Hypertension

Hypertension is a condition in which the blood pressure in the arterial system is persistently elevated. It is typically of two varieties -- primary or secondary. Most people will have primary hypertension, that is, elevated blood pressure resulting from various lifestyle behaviors and genetic factors. Secondary hypertension is an entity that refers an elevated blood pressure from a specific and sometimes, reversible, underlying medical reason.

A blood pressure above >140/80 is generally elevated. Hypertensive urgency refers to an elevation >180/110 without evidence of end organ damage. Hypertensive emergency is a reference to an elevated blood pressure in the setting of end organ damage such as acute coronary syndrome, pulmonary edema, renal failure etc.

90 -95% of hypertensive cases are of the primary variety. The remaining 5-10% have some secondary cause to their hypertension. It is important to recognize that hypertension affects between some 16-37% of the world. One estimate in 2010, concluded that hypertension was a significant factor in some 18% or 9.4 million deaths. (2)

Hypertension is a multifactorial condition that is a result of numerous mechanistic processes throughout the body. The basic pathophysiology of primary hypertension is thought to be related to underlying endothelial dysfunction and inflammation of the arterial vasculature. Lifestyle choices such as diet and exercise play an important role in primary hypertension.

Secondary hypertension is due to underlying processes that raise your systemic blood pressure.  Important pathophysiology to consider include renal dysfunction, endocrine dysregulation and abnormalities in the sympathetic nervous system. Examples of secondary causes include: cushing’s syndrome, hyperthyroidism, renal artery stenosis, coarctation of the aorta and pheochromocytoma.

Patients with hypertension have tremendous variation in presentation. Some patients may be asymptomatic. Others may report headaches, visual changes, chest pain, shortness of breath, abdominal pain, nausea, vomiting, rash, decreased urinary output or even confusion. On examination you may find papilledema, focal neurological deficits, new heart murmur, pulmonary rales or rash.

The complaint of hypertension is typically related to a primary process. It is important for the physician to differentiate whether or not  there is any evidence of end organ damage. The following workup may be considered, and tailored according to the patient’s reported symptoms:

• Head CT (to evaluate hypertensive intracranial bleeds)

• EKG (to evaluate for ventricular hypertrophy and ischemic changes)

• CXR (to evaluate for cardiomegaly and pulmonary edema)

• BMP (to evaluate creatinine looking for renal injury)

1. If the patient is asymptomatic and there is no evidence of end organ ischemia, with a persistently elevated blood pressure, these patients are reasonable to discharge home with strict primary care physician follow-up.

2. If there is evidence of end organ dysfunction, get the appropriate consult, workup and reassess need for admission. Useful agents in the control of specific processes below:

• Aortic dissection → esmolol

• Acute pulmonary edema → nitroglycerin

• Acute coronary syndrome → nitroglycerin, metoprolol

• Acute sympathetic crisis → benzodiazepines/phentolamine

• Acute renal failure → labetalol

• Preeclampsia → labetalol

• Hypertensive encephalopathy → Nicardipine or labetalol

• Acute ischemic stroke → labetalol/nicardipine

It is a well known mantra to not administer beta blockers in the setting of cocaine ingestion. Cocaine has effects on alpha and beta receptors. Using beta blockers will cause there to be unopposed alpha agonism which can lead to severe vasoconstriction. Be aware that labetalol is a beta blocker that has mixed alpha and beta blocker properties. Unlike metoprolol, which is primarily beta, there are some studies which suggest that labetalol is associated with less adverse events.

References

1. Tintinalli’s 7th edition

2. https://en.m.wikipedia.org/wiki/Hypertension