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Biomedical subjects

A B Sanders

Publications and source records attributed to A B Sanders.

At least 73 records · Page 4Linked to original sources
PubMed1991

Hypertensive emergencies.

A hypertensive emergency is a rare event in which an acute elevation of blood pressure causes rapid progressive end-organ damage. Cardiovascular, renal and central nervous system syndromes may be associated with acute blood pressure elevations. Prompt treatment with antihypertensive agents should be initiated while the patient is closely monitored. Lowering the blood pressure too quickly can exacerbate symptoms and decrease organ blood flow. Treatment must be individualized depending on the end organ involved and the patient's clinical status. A general goal is to lower the mean arterial pressure by approximately 20 to 25 percent or reduce the diastolic pressure to 100 to 110 mm Hg over a one-hour period. Medications such as nitroprusside allow minute-to-minute regulation of the patient's blood pressure and clinical symptoms.

Acute Disease↗
PubMed1990

Depletion of myocardial adenosine triphosphate during prolonged untreated ventricular fibrillation: effect on defibrillation success.

We studied left ventricular endomyocardial adenosine triphosphate levels in 13 large mongrel dogs before and during ventricular fibrillation induced cardiac arrest to assess whether myocardial adenosine triphosphate content could predict successful cardiopulmonary resuscitation. Endomyocardial biopsies were performed during sinus rhythm (control), after 15 min of ventricular fibrillation or 10 min of ventricular fibrillation and 5 min of open chest cardiopulmonary resuscitation, after 20 min of ventricular fibrillation and 10 min of open chest cardiopulmonary resuscitation and after 40 min ventricular fibrillation and 15-20 min open chest cardiopulmonary resuscitation. Myocardial adenosine triphosphate was measured utilizing a bioluminescence method adapted for use with endomyocardial biopsies and normalized to protein content. Left ventricular endomyocardial adenosine triphosphate content fell significantly over time from a control level of 8.88 +/- 0.9 micrograms/mg protein to 5.73 +/- 0.5 micrograms/mg protein at 15 min of cardiac arrest, to 3.4 +/- 0.4 micrograms/mg protein after 30 min of cardiac arrest and to 1.98 +/- 0.3 micrograms/mg protein after 60 min of cardiac arrest (P less than 0.001). Adenosine triphosphate levels were significantly different between animals that received 10 min of ventricular fibrillation and successful open chest cardiopulmonary resuscitation and those that received 40 min of ventricular fibrillation and unsuccessful open chest cardiopulmonary resuscitation (4.35 +/- 0.48 vs. 2.11 +/- 0.43 micrograms/mg protein; P less than 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1990

The effect of energy malnutrition in ruminants on experimental infection with Dermatophilus congolensis.

The ability of malnourished and optimally fed animals to resist infection with D. congolensis was assessed by the dose-response to experimental inoculation. The severity of infection, as measured by scoring the lesions, was the same in both groups of lambs. However marked differences were seen between the two groups in the appearance of scabs and in the time taken for them to resolve. The malnourished animals had more persistent, chronic lesions compared with the more obvious, acute type lesions seen on the skin of the healthy controls. These results were probably related to the reduced rates of wool growth and lanolin production found in the malnourished lambs, which may reflect a reduction in the rate of cellular turnover in the skin of these animals.

3-Hydroxybutyric Acid↗
PubMed1990

The role of bicarbonate and fluid loading in improving resuscitation from prolonged cardiac arrest with rapid manual chest compression CPR.

