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.

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.

3 What is a fever?

A bodily temperature >98.6°F (37°C). This is the value traditionally considered “normal,” based on 19th-century data by Wunderlich, who took 1 million axillary temperatures in 25,000 subjects. Yet, many normal people can get higher than 98.6 simply because of exercise or exposure. Moreover, gender differences (temperatures are usually higher in women than men) and swings over time (lowest values between 1–8 AM and highest between 4–9 PM) make “normal” a bit more flexible. A more recent study by Mackowiak et al. indicates that the upper limit of normal should be considered an oral temperature of 99.9°F (37.7°C). Fever, therefore, is anything above it.

4 Which is higher, rectal or oral temperature?

Rectal temperature. The difference is around 1°F (0.55°C) but can be even greater in mouth-breathing or tachypneic patients, whose rectal values may average 1.67°F (0.93°C) more than oral values.

5 Are there any other conditions that can alter oral temperature?

Beside tachypnea (which decreases oral temperature by 0.5°C for every 10 breaths/minute increase in respiratory rate), recent ingestion of cold or hot substances (including smoking a cigarette) may also change it—something well known to anyone who ever tried to play hooky from school (see factitious fever in question 17).

6 What about tympanic membrane temperatures?

They are lower than oral temperatures and better suited to reflect core temperatures. Yet, they can be lowered by cerumen (hence, always check for it) and, depending on time of recording, may exhibit greater swings than other modalities of measurement.

7 What about axillary temperatures?

To Wunderlich’s chagrin, they are very inaccurate and should be avoided. Especially in patients with hemiparesis, where the affected site always exhibits a significantly lower 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:

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:

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:

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:

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:

26 What are the causes of hypothermia?

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

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

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

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:

36 What other findings might help to recognize an arrhythmia?

37 How is blood pressure measured?

It depends. In clinical practice, the standard of measurement is the indirect method, which relies on a blood pressure cuff (sphygmomanometer) and can be either palpatory or auscultatory. The gold standard, however, remains direct determination, based on intra-arterial rigid-walled catheter.

38 Why is it important to measure blood pressure accurately?

Because unrecognized hypertension may lead to cardiovascular disease and thus reduce life expectancy. Hypertension is a common medical problem, affecting as many as 1 of 5 North American adults. It is easily treatable but often clinically silent, at least in its initial phases. Only regular and accurate blood pressure measurements can detect it early enough to initiate therapy. In addition, erroneous pressure overestimates may label a normal person as hypertensive, with significant economic, medical, and psychologic repercussions. Hence, correct and frequent ambulatory measurements are key in every physician’s armamentarium.

39 What does sphygmomanometer mean?

It is Greek for “measure of a weak pulse” (sphygmos, pulse; manos, scanty; metron, measure).

40 Who invented it?

In contrast to failures (that are almost always orphans), the sphygmomanometer has many proud fathers: the French Pierre Potain, the Italian Scipione Riva-Rocci, the Russian Nicolai Korotkoff, and the American Harvey Cushing. Cushing did not really participate in the ideation of the device but was instrumental (no pun intended) in its diffusion to North America. Incidentally, the mercury sphygmomanometer just celebrated his 111th anniversary (it was invented in 1896).

41 Who made the first direct measurement of blood pressure?

Stephen Hales, an English botanist and part-time chemist, who in 1733 decided to sacrifice his mare to see whether indeed a “blood pressure” existed. He cannulated the left carotid of the poor animal and then measured the height of the column of blood extending from her artery into a brass pipe until she finally died. Since the blood rose 8 feet and 3 inches above the level of the left ventricle, Hales concluded that there was indeed something he called “blood pressure,” and suggested that this varied between arteries and veins, cardiac dilations and contractions, and larger and small animals. He published it under the title “Haemasticks,” and then went on to bigger and better things, like telling housewives that putting an inverted teacup in their pies would prevent the crust from getting soggy.

42 Who was Potain? How did he contribute to the measurement of blood pressure?

Pierre Potain was one of the several well-rounded giants produced by 19th-century French medicine. A true humanist who never went to sleep without reading a few pages of his beloved Pascal, he was also an interesting man. As an intern, he survived a rendezvous with cholera (which he contracted during the 1849 epidemic) and then an even more dangerous rendezvous with the Prussians (whom he faced during the 1870 war, fighting as a simple foot soldier). Unscathed by these experiences, Potain went on to become one of Trousseau’s protégés, a great promoter of cardiac auscultation, and a very compassionate teacher (he was famous for answering his own question if an examinee failed to provide the answer in time). Before dying peacefully in his sleep at age 76, he made many landmark contributions: he was the first to describe (and name) the gallop rhythms, the opening snap of mitral stenosis, the tambour S₂ of syphilitic aortitis (“Potain’s sign”), the hepatic pulsatility of tricuspid regurgitation, and the waveform analysis of the internal jugular vein. He even inspired the figure of the great Parisian diagnostician in Proust’s Remembrance of Things Past. His unique contribution to blood pressure measurement consisted of a contraption made of a compressible bulb filled with air and attached by a rubber tube to an aneroid manometer. To measure the blood pressure, the bulb was pressed on the peripheral artery of the patient until the pulse disappeared. The manometric recording at time of pulse disappearance reflected the patient’s systolic blood pressure. Potain also taught Riva-Rocci, the next link in this blood pressure saga.

