Dizzy Spells Complicating Hypertension Management

Three cases are presented where episodic dizzy spells impeded hypertension management. Dizziness is a frequent, often age‐related clinical condition, and patients’ perceptions of these symptoms related to both their blood pressure (BP) and their antihypertensive medications occasionally interfere with clinical management.

Case 1

A 58‐year‐old man was referred to our hypertension clinic for evaluation of difficult to control hypertension and dizzy spells, which he attributed to overmedication. He had been taking antihypertensive medication for approximately 10 months. For his consultation visit, the patient brought an extensive record of home BP readings taken 3 times daily. Home systolic pressures were predominantly 140 to 170 mm Hg, but sporadic systolic pressures were 105 to 110 mm Hg. Every time the systolic pressure got below 120 mm Hg, a dizzy spell lasting up to 90 minutes would occur. He described these episodes as a gradual in onset “unsteadiness” and his wife observed him to be “zombie‐like.” He denied associated vertigo or diaphoresis, and spells were incompletely relieved by sitting or lying down.

Because of his impression that the dizzy spells were associated with lower BPs, he had been gradually cutting back on his antihypertensive medications and had completely stopped amlodipine and atenolol. Nonetheless, the dizzy episodes persisted. He denied any chest complaints or ambulatory lower extremity pain, but he described occasional episodes where the entire left leg transiently became numb. His most recent clinic BPs were 164/78 mm Hg and 171/72 mm Hg. The patient had been taking antidepressant medication for 3 to 4 years, and recently switched to bupropion to coincide with tobacco cessation. Current medications were lisinopril 40 mg daily, hydralazine 25 mg 2 times a day, and bupropion 100 mg 2 times a day. There was a history of hydrochlorothiazide (HCTZ) intolerance with hyponatremia, but hyponatremia was persistent despite discontinuation of HCTZ while continuing antidepressant therapy.

On examination, there was a 10‐mm Hg systolic pressure differential in the arms with 2 determinations: 174/70 mm Hg on the right and 192/78 mm Hg on the left. There were bilateral carotid, supraclavicular, and femoral bruits with trace to absent pedal pulses bilaterally. A 2/6 mid peaking systolic murmur was auscultated in the aortic area. Electrocardiographic findings showed a probable old inferior wall myocardial infarction. Adenosine dual isotope cardiac imaging showed no defects, a magnetic resonance imaging study of the brain revealed an old right posterior parietal stroke, and renal magnetic resonance angiography showed no obstruction. An ambulatory cardiac monitor showed normal sinus rhythm when dizzy episodes were recorded in the patient log.

Amlodipine 5 mg daily was advanced to 10 mg daily, atenolol 25 mg daily was advanced to 50 mg daily, furosemide 10 mg 2 times a day was advanced to 20 mg 2 times a day, and hydralazine was advanced to 50 mg 2 times a day. Follow‐up standing systolic BPs in the office were 134 to 138 mm Hg on the left arm, the arm with the higher pressure. Nonvertiginous nonpostural dizzy spells, mostly characterized as an “unsteadiness” lasting several minutes continued to occur daily but did not significantly interfere with function. These spells continued to be associated with lower home BP levels. However, a follow‐up 24‐hour ambulatory BP recording showed a systolic BP range from 105 to 142 mm Hg with a 24‐hour mean pressure of 122/64 mm Hg.

Case 2

A 77‐year‐old woman was referred to our hypertension clinic for evaluation of difficult to control hypertension and intolerance to antihypertensive medications due to dizzy spells. The patient, accompanied by her son, was a poor historian. She had a prior history of myocardial infarction and 2 coronary stents, a left thalamic stroke, bilateral lower extremity bypass surgery, stage 3 chronic kidney disease, and was wheelchair‐bound due to post‐polio syndrome. Dizziness was poorly articulated but appeared to be chronic, fluctuating, and nonspecific. Spells would occur most of the day. Antihypertensive medications were blamed and she stopped most of them except for lisinopril 20 mg daily. Hyponatremia intolerance to thiazide was noted.

