 60-100 beats/min (regardless of mechanism), cardiac rhythm is not a problem.

3. State the goals in the treatment of cardiac dysrhythmias.

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Primary goal: to control ventricular rate between 60 and 100 beats/min
Secondary goal: to maintain sinus rhythm

4. How important is sinus rhythm?

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It depends on the patient’s ventricular function. Induction of atrial fibrillation in a medical student volunteer causes no measurable hemodynamic effect. Your ventricular compliance is so good that you do not need an atrial “kick” to fill the ventricle completely. Conversely, the worse (the stiffer) the patient’s heart, the more you should try to maintain sinus rhythm. We observed a patient with a 7% left ventricular ejection fraction whose cardiac output decreased by 40% when he spontaneously developed atrial fibrillation.

5. Do you need to be ankle-deep in ECG paper and personally acquainted with Drs. Mobitz, Lown, and Ganong to treat cardiac dysrhythmias in the intensive care unit (ICU)?

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No.

6. When you are called by the ICU nurse to see a patient with an “arrhythmia,” what questions do you ask yourself?

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1. Does the patient really exhibit an arrhythmia? What is the patient doing? Is the stuff that looks like ventricular fibrillation (VF) really just the patient brushing his teeth? Or is the rhythm strip that looks like asystole really just a loose lead? If the patient does exhibit an arrhythmia, ask yourself the following questions.
2. Does the arrhythmia require intervention? Isolated PVCs usually can be ignored safely. Similarly a resting bradycardia in a triathlete is normal. This is the occasion to launch into your “2-second physical exam”-is the patient sweaty and confused or alert and happy?
3. What is a 2-second physical exam? You look into the patient’s eyes, hoping to determine whether he or she is perfusing his or her brain. If the patient looks back at you, you have some time. If the patient requires therapy, ask yourself the following questions.
4. How soon is therapy required? At this point, the patient becomes (paradoxically) irrelevant. The most robust indicator dictating velocity of intervention is not how sick the patient is, but how frightened you are. The dean may have had his carotid arteries firmly ligated years ago. Conversely, to match the surgical residency of your choice, you need to be firing on a lot more cylinders than the dean. You must determine rapidly whether delay in therapy is likely to put the patient at risk. If the cardiac arrhythmia is likely to inflict psychopathologic (hypoxemic) consequences not only on the patient but also, by extension, on his or her extended (societal) family, you should be frightened. If you are frightened, you must ask yourself:
5. What is the safest and most effective therapy?

7. If the patient requires antiarrhythmic therapy, what is the safest and most effective strategy?

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Therapy for cardiac arrhythmias is simple and comprises three comprehensible concepts:

1. If the patient is hemodynamically unstable (the sole determinant of instability is whether you are frightened), cardiovert with 360 J. (For lower energy, see Chapter 2.)
2. If the patient has a wide-complex tachycardia, cardiovert with 360 J.
3. If the patient has a narrow-complex tachycardia, infuse an atrioventricular (AV) nodal blocker IV. If at any time the patient becomes unstable, proceed with cardioversion.

8. In assessing a cardiac impulse, how do you distinguish supraventricular from ventricular origin?

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Supraventricular origin: When an impulse originates above the AV node (supraventricular), it can access the ventricles only through the AV node. The AV node connects with the endocardial Purkinje system, which conducts impulses rapidly (2-3 m/sec). A supraventricular impulse activates the ventricles rapidly (< 0.08 sec, 80 msec, or two little boxes on the ECG paper), producing a narrow-complex beat.
Ventricular origin: When an impulse originates directly from an ectopic site on the ventricle, it takes longer to access the high-speed Purkinje system. A ventricular impulse activates the entire ventricular mass slowly (< 0.08 sec, 80 msec, or two little boxes on the ECG paper), producing a wide-complex beat. (See Figure 3-1.)

Figure 3-1 Wide complex beats are of ventricular origin. Narrow complex beats are of supraventricular origin.

