The importance of transesophageal echocardiography during surgery of the thoracic aorta.

OBJECTIVES: To assess left ventricular dimensions and cardiac output during thoracic and thoracoabdominal aortic aneurysm repair. MATERIAL AND METHODS: Nine patients undergoing thoracic and thoracoabdominal aneurysm repair using direct cross-clamping without shunt or by-pass were studied prospectively. Prior to, during cross-clamping (XC) and after declamping left ventricular cross-sectional areas were monitored with transesophageal echocardiography. A pulmonary artery catheter was used for measurements of cardiac output with the thermodilution technique. RESULTS: Cardiac output increased 43% from baseline during XC (p < 0.01) and was still 55% above baseline at declamping (p < 0.05). Left ventricular end-systolic inner area was reduced 32% during XC (p < 0.01). Pulmonary artery pressures and central venous pressure increased during declamping (p < 0.05). Heart rate increased 38% from 66 beats/ min to 92 beats/min (p < 0.01) and was still 30% elevated at declamping (p < 0.01). CONCLUSION: During thoracic aortic XC, cardiac output is increased and left ventricular end-systolic dimension is reduced. TEE is a valuable supplement to pressure measurements for the evaluation of cardiac function during surgery of the thoracic aorta.

Selective carotid angiography during cross-clamping of the descending thoracic aorta in pigs.

OBJECTIVE: To visualize the intra- and extracranial blood vessels during cross-clamping of the descending thoracic aorta. EXPERIMENTAL DESIGN: Experimental animal study. SETTING: Animal laboratory, University Hospital. MATERIALS: Seven pigs. INTERVENTIONS: Cross-clamping of the descending thoracic aorta for 30 minutes. METHOD: Selective carotid angiography was performed before, during and after cross-clamping. Venous filling time of internal- and external jugular veins, diameter of internal and external jugular veins and internal, external and common carotid arteries and contrast intensity were determined. RESULTS: During cross-clamping the blood flow velocity increased as demonstrated by decreased venous filling time and decreased contrast intensity. In addition, the diameter of the external jugular vein increased and the diameter of the internal carotid artery decreased during cross-clamping. No arteriovenous anastomoses could be detected during the experiment. CONCLUSIONS: Our results indicate increased intra- and extracranial blood flow during cross-clamping of the descending thoracic aorta in pigs.

Cerebral haemodynamics during thoracic- and thoracoabdominal aortic aneurysm repair.

OBJECTIVE: To investigate cerebral haemodynamics during operations for thoracic and thoracoabdominal aortic aneurysms. DESIGN: Prospective clinical study. MATERIAL: 10 patients operated on consecutively with resection for thoracic (5) or thoracoabdominal aortic (5) aneurysms. METHODS: Blood flow velocity of the middle cerebral artery was measured through a temporal approach using a TC Doppler with a 2 MHz probe. Recordings were made during induction of anaesthesia and performed continuously before, during and after cross-clamping of the aorta. RESULTS: Following 10 min. of aortic cross-clamping blood flow velocity of the middle cerebral artery increased from 44 to 55 cm/s (p < 0.01). A further increase to 69 cm/s (p < 0.01) was observed 5 min after declamping. The pulsatility index averaged 0.74 increasing to 1.21 (p < 0.05) at clamping and 0.87 (p < 0.05) after declamping. CONCLUSION: There was an increased blood flow velocity of the middle cerebral artery during cross-clamping of the descending thoracic aorta in patients operated on for thoracic and thoracoabdominal aortic aneurysms. This increase in cerebral blood flow and blood volume could explain the acute increase in cerebrospinal fluid pressure observed during cross-clamping of the thoracic aorta.

Effect of sodium nitroprusside on cerebral haemodynamics during cross-clamping of the descending thoracic aorta in pigs.

