making any diagnosis.
He pointed out that citizens of cities in particular
27
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Psychosomatic medicine has been a specific area of focus within the field of
psychiatry for more than 50 years. The term psychosomatic is derived from
the Greek words psyche (soul) and soma (body). The term literally refers to
how the mind affects the body. Unfortunately, it has come to be used, at
least by the lay public, to describe an individual with medical complaints
that have no physical cause and are “all in your head.” In part due to this
misconceptualization, the American Psychiatric Association’s (APA)
Diagnostic and Statistical Manual of Mental Disorders (DSM), in 1980,
deleted the nosological term psychophysiological (or psychosomatic)
disorders and replaced it with “Psychological Factors Affecting Physical
Conditions” in DSM-5. Nonetheless, the term continues to be used by
researchers and is in the title of major journals in the field (e.g.,
Psychosomatic Medicine, Psychosomatics, and Journal of Psychosomatic
Research). It is also used by the two major national organizations in the
field (the Academy of Psychosomatic Medicine and the American
Psychosomatic Society) as well as international organizations (e.g., the
European Association of Psychosomatic Medicine). In 2003, the American
Board of Medical Specialties and the American Board of Psychiatry and
Neurology approved the specialty of psychosomatic medicine. That
decision recognized the importance of the field and also brought the term
psychosomatic back into common use in the field.
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According to Hippocrates (460 to 370 BC), who selected from the Egyptian
and the Greek traditions, disease originated within the body and was due to
an imbalance in fluid matter. That imbalance could be related to or even
caused by a similar imbalance in the patient’s external environment.
Hippocrates warned the visiting doctor to consider the altitude, the wind
direction, the purity of water supply, and the season of the year before
environments would run to phlegmatic or sanguine temperaments as a
reflection of the city’s coldness or heat. Physical or fluid imbalance could be
caused by emotional upset, too. Hippocrates reported that fear produced
sweat and that shame brought on palpitations of the heart; he urged young
physicians to look at patients with kindly expressions and never with
impatience, because impatience could inhibit the return of health. He is
said to have cured a king of an intestinal lesion by analyzing a dream. It
was Hippocrates who wrote “in order to cure the human body, it is
necessary to have a knowledge of the whole of things.”
In Timaeus, Plato remarked that trouble in the soul could bring trouble
to the body, and, in Charmides, Plato quoted Socrates, who had himself
attributed the words to a Greek king: “As it is not proper to cure the eyes
without the head, nor the head without the body, so neither is it proper to
cure the body without the soul.” Aristotle (384 to 322 BC) observed that the
emotions of anger, fear, courage, and joy affect the body, and Areteus (first
century bc) pinpointed a disturbance of the emotions as one of the six major
causes of paralysis.
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As Edward Shorter discusses in detail in his history of psychosomatic
illness, ways of presenting illness have varied over history, since patients
unconsciously select symptoms that are thought to represent true somatic
illnesses. Prior to 1800, physicians did not conduct clinical evaluations and
could not distinguish somatic from psychogenic illness. As a result, the
diagnoses of hysteria and hypochondriasis could easily be made
erroneously in the presence of true medical illnesses and did not suggest
any specific disease presentations. According to Shorter, “cultural shaping”
of patients’ symptoms began in the middle of the 19th century with the
popular diagnosis of spinal irritation. That diagnosis was made when a
physician believed that spinal cord irritation caused symptoms, and the
patient complained of spine sensitivity as well as peripheral symptoms. As
was the case for previous explanations of illness, spinal irritation was either
an invalid diagnosis for true medical illness or a “code word” for
psychosomatic symptoms. The term “psychosomatic” was first used by
Johann Christian Heinroth in 1818.
In the mid-19th century, after much popularity in Europe and the
United States, the diagnosis of spinal irritation went out of favor. It was
replaced by “reflex neurosis” as an explanation for somatization. That
diagnosis was based on the view that any affected organ could cause
irritation in any other organ in the body. The conceptualization was based
on reflex theory, the notion that nervous connections throughout the body
regulate all bodily organs, independent of free will. The Berlin neurologist
Moritz Romberg was an influential proponent of the view that the uterus
was the cause of hysteria, a reflex neurosis. In this view, hysteria, which
encompassed globus hystericus, hysterical seizures, and other psychogenic
disorders, was due to irritation of the uterus and the ovaries. He believed
that male genitals could also cause hysteria, but that they do so less
commonly because they are less frequently irritated. In the late 19th
century, reflex theory was one of the leading models of nervous illness.
Since physicians promulgated the theory to their patients, it is not
surprising that they found many of their patients to be preoccupied with
their genital organs. Gynecologist August Rheinstadter of Cologne
commented skeptically in 1884:
But now, a true hysteromania, a Furor uterinus, has unfortunately arisen from the previous
reluctance of women to undergo a gynecological examination and from the indifference which
doctors once displayed towards gynecological disease. So that every woman who suffers from
migraine, stomach cramps, or palpitations believes herself to have a uterine illness and indeed
will find some physician willing to indulge her in the treatment of this presumed cause.
In the late 19th century, many physicians in Europe and the United
States believed that gynecologic problems produced hysteria and other
forms of mental illness. As a result, gynecologists performed surgery to
treat hysteria and insanity, including removal of healthy ovaries.
Widespread availability of gynecologic surgery in the United States also led
women to request such surgery to relieve psychosomatic symptoms. In his
history of psychosomatic illness, Shorter notes that some Americans’
“addiction to surgery” was due to practitioners convincing the public that
vague physical symptoms were due to reflex phenomena from peripheral
organs. The nose was the final organ addressed by reflex theory in the late
19th century. One of its chief proponents was Wilhelm Fliess, a Berlin
general practitioner, who greatly influenced Freud.
In the 19th century, hysterical fits were the most common form of
motor hysteria. There were two primary forms: catalepsy and uncontrolled
motor activity such as thrashing about. The psychiatrist Pierre Briquet
described over 400 women with hysterical conversion disorders whom he
had evaluated at the Pitie Hospital in Paris from 1849 to 1859. Many had
multiple unexplained somatic complaints; the diagnosis of Briquet
syndrome ultimately developed into the diagnosis of somatization disorder
and is most similar to the current DSM-5 diagnosis of somatic symptom
disorder.
Hysterical paralysis, often due to stressful life events, was apparently
quite common through the 19th and early 20th centuries. Louis Verhaeghe,
a spa physician in Belgium, wrote in 1850:
How often do we see patients with paralyzed arms, legs, the side of the face or even a more
limited area such as one or two fingers, problems attributable to an unequal distribution of
nervous fluid. It is individuals of a pronounced nervous temperament, subject to hysterical fits,
somnambules, persons subject to shameful habits or who abuse the pleasures of love, who are
most likely to experience these paralyses.
Astasia-abasia was also seen frequently; Silas Wier Mitchell in
Philadelphia referred to it as “hysterical motor ataxia.” One of the most
prominent physicians of the late 19th century, Jean-Martin Charcot
promulgated a highly influential theory of hysteria. He believed that it was
a chronic inherited functional disease of the nervous system. “In the
[hysterical] fit,” he said in 1882, “nothing is left to chance, that to the
contrary everything unfolds according to the rules, which are always the
same and characterize what we see in our outpatients as well as inpatients;
they are valid for all countries, for all epochs, for all races, and are, in short,
universal.” Although his conception of hysteria was widely disseminated,
some physicians who were aware of his ability to suggest symptoms to
vulnerable patients were dubious of his theory. The Swiss neurologist Paul
Dubois wrote in 1904: “Endowed with the spirit of authority,
[Charcot] . . . suggested to them their attitudes and their gestures. Example
is contagious even in sickness, and in the great hospitals of Paris, at La
Salpetriere, all cases of hysteria resemble each other. At the command of
the chief of the staff, or of the interns, they begin to act like marionettes, or
like circus horses accustomed to repeat the same evolutions.” It was not
until near the end of his life that Charcot’s theories became more
psychologically focused.
Within a decade after he died in 1893, Charcot hysteria had virtually
disappeared. Many physicians began to believe that some of his patients
most likely had organic illness. Joseph Babinski’s discovery in 1896 of the
Babinski sign was extremely helpful in distinguishing organic disease from
hysteria. In 1901, he put forward a new conceptualization of hysteria: It was
defined as any symptom that could be induced by suggestion and
eliminated by persuasion.
As the reflex model faded in prominence in the late 19th century, the
most dominant model became one in which central nervous disease was
held responsible for nervous symptoms. In the early 20th century,
psychological theories of somatization became popular, but they became
dominant only in the latter half of the 20th century. “Neurasthenia,” or
tired nerves, was a new diagnosis at the end of the 19th century that was
brought to prominence by George Beard, a New York electrotherapist. A
term applied broadly, the diagnosis encompassed depression, anxiety,
somatization, male hysteria, and chronic fatigue. Wilhelm Stekel, a
Viennese psychoanalyst, coined the term “somatization” in the 1920s.
Sigmund Freud was the principal theoretician to bring psyche and soma
back together. He demonstrated the importance of the emotions in
producing mental disturbances and somatic disorders. His early
psychoanalytic formulations detailed the role of psychic determinism in
somatic conversion reactions. Picking up where the Greeks and Romans
had left off, Freud redignified the study of the emotions as a separate study
and pointed to their relationship with the soma in the new field of
psychiatry. Using Freud’s insight, a number of workers in the early decades
of the 20th century tried to expand the understanding of the
interrelationship of psyche and soma. The influence on adult organ tissue
of various unresolved pregenital impulses was proposed by Karl Abraham
in 1927, the application of the idea of conversion reaction to organs under
the control of the autonomic nervous systems was described by Sandor
Ferenczi in 1926, and the attaching of a symbolic meaning to fever and
hemorrhage was suggested by George Groddeck in 1929.
In the 20th century, somatization symptoms changed from
predominantly neurologic (e.g., hysterical paralysis) to other symptoms
such as fatigue and chronic pain. Edward Shorter attributes this change to
three causes: (1) improvements in medical diagnostic techniques made it
easier to rule out organic causes for neurologic disease; (2) the central
nervous system (CNS) paradigm faded; and (3) social roles changed (e.g.,
the disappearance of the historical notion that “weak” women would be
expected to have fainting spells and paralysis).
Although hysterical neurologic symptoms have remained relatively less
common in the 21st century, CNS explanations of chronic pain and fatigue
are gaining prominence. For example, functional brain research has
demonstrated brain dysfunction and possibly genetic contributions among
some individuals with fibromyalgia and chronic fatigue syndrome. Those
syndromes, while still thought by some to represent somatization variants,
are currently established medical diagnoses.
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Since the mid-20th century, research in psychosomatic medicine and
consultation-liaison psychiatry has taken two interconnected paths.
Psychosomatic medicine research has generally focused on understanding
psychophysiologic mechanisms underlying mind–body relationships.
Consultation-liaison research, however, has largely been directed at
understanding psychiatric problems among clinical populations with
medical illnesses.
In the early 20th century, two theoretical trends developed, one
suggesting that specific emotions led to specific cell and tissue damage, and
the second that generalized anxiety created the preconditions for a number
of not-necessarily predetermined diseases. Cases of shell shock during
World War I and new endocrine studies provided observations for the swell
of interest in theory evidenced in the 1930s.
In the early 1930s, Franz Alexander, who had left Berlin to move to
Chicago where he founded the Chicago Institute for Psychoanalysis,
described how he believed specific psychological conflicts caused specific
somatoform symptoms. Alexander saw conflict as a stress and suggested
that, when conflict presents itself, the individual may suppress the stress
and produce, through the voluntary nervous system, a reaction such as the
conversion reaction described by Freud. However, after suppressing stress,
the individual may, through the autonomic system, keep his or her
sympathetic responses alert for heightened aggression or flight or
parasympathetic responses alerted for heightened vegetative activity.
According to these theories, prolonged alertness and tension can produce
physiological disorders and eventual pathology of visceral organs.
For instance, Alexander postulated that, in a passive-dependent person
without someone to satisfy his or her dependence, stress is created. That
particular stress may stimulate and keep alert the parasympathetic nervous
system, which means that too much gastric acid is secreted, and gastric
hypermotility results, all of which may lead to a peptic ulcer. Another
dependent person with a different genetic set may, in repressing conflict,
stimulate parasympathetic overfunctioning through pathways leading to
colitis or asthma. Still other dependent persons, in seeking to move beyond
dependency, incorporate the stress; such a move entails overstimulation of
the sympathetic system, and the resulting chronic alertness produces
migraine, hypertension, or arthritis.
Although there were multiple case reports supporting Alexander’s
views, it has not been demonstrated that the same specific conflicts are
present in all cases of the same disease. Early methodologically flawed
reports were rooted in psychoanalytic explanations of “psychosomatic”
illnesses. This work had numerous problems, including selection bias,
small sample size, and lack of control groups.
A number of investigators developed the pathway concept of
constellations into other theories involving the whole personality. In 1954,
Flanders Dunbar proposed that the ambitious, hard-driving man would be
prone to coronary occlusion. That personality type is similar to the
competitive, restless, time-haunted, and coronary-bound type A person
proposed by M. Friedman and R. H. Rosenman in 1959. Modern research
has supported the notion that hostility, one component of type A
personality, is a risk factor for the development of coronary artery disease.
A second trend in psychosomatic medicine that began in the middle of
the 20th century has been to investigate what happens to a person in a
nonspecific way when faced with stress. In the 1950s, Harold Wolff and
Stewart Wolf observed that chronic hyperfunction or chronic hypofunction
in the vascular and secretory activities of the mucosa of the gastrointestinal
(GI) and respiratory systems can produce pathology. Overfunctioning of
the mucosa was correlated with hostility, and underfunctioning was
correlated with fear or sadness. The patient’s entire reactive patterning and
his or her life history account for whether he or she reacts to stress by
hyperfunctioning or hypofunctioning.
Other workers in the nonspecific group described various possible
mechanisms by which psychologically induced stress may cause organic
disease in humans and animals. In 1950, Hans Selye thought that the
hypophyseal–adrenocortical axis responded to various types of physical
and psychic stress with hormonal changes that can ultimately cause a
variety of organic diseases, such as rheumatoid arthritis and peptic ulcer.
Selye viewed such diseases as a by-product of the body’s attempt to adapt
to stress from any source.
Experimental psychologists with a learning theory conception of
behavior studied the effects of chronic unrelieved anxiety in humans and
animals and found that gastric hydrochloric acid production increases
under such circumstances. Because such acidity is a precursor of peptic
ulcer, they concluded that chronic anxiety is the variable intervening
between the behavioral and physical events involved in psychosomatic
illness. Modern research does continue to support the role of emotional
factors in peptic ulcer disease (e.g., the work of Levenstein [see below]),
indicating that anxiety leads to poorer ulcer healing.
Beginning in the late 1960s, T. H. Holmes and R. H. Rahe showed that
life crises often precede illness and that there is some correlation between
the intensity of the crisis and the severity of the illness that follows; the
crisis ranked as the most intense by subjects was the death of a spouse.
Other works suggested a giving-up–given-up complex, in which individuals
feel powerless to change their environments or themselves and eventually
lose the will to try, becoming mentally or physically ill, perhaps because of
changes in the immunological and neuroendocrine systems.
As exemplified by the long history of psychosomatic research in pain
and GI disease, the quality of research in the field has evolved significantly
over the past 70 years. Early research efforts were psychoanalytically
oriented case studies of conditions such as ulcerative colitis. Such research
often led to invalid conclusions. For example, one report by A. Johnson and
colleagues in 1947 of a series of 33 patients with rheumatoid arthritis led to
the preliminary conclusion that women with this disorder have “a chronic
inhibited hostile aggressive state as a reaction to the earliest masochistic
dependence on the mother that is carried over to the father and all human
relationships, including the sexual.” Nonetheless, even those authors were
aware of potential methodological limitations of their work: “but these
factors . . . are found so commonly in patients who do not suffer from
arthritis that additional etiologic factors, still unknown, must be
postulated.”
In the mid-20th century, research on the classic psychosomatic illnesses
such as rheumatoid arthritis and peptic ulcer disease used projective
testing such as the Rorschach to identify specific personality traits. Later
studies used structured clinical interviews and objective instruments such
as the Minnesota Multiphasic Personality Inventory (MMPI). In one
leading journal in the field, Psychosomatic Medicine, psychosomatic
research on upper GI syndromes has changed its focus over the past 70
years. For example, psychodynamic and personality research peaked in the
mid-20th century. However, research on stress and interactions between
psychological and medical factors have remained at fairly steady levels over
that time period.
Psychophysiological research began in the first half of the 20th century.
Researchers used techniques such as electromyogram (EMG),
electroencephalogram (EEG), and galvanic skin response to examine
physiologic parameters among individuals with a variety of psychosomatic
illnesses. Research has evolved to the present day to include areas such as
heart rate variability and stress, and the role of the CNS in illnesses such as
fibromyalgia and chronic fatigue syndrome. Pain treatment research has
evolved from less-controlled studies to randomized-controlled studies.
As early as the 1960s, researchers reported on the prevalence of various
psychiatric problems in inpatient and outpatient medical settings.
Methodological variability led to wide variation in estimates of
comorbidity. Early work also reported on the characteristics of patients
referred for psychiatric consultation. R. J. Kahana’s and G. L. Bibring’s
classic work in 1964 emphasized the importance of understanding
personality types to the effective treatment of one’s patients.
Consultation-liaison psychiatry research in the mid-20th century also
elucidated the most common reasons for psychiatric consultation. While
many of those reasons hold true to this day, psychoanalytic influences on
physician consulting behavior have clearly waned in recent years. Consider
Zbigniew Lipowski’s summary in 1967 of the two most common diagnostic
questions asked of the consulting psychiatrist:
1. Is this particular bodily complaint (or set of complaints) explicable as an
expression of psychological ill health, that is, is it partly or wholly
psychogenic?
2. Is the inner experience of psychic change reported by the patient or his
observable behavior explicable as the direct results of, or a psychological
reaction to, organic disease?
However, reasons for requests for assistance in patient management
have seemingly changed very little since Lipowski summarized them in
1967, and will be familiar to all currently practicing psychosomatic
medicine psychiatrists:
1. Suicidal attempt or threat
2. Grossly disturbed behavior, for example, delirium and psychosis
3. Excessive emotional reactions, for example, depression and anger
4. Refusal to cooperate
5. Delayed convalescence
6. Conflict between patient and personnel
7. Patient with psychiatric history
8. Psychiatric side effects of drugs
9. Selection and/or preparation of patients, for example, for surgery
0. Disposition
Although such epidemiologic work has been useful for educational and
staffing purposes, it did not contribute significantly to the advancement of
understanding of mind–body relationships (Table 27.1–1).
