Neural interventions in heart failure Flashcards

1
Q

What is the normal neural control of the heart?

A

heart is autorhythmic- therefore without any neural input the heart will continue to beat
intrinsic HR= 100bpm due to SAN
at rest, parasympathetic input decreases HR to 60-70bpm- slows the SAN activity
maximum HR= 220-age-
- as you age your max HR decreases as it cannot maintain as high a HR

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2
Q

Which is the initial effect of heart failure?

A

it causes decreased cardiac output

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3
Q

What happens in heart failure to attempt to improve cardiac output?

A

neurohumoral activation
- sympathetic system increases to increase vasoconstriction and HR
- renin-angiotensin system is activated to induce sodium and fluid retention
BUT both these effects actually adds further stress to the heart and increases damage therefore potentiating heart failure - progressive disorder

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4
Q

What can cause heart failure?

A

myocardial infarction is the main cause of HF
- blockage of one of the coronary arteries causes part of the heart to die and once you’ve damaged cardiac muscle cells you cant replace them- they are replaced by fibrous scar tissue that is not contractile therefore reducing cardiac output

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5
Q

What does it mean by a compensated heart and a decompensated heart ?

A

compensated heart= a heart that has undergone the neurohumoural changes causing hypertrophy- muscle cells enlarged as they are being told to work harder
decompensated heart= the extra work load induced by neurohumoural changes has caused heart cells to die and be replaced by fibrous tissue making it less contractile- its a floppy heart - thin walls and poor at contracting

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6
Q

What is class 1 heart failure?

A

without limitations of physical activity. Ordinary physical activity does not cause undue fatigue, palpitations to dyspnea - mild

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7
Q

What is class 2 heart failure?

A

slight limitation of physical activity. They are comfortable at rest. ordinary physical activity causes fatigue, palpitations or dyspnea - difficulty breathing

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8
Q

What is class 3 heart failure?

A

marked limitations of physical activity. They are comfortable at rest. Less than ordinary activity causes fatigue, dyspnea or palpitations

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9
Q

What is class 4 heart failure?

A

inability to carry out any physical activity without discomfort. Symptoms are present at rest or minimal exertion

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10
Q

What are the current treatments?

A

Beta-blockers= propanolol- helps to mitigate the effects of the sympathetic nervous system - reduce HR
ACE inhibitors= reduce angiotensin 2 production, reduce it increase in BP both peripherally and centrally

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11
Q

What is an indicator of autonomic function ?

A

heart rate variability
reliant on the fact the heart is not a metadrome
measure cardiovascular autonomic function

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12
Q

What happens to HR when you are breathing?

A

when you breathe in your HR increases slightly whereas as you breathe out your HR decreases slightly

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13
Q

What 2 things can be looked at by measuring the difference between R-R intervals?

A

TIME-DOMAIN= looking at statistical analyses
FREQUENCY DOMAIN= spectral methods to look at oscillation
it provides a measure of the contraction of the ventricles

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14
Q

What are the important peaks in a power spectrum?

A

HF peak= beat to beat changes in HR controlled by parasympathetic nerve- fast chnages in HR
LF peak= controlled by both parasympathetic and sympathetic nervous system - slower changes in HR
look at the ratio between these peaks to get a balance of autonomic balance - low = higher parasympathetic activity
high- low parasympathetic activity

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15
Q

What is microneurography?

A

recording muscle sympathetic nerve activity
- insert electrode into tibular nerve and record the actions potentials upon vasoconstrictor axons
very direct measure

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16
Q

When sympathetic activity is stimulated what is shown in microneurography?

A

increased HR and BP

if you’ve recorded from 1 axon then all the action potentials recorded should overlap perfectly to give you one trace

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17
Q

What should be indicated about baroreflex sensitivity when systolic BP is plotted against R-R interval?

A

as BP increases you should get a decrease in HR and therefore an increase in R-R interval producing a pstitive linear line
BUT if the graph is a horizontal line it indicates that as BP increases the R-R isn’t increasing and so the HR isn’t slowing so there is very little vagal input

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18
Q

With normal baroreflex sensitivity what should be shown about R-R interval ?

A

normal baroreceptor sensitvity should correlate with increase of 3ms in R-R for every 1mmHg increase in BP

19
Q

With impaired baroreflex activity what is shown about the R-R interval?

A

low levels of parasympathetic activity indicated by a change in R-R interval of

20
Q

What is characterised of HF?

A

sympathetic activation and parasympathetic withdrawal

21
Q

What happens to % change in HR when propanolol is given to normal and HF people?

A

HR is decreased in both groups, slightly more in HF but not much
- sympathetic activity is reduced in both groups by relatively similar amounts

22
Q

What happens to the % change HR when propranolol and atropine are given to normal and HF people?

A

normal group have a substanially higher HR but HF group doesn’t increase nearly as much
- this indicates that their parasympathetic activity was low to begin with, therefore blocking with atropine hasn’t made much of a difference

23
Q

What happens to baroreflex sensitivity when propranolol is given ?

