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| 2. |
- Hjalmarsson, Clara, 1969, et al.
(författare)
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Severe heart failure in a unique case of cobalamin-C-deficiency resolved with LVAD implantation and subsequent heart transplantation.
- 2024
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Ingår i: Molecular genetics and metabolism reports. - 2214-4269. ; 39
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Tidskriftsartikel (refereegranskat)abstract
- Introduction Cobalamin c deficiency (cblC), an inborn error of vitamin B12 metabolism, is caused by mutations of the MMACHC gene. It usually leads to a multisystemic disease; 50% of all patients with cblC have various structural heart defects. Severe congestive heart failure (HF) may also occur and its prognosis is poorly documented. Case report We present the case of a young man who had been diagnosed with cblC due to C331T mutation in the MMACHC gene at the age of 3days and had been treated with substitution therapy (OH-Cbl, mecobalamine, carnitine, betaine, and calcium folinate) since then. He had mildly impaired cognitive function; an ectopic hypophysis/pituitary insufficiency, with adequate hormone replacement therapy; obstructive sleep apnea syndrome, treated with CPAP, bronchial asthma, and obesity (BMI of 30). The liver and kidney functions were normal. He developed severe dilated cardiomyopathy and HF at the age of 12y. With medical treatment, his condition improved and he was stable (NYHA class II) for several years. Six years later, his status deteriorated rapidly, as he developed advanced HF, INTERMACS 3. The cardiac ultrasound revealed dilated ventricles with severely depressed ejection fraction (EF), increased filling pressures, and pulmonary hypertension (sPAP 60mmHg). Cardiac MRI showed extremely dilated chambers (LVedv 609mL, RVedv 398mL) with pronounced non-compaction, and a left ventricle EF of 13%. A primary prophylactic ICD and a left ventricular assist device (LVAD/HM3) were implanted, and the patient was subsequently listed for heart transplantation (HTx). After 25months on the waiting list, he underwent an uncomplicated HTx. However postoperatively, he got two episodes of cardiac tamponade, as well as mediastinitis, treated with antibiotics and vaccum assisted closure. He developed severe kidney failure, which fully recovered after two months, and was treated successfully for an early moderate allograft rejection (ISHT 2). At the latest outward visit, twelve months after HTx, the patient was doing excellent. Summary To the best of our knowledge, this is the first ever reported case of a patient with CblC undergoing an LVAD implantation and subsequently a HTx. Although both interventions were complicated with bleeding events, this seems to be a treatment option for advanced HF in patients with CblC.
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| 3. |
- Martinsson, Andreas, et al.
(författare)
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Inspiratory and end-expiratory effects of lung recruitment in the prone position on dorsal lung aeration – new physiological insights in a secondary analysis of a randomised controlled study in post-cardiac surgery patients
- 2022
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Ingår i: British Journal of Anaesthesia. - : Elsevier BV. - 0007-0912 .- 1471-6771. ; 4:December 2022
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Tidskriftsartikel (refereegranskat)abstract
- Background Cardiac surgery produces dorso-basal atelectasis and ventilation/perfusion mismatch, associated with infection and prolonged intensive care. A postoperative lung volume recruitment manoeuvre to decrease the degree of atelectasis is routine. In patients with severe respiratory failure, prone positioning and recruitment manoeuvres may increase survival, oxygenation, or both. We compared the effects of lung recruitment in prone vs supine positions on dorsal inspiratory and end-expiratory lung aeration. Methods In a prospective RCT, 30 post-cardiac surgery patients were randomly allocated to recruitment manoeuvres in the prone (n=15) or supine position (n=15). The primary endpoints were late dorsal inspiratory volume (arbitrary units [a.u.]) and left/right dorsal end-expiratory lung volume change (a.u.), prone vs supine after extubation, measured using electrical impedance tomography. Secondary outcomes included left/right dorsal inspiratory volumes (a.u.) and left/right dorsal end-expiratory lung volume change (a.u.) after prone recruitment and extubation. Results The last part of dorsal end-inspiratory volume after extubation was higher after prone (49.1 a.u.; 95% confidence interval [CI], 37.4–60.6) vs supine recruitment (24.2 a.u.; 95% CI, 18.4–29.6; P=0.024). Improvement in left dorsal end-expiratory lung volume after extubation was higher after prone (382 a.u.; 95% CI, 261–502) vs supine recruitment (–71 a.u., 95% CI, –140 to –2; n=15; P<0.001). After prone recruitment, left vs right predominant end-expiratory dorsal lung volume change disappeared after extubation. However, both left and right end-expiratory volumes were higher in the prone group, after extubation. Conclusions Recruitment in the prone position improves dorsal inspiratory and end-expiratory lung volumes after cardiac surgery.
