| 1. |
- Jörgensen, Kirsten, 1959, et al.
(author)
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Left ventricular performance and dimensions in patients with severe emphysema.
- 2007
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In: Anesthesia and analgesia. - : Ovid Technologies (Wolters Kluwer Health). - 1526-7598 .- 0003-2999. ; 104:4, s. 887-92
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Journal article (peer-reviewed)abstract
- BACKGROUND: Concomitant heart dysfunction during the course of chronic obstructive pulmonary disease is well recognized. The prevailing view is that mainly the right side of the heart is involved. We evaluated left ventricular (LV) function and dimensions in patients with severe emphysema. METHODS: Patients with severe emphysema undergoing lung volume reduction surgery were studied after anesthesia induction (n = 10). Non-emphysematous patients scheduled for lobectomy served as controls (n = 10). LV dimensions were measured with patients in the supine position by transesophageal two-dimensional echocardiography and systemic hemodynamics by a pulmonary artery thermodilution catheter, before and during central blood volume expansion by passive leg elevation. RESULTS: Baseline cardiac index (-25%), stroke volume index (SVI, -32%) stroke work index (-34%) and LV end-diastolic area index (EDAI, -33%) were significantly (P < 0.001) lower in the emphysema group. Passive leg elevation increased SVI and LV area ejection fraction more in the emphysema group than in controls (P < 0.05). The DeltaSVI/Delta pulmonary capillary wedge pressure and the DeltaSVI/DeltaEDAI relationships were significantly (P < 0.05) higher in the emphysema group compared to controls (2.2 +/- 0.71 vs 0.6 +/- 0.2 mL/mm Hg x m2 and 5.8 +/- 0.89 vs 2.8 +/- 0.8 mL/cm2 x m2, respectively). Preload-recruitable stroke work (Deltastroke work index/DeltaEDAI), a load-independent index of systolic LV function, did not differ between the two groups. CONCLUSION: The LV in patients with severe emphysema is hypovolemic, and operates on a steeper portion of the LV function curve, while indices of systolic function are not significantly impaired compared to non-emphysematous controls.
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| 2. |
- Redfors, Bengt, et al.
(author)
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Effects of mannitol alone and mannitol plus furosemide on renal oxygen consumption, blood flow and glomerular filtration after cardiac surgery.
- 2009
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In: Intensive care medicine. - : Springer Science and Business Media LLC. - 1432-1238 .- 0342-4642. ; 35:1, s. 115-22
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Journal article (peer-reviewed)abstract
- OBJECTIVE: Imbalance of the renal medullary oxygen supply/demand relationship can cause hypoxic medullary damage and ischaemic acute renal failure (ARF). The use of mannitol for prophylaxis/treatment of clinical ischaemic ARF is controversial and the effect of mannitol on renal oxygenation in man has not yet been investigated. We evaluated the effects of mannitol on renal oxygen consumption (RVO(2))(,) renal blood flow (RBF) and glomerular filtration rate (GFR) in postoperative patients. DESIGN: Prospective interventional study. SETTING: University hospital cardiothoracic ICU. PATIENTS: Ten uncomplicated mechanically ventilated and sedated postcardiac surgery patients with preoperatively normal renal function. INTERVENTIONS: Mannitol infusion (225 mg/kg + 75 mg/kg/h) and combined mannitol and furosemide infusion (0.25 mg/kg + 0.25 mg/kg/h). MEASUREMENTS AND RESULTS: Systemic haemodynamics were evaluated by a pulmonary artery catheter. RBF and GFR were measured by the renal vein thermodilution technique and by renal extraction of (51)Cr-EDTA, respectively. Mannitol increased urine flow (60%), GFR (20%) and filtration fraction (FF) (20%) with no change in RBF. This was accompanied by an increase in renal sodium reabsorption (18%), RVO(2) (19%) and renal oxygen extraction (21%). When combined with mannitol, furosemide normalised sodium reabsorption, RVO(2), renal oxygen extraction with no change in RBF, while GFR and FF were still elevated compared to control. CONCLUSIONS: In patients with normal renal function, mannitol increases GFR, which increases tubular sodium load, sodium reabsorption and RVO(2) after cardiac surgery. The lack of effect on RBF, indicates that mannitol impairs the renal oxygen supply/demand relationship. Furosemide normalised renal oxygenation when combined with mannitol.