Her BP was 210/65 mm Hg. A plan for gradually increasing her medications in small doses was agreed upon by the patient and promoted by her son. Follow‐up visits were arranged at 2‐week intervals. After about 4 months, systolic BPs of 142 to 146 mm Hg were achieved on a combination of amlodipine 10 mg daily, long‐acting diltiazem 120 mg daily, furosemide 10 mg 2 times a day, and lisinopril 40 mg daily. Dizzy spells continued but were not as bothersome, and overall the patient felt better.

Case 3

An 89‐year‐old woman was referred to our hypertension clinic because of difficult to control systolic BP and recurrent dizzy spells. She resided at an assisted‐living facility and was accompanied by her son. Antihypertensive medications were initiated approximately 5 years earlier. Episodes of poorly characterized dizziness at the assisted‐living facility led to BP determinations that were >200 mm Hg systolic, prompting urgent trips to the emergency department on 2 occasions. However, BPs in the emergency department on those 2 occasions were 140/78 mm Hg and 153/85 mm Hg. Thiazide‐related hyponatremia was recorded. Her only antihypertensive medication was lisinopril 40 mg daily, but she complained of chronic persistent dry cough since starting this medication.

Her standing BP was 154/84 mm Hg. Lisinopril was discontinued with resolution of her cough, and amlodipine was initiated and advanced to 10 mg daily. Follow‐up standing systolic BPs were 134 to 142 mm Hg. With follow‐up office visits, a better description of her dizzy spells emerged, and they were always accompanied by facial flushing, lasting about 30 minutes, and occurred twice weekly. Overall she felt well, and these episodes did not interfere with her function. She and her son were advised not to take home BPs.

Discussion

Prevalence of the Dizziness Complaint

Dizziness is often poorly characterized and a catchment term for a wide assortment of unpleasant sensations. It is also a very common complaint in office practice, with prevalence related to increasing age. A national ambulatory care survey found dizziness to be the main complaint of 2.4% of office visits, ¹ but such surveys substantially underestimate occurrence. Dizziness has been described as a geriatric syndrome, ² and prevalence studies register a complaint of dizziness in about 30% of individuals 65 years and older. ³ Since hypertension is an age‐related disease, clinicians can expect occasional overlap of these conditions.

When reported, dizziness is a frequently reported side effect in hypertension treatment trials. In the Valsartan Antihypertensive Long‐Term Use Evaluation (VALUE) trial, which enrolled patients with a mean age of 67 years, dizziness was a prespecified adverse event and was reported in 16.5% of patients in the valsartan arm vs 14.3% of patients in the amlodipine arm of the trial. ⁴ In a study comparing hypertensive monotherapy with a fixed‐dose combination (FDC), there was significantly more dizziness with the FDC, but the absolute numbers were small and the seriousness of the complaints was unmentioned. ⁵ In the Quinapril Titration Interval Management Evaluation (ATIME) trial, a more rapid drug up‐titration scheme led to more complaints of dizziness than a less rapid drug up‐titration scheme, but there was no difference in hypotension, and the difference in dizzy complaints was not statistically significant, P=.07. ⁶ In the Hypertension Optimal Treatment (HOT) trial, where goal diastolic pressures were 80, 85, and 90 mm Hg, improvement in dizziness compared with baseline was significant in all treatment groups, and lower levels of achieved BP were associated with improved quality‐of‐life scores. ⁷ It should be noted that dizziness is most often a mild transient complaint, and the severity of dizziness is not usually assessed. In the Avoiding Cardiovascular Events through Combination Therapy in Patients Living With Systolic Hypertension (ACCOMPLISH) trial, “any” report of dizziness was recorded in 20.7% of patients in the benazepril/amlodipine arm and 25.4% of patients in the benazepril/hydrochlorothiazide arm of the trial. However, “drug‐related serious” dizziness, hypotension, was reported in only 2 of 5744 (<0.1%) and 5 of 5762 (0.1%) patients in the 2 study arms, respectively. ⁸

What Is the Differential Diagnosis of Dizziness?

