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Extracorporeal life support (ECLS) was used to treat three patients with near-fatal status asthmaticus who did not respond to aggressive medical therapies and mechanical ventilation under controlled permissive hypercapnia. ECLS was instituted in patient 1 because Paco 2 was excessively high and pH was excessively low, in patient 2 because hypoxemia and shock were not responsive to treatment, and in patient 3 because of sustained severe hypotension. ECLS supported adequate gas exchange until pulmonary function improved, diminishing the need for mechanical ventilation and preventing pulmonary complications. Pulmonary dysfunction improved markedly after only 21 to 86 hours of ECLS. Aggressive medical treatments were continued during ECLS. Our findings indicate that ECLS is a useful method for preventing death in patients with near-fatal status asthmaticus.

Three months after implantation of endocardial pacing leads in 10 mongrel dogs, the tensile forces needed to remove 5 tined type and 5 screw-in type leads were compared experimentally. Mean maximum tensile force was 291 +/- 174 g with the screw-in type and 1174 +/- 369 g with the tined type (p < 0.01). Histopathologically, no changes suggesting any myocardial damage due to lead extraction were recognized in cases where screw-in type leads were used. These results support the clinical feasibility of safe and easy manual retraction of infected pacing leads of the screw-in type.

We investigated the factors associated with cerebral dysfunction in patients undergoing extracorporeal life support (ECLS) following conventional advanced cardiac life support (ACLS). The subjects were 9 patients in whom ECLS was started following ACLS because of intractable cardiac arrest. We investigated whether the irreversibility of cerebral dysfunction during ECLS was related to the cardiopulmonary resuscitation (CPR) time, arterial pH and blood gases, hemoglobin concentration (Hb), peak arterial pressure (PAP) before the start of ECLS and total doses of epinephrine and sodium bicarbonate administered during CPR. Two of the 3 patients who recovered consciousness were weaned from ECLS and survived, while all 6 patients who did not recover from coma were not weaned and died. There was no difference in the CPR time, Hb and PAP before the start of ECLS along with total doses of epinephrine and sodium bicarbonate administered during CPR between the patients who recovered consciousness and those who did not. In addition, there was no difference in arterial pH and blood gases except the arterial oxygen tension (PaO2) between the groups. The PaO2 values before the start of ECLS in the patients who remained in coma ranged from 34 to 58 mmHg, whereas those in the patients who recovered consciousness ranged from 132 to 442 mmHg. The PaO2 values before the start of ECLS in the patients who remained in coma were less than 60 mmHg, whereas those in the patients who recovered consciousness were over 60 mmHg. The present study suggests that hypoxemia during CPR may play a major role in severe cerebral dysfunction in patients undergoing ECLS and PaO2 during CPR.

We examined the incidence of nasel MRSA carriers who were admitted to the ICU during about 6 months. The nasal organisms of 25 medical staffs were also examined during this period. Of 83 patients, 8 (9.6%) had MRSA. Of 25 medical staffs, 1 (4%) had MRSA. Patients who had MRSA were isolated to the single room and their nasal cavities were wiped with 10% popidon iodine solution.The routine inspection of nasal organisms in critically-ill patients on admission to the ICU and in staffs was useful to determine MRSA carrier and to prevent the prevalence of MRSA infections.Three adult patients received intravenous infusion of 0.5g vancomycin for 90 minutes twice a day. This prescription was sufficient to maintain the minimum inhibitory concentration of vancomycin for adult patients without impairing renal function.

The purpose of this study was to determine the mortality rate in 527 critically ill patients with multiple organ failure (MOF), treated in our ICU between August, 1986 and January, 1992, and to compare it with the results obtained in a group of patients studied who had been treated between October, 1978 and July, 1986. The relationship between the mortality rate and each type of organ failure and the extent of organ system involvement was also investigated. The overall mortality rate was 25%, and the rate increased with the number of failed organs. Sepsis and disseminated intravascular coagulation were closely associated with the development of MOF. The mortality rate of patients with the failure of two organs in the present study was significantly lower than that found in those in the previous study. Although artificial organ mechanical life support technology other than that for patients with renal failure is still unsatisfactory, these results suggest that the prognosis of patients with MOF is improving.

