Sudden cardiac death is responsible for 300 000 deaths annually in the United States.^(5,6) Sympathetic nervous system activity increases the likelihood of ventricular dysrhythmias⁽⁶⁾ especially when there is prior ischaemic damage. Sympathetic nervous system stimulation, which increases heart rate, can trigger ectopic sites in the myocardium, which override normal conductive pathways, producing potentially fatal dysrhythmias. Either the peripheral sympathetic nervous system or the central nervous system can generate stimuli leading to this phenomenon. Therefore, anxiety and stress may increase the risk of dysrhythmia.⁽⁷⁾ Among individuals with pre-existing heart disease or dysrhythmias, activities which precipitate adrenergic discharge may produce ventricular dysrhythmias—for example, public speaking, road rage, and recall of emotionally charged events.⁽⁸⁾ In one series of patients, psychological stressors were more reliable triggers of dysrhythmias than physical manoeuvres such as carotid sinus massage, hyperventilation, and the Valsalva manoeuvre.⁽⁸⁾ Simple and inexpensive non-pharmacological techniques such as relaxation training, hypnosis, and medication have been shown to improve ventricular dysrhythmias.^{(8, 9)}

Depression has also been associated with lower threshold for ventricular dysrhythmias.⁽¹⁰⁾ Patients with depression exhibit dysregulation of the sympathoadrenal system—hypothalamic corticotropin releasing factor-containing neurons appear to stimulate several autonomic centres involved in regulating sympathetic activity.⁽¹¹⁾ Smith et al.⁽⁸⁾ found that deaths within 18 months of a myocardial infarction were concentrated among depressed patients with 10 or more premature ventricular contractions per hour. In this group of patients, 83 per cent of mortality was due to ‘arrhythmic deaths’.

More than 60 million Americans have hypertension. The prevalence among whites is about 15 per cent, but is over 25 per cent in the African-American population. 95 per cent of people with hypertension have primary, or idiopathic, hypertension. The remaining 5 per cent have secondary hypertension, due to conditions or substances such as renal disease, steroids, or oral contraceptives. Managing hypertension reduces the morbidity and mortality of the condition. Constitutional and stress-related factors contribute to hypertension. Patients with hypertension, in general, have a more prolonged vasoconstrictive response to psychological stress than patients with normotension,⁽¹²⁾ which may result in both short-term and long-term blood pressure elevation due to this interplay of environmental and constitutional factors.⁽¹³⁾

Myocardial ischaemia often leads to myocardial infarction. Acute myocardial infarction can develop at rest or with normal activity. Deaths associated with acute myocardial infarction occur during the first few hours after the onset of symptoms, and are the result of ventricular fibrillation. It is important that patients know the warning signs and seek care promptly when symptoms develop. Unfortunately, as many as 20 per cent of myocardial infarctions are unrecognized. Denial of acute myocardial infarction symptoms and warning signs by individuals, particularly men, are a frequent source of mortality and morbidity. The roles of gender-specific differences in terms of establishing predictors for clinical outcomes is understudied.⁽¹⁴⁾

The most common precipitant of myocardial ischaemia among patients with pre-existing coronary artery disease is stress.⁽¹⁵⁾ Stress-induced ischaemia is more common than ischaemia induced by physical stressors. Recovery from a myocardial infarction is also highly dependent on psychosocial factors. Ruberman et al.⁽¹⁶⁾ demonstrated that postmyocardial infarction patients, who are socially isolated and have high stress levels, have at least four times
the risk of death, compared to their counterparts who have lower levels of stress and isolation. Particularly, lack of a close confidant predicts negative outcomes after myocardial infarction, including further cardiac events.⁽¹⁷⁾ In addition, emotional distress after myocardial infarction is associated with poorer outcomes in terms of quality of life and psychological adjustment.⁽¹⁸⁾

