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_3793_Библиотеки_им_академика_М_И_Перельмана
.pdf
CHAPTER 2 Ethical Issues in the Cardiac Intensive Care Unit 26.e3
https://t.me/medicina_free
86. Jecker NS. Futility and Fairness: A Defense of the Texas
Advance Directive Law. Am J Bioeth. 2015;15(8):43–46.
87. Smedira NG, Evans BH, Grais LS, et al. Withholding and
withdrawal of life support from the critically ill. N Engl J Med.
1990;322(5):309–315.
88. Bastos PG, Knaus WA. APACHE III study: a summary. Intensive
Care World. 1991;8(1):35–38.
89. Appelbaum PS. Clinical practice. Assessment of patients’
competence to consent to treatment. N Engl J Med.
2007;357(18):1834–1840.
90. Gilligan T, Raffin TA. Rapid withdrawal of support. Chest.
1995;108(5):1407–1408.
91. Kleinman A, Eisenberg L, Good B. Culture, illness, and care:
clinical lessons from anthropologic and cross-cultural research.
Ann Intern Med. 1978;88(2):251–258.
92. Kalish R, ed. Death and Dying: Views From Many cultures.
Farmingdale, NY: Baywood; 1980.
93. Bedolla MA. The principles of medical ethics and their
application to Mexican-American elderly patients. Clin Geriatr
Med. 1995;11(1):131–137.
94. Hepburn K, Reed R. Ethical and clinical issues with NativeAmerican elders. End-of-life decision making. Clin Geriatr Med.
1995;11(1):97–111.
95. Marshall P, Thomasma DC, Bergsma J. Intercultural reasoning:
the challenge for international bioethics. Camb Q Healthc
Ethics. 1994;3(3):321–328.
96. Mouton CP, Johnson MS, Cole DR. Ethical considerations with
African-American elders. Clin Geriatr Med. 1995;11(1):113–129.
97. Pellegrino ED. Is truth telling to the patient a cultural artifact?
JAMA. 1992;268(13):1734–1735.
98. Tangwa GB. Between universalism and relativism: a conceptual
exploration of problems in formulating and applying
international biomedical ethical guidelines. J Med Ethics.
2004;30(1):63–67.
99. Yeo G. Ethical considerations in Asian and Pacific Island elders.
Clin Geriatr Med. 1995;11(1):139–152.
100. Katz J. Informed consent in the therapeutic relationship: legal
and ethical aspects. In: Reich W, ed. Encyclopaedia of Bioethics.
Vol. 2. New York: The Free Press; 1978:771–778.
101. Gostin LO. Informed consent, cultural sensitivity, and respect
for persons. JAMA. 1995;274(10):844–845.
102. Carrese JA, Rhodes LA. Western bioethics on the Navajo
reservation. Benefit or harm? JAMA. 1995;274(10):826–829.
103. Carrese JA, Rhodes LA. Bridging cultural differences in medical
practice. The case of discussing negative information with
Navajo patients. J Gen Intern Med. 2000;15(2):92–96.
104. Arato v Avedon, 598 (858 1993).
105. Putensen v. Clay Adams, Inc., 91 319 (1970).
106. Freedman B. Offering truth. One ethical approach to the
uninformed cancer patient. Arch Intern Med.
1993;153(5):572–576.
107. DiMaio JM, Salerno TA, Bernstein R, et al. Ethical obligation of
surgeons to noncompliant patients: can a surgeon refuse to
operate on an intravenous drug-abusing patient with recurrent
aortic valve prosthesis infection? Ann Thorac Surg.
2009;88(1):1–8.
108. Hull SC, Jadbabaie F. When is enough enough? The dilemma of
valve replacement in a recidivist intravenous drug user. Ann
Thorac Surg. 2014;97(5):1486–1487.
109. Kirkpatrick JN. Infective endocarditis in the intravenous drug
user. Virtual Mentor. 2010;12(10):778–781.
110. Abrams DC, Prager K, Blinderman CD, Burkart KM, Brodie D.
Ethical dilemmas encountered with the use of extracorporeal
membrane oxygenation in adults. Chest. 2014;145(4):876–882.
111. Meltzer EC, Ivascu NS, Acres CA, et al. Extracorporeal
membrane oxygenation in adults: a brief review and ethical
considerations for nonspecialist health providers and
hospitalists. J Hosp Med. 2014;9(12):808–813.
112. Kon AA, Davidson JE, Morrison W, et al. Shared Decision
Making in ICUs: An American College of Critical Care
Medicine and American Thoracic Society Policy Statement. Crit
Care Med. 2016;44(1):188–201.
113. Deleted in review.
114. Courtwright AM, Robinson EM, Feins K, et al. Ethics
Committee Consultation and Extracorporeal Membrane
Oxygenation. Ann Am Thorac Soc. 2016;13(9):1553–1558.
115. Adler ED, Goldfinger JZ, Kalman J, Park ME, Meier DE.
Palliative care in the treatment of advanced heart failure.
Circulation. 2009;120(25):2597–2606.
116. Barclay S, Momen N, Case-Upton S, Kuhn I, Smith E. End-oflife care conversations with heart failure patients: a systematic
literature review and narrative synthesis. Br J Gen Pract.
2011;61(582):e49–e62.
