Acute High-Output Heart Failure with Pulmonary Hypertension and Severe Liver Injury Caused by Amlodipine Poisoning: A Case Report.

Acute high-output heart failure (HOHF) with pulmonary hypertension and liver injury caused by amlodipine poisoning is very rare. We report a 52-year-old woman who suffered from severe shock after an overdose of amlodipine. Hemodynamic monitoring showed that while her left ventricular systolic function and cardiac output were elevated, her systemic vascular resistance decreased significantly. At the same time, the size of her right heart, her central venous pressure, and the oxygen saturation of her central venous circulation all increased abnormally. The patient's circulatory function and right ventricular dysfunction gradually improved after large doses of vasopressors and detoxification measures. However, her bilirubin and transaminase levels increased significantly on hospital day 6, with a CT scan showing patchy, low-density areas in her liver along with ascites. After liver protective treatment and plasma exchange, the patient's liver function gradually recovered. A CT scan 4 months later showed all her liver abnormalities, including ascites, had resolved. The common etiologies of HOHF were excluded in this case, and significantly reduced systemic vascular resistance caused by amlodipine overdose was thought to be the primary pathophysiological basis of HOHF. The significant increase in venous return and pulmonary blood flow is considered to be the main mechanism of right ventricular dysfunction and pulmonary hypertension. Hypoxic hepatitis caused by a combination of hepatic congestion and distributive shock may be the most important factors causing liver injury in this patient. Whether amlodipine has other mechanisms leading to HOHF and pulmonary hypertension needs to be further studied. Considering the significant increase of right heart preload, aggressive fluid resuscitation should be done very cautiously in patients with HOHF and shock secondary to amlodipine overdose.

Transition from Intravenous Epoprostenol to Treprostinil Due to Intolerable Side Effects in Patients With Pulmonary Arterial Hypertension.

Intravenous epoprostenol improves exercise capacity and survival in patients with pulmonary arterial hypertension (PAH); however, it has side effects. Reviewing the side effects associated with epoprostenol and treprostinil is essential for improving the long-term treatment strategies for PAH. This retrospective review included patients with PAH who transitioned from intravenous epoprostenol to intravenous treprostinil owing to intolerable side effects, including high cardiac output symptoms, ascites, and thrombocytopenia. Of the 85 patients who received epoprostenol at our hospital between 2013 and 2021, 16 (11 women), with a median age of 33 (range 26 to 40) years (including 12 with idiopathic PAH, 3 with hereditary PAH, and 1 with connective tissue disease pulmonary hypertension), had to switch from intravenous epoprostenol to treprostinil owing to the side effects. After transitioning, epoprostenol-associated intolerable side effects, such as high cardiac output symptoms, ascites, and thrombocytopenia, were ameliorated. In conclusion, for patients with PAH who have intolerable side effects from epoprostenol and have difficulty in continuing treatment, switching from epoprostenol to treprostinil may be an option. Switching treatment leads to better adherence and improved long-term prostacyclin therapy.

A porcine model of hyperdynamic endotoxemia: pattern of respiratory, macrocirculatory, and regional blood flow changes.

Systemic sepsis and multiple organ failure are frequent and often fatal complications after major surgery and trauma. In contrast to the biphasic hemodynamic pattern characteristically seen in patients, most experimental animal models have failed to reproduce the early, hyperdynamic phase of sepsis and endotoxemia. We have designed a standardized model of endotoxemia, which is elicited by continuous IV infusion of Salmonella abortus equi endotoxin in anesthetized juvenile pigs (age 8-12 weeks). The plasma concentration of endotoxin--as evaluated by the LAL test--is significantly elevated within less than half an hour following the start of endotoxin administration and is accompanied by a rapid fall of the leukocyte count in peripheral blood. High cardiac output and low systemic vascular resistance reflect a hypercirculatory state, during which left ventricular filling pressure is maintained by carefully monitored volume substitution (6% dextran 60). In the present investigation, different doses of endotoxin (3.8 and 11.4 micrograms/kg, respectively) were infused intravenously and investigated for their effect on respiratory, macrocirculatory, and regional blood flow alterations. The development of respiratory deterioration depended on the duration of endotoxin administration and on the height of endotoxin plasma levels. In all animals, a high cardiac output was maintained throughout 3.5 hr of endotoxemia. Regional blood flow to the myocardium and liver increased, whereas blood flow to the gastrointestinal tract and the spleen was compromised without difference between both groups. It is concluded that this porcine model should provide the potential for further insight into the early pathophysiological mechanisms involved in the development of multiple organ failure in patients with sepsis and endotoxemia.