ABC | Volume 114, Nº4, April 2020

Statement Luso-Brazilian Position Statement on Hypertensive Emergencies – 2020 Arq Bras Cardiol. 2020; 114(4)736-751 2. Pathophysiological Aspects of Hypertensive Emergency The pathophysiology of HE has not been completely elucidated, and in general, two different mechanisms may play central roles in this process. The first is an imbalance in the vascular autoregulation system leading to reduced perfusion pressure and, consequently, decreased blood flow and increased vascular resistance, resulting in mechanical stress and endothelial injury. 13 The second mechanism is an activation of the renin-angiotensin system resulting in greater vasoconstriction and leading to a vicious cycle of endothelial injury, fibrinoid necrosis of arterioles, and subsequent ischemia. 14 Vascular injury leads to platelet and fibrin deposition, also characterizing a prothrombotic state. 15 Subsequent ischemia results in the release of more vasoactive substances, creating a vicious cycle. 2.1. Autoregulation of Cerebral Blood Flow Knowledge about the mechanism of autoregulation of blood flow to target organs (brain, coronary arteries, and kidneys) is fundamental for improved antihypertensive treatment in cases of HE. Autoregulation of cerebral blood flow (CBF) is maintained by the ratio of cerebral perfusion pressure (CPP) to cerebrovascular resistance (CVR), i.e. , CBF = CPP/CVR (CPP =mean BP - mean venous pressure). CPP is the difference between BP – which helps with tissue blood flow – and venous pressure. With a normal CPP, venous pressure is not important, so CPP is equivalent to BP. Reductions in CPP may be caused by reductions in BP or increased intracranial pressure (ICP), which increases venous pressure. Elevations in ICP may occur as a result of arterial or venous occlusive disease or intracerebral hemorrhage. In normotensive individuals, a wide variation in BP (between 60 and 150 mmHg) may occur without CBF changes. An increase in CPP (or BP) leads to an elevation in CVR, thus protecting the patient against cerebral edema, while reductions in CPP result in decreased CVR, thus protecting the patient from tissue ischemia. When CPP exceeds the upper limit of autoregulation, CBF increases, causing cerebral edema. In contrast, when CPP falls below the lower limit of autoregulation, CBF decreases, causing cerebral ischemia. 16,17 In hypertensive individuals, this relationship is modified in a way that their lower limit of autoregulation is higher compared with normotensive individuals. Thus, improper decrease in CPP can hinder tissue irrigation and, consequently, aggravate the viable ischemic area. For this reason, it is advisable to initially reduce the mean BP by 20 to 25% in relation to the initial values, as this will bring them close to the lower autoregulation limit. 18 Attention should be given to this situation, as most patients with HE have chronic Table 1 – Conditions with target-organ damage characterizing hypertensive emergencies 1-5 Severe hypertension associated with acute complications Cerebrovascular events - Hypertensive encephalopathy - Intracerebral hemorrhage - Subarachnoid hemorrhage - Ischemic stroke Cardiocirculatory events - Acute aortic dissection - Acute pulmonary edema with left ventricular failure - Acute myocardial infarction - Unstable angina Renal disease - Rapidly progressive renal failure Severe adrenergic crisis - Pheochromocytoma crisis - Illicit drug overdose (cocaine, crack, LSD) Hypertension in pregnancy - Eclampsia - Severe preeclampsia - "HELLP" syndrome - Severe hypertension in late pregnancy HELLP: hemolysis, elevated liver enzymes, and low platelet count; LSD: lysergic acid diethylamide. Table 2 – Conditions associated with hypertensive urgency 1-5 Severe hypertension associated with: - Coronary insufficiency - Cardiac insufficiency - Aortic aneurysm - Uncomplicated stroke - Severe epistaxis - Extensive burns - Hypocoagulability states Systemic vasculitis - Perioperative - Preoperative in emergency surgeries - Intraoperative (cardiac surgery, vascular surgery, neurosurgery, pheochromocytoma, etc.) - Postoperative stage III hypertension (organ transplantation, cardiac surgery, vascular surgery, neurosurgery, etc.) Mild/moderate adrenergic crisis - Rebound syndrome (abrupt discontinuation of adrenergic inhibitors) - Drug-food interaction (tyramine vs. MAO inhibitors) - Excessive use of stimulants (amphetamines, tricyclics, etc.) In pregnancy - Preeclampsia - Stage III hypertension MAO: monoamine oxidase. 739