From November 1987 to February 1992, extracorporeal life support (ECLS) was used for four patients undergoing prolonged external cardiac massage following cardiac arrest. Their underlying diseases consisted of acute pulmonary embolism, pulmonary arterial thrombosis due to protein C deficiency, acute inferior left ventricular infarction accompanied by right ventricular infarction and thoracic contusion. After the initiation of ECLS, hemodynamic variables and metabolic acidosis improved in all of the cases. The case of pulmonary embolism and the case of acute myocardial infarction were successfully weaned from ECLS without complications. They were later discharged ambulatory from the hospital. The patient with pulmonary arterial thrombosis, who was comatose, became alert after the initiation of ECLS. However the patient finally died due to diffuse and massive pulmonary arterial thrombosis, which was probably related to protein C deficiency. The patient with thoracic contusion was also comatose before ECLS. He did not recover from the coma and died soon after the disconnection of ECLS. The latter two cases were suspected to have had irreversible organ failures not responsive to mechanical support of both circulation and respiration. We conclude that ECLS is a very useful method for patients requiring prolonged cardiac massage following cardiac arrest.

To examine the sites of release and removal of plasma atrial natriuretic polypeptide plasma levels in the femoral vein, right atrium, pulmonary artery, pulmonary capillary bed, left atrium and aortic root were measured in 11 control subjects and 22 patients with mitral stenosis. Mean plasma natriuretic polypeptide levels in the femoral vein, right atrium, pulmonary artery, pulmonary capillary bed, left atrium and aortic root were, respectively, 64 +/- 29, 124 +/- 72, 103 +/- 44, 83 +/- 30, 106 +/- 46 and 101 +/- 35 pg/ml in the control subjects and 321 +/- 170, 500 +/- 234, 458 +/- 266, 356 +/- 209, 434 +/- 222 and 432 +/- 217 pg/ml in the patients with mitral stenosis. In both the control subjects and the patients with mitral stenosis, there was a significant increase between the femoral vein and the right atrium and between the pulmonary capillary bed and the left atrium and a significant decrease between the pulmonary artery and the pulmonary capillary bed. Blood samples were also taken simultaneously from the pulmonary vein and the pulmonary capillary bed, as well as from the pulmonary artery and the left atrium, in 25 patients (11 control subjects, 5 patients with mitral stenosis and 9 patients with atrial septal defect). There was no difference in plasma atrial natriuretic polypeptide levels between the pulmonary capillary bed and the pulmonary vein in these 25 patients. It is concluded that atrial natriuretic polypeptide 1) is released into the left as well as the right atrium, and 2) is removed by the lungs.

In Japan, liver transplantation from brain dead donors has not yet started. The authors present the first report of a clinical experience with a child with fulminant hepatic failure in whom the combined treatment of plasma exchange and continuous hemodiafiltration using a high-performance polymethylmethacrylate membrane was used successfully to sustain life for a period of as long as 54 days before liver transplantation from a living donor could be performed. The combination of plasma exchange and continuous hemodiafiltration appeared to maintain blood coagulation and level of consciousness effectively. Although the combined use of plasma exchange and continuous hemodiafiltration is still unsatisfactory as an artificial liver support, the authors suggest that this technique may be useful to support the life of a child who awaits liver transplantation.

We report an interesting case of aortic regurgitation. Phonocardiographically, the shape of the diastolic musical murmur in this case changed in each cardiac cycle despite being in sinus rhythm, in the same posture and in the same breathing phase. Experimentally, we were able to obtain a similar noise pattern using an artificial respirator and a hemispherical silicone membrane. We concluded that the irregular and chaotic change in the shape of the diastolic musical murmur in the present case occurred due to irregular swaying of the non-coronary cusp under the influence of the Venturi effect owing to a regurgitant jet stream. (Jpn Circ J 1996; 60: 993 - 997)

We report a case of sudden death due to variant angina during Holter electrocardiogram (ECG) monitoring. The patient, a 60-year-old man, had been aware of chest discomfort lasting less than one minute at midnight 2 days earlier. Because variant angina or arrhythmia was suspected, Holter ECG monitoring was performed. The patient spent a whole day without a recurrence of chest pain before going to bed, but at midnight he developed sudden chest pain, and died immediately after taking a sublingual tablet of isosorbide-dinitrite. Analysis of the Holter ECG revealed ventricular fibrillation after several ventricular premature beats following ST-segment elevation in both the CM5 and NASA leads. This case shows that sudden death from variant angina may occur within a few days after the first onset, and also highlights whether priority should be given to making a definite diagnosis or giving treatment when variant angina is strongly suspected.

We examined histologically whether the severity of arterial stretch injury is related to the degree of subsequent intimal hyperplasia. In six male New Zealand White rabbits, the common carotid artery was hyperextended with a 3F Fogarty balloon catheter. Two weeks later, no proliferative change was evident in the intima in the most hyperextended portion. Paradoxically, however, intimal hyperplasia due to smooth muscle cell proliferation was observed in the moderately extended portions. The intimal hyperplasia appeared to be exacerbated where the arterial stretching was more severe. It is concluded that the severity of arterial stretch injury is closely related to the intimal proliferation of smooth muscle cells.