Rapid manual chest compression (120 compressions/min) CPR has been shown to improve hemodynamics and survival when compared with standard CPR (60 compressions/min) in a canine model of prolonged cardiac arrest. The study showing improved survival with rapid manual CPR empirically included treatment with bicarbonate and initial fluid loading. To determine the role of bicarbonate and fluid loading in the success of rapid manual chest compression CPR, 31 mongrel dogs were studied. After instrumentation with micromanometer-tipped catheters to measure aortic and right atrial pressures, the animals were assigned sequentially to three treatment groups. Group A underwent rapid manual chest compressions at 120 compressions/min, bicarbonate treatment, and initial fluid loading. Group B underwent rapid manual compressions at 120 compressions/min without bicarbonate or fluid loading. Group C underwent standard CPR at 80 compressions/min with bicarbonate and fluid loading. After 30 minutes of ventricular fibrillation, defibrillation was attempted. Seven of 11 dogs in group A survived 24 hours. None of the animals in group B resuscitated or survived. Three of the ten dogs in group C survived 24 hours. Survival with rapid manual CPR without bicarbonate and initial fluid loading was significantly less than when these interventions were used (P less than .01). To examine the separate contribution of bicarbonate and fluid therapy, two additional groups of animals were studied. Fourteen animals (group D) received rapid manual CPR with bicarbonate therapy, and 12 (group E) received rapid manual CPR with fluid loading only.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

End-tidal carbon dioxide monitoring during cardiopulmonary resuscitation. A prognostic indicator for survival.

The effectiveness of ongoing cardiopulmonary resuscitation efforts is difficult to evaluate. Recent studies suggest that carbon dioxide excretion may be a useful noninvasive indicator of resuscitation from cardiac arrest. A prospective clinical study was done to determine whether end-tidal carbon dioxide monitoring during cardiopulmonary resuscitation could be used as a prognostic indicator of resuscitation and survival. Thirty-five cardiac arrests in 34 patients were monitored with capnometry during cardiopulmonary resuscitation during a 1-year period. Nine patients who were successfully resuscitated had higher average end-tidal carbon dioxide partial pressures during cardiopulmonary resuscitation than 26 patients who could not be resuscitated (15 +/- 4 vs 7 +/- 5 mm Hg). The 3 patients who survived to leave the hospital had a higher average end-tidal carbon dioxide partial pressure than the 32 nonsurvivors (17 +/- 6 vs 8 +/- 5 mm Hg). All 9 patients who were successfully resuscitated had an average end-tidal carbon dioxide partial pressure of 10 mm Hg or greater. No patient with an average end-tidal carbon dioxide partial pressure of less than 10 mm Hg was resuscitated. Data from this prospective clinical trial indicate that findings from end-tidal carbon dioxide monitoring during cardiopulmonary resuscitation are correlated with resuscitation from and survival of cardiac arrest.

Blood Gas Monitoring, Transcutaneous↗
PubMed1989

Emergency medicine.

Explore the source record for details and available documents.

Emergency Medical Services↗
PubMed1989

Changes in expired end-tidal carbon dioxide during cardiopulmonary resuscitation in dogs: a prognostic guide for resuscitation efforts.

Expired end-tidal carbon dioxide (PCO2) measurements made during cardiopulmonary resuscitation have correlated with cardiac output and coronary perfusion pressure when wide ranges of blood flow are included. The utility of such measurements for predicting resuscitation outcome during the low flow state associated with closed chest cardiopulmonary resuscitation remains uncertain. Expired end-tidal PCO2 and coronary perfusion pressures were measured in 15 mongrel dogs undergoing 15 min of closed chest cardiopulmonary resuscitation after a 3 min period of untreated ventricular fibrillation. In six successfully resuscitated dogs, the mean expired end-tidal PCO2 was significantly higher than that in nine nonresuscitated dogs only after 14 min of cardiopulmonary resuscitation (6.2 +/- 1.2 versus 3.4 +/- 0.8 mm Hg; p less than 0.05). No differences in expired end-tidal PCO2 values were found at 2, 7 or 12 min of cardiopulmonary resuscitation. A significant decline in end-tidal PCO2 levels during the resuscitation effort was seen in the nonresuscitated group (from 6.3 +/- 0.8 to 3.4 +/- 0.8 mm Hg; p less than 0.05); the successfully resuscitated group had constant PCO2 levels throughout the 15 min of cardiac arrest (from 6.8 +/- 1.1 to 6.2 +/- 1.2 mm Hg). Changes in expired PCO2 levels during cardiopulmonary resuscitation may be a useful noninvasive predictor of successful resuscitation and survival from cardiac arrest.

Animals↗
PubMed1989

Capnometry in emergency medicine.

