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Biomedical subjects

A A Driedger

Publications and source records attributed to A A Driedger.

At least 73 records · Page 4Linked to original sources

Phentolamine in low cardiac output states: an assessment with ECG-gated cardiac scintigraphy.

We examined the effect of parenteral phentolamine in 11 critically ill patients with a low cardiac output state and a high systemic resistance. Because vasodilators often affect left ventricular end-diastolic pressure-volume relationships (compliance) in acute cardiac disease, changes in the pulmonary capillary wedge pressure (WP) may conceivably not reflect the true effect of vasodilators on left ventricular preload. Hence, we measured left ventricular ejection fraction (LVEF) with ECG-gated cardiac scintigraphy and stroke volume by thermodilution before and during phentolamine infusion. We then calculated left ventricular end-diastolic volume index (LVEDVI). Phentolamine infusion was associated with an increase in the mean cardiac index (CI) (1.96 +/- .53 [mean +/- SD] to 2.45 +/- .69 L/min X m2; p less than .0025) whereas the mean WP fell (19.5 +/- 7.5 to 13.5 +/- 7.3 mm Hg; p less than .05). There was no simultaneous change in the mean LVEDVI (100 +/- 48 to 110 +/- 40 ml/m2; p = NS), implying that one of the effects of phentolamine infusion was to improve left ventricular diastolic compliance. Multiple regression analysis suggested that the major effect of phentolamine on stroke volume was mediated by concomitant changes in the LVEDVI (r2 = .64). Therefore, benefit from phentolamine in low cardiac output states is multifactorial and phentolamine likely improves left ventricular compliance in some patients.

Aged↗

Biventricular function in the adult respiratory distress syndrome.

We examined biventricular function in patients with the adult respiratory distress syndrome (ARDS) by a combination of invasively determined pressures and flows and concomitant radionuclide angiography. Right (RVEF) and left (LVEF) ventricular ejection fractions were measured; right and left ventricular end-diastolic (EDVI) and end-systolic (ESVI) volume indices were calculated from the respective ejection fraction and measured thermodilution stroke volume. With an increase in the outflow pressure load on the right ventricle, measured as the mean pulmonary artery pressure (PAP), the RVEF fell (Y = 66.25 -1.01X; r2 = .42; p less than .001) and both the RVEDVI (y = 13.39 + 3.66X; r2 = .33; p less than .001) and RVESVI (Y = 23.9 + 3.57X; r2 = .41; p less than .001) increased. Progressive increases in the PAP also seemed associated with a change in left ventricular end-diastolic pressure-volume relationships: without pulmonary artery hypertension (PAP less than 20 mm Hg) the mean LVEDVI was 87.2 +/- 31.3 ml/m2 (mean +/- SD) and the mean PCWP was 5.0 +/- 2.8 mm Hg; with a mean PAP exceeding 30 mm Hg, the LVEDVI remained constant (90.4 +/- 26.9 ml/m2) although the PCWP was greater than previous (18.5 +/- 5.7 mm Hg; p less than .01). Analysis of right ventricular peak-systolic pressure end-systolic volume ratios implied a concurrent depression in right ventricular contractility at high levels of PAP. However, right ventricular "pump" function to maintain an adequate left ventricular preload remained unaltered regardless of the presence of pulmonary artery hypertension.

Adult↗

The short-term effects of increasing plasma colloid osmotic pressure in patients with noncardiac pulmonary edema.

We infused hyperoncotic albumin (25 or 50 gm of a 50% solution) into patients with noncardiac pulmonary edema (adult respiratory distress syndrome [ARDS]) to evaluate its effect on the transmicrovascular flux from blood to pulmonary edema fluid of two radiotracers--111In-DTPA (mol wt 504) and 125I-human serum albumin (HSA) (mol wt 69,000). Two groups of patients were studied--one with a modest increase in permeability of the pulmonary alveolocapillary membrane to 125I-HSA (group 1) and another with a large increase in permeability to 125I-HSA (group 2). We used furosemide, when necessary, to minimize the effect of albumin infusion to increase the pulmonary microvascular hydrostatic pressure (Pmv), measured clinically as the pulmonary capillary wedge pressure (PCWP). Therapy significantly increased the mean colloid osmotic pressure (COP) in both groups, but not the mean PCWP or calculated Pmv. Albumin had no significant effect on the mean pulmonary transmicrovascular flux of the radiotracers in either group, despite the increase in COP. In individual patients, a change in the Pmv in response to albumin infusion was directly correlated with the change in flux of 111In-DTPA [group 1: delta In-DTPA (%) = 8.66 + 1.4 delta Pmv (%) r = 0.51, P less than 0.02; group 2: delta In-DTPA (%) = -3.43 + 1.6 delta Pmv (%) r = 0.67, P less than 0.01]. A change in the transmicrovascular flux of I-HSA also correlated with a change in the intravascular Starling forces in both groups. We conclude that albumin infusion in patients with ARDS will not augment the pulmonary transmicrovascular flux of low or high molecular-weight solutes when the effect of albumin to increase the Pmv is minimized; nor, however, does an increase in plasma COP significantly reduce the flux of such solutes.