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ƚLJƉĞ͘
WĞƚĞƌ^ŝĨŶĞŽƐ͕:ŽŚŶ͘EĞŵŝĂŚ;ϭϵϳϬͿ͗ůĂďŽƌĂƚĞĚƚŚĞĐŽŶĐĞƉƚŽĨĂůĞdžŝƚŚLJŵŝĂ͘ĞǀĞůŽƉŵĞŶƚĂů
ĂƌƌĞƐƚƐŝŶƚŚĞĐĂƉĂĐŝƚLJƚŽŝĚĞŶƚŝĨLJĂŶĚĞdžƉƌĞƐƐĐŽŶĨůŝĐƚͲƌĞůĂƚĞĚĂĨĨĞĐƚƌĞƐƵůƚŝŶƉƐLJĐŚŽƐŽŵĂƚŝĐ
ƐLJŵƉƚŽŵĨŽƌŵĂƚŝŽŶ͘ŽŶĐĞƉƚŽĨ͞ĂůĞdžŝƚŚLJŵŝĂ͟ŵŽĚŝĨŝĞĚůĂƚĞƌďLJ^ƚŽƵĚĞŵŝƌĞ͕ǁŚŽĂĚǀŽĐĂƚĞĚƚŚĞ
ƚĞƌŵ͞ƐŽŵĂƚŽƚŚLJŵŝĂ͟ƚŚĂƚĞŵƉŚĂƐŝnjĞĚĐƵůƚƵƌĂůŝŶĨůƵĞŶĐĞƐŽŶƵƐĞŽĨƐŽŵĂƚŝĐůĂŶŐƵĂŐĞĂŶĚ
ƐŽŵĂƚŝĐƐLJŵƉƚŽŵƐƚŽĞdžƉƌĞƐƐĂĨĨĞĐƚŝǀĞĚŝƐƚƌĞƐƐ͘
//͘ WƐLJĐŚŽƉŚLJƐŝŽůŽŐŝĐĂů
tĂůƚĞƌĂŶŶŽŶ;ϭϵϮϳͿ͗ĞŵŽŶƐƚƌĂƚĞĚƚŚĞƉŚLJƐŝŽůŽŐŝĐĂůĐŽŶĐŽŵŝƚĂŶƚƐŽĨƐŽŵĞĞŵŽƚŝŽŶƐĂŶĚƚŚĞ
ŝŵƉŽƌƚĂŶƚƌŽůĞŽĨƚŚĞĂƵƚŽŶŽŵŝĐŶĞƌǀŽƵƐƐLJƐƚĞŵŝŶƉƌŽĚƵĐŝŶŐƚŚŽƐĞƌĞĂĐƚŝŽŶƐ͘dŚĞĐŽŶĐĞƉƚŝƐ
ďĂƐĞĚŽŶWĂǀůŽǀŝĂŶďĞŚĂǀŝŽƌĂůĞdžƉĞƌŝŵĞŶƚĂůĚĞƐŝŐŶƐ͘
,ĂƌŽůĚtŽůĨĨ;ϭϵϰϯͿ͗ƚƚĞŵƉƚĞĚƚŽĐŽƌƌĞůĂƚĞůŝĨĞƐƚƌĞƐƐƚŽƉŚLJƐŝŽůŽŐŝĐĂůƌĞƐƉŽŶƐĞ͕ƵƐŝŶŐŽďũĞĐƚŝǀĞ
ůĂďŽƌĂƚŽƌLJƚĞƐƚƐ͘WŚLJƐŝŽůŽŐŝĐĂůĐŚĂŶŐĞ͕ŝĨƉƌŽůŽŶŐĞĚ͕ŵĂLJůĞĂĚƚŽƐƚƌƵĐƚƵƌĂůĐŚĂŶŐĞ͘,Ğ
ĞƐƚĂďůŝƐŚĞĚƚŚĞďĂƐŝĐƌĞƐĞĂƌĐŚƉĂƌĂĚŝŐŵĨŽƌƚŚĞĨŝĞůĚƐŽĨƉƐLJĐŚŽŝŵŵƵŶŽůŽŐLJ͕ƉƐLJĐŚŽĐĂƌĚŝŽůŽŐLJ͕
ĂŶĚƉƐLJĐŚŽŶĞƵƌŽĞŶĚŽĐƌŝŶŽůŽŐLJ͘
,ĂŶƐ^ĞůLJĞ;ϭϵϰϱͿ͗hŶĚĞƌƐƚƌĞƐƐĂŐĞŶĞƌĂůĂĚĂƉƚĂƚŝŽŶƐLJŶĚƌŽŵĞĚĞǀĞůŽƉƐ͘ĚƌĞŶĂůĐŽƌƚŝĐĂů
ŚŽƌŵŽŶĞƐĂƌĞƌĞƐƉŽŶƐŝďůĞĨŽƌƚŚĞƉŚLJƐŝŽůŽŐŝĐĂůƌĞĂĐƚŝŽŶ͘
DĞLJĞƌ&ƌŝĞĚŵĂŶ;ϭϵϱϵͿ͗dŚĞŽƌLJŽĨƚLJƉĞƉĞƌƐŽŶĂůŝƚLJĂƐĂƌŝƐŬĨĂĐƚŽƌĨŽƌĐĂƌĚŝŽǀĂƐĐƵůĂƌĚŝƐĞĂƐĞ͘
dŚĞďĂƐŝĐĐŽŶĐĞƉƚǁĂƐŝŶƚƌŽĚƵĐĞĚďLJ,ĞůĞŶ&ůĂŶĚĞƌƐƵŶďĂƌĂƐĞĂƌůLJĂƐϭϵϯϲ͘
ZŽďĞƌƚĚĞƌ;ϮϬϬϳͿ͗ĞŐŝŶŶŝŶŐŝŶƚŚĞϭϵϳϬƐ͕ĞƐƚĂďůŝƐŚĞĚƚŚĞďĂƐŝĐĐŽŶĐĞƉƚƐĂŶĚƚŚĞƌĞƐĞĂƌĐŚ
ŵĞƚŚŽĚƐĨŽƌƚŚĞĨŝĞůĚŽĨƉƐLJĐŚŽŶĞƵƌŽŝŵŵƵŶŽůŽŐLJ͘
///͘ ^ŽĐŝŽĐƵůƚƵƌĂů
<ĂƌĞŶ,ŽƌŶĞLJ;ϭϵϯϵͿ͕:ĂŵĞƐ,ĂůůŝĚĂLJ;ϭϵϰϴͿ͗ŵƉŚĂƐŝnjĞĚƚŚĞŝŶĨůƵĞŶĐĞŽĨĐƵůƚƵƌĞŝŶƚŚĞ
ĚĞǀĞůŽƉŵĞŶƚŽĨƉƐLJĐŚŽƐŽŵĂƚŝĐŝůůŶĞƐƐ͘dŚĞLJƚŚŽƵŐŚƚƚŚĂƚĐƵůƚƵƌĞŝŶĨůƵĞŶĐĞƐƚŚĞŵŽƚŚĞƌ͕ǁŚŽ͕ŝŶ
ƚƵƌŶ͕ĂĨĨĞĐƚƐƚŚĞĐŚŝůĚƚŚƌŽƵŐŚŚĞƌƌĞůĂƚŝŽŶƐŚŝƉǁŝƚŚƚŚĞĐŚŝůĚͶĞ͘Ő͕͘ŶƵƌƐŝŶŐ͕ĐŚŝůĚƌĞĂƌŝŶŐ͕ĂŶĚ
ĂŶdžŝĞƚLJƚƌĂŶƐŵŝƐƐŝŽŶ͘
dŚŽŵĂƐ,ŽůŵĞƐ͕ZŝĐŚĂƌĚZĂŚĞ;ϭϵϳϱͿ͗ŽƌƌĞůĂƚĞĚƚŚĞƐĞǀĞƌŝƚLJĂŶĚƚŚĞŶƵŵďĞƌŽĨƌĞĐĞŶƚƐƚƌĞƐƐĨƵů
ůŝĨĞĞǀĞŶƚƐǁŝƚŚƚŚĞůŝŬĞůŝŚŽŽĚŽĨĚŝƐĞĂƐĞ͘
/s͘ ^LJƐƚĞŵƐƚŚĞŽƌLJ
ĚŽůƉŚDĞLJĞƌ;ϭϵϱϴͿ͗&ŽƌŵƵůĂƚĞĚƚŚĞƉƐLJĐŚŽďŝŽůŽŐŝĐĂůĂƉƉƌŽĂĐŚƚŽƉĂƚŝĞŶƚĂƐƐĞƐƐŵĞŶƚƚŚĂƚ
ĞŵƉŚĂƐŝnjĞƐƚŚĞŝŶƚĞŐƌĂƚĞĚĂƐƐĞƐƐŵĞŶƚŽĨĚĞǀĞůŽƉŵĞŶƚĂů͕ƉƐLJĐŚŽůŽŐŝĐĂů͕ƐŽĐŝĂů͕ĞŶǀŝƌŽŶŵĞŶƚĂů͕
ĂŶĚďŝŽůŽŐŝĐĂůĂƐƉĞĐƚƐŽĨƚŚĞƉĂƚŝĞŶƚ͛ƐĐŽŶĚŝƚŝŽŶ͘ĂƐŝĐĐŽŶĐĞƉƚŽĨƚŚĞďŝŽƉƐLJĐŚŽƐŽĐŝĂůŵŽĚĞůŝƐ
ŝŵƉůŝĐŝƚŝŶŚŝƐĂƉƉƌŽĂĐŚ͘
ďŝŐŶŝĞǁ>ŝƉŽǁƐŬŝ;ϭϵϳϬͿ͗ƚŽƚĂůĂƉƉƌŽĂĐŚƚŽƉƐLJĐŚŽƐŽŵĂƚŝĐĚŝƐĞĂƐĞŝƐŶĞĐĞƐƐĂƌLJ͘džƚĞƌŶĂů
;ĞĐŽůŽŐŝĐĂů͕ŝŶĨĞĐƚŝŽƵƐ͕ĐƵůƚƵƌĂů͕ĞŶǀŝƌŽŶŵĞŶƚĂůͿ͕ŝŶƚĞƌŶĂů;ĞŵŽƚŝŽŶĂůͿ͕ŐĞŶĞƚŝĐ͕ƐŽŵĂƚŝĐ͕ĂŶĚ
ĐŽŶƐƚŝƚƵƚŝŽŶĂůĨĂĐƚŽƌƐĂƐǁĞůůĂƐƉĂƐƚĂŶĚƉƌĞƐĞŶƚŚŝƐƚŽƌLJĂƌĞŝŵƉŽƌƚĂŶƚĂŶĚƐŚŽƵůĚďĞƐƚƵĚŝĞĚďLJ
ŝŶǀĞƐƚŝŐĂƚŽƌƐǁŽƌŬŝŶŐŝŶƚŚĞǀĂƌŝŽƵƐĨŝĞůĚƐŝŶǁŚŝĐŚƚŚĞLJĂƌĞƚƌĂŝŶĞĚ͘
'ĞŽƌŐĞŶŐĞů;ϭϵϳϳͿ͗ŽŝŶĞĚƚŚĞƚĞƌŵ͞ďŝŽƉƐLJĐŚŽƐŽĐŝĂů͟ĚĞƌŝǀĞĚĨƌŽŵŐĞŶĞƌĂůƐLJƐƚĞŵƐƚŚĞŽƌLJĂŶĚ
ďĂƐĞĚŽŶĐŽŶĐĞƉƚƵĂůŝĚĞĂƐŝŶƚƌŽĚƵĐĞĚŵƵĐŚĞĂƌůŝĞƌďLJůĞdžĂŶĚĞƌĂŶĚDĞLJĞƌ͘
>ĞŽŶŝƐĞŶďĞƌŐ;ϭϵϵϱͿ͗ŽŶƚĞŵƉŽƌĂƌLJƉƐLJĐŚŝĂƚƌŝĐƌĞƐĞĂƌĐŚĚĞŵŽŶƐƚƌĂƚĞƐƚŚĂƚƚŚĞŵŝŶĚʹďƌĂŝŶ
ƌĞƐƉŽŶĚƐƚŽďŝŽůŽŐŝĐĂůĂŶĚƐŽĐŝĂůǀĞĐƚŽƌƐǁŚŝůĞďĞŝŶŐũŽŝŶƚůLJĐŽŶƐƚƌƵĐƚĞĚŽĨďŽƚŚ͘DĂũŽƌďƌĂŝŶ
ƉĂƚŚǁĂLJƐĂƌĞƐƉĞĐŝĨŝĞĚŝŶƚŚĞŐĞŶŽŵĞ͖ĚĞƚĂŝůĞĚĐŽŶŶĞĐƚŝŽŶƐĂƌĞĨĂƐŚŝŽŶĞĚďLJ͕ĂŶĚĐŽŶƐĞƋƵĞŶƚůLJ
ƌĞĨůĞĐƚ͕ƐŽĐŝĂůůLJŵĞĚŝĂƚĞĚĞdžƉĞƌŝĞŶĐĞŝŶƚŚĞǁŽƌůĚ͘
hZZEddZE^
The practice of psychosomatic medicine has evolved considerably since its
early clinical origins and has come to focus on psychiatric illnesses that
occur in the setting of physical health care. In large part this evolution has
occurred as a result of the increased complexity of medicine, the increased
understanding of the relationship of medical illness to psychiatric illness,
and the greater appreciation of mind and body as one. A key outcome of
this has been the granting of subspecialty status for psychosomatic
medicine. Clinical care is now delivered in a variety of health care settings
and utilizes an ever expanding set of diagnostic tools as well as many
effective somatic and psychotherapeutic interventions. Research in the area
has progressed to include a greater understanding of the relationship
between chronic medical conditions and psychiatric disorders and has
examined the pathophysiologic relationships, the epidemiology of
comorbid medical and psychiatric disorders, and the role that specific
interventions play in physiologic, clinical, and economic outcomes.
The extent of the burden caused by co-occurring mental and physical
disorders represents a tremendous public health problem. This was
highlighted by the report from U.S. President George W. Bush’s New
Freedom Commission, Achieving the Promise: Transforming Mental
Health Care in America, which called for closer coordination of the
medical and mental health systems. Further, the Institute of Medicine
(IOM) study, Quality of Healthcare for Mental and Substance Use
Disorders (2005), states: “there is no health care without mental health
care.” There has been increasing awareness that mental disorders may be
both risk factors for and poor prognostic indicators in chronic medical
illnesses such as cardiovascular disease, diabetes, and cancer.
Psychiatric morbidity is very common in patients with medical
conditions, with a prevalence ranging from approximately 20 to 65 percent,
depending on the illness. Patients in the general hospital have the highest
rate of psychiatric disorders when compared to community samples or
patients in ambulatory primary care. For example, compared to community
samples, depressive disorders in the general hospital are more than twice
as common, and substance abuse is two to three times as common.
Delirium occurs in approximately 20 percent of inpatients. Psychiatric
morbidity has serious effects on medically ill patients and is often a risk
factor for exacerbation of their medical conditions. It is well established
that depression is both a risk factor and a poor prognostic indicator in
coronary artery disease. Psychiatric illness worsens cardiac morbidity and
mortality in patients with a history of myocardial infarction, diminishes
glycemic control in patients with diabetes, and decreases return to
functioning in patients experiencing a stroke. Depressive and anxiety
disorders compound the disability associated with stroke. In the context of
neurodegenerative disease such as Parkinson disease or Alzheimer disease,
depression, psychosis, and behavioral disturbances are significant
predictors of functional decline, institutionalization, and caregiver burden.
Hospitalized patients with delirium are significantly less likely to improve
in function compared to patients without delirium. Delirium is associated
with worse outcomes after surgery, even after controlling for severity of
medical illness.
In addition, depression and other mental disorders significantly impact
quality of life and the ability of patients to adhere to treatment regimens
(e.g., in patients with diabetes mellitus). Psychiatric disorders are linked to
nonadherence with antiretroviral therapy, adversely affecting the survival
of human immunodeficiency virus (HIV)-infected patients, and they
worsen the prognosis and quality of life of cancer patients. Finally, they are
linked to nonadherence with safe sex guidelines and with use of sterile
needles in HIV-infected injection drug users, thus having major public
health implications.
Failure to identify, evaluate, diagnose, treat, or achieve symptom
resolution of psychiatric morbidity in medical care settings results in
significantly increased service utilization. For example, depression,
dementia, and delirium are associated with higher utilization of medical
care, both in the hospital (longer lengths of stay) and after discharge. When
delirium is unrecognized and untreated in the hospital, it may result in
unnecessary placement in nursing homes instead of discharge to home.
Untreated depression is associated with higher medical utilization after
hospital discharge and with higher mortality and morbidity in coronary
disease, hypertension, diabetes, and stroke.
d,>/E/>WZd/K&W^z,K^KDd/D//E DĞĚŝĐĂůĐŽŵƉůŝĐĂƚŝŽŶƐŽĨ
The primary objective for psychosomatic medicine is the diagnosis and
treatment of psychiatric disorders in patients with complex medical
conditions. Thus, psychosomatic medicine focuses on a variety of clinical
problems that occur in patients being treated in medical settings, including
primary psychiatric disorders such as delirium and dementia, which occur
as a result of a medical condition; anxiety or depression, which occur in the
setting of chronic medical conditions but may also be due to medical
causes; and somatic symptom disorders (formerly somatoform disorders).
In addition to the care of specific conditions, psychosomatic medicine also
encompasses a variety of other clinical activities that occur in the medical
setting, including evaluation of decision-making capacity, attention to
quality of life and symptom management in chronic and terminally ill
individuals, provision of liaison services to medical staff, and assistance
with management of primary psychiatric conditions such as bipolar
disorder or schizophrenia. Table 27.1–2 summarizes the types of clinical
problems addressed in psychosomatic medicine.
Psychosomatic medicine is practiced in a variety of settings and
encompasses a combination of consultative, treatment, and liaison
activities. Historically, the majority of this work occurred within the
general hospital setting. Largely this has been due to the fact that the
greatest risk factor for requiring psychiatric intervention has been the
severity of the medical illness. However, as more illnesses become chronic
in nature (e.g., cancer and HIV), there has been an increase in delivery of
psychosomatic medicine services in outpatient settings as well. Regardless
of where care is delivered, the basic approaches are similar: To conduct a
psychiatric assessment, provide psychotherapeutic, behavioral, or
pharmacologic interventions to patients, and to work closely with other
medical professionals in a liaison capacity.
dĂďůĞϮϳ͘ϭʹϮ͘
^ƵŵŵĂƌLJŽĨůŝŶŝĐĂůWƌŽďůĞŵƐŝŶWƐLJĐŚŽƐŽŵĂƚŝĐDĞĚŝĐŝŶĞ
dLJƉĞŽĨůŝŶŝĐĂůWƌŽďůĞŵ džĂŵƉůĞ
WƐLJĐŚŝĂƚƌŝĐƐLJŵƉƚŽŵƐ ĞůŝƌŝƵŵ͕ĚĞŵĞŶƚŝĂ
ƐĞĐŽŶĚĂƌLJƚŽĂŵĞĚŝĐĂů
ĐŽŶĚŝƚŝŽŶ
WƐLJĐŚŝĂƚƌŝĐƐLJŵƉƚŽŵƐĂƐĂ ŶdžŝĞƚLJƌĞůĂƚĞĚƚŽĐŚĞŵŽƚŚĞƌĂƉLJ͕ĚĞƉƌĞƐƐŝŽŶƌĞůĂƚĞĚƚŽůŝŵď
ƌĞĂĐƚŝŽŶƚŽŵĞĚŝĐĂů ĂŵƉƵƚĂƚŝŽŶ
ĐŽŶĚŝƚŝŽŶŽƌƚƌĞĂƚŵĞŶƚƐ
WƐLJĐŚŝĂƚƌŝĐĐŽŵƉůŝĐĂƚŝŽŶƐŽĨ ĞƉƌĞƐƐŝŽŶƐĞĐŽŶĚĂƌLJƚŽŝŶƚĞƌĨĞƌŽŶƚƌĞĂƚŵĞŶƚ
ŵĞĚŝĐĂůĐŽŶĚŝƚŝŽŶƐĂŶĚ
ƚƌĞĂƚŵĞŶƚƐ
WƐLJĐŚŽůŽŐŝĐĂůĨĂĐƚŽƌƐ ^ŽŵĂƚŝĐƐLJŵƉƚŽŵĚŝƐŽƌĚĞƌƐ
ĐŽŶƚƌŝďƵƚŝŶŐƚŽŵĞĚŝĐĂů
ƐLJŵƉƚŽŵƐ
EĞƵƌŽůĞƉƚŝĐŵĂůŝŐŶĂŶƚƐLJŶĚƌŽŵĞ͕ĂĐƵƚĞǁŝƚŚĚƌĂǁĂůĨƌŽŵĂůĐŽŚŽůŽƌ
ƉƐLJĐŚŝĂƚƌŝĐĐŽŶĚŝƚŝŽŶƐŽƌ ŽƚŚĞƌƐƵďƐƚĂŶĐĞ
ƚƌĞĂƚŵĞŶƚ
ŽͲŽĐĐƵƌƌŝŶŐŵĞĚŝĐĂůĂŶĚ ZĞĐƵƌƌĞŶĐĞŽĨĚĞƉƌĞƐƐŝǀĞĚŝƐŽƌĚĞƌŝŶƐĞƚƚŝŶŐŽĨĐĂŶĐĞƌƚƌĞĂƚŵĞŶƚ
ƉƐLJĐŚŝĂƚƌŝĐĐŽŶĚŝƚŝŽŶƐ ;ĐŽŶĚŝƚŝŽŶƐŽĐĐƵƌŝŶĚĞƉĞŶĚĞŶƚůLJͿ͖ƐĐŚŝnjŽƉŚƌĞŶŝĂŝŶĂƉĂƚŝĞŶƚǁŝƚŚ
ĞŶĚͲƐƚĂŐĞƌĞŶĂůĚŝƐĞĂƐĞ͘
WƐLJĐŚŝĂƚƌŝĐͬƉƐLJĐŚŽƐŽĐŝĂů ĂƉĂĐŝƚLJĞǀĂůƵĂƚŝŽŶ͖ĞǀĂůƵĂƚŝŽŶƉƌŝŽƌƚŽŽƌŐĂŶƚƌĂŶƐƉůĂŶƚĂƚŝŽŶ
ĂƐƐĞƐƐŵĞŶƚ
s>hd/KEWZK^^/EW^z,K^KDd/D//E diagnostic studies, including computed tomography (CT) or magnetic
Psychiatric assessment in the medical setting includes a standard
psychiatric assessment as well as a particular focus on the medical history
and context of physical health care. In addition to obtaining a complete
psychiatric history, including past history, family history, developmental
history, and a review of systems, the medical history and current
treatments should be reviewed and documented. A full mental status
examination should be completed, and focused neurologic and physical
examinations are often indicated depending on the nature of the presenting
problem.
Several components of the process should be emphasized. First, it is
critical to speak with the referring clinician. In many cases, the reason for
consultation is not clear, and it is often helpful to understand why the
treating team believes the patient might have a psychiatric problem. Such
information can guide the assessment and may provide information about
other concerns the treatment team might have, including the patient’s
behavior and over or under use of treatment, such as pain medication. It
may also reveal the team’s anger or frustration with a particular patient.
Second, collateral information from family members and other health care
providers, including mental health professionals, is important in
understanding any prior history of psychiatric problems and helping the
team plan for ongoing care. Third, while the interview of the patient should
be comprehensive, it also needs to be sensitive to the patient’s medical
status. In many cases, patients in the general medical setting are
experiencing pain or discomfort, distracted by medical problems, or
cognitively compromised. Thus, the interview may need to be focused on
the reason for consultation.
A full mental status examination, including specific focus on cognitive
functioning, should be completed. The mental status should address the
level of consciousness, attention, concentration, memory, executive
function, language, praxis, mood, affect, perception, judgment, and insight.
The Mini-Mental State Examination or Montreal Cognitive Assessment is
often a helpful component because it provides an objective score that can
serve as a baseline for retesting, especially when delirium is a concern. It is
also important to be sure that physical and neurological examinations have
been completed. It is appropriate for the psychiatric consultant to either
complete limited components of these examinations or request the
referring clinicians to perform additional examinations.
The psychiatric consultant should also ensure that appropriate
laboratory and other diagnostic evaluations have been conducted. Basic
chemistry, hematologic, and cardiovascular workup can be supplemented
with other tests, including thyroid function, liver function, vitamin B12,
folate, toxicology, serological tests for syphilis, and HIV testing. Additional
resonance imaging (MRI) scans of the brain, EEG, or lumbar puncture,
may also be indicated.
Another important objective of the psychiatric evaluation is to gain an
understanding of the patient’s experience of his or her illness. In many
cases, this becomes the central focus for both the psychiatric assessment
and interventions. It is often helpful to develop an understanding of the
patient’s developmental and personal history as well as key dynamic
conflicts, which in turn may help to make the patient’s experience with
illness more comprehensible. Such an evaluation can include use of the
concepts of stress, personality traits, coping strategies, and defense
mechanisms. Observations and hypotheses that are developed can help to
guide psychotherapy with patients aimed at diminishing distress and may
also be helpful for the primary medical team in their interactions with the
patient.
Finally, a full report synthesizing the information should be completed
and should include specific recommendations for additional evaluations
and intervention. Ideally, the report should be accompanied by a discussion
with the referring physician.
dZdDEd^h^/EW^z,K^KDd/D//E
A host of interventions have been successfully utilized in psychosomatic
medicine. Specific consideration must be given to medical illness and
treatments when making recommendations for psychotropic medications.
Psychotherapy also plays an important role in psychosomatic medicine and
may vary in its structure and outcomes as compared to therapy that occurs
in a mental health practice.
Psychopharmacologic recommendations need to consider several
important factors. In addition to targeting a patient’s active symptoms,
considering the history of illness and treatments, and weighing the
particular side effect profile of a particular medication, there are several
other factors that must be considered that relate to the patient’s medical
illness and treatment. It is critical to evaluate potential drug–drug
interactions and contraindications to the use of potential psychotropic
agents. Since the majority of psychotropic medications are metabolized in
the liver, awareness of liver function is important. General appreciation of
side effects, such as weight gain, risk of development of diabetes, and
cardiovascular risk, must be considered in the choice of medications. In
addition, it is also important to incorporate knowledge of recent data that
outline effectiveness and specific risks involved for patients with co-
occurring psychiatric and physical disorders. For example, a greater
understanding of the side effects of antipsychotic medications has raised
concerns about the use of these medications in patients with dementia.
