Hypertension

Blood Pressure

The following is mostly redacted from the references provided and is provided as a source reference.

Hypertension is one of the most preventable causes of premature morbidity and mortality worldwide; a major risk factor for ischemic and hemorrhagic stroke, myocardial infarction, heart failure, chronic kidney disease, peripheral vascular disease (PVD), cognitive decline, and premature death. Epidemiological studies suggest that the risk associated with high blood pressure is a continuous relationship, and the risk of cardiovascular events doubles for every 20/10 mmHg rise in blood pressure above 115/70 mmHg, Blood pressure is normally distributed within a population, and there is no natural cut-off point above which hypertension definitively exists and below which it does not.

The Renin-Angiotensin-Aldosterone (RAAS) System

Hypertension-related morbidity can be reduced with effective lifestyle interventions, including diet, exercise, and control of body weight; however, many people require antihypertensive medications to lower blood pressure. Inhibitors of the angiotensin-converting enzyme (ACEIs), blockers of the angiotensin receptor (ARBs), and the direct renin inhibitor (DRI) aliskiren are among approved drug treatments hypertension in adults. While these three drug classes target the renin-angiotensin-aldosterone (RAAS) system, it is not clear that these medications are clinically equivalent. What is the evidence for the comparative long-term benefits and adverse effects of ACEIs, ARBs, and the DRI aliskiren where used for treating hypertension in adults?

There is a high-level evidence that ACEIs and ARBs control blood pressure to a similar extent. Data are, however, more limited for comparisons with the DRI aliskiren. ACEIs and ARBs have similar effects on mortality, major cardiovascular events, quality of life, lipid levels, markers of carbohydrate metabolism (diabetes control), and other adverse events excluding cough. Cough is significantly higher with ACEIs when compared with an ARB.

BP Measurement and Monitoring

According to the recent ACE-Prevention (Assessing Cost-Effectiveness in Prevention) Report, the management of blood pressure and cholesterol is currently inefficient. Prevention should target absolute rather than individual risk factor thresholds. Retrospective analysis of a recent British clinical trial of 163 patients showed that no monitoring—not office, 24hr ambulatory, or home self-monitoring—came within ± 8-10 mmHg of the accuracy obtained with continuous monitoring. A week of self-monitoring was the most accurate, but even this was highly imperfect. Office measurement was impractical for precise assessment, as 10-13 separate measures were required to give the accuracy essential for safely titrating antihypertensives. Meta-analysis of from 28,281 patients newly initiated on ACEi across seven RCTs, even after regular monitoring for 3 months, found it impossible to determine whether resultant blood pressure readings was due to drugs; as most variation in a person’s blood pressure response is a consequence of background day-to-day fluctuations. Estimates are that it would require 90 separate measurements, both before and after starting treatment, to be 95% certain that an apparent decrease of more than 4 mmHg in systolic blood pressure was a true decrease, and about 30 readings to be 95% confident of a 4 mmHg reduction in diastolic blood pressure.

The 10-year cardiovascular risk categories by the European Systematic Coronary Risk Evaluation system (SCORE).

Very high risk	People with any of the following: Documented CVD, either clinical or unequivocal on imaging. • Clinical CVD includes acute myocardial infarction. acute coronary syndrome, coronary or other arterial revascularization, stroke, TIA, aortic aneurysm, and PAD • Unequivocal documented CVD on imaging includes significant plaque (i.e. ≥ 50% stenosis) on angiography or ultrasound; it does not include increase in carotid intima-media thickness • Diabetes mellitus with target organ damage, e.g. proteinuria or with a major risk factor such as grade 3 hypertension or hypercholesterolemia • Severe CKD (eGFR < 30 mL/min/1.73 m2) • A calculated 10 year SCORE of ≥ 10%
High risk	People with any of the following: • Marked elevation of a single risk factor, particularly cholesterol > 8 mmol/L (> 310 mg/dL), e.g. familial hypercholesterolemia or grade 3 hypertension (BP ≥ 180/110 mmHg) • Most other people with diabetes mellitus (except some young people with type 1 diabetes mellitus and without major risk factors, who may be at moderate risk) Hypertensive LVH Moderate CKD eGFR 30-S9 ml/min/1.73 m2) A calculated 10 year SCORE of 5-10%.
Moderate risk	People with: • A calculated 10 year SCORE of ≥ 1 to < 5% • Grade 2 hypertension • Many middle-aged people belong to this category
Low risk	People with: • A calculated 10 year SCORE of < 1%

Data from the BEACH study of Australian general practice activity show that cardiovascular problems account for 20.5 per 100 encounters, with hypertension contributing to 46% of these.