Depression may occur in 31 per cent of patients admitted for acute myocardial infarction.⁽¹⁹⁾ Presence of major depressive disorder in a patient with cardiac disease has a significant association with morbidity and mortality. Carney et al.⁽²⁰⁾ found that major depressive disorder was the best single predictor of myocardial infarction, angioplasty, and death during the 12 months following cardiac catheterization. Patients with a history of myocardial infarction and major depressive disorder are up to three to five times more likely to die within 6 months of discharge than non-depressed patients following infarction.⁽¹⁹⁾ As to how depression increases risk include hypothalamic-pituitary-adrenocortical and/or sympathoadrenal hyperactivity, diminished heart rate responsivity, ventricular instability, myocardial ischaemia due to stress, and alterations in platelet receptors and reactivity.^{(21, 22)} The data are limited, antidepressant treatment, stress management, and relaxation training in patients with coronary artery disease or myocardial infarction and major depression probably reduces mortality.⁽²³⁾

Assessment of the patient’s personality and behavioural style is important because type A behavioural patterns increase the risk of a myocardial infarction.⁽²⁴⁾ The type A behaviour pattern includes ambitiousness, aggressiveness, competitiveness, impatience, muscle tenseness, alertness, rapid and emphatic vocal style, irritation, cynicism, hostility, and an increased potential for anger. Very frequently, such individuals are also hard-working ‘workaholics’ who deny physical or emotional vulnerability. Their self-esteem is often dependent on constant achievement. Unstable cardiac function poses an immediate and ongoing threat to them, and challenges their need to be in control of their environment and bodies. Many clinicians believe that modifying a type A behaviour pattern is an integral part of preventing future myocardial infarctions.⁽²⁴⁾ Group or individual psychotherapy that reduces type A behaviour and other behavioural risks has been shown to lower the incidence of recurrent infarction and cardiac death in patients with a previous myocardial infarction.⁽²⁵⁾

There has been recent attention to the type D personality construct.^{(26, 27)} D behaviour is characterized by inhibition of negative emotions and avoiding social contacts with others. D personality patients may be at increased risk for cardiovascular morbidity and mortality.⁽²⁶⁾ Cortisol may be a mediating factor for this increased risk. D personality predicts cardiac events after controlling for concurrent stress and anxiety.⁽²⁷⁾ Studies are needed to validate this personality construct, further define associations with cardiac outcome, and develop treatment approaches for patients with this personality style.

Asthma affects between 3 and 5 per cent of the population of the United States. The three hallmarks of the disease are airway inflammation, airway hyperresponsiveness, and a partially reversible airway obstruction. It is one of the classic ‘psychosomatic diseases’. Emotional arousal causes changes in airway tone. The severity of an asthma attack is highly correlated with presence of major depressive disorder, panic attacks, general anxiety, and level of fear among children, adolescents, and adults.⁽²⁸⁾ Asthma patients with psychiatric disorders have worse asthma control, more frequent exacerbations, and worse quality of life than asthma patients without psychiatric disorders.⁽²⁹⁾ Education, relaxation, biofeedback, and family therapy have each shown efficacy in the management of asthma.⁽³⁰⁾ Important in the management of asthma is education about the adverse effects of antiasthma medications, which include jitteriness, palpitations, and insomnia. These side effects may require treatment with behavioural and/or psychopharmacological therapies.

Patients with chronic obstructive pulmonary disease (COPD) have slowly progressive airway obstruction. The course of the disease is punctuated by exacerbations due to pulmonary infection, heart failure, and poor compliance with prescribed therapy. Generally affects middle-aged and older patients. They present with dyspnoea, exercise intolerance, cough, and sputum production. Physical examination reveals lung overinflation, prominent use of accessory muscles to augment respiration, diminished breath sounds, and diffuse wheezing. As with asthma, pharmacological treatments for COPD can cause psychiatric symptoms, especially higher doses of steroid medications. Patients with COPD must stop smoking; pulmonary function declines faster in smokers who develop COPD than non-smokers who develop COPD.