Psychosocial interventions also require adaptation when used in this
population. The methods used and the goals of psychosocial interventions
in the medically ill are often determined by the consideration of disease
onset, etiology, course, prognosis, treatment, and understanding of the
nature of the presenting psychiatric symptoms in addition to an
understanding of the patient’s existing coping skills and social support
networks. There are ample data that psychosocial interventions are
effective in addressing a series of identified problems and that such
interventions in many cases are associated with a variety of positive clinical
outcomes.
Every major psychosocial intervention has been used in psychosomatic
medicine, including dynamic, supportive, and behavioral interventions,
delivered in family, group, and individual settings. The goals for
psychosocial interventions vary widely depending on the nature of both the
psychiatric issues and the medical illness. In addition, the specific
intervention will vary based on the illnesses and goals. For instance, while a
goal generally present for all medical illness may be addressing changes in
role and function resulting from illness, addressing concerns regarding
death and dying will be a key concern for those in the terminal phases of an
illness such as cancer. Coping with changes in physical function and pain
are key issues that can be addressed for patients with arthritis. Addressing
barriers to adherence to treatment becomes critical to psychosocial
interventions in patients with diabetes.
An extensive body of research has demonstrated positive clinical
outcomes associated with a variety of interventions. At minimum,
psychosocial interventions have been shown to improve quality of life and
psychiatric conditions; in addition, there is some evidence that
psychosocial interventions may positively impact treatment adherence and
medical outcomes. Interventions aimed at depression in patients with
diabetes have shown not only decreases in depressive symptoms but also
reduction in medical costs of care.
DEd>/^KZZ^/EWZ/DZzZ Various conceptual models of the relationship between medical and
An area of considerable focus has been the successful identification and
management of patients with mental disorders treated in the primary care
setting. Although a variety of interventions aimed at education of primary
care physicians, screening initiatives, and implementation of quality
improvement programs may have short-term benefit, they have not had a
long-term impact on the improvement in detection and treatment of
depression. However, programs that incorporate access to mental health
professionals, combined with education of primary care physicians and use
of a care manager to provide appropriate monitoring and care strategies,
have been shown to be very successful. These programs, known collectively
as “collaborative care,” provide direct evidence-based treatment (e.g.,
psychotherapy and psychopharmacology) with coordination of care
between mental health professionals and the primary care team. A recent
meta-analysis of randomized-controlled trials of collaborative care models
for treating depression in primary care settings showed that they
significantly improved the quality of care for depression, depression
outcomes, patient and provider satisfaction, and increased patient
adherence to the treatment regimen. In addition, similar disease
management programs in medical settings have been shown to effectively
treat panic disorder, late-life depression, depression in individuals with
cancer, and depression in obstetrics and gynecology clinics. This model of
intervention is consistent with the New Freedom Commission on Mental
Health Report, which recommended that “collaborative care models for
identification and treatment of mental disorders across the lifespan should
be widely implemented in primary care settings and reimbursed by public
and private insurers.” Both the APA and the Academy of Psychosomatic
Medicine have recently made integrated care initiatives a high priority for
the field.
Z^Z,/EW^z,K^KDd/D//E
Research in psychosomatic medicine has focused on several key areas that
have contributed to the current understanding of the burdens of co-
occurring psychiatric and medical disorders. Important advances in
psychosomatic medicine research have identified common pathways
between psychiatric illness and physical illnesses, such as cardiovascular
disease or diabetes, bidirectional risk associated with the presence of
psychiatric disorders or medical conditions such as stroke, and the
identification of clinical interventions that can impact both medical and
psychiatric outcomes. However, research in psychosomatic medicine has
been limited by the complexity of research questions that require
investigation of both medical and psychiatric outcomes and the existing
“division” of the research enterprise into separate psychiatric and medical
domains.
physical illness underlie the core research areas. For example, a large body
of epidemiologic work has examined the relationship of depressive
disorders to poor outcomes among patients with cardiovascular disease. In
contrast, in the field of psychoneuroimmunology, basic science techniques
are used to examine the relationship between psychosocial stressors and
immune functioning. Table 27.1–3 presents an overview of conceptual
areas and specific current research areas.
hZZEdW^z,K^KDd/D//EZ^Z, time continuing with key treatment studies, until mechanism studies lead
Psychosomatic medicine is now involved with a wide, ever-expanding to the development of “designer” therapies. Thus, there will be increasing
spectrum of investigations examining the medical illness–psychiatry application of newer research methods from genetics, brain imaging,
relationship. Important contributions have occurred in acquired animal models, pharmacology, psychology, epidemiology, and clinical
immunodeficiency syndrome (AIDS), cancer, transplantation, cardiac, trials.
neurological, pulmonary, renal, GI disease, and obstetrics and gynecology.
d,&/>K&W^z,K^KDd/D//E
In each of these areas, first-generation studies identified the extent and
nature of psychiatric morbidity associated with the most common diseases. The term psychosomatic medicine was first used by Felix Deutsch in the
More sophisticated second-generation cross-sectional epidemiological early 1920s. Organized psychosomatic medicine and consultation-liaison
studies have established the prevalence rates of a broader range of psychiatry had their origins in the publication of the journal Psychosomatic
psychiatric disorders in several medical conditions, as well as newer Medicine in 1939, the founding of the American Psychosomatic Society in
psychiatric syndromes, such as mild traumatic brain injury. 1947, and the journal Psychosomatics in 1960. The Academy of
In some cases, a new body of research has extended the knowledge Psychosomatic Medicine was founded in 1953 and continues to be the
about genetic, neurochemical, and behavioral factors contributing to the organization for consultation-liaison psychiatrists. In 1968, John Schwab
development of psychiatric disorders among complex medically ill published the first consultation-liaison psychiatry textbook.
populations. This work has shown that many different mechanisms are
involved. Examples include the relationships between depression and dĂďůĞϮϳ͘ϭʹϯ͘
diabetes, the location of stroke and major depression, and specific ƵƌƌĞŶƚĂŶĚWŽƚĞŶƚŝĂůZĞƐĞĂƌĐŚŝŶWƐLJĐŚŽƐŽŵĂƚŝĐDĞĚŝĐŝŶĞ
autoantibodies and limbic encephalitis. This research has led to some džĂŵƉůĞƐŽĨ
intervention studies focused on reducing the rate of occurrence of these dLJƉĞƐŽĨ^ƚƵĚŝĞƐ ƵƌƌĞŶƚZĞƐĞĂƌĐŚ džĂŵƉůĞƐŽĨWŽƚĞŶƚŝĂů^ƚƵĚŝĞƐ
disorders, for example, hospital programs that reduce postcardiotomy ƉŝĚĞŵŝŽůŽŐŝĐĂŶĚĐůŝŶŝĐĂůĞƉŝĚĞŵŝŽůŽŐŝĐƐƚƵĚŝĞƐ
delirium. KĐĐƵƌƌĞŶĐĞ͕ŶŽƐŽůŽŐLJ͕ĂŶĚŝŵƉĂĐƚŽĨ KĐĐƵƌƌĞŶĐĞĂŶĚ ZĞůĂƚŝŽŶƐŚŝƉŽĨƉƐLJĐŚŝĂƚƌŝĐ
Of long-standing interest to the psychosomatic medicine field has been ĚŝĨĨĞƌĞŶƚƚLJƉĞƐŽĨƉƐLJĐŚŝĂƚƌŝĐŵŽƌďŝĚŝƚLJ ƉŚĞŶŽŵĞŶŽůŽŐLJ ƉƌŽďůĞŵƐƚŽĚŝƐĂďŝůŝƚLJĂŶĚƋƵĂůŝƚLJ
ŽǀĞƌƚŚĞĐŽƵƌƐĞŽĨŐĞŶĞƌĂůŵĞĚŝĐĂů ŽĨĚĞƉƌĞƐƐŝŽŶ ŽĨůŝĨĞƚŚƌŽƵŐŚƚŚĞĐŽƵƌƐĞŽĨ
the relationship between emotional factors and disease development.
ĐŽŶĚŝƚŝŽŶƐ ŽǀĞƌƚŚĞĐŽƵƌƐĞ WĂƌŬŝŶƐŽŶĚŝƐĞĂƐĞ
Recent studies have demonstrated the dramatic impact of coexisting ŽĨĚŝĂďĞƚĞƐ >ŽŶŐͲƚĞƌŵĞĨĨĞĐƚƐŽĨƉƐLJĐŚŝĂƚƌŝĐ
psychiatric morbidity on the course or outcome of specific medical Wd^ŝŶŝŶĚŝǀŝĚƵĂůƐ ĐŽŶĚŝƚŝŽŶƐŽŶƋƵĂůŝƚLJŽĨůŝĨĞĂĨƚĞƌ
illnesses. Studies have now been extended to examine the effect of ǁŝƚŚƚƌĂƵŵĂƚŝĐ ŽƌŐĂŶƚƌĂŶƐƉůĂŶƚĂƚŝŽŶ
psychiatric comorbidity on health costs. Comorbid psychiatric disorders ďƌĂŝŶŝŶũƵƌLJ
DĞĐŚĂŶŝƐƚŝĐƐƚƵĚŝĞƐ
have been shown to increase the length of hospital stay and
hŶĚĞƌƐƚĂŶĚŝŶŐƚŚĞƌŽůĞŽĨƉƐLJĐŚŽƐŽĐŝĂů͕ ^ŽĐŝĂůŝƐŽůĂƚŝŽŶ /ŶƚĞƌĂĐƚŝŽŶŽĨƐŽĐŝĂůŝƐŽůĂƚŝŽŶ͕
rehospitalization rates in numerous illnesses. Several cost-effectiveness ďŝŽůŽŐŝĐĂů͕ĂŶĚŐĞŶĞƚŝĐĨĂĐƚŽƌƐŝŶƚŚĞ ůĞĂĚŝŶŐƚŽ ŐĞŶĞƚŝĐƉƌĞĚŝƐƉŽƐŝƚŝŽŶ͕ĂŶĚďƌĂŝŶ
studies have demonstrated the value of psychosomatic medicine ĐĂƵƐĂƚŝŽŶŽĨƉƐLJĐŚŝĂƚƌŝĐĂŶĚŵĞĚŝĐĂů ƉŽŽƌĞƌŚĞĂůƚŚ ĚĂŵĂŐĞŝŶƚŚĞĚĞǀĞůŽƉŵĞŶƚŽĨ
interventions in hospital and outpatient populations. In addition, ŵŽƌďŝĚŝƚLJ ŽƵƚĐŽŵĞƐ ŵĂũŽƌĚĞƉƌĞƐƐŝŽŶĂĨƚĞƌƚƌĂƵŵĂƚŝĐ
psychobiologic research continues to focus on emotional factors and illness ĨĨĞĐƚŝǀĞĐŝƌĐƵŝƚƌLJ ďƌĂŝŶŝŶũƵƌLJ
ŝŶĐŚƌŽŶŝĐƉĂŝŶ 'ĞŶĞʹĞŶǀŝƌŽŶŵĞŶƚŝŶƚĞƌĂĐƚŝŽŶƐŝŶ
development in individuals who do not necessarily have psychiatric &ĂŵŝůLJĂĚǀĞƌƐŝƚLJ ƚŚĞĚĞǀĞůŽƉŵĞŶƚŽĨĐŚƌŽŶŝĐ
illnesses. For example, there continues to be important work in the ĂŶĚ ƐƚƌĞƐƐͲƌĞůĂƚĞĚŝůůŶĞƐƐĞƐ
relationship between emotional stressors and the functioning of the ŝŶĨůĂŵŵĂƚŝŽŶ 'ĞŶĞƚŝĐĂƐƐŽĐŝĂƚŝŽŶƐƚƵĚŝĞƐŽĨ
immune system. ĚĞƉƌĞƐƐŝǀĞƐLJŵƉƚŽŵƐĂĨƚĞƌƚŚĞ
ŽŶƐĞƚŽĨĐŚƌŽŶŝĐŵĞĚŝĐĂůŝůůŶĞƐƐ
The future research agenda for the psychosomatic medicine field will
^ƚƵĚŝĞƐŽĨƚŚĞƐŽĐŝĂů͕ƉƐLJĐŚŽůŽŐŝĐĂů͕ WĞƌƐŽŶĂůŝƚLJƚƌĂŝƚƐ 'ĞŶĞƚŝĐƌŝƐŬĨĂĐƚŽƌƐĨŽƌƚŚĞ
likely continue to revolve around these themes. Table 27.1–3 gives ďŝŽůŽŐŝĐĂů͕ĂŶĚŐĞŶĞƚŝĐĨĂĐƚŽƌƐŝŶǀŽůǀĞĚŝŶ ĂƐƉƌĞĚŝĐƚŽƌƐŽĨ ĚĞǀĞůŽƉŵĞŶƚŽĨĐŚƌŽŶŝĐƉĂŝŶ
examples of the types of studies that are anticipated in the next few decades ƚŚĞĞdžƉƌĞƐƐŝŽŶŽĨĂďŶŽƌŵĂůŝůůŶĞƐƐ ŚLJƉŽĐŚŽŶĚƌŝĂƐŝƐ ƐLJŶĚƌŽŵĞƐ
in the psychosomatic medicine field. They are grouped along types of ďĞŚĂǀŝŽƌ͕ƐŽŵĂƚŝĐƐLJŵƉƚŽŵĚŝƐŽƌĚĞƌƐ͕ &ƵŶĐƚŝŽŶĂůďƌĂŝŶ dŚĞƌŽůĞŽĨŚĞĂůƚŚĐĂƌĞƐLJƐƚĞŵ
studies, with specific examples provided within each group. Psychosomatic ĂŶĚĐŚƌŽŶŝĐƉĂŝŶ ŝŵĂŐŝŶŐ ĨĂĐƚŽƌƐŝŶĐŽŶƚƌŝďƵƚŝŶŐƚŽƚŚĞ
ĂďŶŽƌŵĂůŝƚŝĞƐŝŶ ƉĞƌƐŝƐƚĞŶƚƵƚŝůŝnjĂƚŝŽŶŽĨŚĞĂůƚŚ
medicine research is likely to continue to move away from descriptive ĐŚƌŽŶŝĐĨĂƚŝŐƵĞ ĐĂƌĞ
studies and focus increasingly on studies of mechanism, while at the same

^ƚƵĚŝĞƐŽĨƚŚĞĞĨĨĞĐƚƐŽĨŵĞĚŝĐĂůŝůůŶĞƐƐĂŶĚ
ƚŚĞŝƌƚƌĞĂƚŵĞŶƚƐŽŶƚŚĞďƌĂŝŶĂŶĚŽŶƚŚĞ
ĚĞǀĞůŽƉŵĞŶƚŽĨƐĞĐŽŶĚĂƌLJ;͞ŽƌŐĂŶŝĐ͟Ϳ
ƉƐLJĐŚŝĂƚƌŝĐĚŝƐŽƌĚĞƌƐ
DĞĐŚĂŶŝƐƚŝĐƐƚƵĚŝĞƐƚŽƵŶĚĞƌƐƚĂŶĚŚŽǁ
ƉƐLJĐŚŝĂƚƌŝĐŵŽƌďŝĚŝƚLJĂĨĨĞĐƚƐŵĞĚŝĐĂů
ŽƵƚĐŽŵĞƐŝŶƐĞǀĞƌĂůĐŽŶƚĞdžƚƐ
dƌĞĂƚŵĞŶƚƐƚƵĚŝĞƐ
dƌĞĂƚŵĞŶƚƐƚƵĚŝĞƐŽĨƚŚĞĞĨĨŝĐĂĐLJĂŶĚƐĂĨĞƚLJ ŽŐŶŝƚŝǀĞ
ŽĨƉƐLJĐŚŝĂƚƌŝĐƚƌĞĂƚŵĞŶƚƐĂƐĂƉƉůŝĞĚƚŽƚŚĞ
ĐŽŵƉůĞdžŵĞĚŝĐĂůůLJŝůů
dƌĞĂƚŵĞŶƚƐƚƵĚŝĞƐŽĨŚŽǁƚƌĞĂƚŝŶŐ
ƉƐLJĐŚŝĂƚƌŝĐĐŽŶĚŝƚŝŽŶƐĂĨĨĞĐƚŵĞĚŝĐĂů
ŽƵƚĐŽŵĞƐŝŶƚŚĞĐŽŵƉůĞdžŵĞĚŝĐĂůůLJŝůů
ĞǀĞůŽƉŵĞŶƚĂŶĚƐƚƵĚLJŽĨ͞ĚĞƐŝŐŶĞƌ͟
ƉƐLJĐŚŝĂƚƌŝĐƚƌĞĂƚŵĞŶƚƐďĂƐĞĚŽŶĂŶ
ƵŶĚĞƌƐƚĂŶĚŝŶŐŽĨƚŚĞĐĂƵƐĂƚŝŽŶŽĨ
ƉƐLJĐŚŝĂƚƌŝĐŵŽƌďŝĚŝƚLJŝŶƚŚĞĐŽŵƉůĞdž
ŵĞĚŝĐĂůůLJŝůů
^ĞƌǀŝĐĞĚĞůŝǀĞƌLJƐƚƵĚŝĞƐ
^ƚƵĚŝĞƐŽĨƚŚĞĚĞůŝǀĞƌLJŽĨĞĨĨŝĐĂĐŝŽƵƐ
ƉƐLJĐŚŝĂƚƌŝĐƚƌĞĂƚŵĞŶƚƐĨŽƌƚŚĞĐŽŵƉůĞdž
ŵĞĚŝĐĂůůLJŝůůĂĐƌŽƐƐĚŝĨĨĞƌĞŶƚƐĞƌǀŝĐĞ
ƐĞƚƚŝŶŐƐ͕ƐƵĐŚĂƐƉƌŝŵĂƌLJĐĂƌĞ͕ŚŽŵĞͲ
ďĂƐĞĚĐĂƌĞ͕ĂƐƐŝƐƚĞĚůŝǀŝŶŐ͕ŶƵƌƐŝŶŐŚŽŵĞƐ͕
ĂŶĚŽƚŚĞƌůŽŶŐͲƚĞƌŵĐĂƌĞƐĞƚƚŝŶŐƐ
ĂŶĚĐŽŶǀĞƌƐŝŽŶ
/ŶƚĞƌĨĞƌŽŶͲ ŶŝŵĂůŵŽĚĞůƐƚŽƵŶĚĞƌƐƚĂŶĚďƌĂŝŶ
ŝŶĚƵĐĞĚ ŵĞĐŚĂŶŝƐŵƐŝŶǀŽůǀĞĚŝŶĚĞůŝƌŝƵŵ
ĚĞƉƌĞƐƐŝŽŶ ƌĂŝŶŝŵĂŐŝŶŐĂŶĚ
WĂƌĂŶĞŽƉůĂƐƚŝĐ ŶĞƵƌŽƉƐLJĐŚŽůŽŐŝĐĂůƐƚƵĚŝĞƐŽĨ
ůŝŵďŝĐ ƚŚĞďƌĂŝŶĞĨĨĞĐƚƐŽĨǀĂƌŝŽƵƐ
ĞŶĐĞƉŚĂůŝƚŝƐ ĐĂŶĐĞƌĐŚĞŵŽƚŚĞƌĂƉĞƵƚŝĐĂŐĞŶƚƐ
ĞƉƌĞƐƐŝŽŶĂƐĂ ƌĂŝŶŝŵĂŐŝŶŐĂŶĚŐĞŶĞƚŝĐƐƚƵĚŝĞƐ
ƉƌĞĚŝĐƚŽƌŽĨ ŽĨƚŚĞƌŽůĞŽĨĚĞƉƌĞƐƐŝŽŶŝŶƚŚĞ
ƉŽŽƌĂĚŚĞƌĞŶĐĞ ĚĞǀĞůŽƉŵĞŶƚŽĨĐŽŐŶŝƚŝǀĞĚĞĐůŝŶĞ
ƚŽĚŝĂďĞƚĞƐ ůŽŽĚĂŶĚĐĞƌĞďƌŽƐƉŝŶĂůĨůƵŝĚ
ƚƌĞĂƚŵĞŶƚ ďŝŽŵĂƌŬĞƌƐƚƵĚŝĞƐŽĨĞŶĚŽĐƌŝŶĞ͕
ŝŵŵƵŶĞ͕ĂŶĚŽƚŚĞƌĨĂĐƚŽƌƐ
ŝŶǀŽůǀĞĚŝŶƚŚĞĚĞǀĞůŽƉŵĞŶƚŽĨ
ƉŽƐƚƉĂƌƚƵŵĚĞƉƌĞƐƐŝŽŶ
dŚĞĞĨĨŝĐĂĐLJĂŶĚƐĂĨĞƚLJŽĨĞŵĞƌŐŝŶŐ
ďĞŚĂǀŝŽƌĂů ĂŶƚŝĚĞƉƌĞƐƐĂŶƚƚŚĞƌĂƉŝĞƐĨŽƌ
ƚŚĞƌĂƉLJŝŶ ĚĞƉƌĞƐƐŝŽŶĂŶĚĂŶdžŝĞƚLJĂĨƚĞƌ
ƐŽŵĂƚŝĐ ŽƌŐĂŶƚƌĂŶƐƉůĂŶƚĂƚŝŽŶ
ƐLJŵƉƚŽŵ dŚĞĞĨĨŝĐĂĐLJĂŶĚƐĂĨĞƚLJŽĨ
ĚŝƐŽƌĚĞƌƐ ĐŚŽůŝŶĞƐƚĞƌĂƐĞŝŶŚŝďŝƚŽƌƐŽƌ
dŚĞĞĨĨŝĐĂĐLJĂŶĚ ŵĞŵĂŶƚŝŶĞŝŶƚƌĞĂƚŝŶŐ
ƐĂĨĞƚLJŽĨɲͲϮ ƉŽƐƚĐŚĞŵŽƚŚĞƌĂƉLJĐŽŐŶŝƚŝǀĞ
ĂĚƌĞŶŽƌĞĐĞƉƚŽƌ ŝŵƉĂŝƌŵĞŶƚ
ĂŐŽŶŝƐƚƐŝŶ
ƚƌĞĂƚŝŶŐ
ĚĞůŝƌŝƵŵ
dŚĞĞĨĨĞĐƚŽĨ dŚĞĞĨĨĞĐƚŽĨƚƌĞĂƚŝŶŐĚĞƉƌĞƐƐŝŽŶ
ƚƌĞĂƚŝŶŐ ĂĨƚĞƌĐŽƌŽŶĂƌLJĂƌƚĞƌLJďLJƉĂƐƐ
ĚĞƉƌĞƐƐŝŽŶŽŶ ŐƌĂĨƚƐƵƌŐĞƌLJŽŶƚŚĞƌĞĐƵƌƌĞŶĐĞ
ŚĞŵŽŐůŽďŝŶϭĐ ŽĨĐŽƌŽŶĂƌLJĂƌƚĞƌLJĚŝƐĞĂƐĞ
ůĞǀĞůƐŝŶ dŚĞĞĨĨĞĐƚŽĨŝŶƚĞŶƐŝǀĞĚĞƉƌĞƐƐŝŽŶ
ĚŝĂďĞƚŝĐ ƌĞĚƵĐƚŝŽŶŽŶƚŚĞŽĐĐƵƌƌĞŶĐĞŽĨ
ƉĂƚŝĞŶƚƐ ƌĞƚŝŶŽƉĂƚŚLJ͕ŶĞƵƌŽƉĂƚŚLJ͕ĂŶĚ
ŽƚŚĞƌůŽŶŐͲƚĞƌŵĐŽŵƉůŝĐĂƚŝŽŶƐŽĨ
ĚŝĂďĞƚĞƐ
EŽŶĞ dŚĞƉŽƚĞŶƚŝĂůďĞŶĞĨŝƚƐŽĨĚĞĞƉďƌĂŝŶ
ƐƚŝŵƵůĂƚŝŽŶĨŽƌĚĞƉƌĞƐƐŝŽŶŝŶƚŚĞ
ŵĞĚŝĐĂůůLJŝůů͘dŚĞƉŽƚĞŶƚŝĂů
ďĞŶĞĨŝƚƐŽĨĂŵLJůŽŝĚŽƌƚĂƵ
ƌĞĚƵĐŝŶŐƚŚĞƌĂƉLJŽŶƚŚĞ
ŽĐĐƵƌƌĞŶĐĞŽĨůnjŚĞŝŵĞƌ͛Ɛ
ĂƐƐŽĐŝĂƚĞĚŵŽŽĚƐLJŵƉƚŽŵƐ
hƐĞŽĨ dŚĞďĞŶĞĨŝƚƐŽĨŝŵƉůĞŵĞŶƚŝŶŐ
ĐŽůůĂďŽƌĂƚŝǀĞ ͞ĚĞŵĞŶƚŝĂĐĂƌĞ͟ŝŶƚĞƌǀĞŶƚŝŽŶƐŝŶ
ĐĂƌĞƐƚƌĂƚĞŐŝĞƐ ƉƌŝŵĂƌLJĐĂƌĞĂŶĚĂƐƐŝƐƚĞĚůŝǀŝŶŐ
ŝŶƉƌŝŵĂƌLJĂŶĚ ƐĞƚƚŝŶŐƐ
ƐƉĞĐŝĂůƚLJĐĂƌĞ ĞǀĞůŽƉŵĞŶƚŽĨŶĞǁǁĂLJƐƚŽ
ƐĞƚƚŝŶŐƐ ĚĞůŝǀĞƌŵĂŶƵĂůŝnjĞĚ
ƉƐLJĐŚŽƚŚĞƌĂƉŝĞƐŝŶƉƌŝŵĂƌLJĐĂƌĞ
ŽƐƚͲĞĨĨĞĐƚŝǀĞŶĞƐƐŽĨŝŶƚĞŐƌĂƚŝŽŶŽĨ
ŵĞŶƚĂůŚĞĂůƚŚĐĂƌĞŝŶƚŽŵĞĚŝĐĂů
ŚŽŵĞƐ
The origins of consultation-liaison psychiatry fellowships can be traced
to George Engel’s and John Romano’s fellowship program in psychosocial
skills at Rochester University College of Medicine. This program, first
offered in 1946, was offered to nonpsychiatric physicians as well as
psychiatrists. The Massachusetts General Hospital established its first
consultation service in 1954.
