Management of the Hypertensive Dental Patient

Hypertension affects more than a billion people and is the leading risk factor for morbidity and mortality around the globe.^1,2 The lethality of hypertension is attributed to the fact that it is the most common risk factor for cardiovascular disease, which claims roughly 18 million lives a year.^3,4 Despite global efforts to mitigate hypertension, the number of cases has been increasing steadily over the last 25 years.⁵ In 2017, the threshold at which we classify hypertension was reduced to any reading over 130 mmHg systolic blood pressure (SBP) and 80 mmHg diastolic blood pressure (DBP).⁶ This decision was made after studying the importance of early intervention as well as the fact that, with each increased increment of 20 mmHg in SBP, the risk of cardiovascular diseases doubles.^7-9 The association of hypertension with cardiovascular disease is not the only reason for the disease’s high mortality rate. It is also a risk factor for chronic kidney disease, stroke, heart failure, diabetes, dementia and erectile dysfunction.^10,11

The etiology of hypertension falls into 2 major categories: primary/essential and secondary.¹² For adults, close to 95% of hypertension can be attributed to primary causation, meaning there is no identifiable cause. Secondary hypertension, the remaining 5%, is the result of an underlying condition, such as obstructive sleep apnea, adrenal gland tumours, thyroid conditions, kidney disease and congenital blood vessel defects. Certain medications may also be linked to secondary hypertension: oral contraceptives, decongestants and over-the-counter analgesics.^11-14 The pathogenesis of hypertension involves intricate interactions between environmental, genetic and behavioural factors.¹⁵ Risk factors notably include age, family history of cardiovascular disease, smoking, elevated and frequent alcohol consumption, cholesterol, sodium-rich diet and sedentary life style.^11,12,16,17 Pathophysiologic mechanisms that contribute to essential hypertension are salt/volume overload, activation of the renin-angiotensin-aldosterone system and the sympathetic nervous system.^4,12 The pharmacologic action of antihypertensive medications will target these specific systems. However, we also discuss the importance of non-pharmacological intervention as an adjunct to reducing blood pressure.

Hypertension often lacks symptoms, and, for many people, the most common interaction with a health professional is with their dentist. Therefore, dentists play an important role in early recognition, referring for diagnosis and providing council on prevention. The aim of this article is to go beyond simple screening for hypertension and to provide the dentist with a complete guide to managing the care of a hypertensive patient. Aspects of this include restrictions and warnings when certain procedures should be limited, common dentist-prescribed medications and their interaction with antihypertensive medications, oral presentations of hypertension, office blood pressure reading protocol and stress-limiting protocols.

Methods

We carried out a literature review to identify the management of hypertensive patients in a dental setting. Databases in the University of Toronto library system were searched to locate relevant peer-reviewed articles written in English and published in the past 5 years to ensure relevancy. Search words included “hypertensive patients,” “management,” “adverse effects,” “pharmacology,” “classification” and “dentistry.” Dentistry textbooks were also obtained from the University of Toronto Library and reviewed for relevant information. A limitation was the fact that some guidelines are based on best practices from the literature and not derived from a randomized controlled study because of ethical constraints.

Classification

The classification of hypertension has changed many times throughout the years and differs globally. A 2017 update from the American College of Cardiology (ACC) and the American Heart Association (AHA) decreased the threshold at which we classify hypertension.^6,7 This change stems from the fact that recent data have shown that intense blood pressure control in the lower ranges results in reduced fatality rates from cardiovascular events.¹⁸ Previously, prehypertension was described as SBP 120–139 mmHg or DBP 80–89 mmHg. The ACC/AHA has now separated hypertension into 2 categories: elevated (SBP 120–129 mmHg and DBP < 80 mmHg) and stage 1 (SBP 130–139 mmHg or DBP 80–90 mmHg). As a result, all other thresholds have also been lowered (Table 1).