117. Chen-Scarabelli C, Saravolatz L, Hirsh B, Agrawal P, Scarabelli
TM. Dilemmas in end-stage heart failure. J Geriatr Cardiol.
2015;12(1):57–65.
118. Kini V, Kirkpatrick JN. Ethical challenges in advanced heart
failure. Curr Opin Support Palliat Care. 2013;7(1):21–28.
119. Anderson-Shaw L. The unilateral DNR order–one hospital’s
experience. JONAS Healthc Law Ethics Regul. 2003;5(2):42–46.
120. Blinderman CD, Krakauer EL, Solomon MZ. Time to revise the
approach to determining cardiopulmonary resuscitation status.
JAMA. 2012;307(9):917–918.
121. Daeschler M, Verdino RJ, Caplan AL, Kirkpatrick JN.
Defibrillator Deactivation against a Patient’s Wishes:
Perspectives of Electrophysiology Practitioners. Pacing Clin
Electrophysiol. 2015;38(8):917–924.
122. Karnik AM. End-of-life issues and the do-not-resuscitate order:
who gives the order and what influences the decision? Chest.
2002;121(3):683–686.
Physical Examination in the Cardiac
https://t.me/medicina_free
The trouble with doctors is not that they don’t know enough, but that they don’t see enough.
OUTLINE
General Assessment, 27
Vital Signs, 27
Temperature, 28
Respiration, 28
Pulse, 29
Blood Pressure, 30
Weight, 31
Head, Eyes, Ears, Nose, and Throat Examination, 31
Jugular Venous Pulse and Abdominojugular Reflux, 31
Chest and Lung Examination, 32
3
Intensive Care Unit
Hal A. Skopicki, George Gubernikoff, David L. Brown
Sir Dominic J. Corrigan (1802–1880)
Thorax and Heart Examination, 33
Auscultation of the Heart, 34
S1, S2, S3, and S4, 34
Heart Murmurs: Static and Dynamic Auscultation, 35
Abdominal Examination, 37
Neurologic Examination, 38
Vascular Examination, 40
Musculoskeletal and Integument Examination, 40
Conclusion, 40
In the cardiac intensive care unit (CICU), the ubiquitous presence
of advanced technology and highly sensitive laboratory assessments/
testing has resulted in an overreliance on imaging and testing at
the expense of the skills required to examine critically ill patients.
Yet, at the moments of initial patient contact, acute decompensation, and serially after therapeutic interventions, the ability to
integrate an outstanding physical evaluation into the diagnostic
assessment of the patient remains critical. Since, in the words of
William Osler, “Medicine is the art of uncertainty and the science
of probability,” the physical examination should be used in concert
with laboratory analyses and diagnostic imaging, to limit the
uncertainty and increase the probability of optimal patient care.
The ideal physical examination requires time, patience, a quiet
room, and the ability to think and examine simultaneously.
Although these elements are rarely present in the CICU setting,
it is precisely through the tangle of electrocardiogram leads and
intrusive sounds of pumps, cardiac monitors, ventilators, and
conversations that well-prepared physicians can optimize the
management of critically ill patients by focusing their senses
and performing the physical examination to the best of their
abilities.
GENERAL ASSESSMENT
The general assessment should include a broad evaluation of
the patient’s emotional status, appearance, and nonverbal cues.
Although apprehension may be part of a patient’s natural temperament, abrupt-onset or escalating anxiety should elicit serious
diagnostic concern until acute and life-threatening processes
(e.g., escalating ventricular arrhythmias, impeding pulmonary
edema, crescendo angina, extension of a myocardial infarction
[MI], aortic dissection) can be ruled out. Reassuring the patient
may gain time for further investigation. A patient who needs to
sit up to catch his or her breath suggests the presence of pulmonary edema or a large pleural effusion, whereas a patient
who finds relief of chest pain while sitting up and leaning forward
may have acute pericarditis. The inability to get comfortable in
any position often occurs with abdominal and genitourinary
disorders, such as cholecystitis, penetrating ulcers, nephrolithiasis,
ischemic bowel, and colonic obstruction. Cachexia, with decreased
generalized muscle mass or temporal muscle wasting, suggests
long-standing disease and is often seen with heart failure, renal
or hepatic failure, cancer, or nutritional disorders.
VITAL SIGNS
When asked to examine a critically ill patient, careful consideration
of the vital signs is often the difference between successful and
unsuccessful outcomes. Being called on to evaluate a patient
who is acutely decompensated necessitates that the physician
obtain vital signs that are current and accurate. “Tachycardia”
can occur when a cardiac monitor inadvertently counts the T
wave. Similarly, “hypotension” may be urgently reported only
to reveal an improperly situated or sized blood pressure cuff.
A critical aspect of vital sign assessment is the evaluation of
trends. A patient whose heart rate has increased from a consistent
27
CHAPTER 3 Physical Examination in the Cardiac Intensive Care Unit 27.e1
https://t.me/medicina_free
Keywords
physical examination
auscultation
jugular venous pulsations
myocardial infarction
ventricular septal defect
pneumopericardium
pericarditis
pericardial tamponade
Kussmaul’s sign
right ventricular infarction
Valsalva maneuver
acute aortic syndromes
heart failure
mitral regurgitation
aortic regurgitation
tricuspid regurgitation
atrial fibrillation
atrial flutter
heart block
28 PART I Introduction
https://t.me/medicina_free
baseline of 60 to 70 beats/min to 100 beats/min should be a cause for
concern, similar to a patient who appears with an initial heart rate
greater than 120 beats/min. Likewise, a patient with a respiratory
rate that has gone from 12 to 22 breaths/min should be considered
as seriously as one who initially presents with acute tachypnea.