43 Who first thought of the mercury sphygmomanometer?

The Italian Scipione Riva-Rocci, who became interested in noninvasive blood pressure measurement while studying air-filling of the pleural cavity at controlled pressures, a technique pioneered by Forlanini for the control of tuberculosis. In 1896, at age 33, Riva-Rocci came up with the idea of “Un nuovo sfigmomanometro” (a new sphigmomanometer), which he reported in the Gazzetta Medica di Torino. His device was attached to a manometer in which the varying pressures were shown by differences of elevation in a column of mercury rather than by a revolving pointer, as in Potain’s aneroid (or dial) manometer. The idea was quite good for medicine, but may have been fatal for Riva-Rocci, who years later died of a chronic neurologic condition he probably contracted in the laboratory. Still, he had good insights and made several improvements on Potain’s instrument:

44 How did Riva-Rocci’s device reach the United States?

Serendipity. Despite its achievements, Riva-Rocci’s sfigmomanometro might have remained a little Italian secret were it not for Harvey Cushing’s visit to Pavia in 1901. Cushing spent several days with Riva-Rocci at the Ospedale di San Matteo, made a drawing of the instrument, received one as a gift, and brought everything back to Johns Hopkins. The rest is history.

45 What were the problems of Riva-Rocci’s tool? Who perfected the “indirect” method?

Both Riva-Rocci’s and Potain’s devices only provided a systolic reading (by releasing the arterial pulse, after its obliteration). Thirty-year-old Nicolai Sergeievich Korotkoff came to the rescue. As often happens in medical breakthroughs, he actually stumbled onto his discovery of auscultatory recording of blood pressure. A surgeon in the Czar’s army, he had completed a tour of duty in the Russian–Japanese war and was working in St. Petersburg on an animal model of post-surgical arteriovenous fistulae. One day, while listening over a dog’s artery before releasing a tourniquet, he suddenly heard loud sounds. Intrigued, he noticed that these correlated with systole and diastole, and in 1905 reported his observation in the “Izvestie Imp Voiennomedicinskoi Akademii” of St Petersburg. It was a brief report (only 281 words) that suggested that listening for the appearance and disappearance of pulse sounds might serve as a signal for maximal and minimal blood pressure. Written in Russian, the paper did not create much noise in Europe, but stirred quite a ruckus at home, winning Korotkoff an enviable reputation as a madman. It was only after the article finally reached Germany (and from there England) that his auscultatory method replaced the pulse obliteration technique of Riva-Rocci and Potain. Modern measurement of systolic and diastolic blood pressure was finally born. Korotkoff did not enjoy the rewards, though. Arrested during the Russian revolution of 1917, he soon died of TB.

46 What is the systolic pressure?

It is the highest intra-arterial pressure that can be produced during ventricular systole.

47 What is the diastolic pressure?

It is the lowest intra-arterial pressure prior to the next systolic event.

48 What are the various Korotkoff phases?

They are acoustic marks that take place after gradual deflation of the cuff. Validated by intra-arterial recordings, they were first suggested by Goodman and Howell in 1911. They include:

Use phase 1 to determine systolic pressure and phase 5 for diastolic (using phase 4 would overestimate it by close to 20   mmHg).

49 Where (and how) are Korotkoff sounds produced?

They are produced under the distal portion of the cuff, by the systolic reopening of a completely collapsed artery. Note that the sudden tensing of the arterial wall (and its resulting sound) can only occur between systolic and diastolic pressure because values above systolic will keep the artery collapsed, whereas values below diastolic will keep it totally open (and, thus, silent).

50 What is the proper technique for indirect measurement of blood pressure?

The American Heart Association has published guidelines for indirect (auscultatory) measurement (Table 2-2). Italicized parts ought to be paid special attention. Note that you should use the stethoscope’s bell and not the diaphragm (because Korotkoff sounds are low in frequency).

Table 2-2 Technique for Measuring Blood Pressure

Copyright 1993 American Heart Association. Reproduced with permission.

(Adapted from Reeves RA: Does this patient have hypertension? How to measure blood pressure. JAMA 273:1211–17, 1995.)

51 When should blood pressure be measured?

n every significant patient interaction, whether ambulatory or hospital based. Always obtain two or more readings from the same arm, with patient supine or seated. Then record the average value. If diastolic readings differ by more than 5   mmHg, take additional measurements until a stable pressure is reached. Measure blood pressure in both arms at the first visit, and then use the arm with the higher pressure thereafter (the arm with the lower pressure is abnormal). When indicated, also measure the pressure in the lower extremities and/or in different positions (supine versus standing).

52 How about comparison of upper extremities’ pressure?

Blood pressure should be measured at least once in both upper extremities. This requires two independent observers, working simultaneously on the two arms and then switching sides.

53 What is a significant difference between the two arms?

A difference in systolic pressure >10–15   mmHg. If >20, this usually indicates a subclavian artery occlusion, whose etiology varies based on setting. In an acute situation, it usually suggests aortic dissection (with aortic regurgitation in cases of more proximal dissection). In more chronic settings, it would instead indicate a subclavian steal syndrome, wherein blood is “stolen” from the vertebral circulation to feed a hypoperfused arm. Patients with this condition usually present with vertebrobasilar symptoms, such as vertigo, hemiparesis, ataxia, and visual changes. They can also have a diminished arterial pulse and an ipsilateral bruit over the subclavian artery.

54 Which factors can affect the accuracy of blood pressure measurement?

Several, and these can be related to patient, equipment, or examiner (Table 2-3). Conversely, some factors have no effect on blood pressure: menstrual phase, chronic caffeine ingestion, phenylephrine nasal spray, cuff self-inflation, discordance in gender or race of examinee and examiner, thin shirt sleeve under cuff, bell versus diaphragm, cuff inflation per se, hour of day (during work hours), and room temperature.

