Whole-body mathematical model for simulating intracranial pressure dynamics

A whole-body mathematical model (10) for simulating intracranial pressure dynamics. In one embodiment, model (10) includes 17 interacting compartments, of which nine lie entirely outside of intracranial vault (14). Compartments (F) and (T) are defined to distinguish ventricular from extraventricular CSF. The vasculature of the intracranial system within cranial vault (14) is also subdivided into five compartments (A, C, P, V, and S, respectively) representing the intracranial arteries, capillaries, choroid plexus, veins, and venous sinus. The body's extracranial systemic vasculature is divided into six compartments (I, J, O, Z, D, and X, respectively) representing the arteries, capillaries, and veins of the central body and the lower body. Compartments (G) and (B) include tissue and the associated interstitial fluid in the intracranial and lower regions. Compartment (Y) is a composite involving the tissues, organs, and pulmonary circulation of the central body and compartment (M) represents the external environment

Intra-Aortic Balloon Counterpulsation for the Treatment of Ischemic Stroke

Colloid volume expansion has been shown to increase cerebral blood flow to ischemic brain in an animal stroke model and improve recovery in patients. It is, however, potentially hazardous to use in older patients because of frequently associated cardiovascular disease. Intra-Aortic Balloon Counterpulsation might reduce the risks of using volume expansion therapy in the elderly patient. This study was designed to see if Intra-Aortic Balloon Counterpulsation (without volume expansion), in an animal with a normal heart, would increase cerebral blood flow and EEG activity in the ischemic brain. Unilateral cerebral ischemia was produced in baboons (n = 9) after right middle cerebral artery occlusion. A 12 ml intra-aortic balloon catheter was introduced into the descending aorta via the femoral artery prior to middle cerebral artery occlusion. The balloon was positioned distal to the origin of the left subclavian artery and following middle cerebral artery occlusion was inflated with each R wave on the ECG. Cardiac output, cerebral blood flow (by Hydrogen wash-out), computer-mapped EEG, and hemodynamic data were collected prior to middle cerebral artery occlusion and following occlusion both before and during counterpulsation. Intra-Aortic Balloon Counterpulsation produced a significant increase in pulse pressure from 54.7 ± 21 to 70.6 ± 33 mmHg (p = .043). No significant change was seen in cardiac output, mean arterial pressure, or cerebral blood flow. Although the computer- mapped EEG improved and the right (ischemic) hemisphere cerebral blood flow did increase slightly from 16.9 ± 6.5 to 18.3 ± 8.3 ml/100 gm/min, the cerebral blood flow changes were not significant (p=.295). It is possible that the desired increase in cerebral blood flow was not achieved partly because the animals were only 3-4 years old and were difficult to stroke. We believe that there is merit to a follow-up study in older primates with colloid volume expansion where Intra-Aortic Balloon Counterpulsation is used to protect the heart from the deleterious effects of volume expansion and where the cardiac effects of volume expansion and counterpulsation are quantified. Perhaps volume expansion with Intra-Aortic Balloon Counterpulsation will be safer and more effective than either treatment modality alone. (All data reported as mean ± standard deviation

Intra-aortic balloon counterpulsation: a treatment for ischaemic stroke?

Intra-aortic balloon counterpulsation (IABC) augments cardiac output (CO) and pulse pressure (PP) allowing patients with low output heart failure to be supported for a period of time. Augmentation of CO and PP may also be beneficial to the patient with acute cerebral ischaemia. In this paper we investigated the possibility of using IABC to increase local cerebral blood flow (CBF) in ischaemic brain. In 12 anaesthetized mongrel dogs, a canine stroke model was produced by occluding the left internal carotid and middle cerebral arteries with aneurysm clips. Six dogs were then treated with IABC for 2 h, and 6 other dogs acted as controls (no IABC). Haemodynamic data were measured continuously and CBF (microsphere technique) and CO measurements were performed pre- and post-occlusion, and then twice during the treatment period. In the IABC-treated animals, PP increased from 32 ± 5.9 to 39 ± 7.8 mmHg (p < 0.01) but CO and local CBF in the ischaemic brain did not change significantly during IABC. However; in 4 dogs with significant increases in CO due to IABC [1.7 ± 0.3 to 2.8 ± 0.7 l/min (p < 0.05)], local CBF in ischaemic brain also increased significantly from 22 ± 12 to 26 ± 11 cc/100 g/min (p < 0.05). In the control animals, CO and local CBF did not change significantly during the observation period. These data suggest that augmentation of CO and PP by IABC results in an increase in local CBF in ischaemic brain. IABC may be an effective treatment for ischaemic stroke in those patients with compromised cardiac performance whose cardiac output and pulse pressure can be augmented by IABC