Hypertension

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Introduction

Hypertension, or high blood pressure, is a very common chronic condition, affecting 20-25% of adults. It is also very serious, being the leading cause of cardiovascular disease. It is responsible for over 7 million deaths worldwide annually (Perkovic et al, 2009).

 

The lifetime risk for hypertension among middle-aged, normotensive adults is around 90% (Vasan et al, 2002). In Ontario, age- and sex-adjusted prevalence has increased 60% from 1995 to 2005, while incidence increased 26% (Tu et al, 2008).

 

Hypertension is diagnosed with blood pressure readings over 140 systolic or 90 diastolic on at least three occasions.

Normal blood pressure is less than 120 systolic and 80 diastolic, while prehypertension is between 120-139 systolic and 80-89 diastolic.

The JNC-V (Pogue et al, 1996) criteria ranks hypertension as:

 

 

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Causes and Risk Factors

  • essential hypertension
  • secondary hypertension
  • apparent 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 are thought to include:

  • high dietary intake of salt (>2.5 g/day), but only 40-50% of people are salt sensitive
  • stress
  • genetics
  • age
  • race: Black people have increased risk
  • sex - males are more likely
  • smoking
  • sedentary lifestyle
  • persistent stress
  • diabetes mellitus
  • alcohol consumption
  • oral contraceptives and other medications (to find out)

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). S

  • obstructive sleep apnea
  • alcoholism
  • drugs: NSAIDS, OCP, cocaine, steroids, ephedrine, MAOIs
  • renal artery stenosis (at least 50% narrowing of one side)
  • renal parenchymal disease, with Na avidity
  • hyperaldosteronism: sodium retention
  • phaeochromocytoma: high levels of catecholamines
  • Cushing's syndrome
  • thyroxtoxicosis, hypothyroidism
  • hypercalcemia
  • coarctation of the aorta: reduced renal perfusion
  • obesity: increased CO, hyperinsulinemia may increase SVR

 

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:

 

 

 

 

 

 

 

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Pathophysiology

 

 

used with permission, wikimedia

Peripheral resistance is increased by the SNS (stress), hormines such as aldosterone, thyroid hormone, and insulin, as well as paracrine signals including prostaglandins, endothelin, and nitric oxide. A reduced baroreceptor response also occurs. There is increasing evidence that essential hypertension may be a primary defect in Na excretion by the kidney, leading to increased intravascular volume.

 

Hypertension induces structural changes to the vasculature through hypertrophy of resistance vessels. Endothelial dysfunction includes reduced nitric oxide and increased endothelin.

 

It is speculated that excess insulin, as occurs in insulin resistance, may play a role in sodium retention, blood volume expansion, excess norephinephrine production, and smooth muscle proliferation. Hyperglycemia itself also leads to endothelial cell dysfunction, adding to the doubled rates of hypertension in people with diabetes.

 

Systolic pressure rises with age, though the diastolic does not. The elderly often show isolated systolic hypoertension.

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Signs and Symptoms

  • history
  • physical exam

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.

Duration and levels of high blood pressure

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

  • cardiovascular disease
  • stroke/TIA
  • peripheral artery disease
  • kidney disease
  • diabetes

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

 

cardiovascular

  • blood pressure
  • 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

abdominal exam

  • enlarged kidneys
  • masses
  • abdominal aortic pulsation

 

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Investigations

  • lab investigations
  • diagnostic imaging

Lab Investigations

Lab investigations for everyone with hypertension include:

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

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

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Differential Diagnosis

 

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Treatment Options

Intensive control of blood pressure, lipid levels, and hyperglycemia can save the health care system money while preventing death and disability GET STATS (CDC, 2002). There has been remarkable improvement in hypertension control in recent years, with rates ranging from 25-82% (Mohan and Campbell, 2008).

  • lifestyle
  • pharmacological
  • patient motivation
  • resistant hypertension

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 HT interfere with normal mechanisms of blood pressure regulation.

  • angiotensin inhibitors - promote vasodilation and reduced other effects of Ang II
  • diuretics, especially thiazides: promote naturesis and reduce TPR through unknown mechanisms
  • beta blockers - reduce CO, renin production, TPR, and catecholamines
  • calcium channel blockers - promotes vasodilation
  • alpha blockers
  • vasodilators

 

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

More common in:

  • elderly
  • women
  • black race
  • etc

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

medication and illicit drug use

  • NSAIDs
  • sympathomemetics
  • steroids
  • immunosuppressive agents
  • EPO
  • OCs
  • liquorice
  • cocaine, amphetamines
  • herbals: ephedra

weight gain

excessive salt intake or alcohol consumption

secondary causes

 

 

 

 

 

Consequences and Course

Hypertension is a key contributor to disease. Nearly 2/3 of stroke and 1/2 of ischemic heart disease is directly attributable to it (Lawes et al, 2006).

 

  • cardiovascular
  • renal
  • other
  • malignant hypertension

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.

 

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

 

Vascular conditions can include aneurysm, dissection, or peripheral artery disease.

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

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

 

 

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The Case of...

Case #2 - a small story wrapping it all up and asking especially about management.

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Additional Resources

 

 

 

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Topic Development

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