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Periprocedural blood pressure management in neurointerventional surgery
  1. Thabele M Leslie-Mazwi1,
  2. John R Sims1,
  3. Joshua A Hirsch2,
  4. Raul G Nogueira3
  1. 1Department of Neurologic Critical Care, Massachusetts General Hospital, Boston, Massachusetts, USA
  2. 2Department of Interventional Neuroradiology, Massachusetts General Hospital, Boston, Massachusetts, USA
  3. 3Department of Interventional Neuroradiology, Department of Neurologic Critical Care, Massachusetts General Hospital, Boston, Massachusetts, USA
  1. Correspondence to Raul G. Nogueira, MD, Emory Faculty Office Building 80 Jesse Hill Dr. SE, Room 398, Atlanta, GA 30303; rnoguei{at}emory.edu

Abstract

With the increasing range of conditions currently amenable to endovascular therapies, the knowledge of periprocedural blood pressure management is essential for the neurointerventional surgeon. This review discusses the physiology of cerebral blood flow and blood pressure, monitoring options for neurointerventional patients, useful agents for blood pressure elevation and reduction and neuroanesthetic considerations during procedures with an emphasis on practical decision-making. Also included are parameters for conditions typically encountered in the neurointerventional suite based on best available evidence, with reference to blood pressure management before, during and after neurointerventional therapy.

  • Blood pressure
  • neurointerventional
  • endovascular
  • artery
  • hemorrhage
  • malformation
  • angiography
  • intervention

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Introduction

Neurointerventional procedures have expanded in technical applications and into more unstable patient populations. This expansion requires a greater understanding of the indications for blood pressure (BP) parameters and the means for achieving BP control.

Normal BP varies between individuals based on various demographic and genetic factors. BP becomes pathological if either abnormally elevated or too low for adequate tissue perfusion. The 2003 WHO/International Society of Hypertension statement defines hypertension on the basis of the presence of consistent BP >140/90 mm Hg.1 The neurointerventionalist typically encounters BP in the following scenarios:

  1. Preprocedural chronic BP levels

  2. Preprocedural acute BP levels

  3. Intraprocedural BP levels

  4. Postprocedure acute BP levels

  5. Postprocedure chronic BP levels

The optimal management of BP can differ substantially based on the patient's past BP, status of the cerebral vasculature and time from acute events. For instance, there is a good rationale to maintain preprocedural acute elevations of BP when facing symptomatic intracranial stenosis in order to optimize direct and collateral flow. Conversely, high chronic BP in medically treated cases has been related to a higher likelihood of stroke in the affected territory,2 and acutely elevated BP after revascularization can increase the risk of hyperperfusion syndrome.3 These examples illustrate the need for greater awareness of BP management in the neurovascular patient and require knowledge of cerebral pathophysiology. These issues, coupled to the unique features of cerebral BP regulation, demand flexibilty from the neurointerventional specialist over a wide range of conditions. The following review provides an overview of current issues in periprocedural BP management.

Cerebral physiology and BP control in health

The brain requires coupling of energy supply and demand owing to its high level of metabolism. This homeostatic mechanism was first demonstrated by Fog in 1939 in cats, but it was not accepted until 1959 when Lassen described the concept of cerebrovascular autoregulation.4 Despite the many years since that description, there remains only a limited understanding about how this mechanism works at the molecular level.

The microcirculation of the brain has distinct anatomical, physiological and pharmacological features despite its similarities to microcirculation elsewhere in the body. The general principles of fluid dynamics apply: cerebral blood flow (CBF) or CBF (Q) is directly related to pressure (P) and inversely affected by resistance (R): Q=P/R. Thus cerebrovascular autoregulation adjusts to acute flow changes largely by altering resistance and it couples flow to acute metabolic demand via this same mechanism. Coupling supply and demand under physiological and pathological conditions is modulated by the following salient factors:

  1. Perfusion pressure

  2. Metabolic and chemical stimuli

  3. Neural stimuli

Perfusion pressure

The brain maintains a relatively constant cerebral blood flow between perfusion pressures of 50 and 150 mm Hg by pressure-dependent activation of the smooth muscle in the precapillary arterioles. Cerebrovascular smooth muscle possesses the intrinsic capacity to constrict in response to an increase in wall tension and to relax as wall tension decreases. This dampening of perfusion pressures is a process commonly referred to as cerebral autoregulation.5 Release of vasoactive substances such as nitric oxide from the vascular endothelium also plays a role.