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| 3. |
- Swärd, Kristina, 1953, et al.
(author)
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Differential effects of human atrial natriuretic peptide and furosemide on glomerular filtration rate and renal oxygen consumption in humans.
- 2005
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In: Intensive care medicine. - : Springer Science and Business Media LLC. - 0342-4642 .- 1432-1238. ; 31:1, s. 79-85
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Journal article (peer-reviewed)abstract
- OBJECTIVE: Imbalance in the renal medullary oxygen supply/demand relationship can cause hypoxic medullary damage and ischemic acute renal failure. Human atrial natriuretic peptide (h-ANP) increases glomerular filtration rate in clinical acute renal failure. This would increase renal oxygen consumption due to increased tubular load of sodium. Loop diuretics are commonly used in acute renal failure. Data on the effects of loop diuretics on glomerular filtration rate and renal oxygen consumption in humans are, however, controversial. We evaluated the effects of h-ANP and furosemide on renal oxygen consumption, glomerular filtration rate, and renal hemodynamics in humans. DESIGN AND SETTING: Prospective two-agent interventional study in a university hospital cardiothoracic ICU. PATIENTS: Nineteen uncomplicated, mechanically ventilated postcardiac surgery patients with normal renal function. INTERVENTIONS: h-ANP (25 and 50 ng/kg per minute, n=10) or furosemide (0.5 mg/kg per hour, n=9). MEASUREMENTS AND RESULTS: Renal plasma flow and glomerular filtration rate were measured using the infusion clearance technique for (51)Cr-labeled EDTA and paraaminohippurate, corrected for by renal extraction of PAH. h-ANP increased glomerular filtration rate, renal filtration fraction, fractional excretion of sodium, and urine flow. This was accompanied by an increase in tubular sodium reabsorption (9%) and renal oxygen consumption (26%). Furosemide infusion caused a 10- and 15-fold increase in urine flow and fractional excretion of sodium, respectively, accompanied by a decrease in tubular sodium reabsorption (-28%), renal oxygen consumption (-23%), glomerular filtration rate and filtration fraction (-12% and -7%, respectively). CONCLUSIONS: The filtered load of sodium is an important determinant of renal oxygen consumption. h-ANP improves glomerular filtration rate but does not have energy-conserving tubular effects. In contrast, furosemide decreases tubular sodium reabsorption and renal oxygen consumption and thus has the potential to improve the oxygen supply/demand relationship in clinical ischemic acute renal failure.
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| 4. |
- Bragadottir, Gudrun, et al.
(author)
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Low-dose vasopressin increases glomerular filtration rate, but impairs renal oxygenation in post-cardiac surgery patients.
