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Biomedical subjects

J W Standeven

Publications and source records attributed to J W Standeven.

At least 19 recordsLinked to original sources

Assessment of fatigue, monitor placement, and surgical experience during simulated laparoscopic surgery.

BACKGROUND: Laparoscopic surgery requires the surgeon to assume atypical postures for extended periods of time, potentially leading to fatigue and chronic injury. This study assessed the level of muscle activity and compared the effects of fatigue, monitor placement, and surgical experience during simulated laparoscopic surgery. METHODS: Four attending and four resident surgeons repeated a series of four tasks with a View site and a standard operating room monitor. Electromyography (EMG) activity and muscular discomfort scores were obtained before and after a "fatigue session." Two variables, the EMG amplitudes and discomfort scores, were analyzed. RESULTS: The EMG amplitudes generally exceed the recommended threshold limits of acceptable muscular load. EMG data and discomfort scores demonstrated a fatigue response in several muscle groups. Minimal differences between the two monitor positions were seen. Overall, the EMG data and discomfort scores showed less muscle activity and discomfort in the attending surgeons. CONCLUSION: Laparoscopic surgery required a relatively high muscular load, putting surgeons at risk for fatigue and injury. Altering the monitor placement did not reduce the surgeon's risk of fatigue. Experience slightly reduced the level of fatigue, but not enough to reduce the surgeon's risk category.

Adult↗

An inexpensive alternative approach to bone compression analyses.

A new method for testing the compression strength of vertebrae was developed and implemented using minimal resources and time expenditure. The device digitally measured and analyzed the torque and force necessary to load rat lumbar and thoracic vertebrae to failure. The system was calibrated using a series of known lead masses. Similar to other standardized force/compression and torque devices, this method has been shown to provide reliable and reproducible results. Furthermore, although vertebrae were the only specimens used to collect data in these initial studies, this measurement system could be altered quite easily to allow for a variety of test materials.

Animals↗

Effects of intraaortic balloon position on renal artery blood flow.

Debate continues over what happens to renal blood flow when intraaortic balloons are adjacent to the renal arteries. Fourteen dogs were prepared by implanting instruments to measure heart rate; right atrial, pulmonary arterial, carotid arterial, and femoral arterial pressures; cardiac index; mixed venous oxygen saturation; urine output; and left and right renal blood flows. A 12-mL intraaortic balloon was inserted through the left (n = 9) or right (n = 5) femoral artery. The position of the balloon was randomized so that it was initially placed in either the control (thoracic) or renal position (at the level of the renal arteries). Intraaortic balloon pumping was performed for 4 hours in each position. In 8 dogs, at least one of the renal arteries had partial occlusion, 23% to 98% decrease in flow (mean decrease, 66%), while the intraaortic balloon was in the renal position. An intraaortic balloon in the renal position results in lower renal blood flow as well as a high risk (57%) of selective renal artery occlusion. Decreased renal blood flow is not apparent using conventional monitoring, as hemodynamics do not change.

Animals↗

Twelve-year experience with internal mammary artery for coronary artery bypass.

