This is the first article in a series of the most commonly billed diagnoses in primary care outpatient settings. A list of the top 12 billable diagnoses was compiled from information obtained from the CDC and the Centers for Medicare and Medicaid Services (CMS).1,2 Each article will delve into the pathophysiology of disease to gain an in-depth understanding of the process. Disease pathophysiology helps NPs understand the whys: why certain clinical manifestations are present, why specific diagnostic tests are ordered, and why treatments are chosen. Each article will convey a description of the disease and a comprehensive overview of the pathophysiology, as well as the clinical manifestations, diagnostic testing, treatment, and appropriate billing codes. Information is based on the best-available evidence.
Hypertension is the first diagnosis addressed. The prevalence of hypertension among adults (age 20 and above) in the US is 46%, accounting for 116.4 million adults.3 Hypertension increases lifetime risk for angina, myocardial infarction, cardiovascular disease, and cerebrovascular accident.3,4 Other health risks associated with hypertension include heart failure, kidney disease, and visual impairment. Hypertension is the second-ranked preventable cause of death for any reason, just behind cigarette smoking.5 The estimated direct and indirect cost related to hypertension was $55.9 billion between 2014 and 2015 and projected to be $220.9 billion by 2035.3 Additionally, more than 50% of US adults taking antihypertensive medications are not meeting BP goals set by the current guidelines.4 Hypertension is the reason behind nearly 30% of all outpatient visits related to a chronic condition; therefore, it is imperative that NPs have a clear understanding of the disease to appropriately assess, diagnose, and manage patients.6
The 2017 hypertension clinical practice guideline from the American College of Cardiology (ACC) and the American Heart Association (AHA) recommends maintaining a BP below 130/80 mm Hg.7 A diagnosis of hypertension is based on the average of two or more BP readings above 130/80 mm Hg, on two or more occasions.7
The pathogenesis of essential hypertension involves several interacting homeostatic mechanisms. Hypertension is the result of various genetic and environmental factors mediated by neurohormonal effects (see Genetic, environmental, and risk factors).8-10 The primary intermediaries involved in BP regulation are the sympathetic nervous system (SNS), renin-angiotensin-aldosterone system (RAAS), and natriuretic peptides. Hypertension, if left untreated or uncontrolled, can negatively affect the structure and function of multiple organ systems.
A central component in the pathogenesis of essential hypertension is a shift in the pressure-natriuresis relationship.8-10 This means there is increased vascular volume and decreased renal salt excretion. How does this happen? A shift occurs due to a disturbance in one or more of the following intrinsic mechanisms: SNS, RAAS, abnormal release of antidiuretic hormone (ADH), and autoregulation.
BP reacts to changes in the environment to maintain accurate perfusion. The SNS plays an important role in regulating arterial BP (ABP). ABP, a product of cardiac output (CO) and systemic vascular resistance, is essential for organ perfusion. CO is escalated by conditions that increase heart rate, stroke volume, or both.8-10 These effects are apparent during stress or high SNS activity. SNS activity is elevated due to the release of norepinephrine, a potent vasoconstrictor, which causes sympathetic stimulation of the heart. The SNS also interacts with nitric oxide, a vasodilator derived from endothelial cells, to control BP. The effects of decreased nitric oxide production and increased SNS activity include tachycardia, increased peripheral resistance, narrowing of arteries, vascular spasm, insulin resistance, and procoagulant effects leading the way to hypertension.8-10 Over a sustained period, increased SNS activity causes retinol changes, renal disease, cardiac disease, and neurologic disease. Similar effects are seen with RAAS dysfunction when the body maintains high levels of renin, angiotensin II, and aldosterone.8-10
Overactivity of the RAAS ultimately leads to hypertension secondary to increased blood volume and vascular resistance. First, renin reacts with angiotensinogen, converting it to angiotensin I, which then transforms to the potent vasoconstrictor angiotensin II. Angiotensin II targets the arterioles and stimulates the adrenal cortex to secrete aldosterone. This release of aldosterone leads to vasoconstriction and increases blood volume through the retention of sodium and water. Natriuretic hormonal modulation of renal sodium excretion maintains a homeostatic pressure-natriuresis relationship.8-10 The most commonly known natriuretic hormone is the B-type natriuretic peptide, which is released in response to volume and pressure overload. Other natriuretic hormones include the atrial natriuretic peptide, C-type natriuretic peptide, and urodilatin. The main function of the peptides is to decrease BP and control electrolyte homeostasis by inducing diuresis, increasing systemic vasodilation, boosting renal blood flow, suppressing aldosterone, and inhibiting the SNS.8-10 These natriuretic hormones regulate renal sodium excretion and require adequate electrolyte consumption to function properly. This is the significance behind maintaining sufficient intake of potassium, calcium, and magnesium. A deficiency in these electrolytes induces the body to retain sodium, which causes increased volume.8-10 The reabsorption of water by the kidneys occurs with the release of ADH–a compensatory response related to detection of increased blood osmolality or decreased blood volume.8,9 As water is reabsorbed, the blood plasma volume increases, which elevates the BP.
