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Biomedical subjects

A B Groeneveld

Publications and source records attributed to A B Groeneveld.

At least 109 records · Page 6Linked to original sources
PubMed1989

Effect of dopamine vs norepinephrine on hemodynamics in septic shock. Emphasis on right ventricular performance.

The effects of continuously infused dopamine and norepinephrine on hemodynamics, oxygen metabolism, and right ventricular (RV) performance were studied by crossover design in ten patients with septic shock who needed treatment with vasoactive drugs after fluid replacement. Standard hemodynamic measurements were obtained and RV performance assessed before and 1 h after the start of the infusion. All but one patient had pulmonary hypertension, and in seven the RV ejection fraction (RVEF) was lower than 50 percent at baseline. Drugs were titrated to a systolic arterial blood pressure of mean 106 +/- 18 mm Hg for dopamine and 116 +/- 20 mm Hg for norepinephrine (NS). Dopamine infusion increased the cardiac index (CI) 16 percent (p less than 0.02), but heart rate and systemic and pulmonary vascular resistances were unchanged. With norepinephrine CI was unchanged, a heart rate decreased 7 percent (p less than 0.05), and systemic and pulmonary vascular resistance increased 35 and 26 percent, respectively (p less than 0.05). With both drugs, RV volumes and RVEF remained unchanged, and systemic oxygen consumption increased equally (by 19 percent for dopamine and 22 percent for norepinephrine, p less than 0.05); systemic oxygen delivery rose by 17 percent during dopamine infusion and was unchanged during norepinephrine infusion. Norepinephrine increased oxygen extraction vs dopamine (p less than 0.05). There were no differences in urinary output. Norepinephrine may improve the RV oxygen supply/demand ratio, but this potentially beneficial effect on RV ejection fraction may be offset by a concomitant increase in pulmonary vascular resistance and RV afterload. Norepinephrine may not adversely affect the peripheral circulation. In short-term treatment of volume-resuscitated, severe septic shock complicated by pulmonary hypertension and impaired RV performance, norepinephrine may be at least as effective as dopamine.

Adult↗
PubMed1988

Peripheral vascular resistance in septic shock: its relation to outcome.

To support the concept that patients who die of septic shock have a persistent defect in peripheral vascular tone irrespective of cardiac index (CI), a retrospective study was undertaken of 42 patients with documented septic shock. From the patient records, the single lowest CI (t = 2) measured after initial values (t = 1) with concomitantly obtained haemodynamic and metabolic variables was taken. Group 1 consisted of 21 survivors and group 2 of 21 patients, who had died in shock. Initial haemodynamic and metabolic variables were comparable between the groups, reflecting shock with a hyperdynamic circulation and lactic acidemia. At t = 2, median CI measured 3.21.min-1.m-2 in both groups, but mean arterial pressure (MAP) and systemic vascular resistance index (SVRI) were higher in group 1 than 2 (p less than 0.0005). Changes in arterial blood lactate levels also differed significantly. The rankcorrelation between CI and SVRI at t = 2 was significant in group 1 (rs = -0.69, p less than 0.005) but not in group 2 (rs = -0.34). Our data suggest that when CI decreases in septic shock, patients with a fatal outcome have less capability to augment vascular resistance than survivors. Hence, peripheral vascular failure, even if complicated by inability to maintain an elevated CI, may be a major haemodynamic determinant of mortality in septic shock.

Adult↗
PubMed1988

Biventricular performance during volume loading in patients with early septic shock, with emphasis on the right ventricle: a combined hemodynamic and radionuclide study.

The cardiac response to a rapid volume infusion was studied in 18 patients with septic shock accompanied by pulmonary hypertension. Right and left ventricular ejection fractions were measured, and right and left ventricular volume indices were calculated from ejection fractions and stroke volumes before and 30 minutes after the start of the infusion. Responders (13 patients) showed an increase in stroke volume index (SVI) as a result of a mean 30% increase in right ventricular end-diastolic volume index (RVEDVI) and a mean 17% increase in left ventricular end-diastolic volume index (LVEDVI) during volume loading. In the nonresponders (five patients) fluid loading resulted in a decreased or unchanged SVI; this was accompanied by a 7% increase in RVEDVI but no change in LVEDVI, although both the central venous pressure and pulmonary capillary wedge pressure increased. At baseline, nonresponders differed from responders as evidenced by a high central venous pressure and RVEDVI but a lower mean arterial pressure: thus, right ventricular coronary perfusion pressure was lower and right ventricular wall stress may have been higher. Mean pulmonary artery pressure did not differ between the groups. Our data suggest that in some patients with septic shock volume loading does not result in increased forward flow because of right ventricular failure associated with pulmonary hypertension and coronary hypotension.

Fluid Therapy↗
PubMed1987

Increased systemic microvascular albumin flux in septic shock.

