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102 Laboratory Medicine in Psychiatry and Behavioral Science
Dexamethasone suppression test (DST) (continued)
Interfering factors (continued) Drugs that can cause false-positive results include aspirin
overdose, barbiturates, carbamazepine, estrogen, meproba
-
mate, methyprylon, phenytoin, rifampin, and tetracycline.
False-negative results can be seen with adrenal failure, hypo-
pituitarism, and poor metabolism of dexamethasone.
Drugs that can cause false-negative results include high-dose
benzodiazepines, corticosteroids, and cyproheptadine.
Cross-references Adrenocorticotropic Hormone
Cortisol
Cushing’s Syndrome
Nijdam MJ, van Amsterdam JG, Gersons BP, Olff M: Dexamethasone-suppressed cortisol awakening re-
sponse predicts treatment outcome in posttraumatic stress disorder. J Affect Disord 184:205–208, 2015
Scherf-Clavel M, Wurst C, Nitschke F, et al: Extent of cortisol suppression at baseline predicts improve-
ment in HPA axis function during antidepressant treatment. Psychoneuroendocrinology 114:104590,
2020
Vinkers CH, Kuzminskaite E, Lamers F, et al: An integrated approach to understand biological stress sys-
tem dysregulation across depressive and anxiety disorders.J Affect Disord 283:139–146, 2021
https://t.me/med1917
103 Laboratory Tests
Diazepam level
Type of test Blood
Background and explanation
of test
Benzodiazepines are Schedule IV sedative-hypnotic drugs
used to treat anxiety and insomnia. Diazepam is a highly lipo
-
philic benzodiazepine with a short transit through the circu-
lation before being deposited in fatty tissue, where it can
accumulate. It is then released erratically back into the circu
-
lation. Both diazepam and its active metabolite nordiazepam
have long elimination half-lives. Diazepam levels generally
have little clinical significance unless they are extremely high
or low. Levels are rarely checked except to confirm overdose,
noncompliance, or use without a prescription. In the latter
case, a urine drug screen is more often used than a blood level.
Relevance to psychiatry and
behavioral science
Toxicity with chronic benzodiazepine ingestion may mani-
fest as confusion, disorientation, memory impairment,
ataxia, decreased reflexes, and dysarthria. With acute over
-
dose, the patient may exhibit somnolence, confusion, ataxia,
decreased reflexes, vertigo, dysarthria, respiratory depres
-
sion, and coma. More serious consequences usually involve
co-ingestion of alcohol or other sedatives. Administration of
flumazenil does not affect the drug level. Activated charcoal
is no longer recommended as a treatment because of the high
risk of aspiration. Supportive care, including intubation as
indicated, is the mainstay of treatment.
Preparation of patient None needed
Indications • Screening for drug use
• Suspicion of overdose
• Signs of toxicity in treated patient
• Suspected noncompliance with prescribed therapy
Reference range Diazepam 200–1,000 ng/mL
Nordiazepam 100–1,500 ng/mL
Critical value(s) Nordiazepam >2,500 ng/mL
Note:
Administration of flumazenil does not affect drug
level.
Increased levels • Overdose
• Overuse
• Poor metabolism
• Hepatic encephalopathy
Decreased levels Noncompliance with prescribed drug
Interfering factors None noted
Cross-references Benzodiazepines
Urine Drug Screen
ARUP Laboratories: Benzodiazepines, urine, quantitative, in L ab Test Dir ecto ry. Salt La ke C ity, UT, A RUP L ab-
oratories, 2021. Available at: https://ltd.aruplab.com/Tests/Pub/2008291. Accessed November 2021.