From Feb. 1, 1972, to Jan. 30, 1984, 1,000 patients had isolated coronary bypass with at least one internal mammary artery, and 103 of them had bilateral internal mammary artery grafts. There were 1,395 associated vein grafts and 1,158 internal mammary artery anastomoses, for a total of 2,556 grafts (2.5 per patient). Patients were followed up for 1 to 12 years (mean 6.3 years) and 77 patients were lost to follow-up at a mean of 4.0 years. Operative mortality was 1.4%, with 11 of 14 deaths in the first 240 patients (4.6%) and eight of 14 in the 103 patients with bilateral internal mammary artery grafts. There were 93 late deaths, with an actuarial survival rate of 93% at 5 years and 84% at 10 years. Angina occurred at a mean rate of 6.2% +/- 1.2% per year. Perioperative infarction was detected in 37 patients (3.7%). Late infarction occurred in 75 patients, for a mean rate of 1.5% +/- 0.3% per year. Reoperation (or percutaneous transluminal coronary angioplasty) was necessary in 35 patients, for a mean rate of 0.85% +/- 0.28% per year. Graft patency was assessed by 1,029 follow-up catheterizations in 519 patients. The patency rate of the left internal mammary artery was 96.4% at 1 year, 88.1% at 5 years, and 88.1% at 10 years. That of the right internal mammary artery was 92.8% (p = NS) at 1 year, 84.6% (p = NS) at 5 years, and at 10 years the numbers were too small to be meaningful. Comparison of patency rates for all internal mammary artery grafts with vein grafts gave 1 year graft patency rates of 95.7% versus 93.4% (p less than 0.025), 5 year rates of 87.9% versus 74.0% (p less than 0.001), and 10 year rates of 83.0% versus 41.0% (p less than 0.001). Included in these patency data are 20 free internal mammary artery grafts; 16 were studied (mean 2.3 years) and 12 of these 16 (75%) were patent. Of the 58 sequential internal mammary artery grafts, 18 were studied by catheterization (mean interval 2.0 years); 35 of 36 anastomoses were patent and one end-to-side anastomosis was closed. Morbidity and mortality for patients having internal mammary artery grafting are comparable to those of patients having saphenous vein bypass only. The demonstrated superior patency for internal mammary artery grafts supports the routine use of bilateral internal mammary artery grafting.

Actuarial Analysis↗

Cold blood potassium diltiazem cardioplegia.

Despite the use of cold blood potassium (CBK) cardioplegia, the severely impaired myocardium and/or long ischemia time continue to be a challenge. Because of the association of Ca++ with cell injury and death, the use of Ca++ entry blockers is logical. Investigation of cold blood diltiazem (CBD) revealed no advantages over CBK cardioplegia. The combination of potassium and diltiazem is appropriate because of their different mechanisms of action. Ten dogs had 1 hour of myocardial ischemia with topical ice (temperature 7 degrees +/- 2 degrees C) after coronary perfusion with 200 ml of cold blood (5 degrees +/- 1 degree C) containing potassium (30 mEq/L) and diltiazem (400 micrograms/kg). Eight dogs had 2 hours of ischemia after perfusion with 200 ml of cold blood containing potassium (30 mEq/L) and diltiazem (200 micrograms/kg) and reperfusion every 30 minutes with 100 ml of cold blood containing KCl (30 mEq/L) and diltiazem (100 micrograms/kg). Six dogs received the same treatment as the previous group except that diltiazem was increased to 1,600 micrograms/kg for all four perfusions. Baseline studies were repeated after 60 minutes of reperfusion without the use of Ca++ or inotropic agents. Heart rate, peak systolic pressure, velocity of the contractile element (Vce), maximum velocity of contractile element (Vmax), peak +dp/dt, peak -dp/dt, dp/dt over common peak isovolumic pressure, left ventricular compliance, stiffness and elasticity, and heart water were unchanged from control. Coronary vascular resistance was unchanged in Groups 1 and 2 but declined in Group 3. Creatine phosphate was preserved during ischemia; adenosine triphosphate (ATP) declined. With reperfusion there was continued fall in ATP, ADP, and the adenosine pool. Ultrastructure was well preserved. In 16 of 24 dogs defibrillation was not required, whereas all 48 dogs with CBK and all 13 with CBD required defibrillation. These data suggest that the addition of diltiazem to CBK provides more effective cardioplegia (preservation of creatine phosphate), although ATP and the adenosine pool continued to decline with reperfusion.

Adenosine Triphosphate↗

Cold blood-diltiazem cardioplegia.