To assess whether the impairment of neuronal norepinephrine (NE) uptake is involved in the increased NE release observed in the failing heart, we examined the cardiac extractions of NE and epinephrine (E) and their correlation with left ventricular function in 16 patients with anterior transmural old myocardial infarction (OMI) and 18 patients with dilated cardiomyopathy (DCM). The plasma NE and E levels were both increased in OMI and DCM, particularly in the coronary sinus, as compared with those in 16 control subjects (Control). The cardiac NE and E extractions were significantly reduced in OMI (P < 0.001) and in DCM (P < 0.001) as compared with those in the Control (NE: -38 +/- 36% in OMI, -33 +/- 28% in DCM, and 14 +/- 18% in Control; E: 30 +/- 12% in OMI, 32 +/- 17% in DCM, and 54 +/- 8% in Control). However, there was no reduction in the NE and E extraction in the leg in OMI and DCM. Cardiac NE and E extractions both showed significant correlation with the left ventricular ejection fraction (r = 0.685, P < 0.001 and r = 0.609, P < 0.001, respectively). We conclude that, in patients with heart failure, NE release from the heart is increased partially due to the reduction of the cardiac neuronal uptake of NE which is proportional to the severity of left ventricular dysfunction.

There has been no report regarding therapy of extracorporeal life support (ECLS) that showed stunned myocardium echocardiographically and electrocardiographically in patients with acute myocardial infarction. ECLS was performed in eight patients with cardiogenic shock or arrest unresponsive to catecholamines and intra-aortic balloon pumping following myocardial infarction; these patients required prolonged external cardiac massage. After the initiation of ECLS, both blood pressure and metabolic acidosis improved in all patients. Four of eight patients were weaned from ECLS after a mean of 69.3 h, which was far longer than previously reported in patients with ischemic heart disease. Three of these patients survived, and cardiac function recovered to NYHA class II in two of the survivors and class III in the other. The other five patients did not recover from coma during ECLS and died. A marked improvement of ventricular wall motion was seen in two survivors with the disappearance of pathologic Q waves after the initiation of ECLS. No occlusion of the coronary arteries or bypass grafts was observed in any of the survivors. These findings suggested the existence of stunned myocardium with myocardial reperfusion. The recovery of stunned myocardium may be delayed for days or even weeks, hence the extended period of ECLS therapy was theoretically justifiable. We conclude that long-term ECLS is a useful therapeutic method for patients with severe cardiogenic shock that is related to stunned myocardium.

We evaluated the incidence and severity of serum magnesium (Mg) abnormality along with other electrolyte and acid-base disturbances before and during the course of orthotopic liver transplantation (OLT) in pediatric patients. Serum Mg, Na, K, ionized Ca, pH, and blood gas measurements were performed before and hourly during the course of OLT. Hypomagnesemia was frequently observed in children undergoing OLT. Of a total of 30 recipients, 27 (90%) had hypomagnesemia before surgery; the mean serum Mg value at this time was 0.77±0.15 mmol/L. In most of the recipients, the serum Mg value showed a gradual decrease during the course of OLT until magnesium sulfate supplements were administered. On the other hand, the serum Na, K, and ionized Ca levels and acid-base balance were normal before the beginning of surgery. However, hypernatremia, hypokalemia, a decrease in ionized Ca, and metabolic acidosis were commonly observed during the course of OLT. We conclude that electrolyte abnormalities, including hypomagnesemia and metabolic acidosis, commonly develop in children during the course of OLT. The frequent assessment of electrolytes, pH and blood gases is essential for the correction of these abnormalities during the course of OLT.

The use of propranolol is generally contraindicated in patients with congestive heart failure. However, we successfully used a continuous high-dose infusion of propranolol, in combination with the use of extracorporeal life support (ECLS) and intra-aortic balloon pumping (IABP), to treat refractory life-threatening ventricular tachycardia in a patient with postoperative congestive heart failure. The early combined use of ECLS and IABP before irreversible myocardial damage contributed to the successful outcome.

