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14—CUSHING SYNDROME
CUSHING SYNDROME
Central obesity
Absence
Absence of plethora
5.6
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EBM BOX 14.1 Cushing Syndrome*
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Finding (Reference)
Vital signs
Hypertension
Body habitus
Moon faciesf
Dorsal cervical fat pad
Central obesity
Generalized obesity
BMI >30 kg/m
Skin findings
Thin skinfold
5
Plethora
Hirsutism, in women
Ecchymoses
Red or blue striae
5,30
Acne
Extremity findings
Muscle weakness
5,6
Edema
*Diagnostic standard: for Cushing syndrome, elevated daily cortisol or corticosteroid metabolites, or both,
with loss of circadian rhythm and with abnormal dexamethasone suppression.
†
Definition of findings: for hypertension, diastolic blood pressure >105 mm Hg; for central obesity, central
obesity index exceeds 1 or subjective appearance of central obesity sparing the extremities;
skinfold, skinfold thickness on back of hand <1.8 mm (women of reproductive age only).
‡
Likelihood ratio (LR) if finding present = positive LR; LR if finding absent = negative LR.
NS, Not significant.
†
5,6
6
45
5–7
5
2 30,45
15
5,6,30,45
5,6,30
5,6,30,45
5,6,30,45
Sensitivity
(%)
25–38 83–94 2.3 0.8
98 41 1.6 0.1
50 78 2.3 0.6
72–90 62–97 3.0 0.2
4 38 0.1 2.5
31–85 4–26 NS 3.1
78 99 115.6 0.2
83 69 2.7 0.3
31–76 48–79 1.4 NS
38–71 69–94 4.5 0.6
15–52 61–93 1.7 NS
25–52 61–76 NS NS
28–63 69–98 3.8 NS
38–57 56–83 1.8 0.7
Specificity
(%)
Likelihood Ratio‡ if Finding Is
Present Absent
5,6,7
for thin
15
LRs
0.1 0.2 0.5 12510
of moon facies
Generalized obesity
Absence of thin skinfold
In these same studies, one of the more powerful predictors of Cushing syndrome is osteoporosis
(sensitivity of 32% to 63%, specificity of 90% to 97%, positive LR = 8.6, and negative LR = 0.5).
Osteoporosis was identified radiographically in these studies, but it is often apparent at the bedside
from vertebral fractures, kyphosis, and loss of height. Presumably, these bedside findings also accurately identify Cushing syndrome.
Probability
Decrease Increase
Muscle weakness
+45%+30%+15%–15%–30%–45%
Thin skinfold
Ecchymoses
LRs
11
5,6,30
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3—GENERAL APPEARANCE OF THE PATIENT
B. ETIOLOGY OF CUSHING SYNDROME AND BEDSIDE FINDINGS
Patients who take exogenous corticosteroids have the same frequency of central obesity, moon
facies, and bruising as patients with endogenous Cushing, but a significantly lower incidence of
hypertension, hirsutism, acne, striae, and buffalo humps.
Patients with the ectopic ACTH syndrome from small cell carcinoma are more often male,
have Cushing syndrome of rapid onset (over months instead of years), and present with prominent
weight loss, myopathy, hyperpigmentation, and edema.
static disease may suggest this diagnosis.32 In studies of patients with ACTH-dependent Cushing
syndrome, two findings significantly increase the probability of ectopic ACTH syndrome: weight
loss (positive LR = 20) and symptom duration less than 18 months (positive LR = 15). Male sex
increases the probability of ectopic ACTH syndrome a smaller amount (LR = 2.9).
Hirsutism and acne may occur in any woman with endogenous Cushing syndrome, but the
presence of virilization (i.e., male pattern baldness, deep voice, male musculature, clitoromegaly)
argues strongly for adrenocortical carcinoma.
37–39
References may be accessed online at Elsevier eBooks for Practicing Clinicians.
31
25,32,33
e irregular hepatomegaly of meta-
32,34–36
References
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1. Newell-Price J, Bertagna X, Grossman AB, Nieman LK. Cushing’s syndrome. Lancet. 2006;367(9522):
1605–1617.
