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46 CHAPTER 4: Vital Signs, Anthropometric Data, and Pain
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Normal temperature.
Normal body temperature. Internal body temperature is maintained within
a narrow range, ±0.6°C (1.0°F). The population range of this set point varies
from 36.0°C to 37.5°C (96.5–99.5°F), making it necessary to establish a baseline for each patient. Without a baseline, an oral temperature above 37.5°C
(99.5°F) and a rectal temperature over 38.0°C (100.5°F) is considered fever.
Diurnal variation.
temperatures between 3 and 4 , rising slowly to a maximum between 8
and 10 . This pattern is reversed in nightshift workers. Transitioning from
one pattern to the other requires several days.
Regional temperature variation. Heat is produced by cellular metabolism.
The temperature is highest in the liver and lowest at the skin surface. Customarily, body temperature is measured in the rectum, mouth, ear, axilla, or
groin. Among these sites, rectal temperature is ~0.3°C (0.6°F) higher than that
of the oral or groin reading; the axillary temperature is ~0.5°C (1.0°F) less than
the oral value.
Elevated temperature. Increased temperature results from excessive heat
production or impaired heat dissipation. Each mechanism may be a normal
response to physiologic challenge or be due to damage to the thermoregulatory pathways. Fever is a physiologic elevation of the set point for body temperature by the hypothalamus. Pathologic elevations of body temperature,
hyperthermia, results from unregulated heat generation and/or impaired heat
exchange with the environment.
Fever. Release of endogenous pyrogens, particularly interleukin (IL-1), trig-
gered by tissue necrosis, infection, inammation, and some tumors, elevates
the hypothalamic set point leading to increased body temperature. Fevers
often begin with a chill and shivering, which generates heat, accompanied by
cutaneous vasoconstriction reducing heat loss; rigors are particularly severe
chills. Be aware that the skin temperature may be low or normal, while the
core temperature is markedly elevated. The skin becomes warm again when
the new set point is reached. Fever is accompanied by tachycardia in proportion to the temperature elevation. The body returns to normal temperature
through dissipation of heat by ushing and sweating. Night sweats are an
exaggeration of the normal diurnal temperature variation, the sweat marking nocturnal temperature decline. They occur in many chronic infections,
inammatory diseases, and some malignancies, particularly lymphomas.
Fever requires special consideration in immunocompromised, HIV-infected,
and hospitalized patients. Some patients cannot mount a febrile response to
infection, particularly those with renal failure, on high doses of corticosteroids, and the elderly.
CLINICAL OCCURRENCE: Congenital: Familial Mediterranean fever, other
familial periodic fevers, porphyrias; Endocrine: Hyperthyroidism, pheochromocytoma; Degenerative/Idiopathic: Seizures; Infectious: Bacterial, viral,
rickettsial, fungal, and parasitic infections either localized (e.g., SBE) or systemic (occult abscess is common); Inammatory/Immune: Systemic lupus
erythematosus (SLE), acute rheumatic fever, Still disease, vasculitis, serum
Daytime workers, who sleep at night, have minimum
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sickness, any severe local or systemic inammatory process (e.g., sarcoidosis, bullous dermatosis);
cardial infarction, pulmonary infarction, stroke), exercise;
Drug reactions, gout;
Mechanical/Traumatic: Tissue necrosis (e.g., myo-
Metabolic/Toxic:
Neoplastic: Leukemia, lymphomas, and solid tumors;
Psychosocial: Factitious; Vascular: Thrombophlebitis, tissue ischemia and
infarction, vasculitis, subarachnoid hemorrhage.
Fever patterns.
The pattern of temperature uctuations may be a useful di-
agnostic clue.
Continuous fever. The diurnal temperature uctuation is 0.5°C to 1.0°C (1.0°F
to 1.5°F).
Remittent fever. The diurnal uctuation is more than 1.1°C (2.0°F) without
normal readings.
