This 45-year-old woman with a medical history which includes medication-controlled essential hypertension, stage 2 chronic kidney disease, type 2 diabetes mellitus, and a 1 pack-per-day cigarette smoking habit presented to the emergency department with <60 minutes of 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 am she was awoken from sleep very dyspneic, with moderate chest “discomfort” over her left chest and radiated to her back, and was unchanged by position or respirations. She denied any other symptoms such as fever, cough, nausea/vomiting, numbness, or abdominal pain.

Initial vital signs were blood pressure 138/76 mmHg, pulse 87 bpm, respiratory rate 26, SpO2 was 95%. She was afebrile. Her physical exam was unremarkable; there were 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 did improve her chest discomfort. Her chest radiograph was clear. Her presenting electrocardiogram is shown in below.


The patient’s history, presenting complaint, and initial evaluation helps us narrow our differential diagnosis (see Table 1). Waking from sleep with dyspnea, referred to as paroxysmal nocturnal dyspnea, is most commonly associated with congestive heart failure. However, in this patient there is little other evidence of this. She has no history of previous heart disease, her lungs are clear both on exam and imaging which would be the case if there was cardiogenic pulmonary edema, and she does not have lower extremity edema that should develop with vascular congestion. Pneumonia, likewise, is unlikely in a patient without signs/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 Well’s Criteria, and meets all 8 criteria of the PERC Rule for Pulmonary Embolism (see Table 2), which gives her <2% risk of pulmonary embolism.

Differential of nocturnal dyspnea
Pulmonary embolism
Obstructive airway disease
Congestive heart failure
Myocardial ischemia
Gastroesophageal reflux disease
Sleep apnea
Panic attack/Anxiety

PERC Rule for Pulmonary Embolism
Age <50
Heart rate <100 bpm
SpO2 >94%
No prior history of DVT/PE
No hemoptysis
No exogenous estrogen
No clinic signs suggesting DVT
Gastroesophageal reflux disease
Reference: Kline et al. J Thromb Haemost 2006;6:772

The emergency physicians attending to this patient considered myocardial ischemia as 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 is also down-sloping ST-segments in multiple leads. These findings would be consistent with subendocardial ischemia.

For comparison, the figure below shows an ECG obtained 6 months prior 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. However, it is always important to fully evaluate all the parts of and ECG. Take a close look at lead II, shown in close-up below in Figure 3. One striking feature is the lack of P-waves preceding the QRS complex. Following the QRS complex however, there 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. From the AV node, the ventricular depolarization and repolarization conducts normally, and can be seen in the normally aligned QRS complex and T-wave. This is classic for an AVNRT rhythm.


Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common form of paroxysmal supraventricular tachycardia (PSVT). Palpitations and lightheadedness are frequent presenting complaints, but in patients with coronary artery disease or structural heart disease chest pain and dyspnea can occur. There is often no specific inciting event