eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Cardiology

Hypertension

Author: Edwin Rodriguez-Cruz, MD, Assistant Professor, Department of Pediatrics, San Juan Bautista Medical School and Medical Center; Consulting Interventional/Clinical Pediatric Cardiologist, Department of Pediatrics, Hospital El Maestro and San Juan Bautista Medical Center; Consulting Interventional/Clinical Pediatric Cardiologist, Department of Cardiology, Cardiovascular Center of Puerto Rico and the Caribbean and Veterans Affairs Hospital and Medical Center of Puerto Rico
Coauthor(s): Leigh M Ettinger, MD, MS, Clinical Assistant Professor, Division of Pediatric Nephrology, The Joseph M Sanzari Children's Hospital, Hackensack University Medical Center; Adrian Spitzer, MD, Professor, Department of Pediatrics, Albert Einstein College of Medicine; Director of NIH Training Program, Children's Hospital at Montefiore Medical Center
Contributor Information and Disclosures

Updated: Nov 16, 2009

Introduction

Background

Hypertension is a major cause of morbidity and mortality in the United States and in many other countries. The prevalence of hypertension in the United States for people aged 60-69 years is more than 50%. This prevalence increases to approximately 75% among those aged 75 years. Hypertension is now commonly discovered in children. The long-term health risks to these children with hypertension may be substantial.

For children in the United States, extensive normative data for blood pressure (BP) are available. The Task Force on Blood Pressure Control in Children commissioned by the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health developed standards for BP by using the results of 11 surveys of more than 83,000 person visits of infants and children. Approximately equal numbers of boys and girls were surveyed. The percentile curves were first published in 1987 and describe age-specific distributions of systolic and diastolic BPs in infants and children with corrections for height and weight.1

The Third Report of the Task Force, published in 1996, provides further details regarding the diagnosis and treatment of hypertension in infants and children.2 In 2004, the Fourth Report added normative data and adapted the data to growth charts from the Centers for Disease Control and Prevention (CDC) for 2000.3 See 2000 CDC Growth Charts: United States.

In accordance with the recommendations of the Task Force, BP is considered normal when the systolic and diastolic values are less than the 90th percentile for the child's age, sex, and height.

The Fourth Report introduced a new category called prehypertension. The condition is diagnosed when a child's average BP exceeds the 90th percentile but is less than the 95th percentile. Any adolescent whose BP is greater than 120/80 mm Hg is also given this diagnosis, even if their reading is less than the 90th percentile. This classification was created to align the categories for children with the categories for adults from the 2003 recommendations of the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure.

Stage I hypertension is diagnosed if a child's BP is greater than the 95th percentile but less than or equal to the 99th percentile plus 5 mm Hg. A child is classified as having stage II hypertension if their BP is greater than the 99th percentile plus 5 mm Hg.

If the systolic and diastolic classifications cause a discrepancy, the child's condition should be categorized by using the higher value. Table 1 serves as a guide to the practicing physician. Full tables from the NHLBI may be found at Blood Pressure Tables for Children and Adolescents.

Table 1. The 95th Percentiles of Blood Pressure in Children and Adolescents3

Open table in new window

Table
Age, yBP for Girls by Percentile for Height, mm HgBP for Boys by Percentile for Height, mm Hg
50th75th50th75th
1104/58105/59103/56104/58
6111/74113/74114/74115/75
12123/80124/81123/81125/82
17129/84130/85136/87138/87
Age, yBP for Girls by Percentile for Height, mm HgBP for Boys by Percentile for Height, mm Hg
50th75th50th75th
1104/58105/59103/56104/58
6111/74113/74114/74115/75
12123/80124/81123/81125/82
17129/84130/85136/87138/87


Pathophysiology

BP is determined by the balance between cardiac output and vascular resistance. A rise in either of these variables, in the absence of a compensatory decrease in the other, increases mean BP, which is the driving pressure. Several factors regulate cardiac output and vascular resistance.