2. Lacroix A, Feelders RA, Stratakis CA, Nieman LK. Cushing’s syndrome. Lancet. 2015;386(9996):913–927.
3. Cushing H. e basophil adenomas of the pituitary body and their clinical manifestations (pituitary
basophilism) 1932. Obes Res. 1932;2(5):486–508.
4. Freyberg RH, Traeger CH, Patterson M, Squires W, Adams CH, Stevenson C. Problems of prolonged
cortisone treatment for rheumatoid arthritis: further investigation. JAMA. 1951;147(16):1538–1543.
5. Nugent CA, Warner HR, Dunn JT, Tyler FH. Probability theory in the diagnosis of Cushing’s syndrome.
J Clin Endocrinol Metab. 1964;24:621–627.
6. Streeten DHP, Stevenson CT, Dalakos TG, Nicholas JJ, Dennick LG, Fellerman H. e diagnosis of
hypercortisolism. Biochemical criteria differentiating patients from lean and obese normal subjects and
from females on oral contraceptives. J Clin Endocrinol. 1969;29(9):1191–1211.
7. Hiramatsu R, Yoshida K, Sato T. A body measurement to evaluate the pattern of fat distribution in central
obesity. A screening and monitoring technique for Cushing’s syndrome. JAMA. 1983;250(23):3174–3178.
8. Yanovski JA, Cutler Jr. GB. Glucocorticoid action and the clinical features of Cushing’s syndrome.
Endocrinol Metab Clin North Am. 1994;23(3):487–509.
9. Gottlieb NL. Temporal fat pad sign during corticosteroid treatment. Arch Intern Med. 1980;140(11):
1507–1508.
10. Lucena GE, Bennett WM, Pierre RV. “Dewlap”: a corticosteroid-induced episternal fatty tumor. N Engl
J Med. 1966;275(15):834–835.
11. Printen KJ, Blommers TJ. Morbid obesity in Cushing’s syndrome: a nonentity? Am J Surg. 1977;134(5):
579–580.
12. Mayo-Smith W, Hayes CW, Biller BM, Klibanski A, Rosenthal H, Rosenthal DI. Body fat distribution
measured with CT: correlations in healthy subjects, patients with anorexia nervosa, and patients with
Cushing syndrome. Radiology. 1989;170(2):515–518.
13. Isidori AM, Graziadio C, Paragliola RM, etal. e hypertension of Cushing’s syndrome: controversies in
the pathophysiology and focus on cardiovascular complications. J Hypertens. 2015;33(1):44–60.
14. Pivonello R, Isidori AM, De Martino MC, Newell-Price J, Biller BM, Colao A. Complications of Cushing’s
syndrome: state of the art. Lancet Diabetes Endocrinol. 2016;4(7):611–629.
15. Corenblum B, Kwan T, Gee S, Wong NCW. Bedside assessment of skin-fold thickness. A useful mea-
surement for distinguishing Cushing’s disease from other causes of hirsutism and oligomenorrhea. Arch
Intern Med. 1994;154(7):777–781.
16. Wright AD, Joplin GF. Skin-fold thickness in normal subjects and in patients with acromegaly and
Cushing’s syndrome. Acta Endocrinol (Copenh). 1969;60(4):705–711.
17. Stratakis CA, Mastorakos G, Mitsiades NS, Mitsiades CS, Chrousos GP. Skin manifestations of Cushing
disease in children and adolescents before and after the resolution of hypercortisolemia. Pediatr Dermatol.
1998;15(4):253–258.
18. Stratakis CA. Skin manifestations of Cushing’s syndrome. Rev Endocr Metab Disord. 2016;17(3):283–286.
19. Arem AJ, Kischer CW. Analysis of striae. Plast Reconstruct Surg. 1980;65(1):22–29.
20. Urbanic RC, George JM. Cushing’s disease–18 years’ experience. Med (Baltim). 1981;60(1):14–24.
21. Starkman MN, Schteingart DE. Neuropsychiatric manifestations of patients with Cushing’s syndrome.
Relationship to cortisol and adrenocorticotropic hormone levels. Arch Intern Med. 1981;141(2):215–219.
