ضربان قلب و نوسان ضربان قلب در اختلالات هراس، اضطراب اجتماعی، اختلالات اضطرابی وسواس عمومی در ابتدا و در پاسخ به آرام سازی و تنفس سریع

It remains unclear if diminished high frequency heart rate variability (HF-HRV) can be found across anxiety disorders. HF-HRV and heart rate (HR) were examined in panic (PD), generalized anxiety (GAD), social anxiety (SAD), and obsessive–compulsive disorder (OCD) relative to healthy controls at baseline and during anxiety stressors. All disorders evidenced diminished baseline HF-HRV relative to controls. Baseline HRV differences were maintained throughout relaxation. For hyperventilation, PD and GAD demonstrated greater HR than controls. Psychotropic medication did not account for HF-HRV differences except in OCD. Age and sex evidenced multiple main effects. Findings suggest that low baseline HF-HRV represents a common index for inhibitory deficits across PD, GAD, and SAD, which is consistent with the notion of autonomic inflexibility in anxiety disorders. Elevated HR responses to hyperventilation, however, are specific to PD and GAD.

A robust literature examined cardiac psychophysiology at rest and in response to provocation among individuals with anxiety disorders. Most studies focused on panic disorder (PD), and to a lesser extent, on generalized anxiety disorder (GAD) and social anxiety disorder (SAD; see Friedman, 2007). Within these studies, heart rate variability (HRV) and heart rate (HR) were the most common measures of cardiovascular activity. HRV in the high frequency spectrum (HF-HRV) represents an index of respiratory sinus arrhythmia (RSA), which involves regular patterns of HR fluctuations that are linked to the breathing cycle and modulated by the parasympathetic nervous system (Thayer and Lane, 2000). Extensive research demonstrated associations between HRV and various physical diseases, psychopathology, and emotion regulation (e.g.,Camm et al., 1996, Beauchaine, 2001 and Friedman, 2007). Most important, theories have proposed close links between low RSA and psychopathology, especially anxiety disorders. The Polyvagal theory (e.g., Porges, 2007) links autonomic regulation and RSA to a variety of (psycho-) pathological states and behaviors. Adaptive behavior and autonomic responses emerge from the hierarchical organization of different phylogenetic subsystems of the autonomic nervous system with phylogenetically newer systems inhibiting older ones. These inhibition processes are essential for adaptive behavior with (autonomic) variability being associated with healthy responses. Deficits in these inhibitory processes are seen as a risk for emotion dysregulation and psychopathology more generally (Beauchaine, 2001). The related neurovisceral model of cardiac and emotion regulation proposes specific links between cardiovascular variability and anxiety disorders (Thayer and Lane, 2000 and Friedman, 2007). It outlines a central and peripheral network that integrates autonomic, attentional, and affective systems involved in emotion self-regulation. Within this homeodynamic view, healthy physiological variability involves the ability to adaptively react to environmental demands to maintain the stability of an organism. Anxiety disorders (and other affective disorders) are characterized by a rigid emotional response style with responses not reflecting environmental demands. More specifically, this rigid response style expresses as an inability to inhibit inappropriate anxious responses in non-threatening situations. HF-HRV predominantly represents the parasympathetic nervous system output of this integrated network and, thus, serves as an important index of the adaptability and regulatory ability of an organism, with decreased HF-HRV associated with less flexible responding to the environment. Thus, this model predicts that the rigid responding in anxiety disorders is associated with lower HRV. In support, numerous studies demonstrated that relative to non-anxious controls, individuals with anxiety disorders evidence lower HF-HRV at rest or in response to anxiety stressors (Klein et al., 1995, Friedman and Thayer, 1998a and Friedman and Thayer, 1998b). This lower parasympathetic cardiac control has been especially found in PD (see Friedman, 2007). The smaller number of GAD and SAD studies demonstrate more mixed results, with some showing lower HF-HRV at rest or in response to anxiety-related provocation relative to non-anxious controls (Thayer et al., 1996, Thayer et al., 2000 and Grossman et al., 2001) and others showing no differences, particularly for SAD (Kollai and Kollai, 