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Biomedical subjects

R M Prewitt

Publications and source records attributed to R M Prewitt.

53 records · Page 3Linked to original sources
PubMed1984

Volume expansion versus norepinephrine in treatment of a low cardiac output complicating an acute increase in right ventricular afterload in dogs.

The authors investigated the effects of treatment on ventricular performance when cardiac output (CO) was reduced significantly because of an acute increase in pulmonary vascular resistance (PVR). In eight anesthetized, ventilated dogs, the effects of volume expansion (100 ml 6% dextran) on ventricular performance were determined before and after PVR was elevated. Resistance was increased by microembolization of the pulmonary vascular bed with glass beads (80-100 microns). When PVR was normal, volume expansion increased (P less than 0.05) stroke volume (SV) and mean blood pressure (BP). Alternatively, when RV afterload was increased, volume resulted in RV failure, i.e., decrease in SV (P less than 0.01) from 9.1 to 6.3 ml and a decrease (P less than 0.05) in mean BP from 97 to 65 mmHg, despite increased right ventricular end diastolic pressure (RVEDP) (P less than 0.05). Right ventricular dysfunction occurred with volume expansion, despite constant PVR and a decrease (P less than 0.01) in mean pulmonary artery pressure (PAP). In contrast to volume, norepinephrine infusion decreased biventricular filling pressures (P less than 0.01) and increased (P less than 0.01) SV from 6.2 to 11.3 ml. Accordingly, when RV afterload is increased significantly, even a relatively small increase in blood volume may result in RV dysfunction. Alternatively, inotropic agents with pressor effects may be the treatment of choice to increase CO when RV afterload is increased.

Animals↗
PubMed1984

Effect of increased pulmonary vascular resistance on right ventricular systolic performance in dogs.

We tested the possibility that for a given contractile state and right ventricular systolic pressure (RVSP), rate and extent of ventricular shortening would be reduced as resistance to ejection increased. In eight anesthetized, ventilated dogs, we measured RV and pulmonary artery pressure (Ppa), blood pressure, heart rate, cardiac output (CO), and RV dP/dt before (condition 1) and after (condition 2) pulmonary vascular resistance (PVR) was increased by injection of small (80 micron) glass beads. Glass beads caused a large increase (P less than 0.001) in Ppa and in RVSP and, despite increased RV end-diastolic pressure (EDP), CO and stroke volume (SV) were reduced. A third set of measurements was obtained following a further increase in resistance (condition 3). A comparison of condition 2 with condition 3, despite constant RVSP, constant mean Ppa, and increased EDP, showed a marked fall in CO and SV (P less than 0.001) when glass bead injection increased calculated resistance from 21 (condition 2) to 34 (condition 3) mmHg X 1(-1) X min. RV contractility, as assessed by Vmax and peak dP/dt was similar in both conditions. In five additional dogs, we measured the same parameters as before plus instantaneous pulmonary artery flow in all conditions. In a comparison of conditions 2 and 3, despite constant RVSP and increased EDP, peak and total flow (P less than 0.05) were reduced as resistance to RV ejection increased. We conclude that the right ventricle shortens more slowly and to a smaller extent against the same systolic pressure when its resistive afterload increases.

Animals↗
PubMed1984

Direct effects of nitroprusside do not alter gas exchange in canine oleic acid edema.

The authors investigated why intrapulmonary shunt (QS/QT) increases with sodium nitroprusside (SNP) in canine oleic acid pulmonary edema. To determine the effects of flow alone on QS/QT, a peripheral arteriovenous fistula with a variable resistor was employed to increase cardiac output (Q) 26 and 52% above base line in a stepwise fashion (P less than 0.01). To examine the direct effects of SNP, distinct from changes in flow, the drug was given to produce matched increments in Q in each dog (P less than 0.01). To control for time, base-line measurements were obtained before and after each intervention, the sequence of which was alternated. At each increment in Q, SNP and the arteriovenous fistula increased QS/QT a similar amount. The mixed venous O2 tension (P-vO2) followed Q similarly in each group. Pulmonary vascular resistance (PVR) fell more (P less than 0.01) with SNP than with the arteriovenous fistula at identical Q and P-vO2. The authors conclude that, in this model, a direct pharmacological effect of SNP does not contribute to the deterioration in QS/QT. In fact, SNP exerts a pulmonary vasoactive effect that does not adversely affect gas exchange.

Analysis of Variance↗
PubMed1984

Effects of dopamine on cardiopulmonary function and left ventricular volumes in patients with acute respiratory failure.

