ABSTRACT
Despite a rise in blood pressure, cerebral oxygenation decreases following phenylephrine administration, and we hypothesised that phenylephrine reduces cerebral oxygenation by activating cerebral α1 receptors. We studied patients on cardiopulmonary bypass during constant flow. Phenylephrine raised mean arterial pressure (α1 -mediated) from mean (SD) 69 (8) mmHg to 79 (8) mmHg; p = 0.001, and vasopressin raised mean arterial pressure (V1 mediated) from 69 (8) mmHg to 83 (6) mmHg; p = 0.001. Both drugs elicited a comparable decrease in cerebral oxygenation from 61 (7)% to 60 (7)%; p = 0.023 and 61 (8)% to 59 (8)%; p = 0.022, respectively. This implies that after phenylephrine or vasopressin administration, cerebral oxygenation declines as a result of cerebral vasoconstriction, due to either both cerebral α1 and V1 receptors being equipotentially activated or to an intrinsic myogenic mechanism of cerebral vasculature in reaction to blood pressure elevation.
Subject(s)
Cardiopulmonary Bypass , Cerebrovascular Circulation/physiology , Oxygen Consumption/physiology , Vascular Resistance/physiology , Aged , Arterial Pressure/drug effects , Carbon Dioxide/blood , Cardiac Surgical Procedures , Cerebrovascular Circulation/drug effects , Female , Humans , Male , Middle Aged , Oxygen/blood , Oxygen Consumption/drug effects , Partial Pressure , Phenylephrine/pharmacology , Proof of Concept Study , Vascular Resistance/drug effects , Vasoconstriction/drug effects , Vasoconstriction/physiology , Vasoconstrictor Agents/pharmacology , Vasopressins/pharmacologyABSTRACT
Right ventricular function (RVF) is often selectively declined after coronary artery bypass graft surgery. In adult patients with congenital heart disease (CHD) the incidence and persistence of declined RVF after cardiac surgery is unknown. The current study aimed to describe RVF after cardiac surgery in these patients. Adult CHD patients operated between January 2008 and December 2009 in the Academic Medical Centre in Amsterdam were studied. Clinical characteristics, laboratory tests, surgical data and intensive care unit outcome were obtained from medical records. RVF was measured by trans-thoracic echocardiography (TTE) and expressed by tricuspid annular plane systolic excursion (TAPSE), tissue Doppler imaging (RV S') and myocardial performance index (MPI) pre-operatively and direct, at intermediate and late follow up. Of a total of 185 operated, 86 patients (mean age 39 ± 13 years, 54% male) had echo data available. There was a significant fall in RVF after cardiac surgery. TAPSE and RV S' were significantly higher and MPI was significantly lower pre-operatively compared to direct post-operative values (TAPSE 22 ± 5 versus 13 ± 3 mm (P < 0.01), RV S' 11 ± 4 versus 8 ± 2 cm/s (P < 0.01) and MPI 0.36 ± 0.14 vs 0.62 ± 0.25; P < 0.01). There were no significant differences in left ventricular function pre-operatively compared to post-operative values. Right-sided surgery was performed in 33, left-sided surgery in 37 and both sided surgery in 16 patients. Decline in RVF was equal for those groups. Patients with severe decline in RVF, were patients who underwent tricuspid valve surgery. Decline in RVF was associated with post-operative myocardial creatine kinase level and maximal troponin T level. There was no association between decline in RVF and clinical outcome on the intensive care unit. 18 months post-operatively, most RVF parameters had recovered to pre-operative values, but TAPSE which remained still lower (P < 0.01). CHD patients have a decline in RVF directly after cardiac surgery, regardless the side of surgery. Although a gradual improvement was observed, complete recovery was not seen 18 months post-operatively.
Subject(s)
Cardiac Surgical Procedures/adverse effects , Heart Defects, Congenital/surgery , Ventricular Dysfunction, Right/etiology , Ventricular Function, Right , Academic Medical Centers , Adult , Biomarkers/blood , Chi-Square Distribution , Creatine Kinase/blood , Echocardiography, Doppler , Female , Humans , Linear Models , Male , Netherlands , Recovery of Function , Risk Assessment , Risk Factors , Time Factors , Treatment Outcome , Troponin T/blood , Ventricular Dysfunction, Right/blood , Ventricular Dysfunction, Right/diagnostic imaging , Ventricular Dysfunction, Right/physiopathology , Young AdultABSTRACT
Patients with an untreated myocardial infarction may present with serious late complications. 3 patients are described. A 63-year-old woman became progressively more short of breath 4 days after an acute episode of chest pain accompanied by nausea and sweating. It proved to be a cardiogenic shock following a rupture of a papillary muscle. A man aged 65 collapsed 5 days after an episode of back pain and nausea. This was a cardiac tamponade due to rupture of the left ventricle. A woman aged 74 had transient aphasia and during investigations for this was seen to have anomalies on ECG. She had cerebral emboli and a cardiac aneurysm with associated thrombus. All 3 patients recovered following mitral-valve replacement, repair of the rupture and medicinal treatment for the clot, respectively. Around one-third of patients who have a myocardial infarction do not have chest pain but experience shortness of breath, autonomic nervous symptoms (sweating, nausea, vomiting), extreme and inexplicable tiredness and fainting. These atypical symptoms should suggest myocardial infarction. In order to avoid high morbidity and death from complications such as arrhythmias, heart failure, rupture and aneurysm formation it is important that a patient who has had a myocardial infarction should be treated as soon as possible, preferably by reperfusion therapy.