When a hypertension patient complains of dizziness, the dizziness needs to be addressed as an independent problem in order to make certain that the differential diagnosis is sufficiently inclusionary. ⁹ It is clinically useful to categorize the patient’s description of symptoms into 4 categories: (1) vertigo, (2) disequilibrium, (3) presyncope, and (4) lightheadedness (Table). ¹⁰ Vertigo is subdivided into peripheral and central etiologies. Benign positional vertigo is not age related, but is transient, related to changes in head position, and often severe with accompanying nausea and vomiting. Patients with Meniere disease or endolymphatic hydrops, another peripheral cause of vertigo, complain of episodic more persistent vertigo, tinnitus, fluctuating hearing loss, and aural fullness. Thiazide diuretics and sodium restriction are often successful in treating Meniere disease because diuretics reduce the expanded inner ear fluid volume that occurs in this disease, thereby decompressing the inner ear fluid spaces. ¹¹

Table.

 Categorization of Dizziness by Symptom Type

I. Vertigo

A. Peripheral

1. Benign positional vertigo (<1 minute)

2. Meniere disease (>5 minutes to hours, associated with tinnitus, aural fullness, hearing loss)

3. Motion sickness

4. Medications

B. Central (associated with additional neurologic signs)

1. Younger patients: multiple sclerosis

2. Older patients: brainstem or cerebellar ischemia due to stroke or vascular compromise such as vertebral basilar insufficiency

II. Presyncope

A. Cardiac arrhythmia (sudden in onset and nonpositional)

B. Severe aortic stenosis

C. Volume depletion: check postural vital signs

D. Postprandial postural hypotension occurring within 2 hours of eating in older patients

E. Metabolic: anemia, hypoglycemia, hypoxia, hypercapnia

F. Medications

III. Dysequilibrium, unsteadiness

A. Multisensory deficit, ie, vision and peripheral neuropathy, associated with diabetes mellitus

B. Multisensory deficit, ie, vision, hearing, reduced proprioception, associated with aging

C. Parkinson disease

D. Medications

IV. Prolonged vague lightheadedness; swimming or floating feelings

A. Psychiatric: anxiety, depression, hyperventilation, panic attacks, agoraphobia

B. Mixed dizziness syndromes

Central etiologies of vertigo such as brainstem and cerebellar disorders, as well as multiple sclerosis, are usually accompanied by additional “neighborhood” neurologic signs and symptoms over time. Separation of the central etiologies of vertigo is usually related to age with multiple sclerosis occurring in younger individuals and brainstem and cerebellar disease predominantly occurring in older patients. ¹ A common vascular cause of central vertigo in older patients is vertebral basilar insufficiency. In these patients, sudden recurrent vertiginous episodes may last days or weeks, and lightheadedness may follow neck extension. ¹²

Disequilibrium, a feeling of imbalance, is often attributed to sensory impairments. Reduced proprioception, which occurs with aging, reduced vision and hearing, and peripheral neuropathy either idiopathic or associated with systemic disease such as diabetes, all contribute to this category of dizzy complaints. Given the etiologies, disequilibrium dizziness is occasionally seen in older patients receiving antihypertensive therapy. Tinetti and colleagues² suggest that once diagnosed by clinical evaluation, proper management should address the contributing sensory deficits, ie with hearing aids, eyeglasses, and ambulatory assistance to prevent falling. In a 2‐year prospective study, older patients with dizziness were more likely to become disabled than their nondizzy counterparts. ¹³ Presyncope, or impending faint, described as a feeling of faintness, is particularly suggestive of reduced cardiac output when sudden in onset, such as occurring with an arrhythmia. Presyncope may also occur in association with postural hypotension due to reduced plasma volume.