Factors that affect BP include the following:4

  • Cardiac output
    • Baroreceptors
    • Extracellular volume
    • Effective circulating volume
      • Atrial natriuretic hormones
      • Mineral corticoids
      • Angiotensin
    • Sympathetic nervous syndrome
  • Vascular resistance
    • Pressors
      • Angiotensin II
      • Calcium (intracellular)
      • Catecholamines
      • Sympathetic nervous system
      • Vasopressin
    • Depressors
      • Atrial natriuretic hormones
      • Endothelial relaxing factors
      • Kinins
      • Prostaglandin E 2
      • Prostaglandin I 2

Changes in electrolyte homeostasis, particularly changes in sodium, calcium, and potassium concentrations, affect some of the factors shown above. Under normal conditions, the amount of sodium excreted in the urine matches the amount ingested, resulting in near constancy of extracellular volume. Retention of sodium results in increased extracellular volume, which is associated with an elevation of BP. By means of various physical and hormonal mechanisms, this elevation triggers changes in both the glomerular filtration rate and the tubular reabsorption of sodium, resulting in excretion of excess sodium and restoration of sodium balance.

A rise in the intracellular calcium concentration, due to changes in plasma calcium concentration, increases vascular contractility. In addition, calcium stimulates the release of renin, synthesis of epinephrine, and activity of the sympathetic nervous system. Increased potassium intake suppresses production and release of renin and induces natriuresis, decreasing BP. The complexity of the system explains the difficulties often encountered in identifying the mechanism that accounts for hypertension in a particular patient. This difficulty explains why treatment is often designed to affect regulatory factors rather than the cause of the disease.

In a child who is obese, hyperinsulinemia may elevate BP by increasing sodium reabsorption and sympathetic tone.

Frequency

United States

The true incidence of hypertension in the pediatric population is not known. This vagueness partly stems from the somewhat arbitrary definition of hypertension. In adults, hypertension is defined on the basis of data from extensive studies that allowed for correlation of BP with adverse events, such as heart failure or stroke.

Similar studies have not been performed in children, although reports from small populations of children provided compelling evidence of a relationship between hypertension and both ventricular hypertrophy and atherosclerosis. In children, the definition of hypertension is based exclusively on frequency-distribution curves for BP. As a consequence, estimations of the prevalence of pediatric hypertension lack a scientific basis. The number of children who might be defined as having hypertension and the frequency with which they develop complications during adulthood remains unknown.

International

Because of differences in genetic and environmental factors, incidences vary from country to country and even from region to region in the same country.

Mortality/Morbidity

High blood pressure is a precursor of heart attacks and strokes; well established in the adult literature. Children who are obese have approximately a 3-fold higher risk for hypertension than children who are not obese. In studies, as many as 41% of children with high BP have left ventricular hypertrophy.5 Almost 60% of children with persistent elevated BP had relative weights greater than 120% of the median for their sex, height, and age.

Race

The Task Force on Blood Pressure Control in Children noted no differences in BP between African American and Caucasian children. However, peripheral vascular resistance and sensitivity of BP to salt intake appear greater in African American children than in Caucasian children, at any age.

Sex

No significant differences are observed in BP between girls and boys younger than 6 years. From that age until puberty, BP is slightly higher in girls than in boys. At puberty and beyond, BP is slightly higher in male adolescents and men than in comparably aged female adolescents and women.

Age

Height and weight affect BP. However, these relationships do not become evident until children are school aged. The Task Force on Blood Pressure Control in Children considered these factors when they published their normative data in 1987.1

Numerous investigators have noted a correlation between the BP of parents and that of their offspring. Familial aggregation of BP is detectable early in life. Some data relate this association to concomitant obesity in both parent and child.

Clinical

History

A well-taken history provides clues about the cause of hypertension and guides the nature and sequence of ensuing investigations.

  • Relevant information includes the following:
    • Prematurity
    • Bronchopulmonary dysplasia
    • History of umbilical artery catheterization
    • Failure to thrive
    • History of head or abdominal trauma
    • Family history of heritable diseases (eg, neurofibromatosis, hypertension)
    • Medications (eg, pressor substances, steroids, tricyclic antidepressants, cold remedies, medications for attention deficit hyperactivity disorder [ADHD])
    • Episodes of pyelonephritis (perhaps suggested by unexplained fevers) that may result in renal scarring
    • Dietary history, including caffeine, licorice, and salt consumption
    • Sleep history, especially snoring history
    • Habits, such as smoking, drinking alcohol, and ingesting illicit substances
  • Presenting symptoms and signs are not specific in neonates and absent in most older children unless their hypertension is severe.
  • Signs and symptoms that should alert the physician to the possibility of hypertension include the following:
    • Neonates
      • Failure to thrive
      • Seizure
      • Irritability or lethargy
      • Respiratory distress
      • Congestive heart failure
    • Children (Findings in addition to those observed in neonates)
      • Headache
      • Fatigue
      • Blurred vision
      • Epistaxis
      • Bell palsy 

