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M Ghignone

Publications and source records attributed to M Ghignone.

28 records · Page 2Linked to original sources
PubMed1986

Effects of clonidine on narcotic requirements and hemodynamic response during induction of fentanyl anesthesia and endotracheal intubation.

The effects of clonidine, a centrally acting alpha 2-adrenergic receptor agonist, on depth of fentanyl anesthesia and on cardiovascular response to laryngoscopy and intubation were studied. Twenty-four patients undergoing aortocoronary bypass surgery (ACBS) with a history of arterial hypertension, coronary artery disease (NYHA class 3-4), and well-preserved left ventricular function were assigned randomly to either Group 1 (n = 12), who received standard premedication, or Group 2 (n = 12), who received clonidine 5 micrograms X kg-1 po in addition to standard premedication 90 min before estimated induction time. Depth of anesthesia was assessed by on-line aperiodic computerized analysis of the electroencephalogram (Lifescan EEG Monitor). Fentanyl was administered in 250-micrograms increments to shift the EEG to the 0.5-3-Hz frequency range (delta activity) in all subjects. In both groups, the anesthetic regimen effectively prevented hyperdynamic cardiovascular responses to laryngoscopy and intubation. No significant differences in measured or derived hemodynamic variables were observed between the two groups during the awake control period, except for stroke volume index (SVI), which was significantly greater in Group 1, 44 +/- 9 ml X beat-1 X m-2 compared with Group 2, 35 +/- 3.3 ml X beat-1 X m-2 (P less than 0.05). By contrast, fentanyl requirements in Group 2 were significantly reduced by 45% when compared with Group 1, i.e., from 110 +/- 23 to 61 +/- 19 micrograms X kg-1 (P less than 0.001). The authors conclude that at a similar anesthetic depth, as assessed by the EEG shift into the lower frequency range (0.5-3 Hz), a markedly reduced fentanyl dose effectively prevented the hyperdynamic cardiovascular response to laryngoscopy and intubation in the group of patients premedicated with clonidine. This is likely explained by the known synergistic inhibitory action of opiates and alpha 2-adrenoceptor agonists on central sympathetic outflow.

Adult↗
PubMed1986

Malnutrition and respiratory function.

Malnutrition has a tremendous impact on respiratory functions. It affects respiratory muscle performance, lung structure, defense mechanisms, and control of ventilation and predisposes to respiratory failure and prolonged mechanical ventilation. Calling clinicians' attention to this common clinical problem is the first step toward developing a systematic approach to patient care in which correction of malnutrition is an integral part of the therapy. The increased morbidity and mortality in malnourished patients can be better understood when they are superimposed on other disease conditions, such as chronic lung disease, sepsis, trauma, and cardiovascular dysfunction. Most important is the fact that many of the consequences of malnutrition can be partially reversible with appropriate refeeding.

Animals↗
PubMed1985

Effects of vasodilators on canine cardiopulmonary function when a decrease in cardiac output complicates an increase in right ventricular afterload.

In canine oleic acid pulmonary edema, we investigated acute cardiopulmonary effects of nitroprusside (NP) before (NP1), and after (NP2) pulmonary vascular resistance (PVR) was increased via glass bead embolization. In the setting of increased PVR and reduced cardiac output (CO), acute cardiopulmonary effects of NP and hydralazine were compared. Oleic acid increased (p less than 0.05) pulmonary shunt (Qs/Qt) from 15 to 24%, but did not alter PVR. Cardiac output decreased (p less than 0.01) 31% with oleic acid from 4.2 to 2.9 1 X min-1 and systemic vascular resistance (SVR) increased (p less than 0.01). When PVR was normal, NP reduced (p less than 0.05) blood pressure (BP) from 148 to 123 mmHg, decreased SVR 31%, and increased (p less than 0.05) CO and Qs/Qt. Glass bead embolization increased (p less than 0.001) PVR from 2.2 to 20 mgHg X 1-1 X min and reduced (p less than 0.01) CO 23%, from 2.6 to 2 L/min. The Qs/Qt did not increase with embolization. In contrast to effects of NP1, when RV afterload was increased, CO fell (p less than 0.05) with NP2 from 2 to 1.6 1 X min-1. Alternatively, hydralazine improved cardiopulmonary function. In the setting of increased RV afterload, SVR and PVR decreased (p less than 0.01) 48 and 29%, respectively, with hydralazine. Corresponding to the decrease in resistance, CO increased (p less than 0.001) 84% with hydralazine, from 1.9 to 3.5 1 X min-1. Also, BP and Qs/Qt remained constant and arterial O2 tension increased (p less than 0.05) with hydralazine, from 113 to 152 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
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↗
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

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↗