Pulmonary injury after cardiopulmonary bypass.
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Cardiopulmonary Bypass↗
Biomedical subjects
V R Conti
Publications and source records attributed to V R Conti.
Vasodilation and cardiopulmonary bypass: the role of bradykinin and the pulmonary vascular endothelium.
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Bradykinin↗
Primary cardiac malignancy masquerading as mitral valve stenosis.
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Echocardiography↗
Acute normovolemic red cell exchange for cardiopulmonary bypass in sickle cell disease.
A patient with sickle cell disease (hematocrit, 28.5%; hemoglobin S fraction, 79%), required mitral valve repair. Partial red cell removal and blood component sequestration with an autotransfusion device before cardiopulmonary bypass initially decreased the sickle red cell mass. This was followed by an acute one-volume whole blood exchange transfusion performed upon the initiation of cardiopulmonary bypass, resulting in a further reduction. Both techniques yielded fresh autologous plasma for use; sequestration yielded a platelet-pheresis product. Adequate postbypass hemostasis was demonstrated.
Adolescent↗
Air embolism with intraaortic balloon counterpulsation during cardiopulmonary bypass.
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Cardiopulmonary Bypass↗
Relation of unstable angina and myocardial infarction to progression of coronary narrowing in patients undergoing coronary artery bypass grafting (utilizing an internal mammary artery).
We examined the relation of an ischemic syndrome with the progression of coronary disease early (<3 years) after multiple bypass grafting utilizing an internal mammary artery and saphenous vein grafts. Data indicate that an ischemic syndrome is associated with progression of native coronary disease distal to the graft or total occlusion of the saphenous vein graft in most cases.
Aged↗
Automatic internal cardioverter-defibrillator patch erosion into the upper airway presenting as a cavitary lesion.
Erosion of an automatic internal cardioverter-defibrillator (AICD) patch into the lingular bronchus occurred 4 years after implantation; the erosion presented as a cavitary mass associated with hemoptysis and weight loss. On bronchoscopy to evaluate for suspected carcinoma, a cavity was entered through a bronchial defect and the AICD patch clearly identified. The complication was successfully treated with patch removal and fistula closure.
Aged↗
Simple technique of left heart bypass.
Left heart bypass is typically established by left atrial appendage cannulation. We report a technique using inferior pulmonary vein cannulation, which is technically simpler. We have used this technique in 20 cases with reliable venous inflow.
Catheterization, Central Venous↗
Adverse effects of postoperative infusion of shed mediastinal blood.
BACKGROUND: Postoperative infusion of shed mediastinal blood has been used in an effort to decrease blood usage after cardiac operations. Recent experience has suggested that this practice may actually lead to a delayed increase in bleeding. METHODS: In a prospective, randomized study, 40 patients undergoing coronary artery bypass grafting with shed mediastinal blood collected in a cardiotomy reservoir were divided into two equal groups and studied during their first 4 hours in the intensive care unit. Shed mediastinal blood was directly infused in group I (n = 20), whereas in group II (n = 20), it was not. In group II, if a sufficient volume of red cells was present to allow processing (n = 5), washed red cells were infused. Variables studied before and after infusion were the amount of blood lost and infused, homologous blood transfused, complete blood count and differential, serum fibrinogen, fibrin split products, D-dimers, clotting factors, prothrombin time, activated partial thromboplastin time, thromboelastograms, plasma-free hemoglobin, complement factors C3 and C4, creatine kinase and its MB isoenzyme, and body temperature. RESULTS: After infusion of shed mediastinal blood, elevated levels of fibrin split products and D-dimers were found in significantly more patients in group I. The thromboelastogram index was normal in 76% of patients in group II but in only 12.5% in group I. Group I also had an increase in band neutrophils, a greater number of febrile patients, higher serum levels of creatine kinase, its MB isoenzyme, and plasma-free hemoglobin, and greater blood loss during hours 3, 4, and 5 in the intensive care unit. The volume of red cells in shed mediastinal blood (hematocrit, 9% to 10%) was small, resulting in clinically insignificant autotransfusion when infused directly, and insufficient for cell processing in most patients. CONCLUSIONS: These data support those in previous studies that direct infusion of shed mediastinal blood does not save substantial amounts of autologous red cells and can cause a delayed coagulopathy and other adverse effects that may be harmful to patients postoperatively.
