hypertension- management in special situation
TRANSCRIPT
Hypertension –Management in special situation
Dr. Md.Toufiqur Rahman MBBS, FCPS, MD, FACC, FESC, FRCPE, FSCAI,
FAPSC, FAPSIC, FAHA, FCCP, FRCPG
Associate Professor of CardiologyNational Institute of Cardiovascular Diseases,
Sher-e-Bangla Nagar, Dhaka-1207
Consultant, Medinova, Malibagh branchHonorary Consultant, Apollo Hospitals, Dhaka and
STS Life Care Centre, Dhanmondi [email protected]
Summary "Hypertensive urgency" is the situation in which a patient's DBP is >120 mm Hg. If there is acute or rapidly
worsening target organ damage, then the term used is "hypertensive emergency." Hypertensive urgency can be managed as an outpatient, but hypertensive emergency requires admission to a unit with cardiovascular
monitoring facilities, for parenteral antihypertensive therapy.
There are many causes of secondary hypertension, including primary aldosteronism and RAS. Primary
aldosteronism may be caused by an aldosterone producing adenoma of the adrenal gland, or by bilateral adrenal hyperplasia. There is suppressed PRA, increased urinary potassium loss, often but not always with
hypokalemia,and hypertension. Screening for primary aldosteronism is appropriate in patients with hypertension andspontaneous hypokalemia, or in any patient with treatment resistant hypertension. The screening test of choice isthe morning PAC to PRA ratio, which if >20 (with a PAC of ≥12 ng/dl) is suggestive of primary
hyperaldosteronism,and if >70 with a PAC of ≥15 ng/dl and a PRA of ≤1 ng/ml/h is virtually diagnostic.
High resolution CT of the adrenal glands completes the workup.
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Summary RAS may result in hypertension and/or ischemic
nephropathy. Most cases are due to atherosclerosis, but about10% are due to fibromuscular dysplasia, which affects younger persons, particularly women.
The most powerful predictors of the presence of RAS are: age, atherosclerotic cardiovascular disease elsewhere, the presence of anabdominal bruit, recent onset of hypertension or recent loss of BP control, unilateral small kidney, a largeincrease in serum creatinine after an ACE inhibitor or ARB, hypercholesterolemia, cigarette smoking, andabsence of a family history of hypertension
Summary A workup for atherosclerotic RAS should be done only if there is resistant hypertension or if there is
worseningrenal function, and if there is no contraindication to an invasive procedure (renal angioplasty or revascularizationsurgery), and if the patient is willing to accept revascularization. Otherwise, only medical management is advised.
Measurement of peripheral venous PRA at rest or following stimulation with ACE inhibitors lacks the sensitivityand specificity to be useful in screening for RAS.
Useful tests for RAS include radioisotope scanning with ACEinhibition (captopril scintigraphy), Doppler ultrasound, MRA, CTA, and renal arteriography.
In atherosclerotic renovascular hypertension, BP control may be achieved in >90% of cases with medical therapyalone, usually with a combination of antihypertensive drugs, but more invasive man
agement is indicated if thehypertension is refractory to medical therapy with multiple antihypertensive agents at maximum dose, or if there isprogressive deterioration of renal function.
By contrast, in fibromuscular hyperplasia, renal artery angioplasty isthe treatment of choice.OSA is characterized by repetitive interruption of ventilation for 10 seconds or more during sleep cau
sed bycollapse of the pharyngeal airway, and with associated respiratory effort. Persons with hypertension and theclinical features/predisposing factors for OSA, particularly loud snoring, daytime sleepiness, or witnessedapneas, should undergo formal overnight sleep testing ("polysomnography") to make the diagnosis.
Therapy is behavioral, medical, and surgical.
