Colloid volume loading does not mitigate decreases in central blood volume during simulated haemorrhage while heat stressed.

Heat stress results in profound reductions in the capacity to withstand a simulated haemorrhagic challenge; however, this capacity is normalized if the individual is volume loaded prior to the challenge. The present study tested the hypothesis that volume loading during passive heat stress attenuates the reduction in regional blood volumes during a simulated haemorrhagic challenge imposed via lower-body negative pressure (LBNP). Seven subjects underwent 30 mmHg LBNP while normothermic, during passive heat stress (increased internal temperature ∼1◦C), and while continuing to be heated after intravenous colloid volume loading (11 ml kg⁻¹). Relative changes in torso and regional blood volumes were determined by gamma camera imaging with technetium-99m labelled erythrocytes. Heat stress reduced blood volume in all regions (ranging from 7 to 16%), while subsequent volume loading returned those values to normothermic levels. While normothermic,LBNP reduced blood volume in all regions (torso: 22 ± 8%; heart: 18 ± 6%; spleen: 15 ± 8%). During LBNP while heat stressed, the reductions in blood volume in each region were markedly greater when compared to LBNP while normothermic (torso: 73 ± 2%; heart: 72 ± 3%; spleen: 72 ± 5%, all P<0.001 relative to normothermia). Volume loading during heat stress did not alter the extent of the reduction in these blood volumes to LBNP relative to heat stress alone (torso: 73 ± 1%; heart: 72 ± 2%; spleen: 74 ± 3%, all P>0.05 relative to heat stress alone). These data suggest that blood volume loading during passive heat stress (via 11 ml kg⁻¹ of a colloid solution) normalizes regional blood volumes in the torso, but does not mitigate the reduction in central blood volume during a simulated haemorrhagic challenge combined with heat stress.

Propylthiouracil before 131I therapy of hyperthyroid diseases: effect on cure rate evaluated by a randomized clinical trial.

A randomized clinical trial was performed to clarify whether pretreatment with propylthiouracil (PTU) before radioiodine ((131)I) therapy influences the final outcome of this therapy, as has been indicated by retrospective studies. Untreated consecutive hyperthyroid patients with Graves' disease (n = 23) or a toxic nodular goiter (n = 57) were randomized to either PTU (+PTU; n = 39) or no pretreatment (-PTU; n = 41) before compensated (131)I therapy. The median PTU dose was 100 mg, which was discontinued 4 d before treatment. The median (131)I activity was 302 MBq (range, 87-600 MBq). After (131)I therapy, the serum free T(4) index increased in the +PTU group from 97.7 +/- 47.5(+/-sd) nmol/liter at the time of therapy to 152.3 +/- 77.6 nmol/liter at 3 wk (P < 0.001) and 140.4 +/- 75.9 nmol/liter at 6 wk (P < 0.001). In the -PTU group, the serum free T(4) index, which was initially 254.3 +/- 145.7 nmol/liter, decreased significantly to 212.0 +/- 113.0 nmol/liter at 3 wk (P < 0.05) and 165.8 +/- 110.0 nmol/liter at 6 wk (P < 0.005). After 1 yr of follow-up, the treatment failure rate in patients with a toxic nodular goiter was four times higher in the +PTU group than in the -PTU group (nine of 20 vs. three of 25 patients; P = 0.06), whereas the difference among patients with Graves' disease was less obvious (four of six vs. four of nine; P = 0.81). Patients in the +PTU group who were cured had higher serum TSH (s-TSH) levels at the time of (131)I therapy than those who were not cured. By adjusting for a possible interfactorial relationship through a regression analysis, including the s-TSH level and type of disease, only PTU pretreatment had a significant adverse effect on the cure rate (P = 0.03). In conclusion, this randomized trial demonstrates that PTU pretreatment reduces the cure rate of (131)I therapy in hyperthyroid diseases, although this adverse effect seems to be attenuated by the concomitant rise in s-TSH.

Left ventricular function during alcohol intoxication and autonomic nervous blockade.

