Mild hypothermia during prolonged cardiopulmonary cerebral resuscitation increases conscious survival in dogs

OBJECTIVE: Therapeutic hypothermia during cardiac arrest and after restoration of spontaneous circulation enables intact survival after prolonged cardiopulmonary cerebral resuscitation (CPCR). The effect of cooling during CPCR is not known. We hypothesized that mild to moderate hypothermia during CPCR would increase the rate of neurologically intact survival after prolonged cardiac arrest in dogs. DESIGN: Randomized, controlled study using a clinically relevant cardiac arrest outcome model in dogs. SETTING: University research laboratory. SUBJECTS: Twenty-seven custom-bred hunting dogs (19-29 kg; three were excluded from outcome evaluation). INTERVENTIONS: Dogs were subjected to cardiac arrest no-flow of 3 mins, followed by 7 mins of basic life support and 10 mins of simulated unsuccessful advanced life support attempts. Another 20 mins of advanced life support continued with four treatments: In control group 1 (n = 7), CPCR was with normothermia; in group 2 (n = 6, 1 of 7 excluded), with moderate hypothermia via venovenous extracorporeal shunt cooling to tympanic temperature 27 degrees C; in group 3 (n = 6, 2 of 8 excluded), the same as group 2 but with mild hypothermia, that is, tympanic temperature 34 degrees C; and in group 4 (n = 5), with normothermic venovenous shunt. After 40 mins of ventricular fibrillation, reperfusion was with cardiopulmonary bypass for 4 hrs, including defibrillation to achieve spontaneous circulation. All dogs were maintained at mild hypothermia (tympanic temperature 34 degrees C) to 12 hrs. Intensive care was to 96 hrs. MEASUREMENTS AND MAIN RESULTS: Overall performance categories and neurologic deficit scores were assessed from 24 to 96 hrs. Regional and total brain histologic damage scores and extracerebral organ damage were assessed at 96 hrs.In normothermic groups 1 and 4, all 12 dogs achieved spontaneous circulation but remained comatose and (except one) died within 58 hrs with multiple organ failure. In hypothermia groups 2 and 3, all 12 dogs survived to 96 hrs without gross extracerebral organ damage (p < .0001). In group 2, all but one dog achieved overall performance category 1 (normal); four of six dogs had no neurologic deficit and normal brain histology. In group 3, all dogs achieved good functional outcome with normal or near-normal brain histology. Myocardial damage scores were worse in the normothermic groups compared with both hypothermic groups (p < .01). CONCLUSION: Mild or moderate hypothermia during prolonged CPCR in dogs preserves viability of extracerebral organs and improves outcome.     

Second report of an experimental study of cerebrocardiopulmonary resuscitation (CCPR) in dogs with reference to a new continuous brain cooling method, using a Resusci Pump TM-1

In our previous report, the effect of CCPR (an intracarotid hypothermic infusion combined with the existing CPR) has been described by the authors on dogs in which cardiac arrest had been induced by the inhalation of nitrous oxide. This report contains a new continuous brain cooling method, using a Resusci Pump TM-1 which has been newly devised by us and which has a carotid-carotid bypass in order to reduce oxygen consumption and cerebral metabolism while maintaining a continuous cerebral blood flow. Cardiac arrest was induced experimentally by electrical stimulation. The duration of cardiac arrest was 5 to 10 min duration. The continuous brain cooling was carried out during the period of 10-30 min. Through the experiment, we have investigated vital signs, acid base balance, cardiac output, carotid arterial blood flow, oxygen availability of the brain tissue, and regional cerebral blood flow in both groups of CPR and CCPR . As for the clinical signs and cardiac output, there were no significant differences between two groups. Oxygen availability of the brain tissue and regional blood flow were much more improved in CCPR group than in CPR group. The brain was selectively cooled by means of the continuous brain cooling. This resulted in the minimum effect on circulatory and respiratory system as compared to the effects caused by general hypothermia. Furthermore, the continuous brain cooling decreased cerebral metabolism and CMRO2, and prevented a progressive development of cerebral hypoxia Cerebral perfusion at a given constant pressure may protect the brain tissue from the disturbance of cerebral microcirculation. Therefore, we might expect the continuous brain cooling to have a beneficial effect on cerebral respiration, circulation and metabolism.     