Intermittent fever. Fever episodes are separated by days. Examples include
tertian fever of Plasmodium vivax, quartan fever of Plasmodium malariae.
Relapsing fever. Fevers occur every 5 to 7 days in borreliosis and Colorado
tick fever.
Episodic fever. Typical of the familial periodic fevers, fever lasts for days or
longer followed by a remission of at least 2 weeks. [Drenth PPH, van der
Meer JWM. Hereditary periodic fever. N Engl J Med. 2001;345:1748–1757].
Pel–Epstein fever. Characteristic of Hodgkin disease, several days of contin-
uous or remittent fever are followed by afebrile remissions lasting an
irregular number of days.
Fever of unknown origin (FUO). Three conditions dene an FUO: (1) the illness has lasted >3 weeks; (2) the temperature is repeatedly >38.3°C (100.9°F);
and (3) more than three outpatient visits or ≥3 days in the hospital have not
yielded a diagnosis. In the modern era the most common causes of FUO in
immunocompetent patients are noninfectious inammatory diseases, infections, and malignancies, especially hematologic malignancies. However,
fever remains unexplained in almost 50% of patients, especially those with
episodic.
CLINICAL OCCURRENCE: Noninfectious Inammatory Diseases:
Polymyalgia rheumatica, Still disease, SLE, sarcoidosis, Crohn disease, vasculitis (giant cell arteritis, Wegener disease, polyarteritis nodosa);
Infections:
Endocarditis, tuberculosis, urinary tract infection, cytomegalovirus, Epstein–
Barr virus, HIV, subphrenic abscess, cholangitis and cholecystitis; Neoplasms:
Non-Hodgkin lymphoma, Hodgkin disease, leukemia, adenocarcinoma;
Miscellaneous: Habitual hyperthermia, subacute thyroiditis, Addison dis-
ease, drug fever.
Rheumatic fever.
See Chapter 13, page 586.
Pathologic overproduction and impaired dissipation of heat.
Hyperthermia. Unregulated heat production or damage to heat dissi-
pation systems leads to rapid and severe uncompensated temperature
elevation. Common causes of fever rarely produce hyperthermia. More
commonly, the environment, impaired judgment, or toxin exposure is
the direct cause.
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CLINICAL OCCURRENCE: Impaired Heat Loss: High environmental
temperature and humidity, moderately hot weather for a person with
congenital absence of sweat glands, congestive heart failure, heat stroke,
anticholinergic drugs and toxins. Poverty, homelessness, and psychosis
all inhibit the ability to adapt to environmental challenges. Increased
Heat Generation:
drome, heavy exertion in hot and humid environment.
Neuroleptic malignant syndrome. Medications disrupt central dopa-
mine pathways leading to uncontrolled hyperthermia. One to two days
after exposure to a neuroleptic (antipsychotic) drug, the patient develops hyperthermia, rigidity, altered mental status, labile BP, tachycardia,
tachypnea, and progressive metabolic acidosis. Myoglobinuria and
acute renal failure can occur. It can be confused with worsening of the
psychotic state leading to delayed diagnosis and administration of more
neuroleptics.
Malignant hyperthermia. An inherited disorder of muscle sarcoplas-
mic reticulum calcium release produces sustained muscle contraction
on exposure to inhalational anesthetics or succinylcholine. The patient
develops rigidity, hyperthermia, rhabdomyolysis, metabolic acidosis,
and hemodynamic instability. Prompt recognition and treatment is lifesaving.
Heat stroke. Failure of the thermoregulatory system leads to decreased
sweating and rapid increases in core body temperature. Cardiovascular
disease increases risk by restricting the increased cardiac output necessary for skin perfusion. Diuretics and anticholinergic drugs also increase
the risk. The typical victim is a chronically ill adult conned in a hot,
humid environment during heat waves. The patient is often delirious or
comatose; the diagnostic clue is the hot dry skin.