Temperature
Because core body temperature is carefully controlled within a
narrow range, the detection of hyperthermia or hypothermia
offers important clinical clues. Normal oral body temperature
is approximately 37°C (98.6°F) with early morning temperatures
approximately 1°C lower compared with later in the afternoon.
By convention, fever is defined as an oral temperature greater
than 38°C (> 100°F), although it is common practice to consider
temperatures greater than 38.4°C (> 101.1°F) in hospitalized
patients to be clinically significant (albeit without significant
data to support this assumption).
Hyperthermia associated with infection (for patients not
receiving negative chronotropic agents or with intrinsic cardiac
conduction disease) should be accompanied by an increase in
the pulse rate of approximately 8.5 beats/min for each 1°C increase
(the Liebermeister rule).1 The presence of a factitious fever can
be suspected if there isn’t a similar temperature elevation in
voided urine compared with the oral temperature. Although a
hot drink can quickly increase oral temperature up to 2°C, 5
minutes later the increase is only 0.3°C.
2
The pattern of the fever spikes should also be assessed.
Intermittent (returning to normal each day) can occur in septicemia and with abscesses; sustained (with minor daily variation
[i.e., <0.3°C] suggesting gram-negative infections or pneumonia),
remittent (varying > 0.3°C each day but not returning to normal,
which occurs in infective endocarditis), and relapsing (febrile
and afebrile days suggesting the Pel-Ebstein fever of Hodgkin
disease or episodic cholangitis caused by a mobile common bile
duct stone). Once-daily spikes (quotidian fever) occur with liver
abscesses or acute cholangitis; twice-daily spikes (double quotidian
fever) suggest gonococcal endocarditis. Prolonged fever despite
antibiotic therapy can also occur with connective tissue disorders,
drug fever, neoplasm, abscess, or antibiotic-resistant organisms
and superinfection.
The presence of hypothermia (oral temperature <35°C [95°F])
requires confirmation. Drinking ice water reduces the oral temperature up to 0.6°C (1°F) for 5 minutes.
2
False-negative hypothermic
readings can also occur with ear temperatures taken in the presence
of cerumen and oral temperatures recorded in the presence of
tachypnea. Confirmed hypothermia requires the assessment of a
patient’s temperature with a rectal thermometer (which averages
approximately 0.6°C [1°F] higher than the oral temperature). The
differential diagnosis of true hypothermia includes ambient cold
exposure, submersion, hypothyroidism, hypoglycemia, sepsis, and
adrenal insufficiency. With hypothermia from submersion or
exposure, warming to room temperature is necessary for adequate
assessment of end-organ and neurologic function.
Respiration
The respiratory effort, rate, and pattern should be assessed in
ventilated and nonventilated patients. Accessory muscle use is
common with pulmonary edema, chronic obstructive pulmonary
disease (COPD), asthmatic exacerbations, and pneumonia. It
may be detected visually or by palpation over the sternocleidomastoid or intercostal muscles. With acute tachypnea (a respiratory rate greater than 25 breaths/min), an immediate assessment
should be performed to distinguish peripheral cyanosis (dusky
or bluish tinge to the fingers and toes without mucosal or buccal
changes) from central hypoxemia (associated with a bluish tinge
to the lips or mucosa under the tongue). Peripheral cyanosis
may occur with or without hypoxemia, such as in the case of
severe peripheral vasoconstriction. This condition is accompanied
by cold extremities and compromised capillary refill.
Tachypnea, when secondary to hypoxia, should nearly always
be associated with a reflex tachycardia. Although resting tachypnea
may occur with cardiopulmonary disease, it may also be present
in response to fever, pain, anemia, hyperthyroidism, abdominal
distention, respiratory muscle paralysis, obesity, or metabolic
acidosis. When tachypnea accompanies chest pain or collapse,
acute pulmonary embolism should be included in the differential
diagnosis. When tachypnea is present with a history of orthopnea,
it suggests the presence of pulmonary edema, pleural effusion,
or both. When tachypnea is present in a patient being weaned
from a ventilator, tachypnea predicts weaning failure.
3
Hypopnea is defined as less than 10 shallow or slow breaths
per minute. It may be due to severe cardiopulmonary failure,
sepsis, central nervous system (CNS) depressants (e.g., sedativehypnotics, narcotics, and alcohol), or CNS disease (e.g., cerebrovascular accident, meningitis). Hypopnea may also occur
secondary to factors that limit inspiration, such as pericarditis,
pleuritis, or postoperative pain.
Breathing patterns can reveal underlying pathology (Video
3.1, Table 3.1). While most causes of hypoxia usually result in
shallow, rapid respirations, exaggerated deep and rapid respirations were noted by Kussmaul to imply the presence of diabetic
ketoacidosis. Apneic episodes with snoring suggest obstructive
sleep apnea, a potentially treatable contributor to hypertension,
right heart failure, and atrial fibrillation. Cheyne-Stokes breathing,
in which periods of waxing and waning tachypnea and hyperpnea
alternate with apnea, occurs in various cardiac, neurologic, and
pulmonary disorders or from simple oversedation. When CheyneStokes breathing occurs in the setting of uremia or heart failure,
it portends a poor prognosis. Biot breathing is characterized by
irregularly irregular breaths of equal depth that are associated
with periods of apnea. It can be seen in patients with intracranial
disease affecting the medulla oblongata. More severe damage to
the medulla oblongata results in ataxic respiration, the complete
irregularity of breathing, with irregular pauses and increasing
periods of apnea. As this breathing pattern deteriorates further,
it merges with agonal respiration.