It should also be noted that a single elevated blood pressure reading does not justify a specific classification. Classification should be based on an average of ≥ 2 readings on ≥ 2 occasions in a standardized environment using appropriate blood pressure technique. If SBP and DBP readings place the classification in different categories, the higher category should be chosen.¹⁹ Furthermore, persistent elevated blood pressure in a clinical setting in a patient who has no previous elevated reading within a 24-h period should be considered “white coat” hypertension. White coat hypertension can be confirmed with home blood pressure readings of ≤ 135/85 mmHg or 24-h ambulatory readings ≤ 130/80 mmHg.^20,21

From a treatment standpoint, classification is important as it serves as a factor when deciding when pharmacologic therapy should commence. However, the standard practice does not rely solely on blood pressure, but also includes a risk assessment for atherosclerotic cardiovascular disease, 10-year cardiovascular disease and general clinical judgement (Figure 1). If a patient falls within the normal or elevated blood pressure class, pharmacologic treatment is not necessary. The administration of antihypertensives is deemed appropriate for stage 1 hypertensive patients if they also have an atherosclerotic cardiovascular disease or 10-year cardiovascular disease risk assessment ≥ 10%. The initiation of antihypertensive medication is acceptable for a stage 2 hypertensive patient without the need for risk assessment but assessment is still recommended.6 In all classes, the therapeutic target is to lower blood pressure to ≤ 130/80 mmHg. In the case of seniors (over 65 years) with hypertension and other comorbidities, the appropriateness of pharmacologic action relies on other factors, such as clinical judgement, patient preference and a team-based approach. It is extremely important that, regardless of pharmacological treatment, all patients be educated on appropriate lifestyle modifications to reduce blood pressure, enhance antihypertensive therapy and decrease cardiovascular risk.²²

The measurement and classification of hypertension are useful in a dental setting for several reasons. First, it is important to recognize hypertension early to offer intervention, counseling and referral to mitigate progression of the disease; lifestyle modifications play an important part in the control of hypertension, independent of pharmacologic treatment. Second, classification serves as an important indicator as to when certain dental procedures should be suspended. Third, measuring blood pressure at the beginning of appointments — and during — can reveal how dental treatment may affect blood pressure. Blood pressure may change with administration of local anesthetic, general anesthesia or even anxiety over the procedure. We discuss the nuances of these effects below.

Pharmacology of Antihypertensive Drugs

One of the most important aspects of management of the hypertensive patient in a dental setting is a complete medical history, and a significant aspect of the medical history is noting all medications the patient is taking. Antihypertensive medications have a variety of adverse effects that can manifest in the oral cavity.²³ Some of the more frequent ones include xerostomia, lichen planus type lesions, dysgeusia and gingival hyperplasia. Although direct adverse effects are of concern, dentists should also be aware of potential problematic interactions involving the use of vasoconstrictors, such as epinephrine and NSAIDS, as well as the induction of orthostatic hypotension.

A variety of medications are used by hypertensive patients to control their blood pressure (Table 2). The goal in multidrug therapy is to treat the hypertension through multiple mechanisms of action, which may lower the chances of adverse effects and drug resistance by reducing the relative amount of each drug that’s taken. The main classes of medications include angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), calcium channel blockers (CCBs) and thiazide diuretics.²² ACE inhibitors combat hypertension by interfering with the renin-angiotensin-aldosterone system (RAAS). The RAAS is a complex of organs and enzymes that increase blood pressure through a variety of mechanisms, such as increasing blood volume and vasoconstriction. ACE inhibitors block the conversion of angiotensin 1 into angiotensin 2 thus halting the RAAS and decreasing blood pressure.²⁴ ARBs counteract the RAAS through a different mechanism of action. They block the active enzyme (angiotensin 2) from interacting with its receptor, thus preventing vasoconstriction, water retention and aldosterone production and, therefore, decreasing blood pressure.²⁴ CCBs lower blood pressure by acting at the level of the cardiac myocytes and smooth muscle cells in arteries. They block the influx of calcium into these cells allowing for vasodilation and a decrease in cardiac output.²⁴ Thiazide diuretics act at the level of the kidney by inhibiting the reabsorption of sodium and chlorine ions from the distal convoluted tubule by blocking thiazide-sensitive sodium–calcium symporter.²⁴ Blocking this transport allows for a decrease in blood volume and, subsequently, blood pressure.