Malignant hyperthermia, neuroleptic malignant syn-
Heat exhaustion (heat prostration). Exertion in a hot, usually humid, envi-
ronment leads to loss of uid and electrolytes and decreased ability to dissipate body heat. This is classically seen in younger individuals participating
in athletic events or working in hot, humid environments. Symptoms are palpitations, faintness, lassitude, headache, nausea, vomiting, and cramps. Patients have tachycardia, diminished BP, diaphoresis, ashen, cool, moist skin,
and dilated pupils. The core body temperature is elevated, but <40°C (104°F).
Untreated it can lead to heat stroke.
Factitious fever. Common in malingering and Munchausen syndrome, clues
are unexpectedly high temperatures with unusual uctuation, and fever
without other signs of acute illness.
Infections presenting as fever. Fever accompanies many infections and
inammatory diseases. The following are diseases that often present with
fever without localizing symptoms or signs.
Tuberculosis. Infection with Mycobacterium tuberculosis may be limited to
the lung or spread via the lymph nodes or bloodstream to affect any organ.
Primary infection is in the lung and may leave a calcied middle or lower lobe
nodule and hilar lymph nodes (Ghon complex). Progressive primary tubercu-
losis is seen commonly in HIV-infected patients but may occur in otherwise
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healthy people. It presents as progressive lung infection (usually in the lower
lung zones), pleural effusion, and lymphadenopathy. Immunosuppressed
hosts and dark-skinned races have increased risk for early hematogenous
dissemination. Miliary tuberculosis presents with fever, anorexia, and weight
loss and may have hepatomegaly, splenomegaly, and/or lymphadenopathy.
Reactivation tuberculosis most commonly occurs in the lung apices. Patients
present with fever, malaise, night sweats, cough with sputum production,
and lung consolidation and/or cavity formation. Reactivation can also occur
in bones, especially the spine (Pott disease), the peritoneum, meninges, kidneys and urinary tract, lymph nodes, intestine, and pericardium [Tanoue LT,
Mark EJ. Case records of the Massachusetts General Hospital. Case 1–2003. N
Engl J Med. 2003;348:151–161].
Endemic North American fever syndromes.
an undifferentiated febrile illness, are found exclusively or with increased
frequency in certain regions of the United States. In the rst days of illness,
they cannot be clinically differentiated, so travel history is essential for timely
recognition and treatment.
CLINICAL OCCURRENCE: Rocky Mountain spotted fever (RMSF), other
rickettsial infections, babesiosis, ehrlichiosis and anaplasmosis, Lyme disease, Q fever, leptospirosis, relapsing fever, Colorado tick fever, and other
viral exanthems.
Rickettsial spotted fever syndromes.
bites and usually present as systemic disease with headache and rash without
localizing symptoms or signs. Travel and exposure history are essential for
an accurate differential and evaluation. Prompt treatment can be lifesaving.
DDX: RMSF is described below; it produces the archetypical syndrome. The
other rickettsial diseases present in a similar fashion with severe headache,
fever, myalgias, and malaise. Careful history and exam minimize confusion
with babesiosis, Lyme disease, or Ehrlichiosis and anaplasmosis.
Rocky Mountain spotted fever. Rickettsia rickettsii are transmitted by the
bite of an infected tick. The obligate intracellular parasites infect endothelial
cells producing acute systemic illness. The disease is highly endemic to the
Atlantic coastal states. The onset is nonspecic with headache, fever, chills,
myalgias, and asthenia frequently accompanied by nausea, vomiting, and abdominal pain. An erythematous macular rash spreading centrally from the
wrists and ankles may be seen after the third day; the palms and soles may be
affected, and dorsal edema of the hands and feet is characteristic. The lesions
are initially blanching but progress to papules which become non-blanching
purpura. Systemic involvement leads to widespread organ damage and
death in 25% of untreated patients.
Several infections, presenting as
Rickettsia are transmitted by arthropod
Louse-borne typhus (epidemic typhus, trench fever), endemic typhus (murine
typhus), and rickettsialpox. All are endemic to the United States and are also
imported. Rickettsialpox, seen in the Northeastern United States, has a papular erythematous rash at the mite bite site that becomes a necrotic eschar with
regional lymphadenopathy. Nausea and vomiting are highly characteristic of
murine typhus.
