Medicina interna

Internal medicine: hypertensive urgency and emergency

In order to speak of hypertension, we need blood pressure equal to or above 140/90 mmHg for systolic and diastolic values. The European Society of Hypertension further divided blood pressure into several grades, and grade 3 is the one we’re talking about.

Chronic hypertension

There are other degrees of hypertension, but in this case it is a chronic condition, often mild, associated with nonspecific symptoms such as headache or a general sense of discomfort. The main goal in this situation is to modulate and control the chronic blood pressure pattern over time. The scenario is different in acute hypertension, which requires a distinct and more immediate approach.

A chronic condition is one in which the patient still has, at least to some extent, compensatory mechanisms that allow the organism to adapt. This is not always the case in elderly patients, where these compensatory capacities may be exhausted, leading to different degrees of frailty.

In chronic conditions, therapy aims to support and enhance this reduced countervailing capacity of the organism. In acute conditions, the situation is different and requires a distinct approach.

Acute hypertension and hypertensive crisis

In an acute condition there is an acute cause that suddenly precipitates the clinical scenario and therefore we have to rush in our hypertensive intervention. In some cases, for example during a hypertensive crisis in the urgency scenario, we must pay close attention and manage the abrupt increase in blood pressure as soon as possible, but without acting too aggressively.

A hypertensive crisis can be defined as a severe and sudden rise in blood pressure, typically above 180/120 mmHg, which may potentially cause damage to vital organs such as the brain, heart, and kidneys. The crisis can be urgency or emergency.

In summary, a hypertensive crisis is defined as a severe elevation in blood pressure, with systolic values over 180 mmHg and/or diastolic values over 120 mmHg, with or without acute organ damage. We therefore distinguish hypertensive urgency, without organ damage, from hypertensive emergency, with organ damage.

Hypertensive crises account for up to about 5% of emergency department visits. The lifetime risk of experiencing a hypertensive crisis in patients with essential hypertension is approximately 1–2%. We divide hypertensive crises into urgency and emergency based on the presence or absence of acute target-organ injury. Acute cardiorespiratory failure is the one that is much more associated with high mortality, followed by stroke or TIA, followed by aortic dissection, acute chest pain and myocardial infarction.

Hypertensive urgency

Hypertensive urgency is characterized by a marked increase in blood pressure, typically ≥180/120 mmHg, without evidence of acute target-organ damage. Symptoms, if present, are usually mild or nonspecific, such as headache or anxiety, and there is no severe organ involvement. Management does not require emergency interventions: blood pressure can be gradually reduced with oral antihypertensive medications, adjustment of ongoing therapy, and close follow-up.

These patients may present to the emergency department with high blood pressure and anxiety, undergo basic clinical evaluation and observation, receive treatment, and then be safely discharged. It is usually due to poorly controlled hypertension and hospital admission isn’t usually necessary.

In hypertensive urgencies, titratable oral medications are used, and blood pressure is carefully monitored and gradually lowered over 24–48 hours to avoid complications. Certain patients, such as those with stroke, acute atherosclerotic events, or those requiring urgent thrombolytic therapy, may require specialized adjustments. In these situations, beta blockers or alpha blockers may be used orally under supervision, depending on the clinical scenario. In emergencies, intravenous therapy is guided by the associated condition and requires careful monitoring, but the detailed choice of agent is usually managed by the physician.

The only exceptions to rapid reduction are thrombotic microangiopathy, acute kidney injury, or ischemic stroke, where careful management is required to avoid further organ damage.

Hypertensive emergency

Hypertensive emergency, on the other hand, is defined by an acute and severe rise in blood pressure associated with evidence of acute target-organ damage. This may involve the heart, brain, lungs, or kidneys, leading to clinical syndromes such as acute myocardial infarction, acute pulmonary edema, or stroke. In this case, the abrupt elevation in blood pressure is directly responsible for organ injury and requires immediate and intensive management.

