Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2716_Библиотеки_им_академика_М_И_Перельмана
.pdf
CHAPTER
https://t.me/medicina_free
47
Disorders of the Pericardium
KEY TEACHING POINTS
• Acute pericarditis is principally defined by its bedside criteria: combinations
of characteristic chest pain, pericardial rub, and electrocardiographic and
echocardiographic findings. The pericardial rub is less frequent in neoplastic pericarditis
than in other etiologies.
• The diagnosis of cardiac tamponade combines the bedside criteria—elevated neck veins,
tachycardia, pulsus paradoxus—with the echocardiographic criteria. In patients with
pericardial effusions, a pulsus paradoxus greater than 12 mm Hg accurately identifies
those patients whose cardiac output improves after pericardiocentesis.
• The key physical findings of constrictive pericarditis are elevated neck veins, prominent y
descent in venous waveforms, pericardial knock, and hepatomegaly.
PERICARDITIS AND THE PERICARDIAL RUB
I. Introduction
e pericardial rub is a physical sign of pericarditis, or inflammation of the pericardium, which
is caused by a wide variety of disorders, including infections, connective tissue diseases, radiation
injury, myocardial infarction, neoplasia, uremia, and trauma.
In the 1820s, shortly after the introduction of the stethoscope, Collin first described the peri-
cardial rub, as a sound “similar to that of the crackling of new leather.”
II. The Finding
Pericardial rubs are grating, scratching, or creaking sounds that are loudest near the left sternal
border and are most apparent when the patient is sitting upright, leaning forward, and holding
his or her breath in deep exhalation.
rubbed together. Compared with heart murmurs, the pericardial rub has more high-frequency
energy and sounds closer to the ear,2 it may completely disappear during inspiration or expiration,
and up to one-fourth are palpable.
In approximately 50% of patients, the rub has three components per cardiac cycle—one during ventricular systole and two during diastole (mid-diastole and atrial systole).* In approximately
one-third of patients, only two components are heard (usually the atrial and ventricular systolic
rub), and in the remaining 15%, only a single-component ventricular systolic rub is heard.
*
These three components represent the three moments in the cardiac cycle when the ventricle is moving the most.
1
2,3
ey resemble the sound of two pieces of sandpaper being
3,4
3
395
396
https://t.me/medicina_free
9—SELECTED CARDIAC DISORDERS
III. Clinical Significance
A. THE RUB AND PERICARDITIS
Clinical studies of pericarditis require at least two of the following four criteria: (1) pericardial rub,
(2) characteristic pericardial chest pain (precordial pleuritic pain radiating to the trapezius ridge
which is relieved when sitting up), (3) characteristic electrocardiographic changes (diffuse concave ST
elevation, PR segment depression, absence of Q waves), and (4) new or worsening pericardial effusion.
Echocardiography alone cannot be used to diagnose pericarditis, because only 50% to 66% of patients
have detectable pericardial effusions on echocardiography (and most of these effusions are mild).
erefore, because the pericardial friction rub is one of the bedside criteria for the diagnosis of
pericarditis, the diagnostic accuracy of the rub cannot be assessed (see Chapter 1).
B. PERICARDITIS AND FEVER
In Western Europe and the United States, the specific cause of pericarditis is never discovered
in 80% to 90% of cases.8 Such idiopathic cases are often attributed to viral infection. In contrast,
evaluation reveals a specific diagnosis (such as neoplasia, connective tissue disease, tuberculosis,
or bacterial infection) in only 10% to 20% of cases. In one study of 453 patients with acute pericarditis, the presence of fever (temperature >38°C) increased the probability that one of these
specific diagnoses would be found (likelihood ratio [LR] = 4.3) and decreased the probability of
an idiopathic/viral diagnosis (LR = 0.2).
10
C. THE RUB AND PERICARDIAL EFFUSION
5–9
Although the pericardial rub suggests the rubbing together of contiguous pericardial surfaces,
the sound often persists after the accumulation of significant pericardial effusions.
3,11
e rub is
heard, for example, in up to one-fourth of patients with cardiac tamponade (see later). erefore,
the presence of the rub cannot be used to argue against the development of pericardial effusion.