We investigated cardiopulmonary effects of dopamine in patients with acute respiratory failure. Specifically, we wished to test the hypothesis that left ventricular filling pressure (Pcwp) would increase when cardiac output (CO) increased with dopamine. Dopamine (range, 5.5 to 20 micrograms/kg/min) increased blood pressure (BP) (p less than 0.001) Pcwp, CO, and stroke volume (SV) (p less than 0.005). Mean Pcwp increased (p less than 0.005) 45% with dopamine, from 11 to 16 mmHg. Qs/Qt increased with dopamine in association with an increase in mixed venous O2 tension, and arterial O2 tension remained constant. In 8 of these patients, left ventricular end-diastolic volume (LVEDV) and end-systolic volume (ESV) were measured using scintigraphic techniques. The LVEDV increased (p less than 0.01) in each patient after the administration of dopamine, and the mean change was from 134 to 163 ml. Although BP and LV afterload increased in each patient, there was no consistent change in LVESV after dopamine administration, i.e., ESV decreased in 1 patient, remained constant in 3, and increased in 4. Accordingly, because afterload increased in all patients and ESV did not, dopamine probably increased contractility. Because EDV increased in all patients, we concluded that the increase in SV with dopamine is explained by a combination of inotropic and peripheral vascular effects.

Acute Disease↗
PubMed1984

Treatment of shock in a canine model of pulmonary embolism.

Despite the high mortality (greater than 30%) associated with hypotension complicating pulmonary embolism, previous studies have not systematically investigated how best to treat shock resulting from pulmonary embolism. In 24 dogs, we measured relevant hemodynamic parameters before and after shock was produced by intravenously injected autologous blood clots. When systemic blood pressure fell to 70 mmHg, dogs were randomly divided into groups and treated blindly for 1 h. All control dogs and all dogs treated with volume and isoproterenol died. In contrast, all dogs treated with noradrenaline were resuscitated and remained hemodynamically stable for 1 h. This effect of noradrenaline was significant (p less than 0.01, Fisher's exact test). Noradrenaline improved right ventricular performance by increasing blood pressure and improving right ventricular perfusion and/or by a direct increase in contractility. We conclude that in a canine model of pulmonary embolism and shock, noradrenaline may be the drug of choice for acute resuscitation.

Animals↗
PubMed1984

Right ventricular contusion: experimental pathophysiology and treatment in an open-chest canine preparation.

To investigate the pathophysiology and treatment of right ventricular (RV) contusion we assessed biventricular function via volume expansion in eight open-chest, anesthetized, ventilated dogs. Measurements were obtained before and after RV contusion with a captive bolt pistol and during dobutamine infusion. RV contusion depressed both RV and left ventricular (LV) performance as assessed by classical ventricular function curves (p less than 0.05). Dobutamine reduced filling pressure (p less than 0.05) and increased cardiac output (CO) (p less than 0.01) when infused post contusion. Because, on inspection, the LV was not contused, the apparent depression in LV function is most likely due to reduced diastolic compliance secondary to ventricular interdependence. In support of this possibility, in four dogs, LV performance significantly improved (p less than 0.05) when the pericardium was opened. We conclude that RV contusion can depress the relationship between CO and filling pressures in both ventricles and that dobutamine is superior to volume in treating the resultant low cardiac output state.

Animals↗
PubMed1983

Treatment of right ventricular dysfunction in acute respiratory failure.

The pathophysiology and managements of right ventricular (RV) dysfunction in acute respiratory failure (ARF) is complicated. Results presented in this paper indicate that volume expansion may not be appropriate therapy to maintain or increase cardiac output (CO) when flow is reduced because of increased RV afterload. Volume will increase RV wall stress and O2 requirements so that despite increased preload, CO may fall. If RV afterload is significantly increased, such changes can occur despite a relatively normal RV end-diastolic pressure (RVEDP). Further, increased RV afterload and/or volume expansion can result in increased RV volumes and secondary alteration in left ventricular (LV) diastolic mechanics. Such changes, especially if wedge pressure increases, would tend to increase pulmonary edema. Also, because of potential changes in viscosity and pulmonary vascular resistance (PVR), packed red blood cells may not be indicated to increase CO, arterial O2 content and tissue O2 delivery in the setting of ARF. Therapy designed to reduce PVR may be appropriate to increase flow in the setting of increased RV afterload. However, such therapy may also reduce systemic vascular resistance, blood pressure (BP) and RV perfusion pressure. Such changes could lead to RV ischemia and reduced CO. Alternatively, agents which increased RV perfusion and/or contractility will increase CO by reducing RV end-diastolic and end-systolic volumes and may be the treatment of choice to increase flow when RV afterload is elevated.