22. Jeffcoate WJ, Silverstone JT, Edwards CR, Besser GM. Psychiatric manifestations of Cushing’s syn-
drome: response to lowering of plasma cortisol. Q J Med. 1979;48(191):465–472.
23. Kirkman S, Nelson DH. Alcohol-induced pseudo-Cushing’s disease: a study of prevalence with review of
the literature. Metabolism. 1988;37(4):390–394.
24. Veldman RG, Meinders AE. On the mechanism of alcohol-induced pseudo-Cushing’s syndrome. Endocr
Rev. 1996;17(3):262–268.
25. Trainer PJ, Grossman A. e diagnosis and differential diagnosis of Cushing’s syndrome. Clin Endocrinol
(Oxf ). 1991;34(4):317–330.
26. Lo JC, Mulligan K, Tai VW, Algren H, Schambelan M. “Buffalo hump” in men with HIV-1 infection.
Lancet. 1998;351(9106):867–870.
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27. Miller KK, Daly PA, Sentochnik D, et al. Pseudo-Cushing’s syndrome in human immunodeficiency
https://t.me/medicina_free
virus-infected patients. Clin Infect Dis. 1998;27(1):68–72.
28. Aboulafia DM, Bundow D. Images in clinical medicine. Buffalo hump in a patient with the acquired
immunodeficiency syndrome. N Engl J Med. 1998;339(18):1297.
29. Tierney EP, Hanke CW. “Bullfrog neck,” a unique morphologic trait in HIV lipodystrophy: case series
and review of the literature. Arch Dermatol. 2010;146(11):1279–1282.
30. Pecori Giraldi F, Pivonello R, Ambrogio AG, etal. e dexamethasone-suppressed corticotropin-releas-
ing hormone stimulation test and the desmopressin test to distinguish Cushing’s syndrome from pseudoCushing’s states. Clin Endocrinol. 2007;66(2):251–257.
31. Liou TC, Lam HC, Ho LT. Cushing’s syndrome: analysis of 188 cases. Taiwan Yi Xue Hui Za Zhi.
1989;88(9):886–893.
32. Blunt SB, Sandler LM, Burrin JM, Joplin GF. An evaluation of the distinction of ectopic and pituitary
ACTH dependent Cushing’s syndrome by clinical features, biochemical tests and radiological findings.
Q J Med. 1990;77(283):1113–1133.
33. Newell-Price J, Trainer P, Besser M, Grossman A. e diagnosis and differential diagnosis of Cushing’s
syndrome and pseudo-Cushing’s states. Endocr Rev. 1998;19(5):647–672.
34. Su DH, Chang YC, Chang TC, Chang CC, Tsai KS, Huang TS. Characteristics of Cushing’s syndrome
in Taiwanese. J Formos Med Assoc. 2003;102(5):292–298.
35. Valassi E, Santos A, Yaneva M, etal. e European Registry on Cushing’s syndrome: 2-year experience.
Baseline demographic and clinical characteristics. Eur J Endocrinol. 2011;165(3):383–392.
36. Yaneva M, Kalinov K, Zacharieva S. Mortality in Cushing’s syndrome: data from 386 patients from a
single tertiary referral center. Eur J Endocrinol. 2013;169(5):621–627.
37. Bertagna C, Orth DN. Clinical and laboratory findings and results of therapy in 58 patients with adre-
nocortical tumors admitted to a single medical center (1951-1978). Am J Med. 1981;71(5):855–875.
38. Hutter AM, Kayhoe DE. Adrenal cortical carcinoma: clinical features of 138 patients. Am J Med.
1966;41(4):572–580.
39. Luton JP, Cerdas S, Billaud L, etal. Clinical features of adrenocortical carcinoma, prognostic factors, and
the effect of mitotane therapy. N Engl J Med. 1990;322(17):1195–1201.
40. Ross EJ, Linch DC. Cushing’s syndrome—killing disease: discriminatory value of signs and symptoms
aiding early diagnosis. Lancet. 1982;2(8299):646–649.
41. Soffer LJ, Iannoccone A, Gabrilove JL. Cushing’s syndrome: a study of fifty patients. Am J Med. 1961;
30(1):129–146.
