Strain analysis for the identification of hypertensive cardiac end-organ damage in the emergency department

An estimated 26% of ED patients will have an elevated BP with half of these patients having a BP > 160/100 [1, 2]. Distinguishing hypertensive urgency and emergency is challenging as both conditions involve marked elevation of blood pressure (BP, i.e., systolic BP ≥ 180 and/or diastolic BP ≥ 120). Hypertensive emergency is a life-threatening state with evidence of end-organ damage, as opposed to hypertensive urgency, and requires rapid reduction in BP [3, 4]. The heart is the most common organ affected, accounting for 52% of hypertensive emergencies [3]. Strain echocardiography is a relatively new way to measure left ventricular (LV) mechanical function. Unlike conventional 2D echocardiography which relies on visual estimation to assess cardiac contractility, strain echocardiography utilizes computerized speckle-tracking to measure actual tissue deformation of the myocardium. Strain can be measured in the longitudinal, radial and circumferential planes of the left ventricle (LV). Peak longitudinal strain (PLS) is a measurement of the overall longitudinal deformation of the left ventricle from diastole to systole. PLS can be measured from clips captured from standard apical views of the heart [5]. Longitudinal strain has been shown to be more sensitive at identifying hypertensive changes in LV mechanical function than ejection fraction (EF), fractional shortening, mitral E/A ratio, and tissue Doppler mitral annular velocity [5, 6]. Normal strain measurements range from − 15 to − 22% [7]. We present a case where emergency physician (EP) performed point-of-care PLS analysis is used to monitor improvement in LV mechanical function over time for a patient with hypertensive cardiac emergency.

A 41-year-old woman with past medical history of peripartum cardiomyopathy, mitral regurgitation, and hypertension was referred to the emergency department (ED) due to severely elevated blood pressure. Patient reports a one week history of dyspnea, mild chest pressure with exertion, and stated that she had similar symptoms before with her pulmonary embolism more than 10 years ago. Three days prior to the onset of her symptoms, the patient had stopped taking her prescribed hydrochlorothiazide (HCTZ) due to increased urinary frequency, but maintained compliance with losartan. Vital signs at presentation were temperature 37.2 °C, BP 218/150, heart rate 121, respiratory rate 16, and pulse oximetry 100% on room air. On exam, the patient was well-appearing and in no apparent distress. The patient’s lungs were clear to auscultation and she had no S3, jugular vein distention, or lower extremity edema. The remainder of the physical exam was unremarkable. Further testing included labs, an electrocardiogram (EKG), a chest radiograph, and bedside echocardiogram (BSE) performed by ultrasound trained EPs. An apical four-chamber was obtained to calculate peak longitudinal strain (PLS) using only this view. Two initial troponin levels were mildly elevated at 0.08 µg/L, but down-trended thereafter to 0.05 µg/L. There was mild cardiomegaly and increased pulmonary vasculature on chest x-ray, and a new left bundle branch block (LBBB) on EKG. At the time of the initial BSE, BP was 252/163 [mean arterial pressure (MAP) = 170)] and PLS was − 3.5% (Fig. 1). The EF was not calculated, but estimated to be mildly reduced. Six hours later, the BP was 171/94 (MAP = 123) and a repeat BSE was performed and PLS was recalculated. Between the first and second BSE, the patient had received a total of 60 mg IV labetalol, 25 mg PO HCTZ, 40 mg IV furosemide, and was on a nitroglycerine drip at 40 mcg/min. The MAP had been reduced by 27% and the PLS improved to − 14% (Fig. 2). Repeat EKG after the IV medications continued to show a persistent LBBB. The patient was admitted to the cardiac intensive care unit for hypertensive emergency and acute coronary syndrome rule-out. Follow-up outpatient notes indicate that the patient was discharged home the following day and did not get re-admitted to the hospital within 30 days.

Figure 1 reflects the patient before hypertension treatment and Fig. 2 reflects the patient after treatment. Both Figs. 1 and 2 are quad displays of an apical 4-chamber image demonstrating peak longitudinal strain (PLS) of the left ventricle (white arrow). In each figure, top left image (A) is a 2D depiction showing the color coding for each left ventricle (LV) segment and the PLS in the 4-chamber view; bottom left image (B) displays the peak systolic strain for each of the six LV segments in the 4-chamber view; top right image (C) displays strain (y-axis) plotted over time (x-axis) for each of the six color-coded LV segments in a linear graphical display. The white dotted line shows the average of the six strain curves; bottom right image (D) shows the anatomical M-mode display depicting instantaneous strain for the 4-chamber plane with each LV segment color-coded on the y-axis, where the red color represents more negative strain.