Cardiovascular response to acute normovolemic hemodilution in patients with coronary artery diseases: Assessment with transesophageal echocardiography

OBJECTIVE: Preoperative acute normovolemic hemodilution induces an increase in circulatory output that is thought to be limited in patients with cardiac diseases. Using multiple-plane transesophageal echocardiography, we investigated the mechanisms of cardiovascular adaptation during acute normovolemic hemodilution in patients with severe coronary artery disease. DESIGN: Prospective case-control study. SETTING: Operating theater in a university hospital. PATIENTS: Consecutive patients treated with beta-blockers, scheduled to undergo coronary artery bypass (n = 50). INTERVENTIONS: After anesthesia induction, blood withdrawal and isovolemic exchange with iso-oncotic starch (1:1.15 ratio) to achieve a hematocrit value of 28%. MEASUREMENTS AND MAIN RESULTS: In addition to heart rate and intravascular pressures, echocardiographic recordings were obtained before and after acute normovolemic hemodilution to assess cardiac preload, afterload, and contractility. In a control group, not subjected to acute normovolemic hemodilution, hemodynamic variables remained stable during a 20-min anesthesia period.Following acute normovolemic hemodilution, increases in cardiac stroke volume (+28 +/- 4%; mean +/- sd) were correlated with increases in central venous pressure (+2.0 +/- 1.3 mm Hg; R = .56) and in left ventricular end-diastolic area (+18 +/- 5%, R = .39). The unchanged left ventricular end-systolic wall stress and preload-adjusted maximal power indicated that neither left ventricular afterload nor contractility was affected by acute normovolemic hemodilution. Diastolic left ventricular filling abnormalities (15 of 22 cases) improved in 11 patients and were stable in the remaining four patients. Despite reduction in systemic oxygen delivery (-20.5 +/- 7%, p < .05), there was no evidence for myocardial ischemia (electrocardiogram, left ventricular wall motion abnormalities). CONCLUSIONS: In anesthetized patients with coronary artery disease, moderate acute normovolemic hemodilution did not compromise left ventricular systolic and diastolic function. Lowering blood viscosity resulted in increased stroke volume that was mainly related to increased venous return and higher cardiac preload.     

Efficiency of using gelofusine and voluven in acute normovolemic hemodilution during cardiosurgical interventions

The aim of the study was to assess the use of gelofusine and voluven for acute normovolemic hemodilution at cardiac surgery under extracorporeal circulation (EC). Sixty-seven patients with coronary heart disease were examined. Heart rate, total peripheral vascular resistance, pulmonary pressure, pulmonary artery wedge pressure, oxygen delivery and consumption, central venous pressure, arteriovenous oxygen difference, oncotic pressure, and postoperative clinical course were studied. No significant group differences were found in indices, other than arteriovenous oxygen difference, after acute normovolemic hemodilution and in central venous pressure following 6 hours of EC termination. The administration of gelofusine caused a more steady-state oxygen-transport function of the circulatory system. The use of the agent for acute normovolemic hemodilution at cardiac surgery under EC is more economically justified than that of volumen.     

Cardiovascular adjustments and gas exchange during extreme hemodilution in humans

OBJECTIVE: To examine the cardiovascular adjustments and pattern of gas exchange that occur during hemodilution. DESIGN: Nonrandomized prospective study. SETTING: Operating room in a university hospital. PATIENTS: Seven patients undergoing elective aortocoronary artery bypass surgery. INTERVENTIONS: Before initiating cardiopulmonary bypass, the patients' hematocrit levels were decreased to approximately 15%. This hemodilution was done by removing a sufficient amount of autologous blood from the aortic cannula and replacing it with a sufficient amount of crystalloid solution. After the discontinuation of cardiopulmonary bypass, measurements were made at a hematocrit of approximately 15%. Then, after autologous blood infusion, measurements were made at a hematocrit of 20%, followed by more blood infusion to approximately 25% with repeat measurements. MEASUREMENTS AND MAIN RESULTS: The following measurements were made before hemodilution and then at all three levels of hemodilution: heart rate, mean arterial pressure (MAP), right atrial pressure, mean pulmonary artery pressure, pulmonary artery occlusion pressure, and cardiac output. From these measurements, the following derived variables were calculated: cardiac index, systemic vascular resistance, and pulmonary vascular resistance. From measurements of arterial oxygen content, mixed venous oxygen content, and cardiac output, intrapulmonary shunt (Qsp/Qt), oxygen uptake (VO2), oxygen extraction ratio, and oxygen delivery (DO2) were derived. The MAP was lowest (57 +/- 3 [SD] vs. 92 +/- 3 mm Hg) at the lowest hematocrit. The cardiac index was highest (4.0 +/- 0.3 vs. 2.3 +/- 0.6 L/min.m2) at the lowest hematocrit. DO2 was lowest at the lowest hematocrit but VO2 remained constant at all levels of hematocrit. The oxygen extraction ratio increased as hematocrit decreased. With progressive increases in hematocrit, DO2 increased and Qsp/Qt decreased. CONCLUSIONS: The data suggest that, during hemodilution, tissue autoregulation of VO2 and utilization are not impaired, but gas exchange function (Qsp/Qt) is impaired.     

