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Biomedical subjects

P Mair

Publications and source records attributed to P Mair.

At least 37 records · Page 2Linked to original sources
PubMed1998

Myocardial damage after minimally invasive coronary artery bypass grafting on the beating heart.

BACKGROUND: In conventional coronary artery bypass grafting, the rate of perioperative myocardial infarction is reported in the 2% to 6% range; however, significantly higher rates are observed if sensitive myocardial marker proteins are used to detect perioperative myocardial damage. For minimally invasive direct coronary artery bypass grafting, few data are available concerning myocardial marker protein release. METHODS: Fifteen consecutive patients (11 male, 4 female; mean age, 59.6 +/- 8.5 years) received minimally invasive direct coronary artery bypass grafting procedures via minithoracotomy on the beating heart. Electrocardiography and transesophageal and transthoracic echocardiography as well as determination of creatine kinase-MB mass concentration and cardiac troponin I level were used for ischemic monitoring. RESULTS: One patient had a perioperative myocardial infarction according to standard criteria and died despite mechanical circulatory support. Determination of cardiac troponin I level showed small but definitive ischemic damage in 4 of 9 patients (44%) who presented transient ischemic signs intraoperatively or postoperatively. In 2 of these 4 patients pathologic findings could be detected on angiographic restudies. CONCLUSIONS: Subclinical myocardial injury is a common event in minimally invasive coronary artery bypass grafting on the beating heart. Cardiac troponin I could serve as an adequate diagnostic tool for diagnosis of perioperative myocardial infarction in minimally invasive direct coronary artery bypass grafting.

Aged↗
PubMed1998

Forward blood flow during cardiopulmonary resuscitation in patients with severe accidental hypothermia. An echocardiographic study.

BACKGROUND: The mechanism responsible for the forward blood flow associated with external chest compression is still controversial. Evidence for both blood flow caused by direct cardiac compression and blood flow generated by a general increase in intrathoracic pressure has been found in experimental as well as clinical studies. No data are available concerning the mechanism causing forward blood flow in hypothermic patients undergoing cardiopulmonary resuscitation. Therefore, echocardiographic findings during external chest compression in seven hypothermic arrest victims are reported. METHODS: All transesophageal echocardiographic studies performed at the Anaesthesia department between 1994 and 1997 were reviewed and seven hypothermic patients with transesophageal echocardiography performed during cardiopulmonary resuscitation were identified. RESULTS: An open mitral valve or a circumferential reduction in aortic diameter during the compression phase was found in four of seven patients, indicating that primarily an increase in intrathoracic pressure (thoracic pump mechanism) generated forward blood flow. In three patients, mitral valve closure during external chest compression indicated that direct cardiac compression (cardiac pump mechanism) contributed to forward blood flow. Two patients studied during active compression-decompression cardiopulmonary resuscitation demonstrated enhanced right ventricular filling and aortic valve opening during active decompression of the thorax. CONCLUSIONS: In contrast to normothermic arrest victims, an open mitral valve during external chest compression is a common finding during hypothermia, indicating that thoracic pump mechanism is important for forward blood flow during cardiopulmonary resuscitation in hypothermic arrest victims. Aortic valve opening in two hypothermic arrest victims suggests forward blood flow also during active decompression of the thorax with the Cardiopump.

Accidents↗
PubMed1998

Different intracellular compartmentations of cardiac troponins and myosin heavy chains: a causal connection to their different early release after myocardial damage.

We investigated the net myocardial release of creatine kinase isoenzyme MB (CKMB), myoglobin, cardiac troponin T (cTnT), cardiac troponin I (cTnI), and cardiac beta-type myosin heavy chain (beta-MHC) into the coronary circulation after cardioplegic cardiac arrest in humans. Cardiac markers were measured in paired arterial, central venous, and coronary sinus blood in 19 patients undergoing elective coronary artery bypass grafting (CABG) before aortic cross-clamping and 1, 5, 10, and 20 min after aortic declamping. cTnT and cTnI were released into the coronary sinus in parallel to each other and almost simultaneously to myoglobin and CKMB within 20 min of reperfusion. In contrast, no beta-MHC was released in the same patients during the study period. The average soluble cTnT and cTnI pools in right atrial appendages of 11 patients with right atrial and right ventricular pressures within reference values were comparable and were approximately 8% of total myocardial troponin content. The soluble beta-MHC pool was <0.1% in all patients. Our results demonstrate the impact of the different intracellular compartmention of regulatory and contractile proteins on their early release from damaged myocardium.