OBJECTIVE: To assess the effect of sodium nitroprusside on cerebral haemodynamics during cross-clamping of the descending thoracic aorta in pigs. DESIGN: Non-randomised controlled animal study. SETTING: University hospital, Norway. MATERIAL: 17 Pigs. INTERVENTIONS: Cross-clamping of the descending thoracic aorta for 30 minutes. In 8 pigs sodium nitroprusside was given to prevent proximal hypertension (sodium nitroprusside group); 9 pigs were given no sodium nitroprusside (control group). MAIN OUTCOME MEASURES: Intracerebral pressure, sagittal sinus pressure, cerebral flux, and internal carotid artery blood flow. RESULTS: Intracerebral pressure, sagittal sinus pressure, and cerebral flux increased in both groups during cross-clamping of the descending thoracic aorta. There were no differences between the groups in these variables despite significantly lower mean proximal aortic pressure in the sodium nitroprusside group. CONCLUSIONS: Sodium nitroprusside did not affect intracerebral pressure, sagittal sinus pressure, or cerebral flux during cross-clamping of the descending thoracic aorta. Increased cerebral blood flow rather than venous congestion is the most likely cause of increased intracranial pressure during cross-clamping of the descending thoracic aorta.

[Results after surgical treatment of abdominal aortic aneurysm]. / Resultater etter kirurgisk behandling av abdominale aortaaneurismer.

During the period 1983-1993 altogether 403 patients were operated on for abdominal aortic aneurysm. The median age was 69.5 years. 246 were operated on electively whereas 58 had symptoms without rupture and 99 had ruptured aneurysm. The 30 day mortality in the three groups was 4.1, 12.0 and 28.3% respectively. The mortality in hospital was 4.5, 12.0 and 31.3% in the three groups respectively. Coronary artery disease dominated as cause of death in the group as a whole, whereas irreversible shock and complications secondary to haemorrhage were common in the group with ruptured aneurysm. There were no graft infections in this series, and only one superficial infection which healed without complications. Investigation and treatment of coronary artery disease might perhaps decrease the mortality rate in the elective group. These results form a basis against which the results of endovascular treatment should be compared.

Increased left ventricular contractility during cross-clamping of the descending thoracic aorta.

OBJECTIVE: To evaluate how left ventricular (LV) dimensions and contractility and proximal systemic hemodynamics respond during and after 30 minutes of cross-clamping of the descending thoracic aorta. DESIGN: The study was prospective and controlled. SETTING: The study was performed in a university animal laboratory. PARTICIPANTS: Ten pigs (bodyweight: 22 to 30 kg). INTERVENTIONS: The pigs were anesthetized with fentanyl and ketamine, and the heart and aorta were exposed through a left thoracotomy. The aortic root pressure and flow and LV dimensions were monitored with a high-fidelity pressure catheter, a precalibrated ultrasonic transit-time flow probe, and by two-dimensional ultrasound imaging, respectively. MEASUREMENTS AND MAIN RESULTS: After 1 minute of cross-clamping, LV end-diastolic and end-systolic diameters were increased 17% and 32% above baseline (both p < 0.001), respectively, whereas LV fiber shortening was decreased by 35% (p < 0.05) corresponding to the 257% increase in wall stress (p < 0.001). After 5 minutes, LV dimensions, fiber shortening, and wall stress had returned to baseline levels. After 10 minutes, fiber shortening was increased 67% (p < 0.05), although wall stress was maintained at baseline levels. Simultaneously, the aortic mean blood pressure, heart rate, and cardiac output peaked 112% (p < 0.001), 81% (p < 0.001), and 125% (p < 0.01) above baseline, respectively. CONCLUSIONS: Cross-clamping grossly increased systemic afterload grossly and was followed by moderate LV dilation, which resolved after 5 minutes owing to the combined effects of proximal vasodilation, increased myocardial contractility, and tachycardia. This hyperdynamic circulatory state was maintained during cross-clamping and decreased after declamping.

