Hypertension

Essential Hypertension

A specific cause of hypertension is found in 10-15% of patients. The other 85-90% is termed essential, meaning no other medical reason is present. Contributing factors to essential hypertension are thought to include:

• high dietary intake of salt (>2.5 g/day), but only 40-50% of people are salt sensitive
• stress
• genetics : black people have increased risk
• age
• sex - males are more likely
• smoking
• sedentary lifestyle
• diabetes mellitus
• alcohol consumption

Secondary causes

It is more likely if HT onset is <30 or >55, if there is a poor response to treatment, if increase is accelerated, or if there are further clinical signs (electrolyte abnormalities, renal bruits, etc).

Apparent Hypertension

White coat syndrome

• measure home BP

pseudohypertension: calcified brachial arteries

• suspect if BP high and no target organ damage
• may complain of dizziness despite high BP
• Osler's maneuvre:

History

As over 40% of people with hypertension do not know it (Joffres et al, 1997), it is termed 'the silent killer'. However, people may have an occipital headache on awakening, or can complain of vision changes.

Sudden onset would suggest renovascular hypertension.

History should be focused on symptoms of organ damage caused by hypertension:

• cardiovascular disease
• stroke/TIA
• peripheral artery disease
• kidney disease
• diabetes
• snoring, sleep pauses, suggesting sleep apnea

Vascular disease can also point towards renovascular causes for hypertension.

family history

• hypertension
• premature CVD
• stroke
• diabetes
• dyslipidemia

medications

• results and side effects of previous therapy
• commonly prescribed/OTC/illegal medications which can raise bp

social history

• education, work conditions
• finances
• family/friend dynamics
• other sources of stress
• cigarettes, alcohol, other drugs
• diet: sodium and fats

Physical Exam

head and neck

• thyroid exam
• fundoscopy: arteriolar narrowing, arteriovenous nicking, hemorrhages, exudates, papilledema
• arcus senilis in the eyes
• bulging veins of the chest
• supraclavicular fat pad
• buffalo hump
• mood face

cardiovascular exam:

• pulse for arrhythmias, tachycardia
• auscultate carotids for bruits
• assess JVP
• auscultate for murmurs, S3 and S4
• auscultate for renal bruits
• diminished, delayed, absent femoral/pedal pulses
• edema
• signs of peripheral vascular disease

abdominal exam:

• trunkal obesity
• enlarged kidneys
• masses
• abdominal aortic pulsation

skin

• leukonychia
• tremor
• clubbing
• reflexes

Lab Investigations

Lab investigations for everyone with hypertension include:

• urinalysis
• CBC
• electrolytes
• BUN and creatinine
• fasting lipid profile
• fasting blood glucose
• TSH

Other tests should be done for specific patient subgroups, and include:

• diabetes or renal disease: urinary protein excretion
• plasma aldosterone and renin (endocrine)
• 24 hour urine for catecholamines (phaeochromocytoma)

Diagnostic Imaging

ECG for left ventricular dysfunction.

Renal ultrasound if creatinine elevated or other evidence of renal disease.

MRA if renal artery stenosis

or renal captopril scan

Lifestyle

Lifestyle measures are incredibly important in preventing and reducing hypertension. These include:

• reduce foods with added sodium: under 2300 mg/day DASH diet
  • teach about reading labels
• increased potassium intake
• physical activity
• weight loss
• alcohol reduction
• smoking cessation
• stress reduction

Pharmacological

All pharmacological approaches to lowering blood pressure interfere with normal mechanisms of blood pressure regulation.

Combination therapy is increasingly being shown to improve blood pressure. The most important step is to gain buy-in by patients.

Various classes of medication include

• ACE inhibitors - promote vasodilation and reduced other effects of Ang II
  • not women of child-bearing age; not as monotherapy for black patients
• angiotensin receptor blockers
• diuretics, especially thiazides: promote naturesis and reduce TPR through unknown mechanisms
• beta blockers - reduce CO, renin production, TPR, and catecholamines (not for patients >60)
• calcium channel blockers - promotes vasodilation
• alpha blockers
• vasodilators

Specific situations

• Systolic hypertension: thiazide
• CAD: ACE, BB, CCB
• recent MI: BB, ACE
• CHF
• non DM CKD: ACE
• renovascular disease: caution with ACE/ARB

A simple algorithm appears very helpful (Feldman et al, 2009):

1. initial therapy with a low-dose angiotensin-converting enzyme inhibitor/diuretic or angiotensin receptor blocker/diuretic combination
2. up-titration of combination therapy to the highest dose
3. addition of a calcium channel blocker and up-titration
4. addition of a non-first-line antihypertensive agent (beta blocker, alpha blocker)

Medications can be costly, but unnecessarily so. A 25 mg dose of thiazide can be bought for 0.3 cents US (Perkovic et al, 2007). All people of Africa with a 10-year risk of a major cardiovascular event could be treated for ~$20M, making the estimated cost of preventing each major event approximately $200 (Perkovic et al, 2007).

Patient Motivation

Nonadherence to plan is important. Reasons can include:

Resistant Hypertension

Resistant hypertension is defined as...

It is more common in:

• elderly
• women
• black race
• etc

Assess for non-adherence to lifestyle and pharmacological strategies, as well as secondary causes.

Options for managing resistant hypertension include:

• hydralazine: mechanism unknown
• sodium nitroprusside: increases smooth muscle cell [cGMP]
• minoxidil: opens K+ channels

Cardiovascular

Even mild hypertension, slightly above 140/90, if sufficiently prolonged, increases the demands of the heart, which adapts with concentric hypertrophy. This can lead to myocardial dysfunction, ischemic heart disease, atrial fibrillation, heart failure, or sudden death.

Cerebral ischemia or hemorrhagic stroke is most commonly caused by hypertension.

Other vascular conditions can include aneurysm, aortic dissection, or peripheral artery disease.

Even a 2 mmgHg reduction can lead to substantial reductions in mortality (ref).

Renal Complications

Hypertension is one of the most common causes of end stage renal disease.

Renal nephrosclerosis is chronic nephron scarring with glomerulosclerosis, interstitial fibrosis, arteriolar thickening, and hyaline arteriosclerosis.

This can lead to further hypertension, mild proteinuria, bland urinalyis, elevated uric acid, and small kidneys on ultrasound.

other

retinal complications

• grade 1: mild arteriolar narrowing
• grade 2: AV nicking
• grade 3: hemorrhages, cotton wool spots
• grade 4: papilledema

Malignant Hypertension

main article: hypertensive emergency

Marked elevation in BP, usually in patient with long-standing, poorly controlled hypertension

retinal hemorrhages and papilledema

acute renal failure, hematuria, proteinuria

hypertensive encephalopathy (cerebral edema) can lead to headache, nausea, vomiting, confusion, and seizures