Capnometers measure carbon dioxide (CO2) in expired air and provide clinicians with a noninvasive measure of systemic metabolism, circulation, and ventilation. If two of these systems are held relatively constant, changes in CO2 excretion will reflect the third. CO2 measurement has been advocated as a method of ensuring endotracheal intubation. Because the air in the esophagus has very low levels of CO2, the use of capnometers may help prevent unrecognized esophageal intubation in prehospital and emergency department settings. In patients with normal perfusion and ventilation, end-tidal CO2 measurements closely reflect alveolar PCO2. Capnometry may decrease the need for frequent arterial blood gas measurements. A sudden change in end-tidal CO2 measurement may indicate decreased lung perfusion and an early shock state. Thus, capnometry may be useful to monitor critical patients in the ED. In addition, capnometry has potential usefulness as a noninvasive indicator of the efficacy of ongoing CPR efforts. End-tidal CO2 has been shown to correlate with cardiac output, perfusion pressures, and successful resuscitation in experimental models of cardiac arrest. Further clinical studies are needed to define the role of capnometry in emergency medicine.

Breath Tests↗
PubMed1989

Plasma catecholamines and resuscitation from prolonged cardiac arrest.

Plasma catecholamine levels rise markedly with cardiac arrest and attempted resuscitation. We examined whether epinephrine (EPI) or norepinephrine (NE) plasma concentrations could predict resuscitation outcome. In nine mongrel dogs, EPI and NE levels were drawn before cardiac arrest and after 8 and 14 min of cardiac arrest and CPR. Intravenous EPI (1 mg) was given 1 min before the last plasma level was drawn. Catecholamines were quantitated by high-performance liquid chromatography with triple-electrode coulometric electrochemical detection. Plasma catecholamines increased significantly with cardiac arrest, EPI levels increased from a control level of 15.9 +/- 3.0 to 396.0 +/- 63.3 pmol/ml after 8 min of cardiac arrest (p less than .05), and NE levels similarly increased from 4.4 +/- 1.7 to 66.5 +/- 12.0 pmol/ml (p less than .01). Neither the absolute catecholamine plasma concentration nor the response to cardiac arrest of the endogenous catecholamine concentrations could predict outcome, but catecholamine responses to exogenous EPI did correlate with outcome. Animals which were subsequently resuscitated had a greater increase in the plasma EPI concentrations after exogenous EPI than animals that were not resuscitated, a 53-fold vs. a 23-fold increase (p less than .05). Successfully resuscitated animals also had increased NE levels after exogenous EPI, while unsuccessfully resuscitated animals had either no change or a decrease (p less than .02). Successfully resuscitated animals had an increase in coronary perfusion pressure (p less than .01) in response to exogenous EPI, in contrast to those that were not resuscitated. This suggests that the exogenous administration of EPI during prolonged CPR is beneficial despite markedly elevated endogenous catecholamine levels.

Animals↗
PubMed1988

Aortic and right atrial systolic pressures during cardiopulmonary resuscitation: a potential indicator of the mechanism of blood flow.

The absolute difference between aortic and right atrial systolic pressure (systolic pressure gradient) and the difference between the aortic diastolic and right atrial diastolic pressure (coronary perfusion pressure) were evaluated in a series of 63 adult mongrel dogs undergoing five different methods of cardiopulmonary resuscitation (CPR). Fluid-filled pressure monitoring catheters were placed in the ascending aorta and right atrium in each of the animals after induction of anesthesia with morphine sulfate and 1% halothane and oxygen. The animals were then fibrillated with a transvenous electrode catheter that had been introduced into a ventricle. After a "down time" of 3 minutes during which no CPR was performed, the animals' lungs were ventilated, and one of five methods of CPR was initiated. The systolic pressure gradient and coronary perfusion pressure were measured in all animals 1 minute after CPR was begun, and in all but the group undergoing open-chest cardiac massage after 7 minutes and 17 minutes of CPR. The systolic pressure gradient and coronary perfusion pressure were greatest during open-chest cardiac massage (true cardiac compression), intermediate in external mechanical CPR (Thumper) and standard CPR (greater in small dogs than large dogs), and lowest in CPR performed with a combined thoracic and abdominal vest apparatus (predominantly thoracic pump). The observation that the systolic pressure gradient between intrathoracic chambers is largest in open-chest cardiac massage and smallest in vest CPR suggests that similar measurements recorded during the performance of human cardiac resuscitation may be useful in determining the mechanism of blood flow.

