AUTHOR: Tania B. Babar, MD
Normal blood pressure (BP) in adults can be defined as systolic BP <120 mm Hg and diastolic BP <80 mm Hg. Elevated BP is defined as systolic BP between 120 and 129 mm Hg or diastolic BP <80 mm Hg. Hypertension (HTN) can be divided into (1) stage 1: Systolic BP from 130 to 139 mm Hg or diastolic BP from 80 to 89 mm Hg and (2) stage 2: Systolic BP ≥140 mm Hg or diastolic BP ≥90 mm Hg. This definition is based on accurate measurements and average of ≥2 readings on ≥2 occasions.
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Physical examination may be entirely within normal limits, except for the presence of elevated BP. A proper initial physical examination on a hypertensive patient should include the following:
TABLE 3 Clinical Clues to Guide the Investigation in Young Patients With Hypertension That Has a Potentially Hereditary Cause
Specific Conditions | Possible Causes of Familial Hypertension | Clinical Clues |
---|---|---|
Catecholamine-Producing Tumors | ||
Pheochromocytoma/paraganglioma | Familial cases are responsible for <30% of cases, including MEN2A and MEN2B, von Hippel-Lindau disease, neurofibromatosis, and familial paraganglioma syndromes (SDH complex mutations) | Paroxysmal palpitations, headaches, diaphoresis, pale flushing; syndromic features of any of the associated disorders |
Neuroblastomas (adrenal) Aortic or renovascular lesions | 1%-2% of neuroblastomas are familial | |
Coarctation of the aorta | Overrepresented in families but no familial distribution | Asymmetry between upper- and lower-extremity BP, radial-formal pulse delay; associated with Turner syndrome, Williams syndrome, and bicuspid aortic valve |
Renal artery stenosis caused by fibromuscular dysplasia or inherited arterial wall lesions | <10% familial with AD pattern | Abnormal renal vascular imaging results; vascular disease in the carotid territory at an early age; common in neurofibromatosis and Williams syndrome; also present in tuberous sclerosis, Ehlers-Danlos syndrome, and Marfan syndrome |
Parenchymal kidney disease GN | Alport disease (X-linked, AR, or AD), familial IgA nephropathy (AD with incomplete penetrance) | Proteinuria, hematuria, low eGFR |
PKD | ADPKD type 1 or 2, ARPKD | Multiple renal cysts (as few as three in patients under 30 yr) |
Adrenocortical disease Glucocorticoid-remediable aldosteronism (familial hyperaldosteronism type I) | AD chimeric fusion of the 11β-hydroxylase and aldosterone synthase genes | Cerebral hemorrhages at young age, cerebral aneurysms; mild hypokalemia; high plasma aldosterone, low renin |
Familial hyperaldosteronism | AD; unknown defect | Severe type 2 hypertension in early adulthood; high plasma aldosterone, low renin; no response to glucocorticoid treatment |
Familial hyperaldosteronism type III | AD; unknown defect | Severe hypertension in childhood with extensive target-organ damage; high plasma aldosterone, low renin; marked bilateral adrenal enlargement |
Congenital adrenal hyperplasia | AR mutations in 11β-hydroxylase or 21-hydroxylase | Hirsutism, virilization; hypokalemia and metabolic alkalosis; low plasma aldosterone and renin |
Monogenic Primary Renal Tubular Defects | ||
Gordon syndrome | AD mutations of KLHL3, CUL3, WNK1, and WNK4; AR mutations of KLHL3 | Hyperkalemia and metabolic acidosis with normal renal function |
Liddle syndrome | AD mutations of the epithelial sodium channel | Hypokalemia and metabolic alkalosis; low plasma aldosterone and renin |
Apparent mineralocorticoid excess | AD mutation in 11β-hydroxysteroid dehydrogenase type 2 | Hypokalemia and metabolic alkalosis; low plasma aldosterone and renin |
Geller syndrome Hypertension-brachydactyly syndrome | AD mutation in the mineralocorticoid receptor AD mutations in the phosphodiesterase E3A enzyme | Hypokalemia and metabolic alkalosis; low plasma aldosterone and renin; increased BP during pregnancy or exposure to spironolactone |
Unknown mechanisms | ||
Hypertension-brachydactyly syndrome | AD | Short fingers (small phalanges) and short stature; brain stem compression from vascular tortuosity in the posterior fossa |
Essential Hypertension | ||
Polygenic | When obesity or metabolic syndrome is present, the likelihood of essential hypertension is higher |
AD, Autosomal dominant; ADPKD, autosomal dominant polycystic kidney disease; AR, autosomal recessive; ARPKD, autosomal recessive polycystic kidney disease; BP, blood pressure; eGFR, estimated glomerular filtration rate; GN, glomerulonephritis; IgA, immunoglobulin A; MEN, multiple endocrine neoplasia; PKD, polycystic kidney disease; SDH, succinate dehydrogenase.
