autonomic neuropathy and heart disease assesment and treatment

8/7/2019 AUTONOMIC NEUROPATHY AND HEART DISEASE ASSESMENT AND TREATMENT

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AUTONOMIC NEUROPATHY ANDHEART DISEASE ASSESMENT AND

TREATMENT

Dr M S ADITYA


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OVERVIEW OF AUTONOMIC NERVOUS

SYSTEM The principal cardiovascular influences are

mediated through the sympathetic and

parasympathetic systems The interplay between these two systems

determine cardiovascular responses under a

variety of conditions

Autonomic nervous system offers the most

rapid response system


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OVERVIEW OF AUTONOMIC

NERVOUS SYSTEM The reflexes by which blood pressure is

maintained are collectively known as the

baroreflex Arterial baroreceptors (also known as the

high pressure receptors) and

cardiopulmonary receptors (the low pressure

receptors


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NERVOUS SYSTEM ARTERIAL BARORECEPTORS

1. Carotid sinuses

2. Aortic arch3. Origin of right sub clavian artery

Baroreceptors are stretch-dependent

mechanoreceptors that sense changes inpressure, transmitting via afferents to the

nucleus tractus solitarius (NTS) in the brain

stem


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NERVOUS SYSTEM


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CARDIOPULMONARY

BARORECEPTORS Low-pressure receptors in the heart and

venae cavae termed cardiopulmonary

receptors also play a role in blood pressuremodulation

They primarily respond to changes in volume

but also to chemical stimuli

They project via vagal afferents to the NTS

and via spinal sympathetic afferents to the

spinal cord


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BREATHING AND THE

CHEMOREFLEXES The chemoreflexes are modulators of

sympathetic activation and play an important

role in cardiovascular autonomic tone Mediated by

1. Central receptors (hypercapnia)

2. Peripheral receptors(hypoxia) Hypoxemia or hypercapnia results in

hyperventilation and vascular sympathetic

activation


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BREATHING AND THE

CHEMOREFLEXES Inhibitory influences on the chemoreflex

drive are seen with stretch of the pulmonary

afferents and with activation of thebaroreflex

Clinically relevant in situations of sleep apnea


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Diving reflex

Unique state of simultaneous increasedparasympathetic drive to the heart andincreased sympathetic drive to thevasculature

Decreasing oxygen delivery to rest of thebody via increased sympatheticvasoconstriction

Myocardial oxygen demand is decreasedbecause of bradycardia caused by an increasein parasympathetic tone


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CLINICAL PRESENTATION

ORTHOSTATIC HYPOTENSION

SUPINE HYPERTENSION

LABILE HYPERTENSION INAPPROPRIATE TACHYCARDIA

SYNCOPE

CARDIAC ARRHYTHMIAS SUDDEN DEATH


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AUTONOMIC TESTING

1. Orthostatics

2. Valsalva maneuver

3. Baroreflex sensitivity4. Heart Rate Variability

5. Heart Rate Recovery

6. Chemoreflexes7. Tilt Table testing


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ORTHOSTATICS

Orthostatic hypotension is defined as a

decrease of more than 20 mm Hg in systolic

pressure or a decrease of more than 10 mmHg in diastolic pressure after rising to a

standing position from a supine position

Blood pressure and heart rate measurement

should be done once symptoms develop orafter 3 minutes have passed after rising to thestanding position


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Orthostatic hypotension is an inability of the

cardiopulmonary system to maintain

sufficient blood pressure and adequatecerebral perfusion against gravity

Significant decrease in blood pressure

without a corresponding rise in heart rate

suggests abnormal autonomic innervation tothe heart and may represent an underlyingneuropathy


