Brief Overview of Autonomic Function Tests

Editor's Notes

• #3: Food – resting, suddenly danger, mention the changes you need.
• #9: The autonomic nervous system (ANS) is made up of the sympathetic nervous system (SNS) (noradrenergic, adrenergic and cholinergic), the parasympathetic nervous system (PNS) cholinergic and the enteric nervous system. 
• #10: The ANS rules functioning of the milieu intérieur, arterial pressure (AP), heart rate (HR), thermoregulation, breathing, gastriontestinal, urogenital and pupillary system. (1) 
• #14: The terms dysautonomia, and autonomic dysfunction only describe a ANS compromise; however, in the study of one patient with autonomic symptoms it is necessary to identify if the compromise mainly affects  SNS, PNS, the enteric system or all three systems. ANS compromise is present in diseases: 1. Of the central nervous system, such as multiple-system atrophy, 2. of the peripheral nervous, such has diabetic polyneuropathy, 3. primary of the ANS, such as pure autonomic failure. The  ANS compromise may also be functional, with no evidence of  a structural lesion of the autonomic ways, such as  the vasovagal syncope.
• #15: ANS compromise is present in diseases: Central nervous system, such as multiple-system atrophy. Peripheral nervous, such has diabetic polyneuropathy, Primary of the ANS, such as pure autonomic failure. Functional, with no evidence of  a structural lesion of the autonomic ways, such as  the vasovagal syncope.
• #18: In a patient with a suspected autonomic disorder the major aims of investigation are- to determine whether autonomic function is normal or abnormal- to assess the degree of dysfunction, in determining the site of the lesion- to ascertain whether the abnormality is of primary or secondary to recognized disorders, as the prognosis and management will depend on the diagnostic category.- to obtain information on the underlying pathophysiological processes, and effect of stimuli in daily life on autonomic responses as the former are of importance in development of novel treatment, and the latter for ensuring holistic management especially in generalized autonomic disorders.
• #24: The baroreceptors (or pressoreceptors) are stretch receptors located in the carotid sinuses and in the aortic arch. Increases in arterial blood pressure induce vascular stretch and deformation of the walls of the carotid sinus and aortic arch enhances the frequency of firing of baroreceptor nerves (CN IX and X) These fibers release glutamate to excite neurons in the nucleus of the tractus solitarius (NTS) in the medulla which in turn excite neurons in the caudal ventrolateral medulla (CVLM). This causes them to release the inhibitory neurotransmitter aminobutyric acid (GABA) into the rostral ventrolateral medulla (RVLM) to reduce their firing rate to the thoracolumbar intermediolateral horn (IML). Excitatory projections also extend from the NTS to the vagal motor neurons in the nucleus ambiguus and dorsal motor nucleus. Increased baroreceptor discharge inhibits the tonic discharge of sympathetic nerves and excites the vagal innervation of the heart It producing vasodilation of the veins and arterioles throughout the peripheral circulatory system along with a decrease in heart rate and strength of contraction. This causes a reflex decrease in the arterial pressure because of the decrease in both peripheral resistance as well as cardiac output.
• #26: Fig. 3a–f Representative continuous beat-to-beat BP and HR recordings in selected patients demonstrating common abnormal profles on passive head-up tilt table testing. a In initial OH (seen more typically during active standing), a transient drop in BP of >40 mmHg occurs within 5–15 s and recovers within 1 min. b In non-neurogenic OH, there is a sustained decrease in systolic BP of >20 mmHg. In most cases, unless the patient is taking a beta blocker or has a pacemaker, compensatory tachycardia occurs. c In neurogenic OH, there is a larger sustained decrease in systolic BP, typically >30 mmHg, and in most cases compensatory tachycardia is absent. Supine hypertension may be present. A diagnosis of neurogenic OH should be confrmed by detecting inadequate BP responses to the Valsalva maneuver. D In delayed OH, the BP does not reach the threshold for OH within the frst 3 min of head-up tilt, but a further gradual decrease in BP occurs, reaching the criterion for OH beyond 3  min of standing or head-up tilt. e In syncope caused by neurally mediated hypotension, a delayed decrease in BP occurs more suddenly than that of delayed OH. This profle is typical of a vasodepressor response and is accompanied by relative bradycardia. Note the preceding tachycardia (which in this patient qualifes for POTS) and oscillations in BP indicating the sympathoadrenal imbalance typical of the presyncopal prodrome. At the moment of loss of consciousness, the table was returned to the horizontal position and the patient regained consciousness and baseline BP. f In POTS, the HR sharply rises during the frst 30 s of headup tilt and remains elevated as long as the patient is in the upright position. OH does not occur. Oscillations in beat-to-beat BP and HR may be seen while in the head-up position
• #30: DBD tends to decrease with age, the value being around 15-20 beats/min in persons of 20 years of age and 5-10 over the age of 60 years.