Adult↗
PubMed1997

Augmented release of brain natriuretic peptide during reperfusion of the human heart after cardioplegic cardiac arrest.

The aim of the study was to investigate the release of natriuretic peptides during myocardial ischaemia and reperfusion associated with cardioplegic cardiac arrest. Brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) concentrations were measured in paired arterial, central venous and coronary sinus blood samples in 19 patients undergoing elective coronary artery bypass grafting before aortic crossclamping and 1, 5, 10 and 20 min after aortic declamping. Peak myocardial BNP release after aortic declamping was significantly higher than baseline values before aortic crossclamping. Both peak and cumulative BNP release during reperfusion correlated significantly with the severity of ischaemia, as assessed by myocardial lactate production. In 3 patients with perioperative myocardial ischaemia, cumulative and peak myocardial BNP release after aortic unclamping was markedly higher than in the remaining 16 uneventful patients. Myocardial ANP release during reperfusion was not significantly different from baseline values before aortic crossclamping. In conclusion, our data demonstrate a significantly enhanced myocardial BNP release early during reperfusion of the human heart after global ischaemia associated with cardioplegic cardiac arrest.

Adult↗
PubMed1997

Inhalation injury treated with extracorporeal CO2 elimination.

A 38-year-old male was admitted to the intensive care unit with a full-thickness burn involving 30 per cent of his total body surface area (TBSA) and severe inhalation injury. Respiratory failure developed within 54 h and CO2 could not be eliminated, even by very invasive mechanical ventilation. Because of the patient's age and the minor extent of the burned TBSA, we started extracorporeal CO2 elimination (ECCO2-R) and continued ECCO2-R for 30 days, when the patient was weaned from ECC. The clinical course during ECCO2-R was complicated by major bleeding from a thoracotomy tube, from the site of tangential excision and by four septic episodes. Lung biopsy was performed twice on day 29 (during ECCO2-R) and day 58 (after ECCO2-R) after admission and revealed bronchiolitis obliterans without tendency to recovery. The patient died of sepsis with multiorgan failure on day 81 after trauma.

Adult↗
PubMed1996

Cardiac troponin I in the diagnosis of myocardial injury and infarction.

We used a cardiospecific enzymoimmunometric assay to measure cardiac troponin I (cTnI) in samples serially drawn from 78 patients with acute myocardial infarction (AMI), 7 patients with unstable angina (Braunwald class III), 22 multi-traumatized patients, and in 30 athletes after eccentric exercise, as well as in 101 non-traumatic chest pain patients on admission to the emergency department. cTnI assay crossreactivity with crude human skeletal muscle homogenates was < 0.1%. cTnI could not be detected in athletes or multi-traumatized patients except for 2 trauma patients with myocardial damage. Increased cTnI concentrations were found in 6 of 7 patients with unstable angina at rest and in all AMI patients. After AMI, cTnI increased about 3.5 h (median) after the onset of chest pain, reached peak values parallel to CKMB, and stayed increased for at least 4 days. Cardiac troponin T (cTnT) increased and mostly peaked parallel to cTnI. cTnT sensitivity on the 7th day after AMI was significantly higher than that of cTnI. In contrast to cTnI, cTnT mostly showed a second, usually smaller, peak about day 4 after AMI. During the first 4 h after the onset of chest pain and before thrombolytic therapy the sensitivities of myoglobin (0.43) and CKMB mass (0.56) were significantly higher than those of both troponins (cTnI, 0.29; cTnT, 0.25). Areas under receiver operator characteristic curves indicated only moderate diagnostic accuracies of bio-chemical markers for early AMI diagnosis in non-traumatic chest pain patients that cTnI is a highly sensitive and specific marker for myocardial damage which is suitable for early and late diagnosis.

Adult↗
PubMed1996

Percutaneous venoarterial extracorporeal membrane oxygenation for emergency mechanical circulatory support.