A

in normal group they become slightly less sensitive and the HF group become slightly more sensitive but it doesn’t appear to make a huge difference

24
Q

What happens to baroreflex sensitivity when atropine and propranolol are both given ?

25
From the experiments with atropine what is indicated?
promoting parasympathetic activity may help to improve autonomic function
26
What is carotid sinus stimulation?
place electrodes around the carotid sinus in the neck stimulator implanted under chest wall increases sympathetic activity electrically stimulating carotid sinus increases BP- artificially stimulating baroreceptor reflex artificially stimulates parasympathetic activity
27
What has carotid sinus stimulation shown to improve ?
improves left ventricular function
28
What did a canine model using carotid sinus stimulation show?
canine heart failure model was induced by coronary artery microembolisation - mimics myocardial infarction - after 3 months haemodynamics were measured and demonstrated improvements - improved cardiac output - improved left ventricular fraction output - huge decrease in plasma noradrenaline levels
29
With the canine model of heart failure what indicates that the model may not have been the best ?
the models which didn't receive carotid sinus stimulation didn't demonstrated decreased CO
30
What other beneficial effect was demonstrated by baroreflex stimulation ?
attenuated left ventricular remodelling - less fibrosis and enlargements in the cardiomyocytes and the capillaries were closer to cardiomyocytes in the carotid sinus stimulated model
31
What are the acute and chronic effects of baroreflex stimulation in patients?
acute- decreases BP and decreases sympathetic nerve activity so less vasoconstriction chronic- decreases left ventricular mass after 12 months, this was surprising because remodelling go the heart was thought to be irreversible
32
What are some limitations of vagal nerve stimulation ?
invasive and expensive | - orginally developed for epilepsy
33
What % of the cervical vagus nerve are afferent and efferent fibres?
``` afferent= 80%- send info into CNS to alter central autonomic control efferent= 20% - alter efferent fibre activity ```
34
What is the principal of vagal nerve stimulation ?
by activating nerves in the neck the afferent fibres are activated which could alter central autonomic control or it could activate efferent fibres to target organs directly to enhance parasympathetic activity
35
What happened in a study of vagal nerve stimulation in rats?
heart failure model induced by coronary artery ligation- did cause 60% mortality 1 week later an implant vagus stimulator and telemetry device was implanted to record HR and BP 1 week after that VNS treatment started and lasts for 6 weeks VS group of rats had smaller hearts so less enlargement occurred, reduced plasma noradrenaline so less sympathetic activity and reduced release of BNP( released from the heart when its stretched) vs group had much better survival rates - 90% survival compared to 50% in control group
36
What was the canine model for vagal nerve stimulation and what occurred?
model was induced by an inserted pacemaker which drives heart at very high rate to induce hf then they stimulated the right cervical vagal nerve in 8 dogs and 7 were untreated the vs group had much higher parasympathetic activity markers of inflammation, sympathetic activity and RAAS activity were all reduced - reduced neurohumoural effects to reduce progression of hf
37
In a clinical trial of vagus nerve stimulation what happened?
improvements in quality of life measurements - improved the distance in which they could walk at both 3 months and 6 months and they felt better and much happier they also showed improvements in heart rate variability at both 3 months and 6 months and this indicates there is more parasympathetic activity- its an indirect measure
38
From the clinical trial of VNS what was shown in the the new york heart association classes?
- no longer any patient with class 4 - of the 15 that had class 2, by 6 months 10 of them were classified as class 1 symptoms substantially improved
39
What are the limitations of VNS?
cough, neck pain and can affect your voice- horse voice | its invasive so if you are unwell you will not be able to undergo treatment
40
What was the next idea for VNS ?
to try and activate the vagus nerve by cutaneous stimulation the auricular branch of the vagus nerve is able to be stimulated by stimulating the ear
41
What happened when the auricular nerve was stimulated by electrical acupuncture?
10 days later there were drastic improvements there was no need for vasodilators and there was no pain at rest significant improvements in - spontaneous recovery of cardiac sinus rhythm - cardiac insufficiency - stable haemodynamics, sinus rhythm
42
What is tVNS?
transcutaneous vagus nerve stimulation clipped stimulator onto tragus to stimulate auricular branch of vagus- this was tested in healthy individuals acute stimulation of 15 mins of 200microsecond pulse frequency at 30Hz demonstrated beneficial effects- there was a significant decrease in LF/HF ratio demonstrating the promotion of parasympathetic activity- improved heart rate variability also significantly reduced sympathetic vasoconstrictor activity
43
What is the theoretical pathway of the auricular branch ?
its known to project to the NTS So maybe it projects to NTS to reach brainstem to increase parasympathetic outputs such that NTS projects to DMN or maybe to the CVLM to inhibit RVLM to decrease sympathetic output