Fix the Rate First ?

CASE PRESENTATION:
Providers respond to a 68 yo female with a sudden onset of paroxysmal nocturnal dyspnea. The patient reports slight dyspnea on exertion for the past few weeks and endorses a mild, non productive cough. The patient speaks in 2-3 word sentences and appears in severe respiratory distress. The patient denies chest discomfort, nausea, vomiting or fever. The patient is in severe respiratory distress and is profoundly diaphoretic. Another paramedic provider onscene diagnoses SVT and readies adenosine for administration.

EXAM:

BP:     220/120
P:        168
R:        40
Spo2:  88%


12 LEAD ECG:

12 LEAD ECG ANALYSIS:

There is a supraventricular tachycardia. P waves are difficult to discern but the QRS complexes are narrow and occur at regular intervals. Diffuse repolarization abnormalities in the form of biphasic T waves are present in the inferior leads. There is no obvious ST segment elevation.

TREATMENT:

High flow oxygen is administered and an intravenous line is inserted. The senior paramedic recommends against adenosine administration. A total of 1.2 mg of nitroglycerin is administered sublingually. 324 mg of aspirin is administered. As the patient is prepared for transportation, CPAP is started at 10 cm H20. The patient experiences rapid improvement and the hypoxia resolves. A repeat ECG shows sinus rhythm with some lateral ST segment depression. Vital signs following CPAP and NTG are as follows: BP: 180/100, P: 110, R: 22, Sp02: 100%. A chest xray shows cardiomegaly and bilateral opacities consistent with pulmonary edema are present.

DISCUSSION:

Though fixing a fast heart rate can reduce ischemia, it is important to consider the underlying cause of a dysrhythmia. Administration of adenosine could convert this ECG but the SVT is very likely due to the catecholamine surge that accompanies acute pulmonary edema. A reduction in cardiac output and afterload results in improved oxygenation, reduced work of breathing, and resolution of the supraventricular tachycardia. Following a hospitalization for acute heart failure, the patient was discharged to home on an aggressive medical regimen targeted at maintaining an acceptable blood pressure. The prehospital application of CPAP is consistently linked to a reduced endotracheal intubation and improved mortality.

Sinus Tachycardia ?

Providers arrive at the scene of a 5 year old male with chest palpitations. The patient is alert and appears anxious. He is mildly short of breath. Symptoms occured spontaneously and have been present for the last hour. The patient is experiencing associaed nausea. The patient denies LOC, diaphoresis, or recent illness.

BP: 90/palp
P:   200/min, rapid
R:  22 (hyperventilating)
Sp02: Poor waveform

12 Lead ECG

ECG Interpretation and Case Discussion

This patient is clearly experiencing some type of supraventricular tachycardia. Though the QRS complexes are narrow and occur at regular intervals, there is no evidence of an aberrantly (non sinus) conducted p-wave. A close examination of the precordial leads reveals an extra, retrograde "blip" in V1 and V2. Retrograde P's make the diagnosis of a junctional tachycardia more likely. This patient is symptomatic but relatively stable. Appropriate treatment options include:
1) Vagal maneuvers
2) Adenosine 0.1 mg/kg IVP, may repeat at 0.2 mg/kg
3) Synchronized cardioversion 0.5-1 joule/kg

This patient was treated successfully with a rapid administration of adenosine. After a period of observation in the ED that included repeat ECGs, serum electrolytes, and cardiac monitoring, the patient was discharged.

ECG Interpretation

Junctional (supraventricular tachycardia), rate of 200/minute

For rapid, regular, narrow complex rhythms, consider the following:

• Atrial flutter
• SVT
• Sinus tachycardia

A Serial Case

An elderly male patient is transported to the emergency department following a syncopal episode. The patient reported feeling lightheaded, and experienced two witnessed syncopal episodes lasting for several minutes. Symptoms were made worse when standing up. The patient denied chest pain and reported some mild dyspnea. The patient had been in his usual state of health. The patient's medical history is significant for a tibial fracture several months prior.

Vitals:

Afebrile

BP: 72/P

P: 100

R: 24

Sp02: 92%, poor waveform, on NRB

Physical exam:

Pt is diaphoretic and alert.

Lungs are clear bilaterally.

The patient's abdomen is soft and non tender.
No evidence of lower extremity edema.

(Prehospital) 12 lead ECG:

Upon arrival at the hospital, large bore IV access was secured. A FAST (Focused Assessment with Sonography for Trauma) exam revealed no obvious free fluid and no obvious pericardial effusion. The abdominal aorta appeared grossly normal. The patient remained alert and responded to a bolus of IV crystalloid. A repeat ECG was obtained following another pre-syncopal event in the emergency department.

12 Lead ECG Interpretation and Discussion

On the repeat ECG, a sinus rhythm is present. The electrical axis is physiologic. Artifact interferes with the tracing in the inferior limb leads. ST segment elevation is present in aVR, V1, and V2. The ST segments appear horizontal in shape. That particular morphology is concerning for ischemia. While some mild ST segment depression is present in lead I, there are no clear cut reciprocal changes. The evolving changes suggest a septal wall myocardial infarction.

Final Interpretation

Sinus tachycardia, septal ST segment elevation myocardial infarction

(WRONG!)

Case Conclusion

The patient was transported emergently to the cardiac catheterization lab. The patient's coronary arteries were CLEAN and without evidence of disease. An emergent echocardiogram showed a severely dilated right ventricle with concurrent diastolic dysfunction. The clean coronary arteries and echocardiograpghic findings combined point to a massive pulmonary embolism as the cause of the patient's symptoms. Another subtle clue to this diagnosis was the hypoxia that persisted with high flow oxygen administration.

Though not all that elevates is a STEMI, field providers should nevertheless focus on identifying worrisome ST segment changes. The patient's initial ECG was somewhat non-specific. Though close inspection can reveal some slight ST segment elevation of less than 1mm in aVR and V1, it certainly did not meet standardized criteria for STEMI. The second ECG, however, represents a clear-cut evolution. ST segments have become more pronounced (elevated) in the septal leads. The increase in elevation combined with the horizontal plateau of the ST segments in leads V1-V2 suggest an evolving myocardial infarction- or an alternative diagnosis.

The patient presented with a syncopal episode and profound hypotension. Any number of emergent medical conditions can present with those complaints. Pulmonary embolism, internal bleeding, and aortic dissection must be considered in the initial assessment of the hypotensive patient. Unfortunately, there are no "classic" electrocardiographic findings associated with a large PE. That said, the following features can be seen in the setting of a pulmonary embolism.

PULMONARY EMBOLISM ECG FINDINGS

• Sinus tachycardia
• Right bundle branch block or incomplete right bundle branch block
• Deep S wave in lead I, Q wave in lead III, and an interveted T wave in lead III (S1, Q3, T3)
• T wave inversions
• Right axis deviation
• ST segment deviation (depression and elevation)

Sinus tachycardia and right bundle branch block may suggest "heart strain." These are electrical manifestations caused by the right ventricle that is pumping against a greatly increased pulmonary resistance.