The immune system, inflammation, and obesity all play a pivotal role in hypertension. Activation of the immune response system results in a cascade of events causing chronic inflammation. This eventually leads to endothelial cell damage, weakened production of vasodilators, vascular alteration, and smooth muscle contraction.8-10 The chronic inflammation contributes to insulin resistance, reduced natriuresis, autonomic dysfunction, and renal dysfunction.8-10 Obesity, which is linked to chronic inflammation, is associated with hypertension beginning in adolescence.8-10 Obesity is not only a risk factor for hypertension, but contributes to the neurohormonal, metabolic, renal, and cardiovascular complications associated with the disease.8-10 Obesity causes changes in the adipokines (leptin, resistin, adiponectin) and leads to vascular remodeling, insulin resistance, increased RAAS action, and heightened SNS activity.8-10
History, physical exam, and diagnosis
A patient's history is an important component in determining the presence of precipitating or aggravating factors attributable to hypertension. A thorough history should include the individual's social and family background. It is essential to inquire about the presence of environmental or other known risk factors for cardiovascular disease (CVD), such as family history of CVD, tobacco use, high fat and sodium diet, alcohol consumption, recreational drug use, and stress at home or work. Information about prescription and nonprescription medications should be obtained. The presence of clinical manifestations and their durations, including related symptoms such as headache or target organ damage like renal disease, should be documented. It is important to record the initial date of hypertension diagnosis. Finally, it is imperative to document current and previous treatment regimen(s), response to treatment(s), and compliance with medication(s).11
During physical exam (PE), a standard protocol must be used to consistently and accurately measure BP.7,11 At every outpatient visit, it is appropriate to evaluate for signs of end organ damage, established CVD, and evidence of potential causes of secondary hypertension.7 The PE should include a funduscopic exam to evaluate for hypertensive retinopathy.7 It is essential to measure the atherosclerotic cardiovascular disease (ASCVD) risk for all patients with hypertension, regardless of the stage of hypertension.7 Documentation of the ASCVD risk is a key component of quality improvement for patients with hypertension.11
In determining the appropriate diagnosis, BP should be categorized as normal (less than 120/less than 80 mm Hg), elevated (120-129/less than 80 mm Hg), stage 1 hypertension (130-139/80-89 mm Hg), or stage 2 hypertension (greater than or equal to 140/greater than or equal to 90 mm Hg).7 A patient with a systolic BP and diastolic BP in different categories should be designated to the higher category.7
Finally, when documenting the diagnosis of hypertension, it should be noted whether it is essential or secondary and the causal relationship associated with the disease, such as renal or pulmonary.
