Systemic Hpertensiony

Question 1

What is hypertension?

Answer 1

Sustained non physiological rise in diastolic and/or systolic bp
Level of BP associated with greater risk of CV morbidity and mortality relative to general population
Level of BP likely to benefit from ‘treatment’

Question 2

What must you consider about BP levels however?

Answer 2

Substantial variation in BP within population - given level might be associated it’s higher risk in some than others
Consider content of other CV risk factors eg smoking, diabetes, lipids etc

Question 3

NHS/NICE 2011 recommended …. To confirm clinical diagnosis of…

Answer 3

Ambulatory or home blood pressure measure to ABPM, HBPM, to confirm clinical diagnosis of mild/moderate hypertension

Question 4

Ambulatory measurements

Answer 4

Automatic measurement during normal activities
Patient keeps diary of activities
Absence of dipping BP (>10% fall) at night is informative
Associated with OSA, obesity, renal disease, diabetic neuropathy, old age
Gold standard but use limited to secondary care/outpatients at present

Question 5

Home Blood Pressure Measurement

Answer 5

If ambulatory uncomfortable or inconvenient
Patient / carer record manually
At least 2 readings taken at least twice per day morning and evening
Normally for 4-7 days, discard 1st day readings
More widely used than ABPM by GPs

Question 6

What is the white coat effect/hypertension

Answer 6

Elevated BP in a clinical setting >20/20mmHg difference from ABPM
White coat isolated office hypertension - meets criteria for hypertension in a clinical setting but normal when assessed outside this setting - benefits of ambulatory/home monitoring?

Question 7

Does white hypertension matter?

Answer 7

Associated with increased target organ damage and CV risk
Augmented sympathetic nervous activity
75% subsequently develop sustained hypertension within 5 years
Regular follow-up required (at least annually)
When/how to treat?

Question 8

What are the physiological determinants of blood pressure?

Answer 8

Influenced by:
Cardiac output
Systemic vascular resistance - influenced by vascular tone and blood viscosity
Central venous pressure - influenced by blood volume

Question 9

Determinants of systemic vascular resistance

Answer 9

Small arteriolar tone (resistance arterioles) - <450um
Pre-capillary arterioles (auto-regulatory vessels, dynamically change diameter to alter blood flow)-<100um
Altered blood viscosity blood (haematocrit)
80 x (mean arterial pressure - mean central venous pressure)/ cardiac output

Question 10

What causes primary (essential) hypertension

Answer 10

No apparent cause
90-95% of all cases
Occurs in adulthood 40+ years
Associated risks include polygenic predisposition, greater susceptibility to environmental triggers; obesity, physical inactivity, stress, excessive salt or alcohol consumption
Heterogenous condition, reflecting multiple contributing factors
Silent disease, no symptoms at presentation?

Question 11

2 types of primary hypertension

Answer 11

Isolated systolic hypertension (ISH) - more common in elderly affects 25-50% >60
Classical essential hypertension - more common <50 years

Question 12

What is the relationship between BP and age

Answer 12

Systolic BP rises steadily
Diastolic BP falls at 55+
Pulse pressure increases with age
ISH (D<90) is common in older subjects

Question 13

Systolic BP becomes more important beyond….

Answer 13

50 years of age

Question 14

Pathophysiological basis of classical primary hypertension?

Answer 14

Increased systemic vascular resistance
Structural changes to vessels wall (small arterioles)
Impaired baronies sensitivity
Excessive sympathetic nerve activity (+ reduced parasympathetic activity)
Increased cardiac output
Inappropriate RAAS activation

Question 15

Describe the Pathophysiological basis of isolated systolic hypertension?

Answer 15

Exaggerated age-related dilation/stiffening of large arteries
Disruption /disorganisation of elastin and collagen - arteriosclerosis NOT atherosclerosis
Not primarily associated with > systemic vascular resistance
Exacerbated by diabetes - conventional anti hypertensive drugs decr BP making arteries less stiff
Development of specific treatments? Dilate large artery smooth musc? Repair damaged elastin/collagen?

Question 16

What is secondary hypertension

Answer 16

5-10% of all cases
Identifiable cause - eg renal disease, endocrine disease, mono genetic defects such as Liddell syndrome, drugs
More common in younger or those with reistant hypertension - depends on extent of investigation?