A diagnosis can be confirmed, if:

• ambulatory or home BP monitoring indicates an elevated BP; or
• elevated BP at a third office visit.

Lack of effect may be due to white-coat hypertension which can be better detected with ambulatory and home measurements, and decide whether an appropriate level has been reached based on absolute CVS risk profile.

There was no evidence of a difference in patient preferences for GP management, pharmacist management, or telehealth, while there was evidence that participants preferred GP management over self-management. Patients preferred scenarios that had greater reduction in cardiovascular risk, more frequent BP monitoring, and lower costs. Risk was the most important driver of choice.

Commonly Used Antihypertensive Drugs

Thiazide diuretics

Common Adverse Effects: Common: hypotension, muscle cramps, weakness, erectile dysfunction; hypokalaemia, hyponatraemia, hyperglycaemia, hyperlipidaemia, hyperuricaemia. Less Common: allergic reactions (cross sensitivity to other sulfonamide derivatives); photosensitivity; fatigue; blood dyscrasias; azotaemia.

Therapeutic Considerations: monitor serum Creatinine and potassium; generally ineffective in CrCl < 30 mL/min; use cautiously in patients with history of or predisposition to gout (may precipitate gout) or renal impairment (cumulative effects may develop); may change glycaemic control in patient with diabetes or pre-diabetes; consider an alternative antihypertensive for patients with or predisposed to arrhythmias.

chlorthalidone: 50, 100 mg tabs. Initial: 12.5 mg daily. Usual: 12.5-25 mg daily.

Hydrochlorothiazide: 12.5, 25, 50, 100 mg tabs. Initial: 12.5 mg daily. Usual (mono): 12.5 mg to 50 mg once daily; Usual (adjunct): 12.5 mg to 25 mg once daily. Max: 50 mg daily.

Indapamide: 1.25, 2.5 mg tabs. Initial: 1.25 mg once daily. Usual (mono): 2.5 mg once daily; Usual (adjunct): 1.25 mg to 2.5 mg once daily. Max: 2.5-5 mg daily.

Angiotensin-Converting Enzyme Inhibitor (ACE-I)

Common Adverse Effects: Common: dry cough, hyperkalaemia. Less Common: angioedema, precipitation of renal failure in patients with renovascular disease, volume depletion (or diuretic use), or concomitant NSAID use.

Therapeutic Considerations: monitor serum Creatinine and potassium initiation of therapy and periodically; reduce initial dose by 50% if concomitant diuretics (risk of hypotension with hypovolaemia); cough associated with ACEi is dry, hacking and non-productive and typically occurs within months of initiation of therapy; risk factors for hyperkalaemia include; renal dysfunction, diabetes, and concomitant use of potassium supplements, potassium-sparing diuretics or potassium-containing salts; consider a thiazide diuretic or CCB instead of an ACEi or ARB as initial antihypertensive therapy in black patients; for patients who experience reduced antihypertensive effect near the end of the 24-hour dosing interval, divide total daily dosage into two equal doses given every 12 hours or increase once daily dose.

Captopril: 6.25, 12.5, 35, 50, 100 mg tabs. Initial: 12.5-25 mg BID to TID. Usual: 50 mg BID to TID. Max: 450 mg Administer 1 hour prior to meals.

Quinapril (Accupril): 5, 10, 20, 40 mg tabs. Initial: 10 mg once daily. Usual: 10-20 mg once daily. Max: 40 mg daily.

Ramipril: 1.25, 2.5, 5, 10, 15 mg caps. Initial: 2.5 mg once daily. Usual: 2.5-10 mg once daily. Max: 20 mg daily.

Trandolapril: 0.5, 1, 2, 4 mg caps. Initial: 1 mg once daily. Usual: 1-2 mg once daily. Max: 4 mg once daily.

Enalapril: 2.5, 5, 10, 20 mg tabs. Initial: 5 mg once daily. Usual: 10 mg to 40 mg daily as a single dose or two divided doses. Max: 40 mg daily.

Fosinopril (Monopril): 10, 20 mg tabs. Initial: 10mg once daily. Usual: 20 mg once daily. Max: 40 mg daily.