D. THE RUB AND NEOPLASTIC DISEASE
Pericardial rubs are less frequent in neoplastic pericarditis than in other etiologies. For example,
in patients with known cancer who subsequently develop pericardial disease, the presence of a rub
increases the probability that the pericarditis is idiopathic or radiation-induced, not neoplastic
(positive LR = 5.5, negative LR = 0.4).12 In another study of 322 patients presenting with undiagnosed moderate or severe pericardial effusion, the presence of a pericardial rub (among other
inflammatory signs†) increased the probability of a non-neoplastic etiology (LR = 2.3).
13
E. THE RUB AND MYOCARDIAL INFARCTION
A pericardial rub is found in 5% to 20% of patients with acute myocardial infarction, usually appearing
from hospital days 1 to 3.
thrombolytic medications or angioplasty
with rubs have significantly larger myocardial infarctions, lower ejection fractions, more extensive coronary arter y disease, and more complications, including congestive heart failure and atrial arrhythmias.
Nonetheless, in these patients tamponade is rare, even if they receive thrombolytic medications.
†
In this study, “inflammatory signs” were defined as two or more of the following: pericardial rub, characteristic
pericarditis chest pain, fever, or characteristic Electrocardiographic changes.
14–18
e incidence is lowest (i.e., 5% to 7%) in patients receiving immediate
16,18.
Compared with patients who do not develop rubs, patients
14,16,17
16
47—DISORDERS OF THE PERICARDIUM
https://t.me/medicina_free
397
CARDIAC TAMPONADE
I. Introduction
Cardiac tamponade occurs when a pericardial effusion has become so large and tense that intrapericardial pressures exceed the normal filling (i.e., diastolic) pressures of the heart, thus impairing
the diastolic filling of the heart and reducing the cardiac output.
e history of diagnosing tamponade illustrates well the tension that sometimes exists between older
diagnostic standards based on physical signs and newer ones based on clinical imaging. For example,
early descriptions of tamponade, which were based on catastrophic acute intrapericardial hemorrhage,
emphasized hypotension, elevated neck veins, and the small, quiet heart as diagnostic findings (Beck
19,20
triad).
pressure and loud heart tones, the definition of tamponade shifted to emphasize large pericardial effusions, elevated neck veins, pulsus paradoxus, and relief of symptoms and signs after pericardiocentesis.21
Finally, in the 1980s, several echocardiographic criteria for tamponade were introduced,
studies have subsequently shown that relying solely on echocardiographic criteria sometimes identifies
patients who fail to improve symptomatically or physiologically after pericardiocentesis.
but requires synthesis of all the findings, emphasizing especially the ones from physical diagnosis—elevated neck veins, tachycardia, and pulsus paradoxus.
II. The Findings
Later, after it became obvious that many medical patients with tamponade had normal blood
20,22
although
23–25
erefore, the diagnosis of tamponade should not rely solely on the echocardiographic report
26
Table 47.1 presents the physical signs observed in several studies of patients with proven cardiac
tamponade. Most of these patients presented with shortness of breath.
21,27
e definition and
pathogenesis of pulsus paradoxus and elevated neck veins are discussed in Chapters 15 and 36.
TABLE 47.1 ■ Cardiac Tamponade*
Physical Finding
Neck veins
Elevated neck veins 100
Kussmaul sign 0
Arterial pulse
Tachycardia (>100 bpm) 81–100
Blood pressure
Systolic blood pressure greater than 100 mm Hg 58–100
Pulsus paradoxus >10 mm Hg 98
Pulsus paradoxus >20 mm Hg 78
Pulsus paradoxus >30 mm Hg 49
Pulsus paradoxus >40 mm Hg 38
Total paradox 23
Auscultation of heart
Diminished heart tones 36–84
Pericardial rub 27
Other
Hepatomegaly 58
Edema 27
Data from 128 patients from references 21,27,38–40.
*Diagnostic Standard: for tamponade, cardiac output that improved after drainage of pericardial effusion.
†
Definition of finding: for total paradox, palpable pulse disappears completely during inspiration.
‡
Results are overall mean frequency or, if statistically heterogeneous, the range of values.