Aged↗
PubMed1983

Effects of hydralazine and nitroprusside on cardiopulmonary function when a decrease in cardiac output complicates a short-term increase in pulmonary vascular resistance.

We investigated the short-term cardiopulmonary effects of nitroprusside and hydralazine when cardiac output (CO) was reduced by a short-term increase in pulmonary vascular resistance (PVR). In six anesthetized, ventilated dogs, small autologous blood clots, injected over 1 to 2 hr, increased right ventricular afterload. When CO had fallen approximately 40%, dogs were treated with nitroprusside and subsequently with hydralazine. Both drugs reduced biventricular filling pressures (p less than .05), but only hydralazine increased CO and stroke volume (p less than .05). Although mean blood pressure and pulmonary artery pressure remained constant with hydralazine, systemic vascular resistance and PVR decreased (p less than .01). In contrast, although nitroprusside reduced blood pressure and systemic vascular resistance (p less than .01), it did not affect PVR and pulmonary artery pressure. When CO is significantly reduced because of a short-term increase in PVR, hydralazine may be superior to nitroprusside in improving cardiopulmonary function.

Animals↗
PubMed1983

Treatment of canine low pressure pulmonary edema. Nitroprusside versus hydralazine.

In canine oleic acid pulmonary edema, we investigated acute cardiopulmonary effects of different doses of nitroprusside and compared the results with those obtained after intravenously administered hydralazine. Oleic acid increased (p less than 0.05) intrapulmonary shunt (Qs/Qt), increased (p less than 0.01) systemic vascular resistance (SVR), and reduced (p less than 0.05) cardiac output (CO). In the presence of low-pressure pulmonary edema, low-dose nitroprusside (NP1) reduced (p less than 0.01) mean blood pressure (BP) approximately 8%, but with the exception of a small fall in ventricular filling pressure, other parameters remained constant. Compared with control values, a higher dose of nitroprusside (NP2) reduced mean BP 20%, and despite a fall (p less than 0.01) in pulmonary capillary wedge pressure, CO increased (p less than 0.05) 20%. Corresponding to the increase in flow, mean Qs/Qt increased (p less than 0.05) from 26 to 36% with NP2 and arterial O2 tension fell (186 to 166 mmHg, p less than 0.05). Compared with NP2, intravenously administered hydralazine caused a larger (p less than 0.01) change in CO. Despite increased CO and increased (p less than 0.01) mixed venous O2 tension, there was no deterioration in gas exchange with hydralazine. Mean Qs/Qt remained constant and arterial O2 tension, (PaO2) increased (p less than 0.05) from 174 mmHg to 217 mmHg. The increased CO with NP2 and hydralazine is probably explained by the large reduction in systemic vascular resistance. Because Qs/Qt remained constant with hydralazine, the increase in PaO2 is most likely due to the increase in PvO2, which increased because CO increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Effects of hydralazine on cardiopulmonary function in canine low-pressure pulmonary edema.

The authors investigated the acute cardiopulmonary effects of hydralazine in canine low-pressure pulmonary edema. Ninety minutes after oleic acid, right to left shunt (Qs/Qt) had increased from 16-46.7%, and arterial O2 tension decreased from 444-194 mmHg. In the presence of oleic acid pulmonary edema, hydralazine infusion increased cardiac output (CO) and stroke volume (SV) from 3.65-4.9 mmHg . 1 (-1) . min (P less than 0.001) and from 26-31 ml (P less than 0.005), respectively. These changes occurred despite reduced preload as mean pulmonary capillary wedge pressure (PCWP) decreased from 6.6-4.1 mmHg (P less than 0.005). These changes are most likely explained by a reduction in resistive afterload because hydralazine reduced systemic vascular resistance (SVR) from 29.1-20.8 mmHg . 1(-1) . min. Despite improved CO, Qs/Qt remained constant and arterial O2 tension increased (P less than 0.005) with hydralazine. Because Qs/Qt remained constant with hydralazine, the improvement in arterial O2 tension is explained most likely by the increased mixed venous oxygen tension secondary to the increase in CO. To the extent that canine oleic acid edema resembles low-pressure pulmonary edema in patients, hydralazine is a potential agent to reduce PCWP, increase CO and arterial O2 tension.

