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PubMed2001

Systemic toxicity and resuscitation in bupivacaine-, levobupivacaine-, or ropivacaine-infused rats.

We compared the systemic toxicity of bupivacaine, levobupivacaine, and ropivacaine in anesthetized rats. We also compared the ability to resuscitate rats after lethal doses of these local anesthetics. Bupivacaine, levobupivacaine, or ropivacaine was infused at a rate of 2 mg. kg(-1). min(-1) while electrocardiogram, electroencephalogram, and arterial pressure were continuously monitored. When asystole was recorded, drug infusion was stopped and a resuscitation sequence was begun. Epinephrine 0.01 mg/kg was administered at 1-min intervals while external cardiac compressions were applied. Resuscitation was considered successful when a systolic arterial pressure > or =100 mm Hg was achieved within 5 min. The cumulative doses of levobupivacaine and ropivacaine that produced seizures were similar and were larger than those of bupivacaine. The cumulative doses of levobupivacaine that produced dysrhythmias and asystole were smaller than the corresponding doses of ropivacaine, but they were larger than those of bupivacaine. The number of successful resuscitations did not differ among groups. However, a smaller dose of epinephrine was required in the Ropivacaine group than in the other groups. We conclude that the systemic toxicity of levobupivacaine is intermediate between that of ropivacaine and bupivacaine when administered at the same rate and that ropivacaine-induced cardiac arrest appears to be more susceptible to treatment than that induced by bupivacaine or levobupivacaine.

Adrenergic alpha-Agonists↗
PubMed1975

Sepsis, resuscitated hemorrhagic shock and "shock lung:" An experimental correlation.

Dogs were submitted to hermorrhagic shock, resuscitated shock and resuscitated shock plus a pulmonary bacterial insult. Pulmonary familure was absent in dogs submitted only to shock or to shock and its resuscitation. The addition of usually sub-lethal amounts of micro-organisms to the shock-resuscitated lung caused rapid death from pulmonary failure. Pulmonary failure was demonstrated by increased lung weight, hypoxemia, decreased compliance and a hemorrhagic destruction of lung tissue. These findings strongly support recent concepts of an infective genesis of "shock lung" in man.

Animals↗
PubMed1979

Critical evaluation of hypertonic and hypotonic solutions to resuscitate severely burned children: a prospective study.

Children with thermal burns covering 30% or more of the body surface area were alternately resuscitated with either hypertonic lactated saline (HLS) or lactated Ringer's solution (LRS). Parameters sequentially measured and calculated included: 1) serum and urine electrolyte concentrations, 2) serum and urine osmolalities, 3) arterial blood gases, 4) total and fractional serum proteins, 5) blood urea nitrogen, complete blood count and blood sugar concentration, 6) changes in body weight, 7) sodium, potassium and water balance. The water load received by the HLS group was significantly less through 48 hours postburn (49% at 8 hours, 44% at 24 hours and 38% at 48 hours postburn). Although the HLS group received significantly more sodium than the LRS group, there was no difference in sodium balance at 48 hours postburn. This is explained by the fact that the HLS group, at 48 hours postburn, retained significantly less of the administered sodium load (69% vs. 83%). Positive water balance was significantly greater in the LR group for the first 48 hours postburn. This study suggests that current hypotonic fluid regimens for burn resuscitation contain water in excess of that required for proper resuscitation. Severely burned children may be safely and efficiently resuscitated with conventional salt loads and one-third less than usual water loads.

Blood↗
PubMed1991

Small-volume hypertonic saline dextran resuscitation from canine endotoxin shock.

