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Biomedical subjects

R O Russell

Publications and source records attributed to R O Russell.

At least 73 records · Page 4Linked to original sources
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↗
PubMed1980

Dilation of coronary artery stenoses after isosorbide dinitrate in man.

The effect of isosorbide dinitrate (ISDN), 5 mg sublingually, on the diameters of coronary artery stenoses (n = 27) was examined in 20 patients. Another 18 patients with angiographically normal coronary arteries received the same amount of ISDN and were used as controls. Prestenotic and stenotic diameters were measured with a vernier calliper having an accuracy of 0.05 mm. The degree of stenosis was expressed as percentage of cross-sectional area reduction. ISDN caused uniform dilatation of every normal epicardial artery; mean increase in diameter was 21 per cent (range: 17 to 26%). In 18 stenoses (28 to 95% obstruction) there was very little change after ISDN. The mean prestenotic diameter increased from 2.82 +/- 0.48 mm to 3.05 +/- 0.43 mm and the mean stenotic diameter from 1.45 +/- 0.49 mm to 1.59 +/- 0.51 mm. However, in the nine other stenoses (35 to 89% obstruction) the mean degree of obstruction decreased significantly from 68 +/- 15.6 per cent to 47 +/- 15.6 per cent after ISDN. This improvement was a result of a significant increase of the mean stenotic diameter from 1.71 +/- 0.47 mm to 2.41 +/- 0.55 mm, whereas the prestenotic diameter showed only an insignificant increase from 3.17 +/- 0.63 mm to 3.31 +/- 0.58 mm after ISDN. In four patients with two obstructions in different coronary branches ISDN dilated one without significantly affecting the other lesion. From the data we conclude that ISDN can dilate some coronary artery stenoses but that this response may vary from one site to another even in the same patient.

Coronary Disease↗
PubMed1980

Coronary angiography soon after myocardial infarction.

We evaluated 198 consecutive survivors of acute myocardial infarction and performed selective coronary angiography in 117 of 131 (89 percent) patients who were deemed candidates for angiography by clinical criteria. Overall, left main CAD (greater than or equal to 70 percent stenosis) was found in ten patients (8.5 percent), three vessel CAD in 41 patients (35 percent), two vessel CAD in 37 patients (31.5 percent), single vessel disease in 27 patients (23 percent) and zero vessel disease in two patients (2 percent). Factors suggesting multivessel disease included older age, history of prior myocardial infarction, and post-infarction convalescence complicated by angina pectoris. Factors not discriminating between single and multivessel disease were sex, infarct extent (transmural vs non-transmural), (3) infarct location (anterior vs inferior), and post-infarction convalescence complicated by late arrhythmia or heart failure. This study demonstrates that multivessel coronary artery disease is common in survivors of myocardial infarction and is suggested by the occurrence of post-infarction angina and by the history of an antecedent myocardial infarction. Coronary angiography can be performed safely within 30 days after myocardial infarction in patients with an uncomplicated convalescence and with mild risk in those with a complicated convalescence.

Coronary Angiography↗