(Question 1 of 5)

The first question to start the interpretation process is “Are there any ectopic (possible arrhythmic) beats?” If the answer to this question is positive, the report may need to be read differently (see the section “Reading ectopy” later in this chapter). If not, the report is read in the usual manner; see questions two through five, next.

(Question 2 of 5)

The second question in the interpretation process is: “Is the resting P activity above 0.1 bpm²?” This question addresses the possibility that the patient may be at risk for cardiovascular autonomic neuropathy (CAN), which indicates risk of sudden cardiac death. CAN is defined as the parasympathetic measure, RFa <0.1 bpm² (see Fig. 7.2, the pink shaded area in the (resting) baseline response graph). The threshold for CAN is equivalent to the Framingham Heart Study threshold for high risk of a cardiovascular event [1]. If RFa ≥0.1 bpm², then continue to the next question.

CAN MAY BE NORMAL .

CAN simply indicates that the average 85–year-old has a greater mortality risk than the average 45–year-old.

CAN risk is stratified by SB.

Low–normal SB minimizes CAN risk [2].

If not, the patient’s heart may need to be more protected, clinically. RFa <0.1 bpm² indicates that there may not be sufficient parasympathetic tone to slow a ventricular tachyrhythm from progressing. So as to not be an alarmist, it should be noted that RFa <0.1 bpm² may be normal. CAN simply indicates that the average 85-year-old has a greater mortality risk than the average 45-year-old, all else being equal. If the patient is (physiologically) older, including all geriatric and cardiovascular disease patients, or if the patient is post-MI or post-CABG, CAN risk may be normal. For the latter two cases, the risk follows the same 5-year time course as the Framingham Heart Study risk profile [1]. In any case, the geriatric cardiology literature recommends more parasympathetic activity [2–4]. Too much more parasympathetic activity, however, may lead to depression [5–10]. So “a little more” is necessary. As shown in a study detailed elsewhere in this compendium (see Chap. 15), “a little more” parasympathetic activity is defined as low-normal SB (0.4 < SB < 1.0) [11]. This may be established and maintained with therapy by treating the P&S imbalance, CAN, history dependent [12]. Typically, therapy options for CAN begin with titrating sympathetic blockade (e.g., beta-blockers or antihypertensives) if SB is high, or low-dose, anticholinergics (e.g., very low dose, tricyclic antidepressants or SNRIs) if SB is low, thereby establishing or maintaining low-normal SB.

(Question 3 of 5)

The third question is: “Is the patient in balance: is SB between 0.4 and 3.0?” This question addresses whether the patients’ SBs is appropriate for them as individuals. As with everything else in life, balance is key. Proper balance is based on age, disease, therapy, lifestyle, and history. As a “rule of thumb,” for younger adults, high-normal SB (1.0 < SB < 3.0) is typical. After all, they need the extra sympathetic activity to chase after children. For older adults, low-normal SB (0.4 < SB < 1.0) is recommended as this indicates more, resting parasympathetic activity which is known to be cardioprotective and has been shown to reduce comorbidities diagnosed and medications prescribed [2–4]. If the patient is in balance, continue to the next question. If not, and if SB is high (indicating a resting sympathetic excess), consider reducing SB by decreasing anticholinergics or increasing sympathetic blockade, history dependent. If SB is low (indicating a resting parasympathetic excess), consider increasing SB by increasing anticholinergics or decreasing sympathetic blockade, history dependent. If SB is normal, no change in therapy is necessary, assuming normal HR and BP. Follow up in 6 months to ensure their SB remains normal. If intervention is made, follow up in 3 months to document the patient’s responses. Treating abnormal SB treats advanced autonomic dysfunction (DAN in diabetics) and CAN [12].

(Question 4 of 5)

The fourth question is: “Is there standing or Valsalva parasympathetic excess (PE)?” (see Fig. 5.​4). This question addresses the patient’s stability in response to disease, therapy, lifestyle, and history. If the answer is positive, standing or Valsalva PE is associated with difficult to control BP, blood sugar, or hormone levels (e.g., thyroid or estrogen), and symptoms of depression, fatigue, exercise intolerance, persistent weight gain, sleep disturbances, hypertension secondary to autonomic dysfunction, GI upset, dizziness or lightheadedness, and frequent headache or migraine [13]. Standing or Valsalva PE is also associated with clinical conundrums; examples include concurrent depression and hypertension, or fibromyalgia with fatigue and heightened pain sensitivity, or depression and anxiety syndromes, or chronic fatigue with nighttime sleeplessness. There are many, more of course, but in all of these couplets, the first disorder is associated with PE and the second with SE. Both ends of the “seesaw” are high. The “seesaw” is broken (Fig. 7.3). P&S monitoring helps to document the primary P and S dysfunction (e.g., standing or Valsalva PE [13]), guide therapy to restore balance (see General Therapy options, Table 6.​2), and reduce morbidity (relieve secondary symptoms), enabling the physician to be more aggressive with the primary dysfunction. In treating PE, consider titrating low-dose anticholinergic therapy if the patient is not diagnosed with CVD, including hypertension. If the patient is diagnosed with CVD, consider titrating low-dose carvedilol, history dependent [13]. If the patient already has a history of a beta-blocker, consider switching it to carvedilol. The reason for this recommendation is that carvedilol is a double cocktail, and along with its antioxidant properties, it is known to also have an effect in the brainstem, indirectly reducing PE in patients demonstrating advanced autonomic dysfunction or autonomic neuropathy [14–16]. If the answer to the fourth question is “No,” continue to the fifth question.

(Question 5 of 5)

The fifth question is: “Is the standing sympathetic response normal?” (see Fig. 5.​2). This question addresses the reminder of the morbidity issues (and finish addressing quality of life issues). If the answer, in adults, is negative, an abnormal sympathetic response to standing (up right posture) is indicated. Abnormal sympathetic responses to PC is associated with orthostasis (if SW) or syncope (if SE). In many cases, these indications are preclinical, and while the patients may not demonstrate dizziness or lightheadedness, they may demonstrate evening edema, frequent afternoon fatigue or headache, sleep disturbances, or (subclinical) depression or related syndromes. Often, normalizing sympathetic responses to standing also helps to restore the dynamic autonomic balance and helps to relieve some of these other disorders, including elevated BP [17]. If the answer is positive, then the reading of the report is complete. In pediatric patients, SW and SE upon standing does cause dizziness or lightheadedness, but in many cases patients “grow out of it.” If stand sympathetic abnormalities are not interfering with the patient’s lifestyle, then promote proper daily hydration and modifications to lifestyle (e.g., squeezing muscles while standing, etc.), and wait to see if the symptoms reduce.

In the presence of autonomic neuropathy (DAN or CAN, including advanced autonomic dysfunction), the DB and Valsalva responses are expected to be low. As long as they are normal to low, they provide no additional information. They simply suggest or confirm autonomic dysfunction and ALA is recommended. However, if they are high, then additional information may be indicated: