Hyperdynamic therapy: the nurse's role in the treatment of cerebral vasospasm.
Approximately 25,000-30,000 people in North America annually experience subarachnoid hemorrhage due to a ruptured cerebral aneurysm.[5,10] About 10% f people with ruptured cerebral aneurysm die prior to hospital admission. Of those presenting for medical treatment 50-60% die and another 20-30% have varying degrees of permanent ischemic neurological deficits due to cerebral vasospasm.[10,13,24,25]
Neuroscience nurses play an important role in the detection of vasospasm and prevention of permanent deficits following cerebral aneurysm rupture. This article discusses aneurysmal subarachnoid hemorrhage and its relationship to cerebral vasospasm. The use of hyperdynamic therapy and the role of the nurse are presented.
It is not known how or why aneurysms form, or what causes them to rupture. Current theories for the origin of cerebral aneurysms include: weakness within the vessel's intima layer, postnatal deterioration of the intimal layer, trauma to the intimal layer, arterial sclerosis, infection and inflammation.[2,13] Hypertension, smoking, oral contraceptives, alcohol use, cocaine, amphetamine use, intercourse and pregnancy have been associated with aneurysm rupture.[2,5,22]
Rupture of a cerebral aneurysm usually causes bleeding into the subarachnoid space producing a subarachnoid hemorrhage (SAH). Associated signs and symptoms may include: sudden onset of headache, described as " the worst headache of my life," nausea and vomiting, seizures, syncope, decreased level of consciousness and bloody cerebrospinal fluid. Other signs and symptoms that may appear are meningeal irritation characterized by Kerning's sign, Brudzinski's sign and nuchal rigidity, photosensitivity, abnormal extra ocular movements, facial droop, diplopia, aphasia/dysphasia, contralateral pronator drift and hemiparesis.[2,5,13]
Cerebral vasospasm (VSP) accounts for 20-30% of the diffuse ischemic neurologic deficits leading to ischemia, infarction or death in patients with SAH. Vasospasm is described as: 1) clinical, which is evident on neurologic exam without confirmatory diagnostic tests, characterized by confusion, or decreased level of consciousness (LOC), 2) radiographic, angiographically seen as a narrowing of local or diffuse cerebral arteries and may or may not be symptomatic, or 3) symptomatic, when the delayed ischemic neurological deficits correspond to the region of spasm identified on angiogram.[5,6,17,28] Initial diagnosis is made on the basis of signs and symptoms and the exclusion of other sequela with definitive diagnosis by cerebral angiography. Transcranial doppler (TCD) Studies following SAH may be used as a bedside tool to further evaluate VSP.[5,17,28]
The exact pathophysiology of VSP is unclear. Proposed theories underlying VSP are: 1) mechanical factors involving the interaction of the subarachnoid blood on the arterial smooth muscle cells causing unusual contraction, 2) the actual breakdown of the subarachnoid blood leading to the release of oxyhemoglobin, serotonin, prosta-glandin, catecholamines and calcium resulting in arterial spasm, 3) localized reaction due to the irritation caused by the subarachnoid blood or intraoperative trauma leading to proliferation of smooth muscle. VSP is currency under intense exploration.[4,8,10,18,23,28]
The potential for vasospasm corresponds to the Hunt and Hess grades of SAH (Table 1). Grades 0-II have a decreased probability, and grades III-V have an increased likelihood of VSP. The likelihood of VSP also increases in those with a history of hypotension and dehydration, and within 3-14 days posthemorrhage. [5,13,19,28] Table 1. Hunt and Hess Classification of Aneurysms
Grade 0 Unruptured aneurysm Grade 1 Asymptomatic or mild headache and slight nuchal rigidity Grade 2 Mild bleeding -- moderate to severe headache, nuchal rigidity and cranial nerve palsy Grade 3 Moderate bleeding -- patient is lethargic with headache or nuchal rigidity, no hemispheric neurological signs. May also represent a patient who is nearly recovered from hemorrhage and is alert but has residual neurological deficits such as hemiparesis or dysphasia Grade 4 Moderate to severe bleeding -- patient is stuporous, moderate to severe hemiparesis, early decerebrate rigidity Grade 5 Severe bleeding -- patient in deep coma, decerebrate rigidity, moribund appearance