55 How variable can pressure be?

Quite variable. With >2 measurements at each visit, the standard deviation between visits is 5–12   mmHg systolic and 6–8 diastolic. Between-visits variability is greater than within-visit fluctuation. Hence, more visits are needed to ensure diagnostic precision. That is why the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure recommends repeat measurements within 1 month for initial values in the range of 160–179   mmHg systolic or 100–109   mmHg diastolic (stage 2 hypertension), within 2 months for stage 1, within 1 week for stage 3, and immediate evaluation for stage 4. Arrhythmias (especially atrial fibrillation) also may cause beat-to-beat variations in cardiac output and thus increase interobserver variation in blood pressure measurements. Averaging several readings may help.

56 And how about the physician’s expertise?

Although interobserver agreement is usually high for blood pressure measurement, examiners may also be responsible for errors. In fact inter examiners differences of 10/8   mmHg are quite common. A common physician’s error is excessive pressure with the stethoscope (which can lower the diastolic reading). Another error is placing the patient’s arm either higher than the level of the heart (which lowers both systolic and diastolic readings) or lower (which increases them).

57 What is the most common “equipment” error?

The wrong cuff size (shorter cuffs overestimate blood pressure, whereas larger ones underestimate it). Also, aneroid instruments (used by 34% of practices) often go out of calibration, usually downward. In surveys, one third of office devices were off by >10   mm. Hence, the need for periodical recalibration.

58 How do you calibrate an aneroid sphygmomanometer?

gainst a mercury unit, and by using a Y connector to link the cuff to both devices.

59 What is the silent or auscultatory gap?

A finding present in one fifth of elderly patients with hypertension. It consists of a temporary disappearance of Korotkoff sounds after the systolic reading (and during phase II Korotkoff), with sudden reappearance of sounds just above diastolic values. This may underestimate the systolic pressure, unless one simultaneously palpates the radial pulse (which persists throughout the “gap”). The phenomenon was first described by Krylov in 1906, just a year after Korotkoff’s initial report. Its potential clinical relevance was then suggested by Cook and Taussig in 1917.

60 How common is the auscultatory gap? What are its causes?

n a recent study by Cavallini et al., classic gaps were present in 21% of 168 hypertensive patients, otherwise healthy and not on medications. Gaps were associated with female gender, increased arterial stiffness, prevalence of carotid atherosclerotic plaques—all independent variables—and also with older age—not an independent variable. These findings suggest that auscultatory gaps are related to the atherosclerosis and increased arterial stiffness of hypertensive patients. Hence, they may have prognostic relevance, making hypertensive patients with gaps more likely to develop cardiovascular disease, independent of age, blood pressure, and other risk factors.

61 How accurate is blood pressure measurement by sphygmomanometer?

Accurate, but with some limitations:

62 What is the palpatory systolic blood pressure?

The value that coincides with arterial reopening (i.e., the reappearance of peripheral pulse). It can be obtained by palpating either the brachial artery below the cuff or the radial artery at the wrist.

63 Can the palpatory method be used to determine diastolic pressure?

Yes, but with some expertise. The most-used technique consists in feeling the brachial pulse just below the deflating cuff. The point where a sudden decrease in volume (and peak) makes the pulse less bounding coincides with the diastolic blood pressure.

64 Are there differences in systolic pressure determined by palpation versus auscultation?

Yes, but not a lot. Palpatory values are about 7   mmHg lower than auscultatory values. Hence, physicians with hearing impairment may still rely on it to get accurate systolic and diastolic values.

65 How common is hypertension?

Very common. It affects nearly one fourth of the adult U.S. population, in whom it is also the most common outpatient diagnosis. The lifetime risk for hypertension is also quite high: 90% percent of those who, at age 55, do not yet have it will eventually develop it. Still, 30% of affected patients are unaware that they have it, which is sad, since effective blood pressure control is indeed achievable and can substantially reduce the risk of stroke, myocardial infarction, and heart failure.

66 How is hypertension defined?

With great difficulty. Overall, the risk of cardiovascular disease begins at 115/75   mmHg and doubles with each increment of 20   mmHg systolic blood pressure and 10   mmHg diastolic. This means that if a patient’s blood pressure were to increase from 115/75   mmHg to 135/85   mmHg, the risk of stroke and heart attack would double. Hence, even “mild” hypertension should receive serious consideration. And systolic hypertension should not be disregarded either. In fact, in patients older than 50, a systolic pressure >140   mmHg is a more important cardiovascular risk factor than its diastolic counterpart. Overall, general consensus defines hypertension as the blood pressure level above which the risk for stroke and heart disease increases significantly. This threshold is set by the World Health Organization (WHO) at a systolic blood pressure >139   mmHg and/or a diastolic blood pressure >89   mmHg in an adult patient who is not receiving antihypertensive medication and is not acutely ill. Recent evidence, however, shows that this threshold should be lowered to 130/80   mmHg for patients with diabetes, heart failure, or chronic kidney disease.

67 What are the key aspects of the latest guidelines?

The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (released in 2003) is an update of the 1997 guidelines (Table 2-4). It combines stages 2 and 3 hypertension, and it also contains a new category of prehypertension (120/80–139/89   mmHg). Prehypertensive patients are at increased risk of progressing to hypertension (those in the 130/80–139/89   mm Hg range have twice the risk of developing hypertension as those with lower values) and thus should initiate lifestyle modifications. These include weight reduction, a DASH diet (Dietary Approaches to Stop Hypertension), lowering of sodium intake, increased physical activity, moderate consumption of alcohol, and no tobacco.

68 What is pseudo hypertension?

/>An elevated indirect recording of blood pressure in patients with normal intra-arterial measurements. It is uncommon, seen in fewer than 2% of otherwise healthy elderly people.

69 What is the cause of pseudohypertension?

A stiffening of the arterial wall. This leaves the vessel patent (and thus able to produce Korotkoff sounds), even when the cuff pressure has exceeded the systolic blood pressure.

