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Biomedical subjects

C E Rackley

Publications and source records attributed to C E Rackley.

At least 73 records · Page 4Linked to original sources
PubMed1981

Glucose-insulin-potassium induced alterations in individual plasma free fatty acids in patients with acute myocardial infarction.

Total and individual plasma free fatty acids (FFA) were measured on admission and over the next 4 days in 24 patients admitted to the hospital with chest pain and suspected acute myocardial infarction (AMI). In a prospective randomized fashion, the patients were either given an infusion of 300 gm of glucose, 50 units of insulin, and 80 mEq of KCl per liter at a rate of 1.5 ml/kg/hr over the initial 48 hours of hospitalization, or they served as controls receiving conventional therapy. Eleven patients were in the control group and 13 were in the glucose-insulin-potassium (G-I-K) group. Twenty-one of the patients had an AMI by CK-MB rise and ECG changes (in the G-I-K group three did not evolve AMI). The total plasma FFA were 840 +/- 134 microM/L in the controls and 933 +/- 160 microM/L in the G-I-K group initially (prestudy). Total FFA rapidly fell in the G-I-K group and then rebounded when G-I-K was stopped. In contrast, total FFA values fell gradually in the control group over the 4-day period. The individual FFA had similar percentages initially in the two groups. In the control group the percent of individual plasma FFA was unchanged over the period studied, although there was some mild random day-to-day fluctuation. In contrast in the G-I-K group linoleic acid fell both during and after the infusion was stopped (26.8% to 19.1% P less than 0.001). Arachidonic acid doubled in percentage of the total FFA value during G-I-K infusion (3.1% to 6.5%, P less than 0.002) and returned to the control value when it was stopped. Thus G-I-K infusion during AMI reduces the total level of plasma FFA while increasing the percent of arachidonic and decreasing the percent of linoleic acid, observations proposed to reflect improved membrane stability of the ischemic myocardium.

Acute Disease↗
PubMed1981

Coronary revascularization surgery: feasibility after myocardial infarction.

Since coronary revascularization improves prognosis in some patients with multivessel disease, can the potential benefits be extended to "prophylaxis" in selected postinfarction patients as well? These investigators sought the answer on the basis of patient characteristics, types of surgery, survival data, and mode of death in the postinfarction population of 129 patients who had early angiography.

Angiography↗
PubMed1981

Limited exercise testing soon after myocardial infarction. Correlation with early coronary and left ventricular angiography.

Forty-eight patients within 3 weeks of myocardial infarction underwent both limited treadmill graded exercise testing and coronary and left ventricular angiography. Nineteen (90%) of 21 patients with positive exercise tests (greater than or equal to 1 mm ST depression, angina, or both) had multivessel coronary artery disease. In the 27 patients with negative exercise test results, 15 (55%) had multivessel disease, 11 (41%) had single-vessel disease, and one (4%) had no coronary stenosis. Exercise-induced ST segment elevation occurred in 24 patients and predicted a significantly lower ejection fraction and higher angiographic abnormally contracting segment size. Patients experiencing angina during or after exercise had a significantly shorter 2-year survival (54% +/- 21%) than patients without exercise-induced angina (97% +/- 3%) (p less than 0.03). Thus limited exercise testing postinfarction is useful in evaluating the presence of multivessel coronary artery disease and left ventricular dysfunction and predicting long-term survival.

Adult↗
PubMed1981

Advances in the treatment of heart failure.

The intensive care clinician has available techniques for assessing the six major determinants of left ventricular function in patients with heart failure and therapeutic approaches for optimizing these determinants and restoring ventricular performance. With the objective data provided via the thermodilution pulmonary arterial catheter, the schema in Figure 12 can be used as a framework for the hemodynamic management of unstable patients. When the filling pressure is less than 20 mm Hg and the cardiac index is greater than 2.5 L/min/m2, no active hemodynamic intervention is indicated. If the patient has recurrent angina or significant hypertension, the use of sublingual nitrates or other agents is indicated to reduce the afterload. Patients who have a low stroke volume are candidates for volume expansion. Filling pressures above 24 mm Hg need to be reduced. Patients with acute pulmonary venous hypertension will frequently respond to sublingual nitrates and bedrest. Patients with persistent congestive heart failure will require supplemental diuretics and more powerful vasodilators. The management of severe low cardiac output and cardiogenic shock may required the addition of supplemental catecholamines and, in selected patients, the intra-aortic balloon pump. In addition to optimizing the ventricular preload and afterload, the treatment of rate, rhythm and conduction disturbances, and the correction of hypoxia and metabolic disturbances are essential. Finally, the ideal treatment for the management of heart failure is to prevent or at least limit the injury to the ventricular myocardium and to correct reversible causes contributing to the patient's symptoms.