Computed tomography (CT) scans can also help predict the possibility and severity of VSP by pinpointing the location and size of the hemorrhage.[1,2.5] Severe VSP tends to occur in the area of the thickest layers of subarachnoid blood as seen on CT scan, whereas a focal thin hemorrhage has a low likelihood of Vsp.1.5,26 Midline aneurysmal rupture, with hemorrhage in the Sylvian fissure tend to be associated with the most severe VSP. Vasospasm is more prevalent with the rupture of the anterior cerebral and middle cerebral arteries, affecting the cortical motor and sensory areas, Broca's area, internal capsule, temporal lobe and corpus callosum.[1,5,28]
Consequences of Vasospasm
Delayed ischemic deficit from arterial narrowing is the possible consequence of VSP. This is directly related to a decrease in the cerebral blood flow and the cerebral perfusion pressure, and can be complicated by interruption of the blood brain barrier due to surgical intervention and vasogenic edema. The degree of ischemic injury correlates with the severity of the spasm and die vessels involved. If ischemia progresses to infarction, the initial symptoms can become permanent deficits of varying magnitudes.[1,2,6,19] Death can ensue if the ischemia is severe enough to cause edema, midline shift and brain herniation.[11,28]
The initial onset of VSP occurs 3-14 days post SAH, but is most commonly seen between days 5-8 posthemorrhage, and rarely seen after day fourteen. Vasospasm can continue for several weeks and has been known to vacillate between mild and severe over its course.[13,19]
The neuroscience nurse is usually the first to identify deficits during frequent neurological assessments. The neurological assessment should include observing for any of the following: confusion, lethargy, disorientation, change in level of consciousness, new or increased headache, hemiparesis, contralateral pronator drift of upper extremities, seizures, mild rise in basal temperature, labile blood pressure or leukocytosis, which can suggest VSP.[5,6,7,27] One should know that any subtle change from baseline neurological examination, such as confusion, can be the initial sign of VSP until proven otherwise and needs to be addressed promptly.
When clinical VSP is suspected, the patient may first undergo a CT scan to rule out rebleeding, hydrocephalus or surgically-induced infarction as the cause of changed neurological status. A transcranial Doppler (TCD) study, which is easily performed at the bedside, provides information regarding blood flow velocities and direction of flow through major cerebral arteries to determine if vessel narrowing is suggested. An increase velocity, greater than than 120 Vm cm/sec, is indicative of VSP. Serial TCD studies allow treatment to be tailored to patient's response during hyperdynamic therapy.[1,6,27] Angiography may be used to give a definitive diagnosis, confirm specific vessels in spasm and provide treatment via balloon angioplasty and/or papaverine.[1,5,6,28]
One approach currently used for cerebral vasospasm is hyperdynamic therapy, also known as Triple-H therapy, which utilizes induced hypervolemia, hemodilution and hypertension. The therapy is initiated when the first signs and symptoms of VSP are noted or when the potential for VSP is high. The goal is to increase the cerebral blood flow by passively dilating vessels and secondarily increasing cerebral perfusion pressure (CPP) without increasing the intracranial pressure (ICP). To improve the CPP, the mean arterial pressure (MAP) is elevated by increasing the cardiac index and decreasing the systemic vascular resistance.
Increasing intravascular volume and decreasing blood viscosity with colloids and crystalloid, and the utilization of dopamine or dobutamine to increase the MAP may result in an improved CPP. Theoretically, this decreases the severity of vasospasm and prevents or minimizes ischemia.