Dizziness described as lightheadedness suggests the possibility of stress reactions, anxiety, and depression. ¹⁰ The symptom most frequently associated with hyperventilation syndrome is dizziness. ¹⁰ Other concomitant symptoms of panic disorder such as dyspnea, hot flashes, paresthesias, trembling, and tachycardia should be sought. Unlike the other dizziness syndromes, psychological dizziness can also be continuous or long standing. ¹⁴ These patients may benefit from counselling, anxiolytic drugs, or psychiatric referral.

Clinical Workup

The clinical workup for dizziness is highly dependent on the history and physical examination as well as knowledge of the differential diagnosis. Few additional tests are usually required. A Nylen Barany or Dix Hallpike maneuver can be considered to diagnose a peripheral vestibular disorder when the history is not completely clear, and a simultaneous canalith repositioning maneuver can be used for treatment. Vertical nystagmus or the failure of nystagmus to be suppressed by visual fixation suggests a central lesion. Postural vital signs, along with cardiac and neurologic examinations, are necessary. Cardiac arrhythmia monitoring is indicated in the case of episodic presyncope. Thirty seconds of hyperventilation may reproduce symptoms of psychiatric dizziness, ¹ but several studies have demonstrated that hyperventilation may also unmask vestibular dysfunction. ¹⁵ In the absence of associated neurologic signs and symptoms, brain imaging is unlikely to be helpful. ¹ In fact, brain imaging may detect minor incidental abnormalities that can incorrectly be implicated as the cause of dizzy episodes. ¹⁶

All antihypertensive medications can cause dizziness, ¹⁷ and most any oral medication of any type can be associated with dizziness. In Drachman’s informal survey of 20 random oral medications randomly selected from the Physicians Desk Reference, 18 listed dizziness as an adverse effect, and 10 of 20 listed dizziness as among the most frequently associated side effects. ¹ Tinetti found that use of ≥5 medications was a significant risk factor for dizziness in elderly individuals. ² Therefore, when faced with a patient complaining of dizziness, the medication list should be carefully reviewed and nonessential medications removed. Anticholinergic medications in particular should be removed as a potential cause of both dizziness and delirium in older patients. ¹⁸

Application of Clinical Considerations to These 3 Cases

These 3 cases each illustrate common problems hindering successful antihypertensive therapy in patients with dizzy spells. The first case described his spells as an episodic unsteadiness, which according to the classification scheme discussed above, would ordinarily be associated with sensory impairment, although no sensory impairment could be ascertained. The patient attributed these symptoms to intermittently decreased BP but was motivated to work with the hypertension consultant because he also knew that his BPs were predominantly elevated. No etiology of his spells could be determined, but they became less symptomatic and more manageable over time. Many times the correct strategy in elderly patients with dizziness is an impairment reduction strategy to improve function, but not to cure. ² Sometimes, dizzy syndromes may burn out over time. ¹⁹

The second case patient felt that bothersome dizzy episodes were caused by her antihypertensive medications. As is commonly the case, the description of her symptoms was poorly articulated. However, the chronicity of her symptoms suggested a psychiatric etiology. Frequent outpatient follow‐up with support from the patient’s son led to gradual incremental medication up‐titration and BP control using combined dihydropyridine/nondihydropyridine calcium channel blockers and low‐dose furosemide 2 times a day. Her dizzy symptomatology was managed but remained unresolved. However, her quality of life was significantly improved and anxiolytic medications were unnecessary.

The third patient also had poorly described dizzy episodes initially, which later became better defined as fairly classic anxiety attacks associated with facial flushing and transient severe BP elevation. She was advised not to use her home BP monitor, and hypertension was controlled with monotherapy. Her dizziness persisted but became tolerable with reassurance, and she was comforted by her BP control.

In all 3 of these cases, dizzy episodes were managed but continued. Function and quality of life were improved with successful antihypertensive therapy. In all 3 cases, management was marked by scheduled short‐interval follow‐up visits, an empathetic relationship by the clinician, and family support.