Albumins↗

Pulmonary accumulation of polymorphonuclear leukocytes in the adult respiratory distress syndrome.

The polymorphonuclear leukocyte (PMN) plays an integral role in the development of permeability pulmonary edema associated with the adult respiratory distress syndrome (ARDS). This report describes 3 patients with ARDS secondary to systemic sepsis who demonstrated an abnormal diffuse accumulation of Indium (111In)-labeled PMNs in their lungs, without concomitant clinical or laboratory evidence of a primary chest infection. In one patient, the accumulation of the pulmonary activity during an initial pass suggested that this observation was related to diffuse leukoaggregation within the pulmonary microvasculature. A 4th patient with ARDS was on high-dose corticosteroids at the time of a similar study, and showed no pulmonary accumulation of PMNs, suggesting a possible reason for the reported beneficial effect of corticosteroids in human ARDS.

Acute Disease↗

Left ventricular function during graded exercise in patients with coronary artery disease and in control subjects.

The left ventricular function of 30 patients with coronary artery disease and 11 control subjects was studied by electrocardiography gated cardiac blood pool scintigraphy as the participants lay on their backs and either rested or exercised on a cycle ergometer at graded levels on intensity. The control subject showed a progressive increase in ejection fraction from rest (51% +/- 7%) to intermediate (56% +/- 10%, P less than 0.05) and maximum levels of exercise (64% +/- 10%, P less than 0.001). All the patients showed a decrease in ejection fraction from rest (42% +/- 16%) to their maximal level of exercise (36% +/- 11%, P less than 0.001). However, the response of some of the patients to intermediate exercise ranged from a decrease or no change to an increase in ejection fraction. Thus, exercise at maximal intensity is necessary to induce the left ventricular dysfunction that is diagnostic of coronary artery disease.

Coronary Disease↗

Does the pulmonary capillary wedge pressure predict left ventricular preload in critically ill patients?

The construction of a Frank-Starling myocardial function curve relating heart work to left ventricular preload is clinically utilized to assess therapeutic protocols in critically ill patients. The pulmonary capillary wedge pressure (PWP) is the index of left ventricular filling pressure most frequently utilized as representative of left ventricular preload. The authors assessed the relationship between left ventricular preload measured as the left ventricular end-diastolic volume (LVEDV), and the PWP, in acutely ill patients with sepsis and cardiac disease. Within each group, no relationship was found between the LVEDV and the PWP; however, when omitting the effect of PEEP, a modest correlation was noted (r = 0.302; p less than 0.01). Of the left ventricular ejection fraction, LVEDV and PWP, the PWP accounted for less than 5% of the explained variance in the stroke volume index. The PWP is a poor predictor of left ventricular preload, probably because of abnormalities of left ventricular compliance in critically ill patients.

Aged↗

Anatomic and cardiopulmonary responses to trauma with associated blunt chest injury.

Myocardial dysfunction may result from severe trauma. Therefore, left (LV) and right ventricular (RV) function were prospectively assessed by ECG-gated blood pool radionuclide (RN) angiography in 25 consecutive patients who had sustained severe trauma including blunt chest injuries. Focal abnormalities of RV and LV wall motion were defined in 17 patients; 12, RV; two, LV; and three, biventricular. In two patients traumatic tricuspid insufficiency was also demonstrated, and subsequently verified by contrast angiography. Other means to detect myocardial contusion (enzymatic, electrocardiographic, and Tc-99m pyrophosphate scintigraphy) proved to be insensitive when compared to RN angiography. Two of the five deaths in the group were attributed to refractory arrhythmias. Surgical or post-mortem evidence of traumatic myocardial injury was obtained in five instances when RN angiography indicated contusion. Of the 13 patients available for followup examinations, 11 showed complete or partial resolution of the abnormality and two were unchanged. Comprehensive cardiopulmonary monitoring revealed an inverse relationship between right ventricular ejection fraction (RVEF) and pulmonary vascular resistance (PVR) (R2 = 0.42; p < 0.01) and between the PVR and left ventricular ejection fraction (LVEF) (R2 = 0.48; p < 0.01) and left ventricular end-diastolic volume (LVEDV) (R2 = 0.69; p < 0.01). Further, as right ventricular end-diastolic volume (RVEDV) was increased in trauma, left ventricular function and compliance were reduced. In blunt chest trauma RV contusion occurs more frequently than previously recognized and positive RN angiography constitutes prima facie evidence of direct myocardial injury. Further, LV function remains preload dependent, but may be depressed by elevated PVR impeding the blood flow from RV to LV and/or decreases in LV compliance.