Lisinopril (Zestril): 5, 10, 20 mg tabs. Initial: 10 mg once daily. Usual: 10 to 40 mg once daily Max: 80 mg daily.

Angiotensin II Receptor Blockers (ARB)

Common Adverse Effects: Common: hyperkalaemia. Less Common: angioedema, precipitation of renal failure in patients with renovascular disease, volume depletion (or diuretic use), or concomitant NSAID use.

Therapeutic Considerations: monitor serum creatinine and potassium at initiation of therapy and regularly; reduce initial dose if using concomitant diuretics (risk of hypotension with hypovolaemia); risk factors for hyperkalaemia include renal dysfunction, diabetes, and concomitant use of potassium supplements, potassium-sparing diuretics, or potassium-containing salts; consider a thiazide diuretic or CCB instead of an ACEi or ARB as initial antihypertensive therapy in black patients; contraindicated in pregnancy.

candesartan (Atacand): 4, 8, 16, 32 mg tabs. Initial: 8 mg once daily. Usual: 8 to 16 mg daily. Max: 32 mg daily.

eprosartan (Teveten): 400, 600 mg tabs. Initial: 600 mg daily. Max: 800 mg once daily as a single dose or two divided doses.

irbesartan (Avapro): 75, 100, 300 mg tabs.
losartan (Cozar): 25, 50, 100 mg tabs.
olmesartan (Olmetec): 20, 40 mg tabs.
telmisartan (Micardis): 40, 80 mg tabs.
valsartan (Diovan): 40, 80, 160, 320 mg tabs.

Beta₁-Adrenerglc Antagonists (Beta -Blockers)

Non-selective

Common Adverse Effects: Common: bradycardia, fatigue, decreased exercise, tolerance, headache, erectile dysfunction, vivid dreams. Less common: hyperglycaemia, heart failure, heart block, depression. Propranolol has higher lipophilicity than other beta-blockers and is more likely to cause CNS adverse effects, e.g. insomnia, vivid dreams.

Therapeutic Considerations: Avoid non-selective beta-blockers in reactive airways disease (risk of bronchospasm or bronchoconstriction); Initiate cautiously and titrate slowly in patients with heart failure as beta-blockers may worsen heart failure; When discontinuing in chronic users, gradually taper doses over 1-2 weeks (abrupt discontinuation may precipitate cardiac events, sinus tachycardia, and rebound HTN); Consider alternative antihypertensive in patients at high risk of heart block (contraindicated in 2nd or 3rd degree heart block without pacemaker); Avoid in severe PAI;
Avoid beta-blockers as initial antihypertensive therapy in patients > 60 years without other compelling indication.

Propranolol (Inderal): 10, 20, 40, 80, 120 mg tabs.

timolol: 5, 10, 20 mg tabs.

Non-selective with Intrinsic sympathomimetic activity (ISA)

Common Adverse Effects: Common: bradycardia, fatigue, decreased exercise, tolerance, headache, erectile dysfunction, vivid dreams. Less common: hyperglycaemia, heart failure, heart block, depression. Adverse effects specific to labetolol: oedema, postural hypotension, dizziness, nasal congestion.

Therapeutic Considerations: Beta-blockers with ISA have a lesser effect on resting heart rate compared to agents without ISA; Avoid non-selective beta-blockers in reactive airways disease (risk of bronchospasm or bronchoconstriction); Initiate cautiously and titrate slowly in patients with heart failure as beta-blockers may worsen heart failure; When discontinuing in chronic users, gradually taper doses over 1-2 weeks (abrupt discontinuation may precipitate cardiac events, sinus tachycardia, and rebound HTN); Consider alternative antihypertensive in patients at high risk of heart block (contraindicated in 2nd or 3rd degree heart block without pacemaker); Avoid in severe PAI; Avoid beta-blockers as initial antihypertensive therapy in patients > 60 years without other compelling indication.

pindolol (Visken): 5, 10, 15 mg tabs.

labetalol (Trandate): 100, 200 mg tabs.

Beta₁-selective

Common Adverse Effects: Common: bradycardia, fatigue, decreased exercise tolerance, headache, erectile dysfunction, vivid dreams; Less Common: hyperglycaemia, heart failure, heart block, depression; Cardiac selectivity of beta1-selective blockers may result in fewer non-cardiac adverse events.