Arterial blood gases during cardiac arrest: markers of blood flow in a canine model.

Measures of CO2 have been shown to correlate with coronary perfusion pressure and cardiac output during cardiac arrest. We evaluated arterial pH (pHa) relative to blood flow during cardiac arrest in a canine electromechanical dissociation (EMD) model of cardiac arrest using different resuscitation techniques. Following 15 min of cardiac arrest, 24 mongrel dogs received epinephrine with continued CPR or closed-chest cardiopulmonary bypass. Central arterial blood gases, end-tidal carbon dioxide (PetCO2), coronary perfusion pressure and cardiac output were measured. During CPR, prior to epinephrine or bypass, there was no correlation of pHa, PACO2 and PetCO2, with cardiac output or coronary perfusion pressure. Immediately after instituting the resuscitation techniques, both pHa and PaCO2 showed a significant correlation with cardiac output (pHa; R = -0.78, P less than 0.001 and PaCO2; R = 0.87, P less than 0.001) and with coronary perfusion pressure (pHa; R = -0.75, P less than 0.001 and PaCO2; R = 0.75, P less than 0.001). Eventual survivors (n = 15) had an early significant decrease in pHa, base excess and a significant increase in PaCO2 which was not present in non-survivors (n = 9). Neither pHa nor PaCO2 correlate with blood flow under low flow conditions of CPR. However, with effective circulatory assistance, pHa and PaCO2 reflect systemic blood flow and reperfusion washout.     

Intermittent autologous blood perfusion of the brain for prolongation of the total period of total circulatory occlusion during surface-induced hypothermia in dogs

(1) Eighteen anaesthetized dogs were subjected to deep hypothermia and total circulatory occlusion for 1 h. During the circulatory arrest one carotid artery was perfused with blood (2 ml/kg) from either the superior vena cava (12 dogs) or femoral artery (six dogs) every 1o min. (2) After the first 1o min of total circulatory occlusion the PO₂ dropped from 30 mm Hg to 14·4 mm Hg with the venous perfusion and from 380 mm Hg to 13·5 mm Hg with the arterial perfusion. A continued decline occurred during the arrest. (3) The PCO₂ immediately before perfusion had reached 14 mm Hg (venous group) and 9·4 mm Hg (arterial group) and gradually increased during the occlusion. During the circulatory arrest there was only a slight decline in pH from preocclusion values, ranging from 7·79 to 7·73 in both groups. (4) Cerebral angiography during perfusion demonstrated good filling of vessels supplying both cerebral hemispheres. Ten of the 12 dogs in the venous perfusion group were entirely normal postoperatively. The remaining two dogs and three of the six dogs in the arterial perfusion group developed a high stepping gait.     

