Browsing by Author "Bensch, Marc"

Although the mechanisms of neurological disorders after cardiac surgery in neonates are still not fully understood, alterations in blood flow after cardiopulmonary bypass (CPB) may lead to cerebral injury. The aim of the study was the analysis of flow changes in the carotid artery of neonatal piglets after CPB. Ten neonatal piglets (younger than 7 days) were connected to the CPB and further management underwent three steps: (i) cooling to 32 degrees C core temperature within 30?min; (ii) cardiac arrest under cardioplegic myocardial protection for 90?min; and (iii) rewarming to 37 degrees C after cross-clamp release (60?min of reperfusion). In summary, piglets were separated from CPB after a total duration time of 180?min. The blood flow was measured in the left carotid artery by an ultrasonic flow probe before CPB (baseline), immediately after CPB, 30?min, and 60?min after CPB. Additionally, the pulsatility index and the resistance index were calculated and compared. Finally, the relation of the carotid artery flow data with the corresponding pressure data at each time point was compared. After termination of CPB, the carotid artery mean flow was reduced from 28.34?+/-?13.79?mL/min at baseline to 20.91?+/-?10.61?mL/min and remained reduced 30 and 60?min after CPB termination (19.71?+/-?11.11 and 17.64?+/-?15.31?mL/min, respectively). Both the pulsatility and the resistance index were reduced immediately after CPB termination and increased thereafter. Nevertheless, values did not reach statistical significance. In conclusion, the carotid Doppler flow immediately after CPB and mild hypothermia in neonatal piglets was lower than before CPB due to reduced vascular resistance. Additionally, the pressureflow relation revealed that immediately after CPB, a higher pressure is required to obtain adequate flow.

The mortality rate of neonatal piglets after heart surgery is high. Searching for a possible explanation for the death of neonatal piglets early after cardiopulmonary bypass, we analyzed hemodynamic parameters regarding survival and non-survival. Initially, 10 neonatal piglets (younger than 7 days) were connected to cardiopulmonary bypass (CPB). The mean body weight was 2.98+/-0.44 kg. Exposure of the heart was performed through a median sternotomy. After connection to the CPB, the piglets were cooled to 32 degrees C core temperature before the ascending aorta was cross-clamped and the heart arrested (90?min). Thereafter, piglets were re-warmed to 37 degrees C and separated from CPB. During follow-up, the piglets did not receive inotropic support or vasopressors. Piglets who survived at least 2h after termination of CPB were included in the study for further data analysis (n=9). Five piglets died 2.5 to 4.0 h (median: 3.5 h) after CPB; these piglets formed the non-survivors group. Four animals survived the complete follow-up of 6 h after CPB and formed the survivors group. Regarding contractility (dP/dtmax, dP/dtmax/P, and wall thickening) there were not statistically significant differences between the groups. Non-survivors showed prolonged decrease of mean arterial pressure of more than 20% of baseline values, corresponding with a value of below 30?mm?Hg. In conclusion, the death of neonatal piglets early after cardiopulmonary bypass was not determined by low output.

Background: Hemodynamic function may be depressed in the early postoperative stages after cardiac surgery. The aim of this study was the analysis of the myocardial contractility in neonates after cardiopulmonary bypass (CPB) and mild hypothermia. Methods: Three indices of left ventricular myocardial contractile function (dP/dt, (dP/dt)/P, and wall thickening) were studied up to 6 hours after CPB in neonatal piglets (CPB group; n = 4). The contractility data were analysed and then compared to the data of newborn piglets who also underwent median thoracotomy and instrumentation for the same time intervals but without CPB (non-CPB group; n = 3). Results: Left ventricular dP/dt(max) and (dP/dt(max))/P remained stable in CPB group, while dP/dt(max) decreased in non-CPB group 5 hours postoperatively (1761 +/- 205 mmHg/s at baseline vs. 1170 +/- 205 mmHg/s after 5 h; p < 0.05). However, with regard to dP/dt(max) and (dP/dt(max))/P there were no statistically significant differences between the two groups. Comparably, although myocardial thickening decreased in the non-CPB group the differences between the two groups were not statistically significant. Conclusions: The myocardial contractile function in survived neonatal piglets remained stable 6 hours after cardiopulmonary bypass and mild hypothermia probably due to regional hypercontractility.

