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Traumatic Brain Injury and Aeromedical Licensing
Published in Anthony N. Nicholson, The Neurosciences and the Practice of Aviation Medicine, 2017
Those more severely injured will require close observation in the acute admission and post-operative periods. Such care on specialist units affords moment-to-moment monitoring aimed at maintaining vital systems. Patients with brain swelling may need prolonged periods of ventilation until this settles. During this period, the primary target is to control the cerebral perfusion pressure (CPP) which is a function of mean arterial blood pressure, normally ~100 mm Hg, less the intracranial pressure, normally 10 mm Hg (Figure 16.1). This is achieved by introduction of an intracranial pressure monitor and arterial lines. The critical cerebral perfusion pressure is around 60 mm Hg, and efforts are aimed at reducing the intracranial pressure and elevating mean arterial pressure to effect a cerebral perfusion pressure well above the critical level.
Cerebrovascular Effects of Carbon Monoxide
Published in David G. Penney, Carbon Monoxide, 2019
Mark A. Helfaer, Richard J. Traystman
Under conditions of hypoxia, CBF increases because of cerebral vasodilation (Iadecola et al., 1994). In addition, the hemodynamic effects of hypoxia result in an elevated mean arterial blood pressure (MABP), which results in a greater driving pressure into the brain, defined as cerebral perfusion pressure (CPP = MABP-ICP), where ICP is intracranial pressure. The mechanism by which CBF increases with either hypoxic hypoxia or CO hypoxia is controversial. One theory is that there is an oxygen sensor (Traystman et al., 1978) in brain. If this sensor responds to PaO2, then CO hypoxia should not change cerebral vascular resistance (CVR = MABP/CBF), for under these conditions (unlike hypoxic hypoxia), PaO2 is preserved. Traystman et al. (1978) reported that the rise in CBF during a reduction in arterial oxygen content produced by hypoxic hypoxia (low inspired percentage oxygen) was similar to the rise in CBF associated with CO hypoxia for a similar reduction in oxygen content. During this experiment, MABP increased with hypoxic hypoxia, and decreased with CO hypoxia. It was shown that by denervating the carotid bodies, cerebral vascular resistance fell in the hypoxic hypoxia animals to the same degree as in the CO hypoxia animals. Therefore, it was concluded that it is unlikely that the chemoreceptors play a role in either CO or hypoxic hypoxia and that the brain increases its blood flow in response to its oxygen needs with both hypoxic and CO hypoxia in order to maintain CMRO2. This is independent of whether or not the baroreceptors or chemoreceptors are dener-vated. The implications for these findings, illustrated in Figure 3, are that if an oxygen sensor exists, it does not reside in either the baroreceptors or the chemoreceptors.
Numerical analysis of hemodynamic effect under different enhanced external counterpulsation (EECP) frequency for cerebrovascular disease: a simulation study
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2021
Siwei Ye, Ming Yang, Yuanfei Zhu, Xiaochen Gao, Fan Meng, Ruiliang Wu, Bo Yu
The human blood circulation is a highly complex multi-unit impedance network system, which can be analyzed based on an LPM (Mihalef et al. 2017). For ischemic stroke patients, CA ability is critical in maintaining brain health (Moerman and De Hert 2019). In previous studies (Li et al. 2019), researchers simulated the increase in CBF for ischemic stroke patients after EECP. The absolute increasing rate was approximately 35%, and much higher than corresponding data in this study. The potential cause may be the introducing of personal CA ability model. The ability of CA reflects the ability of cerebral circulation to maintain stable blood flow when the external cerebral perfusion pressure changes. Ischemic stroke patients generally have a certain degree of damage compared to healthy people. In this study, the damage degree to CA of patient A was less severe, which is also reflected in the increased CBF caused by EECP.
Devices to enhance organ perfusion during cardiopulmonary resuscitation
Published in Expert Review of Medical Devices, 2021
Matthew A. Bridges, Julie B. Siegel, Joshua Kim, Kristen M. Quinn, Jennie H. Kwon, Brielle Gerry, Taufiek Konrad Rajab
Cardiac arrest is one of the leading causes of morbidity and mortality in the US. In 2019, more than 356,000 people experienced an out-of-hospital cardiac arrest (OHCA) with an overall survival rate of only 10% [1]. A contributing factor to these dismal outcomes is the poor perfusion of vital organs during cardiac arrest. Cardiopulmonary resuscitation (CPR) is the American Heart Association (AHA) recommended treatment for emergent cardiac arrest with the goal of providing circulatory support via chest compressions and ventilatory support via rescue breaths. Without CPR, the survival rate of witnessed cardiac arrest from ventricular fibrillation decreases by 7–10% per minute; however, when CPR is administered, the survival rate decreases by only 3–4% per minute from the time of collapse to defibrillation [2]. The increase in survival is due to perfusion of vital organs, most importantly the heart and the brain, as these tissues have the lowest tolerance to ischemia. In animal models, when the focus of CPR is on increasing coronary perfusion pressure (CPP) and cerebral perfusion pressure (CerePP), survival from cardiac arrest increases [3–5].