†
Frequency (%)
‡
398
https://t.me/medicina_free
9—SELECTED CARDIAC DISORDERS
e three key findings of tamponade are elevated neck veins (100% of patients), tachycardia
(81% to 100% of patients), and pulsus paradoxus >10 mm Hg (98% of patients). In patients with
pericardial effusions, the finding of pulsus paradoxus greater than 12 mm Hg detects tamponade
with a sensitivity of 98%, specificity of 83%, positive LR = 5.9, and negative LR = 0.03 (see
Chapter 15).28 Furthermore, the absence of pulsus paradoxus on analysis of printed pulse oximetry
tracings (see Chapter 15) greatly decreases the probability of tamponade (LR = 0.05).
29
e complication of tamponade in patients with pericarditis greatly increases the probability
that a specific diagnosis will be made (e.g., neoplasia, connective tissue disease, tuberculosis, or
bacterial infection; LR = 21.5).
10
Cardiac tamponade is one of the few causes of elevated neck veins with an absent y descent
(see Chapter 36). is contrasts sharply with the exaggerated y descent of constrictive pericarditis
(see later).
CONSTRICTIVE PERICARDITIS
I. Introduction
Constrictive pericarditis is present when calcification or fibrosis of the pericardium impairs diastolic filling, thus causing elevated venous pressure and reduced cardiac output.
II. The Findings
Table 47.2 presents the physical signs of patients with constrictive pericarditis; most patients pres-
ent with edema, abdominal swelling, and dyspnea.
30–32
e key physical findings are elevated neck
veins (94%), a prominent y descent in venous waveform (57% to 100%, median 94%), pericardial
knock (20% to 94%), and hepatomegaly (53% to 100%).
TABLE 47.2 ■ Constrictive Pericarditis*
30,38,46–48
†
sometimes in
49
Physical Finding Frequency (%)
Neck veins
Elevated neck veins 94
Prominent y descent (Friedreich sign) 57–100
Kussmaul sign 14–50
Arterial pulse
Irregularly irregular (atrial fibrillation) 36–70
Blood pressure
Pulsus paradoxus >10 mm Hg 13–64
Auscultation of heart
Pericardial knock 20–94
Pericardial rub 3–16
Other
Hepatomegaly 53–100
Edema 58–100
Ascites 37–89
Data from 780 patients from references 30,31,36,38,41–49.
*Diagnostic standard: For constrictive pericarditis, surgical and postmortem findings,
combination with hemodynamic findings
†
Results are the overall mean frequency or, if statistically heterogeneous, the range of values.
31,36,41–45
and magnetic resonance imaging findings.
47—DISORDERS OF THE PERICARDIUM
https://t.me/medicina_free
399
A. NECK VEINS
In addition to the elevated venous pressure, the venous waveform displays an unusually prominent
y descent, which, combined with an exaggerated x′ descent, creates two conspicuous dips per car-
diac cycle, making the waveform appear to trace an M or W with each arterial pulse (Friedreich
sign, see Chapter 36). Sometimes these movements are transmitted to the liver, causing it to
pulsate inward twice with each cardiac cycle.
33
e prominent y descent occurs because diastolic filling is only impaired during the last twothirds of diastole. At the moment the tricuspid valve opens (beginning of diastole and beginning
of y descent), the right atrium empties rapidly and without resistance (causing a prominent y
descent), although eventually the relaxing ventricle meets the limits of the rigid pericardial shell
and the pressures again increase.34 is contrasts with tamponade, which impairs diastolic filling
throughout diastole and thus eliminates the y descent.
B. KUSSMAUL SIGN
e Kussmaul sign is the paradoxical increase in venous pressure during inspiration. is sign,
present in 14% to 50% of patients with constriction, is discussed fully in Chapter 36 (an excellent
video of the Kussmaul sign is available in the reference by Mansoor).
35
C. PERICARDIAL KNOCK
e pericardial knock is a loud, high-frequency early diastolic sound heard between the apex and
left lower sternal border. It is discussed in Chapter 42.
D. OTHER FINDINGS
Up to 90% of patients with constrictive pericarditis have systolic retraction of the apical impulse
(see Chapter 38).
