A 60-year-old female without prior cardiac history presented to our ED with chest pain. The pain started 4 days prior to her coming to the ED. She described the pain as fairly severe and left-sided. The pain radiated to her left arm, and she had not had pain this severe before. She called EMS on the day she presented to the ED because the pain had acutely worsened, and she became short of breath.
When EMS arrived to her house, she was found to be quite tachycardic with a rate in the 180s and hypotensive with a SBP in the 70s. Prehospital ECG looked like SVT and the medics gave the patient 6 mg adenosine without change and then 12 mg adenosine. The HR dropped to 140s after that and BP improved to 100s systolic.
Initial ED VS: HR 148, BP 108/66, RR 27, 98% on RA, afebrile
The differential was broad and the ED team initiated a work up with ECG, labs, CXR, and a bedside cardiac ultrasound while making a decision about what to do about the tachycardia.
BSUS done upon arrival showed an unexpected finding:
This is a subcostal 4-chamber view of the heart. Notice the pericardial effusion. The heart is also going very fast. It looks like the left ventricular walls are almost touching each other during systole which is consistent with possible hypovolemia. The ED team questioned whether or not this was tamponade given the clinical presentation. Initial concern was for a possible myocardial free wall rupture with the history of 4 days of chest pain.
The effusion does not look huge on the ultrasound, but even a small effusion, if it accumulates rapidly, can cause tamponade physiology. Chronic effusions can also cause tamponade with certain triggers including hypovolemia and paroxysmal tachycardia. Echocardiography can aid in the diagnosis of tamponade, but it is also a clinical diagnosis.
What are the ultrasonographic findings of cardiac tamponade?
Ultrasonographic B-mode findings of tamponade:
- Right atrial collapse during ventricular systole
- Right ventricular diastolic collapse
- Left ventricular collapse
- Heart swinging in the pericardium
- Dilated IVC without respiratory variation
- Septal shift towards the left ventricle during inspiration
With this image, it is hard to know how to manage the patient. Was the patient dependent on the tachycardic rate, and would dropping that also drop the BP? Was the patient initially hypotensive because of the rate, and would fixing the rate improve her hemodynamics?
The team decided to give fluid boluses and obtain more information after seeing the effusion. Here is the ECG that was obtained in the ED:
The rate is about 158 in this ECG. There is a narrow QRS. P-waves were not appreciated. The patient appears to be in atrial fibrillation. There was no clear ST elevation or depression and no q-waves present. This made a free wall rupture from MI less likely because there was no clear pattern of injury.
Before much IVF had been infused, the ED team did a more complete ultrasound. Here is the IVC:
You can see that it has respiratory variation and is not very dilated. This makes the diagnosis of tamponade less likely.
Here is an apical 4-chamber view:
You can see that the effusion is much less impressive in this view and the heart does not seem to be swinging in the pericardium.
The troponin came back at 0.128. This value was thought to be too low to be from a free wall rupture and was felt to be more consistent with demand ischemia.
The case was discussed with cardiology from the ED and cardiology wanted to obtain a formal echo. She was taken from the ED up to the MICU while awaiting the echo. Her BP remained above 100 systolic and the HR remained in the 140s. Here is what the IVC looked like after a few liters of NS:
You can see that it is now dilated with no respiratory variation.
The formal echo was not felt to be consistent with tamponade. Cardiology recommended starting an infusion of Diltiazem. By the next morning, the patient had converted to sinus rhythm with a normal rate. The patient was found to have a lung mass, which on biopsy was non-small cell lung carcinoma. She was initially doing better and was transferred out of the MICU, but then developed respiratory failure and a severe lactic acidosis thought to be secondary to septic shock from pneumonia in the setting of metastatic lung disease. The shock was refractory to treatment and the patient succumbed to her illness on hospital day 7. No autopsy was performed.
Bottom Line: Diagnosis of tamponade is not as straight forward at it might seem. Cardiac ultrasound can aid in the diagnosis, but must be used in the context of the clinical picture.