Provocation of ventricular tachycardia by an automatic implantable cardioverter defibrillator.
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Biomedical subjects
Publications and source records attributed to M M Kirsh.
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One of the most lethal forms of mediastinitis is descending necrotizing mediastinitis, in which infection arising from the oropharynx spreads to the mediastinum. Two recently treated patients are reported, and the English-language literature on this disease is reviewed from 1960 to the present. Despite the development of computed tomographic scanning to aid in the early diagnosis of mediastinitis, the mortality for descending necrotizing mediastinitis has not changed over the past 30 years, in large part because of continued dependence on transcervical mediastinal drainage. Although transcervical drainage is usually effective in the treatment of acute mediastinitis due to a cervical esophageal perforation, this approach in the patient with descending necrotizing mediastinitis fails to provide adequate drainage and predisposes to sepsis and a poor outcome. In addition to cervical drainage, aggressive, early mediastinal exploration--debridement and drainage through a subxiphoid incision or thoracotomy--is advocated to salvage the patient with descending necrotizing mediastinitis.
A technique is described for bypassing the posterior lateral branch of the right coronary artery by passing the vein graft beneath the inferior vena cava to avoid kinking of the graft.
The myocardial effects of protamine, with and without heparin, were documented in this investigation. Isolated rabbit hearts (n = 30) were retrograde perfused with Krebs-Ringers bicarbonate solution aerated with 95% O2/5% CO2 through the aortic root (37 C, 80 mmHg). Developed left ventricular blood pressure, heart rate, coronary artery flow, contractility as reflected by peak +dp/dt, oxygen extraction (a-vO2), and oxygen consumption (VO2) were measured at baseline and continuously throughout the experiment. Protamine (25 micrograms, 50 micrograms, and 250 micrograms per mL of perfusate) was circulated in the Krebs-Ringers buffer to hearts perfused without heparin (groups I, II, and III) or hearts perfused with heparin added to the buffer solution, 0.1 IU/1.0 microgram protamine (groups IV, V, and VI). Blood pressure 4 minutes after protamine was less in groups III (-23 mmHg) and VI (-28 mmHg) than in groups I (-6 mmHg), II (-18 mmHg), IV (-1 mmHg), and V (-7 mmHg). Heart rate changes (beats/minute) at 4 minutes revealed similar dose-dependent reductions (III and VI: -51, -55; II and V: -36, -36; and I and IV: -20, -16, respectively). Coronary artery flow at 4 minutes was slightly increased in groups III (9 mL/minute) and VI (15 mL/minute), but was relatively unchanged in the other groups. Decreases in contractility were apparent in all groups 4 minutes after protamine was started: group I, -14%; II, -16%; III, -30%; IV, -7%; V, -15%; and VI, -34%. Similarly declines in oxygen extraction and consumption were noted in all groups at the same time period and were greater in groups III (-53%, -44%) and VI (-55%, -49%) than in groups I (-25%, -26%), II (-15%, -12%), IV (-48%, -49%) and V (-15%, -18%), with p less than or equal to 0.05 or p less than or equal to 0.01 compared to baseline. Three of ten hearts exposed to high-dose protamine stopped beating after 5 minutes. This investigation establishes, for the first time, that protamine has dose- and time-specific adverse effects on cardiac contractility. In addition protamine decreases myocardial a-vO2 and VO2. These changes may contribute to certain adverse events accompanying the clinical administration of protamine.
Elevated plasma levels of atrial natriuretic hormone (ANH) have been found in patients during paroxysmal supraventricular tachycardia (SVT) and other clinical syndromes. However, physiologic effects of this endogenous ANH have not been demonstrated. To determine whether the rise in ANH during SVT is associated with either a natriuresis or kaliuresis, urine sodium and potassium levels were measured in five patients at baseline and during SVT simulated by rapid atrioventricular pacing. Plasma ANH levels increased from 149 +/- 35 pmol/L at baseline to 187 +/- 31 pmol/L (p = 0.007) during SVT. Plasma vasopressin and renin levels were unchanged. Urine sodium levels increased 49% from 1.54 +/- 0.66 mEq/hr at baseline to 2.29 +/- 0.89 mEq/hr (p = 0.044) during SVT, and urine potassium levels increased 22% from 4.14 +/- 0.10 mEq/hr to 5.04 +/- 1.25 mEq/hr (p = 0.018). Urine sodium and potassium levels returned to baseline values 1 hour after pacing. Thus elevated plasma levels of ANH during SVT are associated with both a natriuresis and kaliuresis, which may represent physiologic effects of the endogenously secreted hormone.