Therapeutic Considerations: Low doses of beta1·selective beta-blockers may be used in patients with mild to moderate reversible airway disease (ensure access to a bronchodilating beta2·agonist is readily available); Initiate cautiously and titrate slowly in patients with heart failure as beta-blockers may worsen heart failure; When discontinuing in chronic users, gradually taper doses over 1-2 weeks (abrupt discontinuation may precipitate cardiac events, sinus tachycardia, and rebound HTN); Consider alternative antihypertensive in patients at high risk of heart block (contraindicated in 2nd or 3rd degree heart block without pacemaker); Avoid in severe PAI; Avoid beta-blockers as initial antihypertensive therapy in patients > 60 years without other compelling indication.

atenolol (Tenormin): 25, 50, 100 mg tabs. Initial: 25 mg daily. Usual: 50 mg daily as single dose or divided BID. Max: 100 mg daily as single dose or divided BID.

Bisoprolol: 5, 10 mg tabs. Initial: 5 mg once daily. Usual: 10 mg once daily Max: 20 mg once daily.

Metoprolol (Lopressor, Betaloc): 50, 100 mg tabs and 100, 200 mg SR tabs. Initial: 50 mg daily. Usual: 100 to 200 mg daily. Max: 400 mg daily. Regular release: dose BID; Sustained release dose once daily.

Beta1-selectlve with intrinsic sympathomimetic activity (ISA)

Common Adverse Effects: Common: bradycardia, fatigue, decreased exercise tolerance, headache, erectile dysfunction, vivid dreams. Less Common: hyperglycaemia, heart failure, heart block, depression Cardiac selectivity of beta1-selective blockers may result in fewer non-cardiac adverse events.

Therapeutic Considerations: Beta-blockers with ISA have a lesser effect on resting heart rate compared to agents without ISA; Low doses of beta1·selective beta-blockers may be used in patients with mild to moderate reversible airway disease (ensure access to a bronchodilating beta2·agonist is readily available).; Initiate cautiously and titrate slowly in patients with heart failure as beta-blockers may worsen heart failure; When discontinuing in chronic users, gradually taper doses over 1-2 weeks (abrupt discontinuation may precipitate cardiac events, sinus tachycardia, and rebound HTN); Consider alternative antihypertensive in patients at high risk of heart block (contraindicated in 2nd or 3rd degree heart block without pacemaker); Avoid in severe PAI; Avoid beta-blockers as initial antihypertensive therapy in patients > 60 years without other compelling indication.

acebutolol: 100, 200, 400 mg tabs. Initial: 100 mg daily. Usual: 400 mg daily as single dose or divided BID Max: 800 mg daily as single dose or divided BID.

Calcium Channel Blockers (CCB)

Dihydropyridine (DHP)

Common Adverse Effects: Common: Adverse effects related to vasodilation (e.g., pedal oedema, flushing headache, palpitations); Serious: Angina, heart failure, pulmonary oedema, tachycardia, bradycardia, skin rashes.

Therapeutic Considerations: Do not use immediate release DHP-CCBs for acute reduction or BP (strokes have been reported); Do not use immediate release nifedipine to treat essential HTN; DHP·CCBs may worsen heart failure symptoms; Grapefruit juice may increase drug levels and potentiate adverse effects (particularly with felodipine); When discontinuing. taper doses gradually (abrupt withdrawal may provoke chest pain).

amlodipine (Norvasc): 2.5, 5, 10 mg tabs. Initial: 2.5 mg once daily. Usual: 5 to 10 mg once daily. Max: 10 mg daily.
felodipine (Plendil): 2.5, 5. 10 mg ER tabs. Initial: 2.5 mg once daily. Usual: 2.5 to 10 mg once daily. Max: 10 mg daily.
nifedipine (Adalat): 20, 30, 60 mg ER tabs. Initial: 30 mg once daily. Usual: 30 to 60 mg once daily Max: 90 mg daily.

Non-dihydropyridine (non-DHP)

Common Adverse Effects: Common: Headache, peripheral oedema, dizziness, bradycardia, flushing, nausea, constipation Serious: heart block, worsening of heart failure, hypotension, ECG abnormality, asthenia, arrhythmia.