The chronic hypoxia caused by COPD compromises cognition and mood, which, in turn, can produce delirium, mood lability, mood disorders, and restriction in daily activities. Depression is present in 20-60 per cent of COPD patients.⁽³¹⁾ Depression adversely affects treatment adherence and may increase risk for poor outcomes. There is considerable evidence that supplemental oxygen improves cognitive function and quality of life.⁽³⁰⁾ Unfortunately, mood improvement with supplemental oxygen has not been conclusively demonstrated.

Panic attacks are reported in up to 38 per cent of patients with COPD.⁽³²⁾ Benzodiazepines, which are highly effective for controlling panic attacks, have limited usefulness in patients with COPD because they can suppress respiratory function and if used chronically result in tolerance and dependence. Carbon dioxide likely plays a role in promoting panic attacks; carbon dioxide levels increase with COPD disease progression. Antidepressants are useful in patients with COPD who develop panic attacks. Low-dose neuroleptic medications (e.g. 0.5-1.0 mg risperidone orally two to three times daily) are also sometimes used for severe fear and panic, especially in intensive care unit settings (e.g. when weaning the patient from a respirator). Neuroleptics do not directly suppress respiration, though caution must be exercised so that the sedation induced by neuroleptics— potentially combined with other sedating agents—does not reduce respiratory effort beyond that required to maintain adequate oxygenation. Function must also be monitored to ensure that neuroleptic use does not affect cardiac conduction or cause dysrhythmias.

Patients with psychiatric disorders, including bipolar disorder, anxiety disorder, and schizophrenia, are at increased risk for pulmonary embolism.⁽³³⁾ Embolism may account for a portion of the
excess risk of death among people with schizophrenia, even after controlling for blood pressure, cholesterol, body mass index, smoking, exercise, alcohol intake, and education level.⁽³⁴⁾ Most thromboemboli originate in the deep veins of the thigh. The diagnosis of pulmonary embolus is often missed because the clinical findings are non-specific. They include dyspnoea, pleuritic chest pain, haemoptysis, tachypnoea, and wheezing or crackles on pulmonary examination. Number of factors predispose to pulmonary thromboemboli: cancer, stroke, myocardial infarction, congestive heart failure, sepsis, pregnancy, lower extremity fractures, major surgical procedures, polycythaemia vera, and paroxysmal nocturnal haemoglobinuria. Pulmonary emboli are treated with heparin and warfarin. Fibrinolytic drugs and acute embolectomy are used in certain situations. The differential diagnosis of sudden anxiety or a panic attack includes pulmonary embolus.

Apnoea is defined as the complete cessation of respiratory airflow for 10 or more seconds.⁽³⁵⁾ Apnoea can occur during any sleep stage, but is particularly likely to occur during the period of rapid eye movement sleep. It is important to remember that normal people have apnoeic episodes during sleep. When apnoeic events are frequent and prolonged, they lead to chronically disrupted sleep and excessive daytime somnolence. This defines the condition known as sleep apnoea. Sleep apnoea can be central, obstructive, or a mixture of the two. Central sleep apnoea is caused by an abnormal central drive to the respiratory muscles. Congestive heart failure is the most common cause, followed by neurological disorders involving the brainstem and respiratory centres. Obstructive sleep apnoea is more common; obesity is a major risk factor, but is not always present. Aside from disrupted sleep and daytime somnolence, associated symptoms include an inability to concentrate, depressed mood, irritability, and personality changes. The sleeping partner often sleeps in another room because of the individual’s very loud snoring, snorting, gasping, and restlessness. Treatment with continuous positive airway pressure is often effective. Patients should avoid sedatives and alcohol. If obese, they should lose weight.