Orthopnea (shortness of breath while supine) is most commonly present in patients with heart failure and pleural effusion,
but also can occur with ascites, morbid obesity, and diaphragmatic
paralysis. Alternatively, platypnea (shortness of breath when
assuming the upright position) suggests the right-to-left shunting
that occurs with an atrial septal defect or intrapulmonary shunt.
Trepopnea (shortness of breath while lying on one side) occurs
with a right pleural effusion or with unilateral lung or diaphragm
CHAPTER 3 Physical Examination in the Cardiac Intensive Care Unit 29
https://t.me/medicina_free
TABLE 3.1 Breathing Patterns
Respiratory Pattern Consider Eponym/Classification
Deep and rapid Diabetic ketoacidosis Kussmaul respiration
Snoring with episodic apnea Obstructive sleep apnea
Waxing and waning tachypnea/hypopnea alternating with apnea Oversedation Cheyne-Stokes breathing
Heart failure
Severe CNS process
Respiratory failure
Renal disease (uremia)
Irregularly irregular (yet equal) breaths alternating with periods
of apnea
Completely irregular breaths (pauses with escalating periods of
apnea)
No breaths or occasional gasps Severe cardiovascular or neurologic disease Agonal breathing
CNS, Central nervous system.
Damage to the medulla oblongata
(intracranial disease)
Severe damage to the medulla oblongata Ataxic respiration
Biot breathing
disease when the healthy lung is down.
4,5
Bendopnea, or shortness
of breath when bending over, is a sign of heart failure.
Pulse
The pulse should be assessed bilaterally for presence, rate, volume,
contour, and regularity. An initial examination should always
contain a description of the radial and carotid arteries, in addition
to the brachial, femoral, popliteal and pedal pulses. This examination is important for patients with hypotension, claudication,
arterial insufficiency, or cerebrovascular accident and after
intraaortic balloon pump insertion. Assessing the pulse for 30
seconds is more accurate than counting for only 15 seconds.
A discrepancy in bilateral upper extremity pulses (especially
with decreases in rate or volume on the left side) raises the
possibility of aortic dissection, subclavian narrowing secondary
to atherosclerosis, or congenital webs. If such a discrepancy is
present, the examiner should search for evidence of a subclavian
steal phenomenon, detected as a decrease in pulse amplitude
after raising or exercising the affected arm for approximately 45
seconds (the left side is affected 70% of the time; the reduction
in systolic blood pressure is >20 mm Hg 94% of the time).7
Aortic dissection is suggested by the presence of a pulse deficit,
focal neurologic signs, and mediastinal widening on the chest
radiograph.8 Diminished lower extremity pulses are consistent
with coarctation of the aorta or atherosclerotic disease of the
abdominal aorta and/or the arterial supply of the lower extremities. Although the detection of low femoral pulse amplitude (or
its absence) is crucial for assessing the risk-to-benefit ratio in
patients who may require vascular access or device implantation,
its diminution or absence after catheterization or intraaortic
balloon pump implantation requires urgent investigation.
When tachycardia (heart rate >100 beats/min) is present, the
regularity of the rhythm offers important diagnostic clues. Regular
rhythm rates between 125 beats/min and 160 beats/min suggest
sinus tachycardia, the presence of atrial flutter with 2 : 1 block,
or ventricular tachycardia. The presence of intermittent cannon
A waves in the neck veins is highly sensitive, whereas a changing
intensity of the first heart sound (S1) is highly specific for the
detection of ventricular tachycardia.9 Atrial flutter may be
accompanied by rapid undulations in the jugular venous pulse
6
(flutter waves or F waves). Because sinus tachycardia may be
due to correctable causes, such as hypovolemia, hypoxia, infection,
hyperthyroidism, anemia, or anxiety, or may be due to the
pathologic adaptation occurring with chronic heart failure or
myocardial ischemia, integration of these clinical suspicions with
the nature of the underlying rhythm is important. The use of
vagal maneuvers may help differentiate the causes of narrowcomplex tachycardia.
The Valsalva maneuver, performed by asking the patient to
bear down as if “having a bowel movement” or pushing up the
abdomen against the examiner’s hand placed on the middle of
the abdomen, may be more effective than carotid sinus massage,
performed by pressing on the neck at the bifurcation of the
carotid artery just below the angle of the jaw, at terminating
supraventricular tachycardia.
10,11
Paroxysmal supraventricular
tachycardia (nodal reentry and reciprocating tachycardias) may
be interrupted with enhanced vagal tone. Sinus tachycardia, atrial
flutter, and atrial fibrillation may slow only transiently (to reveal
the underlying rhythm), although an abrupt halving of the rate
can occur with atrial flutter. Detection of an irregular tachycardia
on physical examination suggests atrial fibrillation, atrial premature beats, or ventricular premature contractions. In atrial
fibrillation, assessment of the apical rate (counting heartbeats
via auscultation) is more accurate than counting the radial pulse,
accounting for a “pulse deficit.”
