Protamine sulfate, a strong polycationic polypeptide, combined with acidic heparin to form a neutral salt, eliminates the anticoagulating properties of heparin. Heparin reversal with protamine after cardiopulmonary bypass may complicate with adverse hemodynamic effects including systemic hypotension, decreased cardiac output, changes in systemic and pulmonary vascular resistances, anaphylaxis and noncardiogenic pulmonary edema. We recently observed a case of severe pulmonary vasoconstriction with right ventricular failure after protamine administration in 37-year-old woman with mitral stenosis who underwent mitral valvuloplasty. After uneventful termination of cardiopulmonary bypass, administration of protamine was associated with sudden elevation of pulmonary arterial pressure with profound right ventricular distension and systemic hypotension by which heparin-protamine reaction is suspected. After intravenous epinephrine infusion and cardiac massage, these changes were reversed. Although the mechanism of this protamine-heparin induced response is unclear, complement activation and thromboxane release may play a role in the development of pulmonary vasoconstriction.
Adult ; Anaphylaxis ; Arterial Pressure ; Cardiac Output ; Cardiopulmonary Bypass ; Complement Activation ; Epinephrine ; Female ; Heart Massage ; Heart* ; Hemodynamics ; Heparin* ; Humans ; Hypertension, Pulmonary* ; Hypotension ; Mitral Valve Stenosis ; Protamines ; Pulmonary Edema ; Thoracic Surgery* ; Vasoconstriction

BACKGROUND: We examined the ability of thiopental known to have protective effect on brain to prevent brain damage resulting from cerebral ischemia due to global imbalance in cerebral metabolic rate for oxygen and cerebral blood flow during rewarming period in cardiopulmonary bypass. METHODS: Jugular venous oxygen saturation(SjO2) was used as a reflection of cerebral oxygen balance. Thiopental 20 mg/kg(thiopental 10 mg/kg bolus and 10 mg/kg continuous infusion) was received during rewarming from hypothermic cardiopulmonary bypass of 27~30.5degrees C to 36degrees C and SjO2 compared with control group. RESULTS: In 8 patients of the 25 control group(32%) and 7 patients of the 24 thiopental group(29.2%), SjO2 were < or =50% with no difference between groups. Artery-jugular vein oxygen content differences (C(a-j)O2) and O2 extraction ratios increased significantly in SjO2 < or =50% patients suggesting increased oxygen consumption. Awake time prolonged significantly with thiopental. CONCLUSIONS: Thiopental(20 mg/kg) administration during rewarming in cardiopulmonary bypass for cerebral protection is not recommended.
Anesthetics ; Brain ; Brain Ischemia ; Cardiopulmonary Bypass* ; Heart ; Humans ; Oxygen Consumption ; Oxygen* ; Rewarming* ; Thiopental* ; Veins

BACKGROUND: Peripheral nerve injury may produce a syndrome consisting of spontaneous pain, allodynia and hyperpathia. In previous study, we examined the antiallodynic action produced by intrathecal (i.t.) cholinesterase inhibitors (ChEi) in a neuropathic pain rat model and the reversal of antiallodynic state by i.t. atropine, muscarinic antagonist, but not by nicotinic antagonist mecamylamine. The purpose of this study was to determine the selective antagonistic action of four subtypes of muscarinic receptor on antiallodynic state by i.t. ChEi in a rat model of neuropathic pain. METHODS: Sprague Dawley rats were prepared with tight ligation of left L5/L6 spinal nerves with 6-0 black silk and chronic lumbar intrathecal catheters. After obtaining the baseline hindpaw withdrawal scores, edrophonium (100 microgram) or neostigmine (10 microgram) was administered intrathecally. Tactile allodynia was measured using von Frey filaments and allodynic threshold was calculated by the up-down method. Allodynic changes were tested at 15, 30, 45, 60, 90, 120 and 180 minutes. To examine the reversal of antiallodynia and to compare the antagonizing action of antiallodynic state produced by i.t. administration of ChEi, non-selective muscarinic receptor antagonists atropine (10 microgram), M1 antagonist pirenzepine (3 microgram), M2 antagonist methoctramine (3 microgram), M3 antagonist 4-DAMP (3 microgram) and M4 antagonist tropicamide (3 microgram) were injected intrathecally respectively 5 minutes prior to the injection of edrophonium or neostigmine. RESULTS: Antiallodynia produced by i.t. edrophonium was reversed by pretreatment with i.t. methoctramine, 4-DAMP, tropicamide and pirenzepine (P<0.05). On the contrary, antiallodynic state made by i.t. neostigmine was not antagonized by methoctramine, 4-DAMP and tropicamide. M1 antagonist pirenzepine had a moderate, statistically significant (P<0.05) effect on reversal of increased allodynic threshold while atropine showed a complete antagonism. CONCLUSION: These experiments suggest that antialllodynic action of cholinesterase inhibitors is likely due to mediation of spinal muscarinic system and M1 receptor subtype is more likely involved in this mechanism.
Animals ; Atropine ; Catheters ; Cholinesterase Inhibitors ; Edrophonium ; Hyperalgesia ; Ligation ; Mecamylamine ; Models, Animal* ; Negotiating ; Neostigmine ; Neuralgia* ; Peripheral Nerve Injuries ; Pirenzepine ; Rats* ; Rats, Sprague-Dawley ; Receptors, Muscarinic* ; Silk ; Spinal Nerves ; Tropicamide

