Monday, May 31, 2021

Hypertension Case File

Posted By: Medical Group - 5/31/2021 Post Author : Medical Group Post Date : Monday, May 31, 2021 Post Time : 5/31/2021
Hypertension Case File
Eugene C. Toy, MD, Barry C. Simon, MD, Terrence H. Liu, MD, MHP, Katrin Y. Takenaka, MD, Adam J. Rosh, MD, MS

Case 30
A 58-year-old woman comes to see you for her annual check-up. She was diagnosed with prehypertension and was overweight 2 years ago. At that time, you recommended a low sodium, low-calorie diet, exercise, and weight loss. Since that time, she has diligently watched her salt intake, exercised routinely, and lost 20 pounds. She remains compliant with all of her appointments. However, during the past 5 months she has experienced some exertional fatigue, which she attributes to “getting older.” She denies chest pains, orthopnea, paroxysmal nocturnal dyspnea, palpitations, or lightheadedness. She smoked one pack of cigarettes per day for 20 years and quit when she was 45 years old. She drinks one glass of red wine per week on the weekends. Her mother was diagnosed with coronary heart disease at age 60 years while being evaluated for aortic stenosis and has an older brother whom had a myocardial infarction and coronary stents at age 47 years. On examination, the patient is non distressed and overweight, and you calculate her body mass index (BMI) at 28 kg/m3. Her blood pressure is 146/91 mmHg (right arm, sitting) and 150/ 94 (left arm, sitting). There were no postural changes in blood pressure. Her pulse was 73 bpm and regular. There is no thyromegaly or palpable lymphadenopathy. Fundoscopic examination reveals arteriovenous nicking. The cardiac examination reveals a laterally displaced, forceful, and sustained point of maximal impulse (PMI). There is an S4 gallop without any murmur on auscultation. The pulmonary and abdominal examinations are normal. All pulses are brisk and symmetric. Her extremities are warm, noncyanotic, and without clubbing or edema.

 What is the best next step in evaluation?
 What is the best initial therapy?


ANSWER TO CASE: 30
Hypertension

Summary: A 58-year-old hypertensive woman is currently being seen in your office for follow-up. Two years prior you diagnosed her as prehypertensive and overweight. She has done her best to lose weight and watch her salt intake. However, she now has some exertional fatigue for the past 5 months. She denies any angina or positional symptoms related to heart failure. She does not smoke and rarely drinks alcohol. Yet, she does have two first-degree relatives with a diagnosis of coronary heart disease. She remains overweight. Her blood pressure ranges between 140–150 systolic and 90–100 mmHg diastolic. She has evidence of hypertensive retinopathy. Her PMI is forceful and sustained and displaced laterally with an S4 suggesting a hypertrophic left ventricle with reduced compliance.
  • Next Step in Evaluation: Blood chemistries, urinalysis, complete blood cell count, and a 12-lead electrocardiogram (ECG). Other tests include blood calcium, uric acid, fasting triglyceride, low-density lipoprotein cholesterol (LDL-C), hemoglobin A1c percent, thyroid-stimulating hormone (TSH) levels, creatinine clearance, microalbuminuria, 24-hour urinary protein, and limited echocardiography to assess the presence of left ventricular hypertrophy (LVH).
  • Initial Treatment: Start the patient on chlorthalidone (a thiazide diuretic), consider an exercise stress test, and continue to emphasize the importance of lifestyle changes, including a low-sodium diet.

ANALYSIS
Objectives
  1. Know the definition of hypertension and its contribution to cardiovascular comorbidity.
  2. Comprehend the management of and treatment decisions for hypertension.
  3. Recognize the etiologies of secondary hypertension and when it is appropriate to investigate them.

Considerations
This is a 58-year-old woman with hypertension who has physical findings consistent with hypertensive end-organ damage: hypertensive retinopathy and LVH. Additionally, she has a family history of coronary heart disease and has exertional dyspnea and may already have obstructive coronary heart disease. She likely has essential hypertension, although causes for secondary hypertension may need to be explored. Despite the presence of end-organ effects of hypertension, evaluation for other modifiable cardiovascular risk factors is paramount. Lifestyle modification, including a low-calorie and low-sodium diet, weight loss, and aerobic exercise continue to be essential even in the presence of medical treatment. Assessing this patient, we find that she has a blood pressure above 140/90 mmHg and would be classified as having stage 1 hypertension. She also has evidence for end-organ damage from hypertension. This warrants expeditious treatment with one-drug therapy, which, according to current guidelines, should include a thiazide diuretic.