Physical

  • Measurement and recording of blood pressure (BP)
    • Best medical care includes yearly measurement of BP in every child older than 3 years, preferably by means of auscultation with a mercury gravity manometer. Doppler and oscillometric techniques can be used in children in whom auscultatory BP measurements are difficult to obtain. Measurements obtained by using oscillometric devices that exceed the 90th percentile should be repeated with auscultation.
    • Measurements repeated over time are required to obtain meaningful information.
    • Proper cuff size is essential for accurate measurement of BP. The width of the rubber bladder inside the cloth cover should cover at least 40% of the patient's arm circumference at a point midway between the olecranon and the acromion. The length of the bladder in the cuff should cover 80-100% of the circumference of the arm. If a cuff is too small, the next larger cuff size should be used, even if it appears too large.
    • The child should be relaxed and in a comfortable, preferably sitting, position with the child's feet on the floor and the back supported. The patient's right arm should be resting on a supportive surface at the level of the heart. Infants can be examined while supine.
    • The cuff should be inflated at a pressure approximately 20 mm greater than that at which the radial pulse disappears and then allowed to deflate at a rate of 2-3 mm Hg/s.
    • The first Korotkoff sound (ie, appearance of a clear tapping sound) defines the systolic pressure, whereas the fifth Korotkoff sound (ie, disappearance of all sounds) defines the diastolic pressure. The fourth (low-pitched, muffled) sound and the fifth sound frequently occur simultaneously, or the fifth sound may not occur at all. Diastolic BP must be recorded. When Korotkoff sounds can be heard down to 0 mm Hg, the BP measurement should be repeated with less pressure applied to the head of the stethoscope than was applied before.
    • Systolic BP in the lower extremities must be measured when elevated systolic BP in the upper extremities is first noted regardless of whether amplitude of the arterial pulse seems lower in the legs to be lower than that in the arms. Increased systolic pressure in the arm suggests coarctation of the aorta. If found, systolic pressure must also be measured in the left arm and leg. With the patient in the supine position, place a cuff on the calf. The cuff should be wide enough to cover at least two thirds of the distance from knee to ankle. Doppler sonography can be used to detect onset of blood flow, which reflects systolic BP, in the posterior tibial or dorsalis pedis artery. The value should be compared with a similarly obtained Doppler systolic BP in the arm, again with the patient supine.
    • Remember that the artifact of distal pulse amplification causes the measured systolic BP at the brachial artery to be less than that at the posterior tibial or dorsalis pedis artery. This difference may be only a few millimeters in the infant but can rise to 10-20 mm Hg in the older child or adult. Magnitude of this artifact is directly proportional to the pulse pressure. In a patient with chronic aortic regurgitation, for example, the difference in measured systolic pressure may exceed 40 mm Hg. At no time should the systolic pressure in the arm exceed that in the foot. If it does, pressures in both arms and legs should be measured. Consistent recording of high arm systolic pressure indicates aortic coarctation. High pressure in only the right arm suggests that an obstruction is present proximal to origin of the left subclavian artery.
  • Interpretation of BPs
    • Hypertension is defined as average systolic or diastolic BPs greater than those at the 95th percentile (see Table 1). Any child with a BP exceeding the 90th percentile requires scrutiny.
    • Patients with severe hypertension and target-organ damage require immediate attention. For other patients, several measurements of BP should be made at weekly intervals to determine if the elevation is sustained.
    • The average of multiple measurements should be plotted on an appropriate percentile chart. If the average measurement is between the 90th and 95th percentiles (ie, prehypertensive) the child's BP should be monitored at 6-month intervals. If the average BP is greater than the 95th percentile, the child should be evaluated further and therapy considered.
    • Patients with stage I hypertension should be seen again in 1-2 weeks. Those with stage II hypertension should be reevaluated in 1 week or sooner if the patient is symptomatic.
    • White-coat hypertension is diagnosed in a patient who has a BP above the 95th percentile when measured in the physician's office but who is normotensive outside the clinical setting. Ambulatory monitoring of BP usually is required to diagnose white-coat hypertension.
  • Objective of physical examination: A primary objective of the physical examination is to identify signs of secondary hypertension, including the following:
    • Café au lait spots to assess for neurofibromatosis
    • Abdominal mass to assess for Wilms tumor and polycystic kidney disease
    • Epigastric and/or abdominal bruit to assess for coarctation of the abdominal aorta or renal artery stenosis
    • BP difference between upper and lower extremities to assess for coarctation of the thoracic aorta
    • Thyromegaly to assess for hyperthyroidism
    • Virilization or ambiguity to assess for adrenal hyperplasia
    • Stigmata of Bardet-Biedl, von Hippel-Landau, Williams, or Turner syndromes
    • Acanthosis nigricans to assess for metabolic syndrome