In this retrospective study we report our initial experience with percutaneous venoarterial extracorporeal membrane oxygenation in the emergency treatment of intractable cardiogenic shock or pulseless electrical activity. Between January 1994 and July 1995, percutaneous venoarterial extracorporeal membrane oxygenation was attempted in seven patients (pulseless electrical activity, five patients; cardiogenic shock, two patients). In two of the seven patients, efforts at arterial cannulation resulted in cannula perforation at the level of the iliac artery. In the remaining five patients, percutaneous venoarterial extracorporeal membrane oxygenation could be established and was maintained for 3-84 h. Major bleeding remained a common complication during extracorporeal membrane oxygenation despite the use of heparin-coated bypass circuits and was responsible for death during extracorporeal membrane oxygenation in one patient. The remaining four patients could be weaned from mechanical circulatory support within 24 h, two after surgical interventions (resection of right atrial tumor, heart transplantation), one after thrombolytic therapy. In one patient, cardiac function recovered spontaneously after 6 h on venoarterial extracorporeal membrane oxygenation. Three patients were discharged from hospital, two of them made a full recovery, one sustained severe hypoxic brain injury. A few patients with intractable cardiogenic shock or pulseless electrical activity can be resuscitated with the help of emergency percutaneous venoarterial extracorporeal membrane oxygenation. Emergency venoarterial extracorporeal membrane oxygenation is associated with a high rate of complications and its use should therefore be limited to selected patients with a rapidly correctable underlying cardiopulmonary pathology (anatomic, metabolic or hypothermic) who do not respond to conventional advanced cardiac life support.

Emergencies↗
PubMed1996

Important aspects in the treatment of severe accidental hypothermia: the Innsbruck experience.

The purpose of this paper is to review important aspects in the treatment of accidental hypothermia, based on our own experience in rewarming 55 patients with severe accidental hypothermia and a core temperature < 30 degrees C. We used three different methods of rewarming, adjusted to the patients' hemodynamics: airway rewarming, warmed fluids and insulation in patients with stable hemodynamics (group 1, n = 24), peritoneal dialysis in patients with unstable hemodynamics (group 2, n = 7) and extracorporeal circulation in patients with cardiocirculatory arrest (group 3, n = 24). Survival rates were 100% (group 1), 72% (group 2) and 13% (group 3) retrospectively. Published data supporting our strategy and alternative approaches are reviewed. The method used to rewarm a patient with severe accidental hypothermia should be adjusted to the hemodynamic status. The prognosis is excellent in patients in whom no hypoxic event precedes hypothermia and no serious underlying disease exists.

Adult↗
PubMed1996

[A new cardiac pacemaker stimulation technology (autocapture) allows, with unchanged life expectancy, reduction of generator size by half].

Energy delivery (stimulation amplitude) of a pacemaker should be adjusted to the depolarisation threshold of the heart, which is a nonconstant magnitude. As programming of the stimulation amplitude is time-consuming, many pacemakers are never adjusted to the measured threshold referring to energy delivery. The unnecessary energy loss subsequently reduces the longevity of the implanted devices and remains the weak point of modern pacemakers. Autocapture function (automatic stimulation threshold search, subsequently automatic amplitude regulation 0.3 V above measured threshold, evoked response detection to verify the efficacy of every stimulus and back up pulse in case of loss of capture) is for the first time realized in an extremely small, rate adaptive, multiprogrammable single chamber pacemaker (Microny SR+ 2425T). The pulse generator was tested in a multicentric, european clinical investigation study. These pacemakers were implanted in 8 patients (5 male, 3 female) between December 1994 and April 1995. Automatic measurement of Autocapture threshold revealed 0.7 +/- 0.15 V at implantation, 1.5 +/- 0.3 V after 1 month, 1.3 +/- 0.14 V after 6 months and 1.3 +/- 0.14 V 1 year after implantation. A safety margin of 0.3 V is added to the threshold value to secure capture, therefore mean stimulation amplitude is 1.6 V after 12 months implantation time. The Autocapture feature minimizes current drain and that means that this extremely small generator provides a comparable life as the twice as large common generators used at present time.

Aged↗
PubMed1995

[Management of isolated sternum fracture: screening for heart contusion with troponin T].

In all of our reported cases a seat belt injury was the reason for the sternal fracture. Only 4 of 27 patients of this prospective study suffered from a heart contusion. None of our patients showed complications. An isolated sternal fracture with or without heart contusion seems to be of minor clinical significance. Referring to our patients a screening of a heart contusion with CKMB/CK activity and ECG seems to be sufficient when the trauma is not older than 12 hours. The longer persisting plasma concentrations of cardiac troponin T (cTnT) enables a diagnosis of a heart contusion even after a few days.

Adolescent↗
PubMed1995

[Intraoperative calorimetry in aortic bifurcation reconstruction].