42. Erem C, Algün E, Ozbey N, etal. Clinical laboratory findings and results of therapy in 55 patients with
Cushing’s syndrome. J Endocrinol Invest. 2003;26(1):65–72.
43. Boscaro M, Arnaldi G. Approach to the patient with possible Cushing’s syndrome. J Clin Endocrinol
Metab. 2009;94(9):3121–3131.
44. Pecori Giraldi F, Moro M, Cavagnini F. Study the group on the hypothalamo-pituitary-adrenal axis of
Italian Society of Endocrinology. Gender-related differences in the presentation and course of Cushing’s
disease. J Clin Endocrinol Metab. 2003;88(4):1554–1558.
45. León-Justel A, Madrazo-Atutxa A, Alvarez-Rios AI, etal. A probabilistic model for Cushing’s syn-
drome screening in at-risk populations: a prospective multicenter study. J Clin Endocrinol Metab.
2016;101(10):3747–3754.
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CHAPTER
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15
Pulse Rate and Contour
KEY TEACHING POINTS
• Tachycardia (increased heart rate) portends a worse prognosis in many different
conditions, including sepsis, pneumonia, myocardial infarction, acute gastrointestinal
hemorrhage, gallstone pancreatitis, and stroke.
• The two most common abnormalities of pulse contour are pulsus alternans and pulsus
paradoxus. Both are detectable by palpation or by using the blood pressure cuff.
• Pulsus alternans (regular rhythm with alternating strong and weak pulse) indicates severe
left ventricular dysfunction.
• Pulsus paradoxus (inspiratory decline in systolic blood prsessure of more than 10
to 12 mm Hg) appears in cardiac tamponade and severe asthma. In patients with
significant pericardial effusions, the finding of pulsus paradoxus increases probability that
pericardiocentesis will improve cardiac output; its absence decreases probability that
pericardiocentesis will be beneficial.
• In patients with hypovolemic shock, the femoral pulse is the best indicator of cardiac
perfusion.
PULSE RATE
I.
Introduction
Taking the patient’s pulse is one of the oldest physical examination techniques, practiced as long ago
as 3500 BC by ancient Egyptian physicians, who believed a weakening pulse indicated advancing dis-
1
ease.
e pulse was one of Galen’s (ca. 129–200 AD) favorite subjects, occupying several treatises that
directed clinicians to observe the pulse’s speed, force, and duration.
heart rate in disease were by John Foyer (1649–1734), who published his clinical observations in 1707
based on his invention, the pulse-watch.
dia were Adams and Stokes, who, between 1827 and 1846, pointed out that not all seizures and fainting represented disease of the brain but instead could occur because of the slow pulse of heart block.
II. Technique
Most clinicians determine the pulse rate by palpating the radial pulse or, less often, by listening
to the heart tones with the stethoscope (i.e., apical rate). Counting the pulse for 30 seconds and
doubling the result is more accurate than 15 seconds of observation.
rates, especially if the patient has atrial fibrillation, counting the apical rate is more accurate than
counting the radial pulse, and 60 seconds of observation is more accurate than shorter periods.
2,3
e first accurate observations of
3
e first clinicians to establish the significance of bradycar-
4
In patients with fast heart
1
5
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A difference between the radial pulse rate and apical rate (the apical rate always being greater
if there is a difference) is called the pulse deficit. A pulse deficit has traditionally been associated
with atrial fibrillation, although it is a common finding with extrasystoles and all fast heart rates
and by itself has little diagnostic significance.
6,7
4—VITAL SIGNS
III. The Finding
Many textbooks state that the normal sinus rate ranges from 60 beats/min to 100 beats/min, but
evidence indicates that the heart rate of 95% of healthy persons instead ranges from 50 beats/min
to 95 beats/min.8 Bradycardia is a pulse rate less than 50 beats/min; tachycardia is a rate greater
than 100 beats/min.
IV. Clinical Significance
An important role of any vital sign is to provide the clinician an early indication that trouble is
afoot for the patient. EBM Box 15.1 shows that the finding of tachycardia serves this role well.
