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Hypertension –Management in
special situation
Dr. Md.Toufiqur Rahman
MBBS, FCPS, MD, FACC, FESC, FRCPE, FSCAI,
FAPSC, FAPSIC, FAHA, FCCP, FRCPG
Associate Professor of Cardiology
National Institute of Cardiovascular Diseases,
Sher-e-Bangla Nagar, Dhaka-1207
Consultant, Medinova, Malibagh branch
Honorary Consultant, Apollo Hospitals, Dhaka and
STS Life Care Centre, Dhanmondi
drtoufiq19711@yahoo.com
drtoufiq19711@yahoo.com
drtoufiq19711@yahoo.com
drtoufiq19711@yahoo.com
drtoufiq19711@yahoo.com
drtoufiq19711@yahoo.com
drtoufiq19711@yahoo.com
drtoufiq19711@yahoo.com
drtoufiq19711@yahoo.com
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drtoufiq19711@yahoo.com
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drtoufiq19711@yahoo.com
drtoufiq19711@yahoo.com
drtoufiq19711@yahoo.com
drtoufiq19711@yahoo.com
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 aldosteroneproducing 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.
Highresolution CT of the adrenal glands completes the workup.
.
drtoufiq19711@yahoo.com
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 an
abdominal 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, and
absence of a family history of hypertension
drtoufiq19711@yahoo.com
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 angi
oplasty or revascularizationsurgery), and if the patient is willing to accept revascularization. Oth
erwise, 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), Doppl
er 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 antihyper
tensive 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 ca
used 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 ("polys
omnography") to make the diagnosis.
Therapy is behavioral, medical, and surgical.
drtoufiq19711@yahoo.com
Thank you !drtoufiq19711@yahoo.com

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Hypertension- Management in special situation

  • 1. Hypertension –Management in special situation Dr. Md.Toufiqur Rahman MBBS, FCPS, MD, FACC, FESC, FRCPE, FSCAI, FAPSC, FAPSIC, FAHA, FCCP, FRCPG Associate Professor of Cardiology National Institute of Cardiovascular Diseases, Sher-e-Bangla Nagar, Dhaka-1207 Consultant, Medinova, Malibagh branch Honorary Consultant, Apollo Hospitals, Dhaka and STS Life Care Centre, Dhanmondi drtoufiq19711@yahoo.com
  • 17.
  • 22. 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 aldosteroneproducing 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. Highresolution CT of the adrenal glands completes the workup. . drtoufiq19711@yahoo.com
  • 23. 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 an abdominal 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, and absence of a family history of hypertension drtoufiq19711@yahoo.com
  • 24. 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 angi oplasty or revascularizationsurgery), and if the patient is willing to accept revascularization. Oth erwise, 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), Doppl er 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 antihyper tensive 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 ca used 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 ("polys omnography") to make the diagnosis. Therapy is behavioral, medical, and surgical. drtoufiq19711@yahoo.com