The calcium channel blocker, diltiazem, has been studied in the same model used for evaluation of cold blood-potassium cardioplegia. Six dogs (Group 1) had one hour of myocardial ischemia with topical ice (myocardial temperature, 7 degrees +/- 2 degrees C) after coronary perfusion with 200 ml of cold blood (5 degrees +/- 1 degree C) containing diltiazem, 400 micrograms per kilogram of body weight. Seven dogs (Group 2) had two hours of ischemia after perfusion with 200 ml of cold blood containing 200 micrograms/kg and reperfusion every 30 minutes with 100 ml of cold blood and diltiazem, 100 micrograms/kg. Baseline studies were repeated after rewarming and 40 minutes of reperfusion. No inotropic agents or calcium were used. Heart rate, peak systolic pressure, velocity of the contractile element, peak + rate of rise of left ventricular pressure (dP/dt), peak - dP/dt, dP/dt over common peak isovolumic pressure, left ventricular compliance and stiffness, and heart water were unchanged in Group 1. In Group 2, heart rate slowed (p less than 0.025) and compliance decreased (p less than 0.02). In both groups, coronary vascular resistance declined (p less than 0.001) and recovery of adenosine triphosphate (p less than 0.001), adenosine diphosphate (p less than 0.025), and the adenosine pool (p less than 0.001) was impaired. Ultrastructure was well preserved, but myofibrillar lesions were noted in Group 2. Diltiazem cardioplegia was associated with good functional recovery, but there was impairment of high-energy phosphate metabolism.

Adenosine↗

Afterload reduction with hydralazine following valve replacement.

Impedance reduction with hydralazine was evaluated in 23 patients 1 to 3 hours after aortic or mitral valve replacement. Patients were randomly assigned to Group 1 (0.25 mg/kg) or Group 2 (0.5 mg/kg) and responses at 20, 60, and 120 minutes compared with control (paired t test) and mean values for each group compared (t test). In Group 1 significant responses were the fall in mean arterial pressure (78.3 +/- 3.0 to 66.7 +/- 2.2 mm Hg) and systemic vascular resistance (2,808 +/- 264 to 1,823 +/- 164 dynes-sec/cm5); the increase in cardiac index (2.07 +/- 0.13 to 2.71 +/- 0.21 L/min/m2), stroke volume index (26.9 +/- 2.3 to 34.0 +/- 3.3 ml/beat), and heart rate (80.8 +/- 5.8 to 84.2 +/- 6.6 beats/min). Central venous pressure did not change and left atrial pressure decreased at 120 minutes. Group 2 responses were similar except for higher central venous pressure at 20 minutes, higher left atrial pressures at control, 20, and 60 minutes, and lower left ventricular stroke work at control, 20, and 60 minutes. By selectively dilating the arterial system, hydralazine reduces mean arterial pressure and systemic vascular resistance and increases cardiac output with suble filling pressures.

Aortic Valve↗

Cold blood as the vehicle for potassium cardioplegia.

Cold blood with potassium, 34 mEq/L, was compared with cold blood and with a cardioplegic solution. Three groups of 6 dogs had 2 hours of aortic cross-clamp while on total bypass at 28 degrees C with the left ventricle vented. An initial 5-minute coronary perfusion was followed by 2 minutes of perfusion every 15 minutes for the cardioplegic solution (8 degrees C) and every 30 minutes for 3 minutes with cold blood or cold blood with potassium (8 degrees C). Hearts receiving cold blood or cold blood with potassium had topical cardiac hypothermia with crushed ice. Peak systolic pressure, rate of rise of left ventricular pressure, maximum velocity of the contractile element, pressure volume curves, coronary flow, coronary flow distribution, and myocardial uptake of oxygen, lactate, and pyruvate were measured prior to ischemia and 30 minutes after restoration of coronary flow. Myocardial creatine phosphate (CP), adenosine triphosphate (ATP), and adenosine diphosphate (ADP) were determined at the end of ischemia and after recovery. Changes in coronary flow, coronary flow distribution, and myocardial uptake of oxygen and pyruvate were not significant. Peak systolic pressure and lactate uptake declined significantly for hearts perfused with cold blood but not those with cold blood with potassium. ATP and ADP were lowest in hearts perfused with cardioplegic solution, and CP and ATP did not return to control in any group. Heart water increased with the use of cold blood and cardioplegic solution. Myocardial protection with cold blood with potassium and topical hypothermia has some advantages over cold blood and cardioplegic solution.