Alterations in intracranial volume following cross-clamping of the descending thoracic aorta in pigs--an experimental study using MRI.

OBJECTIVES: To determine whether alterations in intracranial volume occurred following cross-clamping of the descending thoracic aorta in pigs. DESIGN AND SETTING: Laboratory animal study. MATERIALS: Eight pigs undergoing cross-clamping of the descending thoracic aorta for 30 min. CHIEF OUTCOME MEASURES: A Philips Gyroscan T5-II Release 3 (0.5 T) was used to obtain intracranial images before cross-clamping, during cross-clamping and after declamping. The ventricular volume was measured on Spin Echo T1-weighted images. The signal intensity of the cerebral tissue was measured on Spin Echo T2-weighted images. Increased signal intensity of the cerebral tissue relative to an external reference was used as an indicator of cerebral oedema. MAIN RESULTS: The ventricular volume decreased to 89% (p < 0.01) of the baseline value after 5 min of cross-clamping. At 5 min after declamping the ventricular volume decreased further to 71% (p < 0.01). At 25 min after declamping the ventricular volume had returned to the baseline value. The signal intensity of the cerebral tissue did not differ from baseline values following aortic cross-clamping. CONCLUSIONS: In this study, ventricular volume decreased following cross-clamping of the descending thoracic aorta. Since no cerebral oedema was observed, the decrease of ventricular volume was most likely due to increased intracranial blood volume.

Effect of sodium nitroprusside on cardiac output during cross-clamping of the descending thoracic aorta in pigs.

Sodium nitroprusside (SNP) is used to control proximal hypertension during cross-clamping of the descending thoracic aorta (XC). To assess the haemodynamic effects of SNP on cardiac output (CO) during XC, 21 pigs were anaesthetized with ketamine and fentanyl. In the control group (n = 11), no vasodilating therapy was given. In the investigation group (SNP group), 2 animals died during the surgical preparation and were excluded, leaving 8 animals in the group (n = 8). In these animals, SNP was infused in order to keep the mean arterial pressure (MAP) at about 100 mm Hg during cross-clamping. In both groups, aorta was cross-clamped for 30 min, and cardiac output (CO) was measured by the thermodilution technique. Following cross-clamping, CO increased 107% in the control group and 96% in the SNP group. There was an increase in heart rate (HR) of 77% in the control group and of 110% in the SNP group, and a reduction in systemic vascular resistance of 41% in the SNP group. Stroke volume (SV) was unchanged in both groups. MAP increased 83% in the control-group. No differences were observed between the two groups regarding central venous pressure or pulmonary artery pressure. Four animals in the SNP group died 5-10 min after release of the aortic clamp. In conclusion, we found equal increase in CO in both groups. The increase in CO was related predominantly to increased HR, whereas SV was largely unaltered. Vasodilation with SNP increased the mortality following clamp removal in this experimental model.

Cerebrospinal fluid production during proximal aortic cross-clamping.

During cross-clamping (XC) of the thoracic aorta, the cerebrospinal fluid pressure (CSFP) increases. The mechanism of the increased CSFP is unknown but increased cerebrospinal fluid (CSF) production has been suggested as one explanation. The aim of this study was to investigate whether the CSF production rate was influenced by proximal XC of the thoracic aorta in an experimental model. Using the ventriculocisternal perfusion method including [14C] inulin, the rate of CSF production was measured before, during and after XC of the thoracic aorta in seven pigs. The CSFP was measured via a catheter in the lateral ventricle and the thoracic aorta was cross-clamped just distal to the left subclavian artery for 30 minutes. Following cross-clamping the CSFP increased from 5 mmHg to 11 mmHg (p < 0.001) and remained elevated during XC. In contrast the CSF production rate was 0.09 ml/min prior to XC and was not significantly altered following XC. In conclusion this experimental study indicates that increased CSF production is not responsible for the increase in CSFP during XC.