In a wide variety of clinical disorders, including septic shock, pneumonia, myocardial infarction,
upper gastrointestinal hemorrhage, gallstone pancreatitis, and pontine hemorrhage, the finding of
tachycardia (variably defined as rate >85 beats/min to >125 beats/min) predicts both increased
complications and worse survival (likelihood ratios [LRs] = 1.5 to 25.4). In patients with myocardial infarction, the increased risk of adverse outcome is a continuum, being greater for patients
with higher heart rates and persisting whether or not the patient has a low ejection fraction, takes
beta-blocker medications, or receives thrombolytic therapy.
increased mortality when detected during the first year after myocardial infarction.28 In patients
with septic shock, the relationship between tachycardia and mortality is independent of whether
the patient receives vasopressor medications,11 and in patients with pontine hemorrhage, tachycardia is a better predictor of mortality than other neurologic findings such as extensor posturing
or the absence of withdrawal to pain.20 e absence of tachycardia, on the other hand, decreases the
probability of hospital mortality in patients with trauma, septic shock, and pontine hemorrhage
(LRs = 0.1 to 0.3; see EBM Box 15.1) and argues against the presence of active bleeding during
endoscopy for upper gastrointestinal hemorrhage (LR = 0.3).
Bradycardia is also an ominous finding in acute disorders. In patients with severe trauma, a
pulse rate of 50 or less predicts mortality with a sensitivity of 17%, specificity of 99%, and positive
LR of 20.7.29 In acutely ill patients presenting to emergency departments for a variety of reasons,
a pulse rate of 40 or less predicts hospital mortality with sensitivity of 9%, specificity of 100%, and
positive LR of 39.1.
Heart rates less than 50 beats/min or greater than 120 beats/min may also indicate heart
rhythms other than sinus rhythm (e.g., complete heart block, atrial flutter), a subject discussed
fully in Chapter 16.
30
13,24–27
Tachycardia continues to predict
ABNORMALITIES OF PULSE CONTOUR
I. Pulsus Alternans
A. THE FINDING
Pulsus alternans describes a regular pulse that has alternating strong and weak beats (Fig. 15.1).
e pulse must be absolutely regular to diagnose pulsus alternans and distinguish it from the
bigeminal pulse, which also has beats of alternating strength although that rhythm is irregular (see
15—PULSE RATE AND CONTOUR
LRs
TACHYCARDIA
if myocardial infarction
Predicting postoperative complications,
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EBM BOX 15.1 Tachycardia, Predicting Patient Outcome
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Likelihood Ratio* if Finding Is
Present Absent
Finding (Reference)
Sensitivity
(%)
Specificity
(%)
Heart rate >85 beats/min
Predicting postoperative
complications, if lung cancer
9
surgery
71 81 3.8 0.4
Heart rate >90 beats/min
Predicting hospital mortality, if
trauma and hypotension
10
94 38 1.5 0.2
Heart rate >95 beats/min
Predicting hospital mortality, if
septic shock
11
97 53 2.0 0.1
Heart rate >100/min
Predicting hospital mortality, if
myocardial infarction
12–16
Predicting active bleeding on urgent
endoscopy, if UGI hemorrhage
Predicting postoperative
complications, if hernia surgery
Predicting complications, if
gallstone pancreatitis
19
6–40 88–98 3.0 0.9
71 86 4.9 0.3
17
54 90 5.6 0.5
18
86 87 6.8 NS
Heart rate >110 beats/min
Predicting hospital mortality, if
pontine hemorrhage
20
70 97 25.4 0.3
Heart rate >125 beats/min
Predicting hospital mortality, if
pneumonia
*Likelihood ratio (LR) if finding present = positive LR; LR if finding absent = negative LR.
NS, Not significant; UGI, upper gastrointestinal.