70 What is Osler’s maneuver?

A bedside test for the detection of pseudohypertension. It is carried out by first inflating the cuff until it obliterates the radial pulse, and then by feeling the radial artery. If the cuff is unavailable, the radial pulse can be obliterated by compressing the brachial artery with the other thumb. The maneuver is positive when the artery remains palpable as a firm “tube” (positive Osler’s sign).

71 What is the significance of a positive Osler’s sign?

Palpability of an artery in the absence of its pulse is a sign of arteriosclerosis. It suggests that both systolic and diastolic pressures might be overestimated (pseudohypertension).

72 How useful is Osler’s sign?

Probably not as much as traditionally taught. It has moderate to modest intraobserver and interobserver agreement, and occurs frequently in the elderly, hypertensive or not. Also, many Osler’s cases do not really have pseudohypertension, since both indirect and intra-arterial recordings actually show lower blood pressure.

73 What is malignant hypertension?

A form of hypertension associated with one or more of the following end-organ damages: rapid deterioration of renal function, retinal hemorrhages or optic nerve involvement, left ventricular failure, myocardial ischemia, or cerebrovascular accidents. This may occur independently of the level of hypertension. Hence, patients with very high pressure may not develop malignant hypertension, whereas those with pressures as low as 180/120   mmHg may present with it.

74 What is pseudohypotension?

A condition seen in shock, where the high peripheral vascular resistance tightens arteries to the point of impairing the generation of Korotkoff sounds. This prevents effective measurement of systolic and diastolic pressures, and may lead to gross underestimation. Both pseudohypertension and pseudohypotension can be counteracted by a direct intra-arterial recording.

75 What is the clinical significance of hypotension?

In acute settings, it always carries a bad prognosis. Data confirm this ominous significance in cases of acute myocardial infarction, pneumonia, and intensive care unit hospitalization in general.

76 What is a mean arterial pressure?

Not a wicked pressure, but instead the sum of systolic plus twice the diastolic pressure, divided by three. This is in recognition of the different durations of systole and diastole (with the latter being usually twice as long as systole), thus contributing unequally to average blood pressure values. Hence, in a patient with a blood pressure of 120/80   mmHg, the mean arterial pressure would be (120 + [2 × 80]) ÷ 3 = 280 ÷ 3 = 93.33.

77 What is a pulse pressure?

It is the difference between systolic and diastolic pressure. Thus, in a patient with a systolic value of 120   mmHg and a diastolic value of 80, the normal pulse pressure is 40.

78 What is a wide pulse pressure? What are its causes?

An abnormally large (“wide”) pulse pressure is one that is greater than 50% of the systolic blood pressure. Hence, in a patient with a systolic of 140   mmHg and a diastolic of 60, the pulse pressure is 80. The most common cause is a hyperkinetic heart syndrome, a high output state characterized by increased stroke volume and low peripheral vascular resistance. This is seen in various conditions, including:

Many of these are characterized by arteriovenous (A-V) fistula(s) that may be large and single (as in PDA), or small and multiple. The latter are seen in Paget’s disease (the fistulas are in the bone); exfoliative dermatitis (the fistulas are in the skin); cirrhosis (the fistulas are both hepatic and extrahepatic); and pregnancy (the entire placenta functions as a big A-V fistula). Shunt from fistulas is then responsible for the high output and hyperdynamic state.

79 What is the significance of a wide pulse pressure in aortic regurgitation (AR)?

If >80   mmHg, it reflects moderate to severe AR—a finding moderately sensitive but highly specific.

80 What is the significance of a wide pulse pressure in only one extremity?

It indicates the presence of an A-V fistula in that extremity. A Branham’s sign would confirm it.

81 What is Branham’s sign?

It is the typical bradycardia that occurs after compression (or excision) of a large A-V fistula. This is caused by inhibition of the Bainbridge reflex, which operates continuously in patients with large fistulas and is responsible for a compensatory increase in heart rate as a result of the higher right atrial pressure commonly induced by the large shunt. This right atrial stretching will then cause compensatory tachycardia through inhibition of vagal influence and activation of sympathetic acceleration. Note that the Bainbridge reflex is also responsible for the supraventricular tachyarrhythmias of patients with acute pulmonary embolism.

82 How does one test for the Branham’s sign?

By inflating a blood pressure cuff over the suspected limb: the heart rate will slow down, only to reaccelerate upon deflation of the cuff (and secondary reopening of the A-V fistula).

83 Who were Branham and Bainbridge?

Henry Branham was a 19th-century American surgeon. Francis Bainbridge (1874–1921) was an English physiologist and a small, quiet, and unimpressive lecturer with interest in exercise.

84 When is a pulse pressure considered “narrow”? What are its causes?

A pulse pressure is abnormally small (“narrow”) if <25% of the systolic value. Hence, a patient with a systolic of 100    mmHg and a diastolic of 90 has a narrow pulse pressure of 10. The most common cause is a drop in left ventricular stroke volume because of obstruction to left ventricular filling (tamponade, constrictive pericarditis) or emptying (aortic stenosis, even though this usually presents with normal pulse pressure). It may also occur in a tachycardia so severe to reduce ventricular filling time, and in shock (because of increased peripheral vascular resistance).

85 What is pulsus paradoxus?

It is an exaggeration of the normal respiratory variation in systolic blood pressure (the diastolic changes little) characterized by a decrease with inspiration and an increase with exhalation. Although these swings are physiologic, in some disease states they may become large enough to be detectable at the bedside, even on simple palpation of a peripheral artery. In this case, the pulse will grow stronger on expiration and weaker on inspiration. It may even disappear.