Wu AHB: Tietz Clinical Guide to Laboratory Tests, 4th Edition. St. Louis, MO, WB Saunders, 2006
https://t.me/med1917
104 Laboratory Medicine in Psychiatry and Behavioral Science
Echocardiogram
Type of test Imaging
Background and explanation
of test
The echocardiogram is a noninvasive means to evaluate the
position and size of the heart, movement of valves and
chamber walls, and blood flow velocity. It can be performed
at the bedside or in the laboratory. In transthoracic echocar
-
diography (TTE), the transducer is placed on the chest, and
pulsed high-frequency sound waves are transmitted
through the chest wall and heart structures. For patients
who are obese or who have chronic obstructive pulmonary
disease, visualization may be poor by this method, so trans-
esophageal echocardiography (TEE) is used, in which the
transducer is inserted into the esophagus after the posterior
pharynx is anesthetized. Different modes of echocardio
-
graphic study are now available, including stress echocardi-
ography. The usual examination takes 30–45 minutes.
Relevance to psychiatry and
behavioral science
Severe left ventricular dysfunction (left ventricular ejection
fraction [LVEF] <35%) may be associated with fatigue, ap
-
parent loss of motivation, and depression. When the LVEF
is ≤25%, the patient is prone to develop delirium with minor
precipitants. Certain psychotropic medications (e.g., clo
-
zapine) are associated with pericardial effusion that can be
seen on echocardiogram.
Preparation of patient For routine echocardiography, no preparation is needed.
For specialized procedures such as TEE or stress echocardi-
ography, lab will provide patient instructions.
Indications •
Evaluating heart valve function
• Evaluating velocity and direction of cardiac blood flow
• Pericardial effusion
• Monitoring patients with known cardiac disease
• Monitoring patients with left ventricular assist devices
Normal result Normal position, size, and movement of heart valves and
chamber walls
Normal heart structures
Abnormal result • Valvular disease: stenosis, insufficiency, prolapse,
regurgitation
• Cardiomyopathy
• Pericardial disease: effusion, tamponade, pericarditis
• Endocarditis
• Cardiac neoplasm
• Intracardiac thrombus
• Coronary artery disease
• Prosthetic valve dysfunction
• Congenital heart disease
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105 Laboratory Tests
Echocardiogram (continued)
Interfering factors Cardiac rhythm disturbance, lung hyperinflation from me-
chanical ventilation, and transducer positioning for Dop-
pler study all affect results.
Cross-references Medical Evaluation for Electroconvulsive Therapy
(Appendix C)
Fauci AS, Braunwald E, Kasper DL, et al (eds): Harrison’s Principles of Internal Medicine, 17th Edition.
New York, McGraw-Hill, 2008
Rose VL: American College of Cardiology and American Heart Association address the use of echocar-
diography. Am Fam Physician 56:1489–1490, 1997
https://t.me/med1917
106 Laboratory Medicine in Psychiatry and Behavioral Science
Electrocardiogram
Type of test Electrophysiology
Background and explanation
of test
The ECG (or EKG) records the electrical activity of the heart,
including voltages generated and the time it takes for these
voltages to flow from one area of the heart to another. The
ECG tracing can be used to identify the anatomical source of
abnormal rhythms, presence of inadequate blood flow (ische
-
mia), destruction of heart muscle (infarction), enlargement of
heart chambers
(atrial and ventricular hypertrophy), delays
in conduction of electrical current, and inflammation of the
tissue surrounding the heart (pericarditis).
The ECG can also
be helpful in evaluating the effects of electrolyte disturbances,
systemic diseases, and medications or drugs that act on the
heart and can assist in the evaluation of implanted pacemaker
and defibrillator functions.
As shown in Appendix C, a normal heart cycle consists of a
P wave, QRS complex, and T wave; a U wave may also be
seen. This cycle is repeated at regular intervals. The P wave
occurs with atrial depolarization, the QRS complex with
ventricular depolarization, and the T wave with ventricular
repolarization. The U wave represents nonspecific recovery
afterpotentials. The ECG is analyzed to determine rate,
rhythm, intervals, voltages, axis, and presence of abnormal
waveforms.
Relevance to psychiatry and
behavioral science
ECG tracings for many patients in psychiatric care show
changes suggestive of ischemia, even in the absence of any
clinical correlates of disease. For example, anxiety and hy-
perventilation can be associated with sinus tachycardia and
ST-segment depression with or without T-wave inversion,
possibly mediated by autonomic function. More significant
ECG abnormalities are seen in patients with eating disor
-
ders with associated electrolyte derangements. In addition,
many psychotropic medications cause ECG abnormalities.