Adolescent↗

Left ventricular function and volume during supine exercise in subjects with coronary artery disease.

Left ventricular function and volume changes during supine isotonic exercise were assessed in 32 patients with coronary artery disease (CAD) and 12 normal subjects by electrocardiographically gated blood pool cardiac scintigraphy. Ejection fraction (EF) in normal subjects was 49 +/- 10% at rest, 54 +/- 10% during intermediate exercise (P less than 0.05 vs. rest), and 62 +/- 14% during maximal exercise (P less than 0.01 vs. rest). In patients with CAD the resting EF was 42 +/- 14%, 43 +/- 23% at intermediate exercise (P = nonsignificant vs. rest) and 36 +/- 11% at maximal exercise (P less than 0.01 vs. rest). Changes of average and maximal ejection rates from rest to exercise were similar to those of EF but had a lesser degree of statistical significance. End-diastolic volume index (EDVI) in patients with CAD, at intermediate exercise was equal to that at rest, but it increased during maximal exercise (P less than 0.01). In normal subjects EDVI did not change with exercise. Thus, during supine exercise the Frank-Starling mechanism is apparent in patients with CAD but not in normal subjects. Analysis of EF response to exercise is a highly sensitive technique to detect CAD provided that adequate exercise is achieved.

Adult↗

Pulmonary microvascular clearance of radiotracers in human cardiac and noncardiac pulmonary edema.

We examined the integrity of the alveolocapillary membrane in human cardiac (hydrostatic) (group 1) and noncardiac (permeability) (group 2) edema by measuring the clearance of two intravenously administered radiotracers from the blood to suctioned bronchoalveolar secretions (BAS), representing pulmonary edema fluid, and compared the clearances to simultaneously measured pulmonary capillary wedge pressure (PCWP) and colloid osmotic pressure (COP), representing the intravascular Starling forces, Pmv and pimv. 111In-labeled diethylenetriamine pentaacetic acid (DTPA), mol wt 504, a hydrophilic radiotracer that equilibrates with extracellular water, and 125I-labeled human serum albumin (HSA), mol we 69,000, were injected intravenously. Samples of blood and BAS were then collected hourly for 405 h, and clearances were calculated. We found the clearance of both radiotracers to be greater in group 2 than in group 1 patients, despite a low mean PCWP-COP gradient, indicating greater alveolocapillary membrane permeability membrane in noncardiac, than in cardiac edema. Furthermore, 111In-DTPA clearance was linearly correlated with the PCWP-COP gradient in both groups (group 1, R2 = 0.726, P less than 0.001; group 2, R2 = 0.879, p less than 0.001 as was the clearance of 125I-HSA in group 2 (R2 = 0.35, P less than 0.027). Clinically, the data suggest that in cardiac and noncardiac pulmonary edema the transmicrovascular flux of small and large solutes may be favorably influenced by therapeutic alterations aimed at widening the intravascular PCWP-COP gradient. However, the greater permeability of the alveolocapillary membrane in noncardiac edema would prohibit any major resolution of edema by simple therapeutic alterations of this gradient.

Capillary Permeability↗

Positive end-expiratory pressure (PEEP) does not depress left ventricular function in patients with pulmonary edema.