- 2009
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In: Acta Anaesthesiol Scand. - : Wiley. - 1399-6576. ; 53:8, s. 1052-9
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Journal article (peer-reviewed)abstract
- BACKGROUND: The beneficial effects of vasopressin on diuresis and creatinine clearance have been demonstrated when used as an additional/alternative therapy in catecholamine-dependent vasodilatory shock. A detailed analysis of the effects of vasopressin on renal perfusion, glomerular filtration, excretory function and oxygenation in man is, however, lacking. The objective of this pharmacodynamic study was to evaluate the effects of low to moderate doses of vasopressin on renal blood flow (RBF), glomerular filtration rate (GFR), renal oxygen consumption (RVO2) and renal oxygen extraction (RO2Ex) in post-cardiac surgery patients. METHODS: Twelve patients were studied during sedation and mechanical ventilation after cardiac surgery. Vasopressin was sequentially infused at 1.2, 2.4 and 4.8 U/h. At each infusion rate, systemic haemodynamics were evaluated by a pulmonary artery catheter, and RBF and GFR were measured by the renal vein thermodilution technique and by renal extraction of 51chromium-ethylenediaminetetraacetic acid, respectively. RVO2 and RO2Ex were calculated by arterial and renal vein blood samples. RESULTS: The mean arterial pressure was not affected by vasopressin while cardiac output and heart rate decreased. RBF decreased and GFR, filtration fraction, sodium reabsorption, RVO2, RO2Ex and renal vascular resistance increased dose-dependently with vasopressin. Vasopressin exerted direct antidiuretic and antinatriuretic effects. CONCLUSIONS: Short-term infusion of low to moderate, non-hypertensive doses of vasopressin induced a post-glomerular renal vasoconstriction with a decrease in RBF and an increase in GFR in post-cardiac surgery patients. This was accompanied by an increase in RVO2, as a consequence of the increases in the filtered tubular load of sodium. Finally, vasopressin impaired the renal oxygen demand/supply relationship.
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| 5. |
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| 6. |
- Jörgensen, Kirsten, 1959, et al.
(author)
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Effects of levosimendan on left ventricular relaxation and early filling at maintained preload and afterload conditions after aortic valve replacement for aortic stenosis.
- 2008
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In: Circulation. - 1524-4539. ; 117:8, s. 1075-81
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Journal article (peer-reviewed)abstract
- BACKGROUND: We determined the effects of levosimendan, a calcium sensitizer, on left ventricular (LV) diastolic function in patients with LV hypertrophy. METHODS AND RESULTS: In this prospective, randomized, blinded study, 23 patients received either levosimendan (0.1 and 0.2 microg x kg(-1) x min(-1); n=12) or placebo (n=11) after aortic valve replacement for aortic stenosis. The effects on LV performance, dimensions, filling patterns, and isovolumic relaxation time, as well as systemic hemodynamics, were assessed by pulmonary artery thermodilution catheterization and transesophageal 2-dimensional Doppler echocardiography. To circumvent the confounding effects of the levosimendan-induced hemodynamic changes on Doppler echocardiographic indexes of LV early relaxation, heart rate and mean arterial and central venous pressures were kept constant during levosimendan/placebo infusion by atrial pacing, vasopressor, and colloid infusions. In the levosimendan group, dose-dependent increases in cardiac output (28%; P<0.001) and stroke volume (26%; P<0.001) and a decrease in systemic vascular resistance (-22%; P<0.001) were observed. There was a trend for an increase in LV ejection fraction (12%; P=0.058) with levosimendan. There were no significant differences in systolic, diastolic arterial, or LV filling pressures or LV end-diastolic area between the 2 groups. Isovolumic relaxation time decreased (-23%; P<0.001), as did the deceleration slope of early diastolic filling (-45%; P<0.01), whereas peak early diastolic filling velocity (16%, P<0.01) and peak late diastolic filling velocity (15%; P<0.001) increased after levosimendan compared with placebo. CONCLUSIONS: Levosimendan, in addition to its inotropic effects, exerts a direct positive lusitropic effect in patients with LV hypertrophy as it shortens isovolumic relaxation time and improves LV filling.
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| 7. |
- Jörgensen, Kirsten, 1959, et al.
(author)
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Reduced intrathoracic blood volume and left and right ventricular dimensions in patients with severe emphysema: an MRI study.