In this situation, the blood pressure reaches the same threshold values, typically ≥180/120 mmHg, but is associated with acute target-organ damage. This may include neurological involvement such as stroke or hypertensive encephalopathy, cardiac complications such as acute heart failure or myocardial infarction, acute kidney injury with sudden renal failure, or aortic dissection. Aortic dissection, in particular, is a dramatic and life-threatening condition, often discussed in vascular surgery, that requires immediate intervention and may rapidly lead to death.

Hypertensive emergency requires immediate intravenous antihypertensive therapy in a monitored setting. Patients must be admitted or kept under prolonged observation in the emergency department, and then transferred to the appropriate specialty unit, such as cardiology, neurology, internal medicine, or directly to the operating room in the case of aortic dissection.

In hypertensive emergencies, we use intravenous medications to lower blood pressure, whereas in hypertensive urgencies, oral medications are typically sufficient. In emergencies, the goal is to reduce the mean arterial pressure by about 20–25% within the first 2–6 hours, aiming for a safe threshold of approximately 160/100 mmHg. The mean arterial pressure is calculated as the diastolic pressure plus one-third of the pulse pressure, systolic minus diastolic. During the first hour, the reduction should be gradual to avoid organ hypoperfusion, while keeping the diastolic pressure around 100 mmHg. Over the next 24 hours, blood pressure should continue to be monitored and maintained within target ranges, with adjustments according to specific organ involvement.

Blood pressure should generally be reduced quickly, but the speed and degree of reduction depend on the specific organ involvement. In thrombotic microangiopathy, blood pressure is lowered gradually over several hours, because peripheral tissue involvement is not as dramatic. In hypertensive encephalopathy, diagnosed by clinical signs and imaging, CT scan, blood pressure should be reduced immediately, aiming for a 20–25% reduction in mean arterial pressure.

In acute ischemic stroke, blood pressure reduction should be more cautious, around 15% in the first hour, to maintain cerebral perfusion. If thrombolytic therapy is indicated, careful maintenance of perfusion is critical. In hemorrhagic stroke, acute coronary syndrome, acute cardiogenic pulmonary edema, and aortic dissection, blood pressure should be reduced immediately, often aiming for systolic values below 140 mmHg. The same approach applies to severe preeclampsia, eclampsia, and HELLP syndrome in pregnant women.

Medications used include beta blockers such as labetalol and esmolol, labetalol is preferred in young women, nitrates like nitroglycerin, certain calcium channel blockers, hydralazine, and centrally acting alpha-2 agonists like clonidine, used cautiously, particularly in encephalopathy. Beta blockers reduce the effects of catecholamines on the heart, nitroglycerin acts as a direct vasodilator, calcium channel blockers induce peripheral vasodilation, and clonidine decreases sympathetic outflow from the central nervous system.

Organ involvement

The involvement of the aorta is mainly acute aortic distention or microangiopathic hemolytic anemia, which is associated but usually is acute aortic distention. One of the most dramatic effects on the brain we can have is transient ischemic attack, TIA. To understand the concept, we can compare it with cardiac ischemia: in the heart, myocardial infarction represents irreversible tissue necrosis, whereas angina is a transient ischemic condition without permanent damage. Similarly, in the brain, a transient ischemic attack is a temporary episode of cerebral ischemia without infarction, in contrast to stroke, which involves permanent tissue injury.

Hypertensive crises involving the brain can also precipitate seizures, particularly in patients with pre-existing atherosclerotic disease, or lead to intracerebral or subarachnoid hemorrhage, which together constitute hemorrhagic stroke. Cerebral infarction, on the other hand, corresponds to ischemic stroke. Therefore, stroke can be classified into two main types: ischemic and hemorrhagic. Hemorrhagic stroke includes intracerebral parenchymal hemorrhage and subarachnoid hemorrhage and is strongly associated with acute increases in blood pressure.