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Babesiosis. Babesia are intracellular protozoa transmitted by infected Ixo-
des ticks. Babesiosis is a worldwide zoonotic infection in which humans are
infected incidentally. They parasitize red blood cells and can be identied
on blood smears.
York, Connecticut, Rhode Island, and Massachusetts. It has been reported
from other locales and imported cases are seen. There is gradual onset of fever, headache, myalgias, and fatigue. There may be hepatosplenomegaly and
hemolysis. A rash does not occur. Coincident infection with other tick-borne
diseases (Lyme and anaplasmosis) should be considered.
Lyme disease. Infection with Borrelia burgdorferi is transmitted by bites of
Ixodes ticks. Initially infection is in the skin with a characteristic rash, but it
disseminates to virtually all organs and tissues within days. If the character-
istic erythema migrans rash is missed or ignored, the patient presents with
fever, headache, myalgias, neck stiffness, arthralgias, and striking fatigue and
malaise. These symptoms may persist for weeks, gradually resolving or being replaced with neurologic symptoms and signs (peripheral neuropathy,
mononeuritis multiplex, cranial neuropathy, aseptic meningitis, or chorea);
Bell palsy is quite common at this stage. Cardiac conduction block with
symptomatic bradycardia may be seen. The most common late manifestation
is an inammatory large joint oligoarthritis, commonly affecting the knee.
Ehrlichiosis and anaplasmosis. Ehrlichia and anaplasma are intracellular
parasites that reproduce in either mononuclear phagocytic cells in the blood
and tissues (Ehrlichia chaffeensis) or granulocytes (Ehrlichia ewingii and
Anaplasma phagocytophilia) forming vacuolar inclusions (morula) visible
on light microscopy. Human monocytotropic ehrlichiosis and ehrlichiosis ew-
ingii are transmitted by the Lone Star tick (Amblyomma americanum) and are
most prevalent in the south-central, southeastern, and Mid-Atlantic States.
Onset of both diseases is nonspecic with fever, headache, malaise, and myalgia often accompanied by nausea, vomiting, and diarrhea. Rash, cough,
and confusion may be seen. A. phagocytophilia is transmitted by bites of the
Ixodes ticks with high concentrations in the northeastern and upper Midwestern states. A high index of suspicion is required to make these diagnoses
promptly.
It is highly endemic in the Atlantic coastal regions of New
Cat-scratch disease.
lated by the scratch, lick, or bite of a healthy cat. The organisms travel to the
regional lymph nodes then disseminate.
aise and headache. Signs include fever, an inoculation site papule or pustule,
followed by painful uctuant regional lymphadenopathy with overlying
erythema. In immunocompromised hosts dissemination can lead to hepatitis
(peliosis hepatitis), osteomyelitis, or meningoencephalitis. Conjunctival infection produces preauricular lymphadenopathy (Parinaud oculoglandular
syndrome).
Leptospirosis.
tion of contaminated water or contact with urine or tissues of infected animals. The onset is abrupt with fever, headache, myalgias, and malaise often
accompanied by conjunctival suffusion. There may be muscle tenderness,
Gram-negative bacilli (Bartonella henselae) are inocu-
Symptoms are nonspecic with mal-
Leptospirosis is a worldwide zoonosis transmitted by inges-
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lymphadenopathy, hepatosplenomegaly, or rashes. History of contact with
contaminated water in the summer or fall is a key to making the diagnosis. Men are more often exposed than women. If not initially recognized and
treated symptoms may subside or disappear for a week only to recur. Severe
disease causes multiorgan failure known as Weil syndrome with jaundice,
renal insufciency, and hemorrhage.
