QA of the Month: November 2013
Congratulations Dr. Nolan Caldwell!
91 year-old male with h/o dementia, depression, HTN presenting as a trauma 97 with full spinal precautions after suffering several un-witnessed falls earlier in the day (eventually found by neighbors). Patient with no recollection of events. No current complaints, including CP/SOB/lightheadedness/weakness/numbness/incontinence/bloody stools.
|HR 100||RR 18||BP 124/71||SpO2 97% RA||T 98.1||Blood Glucose: 152|
Primary survey normal. Secondary survey relevant for 5 cm chin laceration, R eyebrow abrasion, avulsed tooth #10.
Guaiac negative. Hgb 16.4, EKG with NSR at 97, normal intervals, ST elevation in V2 but no other contiguous leads and no reciprocal changes. No previous EKG on file. iSTAT troponin 0.42.
FAST was performed - unremarkable for intra-peritoneal free fluid or pericardial effusion. A focused bedside echo was then performed by Dr. Caldwell with the following images (first is an apical four-chamber view and the second is a para-sternal short axis view):
That’s right, the arrows are pointing to bowing of the inter-ventricular septum toward the LV, interpreted as “RV>LV, bowing of the right ventricle”. On the para-sternal short axis, we see the “D-sign”; moreover, the normally concentric left ventricle looks like the letter “D” because of the RV strain pushing the septum paradoxically.
This caused the patient to obtain a CT angio chest showing bilateral main pulmonary artery emboli and “right ventricle enlargement and bowing of the septum compatible with RV strain”. Heparin was ordered and subsequently discontinued after CT head showed trace blood in the lateral ventricle with no acute ICH. Patient was admitted to medicine with cardiology and neurosurgery consults. tPA was withheld because of hemodynamic stability and questionable head bleed. Elevated troponin was surmised to be secondary to the massive pulmonary embolism, and patient was not taken to the cath lab.
Goal-directed learning points for bedside echocardiography were covered in last months QA of the month. However, here are tips to improve image acquisition:
- Turn patient onto the left lateral decubitus position; this allows the heart to come forward into the chest wall ad improves parasternal and apical views.
- On your apical 4-chamber view, if you are not getting the apex of the heart and a symmetric view of the left and right sides of the heart, chances are you are medial to the apex. Try sliding the probe laterally along the chest wall; you should get a beautiful 4-chamber view.
With regards to bedside echocardiography and pulmonary embolism, here are a few pointers:
- Normal RV:LV ratio is <0.7:1. RV dilatation is defined as RV:LV ratio greater than 1:1
- Other signs of RV dysfunction include tricuspid regurgitation, paradoxical septal motion (as seen with Dr. Caldwell’s “D” sign on the PSS and bowing of the septum on the A4), and McConnell’s sign (RV free wall hypokinesis with apical sparing, also known as the “apical wink”, and named after Stanford cardiologist Michael McConnell).
- Smaller PE’s may not show any R-sided heart abnormalities on the bedside echo, and that’s widely accepted. If you see obvious RV changes with a congruent clinical scenario, the patient likely has a massive or sub-massive PE and a decision to provide thrombolytic therapy should be entertained at this point.
- There are many other causes of RV dilatation, including pulmonary hypertension, chronic COPD, cor pulmonale, dilated cardiomyopathy, among others. It’s integral to take the entire clinical scenario into account before attributing RV dilatation to PE.
- A recent study from Annals of Emergency Medicine (article in press) by Dresden et al. showed that in patients with moderate to high probability of PE, RV dilatation of >1:1 as seen by emergency physicians on bedside echo had a specificity of 98% and a sensitivity of 50%. In other words, get out there and scan some hearts; you never know what you’ll find!
- Josh Ennis, Mansour Jammal, and Laleh Gharahbagian