Cardiac Catheterization↗
PubMed1981

Current status of hemodynamic monitoring: indication, diagnoses, complications.

Indications for hemodynamic monitoring include the need to assess left ventricular function, to estimate patient prognosis, to monitor cardiac performance, to study the cardiac response to drugs, to evaluate new methods of treatment, and to diagnose and treat cardiac dysrhythmias. Diagnoses which may be made or clinically facilitated include cardiogenic shock, hypovolemic shock, right ventricular infarction, ruptured ventricular septum, mitral regurgitation, low cardiac output syndrome, cardiac tamponade, and pulmonary embolism. Potential complications of hemodynamic monitoring include dysrhythmias, balloon rupture, knotting of the catheter, pulmonary infarction, pulmonary artery rupture, infection, and deep vein thrombosis.

Acute Disease↗
PubMed1981

Clinical interventions for the preservation of ischemic myocardium.

The clinical understanding of determinants of mechanical function and oxygen requirements of the myocardium have now been applied to the patient with acute myocardial infarction. Invasive and noninvasive techniques to quantitate afterload, contractile state, preload, and heart rate as well as to assess the metabolic state and infarct size are now available to evaluate a growing list of therapeutic interventions. Thus, the availability of pharmacologic and metabolic agents to support ischemic myocardium and to reduce the eventual loss of contracting myocardium appears promising to the patient with acute myocardial infarction.

Acute Disease↗
PubMed1981

Cardiogenic shock.

Cardiogenic shock is a complication of acute myocardial infarction characterized by reduction in systemic blood pressure and clinical evidence of impaired blood flow to the skin, central nervous system, and kidneys. Circulatory changes of cardiogenic shock result from excessive loss of contracting myocardium and impaired mechanical performance of the left ventricle. Hemodynamic measurements of left ventricular filling pressure (recorded as the pulmonary artery end-diastolic pressure) and the cardiac index can identify four different subgroups with hospital mortality ranging from 13 to 100 percent when managed with available pharmacologic agents. Patients in cardiogenic shock with a normal or near normal left ventricular filling pressure may respond to volume expansion by restoration of blood pressure and organ flow. The pharmacologic management of cardiogenic shock can be effectively enhanced by measuring the changes in cardiac index and left ventricular filling pressure before and after various vasopressor, inotropic, and volume expansion agents. A clinical scheme for the management of cardiogenic shock based on hemodynamic measurements delineates optimal medical management as well as recognition of rupture of the ventricular septum or the papillary muscle. Despite the combined medical and surgical advances in cardiogenic shock, hospital mortality remains high due to the extensive loss of contracting myocardium of the left ventricle.

Cardiotonic Agents↗
PubMed1980

Effects of vasodilators on renal function in severe heart failure.

UNLABELLED: Changes in renal function associated with heart failure (HF) and the response to vasodilator therapy were investigated in 21 patients (pts) with ischemic heart disease. Serial measurements of systemic arterial pressure (AP), pulmonary arterial end diastolic pressure, cardiac index (CI) and effective renal plasma flow (ERPF) were obtained before and after isosorbide dinitrate (ISD) or prazosin (PZ). Baseline ERPF values measured by 131-I-orthoiodohippurate clearance correlated well with CI (r = 83). Pts with low ERPF (< 300 ml/min) had an increase of 20 to 80% in response to vasodilatation. This improvement in ERPF was not dependent on an increase in the Cl. Pts on nonic ISD/PZ with systolic AP < 90 mmHg developed edema and ascites that responded to spironolactone. These data indicate that vasodilators can significantly improve ERPF in pts with low Cl and suggests a specific beneficial effect on the renal vascular bed. SUMMARY: In pts with low cardiac output HF : 1) the ERPF is reduced in proportion to the Cl; 2) vasodilation will improve ERPF independently of the cardiac response although; 3) persistent hypotension and vasodilation may result in a clinical picture of secondary hyperaldosteronism.

Adult↗