Lithium, for example, is associated with T-wave flattening
or inversion in most treated patients, and clozapine can be
associated with ST-segment changes as well as T-wave in
-
version. These psychotropic-related findings are of uncer-
tain significance. On the other hand, many psychotropics
are known to cause prolongation of the QT interval, which
can result in sudden cardiac death due to polymorphic ven-
tricular tachycardia (torsades de pointes). Overdose of medi-
cations such as TCAs and dual-acting antidepressants may
also cause significant ECG changes.
Preparation of patient Patients should abstain from smoking and avoid heavy
meals for ≥30 minutes and should rest for ≥15 minutes be-
fore testing.
Indications •
Routine admission testing for older patients
• Preoperative screening before general anesthesia
• ECT screening in patients older than 50 years or with
previous abnormal ECG or known heart disease
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107 Laboratory Tests
Electrocardiogram (continued)
Indications (continued) • Chest pain or other signs of possible MI
• Syncope
• Irregular pulse
• Initiation of a psychotropic drug that affects cardiac con-
duction (e.g., TCA or antipsychotic)
Reference ranges Rate: 60–100 beats per minute
Rhythm: Normal si nus rhythm or sinus arrhythmia
Intervals:
• PR interval: 120–200 ms
• QRS interval: 80–120 ms
• QT interval: 350–430 ms (varies with heart rate [HR],
sex, time of day)
Vol tages:
• Top of R wave to bottom of S wave: 1 mV
• P wave: 0.1–0.3 mV
• T wave: 0.2–0.3 mV
Axis: + 90° to −30° in adults
Critical findings Ventricular tachycardia: HR>100 with at least three irregular
heartbeats in a row
Ventricular fibrillation: very rapid HR, uncoordinated, fatal
unless treated immediately
Torsades de pointes: bradycardia, prolonged QT, and QRS that
rotates around the isoelectric baseline
Idioventricular rhythm: sustained rhythm with pacemaker
localized to the ventricles, with HR 20–50
Severe bradycardia with HR <40 is often symptomatic.
Acute MI: See Myocardial Infarction in the Diseases and
Conditions chapter.
Abnormal findings • Bradycardia: HR < 60
• Tachycardia: HR >100
• Atrial fibrillation: HR rapid, rhythm irregular; ECG
shows absence of P waves that normally precede QRS
complexes
• Atrial flutter: HR rapid (ventricular rate ~150), QRS nar-
row, ECG baseline has “sawtooth” appearance
• Junctional rhythm: Atrioventricular node takes over as
pacemaker; P waves absent or inverted on ECG or may
appear after QRS complex
• First-degree heart block: PR interval >200 ms; each P wave
followed by QRS
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108 Laboratory Medicine in Psychiatry and Behavioral Science
Electrocardiogram (continued)
Abnormal findings
(continued)
• Second-degree heart block: Some P waves blocked at atrio-
ventricular node and have no following QRS
• Third-degree heart block (complete heart block): complete
dissociation between P waves and QRS
• Bundle branch block (BBB): QRS > 120 ms; right BBB pro-
longs last part of QRS and shifts axis right; left BBB pro-
longs the whole QRS and shifts the axis to the left.
• Left anterior fascicular block (left anterior hemiblock): QRS
<120 ms, left axis deviation (−45° to −90°), qR in I and
augmented Vector Left (aVL) and rS in II, III, and aug
-
mented Vector Foot (aVF)
• QTc prolongation: >450 ms for men and >470 ms for
women; results from delayed repolarization, which
enables early afterdepolarizations and sets the stage for
extrasystoles and possibly torsades de pointes
• Premature ventricular contractions (PVCs) or ventricular
premature depolarizations (VPDs): wide QRS that follows
closely a normal QRS; when PVC occurs after every nor
-
mal QRS, pattern is called bigeminy. When it occurs after
every other normal QRS, pattern is called trigeminy.
When three or more occur in a row, pattern is ventricular
tachycardia.