Therapeutic Considerations: Contraindicated post-MI in patients with moderate or severe left ventricular dysfunction.; Use cautiously in patients with heart failure, or 2nd or 3rd degree heart block without pacemaker; Grapefruit juice may increase drug levels and potentiate adverse effects; When discontinuing, taper doses gradually (abrupt withdrawal may provoke chest pain).

Diltiazem (Cardizem CD): 120, 180, 240, 360 mg ER tabs.

Verapamil (Isoptin / SR): 80, 120 mg tabs and 120, 180, 240 mg ER tabs. Initial: 80 mg TID immediate release; 180 to 240 mg daily sustained release. Usual: 160 mg TID immediate release; 180 to 240 mg BD sustained release. Max: 480 mg daily.

Usual adult doses quoted are for normal renal and hepatic function. Consult product monograph for detailed dosing instructions and dose adjustments for unique patient populations. As per BCGuidelines.ca: Hypertension – Diagnosis and Management: Appendix D (2015).

Diagnosis of Hypertension: algorithm

A 2017 meta-analysis of 4 RCTs (869 patients) evaluated the effectiveness of prescribing spironolactone for patients with resistant hypertension, defined as above-goal blood pressure (BP) despite treatment with at least 3 BP-lowering drugs (at least 1 of which was a diuretic). All 4 trials compared spironolactone 25 to 50 mg/d with placebo. Follow-up periods ranged from 8 to 16 weeks. The primary outcomes were systolic and diastolic BPs, which were evaluated in the office, at home, or with an ambulatory monitor. A statistically significant reduction in SBP occurred in the spironolactone group compared with the placebo group (weighted mean difference [WMD] = -16.7 mm Hg; 95% confidence interval [CI], -27.5 to -5.8 mm Hg). DBP also decreased (WMD = -6.11 mm Hg; 95% CI, -9.34 to -2.88 mm Hg). The evidence from multiple RCTs convincingly shows the effectiveness of spironolactone. Despite the SOR of C because of a disease-oriented outcome, we do treat to blood pressure goals, and therefore, spironolactone is a good option.

RAAS Blockade:  Generally better to use small doses blocking the different components of the RAAS pathway – ACEi /ARB. Risks:  worsening renal function; hyperkalaemia; anaemia.

AT1-receptor antagonists

Several orally active AT1-receptor antagonists are in various stages of clinical development. Losartan is the prototype of the angiotensin II receptor antagonist class. 3 It has been followed by irbesartan, eprosartan and candesartan and others are coming, such as valsartan, telmisartan and tasosartan. By binding to the AT1 receptor, all these drugs prevent the vasoconstrictor and other actions of angiotensin II. The majority of them produce non-competitive or insurmountable antagonism; even with increasing levels of angiotensin II, the blockade cannot be overcome.

The absorption of losartan, candesartan and irbesartan is not affected by food, whereas valsartan’s bioavailability is decreased by food. The drugs vary in their potency, but most of them are very long acting.

Some are prodrugs (losartan, candesartan) that have to be converted to an active compound. Losartan, although itself an antagonist, is converted to EXP3174 which is more potent and much longer acting than the parent compound. AT1 receptor antagonists also vary in their metabolism, some being excreted exclusively by the kidney, whereas others are excreted both by hepatic metabolism and renal excretion.

The drugs have little or no effect on the AT2 receptor. Similarly, they have no significant affinity for other hormone receptors or ion channels.

AT1 receptor antagonists lower the blood pressure of hypertensive patients. Their action is slow in onset avoiding first-dose hypotension, although this may still occur, particularly if patients are salt depleted. The class tends not to affect lipids, blood glucose and, in people with normal renal function, potassium.

Predictor of Hyperkalaemia

• eGFR < 45 mL/min/1.73 m²
• baseline [K⁺] > 4.5 mEq/L on diuretics
• BMI < 26 kg/m² (adipocytes produce aldosterone to a certain extent)

Patients should be instructed to empty their bladder and avoid smoking, caffeine, and exercise for at least 30 minutes before measuring their BP. They should be seated comfortably with their back supported and feet on the ground for 3 to 5 minutes before the readings. The patient and observer should refrain from talking during the rest period and during BP measurement. Cuff size should be appropriate for the individual’s arm circumference, and the cuff should be positioned at heart level (mid-sternum). Guidelines recommend averaging 2 or more readings obtained on 2 or more occasions to obtain the best estimate of BP.