Metabolic and chemical stimuli

This represents the primary mechanism of adaptation of CBF to the local metabolic demands of the brain. Local flow varies directly with local brain function by approximately 10–20% as a function of vasoactive metabolic mediators, including the hydrogen ion, CO2, potassium, adenosine, glycolytic intermediates, phospholipid metabolites and nitric oxide. Arterial partial pressures of oxygen (Pao2) and carbon dioxide (Paco2) directly affect CBF. Indeed, CO2 is one of the most potent regulators of vasoconstriction. At normotension, there is a direct linear increase of CBF over the range of Paco2 from 20 to 80 mm Hg. Over this range, global CBF changes by 2–4% for each mm Hg change in Paco2. Hypotension impairs the response of the cerebral circulation to changes in Paco2. Pao2 has no effect on CBF in the normoxemic range. CBF increases only once Pao2 drops below 50 mm Hg in an effort to keep cerebral oxygen delivery constant.

Neural stimuli

A major difference between other systemic circulations and the cerebral circulation is the relative lack of humoral and autonomic control on normal cerebrovascular tone. Hence, a maximal stimulation of the sympathetic or parasympathetic nerves alters CBF only slightly. However, CNS vessels are invested with a rich network of nerves, and changes in transmural pressure trigger the release of neurotransmitters that provide an important additional means of vascular regulation. Changes in vascular tone in response to neuronal innervation are called neurovascular coupling. When BP exceeds the limit of myogenic autoregulation, the remaining autoregulation in large arterioles and small arteries is dependent on sympathetic autonomic innervation in the adventitia.6 Neurovascular coupling is not constant throughout the brain. As a result of sparse sympathetic innervation, the vertebrobasilar system is less protected than other regions of the brain.

Thus, autoregulation is individually and situationally dependent. The classic autoregulation curve is shifted to the right in hypertensive patients and to the left in physiological hypotension (eg, athletes), prolonged hypercarbia or hypoxia and in neonates. Autoregulation is less effective with increasing age and may be dramatically impaired in various pathological conditions including ischemia, amyloid angiopathy, space-occupying lesions, subarachnoid hemorrhage (SAH) and head injury, an issue of considerable relevance in several neurointerventional scenarios.

BP and autoregulation changes during anesthesia

Knowledge of anesthetic effects of common agents on cerebral physiology is beyond the scope of this review, but several points are noteworthy. Between the many intravenous and inhaled anesthetic agents there are fundamental differences in the influence on cerebrovascular autoregulation that bear relevance to the neurointerventionalist in relation to selection of BP targets.

Inhaled anesthetics generally have a dose-related depressive effect on autoregulation, except sevoflurane which, at clinically relevant doses, does not increase CBF or impair cerebrovascular autoregulation. This makes sevoflurane the preferred agent if inhaled anesthesia is employed during interventional cases. With regard to intravenous agents, propofol preserves autoregulation, which for many neurointerventional procedures makes propofol-based intravenous anesthesia an excellent and often first choice, although caution must be exercised as it may induce dose-dependent hypotension that exceeds autoregulation.7 The combination of remifentanil and propofol induces a dose-dependent metabolism-coupled reduction in CBF with preserved cerebrovascular autoregulation. The combined use of propofol and remifentanil anesthesia has been shown to preserve cerebrovascular resistance and cerebrovascular autoregulation and is also a reasonable choice in interventional procedures where BP is a concern.8 Dexmedetomidine, a pure α2 agonist, has become increasingly used as a sedative to induce ‘conscious sedation’ associated with analgesia and minimal respiratory depression. These characteristics facilitate the need to monitor intermittent neurological evaluations. Its effects on cerebrovascular autoregulation in injured brains are still to be determined, but seem to be minimal in healthy brains.9

There is a paucity of data regarding the impact of the sedation modality on the outcomes of patients undergoing neurointerventional procedures. Specifically in the setting of an acute ischemic stroke (AIS), general anesthesia (GA) may cause delays in time to treatment and result in a greater degree of perfusion pressure drop (at least during the induction time) whereas conscious sedation (CS) may result in patient movement and compromise the safety of the procedure. A recent retrospective analysis of a cohort of 980 patients who underwent endovascular treatment for proximal anterior circulation occlusions within 8 h from onset of stroke symptoms demonstrated no differences in symptomatic and asymptomatic hemorrhage rates between patients treated under GA (used in 44% of patients) versus CS. In addition, the use of GA was significantly associated with higher rates of both poor neurological outcome at 90 days (OR 2.33, 95% CI 1.63 to 3.44, p<0.0001) and overall mortality (OR 1.68, 95% CI 1.23 to 2.30, p<0.001) compared with CS.10 While no definite conclusions can be drawn regarding the superiority of one sedation modality over the other (given the retrospective nature of the data as well as the absence of essential information regarding intra- and periprocedural BP levels, type and dose of the different sedative and anesthetic agents used, differences in delay in time from imaging to treatment, differences in the withdrawal of care rates, etc), these data support the notion that both modalities appear to be at least equally safe.

Techniques for BP monitoring in neurointerventional procedures

Several invasive and non-invasive options for BP monitoring exist. Patients undergoing interventional procedures require continuous hemodynamic monitoring. This is best provided with an indwelling arterial line. The most frequently used is the radial artery catheter because of its well-documented low complication rates and easy access. The most feared complication is hand ischemia due to temporary or permanent occlusion of the artery, although this is a relatively rare event. Other complications such as pseudoaneurysm and sepsis (incidence of 0.09% and 0.13%, respectively) may also occur.