This study evaluated resuscitation of endotoxin shock with 7.5% hypertonic saline dextran (HSD 2400 mOsm) by measuring hemodynamic and regional blood flow responses. Endotoxin challenge (1 mg/kg) in adult dogs caused a significant decrease in mean arterial blood pressure (MABP), cardiac output (CO), left ventricular +/- dP/dt max, and regional blood flow (radioactive microspheres). Cardiocirculatory dysfunction and acid-base derangements persisted throughout the experimental period in untreated endotoxin shock (group 1, n = 10). In contrast both regimens of fluid resuscitation (group 2, n = 11: bolus of 4 mL/kg HSD followed by a constant infusion of lactated Ringer's [LR] to maintain MABP and CO at baseline values; group 3, n = 10; LR alone given as described for group 2) improved regional perfusion and corrected acid-base disturbances similarly in all dogs. Hypertonic saline dextran enhanced all indices of cardiac contraction and relaxation more than LR alone. The total volume of LR required to maintain MABP and CO at baseline values was less in the HSD group (59.2 +/- 6.8 mL/kg) than in the LR alone group (158 +/- 16 mL/kg, p = 0.01). The net fluid gain (infused volume minus urine output and normalized for kilogram body weight) was five times greater in the LR (24.8 +/- 6.2 mL/kg) than in the HSD group (4.6 +/- 1.2 mL/kg, p = 0.01). Lung water was similar in all dogs, regardless of the regimen of fluid resuscitation. Hypertonic saline dextran effectively resuscitates endotoxin shock in this canine model.

Animals↗
PubMedDate not supplied

Cardiac pathology following resuscitative circulatory support. Direct mechanical ventricular actuation versus cardiopulmonary bypass.

Cardiopulmonary bypass (CPB) is currently advocated for treating refractory cardiac arrest. Direct Mechanical Ventricular Actuation (DMVA) is an alternative method that does not contact the blood and has other unique advantages for providing resuscitative circulatory support, including rapid application and relative technical simplicity. The purpose of this study was to assess pathologic changes in the heart following resuscitation with either CPB or DMVA. Dogs (n = 22) received 1 hr of CPB (n = 11) or DMVA (n = 11) following a 12.5 min cardiac arrest. All deaths [4/11 (CPB) vs. 2/11 (DMVA), p = 0.31] occurred during the initial 24 postoperative hours. At 7 days, survivors had magnetic resonance imaging to determine cardiac ejection fraction [46% (CPB) vs. 51% (DMVA), p = 0.39], as well as the presence of cardiac wall motion abnormalities [50% (CPB) vs. 33% (DMVA), p = 0.57] and gross cardiac lesions [17% (CPB) vs. 17% (DMVA)]. The survivor's hearts were then extirpated, fixed, and examined for gross lesions [2/7 (CPB) vs. 0/9 (DMVA), p = 0.17]. Transmural sections of the anterior and posterior papillary muscles were histologically evaluated. The severity and extent of epicardial fibrosis and focal myocyte necrosis did not differ between groups. These data demonstrate that DMVA does not cause more myocardial trauma than CPB when used to provide resuscitative circulatory support. Therefore, the unique attributes of DMVA may improve resuscitation outcome in patients who suffer refractory cardiac arrest, without additional risk of cardiac injury.

Animals↗
PubMed1986

Cardiorespiratory and conjunctival oxygen tension monitoring during resuscitation from hemorrhage.

Placement of an unheated miniaturized oxygen electrode against the palpebral conjunctiva permits noninvasive measurement of tissue oxygen tension. In this study, the relationship between conjunctival oxygen tension (PcjO2) and standard cardiorespiratory variables was examined during a sequential resuscitation protocol after acute hemorrhage. Anesthetized dogs were rapidly bled to a mean arterial pressure of 40 mm Hg and then retransfused with the shed blood in a stepwise fashion. PcjO2 fell to 2% of control values after hemorrhage and did not return to prehemorrhage values until more than 90% of the shed blood had been reinfused. PcjO2 was among the last set of cardiorespiratory variables to return to control values during resuscitation and was the last noninvasive variable to normalize. The ratio of PcjO2 to arterial oxygen tension decreased from a prehemorrhage value of 0.76 +/- 0.05 (SEM) to 0.02 +/- 0.003 after hemorrhage, and did not increase to values greater than 0.50 until resuscitation was more than 90% complete. Conjunctival oxygen monitoring may play an important role in assessing the adequacy of resuscitation after acute hemorrhage.

Animals↗
PubMed1989

Arterial PCO2 as an indicator of systemic perfusion during cardiopulmonary resuscitation.