86 How wide does this swing in systolic pressure have to get to become palpable?

At least 20   mmHg. Of course, an easier and more sensitive way of detection is by blood pressure measurement. In this regard, an abnormal pulsus paradoxus is defined as an inspiratory drop in systolic pressure >12 ± 2    mmHg (some authors even quote lower values, such as 6 ± 3).

87 Why is it called paradoxical?

Because changes in pulse volume are independent of changes in pulse rate. This paradox goes back to the original patients described by Kussmaul in 1873, who had such an inspiratory decrease in systolic pressure to completely lose their peripheral pulse, even though they still maintained consciousness and an apical beat. This was a paradox to Kussmaul; hence, his choice of the Latin term pulsus respiratione intermittens (i.e., “intermittent pulse as a result of respiration”). Pulsus paradoxus had actually already been described in 1669 by the Cornish physician Richard Lower, who reported a case of constrictive pericarditis in his treatise on the heart. Subsequently, the British physician Floyer (the same who recommended measuring the arterial pulse with a portable clock) made a similar observation in asthma, and so did William in 1850. Since none of these (Kussmaul included) had a sphygmomanometer (it had not been invented yet), they had to exclusively rely on the peripheral pulse; hence, Kussmaul’s choice of the term “pulsus.” This, however, has become outdated, not only because it describes an exaggerated physiologic (and not paradoxical) phenomenon, but also because nowadays these respiratory changes are not detected by arterial pulse, but by blood pressure.

88 Describe the pathophysiology of pulsus paradoxus

It is an exaggeration of the inspiratory drop in systolic pressure, and thus in the fullness of the pulse.

All these respiratory variations are physiologic, but in certain pathologic states they become large enough to cause more profound (and detectable) changes in blood pressure and pulse volume.

89 How does one measure pulsus paradoxus?

90 Can pulsus paradoxus be identified on arterial tracing?

Yes, since it causes visible inspiratory and expiratory swings in systolic pressure.

91 Which arteries are best suited for detecting pulsus paradoxus: peripheral or central?

Peripheral (i.e., better at the wrist than at the arm or at the neck) because peripheral arteries magnify elastic swings. Hence, they are very good for detecting pulsus paradoxus and pulsus alternans, but very bad for the parvus and tardus of aortic stenosis.

92 What are the values to remember for pulsus paradoxus?

Age of puberty, age of drinking, and age of driving. In other words, the normal respiratory swing in systolic pressure is usually in the range of a magic number frequently encountered in clinical medicine: age of puberty (but also anion gap, osmolar gap, alveolar–arterial oxygen gradient, Hill’s sign, and pulsus paradoxus)—all 12 ± 2. To stretch this analogy a bit further, we might even say that a pulsus paradoxus can be normal all the way up to 16 (i.e., the age of driving). For values between 16 and 21 (age of drinking), a “pulsus paradoxus” has been reported (albeit not consistently) in:

Values in this range also occur in tamponade, and 30–45% of patients with constrictive pericarditis, but this must have an exudative component and not be completely “dry.” Conversely, values above 21 are due to only two conditions: tamponade and status asthmaticus.

93 What is cardiac tamponade?

It is a medical emergency characterized by a pericardial collection large enough to render intrapericardial pressure greater than intracardiac diastolic pressure. This not only prevents adequate filling of the heart (and thus ventricular ejection), but also creates a situation wherein the cardiac chambers start competing for the limited intrapericardial space. This leads to major respiratory swings in ventricular septa, ventricular filling, and systolic blood pressures.

94 What are the characteristics of pulsus paradoxus in tamponade?

Almost 100% of patients will have a “pulsus” >12   mmHg. This percentage is lower (70%) in more chronic cases, but close to 100% for rapid fluid accumulation. A cut-off of 21   mmHg (age of drinking) will decrease sensitivity (only 78% of tamponade cases have it) but improve specificity.

95 In addition to pulsus paradoxus, what are the other clinical features of tamponade?

They consist of a tetrad, present in close to 100% of patients:

96 What is Beck’s triad?

It is a triad described by the American surgeon Claude Beck (who also pioneered open cardiac massage in patients “too good to die”) and considered, until recently, typical of tamponade:

These findings are still seen in tamponade, but only in very advanced cases. Conversely, the tetrad just outlined (coupled with the presence of a pulsus) is probably a much better tool for early diagnosis.

97 Can pulsus paradoxus be falsely negative in tamponade?

Yes. It may be absent in 2% of cases, usually because of compensatory mechanisms that prevent major septal shifts in inspiration. The most common are:

98 What other conditions can cause pulsus paradoxus >10   mmHg?

See Table 2-5.

Table 2-5 Conditions responsible for pulsus paradoxus >10   mmHg

* Seen in 30–45% of patients, but the condition must have an exudative component and not be completely “dry.”

Modified from Khasnis A, Lokhandwala Y: Clinical signs in medicine: pulsus paradoxus. J Postgrad Med 48:46–49, 2002.

99 What about pulsus paradoxus in airflow obstruction?

Obstructive lung disease (especially status asthmaticus) can indeed cause pulsus paradoxus. The mechanism is probably lung hyperinflation, causing excessive inspiratory pooling of blood, and thus a greater drop in systolic blood pressure. Since this form of pulsus paradoxus depends on respiratory rate and effort, it is not a very sensitive indicator of severe bronchospasm (in fact, only half of status asthmaticus patients have a pulsus >10). It is, however, quite specific, with values >20 usually indicating FEV₁ <0.5–0.7 L. Hence, it can serve as a “poor man’s” spirometer (or peak flow meter) for situations in which these devices are not readily available.

