Secondary Hypertension and Hypertensive Emergency

Today's case involved a hypothetical young woman who presented with headache and hypertension (BP 220/120mmHg).  She had a history of poorly-controlled hypertension, albeit with some medication non-adherence.  There was no evidence of end-organ dysfunction.  There were no intoxicants on history.  On her examination, there were café-au-lait spots and neurofibromas.  She had a mild tremor and no renal bruits.  There was no papilledema, but some A-V nicking in her fundoscopy.  She was treated with intravenous labetalol, with fairly minimal effect on her hypertension.  Her age and hypertension resistance, coupled with her spontaneous hypokalemia, prompted workup for secondary hypertension.  Her urine metanephrines were significantly elevated, and she was diagnosed with pheochromocytoma.

There were multiple learning points:

-The CHEP guidelines can be found at www.hypertension.ca and they detail the indications for investigation of secondary hypertension.

-Common causes include (but are not limited to): endocrine hypertension (pheochromocytoma, hyperaldosteronism or Conn’s syndrome), renal artery stenosis, sleep apnea, alcohol withdrawal, hypercarbia and drug intoxication.

-It can be dangerous to use pure beta-blockade in a patient with catecholamine excess.  The reason for this is that some beta adrenergic receptors cause systemic vasodilatation.  When you block beta receptors selectively, you block that vasodilatation and allow unopposed alpha adrenergic stimulation to paradoxically increase the blood pressure.

-Signs of end-organ damage indicate a hypertensive emergency rather than a hypertensive urgency.  The main distinguishing point is the need for intravenous antihypertensives, which preclude ward management and mandate ICU admission.  Take end-organ damage from head to toe: cerebral hemorrhage/stroke, hypertensive encephalopathy/PRES, aortic dissection, congestive heart failure, pulmonary edema, ruptured AAA, renal damage, etc.  If it’s there, generally an intravenous agent such as labetalol or nitroprusside is useful.  The goal is to reduce the mean arterial pressure by around 25% within the first 24 hours, not to reduce them to normotension.  This is because the cerebral vasculature autoregulates and becomes accustomed to high pressures – a normal pressure to such a hypertensive patient may cause cerebral hypoperfusion and stroke.

Further Reading:

Dasgupta, K., Quinn, R. R., Zarnke, K. B., Rabi, D. M., Ravani, P., Daskalopoulou, S. S., ... & Tremblay, G. (2014). The 2014 Canadian Hypertension Education Program recommendations for blood pressure measurement, diagnosis, assessment of risk, prevention, and treatment of hypertension. Canadian Journal of Cardiology, 30(5), 485-501.