P = flow x resistance
= CO x SVR
What factors affect BP.
The CO affects BP. CO is affected by:
- Blood volume: Na intake, kidney perfusion and function, ineralocorticoids
- Venous return: metabolic demand for O2, vascular capacitance and distensibility of peripheral vessels.
- Rate, afterload, preload and contractility.
- These factors particularly affected by the adrenergic system.
It is also affected by SV which is largely autoregulated, but is also affected by:
- the distensibility of blood vessels (compliance)
- vascular reactivity and reactivity of vascular smooth muscle cells
- degree of adrenergic stimulation
- renin-angiotensin system
- vasodilators such as NO and rostacyclin
- blood viscosity
- growth remodeling and arterial vasculature
Changes in HTN
The alteration in the structure and characteristics of the arterial vessel walls leads to more vigorous responses to vasoconstrictive stimuli.
Over time the wall remodels, thickens and there is increased pulse wave reflection furthing increasing systolic pressure
Chronic hypertensive phase shows increased arterial stiffness, increased PP, increased afterload therefore causing LVH and associated diastolic dysfunction.
When does HTN need to be treated immediately?
If BP is very high, especially with evidence of target organ damage.
What investigations should be performed when diagnosing HTN?
- Baseline ECG
- Renal function including urinalysis
- Fasting lipids and glucose
- About 5% of adults hypertensive
- Drugs: o/c pill, NSAID's etc
- Sleep apnoea
- Endocarine: phaeo, Cushing's, Conn's, hyperthyroidism
Ambulatory BP monitoring values
- Daytime BP <135/85
- Night <120/75
- Overall mean <130/80
- Non-dipper < than 10% fall in night-time BP
Role: exclude 'white coat', review borderline or labile BP, review poor BP control despite 'compliance', increasing target organ damage despite apparent good control.
Target organ damage in HTN
- Accelerated atherosclerosis
- Chronic kidney disease
- Hypertensive retinopathy
Left ventricular hypertrophy in HTN
- Myocytes hypertrophy in respone to increase load
- LVH greater for level of clinical BP if obese or a non-dipper
- LVH reduces diastolic ompliance
- Increased distance from capillaries plus CAD leads to patchy ischaemic damage
- Best quantified with echocardiography
Treatment of HTN
Lifestyle interventions for HTN
- Stop smoking
- Low salt intake (decreases systolic 2 to 4mmHg depending on initial BP.
- Increase dietary K (provided renal function OK)
- Weight control (about 1mmHg for each 1% loss)
- Increased physical activity (benefit 4/2.5)
- Limit alcohol intake
Drugs for HTN
- Use beta blockers or a Ca blocker that slows heart rate and contractility
- Use ace-inhibitor but caution thiazide
- No beta blocker
- Use beta blocker or rate controlling Ca blocker
Heart block or marked bradycardia
- Avoid the above 2 classes
First line drugs for HTN
- ACE inhibitors
- Calcium channel blockers
ACE-inhibitors main side effects
- Angioedema in about 0.5% (never use this class of drug again)
- Cough in about 10%: switch to ARB
In whom are thiazides contraindicated?
Side effects of diuretics.
Hypokalaemia and hyponatraemia.
Common side effect of Ca2+ channel blockers
When is beta blocker the first choice of HTN treatment?
Significant 'stress' factor.
Effective add-on especially to dihydropyradine calcium channel blockers.
What is prazosin useful for?
Benign prostatic hypertrophy.