Animals↗
PubMed1982

Effect of altered resistive load on left ventricular systolic mechanics in dogs.

The authors tested the possibility that end-systolic volume is reduced at a given aortic and left ventricular (LV) pressure when systemic vascular resistance is reduced. In seven anesthetized dogs pretreated with propranolol to block reflex changes in contractility, the authors measured aortic pressure and ventricular volumes under baseline conditions and after reducing resistive load by opening two peripheral arterio-venous shunts. When resistive load was reduced, blood pressure was maintained with plasma volume expansion. Real size biplane ventricular end-diastolic areas were obtained using scintigraphic techniques and end-diastolic volumes were calculated using the area-length equation. Thermodilution stroke volume was subtracted from end-diastolic volume to obtain end-systolic volume. When resistive load decreased, mean ejection rate doubled (P less than 0.01) and left ventricular end-systolic volume decreased (P less than 0.005) despite constant aortic pressure. In seven additional dogs, pretreated with propranolol, the authors measured left ventricular pressure, instantaneous and peak left ventricular flow before and after resistive load was reduced by opening one shunt. Despite constant left ventricular pressures, instantaneous, peak and total flow increased when resistance was reduced. It was concluded that the left ventricle shortens farther and faster during ejection against the same aortic and LV pressure when resistive afterload is reduced.

Animals↗
PubMed1981

Cardiovascular management in acute hypoxemic respiratory failure.

This paper reviews recent data concerning the interactions among pulmonary edema, intrapulmonary shunt and cardiac output in acute hypoxemic respiratory failure. In canine oleic acid edema, a 5 mm Hg reduction in pulmonary wedge pressure significantly reduces edema, but a corresponding increase in colloid osmotic pressure does not. When pulmonary wedge pressure is lowered, cardiac output can be maintained with infusions of nitroprusside, dopamine or dobutamine. Each vasoactive agent improves ventricular pumping function, and the increase in cardiac output is due in part to peripheral circulatory actions of the drugs. Although pulmonary shunt increases with these vasoactive agents, increased shunt is due to their pulmonary vasoactivity but to the associated increase in pulmonary blood flow. Positive end-expiratory pressure reduces venous return by raising right atrial pressure, and it does not depress ventricular pumping function. Rather, positive end-expiratory pressure increases ventricular filling pressure t a given end-diastolic volume; it does not reduce and probably increases edema, yet it reduces shunt by redistributing the edema. These interpretations suggest several goals for cardiovascular management in acute hypoxemic respiratory failure: (1) the lowest pulmonary wedge pressure consistent with adequate cardiac output; and (2) the least positive end-expiratory pressure consistent with saturation of adequate circulating hemoglobin on nontoxic inspired oxygen.

Aged↗
PubMed1981

Effect of positive end-expiratory pressure on left ventricular mechanics in patients with hypoxemic respiratory failure.

When positive end-expiratory pressure (PEEP) is added to intermittent positive pressure ventilation, cardiac output and stroke volume frequently fall despite unchanged or increased transmural left ventricular end-diastolic pressure. To determine whether a part of the fall in stroke volume with PEEP is explained by depressed left ventricular systolic function (increased end-systolic volume at a given end-systolic pressure on PEEP) the authors measured left ventricular end-diastolic volume (EDV), end-systolic volume (ESV), and the corresponding pressures in nine patients with acute hypoxemic respiratory failure. Measurements were made before and after 10 cm H2O PEEP was added to the ventilator. PEEP reduced mean stroke volume from 71 to 62 ml and this was explained entirely by a reduction in end-diastolic volume from 135 to 112 ml (P less than 0.005). Despite reduced EDV, pulmonary wedge pressure increased from 12 to 14 torr on PEEP, indicating reduced diastolic compliance or unstressed volume of the left ventricle in these patients similar to that reported in dogs. The authors conclude that PEEP reduces venous return and cardiac output without depressing left ventricular pumping function because end-systolic volume decreased from 64 to 49 ml on PEEP despite identical blood pressures (78 torr). They speculate that PEEP might improve ventricular performance by increasing intrathoracic pressure and left ventricular pressure relative to systemic blood pressure in extrathoracic vessels.

Adult↗
PubMed1981

Effect of sodium nitroprusside on cardiovascular function and pulmonary shunt in canine oleic acid pulmonary edema.