A femoral artery catheter is also occasionally used for BP monitoring, particularly with an indwelling sheath following a procedure. Temporary occlusion is even less frequent than with radial arterial lines (1% incidence). The incidence rates for other major complications such as pseudoaneurysm and sepsis (0.3% and 0.44%, respectively) are similar to the radial artery. The risk of higher sepsis rates from indwelling femoral catheters remains debatable.11 Femoral artery arterial monitoring is typically discontinued at the time sheath removal is planned.

For the patient who undergoes angiography with an indwelling intracranial pressure (ICP) monitor, it is crucial to focus not just on mean arterial blood pressure (MAP) but on cerebral perfusion pressure (CPP), calculated as CPP=MAP − ICP. No clear data exist to support use of systolic BP or MAP preferentially in BP monitoring. However, following MAP to maintain a CPP ensures that adequate CBF is maintained during diastole in the presence of elevated ICP, particularly in cases of markedly elevated ICP, patients with wide pulse pressures or both. Broad application of trauma guidelines suggests that CPP should be maintained at 50–70 mm Hg to assist the perfusion of ischemic regions of the brain after severe traumatic injury.12

Choice of agents for BP control

BP control for the injured brain needs tight control because it cannot be assumed that autoregulation is intact. Thus, MAP or CPP should be maintained within a relatively narrow range to avoid secondary injury from hypo- or hyperperfusion. It is therefore necessary to select short-acting intravenous agents that can be administered by continuous infusion. Ideally, the selected medication would exhibit reliable dose–response relationships and favorable safety profiles. Both patient-specific and drug-specific factors must be considered to ensure the selection of an appropriate agent. Patient-specific factors to consider when choosing both agent and dose include age, race, volume status and the presence of end-organ disease and other comorbid illnesses. In general, elderly patients may be more sensitive to the effects of these agents so it is prudent to start with a lower dose or infusion rate of these medications in patients aged >65 years.

BP reduction

Dihydropyridines

Dihydropyridines (nicardipine and the newer drug clevidipine) are calcium channel blockers more selective for vascular smooth muscle than myocardium in the order of cerebral, coronary, peripheral muscle and renal vascular smooth muscle. There is little effect on heart rate and no effect on myocardial contractility because of low cardiac muscle or sinoatrial node activity.

Nicardipine

Nicardipine acts on vascular smooth muscle promoting vasodilation. Its protonation in acidic cerebral tissue allows for rapid accumulation in ischemic tissue, localized vasodilation and a reduction in vasospasm. Vasodilation occurs predominantly in small resistance arterioles without large changes in intracranial volume or ICP. Nicardipine is one of most frequently employed antihypertensive agents in the neurointerventional and neurocritical care setting.

Clevidipine

Clevidipine is the first third-generation dihydropyridine, having recently received marketing approval in the USA. Clevidipine has an onset of 2–4 min and a duration of action of 5–15 min. It is inactivated by rapid ester hydrolysis by a serum esterase. Its rapid rate of action and metabolism independent of renal or hepatic function are desirable characteristics in patients with comorbid diseases. Clevidipine may additionally protect against organ reperfusion injury by blocking cellular calcium overload and oxygen free radical-mediated toxicity.

Labetalol

Labetalol is a combined α1- and non-selective β-adrenergic blocker. Its pharmacodynamic action intravenously shows an α to β receptor activity ratio of 1:7. The α1-blocking component minimizes reductions in cardiac output observed with β-blockers alone. Labetalol has a minimal direct effect on cerebral vasculature and is thus not directly associated with increased ICP. Because of the non-selective β-blocker actions, labetalol is contraindicated in patients with reactive airway disease, chronic obstructive pulmonary disease, second- or third-degree atrioventricular block or bradycardia. Caution is needed in heart failure. Onset of action is 2–5 min, with duration of action lasting 2–4 min.

Esmolol

Esmolol is a rapidly acting β1-adrenergic antagonist metabolized by an erythrocyte esterase. Its half-life is 9 min with duration of action of 10–20 min (prolonged slightly in patients with anemia owing to the metabolic pathway). Esmolol is safe in the setting of myocardial ischemia or infarction. With esmolol, bradycardia may be more problematic in elderly patients, demanding either a decrease in the dose or discontinuation of the drug. Contraindications to the use of esmolol include concurrent β-blocker therapy, bradycardia and decompensated heart failure.