From Skorecki K et al: Brenner and Rectors the kidney, ed 10, Philadelphia, 2016, Elsevier.
TABLE 2 Guide to Evaluation of Identifiable Causes of Hypertension
Suspected Diagnosis | Clinical Clues | Diagnostic Testing |
---|---|---|
Chronic kidney disease | Estimated GFR <60 ml/min/1.73 m2 Urine albumin-to-creatinine ratio ≥30 mg/g | Renal sonography |
Renovascular disease | New elevation in serum creatinine, marked elevation in serum creatinine with ACEI or ARB, drug-resistant hypertension, flash pulmonary edema, abdominal, or flank bruit | Renal sonography (atrophic kidney), CT or MR angiography, invasive angiography |
Coarctation of the aorta | Arm pulses >leg pulses, arm BP >leg BP, chest bruits, rib notching on chest radiography | MR angiography, TEE, invasive angiography |
Primary aldosteronism | Hypokalemia, drug-resistant hypertension | Plasma renin and aldosterone, 24-h urine aldosterone and potassium after oral salt loading, adrenal vein sampling |
Cushing syndrome | Truncal obesity, wide and blanching purple striae, muscle weakness | 1 mg dexamethasone-suppression test, urinary cortisol after dexamethasone, adrenal CT |
Pheochromocytoma | Paroxysms of hypertension, palpitations, perspiration, and pallor; diabetes | Plasma metanephrines, 24-h urinary metanephrines and catecholamines, abdominal CT or MR imaging |
Obstructive sleep apnea | Loud snoring, large neck, obesity, somnolence | Polysomnography |
ACEI, Angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; BP, blood pressure; CT, computed tomography; GFR, glomerular filtration rate; MR, magnetic resonance; TEE, transesophageal echocardiography.
From Goldman L, Schafer AI: Goldmans Cecil medicine, ed 24, Philadelphia, 2012, Saunders.
TABLE 1 Blood Pressure Cuff Size and Error in Measurement∗
Cuff Bladder Size | Arm Circumference | ||
---|---|---|---|
28 cm or less | 29-42 cm | 43 cm or more | |
Regular (12 × 23 cm) | Accurate | Overestimates SBP by 4-8 mm Hg DBP by 3-6 mm Hg | Overestimates SBP by 16-17 mm Hg DBP by 10-11 mm Hg |
Large (15 × 33 cm) | Underestimates SBP by 2-3 mm Hg DBP by 1-2 mm Hg | Accurate | Overestimates SBP by 5-7 mm Hg DBP by 2-4 mm Hg |
Thigh (18 × 36 cm) | Underestimates SBP by 5-7 mm Hg DBP by 1-3 mm Hg | Underestimates SBP by 5-7 mm Hg DBP by 2-4 mm Hg | Accurate |
DBP, Diastolic blood pressure reading; SBP, systolic blood pressure reading.
∗Overestimation means that hypertension may be diagnosed in someone with normal blood pressure; underestimation means that the blood pressure reading may be normal in someone who actually has high blood pressure. See text for further discussion.
From McGee S et al: Evidence-based physical diagnosis, ed 4, Philadelphia, 2018, Elsevier.
BOX 1 Causes of Secondary Hypertension
NSAIDs, Nonsteroidal antiinflammatory drugs; PTH, parathyroid hormone; PTHRP, parathyroid hormone-related protein; SSRI, selective serotonin reuptake inhibitor; VEGF, vascular endothelial growth factor.
From Talley NJ et al: Essentials of internal medicine, ed 4, Chatswood, NSW, 2021, Elsevier Australia.