Rapidly induced selective cerebral hypothermia using a cold carotid arterial flush during cardiac arrest in a dog model

PURPOSE: The present study was undertaken to determine whether flushing the carotid artery with normal saline at 4 degrees C (hypothermic carotid arterial flush, HCAF) during cardiac arrest can achieve selective cerebral hypothermia rapidly during cardiac arrest and improve cerebral outcome. METHODS: Ventricular fibrillation (VF) was induced in fourteen dogs and circulatory arrest was maintained for 9 min. Dogs were then resuscitated by cardiopulmonary resuscitation. The dogs were divided into two groups; a control group (n=7), which underwent precisely the same procedure as the experimental group but not HCAF, and an experimental group (HCAF group; n=7), which received HCAF from 8 min after the onset of VF. RESULTS: Two dogs in the control group and in the HCAF group died within 72 h after the recovery of spontaneous circulation (ROSC) due to extracerebral complications. The remaining 10 dogs survived to final evaluation at 72 h post-ROSC. In the HCAF group, tympanic temperature decreased from 37.7 degrees C (37.5-37.8) to 34 degrees C in 1 min (1-1.5) from the start of HCAF and was maintained below 34 degrees C until 6.5 min (3-12) after the start of HCAF, whereas oesophageal and rectal temperatures were maintained above 35 degrees C. Neurological deficit scores (0-100%) at 72 h post-ROSC were 42.4% (27.0-80.6) in the control group and 18.4% (14.0-36.0) in the HCAF group (p<0.05). CONCLUSION: HCAF induced selective cerebral hypothermia rapidly during cardiac arrest and improved neurological deficit scores after 9 min of no blood flow in the described canine cardiac arrest model.     

Determination of safe interval of circulatory arrest from the cerebral metabolic aspect

To determine the safe interval of hypothermic total circulatory arrest, the cerebral metabolic state was evaluated in 30 dogs. Surface cooling was achieved by deep ether anesthesia and the animals were assigned to three equal groups. Group I: 30 min circulatory arrest and surface rewarming. Group II: 60 min circulatory arrest and surface rewarming. Group III: 60 min circulatory arrest and perfusion rewarming. Brain tissue gas tension was monitored and cerebral O2 consumption was calculated. Cerebral O2 consumption reduced with cooling, parallel to the decrease in cerebral blood flow. Rapid increase in Po2, elevation of PCO2, and decrease of pH in the brain tissue were observed during circulatory arrest. Brain tissue PO2 increased significantly after circulatory arrest in Group I, but it remained low during rewarming in Groups II and III. Cerebral O2 consumption was at reduced levels in all groups during rewarming and it remained at 29% of the precooling control level in Group II at the end of rewarming, whereas it recovered to 71% and 57% of the precooling levels in Groups I and III, respectively. It was estimated that cerebral metabolism may be recovered after 30 min circulatory arrest, despite a transient reduction in cerebral O2 consumption. On the other hand, after 60 min circulatory arrest, the recovery of cerebral metabolism was delayed in Group II and organic failure might have occurred in this group. However, even after circulatory arrest for 60 min, cerebral metabolism was recovered in Group III. The safe period of circulatory arrest is considered to be prolonged by use of extra-corporeal circulation.     

Veno-venous extracorporeal blood shunt cooling to induce mild hypothermia in dog experiments and review of cooling methods

Mild hypothermia (33-36 degrees C) might be beneficial when induced during or after insults to the brain (cardiac arrest, brain trauma, stroke), spinal cord (trauma), heart (acute myocardial infarction), or viscera (hemorrhagic shock). Reaching the target temperature rapidly in patients inside and outside hospitals remains a challenge. This study was to test the feasibility of veno-venous extracorporeal blood cooling for the rapid induction of mild hypothermia in dogs, using a simple pumping-cooling device. Ten custom-bred hunting dogs (21-28 kg) were lightly anesthetized and mechanically ventilated. In five dogs, two catheters were inserted through femoral veins, one peripheral and the other into the inferior vena cava. The catheters were connected via a coiled plastic tube as heat exchanger (15 m long, 3 mm inside diameter, 120 ml priming volume), which was immersed in an ice-water bath. A small roller-pump produced a veno-venous flow of 200 ml/min (about 10% of cardiac output). In five additional dogs (control group), a clinically practiced external cooling method was employed, using alcohol over the skin of the trunk and fanning plus ice-bags. During spontaneous normotension, veno-venous cooling delivered blood into the vena cava at 6.2 degrees C standard deviation (SD 1.4) and decreased tympanic membrane (Tty) temperature from 37.5 to 34.0 degrees C at 5.2 min (SD 0.7), and to 32.0 degrees C at 7.9 min (SD 1.3). Skin surface cooling decreased tympanic temperature from 37.5 to 34.0 degrees C at 19.9 min (SD 3.7), and to 32.0 degrees C at 29.9 (SD 5.1) (P=0.001). Heart rates at Tty 34 and 32 degrees C were significantly lower than at baseline in both groups, but within physiological range, without difference between groups. There were no arrhythmias. We conclude that in large dogs the induction of mild systemic hypothermia with extracorporeal veno-venous blood shunt cooling is simple and four times more rapid than skin surface cooling.     