Sodium nitroprusside

Sodium nitroprusside is a short-acting antihypertensive drug with a duration of action of 1–10 min. Its effects appear within a few seconds of intravenous infusion. It produces peripheral and cerebral vasodilation by a direct action on both arterioles and veins. Sodium nitroprusside has also been used to reduce preload and afterload in cases of severe heart failure. As a general rule, treatment should not continue for more than 72 h to avoid the risk of cyanide toxicity. Given its cerebrovenodilatory properties, sodium nitroprusside may directly result in significant increases in ICP. This effect prevents its use in many neurointerventional and neurocritical care scenarios.

Hydralazine

Hydralazine is a peripheral vasodilator that relaxes arteriolar smooth muscle by inhibiting calcium ion release from the sarcoplasmic reticulum, although specific details are not known. Small increases in ICP may occur in patients with impaired cerebral autoregulation, and this agent should be used cautiously in the angiography suite if concerns exist for loss of autoregulatory function. Hydralazine causes reflex sympathetic stimulation that can result in increases in heart rate and ICP. Intravenous onset of action is 10–20 min with a duration of 1–4 h, slightly too long to make it an ideal choice during procedures but potentially useful after a procedure is completed.

Enalaprilat

Enalaprilat is an intravenous ACE inhibitor which blocks the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. Its vasodilatory properties are due to the decreased production of angiotensin II. Administration is associated with a decrease in total peripheral resistance but with little change in heart rate, cardiac output or pulmonary occlusion pressures. In contrast to shorter-acting vasodilators, the dosage of enalaprilat is not easily adjusted. A clinical response is usually seen within 15 min although the peak response may not occur until 4 h after administration. This makes it an agent less suitable for acute changes. Enalaprilat should be avoided in patients with acute myocardial infarction and in patients with bilateral renal artery stenosis. In general, ACE inhibitors are more effective in patients with high renin levels.13 14

BP elevation

The hemodynamic management of hypotension and/or shock is aimed at maintaining oxygen delivery above a critical threshold and increasing MAP. For patients in the neurointerventional suite, BP elevation is typically reflected in the desire to maintain adequate CPP or to maintain perfusion across a critical flow-limiting lesion. Identification of the cause of the fall in BP needs to be the first step in an appropriate therapeutic response.

The CNS is relatively deficient in sympathetic receptors and shows little direct response to pressors. Vasoconstriction to vasopressor therapy may be pronounced in other parts of the vasculature, accompanied by the risk of impaired organ blood flow, particularly in the kidneys. Decreased renal perfusion may make the toxicity of radiocontrast used during the angiographic procedure more pronounced. Exposure to radiocontrast should therefore be limited if possible in patients on pressors. Additionally, local tissue necrosis can result from drug extravasation of some of these agents so a central line is often the preferred route of administration.

Multiple agents are available for increasing MAP. We will review those most frequently used in the neurointerventional suites.

Phenylephrine

Phenylephrine is a potent postsynaptic α receptor agonist with little effect on β receptors, resulting in a rise in systolic and diastolic pressures from peripheral vasoconstriction which can be accompanied by reflex bradycardia (which can be blocked by atropine if required). Cardiac irregularities are rarely seen because of the absence of β receptor effects, even with large doses. As a result of these properties, phenylephrine is one of the most commonly used pressors for hypotensive patients in the neurological intensive care setting and the neurointerventional suite.

Norepinephrine

Norepinephrine is an α adrenergic agonist with similarities to phenylephrine but an expanded range of activity on β receptors. The useful α receptor effect is vasoconstriction. The relevant functions associated with β receptors are cardioacceleration, positive inotropy and bronchial relaxation. The inherent chronotropic effect of norepinephrine is opposed to some extent by reflex slowing secondary to vasoconstriction and elevated BP. However, the chronotropic and inotropic actions of norepinephrine increase the risk of arrthymogenicity, and this agent should be used cautiously in patients with a history of cardiac conduction system disease.

Dobutamine

Dobutamine is a synthetic catecholamine that is used as a positive inotropic agent to increase cardiac stroke output in patients with severe decompensated heart failure. Dobutamine is used primarily in patients with decompensated heart failure due to systolic dysfunction. In the neurointerventional environment this presentation occurs most frequently in patients with high-grade SAH. The drug is effective in both right-sided and left-sided heart failure. Because dobutamine does not usually raise the BP, it is not recommended as monotherapy in patients with cardiogenic shock and should be combined with low-dose norepinephrine or other agent.

Dopamine

Dopamine increases mean arterial pressure primarily by increasing cardiac index with minimal effects on systemic vascular resistance. The increase in cardiac index is due to an increase in stroke volume and, to a lesser extent, to increased heart rate. Use of this agent is limited in the neurointerventional environment but it has indications similar to dobutamine.13 15

Parameters for periprocedural BP limits in particular conditions

The following section touches on the more common conditions encountered and provides the best evidence for periprocedural BP management.

