Hypertensive Emergency - Pathophysiology

Pathophysiology

The pathophysiology of hypertensive emergency is not well understood. Failure of normal autoregulation and an abrupt rise in systemic vascular resistance are typical initial components of the disease process.

Hypertensive emergency pathophysiology includes:

• Abrupt increase in systemic vascular resistance, likely related to humoral vasoconstrictors
• Endothelial injury
• Fibrinoid necrosis of the arterioles
• Deposition of platelets and fibrin
• Breakdown of normal autoregulatory function

The resulting ischemia prompts further release of vasoactive substances, completing a vicious cycle. If the process is not stopped, a vicious cycle of homeostatic failure begins, leading to loss of cerebral and local autoregulation, organ system ischemia and dysfunction, and myocardial infarction.

It is estimated that single-organ involvement is found in approximately 83% of hypertensive emergency patients, two-organ involvement in about 14% of patients, and multi-organ failure (failure of at least 3 organ systems) in about 3% of patients.

The most common clinical presentations of hypertensive emergencies are cerebral infarction (24.5%), pulmonary edema (22.5%), hypertensive encephalopathy (16.3%), and congestive heart failure (12%). Less common presentations include intracranial hemorrhage, aortic dissection, and eclampsia.

Cerebral autoregulation is the ability of the blood vessels in the brain to maintain a constant blood flow. It has been shown that people who suffer from chronic hypertension can tolerate higher arterial pressure before their autoregulation system is disrupted. Hypertensives also have an increased cerebrovascular resistance which puts them at greater risk of developing cerebral ischemia if the blood flow decreases into a normotensive range. On the other hand, sudden or rapid rises in blood pressure may cause hyperperfusion and increased cerebral blood flow, causing increased intracranial pressure and cerebral edema. Hypertensive encephalopathy - characterized by hypertension, altered mentation, and papilledema- is one of the clinical manifestations of cerebral edema and microhemorrhages seen with dysfunction of cerebral autoregulation.

Increased arterial stiffness, increased systolic blood pressure, and widened pulse pressures, all resulting from chronic hypertension, can lead to heart damage. Coronary perfusion pressures are decreased by these factors, which also increase myocardial oxygen consumption, possibly leading to left ventricular hypertrophy. As the left ventricle becomes unable to compensate for an acute rise in systemic vascular resistance, left ventricular failure and pulmonary edema or myocardial ischemia may occur.

Chronic hypertension has a great impact on the renal vasculature, leading to pathologic changes in the small arteries of the kidney. Affected arteries develop endothelial dysfunction and impairment of normal vasodilation, which alter renal autoregulation. When the renal autoregulatory system is disrupted, the intraglomerular pressure starts to vary directly with the systemic arterial pressure, thus offering no protection to the kidney during blood pressure fluctuations. During a hypertensive crisis, this can lead to acute renal ischemia.

Endothelial injury can occur as a consequence of severe elevations in blood pressure, with fibrinoid necrosis of the arterioles following. The vascular injury leads to deposition of platelets and fibrin, and a breakdown of the normal autoregulatory function. Ischemia occurs as a result, prompting further release of vasoactive substances. This process completes the vicious cycle.

Many factors and causes are contributory in hypertensive crises. One main cause is the discontinuation of antihypertensive medications. Other common causes of hypertensive crises are autonomic hyperactivity, collagen-vascular diseases, drug use (particularly stimulants, especially cocaine and amphetamines and their substituted analogues), glomerulonephritis, head trauma, neoplasias, preeclampsia and eclampsia, and renovascular hypertension.

During a hypertensive emergency uncontrolled blood pressure leads to progressive or impending end-organ dysfunction. Therefore, it is important to lower the blood pressure aggressively. Acute end-organ damage may occur, affecting the neurological, cardiovascular, renal, or other organ systems. Some examples of neurological damage include hypertensive encephalopathy, cerebral vascular accident/cerebral infarction, subarachnoid hemorrhage, and intracranial hemorrhage. Cardiovascular system damage can include myocardial ischemia/infarction, acute left ventricular dysfunction, acute pulmonary edema, and aortic dissection. Other end-organ damage can include acute renal failure or insufficiency, retinopathy, eclampsia, and microangiopathic hemolytic anemia.

Extreme blood pressure can lead to problems in the eye, such as retinopathy or damage to the blood vessels in the eye.