We examined the relationship between cardiac output (CO) and mixed venous-arterialPCO

BACKGROUND This study was designed to examine the hemodynamic, renal, and hormonal effects of brain natriuretic peptide (BNP) infusion in patients with congestive heart failure (CHF) and in control subjects. METHODS AND RESULTS We infused synthetic human BNP at a rate of 0.1 micrograms/kg/min. BNP infusion decreased pulmonary capillary wedge pressure (control, from 5 +/- 1 to 2 +/- 1 mm Hg, p less than 0.01; CHF, from 21 +/- 3 to 14 +/- 4 mm Hg, p less than 0.05) and systemic vascular resistance (control, from 1,264 +/- 75 to 934 +/- 52 dyne.sec.cm-5; CHF, from 2,485 +/- 379 to 1,771 +/- 195 dyne.sec.cm-5; p less than 0.01, respectively) and increased stroke volume index (control, from 49.9 +/- 2.7 to 51.5 +/- 2.3 ml/m2, p = NS; CHF, from 25.6 +/- 3.8 to 32.0 +/- 3.9 ml/m2, p less than 0.01). BNP infusion significantly increased urine volume (control, from 2.3 +/- 0.7 to 7.5 +/- 1.9 ml/min; CHF, from 0.8 +/- 0.2 to 5.3 +/- 1.0 ml/min; p less than 0.01, respectively), excretion of sodium (control, from 79.2 +/- 21.6 to 332.8 +/- 70.9 microEq/min; CHF, from 77.4 +/- 20.8 to 753.5 +/- 108.0 microEq/min; p less than 0.01, respectively), and excretion of chloride (control, from 72.5 +/- 18.4 to 256.0 +/- 43.3 microEq/min; CHF, from 74.0 +/- 19.6 to 708.8 +/- 103.3 microEq/min; p less than 0.01, respectively). Urinary excretion of sodium and of chloride in response to BNP infusion was higher in patients with CHF than in control subjects (p less than 0.01, respectively). BNP infusion increased the levels of plasma atrial natriuretic peptide (control, from 65 +/- 11 to 84 +/- 14 pg/ml; CHF, from 262 +/- 65 to 301 +/- 62 pg/ml; p less than 0.05, respectively) and decreased plasma aldosterone concentrations in both groups (control, from 43.3 +/- 12.1 to 27.3 +/- 7.1 pg/ml; CHF, from 91.1 +/- 34.3 to 66.3 +/- 27.2 pg/ml; p less than 0.05, respectively). CONCLUSIONS We conclude that BNP infusion improves left ventricular function in patients with CHF by vasodilation and prominent natriuretic action.

To examine whether atrial natriuretic polypeptide (ANP) is released from the left ventricle in patients with dilated cardiomyopathy (DCM) we measured plasma ANP level in the aortic root (Ao), the anterior interventricular vein (AIV), the great cardiac vein (GCV), and the coronary sinus (CS) in 11 patients with DCM and 18 control subjects. Plasma ANP levels in Ao, AIV, GCV, and CS were 454 +/- 360, 915 +/- 584, 1,308 +/- 926, and 1,884 +/- 1,194 pg/ml, respectively, in the patients with DCM and 108 +/- 42, 127 +/- 55, 461 +/- 224, and 682 +/- 341 pg/ml, respectively, in the control subjects. There was no significant difference in the plasma ANP levels between Ao and AIV in the control subjects. On the contrary, there was a significant (P less than 0.001) step-up in plasma ANP levels between Ao and AIV in patients with DCM. Thus, the difference in ANP levels between Ao and AIV was significantly increased in patients with DCM as compared with the control subjects (461 +/- 248 vs. 19 +/- 59 pg/ml, P less than 0.001). The difference in ANP levels between Ao and CS was also significantly increased in patients with DCM as compared with the control subjects (1,429 +/- 890 vs. 577 +/- 318 pg/ml, P less than 0.001). We conclude that ANP is released in increased amounts into the circulation from the left ventricle as well as from the heart as a whole in patients with DCM.

Effects of cardiac pacing on secretion of atrial natriuretic polypeptide (ANP) were examined in 20 patients during cardiac catheterization under control conditions. The plasma ANP concentration in the coronary sinus (900 +/- 115 pg/ml) was significantly higher than those in the aorta (147 +/- 19 pg/ml) and the femoral vein (105 +/- 15 pg/ml) (p less than 0.001). The plasma ANP concentration was also significantly higher in the aorta than in the femoral vein (p less than 0.001). Its concentration at all three sites significantly increased during cardiac pacing (from 900 +/- 115 to 1461 +/- 218, from 147 +/- 19 to 250 +/- 36, and from 105 +/- 15 to 150 +/- 24 pg/ml, respectively). However, mean right atrial pressure and mean pulmonary capillary wedge pressure showed no significant changes between control conditions and during pacing (5 +/- 1 vs 6 +/- 1, and 8 +/- 1 vs 8 +/- 1 mmHg). Furthermore, there was no significant correlation between ANP secretion and the pressure in both atria. Thus, cardiac pacing can release ANP from the heart without increasing atrial pressure.