Chronic hypertension causes
Chronic Hypertension Microchapters
Chronic hypertension causes On the Web
Secondary hypertension is only responsible for 5% of cases of chronic hypertension whereas primary hypertension (also known as essential hypertension where no identifiable cause is identified) is responsible for 95% of cases. Common causes of secondary hypertension include obstructive sleep apnea, hyperaldosteronism, kidney diseases, excess catecholamines, coarctation of the arota, cushing syndrome among other diseases.
|Primary hypertension |
(also known as essential hypertension)
(95% of the cases)
(5% of the cases)
When a full evaluation yields no clear etiology for the elevated blood pressure, the latter is identified as primary hypertension. Primary or essential hypertension is considered a chronic disease requiring lifelong treatment and follow-up. If an underlying disease is identifiable as the cause, secondary hypertension is diagnosed. Secondary hypertension is a potentially curable condition in most cases. In comparison, the prevalence of primary hypertension is significantly higher than secondary hypertension, where only 5-10% of patients have a secondary etiology Classically, the common age range for the presentation of primary hypertension is 30 to 55 years, but age alone should never warrant a diagnosis of primary hypertension without a proper work-up.
When to Suspect Secondary Hypertension
It is not cost effective to evaluate all hypertensive patients for secondary hypertension.  There are certain clinical scenarios, though, that should prompt further evaluation.
Early Onset Hypertension Under Age 30
Primary hypertension generally first occurs between 30 and 55 years. Onset of hypertension before puberty and before age 30 in the absence of risk factors should raise suspicion for secondary hypertension.
Abrupt Onset of Hypertension in A Normotensive Patient
Rapidly Progressive Hypertension or a Hypertensive Emergency or Urgency
Evaluation of Secondary Hypertension
Evaluation of secondary hypertension
Investigation should be limited for patients with clues suggestive of potentially correctable causes.
❑ Perform noninvasive diagnostic studies
Look for findings suggestive of other identifiable causes
❑ Obstructive sleep apnea
❑ Aortic coarctation
Common Causes of Secondary Hypertension
Common causes of secondary hypertension are often memorized by the mnemonic ABCDE:
|Letter||Causes of Secondary Hypertension|
|A||Accuracy, Apnea, Aldosteronism|
|B||Bruit, Bad Kidneys|
|C||Catecholamines, Coarctation, Cushing’s Syndrome|
|E||Erythropoitin, Endocrine Disorders|
An accurate assessment and re-assessment of blood pressures is an essential first step when a patient presents with high blood pressure. The accuracy of home BP measurements should be confirmed by calibrating the patient's measurement technique with that obtained in the doctor's office.
Obstructive sleep apnea (OSA) is a respiratory disease characterized by repetitive narrowing or collapse of the upper airway during sleep leading to apnea, hypopnea, and a nocturnal decrease in oxygen tension. Symptoms and signs that might suggest OSA include daytime somnolence, obesity, snoring, and morning headache. Patients with sleep apnea also tend to have drug resistant hypertension and may retain sodium. Diagnosis is made by polysomnography. Treatment relies on maintaining airway patency at night and includes, among others, the use of continuous positive airway pressure (CPAP).
Primary (hyporeninemic) and secondary (hyperreninemic) hyperaldosteronism result in excess sodium and water retention with slight hypernatremia along with excretion of potassium resulting in hypokalemia in one half of patients. Common symptoms of hyperaldosteronism include drug resistant hypertension, fatigue, headache, intermittent paralysis, muscle weakness, and numbness. The most common cause of primary hyperaldosteronism is an aldosterone-producing adenoma (an "aldosteronoma"), i.e. Conn’s Syndrome. Secondary hyperaldosteronism is due to an overactive RAAS, as seen in renin-secreting tumors, renal artery stenosis, pheochromocytoma, and other syndromes. The diagnosis is made by measuring the ratio of plasma aldosterone to plasma renin activity. It is elevated in primary hyperaldosteronism and decreased/normal with elevated renin in secondary hyperaldosteronism. It should be noted that obesity can also cause aldosterone levels to be elevated. Treatment depends upon the underlying etiology: surgery to resect an adenoma causing primary hyperaldosteronism and spironolactone, an aldosterone antagonist to treat secondary hyperaldosteronism.
Renovascular hypertension is due to decreased blood supply to the kidneys secondary to renal artery stenosis and it is the most common correctable cause of secondary hypertension. Atherosclerosis of the renal artery (renal artery stenosis) in older patients above 50 years of age and fibromuscular dysplasia in younger patients are the most common etiologies.