Stroke and BP

BP in AIS remains an area of great controversy. Chronic hypertension is clearly an established risk factor for stroke but, in the neurointerventional setting, BP alterations will be encountered in the acute setting. There are conflicting data on what is the best approach to elevated BP in AIS. Dropping elevated BP in AIS is associated with worse outcomes, as demonstrated in the Beta Blocker Stroke Trial (BEST) and Intravenous Nimodipine West European Stroke Trial (INWEST) trials with hyperacute lowering, with better outcomes as seen in the Acute Candesartan Cilextil Therapy in Stroke Survivors (ACCESS) trial with subacute lowering, and no effect as in the National Institute of Neurological Disorders and Stroke Trial (NINDS) intravenous recombinant tissue plasminogen activator (rt-PA) trial (non-randomized hyperacute lowering).16 Some of this discrepancy may be due to the U-shaped relationship between BP levels and outcome measures,17 with patients trending toward worse outcomes when BP is low or normal. Data suggest that the majority (up to 75% in some series) of patients with AIS are hypertensive on presentation. Although hypertension is an underlying risk factor for stroke, hyperacute elevation above baseline values is thought to be a response to the acute arterial occlusion. Upon occlusion, arterioles dilate as a compensatory mechanism to lower resistance to downstream flow. Systemic BP rises in an attempt to perfuse the ischemic region of the brain in which, upon maximal dilation, the flow is directly proportional to BP. In the ischemic penumbra, maximal arterial dilation occurs and/or acute ischemic infarction ensues with resultant loss of the mechanisms of autoregulation. In this scenario, MAP and CBF become directly proportional in that decreases in MAP result in concomitant decreases in CBF.18 The converse has also been shown, that recanalizing occluded cerebral arteries through endovascular means results in a return to normal BP more rapidly than if poor recanalization is achieved.19 The ischemic penumbra is characterized by maximally dilated vessels and therefore is vulnerable to further reductions in BP. This has been demonstrated in humans20 and emphasizes the need for judicious BP management.

Recent studies have shown that higher systolic BP on presentation is associated with lower revascularization rates in patients treated with intravenous rt-PA21 or mechanical thrombectomy.22 Higher pretreatment systolic BP levels have also been associated with poorer degrees of collateral flow on pretreatment angiography and poor collateral flow has been associated with lower recanalization rates after mechanical thrombectomy. The precise mechanisms underlying the relationship between BP, collateral flow and treatment response to reperfusion therapy have yet to be elucidated, but may be related to opposing hydromechanical forces (antegrade BP versus retrograde leptomeningeal collateral flow) creating a trans-clot pressure gradient that defines the degree of thrombus impaction into the cerebrovasculature.22 These observations contrast with the broadly accepted theory that a hypertensive response may protect the brain by increasing perfusion pressure to the penumbral tissue through collateral or partially occluded arteries. Therefore, at present there are conflicting physiological data in terms of BP management in the setting of reperfusion therapies.

On presentation to the neurointerventional suite, the patients with acute stroke may or may not have received intravenous rt-PA. These two scenarios should be handled slightly differently from the standpoint of BP management.

Following intravenous thrombolytic therapy

The immediate risk after treatment with intravenous tPA is hemorrhage. This risk has been shown to correlate with systolic BP levels and MAP, and is the source of the recommendation from the 2007 American Stroke Association guidelines for a systolic BP that should be maintained under 180 mm Hg and diastolic BP under 105 mm Hg in patients who have received thrombolytic therapy.23 Because of the risk of worsened perfusion in the ischemic penumbra, BP should not be lowered unless it exceeds these limits. There are no data on the best agent to use if BP lowering is required. These limits should be maintained throughout the duration of the procedure. In the immediate postprocedure period, no firm data exist to support specific recommendations for BP. BP should be allowed to autoregulate up to systolic BP 180 mm Hg and diastolic BP 105 mm Hg without interference. Risk factors for clinically significant hemorrhagic conversion in acute revascularization trials are use of thrombolytic therapy, dose of lytic agents, edema or mass effect on head CT scan, increased stroke severity by the NIH stroke scale (NIHSS) and age. Other risk factors may be hyperglycemia, concurrent heparin use, timing of therapy and timing of successful recanalization.24

In the absence of intravenous thrombolytic therapy

In the absence of definitive benefit, the American Society of Anesthesiologists and the European Stroke Initiative both recommend against routine lowering of BP unless it repeatedly exceeds 220 mm Hg systolic or 120 mm Hg diastolic in the acute period or is resulting in active end-organ damage such as myocardial infarction.23 This parameter should be carried into the interventional environment in the patient who has not received intravenous tPA. When recanalization commences through the post-treatment period, BP should be brought down to the limits proscribed for patients after thrombolytic therapy, with systolic BP <180 mm Hg and diastolic BP <105 mm Hg. These limits should be maintained by the neurological critical care unit for at least 24 h after the procedure is complete. The expectation should be that BP will gradually trend back towards the patient's normal, and that the process will occur more rapidly in patients who have achieved good angiographic results.