Adult↗
Transient ischemia cannot precondition the rabbit heart against postischemic contractile dysfunction.
BACKGROUND: The rat heart is preconditioned against postischemic contractile dysfunction by a brief period of transient ischemia before a prolonged ischemic period. However, the rabbit heart does not receive such cardio-protection from pretreatment with a single transient ischemia periods. We hypothesized that in the rabbit heart, a multiple cycle of transient ischemia is required to reach a threshold necessary to precondition against postischemic contractile dysfunction. METHODS: To test this hypothesis, we subjected isolated, perfused rabbit hearts to either one 5-minute transient ischemic period or three 5-minute transient ischemic periods followed by a 40-minute period of warm ischemia and 30 minutes of reperfusion. Control hearts (no pretreatment with transient ischemia) were examined simultaneously. Left ventricular developed pressure was measured with an intraventricular balloon. RESULTS: Postischemic recoveries (expressed as percent of preischemic values) of left ventricular developed pressure for the group with one ischemic period and the group with three ischemic periods were 43% +/- 5% (n = 5) and 38% +/- 6% (n = 6), respectively. These values were not significantly different from control values. CONCLUSIONS: Neither one nor three periods of transient ischemia protect the isolated, perfused rabbit heart from postischemic contractile dysfunction. Therefore, the rabbit heart may not have the capacity to be ischemically preconditioned against postischemic contractile dysfunction.
Animals↗
Percutaneous tamponade of inadvertent transthoracic catheterization of the aorta.
During routine placement of a subclavian central venous catheter for cancer chemotherapy, a sheath was inadvertently placed into the aortic arch, through the left lung. We describe a technique for transthoracic compression of the aortic injury using the sheath in conjunction with an occlusion balloon catheter.
Aorta, Thoracic↗
Preconditioning with dobutamine in the isolated rat heart.
The ability of dobutamine to precondition the isolated rat heart against postischemic contractile dysfunction was assessed. Hearts were perfused with varying concentrations of dobutamine for 5 min followed by a 5 min "washout" period and 30 min of global ischemia. The hearts were reperfused for 30 min to assess postischemic function. Dobutamine improved postischemic developed pressure, +dp/dt, heart rate x developed pressure, end diastolic pressure, and coronary flow in a concentration-dependent manner. The concentration of dobutamine showing the maximum protective effect was 10(-6)M. Propranolol administered with dobutamine significantly attenuated the protective effect. The results indicate that transient treatment with dobutamine can precondition the rat heart against ischemia/reperfusion injury. The mechanism of protection appears to involve beta-adrenergic stimulation.
Animals↗
First clinical use of a heparin removal device: an alternative to protamine.
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Adult↗
Air embolism during cardiopulmonary bypass.
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Cardiopulmonary Bypass↗
Transient beta adrenergic stimulation can precondition the rat heart against postischaemic contractile dysfunction.