Regional blood flow distribution in dog during induced hypotension and low cardiac output. Spontaneous breathing versus artificial ventilation.

Respiratory muscle blood flow and organ blood flow was studied in two groups of dogs with radioactively labeled microspheres to assess the influence of the working respiratory muscles on the regional distribution of blood flow when arterial pressure and cardiac output were lowered by pericardial tamponade. In one group (n = 6), the dogs were paralyzed and mechanically ventilated (Mv), while in the other (n = 6), they were left to breathe spontaneously (Sb). Cardiac output fell to 30% of control values during tamponade in both groups and was maintained constant. None of the dogs was hypoxic. Ventilation in the Sb group peaked after 50 min of hypotension, but remained unchanged in the Mv group. Duplicate measurements of blood flow were made during a control period and after 50 min of tamponade (corresponding to the peak ventilation in Sb). Blood flow to the respiratory muscles increased significantly (P less than 0.001) during tamponade in Sb (diaphragmatic flow increased to 361% of control values), while it decreased in Mv. Although the arterial blood pressure and cardiac output were comparable in the two groups, blood flow distribution during tamponade was different. In Sb, the respiratory muscles received 21% of the cardiac output, compared with only 3% in the Mv group. Thus, by muscle paralysis and Mv, a large fraction of the cardiac output used by the working respiratory muscles can be made available for perfusion of other organs during low cardiac output state: blood flows to the liver, brain, and quadriceps muscles were significantly higher during tamponade in the Mv group compared with the Sb group. Similarly, blood lactate at all times after the induction of low cardiac output and hypotension was significantly lower in the Mv animals (P less than 0.005).     

Effects of acute administration of isoproterenol on the systemic and regional blood flow in the dog

The effects of isoproterenol on cardiac output and the blood flow to various parts of the body have been investigated in pentobarbital-anaesthetized dogs, by the microsphere method. Arterial and venous catheterizations were performed for haemodynamic measurements, drug infusions and blood samples. After a stabilization period, control measurements were carried out on the cardiac output, heart rate, blood pressure, expiratory minute volume and blood gases. Radioactive microspheres of 50 μm diameter, labelled with either ⁸⁵Sr or ¹⁴¹Ce, were then injected into the left ventricle. Thereafter the intravenous infusion of isoproterenol (0.5 μg min^?1 kg^?1 was started. Fifteen minutes after initiation of the drug infusion, the same parameters as in the control period were measured and the injection of radioactive microspheres into the left ventricle was repeated. At the end of the experiment, various organs and tissues were removed and weighed and their radioactivity was determined. The fractional distribution of cardiac output and the blood flow to various organs and tissues were calculated by the method after Rudolph &; Heymann (1967). The infusion of isoproterenol resulted in an increase of 57% in cardiac output but changes in regional blood flow varied. The fraction of cardiac output to the myocardium, skeletal muscle and skin were increased, whereas that to the kidney, pancreas and brain decreased. The fraction to the bronchial arteries and splanchnic organs except for the pancreas remained unchanged. The uneven distribution of cardiac output to the various areas may be due mainly to the differences in direct and indirect responses of individual vascular beds to isoproterenol.     

Acute alveolar hypoxia increases bronchopulmonary shunt flow in the dog.

To study the effects of alveolar hypoxia on canine bronchopulmonary shunt flow, a biventricular bypass preparation was employed. The preparation allowed a constant and sensitive measure of changes in pulmonary venous blood flow. In 16 of 18 dogs with intact bronchial arteries, alveolar hypoxia caused an increase in pulmonary venous return both under conditions of constant pulmonary arterial inflow and under conditions of no pulmonary arterial inflow, suggesting bronchopulmonary shunting. This effect was accompanied by systemic vasodilation despite vagotomy and ganglionic blockade, and was abolished by division of all bronchial vessels. Ibuprofen, 3 mg/kg, and indomethacin, 15 mg/kg, in dogs with intact bronchial vessels, abolished both the increase in pulmonary venous return and the systemic vasodilatation caused by hypoxia. Thus, alveolar hypoxia directly augments bronchopulmonary flow, most likely through release of one or more vasodilating prostaglandins.     

