Eight patients with complete A-V block were studied during cardiac pacing at multiple ventricular rates to provide information about the mathematical relationship between Q-T and R-R intervals for each patient.

SYNCHRONIZED, external direct-current (DC) countershock has proved to be a valuable tool for the correction of cardiac arrhythmias since its introduction by Lown and his co-workers in 1962.1,2Sodium thiopental has been used as the anesthetic agent for this procedure in most clinical studies.3-5Recently, Nutter and Massumi6reported using diazepam intravenously for the brief period of analgesia-amnesia necessary for DC countershock. In this laboratory 108 patients have had elective DC countershock, in the period August 1962 to December 1965, under sodium thiopental anesthesia. Analysis of continuous electrocardiograms made before, during, and after the DC countershock disclosed the occurrence of premature ventricular contractions in many patients. In each instance when this additional arrhythmia occurred, it appeared after induction of anesthesia but before the DC countershock was given. The occurrence of this additional arrhythmia was disturbingly frequent. These premature ventricular complexes often persisted for several minutes after the

Clinical and hemodynamic data prior to and during oral guanethidine therapy in two patients with idiopathic hypertrophic subaortic stenosis are presented. In both patients the systolic intraventricular pressure gradient both at rest and during exercise was reduced following continued guanethidine administration. Concomitantly, computed values for left ventricular effective outflow tract area were significantly larger during the guanethidine studies than during the control studies. The symptomatic patient (Case 1) experienced increased work tolerance and diminished dyspnea on exertion. Guanethidine did not prevent the increased intraventricular gradient and reduction of the aortic pulse pressure which occur during isoproterenol infusion or in the contraction following a premature ventricular beat. It is suggested that chronic guanethidine administration, by reducing the systolic obstruction, may be a useful pharmacologic agent in this disorder.

The applicability of the indicator dilution method to the measurement of left ventricular volume has been studied. When compared with angiocardiographic measurements, the dilution technique overestimates volume by an average of 52 and 91% in end diastole and end systole respectively. Studies which demonstrated more rapid indicator washout from the outflow than from the apical portion of human and canine left ventricles suggest that faulty intraventricular indicator dispersion is the major cause of the volume over-estimates yielded by the dilution method. Procedures designed to alter ventricular size by altering venous return produced parallel changes in ventricular circumference and in ventricular indicator washout volume. The indicator dilution method does not provide a measure of left ventricular volume, but may, in carefully designed studies, yield an index of changes in ventricular size.

The occurrence of 2:1 A-V block during right atrial pacing in man provided the opportunity to compare A-V conduction time with and without an intervening atrial depolarization at similar ventricular rates. The presence of the interposed atrial depolarization produced prolongation of the subsequent A-V conduction by 0.03 to 0.13 sec, and thus provided evidence of concealed conduction in the normal human heart.

IMPLANTABLE CARDIAC PACEMAKERS are being used with increasing frequency in the management of patients with symptoms of a complete heart block. Although electromechanical control of heart rate would seem to demand a high level of both knowledge and professional concern regarding interactions between pacemakers and the environment, little information is available in scientific journals. We are, therefore, reporting preliminary observations of the behavior of two brands of pacemakers in several environments which may be encountered by patients. Material and Methods Three pacemakers have been used. Two were designed and made by one of us (R. W. S.) and are of the type used in 26 patients treated in this institution.1,2One of these had the long lead wires intact, the other had them removed to ensure that any induction currents or alterations of function which were detected had originated within the pacemaker unit itself. The third pacemaker, a popular,

NSR mos 1 9a.A.L. 46 F RHD-MSt 1 AF 2 mos 58.0 NSR AF days 1 b.A.L.