The following tests should be performed in all patients with newly diagnosed hypertension: fasting blood glucose, complete blood count, lipid profile, serum creatinine with estimated glomerular filtration rate, serum sodium, potassium, calcium, thyroid-stimulating hormone, urinalysis, and ECG.7 Optional testing can include: echocardiogram, uric acid, and urinary albumin-to-creatinine ratio.7,12,13 Patients should also monitor BP outside the office to confirm the diagnosis of hypertension.7
Hypertension is the most common diagnosis group for outpatient office visits and the use of chronic medications.4,6,14 Both nonpharmacologic and pharmacologic approaches may be necessary for treatment. An important aspect of reducing BP and comorbidities is the discussion of lifestyle modifications with patients at the time of diagnosis and at every subsequent office visit. Dietary modifications include the Dietary Approaches to Stop Hypertension (DASH) diet, salt restriction, potassium supplementation, and limiting alcohol consumption.7 The recommended intake of sodium, according to the AHA, is no more than 2,300 mg per day.15 Reducing that amount to no more than 1,500 mg per day for individuals with hypertension is ideal.15 Improved natriuretic peptide function can be seen with adequate intake of dietary potassium, magnesium, and calcium.9,15 Other lifestyle modifications to be addressed include smoking tobacco or vaping, and physical inactivity. The NP should educate the patient on smoking cessation and offer agents to help the patient quit smoking. The NP also needs to educate patients on the exercise recommendations from the ACC/AHA. The current guidelines suggest adults get at least 150 minutes of moderate-intensity exercise or 75 minutes of vigorous-intensity aerobic activity per week and perform muscle-strengthening activities at least 2 days per week.3 Documentation of patient adherence with lifestyle modifications and medication adherence is imperative for all stages of hypertension.11
The RAAS is associated with end organ effects of hypertension, including coronary artery disease (CAD), renal disease, cardiac hypertrophy, and heart failure. Medications, such as angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), and aldosterone antagonists, oppose the activity of the RAAS and are effective in lowering BP. The 2017 ACC/AHA hypertension guideline recommends nonpharmacologic therapy, as discussed above, for those with elevated BP and for those with stage 1 hypertension without ASCVD or with 10-year ASCVD risk of less than 10%. Pharmacologic monotherapy is recommended for patients with stage 1 hypertension who have ASCVD or a 10-year ASCVD risk of 10% or higher.7 First-line agents used in the initiation of pharmacologic treatment for hypertension are thiazide diuretics, calcium channel blockers, and ACE inhibitors, or ARBs. Combination therapy using two drugs is recommended for patients with stage 2 hypertension, and for those unable to attain goal BP with pharmacologic monotherapy in addition to lifestyle changes.7 Combination pharmacologic therapy recommendation includes adding a medication to the first-line agent already prescribed, but not within the same drug class. Second-line agents can be separate medications or a fixed-dose combination.7
Monitoring BP outside the clinic is important; it guides titration of antihypertensive medications. It is essential to educate patients on the appropriate way to measure BP outside the office and instruct individuals to document the results and bring them to every office appointment. This should be done in conjunction with telehealth counseling or clinical interventions.7,16,17 A team-based care approach should be multidisciplinary and patient-centered, involving collaboration between the patient, the patient's primary care provider, and other professionals, such as cardiologists, pharmacists, dietitians, social workers, and community healthcare workers.7
A patient should be referred to a specialist for known or suspected secondary cause(s) of hypertension, resistant hypertension, or if the BP remains uncontrolled after 6 months of treatment.7 The diagnosis of resistant hypertension is made when treatment is unsuccessful with at least three antihypertensive medications, one of which is a diuretic, or requires four or more medications to control BP.7 Hypertensive crisis or hypertensive emergencies are defined as severe elevations in BP (greater than 180/greater than 120 mm Hg) associated with target organ damage.7 A patient with hypertensive crisis should proceed to the ED for immediate evaluation and treatment.
The International Classification of Diseases, 10th Revision, Clinical Modification (ICD-10-CM) is a morbidity classification published by a joint effort between the CMS and the National Center for Health Statistics.18 It is the standard billing code system that is used to submit diagnosis codes for insurance reimbursement.
Hypertension has billable ICD-10-CM codes spanning I10 to I15 excluding I14 (see ICD codes).18,19 It is important to note and ensure that the first letter in the code is a capital I and not the number 1. In the previous ICD–9th Revision (ICD-9-CM), the codes for essential hypertension were 401.0 (malignant), 401.1 (benign), or 401.9 (unspecified).18,19 The ICD-10-CM code I10, for essential (primary) hypertension, is submitted for individuals who do not have associated cardiovascular or renal comorbid conditions. For patients with a single elevated BP reading, the code R03.0 should be submitted until a formal diagnosis of essential hypertension is established. If an individual has a causal relationship due to cardiovascular or renal disease, the code indicating the type of relationship is required. For example, if a patient has hypertension with systolic congestive heart failure, codes I11.0 (for hypertensive heart disease with heart failure) and I50.2 (for systolic heart failure) should be submitted.18,19 While it is not uncommon for patients with longstanding hypertension to develop renal or cardiac changes, it is important to document the supportive information within the chart.18,19 It is equally imperative to code correctly; the code with the highest specificity will increase reimbursement.
