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Introduction
An 84-year-old man with known history of Stage 31 chronic kidney disease (CKD) and a baseline creatinine (Cr) of 1.5 mg/dl was admitted with shortness of breath (SOB), cough productive of white sputum and bilateral lower extremity edema. Two months before the admission the patient had a new procedure for aortic stenosis (AS) called a “valved conduit” going from his Left Ventricle (LV) to his aorta. He also had a history of hypertension, Type II Diabetes, CABG, Sick Sinus Syndrome, was s/p pacer and atrial fibrillation treated with Amiodarone.
On admission he presented with a blood pressure (BP) of 134/83, with respirations of 22 breaths per minute and a temperature of 36.1°C. Physical examination was notable for bilateral rales and lower extremity edema extending to the mid thighs. Lab results on admission included: WBC 13.5k cells/ml, creatinine 1.6 mg/dl and a BNP of 831 pg/ml. Chest X-ray showed increasing congestion changes from a recent previous study.
The patient was diagnosed with congestive heart failure and pulmonary congestion and was diuresed for 5 days without improvement.
Transthoracic echocardiography showed preserved ejection fraction (EF) and no problems with the newly installed valve conduit. The echocardiogram did demonstrate a patent foramen ovale (PFO) with left-to-right shunting and moderate to severe mitral regurgitation. NICOM was ordered to assess the patient’s intravascular fluid status. A passive leg raise (PLR) test was conducted and the results are summarized in Table 1.
1Moderate reduction in glomerular filtration rate (GFR) (30-59 mL/min/1.73 m2)

Table 1. PLR test results
The hemodynamic responses to PLR were positive, with a 23% increase in SVI (Figure 1), suggesting that the patient was fluid responsive. This result, of course did not coincide with the initial clinical working assumption of pulmonary congestion due to heart failure. In case of acute decompensated heart failure we expect a negative PLR test (see next page). However, the clinical picture was so compelling in support of a diagnosis of heart failure it was decided to perform another test to confirm or refute the conclusion derived from the PLR test. Therefore, a right heart catheterization was performed, which showed only mildly elevated wedge pressure and central venous pressure. These results support the NICOM PLR test that the patient is not suffering from heart failure.

Figure 1. stroke volume index following PLR
Impact On Clinical Management
The diagnosis of heart failure as the cause of the patient’s symptoms was rejected on the basis of the PLR and finally the right heart catheterization which lead to further investigation. A diagnosis of Amiodarone induced lung toxicity (most probably interstitial pneumonitis (IP) mimicking heart failure) was ultimately arrived at. Amiodarone treatment was stopped and a trial of corticosteroids was initiated, with significant improvement in the patient’s clinical picture.
Discussion
In the case presented, the patient was diagnosed with heart failure and pulmonary congestion based on the clinical presentation as well as imaging findings and the BNP levels. However, the fact that the patient didn’t improve after 5 days of diuresis encouraged the clinicians to look for another cause for the patient’s symptoms. As the patient’s initial working diagnosis was heart failure he was expected to have a negative PLR test. This is because in a patient with heart failure and a fluid overloaded state, the patient is operating on the flat portion of the Frank-Starling curve and additional volume recruited from the lower extremity venous system during a PLR is ineffective in increasing cardiac output. However, the patient exhibited a positive PLR, suggesting that he was fluid responsive and most likely not fluid overloaded.
PLR is a bedside maneuver that mobilizes the equivalent of approximately 250 ml of blood sequestered in the calf veins back to the heart. It is quick, safe and reversible. It provides information that very quickly helps to guide therapy. A positive PLR test (increase of ≥10% in SVI or CI) implies that there is sufficient cardiac reserve to pump the increased preload forward; in other words, a positive test indicates that the patient is on the ascending limb of the Frank-Starling curve.
For this patient, the PLR challenge helped to rule out a diagnosis of undertreated heart failure and pulmonary congestion for which there was very compelling clinical evidence. Actually, it was so compelling that additional supportive test was required by the clinicians before they felt they could change the patient’s management. This patient probably presented with a combination of both heart failure and Amiodarone induced lung toxicity. As the heart failure was treated, the symptoms of the lung toxicity were unmasked. The NICOM revealed that the underlying etiology for the dyspnea was no longer heart failure. Indeed, results of the right heart catheterization supported the simple bedside PLR challenge. This compelled the clinicians to undertake additional investigations which arrived at a new diagnosis. Clinical management was changed according to the new diagnosis and the patient improved.
Cheetah Medical wishes to thank Dr. Michael Brumback, MD for contributing the case
