A 45-year-old woman with a history of medication-controlled essential hypertension, stage 2 chronic kidney disease, type 2 diabetes mellitus, and a pack-a-day cigarette habit presented less than 60 minutes after acute onset of severe shortness of breath that awoke her from sleep. She had felt well the previous day, and went to bed with no complaints.
Around 4 a.m., she woke up from sleep very dyspneic, with moderate chest “discomfort” over her left chest that radiated to her back and was unchanged by position or respirations. She denied other symptoms such as fever, cough, nausea, vomiting, numbness, or abdominal pain.
Her blood pressure was 138/76 mm Hg, pulse 87 bpm, respiratory rate 26, and SpO2 was 95%. She was afebrile, and her physical exam was unremarkable: clear breath sounds, no S3 or murmur, and no lower extremity edema. She felt slightly less dyspneic with supplemental oxygen. She was treated with an aspirin orally. A sublingual nitroglycerin improved her chest discomfort, and a chest radiograph was clear. Her presenting electrocardiogram is shown in Figure 1.
The ECG is consistent with a supraventricular tachycardia (SVT), likely to be atypical atrioventricular nodal reentrant tachycardia (AVNRT). The key feature to note is the absence of P waves before the QRS complex and retrograde P-waves evident following the QRS as part of the T-wave. The discomfort in her chest and neck is likely secondary to atrial contraction against the closed AV valves during ventricular systole. She was successfully cardioverted to sinus rhythm with adenosine, and her symptoms resolved.
The patient’s history, presenting complaint, and initial evaluation help us narrow our differential diagnosis. (Table 1.) Waking from sleep with dyspnea, referred to as paroxysmal nocturnal dyspnea, is most commonly associated with congestive heart failure. No other evidence, however, exists in this patient. She has no history of previous heart disease, her lungs are clear on exam and imaging, which would not be the case if there were cardiogenic pulmonary edema, and she does not have lower extremity edema that would develop with vascular congestion. Pneumonia, likewise, is unlikely in a patient without signs or symptoms of infection and normal lung findings.
Spontaneous pneumothorax is essentially excluded by the normal radiograph. Obstructive airway disease such as asthma or COPD is an important consideration. The patient has no documented history of either, but her smoking suggests the possibility. Wheezes were not auscultated on physical exam, but a trial of nebulization is appropriate during the workup. Anemia is unlikely given the rapid onset, but measurement of blood counts is reasonable. She has a low pretest probability for pulmonary embolism using the Wells criteria, and meets all eight criteria of the PERC Rule for Pulmonary Embolism (Table 2), which gives her a risk of less than two percent for pulmonary embolism.
Table 1. Differential for Nocturnal Dyspnea
• Pulmonary embolism
• Obstructive airway disease
• Congestive heart failure
• Myocardial ischemia
• Gastroesophageal reflux disease
• Sleep apnea
• Panic attack/anxiety
Table 2. PERC Rule for Pulmonary Embolism
• Age under 50
• Heart rate under 100
• SpO2 over 94%
• No prior history of DVT/PE
• No hemoptysis
• No exogenous estrogen
• No clinic signs suggesting DVT
Source: J Thromb Haemost 2008;6(5):772.
The emergency physicians attending to this patient considered myocardial ischemia the leading diagnosis. They appropriately treated her with supplemental oxygen and a full-dose aspirin 325 mg orally. The presenting ECG was noted to have ST-segment depression in V5, V6, III, and aVF. There are also down-sloping ST-segments in multiple leads. These findings would be consistent with subendocardial ischemia.
Figure 2 for comparison shows an ECG obtained six months earlier when the patient was not experiencing any symptoms.
The changes noted between baseline ECG and her presenting ECG would be further concern that the patient was experiencing ischemic chest pain. It is always important, however, to evaluate all the parts of an ECG fully. Take a close look at lead II, shown in close-up in Figure 3. One striking feature is the lack of P-waves preceding the QRS complex. Following the QRS complex, however, is an initial negative deflection and then positive deflection of the tracing. This is actually a retrograde P-wave followed by a normal axis T-wave. This retrograde P-wave is generated from the AV node, and conducts up and to the right depolarizing the atria. The ventricular depolarization and repolarization conducts normally from the AV node, and can be seen in the normally aligned QRS complex and T-wave. This is classic for an atrioventricular nodal reentrant tachycardia (AVNRT) rhythm.
AVNRT is the most common form of paroxysmal supraventricular tachycardia. Palpitations and lightheadedness are frequent presenting complaints, but chest pain and dyspnea can occur in patients with coronary artery disease or structural heart disease. No specific inciting event can be pinpointed for the initiation of the arrhythmia, but alcohol, stimulants, or excessive vagal tone can increase the risk.
AVNRT arises because of fast and low conduction pathways through the AV node. (Figure 4.) A normal beat is conducted through the fast pathway, and the slow pathway is blocked because of the refractory period in the distal AV node. If a premature atrial contraction occurs (which is the usual inciting mechanism), the fast pathway is refractory. The slow pathway, while conducting more slowly, has a shorter refractory period, and would have recovered excitability and be able to conduct the premature beat. This initial premature beat would have a longer than normal PR interval if captured on ECG.
Once the conduction down the slow pathway reaches the common point, it will conduct down the bundle of His to the ventricle and retrograde up the fast pathway to the atria. The circuit can become self-sustaining if the slow pathway has recovered from its refractory period by the time the beat has reached the top of the AV node. Various forms of AVNRT exist, but 80-90 percent of the cases have what is labeled typical AVNRT (slow-fast) and have retrograde conduction via the fast pathway. The P-wave in this situation is hidden within the QRS complex or seen as an R wave. Atypical AVNRT occurs in the opposite direction (fast-slow) with retrograde conduction via the slow pathway, and the P-wave can therefore be seen in the ST-segment or as part of the T-wave. Significant ST-segment depression can occur during AVNRT, and represents repolarization changes rather than myocardial ischemia.
Treating the rhythm needs to be divided into acute therapy and prevention of recurrence. Electrical cardioversion would be appropriate, as with all arrhythmias causing hemodynamic compromise. Treatment with adenosine is first-line therapy if the patient is relatively stable. Adenosine, a nucleoside analog, has many effects, but most important here is the ability to prolong the conduction time through the AV node, interrupting the re-entry pathways. It is usually given in 6 mg or 12 mg doses.
Unfortunately, adenosine is unstable in vivo, and is very rapidly metabolized (less than 10 seconds) by red blood cells and endothelium so it is administered by fast push. A typical setup is to have a peripheral IV running 0.9% saline, and inject the adenosine and quickly switch syringes to perform the flush. Alternatively, the adenosine can be combined in a single syringe with 20 ml of 0.9% saline and pushed together all at once.
This patient’s ECG is most consistent with an atypical AVNRT. She was given adenosine 12 mg IV by fast push at bedside while obtaining a 12-lead rhythm strip. She converted to sinus rhythm, and her dyspnea and chest discomfort resolved, as did the sagging ST-segment in the inferior leads. An ECG obtained after treatment is shown in Figure 5. Long-term prevention options include treatment with beta-blockers and possibly additional AV nodal agents versus electrophysiology study/RF ablation.