Hypervolemic hemodilution is achieved by increasing blood volume through infusions of crystalloid (D5NS or D5LR), colloids (albumin, mannitol, fresh frozen plasma), or whole blood, which decrease the blood viscosity. Crystalloids are usually given first at a rate of 125-300 cc/hr depending on the level of hydration, cardiac function and degree of VSP Colloids are added as needed to achieve a positive fluid volume of 1-2 liters per day, maintaining die hematocrit at or below 40%, increasing the pulmonary capillary wedge pressure (PCWP) to 12-18 mm Hg and the central venous pressure (CVP) to 10-12 nm Hg as the desired parameters.[13,17,19,28] In patients with normal cardiac function, enhancing the PCWP to 12-14 nun Hg should result in attaining the necessary effect of hypervolemia. Patients that present with suboptimal cardiac function due to congestive heart failure or recent myocardial infarction should be treated more cautiously, and will require higher filling pressures which can be met by raising the PCWP to 14-18 mm Hg.[15,16]
When hypervolemic therapy does not cause a corresponding increase in blood pressure, vasopressors such as dopamine infused at 5-20 mcg/kg/minute, dobutamine at 5-10 mcg/kg/ minute and phenylephrine up to 180 mcg/minute can be added. To combat the effect of dobutamine decreasing PCWP, colloids are infused at rates up to 30 cc/hr. Patients that respond well to increased PCWP through the use of fluids and vasopressors have cardiac indices (CI) between 5-6 liters/ minute/m[2.8,24]
The hypertension aspect of die therapy is based on the patient's baseline blood pressure if known. Prior to aneurysm clipping systolic blood pressure should be kept below 160 mm Hg, and dopamine and dobutamine should be avoided if Possible due to the potential for rebleeding, increased cerebral edema and increased ICP.[17,19,11] It is preferable to clip the aneurysm prior to the initiation of Triple H therapy if possible to minimize the potential of these occurrences. In patients presenting with moderate to severe VSP where the surgeon chooses to delay aneurysm clipping, the therapy is adjusted to keep SBP 130-150 mm Hg using dopamine or nitroprusside if necessary.[20,21] Surgeons may prefer clipping instead of delaying in the presence of VSP so as to allow more leeway for treatment with Triple H therapy.
After aneurysm clipping the SBP is allowed to increase up to 60 mm Hg above baseline but should be kept below 220-240 mm Hg.[13,15,16,17,19,20] The patient who has a SBP that is greater that 60 mm Hg above baseline or greater than 220-240 mm Hg should be treated by decreasing hypervolemia and hemodilution, and, if necessary add antihypertensive therapy utilizing nitroprusside. Or if a cardiac history exists, nitroglycerine may be used to maintain SBP only 20-60 mm Hg above baseline. Therapy continues until vasospasm has resolved as documented by TCD, angiography or improved neurological status. When vasospasm has resolved the therapy is slowly weaned off starting with the vasopressors and then colloids.[1,7]
The use of calcium antagonists in conjunction with hyperdynamic theraphy is by physician preference. The standard is to use calcium antagonists as soon as the patient is diagnosed with a SAH. Some physicians wait until signs and symptoms of VSP appear, while still others never use them due to the hypotension that may occur [23,26]
Complications of Hyperdynamic Therapy
Treatment with hyperdynamic therapy is not without risk. The patient should be monitored for signs and symptoms of pulmonary edema, congestive heart failure (CHF), cerebral edema and systemic complications of prolonged vasopressor us. Myocardial infarction and hypertensive cerebral hemorrhage may also occur. Continuous cardiac/hemodynamic monitoring and frequent physical and neurological assessments are essential.
Modifying the hypervolemia portion of the therapy is indicated when contraindications to hyperdynamic therapy are present. These contraindications include increased intracranial pressure, cerebral edema, cerebral infarction, pulmonary edema, CHF, recent myocardial infarction, and adult respiratory distress syndrome.[3,7,24]
Obtaining a thorough nursing history and assessment can help to indicate the probability and degree of vasospasm and serve as a baseline when initiating a treatment regimen. A detailed history of events prior to the presenting complaint can help determine the date of initial bleed if prolonged symptomology is present. The history should include all currently prescribed medications and any illicit drug or alcohol use as they may potentiate SAH as well as a full cardiac renal, smoking, diabetes, hypertension and past headaches history. Familial history of aneurysm, brain attack and hypertension should also be noted.
Cardiopulmonary assessment requires special attention to determine complicating conditions such as congestive heart failure, myocardial infarction or pulmonary edema. Medications taken prior to the SAH, such as warfarin sodium or antihypertensives, must be evaluated because of a possible potentiation or extension of the initial bleed and interference with future treatment. Compliance in taking prescribed medications and possibility of uncontrolled hypertension must be considered. A baseline chest x-ray, 12 lead electrocardiogram (ECG) and vital signs should be obtained. Be aware that not all ECG changes are cardiac in origin as SAH may also contribute to cardiac problems. Arrhythmias associated with SAH and VSP may occur from catecholamines released during the breakdown of the extravasated blood. Nonetheless patients with ECG changes should have the event ruled out.
Upon admission, baseline laboratory values such as a full chemistry panel, serum osmolality, bleeding times, complete blood count with differential, liver function tests, arterial blood gases and urinalysis should be obtained. Abnormal conditions should be identified and corrected.
Ongoing nursing assessments during treatment should include hourly neurological and physical assessment, ICP monitoring if a ventriculostomy is present, vital signs and intake and output assessments. If a pulmonary artery catheter is in place, cardiac indices should be monitored according to the patient's condition. A chemistry panel with serum osmolarity every 4-6 hours should be considered if the patient has a high or low urinary output, abnormal serum sodium to rule out diabetes insipidus.
Physician notification is warranted for increased urinary output with a corresponding decrease in specific gravity, laboratory abnormalities, deterioration of neurological status, increased ICP, cardiac performance measures not in the desired parameters and ECG or pulmonary changes. Nursing actions are initiated according to a plan of care (Table 2) as well as new medical directives.
Case Study # 1
JB, a 34-year-old single female employed as an office manager, with a history of migraine headaches and cigarette smoking of one pack per day for 16 years, presented to the physicians office with a complaint of worsening migraine. She was treated with diazepam and acetaminophen with codeine. Two days later she was admitted to the neurosurgical intensive care unit (NSICU) with complaints of the worst headache of her life and generalized seizure. Her initial CT scan revealed diffuse SAH (involving the basilar cisterns, sylvian fissure, anterior hemispheric fissure and temporal tips) with mild to moderate hydrocephalus. Admitting diagnosis was Hunt and Hess grade Ill SAH secondary to possible ruptured cerebral aneurysm. She was oriented to person and time, confused to place and situation and lethargic with periods of severe agitation. Her neurologic exam was: pupils right 4 nun, left 3 mm; both reacted briskly with intact extraocular movements (EOMs); strength in all extremities was normal and SBP was 100-120 mm Hg. Medications after admission included phenytoin, phenobarbital for sedation, nimodipine, dexamethasone (to minimize cerebral edema) and cimetidine. Intravenous fluid (IVFs), of D5NS with 20 mEq of potassium chloride was infused at 100 cc per hour.
A four vessel cerebral angiogram was performed revealing a large posteriorly-directed right internal carotid/posterior communicating aneurysm; right anterior choroidal aneurysm was also noted. Neurological assessment after 24 hours showed orientation to person, place and time, pupils equal and reactive to light (PERL), a new left pronator drift, photosensitivity and nystagmus were noted.
The following day, JB underwent a temporal craniotomy for the clipping of both aneurysms without complication. Postoperatively, she was noted to be increasingly confused, restless, with a left pronator drift and right eyelid ptosis. Her IVFs were increased to 250 cc per hour and a pulmonary artery catheter was placed. Dopamine at 8 mcg/kg/minute to maintain SBP [is greater than] 140 mm Hg was begun and titrated up to 20 mcg/kg/minute. 5% albumin at 250 cc every 6 hours as needed for a SBP less than 150 mm Hg and a mannitol 20 gm bolus was given for immediate plasma expansion. A pitressin infusion was titrated to decrease high urinary output of greater than 500cc per hour and lower serum osmolarity. Her PCWP was 17 mm Hg and CI 6.5 l/minute/[m.sup.2]. She continued to have periods of confusion and restlessness, but showed improvement in left pronator drift during postoperative day 2.
Transcranial Doppler studies were done on postoperative days 3, 4 and 5 showing increased flow velocities in the right middle cerebral artery of greater than 180 Vm cm/sec. Her serum sodium dropped to 128 meq/l and 3% saline was infused at 30 cc/hour for six hours resulting in a sodium level of 132 meq/L. A postoperative angiogram on day 5 indicated severe vasospasm in the right anterior communicating artery (ACA) and middle cerebral artery (MCA). The aneurysm clips were intact without evidence of rebleeding.
Hyperdynamic therapy was continued with gradual weaning of dopamine from 20 mcg/kg/minute and IVFs as VSP improved. A Transcranial Doppler study on day 10 showed moderate vasospasm in the right ACA and MCA. Her neurological status continued to improve but increased confusion was noted whenever SBP decreased to less than 130 mm Hg. Right ptosis and short-term memory deficit continued without change. The PCWP was maintained at 12-18 nun Hg with a CI of 5-7 1/minute/[m.sup.2].
A persistent increase in left pronator drift and confusion were noted on day 13 with a TCD study showing bilateral ACA and MCA spasm with velocities of 145 to 157 Vm cm/sec. Dopamine was reinstituted up to 18 mcg/kg/minute with IVFS increased to greater than 250 cc/hour with normal saline boluses to keep SBP [is greater than] 150 mm Hg. IVFs were further increased to 500 cc/hour and boluses of 5% albumin 250 cc were given to increase PCWP above 12 mm Hg and to maintain SBP greater than 160 mm Hg. Dopamine was slowly weaned off by day 20 but total IVFs continued at 500 cc/hour with improving neurological status. No further pronator drift and a slight improvement in short-term memory were noted. The pulmonary artery catheter was discontinued, and physical and occupational therapy were started.
On day 23, a TCD showed only mild spasm in the right ACA and MCA. Fluids were continued at 250 cc/hour with SBP maintained at [is greater than] 30 mm Hg and neurological improvement continued. Hyperdynamic therapy was discontinued on day 27 with TCD studies no longer showing elevated velocities; neurological status was stable. JB was transferred to the neurosurgical step down unit where physical therapy and occupational therapy continued. She was discharged from the hospital on day 30 with occasional mild headaches and short-term memory loss. Five months after discharge JB was able to return to work on a part-time basis.
Cast Study #2
DM is a 56-year-old female, widow and mother of four, with a history of migraine and a one pack per day smoking history. She initially presented to an outlying hospital with a complaint of a sudden pop in her neck followed by the worst headache of her life, nausea and dizziness. There were no seizures, syncope or photophobic events. She was treated at that time for vascular headache with sumatriptin and discharged home. She continued to complain of headache and followed up with her private physician the next day, who diagnosed a cervical strain and headache, treating her with a soft cervical collar, cyclobenzaprine HCL (Flexeril) and analgesics. Two days later she showed no improvement; a CT scan was done which showed a SAH. The following day (day 5) an angio-gram confirmed a large basilar tip aneurysm. She was transferred to our facility and admitted to the NSICU for further treatment of her Hunt and Hess Grade I SAH.
Her neurological exam upon admission showed her to be alert and oriented. Her pupils were equal and reactive to light with EOMs intact. She was able to follow commands, move all extremities with normal strength and speak clearly.
On admission, IVFs of D5NS with 20 mEq of potassium chloride was started at 100 cc/hour. Medications ordered included phenobarbital for sedation and anti-seizure prophylaxis, nimodipine to minimize VSP and acetaminophen for headache. SBP was maintained in a range of 120-140 mm Hg.
An additional four vessel angiogram was completed showing a large basilar tip aneurysm extending left into the interpeduncular region. A CT scan of the head showed no hydrocephalus or further hemorrhage. Aneurysm clipping was delayed due to the need for coordinating surgical specialities to utilize cardiac by-pass during the surgical clipping. This was the first time this procedure was to be utilized at our facility and time was needed to coordinate the surgical groups and operating room necessary.
Her neurological status remained stable. On day 11, a right subtemporal craniotomy was performed to clip the basilar tip aneurysm; cardiopulmonary bypass was used to decompress the aneurysm. An ICP monitoring device and pulmonary artery catheter were placed while in the operating room. An intraoperative angiogram was done showing the clips in good position with no filling of the aneurysms. The angiogram also showed left vertebral artery narrowing suggestive of VSP.