According to the 2013 ACC/AHA Guidelines for the Management of PAD, diagnostic work-up for renal artery stenosis is indicated in the following conditions:
Class I Recommendations
- Hypertension of any stage before the age of 30
- Stage II hypertension (severe hypertension systolic blood pressure > 180 mm Hg or diastolic blood pressure > 120 mm Hg) in patients older than 55 years. If only mild hypertension is present, then renal artery stenosis is the underlying cause in only 1% of patients , but if the blood pressure is markedly elevated, then the risk of renal artery stenosis goes up 10 to 50 fold.
- Accelerated condition of previously controlled hypertension
- Resistant hypertension
- Malignant hypertension
- New azotemia (50% rise in creatinine that is sustained) within one week after administration of an Angiotensin Converting Enzyme (ACE)inhibitor or ARB
- Unexplained atrophic kidney or asymmetric kidneys that differ by > 1.5 cm. If the kidney is < 9 cm in size, there is a 75% chance that renal artery stenosis is present.
- Severe hypertension, impaired renal function, and recurrent flash pulmonary edema
Class IIa Recommendations
- Unexplained renal failure including patients starting renal replacement therapy
Class IIb Recommendations
- Presence of multi vessel CAD and no clinical clues of ARAS or PAD
- Unexplained CHF or refractory angina
- Severe hypertension in the presence of polyvascular disease (coronary artery disease or peripheral arterial disease)
- A unilateral systolic-diastolic abdominal bruit. Although a bruit is infrequent in documented renal artery stenosis (the sensitivity is only 40% percent) if it is auscultated, it is associated with a very high specificity of 99%.
- The association of race with renal artery stenosis is not clear. Reports that it is observed more often in white patients may be due to reporting bias.
Definitive diagnosis is made by magnetic resonance angiography (MRA) and renal arteriography. Other diagnostic methods include duplex ultrasound scanning, and captopril-augmented radio-isotopic renogram. Treatment is based upon the underlying etiology.
Bad Kidney (Chronic Renal Failure)
Renal parenchymal disease blunts the kidney’s physiological ability to maintain appropriate blood pressure. Notably, hypertension is both a cause and a consequence of renal parenchymal disease; the two are closely associated and may potentiate each other. The diagnosis is made by demonstration of a decreased GFR. The mechanisms by which renal parenchymal disease leads to the development of hypertension are numerous and include activation of the local RAAS, release of vasoconstrictor cytokines, and inappropriate natriuresis for any given blood pressure.
Catecholamine excess occurs in several non-disease states, such as acute stress, the administration of medications with sympathomimetic activity, and illicit drug use such as cocaine and these conditions can be ruled out by thorough history taking. Pheochromocytoma, a tumor of the adrenal gland leading to excess secretion of epinephrine, should be considered in young patients with the triad of intermittent hypertensive episodes causing headache, sweating, and tachycardia. However, pheochromocytoma in older adults or a presentation with sustained hypertension is not uncommon. Diagnostic studies to evaluate pheochromocytoma include measurement of plasma free metanephrines and urinary fractionated metanephrines. The diagnostic value of plasma and urinary catecholamines is of limited value given the very short half-life of catecholamines. Treatment is usually by surgical resection of the secreting tumor with appropriate adrenergic blockade.
Coarctation of the aorta is a congenital heart defect, caused by a narrowing in a segment of the ascending or descending aorta. The diagnosis is often made in a neonate or an infant as a result of a weak femoral pulse or asymmetric brisk brachial pulses. Hypertension occurs as a result of a reduction in the effective circulation at the level of the kidneys which respond by increasing plasma volume which in turn causes hypertension in the upper extremities. Diagnosis is by CT angiography, but can also be made in neonates and infants by ultrasound of the heart and the great vessels. Definitive treatment is by surgical correction and or stenting.
Cushing's syndrome is an endocrine disorder caused by prolonged exposure to high endogenous or exogenous cortisol levels. Hypertension in Cushing’s syndrome has been classically attributed to the mineralocorticoid effects of cortisol. It manifests as an absent fall of nocturnal blood pressure physiologically seen in normotensive subjects with associated disturbance in the adrenocorticotropic hormone-glucocorticoid system. Symptoms of Cushing's syndrome include rapid weight gain, particularly of the trunk and face with sparing of the limbs (central obesity), a round face often referred to as a "moon face" along with central obesity, excess sweating, proximal muscle weakness, ecchymoses, insomnia, reduced libido, impotence, amenorrhoea, infertility and psychological disturbances, ranging from euphoria to psychosis. Depression and anxiety. Although an ideal diagnostic test is not considered yet available, clinicians often assess the 24-hour urinary cortisol excretion, a low-dose dexamethasone suppression test, late evening serum or salivary cortisol, and a CRH a following a dexamethasone suppression test to establish the diagnosis.