OBJECTIVE: The aim was to assess the abilities of exogenous noradrenaline, isoprenaline, and phenylephrine to precondition the isolated rat heart against ischaemic and reperfusion injury. METHODS: The isovolumetric Langendorff rat heart model was used to determine postischaemic recovery of left ventricular function. The hearts were subjected to 30 min of normothermic global ischaemia followed by 30 min reperfusion. Treated hearts were perfused with noradrenaline (10(-7) M), isoprenaline (10(-8) M), or phenylephrine (10(-6) M, 10(-5) M, and 10(-4) M) for 5 min followed by 5 min washout before the 30 min ischaemic period. RESULTS: Control hearts recovered 47.6(SEM 4.3)% of baseline heart rate x developed pressure after 30 min reperfusion, whereas noradrenaline and isoprenaline treated hearts recovered 75.1(4.6) and 76.4(4.6)%, respectively (p < 0.001 v control). Left ventricular end diastolic pressures at the end of reperfusion were 48.8(4.0), 20.0(2.4), and 21.6(2.7)mm Hg for control, noradrenaline treated (p < 0.001 v control), and isoprenaline treated (p < 0.001 v control) hearts respectively. beta Blockade with propranolol during noradrenaline treatment blocked the protective effects. No concentration of phenylephrine used was able to enhance postischaemic heart rate x developed pressure significantly, or result in improved (lower) postischaemic left ventricular end diastolic pressure. During treatment with noradrenaline and phenylephrine (10(-5) M), lactate release was 13.0(1.0) and 11.0(0.9) mumol.5 min-1, respectively (p = NS); these values were significantly (p < 0.001) greater than baseline value of 3.7(0.5) mumol.5 min-1. Immediately before the 30 min ischaemic period, control and phenylephrine treated groups had glycogen levels of 132(14) and 128(5) nmol.mg-1 protein, respectively (p = NS), whereas the glycogen content of the noradrenaline treated group was only 96(5) nmol.mg-1 protein (p < 0.05 v control and phenylephrine treated). CONCLUSIONS: Transient beta adrenergic but not alpha 1 adrenergic stimulation can precondition the isolated perfused rat heart. The mechanism of protection may, at least in part, be due to transient demand ischaemia. Partial depletion of glycogen following treatment may play a role in the observed protective effects.
Adrenergic beta-Agonists↗
Attenuation of postischaemic dysfunction by ischaemic preconditioning is not mediated by adenosine in the isolated rat heart.
OBJECTIVE: The aim was to test the hypothesis that adenosine mediates the cardioprotective effects of ischaemic preconditioning in the isolated rat heart. METHODS: Transient exposure of the hearts to adenosine and the A1 selective agonist, PIA, were tested for the ability to mimic the cardioprotective effects of ischaemic preconditioning in hearts that underwent 40 min normothermic ischaemic followed by 30 min reperfusion. Treated hearts were perfused with 10 or 50 microM adenosine or 10(-7) M R-phenylisopropyladenosine (PIA) for 5 min followed by a 5 min washout period. Preconditioned hearts underwent 5 min of ischaemia and 5 min of reflow prior to the 40 min ischaemic period. The ability of the adenosine receptor antagonist, BW A1433U, to inhibit the cardioprotective effects of ischaemic preconditioning was also tested. The effects of these treatments on metabolite levels and postischaemic haemodynamic function were assessed. RESULTS: Adenosine (50 microM), but not PIA, resulted in enhanced accumulation of lactate after 40 min ischaemia: 122(SEM 8) v 96(5) nmol.mg-1 protein in control hearts (p < 0.002). Adenosine and PIA treatments did not significantly affect myocardial acidosis during ischaemia. Postischaemic contractile function (as assessed by percent recovery of the heart rate x developed pressure) was lower in 50 microM, but not 10 microM, adenosine treated hearts [8.8(2.2)] and PIA treated hearts [11.9(2.5)] than in control hearts [20.4(3.6)] (p < 0.01). Ischaemic preconditioning (1) lowered glycogen levels prior to the 40 min ischaemic period [57(6) v 110(18) nmol glucosyl units.mg-1 protein; p < 0.01]; (2) lowered lactate levels at the end of the 40 min ischaemic period [61(4) v 104(5) nmol.mg-1 protein]; (3) preserved myocardial pH during ischaemia [6.69(0.07) v 6.40(0.07); p < 0.01]; and (4) enhanced recovery of postischaemic contractile function [42.3(4.4)% v 19.7(6.0)%; p < 0.02]. BW A1433U did not prevent these effects of ischaemic preconditioning. CONCLUSIONS: The cardioprotective effects of ischaemic preconditioning are not mediated by adenosine released during the preconditioning period in the isolated rat heart. Also, transient treatment of the heart with A1 adenosine receptor agonists can exacerbate postischaemic contractile dysfunction.