Effects of intra-arterial arginine-vasopressin infusions on peripheral blood flows in conscious dogs

We reported in an earlier study that intravenous infusions of arginine-vasopressin (AVP), 220 pg min-1 kg-1 for 1 h, substantially reduced blood flow to the skin, skeletal muscle, pancreas, colon, small intestine, abdominal fat and myocardium in conscious dogs. In the present study, we infused AVP directly into the artery supplying these organs and tissues in order to determine the relative contribution of local versus systemic mechanisms in the vascular resistance changes previously observed. Regional blood flows were measured with radioactive microspheres in conscious, chronically instrumented dogs before and during intra-arterial infusions of AVP administered into the left axillary artery (n = 6), the left coronary artery (n = 6), and the cranial mesenteric artery (n = 6). The infusion rates were calculated to increase local, target organ plasma concentrations of AVP to the levels reached in our previous study while minimizing systemic changes. Left axillary AVP artery infusion significantly reduced skin and compact bone blood flow, but had no effect on skeletal muscle blood flow. Intracoronary AVP infusion had no effect on myocardial blood flow nor on cardiac output. Intramesenteric AVP infusion had no effect on blood flow to the colon, small intestine and abdominal fat, but significantly reduced blood flow to those areas of the pancreas which received blood from the cannulated artery. Measurements in a limited number of dogs indicated that the local axillary and mesenteric venous levels of AVP were similar when the hormone was infused systemically at a rate of 220 pg min-1 kg-1 or intra-arterially at a lower rate.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of dopamine on intrapulmonary shunt fraction and oxygen transport in severe sepsis with circulatory and respiratory failure.

The hemodynamic response to a dopamine HCl infusion (10 microgram/kg per min) was measured in 25 adult patients with severe sepsis: there were 6 patients with circulatory hyperdynamic states, 9 patients with myocardial failure, and 10 with hypovolemia. Each patient also had acute respiratory failure. Changes of intrapulmonary shunt fraction (Qs/Qt), arterial and mixed venous oxygen tension (PaO2 and PvO2), oxygen transport, and oxygen consumption (VO2) were evaluated before and after dopamine infusion. Dopamine infusion produced clinical improvement and increased cardiac output. The hemodynamic response seemed to differ slightly according to the pattern of circulatory failure: chronotropic effect appeared to be predominant in hyperdynamic states, whereas inotropic effect appeared to be predominant in myocardial failure or hypovolemia. Moreover, in hypovolemic patients we noted a rise in pulmonary capillary wedge pressure suggesting an additional increase in venous return. During this treatment, we also noted a worsening of the Qs/Qt despite the increase in pulmonary blood flow; this worsening did not prevent significant improvements in VO2, but the improvement in PVO2 was offset by increased Qs/Qt and PaO2 remained unchanged.     

Redistribution of peripheral blood flow during acute left ventricular failure in the dog

Acute left ventricular failure was induced in anaesthetized dogs by repeated embolization of the left coronary artery with 57 micron microspheres. Tissue blood flow was measured with isotope-labelled microspheres in two stages of heart failure. With increasing doses of embolizing solution there was a progressive decline in systemic blood pressure and cardiac output. Failure was accompanied by a significant decrease in blood flow in all tissues examined except for intestine, adrenal gland, skin and right ventricle. Overall cardiac output distribution was estimated by combining flow data with data on relative tissue weights obtained from a dissection study in a separate group of dogs. A selective redistribution of cardiac output took place in the failure state. The blood flow was redirected away from the skeletal muscles and the spleen in favour of the intestines, kidneys, heart and brain.     