An extensive list of drugs can be associated with hypertension. The most common agents include immunosuppressive agents, non-steroidal anti-inflammatory drugs, oral contraceptive pills, some weight loss agents, stimulants, monoamine oxidase inhibitors, triptans, ergotamines, and sympathomimetics.
In addition to the association of obesity with hypertension, the 2001 study “Effects on Blood Pressure of Reduced Dietary Sodium and the Dietary Approaches to Stop Hypertension (DASH) Diet” concluded that a high sodium diet above the recommended 100 mmol per day (2.4 g of sodium or 6 g of sodium chloride salt) is associated with hypertension. As a result, reduction of sodium levels below 100 mmol per day and following the DASH diet (rich in vegetables, fruits, with low-fat dairy products) can significantly lower BP. Ingestion of excessive amounts of liquorice can lead to elevation in the blood pressure.
Elevated erythropoietin is typically seen in COPD patients who have functional anemia due to chronic hypoxia and in hematologic disorders such as polycythemia. The pathogenesis of erythropoietin-induced hypertension includes increased hematocrit and blood viscosity, altered sensitivity to vasopressors, dysregulated vasodilatory factors, and vascular cell growth causing arterial remodeling and changes in arterial smooth musculature. Diagnosis and treatment are etiology-dependent.
In addition to the more common endocrine causes of hypertension such as hyperaldosteronism, Cushing’s syndrome, and pheochromocytoma, several other endocrine changes can cause hypertension. Both hypothyroidism and hyperthyroidism can cause hypertension by volume retention and by increased cardiac output, respectively. Also, hyperparathyroidism and hypovitaminosis D can cause hypertension due to poorly understood mechanisms, where parathyroidectomy seems to significantly decrease blood pressure in patients with parathyroid disease and elevated BP. Acromegaly can also be a cause of hypertension.
Causes by Organ System
Causes in Alphabetical Order
- Onusko E (2003). "Diagnosing secondary hypertension". Am Fam Physician. 67 (1): 67–74. PMID 12537168.
- Chiong JR, Aronow WS, Khan IA, Nair CK, Vijayaraghavan K, Dart RA; et al. (2008). "Secondary hypertension: current diagnosis and treatment". Int J Cardiol. 124 (1): 6–21. doi:10.1016/j.ijcard.2007.01.119. PMID 17462751.
- Dosh SA (2001). "The diagnosis of essential and secondary hypertension in adults". J Fam Pract. 50 (8): 707–12. PMID 11509166.
- Hirsch AT, Haskal ZJ, Hertzer NR, Bakal CW, Creager MA, Halperin JL; et al. (2006). "ACC/AHA 2005 Practice Guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease): endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation". Circulation. 113 (11): e463–654. doi:10.1161/CIRCULATIONAHA.106.174526. PMID 16549646.
- Rooke TW, Hirsch AT, Misra S, Sidawy AN, Beckman JA, Findeiss LK; et al. (2011). "2011 ACCF/AHA Focused Update of the Guideline for the Management of Patients With Peripheral Artery Disease (updating the 2005 guideline): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines". J Am Coll Cardiol. 58 (19): 2020–45. doi:10.1016/j.jacc.2011.08.023. PMID 21963765.
- Eckert DJ, Malhotra A (2008). "Pathophysiology of adult obstructive sleep apnea". Proc Am Thorac Soc. 5 (2): 144–53. doi:10.1513/pats.200707-114MG. PMC 2628457. PMID 18250206.
- Silverberg DS, Oksenberg A (1996). "Essential and secondary hypertension and sleep-disordered breathing: a unifying hypothesis". J Hum Hypertens. 10 (6): 353–63. PMID 8872797.
- Victor LD (1999). "Obstructive sleep apnea". Am Fam Physician. 60 (8): 2279–86. PMID 10593319.
- Ganguly A (1998). "Primary aldosteronism". N Engl J Med. 339 (25): 1828–34. doi:10.1056/NEJM199812173392507. PMID 9854120.
- Gordon RD, Stowasser M, Tunny TJ, Klemm SA, Rutherford JC (1994). "High incidence of primary aldosteronism in 199 patients referred with hypertension". Clin Exp Pharmacol Physiol. 21 (4): 315–8. PMID 7923898.