Postoperatively her neurological exam changed significantly. Her pupils were 4 mm and nonreactive; bilateral third cranial nerve palsies and a left hemiparesis were evident she was following simple commands and remained intubated. Cardiac indices were PCWP of 10-12 nun Hg, CI 4.0 1/minute/[m.sup.2] and CVP of 9-14 mm Hg. IVFs were increased to 120 cc/hour and 5% albumin 250 cc was added. Nitroprusside to keep SBP [is less than] 160 nun Hg and [is greater than] 120 mm Hg was also used. On day 12, a TCD study showed the right MCA in mild spasm. Additional medication added at this time included mannitol, dexamethasone and cimetidine. Nitroprusside was weaned off. Her pupils were now unequal with the left 5 mm and reactive, right 6 mm and nonreactive. A CT scan of the head showed a 4.5 x 3.0 cm right temporal lobe hematoma with mass effect requiring evacuation of the hematoma and removal of the ICP monitoring device.
DM's level of consciousness decreased on day 13 and hemiparesis worsened. Treatment continued as above with the IVFs increased to 250 cc/hour. PCWP was 9-14 mm Hg, CI 3.0-4.0 1/minute/[m.sup.2] and CVP 7-11 mm Hg. She was slightly improved over the next few days with extubation, lessening hemiparesis, and improving third cranial nerve palsy. Pupils were unchanged though she had no vision in the right eye. Short-term memory loss and disorientation to place and time were noted. During this period IVFs were increased to a total of 400 cc/hour including normal saline and albumin.
By day 19, the TCD indicated the right MCA to be in the severe VSPrange with a velocity of 247 VM cm/sec requiring the addition of dopamine to 12 mcg/kg/minute and neosynepherine to 50 mcg/kg/minute to keep SBP [is greater than] 170 mm Hg. DM now had slight improvement in the right eye vision; her pupils were equal and reactive to light but the third cranial palsy remained. She was able to follow commands, but had occasional periods of confusion.
By day 22 the TCD showed mild VSP. Dopamine and neosynepherine were weaned off. Fluids were decreased to 300 cc/hour, the pulmonary artery catheter was removed with the last cardiac indices of PCWP of 6-10 mm Hg, CI 3.5 1/minute/[m.sup.2], and CVP 7 mm Hg. She remained unable to open or move her right eye, and was still confused to situation but otherwise oriented. Physical and occupational therapy were initiated.
DM was monitored closely in the NSICU for 2 more days then transferred to the neurosurgical step-down unit where she continued to have short-term memory loss, was unable to open her right eye and continued to have decreased vision. DM was transferred 3 days later to her local hospital for further rehabilitation.
Nurses caring for patients at risk of developing cerebral vasospasm are usually the first to identify the subtle to significant neurological changes through frequent neurological assessments. Understanding cerebral aneurysm rupture and the etiology, signs, symptoms and treatment for cerebral vasospasm is important for a positive patient outcome. Early identification of neurological deficits leads to quick initiation of treatment such as hyperdynamic therapy. Frequent neurological and cardiopulmonary assessment during hyperdynamic therapy are important to prevent or minimize systemic complications and prevent or decrease permanent neurological deficits.
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[1.] Barker E: Pages 282-288 in: Neuroscience Nursing. Mosby Yearbook, 1994.
[2.] Cook HA: Aneurysmal subarachnoid hemorrhage: Neurosurgical frontiers and nursing challenges. AACN Clin Issues 1991; 4(2):665-674.
[3.] Darby JM: Acute cerebral blood flow response to dopamine-induced hypertension after subarachnoid hemorrhage. J Neurosurg 1994; 80:857-864.
[4.] Flynn EP: Cerebral vasospasm following intracranial aneurysm rupture: A protocol for detection. J Neurosci Nurs 1989; 21:348-352.
[5.] Greenberg MS: Pages 711-745 in: Handbook of Neurosurgery, 3rd ed. Greenberg Graphics, 1993.
[6.] Grimes CM: Neurologic aspects of critical care: Cerebral balloon angioplasty for treatment of vasospasm after subarachnoid hemorrhage. Heart Lung 1991; 20(5):431-435
[7.] Hickey JV: Pages 517-530 in: The Clinical Practice Of Neurological and Neurosurgical Nursing, 3rd ed. JB Lippincott Company, 1992.
[8.] Hummel SK: Cerebral vasospasm: Current concepts of pathogenesis and treatment. J Neurosci Nurs 1989; 21:216-224.
[9.] Hunt WE, Hess RM: Surgical risk as related to time of intervention in the repair of intracranial aneurysm. J Neurosurg 1968; 28:14-19.
[10.] Kassell NF, Torner JC, Haley C, Kongable G: The international cooperative study on the timing of aneurysm surgery. Part I: Overall management results. J Neurosurg 1990; 73:18-36.
[11.] Kassell NF, Peerless SJ, Dunvard QJ, Beck DW, Drake CG, Adams HP: Treatment of ischemic deficits from vasospasm with intravascular volume expansion and induced arterial hypertension. Neurosurgery 1982; 11(3):337-342.
[12.] Kocan MJ: Electrocardiographic changes following subarachnoid hemorrhage. J Neurosci Nurs 1988; 20(6):362-365.
[13.] Kopitnik TK, Samson DS: Management of subarachnoid hemorrhage. J Neurology 1993; 56(9):947-959.
[14.] Lemons V, Chehrazi BB, Kauten R., Hein L, Wagner FC Jr: The effect of nimodipine on high-energy phosphates and intracellular pH during cerebral ischemia. J Neurotrauma 1993; 10(1):73-81.
[15.] Levy ML, Rabb CH, Vladimir Z, Giannotta SL: Cardiac performance enhancement from dobutamine in patients refractory to hypervolemic therapy for cerebral vasospasm. J Neurosurg 1993; 79:494-499.
[16.] Levy ML, Giannotta SL: Cardiac performance indices during hypervolemic therapy for cerebral vasospasm. J Neurosurg 1991; 75:27-31.
[17.] Levy ML, Giannotta SL: Induced hypertension and hypervolemia for treatment of cerebral vasospasm. Neurosurg Clin North Am 1990;1 (2):357-365.
[18.] Macdonald E: Aneurysmal subarachnoid hemorrhage. J Neurosci Nurs 1989; 21:313-321.
[19.] Manifold SL: Aneurysmal SAH: Cerebral vasospasm and early repair. Crit Care Nurse 1990; 10(8):62-71.
[20.] Origitano TC, Wascher TM, Reichman HO, Anderson DE: Sustained increased cerebral blood flow with prophylactic hypertension hypervolemic hemodilution ("Triple-H Therapy") after subarachnoid hemorrhage. Neurosurgery 1990; 27(5):729-737.
[21.] Ostsubo H, Takemae T, Inoue T, Kobayashi SH, Sugita K: Normovolemic induced hypertension therapy for cerebral vasospasm after subarachnoid hemorrhage. Acta Neurochir 1990; 103:18-26.
[22.] Rinkel GJE, VanGijn J, Wijdicks EFM: Subarachnoid hemorrhage without detectable aneurysm. Stroke 1993; 24(9):1403-1408.
[23.] Sikes PJ, Nolan S: Pharmacologic management of cerebral vasospasm. Crit Care Nurs Quart 1993; 115(4):78-88.
[24.] Solomon TA: Management of symptomatic cerebral vasospasm. Contemp Neurosurg 1990; 13(1):1-5.
[25.] Solomon RA, Fink ME: Current strategies for the management of aneurysmal subarachnoid hemorrhage. Arch Neurol 1987; 44:769-774.
[26.] Sosnowski C: Nimodipine: The use of calcium antagonists to prevent vasospasm following subarachnoid hemorrhage. J Neurosci Nurs 1990; 22(6):382-384.
[27.] Steinmeier R, Laumer R, Bondar I, Priem R, Fahlbusch R: Cerebral hemodynamics in subarachnoid hemorrhage evaluated by transcranial doppler sonography. Part 2: Pulsatility indices. normal reference values and characteristic in subarachnoid hemorrhage. Neurosurgery 1993; 33(1):10-18.
[28.] Weir B, Macdonald L: Cerebral vasospasm. Clin Neurosurg 1993; 40:40-55.
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|Author:||Campbell, Patricia J.; Edwards, Susan M.|
|Publication:||Journal of Neuroscience Nursing|
|Date:||Oct 1, 1997|
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