21–23
6–33 86–98 2.6 NS
0.1 0.2 0.5 12510
Probability
Decrease Increase
+45%+30%+15%–15%–30%–45%
Predicting hospital mortality,
if pontine hemorrhage
Predicting complications,
if gallstone pancreatitis
if hernia surgery
Predicting active bleeding on
endoscopy, if UGI hemorrhage
Predicting postoperative complications,
if lung cancer surgery
Predicting hospital mortality,
LRs
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4—VITAL SIGNS
Normal pulse
Pulsus alternans
Pulsus bisferiens
Dicrotic pulse
Pulsus paradoxus
Pulsus parvus et tardus
Hyperkinetic pulse
Fig. 15.1 Abnormalities of pulse contour. The normal pulse tracing (top row) is displayed with six tracings of
abnormal pulse contours (bottom rows). Pulsus alternans (second row) is a regular pulse that has alternating strong
and weak beats. Both pulsus bisferiens (third row) and the dicrotic pulse (fourth row) have two beats per cardiac
cycle: in pulsus bisferiens both beats are systolic, whereas in the dicrotic pulse one is systolic and the other diastolic.
Pulsus paradoxus (fifth row) is a pulse whose systolic blood pressure decreases more than 10 to 12 mm Hg during
inspiration. Pulsus parvus et tardus (sixth row) is a pulse that has a small volume and rises slowly. The hyperkinetic
pulse (last row) is a pulse with unusually abrupt and strong force; it may have a normal diastolic blood pressure
(e.g., severe mitral insufficiency) or low diastolic blood pressure (e.g., severe aortic regurgitation). These tracings are
facsimiles of actual pulse tracings made over 100 years ago. See text for pathogenesis and clinical significance.
Inspiration
Chapter 16).31 In rare cases of pulsus alternans, the weak pulse is so small it is imperceptible, with
only half of the beats reaching the radial artery (total alternans).32 Pulsus alternans is often accompanied by alternation of the intensity of heart sounds and murmurs (auscultatory alternans).
Traube first described pulsus alternans in 1872.
34
31,33
B. TECHNIQUE
Palpating the radial pulse or using the blood pressure cuff is the best ways to detect pulsus alternans. When using the blood pressure cuff, the clinician should stop deflating the cuff at the first
appearance of Korotkoff sounds and hold the cuff pressure for several beats just below systolic
15—PULSE RATE AND CONTOUR
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101
pressure. In patients with pulsus alternans, only the Korotkoff sounds belonging to the
blood
strong beats are heard. Further deflation of the cuff allows cuff pressure to fall below the systolic
pressure of the weaker beats, causing the cadence of Korotkoff sounds to suddenly double. e
usual difference in systolic pressure between the strong and weak beats is only 15 to 20
mm Hg.
Pulsus alternans often is most prominent in the several beats immediately after a pause in the
32
heart rhythm. Typically, the pause is caused by a premature beat or the abrupt termination of a
paroxysmal tachycardia.
C.
CLINICAL SIGNIFICANCE
In
patients with normal heart rates, the finding of pulsus alternans indicates severe left ven
tricular
dysfunction, caused by ischemic or valvular heart disease, long-standing hypertension,
or
idiopathic cardiomyopathy.
tion, investigators specifically looked for pulsus alternans after premature beats or 10
pacemaker-induced atrial tachycardia: those with pulsus alternans had worse ejection fractions
and higher left ventricular filling pressures than those without the finding.
In patients with rapid heart rates, pulsus alternans has less significance because even patients
with normal hearts sometimes develop the finding during paroxysmal tachycardia.
35
-
36–38
In
one series of patients presenting for cardiac catheteriza
seconds of
35
39
Moreover,
-
pulsus alternans rarely may reflect an intermittent left bundle branch block that alternates with
ventricular beats having normal conduction.
D.
PATHOGENESIS
ere has been considerable debate regarding whether the primary cause of pulsus alternans is
alternation of intrinsic contractility of the heart (contractility argument) or alternation of filling
40
of the ventricles (hemodynamic argument).
One version of the hemodynamic argument is particularly compelling.
regular pulse, the sum of the length of systole and the length of the subsequent diastole must be
constant. If systole lengthens for any reason, the subsequent diastole must be shorter; if systole
shortens for any reason, the subsequent diastole must be longer. In patients with left ventricular
dysfunction, a sudden increase in ventricular filling (such as that induced by a postextrasystolic
pause) causes the subsequent systole to produce a strong beat, although it takes longer than normal for the weakened heart to eject this blood (i.e., thus lengthening systole). By prolonging systole, the strong beat thus shortens the next diastole, which reduces filling of the heart and causes
the next beat to be weaker. e weaker beat is ejected more quickly, shortening systole and causing
34,41
In patients with a
the next diastole to be longer, thus perpetuating the alternating pulse.