According to traditional teachings, pulsus paradoxus is a not a finding of constrictive pericarditis; however, the studies reviewed in Table 47.2 indicate that pulsus paradoxus does appear,
occurring in 13% to 64% of patients with constrictive pericarditis (see Table 47.2). is seeming
contradiction probably reflects the different definitions of pulsus paradoxus. When pulsus paradoxus is defined as an inspiratory fall in the systolic blood pressure of 10 mm Hg or more (i.e., the
usual definition), 13% to 64% of patients with constriction have the finding; when it is instead
defined as an inspiratory fall of 20 mm Hg or more, no patient has the finding.38 In contrast, the
usual pulsus paradoxus in patients with tamponade is 20 to 50 mm Hg (see Table 47.1).
erefore, mild degrees of pulsus paradoxus (10 to 20 mm Hg) are commonly observed in
patients with constrictive pericarditis, but larger degrees (>20 mm Hg) are not and suggest tamponade or another cause of the finding (see Chapter 15).
References may be accessed online at Elsevier eBooks for Practicing Clinicians.
36,37
21
References
https://t.me/medicina_free
1. Stokes W. An Introduction to the Use of the Stethoscope (Facsimile Edition by the Classics of Cardiology
Library). Maclachlin and Stewart; 1825.
2. Harvey WP. Auscultatory findings in diseases of the pericardium. Am J Cardiol. 1961;7:15–20.
3. Spodick DH. Pericardial rub. Prospective, multiple observer investigation of pericardial friction in 100
patients. Am J Cardiol. 1975;35(3):357–362.
4. McGee SR. Etiology and diagnosis of systolic murmurs in adults. Am J Med. 2010;123(10):913–921.
5. Imazio M, Brucato A, Cemin R, etal. A randomized trial of colchicine for acute pericarditis. N Engl J
Med. 2013;369(16):1522–1528.
6. Permanyer-Miralda G, Sagristá-Sauleda J, Soler-Soler J. Primary acute pericardial disease: a prospective
series of 231 consecutive patients. Am J Cardiol. 1985;56(10):623–630.
7. Zayas R, Anguita M, Torres F, etal. Incidence of specific etiology and role of methods for specific etio-
logic diagnosis of primary acute pericarditis. Am J Cardiol. 1995;75(5):378–382.
8. Imazio M, Gaita F, LeWinter MM. Evaluation and treatment of pericarditis: a systematic review. JAMA.
2015;314(14):1498–1506.
9. LeWinter MM. Clinical practice. Acute pericarditis. N Engl J Med. 2014;371(25):2410–2416.
10. Imazio M, Cecchi E, Demichelis B, etal. Indicators of poor prognosis of acute pericarditis. Circulation.
2007;115(21):2739–2744.
11. Markiewicz W, Brik A, Brook G, Edoute Y, Monakier I, Markiewicz Y. Pericardial rub in pericardial
effusion: lack of correlation with amount of fluid. Chest. 1980;77(5):643–646.
12. Posner MR, Cohen GI, Skarin AT. Pericardial disease in patients with cancer. e differentiation of
malignant from idiopathic and radiation-induced pericarditis. Am J Med. 1981;71(3):407–413.
13. Sagristà-Sauleda J, Mercé J, Permanyer-Miralda G, Soler-Soler J. Clinical clues to the causes of large
pericardial effusions. Am J Med. 2000;109(2):95–101.
14. Tofler GH, Muller JE, Stone PH, etal. Pericarditis in acute myocardial infarction: characterization and
clinical significance. Am Heart J. 1989;117(1):86–92.
15. Lichstein E, Liu HM, Gupta P. Pericarditis complicating acute myocardial infarction: incidence of com-
plications and significance of electrocardiogram on admission. Am Heart J. 1974;87(2):246–252.
16. Wall TC, Califf RM, Harrelson-Woodlief L, etal. Usefulness of a pericardial friction rub after thrombo-
lytic therapy during acute myocardial infarction in predicting amount of myocardial damage. e TAMI
Study Group. Am J Cardiol. 1990;66(20):1418–1421.
17. Dubois C, Smeets JP, Demoulin JC, etal. Frequency and clinical significance of pericardial friction rubs
in the acute phase of myocardial infarction. Eur Heart J. 1985;6(9):766–768.
18. Sugiura T, Nakamura S, Kudo Y, Okumiya T, Yamasaki F, Iwasaka T. Clinical factors associated with
persistent pericardial effusion after successful primary coronary angioplasty. Chest. 2005;128(2):798–803.