TABLE 4 Adrenocortical Causes of Hypertension
ACTH,Corticotropin; HSD, hydroxysteroid dehydrogenase.
From Melmed S et al: Williams textbook of endocrinology, ed 14, 2019, Elsevier.
TABLE 5 Initial Laboratory Evaluation of the Hypertensive Patient to Investigate the Presence of Comorbid Conditions, Secondary Causes, or Established Target-Organ Damage
Test | Clinical Usefulness | ||
---|---|---|---|
Serum creatinine (and estimated glomerular filtration rate) | Assessment of renal function. Identifies parenchymal kidney disease as a possible secondary cause as well as established TOD. | ||
Serum potassium | Low potassium (of renal origin) suggests mineralocorticoid excess (primary or secondary), glucocorticoid excess, Liddle syndrome. High potassium with normal renal function suggests Gordon syndrome. Low levels raise caution about the use of thiazides and loop diuretics. High levels preclude the use of ACEIs, ARBs, renin inhibitors, and potassium-sparing diuretics. | ||
Serum sodium | If high, suggests primary aldosteronism. If low, alerts to the need to avoid thiazide diuretics. | ||
Serum bicarbonate | If high, suggests aldosterone excess (primary or secondary). If low with normal renal function, suggests Gordon syndrome (with high potassium) or primary hyperparathyroidism (with high calcium). | ||
Serum calcium | If high, suggests primary hyperparathyroidism. | ||
Serum glucose | Identifies prediabetes or diabetes. In the appropriate setting, suggests glucocorticoid excess, pheochromocytoma, or acromegaly. | ||
Lipid profile | Identifies hyperlipidemia. | ||
Hemoglobin/hematocrit | If high, in the absence of other hematologic abnormalities or underlying lung disease, suggests sleep apnea. | ||
Urinalysis∗ | Proteinuria and hematuria identify a possible secondary cause (glomerulonephritis). Proteinuria can also be a marker of TOD. | ||
Electrocardiogram | Identifies left ventricular hypertrophy, old myocardial infarction, or other ischemic changes. Identifies conduction abnormalities that may preclude the use of β-blockers or nondihydropyridine CCBs. |
The most recent guidelines do not recommend blood urea nitrogen (BUN) measurement alone.ACEI, Angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; CCB, calcium channel blocker; TOD, target-organ damage.
∗Some organizations recommend screening microalbuminuria as a more sensitive tool to identify early renal injury.
From Skorecki K et al: Brenner and Rectors the kidney, ed 10, Philadelphia, 2016, Elsevier.
Lifestyle modifications (the initial treatment of hypertension should focus on lifestyle modifications [Table 6]):
TABLE 6 Effects of Lifestyle Modifications on Blood Pressure
Lifestyle Modification | Specifics | Level of Evidence | Approximate Reduction in Systolic Blood Pressure |
---|---|---|---|
Weight loss | Maintain BMI <25 kg/m2 | A | 5-20 mm Hg per 10 kg weight loss |
Physical activity | At least 30 min per day | A | ∼5 mm Hg |
Reduce salt intake | Limit sodium to 2.4 g per day | A | ∼5 mm Hg |
Heart-healthy diet, such as DASH | Low-fat diet with fruits and vegetables | A | ∼11 mm Hg |
Potassium supplementation | Preferably as part of dietary modification | A | ∼4 mm Hg |
Stop smoking | A | 1-6 mm Hg | |
Moderation of alcohol consumption | Limit alcohol to ≤2 drinks/day for men and ≤1 drink/day for women | A | ∼4 mm Hg |
A, Supported by one or more high quality randomized trials; BMI, body mass index, DASH, Dietary Approaches to Stop Hypertension.
Modified from Whelton PK, Carey RM, Aronow WS, et al: 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines, J Am Coll Cardiol 71:e127-e248, 2018. In Warshaw G et al: Hams primary care geriatrics, ed 7, Philadelphia, 2022, Elsevier.