End-tidal PCO2 (PetCO2) is a quantitative indicator of pulmonary blood flow generated by precordial compression and therefore predicts resuscitability during CPR. A striking increase in PetCO2 follows return of spontaneous circulation. Since PaCO2 is closely related to alveolar PCO2 (PACO2) and therefore PetCO2, we hypothesized that PaCO2 may itself serve as an indicator of the blood flow generated during CPR. In a porcine model of cardiac arrest, PaCO2 during precordial compression was highly correlated with PetCO2 (r = .89), cardiac output (r = .72), and coronary perfusion pressure (CPP) (r = .74). In 14 successfully resuscitated animals, PaCO2, PetCO2, and CPP during precordial compression were significantly higher than in nine nonresuscitated animals. After restoration of spontaneous circulation, there was a marked increase in PaCO2 to levels exceeding control values, which corresponded to the sharp increase in PetCO2 that is characteristic of successful resuscitation. We therefore confirm that both PetCO2 and PaCO2 correspond to the pulmonary blood flow and therefore cardiac output which is generated by precordial compression during CPR. Moreover, both serve as prognosticators of cardiac resuscitability and early indicators that spontaneous circulation has been restored.

Animals↗
PubMed1990

Five percent human albumin in lactated Ringer's solution for resuscitation from hemorrhagic shock: efficacy and cardiopulmonary consequences.

Using an ovine model of acute hemorrhagic shock, we evaluated the utility of 5% albumin in lactated Ringer's (5% ALR) solution as a resuscitation solution. After instrumentation and obtaining baseline values for BP, mean arterial pressure (MAP), pulmonary capillary wedge pressure (WP), CVP, cardiac output, extravascular lung water (EVLW), and blood gases (mixed venous and arterial), animals were rapidly exsanguinated to an MAP of 50 mm Hg. After 30 min at this pressure, measurements were repeated and 5% ALR was administered until two of three variables (WP, MAP, cardiac output) were restored to baseline values. The administration of 5% ALR was continued as needed to maintain baseline values of these variables. Sixty minutes later, data were again recorded. For induction of shock, 15.7 +/- 5.2 ml of blood/kg body weight was removed. Pulmonary artery pressure, WP, MAP, and cardiac output all significantly decreased with shock. After resuscitation, all values except MAP returned to baseline. The resuscitation volume of 5% ALR was 25.2 +/- 18.4 ml/kg. There were no changes in EVLW or intrapulmonary shunt. Oxygen delivery was significantly compromised during shock but returned to baseline after resuscitation. We conclude that in a model such as ours, 5% ALR can reverse the hemodynamic effects of acute hemorrhagic shock.

Acute Disease↗
PubMed1990

Cerebral electrophysiologic effects of resuscitation with hypertonic saline-dextran after hemorrhage.

When brain injury accompanies hemorrhage, resuscitation with hypertonic saline (HS) improves intracranial pressure (ICP) and elastance; however, its effect on brain function after a traumatic or ischemic insult has not been assessed. This study compares the electrophysiologic response to hemorrhage and resuscitation with 7.5% NaCl + 6% dextran (HSD), 6% hetastarch (HE), or 0.9% NaCl (NS) using somatosensory evoked potentials (SSEP). Resuscitation with HE resulted in a better return of electrocortical function than with either HSD or NS (SSEP grade 2.0 +/- 0.2 for HE vs. 3.2 +/- 0.3 for HSD and 2.9 +/- 0.3 for NS; p less than .01). SSEP response correlated closet with mean arterial pressure (MAP) (r = -.53). There was no correlation between the SSEP response and cardiac index (r = .06) or ICP (r = -.04). HSD blunted the usual early increase in ICP after fluid infusion, and resulted in a lower ICP throughout resuscitation. However, the restoration of MAP and cerebral perfusion pressure (CPP) after HSD infusion was poor. The vasodilatory properties of hypertonic saline have been well described, both in the systemic and in the pulmonary vascular bed. While these characteristic usually are cited as advantages of this solution, in the case of ischemic cerebral dysfunction, this diminished vascular tone prevents early restoration of the MAP and CPP. The result is suboptimal electrocortical recovery after hemorrhage.

Animals↗
PubMed1991

Adequate resuscitation of burn patients may not be measured by urine output and vital signs.