Lymph/plasma (L/P) albumin ratios were followed in a patient with a traumatic thoracic duct lymph fistula, during septic shock when lymph flow was high and at recovery when lymph flow was low. Higher albumin ratios were found during the former. On both occasions, the P-L difference of radioactive counts/min per gram was followed for 6 h after i.v. injection of 51Cr human serum albumin (HSA). Equilibration half times between plasma and lymph amounted to 0.85 h during septic shock and 2.49 h at recovery. The data indicate that systemic microvascular albumin flux had increased during shock in our patient. Increased permeability may have been responsible.

Aged↗
PubMed1987

Influence of rosmarinic acid on opsonization and intracellular killing of Escherichia coli and Staphylococcus aureus by porcine and human polymorphonuclear leucocytes.

The influence of rosmarinic acid on the function of porcine and human polymorphonuclear leucocytes was tested. Rosmarinic acid inhibited the chemiluminescence of PMNL, induced by preopsonized Zymosan or phorbol myristate acetate. The killing of Escherichia coli was inhibited by rosmarinic acid at a concentration of 2 mM, but not that of Staphylococcus aureus. The inhibition of the killing was due to an impaired opsonization, caused by an adverse influence of rosmarinic acid on complement activation. Direct effects of rosmarinic acid on the killing mechanisms of PMNL were not observed.

Animals↗
PubMed1987

The immediate effect of nitroglycerin on total body blood volume distribution in patients with congestive heart failure: a non-invasive study.

The effect of sublingually administered nitroglycerin (0.5 mg) on distribution of blood volume in 16 patients with congestive heart failure (NYHA class II and III), randomly assigned to placebo (N = 8) or nitroglycerin (N = 8) was studied 20 minutes after in vivo labelling of red blood cells with 99m-Tc pertechnetate. Count rates over thorax, abdomen and legs were collected with a large field gamma camera and expressed as percentage changes of baseline value. Changes in count rates, averaged for 5, 10 and 15 minutes after drug administration showed a significant decrease in the nitroglycerin group as compared to the placebo group over the thorax (mean 5%, P less than 0.01) and over the liver (mean 5%, P less than 0.05) and a significant increase over the abdomen (mean 4%, P less than 0.01) and the legs (mean 9%, P less than 0.01). After nitroglycerin, the changes in pulmonary activity were variable and did not differ from the placebo group. These results indicate that nitroglycerin causes a redistribution of blood volume in patients with congestive heart failure. An increase in the vascular capacitance in the abdomen and legs may be responsible for a decrease of blood volume of the thorax and the liver in these patients.

Abdomen↗
PubMed1987

Effects of vasodilators prostaglandin E1 and methylprednisolone on pulmonary hypertension and right ventricular performance during volume loading in porcine septic shock: a combined invasive and radionuclide study.

In 16 anesthetized pigs the cardiovascular effects of prostaglandin E1 and methylprednisolone (MPS) during E. coli sepsis were studied. Gated blood pool scans and hemodynamic studies were simultaneously performed. A control group, group I (n = 4), received volume loading alone; groups II, III, and IV received (each n = 4) volume loading after intravenous administration of MPS, prostaglandin E1, and both MPS and prostaglandin E1, respectively. Groups were formed by randomization, such that the effects of prostaglandin E1 (0.1 microgram/kg/min) and MPS (30 mg/kg) could be analyzed separately and in combination. Eight animals treated with prostaglandin E1 were compared with eight animals not receiving prostaglandin E1. The same method was applied to the MPS group. E. coli infusion resulted in an abrupt increase in pulmonary arterial pressure while systemic blood pressure gradually fell. Cardiac output decreased. Gated blood pool studies showed an increase in right ventricular end-diastolic volume and a decrease in right ventricular ejection fraction. Consequently, right-to-left ventricular end-diastolic volume ratio increased. Pulmonary arterial pressure was lowered in the treatment groups compared to control group. During volume loading right ventricular ejection fraction improved in the prostaglandin E1 group but remained low in the MPS group. Compared to control group, cardiac output did not change and mean systemic arterial pressure significantly decreased in the prostaglandin E1 group. Treatment with prostaglandin E1, MPS, or both drugs and volume loading did not reveal any difference between the four groups with respect to cardiac output, right and left ventricular volumes, and left ventricular ejection fraction. The present study indicates that in a porcine model of E. coli septic shock with acute pulmonary hypertension, prostaglandin E1 and MPS treatment decrease pulmonary vascular resistance but also systemic vascular resistance. Prior to and during volume loading right ventricular ejection fraction increased in the prostaglandin E1 group. However, neither prostaglandin E1 nor MPS improved right ventricular performance and forward flow during volume loading.

Alprostadil↗
PubMed1987

Volume expansion, dobutamine and noradrenaline for treatment of right ventricular dysfunction in porcine septic shock: a combined invasive and radionuclide study.