Eight healthy young subjects (6 men, 2 women) entered a controlled investigation of left ventricular (LV) function during alcohol intoxication and autonomic nervous blockade. Radionuclide cardiography was performed at rest and during upright 50% submaximal bicycle exercise. During alcohol intoxication alone (serum ethanol 30 mmol/liter), heart rate at rest increased by 11% (p less than 0.05) and LV ejection fraction (EF) decreased by 6% because of end-systolic dilation. No significant alcohol-induced hemodynamic changes were observed during exercise. Plasma norepinephrine concentration increased by 29% (p less than 0.05), whereas plasma epinephrine concentration did not change. During subsequent autonomic nervous blockade with intravenous metoprolol and atropine infusion, heart rate at rest further increased and systolic blood pressure decreased. These changes were not, however, significantly different from those of a control experiment in which a nonalcoholic isocaloric drink was substituted for alcohol. Plasma norepinephrine levels at rest and during exercise were 25% and 32% higher (both p less than 0.05), respectively, than those during control conditions. Plasma epinephrine concentrations did not change. These findings suggest that alcohol intoxication has a depressant effect on LV function at rest that stimulates autonomic nervous blockade. The increased sympathetic nervous activity during exercise appears to be a toxic rather than a compensatory effect of alcohol.

Late ventricular dilatation in survivors of acute myocardial infarction.

The purpose of this study was to assess the natural course of left ventricular (LV) volumes in the convalescent phase of acute myocardial infarction (AMI). Fifty-seven patients were examined 2 weeks and approximately 1 year after AMI by a radionuclide method allowing determination of absolute LV volumes. After 1 year the patients had fewer clinical and radiologic signs of heart failure, but median end-diastolic volume index had increased from 92 to 112 ml/m2 (p less than 0.001), median end-systolic volume index from 51 to 65 ml/m2 (p less than 0.001) and median stroke volume index from 39 to 47 ml/m2 (p less than 0.001). Patients with first anterior infarcts had significantly greater increases in end-diastolic volume index, end-systolic volume index and stroke volume index than patients with first inferoposterior infarcts. The increase in LV volumes was significantly greater in patients with clinical manifestations of heart failure than in those without these signs. Notably, changes in LV size had an unpredictable effect on LV ejection fraction.

The effect of the tricyclic antidepressant drug, nortriptyline on left ventricular ejection fraction and left ventricular volumes.

Eight patients with major depression but otherwise healthy underwent radionuclide cardiography before and during nortriptyline treatment. The second examination was performed when the nortriptyline plasma concentration was within the therapeutic range (60-150 micrograms X l-1). Heart rate, arterial blood pressure, left ventricular ejection fraction, left ventricular volumes, systolic pressure-volume ratio, and cardiac output were determined. Heart rate increased in mean by 13% (P less than 0.05). All other variables were unchanged. We conclude that nortriptyline in therapeutic doses produces no major adverse effect on left ventricular function. Routine radionuclide cardiography might be a suitable method to detect among those treated with tricyclic antidepressants the occasional susceptible patient. This may particularly apply to patients with known heart disease and to elderly patients.

Acute plasma expansion: left ventricular hemodynamics and endocrine function during exercise.