Implications for practice
The role of the NP in managing hypertension includes: 1) initial and ongoing assessment, 2) ordering labs and diagnostic testing, 3) pharmacologic and nonpharmacologic management per treatment guidelines, 4) patient education, 5) coordination of care–including referrals, 6) follow-up, and 7) billing services for reimbursement of care and performance measurement.20 NPs are an integral part of a team-based approach to care, which contributes to improved patient outcomes. NPs help increase follow-up opportunities and maintain a judicious focus on cost-effective treatment.20 Furthermore, patient satisfaction with a specified treatment plan and quality of contact with a healthcare professional is linked to medication adherence and compliance with lifestyle behavioral changes.21 NPs see beyond the diagnosis and follow a holistic approach to care. An NP considers the social, cultural, economic, and behavioral elements of an individual with hypertension, and designs a patient-specific treatment plan by being culturally sensitive, examining guidelines, and addressing any relevant social determinants of health.20 This is one of the many ways in which NPs are leading the way to promote change within communities and improve the hypertension quality gap and ethnic disparities.20
2. Rui P, Hing E, Okeyode T. National Ambulatory Medical Care Survey: 2014 state and national summary tables. http://www.cdc.gov/nchs/ahcd/ahcd_products.htm
3. Virani SS, Alonso A, Benjamin EJ, et al Heart disease and stroke statistics-2020 update: a report from the American Heart Association. Circulation
4. Muntner P, Carey RM, Gidding S, et al Potential US population impact of the 2017 ACC/AHA high blood pressure guideline. Circulation
5. Danaei G, Ding EL, Mozaffarian D, et al The preventable causes of death in the United States: comparative risk assessment of dietary, lifestyle, and metabolic risk factors. PLoS Med
6. Rui P, Okeyode T. National Ambulatory Medical Care Survey: 2016 national summary tables. http://www.cdc.gov/nchs/data/ahcd/namcs_summary/2016_namcs_web_tables.pdf
7. 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. Hypertension
. 2018;71(6):e13–e115. http://www.ahajournals.org/doi/10.1161/HYP.0000000000000065
8. Heuther SE, McCance KL, Brashers VL. Understanding Pathophysiology
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11. Casey DE Jr, Thomas RJ, Bhalla V, et al 2019 AHA/ACC clinical performance and quality measures for adults with high blood pressure: a report of the American College of Cardiology/American Heart Association task force on performance measures. Circ Cardiovasc Qual Outcomes
. 2019;12(11):e000057. doi:10.1161/HCQ.0000000000000057. http://www.ahajournals.org/doi/full/10.1161/HCQ.0000000000000057
12. Chobanian AV, Bakris GL, Black HR, et al The seventh report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure: the JNC 7 report. JAMA
13. Mancia G, De Backer G, Dominiczak A, et al 2007 Guidelines for the management of arterial hypertension: the task force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). J Hypertens
14. Yoon SS, Gu Q, Nwankwo T, Wright JD, Hong Y, Burt V. Trends in blood pressure among adults with hypertension: United States, 2003 to 2012. Hypertension
16. Centers for Medicare and Medicaid Services. CMS expands coverage of ambulatory blood pressure monitoring (ABPM). http://www.cms.gov/newsroom/press-releases/cms-expands-coverage-ambulatory-blood-pressure-monitoring-abpm
17. Centers for Medicare and Medicaid Services. Decision memo for ambulatory blood pressure monitoring (ABPM) (CAG-00067R2). http://www.cms.gov/medicare-coverage-database/details/nca-decision-memo.aspx
Official Guidelines for Coding and Reporting. FY2020 ICD-10-CM
19. Beckman KD. How to document and code for hypertensive diseases in ICD-10. Family Practice Management. 2014. http://www.aafp.org/fpm/2014/0300/p5.pdf
20. Himmelfarb CRD, Commodore-Mensah Y, Hill MN. Expanding the role of nurses to improve hypertension care and control globally. Annals of Global Health. https://doi.org/10.1016/j.aogh.2016.02.003
21. Lo SHS, Chau JPC, Woo J, Thompson DR, Choi KC. Adherence to antihypertensive medication in older adults with hypertension. J Cardiovasc Nurs