Oesophageal dysmotility can be demonstrated in 30 per cent of patients with non-cardiac chest pain;⁽³⁶⁾ a significant number of non-cardiac chest pain patients lack any evidence of oesophageal reflux and have reduced perception thresholds for pain. Cases of oesophageal dysmotility often lead to psychiatric consultation. Situational stress has not been conclusively linked to oesophageal dysmotility, but major psychiatric illness has.⁽³⁷⁾ The majority of patients with oesophageal motility disorders have an Axis I psychiatric illness, especially major depressive disorder (52 per cent), generalized anxiety disorder (36 per cent), somatization disorder (20 per cent), and substance-related disorders (20 per cent).⁽³⁸⁾ Smooth muscle relaxants, such as calcium-channel blockers, are superior to psychiatric treatments in improving physiological measures (such as oesophageal motility testing), antidepressants, and behavioural therapies produce more impressive changes in patients’ subjective oesophageal complaints and level of psychological well-being.⁽³⁹⁾

Irritable bowel syndrome (IBS) ranks second only to the common cold as a cause of absenteeism from work,^{(40, 41)} affecting between 8 and 17 per cent of the general population in the United States.⁽⁴⁰⁾ Symptoms include abdominal pain (relieved by defecation), and various forms of disturbed defecation such as altered stool frequency, altered stool form, altered stool passage, passage of mucus, and bloating. Symptoms must be continuous or recur within 3 months to meet the criteria for a diagnosis of irritable bowel syndrome. The severity of this syndrome frequently correlates with periods of emotional stress; the sympathetic nervous system inhibits gastric motility.

The enteric nervous system contains approximately 100 million neurons, close to the same number found in the spinal cord,⁽⁴¹⁾ and more than those distributed to any other organ or physiological system. It therefore, makes sense that the gastrointestinal tract is uniquely sensitive to the neurophysiological aspects of the stress response. With IBS who seek medical care exhibit high rates of psychiatric disorders. The most frequently occurring are panic disorder (26 per cent), generalized anxiety disorder (26 per cent), social phobia (26 per cent), and major depressive disorder (23 per cent).⁽⁴²⁾ Patients with irritable bowel syndrome who are depressed and complain of diarrhoea may benefit from tricyclic antidepressant treatment, at least partially because of their anticholinergic effects. Anxious patients may also benefit from, and well-tolerate buspirone. At least one in eight IBS patients are offered an antidepressant,⁽⁴³⁾ though data suggest that antidepressants are more consistent in improving global measures than specific gastrointestinal symptoms. A group of patients with treatment-refractory irritable bowel syndrome—nearly half had no psychiatric disorder—more than 90 per cent benefited from low-dose antidepressant or antianxiety medications: 92 per cent of patients improved, and 56 per cent experienced complete remission of irritable bowel symptoms.

Inflammatory bowel disease is the collective term for patients who have ulcerative colitis or Crohn’s disease. The aetiology of inflammatory bowel disease is unknown, but it may involve immunological, infectious, or environmental factors.⁽⁴⁴⁾ The primary manifestations of acute ulcerative colitis are rectal bleeding, diarrhoea, urgency, fever, weight loss, and, sometimes, abdominal pain. Crohn’s disease presents with malaise, fever, abdominal pain, and frequently rectal bleeding. Surgical treatment (colectomy) cures ulcerative colitis but not Crohn’s disease. However, surgery is usually a last resort in ulcerative colitis.

Despite the strong beliefs of early psychosomatic theorists, there is no objective evidence that psychiatric disorders cause inflammatory bowel disease. However, patients with this disease and who have psychiatric disorders are more likely to have unexplained physical symptoms in other organ systems, more disability than patients with similar disease severity and no psychiatric disorder, and prior histories of physical and sexual abuse.⁽⁴⁵⁾ Exacerbations of inflammatory bowel disease symptoms are positively associated with major life events and major stressors.^(41,46) Stress-induced alterations in gastrointestinal inflammation may be mediated through changes in hypothalamic-pituitary-adrenal axis function and alterations in bacterial-mucosal interactions, and via mucosal mast cells and mediators such as corticotrophin releasing factor.⁽⁴⁷⁾ Treatment focuses on the identification and treatment of
psychiatric disorders, if found, and on stress management and quality of life issues. Walker et al.⁽⁴⁴⁾ treated inflammatory bowel disease patients who had major depression with an antidepressant and found marked improvement in depression and ability to function. Relaxation, stress management,^{(45, 48)} and hypnotherapy were found to reduce abdominal pain and diarrhoea.