Adenosine Diphosphate↗

Cold-blood potassium cardioplegia: evaluation of glutathione and postischemic cardioplegia.

Potassium (34 mEq/L) cardioplegia was induced with cold blood (CBK) in three groups of six dogs undergoing 60 minutes of myocardial ischemia at a systemic temperature of 27 degrees +/- 2 degrees and a myocardial temperature of 7 degrees +/- 2 degrees C (crushed ice). Group 1 (CBK) animals were reperfused initially with 400 ml cold blood over 8 to 10 minutes at increasing pressures of up to 75 mm Hg. Group II (CBK-K) dogs were reperfused in the same manner as Group I with the addition of potassium chloride, 30 mEq/L. In Group III (CBKG-KG) glutathione, 30 mg/100 ml, was added to both the pre- and postischemic perfusions with CBK. After 30 minutes of reperfusion control studies were repeated. Heart rate, peak systolic pressure, rate of rise of left ventricular pressure, maximum velocity of contractile element, pressure-volume curves, coronary flow distribution, muscle stiffness, and heart water were not significantly different from control values. Total coronary flow and myocardial uptake of oxygen, lactate, and pyruvate did not serve to separate the three groups; the same was true for right ventricular creatine phosphate, adenosine triphosphate, and adenosine diphosphate during ischemia and recovery. Ultrastructural myofibrillar lesions were noted in all groups. thus, postischemic cardioplegia and use of a physiological reducing agent do not enhance CBK cardioplegia with topical and systemic hypothermia.

Adenosine Diphosphate↗

Topical cardiac hypothermia: the effect of methylprednisolone sodium succinate.

We evaluated the effects of methylprednisolone sodium succinate (MPSS) on 60 minutes of myocardial ischemia during profound (5 degrees C) topical cardiac hypothermia (ice chips) in a canine right heart bypass preparation. The ventricular function curve shifted to the right and downward, but not significantly, after ischemia, and stroke work declined significantly for both control and treated dogs. Contractility (rate of rise of left ventricular pressure and maximum velocity of the contractile element) declined for both groups but not significantly. Total coronary flow, oxygen consumption, and metabolism of lactate and pyruvate were not different for control and treated dogs. Ultrastructure of the outer and inner myocardium did not demonstrate benefit from MPSS. Intracellular and extracellular edema of moderate severity was slightly worse in the subendocardium, and reversible mitochondrial injury of a mild to moderate degreee was symmetrically present. Ice-related injury was not noted. We were unable to deomonstrate that pretreatment with MPSS favorably alters cardiodynamics or ultrastructure after 60 minutes of profound topical cardiac hypothermia.

Animals↗

Myocardial protection by intermittent perfusion with cardioplegic solution versus intermittent coronary perfusion with cold blood.

The myocardial protection provided by cardioplegic solution using buffered, isosmotic potassium (30 mEq. per liter) was compared with intermittent cold coronary perfusion for 2 hours of aortic cross-clamping in dogs. The cardioplegic solution (Group CS) or cold blood (Group CB) was infused every 15 minutes through a cooling coil to reduce the perfusate temperature to 5 degrees C. Myocardial function after 30 minutes of reperfusion and rewarming was reduced in Group CB with a significant reduction in peak systolic pressure at a left ventricular (LV) balloon volume of 20 ml. and a significant reduction of dp/dt. In contrast, in Group CS, LV function was unchanged from the base-line period. LV compliance also was significantly reduced in Group CB while being unchanged in Group CS. Myocardial extravascular water content, obtained by dessication, was significantly higher in Group CB than in Group CS, which may explain the reduction in compliance. Electron microscopy showed normal ultrastructure in Group CS but extracellular edema in Group CB. Total coronary blood flow showed a sustained increase during reperfusion in both groups. Oxygen consumption rose with rewarming to base-line levels in both groups, whereas lactate and pyruvate consumption was reduced in both groups, particularly Group CB. Cardioplegic solution thus appears to be superior to the intermittent perfusion of cold blood for myocardial protection. The addition of potassium arrest, by markedly reducing myocardial metabolism, improves the protection afforded by cold blood perfusion alone.