19. Beck CS. Two cardiac compression triads. JAMA. 1935;104(9):714–716.
20. Fowler NO. Cardiac tamponade. A clinical or an echocardiographic diagnosis? Circulation. 1993;87(5):
1738–1741.
21. Guberman BA, Fowler NO, Engel PJ, Gueron M, Allen JM. Cardiac tamponade in medical patients.
Circulation. 1981;64(3):633–640.
22. Himelman RB, Kircher B, Rockey DC, Schiller NB. Inferior vena cava plethora with blunted respi-
ratory response: a sensitive echocardiographic sign of cardiac tamponade. J Am Coll Cardiol. 1988;
12(6):1470–1477.
23. Levine MJ, Lorell BH, Diver DJ, Come PC. Implications of echocardiographically assisted diagnosis
of pericardial tamponade in contemporary medical patients: detection before hemodynamic embarrassment. J Am Coll Cardiol. 1991;17(1):59–65.
24. Materazzo C, Piotti P, Meazza R, Pellegrini MP, Viggiano V, Biasi S. Respiratory changes in trans-
valvular flow velocities versus two-dimensional echocardiographic findings in the diagnosis of cardiac
tamponade. Ital Heart J. 2003;4(3):186–192.
25. Mercé J, Sagristà-Sauleda J, Permanyer-Miralda G, Evangelista A, Soler-Soler J. Correlation between
clinical and Doppler echocardiographic findings in patients with moderate and large pericardial effusion:
implications for the diagnosis of cardiac tamponade. Am Heart J. 1999;138(4 Pt 1):759–764.
26. Hancock EW. Cardiac tamponade. Heart Dis Stroke. 1994;3(3):155–158.
400.e1
27. Markiewicz W, Borovik R, Ecker S. Cardiac tamponade in medical patients: treatment and prognosis in
https://t.me/medicina_free
the echocardiographic era. Am Heart J. 1986;111(6):1138–1142.
28. Curtiss EI, Reddy PS, Uretsky BF, Cecchetti AA. Pulsus paradoxus: definition and relation to the severity
of cardiac tamponade. Am Heart J. 1988;115(2):391–398.
29. Doukky R, Improvola G, Shih MJ, etal. Usefulness of oximetry paradoxus to diagnose cardiac tampon-
ad e. Am J Cardiol. 2019;123(3):498–506.
30. Evans W, Jackson F. Constrictive pericarditis. Br Heart J. 1952;14(1):53–69.
31. Wood P. Chronic constrictive pericarditis. Am J Cardiol. 1961;7:48–61.
32. Cameron J, Oesterle SN, Baldwin JC, Hancock EW. e etiologic spectrum of constrictive pericarditis.
Am Heart J. 1987;113(2 Pt 1):354–360.
33. Coralli RJ, Crawley IS. Hepatic pulsations in constrictive pericarditis. Am J Cardiol. 1986;58(3):370–373.
34. Shabetai R, Fowler NO, Guntheroth WG. e hemodynamics of cardiac tamponade and constrictive
pericarditis. Am J Cardiol. 1970;26(5):480–489.
35. Mansoor AM, Karlapudi SP. Images in clinical medicine. Kussmaul’s sign. N Engl J Med. 2015;372(2):e3.
36. el-Sherif A, el-Said G. Jugular, hepatic, and praecordial pulsations in constrictive pericarditis. Br Heart J.
1971;33(2):305–312.
37. Boicourt OW, Nagle RE, Mounsey JPD. e clinical significance of systolic retraction of the apical
impulse. Br Heart J. 1965;27(3):379–391.
38. Lange RL, Botticelli JT, Tsagaris TJ, Walker JA, Bani M, Bustamante RA. Diagnostic signs in com-
pressive cardiac disorders: constrictive pericarditis, pericardial effusion, and tamponade. Circulation.
1966;33(5):763–777.
39. Reddy PS, Curtiss EI, O’Toole JD, Shaver JA. Cardiac tamponade: hemodynamic observations in man.
Circulation. 1978;58(2):265–272.
40. Brown J, MacKinnon D, King A, Vanderbush E. Elevated arterial blood pressure in cardiac tamponade.
N Engl J Med. 1992;327(7):463–466.
