Hypertensive Crisis in an Era of Escalating Health Care Changes

Theresa P. Yeo; Sherry A. Burrell


Journal for Nurse Practitioners. 2010;6(5):338-346. 

In This Article

Pathogenesis of Hypertensive Crises

The following mechanisms that produce hypertensive crisis have been identified: dysfunction of the renin-angiotensin-aldosterone system, high-sodium-volume dependence, acute baroreflex failure, and autodysregulation.

Dysfunction of the Renin-angiotensin-aldosterone System

The renin-angiotensin-aldosterone system normally maintains homeostasis of blood pressure.[23] When renin is overproduced, it stimulates the continual release of angiotensin II, a powerful vasoconstrictor, which results in increased systemic BP and increased vascular resistance. High plasma renin levels (> 0.65 ng/mL/hour) occur in uncomplicated "R" type HTN and hypertensive crisis. This cycle can be interrupted by β-blockers, angiotensin-converting enzyme inhibitors (ACEIs), or by removal of an ischemic kidney.[23]

High-sodium-volume Dependence

In contrast, in the high sodium-volume-dependent forms of HTN, called "V" type HTN, plasma renin levels are normal or low. The V forms of HTN respond well to diuretics, aldosterone antagonists, calcium-channel blockers, and alpha-adrenergic antagonists.[23] Although classifying HTN according to plasma renin levels is useful, this information is usually not available at the time of hypertensive crisis.

Acute Baroreflex Failure

The arterial baroreflex effect to help maintain BP homeostasis and to prevent excessive fluctuations has been known since ancient times.[24] Acute baroreflex failure is generally related to surgery and accidental loss of glossopharyngeal or vagus nerve function and is seen usually in the acute care in-patient setting. Other acute causes of baroreflex failure include unilateral or bilateral carotid endarterectomy; brain stem stroke; genetic disease of chromaffin tissue; pheochromocytoma; or radiation therapy for head, neck, and throat carcinoma.[24] The incidence of postoperative hypertensive crisis varies depending on the surgical population and has been reported as being between 4% and 35%. In such cases, the systolic BP may exceed 300 mmHg. Urgent treatment is required with the centrally and peripherally acting agent clonidine to limit sympathetic surges and pacemaker placement may be required for severe bradycardia or heart block.


Malignant HTN develops when an abrupt increase in systemic vascular resistance causes endothelial injury and fibrinoid necrosis of the arterioles.[20] The resultant vascular insult leads to deposition of platelets and fibrin. When the systolic BP reaches approximately 170 mmHg, the auto-regulatory mechanisms of the central nervous system (CNS) are overwhelmed, resulting in increased intracranial pressure (ICP) from cerebral edema, headache, possible seizure activity, encephalopathy, and retinal disease. Papilledema is often observed on ophthalmic examination. (Of note, the presence or absence of papilledema does not predict survival from HTN crisis.)[25] The feedback system of the kidney, particularly the efferent arterioles, is also overwhelmed, producing proteinuria with subsequent decreased urinary output and eventual renal failure.