, Rohit Arora3, 4, Nicholas L. DePace5 and Aaron I. Vinik6
(1)
Autonomic Laboratory Department of Cardiology, Drexel University College of Medicine, Philadelphia, PA, USA
(2)
ANSAR Medical Technologies, Inc., Philadelphia, PA, USA
(3)
Department of Medicine, Captain James A. Lovell Federal Health Care Center, North Chicago, IL, USA
(4)
Department of Cardiology, The Chicago Medical School, North Chicago, IL, USA
(5)
Department of Cardiology, Hahnemann Hospital Drexel University College of Medicine, Philadelphia, PA, USA
(6)
Department of Medicine, Eastern Virginia Medical School Strelitz Diabetes Research Center, Norfolk, VA, USA
Pulmonary testing, including pulmonary function tests and blood gas tests, is augmented by P&S testing, not simply autonomic testing, but actual P&S testing. As you know, bronchial diameter is directly and uniquely controlled by sympathetic activity. Ventilatory activity is under parasympathetic control.
Pulmonary function tests and blood gas tests determine the net result of both bronchial diameter and ventilatory activity. Simple autonomic testing provides information on the net results of both P and S activity. This is no more information than pulmonary function testing. However, P&S testing augments pulmonary function testing by differentiating P and S activity and the bronchial smooth muscle activity and the activity of the ventilatory muscles.
P&S monitoring responses measured during clinical stimuli at rest and during DB, Valsalva, and PC challenges provide more information regarding patient responses to therapies and disease.
Abnormal responses to DB indicate vagal or parasympathetic dysfunction, indicating that the vagus is “struggling” to ventilate. This has aided in detecting, differentiating, and documenting pulmonary or upper respiratory disorder.
Abnormal Valsalva responses are associated with sleep apnea or the early effects of excessive beta-2 agonist (bronchodilator) use.
Resting autonomic balance (SB) provides objective data regarding patient response to medication. Titration of therapy and patient compliance balances P and S activity. This includes:
An objective and physiologic measure of patient compliance with CPAP or Bi-PAP therapy in sleep apnea. Resting autonomic responses indicate mortality risk.
A (possibly earlier) indication of SE due to the patient’s excessive use of a beta-2 agonist, possibly before the onset of high BP, hypertension, or heart disease.
P&S responses to PC (standing) indicate morbidity risk in response to chronic diseases, including COPD, asthma, sleep apnea, chronic bronchitis, emphysema, and lung cancer.
Examples of expected therapy responses include:
A greater sympathetic response to beta-2 agonist
A reduced sympathetic response to CPAP or Bi-PAP therapy
A reduced sympathetic response to beta-blockers and antihypertensives
A reduced parasympathetic response to anticholinergics (including antidepressants, antipsychotics, anxiolytics)
COPD and Asthma
P and S regulation of HR is altered in subjects with bronchial asthma [1]. Medications utilized by respiratory disorder patients are now self-administered. These medications include sympathomimetics, which in larger or more frequent dosing may affect cardiovascular function and possibly place the patient at risk for heart disease or hypertension. P&S monitoring helps the pulmonologist maintain P&S balance, preventing potential cardiovascular dysfunction.
Chronic obstructive pulmonary disease (COPD) is associated with PE or high respiratory frequency during DB, indicating the additional effort required of the vagus nerve to ventilate the patient. A well-documented and continually growing concern about COPD is the early onset of heart disease. P&S evidence indicates that the heart disease is associated with SE. The SE may be a result of the PE or it may be a consequence of the patient’s habits with therapy. Upon routine checkup with P&S monitoring, if the patient demonstrates SE, even before an increase in BP, and the patient is prescribed a beta-2 adrenergic agonist (bronchodilator), then the SE may be a consequence of the (possibly excessive) use of the beta-2 agonist. If the patient frequently pre-doses or panic doses themselves, then the excess agonist travels directly to the heart where it stimulates the heart. For those patients who demonstrate persistent SE, the beta-2 stimulation may have consequences similar to chronic low-level adrenaline from a stressful lifestyle. The SE may be the sign for the physician to counsel the patient on the dangers of excessive use of a beta-2 agonist or modify the patient’s therapy so that the physician has more control over the patient’s self-dosing.
COPD and asthma may be contraindicated for therapies that are common in the treatment of heart diseases. The beta-adrenergic system contains beta-1 and beta-2 receptors that are found in varying concentrations in the heart and lung. Beta-1 adrenergic receptors and beta-2 adrenergic receptors coexist in the heart, generally in a ratio of 3:1, respectively. Beta-2 receptors are also present on adrenergic nerve terminals in the heart, where they facilitate norepinephrine release. The stimulation of either receptor results in positive inotropic and chronotropic responses, cardiac myocyte growth, and cardiac toxicity. Beta-2 receptors are found predominately in bronchial and vascular smooth muscle and adrenergic nerves. Beta-2 agonists, such as albuterol and salmeterol, are widely used as bronchodilators in the treatment of asthma and COPD.
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