General Treatment of Stroke in Intensive Care Setting

Blood Pressure Management

Elevated blood pressure (BP) is common in patients presenting with ischemic stroke; about 85% will be hypertensive and almost half will have a BP greater than 160 mm Hg . The underlying mechanism of hypertension in stroke is thought to stem from the cerebral ischemic response, a derivative of the diving reflex. Many studies have demonstrated a U-shaped curve when it comes to BP—patients with low pressure, a systolic BP less than 140 mm Hg, have a worse outcome as do those with high pressure, a systolic BP more than 180 mm Hg; however, the exact reasons for this are complex and poorly understood. In patients who have received intravenous tissue plasminogen activator (t-PA), it is clear that the risk of hemorrhagic transformation correlates with high BP. In these patients, the target BP is less than 185/110 mm Hg before t-PA can be administered and less than 180/105 mm Hg for the next 24 h after administration . For patients who have not received thrombolysis, the conventional thinking has been to not treat hypertension unless the BP is very high. In theory, patients with persistent vessel occlusions may be pressure dependent and their condition may worsen if the BP is lowered too much. Recent randomized trials have challenged this view ; however, current guidelines recommend only treating hypertension when the systolic BP is greater than 220 mm Hg. In the setting of intra-arterial intervention, there are no guidelines as to what the optimal BP target should be. In general, before revascularization, and in the setting of poor collaterals, maintaining a systolic BP greater than 150 mm Hg to optimize perfusion is reasonable. After revascularization, the goal is to maintain the systolic BP close to normal and consider targeting an even lower pressure (systolic BP less than 140 mm Hg) if risk factors for hemorrhage are present, including diabetes mellitus, prolonged time to puncture, use of intravenous or intra-arterial t-PA, atrial fibrillation, and high NIHSS (National Institutes of Health Stroke Score) .

BP management in patients with intracerebral hemorrhage (ICH) has also been controversial. As arterial pressure may be a driving force in hematoma expansion, lowering the BP acutely would seem beneficial. Lowering it too much, however, has raised concerns that patients’ condition may worsen from reduced cerebral perfusion, especially in the setting of elevated intracranial pressure (ICP). A recent randomized control trial did demonstrate a benefit from targeting a systolic BP of less than 140 mm Hg . More studies are needed but current guidelines suggest that this approach is safe and can be effective for improving functional outcomes .

Respiratory Care

Many patients with severe stroke require intubation because of respiratory failure, mainly because of poor airway control. Impaired oxygenation is also common from aspiration, atelectasis, or pulmonary edema. The FiO ₂ should be adjusted to maintain an oxyhemoglobin saturation greater than 94%. In general, a protective ventilator strategy, extrapolated from patients with acute respiratory distress syndrome, is used targeting tidal volumes <6 mL/kg and sufficient positive end-expiratory pressure (PEEP) to prevent alveolar collapse while maintaining low plateau pressures. Excessively high PEEP levels should be avoided, as they may decrease cerebral venous outflow, cardiac output, and BP and result in impaired cerebral perfusion. Patients should be ventilated to maintain a normal Pa co ₂ ; hyperventilation should be avoided because it can result in cerebral vasoconstriction and reduced cerebral blood flow (CBF).

Sedation and Analgesia

Every attempt should be made to minimize sedation. Minimizing sedation, including daily sedation interruption trials, has been associated with a shorter duration of mechanical ventilation and a shorter ICU length of stay. When sedation is needed, nonbenzodiazepine sedatives (such as propofol or dexmedetomidine) are recommended. Deep sedation with benzodiazepines (such as midazolam or lorazepam) has been linked with increased delirium and worse long-term cognitive outcomes . Narcotics, such as morphine, fentanyl, and remifentanil, should also be considered for analgesia.