OBJECTIVE: To compare vital sign and urine output monitoring of seriously burned patients with invasive monitoring during early resuscitation. DESIGN: Retrospective review. SETTING: A university hospital burn unit. PATIENTS: Fourteen seriously burned patients who had pulmonary arterial monitoring. Monitoring data were compared at baseline and after fluid challenges. RESULTS: There was no correlation between invasively derived physiologic variables and vital signs and urine output. Vital signs and urine output changed little after fluid challenge, while variables from invasive monitoring demonstrated significant change. In half of the patients, oxygen consumption increased after fluid challenge; vital signs and urine output did not distinguish these patients. CONCLUSIONS: The use of urinary output and vital signs to guide initial burn resuscitation may lead to suboptimal resuscitation. Invasive cardiorespiratory monitoring may be necessary to optimize resuscitation of seriously burned patients.

Adolescent↗
PubMed1991

Pentoxifylline in resuscitation of experimental hemorrhagic shock.

BACKGROUND: Pentoxifylline improves survival in animal models of hemorrhagic shock. The purpose of this study was to determine the physiologic effects of pentoxifylline in hemorrhagic shock that may be responsible for improved survival. METHODS: Randomized, prospective, blinded trials in Sprague-Dawley rats subjected to hemorrhage and resuscitation, with or without pentoxifylline. RESULTS: Pentoxifylline had no effect on BP or cardiac output. However, tissue oxygenation and oxygen consumption were increased with pentoxifylline resuscitation. Pentoxifylline resuscitation also significantly decreased polymorphonuclear leukocyte adhesiveness. CONCLUSIONS: Pentoxifylline improves tissue oxygenation and oxygen consumption posthemorrhage and this effect is not due to increased cardiac output. Therefore, it must be due to improved microcirculatory blood flow. This effect may be due to decreased polymorphonuclear leukocyte adhesiveness induced by pentoxifylline resuscitation.

Animals↗
PubMed1991

Resuscitation fluids for the treatment of hemorrhagic shock in dogs: effects on myocardial blood flow and oxygen transport.

BACKGROUND AND METHODS: The efficacy of using colloids vs. crystalloids in the treatment of hemorrhagic shock remains controversial. An important aspect in the treatment of hemorrhagic shock is the reestablishment of normal myocardial blood flow after fluid resuscitation. This study, therefore, was designed to investigate the effect of resuscitation with different plasma substitutes on myocardial blood flow and oxygen transport after acute hemorrhage in dogs. Forty-three dogs were anesthetized and bled into a heparinized Wiggers' reservoir to a mean arterial pressure of 35 mm Hg. The animals were maintained at this level of hypotension for 90 mins, whereupon the animals were infused with one of five randomly selected fluids: a) succinylated gelatin (Gelofusine); b) urea-linked gelatin (Haemaccel); c) 6% hetastarch (Hespan); d) lactated Ringer's solution; or e) shed blood. Myocardial blood flow was measured using the radiolabeled microsphere technique. RESULTS: Resuscitation with succinylated gelatin, urea-linked gelatin, and hetastarch resulted in significant hemodilution. However, infusion of these fluids resulted in a compensatory hyperemia that increased myocardial blood flow and maintained oxygen transport at preshock values. No hyperemia was observed with reinfusion of shed blood. Resuscitation with lactated Ringer's solution produced significant hemodilution without hyperemia and, consequently, a significant decrease in oxygen transport. CONCLUSIONS: These results suggest that in lieu of blood, the artificial colloids are more effective than crystalloids in restoring myocardial blood flow and oxygen transport after acute experimental hemorrhage in dogs.

Animals↗
PubMed1995

Hypertonic saline-dextran resuscitation from hemorrhagic shock induces transient mixed acidosis.