9. Extra credit: Correlate the ECG with cardiomyocyte membrane ion flux.

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See Figure 3-2.

10. Do all wide-complex beats derive from the ventricles?

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No, but most do. An impulse of supraventricular origin that is conducted with aberrancy through the ventricle can take enough time to make it a wide-complex beat. In one study, 89% of 100 patients presenting to an emergency department with a wide-complex tachycardia eventually proved to exhibit ventricular tachycardia, whereas 11% were diagnosed with supraventricular tachycardia with aberrancy.

Figure 3-2 Typical action potential of a cardiac myocyte, the ionic shifts responsible for each phase, and correlation with the surface ECG. A, Phase 0 = rapid depolarization, characterized by rapid influx of sodium (Na+) through the voltage-gated Na+ channels. B, Phase 1 = brief repolarization, characterized by transient influx of chloride (Cl-). C, Phase 2 = plateau phase, characterized by a rapid rise in calcium (Ca2+) permeability through L-type Ca2+ channels. Phase 3 = repolarization with potassium (K+) exiting the cell. D, Slow depolarization of pacemaker cells caused by slow influx of Na+ (From Meldrum DR, Cleveland JC, Sheridan BC, et al: Cardiac surgical implications of calcium dyshomeostasis in the heart. Ann Thorac Surg 61:1273-1280, 1996, with permission.)

11. What do you do if you cannot tell whether a ventricular complex is wide or narrow?

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Acutely and transiently (for 5 seconds) block the AV node by giving 6 mg of adenosine IV; if the ventricular complex persists, it is ventricular. If the ventricular complex stops, it was supraventricular.

12. To prevent lots of supraventricular impulses from getting to the ventricles, how do you block the AV node pharmacologically?

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In seconds: give 6 mg adenosine IV push.
In minutes: draw up 10 mg verapamil (calcium channel blocker) in 10 mL of saline and give 1 mL/min IV.
In hours: put 0.5 mg digoxin in 100 mL of Ringer’s lactate and infuse by IV drip over 30 minutes.

KEY POINTS: CHARACTERIZATION OF CARDIAC DYSRHYTHMIAS

1. Supraventricular origin: when an impulse originates above the AV node, it can access the ventricles only through the AV node to reach the Purkinje system, which conducts and activates the ventricles rapidly, producing a narrow-complex beat (< 2 small boxes on ECG).
2. Ventricular origin: when an impulse originates from an ectopic site on the ventricle, it takes longer to access the high-speed Purkinje system. A ventricular impulse activates the entire mass, slowly producing a wide-complex beat (> 2 small boxes on ECG).
3. Not all wide-complex beats are ventricular in origin.
4. To distinguish ventricular from supraventricular tachycardia, transiently block AV node with adenosine IVP. If ventricular complex persists, it is ventricular tachycardia; if the complex stops, it is supraventricular tachycardia.

13. Why give digoxin?

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Digoxin is an effective AV nodal blocker, but it makes cardiomyocytes more excitable. By giving digoxin, you make supraventricular impulses more likely; but by blocking the AV node, you render these impulses less dangerous.

14. Why infuse digoxin over 30-60 minutes IV?

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Studies indicate that a big pulse of digoxin (IV push) concentrates in the myocardium, making the myocytes hyperexcitable. Digoxin infused more slowly avoids this problem.

15. List the steps in calling a dysrhythmia by name.

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* Bradycardia: < 60 beats/min
* Tachycardia: 100-250 beats/min
* Flutter: atrial or ventricular rate 250-400 beats/min
* Fibrillation: atrial or ventricular rate > 400 beats/min

References
WEB SITE
http://www.americanheart.org/presenter.jhtml?identifier=10000056#P
BIBLIOGRAPHY
Harken AH: Cardiac dysrhythmias. In Wilmore DW, Cheung L, Harken AH, et al (eds): Scientific American Surgery. New York, Scientific American, 1999.