TABLE 7 Antihypertensive Drugs
Drug Class | Mechanism of Action | Possible Adverse Effects |
---|---|---|
Thiazide-like diuretics Chlorthalidone Hydrochlorothiazide Indapamide | Inhibit sodium and chloride reabsorption in the kidney, reducing intravascular volume and peripheral vascular resistance | Volume depletion hypotension, hyponatremia, hypokalemia, hypomagnesemia, hyperuricemia (gout), hyperglycemia, renal impairment |
Potassium-sparing diuretics Triamterene Spironolactone | ||
Angiotensin-converting enzyme inhibitors (ACE inhibitors) Benazepril Captopril Fosinopril Lisinopril Ramipril | Inhibits ACE, interfering with conversion of angiotensin I to angiotensin II, reducing vasoconstriction | Hyperkalemia (with impaired renal function), cough, angioedema, rash, renal impairment, altered taste |
Angiotensin II receptor blockers (ARB) Candesartan Irbesartan Losartan Valsartan | Antagonizes angiotensin II AT1 receptors, reducing vasoconstriction | Hyperkalemia, renal impairment Do not use an ACE inhibitor and an ARB simultaneously |
Beta-Blockers | Sinus bradycardia, heart block, fatigue, bronchospasm, hyperglycemia, confusion. Not recommended as first-line agents unless the patient has ischemic heart disease or heart failure | |
Beta1 Selective Metoprolol | Selectively antagonizes β-1 adrenergic receptors | |
Dual acting Carvedilol Labetalol | Antagonizes α-1, β-1, and β-2 adrenergic receptors | |
Calcium channel blockers- Nondihydropyridines Diltiazem Verapamil | Prolong AV node refractory period and have negative inotropic effect; less effective as vasodilators | Sinus bradycardia, heart block, heart failure, rash, GERD, constipation, gingival hyperplasia |
Calcium channel blockers- Dihydropyridines Amlodipine Felodipine Nicardipine Nifedipine | Inhibit calcium influx, relaxing vascular smooth muscle and decreasing peripheral resistance causing vasodilation with little or no negative effect upon cardiac contractility or AV nodal conduction | Peripheral edema |
Alpha-adrenergic agonists, centrally acting Methyldopa Clonidine | Stimulates α-2 adrenergic receptors centrally | Sedation, dry mouth, constipation. Avoid in older adults because of central nervous system adverse effects |
Alpha1 selective adrenergic antagonists, peripherally acting Doxazosin Prazosin Terazosin | Antagonizes peripheral α-1 adrenergic receptors | Orthostatic hypotension. Consider in patients with benign prostatic hypertrophy |
GERD, Gastroesophageal reflux disease.
From Warshaw G et al: Hams primary care geriatrics, ed 7, Philadelphia, 2022, Elsevier.
TABLE 8 Antihypertensive Choice in the Setting of Cardiovascular Comorbidity
COMPELLING INDICATION | DIURETIC | BB | ACEI | ATRA | CCB | ALDO ant |
---|---|---|---|---|---|---|
Heart failure | ✓ | ✓ | ✓ | ✓ | ✓ | |
Post myocardial infarction | ✓ | ✓ | ✓ | |||
High risk of coronary artery disease | ✓ | ✓ | ✓ | ✓ | ||
Diabetes | ✓ | ✓ | ✓ | ✓ | ✓ | |
Chronic kidney disease | ✓ | ✓ | ||||
Recurrent stroke prevention | ✓ | ✓ |
ACEI, Angiotensin-converting enzyme inhibitor; ALDO ant, aldosterone antagonist; ATRA, angiotensin II receptor antagonist, BB, beta-adrenoceptor antagonist; CCB, calcium-channel blocker.
From Talley NJ et al: Essentials of internal medicine, ed 4, Chatswood, NSW, 2021, Elsevier Australia.
The therapeutic approach varies with the cause of the renovascular hypertension (RVH) (refer to Renal Artery Stenosis for additional information).
TABLE 9 Drugs Used to Treat Hypertension in Pregnancy
Drug | Starting Dose | Maximum Dose | Comments |
---|---|---|---|
Acute Treatment of Severe Hypertension | |||
Hydralazine | 5-10 mg IV every 20 min | 20 mg∗ | Avoid in cases of tachycardia and persistent headaches |
Labetalol | 20-40 mg IV every 10-15 min | 220 mg∗ | Avoid in women with asthma or congestive heart failure |
Nifedipine | 10-20 mg PO every 30 min | 50 mg∗ | Avoid in case of tachycardia and palpitations |
Long-Term Treatment of Hypertension | |||
Methyldopa | 250 mg bid | 4 g/day | |
Labetalol | 100 mg bid | 2400 mg/day | |
Nifedipine | 10 mg bid | 120 mg/day | |
Thiazide diuretic | 12.5 mg bid | 50 mg/day |
bid, Twice daily; IV, intravenous.