In 2003, the American Board of Medical Specialists approved
psychosomatic medicine as a subspecialty field of psychiatry. Historically,
psychosomatic medicine was known as consultation-liaison psychiatry, and
it represented the care delivered by psychiatrists to patients with co-
occurring medical and psychiatric problems who were treated primarily in
medical settings. The approval of the subspecialty was both a response to
and an opportunity for the field to highlight and expand the foundation in
clinical care, research, teaching, and other scholarly activities related to the
care of this special patient population. Although psychosomatic medicine
specialists do not provide all, or even most, of the care to this patient
population, the presence of the subspecialty clearly has had a positive
impact on general training, research, and academic psychiatry.
Psychosomatic medicine, as defined and characterized by the
subspecialty, is practiced by psychiatrists. The Academy of Psychosomatic
Medicine has over 1,200 members and approximately 3,000 psychiatrist
members of the APA state that they are interested in or spend a substantial
amount of time providing consultation in a general hospital setting. Other
mental health professionals also provide care for this population.
Psychologists have long served in the general medical setting providing
assessments, psychotherapeutic and behavioral interventions, and
conducting research. The health psychology section of the American
Psychological Association has over 3,500 members. In addition, social
workers and nurses participate in care for these patients. In many settings,
psychosomatic medicine psychiatrists function as part of multidisciplinary
teams, which include psychiatry, psychology, nursing, and social work. In
most cases, these teams work within medical specialty settings that provide
care to special populations such as those with HIV, cancer, cardiovascular
disease, transplant, and diabetes.
The APA formed the Council on Psychosomatic Medicine in 2004 in
response to the approval of the subspecialty. The APA Council and the
Academy of Psychosomatic Medicine, as well as other organizations, have
participated actively in the development of clinical standards, addressed
issues related to access to care and reimbursement, and provided education
to members, trainees, medical professionals, and the public. Care of special
populations such as those with cancer, HIV, transplant, and obstetrics and
gynecology is the focus of other organizations (e.g., American Psychosocial
Oncology Society and North American Society for Psychosocial Obstetrics
and Gynecology). Research is a core interest for some organizations,
including the American Psychosomatic Society. In addition to the
organizations in the United States, there has been growing interest in the
field internationally (e.g., The European Association of Psychosomatic
Medicine).
Education and training in psychosomatic medicine are integrated
throughout the psychiatry curriculum in medical school and general
psychiatric training. Starting in 1961, the Accreditation Council for
Graduate Medical Education (ACGME) addressed the need for psychiatric
residents to have contact with other services besides psychiatry, including
medicine, pediatrics, and neurology. By the 1980s, the ACGME’s Residency
Review Committee (RRC) required all psychiatry residency programs to
provide teaching and experience in consultation liaison psychiatry. The
current RRC requirements require at least 2 months of full-time work in
which residents consult under supervision on other medical and surgical
services.
Currently, there are 58 ACGME-accredited psychosomatic medicine
fellowship programs in the United States, an increase of 50 percent in the
past 8 years. The ACGME program requirements for psychosomatic
medicine fellowships can be found on their website (www.acgme.org).
Table 27.1–4 lists the clinical activities in which psychosomatic medicine
fellows must demonstrate competence. In addition, there are also 36
residencies that combine psychiatry with internal medicine, family
practice, pediatrics, and neurology.
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WK>/z
Despite an abundance of evidence that a variety of psychiatric and
psychosocial interventions have positive economic and clinical outcomes
for patients with co-occurring psychiatric and medical problems, access to
and reimbursement for psychiatric and other mental health services are
severely limited. Reimbursement for these services is complex due to the
separation of mental health and physical health benefits in most private
and public insurance coverage. Even in areas where there is reimbursement
for mental health services, it is often administered through a mental health
carve-out that separates reimbursement for these services from the medical
care reimbursement, resulting in patients not being able to receive care in
the medical setting or have access to professionals with the appropriate
expertise to treat psychiatric conditions in the context of complex medical
illnesses.
dĂďůĞϮϳ͘ϭʹϰ͘
WĂƚŝĞŶƚĂƌĞdžƉĞƌŝĞŶĐĞƐŝŶWƐLJĐŚŽƐŽŵĂƚŝĐDĞĚŝĐŝŶĞZĞƋƵŝƌĞĚŽĨůů
WƐLJĐŚŽƐŽŵĂƚŝĐDĞĚŝĐŝŶĞ&ĞůůŽǁƐ
ϭ͘ ǀĂůƵĂƚŝŽŶŽĨƉƐLJĐŚŝĂƚƌŝĐĐŽŵƉůŝĐĂƚŝŽŶƐŽĨŵĞĚŝĐĂůŝůůŶĞƐƐĞƐ
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ŶĞǁƐƵƌŐŝĐĂůŽƌŵĞĚŝĐĂůƉƌŽĐĞĚƵƌĞƐ͕ƚƌĂŶƐƉůĂŶƚĂƚŝŽŶ͕ĂŶĚĞdžƉĞƌŝŵĞŶƚĂůƚŚĞƌĂƉŝĞƐ
ϯ͘ ǀĂůƵĂƚŝŽŶŽĨƚLJƉŝĐĂůĂŶĚĂƚLJƉŝĐĂůƉƌĞƐĞŶƚĂƚŝŽŶƐŽĨƉƐLJĐŚŝĂƚƌŝĐĚŝƐŽƌĚĞƌƐƚŚĂƚĂƌĞĚƵĞƚŽŵĞĚŝĐĂů͕
ŶĞƵƌŽůŽŐŝĐĂů͕ĂŶĚƐƵƌŐŝĐĂůŝůůŶĞƐƐĞƐ
ϰ͘ ǀĂůƵĂƚŝŽŶĂŶĚŵĂŶĂŐĞŵĞŶƚŽĨĚĞůŝƌŝƵŵ͕ĚĞŵĞŶƚŝĂ͕ĂŶĚƉƐLJĐŚŝĂƚƌŝĐĚŝƐŽƌĚĞƌƐĚƵĞƚŽŵĞĚŝĐĂůŝůůŶĞƐƐ
ϱ͘ ǀĂůƵĂƚŝŽŶĂŶĚŵĂŶĂŐĞŵĞŶƚŽĨĂĐƵƚĞƉĂŝŶ͕ĐŚƌŽŶŝĐƉĂŝŶ͕ĂŶĚƐŽŵĂƚŝĐƐLJŵƉƚŽŵĚŝƐŽƌĚĞƌƐ
ϲ͘ ǀĂůƵĂƚŝŽŶĂŶĚŵĂŶĂŐĞŵĞŶƚŽĨƉĂůůŝĂƚŝǀĞĐĂƌĞĂŶĚĞŶĚͲŽĨͲůŝĨĞŝƐƐƵĞƐ
ϳ͘ ǀĂůƵĂƚŝŽŶĂŶĚŵĂŶĂŐĞŵĞŶƚŽĨŝƐƐƵĞƐŝŶĂĚũƵƐƚŝŶŐƚŽƚŚĞĞŵŽƚŝŽŶĂůƐƚƌĞƐƐĞƐŽĨŵĞĚŝĐĂůŝůůŶĞƐƐ
ϴ͘ ƐƐĞƐƐŵĞŶƚŽĨĐĂƉĂĐŝƚLJƚŽŐŝǀĞŝŶĨŽƌŵĞĚĐŽŶƐĞŶƚĨŽƌŵĞĚŝĐĂůĂŶĚƐƵƌŐŝĐĂůƉƌŽĐĞĚƵƌĞƐŝŶƚŚĞ
ƉƌĞƐĞŶĐĞŽĨĐŽŐŶŝƚŝǀĞŝŵƉĂŝƌŵĞŶƚ
ϵ͘ WƌŽǀŝƐŝŽŶŽĨƉƐLJĐŚŽƐŽĐŝĂůŝŶƚĞƌǀĞŶƚŝŽŶƐ͕ŝŶĐůƵĚŝŶŐƉƐLJĐŚŽƚŚĞƌĂƉĞƵƚŝĐŝŶƚĞƌǀĞŶƚŝŽŶƐ͕ĂƉƉƌŽƉƌŝĂƚĞĨŽƌ
ƚŚĞŵĞĚŝĐĂůůLJŝůů
ϭϬ͘ ƉƉƌŽƉƌŝĂƚĞƵƐĞŽĨƉƐLJĐŚŽĂĐƚŝǀĞŵĞĚŝĐĂƚŝŽŶŝŶŵĞĚŝĐĂů͕ŶĞƵƌŽůŽŐŝĐ͕ŽďƐƚĞƚƌŝĐĂů͕ĂŶĚƐƵƌŐŝĐĂů
ĐŽŶĚŝƚŝŽŶƐ
ϭϭ͘ ƐƐĞƐƐŝŶŐĂŶĚŵĂŶĂŐŝŶŐƐƵŝĐŝĚĂůŝƚLJĂŶĚŽƚŚĞƌŚŝŐŚͲƌŝƐŬďĞŚĂǀŝŽƌŝŶƚŚĞŵĞĚŝĐĂůƐĞƚƚŝŶŐ
ϭϮ͘ /ŶƚĞƌĂĐƚŝŽŶƐďĞƚǁĞĞŶƉƐLJĐŚŽƚƌŽƉŝĐŵĞĚŝĐĂƚŝŽŶƐĂŶĚƚŚĞĨƵůůͲƌĂŶŐĞŽĨŵĞĚŝĐĂƚŝŽŶƐƵƐĞĚĨŽƌĂǀĂƌŝĞƚLJ
ŽĨŵĞĚŝĐĂůĂŶĚƐƵƌŐŝĐĂůĐŽŶĚŝƚŝŽŶƐ
ϭϯ͘ ŽůůĂďŽƌĂƚŝŽŶǁŝƚŚŽƚŚĞƌƉŚLJƐŝĐŝĂŶƐĂŶĚŽƚŚĞƌŵĞŵďĞƌƐŽĨƚŚĞŵƵůƚŝĚŝƐĐŝƉůŝŶĂƌLJƚƌĞĂƚŵĞŶƚƚĞĂŵ
ϭϰ͘ dĞĂĐŚŝŶŐŽƚŚĞƌƉŚLJƐŝĐŝĂŶƐĂŶĚŽƚŚĞƌŵĞŵďĞƌƐŽĨƚŚĞŵƵůƚŝĚŝƐĐŝƉůŝŶĂƌLJƚĞĂŵŚŽǁƚŽƌĞĐŽŐŶŝnjĞĂŶĚ
ƌĞƐƉŽŶĚƚŽǀĂƌŝŽƵƐƉƐLJĐŚŝĂƚƌŝĐĚŝƐŽƌĚĞƌƐ
ϭϱ͘ >ĞĂĚŝŶŐĂŶŝŶƚĞŐƌĂƚĞĚƉƐLJĐŚŽƐŽĐŝĂůŚĞĂůƚŚĐĂƌĞƚĞĂŵŝŶƚŚĞŵĞĚŝĐĂůƐĞƚƚŝŶŐ
ĚĂƉƚĞĚĨƌŽŵ'DWƌŽŐƌĂŵZĞƋƵŝƌĞŵĞŶƚƐĨŽƌ'ƌĂĚƵĂƚĞDĞĚŝĐĂůĚƵĐĂƚŝŽŶŝŶWƐLJĐŚŽƐŽŵĂƚŝĐ
DĞĚŝĐŝŶĞ͘ǀĂŝůĂďůĞĂƚ
ŚƚƚƉ͗ͬͬǁǁǁ͘ĂĐŐŵĞ͘ŽƌŐͬWŽƌƚĂůƐͬϬͬW&ƐƐĞƚƐͬWƌŽŐƌĂŵZĞƋƵŝƌĞŵĞŶƚƐͬϰϬϵͺƉƐLJĐŚŽƐŽŵĂƚŝĐͺŵĞĚͺϮϬϭϲͺϭͲ
zZ͘ƉĚĨ
Recent developments, largely driven by components of the Affordable
Care Act (ACA), may provide support to evidence-based psychiatric
interventions in the medical setting. The ACA requires mental health be
included in the “essential benefit” and therefore extends the reach of
mental health parity across the majority of health plans. It also includes a
number of components that promote mental health care in primary care
and other medical settings, such as the patient centered medical home,
which includes requirements for behavioral health screening and
interventions. In addition, new financing arrangements such as
accountable care organizations (ACOs), value based purchasing and pay for
performance create incentives for organizations to incorporate mental
health care more effectively. In the ACO setting, where there is payment for
a population rather than on a fee for service basis, psychiatrists who
provide care across the health system can demonstrate both economic and
clinical value and can be paid accordingly. However, there is still a need to
better characterize these economic models and define the role of the
psychiatrist in quality measures in order to assure full access to these
services. Recent attention to these types of issues by the APA, including a
commissioned Milliman report, highlighted the economic impact of
integrated medical-behavioral health care. Expanded use of collaborative
care models, including adoption of reimbursement strategies to pay for the
components of care, illustrates some of the increased interest in the field.
In summary, there has been an increasing call to action to improve mental
health care for the medically ill and there continues to be room for
improving current delivery systems to achieve that aim.
Editor’s note: The founding editor of this textbook, Harold I. Kaplan, M.D., had a long-
standing interest in psychosomatic medicine and the history of psychiatry. He wrote the section
on the history of psychosomatic medicine for the first edition of this textbook and for each
subsequent edition thereafter until his death in 1998. This chapter includes some of his original
work.
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Lichtman JH, Froelicher ES, Blumenthal JA, et al. Depression as a risk factor for poor prognosis
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*Lipsitt DR. Consultation-liaison psychiatry and psychosomatic medicine: the company they
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ŸϮϳ͘ϮĂƌĚŝŽǀĂƐĐƵůĂƌŝƐŽƌĚĞƌƐ
WdZ͘^,W/ZK͕D͕͘͘EDZ͘Z/d,&/>͕D͘͘
Cardiovascular disorders are the leading cause of death in the United States
and the industrialized world, and ischemic heart disease is one of the
leading causes of worldwide disability burden. Psychiatric problems
contribute to the development of cardiovascular disease and develop as
complications of it. Comorbidity poses a treatment challenge for cardiology
and psychiatry. Behavioral risk factors, such as smoking, failure to exercise,
and failure to adhere to treatment and lifestyle recommendations, are
clearly exacerbated by psychological stress, depression, and anxiety, and
may benefit from psychiatric treatment. Moreover, psychiatric disorders
are common in many cardiac patients and require intervention not only to
improve adherence to and outcomes of medical therapy, but also to relieve
suffering due to the psychiatric illnesses themselves. From an
epidemiological standpoint, the most important categories of
cardiovascular disease include coronary artery disease (CAD), congestive
heart failure (CHF), arrhythmias, and stroke; the chapter also includes
some discussion of other conditions of interest. Here, brief presentation of
background information on these cardiovascular conditions is
accompanied by discussion of psychological conditions and psychiatric
disorders as risk factors for their development and course. The discussion
then turns to psychiatric comorbidity with established cardiovascular
disease and relevant treatment issues.
KZKEZzZdZz/^^
ĞĨŝŶŝƚŝŽŶĂŶĚŽŵƉĂƌĂƚŝǀĞEŽƐŽůŽŐLJ
Atherosclerotic CAD is a progressive illness characterized by the formation
of atherosclerotic plaque in one or more of the coronary arteries. Angina
pectoris is the major symptom of coronary disease. Acute episodes of
illness occur owing to formation of thrombus on the surface of a disrupted
atherosclerotic plaque, leading to total or subtotal occlusion of the affected
coronary artery, abrupt myocardial ischemia, and, if not rapidly corrected,
myocardial cell death. The resulting acute coronary syndromes—unstable
angina, myocardial infarction (MI), and cardiac arrest—lead to death or
progressive disability due to recurrent pain, cardiac arrhythmias, and CHF.
Atherosclerosis generally begins early in life but is not clinically evident
until mid-adult life, and behavioral factors clearly affect the development of
CAD.
ƉŝĚĞŵŝŽůŽŐLJ
Approximately one-third of all adults older than 35 years of age ultimately
die of cardiovascular disease, most often of complications of CAD. In the
United States, the incidence of CAD is more than 5 million cases per year,
and more than 600,000 persons per year have a first MI. One-fifth of
survivors of an acute infarction die within 1 year. Public health education
campaigns and more effective treatments have reduced CAD mortality, but
not its incidence. Established risk factors for coronary disease include
family history, male sex, hypertension, hyperlipidemia, diabetes, sedentary
lifestyle, obesity, and smoking. Premenopausal women have reduced risk
compared to men, but the incidence of clinically significant disease rises
after menopause to match that of men. A variety of additional metabolic,
nutritional, and inflammatory factors have been identified as risk factors
for incident coronary disease. Psychological factors have increasingly been
recognized to contribute to the risk of incident coronary disease and for
disease progression. Notably, depression is independently associated with
an almost doubled risk of the development of CAD.
ŝĂŐŶŽƐŝƐĂŶĚůŝŶŝĐĂů&ĞĂƚƵƌĞƐ
The prototypical feature of CAD is chest pain, typically on exertion, but
often there are no symptoms until an acute coronary event occurs. The
typical presentation of myocardial ischemia includes substernal chest pain,
often described as pressure or burning, with radiation to the shoulders,
back, neck, jaw, or left arm; diaphoresis; nausea; light-headedness; or
palpitations; and occurs with or after exertion, eating, or psychological
arousal. Many patients, especially women (for unknown reasons), have
atypical presentations, often without chest pain but with abdominal pain,
fatigue, anxiety, shortness of breath, or dizziness as the presenting
complaint. Characteristic abnormalities may be evident on the resting
electrocardiogram (ECG), such as ST segment depression, left bundle
branch block or left ventricular hypertrophy, or, in acute coronary
syndromes or completed MI, ST segment elevation, pathological Q waves,
and T wave inversions, but the resting ECG is often normal. Further
diagnostic evaluation typically may include exercise stress testing, with or
without echocardiography or radioisotope imaging, and cardiac
catheterization. The diagnosis of acute MI generally rests on a combination
of acute symptoms or characteristic ECG changes along with new elevation
in serum levels of cardiac enzymes (troponin and creatine phosphokinase
[CPK]).
ŝĨĨĞƌĞŶƚŝĂůŝĂŐŶŽƐŝƐ
The differential diagnosis of CAD is extensive. Shortness of breath occurs in
primary lung disease, CHF without significant coronary disease,
pericarditis, and psychiatric disorders including anxiety and somatic
symptom disorders. Chest pain occurs in pericarditis, peptic ulcer disease,
gastroesophageal reflux disease, hiatal hernia, functional heartburn, and
esophagitis; in pulmonary embolism, pleuritis, pleural effusion, and
pneumonia; after rib fracture; and also, again, in psychiatric disorders.