100 How does pulsus paradoxus behave in intubated and mechanically ventilated patients?

It may present as respiratory variations in the baseline tracing of pulse oximetry (with the height of oscillation correlating with the severity of pulsus and the degree of auto-PEEP [positive end-expiratory pressure]). Hence, pulse oximetry assessment of pulsus paradoxus can provide a useful noninvasive monitor of air trapping severity. Still, beware that positive pressure ventilation can reverse the respiratory changes in intrathoracic pressure, so that the lowest systolic blood pressure will be recorded during expiration (reversed pulsus paradoxus—see question 101), rather than inspiration. Although the correlation between pulsus paradoxus and pulse oximetry recordings might not be influenced by the state of respiration (spontaneous or mechanical ventilation), reversed pulsus paradoxus is not a good indicator of disease severity in patients receiving mechanical ventilation because the magnitude of the pulsus depends (at least in part) on the applied ventilatory pressures.

101 What is “reversed” pulsus paradoxus?

A drop in systolic pressure that coincides with expiration rather than inspiration. This is typical of HOCM (hypertrophic obstructive cardiomyopathy), where the ventricle is too stiff to adequately fill. It also can be seen in patients with left ventricular failure who are on positive pressure ventilation (PPV). In this case, PPV displaces the wall of the ventricle inward during systole, thus assisting ventricular emptying and causing a slight rise in systolic pressure during mechanical inspiration. Note that a reversed pulsus paradoxus in ventilated patients is a sensitive indicator of hypovolemia. Finally, a reversed pulsus paradoxus can also be seen in patients with isorhythmic dissociation. The atrial activity precedes the ventricular activity during inspiration, and follows it during expiration. The atrial contribution during inspiration increases stroke volume, while the lack of it during exhalation decreases it.

102 What is pseudo-pulsus paradoxus?

It is a term used by Salel et al. to describe a patient with isorhythmic dissociation from complete heart block who was misdiagnosed as having pulsus paradoxus. This was in reality due to increased sinus rate from inspiration, which temporarily positioned the P waves in front of the QRS, thus synchronizing (and maximizing) atrioventricular contraction. The misdiagnosis can be avoided by strictly adhering to the guidelines for pulsus paradoxus laid down by Gauchat and Katz:

103 What is the usefulness of Kussmaul’s sign in pulsus paradoxus?

Kussmaul’s sign is a paradoxical increase in venous distention (and pressure) during inspiration (see Chapter 10, The Cardiovascular Exam). This should not be confused with the exaggeration of the normal expiratory increase in venous pressure that is often seen in patients with pulmonary disease. Instead, Kussmaul’s sign reflects some sort of obstruction to right-sided venous return, like superior vena cava syndrome, tricuspid stenosis, right ventricular hypertrophy or infarction, constrictive pericarditis, pulmonary emboli, and severe pulmonary hypertension. Of interest, patients with tamponade do not demonstrate Kussmaul’s sign; yet, they do demonstrate pulsus paradoxus. Conversely, “pulsus” (albeit one that is never >21   mmHg) may occur in some patients with Kussmaul’s.

104 What is Trousseau’s sign?

There are actually two Trousseau’s signs:

105 What are the causes of an “obstetrician’s hand”?

Those predisposing to tetany: alkalemia, hypocalcemia, hypomagnesemia, or hypophosphatemia.

106 How can one trigger carpal spasm in patients with “latent” tetany?

107 Who was Trousseau?

Armand Trousseau (1801–1867) was one of the great leaders of 19th-century Parisian medicine. Among his “firsts” were the performance of tracheostomy (in France), the use of thoracentesis, and the creation of the term “aphasia.” Trousseau was a superb clinician, a much beloved teacher, and a lecturer who could present cases with the elegance of a novelist. He popularized eponyms such as Addison’s, Graves’, and Hodgkin’s disease and was a passionate advocate of bedside teaching through clinical demonstration. Totally adored by students and colleagues alike, he trained, among others, Potain, Lasegue, Brown-Sequard, and Da Costa. Trousseau was also active in politics, especially after the revolution of 1848, holding important positions, including a membership in the legislative body. His advice to students still stands 150 years after his death: “Observe the practice of many physicians; do not implicitly believe the mere assertion of your master; be something better. Do not fear to confess your ignorance. In truth, it seems that the words ‘I do not know’ stick in every physician’s throat. Take care not to fancy yourself as a physician as soon as you have mastered scientific facts; they only afford to your understanding an opportunity of bringing forth fruit, thus elevating you to the high position of a man of art.”

108 Who was Chvostek?

Frantisek Chvostek (1835–1884) was a Moravian-born Austrian surgeon who described the homonymous sign in 1876. His field of interest, however, was the pathology and treatment of neurologic disease, where he even experimented with electrotherapy.

109 What is the Rumpel-Leede sign?

It is an old test of capillary fragility, carried out by raising the venous pressure in the forearm through either inflation of a blood pressure cuff or the closing of a tourniquet. The test is positive when it causes petechial eruptions (presumably because of fragile capillaries bursting open). It is named after the two physicians who first described it at the turn of the century: the German Theodore Rumpel and the American Carl Leede. Yet, it is often referred to as the Hess test, from Alfred Hess (1875–1933), the American who first noticed it while treating scorbutic children.

110 What is Hill’s sign?

A sign of severe aortic regurgitation, first described in 1909 by the British physician Leonard Hill. It is characterized by an exaggerated difference in systolic pressure between upper and lower extremities. Note that there is already a physiologic difference of around 12 ± 2    mmHg (with legs having higher systolic pressure than arms). Conversely, a difference of >20 and <40 is considered pathologic, but with low specificity and sensitivity for AR. A difference of >60   mmHg has high specificity (and a very high positive likelihood ratio) for severe AR, but a sensitivity of only 40%.