Oxygen uptake (VO2) and carbon dioxide elimination (VCO2) can be measured with an indirect calorimeter, this method is well established in routine monitoring of ICU patients to evaluate metabolic state as a reflection of stress. In various experimental studies it was demonstrated that anaesthetics can influence whole-body metabolism. The purpose of this study was to examine whether indirect calorimetry can be used intraoperatively during routine anaesthesia and whether presumable changes in metabolism can be detected immediately. Abdominal aortic cross-clamping changes circulation, nutritional supply of the lower extremities and thus VO2 and VCO2. We therefore used this operation for our study. METHOD. Eleven patients, mean age 64 years, undergoing reconstruction of the aortic bifurcation, were studied. After premedication with piritramid and atropine, total intravenous anaesthesia (TIVA) was performed with fentanyl and midazolam after an induction with thiopental. Patients were ventilated with a Servo-Ventilator 900 D and a constant FiO2 of 0.5, without N2O. Routine monitoring consisted of ECG, pulsoximetry, CVP and continuous AP. VO2 and VCO2 were measured with a Deltatrac (Datex), and data were registered every minute. For statistical evaluation we used a Wilcoxon-Ranksum test for matched pairs, p < 0.05 was considered significant. Data from specific time (5 min after intubation, 5 min before clamping; 5, 10 and 15 min after clamping, before declamping and 5 and 10 min after declamping and at the end of surgery) were calculated. In addition to absolute values, we compared the measured VO2 and VCO2 to baseline (5 min before clamping = MP2). RESULTS. Mean operating time was 139 min +/- 37; aortic cross-clamping time for the first extremity was 38 min and 55 min for the second. As expected, there was a significant decrease in VO2 (90% of baseline) and VCO2 (75% of baseline) during aortic cross-clamping. After declamping VO2 again rose to 110% of baseline, or to 103% for the second limb. VCO2 increased to only 90% and 82%, respectively. At the end of surgery VO2 reached baseline, whereas VCO2 remains at 83%. The respiratory quotient VCO2: VO2 was markedly reduced from 0.95 +/- 0.156 to 0.73 +/- 0.06 during surgery. The Deltatrac showed every change in VO2 without delay; changes in VCO2 seem to occur somewhat retarded. DISCUSSION. Aortic cross-clamping leads to a marked decrease in VO2 and VCO2 reflecting the temporary reduction in whole-body metabolism. Declamping results in a compensatory rise, especially in VO2. VCO2 seems to increase less after declamping, perhaps due to the CO2 pool of the organism or to a change in metabolism from carbohydrate to mainly fat oxidation. The results of this study demonstrate that indirect calorimetry can easily be performed during anaesthesia and surgery. Preconditions are a non-rebreathing system without airleak, constant FiO2 < 0.6 and no use of nitrous oxide.

Aged↗
PubMed1995

Cardiac troponin T release in multiply injured patients.

Cardiac troponin T (cTnT), a new marker of myocardial tissue damage, was investigated in 32 consecutive multiply injured patients. cTnT, creatine kinase (CK) and CK isoenzyme MB (CK-MB) mass concentrations were measured immediately after admission, 12 and 24 h later and daily thereafter for 4 days. We found a moderate increase in cTnT in 22 patients (72 per cent; peaks: 0.6-5.1 micrograms/l). In only four of these 22 patients did the CK-MB mass/CK index indicate myocardial injury. ST-T alterations and arrhythmias did not occur significantly more frequently in patients with increased cTnT plasma concentrations or positive CK-MB mass/CK index. We found a moderate increase in cTnT in 72 per cent of all patients with multiple injuries, but we found no association between an increase in cTnT and the occurrence of electrocardiographic changes and arrhythmias.

Adolescent↗
PubMed1995

Hemodynamics and oxygen metabolism in the pig during long-term hypothermia: comparison of 2 pH strategies.

The aim of this study was to investigate the influence of acid-base management (pH stat or alpha stat) on hemodynamics and oxygen metabolism during long-term hypothermia in the pig. Seventeen female pigs were anesthetized, slowly cooled to 28 degrees C with cooling mats and kept at this temperature for 36 h. Thereafter, slow rewarming was performed with inhalation of a 40 degrees C warm air/oxygen mixture and insulation. Eight of the 17 pigs were ventilated according to the pH stat strategy and 9 according to the alpha stat strategy. Both groups were compared 4 times each for hemodynamics and metabolism during cooling, hypothermia and rewarming. The 2 strategies showed no significant difference in cardiac output, heart rate or mean arterial pressure. The only difference in hemodynamics was observed in mean pulmonary artery pressure and pulmonary artery resistance during hypothermia, showing higher values in pH stat animals. As for oxygen metabolism, oxygen consumption during hypothermia was significantly higher in alpha stat animals. Long-term hypothermia with spontaneous circulation revealed significant differences in oxygen metabolism and pulmonary artery pressure as well as resistance between alpha and pH stat acid-base management. These differences may be of importance when using moderate hypothermia in a clinical or experimental setting.

Acid-Base Equilibrium↗