Approach To:
Hypertension

DEFINITIONS
Essential hypertension: A form of hypertension without identifiable cause. This also happens to be the most prevalent form of hypertension, representing approximately 95% of patients with hypertension. This is synonymous with idiopathic or primary hypertension.

Secondary hypertension: In contrast to essential hypertension, this is a form of hypertension with an identifiable cause. It is much less prevalent, representing nearly 5% of all patients with hypertension. Causes include various renal, endocrine, malignant, or drug-induced pathologies.

Lifestyle modification: This is the hallmark of treating a patient with hypertension. It consists of weight reduction, exercise, and diet. Weight loss of approximately 10 pounds may reduce both systolic and diastolic blood pressures by nearly 2–3 mmHg and may avert the need for medical therapy. Increases in physical activity may lead to reduction of systolic and diastolic blood pressures by nearly 7 mmHg independent of weight reduction. Benefits of salt reduction have been demonstrated. Low-salt diets are recommended in most patients with hypertension.

Hypertensive emergency: Defined as severe hypertension (>180/120 mmHg) with evidence of acute end-organ damage. Typical emergencies include encephalopathy, thrombotic or hemorrhagic cerebrovascular accident, acute aortic dissection, myocardial ischemia/infarction, acute renal failure, retinal hemorrhages or papilledema, and eclampsia. Severe hypertension without the presence of endorgan damage does not constitute a hypertensive emergency. This syndrome implicates immediate lowering of the patient’s blood pressure, typically with parenteral agents, while monitoring the patient in an intensive care unit (ICU).

Hypertensive urgency: Unlike a hypertensive emergency, this is defined as severe hypertension without end-organ damage. Blood pressure, therefore, can be lowered more slowly over a period of days to weeks. Patients may be treated with oral antihypertensives and typically treated as outpatients.


CLINICAL APPROACH

Initial Evaluation and Management
High-to-normal blood pressures ranging from 120 to 139 mmHg systolic and 80 to 89 mmHg diastolic are considered to be prehypertension (Table 30-1). This entity 

hypertension classification for adults

does confer some increased risk for cardiovascular disease. Stage I hypertension is diagnosed with two or more consecutive blood pressure measurements of ≥140 mmHg systolic or ≥90 mmHg diastolic. Stage II hypertension is diagnosed with two or more consecutive blood pressure measurements of ≥160 mmHg systolic or ≥100 mmHg diastolic. Hypertension is also defined as the need for antihypertensive therapy.

The most common form of hypertension is idiopathic hypertension, which is the cause of approximately 95% of high blood pressure. The remaining 5–7% of cases of hypertension are related to secondary causes of hypertension (Table 30-2),

common secondary causes of high blood pressure

which may be reversible. Therefore, it is of great importance to be familiar with the presenting findings and potential laboratory abnormalities that may be associated with various causes of secondary hypertension. Secondary causes of hypertension should be suspected when patients present with: (1) hypertension at age <30 years or >55 years; (2) previously well-controlled hypertension that becomes poorly controlled; (3) sudden-onset or aggressive hypertension; or (4) an abdominal aortic bruit and clinical features suggestive of bilateral renal artery stenosis. Clinical features of renal artery stenosis include resistant hypertension (hypertension requiring the use of three or more antihypertensive medications), multiple episodes of flash pulmonary edema, renal failure with unknown cause (especially with normal urine sediment or without proteinuria), and renal failure associated with the use of either angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin-receptor blockers (ARBs).

Cardiac Risk Factors and Evaluation for Target Organ Damage
One of the hallmarks of treating a patient with newly diagnosed hypertension is evaluation and treatment of other cardiac risk factors in addition to identification of end-organ dysfunction (Table 30-3). Results from these investigations will guide therapy. Classical risk factors for the development of cardiovascular diseases include age, gender, smoking status, diabetes mellitus, LDL-C, HDL-C, and presence of hypertension. Other factors that determine risk include chronic renal diseases and family history of premature coronary heart disease. In order to determine end-organ damage to the eyes, kidneys, heart, brain, and peripheral vasculature, studies including urinalysis, complete blood cell count, blood chemistries, and ECGs need to be completed (Table 30-4). Treatment of hypertension is guided by the level of hypertension in addition to other cardiac risk factors or the development of end organ damage.
 
