Elevated blood pressure is common in acute phase, and approximately 60% of patients have systolic blood pressure greater than 140 mmHg on presentation. The percentage is even higher when the patients have a history of hypertension. The suggested mechanisms of blood pressure surges are partly explained by an increase in plasma catecholamine, anxiety, and noxious stimuli including severe pain or bladder distention. In addition, an increase in intracranial pressure often leads to additional blood pressure elevation in severe stroke (Cushing phenomenon). Regardless of its cause, acute blood pressure elevation is associated with poor neurologic outcome.

Cerebral autoregulation means cerebral blood flow is maintained in a constant level despite the changes in blood pressure (more correctly cerebral perfusion pressure, which is defined as mean arterial pressure minus intracranial pressure) (Fig. 14.1). In cases with intact autoregulation, an increase in blood pressure leads to vasoconstriction which increases vascular resistance and maintains constant cerebral blood flow. By contrast, progressive drop in blood pressure induces vasodilation which decreases vascular resistance and helps with constant blood flow [2]. In patients with acute ischemic stroke, cerebral autoregulation is often disturbed. With disturbed autoregulation, cerebral blood flow is more directly dependent on blood pressure, and a decrease in blood pressure may lead to concomitant decrease in cerebral blood flow, which may aggravate perfusion deficit in the penumbra area. The status of autoregulation on each patient can be identified using correlation analysis between continuous blood pressure and intracranial pressure (pressure reactivity index, PRx) or cerebral blood flow (flow reactivity index, FRx). If patients’ autoregulation status is not known, abrupt drop in blood pressure should be avoided not to aggravate perfusion deficit just in case the patient have disturbed autoregulation. In a healthy person, within the ranges of mean arterial pressure between 60 mmHg and 150 mmHg, cerebral blood flow remained constant based on with autoregulation physiology.

Patients who are treated with intravenous tissue plasminogen activator (t-PA) therapy, blood pressure should be controlled under 180/105 mmHg. In general, there is no sweet spot for pressure in treating patients with acute ischemic stroke. Based on American Stroke Association guidelines, it is reasonable to start using blood pressure-lowering drugs from 220 to 120 mmHg, which is 150 mm Hg in terms of mean arterial pressure. Blood pressure above this level can be in the autoregulatory breakthough zone, which requires lowering blood pressure.

Most commonly used blood pressure-lowering drugs are intravenous injections including labetalol (10–20 mg bolus) or nicardipine (infusion at a rate of 3–5 mg/h or bolus injection of 1–2 mg based on pressure level). In refractory cases, nitroprusside injection may be tried, but it has rarely been used in stroke patients because nitroprusside has an unpredictable effect on blood pressure and has rebound hypertension which may actually aggravate ICP surges.

When patients are treated with t-PA, blood pressure is strictly controlled under 180/105 mmHg because high blood pressure is associated with hemorrhagic transformation [3]. However, it is unknown whether more intensive blood pressure control is beneficial to the patients treated with t-PA or not. In ENCHANTED trial (part B), effectiveness of intensive blood pressure lowering (SBP 130–140 mmHg) were compared with standard treatment (SBP < 180 mmHg), which will be published in the near future [4]. Moreover, in patients with intra-arterial thrombectomy with complete recanalization, appropriate blood pressure level is not known. Those patients may not require high blood pressure to optimize perfusion and may need strict blood pressure control to prevent hemorrhagic transformation. This should be addressed in the upcoming clinical trials.

Investigation of potential embolic source is the most important diagnostic step in evaluating patients with acute ischemic stroke [6]. Evaluating methods include transthoracic echocardiography (TTE), transesophageal echocardiography (TTE), and heart rhythm monitoring (electrocardiogram or Holter monitoring). Current evidence suggests that even longer monitoring, up to several weeks using implantable loop recorder, may detect more atrial fibrillation in high-risk patients.

TTE is generally performed as a screening test to find cardiac embolic sources. Well known embolic sources are described in Table 14.2. If indicated TEE can be performed (Fig. 14.3). TEE is superior to TTE in identifying small embolic sources located in the posterior part, such as valve vegetation, left atrial appendage thrombus, patent foramen ovale, or aortic atheroma. However, TEE also has limitations; high intra and interrater variability, not always available at any time, may require patients’ cooperation. Therefore, patients with severe stroke may not tolerate TEE due to poor cooperation. Cardiac multidetector CT (MDCT) has roles in identifying intra- or extracardiac embolic sources because MDCT has less interrater variability and has better visualization of aortic arch atheroma [7]. Therefore, those who cannot tolerate TEE, cardiac MDCT can be used as an alternative in evaluating intracardiac or extracardiac embolic sources.