BACKGROUND: Pulmonary hypertension (PH) associated with end stage liver disease is rare but the risk of hemodynamic deterioration during liver transplantation may be high. This study was done to characterize the pulmonary hemodynamics during liver transplantation and to seek the relationship between pulmonary artery pressure (PAP) and other hemodynamic variables. METHODS: One hundred patients undergoing liver transplantation were chosen and we divided patients into normal and PH groups (mean pulmonary artery pressure [MPAP] > 25 mmHg). Hemodynamic data was collected throughout the surgery. Studied variables between groups were analyzed with an unpaired t-test. The relationship between MPAP and other hemodynamic variables was analyzed with a linear regression test. Survival analysis was performed by cumulative survival analysis (Logrank test). RESULTS: Incidence of PH during liver transplantation was 34%, and true PH (pulmonary vascular resistance index [PVRI] > 150 dyne.sec/cm5/m2, MPAP > 25 mmHg) was 7%. MPAP, systemic vascular resistance index, cardiac index, right ventricular ejection fraction, maximum elastance, central venous pressure (CVP), pulmonary artery occlusion pressure (PAOP), and right ventricular end-diastolic volume index were significantly higher in the PH group. In the PH group, right ventricular function curve was abnormal. MPAP correlated significantly with PAOP, and CVP (P < 0.01). One year survival rate showed no significant difference between groups (Logrank test P = 0.49). CONCLUSIONS: Episodes of increased pulmonary artery pressure during liver transplantation was not infrequent. PAP was more dependent on preloads. In patients with high PAP, RV diastolic dysfunction was usually observed. Early mortality rate after liver transplantation was not associated with PH.
Central Venous Pressure ; End Stage Liver Disease ; Hemodynamics ; Humans ; Hydrogen-Ion Concentration ; Hypertension, Pulmonary ; Incidence ; Linear Models ; Liver Transplantation* ; Liver* ; Mortality ; Pulmonary Artery* ; Stroke Volume ; Survival Rate ; Vascular Resistance ; Ventricular Function, Right

BACKGROUND: In some studies, 5 microgram/kg clonidine premedication was claimed to enhance the pressor effects of ephedrine in anesthetized patients. We studied hemodynamic responses to intravenous responses, themselves responses to intravenous ephedrine in patients who received clonidine 3 microgram/kg. METHODS: 40 ASA pysical status I or II patients were randomly assigned to either the clonidine group (n = 20), receiving oral clonidine 3 microgram/kg 90 min before general anesthesia, or the control group (n = 20), receiving no clonidine. Hemodynamic measurements were made at one-minute intervals for ten minutes after ephedrine 0.1 mg/kg was injected as a bolus. RESULTS: The magnitude of maximal systolic blood pressure increases in the clonidine group (13.2+/-9.3%) was no different in the control group (12.4+/-12.3%). There were no difference in the pressor effect and duration of response of ephedrine in both groups. CONCLUSIONS: The pressor effect of ephedrine is not enhanced in patients given 3 microgram/kg clonidine premedication during general anesthesia.
Anesthesia, General ; Blood Pressure ; Clonidine* ; Ephedrine* ; Hemodynamics ; Humans ; Premedication*

