Acute myocarditis generally shows varied clinical courses. Some cases develop cardiogenic shock induced by low output syndrome or life-threatening arrhythmia, such as ventricular tachycardia, ventricular fibrillation, asystole, and complete atrioventricular block, resulting in a poor prognosis. Recently, mechanical cardiopulmonary support systems (intraaortic balloon pumping, IABP; percutaneous cardiopulmonary support, PCPS; and ventricular assistant device, VAS) have been proposed as lifesaving treatments of acute fulminant myocarditis.
It is important to use PCPS referring to standardized indicators of circulatory failure and cardiac function. Especially, it is necessary to adjust an appropriate flow support level to promote recovery from environmental insufficiency and to prevent complications associated with PCPS, such as leg ischemia and multiple organ failure.

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This study was designed to investigate the effects of low-dose α-human atrial natriuretic peptide (α-hANP) on hemodynamics, urination and cerebral blood flow in ten patients after cardiac surgery. We assessed cerebral blood flow in the carotid siphon by means of transcranial Doppler sonography (TCD). We measured the peak systolic blood flow velocity (Vs), the end-diastolic blood flow velocity (Ved) and the mean blood flow velocity (Vm), and calculated the pulsatility index (PI) in the left carotid siphon using 2MHz transcranial Doppler ultrasound system. After baseline measurement, the α-hANP loading dosage was increased from 0.025 to 0.05μg·kg^-1·min^-1 every 60 minutes. Hemodynamics, urine volume, Vs, Ved, Vm and PI were measured at each last point. There were no significant changes in hemodynamics (heart rate, mean arterial pressure, central venous pressure, pulmonary artery wedge pressure, cardiac index, systemic vascular resistance index), Vs, Ved, Vm and PI. Urine volume significantly increased from the baseline (129±82ml·hr^-1) to 238±101ml·hr^-1 at the infusion rate of 0.05μg·kg^-1·min^-1. In conclusion, we demonstrated that low-dose α-hANP led to an increase of urination without changes of hemodynamics and cerebral blood flow in the patients after cardiac surgery.

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Both the production of nitric oxide (NO) through the inducible NO synthase (iNOS) pathway and the production of carbon monoxide (CO) through the inducible heme oxygenase (HO-1) pathway have been implicated as major contributors in the process of endotoxin shock. It is proposed that there is a reciprocal action between NO and CO, because both of them bind to heme moiety of guanylyl cyclase to produce cGMP during endotoxin shock. Using a rat endotoxin shock model, the effects of iNOS inhibitor (L-canavanine, CAN) and HO inhibitor (zinc protoporphyrin, ZPP) on the blood concentration of nitrosyl hemoglobin (NO-Hb) and carboxy-hemoglobin (CO-Hb) were studied. CAN attenuated the endotoxin-induced hypotension and only inhibited the increase in NO-Hb. ZPP also abrogated hypotension, but only inhibited the increase in CO-Hb. These data suggest that both inhibition of iNOS pathway and HO-1 pathway are useful for the treatment of hypotension. However, both pathways work on the vascular smooth muscle independently during endotoxin shock.

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We report a case of acquired coagulopathy due to endogenous inhibitors of factor VIII in the clinical course of cervical spinal cord injury. The patient was a 44-year-old man who sustained dislocation and fracture of the 4th cervical vertebra and underwent surgical fixation of the fractured spine. He was transferred to the intensive care unit (ICU) for respiratory management. On the ICU day 21, gross hematuria with an abrupt onset was followed by anuria, which required continuous hemodiafiltration for a week to restore diuresis with persisted hematuria. The assay detected inhibitors of factor VIII (6 Bethesda unit·ml^-1) to counteract factor VIII activity (less than 1.6%) which might result in persistent bleeding from the urinary tract. Bleeding was controlled completely on the ICU day 69 not solely with infusion of factor VIII concentrates but with combination of plasma exchange (from the ICU day 48, 4 times in total) and administration of prednisolone and cyclophosphamide. In summary, we described an unusual case of acquired coagulopathy resulting from endogenous inhibitors of factor VIII with unknown etiology. Although bleeding symptoms were limited to hematuria in this case, our prompt diagnosis should have been followed also promptly by plasma exchange combined with immunosuppressant and steroid therapy to minimize bleeding sequelae.

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A 6-year-old girl was admitted to the pediatric ward because of her behavioral abnormalities such as “diurnal sleepnessnocturnal irritation” rhythm, choreic movements and generalized muscle rigidity. Several medicines including diazepam and phenytoin were given for her convulsive attack. On the 11th hospital day, she was transferred to the ICU, because of progressive disturbance of consciousness, hyperthermia (42°C), hyper- “creatinine phosphkinase (CPK)” -emia and anuria. The patient was suspected as neuroleptic malignant syndrome.
Forced cooling, administration of dantrolene, continuous hemofiltration, and plasma exchange were performed. On the 15th day, the CPK concentration decreased from 312, 480U·l^-1 on the day of ICU admission to 38, 880U·l^-1. Continuous propofol infusion (3mg·kg·hr^-1) was started on the 15th day to facilitate mechanical ventilation and finally stopped on the 27th day becaus of the suspicion that propofol was attributable to lasting hyper- “CPK” -emia in the range between 4, 000 and 8, 000U·l^-1. The CPK concentrations remarkably decreased after the cessation of propofol to less than 1, 000U·l^-1 on the 30th day and kept decreasing. We suggest that propofol should not be used for sedation in children even within the recommended dosage because of the possible contribution of rhabdomyolysis.

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To treat type-A acute aortic dissection (Stanford system), the ascending aorta was replaced with a graft using retrograde cerebral perfusion with deep-hypothermic circulatory arrest. This patient later developed rhabdomyolysis. The patient was a 55 year-old man who was 169cm tall, weighed 120kg and body mass index (BMI) 42.0kg·m^-2. Red urine was first detected during surgery and persisted after that point. At two days after surgery, the levels of creatine phosphokinase (CPK) and creatinine were 22, 320U·l^-1 and 2.2mg·dl^-1, respectively. The levels of serum and urinary myoglobin were 43, 000 and 850, 000ng·ml^-1, respectively. Due to massive infusion, transfusion, diuretic administration and active body position change, renal insufficiency improved and the patient was discharged from the ICU 18 days after the surgery. However, the patient died of sepsis on postoperative day 40. There is a risk of rhabdomyolysis following extracorporeal circulation or circulatory arrest in morbidly obese patients. We suppose the physical pressure imposed by the patient's body weight may be a worsening factor. Active body position change during prolonged bed rest would be effective.

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We experienced a case of acute myocardial infarction with cardiogenic shock caused by a total occlusion of left main trunk. The case was a 51-year-old man.
Percutaneous transluminal coronary angioplasty (PTCA) was accomplished under the support of intraaortic balloon pumping (IABP) and percutaneous cardiopulmonary support (PCPS), but yet he had severe heart failure and could not be weaned off the PCPS. We decided to adapt left ventricular assist device (LVAD) to him on the 8th hospital day in order to maintain hemodynamics and the patient was finally weaned from the device on the 18th hospital day although he suffered renal failure. This case shows that the mechanical cardiac assist devices offer the opportunity for recovering the damaged heart and provide time to choose another option such as transplantation.

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