41. Tyberg TI, Goodyer AVN, Langou RA. Genesis of pericardial knock in constrictive pericarditis. Am J
Cardiol. 1980;46(4):570–575.
42. Schiavone WA. e changing etiology of constrictive pericarditis in a large referral center. Am J Cardiol.
1986;58(3):373–375.
43. Talreja DR, Edwards WD, Danielson GK, etal. Constrictive pericarditis in 26 patients with histologi-
cally normal pericardial thickness. Circulation. 2003;108(15):1852–1857.
44. Kumawat M, Lahiri TK, Agarwal D. Constrictive pericarditis: retrospective study of 109 patients. Asian
Cardiovasc orac Ann. 2018;26(5):347–352.
45. Mutyaba AK, Balkaran S, Cloete R, etal. Constrictive pericarditis requiring pericardiectomy at Groote
Schuur Hospital, Cape Town, South Africa: causes and perioperative outcomes in the HIV era (1990-
2012). J orac Cardiovasc Surg. 2014;148(6):3058–3065. e1.
46. Paul O, Castleman B, White PD. Chronic constrictive pericarditis; a study of 53 cases. Am J Med Sci.
1948;216(4):361–377.
47. Mounsey P. e early diastolic sound of constrictive pericarditis. Br Heart J. 1955;17(2):143–152.
48. Ling LH, Oh JK, Schaff HV, etal. Constrictive pericarditis in the modern era: evolving clinical spectrum
and impact on outcome after pericardiectomy. Circulation. 1999;1000(13):1380–1386.
49. Fernandes F, Melo DTP, Ramires FJA, etal. Importance of clinical and laboratory findings in the diagno-
sis and surgical prognosis of patients with constrictive pericarditis. Arq Bras Cardiol. 2017;109(5):457–465.
400.e2
CHAPTER
https://t.me/medicina_free
48
Congestive Heart Failure
KEY TEACHING POINTS
• In patients with chest pain or dyspnea, the following physical signs increase
probability of elevated left heart filling pressure and cardiac dyspnea: positive
abdominojugular test, abnormal Valsalva response, displaced apical impulse, heart
rate greater than 100 beats/min, the third heart sound, elevated neck veins, and a
positive bendopnea test.
• A normal Valsalva response and negative abdominojugular test decrease probability of
elevated left heart filling pressure.
• The following physical signs are accurate signs of low ejection fraction: Cheyne-Stokes
respirations, displaced apical impulse, abnormal Valsalva response, elevated neck veins,
and third heart sound.
I. Introduction
Heart failure is a clinical syndrome characterized by impaired ventricular performance, elevated
diastolic filling pressure, and diminished exercise capacity. Patients with heart failure and ventricular disease may have a low ventricular ejection fraction (systolic dysfunction) or normal ejection
fraction (diastolic dysfunction).
Clear descriptions of the signs of heart failure date to the Middle Ages.1 In the 17th century,
just after Harvey published his discovery of the circulation of blood, clinicians began to correlate
the pathologic observation of large heart chambers and congested lungs with the clinical observations of dyspnea and edema.
II. The Findings
Many of the findings of heart failure are discussed fully in other chapters of the book, including pulsus alternans and the dicrotic pulse (see Chapter 15), Cheyne-Stokes respirations
(see Chapter 19), crackles (see Chapter 30), elevated neck veins (see Chapter 36), the abdomi-
nojugular test (see Chapter 36), displaced apical impulse (Chapter 38), and third heart sound
(see Chapter 41).
is chapter reviews two findings not discussed extensively elsewhere, the bendopnea test
and the abnormal Valsalva response, and then presents the diagnostic accuracy of all findings of
congestive heart failure.
2
401
402
https://t.me/medicina_free
9—SELECTED CARDIAC DISORDERS
A.
BENDOPNEA TEST
1.
The Finding
Bendopnea describes shortness of breath that develops when a seated patient bends over. In 2013,
clinicians began investigating this symptom in heart failure patients, most of whom had advanced
disease with significant dyspnea on exertion.
3,4
Researchers have developed a specific bedside test to determine whether or not bendopnea
is present: e patient sits in a chair and is asked to bend forward at the waist “as if putting on
their socks or shoes.” e clinician then times the interval between bending over and the onset of
shortness of breath (if it develops). If this interval is less than 30
seconds, bendopnea is present.