1992 and Mauss et al., 2003). The sole published study examining HRV in obsessive–compulsive disorder (OCD) (Slaap et al., 2004) found no HRV differences between OCD and control patients. This study, however, also reported null findings on HRV differences between PD and control patients, contradicting much of the literature and suggesting that sample or other study-specific variables may account for the findings. Overall, findings regarding lower HRV at rest across anxiety disorders remained mixed. Recent studies also demonstrated stronger HRV reactivity to certain stimuli or tasks in anxiety disorders. PD patients, for example, showed a larger decrease in HRV in response to panicogenic substances like sodium lactate or yohimbine (Yeragani et al., 1992 and Yeragani et al., 1994), or a stronger increase in sympathetic-parasympathetic ratios after isoproterenol (Pohl and Yeragani, 2001). These elevated task-specific effects on HRV are also evident in other anxiety disorders. For example, similar effects were found for individuals with dental phobia when confronted with phobia-relevant stimuli (Johnsen et al., 2003), for PTSD patients during speech or mental arithmetics (Keary et al., 2009), or for general measures of anxiety (Shinba et al., 2008). Particularly within homeostatic approaches, differences between individuals with and without anxiety disorders in tonic and phasic HR have been investigated. Despite mixed findings, many studies demonstrate higher HR at baseline and in response to anxiety-related stressors among individuals with anxiety disorders controls (see Aikins and Craske, 2010). Thus, the rigid response style with little variability in anxiety disorders is not only observable as low tonic HRV (e.g., at rest or during relaxation), but also as an inadequate over-reactivity in HR and HRV to certain tasks and stimuli. So far, most studies have focused on HF-HRV or HR differences among individuals with one anxiety disorder (versus controls) or have compared two anxiety disorder groups (Asmundson and Stein, 1994 and Friedman and Thayer, 1998b). A notable exception investigated more than two anxiety disorders within a single sample, but did not investigate HF-HRV in response to anxiety-related provocation (Licht et al., 2009). While yielding important information, this narrow focus limits the capacity to examine HF-HRV and HR differences across the full spectrum of the anxiety disorders. Including a broader range of anxiety disorders would enable investigation of disorder-specific versus shared features of cardiac psychophysiology. A finding of similar features of cardiac psychophysiology across different nosological categories would favor a functional perspective of anxiety disorders (van Praag et al., 1990). The present study, therefore, examined HF-HRV and HR differences among individuals with a DMS-IV (American Psychiatric Association, 2000) anxiety disorder at baseline and in response to two distinct anxiety-related experimental tasks, hyperventilation and relaxation. A recent finding might suggest that association between anxiety disorders and low HRV is accounted for by antidepressant medication use (Licht et al., 2009). This finding calls into question the theorized mechanism of HRV and HR abnormalities in anxiety disorders, and at the very least, suggests that analyses should account for different covariates like psychotropic medication use as well as comorbid mood disorders (Rottenberg, 2007). Therefore, we tested and controlled for the effects of psychotropic medication use and comorbid mood disorders, as well as the contributions of age, sex, and respiration, each of which can affect HRV (Grossman et al., 2001, Burriss et al., 2007, Rottenberg, 2007 and Licht et al., 2009). In sum, the present study investigated the following questions: (1) Do patients with an anxiety disorder (all anxiety disorder patients combined) show lower HF-HRV or higher HR at resting baseline than a non-anxious control group (CG)?; (2) Are these differences evident across the different subdivided anxiety disorder groups (ADGs; PD, GAD, SAD, OCD)?; (3) Do anxiety disorder patients combined and the subdivided ADGs show lower HF-HRV responses and/or greater HR responses during the two anxiety-related tasks than the CG?; (4) Is lower HF-HRV and/or higher HR associated with higher symptom severity?; and (5) Are potential differences in HF-HRV and HR solely explained by relevant demographic variables (age, sex), differences in respiration (for HF-HRV) or certain clinical variables (comorbid mood disorder or psychotropic medication use)?