It is estimated that 5% of patients with heart failure (HF) will progress to end-stage disease refractory to medical therapy and might require prolonged hospitalisation with inotropic support. We present the case of a patient with end-stage HF who was admitted with cardiogenic shock. During his hospitalisation, he required prolonged intravenous vasopressor therapy due to refractory hypotension. He did not qualify for heart transplantation or left ventricular-assist device strategies. Midodrine was started as a last resort attempt to wean off vasopressors. After 5 days of therapy, the patient was weaned entirely off vasopressors and was discharged home for hospice care. By the time of discharge, he was tolerating low-dose carvedilol along with midodrine. We propose midodrine as a reasonable alternative for patients with end-stage HF with reduced ejection fraction and refractory hypotension, who are dependent on intravenous vasoactive drugs and are not candidates for advanced HF therapies.

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A 45-year-old man with no systemic illnesses was found by his neighbor lying unconscious and with recurrent involuntary movements, reason for which he was endotracheally intubated and brought to our institution. Upon evaluation, we found an acutely ill-looking man, with decreased level of consciousness (Glasgow coma scale 11) off sedation, on mechanical ventilator support with adequate oxygenation. Physical exam was remarkable for fever, scalp lacerations with old sutures, generalized rigidity and diaphoresis, with clear lungs and no abnormal heart sounds. Laboratory results showed no leukocytosis or leukopenia, but normocytic normochromic anemia; there were no electrolyte disturbances and negative toxicology screen. Head CT without intravenous contrast showed no findings suggesting bleeding, ischemia or space occupying lesions but reported parenchymal disease, and old skull and maxillofacial fractures. Patient's neighbor referred that he was hospitalized 2 weeks ago at another institution with seizures that apparently caused him a 12-feet fall at work. Reevaluation showed a positive Kernig and Brudzinski signs. Lumbar puncture was performed. The opening pressure was markedly elevated (> 30 cm H 2 O) and cerebrospinal fluid (CSF) analysis was consistent with fungal infection. He was promptly started in empiric antifungal therapy with amphotericin and flucytosine while waiting for CSF culture results. Meanwhile, serial lumbar punctures were performed to decrease intracranial pressure. HIV tests were sent and resulted positive. CSF culture showed Cryptococcus neoformans, and CSF cryptococcal antigen titer was positive in 1:32 dilutions. Diagnosis of severe cryptococcal meningoencephalitis was confirmed. Cryptococcus neoformans is one of the leading opportunistic infections seen in untreated patients with HIV and is uniformly fatal within approximately 2 weeks if untreated. Our patient's prognosis was poor since admission; however, we just cannot stop thinking that maybe his prognosis could have been different if meningitis was even suspected and confirmed during patient's previous hospitalization for seizures 2 weeks ago.