Nonetheless, the hemodynamic argument does not explain how pulsus alternans ever gets
started when there is no pause in the rhythm from an extrasystole or termination of a tachycardia.
Most experts now believe that alternation of intrinsic contractility is the fundamental problem
in pulsus alternans, because alternation can even be demonstrated in vitro in isolated muscles at
constant length and resting tension.
37,38
Once alternans begins, however, the hemodynamic effects
probably contribute to the alternating amplitude of the pulse.
II. Pulsus Bisferiens
A. THE FINDING
Pulsus bisferiens (Latin bis, meaning “twice” and Latin ferire, meaning “to beat”) has two beats per
cardiac cycle, both of which occur in systole (the first beat is called the percussion wave; the second,
the tidal wave, see Fig. 15.1).
31
Descriptions of pulsus bisferiens appear in the writings of Galen.
42
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4—VITAL SIGNS
B. TECHNIQUE
Pulsus bisferiens is detected by palpating the brachial or carotid pulse with moderate compression of the vessel, or by using the blood pressure cuff.43 When using the blood pressure cuff, the
clinician hears a quick double tapping sound instead of the typical single sound (the clinician can
mimic the double sound by saying “pa-da…pa-da” as fast as possible).
44
C. CLINICAL SIGNIFICANCE
Pulsus bisferiens is a finding in patients with moderate-to-severe aortic regurgitation.
bisferiens also occurs in patients with combined aortic stenosis and regurgitation, though the
principal lesion is usually the regurgitation and the stenosis is mild.
cases of the finding in severe aortic stenosis.
43
42,45,46
ere are exceptional
Pulsus bisferiens is sometimes described in patients with hypertrophic cardiomyopathy,47
although almost always as a finding seen on direct intraarterial pressure tracings, not as one palpated at the bedside.
48,49
42,44,45
Pulsus
D. PATHOGENESIS
e bisferiens pulse probably results from rapid ejection of blood into a flexible aorta. Because
of the Venturi effect, the rapidly moving bloodstream temporarily draws the walls of the aorta
together, reducing flow momentarily and producing a notch with two systolic peaks in the waveform (in hypertrophic cardiomyopathy, the Venturi effect draws the anterior leaflet of the mitral
valve and the interventricular septum together.).
50 years ago, direct evidence supporting it is difficult to find.
43,50
Although this hypothesis was proposed over
III. Pulsus Paradoxus
A. THE FINDING
Pulsus paradoxus is an exaggerated decrease of systolic blood pressure during inspiration (see Fig.
31,51
15.1).
ing 10 mm Hg, a better threshold may be 12 mm Hg, which is the upper 95% confidence interval
for inspiratory decline in normal persons (i.e., the average inspiratory decrease in systolic pressure of
normal persons is 6 ± 3 mm Hg).52 In patients with pulsus paradoxus, the systolic blood pressure and
pulse pressure fall dramatically during inspiration, though the diastolic blood pressure changes little.
Kussmaul called the finding “paradoxical” because the pulse of his patients disappeared during inspiration even though the apical beat persisted throughout the respiratory cycle. e term is unfortunate, because the finding is nothing more than an exaggeration of normal physiologic change.
B. TECHNIQUE
When checking for pulsus paradoxus, the clinician should have the patient breathe quietly and
regularly, because even normal persons can induce a pulsus paradoxus with vigorous respirations.
Pulsus paradoxus is detected by palpating the pulse or using the blood pressure cuff, although only
paradoxical pulses exceeding 15 to 20 mm Hg are palpable.
use the blood pressure cuff, which has the added advantage of quantifying the finding (Fig. 15.2).
the tracing’s baseline.57 e amplitude of this oscillation correlates with the severity of pulsus
Although the usual definition is an inspiratory decrease in systolic blood pressure exceed-
51,52
In 1873, Kussmaul first described pulsus paradoxus in three patients with pericardial disease.
55,56
For this reason, most clinicians
53,54
Pulsus paradoxus also has been noted in pulse oximetry tracings as respiratory movement of
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