111 Is Hill’s sign real?

No. The “normal” difference in systolic pressure between foot and arm is only present on indirect recording. By direct intra-arterial measurement there is no discrepancy.

112 What is the mechanism of Hill’s sign?

It’s not entirely clear. According to one theory, a high stroke volume generates a summation between the regular pulse wave of the aortic pressure and a rebound wave from the periphery. Because of the rebound wave’s characteristics, the summation only occurs in the legs.

113 So what about Hill’s sign in AR?

It also is not real. There are no intra-arterial differences in systolic pressure between upper and lower extremities. Hence, the differences at the cuff are just a sphygmomanometric artifact, most likely due to enhanced transmission of pressure wave. Still, it can predict AR severity.

114 Is Hill’s sign specific for AR?

No. It also can be encountered in other hyperdynamic states (previously discussed).

115 How do you perform Hill’s test?

By measuring in the supine patient the systolic pressure at the foot, and then subtracting the one recorded at the arm. The pressure at the foot is obtained by wrapping the cuff around the calf and then palpating either the dorsalis pedis or the tibialis posterior (whichever value is higher).

116 What causes the systolic pressure to be less in the lower than in the upper extremities?

It depends on the age of the subject. In elderly individuals, the most common cause is aortic obstruction (atherosclerotic), or dissection. In younger patients, the predominant reason is instead aortic coarctation. In this case, the lower extremities also have reduced and delayed pulses, and a systolic blood pressure at least 6   mmHg lower than that in the upper extremities.

117 What is the standard bedside test for assessing chronic lower extremity ischemia?

The ankle–brachial pressure index (ABPI), also known as the ankle-to-arm systolic pressure index (AAI).

118 How is the ABPI measured?

According to the guidelines of the Standards Division of the Society of Interventional Radiology:

1. With the patient supine, measure brachial and ankle systolic pressure by handheld Doppler.

2. To obtain an ABPI, divide the highest systolic pressure of the dorsalis pedis (or tibialis posterior) for each foot by the highest systolic pressure at the arm. For example:

To obtain the left ABPI, first measure the systolic brachial pressure in both left and right arms. Select the higher value as your brachial artery pressure measurement. There should be a difference of less than 10    mmHg between each brachial pressure measurement.

Next, measure the left dorsalis pedis (or tibialis posterior) arterial systolic pressures. Select the higher of these two values as the ankle pressure measurement.

Then, divide the selected ankle pressure measurement by the previously selected brachial artery systolic pressure measurement.

Normal values range between 0.97 and 1.1; values <0.97 identify patients with angiographically proven occlusions or stenoses, with 96% sensitivity and 94–100% specificity. Most patients with claudication will have an ABPI between 0.5 and 0.8, whereas those with pain at rest will have values <0.5. Indexes <0.2 are associated with ischemic or gangrenous extremities.

119 Can the ABPI be misleading?

Yes, because it only measures pressure at the ankle and therefore does not account for possible distal occlusions, such as microemboli or small atherosclerotic plaques. Moreover, the ABPI may be falsely elevated in Mönckeberg’s sclerosis, the medial wall calcification of many diabetic patients. In this condition, the ABPI reflects more the ability of the heavily calcified vessel to resist compression than the true blood flow (and pressure) within it. In these patients, toe pressure determinations may more accurately reflect lower extremity perfusion.

120 Who was Hill?

Sir Leonard Hill (1866–1952) was an English physiologist who modified the original Riva-Rocci mercury sphygmomanometer by using a pressure gauge. In 1923, he won the Nobel Prize in physiology for his studies of heat production and muscle metabolism.

121 What is the Valsalva’s maneuver? How does it modify blood pressure?

Valsalva is a great little test for assessing the reflex autonomic control of the cardiovascular system, both sympathetic and vagal. It does so by modifying blood pressure, heart rate, and venous return—all as a result of respiratory swings in intrathoracic pressures. It can be difficult to perform, though, and thus should always be well explained to the patient, especially the need to keep on straining until told to stop, and to breathe as quietly as possible after stopping straining. Valsalva consists of two major periods, comprising a total of four phases (Fig. 2-1):

Period 1: a held (or strain) period. This is carried out by asking the patient to fully inspire and then forcefully exhale against closed glottis for at least 10 seconds. It can be easily accomplished by having the patient “bear down as if having a bowel movement,” or alternatively, by placing a fist onto the midabdomen of a supine patient and then having him or her strain against it (it could even be accomplished more formally by having the patient blow for 10 seconds against an aneroid manometer at a constant pressure of 40    mmHg). Whatever the technique, the resulting strain causes an increase in intrathoracic pressure, a drop in venous return, a reduction in left ventricular diameter, and a fall in cardiac output. These can be quite dramatic (in fact, when first experimenting with Valsalva’s, Weber, in typical Teutonic fashion, managed to give himself a syncope and a seizure; then he recovered and wrote the paper). This “strain” comprises two phases:

Phase I: After onset of straining, systolic pressure increases (due to aortic compression), and heart rate decreases (due to reflex bradycardia from baroreceptor activation).

Phase II: Characterized instead by a drop in venous return because of straining-induced compression of the vena cava. This eventually leads to a fall in cardiac output, a secondary fall in aortic pressure (which therefore slowly returns to the baseline level), and a secondary increase in heart rate (still mediated by the baroreceptor reflex). During the rest of the straining period, the arterial mean and pulse pressures continue to slowly fall, and the heart rate continues to slowly increase.

Period 2: a release period. This is carried out by asking the patient to stop bearing down, or alternatively, by releasing the fist pressure on the abdomen. It also comprises two phases:

Phase III: As soon as straining is released (and the subject starts breathing again), there is a small but transient drop in systolic pressure due to sudden loss of aortic compression. This, in turn, causes a further reflex acceleration of the heart rate.