• #32: It was Karl Ludwig, in 1847, who first noted that the heart rate increased with inspiration and decreased with expiration. This phenomenon called sinus arrhythmia occurs normally and is mediated by the parasympathetic output to the heart. During inspiration, the stretch receptors in the lungs are stimulated and send impulses through the vagus, causing inhibition of the cardio-inhibitory area in the medullary oblongata(24,91,92). In addition, the fall in intrathoracic pressure on inspiration causes an increase in the venous return to the right side of the heart, resulting in stretch of the low-pressure atrial receptors and elicits the Bainbridge reflex. Moreover, there is spillover of impulses from the respiratory center to the cardiac center in the medulla. All these factors lead to a decrease in the tonic vagal discharge responsible for keeping the heart rate slow, thereby leading to a rise in heart rate on inspiration(5,28,29). This variation in heart rate is more pronounced at a breathing rate of 5 to 6 breaths per 104 minute(93). The difference between the average of the largest accelerations during inspiration and the average of the largest decelerations during expiration is calculated in beats per minute(73).
• #38: In patients with mild sympathetic dysfunction, there is a reduced and/or delayed recovery after 7s in phase II and reduced and/or delayed phase IV overshoot. Severe sympathetic dysfunction is characterised by a continued fall in blood pressure throughout the expiratory effort with no evidence of a late phase II blood pressure recovery and absent overshoot in phase IV.
• #39: 50 percent 1 min debilated )
• #42: from the skin as well as emotional arousal.
• #48: This represents the net effect of the parasympathetic (vagus) nerves, which slow HR, and the sympathetic nerves, which accelerate it.
• #50: Acute changes in BP are restored via the baroreflex. A change in BP is detected by arterial baroreceptors, which signal to the medulla. This triggers a compensatory change in HR, and thus cardiac output [CO], via reciprocal modulation of sympathetic and vagal activity to the cardiac sinoatrial node. There is also a change in sympathetic outflow to peripheral arterioles, resulting in a compensatory change in total peripheral vascular resistance (TPR). Very-low-frequency (VLF; red box) blood pressure variability (BPV) occurs due to myogenic responses creating a VLF oscillation in peripheral arteriolar tone and thus TPR. The VLF BPV activates the baroreflex leading to compensatory VLF HRV. Low-frequency (LF) BPV and HRV originate from baroreflex loop resonance (red box). At the resonant frequency, the time delay in this negative feedback loop means the input and output are in phase, generating self-sustained oscillations. High-frequency (HF) BPV and HRV correspond to respiration (red box). The mechanical changes during respiration lead to HF BP oscillations (inspiration lowers intrathoracic pressure, leading to increased venous return, stroke volume [SV], and, therefore, CO), which then activate the baroreflex to produce compensatory HR oscillations
• #52: HRV has been used to study the Risk of cardiac electrical instability after myocardial infarction (Bigger et al 1991) To diagnose diabetic neuropathy To assess re-innervations after cardiac transplantation (Sands et al 1989)
• #61: Both SNS and PNS activity contribute to SDNN and it is highly correlated with ULF, VLF and LF band power, and total power  In short-term resting recordings, the primary source of the variation is parasympathetically-mediated RSA, especially with slow, paced breathing (PB) protocols (12). In 24 h recordings, LF band power makes a significant contribution to SDNN The SDNN is the "gold standard" for medical stratification of cardiac risk when recorded over a 24 h period SDANN is not a surrogate for SDNN since it is calculated using 5 min segments instead of an entire 24 h time series (9) and it does not provide additional useful information
• #64: This is analogous to a prism that refracts light into its component wavelengths  Power is the signal energy found within a frequency band.
• #65: which divides the absolute power for a specific frequency band by the summed absolute power of the LF and HF bands. 
• #66: The VLF band (0.0033–0.04 Hz) requires a recording period of at least 5 min, but may be best monitored over 24 h. Within a 5-min sample, there are about 0–12 complete periods of oscillation The ULF band (≤0.003 Hz) indexes fluctuations in IBIs with a period from 5 min to 24 h and is measured using 24 h recordings (10). The VLF band (0.0033–0.04 Hz) is comprised of rhythms with periods between 25 and 300 s. The LF band (0.04–0.15 Hz) is comprised of rhythms with periods between 7 and 25 s and is affected by breathing from ~3 to 9 bpm. Within a 5 min sample, there are 12–45 complete periods of oscillation (9). The HF or respiratory band (0.15–0.40 Hz) is influenced by breathing from 9 to 24 bpm (11). The ratio of LF to HF power (LF/HF ratio) may estimate the ratio between sympathetic nervous system (SNS) and parasympathetic nervous system (PNS) activity under controlled conditions. Total power is the sum of the energy in the ULF, VLF, LF, and HF bands for 24 h and the VLF, LF, and HF bands for short-term recordings