Often, no diagnosis can be established to account for chest pain, and
musculoskeletal pain or costochondritis is invoked, especially if the pain
can be reproduced by manual pressure on the costochondral junction.
Palpitations occur in cases of CAD but also in mitral valve prolapse, in
patients with arrhythmias due to other causes, in hyperthyroidism, and in
many patients with somatic symptom preoccupation, panic, and anxiety
disorders. Ectopic beats also occur in normal individuals with no evidence
of medical or psychiatric disorder.
ŽƵƌƐĞĂŶĚWƌŽŐŶŽƐŝƐ
One-third of patients experiencing their first MI die within 1 hour of the
onset of symptoms. Evolving trends in coronary care have reduced the
short-term mortality of patients with acute coronary syndrome who survive
long enough to be hospitalized. In survivors, recurrent cardiac events occur
with an incidence of 10 to 20 percent per year, and the 1-year mortality
after MI is 20 percent. Current practice in the treatment of acute coronary
syndromes attempts urgent thrombolysis or revascularization by
angioplasty, stent placement, or coronary artery bypass graft (CABG)
surgery; β-adrenergic blockade; statin therapy to stabilize plaque; and
aspirin or antiplatelet drugs.
dƌĞĂƚŵĞŶƚ
Preventive measures in treatment of coronary disease include the use of
aspirin as an antiplatelet drug, exercise, lipid-lowering therapy with statin
drugs, abstinence from or cessation of smoking, blood pressure control,
and maintenance of normoglycemia. Standard pharmacotherapy for CAD
generally includes β-adrenergic blockade, aspirin, statins, and angiotensin-
converting enzyme (ACE) inhibitors or angiotensin receptor blockers, as
well as primary preventive measures. Complications of acute or progressive
disease, such as arrhythmias and CHF, must also be treated.
WƐLJĐŚŽůŽŐŝĐĂů&ĂĐƚŽƌƐĨĨĞĐƚŝŶŐŽƌŽŶĂƌLJƌƚĞƌLJŝƐĞĂƐĞ
Depression, vital exhaustion, anxiety, type A behavior, hostility, anger, and
acute and chronic mental stress have been evaluated as risk factors for the
development and expression of coronary disease. Negative affect in general,
low socioeconomic status, and low social support have been shown to have
significant relationships with each of these individual psychological factors,
and some investigators have proposed these latter characteristics as more
promising indices of psychological risk. Data from the Normative Aging
Study demonstrate a dose–response relationship between negative
emotions (a combination of anxiety and depression symptoms) and
incident coronary disease. Posttraumatic stress disorder (PTSD) is
increasingly recognized as a risk factor for heart disease.
patients with pre-existing CAD also demonstrate a doubling of risk of
adverse coronary disease-related outcomes, including MI, revascularization
procedures for unstable angina, and death, in association with depression.
A study of 1,002 stable outpatients with coronary disease showed that
depression more strongly predicts impairment in quality of life and
physical functioning than reduced ejection fraction or exercise-induced
myocardial ischemia. A dose–response relationship appears to exist
between the severity of depression symptoms after acute MI or unstable
angina and the risk of death over 5-year follow-up, even after controlling
for other significant prognostic factors (Fig. 27.2–1), an observation
replicated in many studies. Depression immediately after CABG surgery,
marked depression 6 months after CABG surgery, and persistence of even
moderate depression symptoms beginning before surgery at 6-month
postoperative follow-up, all predict increased risk of death over 5- to 10-
year follow-up.
Major adverse cardiac events associated with depression in patients
with established CAD include recurrent infarction and sudden cardiac
death. The co-occurrence of depression and frequent premature ventricular
contractions after MI appears to substantially increase the risk of
ventricular tachyarrhythmias; the mortality associated with these
arrhythmic events may be reduced in contemporary cardiology practice
because of the increased use of implantable defibrillators for both
secondary and primary prevention of tachyarrhythmia-related sudden
cardiac death. Although several trials have failed to demonstrate a
significant effect of treatment of depression on mortality and cardiac
outcomes, a recent meta-analytic review found that serotonin reuptake
inhibitor treatment does modestly reduce the risk of recurrent cardiac
events and mortality.

ĞƉƌĞƐƐŝŽŶ͘ Depression is strongly associated with increased risk for

the development and progression of CAD. Numerous large-scale,
prospective, epidemiological studies of nonclinical community-dwelling
subjects yield converging estimates of increased relative risks of incident
MI and cardiac-related mortality of approximately 1.5 to 2.0 in association
with depression. This finding holds even after controlling for smoking, a
potent risk factor for cardiovascular morbidity and mortality that is far
more prevalent in those with depression than in the population at large,
and the effect of depression continues to be present even in long-term
follow-up over 10 to 20 years. Meta-analyses of numerous studies of

&/'hZ Ϯϳ͘Ϯʹϭ͘ >ŽŶŐͲƚĞƌŵ ƐƵƌǀŝǀĂů ĂĨƚĞƌ ŵLJŽĐĂƌĚŝĂů ŝŶĨĂƌĐƚŝŽŶ ŝŶ ƌĞůĂƚŝŽŶ ƚŽ ĞĐŬ
ĞƉƌĞƐƐŝŽŶ/ŶĚĞdž;/ͿƐĐŽƌĞĚƵƌŝŶŐŚŽƐƉŝƚĂůŝnjĂƚŝŽŶ͘;&ƌŽŵ>ĞƐƉĞƌĂŶĐĞ&͕&ƌĂƐƵƌĞ^ŵŝƚŚE͕
dĂůĂũŝĐD͕ŽƵƌĂƐƐĂD'͘&ŝǀĞͲLJĞĂƌƌŝƐŬŽĨĐĂƌĚŝĂĐŵŽƌƚĂůŝƚLJŝŶƌĞůĂƚŝŽŶƚŽŝŶŝƚŝĂůƐĞǀĞƌŝƚLJĂŶĚ
ŽŶĞͲLJĞĂƌ ĐŚĂŶŐĞƐ ŝŶ ĚĞƉƌĞƐƐŝŽŶ ƐLJŵƉƚŽŵƐ ĂĨƚĞƌ ŵLJŽĐĂƌĚŝĂů ŝŶĨĂƌĐƚŝŽŶ͘ ŝƌĐƵůĂƚŝŽŶ͘
ϮϬϬϮ͖ϭϬϱ͗ϭϬϰϵ͕ǁŝƚŚƉĞƌŵŝƐƐŝŽŶ͘Ϳ
Conversely, poor response to antidepressant treatment after an MI is
associated with higher risk of subsequent cardiac events and death.
Secondary analyses of three large trials of depression interventions in
patients with CAD have found that patients who do not experience
improvement in depression symptoms have significantly higher risk of
cardiac death than those whose depression symptoms improved.
WK^^/>D,E/^D^͘ The mechanisms by which depression may increase
coronary disease risk have not been established, but potential mechanisms
may be organized into behavioral and biological pathways. Behavioral
mechanisms include social isolation, physical inactivity, poor adherence,
and smoking. The relationship between cigarette smoking and mental
illness, particularly depression, has been well documented. History of
depression is associated with lifetime risk of smoking, current smoking,
and lower successful quit rate. As the prevalence of smoking trends
downward in the United States, these associations have strengthened.
Biological pathways include links of depression with abnormal
neuroendocrine and autonomic function, smoking, and platelet
dysfunction.
Hypothalamic–pituitary–adrenal (HPA) axis dysregulation in
depression is manifest by elevated levels of circulating cortisol and loss of
the usual diurnal variation in cortisol level. Elevated cortisol has toxic
effects on the coronary artery endothelium and plays a role in plaque
development.
Autonomic dysregulation with diminished cardiac vagal modulation
and increased sympathetic nervous system activation occurs in depression.
This may provide a substrate for increased arrhythmic activity and sudden
death. Heart rate variability, an index of cardiac autonomic control, is
reduced in depression, and reduced variability has been shown to be a
predictor of sudden death in cardiac patients.
Disordered platelet aggregation, leading to increased thrombus
formation, may also play a role in increasing risk of coronary events in
depression. Measures of in vivo platelet activation and platelet aggregation
show that depressed patients exhibit greater prothrombotic activity at
baseline and greater platelet activation by orthostatic challenge.
Serotonergic antidepressants, especially those with high affinity for the
serotonin reuptake transporter, reduce platelet activation, and several
studies indicate that they reduce the likelihood of first MI.
dLJƉĞĞŚĂǀŝŽƌWĂƚƚĞƌŶ͕ŶŐĞƌ͕ĂŶĚ,ŽƐƚŝůŝƚLJ͘ The relationship between
a behavior pattern characterized by easily aroused anger, impatience,
aggression, competitive striving, and time urgency (type A) and coronary
heart disease dominated studies in psychosomatic cardiology in the 1970s
and 1980s. Several large prospective epidemiological studies found the type
A pattern to be associated with a nearly twofold increased risk of incident
MI and coronary disease-related mortality. Hostility as a core component
of the original type A concept has received considerable empirical support
as a predictor of coronary heart disease outcomes. Low hostility is
associated with low coronary disease risk in studies of workplace
populations. High hostility is associated with increased risk of death in 16-
year follow-up of survivors of a previous MI. In addition, hostility is
associated with several physiological processes that, in turn, are associated
with coronary disease, such as reduced parasympathetic modulation of
heart rate, increased circulating catecholamines, increased coronary
calcification, and increased lipid levels during interpersonal conflict.
Conversely, submissiveness has been found to be protective against
coronary disease risk in women. Adrenergic receptor function is down-
regulated in hostile men, presumably an adaptive response to heightened
sympathetic drive and chronic overproduction of catecholamines due to
chronic and frequent anger. A recent meta-analysis of psychological
interventions for patients with CAD found that those that targeted type A
behavior had the strongest effects on cardiovascular outcome. A 2011
randomized clinical trial in post-MI patients found that a 1-year, 20-session
group cognitive-behavioral therapy (CBT) stress management program that
included a strong emphasis on reduction in anger dramatically reduced
fatal and nonfatal recurrent cardiovascular events, recurrent MI, and all-
cause mortality over an 8-year follow-up period. This finding is consistent
with prior studies showing that group therapy for type A behavior
modification was associated with reduced reinfarction and mortality in
post-MI patients and that type A behavior modification therapy reduces
episodes of silent myocardial ischemia.
sŝƚĂů džŚĂƵƐƚŝŽŶ͘ Vital exhaustion, a state of fatigue associated with
loss of energy, increased irritability, and demoralization (e.g., decreased
interest in work, pessimism, and burnout) has been identified as a risk
factor for incident coronary disease and cardiac events in patients with
CAD in European, predominantly Dutch, studies. Because the vital
exhaustion concept overlaps with depression, its independent contribution
remains uncertain.
ĐƵƚĞ DĞŶƚĂů ^ƚƌĞƐƐ͘ Mental stress induces arterial endothelial
dysfunction, with impaired flow-mediated vasodilatation; paradoxical
vasoconstriction during stress occurs in atherosclerotic arterial segments.
Acute mental stress has a significant effect on coronary artery blood flow
that may be of significance in patients with pre-existing coronary disease.
States of fear, excitement, and, especially, acute anger reduce blood flow
through atherosclerotic coronary segments, provoke coronary spasm, and
are associated with abnormal left ventricular wall motion and ECG
evidence of myocardial ischemia. Mental stress-induced ischemia is
associated with increased risk of subsequent cardiac events in patients with
known coronary disease and may occur even in patients who do not
demonstrate evidence of ischemia during exercise stress testing. Relaxation
training can alter autonomic activation during mental stress, implying a
potential therapeutic role for such training in stress-induced ischemia.
There is also evidence that sertraline treatment reduces myocardial
ischemia induced by mental stress.
ůŝŶŝĐĂůsŝŐŶĞƚƚĞ
A 55-year-old man with a history of coronary disease and major depressive disorder reported
daily episodes of angina associated with anger provoked by interpersonal conflicts. Angina
ceased after he began treatment with sertraline.
Triggering of acute cardiac events, including acute MI and sudden
cardiac death, by acute mental stress has been demonstrated in
epidemiological studies of earthquakes and other natural disasters,
sporting events such as World Cup football matches, bombings, and acts of
terrorism such as the destruction of the World Trade Center in 2001.
Ecological momentary assessment studies with periodic ratings of mood,
stress, and affect correlated with ambulatory ECG recordings, and
retrospective reviews of events preceding acute coronary events also
indicate that acute emotional stress is a frequent trigger of MI. Between 1
and 4 percent of MI and between 20 and 40 percent of sudden cardiac
deaths may be precipitated by acute emotional stressors.
ŚƌŽŶŝĐ DĞŶƚĂů ^ƚƌĞƐƐ͘ Chronic mental stress, such as job or marital
strain, also contributes to the development and the progression of CAD.
One study of over 9,000 British civil servants found that persistently
difficult close social relationships independently contributed to the risk of
new CAD. In a study of over 900 men and women who returned to work
after their first MI, job strain (high demand plus low decision latitude)
independently doubled the risk of recurrent cardiac events in the next 6
years. In the largest case control study of predictors of MI, the
INTERHEART study found that among 11,119 cases of MI in 52 countries,
psychosocial factors, defined as a combination of stress and depression,
ranked as the third-highest predictor of MI, raising the risk of MI by an
odds ratio of 2.67, similar to smoking and diabetes.
WŽƐƚƚƌĂƵŵĂƚŝĐ^ƚƌĞƐƐŝƐŽƌĚĞƌ͘ The impact of PTSD on the development
and course of cardiovascular and cerebrovascular disease has become a
topic of considerable recent investigation, along with current recognition of
the high prevalence of PTSD in recent combat veterans. Military veterans
with PTSD have increased risk of the development of CAD, heart failure,
and peripheral vascular and cerebrovascular disease. The effects remain
significant after adjustment for smoking, depression, and other CAD risk
factors. Both behavioral and physiological processes are likely to be
involved as mediators of risk of cardiovascular disease, including smoking,
difficulty adhering to healthy lifestyle, and autonomic dysfunction with
abnormal sympathetic nervous system activation. Even after adjustment
for medication adherence, PTSD is associated with increased morbidity and
mortality.
^ĐŚŝnjŽƉŚƌĞŶŝĂĂŶĚŝƉŽůĂƌ/ůůŶĞƐƐ͘ Persons with severe mental disorders
such as bipolar disorder, schizophrenia, and schizoaffective disorder tend
to die at a younger age than the general population, with doubling of
mortality risk due to cardiovascular disease. In bipolar disorder,
notwithstanding the high rate of death by suicide and accidents,
cardiovascular disease is the leading cause of death. Onset of
cardiovascular morbidity is earlier in people with bipolar disorder at least
in part as a result of higher rates of unhealthy behaviors, common
medication side effects, and problems with access to medical care.
Individuals with severe mental illness are more likely to engage in
several behaviors that are known to increase the risk of cardiovascular
disease. Smoking is highly prevalent in individuals with severe mental
illness, which leads to vascular endothelial damage and systemic
inflammation. Negative symptoms in patients with schizophrenia are
associated with physical inactivity that itself raises cardiovascular disease
risk and is related to poor diet and obesity. For patients with bipolar and
schizoaffective disorder, hypomanic and manic episodes are associated
with the increased risk of substance use, which in turn increases
cardiovascular disease risk. Interestingly, the association between episodes
of mania and hypomania and cardiovascular risk may not depend solely on
altered behavior; lipid metabolism in individuals with bipolar disorder is
an area of ongoing research into a potential link between the
pathophysiology of bipolar disorder and cardiovascular disease.
Various medications used to treat persons with severe mental illness
can contribute to cardiovascular disease risk. Many second-generation
antipsychotics, including clozapine, olanzapine, and risperidone, are
associated with rapid weight gain that can lead to metabolic syndrome
(hypertension, dyslipidemia, increased abdominal fat, insulin resistance,
and hyperglycemia). Mood stabilizers such as valproic acid and lithium are
also associated with weight gain.
It has been noted that patients with serious mental illness who
experience an acute MI are less likely than the general population to receive
appropriate treatment, including both medications and revascularization
procedures. Most individuals with bipolar disorder and schizophrenia
receive inadequate medical care to mitigate their increased risk of
cardiovascular morbidity and mortality. Those with severe mental illness
are less likely to have a primary care physician and more likely to have
difficulty maintaining continuous insurance coverage. Despite numerous
practice guidelines with agreed-upon recommendations for screening of
modifiable cardiovascular risk factors, many patients are not screened or
treated adequately. For example, among the patients with chronically
treated schizophrenia entering the Clinical Antipsychotic Trials of
Intervention Effectiveness (CATIE) study, 88 percent of patients with
dyslipidemia, 62 percent of patients with hypertension, and 30 percent of
patients with diabetes were not being treated with medications for these
conditions. These data underscore the need for better coordination
between mental and physical health services, potentially through systems
of integrated care and/or colocalized psychiatric and medical services.
Baseline assessments for these patients should include a thorough medical
history, anthropometric assessments, thyroid testing, fasting plasma
glucose, fasting blood lipid panel, baseline ECG, and resting blood
pressure.
Z/ZZ,zd,D/^E^hEZ/d,
ĞĨŝŶŝƚŝŽŶĂŶĚŽŵƉĂƌĂƚŝǀĞEŽƐŽůŽŐLJ
Among the many subtypes of cardiac arrhythmia, of greatest importance to
psychiatrists are sinus node dysfunction and atrioventricular (AV)
conduction disturbances resulting in bradyarrhythmias, atrial fibrillation,
and tachyarrhythmias. Bradycardia, defined by a heart rate of less than 60
beats per minute, may occur in normal subjects, especially trained athletes,
but also occurs pathologically in hypothyroidism, severe liver disease, and
vasovagal syncope, and during a variety of metabolic disturbances.
Idiopathic primary sinoatrial node degeneration and pharmacologically
induced dysfunction are the most common causes of bradycardia.
Symptomatic patients typically present with dizziness or syncope.
Bradyarrhythmias also occur in patients with heart block due to impaired
conduction through the AV conduction system, especially AV nodal block.
Sinus node dysfunction including sinus arrest is a known adverse effect of
lithium and can result in clinically significant bradycardia and syncope.
Selective serotonin reuptake inhibitors (SSRIs) may impair sinus node
function, and at high doses tricyclic antidepressants may impair AV nodal
conduction, leading to complete heart block. Serotonin reuptake inhibitors
taken together with β-adrenergic blockers or vagomimetic compounds may
have additive effects to slow the heart rate, sometimes exacerbated if the
serotonergic agent also inhibits the hepatic metabolism of the beta-blocker,
augmenting its effect.
Atrial fibrillation is the most common cardiac arrhythmia in clinical
cardiology practice; it is an irregularly irregular heart rhythm characterized
by disorganized depolarization of atrial myocytes, so that the AV node is
stimulated in a rapid irregular manner. The ventricular response and
resulting heartbeat can be extremely rapid, with palpitations and
symptoms of reduced cardiac output. Disorganized atrial systole reduces
the efficiency of ejection of atrial contents into the ventricles, further
reducing cardiac output (“loss of ‘atrial kick’”). Inefficient atrial emptying
promotes thrombus formation within the atrium, with resulting fivefold
increased risk of embolic stroke and twofold increased risk of death. Atrial
fibrillation can occur as a consequence of hyperthyroidism, in mitral valve
disease, after cardiac surgery, after MI, and in CHF. Atrial fibrillation is
treated with rhythm or rate control using beta-blockers, calcium channel
blockers, cardioversion, or ablation. Anticoagulation reduces the risk of
embolic events but increases the risk of bleeding. Sadness, anxiety, acute
stress, panic disorder, and anger-hostility have been associated with
increased risk of incident atrial fibrillation; in one study, self-reported
happiness was negatively associated with risk.
Ectopic atrial premature beats and ventricular premature beats are
common, occurring in more than 50 percent of adults during 24-hour ECG
monitoring. In isolation, they are of no pathological significance but may be
perceived as flutters in the chest, skipped beats, palpitations, or abnormally
vigorous beats. These sensations exist in a circular relationship with
anxiety: Awareness of unusual heartbeats often provokes vigilance and
anxiety about body sensations, and anxiety is a potent stimulus for
increased frequency of premature beats. Paroxysmal supraventricular
tachycardia due to an ectopic atrial pacemaker frequently presents with
anxiety associated with tachycardia and palpitations and may be
misdiagnosed as a panic attack.
Sustained ventricular tachycardia and ventricular fibrillation are lethal
arrhythmias; patients with CAD or completed MI who have frequent
premature ventricular depolarizations are at risk of cardiac arrest due to
one of these forms of arrhythmia. About half of all cardiac deaths are
sudden cardiac deaths, and half of cases had no previously known heart
disease.
WĂƚŚŽƉŚLJƐŝŽůŽŐLJŽĨsĞŶƚƌŝĐƵůĂƌdĂĐŚLJĂƌƌŚLJƚŚŵŝĂƐ͘ Malignant ventricular
arrhythmias may occur as an electrical accident in individuals with no
structural heart disease but more often occur in those with underlying
heart disease. Because conduction of myocardial depolarization may be
delayed in regions of myocardial tissue damage, regions distal to the
affected area may be stimulated to depolarization while adjacent tissue is
undergoing repolarization, setting off a premature depolarization of the
adjacent tissue that may precipitate ventricular fibrillation. The rate of local
repolarization and readiness to initiate the next cardiac cycle is modulated
by local innervation of the heart by branches of the sympathetic and
parasympathetic nervous systems. In general, sympathetic fibers
predominate in the left ventricular myocardium and have the effect of
increasing irritability and stimulating depolarization. Parasympathetic
fibers predominate in the innervation of the specialized cardiac conduction
system and have the effect of slowing heart rate and reducing automaticity.
Lethal ventricular tachyarrhythmias are more likely to occur in the
setting of structural heart disease (e.g., after an MI) but also are related to
genetic disorders regulating ion channels that control ventricular
depolarization and repolarization, such as congenital long QT syndrome
and Brugada syndrome. These latter disorders are sometimes clinically
silent until “unmasked” by medications including lithium, tricyclic
antidepressants, and phenothiazines.