The purposes of the present study were 1) to explore if volume loading in combination with dobutamine or noradrenaline would be superior to volume loading alone in the treatment of right ventricular (RV) dysfunction in septic shock complicated by acute pulmonary hypertension and 2) to determine whether noradrenaline would be superior to dobutamine because of its vasoconstrictor effects on the peripheral circulation, resulting in increased RV coronary perfusion pressure. Experiments were performed on 21 anesthetized, ventilated pigs. Gated blood pool studies and hemodynamic measurements were performed simultaneously. All animals were given 3-4 X 10(8)/kg live E. coli bacteria, resulting in an abrupt increase in pulmonary arterial pressure and a decrease in arterial pressure, cardiac output, and RV ejection fraction. Right ventricular end-systolic volume was unchanged; RV end-diastolic volume and RV coronary perfusion pressure fell. After randomization, the control group (I, n = 5) was subjected to volume loading, and treatment groups (each n = 8) received volume loading in combination with dobutamine (group II, 5-10 micrograms/kg/min) or noradrenaline (group III, 0.25-0.50 micrograms/kg/min). In contrast to volume loading alone, dobutamine and noradrenaline increased cardiac output and RV ejection fraction, but only noradrenaline restored mean arterial pressure. Noradrenaline improved RV contractility, as judged from the RV end-systolic pressure-volume relationship, probably because it increased the RV perfusion. Thus, noradrenaline in combination with volume loading may be the treatment of choice to improve RV performance in porcine septic shock associated with pulmonary hypertension.

Animals↗
PubMed1987

Relation of arterial blood lactate to oxygen delivery and hemodynamic variables in human shock states.

A retrospective study of 50 patients with circulatory shock and serial hemodynamic and metabolic measurements was undertaken. From the patient records, values for first measured cardiac index (CI) (t = 1) and highest CI (t = 2) with concomitantly obtained hemodynamic and metabolic variables and with arterial blood lactate levels (ABL), measured within 1.5 hours of t = 1 and t = 2 were taken. Nineteen patients had nonseptic shock (NSS), and 31 had septic shock (SS). Mortality rates were equivalent. At both t = 1 and t = 2, CI and O2 delivery (DO2) were higher and systemic vascular resistance index (SVRI) was lower in SS than in NSS. Although increases in DO2 were significant and not different between the groups and initial ABL values were similar, ABL had declined 50% in NSS but had not changed in SS (p less than 0.0001). From the hemodynamic and metabolic variables investigated in NSS, changes in ABL only correlated with changes in arterial oxygen content (CaO2; r = -0.65; p less than 0.01). Changes in ABL did not correlate with changes in DO2 in both groups. In SS, changes in ABL best correlated with changes in SVRI (r = -0.54; p less than 0.01). Our data suggest that anaerobic metabolism, reflected by ABL, decreases in response to an increase in CaO2, CI, and thus DO2 in NSS but not in hyperdynamic SS. Anaerobic metabolism in the latter may relate to peripheral vasodilation, associated with peripheral "functional" shunting of blood transported oxygen, rather than to insufficient DO2.

Arteries↗
PubMed1986

Progressive and fatal course of a patient with a multifocal leiomyomatous tumor.

The case history of a 53-yr-old woman exhibiting the progressive appearance of several hundreds of subcutaneous leiomyomatous tumors in a 15-yr period is presented. The occurrence of multiple tumors in the gastrointestinal tract, mesentery, and retroperitoneum, necessitated several laparotomies because of pain and chronic blood loss. On light microscopy high mitotic activity, which is generally a characteristic of sarcoma, was only encountered in lesions, surgically removed a few months before death. It is argued that our patient suffered from multiple leiomyomatous tumors with progressive growth capacity, which may represent a multifocal origin rather than a metastasized sarcoma.

Duodenum↗
PubMed1986

Hemodynamic determinants of mortality in human septic shock.

To assess the relative importance of cardiac versus peripheral vascular failure in patients dying of septic shock, a series of 42 patients with documented septic shock was retrospectively evaluated. Patients were included in the study if serial hemodynamic and metabolic studies had been performed: the first one within 12 hours after onset of septic shock and the last one within 12 hours (median 2 hours; range 0.1 to 12 hours) before death in nonsurvivors. Nonsurvivors were included only if they died in shock. From the patient records the first, highest, and last measured cardiac indexes (CI) (t = 1, t = 2, and t = 3) with concomitant hemodynamic and metabolic variables were obtained. Group I (n = 21) consisted of survivors and group II (n = 21) of nonsurvivors. Group II was divided into three subgroups: group IIa (n = 4) consisted of nonsurvivors with liver cirrhosis, group IIb (n = 9) patients with final CI less than 4 1 X min-1 X m-2, and group IIc (n = 8) patients with final CI greater than 4 1 X min-1 X m-2. At t = 1 no significant differences in hemodynamic variables were found between groups I and II, and all patients, whether surviving or not, were able to increase CI to similar levels. At t = 3 group II showed a marked decrease in mean arterial pressure and systemic vascular resistance index compared with group I (p less than 0.001), whereas CI did not differ significantly. The nonsurvivors showed progressive lactic acidemia. Even group IIb patients showed persistent vasodilation despite a decrease in CI. Our data suggest that many patients in septic shock die as a result of peripheral vascular rather than cardiac failure, since persistent vasodilation, irrespective of CI, was a major hemodynamic determinant in nonsurvivors, of whom 57% maintained a high CI until shortly before death.

Adult↗