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Valsalva maneuver

Described by Antonio Maria Valsalva

He described the Eustachian tube and the

maneuver to test its patency Phases are

1. Initial pressure rise

2. Reduced venous return and compensation3. Pressure release

4. Return of cardiac output


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VALSALVA MANEUVER

Patient will blow continuously into a closed

system for 12 seconds at 40 mm Hg and the

fastest heart rate during the maneuver isdivided by the slowest heart rate immediately

afterward

A quotient of less than 1.4 is suggestive of

autonomic impairment


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BAROREFLEX SENSITIVITY

Measure of parasympathetic input to sinus

node

Measures the reflex increase in R-R interval inresponse to an increase in blood pressure

Baroreflex sensitivity decreases with

sympathetic dominance and increases withparasympathetic dominance


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METHOD

Intravenous injection bolus of phenylephrine isgiven which increases the pressure by 20-30mmhg

A linear relationship occurs between the increasein R-R interval and increase in systolic BP

Slope is used to quantify the sensitivity ofarterial baroreflex

Typically steep in healthy individuals , butflattens with increasing age and cardiovasculardisease


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METHOD (OTHER)

FINAPRES ( finger arterial pressure device)

was used in ATRAMI (Autonomic tone and

reflexs after MI) study Spectral techniques have been used to

quantitate beat to beat oscillations in BP and

R-R intervals to obviate the need for

phenylephrine infusion


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HEART RATE VARIABLITY

The phenomenon being measured in heart

rate variability is that of the oscillation in the

interval between consecutive heart beats, aswell as the variance of heart rates

Heart rate variability studies the oscillation of

both heart rate and R-R intervals

Measurement of variablilty is by various

methods important being time domain and

freqeuency domain


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Time Domain Measurement

Calculated by analyzing the time series of

beat-to-beat intervals from ECG or arterial

pressure tracings An example of time domain measurement of

heart rate variability is calculation of the

standard deviation of beat-to-beat intervals

The time domain graph of a value shows how

the signal changes over time


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FREQUENCY DOMAIN MEASUREMENT

Shows how much of a signal lies within given

frequency bands over a range of frequencies

Spectral density analysis is the most commonfrequency domain method used and involvesmeasurement of how the power of a signal or

time series is distributed with frequency


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FREQUENCY DOMAIN MEASUREMENT

The frequency bands in humans are the high frequency (HF)band, the low frequency (LF) band, the very low frequency(VLF) band, and the ultra low frequency (ULF) band, eachhas its own physiologic correlate

HF band lies between 0.15 and 0.4 Hz and is driven byrespiration, appearing to derive mainly from vagal activity.

LF band, lies between 0.04 and 0.15 Hz, derive from vagaland sympathetic activity and is believed to reflect delay inthe baroreceptor loop.

VLF band lies between 0.0033 and 0.04 Hz and has beenattributed to physical activity.

ULF band lies between 0 and 0.0033 Hz and is associatedwith day/night variation.


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HEART RATE VARIABILITY

The utility of heart rate variability as a

measure of autonomic function and as a

predictor of mortality has been suggested bymultiple studies

Heart rate variability has been as an

independent predictor of mortality after

myocardial infarction and as an early warningsign for diabetic neuropathy


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HEART RATE RECOVERY

During exercise initially heart rate increase isbecause o vagal withdrawal and later stagedue to sympathetic influence

The rate at which the heart rate returns tobaseline, measured over the first minute afterexercise, is termed the heart rate recovery

A delayed heart rate recovery is a marker ofdecreased vagal activity, which has beenshown to be an independent risk factor forsudden cardiac death


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TILT TABLE TESTING

The purpose is to diagnose possibledysautonomic causes of syncope

Patients are strapped to a tilt table and are

suspended at angles anywhere from 60 to 90degrees

Patients may be given Isoproterenol to makethem more susceptible to syncope

Symptoms, blood pressure, heart rate,electrocardiographic findings, and bloodoxygen saturation are recorded