Alternative symptoms, such as lightheadedness and fullness in the head, chest, or abdomen do not
constitute a positive test.
a median interval of only 8 to 12
2.
Pathogenesis of Bendopnea
4
In clinical studies of patients with a positive test, dyspnea appears after
seconds.
4,5
e cause of bendopnea is elevated left heart filling pressure. Compared to those without bendopnea, patients with bendopnea have more orthopnea, more paroxysmal nocturnal dyspnea, and
higher pulmonary capillary wedge pressure.
3,4
e action of bending over increases filling pressure
even more, an increment sufficient to cause significant dyspnea in those with the positive bendopnea test.
4
Even so, the actual mechanism for increment in cardiac pressure with bending over
is controversial. Some investigators believe it is due to an increase in intrathoracic pressure in the
bended position,
the abdominojugular test).
frequency, waist circumference, or body habitus.
B.
THE VALSALVA RESPONSE
1.
Introduction
4,6
whereas others believe it results from increased abdominal pressure (similar to
7
e symptom is not explained by differences in cardiac output, ascites
4,5
4
e Valsalva maneuver consists of forced expiration against a closed glottis after a full inspira-
8
tion.
e Valsalva response refers to the changes in blood pressure and pulse that occur during
both the strain phase of the maneuver and the recovery period after the strain is released.
Valsalva
dle ear.
use
it to interrupt his arterial pulse at will (an experiment he eventually abandoned after
fainting and developing convulsions).
introduced his maneuver in 1704 as a technique to expel pus from the mid
8–10
e maneuver was forgotten, however, until 1859, when Weber showed he could
9
Beginning in the 1950s, many different investigators
-
reported that the Valsalva response was distinctly abnormal in patients with congestive heart
11–15
failure.
2.
Technique
To perform the maneuver, the patient should take a deep breath in and bear down, as if straining
to have a bowel movement. e clinician measures the Valsalva response by using a blood pressure cuff, as described below. In clinical studies, the straining phase is standardized by having the
patient’s mouthpiece connected to a pressure transducer, which should demonstrate an increment
of 30 to 40 mm Hg for at least 10 seconds.
system surgery or hemorrhage. It is also unwise to perform the maneuver in patients with
acute coronary ischemia, because it may induce arrhythmias, although in patients with chronic
ischemic heart disease the maneuver is safe and was once even used to terminate episodes of
angina.
e Valsalva maneuver is contraindicated in patients with recent eye or central nervous
16
48—CONGESTIVE HEART FAILURE
https://t.me/medicina_free
403
3. The Normal Valsalva Response
e normal Valsalva response is divided into four phases (Fig. 48.1).8 In phase 1, the arterial
systolic blood pressure rises briefly because increased intrathoracic pressure is transmitted directly
to the aorta. In phase 2, blood pressure falls because of reduced venous return during continuing
straining. In phase 3, just after release of straining, pressure falls further because of temporary
pooling of blood in the pulmonary veins. In phase 4, the arterial pressure overshoots to levels
above the control values, primarily because of reflex sympathetic activity induced by previous
hypotension. e changes in heart rate are exactly out of phase with the blood pressure: the heart
rate increases during phases 2 and 3 and decreases during phase 4.
NORMAL
Cuff pressure
15 mm Hg
Systolic BP
Valsalva strain:
10 seconds
1
2
Valsalva release:
4
Korotkoff sounds
ABSENT PHASE 4
OVERSHOOT
SQU
ARE WAVE
Fig. 48.1 The Valsalva Response. The solid line in each drawing depicts changes in systolic blood pressure
over time during the Valsalva maneuver. The three types of Valsalva responses are normal (top), absent phase
4 overshoot (middle), and square wave (bottom). The clinician distinguishes these responses by inflating the
blood pressure cuff 15 mm Hg above the patient’s resting systolic blood pressure BP; (horizontal dotted line)
and listening for Korotkoff sounds. Korotkoff sounds appear in phase 1 and 4 in the normal response, in phase
1 only in the absent phase 4 overshoot response, and in phases 1 and 2 only in the square wave response.
See the text.
3
Соседние файлы в папке Библиотека им академика М.И. Перельмана