The enzyme xanthine oxidase has been implicated as a generator of toxic oxygen metabolites that contribute to ischemic injury. Because substantial species variability has been demonstrated and because there are minimal human data available, the relevance of xanthine oxidase to human heart damage has been in doubt. We report the absence of xanthine oxidase activity in nine human heart biopsy specimens obtained during cardiac surgery, and in two larger samples obtained during heart transplantation. A sensitive radiochemical assay was used to assess enzyme activity. Our findings imply that oxygen free radicals generated by xanthine oxidase are not relevant in terms of human myocardial injury.
The adequacy of retrograde delivery of cardioplegic solution to the right ventricle and interventricular septum is controversial. To address this issue quantitatively, we infused blood cardioplegic solution labeled with radioactive microspheres (15 microns diameter) into the coronary sinus (n = 8 dogs) at a pressure of 51 +/- 1 mm Hg (mean +/- standard error of the mean) to be compared with the same quantity of labeled cardioplegic solution (20 ml/kg) delivered through the aorta (n = 6 dogs) at 97 +/- 7 mm Hg. Both methods of delivery produced cardiac arrest, but retrograde infusion required a significantly longer time to complete the infusion (6.2 +/- 0.8 minutes versus 1.5 +/- 0.1 minutes, p less than 0.01). Greater than 99% of the microspheres passing through the vasculature of the left ventricle were trapped in the left ventricular myocardium with antegrade infusion, and the distribution of the cardioplegic solution was uniform. Antegrade delivery (cardioplegic flow x infusion time) averaged approximately 3.0 to 4.0 ml/gm, except at the apex, where delivery averaged approximately 2.0 ml/gm. With retrograde infusion, 93% of the microspheres perfusing the left ventricle were trapped and delivery of the cardioplegic solution was not uniform. In the anterolateral free wall, delivery of cardioplegic solution averaged between 1.5 and 2.9 ml/gm (p less than 0.001 compared with antegrade) and only 0.6 to 0.8 ml/gm in the posteroseptal region of the basal left ventricle (p less than 0.001 compared with the antegrade group and anterolateral samples of the retrograde group). In the middle portion of the right ventricle, antegrade trapping of microspheres was 99% and delivery of cardioplegic solution averaged approximately 2.0 ml/gm. With retrograde delivery, only 16.5% (range 11.8% to 26.0%) of the microspheres passing through the right ventricular vasculature were trapped in the right ventricular myocardium, which indicates that substantial shunting had occurred. Corrected for the high shunt fraction, retrograde delivery of cardioplegic solution to the middle portion of the right ventricle averaged only 0.5 ml/gm (p less than 0.01). Retrograde delivery to the atrial septum and right atrium was also low. Because retrograde delivery of cardioplegic solution was markedly nonuniform, we conclude that inadequate cardioplegic delivery to the middle portion of the right ventricle and posteroseptal portion of the left ventricle could result with cardioplegic infusion through the coronary sinus.
Coronary artery spasm during the early postoperative period following cardiopulmonary bypass for coronary artery surgery can be an unrecognized cause of sudden, severe cardiopulmonary collapse. The literature regarding perioperative coronary artery spasm is reviewed, and methods of prevention, diagnosis, and treatment are suggested. Preoperative angina at rest appears to be an important identifying factor in patients who experience postoperative coronary spasm. Anatomically, the presence of a relatively normal, dominant right coronary may also indicate increased risk for early post-coronary bypass spasm. Acute hypotension is often the first sign of coronary artery spasm, and conventional treatment methods may only worsen the vasospastic reaction. Peripheral intravenous nitroglycerin infusion has often been unsuccessful treatment while intragraft or intracoronary nitroglycerin injection or administration of calcium channel-blocking drugs, or both, has proven to be effective in reversing the coronary artery spasm and ventricular dysfunction. Reluctance to use vasodilating agents must be overcome, even in the face of hypotension, when evidence of spasm is present.
A new technique of occlusion of the venae cavae utilizing a cannula with an inflatable balloon cuff is described.