Hypertension Case File

Evaluation of hypertension

Therapy
The treatment of hypertension reduces the incidence of hypertension progression, heart failure, stroke, and chronic renal insufficiency. In addition to medical therapy, weight reduction, exercise, and diet are essential to lowering blood pressure. When initiating pharmacologic treatment, a low dose of drug should be chosen, then titrated upward on a schedule reflecting the patient’s age, response, and medical need. The optimal target for blood pressure lowering is typically <140/90 mmHg unless the patient with hypertension has diabetes mellitus or renal insufficiency, in which case the target would need to be lowered to <130/80 mmHg. Although some patients respond to single-drug therapy, often two or more antihypertensive drugs may be required. Additional considerations include patient demographic, cost, quality of life, and the presence of other medications that may cause pharmacological interactions. The armamentarium of oral blood pressure–lowering medications is extensive (Table 30-5).

In patients without compelling contraindications, thiazide diuretics (viz., chlorthalidone and indapamide) should be considered as first-line agents in patients with hypertension. Because they were originally shown to reduce mortality, diuretics and beta-blockers are common first choices in uncomplicated hypertension. However, in the setting of heart failure or diabetes, ACE inhibitors should be included as first-line agents. Long-acting blood pressure medications are typically preferred to shorter-acting medications because they promote adherence, reduce cost, and confer increased blood pressure control.

Selected Causes of Secondary Hypertension
The most common etiology of secondary hypertension is chronic renal insufficiency. The most common renal diseases associated with hypertension are polycystic kidney disease, hypertensive nephrosclerosis, renal vascular disease, and chronic glomerulonephritis. Renal artery stenosis is caused by obstructive atherosclerotic plaques

various antihypertensive agents

in the renal arteries. Patients may present with the onset of significant hypertension at age >55 years old, and may have accelerated hypertension, newly resistant hypertension, recurrent flash pulmonary edema, and abdominal bruit. In younger patients (typically <30 years old), narrowing of the renal arteries may be related to fibromuscular dysplasia. These can usually be detected depending on the clinical setting and some additional diagnostic testing. For instance, renal ultrasound is useful in diagnosing polycystic kidney disease and suggesting the presence of chronic renal disease, depending on the size and echogenicity of the renal parenchyma. In patients with suspected renovascular hypertension, diagnostic studies include ACEI-enhanced radionuclide renal scans, duplex Doppler flow studies, and magnetic resonance angiography (MRA). Once a flow-limiting lesion is identified, either surgical or percutaneous intervention may be considered.

Pheochromocytoma should be considered in patients with irregular episodes of severe hypertension that may be accompanied by headaches, perspiration, and pallor. This is a tumor that releases high levels of catecholamines typically producing hypertension. Commonly, 9/10 arise from the adrenal medulla and 1/10 arise from extra adrenal sympathetic ganglia. The majority of pheochromocytomas release norepinephrine. Additionally, patients with these tumors may experience orthostatic hypertension. Uncommonly, pheochromocytoma is associated with other endocrine neoplasms such as parathyroid adenomas and medullary thyroid cancer as part of multiple endocrine neoplasia type II A or type II B from mutations in the RET oncogene. As such, nearly 25% of pheochromocytomas may be familial, thus stressing the importance of a thorough family history. They may be diagnosed by plasma or urine levels of free normetanephrines or metanephrines.

Hyperthyroidism should always be considered in a patient presenting with hypertension, recent weight loss, and symptoms of nervousness, anxiety, heat intolerance, diarrhea, excessive perspiration, and muscle weakness. As such, measuring a serum thyroid-stimulating hormone (TSH) in the setting of elevated thyroid hormones (eg, free T4) is diagnostic. Clinical characteristics include a widened pulse pressure characterized by increased systolic blood pressure in the face of lowered diastolic blood pressure and a hyperdynamic PMI. The patient’s skin may be warm to the touch, the patient may be tremulous, and there may be thyroid enlargement or nodules on thyroid examination.