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CLASSIFICATION OF

DYSAUTONOMIAS PRIMARY

1. ACUTE

2. CHRONIC SECONDARY

AUTOIMMUNE

CONGENITAL


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PRIMARY CHRONIC AUTONOMIC

FAILURE Chronic autonomic failure is distinguishable

from acute-onset autonomic dysfunction

syndromes by its progressive nature andprognosis

Chronic autonomic failure may be subdivided

into secondary and primary failure, with

secondary failure being far more common


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PRIMARY CHRONIC AUTONOMIC

FAILURE Pure autonomic failure

Multiple system atrophy

Parkinson disease Overlap among these three syndromes exists

Treatment differs among them


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Pure Autonomic Failure

Pure autonomic failure involves orthostatichypotension in the absence of symptoms orsigns of central neurodegeneration

Dysfunction occurs at the level of peripheralneurons

The functional error lies in available levels of

norepinephrine, which are low when supineand rise minimally with standing

No direct effect on longevity occurs in thesepatients


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Multiple System Atrophy

Multiple system atrophy includes autonomic

failure with signs and symptoms of

progressive central neurodegeneration Aside from orthostatic hypotension, findings

may include impotence, loss of sweating,

abnormal pupillary responses, reduced

intraocular pressure, sleep apnea, and urinaryincontinence


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Multiple System Atrophy

Some patients may suffer from orthostaticangina which worsens with NTG

Because of the slow progression andchronicity patients tolerate precipitous fall inBP well

Tend have severe supine hypertension

Movement disorders similar to parkinsonismare seen, however disease course isunrelenting, ultimately leading to decreasedlife time


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Parkinson Disease

Distinguished from MSA by responsiveness to

DOPA agonists

Neuroimaging techniques using123

I-metaiodobenzylguanidine (123I-MIBG) and 6-(18F)fluoro-dopamine help to distinguish

between the three entities

Allows for visualization of cardiacsympathetic innervation using scintigraphy,

SPECT or PET


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Parkinson Disease

In pure autonomic failure and parkinsonism

there will be evidence of cardiac sympathetic

denervation whereas in MSA innervation isintact


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TREATMENT

Lifestyle changes along with drug therapydepending on severity of symptoms

LIFESTYLE

1. Carbohydrate ingestion can decrease bloodpressure and encouraged during night time

2. Caffeine or somatostatin can be added

daytime to decrease the food associateddecrease in BP

3. Water intake and physical maneuvers canimprove daytime BP


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TREATMENT

DRUG THERAPY

1. Fludrocortisone, 0.05 to 0.2 mg twice daily, andadding sodium to the diet can help with volume

expansion2. In patients with sympathetic cardiac denervation,Midorine (an alpha-adrenoreceptor agonist) or L-threo-3,4-dihydroxyphenylserine (a norepinephrineprecursor converted by parenchymal cells) are

useful3. Multiple system atrophy in whom sympatheticinnervation is intact may benefit from use of asympathomimetic amine or alpha-2-adrenoreceptor blocker


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SECONDARY AUTONOMIC FAILURE

DIABETES

AMYLOIDOSIS

PARANEOPLASTIC SYNDROMES VITAMIN B12 deficiency

HIV

HEAVY METAL INTOXICATION, Copper,Lead, Mercury and Thallium


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SECONDARY AUTONOMIC FAILURE

DIABETES1. Cardiovascular complications secondary to

dysfunction of autonomic control have been

described in patients with and withoutorthostatic hypotension2. Heart rate variability may help in detection of

Diabetic autonomic neuropathy3. Both afferent and efferent, as well as

sympathetic and parasympathetic, componentscontribute to the autonomic dysregulationassociated with diabetes

4. Better glucose and BP control advocated


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AUTOIMMUNE AUTONOMIC FAILURE

Severe autonomic failure may result from

autoimmune damage to neurons

Disease progression is variable Catecholamines are usually low and rise

minimally with standing

Autonomic dysfunction may be seen as a

complication in severe cases of Guillain-Barrsyndrome


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CONGENITAL AUTONOMIC FAILURE

