Neural interventions and cardiovascular disease- HYPERTENSION Flashcards
What are the 3 techniques for treating drug resistant hypertension ?
carotid sinus stimulation
renal nerve denervation
deep brain stimulation
What is hypertension a major risk factor for ?
stroke, myocardial infarction, heart failure, kidney disease, peripheral vascular disease, cognitive decline and premature death
What is the prevalence of hypertension at 45-54 years and? 75years?
as you get older the prevalence increases
45-54= men- 33% and women- 25%
>75 = men- 73% and women- 64%
What is primary hypertension?
also known as essential hypertension
it is hypertension with an idiopathic cause
90%of people with hypertension have primary hypertension
How many people worldwide are affected by hypertension ?
1 billion people - one of the biggest costs to the NHS
if it is left untreated it can lead to serious disease states
Define hypertension:
BP has a skewed normal distribution within the population and the currently accepted model assumes risk is continuously related to BP
What is stage 1 hypertension ?
in surgery, BP is >140/90mmHg or HBPM/ABPM is >135/85mmHg- these results indicate a potential risk of suffering hypertension
wouldn’t necessarily receive treatment but suggestions of changes in diet and exercise
What is stage 2 hypertension ?
in surgery BP is >160/100mmHg or ABPM/HBPM is >150/95mmHg
- likely to be prescribed anti-hypertensive drugs
What is stage 3 hypertension ?
in surgery BP is >180/110mmHg or higher
admit to hospital and administer treatment straight away because it is at a level that may cause organ damage
How can you reduce vascular constriction ?
using calcium channel blockers- they block the influx of calcium ions induced by the sympathetic nerve releasing noradrenaline to bind to alpha-1 R which causes calcium channels to open
Why are beta-blockers useful ?
they act upon the heart to reduce rate and strength of contraction - this helps to reduce BP
What are the current treatments that act on the renin-angiotensin system ?
ACE inhibitors= they reduce the circulating levels of angiotensin 2 which prevents it activating the suprarenal gland causing the release of aldosterone which maintains fluid and sodium retention
it also prevents it acting on the NTS, CVLM causing central activation of sympathetic activity and furthermore it prevents it acting on the arterial walls and causing vasoconstriction
Why do we need new therapies for hypertension ?
because a large number of patients dont respond to the current therapies
What did a study demonstrate about the standard treatments?
found that if they gave the current standard treatments more aggressively from the start then it causes a greater decline in BP then if they are given at much lower doses
What can you do to the basal tone of sympathetic control on blood vessels ?
if you decrease the basal tone then you can cause vasodilation causing smooth muscle to relax and subsequently reducing BP
if you increase the basal tone on the arterial walls you can enhance the vasoconstriction and therefore increase BP
thought that maybe essential hypertension is being caused by increased sympathetic activity
How was human sympathetic nerve activity measured in leeds?
using the common peroneal nerve just behind the knee they inserted a recording electrode and then just below a reference electrode is inserted
the activity in this nerve is representative of sympathetic activity because the activity is going to smooth muscle but also skin which is a slight limitatoin of the process
record the action potentials in the nerve
What was the difference in MSNA in different groups of patients with normotsive, stage 2 and 3 hypertension ?
normotensive group= about 40 bursts per 100bpm
stage 2 group= nearly 60 bursts per 100bpm
stage 3 group= nearly 70 bursts per 100bpm
there is a correlation between sympathetic nerve activity and increased BP - as BP increases, sympathetic nerve activity increases
What was shown in the carotid sinus stimulation experiment in rabbits?
they cut their carotid sinus nerves and inserted an electrode to stimulate just that nerve
as they increase the stimulus intensity it caused a much greater drop in BP
What did the dog model of carotid sinus stimulation show ?
the hypertensive dogs which had carotid sinus stimulation had the greatest drop in BP compared to all other control groups and this decrease was maintained
What happened in the 60s when they carried out carotid sinus stimulation in humans?
a receiver was placed under the skin and then they put a transmitter on the skin to activate it, this caused stimulation of the leads around the carotid sinus
limitations of this treatment are that the battery pack will only last a couple of years and it caused quite a few side effects, with some people even dying
as it was in the 60s, the idea was good but unfortunately they didn’t have the technology to carry it out
What is the rheos system ?
the electrodes are wrapped around the whole carotid sinus so the whole structure is stimulated
- causes stimulation of baroreceptors in carotid sinus to stimulate a decrease in BP
What did the rheos system show?
once it is turned on you get a substantial decrease in BP and HR and sympathetic activity drops almost to zero
once you switch it off you get a sudden rise in BP and sympathetic activity
What did a long term study of the rheos system show?
measuring the effects of this system on both SBP and DBP each year for 3 years demonstrated that the effects are maintained
The rheos system stimulates the whole carotid sinus so what were they worried about and how did the test to see if these effects were present ?
if you are stimulating the whole carotid sinus you may also be activating chemoreceptors which will affect respiration and cause an increase in sympathetic activity and therefore the effects upon BP will be counteracted
took measures of respiration
- measured tidal co2 volume and didn’t see much of a change
- measure MAP at different frequencies and this demonstrated those at at higher voltages were more effective at reducing BP
