Vital Signs

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Chapter 2 Vital Signs

“Immediately below a completely compressed artery (with obliteration of the lumen) no sounds are heard. As soon as the first drop of blood escapes from under the site of pressure, we hear a clapping sound very distinctly. This sound is heard when the compressed artery is released and even before the appearance of pulsation in the peripheral branches.”

N.S. Korotkoff, on methods of studying blood pressure. Bull Imperial Acad Med St. Petersburg 11:365, 1905.

“Humanity has but three great enemies: Fever, Famine and War. Of these by far the greatest, by far the most terrible, is fever.”

Sir William Osler, JAMA 26:999, 1896.

“A quartan fever kills old men and heals young.” — Italian proverb

Generalities

Measuring vital signs is the initial but still essential part of bedside examination. Unfortunately, this task is often relegated to nonphysicians, sometimes even technicians. Yet, as the word implies, vital signs can provide a wealth of crucial information, some requiring special skills and knowledge.

A. Vital Statistics

1 What are the vital statistics?

They are weight and height, both important measurements (see Chapter 1, General Appearance, questions 30–49). In contrast to vital signs, vital statistics are usually stable and thus less clinically helpful.

B. Vital Signs

2 What are the vital signs?

They are crucial (and thus vital) measurements that should be obtained in every meaningful patient interaction. They include heart rate and rhythm, respiratory rate, temperature, and blood pressure. To these, hemoglobin oxygen saturation (O₂ sat) has been recently added.

C. Temperature

8 How long does it take for a thermometer to equilibrate when placed under the tongue?

Three minutes with the old mercury thermometers, and around one with the newest models.

9 What is the clinical significance of a fever?

It usually indicates the presence of an infection. Fever, however, can also be present in inflammatory processes (like autoimmune diseases), cancers, drug reactions, or even environmental exposure (heat stroke). They may also occur in dysmetabolic and endocrine disorders, such as Graves’ disease and Addisonian crisis.

10 What are the most commonly encountered fever patterns?

There are four classic ones:

Sustained or continued (little variability from day to day): This used to be the pattern of lobar pneumonia, steady until abruptly resolving by either crisis or death. Nowadays, a sustained pattern is mostly seen in gram-negative sepsis, but also in central nervous system (CNS) diseases.

Intermittent: With complete resolution between episodes (see later)

Remittent: Abating every day, but still not completely resolving. This used to be the pattern of typhoid fever.

Relapsing: With a series of febrile attacks, each lasting several days, and all separated by afebrile intervals of about the same length. A relapsing fever is usually infectious (brucellosis, borreliosis, or relapsing typhoid, but also tuberculosis [TB]), but can occur in Hodgkin’s, too, or familial Mediterranean fever.

11 What are the most common fever types?

Intermittent or remittent. In fact, since the introduction of antibiotics, all the aforementioned associations have become more historic than diagnostic. Yet, a continued pattern in the face of antibiotics should still suggest four primary explanations:

Resistant organism

Closed space infection

Superinfection

Allergic reaction

It might also suggest a noninfectious etiology, such as an occult neoplasm or autoimmune disease.

12 What are the main types of “intermittent” fever?

The classic ones are those of malaria, one of the three great medical killers of mankind (the others being TB and HIV, plus, of course, war and organized religion). Intermittent malarial fevers vary considerably, based on organism involved:

Quotidian fever: From the Latin quotidianus, daily. This is a fever whose paroxysm (and resolution) occurs every day. It is usually caused by a double tertian malaria, due to infection by two distinct groups of Plasmodium vivax, alternately sporulating every 48 hours. It may also be caused by the most pernicious malarial parasite (P. falciparum), combined with vivax, or by two distinct falciparum generations that mature on different days, thus resulting in a fever that occurs twice a day. Note that a double quotidian fever is a daily two-spikes fever that is not malarial, but gonococcal. It used to be present in 50% of endocarditis cases, but today is mostly extinct.