12
Bradycardia (heart rate <50 beats/min) may be appropriate
in trained athletes, but should be asymptomatic and associated
with a gradual increase in heart rate with exercise.13 Detection
of a regular bradycardia in a patient with fatigue, mental status
changes, or evidence of impaired peripheral perfusion or pulmonary congestion raises the possibility of pharmacologic toxicity
(i.e., digoxin, β-blockers, or calcium channel blockers), hypothermia (owing to hypothyroidism or exposure), or an atrioventricular nodal or ventricular escape rhythm that occurs with
complete heart block or sick sinus syndrome.
Appreciation of the pulse volume and contour is also informative (Table 3.2). Tachycardia with a bounding pulse is present
with septic shock (owing to the acute reduction in afterload),
hyperthyroidism, or—in combination with the sudden collapse
of the pulse—with chronic aortic insufficiency (a “water hammer”
30 PART I Introduction
https://t.me/medicina_free
TABLE 3.2 Pulse Characteristics
Pulse Description Consider
Bounding Septic shock, hyperthyroidism, chronic AI
Weak and thready Severe LV dysfunction, hypovolemia,
severe MR, complete heart block,
pericardial effusion
Slow rising and weak Severe AS
Alternating between strong
and weak
Double tap (pulsus bisferiens) Hypertrophic cardiomyopathy, AS with AI
AI, Aortic insufficiency; AS, aortic stenosis; LV, left ventricular; MR,
mitral regurgitation.
LV dysfunction, pericardial tamponade
pulse). Consistent with the presence of chronic aortic insufficiency
is the accentuation of the radial pulse when the examiner lifts
the whole arm above the patient’s head (Mayne’s sign). A weak
and thready pulse may be present with severe LV dysfunction,
hypovolemia, severe mitral regurgitation, or complete heart block.
A weak and slow-rising carotid pulse (pulsus parvus et tardus)
is consistent with a diagnosis of severe aortic stenosis, whereas
a regular pulse that alternates between weak and strong (pulsus
alternans) occurs with LV dysfunction or, when weakening of
the pulse is associated with inspiration, pericardial tamponade.
A “double tap” of the pulse during systole (pulsus bisferiens), a
small one followed by a stronger and broader one, can occur
with either hypertrophic cardiomyopathy or the combination
14,15
of aortic stenosis and aortic insufficiency.
In the presence of
a bisferiens pulse, two soft and rapid sounds can be auscultated
with each cardiac cycle as the brachial artery is compressed by
a blood pressure cuff proximally.
16
Irregular rhythms are classified as either regularly irregular,
in which the irregular beat can be anticipated at a fixed interval,
or irregularly irregular, in which the irregular beat occurs without
predictability. A regularly irregular pulse commonly occurs with
second-degree atrioventricular block (either Mobitz I or II,
depending on whether the PR interval is constant or lengthening
before the dropped beat) or with interpolated ventricular premature beats. On the physical examination, the PR interval can
be visualized as the distance between the a wave and c wave on
the jugular venous pulse (JVP). This distance, before and after
the dropped beat, can be diagnostic when the electrocardiogram
(ECG) is unable to differentiate between Mobitz type I and Mobitz
type II second-degree block. When an interpolated ventricular
premature beat is present, it may be accompanied by a weakened
pulse (owing to inadequate ventricular filling) that occurs at a
fixed interval from the regular pulse.
An irregularly irregular pulse implies that the examiner cannot
anticipate when the next beat will occur and may be due to
ventricular premature beats, atrial premature beats, multifocal
atrial tachycardia, or atrial fibrillation. Although ventricular
premature beats and atrial fibrillation are associated with a pulse
deficit (in which the auscultated apical rate is greater than the
palpable radial pulse), the impulse that follows a ventricular
premature beat should be stronger. It is clinically relevant to
realize that significant numbers of ventricular premature beats
can compromise cardiac output. Alternatively, if the beat following
a ventricular premature beat is diminished (Brockenbrough sign),
hypertrophic cardiomyopathy or severe LV dysfunction should
be considered. No pulse deficit (or compensatory pause) should
be present with atrial premature beats or multifocal atrial
tachycardia. The physician can differentiate atrial premature beats
from ventricular premature beats by tapping out the rhythm
with one’s finger. Atrial premature beats result in a beat that
occurs while the finger is “up.” Although a ventricular premature
beat also occurs with the finger in the “up” position, the pulse
resumes on the second down beat after the compensatory pause.
Blood Pressure
In the CICU, there is no rule defining “normal” blood pressure.
Adequate blood pressure varies by patient and clinical status but
is generally believed to consist of a mean perfusion pressure of
at least 60 mm Hg and the absence of end-organ hypoperfusion.
For accurate assessment, an adequately sized blood pressure cuff
must be used (there are lines on all blood pressure cuffs to indicate
adequate sizing) and should be correctly situated around the
bicep (and not over clothing). A blood pressure obtained with
a cuff that is too short or narrow, especially if the patient is
obese or has an enlarged upper arm, may result in a factitiously
elevated blood pressure.