The authors investigated the acute effects of nitroprusside on intrapulmonary shunt (Qs/Qt), cardiac output, and left ventricular function in dogs with normal lungs, and again after they developed oleic acid pulmonary edema. Before oleic acid, nitroprusside reduced pulmonary capillary wedge pressure (PCWP) and stroke volume, and there were no changes in Qs/Qt. Ninety minutes after oleic acid, PCWP, Qs/Qt, and systemic vascular resistance increased and stroke volume decreased. Then nitroprusside increased cardiac output by 35 per cent and increased Qs/Qt from 12 to 18 per cent. After oleic acid, stroke volume increased on nitroprusside from 18 to 23 ml (P less than 0.05) despite reduced preload, as PCWP decreased from 10.4 to 4.4 torr on nitroprusside (P less than 0.05). Increased stroke volume may be explained by the reduction in resistive afterload, as nitroprusside reduced systemic vascular resistance from 60 to 34 torr . l-1 . min. To the extent that canine oleic acid pulmonary edema represents low pressure edema in patients, nitroprusside is a potential treatment to reduce PCWP, pulmonary microvascular pressure, and pulmonary edema while maintaining cardiac output.

Animals↗
PubMed1981

Treatment of acute low pressure pulmonary edema in dogs: relative effects of hydrostatic and oncotic pressure, nitroprusside, and positive end-expiratory pressure.

Severe pulmonary edema sometimes develops despite normal pulmonary capillary wedge pressure (Ppw). The equation describing net transvascular flux of lung liquid predicts decreased edema when hydrostatic pressure is reduced or when colloid osmotic pressure is increased in the pulmonary vessels. We tested these predictions in a model of pulmonary capillary leak produced in 35 dogs by intravenous oleic acid. 1 h later, the dogs were divided into five equal groups and treated for 4 h in different ways: (a) not treated, to serve as the control group (Ppw = 11.1 mm Hg); (b) given albumin to increase colloid osmotic pressure by 5 mm Hg (Ppw = 10.6 mm Hg); (c) ventilated with 10 cm H(2)O positive end-expiratory pressure (Peep) (transmural Ppw = 10.4 mm Hg); (d) phlebotomized to reduce Ppw to 6 mm Hg; (e) infused with nitroprusside, which also reduced Ppw to 6 mm Hg. Phlebotomy and nitroprusside reduced the edema in excised lungs by 50% (P< 0.001), but Peep and albumin did not affect the edema. Pulmonary shunt decreased on Peep and increased on nitroprusside, and lung compliance was not different among the treatment groups, demonstrating that these variables are poor indicators of changes in edema. Cardiac output decreased during the treatment period in all but the nitroprusside group, where Ppw decreased and cardiac output did not. We conclude that canine oleic acid pulmonary edema is reduced by small reductions in hydrostatic pressure, but not by increased colloid osmotic pressure, because the vascular permeability to liquid and protein is increased. These results suggest that low pressure pulmonary edema may be reduced by seeking the lowest Ppw consistent with adequate cardiac output enhanced by vasoactive agents like nitroprusside. Further, colloid infusions and Peep are not helpful in reducing edema, so they may be used in the lowest amount that provides adequate circulating volume and arterial O(2) saturation on nontoxic inspired O(2). Until these therapeutic principles receive adequate clinical trial, they provide a rationale for carefully monitored cardiovascular manipulation in treating patients with pulmonary capillary leak.

Albumins↗
PubMed1979

Effect of positive end-expiratory pressure on ventricular function in dogs.

Artificial ventilation with positive end-expiratory pressure (PEEP) reduces venous return by raising intrathoracic pressure. To determine whether PEEP decreases cardiac output further by depressing myocardial function, we constructed Starling curves, using rapid dextran infusion in 7 anesthetized dogs ventilated with zero (ZEEP) and 20 cm PEEP. The changes in stroke volume and in left ventricular stroke work (LVSW) when PEEP was added or removed were significantly greater than could be attributed to the corresponding change in transmural left ventricular end-diastolic pressure (LVEDPTM) on these Starling curves. To the extent that PEEP did not alter left ventricular diastolic volume-pressure characteristics, these data indicated PEEP depressed ventricular function. Identical changes with PEEP in cardiac output (-30%), esophageal pressure (+10 cmH2O), and left ventricular function were observed after pulmonary edema was induced with oleic acid. These results confirm and extend recent suggestions that high levels of PEEP depress left ventricular function in dogs, accounting for about half of the reduction in cardiac output before and during acute pulmonary edema.

Animals↗