Tertian fever: From the Latin tertianus, third. This is a P. vivax fever that recurs every third day, counting the day of an episode as the first. Hence, it occurs every 48 hours (every other day).

Quartan fever: From the Latin quartanus, fourth. This is a P. malariae fever that recurs every fourth day, counting the day of an episode as the first. Hence, it occurs every 72 hours. Note that a double quartan is instead an infection with two independent groups of quartan parasites, so that the febrile paroxysms occur on two successive days, followed by one without fever.

Malignant tertian fever: This is the fever of P. falciparum (falciparum fever, or aestivo-autumnal fever, or Roman fever because it was a common ailment in the countryside of Rome up to World War II). It is characterized by 48-hour paroxysms of a severe form of malaria, occurring with acute cerebral, renal, or gastrointestinal manifestations. These are usually due to clumping of the infected red blood cells, causing secondary capillary obstruction and ischemia.

13 What are the other most common types of intermittent fever?

They are Charcot’s intermittent fever and “hectic” fever.

14 What is Charcot’s intermittent fever?

It is a special intermittent fever that is usually accompanied by chills, right upper-quadrant pain, and jaundice. It is due to stones transiently obstructing the common duct.

15 What is a “hectic” fever?

From the Greek hektikos (habitual), this is a form of intermittent fever characterized by wide swings, usually greater than 2.5°F (1.4°C). It has a typical daily afternoon spike, often accompanied by facial flushing, and is traditionally linked to active tuberculosis.

16 What is Pel-Ebstein fever?

It is the fever of 16% of Hodgkin’s cases. It is characterized by episodes lasting for hours or days, followed by afebrile periods of days and even weeks. It is, therefore, a typical relapsing fever. It was first described in the 19th century by the Dutch Pieter Pel and the German Wilhelm Ebstein. The latter is probably better remembered for his extracurricular interests, ranging from arts and literature to history. He even wrote a couple of books on the diseases of famous Germans (including Luther and Schopenhauer) and a medical reinterpretation of the Bible.

17 What is factitious fever?

A self-induced and artificial fever (from the Latin factitius, made by art). This can occur in many ways, the most common being the ingestion (and mouth holding) of hot liquids prior to a temperature check. Factitious fever can often (but not always) be counteracted by measuring rectal temperature (which may even serve as a punitive deterrent) or urinary temperature on voiding. If doing so, remember that urinary temperature is a little lower than oral temperature.

18 Are there any other terms in this alphabet soup of “fevers”?

Quite a few, once again primarily of historic value. For a smorgasbord:

Ephemeral fever: A febrile episode lasting only a day or two

Epimastical fever: From the Greek epakmastikos, coming to a height. A fever that increases steadily until reaching an acme, and then declines by crisis or lysis (crisis indicates a sudden drop, whereas lysis indicates a more gradual defervescence).

Exanthematous fever: A fever associated with an exanthem, i.e., a skin rash

Fatigue (exhaustion) fever: An elevation of body temperature that follows excessive and continued muscular exertion. It may last sometimes for up to several days.

Miliary fever: An infectious fever characterized by profuse sweating and the production of sudamina (i.e., minute vesicles of fluid retention in sweat follicles, a.k.a. “milia”). Typical of past epidemics.

Monoleptic fever: A continued fever that has only one paroxysm

Polyleptic fever: From the Greek poly (multiple) and lepsis (paroxysm). A fever that occurs in two or more paroxysms, as typically seen in malaria.

Undulant fever: The long and wavy temperature curve of brucellosis

19 What is an “essential” fever?

One with an unknown etiology, whether ultimately due to infection or other processes. It is defined as a temperature of at least 100.4°F (or 38°C), lasting 3 weeks or longer, and with no identifiable cause—often referred to as FUO (fever of unknown origin).