In 11 healthy subjects (8 males and 3 females, age 21-59 yr) left ventricular end-diastolic (LVEDV) and end-systolic (LVESV) volumes were measured in the supine position by isotope cardiography at rest and during two submaximal one-legged exercise loads before and 1 h after acute plasma expansion (PE) by use of a 6% dextran solution (500-750 ml). After PE, blood volume increased from 5.22 +/- 0.92 to 5.71 +/- 1.02 (SD) liters (P < 0.01). At rest, cardiac output increased 30% (5.3 +/- 1.0 to 6.9 +/- 1.6 l/min; P < 0.01), stroke volume increased from 90 +/- 20 to 100 +/- 28 ml (P < 0.05), and LVEDV increased from 134 +/- 29 to 142 +/- 40 ml (NS). LVESV was unchanged (44 +/- 11 and 42 +/- 14 ml). Heart rate rose from 60 +/- 7 to 71 +/- 10 beats/min (P < 0.01). The cardiac preload [central venous pressure (CVP)] was insignificantly elevated (4.9 +/- 2.1 and 5.3 +/- 3.0 mmHg); systemic vascular resistance and arterial pressures were significantly reduced (mean pressure fell from 91 +/- 11 to 85 +/- 11 mmHg, P < 0.01). Left ventricular peak filling and peak ejection rates both increased (19 and 14%, respectively; P < 0.05). During exercise, cardiac output remained elevated after PE compared with the control situation, predominantly due to a 10- to 14-ml rise in stroke volume caused by an increased LVEDV, whereas LVESV was unchanged. CVP increased after PE by 2.1 and 3.0 mmHg, respectively (P < 0.05).2+ remained unchanged during exercise compared with rest after PE in

Effects of autonomic blockade on cardiac function at rest and during upright exercise in humans.

The cardiac function was studied by radionuclide cardiography in eight healthy subjects at rest and during submaximal upright exercise before and after autonomic blockade with metoprolol and atropine. At rest the median stroke volume was reduced by 21% during autonomic blockade (P less than 0.01), but cardiac output was maintained by a concomitant increase in heart rate. The systolic blood pressure was reduced from 120 to 105 mmHg (P less than 0.01), and left ventricular ejection fraction was reduced from 61 to 56% (P less than 0.05). After autonomic blockade the heart rate reached during exercise was the same. Stroke volume and cardiac output were maintained through cardiac dilation. The increase in left ventricular end-diastolic volume was 31 vs. 10% during control conditions (P less than 0.01). The systolic blood pressure was reduced from 174 to 135 mmHg (P less than 0.01). Left ventricular ejection fraction was reduced from 75 to 67% (P less than 0.05), but the increase from rest to exercise was preserved. Total peripheral resistance was reduced by 17% (P less than 0.05). These findings suggest that the heart possesses intrinsic mechanisms to maintain cardiac output during submaximal upright exercise. End-diastolic dilation results in a preserved stroke volume despite a reduced contractility.

Accuracy of left ventricular ejection fraction determined by the nuclear stethoscope.

We assessed left ventricular ejection fraction 47 times in 21 patients with sinus rhythm by a portable non-imaging nuclear probe. After 99mTc blood pool labelling, left ventricular ejection fraction was determined by probe in two different ways: on a beat-to-beat basis, and by the so-called ventricular function mode, based on the gated equilibrium principle, and subsequently compared with left ventricular ejection fraction measured by gated equilibrium radionuclide angiocardiography using a gamma camera. Left ventricular ejection fraction by probe correlated well with left ventricular ejection fraction by gamma camera: beat-to-beat versus gamma camera: r = 0.90, y = 0.75x + 0.12; ventricular function versus gamma camera: r = 0.88, y = 0.87x + 0.08. Also, left ventricular ejection fraction values determined by the two probe methods correlated closely: r = 0.97, y = 0.83x + 0.07. Compared with the gamma camera, the probe overestimated slightly the small values of left ventricular ejection fraction and underestimated high values. Correct determination of left ventricular ejection fraction by a non-imaging probe depends on correct positioning over the left ventricle and selection of a proper background activity level. The main application of this instrument is probably non-invasive bedside determination and monitoring of changes of left ventricular function occurring spontaneously or caused by cardiac arrhythmias or treatment with cardiac drugs.

Accuracy of absolute left ventricular volumes and cardiac output determined by radionuclide cardiography.