Animals↗
PubMed1988

Oxygen free radicals and myocardial reperfusion injury.

Diseases involving tissue reperfusion following ischemia are gaining significance in emergency medicine. The significance of reperfusion injury and the probable role of oxygen-derived free radicals has been described in many tissues, particularly the heart. During myocardial reperfusion a burst of oxygen-derived free radicals overwhelms normal cellular defenses. These radicals may have several detrimental effects. They can oxidize lipids, leading to membrane dysfunction. They can also alter nucleic and other proteins. Cellular dysfunction and death may ensue. Prevention of oxygen-derived free radical injury appears possible and may be feasible for several disease processes, including myocardial reperfusion after infarction.

Animals↗
PubMed1988

Acid-base balance in a canine model of cardiac arrest.

Our study was performed to determine the pattern of arterial, venous, and cerebral spinal fluid (CSF) acidosis in a canine model of cardiac arrest and resuscitation; and the effect of bicarbonate treatment on arterial, venous, and CSF acidosis. Animals were instrumented to sample arterial blood, mixed venous blood, and CSF through a cisternal catheter. Following six minutes of ventricular fibrillation, manual CPR efforts were begun and continued for 30 minutes of cardiac arrest. Arterial, mixed venous, and CS fluids were sampled at baseline, six, 12, 18, 24, 27, and 30 minutes. Ten experimental dogs received sodium bicarbonate (2 mEq/kg) at 20 minutes of cardiac arrest, while ten animals in the control group received no alkali treatment. The experimental group showed a significantly higher arterial (7.79 +/- 0.20 vs 7.46 +/- 0.16 at 30 minutes) and venous pH (7.34 +/- 0.12 vs 7.19 +/- 0.10 at 24 minutes) following bicarbonate administration. This higher pH occurred despite a concomitant increase in arterial (31 +/- 10 vs 19 +/- 9 mm Hg at 27 minutes; 31 +/- 9 vs 10 +/- 8 at 30 minutes) and venous (104 +/- 30 vs 63 +/- 10 mm Hg at 24 minutes) pCO2. CSF analysis showed a gradually worsening acidosis. However, CSF pH (7.12 +/- 0.14 vs 7.16 +/- 0.23 at 30 minutes) and pCO2 were not significantly changed by the administration of bicarbonate.

Acidosis↗
PubMed1988

Influence of compression rate on initial success of resuscitation and 24 hour survival after prolonged manual cardiopulmonary resuscitation in dogs.

The influence of chest compression rate on initial resuscitation success and 24 hr survival after prolonged manual cardiopulmonary resuscitation (CPR) was investigated in 26 morphine-anesthetized dogs (17 to 30 kg). After placement of aortic and right atrial micromanometers and induction of ventricular fibrillation, manual CPR was commenced immediately and continued for 30 min. One group of 13 dogs underwent manual CPR at a compression rate of 60/min, and the other group at a rate of 120/min. The compression durations in the two groups were not significantly different (51.7 +/- 1.8% at 60/min vs 51.6 +/- 1.9% at 120/min). No drugs other than sodium bicarbonate were administered during CPR. A maximum of three attempts was permitted to defibrillate the heart. Successfully defibrillated animals were followed for 24 hr, during which time no treatment, other than naloxone, was given to reverse the effects of morphine. Arterial blood pH, PCO2, and PO2 were not significantly different in the two groups throughout the CPR period. When compared with the compression rate of 60/min, the compression rate of 120/min produced more successfully defibrillated animals (12/13 at 120/min vs 2/13 at 60/min, p less than .002) and more 24 hr survivors (8/13 at 120/min vs 2/13 at 60/min, p less than .03). All 24 hr survivors were conscious and able to sit, stand, and drink normally. One 24 hr survivor in each group had difficulty walking. Improved survival with the high-rate compression technique was consistent with the significantly higher mean aortic (systolic and diastolic) and coronary perfusion pressures attained with high-rate compressions (all p less than .002). Although the clinical applicability of these findings has yet to be demonstrated, they provide empirical support for the recent decision to increase the chest compression rate for manual CPR recommended by the American Heart Association, and indicate that the hemodynamic and survival benefits of faster compression rates in this experimental preparation were not dependent on covariant alterations in compression duration.

