Hypertension Flashcards
Autonomic Vasomotor Nerves
Sympathetic vasoconstrictor nerves
Sympathetic vasodilator nerves
Parasympathetic vasodilator nerves
Sympathetic Vasoconstrictor Nerves
Noradrenaline
Alpha-1 adrenergic receptors
Vascular smooth muscle
Increase in Ca2+
Vasoconstriction
Sympathetic Vasodilator Nerves
Sympathetic cholinergic
- sweat glands
- cutaneous vasodilation
Parasympathetic Vasodilator Nerves
Parasympathetic cholinergic
NO production
- salivary glands
- external genitalia
How do you calculate mean arteriole pressure (MAP)?
MAP = Diastolic + 1/3 Pulse Pressure
During diastole why does aortic BP remain higher than left ventricular pressure?
During systole the wall of the aorta stretches storing energy
During diastole the energy is returned to the blood which is unable to flow backwards due to closing of the aortic valve
What are the main factors determining mean arterial blood pressure?
Cardiac output
Total peripheral resistance
By changing the diameter of the arterioles, MAP can be rapidly modified on a beat by beat process
Baroreceptors
Changes in arterial blood pressure cause the amount of stretch of aortic and carotid baroreceptors to change
Baroreceptor Reflex - parasympathetic neurons
Parasympathetic neurons synapse on the SA and AV nodes. SA node effects reduce heart rate and so cardiac output decreases
Baroreceptor Reflex - sympathetic neurons
Sympathetic neurons synapse on the SA node (increases heart rate) and on ventricular muscle (increases force of contraction), so cardiac output increases
They also synapse on arterioles causing peripheral vasoconstriction which increases TPR and, so, blood pressure
They also cause venoconstriction, which shunts venous blood into the arteries
Specific Stimuli
Specific stimuli can trigger physiological mechanisms that can override the normal physiological control of MAP, leading to sudden drops in blood pressure
E.G. sight of blood, fear, pain etc. could lead to fainting
Vasovagal Syncope
1) Intense increase in cholinergic / sympathetic vasodilator supply to skeletal muscle arterioles –> decrease in TPR
2) Intense increase in output from inhibitory cardiovascular control centre —> decrease in HR
Overall, combined effect cause a rapid decrease in BP and reduced flow to brain –> lose consciousness (fainting)
Primary Hypertension
No identifiable cause, tends to gradually develop over years
Prevalence increases with age
Patients < 40 = high cardiac output with normal peripheral resistance
Older patients = normal/reduced cardiac output but high peripheral resistance
Secondary Hypertension
Caused by an underlying condition
Tends to appear suddenly
Linked to:
- sleep apnoea
- kidney problems
- adrenal gland tumours
- thyroid problems
- drugs (prescription, contraceptive, illegal, OTC)
Accelerated / Malignant Hypertension
Medical emergency
Requires urgent treatment
Recent onset of high blood pressure carrying significant cardiovascular risk and with evidence of end organ damage