We determined left ventricular (LV) volumes and derived variables by gated equilibrium radionuclide imaging at rest and during exercise in 12 patients without valve disease or intracardiac shunts. LV volume was determined as the product of the background-corrected LV count rate and an individual attenuation correction factor divided by the count rate in peripheral blood. Attenuation correction was based on measurement of LV depth within the chest from an initial first pass study in the left lateral view and a linear attenuation coefficient of 0.156 cm-1 determined in phantom studies. The average LV depth was 8.0 cm (range 6.9-9.1) in agreement with an average depth measured by echocardiography of 8.2 cm (6.3-9.4), P much greater than 0.05. The correlation between radionuclide (RC) and simultaneous thermodilution (TD) measurements was for cardiac output (CO): r = 0.95; CO (RC) = 1.00 X CO (TD) + 0.10 1/min with a standard error of the estimate (SEE) of 0.79 1/min; for stroke volume (SV): r = 0.90; SV(RC) = 0.93 X SV (TD) + 5 ml; SEE = 8 ml; for end-diastolic volume (EDV): r = 0.96; EDV(RC) = 1.06 X EDV(TD) -14 ml; SEE = 27 ml; and for end-systolic volume (ESV): r = 0.98; ESV(RC) = 1.05 X ESV (TD) -6 ml; SEE = 20 ml. The interobserver variation, expressed as the coefficient of variation, was for cardiac output 6%, for stroke volume 6%, for end-diastolic volume 4%, and for end-systolic volume 5%. This method permits non-invasive determination of LV volume and total LV output per beat based exclusively on data obtained during radionuclide imaging.

Does the decrease in heart rate prevent a detrimental decrease of the end-systolic volume during central hypovolemia in man?

Central hypovolemia occurring with epidural anesthesia was investigated by measurement of hemodynamic and endocrine variables in 10 patients. Responses fell into two categories. Four patients experienced a hypotensive bradycardic episode after seventeen +/- four minutes. In this group epidural anesthesia initially induced a tendency toward an increase in heart rate from 65 +/- 4 to 73 +/- 5 beats/min concomitantly with decreases in end-diastolic (172 +/- 22 to 138 +/- 16 mL), end-systolic (67 +/- 12 to 51 +/- 9 mL), and stroke (105 +/- 10 to 85 +/- 7 mL) volumes (radionuclide cardiography). A subsequent decrease in mean arterial pressure from 76 +/- 3 to 67 +/- 4 mmHg was associated with a decrease in venous return as reflected by the decrease in cardiac output from 6.1 +/- 0.4 to 4.7 +/- 0.7 L/min. In this situation when the venous return was critically reduced, the heart rate was 49 +/- 4 beats/min and no further reduction in end-diastolic and end-systolic volumes was observed. The observed endocrine changes were compatible with a response to central hypovolemia. In the other 6 patients the reaction to epidural anesthesia did not induce statistically significant changes in hemodynamic and endocrine variables. It is concluded (1) that the decrease in heart rate associated with central hypovolemia during epidural anesthesia seems to be elicited when the left ventricular end-systolic volume is decreased by about 25% and (2) that a further decrease in end-systolic volume during progressive central hypovolemia is avoided possibly as a direct consequence of the slowing of the heart.

[Myocardial scintigraphy and coronary arteriography in patients with known or suspected stable angina pectoris]. / Myokardiescintigrafi og koronararteriografi hos patienter med kendt eller formodet stabil angina pectoris.

INTRODUCTION: Myocardial perfusion imaging (MPI) demonstrates regional hypoperfusion, whereas coronary angiography shows anatomical stenoses in epicardial arteries. Both modalities are potentially relevant in patients with stable angina pectoris. MATERIALS AND METHODS: MPI was undertaken before angiography in 86 randomly selected patients with stable angina pectoris. RESULTS: Of 78 adequately stressed patients, MPI was normal in 28 (36%) and showed reversible and irreversible perfusion abnormalities in 30 (38%) and 20 patients (26%), respectively. Coronary angiograms were normal in 28 (36%) and revealed at least one > or = 50% stenosis in 50 patients (64%) (16 with single vessel and 34 with multivessel disease). With angiography as reference, the sensitivity and specificity of MPI in the detection of coronary artery disease were 88% and 93%, respectively. DISCUSSION: Patients with stable angina pectoris and a normal MPI have a very low risk of cardiac events and do not usually require invasive investigation and therapy. Reversible ischaemia and irreversible ischaemia with viable tissue call for coronary revascularisation.