Although palpation of pulses is commonly used in emergency
situations to estimate systolic blood pressure (i.e., palpation of
a radial pulse suggests a minimum systolic blood pressure of
80 mm Hg; a femoral pulse, a blood pressure of at least 70 mm
Hg; and a carotid pulse, a blood pressure of at least 60 mm Hg),
the overall accuracy of this estimation has been questioned.19
To obtain the palpable systolic blood pressure, the cuff should
first be inflated until the radial pulse is no longer palpable (usually
150 to 200 mm Hg) and then slowly deflated (2 to 3 mm Hg
per second) until the pulse returns.
For the auscultatory blood pressure, inflation should be
repeated (inflate the cuff to 10 mm Hg above the palpable systolic
blood pressure) and listen for the first and fifth (last audible)
Korotkoff sounds during slow cuff deflation. The diastolic blood
pressure may be difficult, if not impossible, to appreciate in the
presence of fever, severe anemia, aortic insufficiency, thyrotoxicosis, vitamin B1 deficiency, or Paget disease. For patients in
atrial fibrillation or with significant ventricular arrhythmias, a
relatively accurate blood pressure assessment is obtained by
averaging three individual readings.
In patients with LV systolic dysfunction, multiple etiologies of
hypotension require assessment during the physical examination.
Although hypotension may be caused by overly aggressive diuresis,
it may also occur because of volume overload. The presence of
a tachycardia with orthostatic hypotension (a blood pressure
decrease of >
20 mm Hg systolic or >10 mm Hg diastolic when the
patient is assessed first in the supine position and then again after
2 minutes with the patient standing or sitting with legs dangling)
is consistent with volume depletion. The differential diagnosis
of hypotension includes factors that reduce systemic vascular
resistance (e.g., infection, inflammation, adrenal insufficiency,
anesthetic agents, atrioventricular malformations, and vascular
insufficiency), stroke volume (e.g., hypovolemia; aortic stenosis;
severe mitral regurgitation; ventricular arrhythmias; and LV
17,18
CHAPTER 3 Physical Examination in the Cardiac Intensive Care Unit 31
https://t.me/medicina_free
dysfunction owing to infarction, ischemia, or a cardiomyopathy),
and heart rate (e.g., heart block or pharmacologic bradycardia).
Hypotension without a concomitant increase in the pulse
rate (in the absence of medications that can blunt a heart rate
response) raises the possibility of autonomic dysfunction. The
presence of a pulsus paradoxus (a >10 mm Hg decrease in
systolic blood pressure occurring at end expiration with the
patient breathing normally) can occur with cardiac tamponade
(very sensitive when occurring with tachycardia, jugular venous
distention, and an absent y descent),
(occurring with jugular venous distention that persistently augments with inspiration, a pericardial knock, hepatomegaly, and
an exaggerated y descent),22 severe hypertension, pulmonary
embolism, COPD, and severe obesity.
With appropriate clinical scenarios, blood pressure should
also be assessed in both arms and one leg. Leg blood pressure
can be assessed by placing the blood pressure cuff around the
calf and using the dorsalis pedis pulse for auscultation or Doppler
interrogation. A systolic blood pressure difference greater than
10 mm Hg between arms suggests aortic dissection, proximal
aortic aneurysm, or subclavian artery stenosis. With coarctation
of the aorta, arm blood pressures are greater than blood pressures
in the legs (this may also be accompanied by underdeveloped
lower extremity musculature compared with upper extremity
musculature). Leg blood pressure that is more than 15 mm Hg
higher than arm blood pressure suggests aortic dissection, aortic
insufficiency, or a proximal vasculitis (i.e., giant cell or Takayasu
arteritis).
The pulse pressure (systolic blood pressure – diastolic blood
pressure) may also be informative. A low pulse pressure may be
present with the decreased stroke volume of hypovolemia,
tachycardia, severe aortic or mitral stenosis, pericardial constriction, or cardiac tamponade. With appropriate clinical suspicion,
it has a high sensitivity and specificity to predict a cardiac index
less than 2.2 L/min per m2 when the pulse pressure divided by
the systolic pressure is less than 0.25. A wide pulse pressure
(>60 mm Hg) can be seen with hyperthermia but may also suggest
severe chronic aortic insufficiency or high output failure owing
to severe anemia, thyrotoxicosis, atrioventricular malformation,
sepsis, vitamin B1 deficiency, or Paget disease. If the wide pulse
pressure is present in just one arm, a search for an atrioventricular
fistula distal to the site of the blood pressure cuff should be
undertaken.
20,21
constrictive pericarditis
Weight
The daily weight is an important vital sign. Ideally, patients should
be weighed on a scale and not in the bed to obtain the most
accurate measurement. Monitoring the daily weight often proves
to be especially helpful for patients in whom volume overload
or hypovolemia is a clinical concern. When a weight appears
inconsistent with prior weights or the clinical history, the clinician
should not hesitate to have the patient reweighed. Noting an
increase in weight may be crucial to discern the presence of
volume overload in a patient with shortness of breath, whereas
loss of weight should occur in patients being diuresed. A weight
gain despite the presence of effective diuresis suggests increased
fluid intake, either orally or via the intravenous route.
HEAD, EYES, EARS, NOSE, AND
THROAT EXAMINATION
In the presence of an endotracheal or nasogastric tube, the
physician first should ensure that the tube is not causing a
pressure injury. If the patient has a central line or pulmonary
artery catheter, the physician must ensure that it is secured and
uninfected. The head, eyes, ears, nose, and throat examination
can also suggest the presence of several syndromes.