20 What are the causes of an essential fever?

FUO in adults is most commonly due to infection, either closed space (abscess) or disseminated (malaria, tuberculosis, HIV, endocarditis, fungemia). Other less common causes include cancer (particularly lymphomas, hypernephromas, hepatomas, and hepatic metastasis of extrahepatic tumors); autoimmune diseases (collagen vascular diseases and vasculitis); and drug reactions. Patients with iatrogenic fever often have temperature/pulse dissociation, appear well in spite of high fever, and have other allergic signs, like skin rash or eosinophilia.

21 What is a temperature/pulse dissociation?

A rise in temperature that is not matched by an equivalent rise in heart rate. Normally, for each degree of temperature increase there is a 10 beats/minute increase in heart rate. This, however, may not always occur. Fever with relative bradycardia has a narrow differential diagnosis, usually infectious (including, among others, salmonellosis and typhoid fever, brucellosis, legionellosis, mycoplasma pneumonia, and meningitis with increased intracranial pressure), but possibly iatrogenic (like a drug fever) or simply the use of digitalis or beta blockers.

22 What are the causes of extreme pyrexia?

Very high temperatures (>105°F, or 40.6°C) are usually due to neurologic thermodysregulations (i.e., central fever). These include heat stroke, cerebrovascular accidents, or major anoxic brain injury following a cardiac arrest. Malignant hyperthermia and neuroleptic malignant syndrome are other important causes of very high fevers of central origin, often raising temperature >106°F (or 41.2°C). Fevers of this degree can be due (but often not) to an infectious process like gram-negative sepsis. The exception is a CNS infection, such as meningitis or encephalitis.

23 What are the causes of an inappropriately low fever?

Fever lower than expected is typical of patients with chronic renal failure (especially if uremic), but also of those receiving antipyretics (such as acetaminophen) and nonsteroidal anti-inflammatory agents. Inappropriately low temperature may also be caused by shock.

24 What other physical findings may help identify the cause of a fever?

Anhidrosis argues in favor of either heat stroke or drugs interfering with diaphoresis.

Muscle rigidity suggests neuroleptic malignant syndrome or malignant hyperthermia.

Jaundice may be seen in bacterial infections, independent of their direct involvement of the hepatobiliary system (such as cholangitis or hepatitis, see question 14).

Shaking chills argue only modestly in favor of bacteremia. Conversely:

Historic predictors (such as diabetes mellitus and old age) plus the degree of leukocytosis and the presence of hypotension argue very strongly in favor of bacteremia.

25 What is hypothermia?

It is a core temperature below 98.6°F (37°C). Yet, given the normal fluctuations, true hypothermia is considered anything below 95°F (35°C). At this low level of temperature, the body usually becomes unable to generate heat, and thus core temperature continues to fall. In fact, at 86°F (30°C), body temperature equilibrates with the environment. Based on this premise:

Mild hypothermia is a core temperature of 89.6–95°F (32–35°C).

Moderate hypothermia is one of 82.4–89.6°F (28–32°C).

Profound hypothermia is one less than 82.4°F (<28°C). Temperatures of this degree are missed by routine thermometers and thus require thermistors.

26 What are the causes of hypothermia?

Various. Based on its mechanism, hypothermia is usually classified as:

Primary (typically due to accidental exposure)

Secondary (due instead to failure of thermoregulation)

Depending on its setting, the most common cause of hypothermia is overwhelming sepsis or environmental exposure. Other major causes include cerebrovascular accidents (anorexia nervosa, multiple sclerosis, stroke, coma of any cause, spinal cord injury), low cardiac output following acute myocardial infarction, endocrine disorders (hypoglycemia, hypothyroidism, panhypopituitarism, adrenal insufficiency), and intoxication (drugs and alcohol). Note that patients who appear hypothermic to touch are often simply peripherally vasoconstricted.

27 What are the signs and symptoms of hypothermia?

They vary, depending on the degree of hypothermia and the type of underlying disorder (a stroke, for example, may obscure the signs of hypothermia). Moreover, symptoms and signs are often a continuum, and there is major variability among patients (Table 2-1).