BACKGROUND: Mannitol is widely used in neurosurgical patients and may induce an increase in serum potassium concentration according to doses and administration rates with unknown mechanism. The treatment of hyperkalemia is aimed at eliminating the causes and includes calcium, sodium bicarbonate, glucose with insulin, loop diuretics and hyperventilation. This study was undertaken to observe the effects of hyperventilation on the serum potassium concentration following infusion of mannitol (2.0 gm/kg). METHODS: We studied 30 patients who were operated brain aneurysm clipping surgery and were divided into 3 groups (n=10). In control group, mild hypocapnia was maintained (PaCO2, 32 2 mmHg) before and after mannitol infusion. In group I, moderate hypocapnia was maintained (PaCO2, 27 2 mmHg) before and after mannitol infusion. In group II, mild hypocapnia (PaCO2, 32 2 mmHg) was maintained before 30 minutes of mannitol infusion and moderate hypocapnia (PaCO2, 27 2 mHg) after mannitol infusion. We started infusion of 20% mannitol with a dosage of 2.0 gm/kg, 15~20 min after cranium was opened. RESULTS: The changes of serum potassium were as follows (Mean SD mEq/l) (just before and 15min, 30min, 60min after mannitol infusion): 3.79 0.48, 4.66 0.60, 4.44 0.48, 4.13 0.40 (Control group), 3.62 0.18, 3.63 0.42, 4.14 0.51, 3.95 0.33 (Group I), 3.76 0.20, 3.91 0.15, 4.11 0.30, 4.04 0.23 (Group II). After 15 minutes of mannitol infusion, the serum potassium levels of group I and II were lower than that of control group (p<0.05) and there was no significant difference between group I and II. CONCLUSIONS: These results suggest that hyperventilation may blunt the increase in serum potassium concentration following rapid infusion of high dose mannitol.
Calcium ; Glucose ; Humans ; Hyperkalemia ; Hyperventilation* ; Hypocapnia ; Insulin ; Intracranial Aneurysm ; Mannitol* ; Potassium* ; Skull ; Sodium Bicarbonate ; Sodium Potassium Chloride Symporter Inhibitors

BACKGROUND: Fulminant hepatic failure is characterized by rapid progressive liver failure with the onset of encephalopathy within a few weeks of the appearance of jaundice. This illness is frequently complicated by hemodynamic instability, multiple organ dysfunction and intracranial hypertension associated with cerebral edema, which is the most common cause of death in this condition. We reviewed 8 cases of liver transplantation with fulminant hepatic failure with respect to anesthetic management and neurologic monitoring. METHODS: We analyzed anesthetic management, intracranial pressure (ICP), cerebral perfusion pressure (CPP), jugular venous oxygen saturation (SjvO2) and hemodynamics retrospectively during liver transplantation in 8 patients with fulminant hepatic failure. Intracranial hypertension was defined as an ICP >or= 20 mmHg for at least 5 minutes. The goal of management is to keep the CPP above 40 - 50 mmHg and ICP below 30 - 40 mmHg. There were 3 cases of hepatorenal syndrome and continous veno-venous hemodiafiltration (CVVHD) was used in 2 cases. RESULTS: All patients showed characteristic hyperdynamic circulation with severe vasodilation and vasopressive drugs were needed to maintain CPP. The episodes of intracranial hypertension occurred in all patients during transplantation. To decrease ICP, medical therapy with mannitol, furosemide and thiopental infusion were required. Intracranial hemorrhagic complications occurred in 3 cases. SjvO2 decreased transiently below 60% in 3 cases. However, it was improved with an increase of PaCO2 by hypoventilation and maintained above 60 - 80% in all cases. CONCLUSIONS: This data suggests that there is a risk of brain injury secondary to elevated ICP and low CPP during liver transplantation. ICP, CPP and SjvO2 monitoring in patients with fulminant hepatic failure can be useful for the prompt recognition of intracranial hypertension and for guiding therapy. However, correction of the coagulopathy before placement of the ICP tranducer must be performed to prevent hemorragic complications.
Anesthesia* ; Brain Edema ; Brain Injuries ; Cause of Death ; Furosemide ; Hemodiafiltration ; Hemodynamics ; Hepatorenal Syndrome ; Humans ; Hypoventilation ; Intracranial Hypertension ; Intracranial Pressure* ; Jaundice ; Liver Failure ; Liver Failure, Acute* ; Liver Transplantation* ; Liver* ; Mannitol ; Oxygen* ; Perfusion ; Retrospective Studies ; Thiopental ; Transplantation ; Vasodilation