Animals↗
PubMed1988

Myocardial salvage: pharmacologic treatment.

We have attempted to review the role of pharmacologic agents in the treatment of patients with acute myocardial infarction for the purposes of limiting infarct size. At this time, the beta-blocking agents and nitroglycerin have been the most extensively studied in clinical trials and should be part of our overall pharmacologic approach to patients with acute myocardial infarction. Treatment, however, needs to be individualized, depending on the resources available within one's hospital and community. The early treatment of patients with acute myocardial infarction is undergoing a revolution. Whereas a decade ago we were satisfied with simply monitoring patients for malignant arrhythmias, now we are aggressively attempting to limit infarct size and reperfuse myocardium. In all these proposed treatments for myocardial salvage, time is a crucial element. Therefore, emergency physicians and paramedics become a vital link to begin appropriate treatment leading to myocardial salvage and reperfusion. We must begin to think of all patients with symptoms of acute myocardial infarction as candidates for aggressive attempts at myocardial salvage. These attempts will only take place with well-coordinated, multidiscipline efforts involving cardiologists, cardiothoracic surgeons, emergency physicians, paramedics, and critical care teams. Our challenge over the next few years will be to develop efficient systems so that all patients with acute myocardial infarction can receive optimal care.

Adrenergic beta-Antagonists↗
PubMed1987

Open-chest cardiac massage after closed-chest compression in a canine model: when to intervene.

Open-chest cardiac massage appears beneficial in improving hemodynamics during resuscitation efforts and in improving resuscitation success. The time between cardiac arrest and the initiation of open-chest cardiac massage is crucial. It would appear that if initiation of open chest cardiac massage is delayed for more than 20 min from the onset of cardiac arrest, little or no successful outcome can be expected. Further techniques for assessing the adequacy of closed-chest compression CPR are needed. Such techniques would allow early identification of ineffective resuscitation efforts and provide the opportunity for early change to other, presumably more effective, techniques.

Animals↗
PubMed1987

Neurologic benefits from the use of early cardiopulmonary resuscitation.

The efficacy of bystander CPR in resuscitation from cardiac arrest when defibrillation is available within five to six minutes has been questioned. Epidemiologic studies from different cities have shown conflicting results. We conducted a study to determine the effect of early CPR versus no CPR on resuscitability, 24-hour survival, and neurologic deficit in an animal model of cardiac arrest. Twenty-two mongrel dogs were subjected to five minutes of electrically induced ventricular fibrillation. In 11 dogs, closed-chest massage and ventilation with room air was begun immediately and was continued for five minutes. The other 11 dogs received no CPR. At five minutes defibrillation was attempted and advanced cardiac life support (ACLS) protocols were followed until the animal was resuscitated or died. No statistical difference in resuscitability or 24-hour survival between the two groups was demonstrated. Eight of 11 "early CPR" animals were resuscitated and survived 24 hours; six of 11 "no CPR" dogs were resuscitated, and five lived for 24 hours. A significant difference was demonstrated by the Student t test in neurologic deficit and ease of resuscitation. "Early CPR" dogs had no neurologic deficit, while "no CPR" dogs had a 41% deficit (P less than .01). "Early CPR" dogs were resuscitated in significantly less time once ACLS was started (29 versus 317 seconds), and required less electrical energy (100 versus 560 J), fewer countershocks (1.3 versus 4.0), and less epinephrine (0.1 versus 1.7 mg) than did "no CPR" animals. In this animal model of cardiac arrest, early CPR was shown to be beneficial to neurologic function and ease of resuscitation, even when ACLS was provided within five minutes.

Animals↗