Relapsing fever.
organisms can change their antigenic coating of variable major proteins causing escape from an initially effective immune response producing a relapsing
illness. Tick-borne relapsing fever is a zoonotic infection. The patient presents
with fever, myalgias, chills, nausea, vomiting, and arthralgias. Abdominal
pain, cough, photophobia, neck stiffness, and rash are less common. Delirium
can accompany the high fever. The illness reaches a crisis in 3 to 5 days when
the fever peaks with chills followed by lysis of fever, diaphoresis, and hypotension. Relapse occurs with the next antigenic variant after 7 to 9 days.
Each crisis is equivalent to a Jarisch–Herxheimer reaction.
relapsing fever is transmitted by the human body louse. The symptoms are
similar. It is endemic to portions of Ethiopia but has caused major epidemics
in wartime Europe.
Q fever. This is a zoonotic infection with Coxiella burnetii transmitted by
infected cattle, goats, and sheep, especially via products of conception during
delivery, and infected milk. Both inhalation and ingestion of organisms pro-
duce infection. The illness has protean manifestations. Common symptoms
are fever, severe fatigue and headache, cough, nausea, and vomiting. Diarrhea and rash may be present. Presentations include an inuenza-like illness,
pneumonia, hepatitis, meningoencephalitis, and culture negative endocarditis. Chronic disease with hepatosplenomegaly implies persistent endocardial
infection. Diagnosis is difcult, requiring a high index of suspicion, and usually made by serology.
Colorado tick fever. Colorado tick fever virus is transmitted by infected
wood ticks (Dermacentor andersoni) in the northern Rocky mountain states
from late spring to fall. It causes a biphasic illness manifest as fever, myalgia,
headache, and occasionally meningoencephalitis and rash. It is self-limited.
Borrellia spp. infects humans from louse or tick bites. The
DDX: Louse-borne
Fever in returning travelers. This frequent problem is associated with rapid
global air travel. Patients present with fever and a history of travel to exotic,
usually tropical, locations. In addition to common illnesses, a host of unusual
infections are possible.
Dengue. The four dengue viruses are transmitted by Aedes mosquitoes well
adapted to tropical and subtropical urban environments worldwide. Common in travelers returning from the Caribbean, patients present with fever,
headache, back pain, and severe myalgias (break-bone fever). Dengue hemorrhagic fever is potentially fatal.
Chikungunya. Extensively distributed in the tropics and subtropics, it is transmitted by Aedes mosquitoes. Key features include polyarthralgia, myalgias,
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rash, and thrombocytopenia. Polyarthralgia begins 2 to 5 days after onset
of fever and commonly involves multiple joints. Rash is usually macular or
maculopapular often starting on the limbs and trunk.
Zika virus. Found mostly in South and Central America, the Caribbean,
sub-Saharan Africa, and South and Southeast Asia, it is transmitted by Aedes
mosquitoes. Key features include myalgia, pruritic rash, arthralgia, nonpurulent conjunctivitis, and thrombocytopenia.
Malaria.
dium falciparum are transmitted by Anopheles mosquitoes. Initial hepatocyte
infection is followed by invasion of erythrocytes. Cyclical release of mature
merozoites from ruptured erythrocytes produces cyclical fever. Plasmodi-
um falciparum infection can produce severe hemolysis, hypoglycemia, and
obstruction of cerebral capillaries (cerebral malaria). P. vivax and P. ovale can
persist in the liver causing relapsing infections. Patients present with fever,
headache, malaise, and myalgias. Nausea, vomiting, and abdominal pain
may be present, and progression to delirium and coma can occur. Prompt
diagnosis relies on the travel history and examination of blood smears by
trained personnel.
but blood smears are negative.
Typhoid Fever.
fection follows ingestion of contaminated food or water. The incubation period is 3 days to as much as 60 days. Symptoms are chills and prolonged,
persistent fever, prostration, cough, epistaxis, and constipation or diarrhea.
There is slowly progressing lassitude, abdominal distention and tenderness,
splenomegaly, and rose spots on the trunk and chest. Delirium may occur.