Even though the concern that BP may affect hemorrhagic conversion after interventional procedures is not fully supported by the current literature data, we often aim for lower postprocedural BP levels in patients who have achieved good degrees of reperfusion (≥thrombolysis in cerebral ischemia 2b) under the assumption that the risk of reperfusion injury is theoretically higher than the chances of collateral dependence in this setting.

Vascular stenosis

Endovascular angioplasty and/or stenting are utilized for stenosis of the extracranial (cervical) and occasionally intracranial arteries. Despite some similarities in periprocedural BP management, these two entities will be dealt with separately.

Carotid stenoses and BP

In recent years carotid artery stenting has emerged as an alternative to carotid endarterectomy. Before the procedure the patient should be maintained at normal BP unless their examination has acutely demonstrated BP dependence, in which case the lowest BP tolerated is preferred. During the angioplasty, allowing slight BP elevation is not unreasonable to compensate for the period of vascular occlusion by the balloon. However, BP should be controlled at preprocedure levels immediately after angioplasty is performed.3

After stent placement BP can either rise or fall, but these changes are usually transient. Bradycardia can also be observed from baroreceptor stimulation in the carotid body. This variability should be anticipated and can be managed with intravenous infusions of antihypertensive or pressor agents as needed. The occasional patient in whom this response is not transient will usually require step-down or admission for maintenance of ongoing pressor therapy.

In the postprocedure period, control of BP is of paramount importance. Hyperperfusion syndrome (possibly complicated by intracranial hemorrhage) is well described after carotid endarterectomy with an incidence of 1.1%. Figures for the incidence of these complications after stenting are yet to be well-defined, but are likely to be similar to the rates seen with endarterectomy. Current understanding is that the chronic hypoperfusion induced by severe carotid artery disease causes a compensatory dilation of cerebral resistance vessels distally to maintain CBF through the normal autoregulatory response.25 This dilation leads to the loss of autoregulatory ability in response to BP changes. Relieving the proximal carotid stenosis by stent placement results in an increase in CBF, hence hyperperfusion. This syndrome is preventable and therefore preprocedural identification of risk factors for hyperperfusion is crucial. These factors include ICA stenosis >90%, significant contralateral ICA disease or occlusion, poor collateral flow through the circle of Willis or leptomeningeal vessels, hypertension and recent stroke or cerebral ischemia.26 During the procedure, in addition to direct BP control, the risk of hyperperfusion syndrome developing can be reduced by limiting the duration of balloon inflation and deploying embolic prevention devices to minimize procedural brain ischemia.3 Patients at high risk for postprocedural hyperperfusion should be maintained normotensive. However, some have suggested that even normal BPs may be deleterious in patients at high risk for hyperperfusion.27 Staff should be made aware of the importance of BP control and should frequently monitor for the development of clinical features of the hyperperfusion syndrome. These include an ipsilateral throbbing headache (frontal, temporal or retro-orbital), nausea, vomiting, seizures and focal deficits. In patients who develop clinical symptoms of hyperperfusion or have a documented middle cerebral artery velocity on transcranial doppler TCD of twice their baseline, consider withholding antiplatelet or anticoagulant agents until the BP is optimally controlled and symptoms have receded.28

β Blockers are a good choice for BP control in these patients unless bradycardia limits their use, in which case nicardipine can be used. After the procedure BP has to be controlled for at least 2 weeks and the neurointerventionalist must communicate this to the patient, family and care team.26 The key is prevention, and this is most readily accomplished by vigilant control of systemic BP both peri- and postprocedurally.

Intracranial vascular stenoses and BP

The optimal treatment for patients with symptomatic intracranial atherosclerosis disease (ICAD) is unknown. Percutaneous transluminal intracranial angioplasty has reported good angiographic and short- and mid-term clinical outcomes that are improved compared with the natural stroke history in patients with symptomatic ICAD.29 Previous practice advocated allowing patients with ICAD to be maintained at higher BP to avoid hypoperfusion. However, a recent post hoc analysis of the Warfarin-Aspirin Symptomatic Intracranial Disease (WASID) trial has shown that patients in whom BP remains chronically elevated actually experience an increased risk of stroke in the same territory, probably due to the effects of elevated BP on the progression of atherosclerosis.2 The optimal timing of BP reduction remains an issue, but these patients should ideally be normotensive coming into the angiography suite, unless they have an examination demonstrating BP dependency. Risks of reperfusion injury that resembles hyperperfusion syndrome have been documented since the first report in the literature about this phenomenon after stenting.30 Identifying these patients before the procedure by evaluation with diffusion-weighted MRI might be useful to identify areas of subtle infarction potentially at risk for reperfusion injury. Perfusion studies (Xe-CT, single-photon emission CT or perfusion MRI) might allow estimation of the degree of revascularization needed to improve but not overwhelm the vascular territory. In the absence of sophisticated imaging, the extent of periventricular white matter disease on imaging may be a proxy to identify patients with impaired autoregulation. In patients identified as being at risk in the periprocedural period, very tight control of BP is required after the procedure in the normotensive to slightly hypotensive range. In the particularly high-risk patient the interventional procedure may be modified, with perhaps less aggressive staged angioplasty with only small incremental improvements in a focal stenosis (a technique advocated previously to reduce the risk of procedural rupture). This may reduce risk of hyperperfusion by allowing restoration of autoregulation, although firm data are lacking. In that setting, BP should be kept normotensive to hypotensive.31