Cardiac tamponade is a life-threatening predicament which demands early recognition and immediate treatment. We report a case of iatrogenic intraoperative cardiac tamponade during an orthotopic liver transplantation. A 55 year-old man was scheduled for an orthotopic liver transplantation due to hepatocellular carcinoma. During the anhepatic period, the patient's vital signs remained stable, but the central venous pressure and pulmonary artery diastolic pressure were increased. However, immediately after reperfusion, sudden hypotension and tachycardia developed. Fluid volume resuscitation and epinephrine injection led only to a transient improvement of the blood pressure. It took approximately 30 minutes to realize the possibility of the cause of hypotension might be due to cardiac tamponade rather than post-reperfusion syndrome. After an emergent transdiaphragmatic pericardiocentesis, we found that the cause of the cardiac tamponade was tearing of an epicardial coronary vein. Evacuation of a massive hematoma resulted in a rapid improvement in the patient's cardiovascular status. The patient has made an uneventful recovery.
Blood Pressure ; Carcinoma, Hepatocellular ; Cardiac Tamponade* ; Central Venous Pressure ; Coronary Vessels ; Epinephrine ; Hematoma ; Humans ; Hypotension ; Liver Transplantation* ; Liver* ; Middle Aged ; Pericardiocentesis ; Pulmonary Artery ; Reperfusion* ; Resuscitation ; Tachycardia ; Vital Signs

Hepatopulmonary syndrome is essentially the triad of liver disease, pulmonary vascular dilations and abnormal arterial oxygenation, which can result in severe hypoxia. We managed two cases of 9 and 49-year-old males for liver transplantation with hepatopulmonary syndrome. Preoperative evaluation showed decreased diffusion capacity of carbon monooxide and severe hypoxemia, while breathing room air (PaO2 < 60 mmHg) but they responded to oxygen therapy. The pulmonary vascular resistance was low, consistent with an intrapulmonary vascular shunt but the pulmonary artery pressure was normal, reflecting a high cardiac output. Intraoperative oxygenation was satisfactory (PaO2 of 100 - 200 mmHg) in spite of a high shunt fraction (Qs/Qt 18.5 +/- 9.2%). This means that the impairment in gas exchange is not the result of a true shunt, suggesting the presence of a functional shunt, which is characterized by diffusion-perfusion impairment. The intraoperative course was uneventful in the two patients and they are in a successful postoperative course. In case 1, the hypoxemia was resolved promptly, but in case 2, it was persistent for sixteen months after transplantation. The hypoxemia itself in hepatopulmonary syndrome is not regarded as a contraindication to liver transplantation. (Korean J Anesthesiol 2001; 40: 677 ~ 683)
Anesthesia* ; Anoxia ; Carbon ; Cardiac Output, High ; Diffusion ; Hepatopulmonary Syndrome* ; Humans ; Liver Diseases ; Liver Transplantation* ; Liver* ; Male ; Middle Aged ; Oxygen ; Pulmonary Artery ; Respiration ; Vascular Resistance

Protein C exerts anticoagulant effects by inactivating factor Va and VIIIa and stimulating fibrinolysis. The homozygous protein C deficiency is extremely rare and often results in life threatening thrombosis and purpura fulminans with necrotic cutaneous lesions. A child with homozygous protein C deficiency was treated at 6 months by a living-related liver transplantaion. After induction of anesthesia, we started an FFP infusion for protein C replacement and a low molecular weight heparin continuous infusion to prevent thrombosis. A complete reconstitution of protein C activity and resolution of the thrombotic condition occured postoperatively. So we report this case with a brief review of the literature.
Anesthesia* ; Child ; Factor Va ; Fibrinolysis ; Heparin, Low-Molecular-Weight ; Humans ; Liver Transplantation* ; Liver* ; Protein C Deficiency* ; Protein C* ; Purpura Fulminans ; Thrombosis