Measurement of home BPs allows for identification of patients with white-coat but also a masked hypertension more prevalent in patients with reduced kidney function, associated with target-organ damage and adverse outcomes.  Newer devices allow for measurement of BP at night and telemonitoring with automatic transmission of BPs to providers.

Hypertension – pathological classification

Following documentation of hypertension and clinical assessment of likely cause, further investigation may be indicated: Creatinine, Electrolytes, Urinalysis, Urine microscopy.

• Essential (idiopathic)
• Renal disorders/disease:
  • Glomerulonephritis
  • Renal tubulo-interstitial disorders
  • Renal artery stenosis: confirmatory tests include measurement of renal vein Renin by selective catheterisation – consult pathologist.
  • Polycystic kidney disease
• Pregnancy-induced hypertension: Urate, Protein urine.
• Endocrine disorders:
  • Cushing’s syndrome
  • Hyperthyroidism
  • Phaeochromocytoma
  • Hyperaldosteronism
• Oestrogen therapy:
  • Oral contraceptives
• Alcoholism

In patients older than 80 years, a threshold of ≥ 160 / ≥ 90mmHg is advised for all groups, equally in diabetes, CAD, CKD or stroke. There are specific underlying mechanisms of HTN in older persons, including mechanical hemodynamic changes, arterial stiffness, neurohormonal and autonomic dysregulation, and the aging kidney. In CAD, diastolic BP should not be lowered < 70 mmHg as myocardial perfusion may be impaired in lower values, while at the other end of the spectrum treatment is recommended at the threshold of high-normal BP of 130–139/85–89 mmHg, as these patients are already considered very high risk.

In the INVEST sub-study, the adjusted hazard ratio for primary outcomes showed a J-shaped relationship between each age group with on-treatment SBP and DBP. The SBP at the hazard ratio nadir increased with aging, highest for the elderly (140 mmHg). Nevertheless, DBP at the hazard ratio nadir was slightly decreased for the very old (70 mmHg).

Thiazide diuretics, angiotensin-converting-enzyme inhibitor (ACEI), angiotensin II receptor blockers (ARB), and calcium channel blocker (CCB), have all shown benefit on CVD outcomes in older age patients. Unless clinically indicated by comorbidities, beta blockers should not be used as first line medications because they may worsen CVD outcomes in those over 60 years of age. Loop diuretics and alpha-blockers should also be avoided given their association with falls.

When to start drug treatment for hypertension²

Heart Foundation in M. Nelson, “Drug treatment of elevated blood pressure,” Aust Prescr  33; 2010, 109. Available at https://doi.org/10.18773/austprescr.2010.055.

Causes of Postural Syncope: a practical differential

• Vasovagal syncope
• Postural tachycardia syndrome (POTS)
• Autonomic failure
• Persistently low supine systolic blood pressure
• Initial orthostatic hypotension

Disorders of circulatory control are frequently disabling and difficult to treat.

Physiological classification of transient loss of consciousness

Postural tachycardia syndrome

Postural tachycardia syndrome (POTS) is a perplexing condition of mostly young women only recently identified in the medical literature. Postural tachycardia syndrome is characterised by fatigue, palpitations, exercise intolerance, light-headedness, visual blurring, chest pain, inability to concentrate, and episodic syncope or presyncope (i.e., the sensation that fainting may occur without actual syncope). Anxiety and depression are frequent comorbidities. A hallmark of POTS is that, during syncope, blood pressure is maintained or falls only minimally, while heart rate increases dramatically: an increase in heart rate of at least 30 beats per minute after 10 minutes of standing, or a heart rate of above 120 beats per minute with prolonged standing, suggests the diagnosis. The onset of POTS is often abrupt and, in about 50% of cases, follows a minor infection. POTS appears to be a manifestation of sympathetic nervous system hyperactivity during standing.

Hypotension in Elderly

Postprandial hypotension in geriatric patients is an underrecognized cause of syncope. The mechanism is unclear, but it appears to be related to reduced sympathetic response to a meal. Ambulatory BP monitoring and symptoms can give a diagnose. The patient can be advised to increase water intake before eating or substituting six smaller meals daily for three larger meals. Older adults have an increase frequency of postprandial hypotension. Patients with HF, syncope, Parkinson’s disease, end-stage renal disease on dialysis, autonomic dysfunction can have postprandial hypotension. Frail older adults with postprandial hypotension increase their postprandial BP and heart rate when walking.