OBJECTIVE: To evaluate the magnitude and mechanism of potential metabolic acidosis after resuscitation with 7.5% sodium chloride/6% dextran-70. DESIGN: Blinded, randomized, control trial. SETTING: Laboratory setting. SUBJECTS: Sixteen healthy Yorkshire swine. INTERVENTIONS: Anesthetized, mechanically ventilated swine underwent 90 mins of hemorrhagic hypotension (mean arterial pressure of 50 to 55 mm Hg), and a lactic acid infusion (1.5 to 2.4 mmol/kg) was given during the last 60 mins of hemorrhage to produce pretreatment acidosis. The pigs were then given either 4 mL/kg of intravenous normal saline (n = 8) or 7.5% sodium chloride/6% dextran-70 (n = 8). Groups then received isotonic lactated Ringer's solution to restore and maintain cardiac output for 120 mins. MEASUREMENTS AND MAIN RESULTS: There was no difference between groups during baseline or shock for any parameter. At the end of shock, arterial pH and base balance were below baseline values. During resuscitation, cardiac output was reached and maintained in both groups. One minute after infusion of hypertonic saline/dextran, there was a significant but transient decrease in arterial pH (from 7.407 +/- 0.015 to 7.339 +/- 0.025) and base balance (from -6.5 +/- 0.7 to -9.9 +/- 1.0 mmol/L). These changes returned to shock levels by 10 mins and then normalized to baseline levels. Hypertonic saline dextran resulted in an immediate hypernatremia, hyperchloremia, and hypokalemia, a decrease in inorganic strong ion difference (calculated as sodium plus potassium minus chloride concentrations), and no immediate change in anion gap. The normal saline group did not show an initial transient decrease in pH and base balance during resuscitation. Plasma lactate, total protein, and hemoglobin concentrations decreased equally in both groups, although they decreased more quickly with hypertonic saline/dextran. CO2 temporarily and insignificantly increased in arterial blood slightly more after the administration of hypertonic saline/dextran. By 120 mins, acid-base, electrolyte and protein changes were normalizing with hypertonic saline/dextran, while pH, base balance, and protein were decreasing below shock values in animals initially treated with normal saline. CONCLUSIONS: Hypertonic saline/dextran caused an immediate, transient acidemia, which was primarily due to a hyperchloremic, hypokalemic, metabolic acidosis with normal anion gap and decreased inorganic strong ion difference, but which was partially due to a mild transient respiratory acidosis. The acidemia was transient because of the offsetting alkalotic effects of decreasing serum protein, normalization of electrolytes, and transient nature of the increase in CO2. Lactic acidosis was not the cause of the acidemia. Over time, the acid-base status appeared to be improved more effectively with hypertonic saline/dextran than with isotonic saline resuscitation.

Acid-Base Equilibrium↗
PubMed1996

Selective brain cooling in infant piglets after cardiac arrest and resuscitation.

OBJECTIVES: To test the hypothesis that selective brain cooling could be performed in an infant model of cardiac arrest and resuscitation without changing core temperature and to study its acute effects on regional organ blood flow, cerebral metabolism, and systemic hemodynamics. DESIGN: Prospective, randomized, controlled study. SETTING: Research laboratory at a university medical center. SUBJECTS: Fourteen healthy infant piglets, weighing 3.5 to 6.0 kg. INTERVENTIONS: piglets were anesthetized and mechanically ventilated, and had vascular catheters placed. Parietal cortex (superficial brain), caudate nucleus (deep brain), esophageal, and rectal temperatures were monitored. All animals underwent 6 mins of cardiac arrest induced by ventricular fibrillation, 6 mins of external cardiopulmonary resuscitation (CPR), defibrillation, and 2 hrs of reperfusion. Normal core temperature (rectal) was regulated in all animals. In seven control animals (group 1), brain temperature was not manipulated. In seven experimental animals (group 2), selective brain cooling was begin during CPR, using a cooling cap filled with -30 degrees C solution. Selective brain cooling was continued for 45 mins of reperfusion after which passive rewarming was allowed. Regional blood flow (microspheres) and arterial and sagittal sinus blood gases were measured prearrest, during CPR, and at 10 mins, 45 mins, and 2 hrs of reperfusion. MEASUREMENTS AND MAIN RESULTS: Rectal temperature did not change over time in either group. In group 1, brain temperature remained constant except for a decrease of 0.6 degrees C at 10 mins of reperfusion. In group 2, superficial and deep brain temperatures were lowered to 32.8 +/- 0.7 (SEM) degrees C and 34.9 +/- 0.4 degrees C, respectively, by 15 mins of reperfusion. Superficial and deep brain temperatures were further lowered to 27.8 +/- 0.8 degrees C and 31.1 +/- 0.3 degrees C, respectively, at 45 mins of reperfusion. Both temperatures returned to baseline by 120 mins. Cerebral blood flow was not different between groups at any time point, although there was a trend for higher flow in group 2 at 10 mins of reperfusion (314% of baseline) compared with group 1 (230% of baseline). Cerebral oxygen uptake was lower in group 2 than in group 1 (69% vs. 44% of baseline, p=.02) at 45 mins of reperfusion. During CPR, aortic diastolic pressure was lower in group 2 than in group 1 (27 +/- 1 vs. 23 +/- 1 mm Hg, p = .007). Myocardial blood flow during CPR was also lower in group 2 (80 +/- 7 vs. 43 +/- 7 mL/min/100 g, p=.002). Kidney and intestinal blood flows were reduced during CPR in both groups; however, group 2 animals also had lower intestinal flow vs. group 1 at 45 and 120 mins of reperfusion. CONCLUSIONS: Selective brain cooling by surface cooling can be achieved rapidly in an infant animal model of cardiac arrest and resuscitation without changing core temperature. Brain temperatures known to improve neurologic outcome can be achieved by this technique with minimal adverse effects. Because of its ease of application, selective brain cooling may prove to be an effective, inexpensive method of cerebral resuscitation during pediatric CPR.