Causes

Hypertension can be primary (ie, essential) or secondary.

  • In general, the younger the child and the higher the BP, the greater the likelihood that hypertension is secondary to an identifiable cause. A secondary cause of hypertension is most likely to found before puberty. After puberty, hypertension is likely to be essential.
  • A review of literature revealed that 78% of 563 young patients with secondary hypertension had a renal parenchymal abnormality. In the remaining 22%, the cause of hypertension, in order of frequency, was renal artery stenosis, coarctation of the aorta, pheochromocytoma, and a variety of other conditions.
  • Table 2. Common Causes of Hypertension by Age

    Open table in new window

    Table
    InfantsChildrenAdolescents
    1-6 y7-12 y
    • Thrombosis of renal artery or vein
    • Congenital renal anomalies
    • Coarctation of the aorta
    • Bronchopulmonary dysplasia
    • Renal artery stenosis
    • Renal parenchymal disease
    • Wilms tumor
    • Neuroblastoma
    • Coarctation of the aorta
    • Renal parenchymal disease
    • Renovascular abnormalities
    • Endocrine causes
    • Essential hypertension
    • Essential hypertension
    • Renal parenchymal disease
    • Endocrine causes
    InfantsChildrenAdolescents
    1-6 y7-12 y
    • Thrombosis of renal artery or vein
    • Congenital renal anomalies
    • Coarctation of the aorta
    • Bronchopulmonary dysplasia
    • Renal artery stenosis
    • Renal parenchymal disease
    • Wilms tumor
    • Neuroblastoma
    • Coarctation of the aorta
    • Renal parenchymal disease
    • Renovascular abnormalities
    • Endocrine causes
    • Essential hypertension
    • Essential hypertension
    • Renal parenchymal disease
    • Endocrine causes

More on Hypertension

Overview: Hypertension
Differential Diagnoses & Workup: Hypertension
Treatment & Medication: Hypertension
Follow-up: Hypertension
Multimedia: Hypertension
References

References

  1. [Guideline] Task Force. Report of the Second Task Force on Blood Pressure Control in Children--1987. Task Force on Blood Pressure Control in Children. National Heart, Lung, and Blood Institute, Bethesda, Maryland. Pediatrics. Jan 1987;79(1):1-25. [Medline].

  2. [Guideline] Task Force. Update on the 1987 Task Force Report on High Blood Pressure in Children and Adolescents: a working group report from the National High Blood Pressure Education Program. National High Blood Pressure Education Program Working Group on Hypertension Control. Pediatrics. Oct 1996;98(4 Pt 1):649-58. [Medline].

  3. [Guideline] NHLBI. National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents. The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. Pediatrics. Aug 2004;114(2 Suppl 4th Report):555-76. [Medline][Full Text].

  4. Gruskin AB. Factors affecting blood pressure. In: Drukker A, Gruskin AB, eds. Pediatric Nephrology: Pediatric and Adolescent Medicine. 3rd ed. Basel, Switzerland: Karger; 1995:1097.

  5. Hanevold C, Waller J, Daniels S, Portman R, Sorof J. The effects of obesity, gender, and ethnic group on left ventricular hypertrophy and geometry in hypertensive children: a collaborative study of the International Pediatric Hypertension Association. Pediatrics. Feb 2004;113(2):328-33. [Medline].

  6. [Guideline] University of Michigan Health System. Essential hypertension. Ann Arbor (MI): University of Michigan Health System; 2009 Feb. [Full Text].