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| 4. |
- Martinsson, Andreas, et al.
(författare)
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Lung recruitment in the prone position after cardiac surgery: a randomised controlled study.
- 2021
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Ingår i: British journal of anaesthesia. - : Elsevier BV. - 1471-6771 .- 0007-0912. ; 126:5, s. 1067-1074
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Tidskriftsartikel (refereegranskat)abstract
- Atelectasis after cardiac surgery is common and promotes ventilation/perfusion mismatch, infection, and delayed discharge from critical care. Recruitment manoeuvres are often performed to reduce atelectasis. In severe respiratory failure, recruitment manoeuvres in the prone position may increase oxygenation, survival, or both. We compared the effects of recruitment manoeuvres in the prone vs supine position on lung aeration and oxygenation in cardiac surgical patients.Subjects were randomised to recruitment manoeuvres (40 cm H2O peak inspiratory pressure and 20 cm H2O PEEP for 30 s) in either the prone or supine position after uncomplicated cardiac surgery. The co-primary endpoints were lung aeration (end-expiratory lung volume measured by electrical impedance tomography (arbitrary units [a.u.]) and lung oxygenation (ratio of arterial oxygen partial pressure to fractional inspired oxygen [Pao2/FiO2 ratio]). Secondary outcomes included postoperative oxygen requirement and adverse events.Thirty subjects (27% female; age, 48-81 yr) were recruited. Dorsal lung tidal volume was higher after prone recruitment manoeuvres (363 a.u.; 95% confidence intervals [CI], 283-443; n=15) after extubation, compared with supine recruitment manoeuvres (212 a.u.; 95% CI, 170-254; n=15; P<0.001). Prone recruitment manoeuvres increased dorsal end-expiratory lung volume by 724 a.u. (95% CI, 456-992) after extubation, compared with 163 a.u. decrease (95% CI, 73-252) after supine recruitment manoeuvres (P<0.001). The Pao2/FiO2 ratio after extubation was higher after prone recruitment manoeuvres (46.6; 95% CI, 40.7-53.0) compared with supine recruitment manoeuvres (39.3; 95% CI, 34.8-43.8; P=0.04). Oxygen therapy after extubation was shorter after prone (33 h [13]) vs supine recruitment manoeuvres (52 h [22]; P=0.01). No adverse events occurred.Recruitment manoeuvres in the prone position after cardiac surgery improve lung aeration and oxygenation.NCT03009331.
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| 5. |
- Nygren, Andreas, 1967, et al.
(författare)
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Autoregulation of human jejunal mucosal perfusion during cardiopulmonary bypass.
- 2006
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Ingår i: Anesthesia and analgesia. - 1526-7598. ; 102:6, s. 1617-22
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Tidskriftsartikel (refereegranskat)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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| 7. |
- Nygren, Andreas, 1967, et al.
