Case Details

A 67-year-old man presented to the Emergency Department with left-sided weakness and slurred speech. A CT head showed no acute abnormalities, however, a CT angiogram showed stenosis of the M2 segment of the right MCA without occlusion. Acute dyspnea prompted a CT scan of his chest to assess for possible pulmonary embolism (PE). No PE was noted, but a large left ventricular thrombus was identified. He was outside the window for tPA and thrombectomy was deferred given the lack of large vessel occlusion. His wife reported that he does not go to the doctor, and was unaware of any past medical history. He smokes 1.5 packs per day.

Bedside echocardiography was performed which confirmed the presence of a large left ventricular thrombus (Figure 1). Left ventricular ejection fraction (LVEF) was estimated to be <20% (Figure 2). Upon further questioning, he stated that he had been feeling weak and short of breath for about 1 week prior to his acute stroke symptoms.

He was admitted to the neuro ICU and cardiology was consulted for his heart failure with reduced ejection fraction (HFrEF). This presented challenges in management, as his M2 stenosis would benefit from an increase in blood pressure to ensure adequate perfusion of his brain; however, his HFrEF would benefit from reduced blood pressure to decrease afterload and decrease the work of the left ventricle. A balance was struck, using diuresis to reduce LV afterload with close monitoring of his neurological status. He was placed on BiPAP to reduce his work of breathing, eventually transitioning to high flow nasal cannula and then to regular nasal cannula. Systemic anticoagulation with a continuous infusion of unfractionated heparin was started to prevent further exacerbation of his LV thrombus or clotting in his cerebral arteries.

His neurological condition improved to the point where he could be transferred out of the ICU. He was eventually transferred from the stroke neurology service to the hospital medicine service with cardiology following. He was deemed a poor candidate for advanced heart failure therapies based on his neurological prognosis.

Using Bedside Echocardiography to Estimate LV Function

Bedside echocardiography was performed in this case by the Neuro ICU Nurse Practitioner prior to the availability of a formal echocardiography study. There are a number of ways to use echocardiography to assess LVEF; however, three methods are most applicable to bedside echocardiography performed by the intensivist. Fractional shortening (FS), E-point Septal Separation (EPSS), and “eyeballing” are all methods that can be used to estimate LVEF at the bedside in the absence of a formal echocardiogram.

FS is calculated by measuring the percentage change in left ventricular diastolic diameter during systole.1 The diameter of the LV at end-systole (LVESD) and again at end-diastole (LVEDD) are measured in the parasternal long axis (PLAX) view in M-mode, placing the M-mode cursor immediately distal to the tips of the mitral valve (Figure 2). FS can then be calculated from these measurements using the following formula:

FS (%) = (LVEDD - LVESD / LVEDD) * 100

FS is inaccurate if LV geometry is abnormal, such as in the presence of regional wall motion abnormalities. However, under the proper conditions, LVEF roughly correlates to 2x the FS. In this case, FS was calculated to be 9%. This suggests approximated EF of 18%.

EPSS is the distance between the tip of the anterior leaflet of the mitral valve and the interventricular septum at its closest point during diastole. Similar to FS, EPSS is measured using M-Mode in the PLAX view; in this case the cursor is placed on the tip on the anterior leaflet of the mitral valve (Figure 3). EPSS in this patient was 17.2mm. Normal LV function is associated with an EPSS of < 7mm, 7-13mm represents mild-moderate dysfunction (LVEF 30-50%), while > 13mm represents severe dysfunction (EF<30%).

Finally, “eyeballing,” i.e. visual estimation for LV function, has been shown to correlate well with LVEF. Multiple studies have shown that non-cardiologists, with proper training and experience, can visually estimate LVEF.2-4 This is a simpler and less time-consuming method, though requires an experienced provider. To estimate the EF with this method, observe the inward movement and thickening of the myocardium, the movement of the mitral valve, and the geometry of the ventricle (Figures 4 & 5). As you may be able to tell, this is essentially a subjective assessment of the objective data we measured in both FS and EPSS. With experience, the intensivist can develop good skill for estimating the EF based on a subjective assessment. Table 1 compares visual assessment to approximate EF calculations.

Conclusion

Estimation of the EF can be an essential skill for the neurointensivist. In this particular case, it is likely that the low EF was a significant contributor to the patient’s acute ischemic stroke as the severely depressed EF led to inadequate perfusion through the stenosed MCA. Additionally, in low flow states such as caused by severe HFrEF, thrombi can form in the left ventricle. If left untreated or unrecognized, these thrombi can embolize to the cerebral circulation, leading to acute ischemic stroke. In the case of this patient, it was not determined if embolization had occurred, however the fact that no obstruction was identified on CT angiogram leads us to suspect that his stroke was secondary to poor perfusion. Knowing his EF and being able to serially assess it and the response to therapy without requiring multiple formal echocardiograms was essential in the management of this patient. It allowed us to balance diuresis and afterload reduction with the needs of his cerebral perfusion and assess the results in real-time.

Figures

Figure 2: Parasternal Long-Axis view of the heart with Fractional Shortening (FS) calculations

Figure 3: Parasternal Long-Axis view of the heart with E-Point Septal Separation (EPSS) calculations

Table 1

Source: 123Sonography.com, https://123sonography.com/ebook/left-ventricular-function