  7. Bartosh SM, Aronson AJ. Childhood hypertension. An update on etiology, diagnosis, and treatment. Pediatr Clin North Am. Apr 1999;46(2):235-52. [Medline].

  8. Falkner B, Gidding SS, Portman R, Rosner B. Blood pressure variability and classification of prehypertension and hypertension in adolescence. Pediatrics. Aug 2008;122(2):238-42. [Medline].

  9. Gerber LM, Stern PM. Relationship of body size and body mass to blood pressure: sex-specific and developmental influences. Hum Biol. Aug 1999;71(4):505-28. [Medline].

  10. Hindmarsh PC, Brook CG. Evidence for an association between birth weight and blood pressure. Acta Paediatr Suppl. Feb 1999;88(428):66-9. [Medline].

  11. Lauer RM, Connor WE, Leaverton PE, Reiter MA, Clarke WR. Coronary heart disease risk factors in school children: the Muscatine study. J Pediatr. May 1975;86(5):697-706. [Medline].

  12. Moore VM, Cockington RA, Ryan P, Robinson JS. The relationship between birth weight and blood pressure amplifies from childhood to adulthood. J Hypertens. Jul 1999;17(7):883-8. [Medline].

  13. Simsolo RB, Romo MM, Rabinovich L, et al. Family history of essential hypertension versus obesity as risk factors for hypertension in adolescents. Am J Hypertens. Mar 1999;12(3):260-3. [Medline].

  14. Sorof JM, Lai D, Turner J, Poffenbarger T, Portman RJ. Overweight, ethnicity, and the prevalence of hypertension in school-aged children. Pediatrics. Mar 2004;113(3 Pt 1):475-82. [Medline].

Further Reading

Keywords

hypertension, pediatric hypertension, infantile hypertension, adolescent hypertension, prehypertension, high blood pressure, high BP, elevated BP, hypertensive, prehypertensive, white-coat hypertension, treatment, diagnosis

Contributor Information and Disclosures

Author

Edwin Rodriguez-Cruz, MD, Assistant Professor, Department of Pediatrics, San Juan Bautista Medical School and Medical Center; Consulting Interventional/Clinical Pediatric Cardiologist, Department of Pediatrics, Hospital El Maestro and San Juan Bautista Medical Center; Consulting Interventional/Clinical Pediatric Cardiologist, Department of Cardiology, Cardiovascular Center of Puerto Rico and the Caribbean and Veterans Affairs Hospital and Medical Center of Puerto Rico
Edwin Rodriguez-Cruz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Heart Association, American Medical Association, American Society of Echocardiography, Puerto Rico Medical Association, Society of Cardiac Angiography and Interventions, and Society of Pediatric Echocardiography
Disclosure: Nothing to disclose.

Coauthor(s)

Leigh M Ettinger, MD, MS, Clinical Assistant Professor, Division of Pediatric Nephrology, The Joseph M Sanzari Children's Hospital, Hackensack University Medical Center
Disclosure: Nothing to disclose.

Adrian Spitzer, MD, Professor, Department of Pediatrics, Albert Einstein College of Medicine; Director of NIH Training Program, Children's Hospital at Montefiore Medical Center
Adrian Spitzer, MD is a member of the following medical societies: American Academy of Pediatrics, American Federation for Medical Research, American Pediatric Society, American Society of Nephrology, American Society of Pediatric Nephrology, International Society of Nephrology, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Medical Editor

Ira H Gessner, MD, Professor Emeritus, Pediatric Cardiology
Ira H Gessner, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Pediatric Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

John W Moore, MD, MPH, Professor of Clinical Pediatrics, Section of Pediatric Cardiology, Department of Pediatrics, University of California San Diego School of Medicine; Director of Cardiology, Rady Children's Hospital
John W Moore, MD, MPH is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

CME Editor

Gilbert Z Herzberg, MD, Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College; Consulting Staff, Department of Pediatrics, Sound Shore Medical Center
Gilbert Z Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Chief Editor

Steven R Neish, MD, SM, Director of Pediatric Cardiology Fellowship Program, Associate Professor, Department of Pediatrics, Baylor College of Medicine
Steven R Neish, MD, SM is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and American Heart Association
Disclosure: Nothing to disclose.

 
 
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