(författare)
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Norepinephrine and intestinal mucosal perfusion in vasodilatory shock after cardiac surgery
- 2007
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Ingår i: Shock. - : Ovid Technologies (Wolters Kluwer Health). - 1073-2322. ; 28:5, s. 536-543
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Tidskriftsartikel (refereegranskat)abstract
- Patients with norepinephrine-dependent vasodilatory shock after cardiac surgery (n = 10) were compared with uncomplicated postcardiac surgery patients (n = 10) with respect to jejunal mucosal perfusion, gastric-arterial PCO2 gradient, and splanchnic oxygen demand/supply relationship. Furthermore, the effects of norepinephrine-induced variations in MAP on these variables were evaluated in vasodilatory shock. Norepinephrine infusion rate was randomly and sequentially titrated to target MAPs of 60, 75, and 90 mmHg (0.25 +/- 0.24, 0.37 +/- 0.21, and 0.55 +/- 0.39 mug/kg per minute, respectively). Data on jejunal mucosal perfusion, jejunal mucosal hematocrit, and red blood cell (RBC) velocity (laser Doppler flowmetry) as well as gastric-arterial PCO2 gradient (gastric tonometry) and splanchnic oxygen and lactate extraction (hepatic vein catheter) were obtained. Splanchnic oxygen extraction was 71 +/- 16% in the vasodilatory shock group and 41 +/- 9% in the control group (P < 0.001), whereas splanchnic lactate extraction did not differ between the two groups. Jejunal mucosal perfusion (61%; P < 0.001), RBC velocity (35%; P < 0.01), and arterial-gastric mucosal PCO2 gradient (150%; P < 0.001) were higher in the vasodilatory shock group compared with those of the control group. Jejunal mucosal perfusion, jejunal mucosal hematocrit, RBC velocity, arterial-gastric mucosal PCO2 gradient, splanchnic oxygen extraction, and splanchnic lactate extraction were not affected by increasing infusion rates of norepinephrine. In patients with norepinephrine-dependent vasodilatory shock after cardiac surgery, intestinal mucosal perfusion was higher, whereas splanchnic and gastric oxygen demand/supply relationships were impaired compared with postoperative controls, suggesting that intestinal mucosal perfusion is prioritized in vasodilatory shock. Increasing MAP from 60 to 90 mmHg with norepinephrine in clinical vasodilatory shock does not affect intestinal mucosal perfusion and gastric or global splanchnic oxygen demand/supply relationships.
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| 8. |
- Nygren, Andreas, 1967, et al.
(författare)
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Norepinephrine causes a pressure-dependent plasma volume decrease in clinical vasodilatory shock.
- 2010
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Ingår i: Acta anaesthesiologica Scandinavica. - : Wiley. - 1399-6576 .- 0001-5172. ; 54:7, s. 814-20
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Recent experimental studies have shown that a norepinephrine-induced increase in blood pressure induces a loss of plasma volume, particularly under increased microvascular permeability. We studied the effects of norepinephrine-induced variations in the mean arterial pressure (MAP) on plasma volume changes and systemic haemodynamics in patients with vasodilatory shock. METHODS: Twenty-one mechanically ventilated patients who required norepinephrine to maintain MAP > or =70 mmHg because of septic/postcardiotomy vasodilatory shock were included. The norepinephrine dose was randomly titrated to target MAPs of 60, 75 and 90 mmHg. At each target MAP, data on systemic haemodynamics, haematocrit, arterial and mixed venous oxygen content and urine flow urine were measured. Changes in the plasma volume were calculated as 100 x (Hct(pre)/Hct(post)-1)/ (1-Hct(pre)), where Hct(pre) and Hct(post) are haematocrits before and after intervention. RESULTS: Norepinephrine doses to obtain target MAPs of 60, 75 and 90 mmHg were 0.20+/-0.18, 0.29+/-0.18 and 0.42+/-0.31 microg/kg/min, respectively. From 60 to 90 mmHg, increases in the cardiac index (15%), systemic oxygen delivery index (25%), central venous pressure (CVP) (20%) and pulmonary artery occlusion pressure (33%) were seen, while the intrapulmonary shunt fraction was unaffected by norepinehrine. Plasma volume decreased by 6.5% and 9.4% (P<0.0001) when blood pressure was increased from 60 to 75 and 90 mmHg, respectively. MAP (P<0.02) independently predicted the decrease in plasma volume with norepinephrine but not CVP (P=0.19), cardiac index (P=0.73), norepinephrine dose (P=0.58) or urine flow (P=0.64). CONCLUSIONS: Norepinephrine causes a pressure-dependent decrease in the plasma volume in patients with vasodilatory shock most likely caused by transcapillary fluid extravasation.
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| 9. |
- Nygren, Andreas, 1967, et al.
(författare)
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Vasopressin decreases intestinal mucosal perfusion: a clinical study on cardiac surgery patients in vasodilatory shock.