Animals↗
PubMed1996

Effects of graded doses of vasopressin on median fibrillation frequency in a porcine model of cardiopulmonary resuscitation: results of a prospective, randomized, controlled trial.

OBJECTIVE: To assess the effects of graded doses of vasopressin vs. saline on median fibrillation frequency and defibrillation success in a porcine model of cardiopulmonary resuscitation. DESIGN: Prospective, randomized, controlled trial. SETTING: Animal laboratory in a university medical center. SUBJECTS: Twenty-eight domestic pigs (body weight between 26 and 31 kg), aged 12 to 14 wks. INTERVENTIONS AND MAIN RESULTS: After 4 mins of ventricular fibrillation and 3 mins of closed-chest cardiopulmonary resuscitation, the animals were allocated to receive either 0.2 U/kg of vasopressin (n = 7), 0.4 U/kg of vasopressin (n = 7), 0.8 U/kg of vasopressin (n = 7), or 10 mL of saline (n = 7, control group). Using radiolabeled microspheres, myocardial blood flow rates during cardiopulmonary resuscitation-before drug administration and 90 secs and 5 mins after drug administration-were as follows in the four groups (mean +/- SEM): 18.8 +/- 0.9, 17.2 +/- 1.1, and 14.6 +/- 1.4 mL/min/100 g in the control group; 17.8 +/- 2.2, 49.6 +/- 6.3 (p < .01 vs. control group), and 29.4 +/- 3.1 mL/min/100 g (p < .05 vs. control group) in the group receiving 0.2 U/kg of vasopressin; 17.1 +/- 1.0, 52.4 +/- 7.5 (p < .01 vs. control group), and 52.2 +/- 5.8 mL/min/100 g (p < .001 vs. control group) in the group receiving 0.4 U/kg of vasopressin; and 18.1 +/- 1.6, 94.9 +/- 9.2 (p < .001 vs. control group), and 57.2 +/- 6.3 mL/min/100 g (p < .001 vs. control group) in the group receiving 0.8 U/kg of vasopressin. Using spectral analysis, median frequencies of ventricular fibrillation-before drug administration and 90 secs and 5 mins after drug administration-were as follows in the four groups: 9.6 +/- 0.4, 8.5 +/- 0.8, and 7.2 +/- 1.0 Hz in the control group; 9.7 +/- 0.5, 12.9 +/- 0.8 (p < .01 vs. control group), and 12.7 +/- 0.8 Hz (p < .001 vs. control group) in the group receiving 0.2 U/kg of vasopressin; 10.3 +/- 0.2, 12.7 +/- 0.9 (p < .01 vs. control group), and 12.8 +/- 0.7 Hz (p < .001 vs. control group) in the group receiving 0.4 U/kg of vasopressin; and 10.0 +/- 0.9, 14.1 +/- 0.9 (p < .001 vs. control group), and 12.5 +/- 0.9 Hz (p < .001 vs. control group) in the group receiving 0.8 U/kg of vasopressin at the same points in time. Median frequency before the first defibrillation attempt was 12.3 +/- 0.4 Hz in the resuscitated animals (n = 19) and 8.2 +/- 1.2 Hz in the nonresuscitated animals (n = 9) (p < .001). CONCLUSIONS: This study contributes to the characterization of the effect of increasing global myocardial blood flow on median fibrillation frequency after administration of graded doses of vasopressin in a porcine model of ventricular fibrillation. Interventions such as vasopressor treatment that increase fibrillation frequency improve the chance of successful defibrillation.