Table 2-1 Signs and Symptoms of Hypothermia

Mild Hypothermia	Moderate Hypothermia	Severe Hypothermia
Confusion	Level of consciousness diminishes	Unresponsiveness or coma
Tachypnea	Delirium	May appear dead*
Tachycardia	Bradycardia	Loss of reflexes
Vasoconstriction	Bradypnea	Very cold skin
Lethargy	Shivering stops	Hypotension
Shivering	Reflexes slowed	Pulmonary edema
Ataxia	Cold diuresis	Respiratory failure
Dysarthria		Profound acidemia and ventricular fibrillation
Loss of fine motor coordination

* Hence, you are never dead until you are warm and dead (see Chapter 20, Coma).

D. Heart Rate and Rhythm

28 What is the history behind the measurement of heart rate through the arterial pulse?

Interpretation of a weak pulse as a bad prognostic indicator goes all the way back to third-millennium Egypt, but only in Ptolemaic and Hellenistic Alexandria (third and second century BC) did such knowledge eventually get applied to the heart rate. The two leading figures of the time were Herophilus of Chalcedon and his rival Erasistratus of Cos, both Hippocratic Greeks who had moved to Egypt to perform dissections, practice medicine, and conduct research. Erasistratus gave heart valves the names they still carry today and eventually committed suicide because of incurable cancer. Herophilus described not only the duodenum (which he named after the Greek word for 12 fingers, the measurement of its length), but also the liver, spleen, circulatory system, eye, brain, and genital organs. He gave great importance to drugs (“the hands of God”) and was the first to suggest that physicians could be guided diagnostically by the arterial pulse, which he counted by using a portable water clock. Influenced by musical theories, he even developed a classification of pulse characteristics, based on rate, rhythm, strength, and amplitude.

Five hundred years later, the Romans perfected this knowledge through the work of Galen, who defined the diagnostic significance of the pulse in terms of force, length, and speed. Half a millennium later, the Chinese developed an even more complicated classification, requiring analysis of the pulse at various sites and simultaneous timing with the physician’s own respiration. Four pulsations to each respiratory cycle constituted the normal adult rate. To avoid possible distractions, practitioners were asked to banish all extraneous thoughts prior to an exam and to conduct their assessments in the morning (and on an empty stomach).

Things got a little easier in the 18th century, when the British physician John Floyer (1649–1734) asked a local watchmaker to build him a portable clock with a special second hand that ran exactly for 1 minute. This allowed him to accurately determine the speed of the pulse and to publish in 1707 “The Physician’s Pulse Watch,” a little treatise that suggested the use of the watch for a more objective determination of the pulse. Floyer also had other and more eccentric interests. One, for example, involved Dr. Samuel Johnson, whom he examined as a 5-year-old child, eventually recommending a healthy dose of “Royal Touch” as remedy against various evils (Dr. Johnson’s mother complied, and so did Queen Anne, who touched and reportedly “healed” the child). Other eccentricities concerned a lifelong fascination with minerals, vegetables, and animals (he wrote a book about discovering their virtues through taste and smell) and a similarly lifelong fascination with cold bathing (he wrote a book on that, too). Maybe because of all this baggage, Floyer’s recommendations on the pulse went mostly unheard, so that for decades practitioners continued to rely more on their “feel” of the pulse, than on an objective assessment of rate and rhythm.

It was only during the mid-19th century that measurement through a watch became the standard of medical care. That was also the time when Adams and Stokes made the connection between an inappropriate slowing of the pulse and some episodes of syncope and seizure, thus shifting attention from the brain to the heart (and to physical exam).