Ninety-three consecutive patients undergoing coronary artery bypass grafting (CABG) were followed prospectively to ascertain the natural history and determinants of new postoperative conduction defects. Each patient was followed in the postoperative period with serial electrocardiograms and continuous monitoring. In the last 70 patients, a technetium pyrophosphate scan was obtained 48 to 72 hours after operation. Postoperatively, new bundle-branch or fascicular block developed in 42 patients (45%) and third-degree atrioventricular (AV) block, in 4 (4%). The occurrence was compared with patient age, preoperative bundle-branch block or fascicular block, number of diseased arteries, number of bypassed arteries, total time of cardiopulmonary bypass, aortic cross-clamping time, occurrence of a preoperative or perioperative myocardial infarction, and presence of disease in the left anterior descending or right coronary artery. Only the number of bypassed arteries, the total time of cardiopulmonary bypass, and the aortic cross-clamping time were related to the development of postoperative conduction defects (all, p less than .05). The conduction defect resolved partially or completely by the time of hospital discharge in 54% of patients. In the 4 patients with third-degree AV block, AV block resolved on postoperative day 2 in 1 patient and resolved transiently for up to 5 days or persisted in 3 patients. At two months of follow-up, all 3 patients discharged in third-degree AV block with a permanent pacemaker were no longer in AV block. In conclusion, following CABG, the occurrence of new AV conduction defects is related to the number of vessels bypassed, the cardiopulmonary bypass pump time, and the aortic cross-clamping time.(ABSTRACT TRUNCATED AT 250 WORDS)
Thirty-three patients undergoing elective myocardial revascularization were prospectively randomized into two study groups (Group S and Group P) to permit evaluation of the effects of shivering on oxygen consumption per minute (VO2), carbon dioxide production per minute (VCO2), and hemodynamic performance. Group S was allowed to shiver during the postoperative rewarming period, and Group P received hourly injections of pancuronium bromide and Metubine (metocurine) sulfate with sedation to block the shivering response. Group S demonstrated significantly higher increases in VO2 and VCO2, lower systolic blood pressure and mixed venous oxygen saturation, and a greater use of inotropic support than the patients in Group P. Suppression of the shivering response minimized increases in VO2 and VCO2, improved hemodynamic stability, and resulted in a decreased need for inotropic support.
Four hundred twenty-six patients with esophageal atresia with or without tracheoesophageal fistula have been primarily cared for at the University of Michigan Medical Center since Cameron Haight's initial experience with this entity. Over the period of observation, the incidence of new cases as well as the number of associated anomalies has remained constant. The long-term survival of these patients has steadily improved over the past half-century from 36% in the pre-1950 era to 84% during the most recent 20 years. Conversely, operative mortality has shown a progressive decline from 56% early in the authors' series to 6.9% more recently, despite a steady increase in the proportion of high-risk neonates seen at the University of Michigan Medical Center during this time span. In the last 9 years, there have been no postoperative deaths in group A or B risk infants (36 patients), while the rate has been 18.2% in group C risk babies (27 patients); almost all of these deaths were due to severe associated anomalies. During the last 10 years, the authors have changed their technique of anastomosis from a two- to a one-layer method while still advocating a primary repair via an extrapleural approach. Although this change has resulted in a modest increase in the rate of anastomotic leak (17% vs. 6.2%, p less than 0.03), the leaks have been small and asymptomatic because of the extrapleural approach and, as a result, have been managed conservatively without any untoward sequelae. Conversely, there has been a significant decrease in the rate of stricture formation with the one-layer anastomosis (4.3% vs. 23.3%, p less than 0.002). While this may in part be explained by the change in anastomotic technique, it is felt that the more aggressive diagnosis and surgical management of gastroesophageal reflux (seen in 37.9% of our recent group) have contributed greatly to this decrease. The steady improvement in survival over this 50-year period, in spite of the increasing number of high-risk infants, is attributable to major improvements in neonatal care before, during, and after operation.
We evaluated whether supplemental pharmacologic interventions that altered formation or degradation of reactive oxygen metabolites, when added to hypothermic crystalloid cardioplegic solution (procaine-free St. Thomas' Hospital solution), alter postischemic function of isolated rabbit hearts. Hypoxic, substrate-free cardioplegic solutions cooled to 27 degrees C were perfused through isolated rabbit hearts for 5 minutes before and after an uninterrupted 2 hour period of global ischemia at 27 degrees C. Hearts were then reperfused with standard buffer for 1 hour at 37 degrees C. In some experiments, the cardioplegic solution was supplemented with the following: superoxide dismutase (30 micrograms/ml; degrades superoxide anion); catalase (1.7 micrograms/ml; degrades hydrogen peroxide); allopurinol (1 mmol/L; inhibits xanthine oxidase); or deferoxamine (Desferal, 0.5 mmol/L; selectively chelates ferric iron). Postreperfusion contractile parameters of supplemented hearts, including left ventricular pressure development and its first derivative, left ventricular compliance, spontaneous heart rate, and coronary vascular resistance, were statistically compared to data obtained from hearts arrested with unsupplemented cardioplegic solution. Catalase supplementation provided statistically significant improvement of most functional parameters; somewhat less protection was obtained with allopurinol. Deferoxamine provided little added protection except for the ability to prevent ischemia-induced increases of coronary vascular resistance. There was no evidence of added protection by superoxide dismutase. The data suggest that an important component of ischemia-induced cardiac cell damage in an asanguineous setting is hydrogen peroxide-dependent, and interventions that either inhibit production of superoxide anion or degrade hydrogen peroxide offer best protection. They may be clinically efficacious additives to crystalloid cardioplegic solutions.