Xerostomia

Commonly known as dry mouth, xerostomia is the most commonly reported adverse effect of antihypertensive medication.²³ Xerostomia tends to increase with the amount of anti-hypertensive drug taken; thus, the likelihood of developing adverse effects would also likely increase. Xerostomia is associated with the development of dental caries. Salivary flow plays a crucial role in the buffering effect needed to balance the demineralization/remineralization process taking place in the oral cavity. Without adequate salivary flow, the oral environment favours demineralization, leading to dental caries.²⁷ Other negative effects of xerostomia include increasing susceptibility to halitosis, oral/pharyngeal infections, gingivitis and bleeding/ulceration events.²⁸ Non-pharmacologic management may involve drinking more water and using oral lubricants, gums, pastes and sprays.²⁹ Changing the brand of antihypertensive medication or prescribing parasympathomimetic agents, such as pilocarpine, cevimeline, bethanechol chloride or anethole trithione, has also been shown to be an effective treatment option.^30,31

Oral Lichenoid Reaction

The etiology of oral lichen planus (OLP) is not well understood; however, its histology and clinical presentation are identical to that of a oral lichenoid reaction (OLR).³² OLR is a well observed adverse drug reaction to a variety of antihypertensive medications (Table 2).³³ It can present as bilateral white papules forming reticular or annular plaque-like patterns on the buccal mucosa, palate, gums and tongue. It may also present as erythematous erosive and ulcerative lesions.³⁴ OLR creates an unpleasant environment for patients causing a burning sensation, bleeding, pain and general discomfort associated with the patches.

A variety of management strategies exist for symptomatic OLR lesions, including non-pharmacologic approaches, such as limiting mechanical trauma that may be induced by an ill-fitting prosthesis. Pharmacologic treatment with topical corticosteroids, such as clobetasol, have also proven to be effective.³² Although OLR can be a serious adverse effect, stopping or changing the offending antihypertensive often resolves the condition.³³ 

Dysgeusia

Some degree of taste alteration has been reported in roughly 30% of patients prescribed antihypertensive and antihyperlipidemic drugs.³⁴ Although dysgeusia presents no immediate threat to oral health from a clinical standpoint, it can have implications for the psychological well-being of the patient. Dysgeusia may affect a patient’s quality of life or influence his/her appetite and body weight, leading to more severe physiologic consequences.³⁵

Management of dysgeusia may closely follow that for xerostomia as prolonged xerostomia can also lead to dysgeusia.³⁶ Therefore, use of the previously mentioned sialagogues is appropriate. However, dysgeusia may be independent of xerostomia and require alternative management. Although research is limited, alpha lipoic acid and zinc supplementation have been shown to improve taste perception.³⁷ In addition to pharmacologic treatment, lifestyle modifications may also alleviate antihypertensive-induced taste alteration, e.g., avoiding metallic silverware and bitter tasting foods, increasing the consumption of flavourful high-protein foods.³⁸

Gingival Hyperplasia

Gingival hyperplasia — aka gingival overgrowth or gingival enlargement — is an often-observed adverse reaction to calcium channel blockers, affecting 20–75% of patients.³⁹ The effect varies with type of calcium channel blocker as well as the oral health status of the patient. It should also be noted that gingival overgrowth can be observed in about 50% of patients who take phenytoin (a class 1 anti-arrhythmic drug).³⁴ Although tissue overgrowth is benign, it can impact mastication, phonation and general esthetics and compromise quality of life.⁴⁰ Gingival overgrowth can also create an uncomfortable oral environment, as tissue can become inflamed with the accumulation of plaque under enlarged gums where it is not easily removed.⁴¹

Potential management of gingival hyperplasia can be mitigated by removing the pro-inflammatory agents, by increasing oral hygiene regimes and using chlorhexidine or folic acid rinses. This approach is usually intended for patients who are trying to prevent the disease before onset and less so for management.³³ A more appropriate non-surgical modality is subgingival scaling and root planing, supplemented with oral hygiene instruction and frequent recalls.⁴² Surgical intervention via gingivectomy is the most effective treatment; however, as recurrence is common, this is recommended only for severe cases.^33,42 In addition to the aforementioned treatment modalities, substitution of the offending agent should be considered where medically appropriate.