Phase IV: When the vena cava compression completely resolves, venous return suddenly increases. This causes a rapid rise in cardiac output, which, in turn, makes the systolic pressure overshoot above baseline values (due to increased systemic resistance from phase II sympathetic activation) and heart rate to drop (because of baroreceptor reflex).

Figure 2-1 Blood pressure response to Valsalva’s maneuver in normal individuals (A) and patients with congestive heart failure (B and C).

This normal hemodynamic response to Valsalva can be quite altered in congestive heart failure.

122 How good is Valsalva for detecting congestive heart failure?

Very good. Valsalva has excellent specificity and sensitivity (90–99% and 70–95%, respectively) for detecting left ventricular dysfunction, either systolic or diastolic. It also has significant likelihood ratios (both negative and positive—the latter being 7.6). To perform the test, inflate the blood pressure cuff 15   mmHg above the patient’s resting systolic pressure, and then maintain this value throughout the 10 seconds of strain and the 30 seconds of release. While doing so, auscultate over the brachial artery, looking for Korotkoff’s sounds. When the patient starts straining, a normal response consists of an initial increase in systolic pressure with clear-cut sounds (phase I); this is then followed by a drop in systolic pressure with disappearance of sounds (phase II) and then, after release of straining, by an overshooting in pressure with reappearance of sounds (phase IV). Note that Korotkoff’s sounds should always be heard during phase I. If not, the patient has failed to adequately increase intrathoracic pressure. Patients with heart failure have instead a quite different response: they either maintain sounds throughout the entire 40 seconds of the maneuver (as a result of an increase in systolic pressure that matches the increase in intrathoracic pressure—square wave response), or they fail to gain them back after strain release (because of the failing ventricle’s inability to produce a systolic pressure overshoot after the hypotension induced by straining—absent overshoot). In fact, the degree of overshoot is directly related to left ventricular ejection fraction, and thus provides a marker for systolic dysfunction. Note, however, that an abnormal Valsalva response may also reflect high filling pressures (and thus provide a marker for diastolic dysfunction).

123 In addition to an abnormal Valsalva response, are there other findings that might diagnose congestive heart failure (CHF)?

Yes, and they involve most of the five “fingers” of the cardiovascular exam (see Chapter 20, Cardiovascular Examination). On the venous side, for example, the presence of either end-inspiratory crackles or distended neck veins has high specificity (90–100%) but low sensitivity (10–50%) for increased left-sided filling pressure due to either systolic or diastolic dysfunction. Of these two signs, only an elevated jugular venous pressure has a significant positive likelihood ratio (3.9). Positive abdominojugular reflux has equally high specificity, but better sensitivity (55–85%), and an even stronger likelihood ratio (8.0). S₃ gallop, downward and lateral displacement of the apical impulse, and peripheral edema also have high specificity (>95%) but low sensitivity (1–40%) for elevated diastolic filling pressures; of them, only the S₃ and the displaced apical impulse have a positive likelihood ratio (5.7 and 5.8, respectively). Given their negative likelihood ratios, only an absent abdominojugular reflux and an abnormal Valsalva response argue against the presence of high filling pressures. Finally, S₄ has high sensitivity (71%), but low specificity (50%), and nonsignificant likelihood ratios.

124 And what about patients with “systolic” dysfunction?

They not only have high diastolic filling pressure (the hallmark of heart failure, whether systolic or diastolic), but also low ejection fraction (<50%). Hence, they present with both dyspnea and fatigue. Of all bedside signs, only an abnormal Valsalva response has high sensitivity and specificity for their identification (>70% and >90%, respectively, with a positive likelihood ratio of 7.6). S₃ and displaced apical impulse have positive likelihood ratios (3.8 and 5.7, respectively) but specificities that are much higher than sensitivity (>90% and 10–50%, respectively). Hence, absence of these findings does not exclude an ejection fraction <50% (although absence of S₃ does exclude an ejection fraction <30%). All other signs (crackles, distended neck veins, peripheral edema, hepatomegaly, mitral regurgitation) have high specificity (>90%) but sensitivity too low for significant likelihood ratios. The PPP (proportional pulse pressure) is another finding with excellent sensitivity (91%) and specificity (83%) for identifying low cardiac index (CI). It is calculated by dividing the arterial pulse pressure by the systolic blood pressure. In dilated cardiomyopathy, a PPP <0.25 has a positive likelihood ratio of 5.4 for CI of 2.2 L/min/m².

125 Can physical exam predict outcome in patients with CHF?

Yes. CHF findings are valuable and independent predictors of worse clinical outcome. For example, ischemic heart disease patients with S₃ have a 1-year mortality that is much higher than those without it (57% versus 14%). The same applies to a displaced apical impulse (1-year mortality of 39% if present and 12% if absent).

126 Who was Valsalva?

Antonio Valsalva (1666–1723) was a professor of anatomy in Bologna, a student of Malpighi, and himself the teacher of Morgagni. He developed his maneuver as a bedside tool for cleaning and inflating the eustachian tube, and reported it in 1704 in a book on the ear. Weber rediscovered it 150 years later, mostly for its effects on cardiac physiology, and the rest is history.

127 What are the diagnostic and therapeutic uses of Valsalva?

Two major diagnostic applications:

Valsalva also has four therapeutic applications:

As for its use in angina, keep in mind that this has to be done with great care, since Valsalva profoundly affects venous return and cardiac output (remember the syncope and seizure of Weber while experimenting with it) and thus may have untoward effects not only in patients with severe coronary artery disease or recent myocardial infarction, but also in patients with moderate to severe hypovolemia and recent surgery/hemorrhage of the eye or central nervous system.

Respiratory Rate and Rhythm