3. Hypertensive disease, mechanisms & consequences Flashcards
Consequences for hypertension
1 risk factor for death
Hypertension -> increased wall tension -> stimulates growth factors/hormones such as Ang II, VGF, endothelin, oxidative stress -> remodelling - thicker, stiffer wall, smaller lumen
- Results in hypertrophy in the left wall of the heart & blood vessels
- Poor blood supply to organs resulting in the heart having to work harder
Cardiovascular risk factors - NZ screening guidelines
Asymptomatic with no known risks
- 1st screening: males 45 years, females 55 years
High risk (genetics or co-morbidities):
Maori, Pacific or South-Asian:
- 1st screening: males 30 years, females 40 years
Family history risk factors:
- 1st screening: males 35 years, females 45 years
Cardiovascular risk factors - NZ treatment guidelines
- If BP >170/100 mmHg usual to treat regardless of overall risk
- If total CVD risk is 5-15% discuss treatment options, initiate lifestyle changes
- If total CVD risk is 15+% blood pressure lowering treatment is strongly
Incidence of hypertension increases with age:
- Below ~60 years males have the greater incidence
- Above ~60 years females have the greater incidence
Lifestyle changes such as regular exercise will reduce developing and help with hypertension
Cardiovascular system basics - pressure
P = CO x R
Pressure (P) regulated/constant so that tissues aren't damaged Cardiac output (CO) is total blood flow which is set & regulated by the bodies needs Increase in total peripheral resistance (R) leads to an upstream increase in pressure to maintain flow
Blood pressure
Force exerted by the blood against any unit area of vessel wall
- Means systemic arterial pressure ~100 mmHg
- Systolic ~120 mmHg
- Diastolic ~90 mmHg
Tends to increase with age
Determinants of arterial pressure
BP/MAP = CO X TPR
Cardiac output:
Cardiac:
- HR
- Inotropic state
- Neural
- Hormonal
Renal Fluid Volume Control:
- Renin-Angiotension
- Pressure natriuresis
- Aldosterone
- Atrial natriuretic factor
Peripheral resistance:
Sympathetic nervous system:
- Vasoconstrictor (alpha)
- Vasodilator (beta)
Humoral:
- Vasodilator
- Prostaglandins
- Kinins
- Vasoconstrictor
- Angiotension
- Catecolamines
Local auto regulation
BP is sensed variable
SV, HR & TPR is controlled variable
Hypertension - factors
Increase in Cardiac output:
- Hypervolaemia (excess total body sodium & water)
- Stress
Increase in systemic vascular resistance:
- Stress
- Artherosclerosis
- Renal artery disease (increased Ang II)
- Thyroid dysfunction
- Diabetes
- Cerebral ischaemia
Resistance & the r4 factor
For steady laminar flow in a rigid tube:
Resistance (R) is proportional to:
- Tube length (L)
- Viscosity of the fluid (n)
Resistance (R) is inversely proportional to:
- Radius raised to the 4th power (r4)
R = 8nl / πr4
A small change in the radius of blood vessels has a large effect on resistance
Contractile state of vascular smooth muscle is controlled by:
- Vascular endothelial cells (e.g. NO)
- Mediators released locally from sympathetic nerve terminals (e.g. noradrenaline)
- Circulating hormones (e.g. Vasopressin, Angiotensin II)
Factors affecting cardiac output
- Increasing heart rate will increase output (stroke volume constant)
- Increasing filling of the heart (preload) increases output (Starling’s Law of the Heart)
- Increasing afterload (arterial pressure will increase output) assuming the heart can relax sufficiently to fill
- Increased sympathetic activity or calcium availability increases contractility & thus stroke volume
Neural-hormonal interactions in hypertension
- Increase in Ang II
- Increase in Sympathetic activity
- Increase in blood volume
- Increase in free radicals
- Decrease in NO
- Decrease in Baroreceptor sensitivity
Beta-adrenergic stimulation -> increased intracellular calcium -> increased force development (SV)
Determinants of pulse pressure
Pulse pressure = systolic pressure - diastolic pressure
Systolic pressure:
- Aortic compliance
- Stroke volume (& ejection rate)
Diastolic pressure: - Aortic compliance - Diastolic run off: \+ Heart rate \+ TPR
Aortic pulse pressure : Systole & Diastole
Systole: Ventricular contraction enables blood flow through arteries
Diastole: Ventricular relaxation allows filling. Blood flow continues due to elastic recoil if arteries (compliant nature)
Compliance (∆V/∆P) of the aorta
- Decreases with age
- Pulse pressure increases with age due to decreased compliance
Decreased compliance results in:
- Increases in systolic pressure
- Decrease in diastolic pressure
Stroke volume
- Increasing SV delivered to aorta increases the arterial pulse pressure
SV is determined by:
- Preload
- Afterload
- Chronotropy
- Inotropy
Systolic pressure can increase in exercise