ŝĂŐŶŽƐŝƐ
Diagnosis of cardiac arrhythmias depends on the ability to record the
rhythm disturbance. Because the resting ECG is most often normal or
shows isolated premature contractions in patients with episodic rhythm
disturbances, ambulatory ECG monitoring may be needed to establish the
diagnosis. Provocative electrophysiological testing may be used to attempt
to induce arrhythmias; depending on the nature of the resulting
arrhythmias, if present, therapies may include ablation of the focus of
ectopic activity, implantation of an automatic cardiac defibrillator, or
antiarrhythmic drug therapy. Indications for defibrillator implantation
have been broadened to include not only secondary prevention for patients
with previous episodes of sudden cardiac death/ventricular
tachycardia/ventricular fibrillation but also primary prevention for patients
with reduced left ventricular ejection fraction due to ischemic or
nonischemic heart disease.
WƐLJĐŚŽůŽŐŝĐĂů&ĂĐƚŽƌƐĨĨĞĐƚŝŶŐƌƌŚLJƚŚŵŝĂ
Because autonomic cardiac modulation is profoundly sensitive to acute
emotional stress, such as intense anger, fear, or sadness, it is not surprising
that acute emotions can stimulate arrhythmias. Instances of sudden cardiac
death related to sudden emotional distress have been noted throughout
history in all cultures. In community samples depression, phobic anxiety
and mixed anxiety symptoms increase the risk of sudden cardiac death.
After the destruction of the World Trade Center in New York in 2001,
patients with implanted defibrillators had sharply increased frequency of
ventricular tachycardia events. In post-MI patients with ventricular ectopy,
comorbid depression is associated with significantly increased rates of
ventricular tachycardia–ventricular fibrillation. Psychiatric conditions
treated with antipsychotic drugs and citalopram are also associated with
increased risk of ventricular tachyarrhythmias, due to the adverse effect of
the psychiatric medication on cardiac conduction. The effect of
psychotropic drugs on the QT interval and arrhythmia risk is discussed
below. Depression is associated with increased mortality in patients who
have received an implanted defibrillator for the prevention of sudden
cardiac death.
KE'^d/s,Zd&/>hZ͕,ZddZE^W>Ed͕E^^/^ds/^
ĞĨŝŶŝƚŝŽŶĂŶĚŽŵƉĂƌĂƚŝǀĞEŽƐŽůŽŐLJ
CHF is an end result of many forms of heart disease and represents the
most common final pathway toward disability and mortality. Heart failure
with reduced ejection fraction (systolic dysfunction) occurs after MI. Heart
failure with preserved ejection fraction (diastolic dysfunction), with
impaired ventricular filling or elevated filling pressure, is increasingly
recognized and may be due to infiltrative disease, hypertension with
resultant chronic ventricular hypertrophy and increased ventricular wall
stiffness, or other causes. Shortness of breath, reduced exercise tolerance,
and peripheral edema are typical symptoms of heart failure. Hepatic
congestion and cardiac cirrhosis occur as complications of elevated central
venous pressure. Renal dysfunction occurs secondary to poor renal
perfusion and impaired venous drainage, and may be exacerbated by
diuretic-induced dehydration. Heart failure patients may struggle with
oscillation between the extremes of being “too wet” or “too dry.” Treatment
of heart failure patients usually includes ACE inhibitors or angiotensin
receptor blockers, β-adrenergic blocking agents, spironolactone, and
diuretics. Diastolic dysfunction tends to be more refractory to treatment.
Heart transplantation and left ventricular assist devices (LVADs) are
options for refractory cases. Apart from their evaluation as heart transplant
candidates, there has been relatively little study of the psychiatric problems
of heart failure patients. Clinically, it appears that adjustment disorders,
depression, and anxiety are relatively common problems in this population.
Disorders of alertness and cognition occur in patients with hypotension,
hyponatremia, hepatic failure, and renal failure secondary to heart failure.
Diagnosis of psychiatric disorders in patients with CHF requires clinical
judgment, as symptoms of heart failure may confound the psychiatric
presentation. Dyspnea and orthopnea, for example, may resemble panic,
and orthopnea, in particular, may interfere with sleep. Hopelessness,
decreased self-esteem, suicidal ideation, and other cognitive aspects of
affective illness are not normally present in heart failure patients and may
help make the distinction.
ƉŝĚĞŵŝŽůŽŐLJ
Recent data continue to demonstrate that more than 500,000 people
develop CHF per year in the United States, and heart failure is cited as the
principal cause in 40,000 deaths and as a contributing factor in 250,000
deaths per year.
ƚŝŽůŽŐLJ
Neurohormonal activation, with a chronic state of sympathetic nervous
system activation, is a hallmark of the development of heart failure and
promotes ventricular remodeling, the dilatation of the left ventricle
associated with reduced ventricular contractility. MI, hypertension, and
mitral and aortic valve disease are among the most common known causes
of heart failure, but dilated cardiomyopathies have many other etiologies,
including viral cardiomyopathy, toxicity of adriamycin, cocaine and other
agents, genetic disorders, and inflammatory disorders, such as giant cell
myocarditis. Almost one half of all nonischemic cardiomyopathy is
idiopathic. Restrictive (e.g., constrictive pericarditis), obstructive (e.g.,
asymmetrical septal hypertrophy and hypertrophic subaortic stenosis), and
infiltrative diseases (e.g., systemic amyloidosis) also result in heart failure.
ŝĂŐŶŽƐŝƐĂŶĚůŝŶŝĐĂů&ĞĂƚƵƌĞƐ
Patients typically present with complaints of shortness of breath or
dyspnea on exertion, diminished exercise tolerance, fatigue, or edema.
Rales, abnormal heart sounds (especially S3 gallop), displacement of the
point of maximal impact of the heart on the chest wall, neck vein
distention, hepatic enlargement, and lower extremity edema may be
present on physical examination. Echocardiography or ventriculography
demonstrates ventricular dilatation (in many cases) and decreased
contractility. Cardiopulmonary exercise stress testing demonstrates
decreased capacity to utilize oxygen. B-type natriuretic peptide levels mark
severity of physiological derangement.
ŝĨĨĞƌĞŶƚŝĂůŝĂŐŶŽƐŝƐ
Hypothyroidism, pulmonary disease, renal disease, and liver disease may
present with symptoms resembling those of heart failure, such as shortness
of breath, edema, and fatigue. Psychiatric disorders must also be included
in the differential diagnosis of heart failure. Fatigue and low energy may be
presenting complaints in depression and generalized anxiety disorder, and
shortness of breath may be the presentation of somatoform and panic
disorders.
ŽƵƌƐĞĂŶĚWƌŽŐŶŽƐŝƐ
CHF is a progressive condition with an approximately 50 percent 5-year
mortality. Classification schemes for staging of CHF are shown in Table
27.2–1. To some degree, prognosis depends on the underlying cause and
the possibility of reversing the pathophysiological derangement. Some
forms of infectious and inflammatory myocarditis are completely
reversible. Ventricular contractility may be impaired by reversible coronary
vascular insufficiency; angiography and positron emission tomography
may identify patients with viable myocardium who will experience
improved ventricular function after a revascularization procedure. For
most patients, however, who have idiopathic dilated cardiomyopathy or MI
with ventricular dysfunction, the course tends to be one of stable or
gradually downhill functional status punctuated by acute episodes of fluid
overload or cardiac arrhythmia, precipitating admission. Comorbid
depression is associated with higher morbidity and mortality.
dƌĞĂƚŵĞŶƚ
Mainstays of therapy for CHF are diuretics, ACE inhibitors or angiotensin
receptor blockers, and β-adrenergic blocking agents; the role of digoxin has
diminished, as some studies suggest that it increases mortality. Many trials
of agents with positive inotropic effects have failed to establish a survival
benefit. Cardiac arrhythmias occur at increased frequency in patients on
inotropic agents. Nevertheless, intravenous (IV) dobutamine (Dobutrex),
milrinone (Primacor), and similar medications are sometimes prescribed
for severely ill patients who would otherwise succumb to low-output states.
Heart transplantation is an option limited by donor supply to a small
fraction of those who might benefit from it. In the absence of significant
improvement in survival with new medications in recent years, and given
the limited number of patients who can receive transplants, the survival
benefit provided by ventricular assist devices has led to their increased use
not only for “bridge to transplantation” but also as “destination” therapy.
dĂďůĞϮϳ͘Ϯʹϭ͘
,ĞĂƌƚ&ĂŝůƵƌĞůĂƐƐŝĨŝĐĂƚŝŽŶ
EĞǁzŽƌŬ,ĞĂƌƚƐƐŽĐŝĂƚŝŽŶ ŵĞƌŝĐĂŶ,ĞĂƌƚƐƐŽĐŝĂƚŝŽŶ
&ƵŶĐƚŝŽŶĂůĐůĂƐƐŝĨŝĐĂƚŝŽŶ WƌŽŐŶŽƐƚŝĐĐůĂƐƐŝĨŝĐĂƚŝŽŶ
ůĂƐƐ/͗ƐLJŵƉƚŽŵĂƚŝĐ ^ƚĂŐĞ͗WƌĞƐĞŶĐĞŽĨƌŝƐŬĨĂĐƚŽƌƐ
 ^ƚĂŐĞ͗^ƚƌƵĐƚƵƌĂůŚĞĂƌƚĚŝƐĞĂƐĞǁŝƚŚŽƵƚƐLJŵƉƚŽŵƐ
ůĂƐƐ//͗DŝůĚƐLJŵƉƚŽŵƐǁŝƚŚ ^ƚĂŐĞ͗^ƚƌƵĐƚƵƌĂůŚĞĂƌƚĚŝƐĞĂƐĞǁŝƚŚĐƵƌƌĞŶƚƐLJŵƉƚŽŵƐŽƌƉƌĞǀŝŽƵƐ
ŵŽĚĞƌĂƚĞĞdžĞƌƚŝŽŶ ƐLJŵƉƚŽŵƐƚŚĂƚŚĂǀĞƌĞƐƉŽŶĚĞĚƚŽƚŚĞƌĂƉLJ
ůĂƐƐ///͗DŝůĚĞdžĞƌƚŝŽŶůŝŵŝƚĞĚ
ďLJƐLJŵƉƚŽŵƐ
ůĂƐƐ/s͗^LJŵƉƚŽŵƐĂƚƌĞƐƚ ^ƚĂŐĞ͗^LJŵƉƚŽŵƐĂƌĞƌĞĨƌĂĐƚŽƌLJƚŽĐŽŶǀĞŶƚŝŽŶĂůƚƌĞĂƚŵĞŶƚĂŶĚ
ƌĞƋƵŝƌĞĂƐƐŝƐƚĚĞǀŝĐĞ͕ƚƌĂŶƐƉůĂŶƚŽƌƉĂůůŝĂƚŝǀĞĐĂƌĞ
,ĞĂƌƚ dƌĂŶƐƉůĂŶƚĂƚŝŽŶ͘ Heart transplantation is available to between
2,000 and 2,500 patients annually in the United States. It provides
approximately 75 percent 5-year survival for patients with severe heart
failure, who would otherwise have a less than 50 percent 2-year survival.
Candidates for heart transplantation typically experience a series of
adaptive challenges as they proceed through the process of evaluation,
waiting, perioperative management, postoperative recuperation, and long-
term adaptation to life with a transplant. These stages of adaptation
typically are accompanied by anxiety, depression, elation, and working
through of grief. Mood disorders are common in transplant recipients.
>ĞĨƚsĞŶƚƌŝĐƵůĂƌƐƐŝƐƚĞǀŝĐĞƐ͘ LVADs are approved as a bridge to heart
transplantation and also for long-term treatment of CHF. First- and
second-generation devices consist of a conduit that drains the left ventricle
of the heart, connected to a mechanical pump implanted in the abdomen,
which, in turn, drains into a conduit connected to the ascending aorta.
Some newer devices use a small axial flow pump implanted inside the
pericardium that drains the left ventricle and empties into the ascending
aorta. The power for the pump is supplied by an external power source,
such as a battery that can be worn on a vest, permitting the patient to
ambulate freely. It has not yet been possible to produce a totally
implantable device with no need to traverse the skin. Patients with LVADs
may recover from the clinical complications of left ventricular functional
impairment, with improved renal, hepatic, cerebral, and peripheral
circulation leading to improved exercise tolerance, functional capacity, and
general well-being. They are subject to complications, such as bleeding,
infection, anorexia, and stroke. Depression and organic mental syndromes
occur frequently. Prior cerebrovascular disease appears to be a risk factor
for psychiatric and neuropsychiatric complications in patients with LVADs.
Caregiver burden is substantial for family members of assist device patients
when they are discharged from the hospital. The neuropsychiatric and
quality-of-life effects of VAD therapy depend on pump design and are likely
to continue to evolve over the near future.
WƐLJĐŚŽůŽŐŝĐĂů&ĂĐƚŽƌƐĨĨĞĐƚŝŶŐŽŶŐĞƐƚŝǀĞ,ĞĂƌƚ&ĂŝůƵƌĞ
Relatively little attention has been paid to the role of psychological factors
in heart failure. However, depression has been recognized as a risk factor in
heart failure incidence and mortality, and the role of psychological factors
in outcome after heart transplantation has been explored. Poor self-care
related to depression has been highlighted as a factor in poor outcome in
heart failure, along with fatigue, denial, lack of knowledge, and impaired
cognitive function.
ĞƉƌĞƐƐŝŽŶĂŶĚWƌŽŐŶŽƐŝƐŝŶŽŶŐĞƐƚŝǀĞ,ĞĂƌƚ&ĂŝůƵƌĞ͘ In a prospective,
longitudinal study of 4,538 hypertensive patients older than 60 years of
age, with a 4.5-year follow-up, CHF developed in 8.1 percent of patients
with high depression symptoms versus 3.2 percent of patients with low
depression symptoms. Adjusting for demographic and medical variables
predicting development of heart failure, including incident MI during the
follow-up period, depression was associated with almost threefold
increased risk of the development of heart failure.
Several studies, involving more than 1,000 patients in total, have
demonstrated the substantial prevalence and prognostic significance of
depression symptoms and major depressive disorder in patients with CHF.
In one study, comorbid major depression increased 1-year mortality more
than threefold in patients with New York Heart Association class III and IV
heart failure. In a second study, 14 percent of hospitalized patients with
CHF met criteria for major depression, and 39 percent had Beck
Depression Index scores of greater than 10. One-year mortality was 16
percent; major depression was associated with more than doubling of
mortality at 3-month and 1-year follow-up, even after adjusting for other
prognostic factors. A retrospective study with 5-year follow-up of 396
patients with CHF due to nonischemic dilated cardiomyopathy identified
21 percent as clinically depressed; of these, 60 percent were receiving
antidepressants. Mortality at 5 years was 36 percent in depressed patients
versus 16 percent in nondepressed patients, with a statistically significant,
threefold increased risk of death for the depressed patients after adjusting
for other factors. As with CAD, depression hastens the development of and
the mortality associated with CHF. In a randomized trial, sertraline
treatment of depression in patients with CHF did not result in improved
depression or survival; in a smaller study, paroxetine was superior to
placebo for improvement in depression symptoms. In a recent trial,
cognitive behavioral therapy improved depression but not heart failure self-
care in a heart failure patients with depression. A recent animal study
found that, independent of its antidepressant effects, paroxetine protects
against pathological changes in left ventricular structure and function in
the setting of heart failure due to MI.
ĨĨĞĐƚ ŽĨ WƐLJĐŚŽƐŽĐŝĂů &ĂĐƚŽƌƐ ŽŶ ŽŵƉůŝĂŶĐĞ ĂŶĚ ^ƵƌǀŝǀĂů ŝŶ ,ĞĂƌƚ
dƌĂŶƐƉůĂŶƚWĂƚŝĞŶƚƐ͘ An emerging body of evidence has demonstrated that
preoperatively assessed psychosocial variables predict not only psychiatric,
but also medical, outcomes after heart transplantation. Personality
disorders, substance abuse disorders, dimensional measures of coping
skills and social support, and clinically assessed compliance history have
been linked to the increased risk of poor postoperative compliance,
rejection episodes, and increased mortality. The use of psychiatric
assessment of transplant candidates may identify opportunities for
intervention before transplantation with subsequent improvement in
outcome. Depression and PTSD after heart transplantation are associated
with heightened mortality.
,zWZdE^/KE
ĞĨŝŶŝƚŝŽŶĂŶĚŽŵƉĂƌĂƚŝǀĞEŽƐŽůŽŐLJ
Hypertension is defined by elevation of blood pressure, typically (but
arbitrarily) with a cutoff of 120 to 140 mm Hg, for systolic blood pressure,
or more than 80 to 90 mm Hg, for diastolic blood pressure, on repeated
measurements, at rest, over time. Blood pressure normally increases
during exertion and falls during sleep (“nocturnal dipping”). Typically,
hypertension is an asymptomatic chronic condition that eventually results
in increased risk of CAD, MI, cardiomyopathy, renal failure, peripheral and
cerebral vascular disease, and stroke.
ƉŝĚĞŵŝŽůŽŐLJ
The prevalence of hypertension in the United States is high, in the range of
20 to 50 percent of adults, depending on the population examined and
cutoff criteria for diagnosis employed. The highest incidence is in the third
through fifth decades of life. Epidemiological risk factors for the
development of hypertension include male sex, family history, nonwhite
race, and high dietary sodium intake. The role of psychosocial risk factors
in the development of hypertension is controversial. Anxiety, acute mental
stress, chronic anger, and job strain have been associated with risk of
hypertension, but epidemiological studies have not yielded consistent
associations. Acute mental stress is associated with transient increased
blood pressure and underlies the phenomenon of white-coat hypertension,
the propensity to manifest elevation of blood pressure during physical
examination, although blood pressure is normal at other times; the
patient’s anxiety about the result of the blood pressure measurement has
the effect of momentarily increasing blood pressure. For this reason, blood
pressure should be recorded repeatedly to allow habituation to the
situation before hypertension is considered to be present.
ƚŝŽůŽŐLJ
More than 90 percent of patients with hypertension have idiopathic or
essential hypertension. Familial and genetic influences are evident.
Pathophysiologically, sympathetic nervous system activation and renin-
angiotensin system activation are important determinants of elevation of
blood pressure. Vasoconstriction mediated by the smooth muscle media
layer of the vessel walls of small arterioles is the primary moment-to-
moment regulator of blood pressure. Renal function—the regulation of
sodium, potassium, and free water excretion—provides more long-term
regulation of blood pressure.
ŝĨĨĞƌĞŶƚŝĂůŝĂŐŶŽƐŝƐ
In addition to essential hypertension, renal, vascular, and endocrine
disorders are the most common causes of hypertension. Renal artery
stenosis, adrenal adenomas (Cushing syndrome), and pituitary adenomas
(Cushing disease) result in hypertension, with characteristic findings on
neuroendocrine testing and clinical examination; in these illnesses,
hypertension responds to correction of the lesion. In pheochromocytoma,
paroxysmal hypertension results from surges of epinephrine secretion from
the neuroendocrine tumor.
ŽƵƌƐĞĂŶĚWƌŽŐŶŽƐŝƐ
Although hypertension is often clinically silent for decades, it may
eventually lead to stroke—ischemic or hemorrhagic—cardiac disease, or
renal failure. Symptoms of hypertension, when present, may include chest
discomfort, headache, and dizziness.
dƌĞĂƚŵĞŶƚ
Mainstays of pharmacotherapy of hypertension include diuretics, ACE
inhibitors and angiotensin II blockers, β-adrenergic blockers, and calcium
channel blockers. Low-salt diet, weight loss, and exercise help reduce blood
pressure.
WƐLJĐŚŽůŽŐŝĐĂů&ĂĐƚŽƌƐĨĨĞĐƚŝŶŐ,LJƉĞƌƚĞŶƐŝŽŶ
“Does tension cause hypertension?” Psychodynamic theories of
hypertension from the 1950s have been discredited, and empirical studies
of psychological factors contributing to the development of hypertension
have yielded mixed results. Laboratory and ambulatory monitoring studies
clearly demonstrate that acute mental stress results in transient elevation
of systolic and diastolic blood pressure. Some studies have found that these
transient hemodynamic responses predict increased blood pressure and
incident hypertension over long-term follow-up. Some recent, large,
population-based cohort studies, examining stress, negative affect, and
anxiety as predictors of incident hypertension, have found a positive
association, with 1.5- to 3-fold increased risk, while others have found
none, or even a negative association. A small study of individualized stress
management for patients with hypertension showed improvement in blood
pressure as a result of the intervention, with reduction in blood pressure
correlated with reduced stress and improved coping with anger.
^zEKW Heart disease is an important prognostic indicator in syncope. In
ĞĨŝŶŝƚŝŽŶĂŶĚŽŵƉĂƌĂƚŝǀĞEŽƐŽůŽŐLJ
Syncope is defined as a sudden, transient loss of consciousness with
associated loss of postural tone, followed by spontaneous recovery, and is
due to temporary reduction in cerebral blood flow. Long-term follow-up
from the Framingham Heart Study found the incidence of first report of
syncope to be 6.2 cases per 1,000 person-years. Approximately 3 percent of
emergency room visits and 1 to 6 percent of hospital admissions are for
syncope. Mechanisms of syncope include disruption in vascular tone or
inadequate blood volume, heart rhythm disorders, perfusion failure in
aortic stenosis or severe pulmonary hypertension, or primary
cerebrovascular insufficiency (usually vertebrobasilar insufficiency).
Disruption in autonomic tone is most common and vasovagal syncope, also
referred to as vasodepressor or neurocardiogenic syncope, and postural
hypotension account for 30 to 50 percent of all cases of syncope. Syncope
can occur as a single episode or can be recurrent and chronic.
Approximately 30 to 40 percent of syncope is idiopathic. It is most
important to detect bradyarrhythmias and ventricular tachyarrhythmias as
an underlying cause, because these are usually associated with underlying
structural heart disease and carry increased mortality risk.
ŝĂŐŶŽƐŝƐĂŶĚůŝŶŝĐĂů&ĞĂƚƵƌĞƐ
Physical examination, including supine and standing blood pressure, and
ECG are the basic examinations for patients with syncope. Abnormal ECG
or structural heart disease often dictates stress testing, echocardiography,
ambulatory monitoring, or electrophysiological (EP) study. In the absence
of structural heart disease, the most likely cause of syncope is one of the
neurally mediated syndromes. Tilt testing with or without isoproterenol
infusion or sublingual nitroglycerine helps demonstrate orthostatic
hypotension and neurocardiogenic syncope, but results of tilt testing are
often irreproducible, and specificity and sensitivity of tilt testing are
disappointing.
ŝĨĨĞƌĞŶƚŝĂůŝĂŐŶŽƐŝƐ
Drop attacks, dizziness, and vertigo do not cause loss of consciousness.
