1. “I have a lot of experience differentiating SVT with aberrancy from VT – I’m really on top of the various criteria you can use to tell one from the other.” That’s great! Until the 54-year-old male who you were “sure” had SVT drops his blood pressure to 50/30 after you give him diltiazem and requires aggressive resuscitation and ICU admission. There are no criteria that are fool proof in differentiating SVT with aberrancy from VT. When the diagnosis is not 100% known to be SVT, a wide complex arrhythmia must be treated as VT. Medications used to treat SVT (diltiazem, verapamil) can be lethal in a patient with VT.
2. “I can’t believe that patient submitted a complaint. Adenosine was the indicated treatment for his SVT and I administered it right after he rolled in the door.” It’s true that adenosine was an appropriate treatment, but patients appreciate forewarning of the side effects of medications. It is good practice to initiate treatment promptly, but take a minute to include patients in the overall plan and prepare them before administering medications that cause a sense of impending doom or death.
3. “That lady had “psych” written all over her – a history of depression, anxiety, and frequent ED visits for palpitations.” Palpitations should not routinely be attributed to anxiety. Often, an ECG and telemetry monitoring in the ED will not document a dysrhythmia but Holter monitoring or event recorders might. It has been well documented that many patients, especially females, with SVT are initially misdiagnosed with anxiety. Referring these patients for additional testing may ultimately lead to a diagnosis, treatment that controls symptoms, and fewer visits to the ED.
4. “Young people can tolerate rapid heart rates; I never use electrical cardioversion because those young whipper-snappers never seem unstable – a blood pressure of 95/50 is normal for them.” While younger patients may be better able to tolerate rapid ventricular response in SVT, there is still potential for precipitous deterioration. Atrial fibrillation in WPW syndrome is an inherently unstable rhythm where heart rates may be 300 bpm and the potential for deterioration to ventricular fibrillation is real. If there is a history of WPW syndrome or ECG findings consistent with WPW syndrome and atrial fibrillation, do not hesitate to cardiovert if there is any hint of hemodynamic instability.
5. “The elderly gentleman with a history of myocardial infarction (MI) had shortness of breath and an irregular rhythm on ECG with a rate of 120. I knew he wouldn’t tolerate a heart rate of 120 for very long so I administered metoprolol for rate control.” Unfortunately, that patient had a history of severe COPD in addition to coronary artery disease; the ECG showed MAT (not atrial fibrillation) and the patient had profound bronchospasm in response to treatment with a β-blocker. In both MAT and NPJT, the best course of action is to treat the underlying precipitant of the SVT rather than the heart rate and to avoid medications that are relatively contraindicated. In this case, treatment of the underlying COPD may have relieved the patient’s symptoms of shortness of breath and terminated or slowed the MAT.
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