Hypertension in Athletes

There is no fundamental difference in the approach to the medical therapy of hypertension in athletes compared with the general population. However, some second-line therapies are best avoided. In athletes, diuretics are relatively contraindicated, as they can impair athletic performance due to volume depletion, and they are prohibited by many of the governing bodies in sport because they may be used to prevent detection of performance enhancing drugs. In addition, beta blockers decrease heart rate and thus can reduce exercise tolerance; they too are prohibited in some sports. Angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), and long-acting dihydropyridine calcium channel blockers are better choices for athletes as they do not impede athletic performance and are permissible under the rules of most governing bodies in sport. Apart from creatine, other performance-enhancing drugs that can produce elevations in blood pressure (BP) include human growth hormone, androgens (anabolic steroids), and erythropoietin. Animal studies have reported that supplemental testosterone reduces body fat and improves insulin sensitivity but also causes increased BP. Stimulants can increase BP and clinicians should ask athletes about their use of both licit and illicit substances. Common stimulants include caffeine, nicotine, ephedra-containing over-the-counter decongestants, ephedra-containing herbal remedies, and amphetamines. Athletes diagnosed with prehypertension or Stage 1 hypertension without signs of end organ damage have no restrictions on their participation in sport.

References

• Agency for Healthcare Research and Quality (AHRQ). “Clinician Research Summary: ACEIs, ARBs, or DRI for Adults With Hypertension.” www.ahrq.gov. 
• Guidelines & Protocols Advisory Committee. BC Guidelines: Hypertension – Diagnosis and Management. Mar 1, 2015. BCGuidelines.ca.
• Bergler-Klein, Jutta and Bergler-Klein, Jutta. What’s new in the ESC 2018 guidelines for arterial hypertension : The ten most important messages. Wiener klinische Wochenschrift 131 (7-8); 2019: 180–185. [online]. https://doi.org/10.1007/s00508-018-1435-8.  
• Cohney, Schlomo. “Taking the tension out of Hypertension: Improving Patient Outcomes.”
• Dixit, Sameer and DiFiori, John P. “Hypertension in athletes.” UpToDate. Jan 21, 2016. Available at http://www.uptodate.com/contents/hypertension-in-athletes?topicKey=SM%2F94700&elapsedTimeMs=4&view=print&displayedView=full.
• Fletcher, Benjamin; Hinton, Lisa; McManus, Richard and Rivero-Arias, Oliver.  “Patient preferences for management of high blood pressure in the UK: a discrete choice experiment.” British Journal of General Practice. Online First 2019. DOI: https://doi.org/10.3399/bjgp19X705101.
• Lyon, Corey; Utter, Brigitte and DeSanto, Kristen. “Q: How effective is spironolactone for treating resistant hypertension?” Online Exclusive. Journal of Family Practice 68 (5), Jun 1, 2019. http://link.galegroup.com/apps/doc/A592903817/AONE?u=usyd&sid=AONE&xid=e9de9f64.
• Nelson, Mark. Drug treatment of elevated blood pressure.” Aus Prescr 33(4); 2010: 108-12. www.australianprescriber.com.
• Oliveros, Estefania; Patel, Hena; Kyung, Stella; Fugar, Setri; Goldberg, Alan; Madan, Nidhi and Williams, Kim A. “Hypertension in older adults: Assessment, management, and challenges.” Clinical Cardiology 43; 2020: 99–107. DOI: 10.1002/clc.23303.
• RCPA Manual. “Hypertension.” The Royal College of Pathologists of Australasia. Dec 2, 2014. http://www.rcpa.edu.au/Library/Practising-Pathology/RCPA-Manual/Items/Clinical-Problems/H/Hypertension.
• Reid, Christopher M. and Nelson, Mark R. “Optimising the Management of Hypertension.” Medicine Today 6(12); 2005: 12-8.
• Saiz LC, Gorricho J, Garjón J, Celaya MC, Erviti J, Leache L. Blood pressure targets for the treatment of people with hypertension and cardiovascular disease. Cochrane Database of Systematic Reviews 2018, Issue 7. Art. No.: CD010315. DOI: 10.1002/14651858.CD010315.pub3.
• Vaddadi, Gautam; Lambert, Elisabeth; Corcoran, Susan J. and Esler. Murray D.  “Postural syncope: mechanisms and management.” MJA187(5); 2007: 200-304.