Cardiac Output
The human heart is capable of beating without any nerve function at all, as heart transplants demonstrate. However, increases and decreases in the rate and strength are regulated by the ANS, and to a lesser extent the endocrine system. Contraction strength can also be modulated by the “Frank-Starling” mechanism.
The Frank-Starling law of the heart states the more blood that flows into the ventricle during the diastolic phase (end diastolic volume or EDV), the more the myocardium will stretch. Greater stretch and greater EDV will increase the stroke volume of the following contraction during the systolic phase, and this effect is independent of neural input.
The heart is innervated by both the sympathetic and parasympathetic systems. It receives sympathetic fibers from the upper thoracic region, approximately levels T1-T5. One area of rich innervation is the sino-atrial node (S-A node), otherwise known as the “pacemaker”. As its nickname suggests, ANS activity at the S-A node regulates heart rate. Sympathetic fibers throughout the muscle help regulate the contraction strength.
Total cardiac output is found by multiplying heart rate by stroke volume. The factors that can influence cardiac output are visualized in the following diagram:
The Regulation of Cardiac Output Factors that stimulate cardiac output are shown as solid arrows, factors that inhibit cardiac output are shown as dashed arrows.
So, an increase in sympathetic tone will increase both heart rate and contraction strength. An increase in parasympathetic tone has the opposite effect. The ANS may operate reciprocally or co-actively on the heart. Sympathetic tone has an influence on heart rate at rest, during exercise, and from emotions. Maximum heart rate from strenuous exercise is associated with a large increase in sympathetic tone.
Schematic of Cardiac Innervation
Based on this diagram, it might seem that a T2 sympathectomy would cause less cardiac denervation than would, say T2-T4. However, this is not necessarily true, owing to the T2 “bottleneck” effect described earlier. (see Hyndman et al. 1942). In fact, bilateral thoracic sympathectomy, regardless of level(s), produces a reduction in the density of cardiac fibers (see Goldstein et al. 2005).
The heart receives SNS innervation from the upper thoracic region of the sympathetic chain, thus ETS surgery is easily predicted to cause partial cardiac denervation. Cardiac denervation is well-established in the literature, even characterized as “a safe, fast, cheap and efficient method for cardiac sympathetic denervation” (Drott et al. 1994).
PET Scans
Flourodopamine PET Scan of Heart After T2-T4 ETS The horseshoe-shaped area shows intact sympathetic activity around the left ventricle. According to the NIH scientists, this amount is below normal. PET scans of normal heart innervation are sought for comparison.
Radioactivity in SNS Heart Terminals Over Time During PET Scanning This shows amount of radioactivity, and therefore the amount of intact sympathetic nerve function in the heart. Normal subjects are represented by solid squares, bilateral ETS patients by solid circles, and patients with Pure Autonomic Failure by hollow circles. Patients with unilateral ETS are shown as hollow squares, and these appear much closer to the normal range.
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This seems to conflict with earlier reports that unilateral ETS denerved the heart regardless of operated side (see Abraham et al. 2001). In any case, it is confirmed that bilateral ETS significantly denerves the heart.
“Bilateral upper thoracic sympathectomy partly decreases cardiac sympathetic innervation density.” (Goldstein et al. 2005)
Empirical Status: Confirmed.
Empirical Status: Confirmed.
“After the [T2-T4 ETS], a significantly reduced heart rate at rest (12%), during exercise and during recovery after exercise was found” (Drott et al. 1994)
A 1986 study entitled “Cardiovascular changes after bilateral upper dorsal sympathectomy” found that heart rate at rest and after effort were both “blunted” (see Papa et al. 1986). From Japan in 2002:
“The [2002] study demonstrated that, at rest after ETS, heart rate, arterial pressure, and the rate–pressure product decreased.”(Nakamura et al. 2002)
“The change induced by exercise for each of heart rate, cardiac index, systemic vascular resistance, and the rate–pressure product after ETS was less than that before ETS” (Nakamura et al. 2002)
ETS surgeon Rafael Reisfeld has reported that his ETS patients “should know that their heart rate could potentially not go above 135 bpm” (Reisfeld 2004), whereas 180-200 BPM is considered normal maximal heart rate for adults. The formula “220 minus your age” is frequently employed by exercise instructors to estimate target maximum heart rate.
Baroreflex
The baroreflex is a negative-feedback loop that helps the body maintain proper blood pressure under changing conditions. Special cells called baroreceptors are located inside the aorta and other large arteries near the heart. Baroreceptors have the ability to detect changes in blood pressure, and send this information to the control center. If a drop in blood pressure is detected (e.g. when standing up), the hypothalamus will respond by increasing the heart rate to compensate. If high blood pressure is detected, heart rate will be slowed.
Sensory stimuli from the barorecpetors in the carotid sinus and the aortic arch acting via the control center, affect the activity of the sympathetic and parasympathetic nerve fibers in the heart. (See Human Physiology, Eighth Edition, Stuart Ira Fox)
Structures Involved in the Baroreceptor Reflex
Empirical Status: Confirmed.
“Endoscopic thoracic sympathectomy suppresses baroreflex control of heart rate in patients with essential hyperhidrosis.” (Kawamata et al 2004). Presumably ETS would suppress baroreflex control of heart rate in patients without essential hyperhidrosis also.
Cardiac Response to Exercise After ETS
In 2002 a group of Japanese surgeons studied the cardiac effects of ETS at rest and during sub-maximal exercise. Maximal exercise was not studied. Below are their charts, showing reductions in essentially every measure.
CI, cardiac index; HR, heart rate; MAP, mean arterial pressure; RPP, rate–pressure product; SI, stroke index; SVR, systemic vascular resistance. *p<0.05 vs before ETS; **p<0.01 vs before ETS.
Effects of ETS on Percent Changes in Hemodynamic Variables with Exercise
The authors measured heart rate, arterial pressure, stroke volume and vascular resistance. Cardiac index is found by multiplying rate by stroke and adjusting for body size. Stroke index is stroke volume adjusted for body size. Rate-pressure-product is found by multiplying rate by pressure. These values were taken at rest (baseline) and during light exercise, both before ETS, and one year after ETS. This chart shows the percentage of change from baseline that occurs during exercise. (see Nakamura et al. 2002)
Clearly, ETS surgery reduces every aspect of cardiac response to exercise.
This study also discovered a decrease in the blood levels of catecholamines adrenaline and noradrenaline. This means that ETS must somehow affect the function of the adrenal medulla, and is discussed in Section III, Changes to Systemic Function.
Empirical Status: Confirmed.
“Cardiac denervation results in a sensitization of the heart to catecholamines.” (Bernston et al. 1991 ; see also Vatner et al. 1985).