At the renal level, hypertensive emergencies can cause acute kidney injury, primarily due to hemodynamic alterations induced by the abrupt rise in blood pressure.

Ocular involvement is less frequent but may occur, presenting as papilledema due to optic disc edema, retinal edema, or retinal hemorrhages. These conditions can be severe and may lead to visual impairment or even retinal detachment.

Pregnancy: preeclampsia and eclampsia

A special hypertensive emergency occurs in pregnancy: preeclampsia and eclampsia. Preeclampsia is characterized by new-onset hypertension, placental circulation disturbances, and proteinuria due to renal involvement. Eclampsia represents the progression to seizures and is a dramatic condition typically occurring in the third trimester. This syndrome poses significant risks to both the mother and the fetus and requires strict monitoring and urgent management.

Usually, there is a single organ involvement in 83% of cases, two organ involvement in 14% of cases, and more organ involvement is very rare, 3% of cases.

In pregnant women, hypertension can occur in those who were already hypertensive before pregnancy or develop as a result of pregnancy.

Preeclampsia is characterized by blood pressure equal to or greater than 160/110 mmHg measured on at least two occasions, four hours apart, after 20 weeks of gestation. It may be associated with proteinuria, either defined as more than 300 mg in a 24-hour urine collection or as a spot urine protein/creatinine ratio of 0.3 mg/dL or higher.

Preeclampsia can also present with additional severe features, including a low platelet count, elevated liver enzymes with right upper quadrant or epigastric pain unresponsive to medication, renal injury with elevated serum creatinine, or visual disturbances.

Eclampsia occurs when preeclampsia is complicated by new-onset generalized seizures in a woman without a prior seizure disorder. Blood pressure is often elevated in these cases and may reach levels seen in hypertensive emergencies.

HELLP syndrome is a severe variant of preeclampsia that may occur with or without marked blood pressure elevation, characterized by hemolysis, elevated liver enzymes, and low platelet count, often with increased bilirubin from hemolysis. These conditions frequently involve multiple organ systems, representing a poly-organ dysfunction scenario. While not all hypertensive pregnant patients meet the criteria for a hypertensive emergency, preeclampsia, eclampsia, and HELLP syndrome often require urgent blood pressure management due to their effects on parenchymal organs.

Predisposition

Several conditions predispose to hypertensive crisis. First of all, essential hypertension is the most common underlying condition. Most patients who experience a hypertensive crisis are already hypertensive, although not all hypertensive patients will develop a crisis. Occasionally, a hypertensive crisis may occur in individuals without a previous diagnosis of hypertension; in these cases, the crisis leads to the first diagnosis of hypertension. It is uncommon for a truly normotensive individual to develop a hypertensive emergency, but transient severe blood pressure elevation may occur, more often as an urgency.

Endocrinological disorders are important predisposing factors. These include Cushing syndrome, due to excess corticosteroid production; primary hyperaldosteronism, characterized by excess aldosterone; pheochromocytoma and paraganglioma, tumors that secrete catecholamines; and rare renin-secreting tumors. All of these conditions can lead to severe hypertension and increase the risk of hypertensive crisis.

Renal and renovascular diseases are also major contributors. Renal artery stenosis and other causes of secondary hypertension predispose patients to hypertensive crises, particularly in those with long-standing uncontrolled hypertension.

Certain inflammatory and immunological diseases, especially large- and medium-vessel vasculitides such as Takayasu arteritis and polyarteritis nodosa, can predispose to hypertensive crises due to vascular involvement.

Disorders of the central nervous system, including brain tumors, cerebral edema, intracranial hemorrhage, and spinal cord injury, may trigger hypertensive crises and further worsen neurological damage.

Drug-related causes are frequent. The use or abuse of cocaine, amphetamines, monoamine oxidase inhibitors, and other sympathomimetic drugs can precipitate a hypertensive crisis. Abrupt withdrawal or poor adherence to antihypertensive therapy is a very common trigger. Over-the-counter sympathomimetic agents such as nasal decongestants, excessive licorice consumption, lead intoxication, and some antidepressants, including selective serotonin reuptake inhibitors in specific contexts, may also contribute.