Obstructive sleep apnea (OSA) is a frequent cause of hypertension as well. Obstructive sleep apnea is characterized by episodic collapse and subsequent obstruction of the upper airway during sleep, due to intermittent loss of normal tonic constrictor tone of the upper airway dilator muscles. The precise mechanism for this intermittent obstruction is not known, but obesity (particularly visceral or central obesity) is a clear causal factor. Anatomically small upper airways and a large neck circumference also confer risk. OSA is characterized by repetitive airway obstruction and arousals from sleep that typically result in decreased blood oxygen tension and increased sympathetic nervous system activation. Over time, this results in the development of systemic vasoconstriction, systolic hypertension, and pulmonary hypertension. Frequent symptoms include unexplained daytime sleepiness, restless sleep, and loud snoring. Patients with this disorder may have trouble concentrating and experience mood changes. Interrogating the patient’s sleeping partner may be key to pinpointing this diagnosis. This is commonly diagnosed by a sleep study.

Cushing syndrome and other glucocorticoid excess states, including chronic steroid therapies, are associated with blood pressure elevations. Common symptoms include muscle weakness, fatigue, easy bruising, thinning skin, decreased muscle mass in the face of increased truncal obesity, purple striae, buffalo hump, moonlike facies, acne, and possible psychiatric symptoms including anxiety, depression, irritability, and headaches. Hypertension in this setting typically arises from excess glucocorticoid- stimulating mineralocorticoid receptors. This is commonly diagnosed by both family history and a dexamethasone suppression test.

Coarctation of the aorta may be present in younger patients with difficult-to-control hypertension and should be considered as a potential diagnosis. This is characterized by a congenital narrowing of the aortic lumen near the ligamentum arteriosum. It is typically associated with other cardiac defects, which include bicuspid aortic valves, ventricular septal defects, valvular and subvalvular aortic stenoses, patent ductus arteriosus, and congenital malformations of the mitral valve. When patients with coarctation of the aorta survive to adulthood, symptoms may often be minimal or nonspecific. They include nosebleeds, headaches, cool extremities, leg weakness, or claudication with exertion. Cardiac examination may reveal a systolic murmur at the upper left sternal border that radiates to the intrascapular area located either anterior or posterior to the position of the coarctation. Upper extremity hypertension is commonly present and may be associated with delayed and diminished femoral arterial pulsations. This may be diagnosed with transthoracic echocardiography or computed tomography angiography.

Hypertensive Crises
Hypertensive crises are defined as either hypertensive emergencies or hypertensive urgencies. These entities are rare, with only approximately 1% of patients with poorly treated essential hypertension progressing to crisis phase. Subjects with secondary hypertension are at higher risk for a hypertensive crisis. Both prompt recognition and treatment are critical, as progression of a hypertensive crisis can cause acute renal, cardiovascular, ocular dysfunction, and even death. It is important to note that hypertensive emergency is defined by the presence of rapidly progressive end-organ damage, not by the actual blood pressure reading. A patient with an acute aortic dissection with a blood pressure of 140/85 mmHg merits ICU admission and parenteral antihypertensive therapy, while an asymptomatic patient without acute end-organ dysfunction with chronic hypertension and blood pressure of 195/105 mmHg does not.

This evaluation of a patient experiencing a hypertensive crisis should concentrate on those organ systems that can be acutely affected: cardiovascular, neurologic, renal, and ocular. In order to assess the pace and contributing factors of the hypertensive crisis, a careful history should be taken focusing on the symptom chronology; any history of chronic hypertension with additional focus on looking for secondary causes; a thorough medication history (eg, NSAIDs, oral contraceptives, immunosuppressants); a detailed social history emphasizing the use of illicit drugs (eg, cocaine, methamphetamine); and a smoking history. Physical examination should involve bilateral blood pressure readings in both the upper extremities and lower extremities. In addition, optic funduscopy, a thorough neurological assessment, cardiopulmonary examination, and vascular examination should be completed in order to look for any signs of end-organ dysfunction.