∗If desired blood pressure levels are not achieved, switch to another drug.
From Gabbe SG: Obstetrics, ed 6, Philadelphia, 2012, Saunders.
Therapy: The choice of therapeutic agents varies with the cause. IV medications are preferred in hypertensive emergencies.
TABLE 10 Treatment of Hypertensive Crisis: Intravenous Medications
Drug Name and Mechanism of Action | Indications/Advantages/Dose | Disadvantages/Adverse Effects/Metabolism Cautions |
---|---|---|
Sodium Nitroprusside | ||
Nitric oxide compound; vasodilation of arteriolar and venous smooth muscle Increases cardiac output by decreasing afterload | Useful in most hypertensive emergencies Onset of action immediate, duration of action 1-2 min Dose: 0.25 μg/kg/min Maximum dose: 8-10 μg/kg/min | Contraindicated in high-output cardiac failure, congenital optic atrophy. Anemia and liver disease at risk of cyanide toxicity: Acidosis, tachycardia, change in mental status, almond smell on breath. Risk of thiocyanate toxicity with renal disease: Psychosis, hyperreflexia, seizure, tinnitus. Cautious use with increased intracranial pressure. Do not use maximum dose for >10 min. Crosses the placenta. |
Nitroglycerin | ||
Directly interacts with nitrate receptors on vascular smooth muscle Primarily dilates venous bed Decreases preload | Use with symptoms of cardiac ischemia, perioperative hypertension in cardiac surgery Initial dose: 5 μg/min Maximum dose: 100 μg/min | Contraindicated in angle-closure glaucoma, increased intracranial pressure. Blood pressure decreased secondary to decreased preload, cardiac output-avoid when cerebral or renal perfusion compromised. Caution with right ventricular infarct. |
Labetalol | ||
β- and α-Adrenergic blockade α:β-Blocking ratio is 1:7 | Onset of action 2-5 min, duration 3-6 h Bolus 20 mg, then 20-80 mg every 10 min for maximum dose 300 mg Infuse at 0.5-2 mg/min | Avoid in bronchospasm, bradycardia, congestive heart failure, greater than first-degree heart block, second/third trimester pregnancy. Use caution with hepatic dysfunction, inhalational anesthetics (myocardial depression). Enters breast milk. |
Esmolol | ||
Cardioselective β1-adrenergic blocking agent | Use with aortic dissection Use during intubation, intraoperative, and postoperative hypertension Onset of action 60 sec, duration 10-20 min, 200-500 μg/kg/min for 4 min, then infuse 50-300 μg/kg/min | See labetalol. Not dependent on renal or hepatic function for metabolism (metabolized by hydrolysis in red blood cells). |
Fenoldopam | ||
Postsynaptic dopamine-1 agonist; decreases peripheral vascular resistance; 10 times more potent than dopamine as vasodilator | May be advantageous in kidney disease, increases renal blood flow, increases sodium excretion, no toxic metabolites Initial dose: 0.1 μg/kg/min, with titration every 15 min No bolus | Contraindicated in glaucoma (may increase intraocular pressure) or allergy to sulfites; hypotension, especially with concurrent β-blocker. Check serum potassium every 6 h. Concurrent acetaminophen may significantly increase blood levels. Dose-related tachycardia. |
Hydralazine | ||
Primarily dilates arteriolar vasculature | Primarily used in pregnancy/eclampsia Dose: 10 mg every 20-130 min; maximum dose 20 mg Decreases blood pressure in 10-20 min Duration of action 2-4 h | Reflex tachycardia; give β-blocker concurrently. May exacerbate angina. Half-life 3 h, affects blood pressure for 100 h. Depends on hepatic acetylation for inactivation. |
Phentolamine | ||
α-Adrenergic blockade | Used primarily to treat hypertension from excessive catecholamine excess (e.g., pheochromocytoma) Dose: 5-15 mg Onset of action 1-2 min, duration 3-10 min | β-Blockade is generally added to control tachycardia or arrhythmias. As in all catecholamine excess states, β-blockers should never be given first, as the loss of β-adrenergically mediated vasodilation will leave α-adrenergically mediated vasoconstriction unopposed and result in increased pressure. |