• ST-segment changes: normal ST segment serves as isoelec-
tric line on ECG tracing. ST-segment depression (below
baseline) may indicate ischemia. ST-segment elevation
may indicate infarction.
Interfering factors Age: T-wave inversion in leads V1–V3 may be normal finding
into second decade (third decade in Blacks).
Sex: Females often exhibit slight ST-segment depression.
Race: ST-segment elevation and T-wave inversion that disap-
pears with maximal exercise may be seen in Blacks.
QRS axis shifts leftward with obesity, ascites, and pregnancy.
Variations of normal anatomical heart position may affect
axis.
Inaccurate lead placement affects test results.
Reversal of limb leads may suggest infarction or dextrocardia
(heart in right chest).
Deep breathing shifts position of heart.
Cross-references Additional Cardiac-Related Information (Appendix C)
Myocardial Infarction
Dubin D: Rapid Interpretation of EKGs, 3rd Edition. Tampa, FL, Cover, 1984
Fauci AS, Braunwald E, Kasper DL, et al (eds): Harrison’s Principles of Internal Medicine, 17th Edition.
New York, McGraw-Hill, 2008
https://t.me/med1917
109 Laboratory Tests
Electroencephalogram (EEG)
Type of test Neurophysiology
Background and explanation
of test
The EEG records electrical potential differences between
electrode pairs on the scalp or between a scalp electrode and
a reference electrode. These potentials reflect underlying
electrical activity in the cerebral cortex and, indirectly, that
of deeper structures. Electrodes are attached to the scalp in
an array known as the 10-20 system, and several different
patterns of electrode pairing (“montages”) are captured
during each recording session. Reference electrodes are
placed on the ear or mastoid process or an averaged refer
-
ence is created electronically. Ideally, recordings capture the
fully awake, drowsy, and sleeping states. To achieve the
sleep state, the patient might require sleep deprivation on
the night before the
test.
Stimulation procedures performed during the test include
hyperventilation and photic stimulation, which are de-
signed to elicit epileptiform patterns. If the referring ques-
tion relates to a specific provocation (e.g., seizures when
listening to music), the provocation should be simulated
during testing. To capture epileptiform or ictal activity aris
-
ing from temporal lobes (e.g., in partial seizures), anterior
temporal (T1 and T2) and ear electrodes may be used; naso-
pharyngeal electrodes offer no advantage and are uncom-
fortable for the patient. If the referring question relates to
encephalopathy, the patient may require specific alerting
procedures; for example, they may be asked to count back
-
ward from 20, or the technician might provide a tapping
stimulus to maintain wakefulness. Standard EEG frequen-
cies recorded range from 0.5 Hz to ~35 Hz, with frequencies
divided into bands as follows:
delta=0.5–4 Hz
theta=5–7.5 Hz
alpha=8–12 Hz
beta=13–35 Hz
Higher frequencies often represent artifactual muscle
activity.
Relevance to psychiatry and
behavioral science
In psychiatric practice, the EEG finds greatest utility in the
diagnosis and differential diagnosis of delirium. It is exqui-
sitely sensitive to the changes in brain metabolism and ac-
tivity accompanying the clinical signs and symptoms of
delirium, showing generalized slow-wave activity in the
delta and theta ranges, slowing of the posterior dominant
frequency, disorganization of the background rhythm, and
loss of reactivity to eye opening and closing. The EEG can be
used to distinguish delirium from primary psychosis be-
cause it is usually normal in the latter condition. It can be
used to detect the presence of delirium superimposed on de-
mentia, in which case the amount of slow-wave activity may
be greatly increased over the baseline tracing.
https://t.me/med1917
110 Laboratory Medicine in Psychiatry and Behavioral Science
Electroencephalogram (EEG) (continued)
Relevance to psychiatry and Serial EEGs can be helpful in gauging response to treatment
behavioral science (continued) of delirium, with serial studies showing improvement in
slowing and increase in mean frequency when treatment is
successful.