- 2009
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Ingår i: Acta anaesthesiologica Scandinavica. - : Wiley. - 1399-6576 .- 0001-5172. ; 53:5, s. 581-8
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Low to moderate doses of vasopressin have been used in the treatment of cathecholamine-dependent vasodilatory shock in sepsis or after cardiac surgery. We evaluated the effects of vasopressin on jejunal mucosal perfusion, gastric-arterial pCO2 gradient and the global splanchnic oxygen demand/supply relationship in patients with vasodilatory shock after cardiac surgery. METHODS: Eight mechanically ventilated patients, dependent on norepinephrine to maintain mean arterial pressure (MAP) > or = 60 mmHg because of septic/post-cardiotomy vasodilatory shock and multiple organ failure after cardiac surgery, were included. Vasopressin was sequentially infused at 1.2, 2.4 and 4.8 U/h for 30-min periods. Norepinephrine was simultaneously decreased to maintain MAP at 75 mmHg. At each infusion rate of vasopressin, data on systemic hemodynamics, jejunal mucosal perfusion, jejunal mucosal hematocrit and red blood cell velocity (laser Doppler flowmetry) as well as gastric-arterial pCO2 gradient (gastric tonometry) and splanchnic oxygen and lactate extraction (hepatic vein catheter) were obtained. RESULTS: The cardiac index, stroke volume index and systemic oxygen delivery decreased and systemic vascular resistance and systemic oxygen extraction increased significantly, while the heart rate or global oxygen consumption did not change with increasing vasopressin dose. Jejunal mucosal perfusion decreased and the arterial-gastric-mucosal pCO2 gradient increased, while splanchnic oxygen or lactate extraction or mixed venous-hepatic venous oxygen saturation gradient were not affected by increasing infusion rates of vasopressin. CONCLUSIONS: Infusion of low to moderate doses of vasopressin in patients with norepinephrine-dependent vasodilatory shock after cardiac surgery induces an intestinal and gastric mucosal vasoconstriction.
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| 10. |
- Nygren, Andreas, 1967, et al.
(författare)
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Vasopressors and intestinal mucosal perfusion after cardiac surgery: Norepinephrine vs. phenylephrine.
- 2006
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Ingår i: Critical care medicine. - 0090-3493. ; 34:3, s. 722-9
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: To evaluate the potential differential effects of norepinephrine, an alpha1-, beta1-, and beta2-receptor agonist, to the alpha1-agonist phenylephrine on jejunal mucosal perfusion, gastric-arterial PCO2 gradient, and the global splanchnic oxygen demand-supply relationship after cardiac surgery. DESIGN: A randomized, prospective, interventional crossover study. SETTING: A university cardiothoracic intensive care unit. PATIENTS: Ten patients were studied during propofol sedation and mechanical ventilation after uncomplicated coronary artery bypass surgery. INTERVENTIONS: Each patient received randomly and sequentially norepinephrine (0.052+/-0.009 microg/kg/min) and phenylephrine (0.50+/-0.22 microg/kg/min) to increase mean arterial blood pressure by 30%. MEASUREMENTS AND MAIN RESULTS: Data on jejunal mucosal perfusion, jejunal mucosal hematocrit, and red blood cell velocity (laser Doppler flowmetry) as well as gastric-arterial Pco2 gradient (tonometry) and splanchnic oxygen extraction were obtained before (control) and during a 30-min drug infusion period after the target mean arterial blood pressure was reached. The procedure was sequentially repeated for the second vasopressor. Both drugs induced a 40-46% increase in systemic vascular resistance with no change in cardiac index. Neither jejunal mucosal perfusion, jejunal mucosal hematocrit, red blood cell velocity, nor gastric-arterial Pco2 gradient was affected by any of the vasopressors. Splanchnic oxygen extraction increased from 38.2% to 43.1% (p<.001) with norepinephrine and from 39.3% to 47.5% (p<.001) with phenylephrine. This increase was significantly more pronounced with phenylephrine compared with norepinephrine (p<.05). Mixed venous-hepatic vein oxygen saturation gradient increased with both drugs (p<.01), and the increase was more pronounced with phenylephrine (p<.05). Splanchnic lactate extraction was not significantly affected by any of the vasopressors. CONCLUSIONS: Phenylephrine induced a more pronounced global alpha1-mediated splanchnic vasoconstriction compared with norepinephrine. Neither of the vasoconstrictors impaired perfusion of the gastrointestinal mucosa in postcardiac surgery patients. The lack of norepinephrine-induced, alpha1-mediated impairment of gastrointestinal perfusion is not explained by a beta2-mediated counteractive vasodilation but instead by possible mucosal autoregulatory escape.
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