The objective of this study was to test the hypothesis that cytotoxic oxygen metabolites participate in lytic cardiac cell damage, detected as creatine kinase release, upon reoxygenation of hypoxic, isolated buffer-perfused hearts (oxygen paradox). Perfusate additives included: superoxide dismutase (30 mg/l); catalase (2 mg/l); deferoxamine (0.5 mM); and allopurinol (1 mM). Creatine kinase release upon reoxygenation was reduced, to levels not significantly different from nonhypoxic controls, by adding either catalase, allopurinol or deferoxamine to the buffer during hypoxia. Reduced creatine kinase leakage was not accompanied by parallel preservation of ventricular function or coronary vascular resistance. Administration of catalase during hypoxia was superior to administering it only during reoxygenation. Treatment with catalase during both hypoxia and reoxygenation provided no more protection than administration only during hypoxia. The data suggest that an important component of hypoxia-induced cardiac cell damage is due primarily to hydrogen peroxide, which may then form hydroxyl radical. Superoxide anion plays an important role as a precursor of these species, but added superoxide dismutase alone did not significantly reduce creatine kinase loss. The data also suggest that damage resulting in creatine kinase release upon reoxygenation occurs during oxygen deprivation, and it is mediated in part by cytotoxic oxygen metabolites.
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During the period 1955 to 1975, 63 consecutive cases of apical lung carcinoma were treated in the Radiation Therapy Division of the University of Michigan Medical Center (UMMC). Supervoltage external radiation alone or combination of radiation and surgery were the main modalities of treatment used in these patients. Our results show 27.9% and 20.9% 3 and 5 years actuarial survival, respectively, in patients who received 5000 to 6000 cGy (rad) of radiation alone. Survival was better in T2 lesions (24.9%) as compared with T3 lesions (7.9%) and in those patients who had no regional adenopathy (30.2% in T2, N0 lesions and 11.6% in T3, N0 lesions). Local osseous and nervous extensions also carried poor prognosis. The results with preoperative irradiation were no better than radiation therapy alone.
At the present time, heparin assays are based on biologic measures of activity. They are time-consuming, difficult to reproduce, and require special devices. We have developed a colorimetric assay for chemical heparin in plasma based on the metachromasia of azure A in the presence of heparin. One milliliter of plasma is added to 1 ml of 0.08 percent azure A, vortex mixed, and read at 620 nm in a spectrophotometer. To evaluate the clinical utility of this assay, we compared it to two biologic assays of heparin effect, activated PTT and activated clotting time, and to heparin levels determined by protamine titration in 113 samples from 28 patients undergoing cardiopulmonary bypass. The activated PTT in 94 of 113 samples was greater than 600 seconds, making this test not useful due to the time required and the lack of an end point. The activated clotting time of 80 samples was less than 600 seconds. The azure A measurement of heparin concentration correlated well in this group (correlation coefficient of 0.88, p less than or equal to 0.0001). Protamine titration determinations also had excellent correlation with azure A measurements in the 111 samples tested (correlation coefficient of 0.85, p less than or equal to 0.0001). The azure A assay correlates well with the standard measures of both heparin activity and heparin concentration. It is more rapid, simple, and less expensive than either of these, and it does not depend on a bioassay of coagulation as an end point. Chemical heparin measurements with azure A may be more useful clinically than the biologic assays in determining the reversal dose of protamine.
A complication of cardiac surgical procedures is postoperative low cardiac output syndrome. Treatment with norepinephrine plus phentolamine (N + P) is beneficial, but the effect of these agents on regional organ blood flow has not been evaluated. Therefore, in 6 dogs with long-term instrumentation, pentobarbital was infused to simulate low cardiac output (32 + 10% of the conscious control level). Infusions of N + P at 0.2, 0.5, and 1.0 microgram/kg/min restored cardiac pump performance to conscious control levels. Regional blood flows, determined with tracer-labeled microspheres, were substantially reduced in the low cardiac output state but increased to values not markedly different from control levels in all organs studied except stomach fundus during infusion of N + P. The pressure-work index, an indirect measure of myocardial oxygen consumption, did not increase to more than the conscious level except at the highest dose. The data demonstrate that simultaneous infusion of N and P is capable of successfully improving cardiac pump performance with restoration of vital organ perfusion and without evidence of excessive myocardial oxygen consumption.