Adenosine↗
Ischemic preconditioning attenuates acidosis and postischemic dysfunction in isolated rat heart.
The hypothesis that brief ischemia (preconditioning) protects the isolated heart from prolonged global ischemia was tested. Isovolumic rat hearts were preconditioned with either 5 min of ischemia followed by 5 min of perfusion (P1) or two 5-min episodes of ischemia separated by 5 min of perfusion (P2). Control hearts received no preconditioning. All hearts received 40 min of sustained ischemia and 30 min of reperfusion. Preconditioning (P1 or P2) significantly (P less than 0.0005) improved recovery of the rate-pressure product; percentage recoveries were 17.8 +/- 3.2 (n = 14), 59.9 +/- 5.5 (n = 6), and 46.4 +/- 4.7 (n = 8) for control, P1, and P2, respectively. Improved functional recovery of preconditioned hearts was associated with reduced end-diastolic pressure and improved myocardial perfusion. During the 40-min ischemic period, myocardial pH decreased from approximately 7.4 to 6.3 +/- 0.1 (n = 7) in the control hearts and to 6.7 +/- 0.1 (n = 7) in the preconditioned hearts (P less than 0.01). Also during the 40-min ischemic period, myocardial lactate (expressed as nmol/mg protein) increased to 146 +/- 11 (n = 7) and 101 +/- 12 (n = 8) in control and preconditioned hearts, respectively (P less than 0.02). The results demonstrate that a brief episode of ischemia can protect the isolated rat heart from a prolonged period of ischemia. This protection is associated with decreased tissue acidosis and anaerobic glycolysis during the sustained ischemic period.
Acidosis↗
Postischemic recovery of mitochondrial adenine nucleotides in the heart.
BACKGROUND: Adenine nucleotides (AdNs) are lost from the mitochondrial fraction of the heart cell during ischemia. It is unknown whether this pool of AdNs can be replenished after reperfusion. The purpose of this study was to evaluate the postischemic recovery of the mitochondrial AdN pool. METHODS AND RESULTS: The left anterior descending coronary artery (LAD) of the canine heart was occluded for 30 minutes followed by either no reflow, 30-minute reflow, 1-day reflow, or 7-day reflow. Systolic shortening in the LAD-supplied region was absent during occlusion but recovered to approximately 30% of preocclusion values during early reperfusion. Mitochondrial and tissue AdNs (ATP, ADP, and AMP) were determined in the LAD-supplied and left circumflex-supplied (control) regions of the heart. The AdN content (expressed as percent of control values) of mitochondria from the LAD region was 55 +/- 10% (p less than 0.002), 64 +/- 7% (p less than 0.001), 81 +/- 6% (p less than 0.03), and 94 +/- 8% for the no-reflow, 30-minute-reflow, 1-day-reflow, and 7-day-reflow groups, respectively. The AdN content (expressed as percent of control values) of tissue samples from the LAD region was 52 +/- 9% (p less than 0.002), 48 +/- 12% (p less than 0.02), 68 +/- 5% (p less than 0.002), and 70 +/- 9% for the no-reflow, 30-minute-reflow, 1-day-reflow, and 7-day-reflow groups, respectively. There was a good correlation between mitochondrial and tissue AdN (r = 0.95). Using initial exchange rates, adenine nucleotide translocase activities of mitochondria from the LAD and control regions were not significantly different. State 3 respiration of LAD mitochondria was depressed (approximately 25%, p less than 0.05) only in the no-reflow group. Acceptor control ratios of the LAD mitochondria were not significantly different from control values in any group. CONCLUSIONS: After 30 minutes of regional ischemia, postischemic restoration of the mitochondrial AdN pool occurs between 1 and 7 days; this restoration is preceded by recovery of respiratory and adenine nucleotide translocase functions. Although the abnormally low levels of AdN persist in the mitochondrial compartment during the early reperfusion period, postischemic contractile dysfunction cannot be explained by depressed mitochondrial respiratory activity.
Adenine Nucleotides↗