低温关胸心肺转流行心肺复苏的实验研究

目的　观察狗心脏停搏15min后深低温(26℃～27℃)和浅低温(33℃～34℃)关胸心肺转流(CPB)对心肺复苏(CPR)的影响。方法　10只麻醉狗,分2组,每组各5只。第1组为浅低温组,第2组为深低温组,用10%氯化钾静注后,使心脏停搏15min,然后用动静脉插管方法立即行关胸心肺转流。第1组食道温度降至33℃～34℃,第2组降至26℃～27℃,15min后逐渐升温至正常范围(36℃～37℃)。复苏期间监测心电图、平均动脉压、中心静脉压和瞳孔直径,3h后观察颅内压和最终效果。结果　第1组全部恢复自主循环(100%),第2组仅3只(60%)恢复自主循环;第1组的自主循环恢复时间为(444±192.2)sec,明显短于第2组(1980±681.5)sec(P＜0.05),其复苏后3h颅内压为(2.4±0.44)cmH     

The importance of colloid osmotic pressure during open heart surgery in infants

Fifty-five infants with transposition of the great arteries and with total anomalous pulmonary venous return underwent intracardiac repair under combined surface/perfusion hypothermia and total circulatory arrest in 1975 to 1983. Although cardiopulmonary bypass (CPB) time is limited when hypothermic circulatory arrest is employed, fluid balance derangement is one of the major postoperative complications. Fluid balance at the end of CPB averaged +299.5 ml (+63.4 ml/kg) when hemodilution with lactated Ringer's was utilized (Group A). Since colloid osmotic pressure (COP) plays an important role in regulating fluid balance, colloid hemodilution prime (whole blood and plasma) was employed in the last 3 years (Group B). COP and total protein concentration during CPB with colloid prime were maintained at around 19 mmHg and 5 g/100 ml, respectively. In Group B, fluid balance at the end of CPB averaged +81.1 ml (+16.3 ml/kg) and was significantly less than in Group A (p less than 0.01). The ICU stay period for survivors in Group B (average 10.9 days) was reduced to half the period in Group A (average 20.6 days) (p less than 0.05). The mortality rate in Group A was 42%, whereas 23% in Group B. It was concluded that well-maintained COP levels during CPB with colloid hemodilution prime reduced fluid accumulation in the body and made patient care easier following open heart surgery in infants.     

Fluid loading with whole blood or Ringer's lactate solution during CPR in dogs

The influence of fluid loading during CPR on oxygen uptake and blood flow was investigated in 18 dogs (12-26 kg). Blood flows were measured with radioactive microspheres at 5 (control CPR), 13 and 20 min after the initiation of ventricular fibrillation and CPR. After 10 min, 9 dogs received a rapid infusion of whole blood (11 ml/kg, i.v.) and 9 dogs received Ringer's solution (11 ml/kg, i.v.). Oxygen uptake was not significantly altered by fluid loading with either whole blood or Ringer's solution. Fluid loading increased cardiac output 34% over the 5 min control value. However, left ventricular perfusion decreased to 74% and brain flow decreased to 65% of control. At 20 min, cardiac output and brain flow returned to near control values, while left ventricular flow remained low. Changes in organ perfusion can be explained in part by the concurrent changes in blood pressures. Central venous diastolic pressure increased significantly (from 9 to 14 mmHg) after fluid load. However, central arterial diastolic pressure did not rise proportionately (from 32 to 34 mmHg). Hence, the central A-V diastolic pressure difference decreased. Although fluid loading during CPR improved cardiac output, flow to the heart and brain decreased. Further, there was no increase in oxygen consumption, indicating that fluid loading did not improve metabolic status.     

Cerebral cortical perfusion during and following resuscitation from cardiac arrest in dogs

Perfusion of the cerebral cortex during closed chest CPR in dogs, generating systolic pressures of 60 to 70 mmHg, is only 10% of pre-arrest blood flow. In contrast, internal cardiac massage produces normal cortical perfusion rates. Following a 20-min perfusion arrest, during pressure controlled reperfusion, cortical flow rates decay to less than 20% normal after 90 min of reperfusion. This appears to be due to increasing cerebral vascular resistance, and is not due to rising intracranial pressure. The post-arrest cortical hypoperfusion syndrome is prolonged with cortical flow remaining below 20% normal up to 18 hr post arrest. The use of a variety of calcium antagonists, including flunarizine, lidoflazine, verapamil, and Mg²⁺, immediately post-resuscitation maintains cerebral vascular resistance and cortical perfusion at normal levels. A prospective blind trial of the calcium antagonist lidoflazine following a 15-min cardiac arrest in dogs and resuscitation by internal massage, demonstrates amelioration of neurologic deficit in the early post-resuscitation period.