Complications include localized infections (gallbladder, bone, liver, spleen,
endocarditis, pneumonia, meningitis, and orchitis), gastrointestinal bleeding
and bowel perforation with peritonitis.
Brucellosis.
melitensis (goats), or canis (dogs) is acquired by exposure to unpasteurized
milk, and contaminated meat or other animal tissues. Lassitude and weight
loss accompany recurrent fever and sweating, undulant fever. Back and joint
pains are common. Physical ndings include splenomegaly, lymphadenopathy, and tender bones or joints. The disease may be acute or chronic [Drapkin
MS, Kamath RS, Kim JY. Case 26–2012: a 70-year-old woman with fever and
back pain. NEJM. 2012;367:754; Vogt T, Hasler P. A woman with panic attacks
and double vision who liked cheese. Lancet. 1999;354:300].
P. vivax, Plasmodium ovale, P. malariae P. knowlesi, and Plasmo-
DDX: Dengue fever may present a similar clinical picture,
Disseminated Salmonella typhi or Salmonella paratyphi in-
Systemic infection with Brucella abortus (cattle), suis (pigs),
Rickettsiosis. Rickettsial infections endemic to other countries, as well as
those endemic to North America, may be imported. Fever, headache, myalgias, and rash are characteristic of the spotted fever syndromes (e.g., Boutonneuse fever). In addition, cough is a prominent symptom in scrub typhus
imported from Australia, the southern Pacic region and southern and
southeast Asia. An inoculation eschar from the mite bite and regional lymphadenopathy typical of ulceroglandular syndromes may be present (Chapter 6,
page 142). Because the mite vector frequently bites in moist areas of the body
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that are usually covered, such as the genitalia, the perineum, and the area
beneath the breasts, the eschar of scrub typhus is often missed. An eschar
should be specically sought. In travelers returning from southern Africa,
one or more eschars may point to the relatively benign African tick typhus
(caused by Rickettsia africae). In those returning from South or Southeast
Asia, an eschar suggests scrub typhus (Orientia tsutsugamushi infection), a
potentially fatal disease
Lowered body temperature.
Hypothermia. Decreased hypothalamic set point, insufcient heat genera-
tion, and excessive heat loss due to behaviors and environmental conditions
all lead to a sustained decline in core temperature. Low body temperature
impairs cellular metabolism and brain function, particularly judgment, and
the combination prevents protection from continued exposure leading to
fatal hypothermia.
complete recovery is possible from rapid and sustained cooling, even when
the patient appears clinically dead. This is especially true for cold-water immersion (drowning). Relative or absolute hypothermia in situations where
fever would be expected, e.g., severe infection, is a poor prognostic sign. Core
temperature is usually lower in older adults making them particularly susceptible to decreased environmental temperatures.
CLINICAL OCCURRENCE: Endocrine: Hypothyroidism; Degenerative/
Idiopathic: Advanced age, seizures; Infectious: Sepsis; Mechanical/Traumatic:
Exposure and immersion, hypothalamic injury from trauma or hemorrhage,
burns; Metabolic/Toxic: Hypoglycemia, drug overdoses; Neoplastic: Brain
tumors; Psychosocial: Poverty, homelessness, and psychosis impair the ability to adapt to environmental challenges; Vascular: Stroke.
The Pulse: Rate, Volume, and Rhythm. The heart’s normal pacemaker is the
sinoatrial (SA) node in the right atrial wall near the superior vena cava (Fig.
4-1). It generates regular depolarization waves that spread rapidly through
both atria. The atrioventricular (AV) node, located in the posterior interatrial
septum, delays the impulse during atrial systole prior to its entering the His
bundle. The His bundle divides into right and left branches on either side of
the interventricular septum exciting the right and left ventricular myocardium nearly simultaneously. Changes in atrial or ventricular excitation or AV
conduction alter the cardiac rate and/or rhythm.
ejects blood into the aorta producing a pulse wave through the arteries whose
speed varies with the ejection force and elasticity of the arteries. The pulse’s
rate and rhythm are functions of the active pacemaker and depolarization
pattern in the conduction system and myocardium.