In adults, a large skull suggests Paget disease (with associated
high-output heart failure) or acromegaly (with frontal bossing
and large features). A high arched palate, associated with a wide
pulse pressure and pectus excavatum, is consistent with Marfan
syndrome. Coarse hair texture or hair loss from the head, axilla,
or pubic region suggests hypothyroidism. Temporal artery tenderness suggests temporal arteritis.
Eyelid xanthelasma or a corneal arcus may occur with either
hypercholesterolemia or diabetes mellitus. Yellowed sclera are
seen with hyperbilirubinemia, whereas blue sclera can be seen
in Marfan and Ehlers-Danlos syndromes. Dry, puffy, and sunken
(enophthalmic) eyes are consistent with hypothyroidism, whereas
exophthalmic eyes (white sclera visible between the margin of
the upper eyelid and the corneal limbus with the patient looking
downward) associated with a lid lag (an immobility or lagging
of the upper eyelid on downward rotation of the eye) and lid
retraction (widening of the palpebral fissure) are associated with
hyperthyroidism. Periorbital edema is seen with the hypoalbuminemia of hepatic disease, a protein-losing nephropathy, or
the superior vena cava syndrome. The lack of periorbital edema
with diffuse peripheral edema is a distinguishing feature of a
cardiac versus hepatic or renal causes of peripheral edema. It
is due to the inability of patients with heart failure and severe
volume overload to elevate their upper torso to breathe more
comfortably. Conjunctival pallor is a very specific sign of anemia;
this diagnosis is reinforced by the presence of concomitant palmar
and palmar crease pallor.
When firmly palpating the patient’s thyroid gland with the
neck flexed (to relax the sternohyoid and sternocleidomastoid
muscles), significant findings can include an enlarged thyroid
(size appreciated larger than an inch) and the presence of nodules
(4% prevalence; most are benign). It is important to note the
size and site of these nodules for follow-up examinations.
swallowing, the thyroid gland rises upward with the trachea to
allow location of a neck mass either within or outside the thyroid
gland.
23
24
During
JUGULAR VENOUS PULSE AND
ABDOMINOJUGULAR REFLUX
The internal jugular venous pulse (JVP) is a useful manometer
for central venous or right atrial pressure (Video 3.2). However,
it is accurate only in indicating intravascular volume status and
pulmonary capillary wedge pressure (PCWP) in the absence of,
among other things, tricuspid stenosis, right ventricular (RV)
dysfunction, pulmonary hypertension, and a restrictive or
constrictive cardiomyopathy. The JVP should be sought by first
asking the patient to lift the chin up and turn to the left against
32 PART I Introduction
Carotid pulse
Venous pulse
Heart sounds
EKG
PT
QRS
https://t.me/medicina_free
Fig. 3.1 Timing of jugular venous pressure. ECG, Electrocardiogram.
the resistance of the examiner’s right hand. Within the triangle
formed by the visible heads of the sternocleidomastoid muscle
and the clavicle, the examiner should then search, with the neck
muscles relaxed, for the weak impulses of the jugular vein along
a line from the jaw to the clavicle. Shining a tangential light
from slightly behind the neck can accentuate the visibility of
the transmitted venous impulses. Simultaneous palpation of the
radial pulse, assuming that the patient is in sinus rhythm, allows
detection of a neck pulsation (a wave) immediately preceding
the peripheral pulse (Fig. 3.1). Alternatively, one can visualize
the x descent as an inward movement along the line of the jugular
vein that occurs simultaneously with the peripheral pulse.
In patients with presumed volume overload, jugular venous
distention may be best assessed with the patient sitting upright,
a position in which the clavicle is approximately 7 to 8 cm above
the right atrium (equivalent to the upper limit of normal for
right atrial pressure, 5 to 7 mm Hg). The 7 to 8 cm is added to
the maximal vertical distance at which any venous pulsations
are seen above the clavicle to estimate the right atrial pressure.
If the JVP cannot be appreciated in the upright position, an
attempt can be made to visualize it sequentially with the upper
body at a 45-degree angle (where only 4 to 5 cm is needed to
the distance above the clavicle where the venous pulsations were
seen). If venous pulsations are still difficult to discern, either of
two extremes may be present: either there is no elevation of the
right atrial pressure or the jugular venous pressure is so far above
the angle of the jaw, even in the upright position, it is lost in
the hairline. The ear lobe should always be assessed for movement
in these cases.
A low right atrial pressure may be investigated further by
increasing right atrial filling (i.e., with deep inspiration or passive
leg elevation). The left internal jugular vein is less useful than
the right internal jugular vein for estimation of right atrial pressure
because of the presence of valves impeding venous return or
compression of the innominate vein. When it must be used,
right atrial pressure should be considered approximately 1 cm
lower than the visualized left internal jugular pulse.
the external jugular veins should be avoided in assessing jugular
venous pressure because of the extreme angle with which they
contact the superior vena cava and their occasional absence or
diminution in the presence of elevated catecholamine levels.
Although the value of sequential assessment of the JVP has
been confirmed by studies of patients with LV dysfunction,28
patients undergoing cardiac catheterization for dyspnea or chest
pain,29 and patients with suspected chronic heart failure,
CA
X
X
V
'
Y
is important to confirm these findings with additional signs of
volume overload in the acute setting.