Animals↗
PubMed1997

Adverse effects of interrupting precordial compression during cardiopulmonary resuscitation.

OBJECTIVES: In the current operation of automated external defibrillators, substantial time may be consumed for a "hands off" interval during which precordial compression is discontinued to allow for automated rhythm analyses before delivery of the electric countershock. The effects of such a pause on the outcomes of cardiopulmonary resuscitation were investigated. DESIGN: Prospective, randomized, controlled animal study. SETTING: Research laboratory. SUBJECTS: Male Sprague-Dawley rats. INTERVENTIONS: Ventricular fibrillation was electrically induced in 25 Sprague-Dawley rats. After 4 mins of untreated ventricular fibrillation, precordial compression was begun and continued for 6 mins. Animals were then randomized to receive an immediate defibrillation shock or the defibrillation attempt was delayed for intervals of 10, 20, 30, or 40 secs. MEASUREMENTS AND MAIN RESULTS: Immediate defibrillation restored spontaneous circulation in each instance. When defibrillation was delayed for 10 or 20 secs, spontaneous circulation was restored in three of five animals in each group. After a 30-sec delay, spontaneous circulation was restored in only one of five animals (p < .05). No animal was successfully resuscitated after a 40-sec delay (p < .01). With increasing delays, 24- and 48-hr survival rates were correspondingly reduced. CONCLUSIONS: During resuscitation from ventricular fibrillation, prolongation of the interval between discontinuation of precordial compression and delivery of the first electric countershock substantially compromises the success of cardiac resuscitation. Accordingly, automated defibrillators are likely to be maximally effective if they are programmed to secure minimal "hands off" delay before delivery of the electric countershock.

Animals↗
PubMed1997

Delayed hyperemia causing intracranial hypertension after cardiopulmonary resuscitation.