- 2007
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In: Chest. - : Elsevier BV. - 0012-3692. ; 131:4, s. 1050-7
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Journal article (peer-reviewed)abstract
- BACKGROUND: Left ventricular (LV) filling is impaired in patients with severe emphysema manifesting in small end-diastolic dimensions. We hypothesized that the hyperinflated lungs of these patients with high intrinsic positive end-expiratory pressure will decrease intrathoracic blood volume (ITBV) and ventricular preload. We therefore measured ITBV, and LV and right ventricular (RV) dimensions and function using MRI techniques in patients with severe emphysema. METHODS: Patients with severe emphysema (n = 13) and matched healthy volunteers (n = 11) were included. The magnetic resonance (MR) examination consisted of three parts: (1) evaluation of RV and LV dimensions and function and interventricular septum curvature using cine MRI; (2) quantification of aortic flow using MR phase velocity mapping; and (3) calculation of the cardiopulmonary peak transit time (PTT) from the pulmonary artery to the ascending aorta using contrast-enhanced, time-resolved, two-dimensional MR angiography. RESULTS: There were no differences between the groups regarding age, height, or weight. In the emphysema patients, ITBV index (- 35%), LV end-diastolic volume index (LVEDVI) [- 21%], RV end-diastolic volume index (- 20%), cardiac index (- 22%), and stroke volume index (SVI) [- 40%] were lower compared to control subjects. LV and RV end-systolic volumes, LV wall mass, septal curvature, and PTT did not differ between the groups. LVEDVI (r = 0.83) as well as SVI (r = 0.82) correlated closely to ITBV index. SVI correlated closely to LVEDVI (r = 0.84). CONCLUSIONS: LV and RV performance is impaired in patients with severe emphysema because of small end-diastolic dimensions. One possible explanation for the decreased biventricular preload in these patients is intrathoracic hypovolemia caused by hyperinflated lungs.
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| 8. |
- Nygren, Andreas, 1967, et al.
(author)
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Autoregulation of human jejunal mucosal perfusion during cardiopulmonary bypass.
- 2006
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In: Anesthesia and analgesia. - 1526-7598. ; 102:6, s. 1617-22
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Journal article (peer-reviewed)abstract
- Animal studies have suggested that autoregulation of intestinal blood flow is severely impaired during cardiopulmonary bypass (CPB). We investigated the jejunal mucosal capacity to autoregulate perfusion during nonpulsatile CPB (34 degrees C) in 10 patients undergoing elective cardiac surgery. Changes in mean arterial blood pressure (MAP) were induced by altering the CPB flow rate randomly for periods of 3 min from 2.4 L/min/m2 to either 1.8 or 3.0 L/min/m2. Jejunal mucosal perfusion (JMP) was continuously recorded by laser Doppler flowmetry. A typical pattern of flow motion (vasomotion) was recorded in all patients during CPB. Variations in CPB flow rates caused no significant changes in mean JMP, jejunal mucosal hematocrit, or red blood cell velocity within a range of MAP from 50 +/- 15 to 74 +/- 16 mm Hg. The vasomotion frequency and amplitude was positively correlated with CPB flow rate. IV injections of prostacyclin (10 microg, Flolan) blunted vasomotion and increased JMP from 192 +/- 53 to 277 +/- 70 (P < 0.05) perfusion units despite a reduction in MAP from 59 +/- 12 to 45 +/- 10 mm Hg (P < 0.05). Prostacyclin-induced vasodilation resulted in loss of mucosal autoregulation (pressure-dependent perfusion). We conclude that autoregulation of intestinal mucosal perfusion is maintained during CPB in humans.
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| 9. |
- Thorén, Anders, 1955, et al.
(author)
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Cardiopulmonary bypass in humans--jejunal mucosal perfusion increases in parallel with well-maintained microvascular hematocrit.