Orthostatic Hypotension

Orthostatic hypotension is the sustained reduction of SBP by at least 20 mmHg or of DBP by at least 10 mmHg within 3 minutes of standing or head‐up tilt to at least 60° on a tilt table.⁴³ A patient taking antihypertensive medication may often experience light-headedness or syncope on standing after prolonged dental procedures in the supine position. The failure of the autonomic nervous system to adequately perfuse cerebral arteries creates a brief moment when the patient could trip, fall and harm themselves. Orthostatic hypotension can be managed simply by allowing the patient to sit upright for a few minutes followed by assistance on standing.⁴⁴ This allows for adequate cerebral profusion to occur, mitigating the risk of syncope.

NSAIDS

Non-steroidal anti-inflammatory drugs (NSAIDs) are often prescribed in a dental setting for their analgesic and anti-inflammatory properties.²² Furthermore, NSAIDs make up 5–10% of all prescriptions across all health care professions.⁴⁵ The use of NSAIDs, while helpful in mitigating pain, can attenuate the effects of antihypertensive medications for prolonged periods.⁴⁶ The average rise in blood pressure with chronic NSAID use is 5 mmHg, which over a long enough time can increase a patient’s risk of other cardiovascular disease, including heart failure.⁴⁵

The management of this potentially detrimental reaction is to limit the duration of treatment with NSAIDs to 5 days, as the use of NSAIDs for a few days shows almost no clinical relevance.^22,47 In addition to limiting duration, other analgesics, such as paracetamol, may be prescribed to avoid this effect.²⁰

Vasoconstrictors

The use of vasoconstrictors, such as epinephrine, in local anesthesia is paramount in performing successful clinical dentistry. The added vasoconstrictor aids in providing profound anesthesia to the focus area by mitigating systemic uptake, thus extending duration of action and providing local hemostasis. In addition, the dulling of sensory nerve fibres can alleviate stress experienced by the patient which would increase blood pressure from the release of catecholamines.⁴⁸ However, the administration of vasoconstrictors into the circulation system can also cause an increase in blood pressure; therefore, special consideration must be given to the hypertensive patient.

Much research has been done on this topic and it concludes that administration of local anesthetic containing vasoconstrictors shows little clinical relevance if done within accepted guidelines ^49-51 In fact, the appropriate administration of local anesthetic containing a vasoconstrictor far outweighs the risk by limiting stress-induced increases in blood pressure resulting from dental pain and anxiety. The effects of vasoconstrictors on systemic blood pressure is dose dependant.⁵² Therefore, procedures of long duration to multiple quadrants using epinephrine should be completed independently, while maintaining diligent supervision of blood pressure. The use of 1 to 2 cartridges of local anesthetic with 1:80 000, 1:100 000 or 1:200 000 of epinephrine in patients with controlled hypertension and/or coronary disease is generally considered safe.^26,53-55 In general, keeping the dose of vasoconstrictor below 0.04 mg per appointment is a safe practice for patients with hypertension.⁵⁶ Although this rule generally applies to patients with uncontrolled hypertension and/or cardiovascular disease, the state of a patient’s control is variable and the best practice may be to limit epinephrine in all cases and focus on the establishment of profound anesthesia with plain anesthetics.²¹ Consequently, the amount of epinephrine in the local anesthetic should be 1:100 000 or 1:200 000 to limit its delivery.²² Also, aspiration before injection to mitigate system load is of vital importance. It should also be noted that the use of even 1 cm of retraction cord impregnated with epinephrine can administer a dose equivalent to about 11 cartridges (2% lidocaine, 1:100 000 epinephrine) of local anesthetic and, therefore, should be absolutely contraindicated for the hypertensive patient.^20,22,57

Patient Management

The management of hypertensive patients requires a delicate combination of accurate record keeping, detailed knowledge and extensive preparation. The first step to patient management is identification and classification. A complete medical history encompassing all prior aliments with up-to-date drug history is required to become familiar with any relevant adverse drug reactions or common dental interactions (Table 2). In addition, blood pressure should be measured before any treatment and documented for both new and returning patients. Intermittent blood pressure measurement over the duration of the appointment is advisable for diagnosed hypertensive patients as blood pressure can change dramatically during treatment.⁵⁸ Such measures are especially indicated for more complicated dental procedures that are stress inducing, such as long-duration restorative procedures, oral/periodontal treatments and the placement of dental implants. Although fluctuations in blood pressure pose a relatively low risk to non-hypertensive ind…