OBJECTIVE: To clarify whether early or delayed failure of cerebral perfusion after cardiopulmonary resuscitation (CPR) occurs in humans and contributes to secondary brain damage. DESIGN: Prospective, repeated-measures study. SETTING: Intensive care unit of Hiroshima University School of Medicine. PATIENTS: Eight comatose patients who had undergone successful resuscitation from cardiac arrest. INTERVENTIONS: All patients underwent transcranial Doppler sonography examination. The intracranial cerebral pressure (ICP) and jugular venous oxygen saturation (SO2) also were continuously monitored in five patients and three patients, respectively. MEASUREMENTS AND MAIN RESULTS: In each patient, we measured the mean flow velocity of the middle cerebral artery transcranially and the mean flow velocity of the internal carotid artery, high in the neck, using transcranial Doppler sonography. The pulsatility index for each measurement was also calculated. The first examinations were performed within 4 to 12 hrs of CPR, and repeat examinations were performed approximately every 12 hrs. The initial mean flow velocities of the middle cerebral artery and the initial mean flow velocities of the internal carotid artery were relatively low, with relatively high pulsatility indices. The mean flow velocities of the middle cerebral artery began to increase at 12 to 24 hrs after CPR and peaked 24 to 120 hrs after CPR. A simultaneous increase in mean flow velocities of the internal carotid artery was observed during this period. The pulsatility index in both arteries dropped significantly during peak mean flow velocity of the middle cerebral artery. In six of seven patients with an abnormal increase (> 100 cm/ sec) in peak mean flow velocity of the middle cerebral artery, the ratio of mean flow velocity of the middle cerebral artery to mean flow velocity of the internal carotid artery was < 3. This value tended to be lower in patients with poor outcomes. An increased mean flow velocity of the middle cerebral artery, with a ratio of < 3 for mean flow velocity of the middle cerebral artery to mean flow velocity of the internal carotid artery, was defined as hyperemia. Although the mean flow velocity of the internal carotid artery was not measured, another patient with an abnormal increase in mean flow velocity of the middle cerebral artery revealed a high jugular venous SO2 value of 83.5%, also representing hyperemia. All ICP values were within the normal range 4 to 12 hrs after CPR and tended to increase before peak mean flow velocity of the middle cerebral artery. The two patients with the lowest ratios of mean flow velocity of the middle cerebral artery to mean flow velocity of the internal carotid artery showed significant increases in ICP after the peak mean flow velocity of the middle cerebral artery. These two patients subsequently developed brain death. CONCLUSIONS: Delayed hyperemia occurs in humans after resuscitation from cardiac arrest. Our data suggest that this delayed hyperemia can lead to intracranial hypertension and occasionally acute brain swelling, contributing to a poor outcome. A high mean flow velocity of the middle cerebral artery with a low ratio of mean flow velocity of the middle cerebral artery to mean flow velocity of the internal carotid artery may be predictive of critical hyperemia. As an indirect method of measuring cerebral blood flow transcranial Doppler sonography can be used to adjust treatment for failure of cerebral perfusion after resuscitation.

Blood Flow Velocity↗
PubMed1998

Comparison of sodium bicarbonate, Carbicarb, and THAM during cardiopulmonary resuscitation in dogs.

OBJECTIVES: During cardiopulmonary resuscitation (CPR), elimination of CO2 was shown to be limited by low tissue perfusion, especially when very low perfusion pressures were generated. It has therefore been suggested that sodium bicarbonate (NaHCO3), by producing CO2, might aggravate the hypercarbic component of the existing acidosis and thereby worsen CPR outcome. The objectives of this study were to evaluate the effects of CO2 producing and non-CO2 producing buffers in a canine model of prolonged ventricular fibrillation followed by effective CPR. DESIGN: Prospective, randomized, controlled, blinded trial. SETTING: Experimental animal research laboratory in a university research center. SUBJECTS: Thirty-eight adult dogs, weighing 20 to 35 kg. INTERVENTIONS: Animals were prepared for study with thiopental followed by halothane, diazepam, and pancuronium. Ventricular fibrillation was electrically induced, and after 10 mins, CPR was initiated, including ventilation with an FIO2 of 1.0, manual chest compressions, administration of epinephrine (0.1 mg/kg every 5 mins), and defibrillation. A dose of buffer, equivalent to 1 mmol/kg of NaHCO3, was administered every 10 mins from start of CPR. Animals were randomized to receive either NaHCO3, Carbicarb, THAM, or 0.9% sodium chloride (NaCl). CPR was continued for up to 40 mins or until return of spontaneous circulation. MEASUREMENTS AND MAIN RESULTS: Buffer-treated animals had a higher resuscitability rate compared with NaCl controls. Spontaneous circulation returned earlier and at a significantly higher rate after NaHCO3 (in seven of nine dogs), and after Carbicarb (six of ten dogs) compared with NaCl controls (two of ten dogs). Spontaneous circulation was achieved twice as fast after NaHCO3 compared with NaCl (14.6 vs. 28 mins, respectively). Hydrogen ion (H+) concentration and base excess, obtained 2 mins after the first buffer dose, were the best predictors of resuscitability. Arterial and mixed venous Pco2 did not increase after NaHCO3 or Carbicarb compared with NaCl. CONCLUSIONS: Buffer therapy promotes successful resuscitation after prolonged cardiac arrest, regardless of coronary perfusion pressure. NaHCO3, and to a lesser degree, Carbicarb, are beneficial in promoting early return of spontaneous circulation. When epinephrine is used to promote tissue perfusion, there is no evidence for hypercarbic venous acidosis associated with the use of these CO2 generating buffers.

Animals↗