Seizures can be difficult to distinguish from syncope, but a preceding aura,
prolonged loss of consciousness for more than 5 minutes, and rhythmic
movements during loss of consciousness are characteristic of seizures.
Pain, micturition, defecation, exercise, and stress as precipitating events
are more characteristic of syncope than of seizures.
ŽƵƌƐĞĂŶĚWƌŽŐŶŽƐŝƐ
particular, patients with syncope with associated left ventricular
dysfunction and CHF have significant 1-year mortality risk. Older age,
ventricular arrhythmias, abnormal ECG, and heart failure contribute
additive mortality risk in patients with syncope. Long-term follow-up data
indicate no increase in mortality or MI risk for patients with vasovagal
syncope or orthostatic hypotension but increased risk of death and MI for
patients with syncope due to underlying heart disease, neurological disease,
or syncope of unknown cause.
dƌĞĂƚŵĞŶƚ
Treatment addresses the underlying cause of syncope, when possible. For
the majority of patients with idiopathic syncope or neurocardiogenic
syncope, orthostatic hypotension, or vasovagal syncope, or a combination
of these, behavioral interventions include instruction about avoiding
precipitants and lying down when premonitory symptoms arise. Alcohol
consumption, sleep deprivation, fasting, dehydration, and prolonged
standing should be avoided.
Both beta-blockers and β-adrenergic agonists have been used for
pharmacological treatment of syncope, but clinical trials are lacking or have
shown at best equivocal efficacy. Permanent pacemakers may be the best
option for patients with recurrent syncope with significant functional
impairment, particularly if cardiac monitoring or tilt testing has
demonstrated bradycardia. Orthostatic hypotension can be treated with
compression stockings, α-adrenergic agonists, and salt supplements or
fludrocortisone.
WƐLJĐŚŽůŽŐŝĐĂů&ĂĐƚŽƌƐĨĨĞĐƚŝŶŐ^LJŶĐŽƉĞ
Although anxiety and acute emotional stress are recognized as precipitants
of syncope, the prevalence of these factors in syncope is unknown. Anxiety
and panic disorder are common in patients with recurrent syncope, but
whether they were present before syncope or only after has not been well
established. One study found no difference between syncope patients with
and without positive tilt table tests in rates of panic and generalized anxiety
disorder, but identified depression as a predictor of recurrent syncope over
3-year follow-up. It should be noted that some clinicians distinguish
hysterical fainting from syncope by the absence of pallor, hypotension, or
bradycardia during the hysterical faint, but the prevalence of this condition
and its relationship to psychological factors or psychiatric diagnoses are not
clear.
d<Kd^hKZ/KDzKWd,z
Takotsubo cardiomyopathy, also known as apical ballooning syndrome,
stress cardiomyopathy, or broken-heart syndrome, is an unusual disorder,
but notable on account of the frequently noted role of acute psychological
stress in most cases. Cases typically present with sudden onset of chest pain
and left ventricular dysfunction, do not have angiographic or enzyme
evidence of an MI, and demonstrate characteristic ballooning of the left
ventricular apex with echocardiography or angiography. The history
typically reveals sudden psychological shock immediately preceding the
event, such as receiving news of the death of a loved one, surprise birthday
parties, or witnessing a traumatic event. Retrospective case-control studies
suggest that premorbid social isolation, anxiety, depression, and family
history of anxiety or depression are more common in patients with stress
cardiomyopathy than in age- and sex-matched MI patients or community
dwelling nonpatients. Left ventricular function usually recovers over a few
days to weeks. The transient changes in cardiac function have been
attributed to a surge in circulating catecholamines and sympathetic
nervous system activation associated with the sudden psychological
stressor.
KE'E/d>,Zd/^^ prophylaxis.
Congenital heart defects occur in 1 percent of live births. Since the 1970s,
advances in cardiac surgery have enabled patients who would previously
have died in childhood to reach adulthood. Most of these patients have
residual abnormalities of circulation, due to uncorrected problems or to
surgical modification of circulation. Late complications include right to left
shunts with cyanosis, sinus and AV node dysfunction, arrhythmias, heart
block, valvular dysfunction, and risk of endocarditis. Ventricular
dysfunction can also occur with right or left heart failure. Adjustment and
developmental problems appear to be common in patients with congenital
heart disease. Cognitive problems may occur as a result of congenital right-
to-left shunting with resulting systemic cyanosis and impaired cerebral
oxygenation.
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The relationship between valvular heart disease and psychiatric disorder
has been a matter of considerable interest over the past several decades. In
panic disorder, mitral valve prolapse is detected in 10 to 25 percent of
patients studied with echocardiography. However, prolapse also occurs in a
substantial portion of the population without panic disorder, and the
nature of the relationship remains uncertain. The subjective experience of
valve prolapse (e.g., fluttering and chest pressure) may be a trigger for
panic sensations; alternatively, the association may be purely coincidental.
Obsessive-compulsive disorders (OCDs), tic disorders, and Tourette
syndrome are associated with poststreptococcal immune system–mediated
inflammatory responses that are similar to those leading to
glomerulonephritis and rheumatic heart disease, a finding stimulated by
consideration of the tic-like quality of movement disorders occurring in
rheumatic fever. This association would lead to the expectation of an excess
of rheumatic valvular heart disease in patients with the OCD spectrum
disorders.
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Stroke is the second leading cause of death worldwide, and the fourth
leading cause in the United States, accounting for 5 percent of deaths. Most
strokes are due to atherosclerotic disease, with risk factors similar to those
for coronary disease. Embolic events and primary intracranial hemorrhage
are other causes of stroke. Study of the relationship between stroke and
psychiatric illness has focused primarily on depression as an effect of
stroke; the incidence of poststroke depression appears to be in the range of
20 to 50 percent at 1 month to 1 year after the index event. However, other
questions of interest include the effect of psychological factors on the risk
of stroke incidence and recovery from stroke, the relationship between
stroke lesion location and incidence of depression, and possible
Depression is a risk factor for stroke. In NHANES I, depression
predicted stroke in models adjusting for age and other stroke risk factors in
white men and blacks of both sexes, with relative risks ranging from 1.68 to
2.60. For white women, the effect of depression was of borderline
significance. In the Women’s Health Initiative Study, SSRI antidepressants
increased the risk of hemorrhagic stroke in postmenopausal women.
A previous history of depression, previous history of other psychiatric
illness, dysphasia, functional impairment, living alone, and social isolation
are the most important predictors of depression after stroke. Lesion
laterality is not a good predictor of depression risk. Worsening of
depression symptoms over time after stroke is associated with subcortical
white matter lesions, and persistent symptoms with small basal ganglia
lesions or large cerebral cortical lesions.
Depression after stroke appears to have a negative effect on functional
outcome, independent of the severity of the stroke itself as judged by other
measures. In the short term, depression impairs reacquisition of mobility
and capacity for activities of daily living, even in patients receiving
antidepressant treatment. This effect persists in studies looking at outcome
as long as 15 months after stroke.
Given the high incidence, prevention of depression in poststroke
patients has been a matter of investigation. Some studies have
demonstrated prophylactic benefits from sertraline, fluoxetine (Prozac),
and nortriptyline. Treatment of depression in poststroke patients with
nortriptyline and serotonin reuptake inhibitors is safe and effective but has
not been shown to reduce poststroke mortality. In a randomized controlled
trial, fluoxetine was superior to placebo in its effect on motor recovery over
6 months after stroke. This effect was independent of an effect on
depression.
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Clozapine treatment is associated with myocarditis, with reported
incidence varying from <0.05 to 1 percent. Signs and symptoms include
flu-like illness, chest pain, tachycardia, hypotension, palpitations, and
dyspnea. Arrhythmias and heart failure may occur. About 50 percent of
cases recover completely, while 10 percent have significant persistent heart
failure symptoms or other complications. Fever during the first 6 weeks of
clozapine treatment may be a sign of early myocarditis. Occurrence is
idiosyncratic and may involve allergic or autoimmune responses.
&hEd/KE>Z/^zDWdKD^
Somatic symptom disorder, panic disorder, anxiety, and depression can all
present with somatic complaints and represent a substantial issue in
ambulatory and emergency cardiology practice. In studies of patients
presenting with the chief complaint of palpitations, these diagnoses
account for approximately 30 percent of cases. In this population,
psychiatric disorder is associated with more frequent recurrent symptoms,
emergency room visits, hypochondriacal concerns, and impairment in
activities of daily living. Similarly, chest pain is a common presentation for
panic disorder. In a study of 1,999 consecutive patients presenting with
chest pain, panic disorder was diagnosed in 38 percent. Patients without
CAD were twice as likely to receive a panic disorder diagnosis. Panic
patients were younger, more likely to be female, and more likely to be
unemployed. In another study of individuals presenting to the emergency
room with chest pain, variables associated with panic disorder included
absence of CAD, female sex, atypical quality of chest pain, younger age, and
high level of self-reported anxiety.
W^z,/dZ/WZK>D^/EWd/Ed^t/d,Z//^^
Psychiatric disorders frequently occur as complications or as comorbid
conditions in individuals with cardiovascular disease. Depression, anxiety,
delirium, and cognitive disorders are especially prevalent problems.
Surveys of ambulatory cardiology practice patients with documented heart
disease indicate a point prevalence of 5 to 10 percent with anxiety
disorders, predominantly panic attacks and phobias, and 10 to 15 percent
with affective disorders, predominantly major depressive episodes, minor
depression, or dysthymia. Major depressive disorder occurs in 15 to 20
percent of patients after MI. PTSD is increasingly recognized as a
complication and comorbidity in patients with heart disease.
WƐLJĐŚŝĂƚƌŝĐŽŵƉůŝĐĂƚŝŽŶƐŽĨƌƌŚLJƚŚŵŝĂƐ
Ventricular arrhythmias may be asymptomatic or may cause palpitations,
light-headedness, dizziness, syncope, or sudden cardiac death. Patients
who experience life-threatening rhythm disturbances are prone to
secondary adjustment, mood, and anxiety disorders. The cardiovascular
symptoms may lead to profound disruption of social roles and capacity for
autonomous functioning. Even patients without symptoms may be
counseled to avoid activities such as driving, which may be hazardous in
the event of an arrhythmic event. Psychodynamically, because of the
recurring, unpredictable, and sudden quality of the course of illness, fear of
exertion, issues of dependence on others, and loss of control are especially
prominent, as well as anxiety about death itself.
Treatment of cardiac rhythm disorders can engender psychiatric
complications. Many antiarrhythmic agents have psychiatric side effects,
including delirium, hallucinations, paranoid ideation, and mood
disturbance. Automatic implanted cardioverter-defibrillators (AICDs) have
supplanted chronic antiarrhythmic medical therapy in most patients who
have experienced ventricular tachycardia–ventricular fibrillation.
Unfortunately, inappropriate shocks are commonplace. Cardioversion by
an AICD may occur in a conscious patient, who experiences the sensation
of one or more powerful shocks or blows to the chest. Although most
patients with AICD seem satisfied with their devices, approximately 10
percent of patients develop clinically significant anxious or depressed mood
symptoms, including panic and agoraphobia and symptoms of
posttraumatic stress associated with AICD discharges. Avoidance behaviors
and anxiety in the setting of discharge-associated stimuli reduce quality of
life for patients who have experienced shocks during ordinary activities
such as sexual relations, showering, and low-intensity exercise. Risk factors
for psychiatric complications in patients with AICD include defibrillator
discharges early after implantation, repetitive discharges, and a high
cumulative number of discharges, along with patient factors such as
neuroticism and premorbid anxiety. PTSD in cardiac patients is discussed
further below.
WƐLJĐŚŝĂƚƌŝĐŽŵƉůŝĐĂƚŝŽŶƐŽĨĂƌĚŝĂĐ^ƵƌŐĞƌLJ
Valve replacement was among the first of the open-heart surgeries to be
developed, and pioneering work in psychiatric aspects of cardiovascular
surgery demonstrated a high prevalence of delirium in early
postcardiotomy patients. This delirium could be attributed to toxic or
metabolic processes in many cases; prolonged exposure to the intensive
care unit (ICU) environment with sleep deprivation, sensory stimulation,
and simultaneous monotony led to the phenomenon of delirium after a
lucid interval (so-called ICU psychosis), but shortened ICU stays and better
attention to maintenance of day–night cycles, noise reduction, and the
provision of privacy have greatly reduced the extent of this phenomenon.
CABG surgery is one of the most frequently performed operations in the
United States. Except for patient with disease of the left main and left
anterior descending coronary arteries, CABG does not have an advantage
over medical management of CAD with respect to survival, but surgery may
be more effective than medication for amelioration of angina symptoms
and improvement in exercise tolerance, functional capacity, and overall
quality of life. Psychiatric complications after CABG have been noted since
its inception and persist despite improvements in cardiopulmonary bypass,
anesthetic, and surgical technique. Delirium after surgery is common and is
discussed below. Persistent, subtle memory and cognitive impairment may
occur after CABG. Predictors of stroke, death, and adverse neuropsychiatric
outcome include older age, proximal aortic atherosclerosis, prior history of
neurological disease, systolic hypertension, pulmonary disease, and
excessive alcohol use. Adverse cerebral outcomes substantially increase
hospitalization duration, in-hospital mortality, and the need for discharge
to institutional supportive care. Although embolic events associated with
cardiopulmonary bypass have long been associated with adverse cerebral
outcomes, cardiac surgery performed “off-pump,” that is, without
cardiopulmonary bypass, has not been found to result in significant
improvement in the rate of cognitive impairment or neuropsychiatric
adverse outcome.
ĞůŝƌŝƵŵ
Delirium is a common problem in severely ill cardiac patients. Three main
categories of patients are at risk: patients with severe CHF, patients
receiving antiarrhythmic agents for tachyarrhythmias early after MI or
cardiac surgery, and patients who have had cardiac surgery. In patients
with CHF, delirium commonly results from hypoxia, hyponatremia, liver
failure, or azotemia, as pulmonary congestion and poor end-organ
perfusion progress. Patients receiving lidocaine and procainamide—now
rarely employed–may appear psychotic or delirious even at nominally
therapeutic blood levels. In postoperative patients, the clinical picture may
include all of these elements; in addition, cerebrovascular hypoperfusion
during surgery, infection, sedatives, and narcotics may contribute to
delirium. Management relies on correcting the underlying abnormality
while treating psychosis or agitation with antipsychotic agents. Other
sedatives should generally be avoided, although the agitated patient may
benefit from concurrent administration of lorazepam (Ativan) with
haloperidol. IV haloperidol can be administered frequently, provided that
hemodynamic and ECG monitoring is in place. High doses, however, may
be associated with arrhythmias, including torsade de pointes (TdP), due to
prolonged cardiac conduction. (Conduction disturbance associated with
psychotropics and resulting risk of ventricular tachycardia–ventricular
fibrillation is discussed below.) It should be noted that no antipsychotic
drug has an indication for the treatment of delirium, and that the U.S. Food
and Drug Administration (FDA) has mandated a warning label about the
risk of ventricular tachyarrhythmias associated with antipsychotic drug use
in the management of agitation in the elderly. Nevertheless, off-label use of
antipsychotic agents remains widespread in the absence of any apparently
better alternative therapy for the agitated postoperative patient. Use of
dexmedetomidine (in place of opiates, propofol, and benzodiazepines) for
sedation and pain control, sedative interruption, and early mobilization are
management options that appear to reduce incidence of delirium after
cardiac surgery.
ĞƉƌĞƐƐŝŽŶ
About 20 percent of patients after acute coronary syndromes, with stable
coronary disease, and with CHF meet criteria for major depressive
disorder; more have elevated depressive symptoms. Although some
clinicians erroneously believe that depressed mood is normal in patients
with medical illness and wanes spontaneously over time after an acute
event, the syndrome of major depression persists in a large portion of
patients who appear depressed after an acute coronary event. Persistence of
depression confers elevated risk of adverse cardiac events and mortality.
Mild-to-moderate degrees of depression occur in approximately one-
third of patients after coronary bypass surgery but may remit within weeks
to months. Depressive symptoms are present in almost 40 percent of
patients with CABG 6 months after surgery, but the presence of depression
in the early postoperative period is not well correlated with depression at 6-
month follow-up. Persistent or worsening depression is associated with
increased mortality at 3-year follow-up. Subtle changes in cognition are
frequently associated with depression after coronary bypass surgery. The
linkage of cognitive and affective disturbances after CABG may be
attributable to small vessel cerebrovascular changes seen in many elderly
with depression.
sĂƐĐƵůĂƌ ĞƉƌĞƐƐŝŽŶ͘ Middle-aged and older depressed patients with
no clinical history of stroke have a high rate of cerebral white matter
infarcts, leading to the “vascular depression” hypothesis that some cases of
depression are caused by multiple small infarcts that do not lead to obvious
motor or sensory impairments. A diagnosis of vascular depression requires
evidence of vascular disease and late-onset depression (over 50 years old)
or a change in the course of depression in people who had early onset
depression. Unlike typical major depressive disorder, vascular depression
is not epidemiologically associated with female sex or family history of
affective disorder. Some evidence suggests that vascular depression is less
likely to respond to antidepressant medications than typical major
depression.
dƌĞĂƚŵĞŶƚ ŽĨ ĞƉƌĞƐƐŝŽŶ͘ Tricyclic antidepressants cause orthostatic
hypotension and cardiac conduction disturbances. In combination with
diuretics, vasodilators, or benzodiazepines, their effect on blood pressure is
exaggerated. In toxic levels, they may precipitate ventricular arrhythmias,
but, at therapeutic doses, they exhibit type 1A antiarrhythmic properties,
similar to those of quinidine (Cardioquin). Studies of type 1 antiarrhythmic
therapy for patients with MI and ventricular ectopy demonstrated that
antiarrhythmic therapy was associated with increased mortality.
Consequently, tricyclic agents are no longer recommended as first-line
drugs in the treatment of depression in patients with ischemic heart
disease. Cardiovascular effects of serotonergic antidepressants in patients
with impaired left ventricular function, including patients with CAD and
prior MI, are lowering of heart rate by 2 to 4 beats per minute and,
possibly, increased left ventricular ejection fraction. Except for dose-related
increased ventricular repolarization time associated with citalopram, they
have no significant effect on cardiac conduction, blood pressure, or
arrhythmias. Compared to side effect rates observed with nortriptyline
treatment, side effects occur less frequently and result in lower rates of
treatment discontinuation in depressed heart disease patients treated with
serotonin reuptake inhibitors. Bupropion in high doses may be associated
with increased blood pressure and ventricular ectopic activity. Trazodone
(Desyrel) and nefazodone (Serzone) may be associated with occasional
ventricular ectopy and orthostatic hypotension. Venlafaxine (Effexor) in
higher doses is associated with sustained elevations of blood pressure
(Table 27.2–2).
In patients with acute coronary syndromes (unstable angina and MI),
the sertraline antidepressant heart attack randomized trial (SADHART)
demonstrated that sertraline was a safe and effective treatment of major
depression. Sertraline was indistinguishable from placebo with respect to
hemodynamic, ECG, and inotropic effects but was associated with a higher
rate of response to treatment, better quality of life, and a trend toward
fewer adverse cardiac events. The antidepressant effect was most
pronounced in patients with more severe depression, with prior episodes of
depression before the index cardiac event, and with onset of the current
episode before the index event. Several other small trials have tended to
show a beneficial effect of sertraline on depression after MI. The CREATE
trial showed that citalopram, like sertraline, is effective when combined
with clinical management for the treatment of major depression in patients
with CAD; in contrast, interpersonal psychotherapy was not more effective
than clinical management without psychotherapy. In another trial enrolling
patients with depression up to 12 months after MI, mirtazapine was not
more effective than placebo as measured by change in the Hamilton Rating
Scale for Depression, but was modestly more effective as determined by
self-rating depression scales. Recently, a large Korean study demonstrated
safety and efficacy for escitalopram treatment of depression in the first 3
months after an acute coronary syndrome. Several recent collaborative care
model studies, employing stepped-care interventions and incorporating
patient preferences in the choice of initial treatment, have demonstrated
good results with respect to patient satisfaction, mood, and quality of life
outcomes, in patients with depression following admission for CAD or
CHF, in patients with recent acute coronary syndromes, and in post-CABG
patients (Bypassing the Blues Trial). In contrast, randomized placebo
controlled trials of sertraline and escitalopram for depression in heart
failure patients have not shown benefit with respect to either
cardiovascular or mood outcome.
dĂďůĞϮϳ͘ϮʹϮ͘
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ĂƌŝƉŝƉƌĂnjŽůĞ;ďŝůŝĨLJͿ
Aerobic exercise has also been demonstrated to significantly reduce
depression symptoms in patient with depression and CAD and depression
and CHF, and rehabilitation and stress management interventions that
include exercise have demonstrated beneficial effects on recurrent
cardiovascular morbidity and mortality in patients with CAD and CHF,
whereas psychotropic medications and psychological interventions without
exercise components have not.
Experienced psychosomatic medicine psychiatrists often use stimulants
as (off-label) primary or adjunctive treatment of medically ill patients with
depressed mood and psychomotor retardation; this may include patients
who have had cardiac surgery and patients with coronary disease or heart
failure. Unstable myocardial ischemia, uncontrolled hypertension, and
tachyarrhythmias are obvious contraindications. Even with doses of 20 to
30 mg/day, the effects of methylphenidate on heart rate and blood pressure
are minimal. Recent studies find no evidence of increased cardiovascular
morbidity associated with stimulant use in large cohorts of young adults
treated with stimulants for attention deficit disorder.
ŶdžŝĞƚLJ
Although the prevalence of anxiety symptoms is high in patients with acute
MI, established CAD, heart failure, and arrhythmias, the treatment of
anxiety disorders has received little attention in randomized trials.
Psychological interventions to reduce anxiety symptoms in patients with
cardiovascular disease were found to be beneficial in recent meta-analyses.
By and large, these studies do not specifically target persons with high
anxiety symptom levels or anxiety disorders. A common anxiety problem in
patients who have had acute coronary events, heart failure, cardiac surgery,
or implanted defibrillator placement is fear of resumption of sexual
activity; in fact, sexual activity is safe for most patients with heart disease,
and the American Heart Association has published guidelines for
counseling, including advice about energy requirements, situations, and
positioning most conducive to comfortable and safe sexual activity in the
setting of heart disease. In the absence of randomized trials for anxiety
specifically in cardiovascular disorder, it is reasonable to utilize treatments
of anxiety established in other clinical settings, with an appreciation of the
potential adverse cardiovascular effects of psychotropic medications
(discussed below). As patients may be reluctant to initiate discussion of
anxiety-provoking topics such as sexuality, open-ended questions
exploratory questions by the physician, psychiatrist, or other health
professional about fears and anxiety may be welcomed as “giving
permission” for discussion.
