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Chronic hydrocephalus-induced changes in cerebral blood flow: mediation through cardiac effects
Stephen M Dombrowski1, Soren Schenk, Anna Leichliter
1Department of Neurological Surgery, Pediatric and Congenital Neurological Surgery, The Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA. dombros@ccf.org
Insights
Chronic hydrocephalus (CH) significantly impacts cardiac output (CO) and cerebral blood flow (CBF) over time. This study reveals a decline in CO and CBF in CH, linked to impaired cardiac function, not just intracranial pressure.
Area of Science:
- Neuroscience
- Cardiovascular Physiology
- Cerebrovascular Research
Background:
- Decreased cerebral blood flow (CBF) in hydrocephalus is typically attributed to increased intracranial pressure (ICP), ventricular enlargement causing vascular compression, or impaired metabolism.
- The role of cardiac function and systemic blood flow in chronic hydrocephalus (CH) has been under-explored.
- Understanding these systemic effects is crucial for a comprehensive view of CH pathophysiology.
Purpose of the Study:
- To investigate the relationship between the duration and severity of chronic obstructive hydrocephalus (CH) and key hemodynamic parameters.
- To assess cardiac output (CO), CBF, myocardial tissue perfusion (MTP), and peripheral blood flow (PBF) in an experimental CH model.
- To explore correlations between hydrocephalus severity, intracranial compliance (ICC), and oxygen delivery to the brain.
Main Methods:
- Utilized an experimental model of chronic obstructive hydrocephalus in canines.
- Measured CO, CBF, MTP, and PBF using the microsphere injection method over 16 weeks.
- Assessed cardiac output via Swan-Ganz thermodilution, and measured intracranial compliance (ICC) and oxygen delivery to the prefrontal cortex (PFC).
Main Results:
- An initial postoperative reduction in CO, CBF, MTP, and PBF was observed in both CH and control groups, with recovery in controls but continued decline in CH animals.
- CBF was positively correlated with CO but showed no significant relationship with cerebrospinal fluid (CSF) volume or pressure.
- Decreased CBF correlated with reduced oxygen in the PFC; decreased CO was inversely related to ventriculomegaly and positively related to increased ICC.
Conclusions:
- Chronic hydrocephalus exerts a significant influence on cardiac output and cerebral blood flow, particularly in later stages.
- The observed decline in cardiac function in CH warrants consideration in its pathophysiology and clinical management.
- Further research is needed to elucidate the mechanisms behind the late deterioration of cardiac function in hydrocephalus.
Abstract:
Decreased cerebral blood flow (CBF) in hydrocephalus is believed to be related to increased intracranial pressure (ICP), vascular compression as the result of enlarged ventricles, or impaired metabolic activity. Little attention has been given to the relationship between cardiac function and systemic blood flow in chronic hydrocephalus (CH). Using an experimental model of chronic obstructive hydrocephalus developed in our laboratory, we investigated the relationship between the duration and severity of hydrocephalus and cardiac output (CO), CBF, myocardial tissue perfusion (MTP), and peripheral blood flow (PBF). Blood flow measures were obtained using the microsphere injection method under controlled hemodynamic conditions in experimental CH (n=23) and surgical control (n=8) canines at baseline and at 2, 4, 8, 12, and 16 weeks. Cardiac output measures were made using the Swan-Ganz thermodilution method. Intracranial compliance (ICC) via cerebrospinal fluid (CSF) bolus removal and infusion, and oxygen delivery in CSF and prefrontal cortex (PFC) were also investigated. We observed an initial surgical effect relating to 30% CO reduction and approximately 50% decrease in CBF, MTP, and PBF in both groups 2 weeks postoperatively, which recovered in control animals but continued to decline further in CH animals at 16 weeks. Cerebral blood flow, which was positively correlated with CO (P=0.028), showed no significant relationship with either CSF volume or pressure. Decreased CBF correlated with oxygen deprivation in PFC (P=0.006). Cardiac output was inversely related with ventriculomegaly (P=0.019), but did not correlate with ICP. Decreased CO corresponded to increased ICC, as measured by CSF infusion (P=0.04). Our results suggest that CH may have more of an influence on CO and CBF in the chronic stage than in the early condition, which was dominated by surgical effect. The cause of this late deterioration of cardiac function in hydrocephalus is uncertain, but may reflect cardiac regulation secondary to physiologic response or brain injury. The relationship between cardiac function and CBF should be considered in the pathophysiology and clinical treatment of CH.
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