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Blood pressure (BP)

The increase in mean arterial blood pressure (MABP) during global cerebral ischemia constitutes a compensatory and protective mechanism, regulated by the Central Nervous System, in response to the accumulation of different toxic compounds in the brainstem 1)

Sometimes referred to as arterial blood pressure, is the pressure exerted by circulating blood upon the walls of blood vessels, and is one of the principal vital signs. When used without further specification, “blood pressure” usually refers to the arterial pressure of the systemic circulation. During each heartbeat, blood pressure varies between a maximum (systolic blood pressure) and a minimum (diastolic) pressure.

The blood pressure in the circulation is principally due to the pumping action of the heart.

Differences in mean blood pressure are responsible for blood flow from one location to another in the circulation. The rate of mean blood flow depends on the resistance to flow presented by the blood vessels. Mean blood pressure decreases as the circulating blood moves away from the heart through arteries and capillaries due to viscous losses of energy.

Mean blood pressure drops over the whole circulation, although most of the fall occurs along the small arteries and arterioles.

Gravity affects blood pressure via hydrostatic forces (e.g., during standing), and valves in veins, breathing, and pumping from contraction of skeletal muscles also influence blood pressure in veins.

Normal blood pressure

Normal blood pressure at rest is within the range of 100-140mmHg systolic (top reading) and 60-90mmHg diastolic (bottom reading). High blood pressure is said to be present if it is often at or above 140/90 mmHg.

Importance

One of the factors that determines cerebral perfusion pressure.

Elevated blood pressure (BP) is a strong predictor of poor outcome in both intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH). Data from a landmark clinical trial INTERACT 2, wherein 2839 participants enrolled with spontaneous ICH were randomly assigned to receive intensive (target systolic BP <140 mmHg) or guideline recommended BP lowering therapy (target systolic BP <180 mmHg), showed that intensive BP lowering was safe, and more favorable functional outcome and better overall health-related quality of life were seen in survivors in the intensive treatment group. These results contributed to the shift in European and American guidelines towards more aggressive early management of elevated BP in ICH. In contrast, the treatment of BP in SAH is less well defined and more complex. Although there is consensus that hypertension needs to be controlled to prevent rebleeding in the acute setting, induced hypertension in the later stages of SAH has questionable benefits 2).

Evidence supports early intensive blood pressure (BP) lowering in acute intracerebral hemorrhage, but uncertainty persists over whether potential benefits and harms vary according to the magnitude of BP reduction.

BP variability is independently and linearly associated with the development of neurologic deterioration in acute stage of ischemic stroke 3).

BP is positively associated with risk of vascular dementia, irrespective of preceding transient ischemic attack or stroke. Previous reports of inverse associations in old age could not be confirmed 4).

Monitoring

Monitoring of blood pressure (BP) during procedures is variable, depending on multiple factors. Common methods include sphygmomanometer (BP cuff), separate radial artery catheterization, and side port monitoring of an indwelling sheath. Each means of monitoring has disadvantages, including time consumption, added risk, and signal dampening due to multiple factors.

see Arterial line


A new technology involving a 330 µm fiber optic sensor embedded in the wall of a sheath structure was tested against both radial artery catheter and sphygmomanometer readings obtained simultaneous with readings recorded from the pressure sensing system (PSS). Correlations and Bland-Altman analysis were used to determine whether use of the PSS could substitute for these standard techniques.

The results indicated highly significant correlations in systolic, diastolic, and mean arterial pressures (MAP) when compared against radial artery catheterization (p<0.0001), and MAP means differed by <4%. Bland-Altman analysis of the data suggested that the sheath measurements can replace a separate radial artery catheter. While less striking, significant correlations were seen when PSS readings were compared against BP cuff readings.

The PSS has competitive functionality to that seen with a dedicated radial artery catheter for BP monitoring and is available immediately on sheath insertion without the added risk of radial catheterization. The sensor is structurally separated from the primary sheath lumen and readings are unaffected by device introduction through the primary lumen. Time delays and potential complications from radial artery catheterization are avoided 5).

Treatment

There are anatomical and physiological evidences that the ventrolateral (VL) region of the medulla plays an important role in blood pressure regulation and that dysfunction at this level may generate hypertension (HT). Vascular compression by a megadolicho-artery from the vertebrobasilar arterial system at the root entry/exit zone (REZ) of the glossopharyngeal (IXth) and vagal (Xth) cranial nerves (CNs) and the adjacent VL aspect of the medulla has been postulated as a causal factor for HT from neurogenic origin. The first attempts at microvascular decompression (MVD) of the IX-Xth CNs together with the neighbouring VL brainstem was revealed promising. Established criteria for indication of MVD as an aetiological treatment of apparent essential HT are still needed 6).

1)
Herguido M, Carceller F, Madero R, Roda J. Animal survival related to acute blood pressure response in global cerebral ischemia in rats. Neurol Res. 1997 Aug;19(4):417-419. PubMed PMID: 27819547.
2)
Carcel C, Sato S, Anderson CS. Blood Pressure Management in Intracranial Hemorrhage: Current Challenges and Opportunities. Curr Treat Options Cardiovasc Med. 2016 Apr;18(4):22. doi: 10.1007/s11936-016-0444-z. PubMed PMID: 26909816.
3)
Chung JW, Kim N, Kang J, Park SH, Kim WJ, Ko Y, Park JH, Lee JS, Lee J, Yang MH, Jang MS, Oh CW, Kwon OK, Jung C, Kim BJ, Han MK, Gorelick PB, Bae HJ. Blood pressure variability and the development of early neurological deterioration following acute ischemic stroke. J Hypertens. 2015 Jul 31. [Epub ahead of print] PubMed PMID: 26237556.
4)
Emdin CA, Rothwell PM, Salimi-Khorshidi G, Kiran A, Conrad N, Callender T, Mehta Z, Pendlebury ST, Anderson SG, Mohseni H, Woodward M, Rahimi K. Blood Pressure and Risk of Vascular Dementia: Evidence From a Primary Care Registry and a Cohort Study of Transient Ischemic Attack and Stroke. Stroke. 2016 Jun;47(6):1429-35. doi: 10.1161/STROKEAHA.116.012658. Epub 2016 May 10. PubMed PMID: 27165956.
5)
Purdy PD, South C, Klucznik RP, Liu KC, Novakovic RL, Puri AS, Pride GL, Aagaard-Kienitz B, Ray A, Elliott AC. Use of a pressure sensing sheath: comparison with standard means of blood pressure monitoring in catheterization procedures. J Neurointerv Surg. 2016 Jul 15. pii: neurintsurg-2016-012536. doi: 10.1136/neurintsurg-2016-012536. [Epub ahead of print] PubMed PMID: 27422970.
6)
Sindou M. Is There a Place for Microsurgical Vascular Decompression of the Brainstem for Apparent Essential Blood Hypertension? A Review. Adv Tech Stand Neurosurg. 2015;42:69-76. PubMed PMID: 25411145.
blood_pressure.txt · Last modified: 2016/11/12 10:41 (external edit)