A specific anatomical condition is coarctation of the aorta, a congenital narrowing of the aorta, which causes severe hypertension proximal to the obstruction and predisposes to hypertensive crises.

Clinical presentation and triggers

Regarding clinical presentation, symptoms depend largely on the presence and type of target-organ involvement. If myocardial infarction occurs, chest pain predominates. In stroke, neurological deficits such as motor, sensory, or speech disturbances are present. However, many patients present with nonspecific symptoms related to the acute rise in blood pressure. Common manifestations include headache, epistaxis, dizziness or faintness, psychomotor agitation, chest pain related to ischemia, and dyspnea, which is often exacerbated by anxiety.

Hypertensive crises without acute target-organ damage, that is hypertensive urgencies, are most commonly due to poorly controlled essential hypertension. These cases usually do not require hospital admission. Management consists of observation, adjustment of oral antihypertensive therapy, and outpatient follow-up. Intravenous antihypertensive drugs are not required.

Historically, two terms were used: malignant hypertension and accelerated hypertension. Malignant hypertension was characterized by very high blood pressure, renal failure, and severe retinopathy with papilledema, proteinuria, and a high mortality rate. Accelerated hypertension referred to a rapid rise in blood pressure associated with target-organ damage. Over time, these concepts evolved into the modern definition of hypertensive emergency: severe hypertension, typically ≥180/120 mmHg, associated with acute target-organ damage, more than 3.

Triggers of hypertensive crises include non-adherence or withdrawal of therapy, under-treatment, untreated hypertension, emotional stress, increased salt intake, drug use, and sympathomimetic medications. These factors can cause an abrupt rise in blood pressure in both known hypertensive patients and previously undiagnosed individuals.

Pathophysiologically, these triggers lead to failure of vascular autoregulation and endothelial dysfunction. There is excessive activation of the renin–angiotensin system, intense vasoconstriction, inflammation, hypoperfusion, hemolysis, thrombogenesis, and perivascular edema. This cascade may or may not result in acute hypertension-mediated organ damage.

When autoregulation fails, microvascular damage occurs in organs such as the brain, heart, kidneys, and retina. Endothelial injury exposes subendothelial tissue, activating platelets and the coagulation cascade, leading to ischemia and further organ dysfunction. Autoregulation becomes shifted toward higher pressure levels, perpetuating the vicious cycle.

Clinically, if severe blood pressure elevation occurs without acute organ damage, the condition is classified as hypertensive urgency. If acute hypertension-mediated organ damage is present, such as acute coronary syndrome, cardiogenic pulmonary edema, stroke, hypertensive encephalopathy, aortic dissection, acute renal failure, or in pregnancy severe preeclampsia or eclampsia with HELLP syndrome, the condition is classified as hypertensive emergency.

In hypertensive urgency, blood pressure reduction is gradual and achieved with oral medications. In hypertensive emergency, treatment is guided by the affected organ system and requires rapid but controlled blood pressure reduction using intravenous antihypertensive agents in a monitored setting.

Diagnosis

To make a diagnosis, the diagnostic measures should be associated with a therapeutic measure, either orally or in an emergency. In an emergency, intravenous therapy plus the specific therapy for the condition associated with the emergency is also considered. For example, severe hypertension grade 3, according to the European Society of Hypertension classification, plus acute organ damage constitutes a hypertensive emergency.

The symptoms of this emergency are predominantly related to the affected organ. If the heart is involved, chest pain, acute dyspnea, angina or acute myocardial infarction, acute pulmonary edema, or acute heart failure are more common symptoms. All the tests we choose are suggested by the dominant clinical scenario, which is the consequence of the organ involved. Therefore, we can use ECG, fundoscopy, Hb, platelets, etc. The kidney involvement is checked by creatinine.