Systemic Hpertensiony Flashcards
What is hypertension?
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’
What must you consider about BP levels however?
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
NHS/NICE 2011 recommended …. To confirm clinical diagnosis of…
Ambulatory or home blood pressure measure to ABPM, HBPM, to confirm clinical diagnosis of mild/moderate hypertension
Ambulatory measurements
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
Home Blood Pressure Measurement
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
What is the white coat effect/hypertension
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?
Does white hypertension matter?
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?
What are the physiological determinants of blood pressure?
Influenced by:
Cardiac output
Systemic vascular resistance - influenced by vascular tone and blood viscosity
Central venous pressure - influenced by blood volume
Determinants of systemic vascular resistance
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
What causes primary (essential) hypertension
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?
2 types of primary hypertension
Isolated systolic hypertension (ISH) - more common in elderly affects 25-50% >60
Classical essential hypertension - more common <50 years
What is the relationship between BP and age
Systolic BP rises steadily
Diastolic BP falls at 55+
Pulse pressure increases with age
ISH (D<90) is common in older subjects
Systolic BP becomes more important beyond….
50 years of age
Pathophysiological basis of classical primary hypertension?
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
Describe the Pathophysiological basis of isolated systolic hypertension?
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?
What is secondary hypertension
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?
What to do in secondary hypertension?
Identify and treat specific cause if possibke
Eg stunting for renal artery stenosis
Adrenalectomy or aldosterone antagonists for adrenal tumours, hyperplasia etc
What are the consequences of untreated or inadequately treated hypertension?
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
What are the manifestations of consequences of hypertension
<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
Hypertension-related organ damage depends on:
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
Manifestation of consequences of hypertension
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
Consequences of hypertension
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
What are the benefits of treating hypertension
Reduced incidence of:
Stroke
Heart attack
Renal failure
Heart failure
Retinopathy
Peripheral artery disease
Complications of diabetes
How should we routinely investigate hypertension?
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
Routine investigations: Target organ damage heart
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?
Routine investigations: target organ damage - renal dysfunction
Serum creatinine, urea
Proteinuria
Microalbuminuria (Micral test 2)
(Haematuria)
Routine investigations
Fundoscopy (early signs of arteriolar narrowing)
CNS screen (cognitive tests)
Glucose, lipids, BMI (CV risk)
Preliminary screen for secondary causes?
Follow up investigations
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)
Novel investigations (experimental)
• 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