Cerebral aneurysm and BP

Cerebral aneurysms are encountered in three scenarios during interventional procedures:

  1. Unruptured, during diagnostic angiogram or therapeutic coiling

  2. Acutely ruptured, during diagnostic angiogram or therapeutic coiling

  3. During vasospasm assessment or therapy

Unruptured, during diagnostic angiogram or therapeutic coiling

BP parameters during evaluation and treatment of unruptured aneurysm should follow standard guidelines. Patients should be maintained in the normotensive range for the majority of the procedure. Allowing slight BP elevation during balloon occlusion may be helpful in compensating for transient alterations of flow in the cases where balloon-assisted coiling is required. However, during the coiling process, keeping BP slightly lower may reduce the transmural pressure the aneurysm experiences. These are both theoretical considerations and lack supportive data.

Acutely ruptured, during diagnostic angiogram or therapeutic coiling

The risk of a ruptured aneurysm rebleeding is approximately 20% in the first 2 weeks and 30% in the first month.32 Patients with poor grade SAH resemble, in many respects, patients after brain trauma where CPP needs to be maintained in the face of elevated ICP. Systolic BP >160 mm Hg or MAPs >130 mm Hg have been correlated with very early rebleeding, presumably by increasing transmural pressure and dislodging clot from the aneurysm dome. This is balanced by the fact that MAPs <70 mm Hg may exacerbate acute brain injury because of impairment in cerebral perfusion. A reasonable BP target in the acute ruptured aneurysm case is a MAP of 80–130 mm Hg or systolic BP of 90–140 mm Hg. In the absence of ICP elevation, systolic BP rather than MAP is perhaps the most desired parameter as this will directly limit the maximum transmural pressure. To illustrate, two patients with BP of 170/40 and 140/56 both have MAPs of 84 but the latter patient has a lower maximal transmural pressure. If ICP monitoring is available (eg, bolt or external ventricular drain), aiming for CPP targets 50–70 mm Hg are reasonable, attempting not to violate the upper limits of MAP and systolic BP targets.33 After the aneurysm has been secured, BP can be allowed to autoregulate with more liberal goals.

During vasospasm assessment or therapy

Fifty to 70% of patients with SAH will develop radiographic vasospasm, but only half will develop symptoms of delayed ischemic deficit.34 Volume contraction can further aggravate marginal CBF as a result of vasoconstriction. Prior to the patient's arrival in the angiography suite, typical therapy involves elevation of BP either by allowing the patient to autoregulate higher or using vasopressors to achieve higher goals. Central venous pressure is also increased using colloid and crystalloid infusions.35 However, recent data suggest that induced hypervolemia is an ineffective approach and may actually be detrimental.36 Indeed, moderate induced hypertension with euvolemia has been shown to improve brain oxygenation and appears to be superior and safer than either hypervolemia/hemodilution or aggressive hypertension/hypervolemia/hemodilution therapy.37 38 Moreover, cardiac output optimization with dobutamine has been shown to reverse flow deficits from SAH-induced vasospasm independent of BP, and this approach may be safer and better tolerated than induced hypervolemia or pharmacological BP augmentation with phenylephrine.39

Patients with vasospasm typically are significantly hypertensive on presentation to the angiography suite, with systolic BP as high as 200–240 mm Hg. Pressures should be maintained at these high levels during the procedure, with particular attention to the fact that intra-arterial infusion of nicardipine, verapamil, nimodipine and papaverine may cause transient drops in systemic BP often necessitating additional intravenous pressor doses. Given its positive inotropic effect, milrinone may be an alternative in patients who develop significant hypotension with other intra-arterial vasodilators. Caution must be exercised in patients who already have areas of delayed cerebral ischemia due to the risk of hemorrhagic conversion of the ischemic bed, which is likely to be exacerbated by elevated BP. In situations in which the arterial feeders into an area of partial ischemia are dilated via interventional approaches after treatment, the systolic BP should be lowered to <180 mm Hg if possible.

