Diagnosis and Treatment of Anxiety in the Intensive Care Unit Patient

Shelley A. Holmer

Robert M. Tighe

Anxiety is a normal, adaptive biological response to threat. It occurs when a person feels helpless and apprehensive about an uncertain future due to a perceived inability to predict or control a desired outcome. In contrast, pathologic anxiety is normal anxiety run amok. It occurs spontaneously or amid usually benign circumstances, is excessive in intensity or duration, and impairs functioning and behavior. Anxiety manifests in a variety of ways, resulting in physical, affective, behavioral, and cognitive symptoms and signs (Table 198.1).

Patients admitted to the intensive care unit (ICU) commonly experience anxiety in response to pain, invasive procedures, an unfamiliar setting, and the fear of death. In moderation, anxiety
can promote healthful behaviors, just as pain can lead to protection from future injury. In excess, however, anxiety can complicate diagnosis, interfere with treatment, and contribute to poor outcomes by increasing both morbidity and mortality. Anxiety can complicate the clinical picture, as symptoms and signs of many medical problems overlap with those of anxiety (e.g., chest pain, palpitations, tachycardia, diaphoresis, tremulousness). Overwrought patients may refuse tests or procedures they fear will cause pain or will lead to bad news. Patients with phobias of blood, needles, and confined spaces (e.g., as in computed tomography and magnetic resonance imaging machines) may forego necessary interventions. Pathologic anxiety may contribute to the need for ICU admission in the first place.

Table 198.1 Symptoms and Signs of Anxiety

Physical
   Tachycardia
   Tachypnea
   Hypertension
   Diaphoresis
   Light-headedness
   Tremulousness
Affective
   Uneasiness
   Edginess
   Nervousness
   Fright
   Panic
   Terror

Behavioral
   Restlessness
   Agitation
   Compulsiveness
   Avoidance
   Noncompliance with diagnostic or therapeutic interventions
   Fidgetiness
Cognitive
   Apprehension
   Worry
   Fear of emotional or bodily damage
   Denial
   Obsessiveness
   Preoccupation with harm
   Thoughts about death

This chapter reviews the physiologic concomitants of anxiety, medical causes of anxiety, critical medical conditions particularly affected by anxiety, anxiety disorders specific to the ICU setting, and the treatment of anxiety.

Physiologic Expressions of Anxiety

The physiologic expressions of anxiety are myriad. By activating the fight or flight response, anxiety recruits the entire autonomic nervous system to respond to an unknown enemy. Multiple organ systems—endocrine, gastrointestinal, musculoskeletal, immune, cardiovascular, and respiratory—are involved [1]. Anxiety increases blood levels of cortisol, prolactin, and growth hormone [2]. A disquieted patient has enhanced gastric motility and gastric secretions, vasoconstriction of the splanchnic and cutaneous circulations, and vasodilation of striated muscle groups [3]. Anxiety also has direct effects on the immune system: a reduction in the chemotaxis of lymphocytes and neutrophils, a decrease in the phagocytic ability of neutrophils, and an increase in plasma levels of tumor necrosis factor α and superoxide anion [4]. This suggests a complex physiologic effect of anxiety in the critically ill population.

The organ systems adversely affected by anxiety of most concern to the intensivist are the cardiovascular and respiratory systems. Anxiety affects the cardiovascular system by altering normal autonomic tone, manifested as increases in heart rate, blood pressure, cardiac output, and cardiac irritability [1]. The stress of simply being hospitalized augments urinary excretion of catecholamines, which represents activation of the sympathetic nervous system and contributes to cardiac arrhythmias [5]. In the fight or flight response, augmentation of cardiac output prevents cardiovascular collapse, but, in heart failure and myocardial infarction (MI), excessive cardiac output can be detrimental. Anxiety increases respiratory rate, tidal volume, and airway resistance [6] and can induce hyperventilation and syncope. These data suggest that anxiety, while exacting a psychological toll, also significantly alters cardiorespiratory physiology, especially in the critical care setting.

