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Critical Care in the ED: Mechanical Ventilation, Sepsis, Neurological Hypertensive Emergencies, and Pressors in Shock

Emergency Medicine. 2015 March;47(3):104-119
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The tremendous overlap between the specialties of emergency medicine and critical care medicine is particularly apparent in the initial resuscitation of critically ill patients—a vulnerable population in which the early period of care has significant impact on outcomes.


Blood Pressure Management for Select Neurological Emergencies

Patients with ischemic stroke, spontaneous intracerebral hemorrhage (ICH), and aneurysmal subarachnoid hemorrhage (SAH) often present with elevated blood pressures (BPs).34-36 In caring for these patients, EPs face the question of how, or even if, the patient’s BP should be managed. What are the appropriate BP targets for each of the aforementioned pathologies? Does aggressive BP management benefit or harm the patient?

Background

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The relationship between hypertension and stroke is different for each stroke type. Retrospective data show a U-shaped relationship between BP and mortality in ischemic stroke, with the highest mortality observed at both extremes of the BP curve.34 Data also suggest increased mortality when ICH is accompanied by hypertension.35 Hypertension may also be associated with a higher risk of rebleeding in patients with SAH due to aneurysms.36 Because of the variable relationship between stroke and hypertension, therapeutic recommendations for each type of stroke can be confusing.

Current Literature and Evidence-Based Guidelines

Firm evidence to make therapeutic recommendations remains elusive. The recent American Heart Association (AHA) guidelines covering ischemic stroke, ICH, and SAH were published between late 2010 and early 2013, and several trials investigating the role of BP control in ischemic and hemorrhagic stroke have subsequently been published.37-41

When the Cochrane Collaboration updated its systematic review on vasoactive medications in stroke in 2014 to include recent evidence,42 it ultimately concluded that lowering BP does not improve mortality, neurological deterioration, or quality of life regardless of stroke type, and suggest that further investigations should be undertaken.9 However, the Cochrane authors noted that two recent trials showed a statistically significant association between improved quality of life and BP reduction within 6 hours of stroke onset.38-39 Although the data were compiled from just 2,835 patients of the 15,432 included in the entire Cochrane review, it suggested that interventions initiated in the ED may contribute to any potential beneficial outcomes from intensive BP control.

Ischemic Stroke

The China Antihypertensive Trial in Acute Ischemic Stroke (CATIS) investigated the initiation of BP-control measures within 48 hours of onset of ischemic stroke in approximately 4,000 patients and found no significant difference in death or disability between the group that received BP-control interventions and the group that did not.37 The Rapid Intervention With Glyceryl Trinitrate in Hypertensive Stroke Trial (RIGHT) included patients with both ischemic and hemorrhagic strokes. Though it studied only 41 patients, this trial suggests that early BP control is safe and may be associated with lower disability.38 These findings are bolstered by the more recent Efficacy of Nitric Oxide in Stroke (ENOS) trial showing a similar safety profile for BP control in both ischemic and hemorrhagic strokes, though the mean difference in systolic BP after therapy was a mere 7 mm Hg.40 The combined data from the RIGHT and ENOS trials offer little to clarify the question of appropriate BP control.

For now, the EP is left with the AHA/American Stroke Association (ASA) guideline’s recommendation “not to lower the BP during the initial 24 hours of acute ischemic stroke unless the BP is greater than 220/120 mm Hg.”34 The recommendation differs in cases when a patient receives thrombolytics and hemorrhagic transformation is a risk. There have been no new data to change the AHA/ASA’s recommendations for patients receiving thrombolytics. In such cases, the EP should ensure the patient’s BP is below 185/110 mm Hg prior to thrombolytic administration and below 180/105 mm Hg during therapy.34 A variety of agents is available to lower BP in this situation, and includes IV labetalol, nicardipine, esmolol, and others.

Intracerebral Hemorrhage

The recent literature on blood pressure control in ICH has also increased since the most recent AHA/ASA recommendations. The Second Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial (INTERACT-2 included over 2,800 patients randomized to intensive early therapy to reduce BP to less than 140 mm Hg or less than 180 mm Hg and found no significant difference in mortality or safety between the two groups, though intensive therapy was associated with less disability.39 The Intracerebral Hemorrhage Acutely Decreasing Arterial Pressure Trial (ICH-ADAPT) trial further clarified the issue of safety during intensive BP control by showing no decrease in perihematomal cerebral blood flow in patients whose BP control was targeted to less than 150 mm Hg compared to those whose BP was less than 180 mm Hg, suggesting that aggressive BP reduction does not cause iatrogenic ischemic stroke.41

These combined data suggest that intensive BP management is safe for patients with ICH, providing reassurance for the AHA/ASA guideline recommendation that “in patients…with a systolic BP of 150 to 220 mm Hg, acute lowering of systolic BP to 140 mm Hg is probably safe.”35 Whether this improves patient outcomes remains unclear. Again, multiple agents are available for BP control, including IV labetalol or nicardipine, with no agent identified as superior in producing better patient outcomes. A continuous infusion is recommended if several boluses are ineffective in achieving and maintaining the target BP, as BP variability has been associated with poorer outcomes.43