29 How should the pulse be examined?

It depends. If you are simply assessing rate and rhythm, the best (and most accurate) technique is to count the pulse at the wrist for 30 seconds, and then double the figure. Alternatively, you could count the apical rate, which is more accurate in situations of pronounced tachycardia, especially atrial fibrillation (where pulse deficit commonly occurs). In this case, counting 60 seconds may further improve accuracy. Finally, if you want to assess the characteristics of the waveform, then you should assess the pulse of a central artery (see Chapter 10, questions 3–56).

30 What is a pulse deficit?

It is the absence of a palpable arterial pulse despite a precordial heartbeat. This is expressed as apical rate minus pulse rate per minute. A pulse deficit is very common in atrial fibrillation, since some ventricular contractions may be too weak to empty into the aorta and cause a waveform. Missed pulses also can be encountered after premature beats, or in other tachycardic states. Hence, always measure heart rate over both precordium and wrist, especially in tachycardia.

31 So what is a normal heart rate?

The traditionally reported range is 60–100/minute, even though 50 is probably a more accurate lower boundary. Hence, anything <50 is bradycardia, whereas anything >100 is tachycardia.

32 In addition to rate, which other characteristics should be assessed in a pulse?

Its regularity—and if the pulse is irregular, whether the irregularity itself is regular or irregular. This is especially important in the evaluation of tachycardia.

33 What is the clinical significance of tachycardia?

Usually ominous. Common in infection and ischemia, a sinus tachycardia predicts poor outcome in pneumonia, sepsis, pontine hemorrhage, myocardial infarction, gallstone pancreatitis, and congestive heart failure.

34 What bedside information can help to evaluate an arrhythmia?

In times of electrocardiograms (ECGs), it seems almost anachronistic to discuss the physical examination of arrhythmias. Yet a thorough and astute exam, comprising an assessment of arterial pulse (especially when coordinated with apical impulse—see pulse deficit in question 30), venous waveform, and characteristics of heart sounds, can often deliver a diagnosis.

35 What are the features of the pulse one should consider when evaluating arrhythmias?

Its regularity (or lack thereof) and its response to vagal maneuvers. In this regard:

A regularly irregular tachycardia is a sign of bigeminy or trigeminy. But it can also indicate atrial flutter with variable atrioventricular block (in this case, look for flutter waves in the neck veins) or a second-degree heart block in which skipped beats occur at regular intervals.

An irregularly irregular tachycardia is most commonly seen in atrial fibrillation. This is differentiated from frequent premature contractions because the latter may present with occasional cannon “A” waves (see Chapter 10, questions 78–88).

A regularly regular tachycardia can be due to atrial flutter (with constant A-V block), paroxysmal atrial tachycardia, ventricular tachycardia, and, of course, sinus tachycardia. Response to vagal maneuvers might be helpful in separating these entities.

A tachycardia that resolves abruptly after either Valsalva’s maneuver or carotid artery massage is a paroxysmal atrial tachycardia (typically associated with a unique feeling of “pounding in the neck” due to the simultaneous occurrence of carotid pulsations and cannon “A” waves).

One that only slows down is usually sinus tachycardia.

One that halves in rate is typically atrial flutter.

Ventricular tachycardia is usually unchanged by vagal maneuvers. Ventricular tachycardia, however, typically presents with findings of atrioventricular dissociation, such as cannon “A” waves, and variable intensity of S₁.

36 What other findings might help to recognize an arrhythmia?

The presence and characteristics of a pause between heartbeats. A pause preceded by a premature beat, for example, usually indicates an atrial (or a ventricular) premature contraction, whereas one not preceded by a premature beat usually indicates a heart block.

A premature beat associated with a cannon “A” wave on venous exam (see Chapter 10, questions 86 and 87) usually indicates an atrial contraction against a closed tricuspid valve and, therefore, a ventricular rather than an atrial premature contraction. Cannon “A” waves might also consistently occur in paroxysmal atrial tachycardia due to the almost simultaneous contraction of atria and ventricles in this condition. Conversely, they might occur randomly in complete heart block.