Arteriovenous malformations and BP

Arteriovenous malformations (AVMs) are increasingly being detected in the unruptured state, probably related to the expansion of modern non-invasive imaging techniques. Common presentations are hemorrhage or seizure. Treatment has evolved, with wider endovascular options and increased combined modality treatment protocols.40 There are two opposing theories in relation to the hemodynamics of AVM therapy. According to the Normal Perfusion Pressure Breakthrough (NPPB) Theory, postoperative hemorrhage and edema are caused by a failure in autoregulation in the ischemic brain around the AVM. The rationale is that chronic hypoperfusion in the brain surrounding an AVM leads to maximal chronic vasodilation which results in an inability to vasoconstrict in response to the normal cerebral perfusion pressure after the AVM has been embolized or resected. According to this theory, staged reduction of AVM and aggressive BP reduction are essential to prevent malignant postoperative hemorrhage and edema. However, many intraoperative studies have shown maintained autoregulation in the region surrounding an AVM both before and immediately after its resection, even in cases subsequently complicated by edema and hemorrhage. Conversely, the Occlusive Hyperemia Theory hypothesizes that malignant postoperative hemorrhage and edema are caused by either arterial stagnation and obstruction or venous outflow obstruction, which are direct results of embolization or resection of the AVM. In this situation, postoperative hypotensive therapy could therefore be more deleterious than beneficial.

In the setting of intraprocedural sacrifice of an en passage feeding vessel, low or even normal BP may result in ischemic deficits due to poor collateral perfusion pressure. Careful analysis of the angiographic data is therefore mandatory in defining the BP goal on any given patient. Periprocedural BP approaches for the unruptured and ruptured AVM are discussed below.

Unruptured arteriovenous malformations

Because unruptured AVM treatment is usually non-emergent, pre-existing medical conditions should be optimized, including chronic hypertension. Ten per cent of patients with AVM have lesions complicated by intracranial aneurysms, and elevated BP (transiently or long-term) may increase transmural pressure and the risk of rupture. However, the risk of AVM rupture during induction is probably low, based on inferential evidence. During open procedures, induced hypotension is not infrequently used during the AVM resection, especially in large AVMs that have a deep arterial supply,41 and this technique may be applied to interventional cases to slow flow through the fistula. Heidenreich et al reported on the bleeding complications after 125 consecutive AVM embolizations performed on 66 patients using n-butyl cyanoacrylate as the embolic agent. Intracerebral hemorrhages occurred in seven patients. After adjusting for age and extent of AVM reduction, significant differences in outcome were found between patients monitored in the interdisciplinary operative ICU compared with those in the medical ICU or stroke unit. This difference in outcome was thought to be potentially related to tighter BP control. A partial AVM reduction of >60% (OR 18.8) and older age (OR 2.5 for every decade) were strong risk factors for hemorrhage.42 Therefore, in general, aggressive BP control to a level that at least approximates the normal range is sound practice in the absence of mitigating circumstances.

Ruptured arteriovenous malformations

In the event of acute endovascular evaluation and treatment of ruptured AVMs, management of BP during the procedure should be along the lines of management of any patient with intracerebral hemorrhage (ICH)—that is, BP should be kept controlled due to concerns for expansion of the bleed, which is especially true for hemorrhage resulting from a ruptured aneurysm in which the risk of continued bleeding or rebleeding is presumed to be highest. Concerns that aggressive BP reduction might exacerbate perihematomal ischemia have been difficult to prove in patients with ICH, but may be more of an issue in patients with AVM owing to possible impaired autoregulation in the brain tissue around the bleeding AVM. Hence, overly aggressive BP reduction may theoretically induce additional ischemic insults in these patients. It seems reasonable to aim for a periprocedural systolic BP of 100–160 mm Hg or MAP <130 mm Hg, as per the American Heart Association guidelines for ICH.43 However, many physicians will advocate lower BP goals, mostly when aggressive embolization or complete resection is performed. A summary of the American Heart Association guidelines for periprocedural BP management in AVM treatment is shown in box 1.

Box 1

Box 1 Summary of the American Heart Association guidelines for periprocedural BP management in AVM therapy40

  • Direct transduction of arterial pressure is indicated for intracranial embolization procedures, especially with manipulation of systemic pressure with vasoactive agents.

  • Profound deliberate systemic hypotension may be induced while the interventionist prepares the glue for injection. Hypotension slows the flow through the fistula and provides for a more controlled deposition of embolic material, particularly the cyanoacrylates.

  • In the setting of inadvertent vascular occlusion, a method to increase distal perfusion is BP augmentation with or without direct thrombolysis.

  • The systemic BP may be increased to drive collateral flow to the ischemic area as a temporizing measure. Deliberate hypertension in the face of symptomatic cerebral ischemia from vascular occlusion during AVM embolization should not be avoided because of fear of rupturing the malformation.

Conclusions

Firm parameters and level 1 evidence are lacking for BP recommendations for many of the conditions treated by endovascular means. This review is based on best available data. More research is needed on patients in the angiographic environment to produce recommendations derived for prospective multicenter randomized trials as a means of better informing the specialty in the future and providing safer more effective patient care.

References

Footnotes

  • Competing interests None.

  • Provenance and peer review Commissioned; not externally peer reviewed.

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