In a hypertensive emergency, the main goal of therapy is to lower mean arterial
pressure (MAP) in a safe and predictable manner. With a few exceptions (eg, aortic dissection or pulmonary edema), blood pressure should be lowered targeting a map reduced by 25% within minutes to hours of presentation. Normal blood pressure levels should be targeted over the coming days to weeks. Emergent blood pressure reduction is typically attained by intravenous agents such as sodium nitroprusside, labetalol, nitroglycerin, nicardipine, or hydralazine. Once the blood pressure is controlled with intravenous agents, then transition to an oral antihypertensive regimen can be initiated.

In contrast, methods for managing hypertensive urgencies are different. Most patients with hypertensive urgency have chronically poorly controlled hypertension and are typically in little danger of progression to a hypertensive emergency. Therefore, patients can be managed with titration of oral antihypertensive agents as appropriate. The main danger in managing these patients is overzealous treatment of these patients and inducing hypotension.


CASE CORRELATION
  • See also Case 1 (acute coronary syndrome/STEMI), Case 2 (acute coronary syndrome/NSTEMI), Case 4 (chronic coronary artery disease), Case 8 (hypertrophic obstructive cardiomyopathy), Case 17 (advanced heart failure), and Case 24 (preoperative risk evaluation).

COMPREHENSION QUESTIONS

30.1 Which of the following blood pressure–lowering medication classes is a preferred agent in a hypertensive patient with diabetes mellitus?
A. Thiazide diuretics
B. ACE inhibitors
C. Alpha-blocking agents
D. Nitrates
E. Calcium channel blockers

30.2 A 42-year-old man has hypertension and is poorly controlled on three agents. He mentions that he was followed by his pediatrician for coarctation of the aorta during his childhood. Which of the following cardiac abnormalities is associated with aortic coarctation?
A. Tetrology of Fallot
B. Ebstein’s anomaly
C. Bicuspid aortic valve
D. Tricuspid atresia
E. Truncus arteriosus

30.3 A 60-year-old woman is in your office for follow-up after a recent cholecystectomy. While in recovery from surgery she became very hypertensive and dyspneic, requiring nitroglycerin and a loop diuretic. She developed hypertension only in her late 50s. In your office her blood pressure is 158/95 mmHg. You hear an abdominal bruit with a present diastolic component on examination. Which of the following studies would reveal the etiology of her secondary hypertension?
A. Transthoracic echocardiography
B. Coronary angiography
C. Duplex Doppler renal ultrasonography
D. Electrocardiogram
E. Chest x-ray


ANSWERS

30.1 B. ACE inhibitors or ARBs are the preferred antihypertensive medications in patients with diabetes mellitus.

30.2 C . Aortic coarctatons are commonly associated with bicuspid aortic valves, ventricular septal defects, valvular and subvalvular aortic stenoses, patent ductus arteriosus, and congenital malformations of the mitral valve.

30.3 C . Her history of flash pulmonary edema, incidence of hypertension after 55 years, and abdominal bruit all suggest that she may have renovascular hypertension caused by renal artery stenosis. Of the answer choices, the best study confirming the diagnosis would be duplex Doppler renal ultrasonography.


CLINICAL PEARLS

 Detection of hypertension begins with two separate blood pressure measurements on two separate occasions that are greater than 140 mmHg systolic or 90 mmHg diastolic.

 When evaluating a patient with hypertension, it essential to evaluate for and treat other cardiac risk factors in addition to identifying end-organ dysfunction.

 Nearly all cases of hypertension are related to essential hypertension. However, given the clinical scenario, evaluation for secondary causes may be appropriate.

 The most common cause of secondary hypertension is related to chronic renal parenchymal or vascular disease.

 In addition to medical treatment, lifestyle modifications, including diet, exercise, and weight reduction, are paramount in reducing blood pressure and the incidence of cardiovascular morbidity and mortality.

⯈ Unless there are other compelling indications, thiazide diuretics such as chlorthalidone or indapamide should be considered as first-line agents in uncomplicated hypertension.

References

ALLHAT. Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). JAMA. 2002;288(23):2981–2997. 

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. 2003;289(19):2560–2572. 

Yusuf S, Sleight P, Pogue J, Bosch J, Davies R, Dagenais G. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. N Engl J Med. 2000;342(3):145–153.

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