Hypothermia protects tissues from ischemic injury, so
Left ventricular contraction
Examining the pulse.
Palpation. Palpate the carotid, radial, femoral, posterior tibial, and dorsalis
pedis arteries (Fig. 4-2). Assess rate and rhythm in the radial, carotid, or femoral artery. Pulse contour and volume are discussed in Chapter 8, page 334,
and Fig. 8-42.
Normal rate and rhythm. Normal sinus rhythm (NSR) is regular at a pulse
rate between 55 and 100 beats per minute (bpm). Infants and children have
higher rates; consult pediatric references for normal ranges. Well-conditioned
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FIG. 4-1Disturbances of Cardiac Rate and Rhythm I. A. Diagram illustrating the spread of excita-
tion over the heart. The stimulus starts in the SA node and spreads throughout the walls of the atria, finally reaching
the AV node, where there is a short delay. The stimulus then proceeds down the His bundle by its two branches along
the right and left wall of the interventricular septum to the apex, spreading from there to the muscle of the right and
left ventricles. The atria contract before the impulse the leaves the AV node; ventricular systole occurs when the impulse
has spread over the ventricles. Note that the heart sounds resulting from ventricular systole are the only physical signs
of this process. B. Atrial premature beat originating outside the SA node, an ectopic beat. This is followed by a short compensatory pause that cannot ordinarily be detected. C. An ectopic ventricular beat with a
detectable compensatory pause. D. Respiratory or sinus arrhythmia. The heart rate accelerates near the
height of inspiration; this acceleration originates in the SA node. In any dysrhythmia, the heart sounds of a beat following
a shortened interval are often fainter than normal; beats following an abnormally long pause are louder than normal.
E. Ventricular rates.
athletes have resting rates into the low forties. Deconditioned adults may
have rates approaching 100 bpm. Ventricular diastole is longer than systole
at rates <100 bpm. They become equal at about 100 bpm and, at >100 bpm,
systole is longer. Rates <55 bpm are bradycardias and those >100 bpm, tachy-
cardias. Exertion accelerates the rate to a maximum of 200 bpm in young,
healthy adults. The maximum achievable heart rate declines predictably with
age. The pulse rhythm is normally regular with slight respiratory variation.
Vagus stimulation by breath holding, Valsalva, or carotid sinus massage
slows the rate.
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FIG. 4-1 (Continued)
Variations in rate and rhythm. The signs of heart action are practically all
ventricular (Fig. 4-1E); the atria produce only the atrial components of neck
vein pulsations, the fourth heart sound, the variably loud rst heart sound
accompanying AV dissociation, and ventricular lling sounds associated
with atrial contraction sometimes heard with AV block. Rhythm disorder
hypotheses are grouped by heart rate (slow, normal, fast) and pattern (regular, irregular in consistent pattern—regularly irregular, or irregular without
pattern—irregularly irregular).
exam must be conrmed or refuted by an ECG.
Slow regular rhythms. Rates <55 bpm suggest sinus bradycardia, second-
degree AV block (Fig. 4-3A), and third-degree AV block with junctional or
ventricular escape rhythms (Fig. 4-3B).
Regular rhythms with rates >120 bpm. Sinus tachycardia, atrial utter with
2:1 AV block, paroxysmal supraventricular tachycardia (PSVT) (Fig. 4-3C),
and ventricular tachycardia (VT) are possibilities.
gal stimulation is a clue to the rhythm. In utter, the rate slows stepwise. Paroxysmal atrial tachycardia (PAT) does not slow but can convert to a normal
rate. Sinus rhythm gradually slows and VT does not change.
Regular rhythms with rates of 60 to 120 bpm.
accelerated junctional rhythm (non-paroxysmal junctional tachycardia), atrial
All rhythm disorders suspected by physical
DDX: The response to va-
These include sinus rhythm,
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