Cooling before circulatory arrest or ischemic arrest has been reported to influence myocardial performance in isolated neonatal hearts. The aim of the present study was to analyze indices of myocardial contractility and relaxation in an in vivo neonatal model after deep hypothermic circulatory arrest (DHCA). DHCA (18 degrees C; DHCA group; n = 8) or mild hypothermic cardiopulmonary bypass ([MH-CPB] 32 degrees C; MH-CPB group; n = 10) was applied in newborn piglets. After reperfusion (60 and 120 min), left ventricular dP/dt(max) increased in DHCA and MH-CPB, while -dP/dt(max) decreased slightly in DHCA and increased in MH-CPB. Nevertheless, the differences between the two groups did not reach statistical significance. In conclusion, left ventricular contractility remained stable after reperfusion following DHCA, to some degree at the expense of the diastolic function.

Background: Early after neonatal cardiac surgery hemodynamic dysfunction may be evident. However, still is not clear if dysfunction and outcome is related to visible myocardial alterations. The aim of the present study was the histological analysis of myocardial tissue of neonatal piglets after cardiopulmonary bypass (CPB) and cardioplegic arrest. Methods: Neonatal piglets (younger than 7 days) were connected to CPB for 180 min, including 90 min of cardioplegic heart arrest at 32 degrees C. After termination of CPB the piglets were observed up to 6 h. During this observational period animals did not receive any inotropic support. Some piglets died within this period and formed the non-survivors group (CPB-NS group) and the remaining animals formed the CPB-6 h group. Myocardial biopsies (stained with H&E) were scored from 0 to 3 regarding histological alterations. Then, the histological data were evaluated and compared to the probes of animals handled comparable to previous piglets but without CPB (non-CPB group; n = 3) and to sibling piglets without specific treatment (control; n = 5). Results: In the first hours after CPB six piglets out of 10 died (median 3.3 h). The animals of CPB-6 h group (n = 4) were sacrificed at the end of experiments (6 h after CPB). Although the myocardial histological score of CPB-6 h group and CPB-NS group were higher than non-CPB group (2.0 +/- 0.8, 1.5 +/- 0.9, and 0.8 +/- 0.3 respectively), these differences were statistically not significant. But compared to control animals (score 0.3 +/- 0.5) the scores of CPB-6 h and CPB-NS groups were significantly higher (p < 0.05). Between the left and the right ventricular tissue there were no significant differences. Conclusions: Myocardial tissue alterations in newborn piglets are related to the surgical trauma and potentiated by cardiopulmonary bypass and ischemia. However, outcome is not related to the degree of tissue alteration.

Cardiac function and hemodynamics are frequently decreased during the first hours after heart surgery, resulting in inotropic support for treatment and prevention of further hemodynamic deterioration. The aim of this study was analysis of hemodynamics of neonatal piglets who survived early postoperative course after cardiopulmonary bypass (CPB) and cardioplegic arrest without the use of inotropic drugs. Newborn piglets (younger than 7 days) were placed on mild hypothermic CPB (32 degrees C) for 180 minutes, including 90 minutes of cardioplegic arrest. Hemodynamics were examined after, termination of CPB and none of the animals received any inotropic support. After 6 hours, survived animals were euthanized (CPB group, n = 4). For control, neonatal piglets were examined for the same time interval after surgery without CPB (control group, n = 3). Systolic left-ventricular pressure increased after CPB, mean arterial blood pressure and amplitude of left ventricular wall thickness decreased. Compared with control group, systolic left-ventricular pressure in CPB group was higher (p < 0.05). Present data demonstrated hemodynamic depression after cardiac procedures in survived neonatal animals. Although the effects may not be solely attributed to CPB and myocardial ischemia effects may be potentiate by CPB. ASAIO journal 2009; 55:93-95.