Medical Causes of Anxiety

Because failure to identify and treat organic (i.e., medical or secondary) causes of anxiety can result in increased morbidity and mortality, the distinction between organic and functional (i.e., psychiatric or primary) causes is vitally important. The presence of an organic cause is suggested when anxiety occurs autonomously in the absence of an apparent psychologically charged situation or of a discrete physical event (e.g., acute pain or tachyarrhythmia). However, in any given patient, determination of what constitutes an appropriate or sufficient psychological precipitant for anxiety is difficult. Life history, cultural background, and prior behavioral conditioning are often unknown to clinicians in the fast-paced ICU setting. Therefore, when anxiety is present and no clear psychological or medical cause is obvious, a thorough search for an organic cause is indicated.

Table 198.2 Common Medical Causes of Anxiety

Neurologic
   Delirium
   Substance withdrawal syndromes
   Complex partial seizures
   Traumatic brain injury
   Pain
Cardiac
   Acute myocardial infarction
   Shock
   Paroxysmal tachycardia
Metabolic
   Hypoglycemia
   Hyperthyroidism
   Pheochromocytoma
   Cushing’s syndrome
   Addison’s disease

Respiratory
   Respiratory failure
   Asthma
   Hypoxia
   Hyperventilation
   Pneumothorax
   Pulmonary edema
   Pulmonary embolism
Toxic
   Illicit drug intoxication
   Anticholinergic intoxication
   Prednisone
   Isoniazid
   Caffeine

Anxiety is a symptom of hundreds of medical conditions; Table 198.2 provides a list of conditions common in the ICU. Two syndromes that are particularly difficult to distinguish from primary anxiety are delirium and substance withdrawal.

Delirium

Treating delirious patients solely with anxiolytics (e.g., benzodiazepines) can exacerbate their confusion, so it is important to distinguish delirium from anxiety by doing a brief cognitive examination. In delirium, performance of tasks of attention, orientation, memory, and language is often impaired; rarely does an anxious patient have these deficits. By definition, delirium always has a medical cause; therefore, determination of its cause, rather than simply treating its symptoms, is vital. Recognition and management of delirium are discussed in Chapter 197.

Substance Withdrawal Syndromes

Because withdrawal from central nervous system depressants (e.g., opioids, benzodiazepines, alcohol) can be life-threatening, it should always be high on the differential diagnosis of anxiety. This diagnosis can be missed because patients either underreport their substance use or are unable to communicate. Patients can also withdraw from sedatives and opioids prescribed during a lengthy period of mechanical ventilation. Recognition and treatment of withdrawal syndromes are discussed in Chapter 145.

Scenarios in Which Anxiety Significantly Affects Outcomes of Medical Illness

Acute Myocardial Infarction

As heart disease remains the leading cause of mortality in the United States, acute coronary syndrome is a common reason for admission to the coronary care unit (CCU). Prevention and treatment have focused on awareness and alteration of traditional risk factors (e.g., hyperlipidemia, hypertension, family history). A developing literature supports consideration of psychosocial factors as well, most frequently, anxiety, depression, and personality traits [7,8,9,10,11].

Anxiety is a frequent occurrence in the CCU, both related to MI itself and as a premorbid condition contributing to the development of MI [12]. In the general hospital, anxiety has been noted to occur in 24% to 31% of patients after MI [13]. The stress of being cared for in an ICU, particularly the relinquishing of control and privacy, in addition to dealing with a potentially life-threatening disease, contribute to anxiety in this setting [9]. Anxiety in the CCU after MI rapidly rises and peaks within the first 12 hours; declines, though persists, during the next 36 hours; and then increases again as patients face transfer out of the CCU and ultimately discharge from the hospital [14]. Physicians and nurses often under-recognize anxiety and underestimate its severity after MI [15]. Anxiolysis should be an early consideration in post-MI patients.

Physiologically, anxiety-disordered patients have decreased heart rate variability, which may result in an alteration in cardiac autonomic tone [16,17], either by heightened sympathetic stimulation or diminished vagal control [7]. Enhanced sympathetic stimulation is associated with arrhythmias [18], and reduced vagal control is linked with impairment in the baroreflex control of the heart; both perturbations are associated with sudden death [19]. These physiologic changes may explain why anxiety—especially phobic anxiety—enhances risk for sudden death [20,21]. In addition, elevated anxiety is associated with poor implementation of important risk-reducing recommendations after MI, particularly stress reduction, greater socialization, smoking cessation, and adherence to carrying supplies [22].