Article1 April 1963A Correlation of Clinical and Hemodynamic Studies in Patients with Mild and Severe Anemia with and without Congestive FailureJOHN S. GRAETTINGER, M.D., F.A.C.P., ROBERT L. PARSONS, M.D., JAMES A. CAMPBELL, M.D., F.A.C.P.JOHN S. GRAETTINGER, M.D., F.A.C.P., ROBERT L. PARSONS, M.D., JAMES A. CAMPBELL, M.D., F.A.C.P.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-58-4-617 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptCastle and Minot emphasized in 1936 that anemic patients "may show, while at complete rest, very little discomfort from a reduction of the red blood cells and hemoglobin values to about one-fifth of normal" (1). Blumgart and Altschule, in a major compilation of the data concerning the adjustments of the cardiovascular system to chronic anemia (2), emphasized that the bulk of the data available were obtained from patients in the basal state. The presently available hemodynamic data (3-7), with few exceptions (8-10), have been measured in resting patients, and it has been widely accepted since the work of Brannon, Merrill,...References1. CASTLEMINOT WBGR: Pathological Physiology and Clinical Description of the Anemias, Oxford University Press, New York, 1936, p. 2. Google Scholar2. BLUMGARTALTSCHULE HDMD: Clinical significance of cardiac and respiratory adjustments in chronic anemia. Blood 3: 329, 1948. CrossrefMedlineGoogle Scholar3. SHARPEY-SCHAFER EP: Cardiac output in severe anemia. Clin. Sci. 5: 125, 1944. Google Scholar4. BRANNONMERRILLWARRENSTEAD ESAJJVEA: The cardiac output in patients with chronic anemia as measured by the technique of right atrial catheterization. J. Clin. Invest. 24: 332, 1945. CrossrefMedlineGoogle Scholar5. NIELSEN HE: The circulation in anemic conditions. Acta Med. Scand. 81: 571, 1934. CrossrefGoogle Scholar6. LILJESTRANDSTENSTROM GN: Clinical studies on the work of the heart during rest. II. The influence of variations in the haemoglobin content on the blood flow. Acta Med. Scand. 63: 130, 1925. CrossrefGoogle Scholar7. STEWARTCRANEDEITRICK HJHFJE: Studies of the circulation in pernicious anemia. J. Clin. Invest. 16: 431, 1937. CrossrefMedlineGoogle Scholar8. LEIGHTSNIDERCLIFFORDHELLEMS LTHGOHK: Hemodynamic studies in sickle cell anemia. Circulation 10: 653, 1954. CrossrefMedlineGoogle Scholar9. BISHOPDONALDWADE JMKWOL: Circulatory dynamics at rest and on exercise in the hyperkinetic states. Clin. Sci. 14: 329, 1955. MedlineGoogle Scholar10. SPROULEMITCHELLMILLER BJJHWF: Cardiopulmonary physiological responses to heavy exercise in patients with anemia. J. Clin. Invest. 39: 378, 1960. CrossrefMedlineGoogle Scholar11. GRAETTINGERMUENSTERSELVERSTONECAMPBELL JSJJLAJA: A correlation of clinical and hemodynamic studies in patients with hyperthyroidism with and without congestive failure. J. Clin. Invest. 38: 1316, 1959. CrossrefMedlineGoogle Scholar12. HUCKABEE WE: Relationships of pyruvate and lactate during anaerobic metabolism. II. Exercise and formation of O2-debt. J. Clin. Invest. 37: 255, 1958. CrossrefMedlineGoogle Scholar13. MENDLOWITZ M: The effect of anemia and polycythemia on digital intravascular blood viscosity. J. Clin. Invest. 27: 565, 1948. CrossrefMedlineGoogle Scholar14. LEVY MN: The influence of erythrocyte concentration upon the pressure-flow relationships in the dog's hind limb. Circ. Res. 1: 247, 1953. CrossrefMedlineGoogle Scholar15. RICHARDSONGUYTON TQAC: Effects of polycythemia and anemia on cardiac output and other circulatory factors. Amer. J. Physiol. 197: 1167, 1959. CrossrefGoogle Scholar16. SUNAHARABECK FAL: Cardiovascular effects of acutely produced anemia in the normal dog. Amer. J. Physiol. 176: 193, 1954. Google Scholar17. MUENSTERGRAETTINGERCAMPBELL JJJSJA: Correlation of clinical and hemodynamic findings in patients with systemic arteriovenous fistulas. Circulation 20: 1079, 1959. CrossrefMedlineGoogle Scholar18. CAMPBELLSELVERSTONEDONOVAN JALADL: Studies on the high output cardiac failure of occidental beri-beri. J. Clin. Invest. 30: 632, 1951. Google Scholar19. GRAETTINGERCAMPBELL JSJA: The hemodynamic common denominators of the syndrome of chronic congestive failure. J. Lab. Clin. Med. 54: 819, 1959 (abstract). Google Scholar20. SAMETFRITTSFISHMANCOURNAND PHWAFA: The blood volume in heart disease. Medicine 36: 211, 1957. CrossrefMedlineGoogle Scholar21. GIBSONHARRISSWIGERT JSAWVW: Clinical studies of the blood volume. VIII. Macrocytic and hypochromic anemias due to chronic blood loss, hemolysis and miscellaneous causes, and polycythemia vera. J. Clin. Invest. 18: 621, 1939. CrossrefMedlineGoogle Scholar22. GREGERSONRAWSON MIRA: Blood volume. Physiol. Rev. 39: 307, 1959. CrossrefMedlineGoogle Scholar23. SHARPEY-SCHAFER EP: Transfusion and the anaemic heart. Lancet 2: 296, 1945. CrossrefGoogle Scholar24. EICHNAFARBERBERGERRADERSMITHALBERT LWSJARBWWRE: Non-cardiac circulatory congestion simulating congestive heart failure. Trans. Ass. Amer. Physicians 66: 72, 1954. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Chicago, IllinoisFrom the Section of Cardio-Respiratory Diseases, Department of Medicine, Presbyterian-St. Luke's Hospital, Chicago, and the Department of Medicine, University of Illinois College of Medicine, Chicago, Illinois.This work was supported in part by grants from the United States Public Health Service, National Institutes of Health (H-404 and H-5579), and by the Schweppe Foundation.Dr. Parsons was a Schweppe Fellow in Cardiology, 1959-1960.Requests for reprints should be addressed to John S. Graettinger, M.D., 1753 West Congress Parkway, Chicago 12, Illinois. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByEffect of Intra- and Post-Operative Fluid and Blood Volume on Postoperative Pulmonary Edema in Patients with Intraoperative Massive BleedingA STUDY OF LIPID PROFILE IN ANEMIA PATIENTS- CASE-CONTROL STUDY IN INDIAN PATIENTS DONE IN THANJAVUR MEDICAL COLLEGE, TAMIL NADUCardiovascular Adaptations to Anemia and the Vascular Endothelium in Sickle Cell Disease PathophysiologyIron Deficiency Without Anemia Is Associated with Anger and Fatigue in Young Japanese WomenThe PhysioFlow Thoracic Impedancemeter Is Not Valid for the Measurements of Cardiac Hemodynamic Parameters in Chronic Anemic PatientsComparison of biventricular dimensions and function between pediatric sickle-cell disease and thalassemia major patients without cardiac ironAssessment of Tissue OxygenationCardiovascular Function and Dysfunction in Sickle Cell AnemiaPathophysiology and Clinical Recognition of Heart FailureHow to Decrease Cardiovascular Mortality in Renal Transplant RecipientsTolerance of Acute Anemia: The Anesthesiology PerspectiveHigh-Output Cardiac Failure in a Patient with Prostate CancerCauses of Anemia in Cancer PatientsAssessment of Cardiac Index in Anemic PatientsHigh-output heart failure resulting from a remote traumatic aorto-caval fistula: Diagnosis by echocardiographyDas Herz bei hämatologischen ErkrankungenA case of progressive congestive heart failure secondary to severe anemia in a patient presenting with uterine hemorrhageAngina pectoris bei extrakoronaren ErkrankungenEffects of increasing blood hemoglobin levels on systemic hemodynamics of acutely anemic cirrhotic patientsAngina pectoris beim LeiomyomMultiple myeloma associated with serum amino acid disturbance and high output cardiac failurePhysiologic Effects of Normovolemic Anemia: Implications for Clinical MonitoringHigh cardiac output state in patients with multiple myeloma: Case report and review of the literatureAngina Pectoris Caused by Pernicious AnemiaOther Causes and Contributing Factors to Congestive Heart FailurePathogenesis of oedema in chronic severe anaemia: studies of body water and sodium, renal function, haemodynamic variables, and plasma hormones.Reduced inhibition of endothelial-derived relaxing factor causes the hyperdynamic circulation in chronic severe anemiaSudden death in a young athleteUse of blood transfusion in management of anemiaCardiac involvement in aidsPrevalence and clinical characteristics of a high cardiac output state in patients with multiple myelomaEmergencies in continuous dialysis patients: Diagnosis and managementCardiac manifestations of human immunodeficiency virus infection: A two-dimensional echocardiographic studyCardiac Complications in Thalassemia Syndromes: Clinical and Radiological ConsiderationsHigh-Output Cardiac Failure in Patients with Multiple MyelomaVentricular function in cirrhosis and portasystemic shunt: A two-dimensional echocardiographic studyEffect of Different Amounts of Blood Transfusion Given at Different Speeds on Left Ventricular Filling Pressure in Cases of Chronic Severe AnemiaAngioaccessA Comparative Study of Conventional vs Rapid Speed of Blood Transfusion in Cases of Chronic Severe AnemiaHerzinsuffizienzSystolic time intervals in anemic children with or without congestive heart failureCardiac Complications of Regular Dialysis TherapyHemodilution - New Clothes for an Anemic EmperorCardiac Complications of Regular Dialysis TreatmentSystolic time intervals in chronic anemiaDialysis Fistula and Heart FailureBARUCH J. HURWICH, M.D.Hypertension in Chronic Renal FailureCardiovascular effects of anemiaMyocardial anaerobiosis in anemia in ur?mic manHemodynamics of Uremic AnemiaObservations on Major Circulatory Problems in Severe Anaemia in PregnancyUncommon or commonly unrecognized causes of heart failureHyperthyroidism as a high cardiac output stateHemodynamic Studies in Chronic UremiaThe Hemodynamic Response to Chronic AnemiaChest Pain in the Surgical PatientCirculatory haemodynamics after blood transfusion in chronic severe anaemia.Hemodynamic Effects of Blood Transfusion in Chronic AnemiaDextran-exchange anemia and reduction in blood viscosity in the heart-lung preparation 1 April 1963Volume 58, Issue 4Page: 617-626KeywordsAnemiaHemodynamicsHemoglobinHospital medicineMedical servicesRed blood cellsResearch design Issue Published: 1 April 1963 PDF DownloadLoading ...

Serial orthopedic and hemodynamic measurements made in a child before, during, and after the creation of a systemic arteriovenous fistula to promote growth of a shortened leg are reported. The mechanisms and associated clinical phenomena of the hemodynamic load imposed by the fistula are discussed. This procedure may be, to date, the most effective method for diminishing the disparity between the lengths of two limbs. In a child with a normal heart the creation of such a fistula may impose no cardiac hazard. However, in some children, especially those with cardiac disease, there may be serious cardiovascular consequences. This procedure requires at all stages the close collaboration of the orthopedic surgeon, the vascular surgeon, and the cardiologist.