- Chade AR, Rodriguez-Porcel M, Grande JP, Krier JD, Lerman A, Romero JC; et al. (2002). "Distinct renal injury in early atherosclerosis and renovascular disease". Circulation. 106 (9): 1165–71. PMID 12196346.
- Anderson JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Curtis LH; et al. (2013). "Management of patients with peripheral artery disease (compilation of 2005 and 2011 ACCF/AHA guideline recommendations): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines". Circulation. 127 (13): 1425–43. doi:10.1161/CIR.0b013e31828b82aa. PMID 23457117.
- Lewin A, Blaufox MD, Castle H, Entwisle G, Langford H (1985). "Apparent prevalence of curable hypertension in the Hypertension Detection and Follow-up Program". Arch Intern Med. 145 (3): 424–7. PMID 3872106.
- Turnbull JM (1995). "The rational clinical examination. Is listening for abdominal bruits useful in the evaluation of hypertension?". JAMA. 274 (16): 1299–301. PMID 7563536.
- Svetkey LP, Kadir S, Dunnick NR, Smith SR, Dunham CB, Lambert M; et al. (1991). "Similar prevalence of renovascular hypertension in selected blacks and whites". Hypertension. 17 (5): 678–83. PMID 2022411.
- Wofford MR, King DS, Wyatt SB, Jones DW (2000). "Secondary Hypertension: Detection and Management for the Primary Care Provider". J Clin Hypertens (Greenwich). 2 (2): 124–131. PMID 11416635.
- AbuRahma AF, Srivastava M, Mousa AY, Dearing DD, Hass SM, Campbell JR; et al. (2012). "Critical analysis of renal duplex ultrasound parameters in detecting significant renal artery stenosis". J Vasc Surg. 56 (4): 1052–9, 1060.e1, discussion 1059-60. doi:10.1016/j.jvs.2012.03.036. PMID 22595689.
- Aitchison F, Page A (1999). "Diagnostic imaging of renal artery stenosis". J Hum Hypertens. 13 (9): 595–603. PMID 10482969.
- Soergel M, Schaefer F (2002). "Effect of hypertension on the progression of chronic renal failure in children". Am J Hypertens. 15 (2 Pt 2): 53S–56S. PMID 11866231.
- Lenders JW, Pacak K, Walther MM, Linehan WM, Mannelli M, Friberg P; et al. (2002). "Biochemical diagnosis of pheochromocytoma: which test is best?". JAMA. 287 (11): 1427–34. PMID 11903030.
- Imai Y, Abe K, Sasaki S, Minami N, Nihei M, Munakata M; et al. (1988). "Altered circadian blood pressure rhythm in patients with Cushing's syndrome". Hypertension. 12 (1): 11–9. PMID 3397172.
- Yudofsky, Stuart C. (2007). The American Psychiatric Publishing Textbook of Neuropsychiatry and Behavioral Neurosciences (5th ed.). American Psychiatric Pub, Inc. ISBN 1585622397. Unknown parameter
- Contreras LN, Hane S, Tyrrell JB (1986). "Urinary cortisol in the assessment of pituitary-adrenal function: utility of 24-hour and spot determinations". J Clin Endocrinol Metab. 62 (5): 965–9. PMID 3958132.
- NUGENT CA, NICHOLS T, TYLER FH (1965). "Diagnosis of Cushing's Syndrome; Single Dose Dexamethasone Suppression Test". Arch Intern Med. 116: 172–6. PMID 14315650.
- Raff H, Raff JL, Findling JW (1998). "Late-night salivary cortisol as a screening test for Cushing's syndrome". J Clin Endocrinol Metab. 83 (8): 2681–6. PMID 9709931.
- Yanovski JA, Cutler GB, Chrousos GP, Nieman LK (1993). "Corticotropin-releasing hormone stimulation following low-dose dexamethasone administration. A new test to distinguish Cushing's syndrome from pseudo-Cushing's states". JAMA. 269 (17): 2232–8. PMID 8386285.
- Sacks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, Harsha D; et al. (2001). "Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group". N Engl J Med. 344 (1): 3–10. doi:10.1056/NEJM200101043440101. PMID 11136953.
- Vaziri ND (1999). "Mechanism of erythropoietin-induced hypertension". Am J Kidney Dis. 33 (5): 821–8. PMID 10213636.
- Chopra S, Cherian D, Jacob JJ (2011). "The thyroid hormone, parathyroid hormone and vitamin D associated hypertension". Indian J Endocrinol Metab. 15 Suppl 4: S354–60. doi:10.4103/2230-8210.86979. PMC 3230087. PMID 22145139.