Two groups demonstrated that anxiety, independent of depressive symptoms, was associated with in-hospital complications after acute MI, including recurrent ischemia, reinfarction, congestive heart failure, and ventricular arrhythmias [9,10]. Further trials are required to determine the nature of this relationship; whether the effect of anxiety is “dose”-dependent; and whether effective anxiety treatment improves cardiac outcomes acutely.

Several studies have looked at the correlation between anxiety and post-MI outcomes in the long term. Some [12,23,24], but not all [25,26,27,28], prospective trials demonstrated that high levels of anxiety predicted cardiac events (unstable angina, reinfarction) and/or mortality. Meyer et al. [11] showed that anxiety predicted greater mortality in post-MI patients only if left ventricular function was reduced. These reports suggest that the data for hard cardiac endpoints over the long term remain unclear.

Weaning from Mechanical Ventilation

Respiratory failure and consequent need for mechanical ventilation are common causes of admission to the ICU. Nearly three fourths of patients resume spontaneous, unassisted breathing with little difficulty [29]. However, patients who require prolonged mechanical ventilation have longer hospital stays, face higher morbidity and mortality, and require lengthier rehabilitation. Therefore, the goal is to wean patients as soon as possible.

The experience of shortness of breath has been well associated with anxiety and is one of the most commonly reported symptoms in panic disorder. In fact, anxiety and panic have been shown to lead to hyperventilation, which, when performed voluntarily, induces panic attacks and mediates a wide variety of psychosomatic symptoms [6]. Chronic hyperventilation due to anxiety and panic leads to hypocapnia and slowed recovery from changes in respiratory status. The integral connection between anxiety and respiratory physiology suggests anxiety may contribute to respiratory failure.

Given the limitations of communication and easy fatigability in patients with critical illness, the evaluation of anxiety in this setting remains difficult. Nearly 60% of patients on a ventilator may experience moderate levels of anxiety. The highest levels occur in patients intubated for primary respiratory disorders (e.g., chronic obstructive pulmonary disease [COPD]) and in those on prolonged (> 22 days) artificial ventilation, the very groups who are most at risk for difficulty weaning from mechanical ventilation [30].

Although the physiologic measures used to determine readiness to wean from the ventilator are well known and several of them have been studied closely in clinical trials, information about the effect of the patient’s psychological state, specifically anxiety, on weaning from the ventilator is scant. Anxiety may cause shortness of breath and a fear of death or abandonment, especially as ventilatory support is withdrawn. This can stimulate the sympathetic nervous system; cause bronchoconstriction; and increase airway resistance, work of breathing, and oxygen demand. This cascade can become a perpetuating cycle of anxiety, muscle fatigue, and thus weaning failure [31].

Anxiety should be considered in all patients during the weaning process, especially those who are intubated for primary respiratory causes and for a prolonged period. Given the paucity of data regarding the effect of anxiety on ventilator weaning, no clear treatment guidelines exist; however, it is well appreciated that weaning should be approached from a multidisciplinary standpoint. Treatment includes pharmacologic, environmental, and educational approaches, and is enhanced when both patient and nursing staff are involved in the decision to wean and in the process of weaning.

Because anxiety and respiratory distress due to fatiguing respiratory muscles can produce similar cardiorespiratory manifestations, it is important to try to distinguish between these two syndromes. Only if one is convinced that anxiety is the cause should one consider pharmacotherapy for anxiety because pharmacotherapy with benzodiazepines can potentially prolong weaning due to central pump fatigue from respiratory depression (see Chapter 60 on Mechanical Ventilation Part III: Discontinuation). Although this class of medications is associated with respiratory depression and altered level of consciousness, benzodiazepines can be quite effective when used judiciously in the correct setting. Neuroleptics are less associated
with respiratory depression and may be more beneficial than benzodiazepines, especially for patients whose weaning failure is due to fear or to delirious agitation.

More recent evidence suggests a role for dexmedetomidine, an α₂-adrenergic receptor agonist, which causes a rapid onset of sedation and analgesia but not respiratory depression [32,33,34]. The lack of respiratory-depressant effects allows patients to be extubated while remaining on dexmedetomidine, whereas benzodiazepines require discontinuation or reduction prior to extubation. Though not specifically studied in anxious patients, dexmedetomidine demonstrates adequate sedation and decreased time on the ventilator, suggesting that it may be a useful agent in the anxious patient attempting to wean from the ventilator.

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