WŽƐƚƚƌĂƵŵĂƚŝĐ^ƚƌĞƐƐŝƐŽƌĚĞƌ
Acute coronary events and their treatment can themselves be traumatic
events; dramatic, painful, and intensely frightening experiences such as the
abrupt onset of intense physical symptoms or emergency resuscitation
procedures may be the stimulus for intrusive flashback experiences. Up to
15 percent of patients are likely to develop PTSD in the year after an MI or
cardiac surgery, most commonly between 3 and 6 months after the cardiac
event. Affected patients may also experience significant depression
symptoms and may be less likely to adhere to medications and behavioral
care. PTSD is also associated with subjective stress and functional
impairment, failure to return to work, and poor quality of life. Clinically
significant PTSD symptoms induced by acute coronary syndromes are
associated with twofold increased risk of recurrent cardiac events and
mortality.
Risk factors for the development of cardiac-related PTSD include prior
history of PTSD, depression, or generalized anxiety disorder. Some studies
suggest that subjective perceptions of danger or potential for life-threat are
not as important as perceptions of control or mastery, especially a general
sense of control over life events, in determining the risk of the development
of PTSD in cardiac patients. Social support during convalescence may
reduce the incidence of PTSD.
Cardiac events such as MI differ from other traumatic events in
important ways. The life-threatening experience comes from within rather
than outside the body, so that instead of directing vigilance to external
sources of danger, the cardiac patient may instead become hypervigilant
about and preoccupied with somatic signals of disease, resembling patients
with the somatosensory amplification experience seen in patients with
panic and illness anxiety. Cardiac patients with PTSD have higher rates of
somatic symptoms than those without it and are more likely to make
repeated visits to emergency departments. Anxious apprehension about
future events may appear similar to the uncontrollable worry associated
with generalized anxiety disorder. Cardiac medicines themselves may be
reminders of the traumatic event; adherence problems may represent the
avoidance of cues to intrusive flashbacks, a hallmark PTSD symptom.
Furthermore, PTSD symptoms may co-occur with depression, anger,
anxiety, and substance use disorder problems, complicating treatment.
Treatment of PTSD in cardiac patients follows the general guidelines for
the treatment of PTSD with psychotherapy, focusing on review of the
traumatic events, and use of SSRIs, with appreciation for adverse effects of
medication as discussed below. A recent trial found telephone-based CBT
reduced PTSD symptoms in ICD patients, but did not result in an effect on
the rate of ICD discharge.
,ĞĂƌƚdƌĂŶƐƉůĂŶƚĂƚŝŽŶ
Although quality of life improves in most respects for most patients who
undergo heart transplantation, myriad difficulties can occur. Common
medical problems of transplant survivors include infections, graft rejection,
graft CAD, renal insufficiency, hypertension, and adverse effects of
immunosuppressive drugs, including osteoporosis. Return to work is
problematic, and other social role functioning may remain limited, even
after physical recovery from heart transplant surgery. Family adjustments
to shifting patterns of chronic illness and recovery may be chaotic and
upsetting. Sexual dysfunction affects one-third or more of heart transplant
recipients. Psychiatric difficulties in heart transplant patients include
primary and secondary mood disorders, delirium, pain, addiction to
analgesic and anxiolytic agents, and anxiety. Tacrolimus and cyclosporine
may induce a variety of neuropsychiatric problems including peripheral
neuropathy pain, headache, altered mental status, and seizures.
Serotonergic antidepressants and nortriptyline are generally well tolerated
in heart transplant recipients with depression.
WĂƚŝĞŶƚƐǁŝƚŚŽŶŐĞŶŝƚĂů,ĞĂƌƚŝƐĞĂƐĞ
The psychiatric status of patients with congenital heart disease has received
little systematic study, but the clinical experience of cardiologists involved
in their care suggests that many experience enduring psychological
sequelae. MRI studies of neonates with congenital heart disease before
surgery demonstrate abnormalities of structure and function
(periventricular leukomalacia, infarcts, and elevated lactate levels), and
follow-up after surgery demonstrates new lesions in more than two-thirds
of patients. The significance of these early brain lesions for subsequent
cognitive and emotional development is uncertain. Children with
congenital heart disease have been reported to demonstrate mild cognitive
deficits, increased anxiety, more body-image concerns, and lower self-
confidence than age-matched peers. Exclusion from peer-group activities,
maternal anxiety, cyanosis, and pain has been linked to higher levels of
anxiety and lower quality-of-life ratings. For late adolescent and young
adult patients, sexuality, childbearing, risk of having offspring with
congenital heart disease, employability, and health insurance issues are
dominant concerns. Surveys of adult patients attending congenital heart
disease clinics demonstrate self-report of quality of life to be worse than
population norms, particularly for those with cyanotic conditions, but one
study found that psychopathology was lower in adult patients with
congenital heart disease than in a matched sample of patients with
orthopedic disorders.
^ƚƌĞƐƐDĂŶĂŐĞŵĞŶƚ
Psychological intervention including various stress management
techniques is widely included in cardiac rehabilitation programs, without
selection for patients with significant psychopathology. Overall, these
programs appear to have beneficial effects on indices of psychological well-
being; findings vary with respect to the effects on recurrent cardiac events
and mortality. Although a 2000 meta-analysis of 23 trials including over
3,000 subjects noted improvement in both psychological and somatic
disease outcomes in association with psychosocial treatments, a 2013
review concluded that psychological treatments without exercise
rehabilitation components did not improve somatic disease outcomes. Sex-
segregated stress management programs for patients with CAD may
improve outcomes.
KƚŚĞƌ/ƐƐƵĞƐŝŶdƌĞĂƚŝŶŐWƐLJĐŚŝĂƚƌŝĐŝƐŽƌĚĞƌƐŝŶWĂƚŝĞŶƚƐǁŝƚŚĂƌĚŝŽǀĂƐĐƵůĂƌ
ŝƐĞĂƐĞ
WƐLJĐŚŝĂƚƌŝĐ^ŝĚĞĨĨĞĐƚƐŽĨĂƌĚŝŽǀĂƐĐƵůĂƌDĞĚŝĐĂƚŝŽŶƐ͘ A few drugs used
in the treatment of cardiovascular disorders have psychiatric side effects
that should be kept in mind when assessing differential diagnosis of
psychopathology in patients with cardiovascular disease. Some of these
effects are listed in Table 27.2–3. Amiodarone deserves special mention
because it is widely used for patients with arrhythmia control and can cause
profound hypothyroidism in just a few months. Symptoms can include
cognitive dulling and depressed mood and may be misattributed to
depression or underlying heart failure; correction of the hypothyroid state
may be neglected. In addition, amiodarone inhibits hepatic drug
metabolism via cytochromes P450 3A4, 2D6, and 2C9, potentially
increasing blood levels of many psychotropic agents metabolized through
these enzyme systems, and increasing the likelihood of toxicities including
QT prolongation and arrhythmic events. The calcium channel blocker
diltiazem is also a strong inhibitor of the 3A4 system with potential for
toxic drug interactions.
ĂƌĚŝĂĐ ^ŝĚĞ ĨĨĞĐƚƐ ŽĨ WƐLJĐŚŝĂƚƌŝĐ DĞĚŝĐĂƚŝŽŶƐ͘ Two especially
important issues in use of psychotropic medications in cardiac patients are
QT interval prolongation and risk of malignant ventricular arrhythmias,
and bleeding risk associated with SSRIs in patients using antiplatelet
agents or warfarin.
Yd/EdZs>WZK>KE'd/KEEsEdZ/h>Zd,zZZ,zd,D/^͘ The QT interval
represents the duration of ventricular depolarization and repolarization.
The QT interval, corrected for heart rate (QTc), is normally less than 450
msec. Prolongation of the QTc interval is associated with progressively DĞdžŝůĞƚŝŶĞ;DĞdžŝƚŝůͿ ĞůŝƌŝƵŵ
ŵŝŽĚĂƌŽŶĞ;ŽƌĚĂƌŽŶĞͿ ,LJƉŽƚŚLJƌŽŝĚƐƚĂƚĞ͕ǁŝƚŚĂƐƐŽĐŝĂƚĞĚĚĞƉƌĞƐƐŝŽŶ
increasing risk of TdP, a form of malignant ventricular tachycardia; QTc
interval of 500 msec is associated with double the risk of QTc of 400 msec.
Risk factors for abnormal QT interval prolongation include congenital long Among serotonin reuptake inhibitors, citalopram stands out in that
QT syndrome, hypokalemia, hypomagnesemia, AV nodal block, low left increasing dose of citalopram is associated with increasing QTc interval;
ventricular ejection fraction, alcohol and cocaine use, advanced age, and the FDA requires a label warning against doses above 40 mg/day due to
female sex. A history of unexplained syncope, seizure, or arrhythmia, or concern about TdP, although large population studies show that the
family history of sudden cardiac death, should provoke careful scrutiny for absolute risk of arrhythmias due to high-dose citalopram is very low.
congenital long QT syndrome. The QTc interval is an imperfect index of >/E'͘ SSRI antidepressants inhibit platelet storage of serotonin and
risk of TdP and sudden cardiac death: some drugs that prolong the QTc may prolong bleeding in occasional patients via an effect on platelets. They
interval have never been associated with cases of torsades; QTc varies do not have a systematic effect on coagulation, as measured by the
according to the method used to calculate it; and there is natural diurnal prothrombin time test, even in patients treated with warfarin (Coumadin).
variation in QTc. However, several first-generation antipsychotic drugs Bleeding risk is increased in patients treated with concomitant SSRIs,
prolong the QTc and are clearly associated with increased risk, including, antiplatelet agents, and warfarin. There is about a 1.5- to 2-fold increased
thioridazine (Mellaril), mesoridazine (Serentil), haloperidol (Haldol) risk of hospitalization for bleeding events when SSRIs are combined with
(particularly in IV formulation), and pimozide (Orap). Among second- antiplatelet agents or warfarin, and an estimated 36 treatment-years
generation antipsychotics, aripiprazole uniquely does not prolong the QTc, needed to cause one additional hospitalization. The benefit of SSRI therapy
while most other second-generation agents do, to varying degrees. may justify this risk in selected patients.
Ziprasidone (Geodon) is associated with the greatest QTc prolongation of
the second-generation antipsychotics, yet has been associated with TdP in
only two case reports. For patients who do not have heart disease, none of dĂďůĞϮϳ͘Ϯʹϰ͘
the second-generation antipsychotics has a well-established risk of TdP ^ƵďƐƚĂŶĐĞƐdŚĂƚWƌŽůŽŶŐƚŚĞYd/ŶƚĞƌǀĂů
when taken at recommended doses; only when other QT-prolonging ůĐŽŚŽů ,ĂůŽĨĂŶƚƌŝŶĞ
conditions are present do these medications seem to pose increased risk. ŵŝŽĚĂƌŽŶĞ <ĞƚŽĐŽŶĂnjŽůĞ
njŝƚŚƌŽŵLJĐŝŶ >ĞǀŽĨůŽdžĂĐŝŶ
These other conditions include the risk factors already listed above such as
ŚůŽƌŽƋƵŝŶĞ DĞƚŚĂĚŽŶĞ
structural heart disease, advanced aged, and electrolyte disturbances; the ŝƐĂƉƌŝĚĞ;ǁŝƚŚĚƌĂǁŶĚƵĞƚŽdĚWͿ DŽdžŝĨůŽdžĂĐŝŶ
combination of a second-generation antipsychotic with other drugs known ŝƚĂůŽƉƌĂŵ WĞŶƚĂŵŝĚŝŶĞ
to prolong the QT interval (see Table 27.2–4); pharmacodynamic ůĂƌŝƚŚƌŽŵLJĐŝŶ WƌŽĐĂŝŶĂŵŝĚĞ
interactions that inhibit the metabolism of the QT prolonging antipsychotic ŽĐĂŝŶĞ YƵŝŶŝĚŝŶĞ
thereby increasing its blood level; and medication overdose. Drugs that ŝƐŽƉLJƌĂŵŝĚĞ YƵŝŶŽůŽŶĞƐ
inhibit metabolism of these antipsychotic agents may exacerbate QT ŽĨĞƚŝůŝĚĞ ^ŽƚĂůŽů
interval prolongation and increase the risk of arrhythmia. Cardiac patients ƌLJƚŚƌŽŵLJĐŝŶ dĂŵŽdžŝĨĞŶ
being treated with antipsychotic medications that prolong the QT interval &ůƵĐŽŶĂnjŽůĞ dĞƌĨĞŶĂĚŝŶĞ;ǁŝƚŚĚƌĂǁŶĚƵĞƚŽdĚWͿ
&ƵƌŽƐĞŵŝĚĞ sĂŶĚĞƚĂŶŝď
should be monitored with periodic ECGs.
Additional cardiovascular effects of psychotropic drugs are listed in
dĂďůĞϮϳ͘Ϯʹϯ͘ Table 27.2–2.
^ŽŵĞWƐLJĐŚŝĂƚƌŝĐ^ŝĚĞĨĨĞĐƚƐŽĨĂƌĚŝŽǀĂƐĐƵůĂƌƌƵŐƐ
DĞĚŝĐĂƚŝŽŶ ĨĨĞĐƚƐ ƌƵŐ /ŶƚĞƌĂĐƚŝŽŶƐ ĂŶĚ ƚŚĞ LJƚŽĐŚƌŽŵĞ ^LJƐƚĞŵ͘ Pharmacodynamic
ŝŐŽdžŝŶ;>ĂŶŽdžŝŶͿ sŝƐƵĂůŚĂůůƵĐŝŶĂƚŝŽŶƐ effects may be additive or offsetting; for example, both SSRIs and beta-
ŶŐŝŽƚĞŶƐŝŶͲĐŽŶǀĞƌƚŝŶŐĞŶnjLJŵĞŝŶŚŝďŝƚŽƌƐ DŽŽĚĞůĞǀĂƚŝŽŶ blockers slow heart rate, and the combination may result in symptomatic
dŚŝĂnjŝĚĞĚŝƵƌĞƚŝĐƐ DŽŽĚĞůĞǀĂƚŝŽŶ͕ĞƌĞĐƚŝůĞĚLJƐĨƵŶĐƚŝŽŶ bradycardia. Pharmacokinetic effects can increase or decrease drug effect
ɴͲĚƌĞŶĞƌŐŝĐďůŽĐŬĞƌƐ &ĂƚŝŐƵĞ͕ƐĞdžƵĂůĚLJƐĨƵŶĐƚŝŽŶ or toxicity; for example, lithium (Eskalith) levels may be affected by the use
>ŝĚŽĐĂŝŶĞ;ĂůĐĂŝŶĞͿ ĞůŝƌŝƵŵ
of diuretics affecting the proximal renal tubule (thiazides) and by ACE
inhibitors, leading to lithium toxicity.
Fluoxetine, fluvoxamine, nefazodone, and bupropion are cytochrome
inhibitors that may affect metabolism of cardiac medications, causing
toxicity; for example, cytochrome P450 2D6 inhibitors such as bupropion,
fluoxetine, and paroxetine may interfere with beta-blocker metabolism.
Sertraline and paroxetine have weaker cytochrome inhibiting effects.
Conversely, barbiturates and carbamazepine are enzyme inducers and may
lower the effectiveness of relevant substrates. Online resources are readily
available to search for pharmacokinetic and pharmacodynamic drug
interactions.
ůŝŶŝĐĂůsŝŐŶĞƚƚĞ
An 86-year-old man with recurrent atrial fibrillation, mitral insufficiency, parkinsonism, mild
cognitive impairment, and a history of MI and hip fracture was treated for recurrent
depression with sertraline 150 mg daily. Concomitant medications included metoprolol
(Lopressor), propafenone (Rythmol), hydrochlorothiazide (Esidrix) and triamterene
(Dyrenium), atorvastatin (Lipitor), warfarin, levothyroxine (Levoxyl), levodopa and carbidopa
(Sinemet), lansoprazole (Prevacid), tamsulosin (Flomax), and donepezil (Aricept). A
permanent pacemaker had been implanted. After several months of remission of depression
symptoms, sertraline was withdrawn due to sexual side effects. When depression symptoms
subsequently recurred, he was treated with bupropion sustained-release tablets, in gradually
escalating doses. He developed severe light-headedness on standing, and his blood pressure
fell to 95/60, with paced heart rate of 60 beats per minute. Despite decreased bupropion dose,
he continued to experience hypotension and dizziness until bupropion was discontinued,
leading to complete resolution of symptoms and normalization of blood pressure. The
psychiatrist hypothesized that bupropion, a potent inhibitor of the cytochrome 2D6 system,
had interfered with metabolism of metoprolol, increasing the hypotensive effect of the beta-
blocker.
ůĞĐƚƌŽĐŽŶǀƵůƐŝǀĞdŚĞƌĂƉLJ͘ Electroconvulsive therapy (ECT) is a highly
effective treatment of severe depressive and manic episodes. During ECT,
initial vagally mediated bradycardia is followed by substantial increases in
heart rate and blood pressure. Patients with ischemic heart disease or
ventricular arrhythmias are at increased risk of MI or ventricular
tachyarrhythmias. Atropine (AtroPen) is commonly used to reduce airway
secretions during ECT and may reduce the extent of bradycardia but may
exacerbate tachyarrhythmias. β-Adrenergic blocking agents, conversely,
may precipitate heart block. Few studies have systematically controlled
concurrent treatment and cardiac diagnoses in assessing effects of ECT in
cardiac patients, but available information suggests that patients with
cardiac disease are more likely than comparison patients without heart
disease to experience cardiovascular complications during ECT. Most
complications are transient, however, and do not necessarily preclude use
of this modality. ECT has been used successfully in patients with heart
transplants.
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ŸϮϳ͘ϯ'ĂƐƚƌŽŝŶƚĞƐƚŝŶĂůŝƐŽƌĚĞƌƐ
>hEZtKd,͕W,͕͘͘:D^<͘Zh&&>͕͘^Đ͕͘D͘͘͘^͕͘ED͘&ZDZ͕W,͘͘
/EdZKhd/KE
There is an intimate relationship between the GI tract and the psyche. For
example, stress or anxiety may modulate GI function and result in
disturbances of function such as diarrhea, bloating, nausea, and
discomfort. Indeed, the influence that anxiety may exert on the GI tract is
often reflected in phrases that are in common parlance such as “butterflies
in my stomach” and “gut wrenching.” However, it was not until the 19th
century that such observations began to be objectively examined. William
Beaumont (1785 to 1853), an early pioneer of GI physiology, isolated
hydrochloric acid from gastric secretions and described the influence of
emotions on gastric acid secretion. While the techniques used to
interrogate the anatomy and physiology of the GI tract function have
advanced, the relationship between the psyche and GI function, both in
health and disease, remains prominent in modern clinical practice and
research. Research from a diverse array of disciplines, coupled with
technological advances particularly in functional neuroimaging, has
provided an increasing body of evidence for the proposal of a gut–brain
axis; a bidirectional intercommunication between the gut and the brain,
which has gained widespread acceptance as the germane construct for
providing an explanation of the normal, acute, and chronic alterations in
digestive tract function. Moreover, this model of circuitous communication
has provided a biological construct to underpin the biopsychosocial
concept of GI disorders by facilitating the integration of many contributing
factors whether they are biological, psychological, or social in nature.
In many ways, considering the essence of the construct of the gut–brain
axis, it should come as no surprise that many GI disorders are comorbid
with psychiatric disorders. The aims of this section are to provide the
reader with a summary of both inflammatory bowel disease (IBD) and the
so-called functional GI disorders, itself comprising of a number of distinct
disorders, as many of these patients are routinely referred to the
psychiatrist. There has been an appreciable interest into developing a
mechanistic-based understanding of the pathophysiology of functional GI
disorders over the recent past, largely as a consequence of the clinical
burden that such patients exert. Within secondary care, more than one-
third of new patients are diagnosed as having one or more functional GI
disorders. The functional GI disorders are a heterogeneous group
consisting of in excess of 25 separate disorders, defined according to the
Rome multinational consensus as “variable combinations of chronic or
recurrent GI symptoms which are not explained by structural or
biochemical abnormalities.” Functional GI disorders are characterized by
chronic abdominal pain and discomfort in the absence of any physical,
biological, or anatomical abnormalities. The most prevalent functional GI
disorder is irritable bowel syndrome (IBS), with a reported prevalence in
excess of 10 percent in the adult population, peaking in the second, third,
and fourth decades of life with a female preponderance. The Rome process,
which has developed in an iterative fashion in a manner not dissimilar to
the Diagnostic and Statistical Manual of Mental Disorders, has generated
considerable debate among gastroenterologists who are used to making
diagnoses on the basis of observable pathological abnormalities.
Regrettably, this often translates into clinical practice that symptoms based
upon demonstrable abnormalities, visualized perhaps through endoscopic
or cross-sectional imaging, are “real,” whereas other complaints may be
dismissed as functional with a large psychiatric component. The
psychiatrist must remain mindful that this message may have been
transmitted, unwittingly, to patients prior to referral, making some patients
reticent when asked about many areas of their psychiatric history.
Nevertheless, despite protestations from the gastroenterologist, the
psychiatrist does have a pivotal role in the management of patients with GI
disorders, and those who are particularly refractory to standard medical
therapy.
The chapter will be structured around examining both “organic” and
“functional” disorders of the digestive tract. The seemingly arbitrary split of
gastroenterological disorders in “organic” or “functional” based upon the
presence or absence of a particular biomarker remains the dominant model
in specialist practice, although such dualism has marked limitations. For
instance, peptic ulcer disease was considered to be a psychosomatic
disorder prior to the identification of Helicobacter pylori. Furthermore,
while the identification of colonic inflammation may be consistent with a
diagnosis of gastroenteritis or IBD, many patients continue to remain
symptomatic even in the context of mucosal healing and resolution of
inflammation. This has led to the proposal that IBD and IBS in reality
represent a similar disease at differing ends of a spectrum where central
and peripheral factors are involved in symptom generation. This chapter
will be structured around describing the epidemiology, putative
pathogenesis, and broad management of both “organic” and “functional”
GI disorders. Each disorder will be further illustrated with a clinical case to
illustrate important practice points as well as a focus on the pivotal role of
the psychiatrist in successfully managing such patients.
/E&>DDdKZzKt>/^^
The two major types of IBD encountered in clinical practice are Crohn
disease (CD) and ulcerative colitis (UC), with the former potentially