- 2005
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In: Acta anaesthesiologica Scandinavica. - : Wiley. - 0001-5172 .- 1399-6576. ; 49:4, s. 502-9
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Journal article (peer-reviewed)abstract
- BACKGROUND: An imbalance between splanchnic oxygen supply and demand occurs during cardiopulmonary bypass (CPB) in man, which might disrupt the intestinal mucosal barrier function. The aim of the present study was to evaluate the effects of mild hypothermic CPB on intestinal mucosal perfusion in man undergoing cardiac surgery. Additionally we aimed to identify variables, which independently could predict changes of intestinal mucosal microcirculatory variables during CPB. METHODS: Jejunal mucosal perfusion (JMP), jejunal mucosal hematocrit (JMHt), red blood cell (RBC) velocity and arteriolar vasomotion using endoluminal jejunal laser Doppler flow metry were studied in eight cardiac surgical patients before and during CPB at a temperature of 34 degrees C. RESULTS: Cardiopulmonary bypass and the accompanied hemodilution (25-30%) induced a 44% increase in JMP (P < 0.05) and a 42% increase in RBC velocity (P < 0.01), with no change in JMHt. The oscillation amplitude of JMP, at a fundamental frequency of 2.8 cycles min(-1), increased with 175% (P < 0.05) during CPB. Splanchnic oxygen extraction increased by 64% during CPB (P < 0.05). Stepwise multiple regression analysis identified systemic hematocrit, arterial O2 and CO2 tension and splanchnic oxygen extraction as independent predictors of RBC velocity during CPB (R2=0.63, P < 0.001). The oscillation amplitude of JMP was predicted by RBC velocity and splanchnic oxygen extraction (R2= 0.68, P <0.0001). CONCLUSIONS: The increase in RBC velocity and enhanced arteriolar vasomotion, as well as maintained jejunal mucosal hematocrit, are microcirculatory, compensatory mechanisms for the splanchic oxygen supply/demand mismatch seen during cardiopulmonary bypass in humans.
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| 10. |
- Lidén, Hans, 1971, et al.
(author)
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Does pretransplant left ventricular assist device therapy improve results after heart transplantation in patients with elevated pulmonary vascular resistance?
- 2009
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In: European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery. - : Oxford University Press (OUP). - 1873-734X. ; 35:6
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Journal article (peer-reviewed)abstract
- OBJECTIVE: Pulmonary hypertension (PH), defined as a pulmonary vascular resistance (PVR) >2.5 Wood units (WU) and (or) a transpulmonary gradient (TPG) >12 mmHg, is an established risk factor for mortality in heart transplantation. Elevated PVR in heart transplant candidates can be reduced using a left ventricular assist device (LVAD), and LVAD is proposed to be the treatment of choice for candidates with PH. We analyzed the effect on PVR of pretransplant LVAD therapy in patients with PH and compared posttransplant outcome with matched controls. Long-term survival was compared between heart transplant recipients with mild, moderate or severe PH and patients with no PH. METHODS: Heart transplant recipients 1988-2007 (n=405) were reviewed and divided into two groups with respect to pretransplant PVR: <2.5 WU (n=148) and >2.5 WU (n=158). From the group with PH, patients subjected to pretransplant LVAD therapy (n=11) were analyzed with respect to PVR at implant and at transplant and, with respect to outcome, compared to matched historical controls (n=22). Patients with PH without LVAD treatment (n=147) were stratified into three subgroups: mild, moderate and severe PH and survival according to Kaplan-Meier was analyzed and compared to patients with no PH. RESULTS: LVAD therapy reduced PVR from 4.3+/-1.6 to 2.0+/-0.6 WU, p<0.05. Three cases of perioperative heart failure required mechanical support whereas one control patient developed perioperative right heart failure requiring mechanical support. The incidence of other perioperative complications was comparable between groups. There was no difference in survival between LVAD patients and controls, 30-day survival was 82% and 91%, respectively and 4-year survival was 64% and 82%, respectively. CONCLUSIONS: Pretransplant LVAD therapy reduces an elevated PVR in heart transplant recipients, but there was no statistically significant difference in posttransplant survival in patients with PH with, or without LVAD therapy. The study revealed no differences in survival in patients regardless of the severity of the PH.
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