Nicardipine | ||
Dihydropyridine calcium channel blocker; inhibits transmembrane influx of calcium ions into cardiac and smooth muscle | Onset of action 10-20 min, duration 1-4 h Initial dose: 5 mg/h to maximum of 15 mg/h | Avoid with congestive heart failure, cardiac ischemia. Adverse effects include tachycardia, flushing, headache. |
Clevidipine | ||
Short-acting dihydropyridine calcium channel antagonist | Initial dose: 1 mg/h; can be increased to 21 mg/h | Reduces blood pressure without affecting cardiac filling pressures or causing reflex tachycardia. |
Enalaprilat | ||
Angiotensin-converting enzyme inhibitor | Onset of action 15-20 min, duration 12-24 h Dose: 1.25-5 mg every 6 h | Response not predictable, with high renin states may see acute hypotension. Hyperkalemia in setting of reduced glomerular filtration rate. Avoid in pregnancy. |
Trimethaphan | ||
Nondepolarizing ganglionic blocking agent; competes with acetylcholine for postsynaptic receptors | Used in aortic dissection Dose: 0.5-5 mg/min | Does not increase cardiac output. No inotropic cardiac effect. Disadvantages include parasympathetic blockade, resulting in paralytic ileus and bladder atony and development of tachyphylaxis after 24-96 h of use. |
From Vincent JL et al: Textbook of critical care, ed 7, Philadelphia, 2017, Elsevier.
The following are important points to remember when treating hypertensive emergencies:
TABLE 11 Guidelines for Blood Pressure Management in the Most Common Conditions Treated in the Neurologic-Neurosurgical Intensive Care Unit
Diagnosis | Recommendation | ||
---|---|---|---|
Acute ischemic stroke | Establish and maintain BP <185/110 mm Hg before receiving intravenous thrombolysis | ||
Keep <180/105 mm Hg if thrombolysis | |||
Treat only BP >220/120 mm Hg if no thrombolysis | |||
Keep <180/105 mm Hg following endovascular clot retrieval | |||
Intracerebral hemorrhage | Keep SBP <180 and MAP <130 mm Hg | ||
(ideal SBP <160 mm Hg) | |||
Subarachnoid hemorrhage | Keep SBP <160 mm Hg before aneurysm treated | ||
Do not lower BP after aneurysm treated | |||
Traumatic brain injury | Keep adequate MAP to maintain CPP 60-70 mm Hg Suggested SBP goals: >100 mm Hg (ages 50-69 yr) or >110 mm Hg (ages 15-49 yr) |
BP, Blood pressure; CPP, cerebral perfusion pressure; MAP, mean arterial pressure; SBP, systolic blood pressure.
From Jankovic J et al: Bradley and Daroffs neurology in clinical practice, ed 8, Philadelphia 2022, Elsevier.
TABLE 12 Indications for Specialist Referral for Patients With Hypertension
Urgent Treatment Needed | |||
Accelerated hypertension (severe hypertension with grade III-IV retinopathy) | |||
Particularly severe hypertension (>220/120 mm Hg) | |||
Impending complications (e.g., transient ischemic attack, left ventricular failure) | |||
Possible Underlying Cause | |||
Any clue in history or examination of a secondary cause (e.g., hypokalemia with increased or high-normal plasma sodium) | |||
Elevated serum creatinine | |||
Proteinuria or hematuria | |||
Sudden onset or worsening of hypertension | |||
Young age (any hypertension <20 yr; needing treatment <30 yr) | |||
Therapeutic Problems | |||
Multiple drug intolerances | |||
Multiple drug contraindications | |||
Persistent nonadherence or nonconcordance | |||
Special Situations | |||
Unusual blood pressure variability | |||
Possible white coat hypertension | |||
Hypertension in pregnancy |
From Floege J et al: Comprehensive clinical nephrology, ed 4, Philadelphia, 2010, Saunders.
High Blood Pressure (Patient Information)
High Blood Pressure-Child (Patient Information)
Eclampsia (Related Key Topic)
Pheochromocytoma (Related Key Topic)
Preeclampsia (Related Key Topic)
Renal Artery Stenosis (Related Key Topic)