First autonomic disorder associated with a

defined genetic abnormality was dopamine

beta-hydroxylase deficiency Dopamine beta-hydroxylase converts

dopamine to norepinephrine in vesicles in

noradrenergic neurons

Marked orthostatic hypotension with ablunted rise in heart rate


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CONGENITAL AUTONOMIC FAILURE

Excess quantities of dopamine which is

released in place of Norepinephrine causes

in urinary Na excretion , ptosis and Nasalstuffiness

Dihydroxyphenylserine has been used with

some benefit


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Baroreflex Failure

CAUSES

1. SURGERY

2. RADIATION3. CEREBROVASCULAR ACCIDENT

Failure results from damage to afferent

neuronal input (via the vagus andglossopharyngeal nerves) or from damage

to brain stem nuclei or interneurons


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Baroreflex Failure

Presentation is similar to pheochromocytoma

with extreme lability in BP

Carotid endarterectomy surgery is associatedquite often with these manifestations

Severe hypotension and bradycardia may

occur during sleep

Heart rate and blood pressure changetogether


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Baroreflex Failure

Diagnostically, patients may show a

depressor response to a small dose of

clonidine but no heart rate response todepressor or pressor infusions, even though

heart rate will change with sedation or

cortical stimuli.

Treatment with clonidine, benzodiazepines,methyl dopa


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ORTHOSTATIC INTOLERANCE

POTS (Postural Tachycardia Syndrome)

1. Characterized primarily by orthostatic

symptoms, tachycardia, and the absence ofsignificant hypotension

2. Decreased responsiveness of the baroreflex

arc to hypotension and a decrease in

transmission of appropriate sympatheticinput to the vasculature


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POTS (Postural Tachycardia

Syndrome) Orthostatic tachycardia greater than 30

beats/min

Transient systolic blood pressure decrease ofgreater than 20 mm Hg, with recovery withinthe first minute of tilt

Standing plasma norepinephrine greater

than 600 pg/ml

Severe orthostatic symptoms


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POTS (Postural Tachycardia

Syndrome In these patients there is a reduction in the

baroreflex index in the presence of alpha and

beta receptor hypersensitivity Blood flow in the middle cerebral artery

during a head-up tilt test can be assessed


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DISORDERS OF INCREASED

PARASYMPATHETIC TONE Increased parasympathetic tone may be seen

in

PHYSIOLOGIC1. NON-REM sleep

2. ATHLETES

PATHOLOGIC1. Spinal cord trauma

2. Weight loss


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DISORDERS OF INCREASED

SYMPATHETIC OUTFLOW Neurogenic essential hypertension

Panic disorder

Congestive heart failure Obstructive sleep apnea

Sleep

Bed rest


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Neurogenic Essential

Hypertension Factors such as insulin resistance, impaired

baroreceptor gain cause sympathetic

activation and increased heart rate andvasoconstriction


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CONGESTIVE HEART FAILURE


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Obstructive Sleep Apnea

An increase in sympathetic outflow occurs

during both sleep and waking hours in

patients with obstructive sleep apnea

Continuous positive airway pressuretreatment during sleep appears to attenuate

sympathetic outflow even during daytime

wakefulness


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SLEEP

During non-REM sleepparasympathetic tonedominates

During REM sleepsympathetic surgesmight occur partly

accounting for theincrease in numbercardiac events in earlyhours


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syncope

AORTIC STENOSIS

HOCM

INFERIOR WALL MI

RENAL FAILURE AND HEMODIALYSIS


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SUMMARY

Clinical presentation remains the key before

extensive investigation is taken up

Simple tests like orthostatics, valsalva, tilttable can used as screening tools

Dysautonomias coexist with various disease

entities

Management is centered treating the cause,volume expansion and drugs (

sympathomimmtics, alpha blockers etc)

autonomic neuropathy and heart disease assesment and treatment

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