Question 17

What to do in secondary hypertension?

Answer 17

Identify and treat specific cause if possibke
Eg stunting for renal artery stenosis
Adrenalectomy or aldosterone antagonists for adrenal tumours, hyperplasia etc

Question 18

What are the consequences of untreated or inadequately treated hypertension?

Answer 18

Progressive damage to large and small BVs
- structural and fucntional changes, impaired auto-regulation, altered sheer stress, remodelling, thickening, stiffening, impaired dilation, disrupted capillary permeability
>end organ damage due to haemodynamic stress
- eg heart (incr cardiac workload, impaired perfusion, ischaemia, apoptosis, arrhythmias etc)
- also kidney, CNS, retina etc

Question 19

What are the manifestations of consequences of hypertension

Answer 19

<15% of patients with established hypertension demonstrate related morbidity and mortality
>85% chronic stable disease, no gross clinical events, protective mechanisms? (Auto-regulation of blood flow to organs? Adaptation of organs to higher pressure?)
Examples: heart LVH to normalise wall stress; kidney constriction of renal afferent arteriole to normalise intraglomerular pressure

Question 20

Hypertension-related organ damage depends on:

Answer 20

Extent higher BP (haemodynamic stress)
Underlying biochemical stress
Ability of organ to withstand stress (coping mechanisms)
Insufficiency/derangement of coping mechanism -> maladaptation
Examples: heart excessive LBH -> LV dysfunction/failure; kidney chronic constriction of renal afferent arteriole -> renal dysfunction/failure

Question 21

Manifestation of consequences of hypertension

Answer 21

Vascular disease - aortic aneurysm, occlusive peripheral vascular disease
Cerebovascular disease - transient ischaemic attack, stroke, multi-infarct dementia
Cardiac disease - angina, myocardial infarction, LVF, sudden cardiac death
Progressive renal failure
Retinopathy

Question 22

Consequences of hypertension

Answer 22

Must be considered in contact of other risk factors: long term hypertensives often other CV factors eg diabetes, LVH, obesity decr HDL incr LDL cholesterol
Untreated hypertensives present acutely with stroke MI, acute renal or heart failure

Question 23

What are the benefits of treating hypertension

Answer 23

Reduced incidence of:
Stroke
Heart attack
Renal failure
Heart failure
Retinopathy
Peripheral artery disease
Complications of diabetes

Question 24

How should we routinely investigate hypertension?

Answer 24

Bp measured in both arms with appropriately sized cuff
Auscultation of carotid, renal arteries (narrowing)
Auscultation of heart (rate/rhythm)
Full CV history/symptoms - previous MI, stroke, angina, heart failure etc

Question 25

Routine investigations: Target organ damage heart

Answer 25

ECG (LVH, arrhythmia, previous MI)
Deep S or QS waves from cavity leads or leads overlying non-hypertrophied ventricle (V1)
Tall R waves in leads recording from epicardial surface of hypertrophied ventricle (V5)
Pathological Q wave (increased amplitude and duration) indicative of previous MI?

Question 26

Routine investigations: target organ damage - renal dysfunction

Answer 26

Serum creatinine, urea
Proteinuria
Microalbuminuria (Micral test 2)
(Haematuria)

Question 27

Routine investigations

Answer 27

Fundoscopy (early signs of arteriolar narrowing)
CNS screen (cognitive tests)
Glucose, lipids, BMI (CV risk)
Preliminary screen for secondary causes?

Question 28

Follow up investigations

Answer 28

ABPM/HBPM
Echo, cardiac MRI (LVH, altered filling, emptying)
Excessive stress test for myocardial ischaemia/reduced coronary flow reserve
Carotid ultrasound (thickness, plaque burden)
Cerebral MRI (micro bleeds, infarcts)
Ankle-brachial pressure index (PAD)

Question 29

Novel investigations (experimental)

Answer 29

• central vs. brachial BP relationship – more predictive of organ damage?
• blood pressure variability, morning and exercise-induced surges? – relationship to cardiovascular risk? – routine clinical application?
• pulse wave velocity (carotid-femoral) – indicator of large artery stiffening