Another use of the EEG in psychiatry is to help distinguish
seizures from pseudoseizures if the ictal event can be cap
-
tured during the recording and neither spike nor spike-and-
wave activity is seen. Caveats here relate to the fact that the
interictal EEG may be completely normal, that patients who
have pseudoseizures may also have true seizures, and that
some patients who have convincing signs and symptoms
but no EEG correlates may, in fact, have deep epileptogenic
foci, with activity captured only by depth recording. When
the EEG is used for the workup of “mental status changes”
or confusional states, it may capture non-convulsive status
epilepticus, a condition disproportionately affecting elderly
females who present in an ongoing oneiric state or stupor. In
these cases, the EEG shows sustained ictal activity.
Characteristic EEG changes are also seen in sporadic CJD
and in subacute sclerosing panencephalitis. In addition, the
EEG may detect toxic effects of drugs such as lithium, in
which case a disorganized rhythm, interspersed slow-wave
activity, and triphasic waves may be seen.
Preparation of patient Some patients need reassurance that the EEG only records
electrical activity and does not deliver an electrical stimulus.
The process of electrode application should be explained;
this often includes use of collodion, an adhesive gel that re
-
quires vigorous cleansing for removal. Patients should
avoid sedatives before testing. If a hypnotic is required to
capture sleep during test, chloral hydrate is often used in
preference to alternatives; other sedatives have been stud-
ied, but no consensus has been achieved as to superiority.
Sleep deprivation may be needed to ensure an adequate
sleep sample is obtained (e.g., in the case of suspected sei-
zures). Sleep deprivation protocol is to awaken patient at
4:00
A.M. and then keep them awake without naps or stimu-
lants until the time of testing.
Indications •
Confirming diagnosis of delirium
• Distinguishing delirium from catatonia
• Monitoring course of delirium (serial studies)
• Detecting presence of epileptiform or ictal activity
• Monitoring efficacy of antiepileptic drugs
• Diagnosing non-convulsive status epilepticus
• Diagnosing CJD
• Diagnosing subacute sclerosing panencephalitis
• Providing evidence for lithium toxicity
https://t.me/med1917
111 Laboratory Tests
Electroencephalogram (EEG) (continued)
Indications (continued) • Various indications in critical care: evaluating coma,
confirming brain death
• Aiding in the diagnosis of functional neurological symp-
tom disorders (e.g., suspected pseudoseizures)
Normal patterns • Posterior dominant (alpha) frequency 8–12 Hz
• Presence of beta activity during wakefulness, prominent
in frontal areas
• Abundant theta and delta slow-wave activity only in
drowsiness and sleep
• Frontal intermittent rhythmic delta activity (FIRDA)
only in transitions to and from sleep
• In drowsiness and light sleep: vertex sharp waves
• In stage 2 sleep: sleep spindles, K complexes
• No epileptiform activity or focal slowing
• No abnormalities elicited by hyperventilation or photic
stimulation
Abnormal patterns Spike, spike-and-slow-wave complexes, slow waves in the
awake state, focal slowing, periodic patterns, triphasic
waves; FIRDA outside of transitions. Abnormalities may
only be seen with stimulation procedures.
Interfering factors For intermittent EEG abnormalities, single EEG may be a
low-yield procedure. This is particularly true for epilepti-
form or ictal (seizure) activity when clinical manifestations
do not appear during EEG recording or when provoking
stimulus cannot be simulated in the laboratory.
For seizure activity, yield increases with sleep deprivation,
greater number of EEG recordings, and longer times of re-
cording. For this purpose, ambulatory (24-hour) EEG or
EEG telemetry may be used for monitoring.
EEG study that does not include wakefulness, drowsiness,
and at least stage 2 sleep along with hyperventilation and
photic stimulation is considered incomplete for detection of
epileptiform activity.
EEG study that does not explicitly produce and document
alerting stimuli is considered incomplete for patients with a
depressed level of consciousness (e.g., suspected delirium).
Many psychotropic drugs affect EEG, usually introducing
either slow-wave activity (e.g., antipsychotics and mood
stabilizers) or beta activity (e.g., sedative-hypnotics and
alcohol).
Cross-references Creutzfeldt-Jakob Disease
Delirium
Quantitative Electroencephalogram
Seizures
https://t.me/med1917
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