We evaluated the effects of positive end-expiratory pressure (PEEP) on left ventricular function in 15 patients with acute respiratory insufficiency secondary to pulmonary edema with invasive (pressure; flow) measurements and radionuclide angiography (RA). Using RNA allowed a definition of the left ventricular ejection fraction (LVEF), and then calculation of the left ventricular end-diastolic volume (LVEDV), both before and after PEEP. With a mean PEEP of 14.2 +/- 1.8 cm H2O (mean +/- SD) (range, 10 to 15), a fall in the cardiac index (4.34 +/- 1.5 to 3.84 +/- 1.4 L/min/M2; p less than 0.001) was accompanied by a significant decrease in the stroke volume index (42 +/- 13 to 39 +/- 12 ml/beat M2; p less than 0.01) and pulse rate (103.4 +/- 14.3 to 98 +/- 13.5 beats/min; p less than 0.01). The decrease in the stroke volume index was primarily due to a significant decrease in left ventricular preload (LVEDV) from 85.9 +/- 19 to 71.4 +/- 21.4 ml/m2 (p less than 0.01). Simultaneously, the mean LVEF increased from 0.47 +/- 0.10 to 0.53 +/- 0.08 (p less than 0.05), despite a significant increase in the systemic vascular resistance (1,619 +/- 575 to 1,864 +/- 617 dynes . s. cm-5/M2; p less than 0.01). We concluded that the use of PEEP in patients with acute pulmonary edema, to the degree used in this study, may depress cardiac output by simply decreasing left ventricular preload. We were unable to produce any evidence that would support a change in the contractile state of the left ventricle as a cause of depressed forward flow with the use of PEEP.

Angiography↗

Alveolo-capillary permeability in human septic ARDS. Effect of high-dose corticosteroid therapy.

High-dose corticosteroid therapy has been advocated as adjunctive therapy in the adult respiratory distress syndrome (ARDS). We evaluated the effect of pharmacologic doses of corticosteroid (methylprednisolone and dexamethasone) on alveolo-capillary permeability in human septic ARDS by examining the change in appearance of intravenously administered iodine 131 (131I) human serum albumin (I-HSA) into broncho-alveolar secretions, before and after corticosteroid administration. Of 19 patients examined, in 14 (group 1) the clearance of I-HSA was reduced by corticosteroid (pre, .204 +/- .08 ml;/hr; post, .096 +/- .01 ml/hr; P less than .001), while in five (group 2) it was unaffected (pre, .23 +/- .02 ml/hr; post, .215 +/- .01 ml/hr; P=NS). Group 2 patients were more severely ill than group 1 patients in that their mean intrapulmonary shunt fractions and mean pulmonary artery pressures were higher. We conclude that high-dose corticosteroid therapy may reduce alveolo-capillary permeability in human septic ARDS if used early in the course of the illness.

Bronchi↗

The hemodynamic effect of rapid fluid infusion in critically ill patients.

The response to a rapidly administered volume infusion (250 ml of 5% albumin over 30 minutes) was studied in 28 critically ill patients. Cardiovascular responses were assessed by means of invasive hemodynamic parameters (i.e., cardiac index [CI], central venous pressure [CVP], pulmonary artery pressure [PAP], and pulmonary capillary wedge [PCWP] pressure as well as radionuclide [RN] angiography). This allowed for the simultaneous measurement of right (RVEF) and left (LVEF) ejection fractions, and right (RVEDV) and left end-diastolic (LVEDV) and end-systolic (LVESV) volumes. Twenty patients responded (R) to volume infusion by demonstrating an increase in stroke volume. This response was secondary to an increase in LVEDV in 11 (R-1) and an increase in the LVEF in nine (R-2). Neither response was predictable before treatment. The responders also demonstrated a significant decrease in heart rate (P less than 0.05). The increased ejection fraction in some responders (R-2) was associated with a decrease in systemic vascular resistance index (SVRI) (P less than 0.05) and LVESV (P less than 0.05) suggesting a reduced afterload secondary to peripheral vasodilation concomitant on volume change. The PCWP appeared to be related more to right ventricular (RV) loading factors (i.e., CVP, RVEDV, and pulmonary vascular resistance [PVRI] [R2 = 0.85, P less than 0.005]) then to the LVEDV (P = NS). Left ventricular (LV) loading with volume infusion appeared to be dependent on both RV performance and the PVRI in some patients, since responders who increased the LVEDV (R-1) were characterized by a simultaneous increase in RV stroke work and decrease in PVRI. The response to fluid infusion in critically ill patients is complex with both increases in LVEF and LV preload contributing to its beneficial effect. Clinical assessment of LV filling pressures (PCWP) does not accurately predict the response to volume infusion and does not allow a reliable assessment of the LV preload. This is most likely due to the broad range of LV compliance characteristics noted in critically ill patients. RV function also appears to be important in the clinical response to volume challenge.

Blood Pressure↗