Animals↗

Coronary venous arterialization: acute hemodynamic, metabolic, and chronic anatomical observations.

Nine dogs that had anastomosis of the internal mammary artery (IMA) to the left anterior descending coronary vein (LADV) were studied acutely on right-heart bypass. Occlusion of the left anterior descending coronary artery (LADA) and LADV without venous arterialization resulted in a significant decline in stroke work, total coronary flow, and myocardial oxygen uptake; with reactive hyperemia an increase in lactate and pyruvate consumption resulted. Occlusion of the LADA and LADV with VA did not change these variables greatly, except for a marked increase in total coronary flow with reactive hyperemia. Chronic venous arterialization in 14 dogs was associated with a 14% mortality, while 10 controls had a 40% mortality. Dogs were killed at six weeks, and prior angiography in 9 showed patency of the IMA to the heart without filling of cardiac veins. All dogs had infarcts in the distribution of the LADA; these infarcts were smaller in dogs with venous arterialization. The anastomoses were obliterated by mature or maturing fibrous tissue, with alteration of the vein so that it was frequently not discernible, while the IMA was well preserved. Distal veins had foci of intimal proliferation, subintimal fibrosis, and medial hypertrophy. Although venous arterialzaiton provides protection for the acutely ischemic myocardium, this effect does not persist, perhaps because of anastomotic occlusion due to fibrous proliferation.

Animals↗

A servo controlled transapical left ventricular to aortic assist device with implantable canulae.

A servo controlled transapical LV to aortic bypass system employing a roller pump was evaluated. The pump achieved complete LV decompression with reduction of LV pressure below systemic pressure. The servo control was responsive to LA pressure and allowed stable complete bypass during interventions designed to raise and lower LA pressure. A permanently implantable transapical LV cannula and aortic cannula without obturators was evaluated with and without anticoagulants. The teflon felt surface 'healed' rapidly and developed a multi-layered fibrous pseudointima. Anticoagulants appeared to avoid excessive thrombus formation at the cannula sites and embolization.

Animals↗

The effect of left atrial-to-aortic assistance on infarct size.

Left atrial-to-aortic (La-A) assistance is effective in supporting the failing circulation. This study evaluated its effect in salvaging ischemic myocardium in both large and small infarct models. In a control group, good correlation was shown between measurements of infarct size by ST-segment mapping at 20 minutes, triphenyl tetrazolium chloride staining at 5 hours, and the distribution of radioactive microspheres (P less than 0.01). A servo controlled assist pump was used which controlled pump speed according to the left atrial pressure. This allowed greater degrees of bypass for prolonged periods with reduced risk of air embolism. La-A assistance reduced systolic left ventricular pressure, and reduced the pressure time index (P less than 0.05). La-A assistance did not reduce infarct size measured by ST-segment mapping in a large infarct model when instituted before occlusion or 20 minutes after occlusion. Triphenyl tetrazolium chloride staining, however, showed less severe and homogenous damage in the assisted group as compared to controls. Electron microscopy confirmed the patchy nature of the ischemia. In a small infarct model, La-A assistance reduced nST from 6.3 +/- 0.8 to 3.8 +/- 1.5 and ST from 4.9 +/- 0.6 to 2.7 +/- 0.9 (P less than 0.05). The endocardial to epicardial ratio in the ischemic area fell from 0.69 +/- 0.05 to 0.43 +/- 0.05 in the control group (P less than 0.05) and a similar fall occurred in the assisted groups. La-A assistance is thus effective in reducing myocardial ischemia in a small infarct model, but appears to be less effective in a large infarct model.

Animals↗