33,34
When an increasing
creatinine value is seen despite the presence of an elevated jugular
30–32
it
venous pressure (with or without diuresis), the differential
S
1
S
2
diagnosis includes refractory LV dysfunction requiring inotropic
support, severe RV dysfunction, restrictive or constrictive cardiomyopathy or right heart failure, or underlying renal dysfunction (cardiorenal syndrome) or renovascular disease. With RV
dysfunction, the assessment of JVP as a measure of PCWP
becomes progressively less accurate. The JVP measured in cm
of H2O is converted to mm Hg by multiplying by 0.735.
Abdominojugular reflux is present when the height of the
neck vein distention, visualized with the patient’s neck at a
45-degree angle, is increased by at least 3 cm (and maintained
for approximately 15 seconds) during a steady pressure of
approximately 20 to 35 mm Hg applied over the right upper
quadrant or mid-abdomen. (You can learn what exerting 20 to
35 mm Hg of pressure feels like by compressing an inflated blood
pressure cuff against a flat surface until the sphygmomanometer
reads 30 mm Hg; Video 3.2.) It is important to instruct patients
not to hold their breath because the Valsalva maneuver negates
the effect of abdominal pressure. The increased abdominal
pressure on the mesenteric or splanchnic veins increases venous
return to the RV. With RV or biventricular heart failure (and
the limited ability to increase RV and LV output), distention of
the internal jugular vein occurs. A positive abdominojugular
reflux may also occur with tricuspid stenosis, tricuspid insufficiency, constrictive pericarditis, restrictive cardiomyopathy,
pulmonary hypertension, and mitral stenosis. Although limited
data are available in the CICU setting, abdominojugular reflux
in patients presenting to the emergency department had a low
sensitivity (33%) but a high specificity (94%; P = .028) for the
diagnosis of heart failure. However, its sensitivity significantly
increases in patients with known chronic congestive heart failure32;
when the abdominojugular reflux is absent, it cannot be taken
as evidence against the diagnosis of heart failure.
35
CHEST AND LUNG EXAMINATION
The thorax should first be examined for the presence of an old
sternotomy (suggesting prior coronary artery bypass grafting,
valve replacement, or other heart surgery) or thoracotomy scars
(suggesting prior pulmonary pathology). If the patient is intubated, the physician needs to ensure that both sides of the chest
are expanding evenly (Video 3.3).
Although Laënnec’s invention of the stethoscope rendered
obsolete the need for the physician to place the ear directly against
25,26
Likewise,
the chest wall to appreciate heart and lung sounds, modern
technology has yet to replace the need for daily auscultation of
the lungs via the stethoscope (Table 3.3). The waning ability of
physicians to appreciate abnormalities in the lung examination
undoubtedly limits the information available for patient manage-
27
36
The lungs should be auscultated in an alternating and
ment.
CHAPTER 3 Physical Examination in the Cardiac Intensive Care Unit 33
https://t.me/medicina_free
TABLE 3.3 Auscultation of the Lungs
Breath Sound Consider
Rhonchi
Diffuse COPD
Localized Pneumonia, tumor, foreign body
Stridorous Large airway obstruction
Wheezes
Expiratory Reactive small airway obstruction (asthma, allergies,
β-blockers)
De novo Nonasthmatic causes (mass, pulmonary embolism,
pulmonary edema, aspiration, foreign body)
Crackles or rales Pulmonary edema, interstitial lung disease, COPD,
amiodarone toxicity
COPD, Chronic obstructive pulmonary disease.
comprehensive fashion (Videos 3.4A and 3.4B). Although the
diaphragm of the stethoscope is used to detect most normal and
pathologic lung sounds, the bell is more advantageous for detecting the rhonchi associated with primary tuberculosis or fungal
disease in the apices.
Crackles (or rales) are discontinuous lung sounds (that sound
like Velcro being pulled apart) generated when abnormally closed
alveoli snap open, usually at the end of inspiration (Audio 3.1).
37
However, “clear lungs” may be present in 25% of patients presenting with heart failure.31 The Boston Criteria for Heart Failure
gives 1 point if the crackles are basilar and 2 points if they extend
further.38 Crackles have a low sensitivity but high specificity to
predict the presence of LV dysfunction or an elevated PCWP.
29,30,32
Crackles may also be caused by interstitial lung disease, amiodarone toxicity, pulmonary fibrosis, or COPD (Audio 3.2).
39
Rhonchi (coarse, dry, leathery sounds) are present in the
setting of large airway (bronchial) turbulent flow caused by
inflammation and congestion and are associated most commonly
with pneumonia or COPD. When detected, it should be noted
whether they occur during inspiration or expiration and whether
they are generalized or localized. Diffuse rhonchi suggest generalized airway obstruction that occurs with COPD. Localized rhonchi
suggest pneumonia or obstruction owing to tumor or a foreign
body. Generally, rhonchi caused by mucous secretions subside
or disappear altogether with coughing. Stridor refers to loud,
audible inspiratory and, possibly, expiratory rhonchi that suggest
extrathoracic large airway obstruction (Audio 3.3).
The presence of wheezes (continuous and high-pitched musical
sounds) that occur during expiration often denotes reactive small
airway obstruction (Audio 3.4). Because airway size is reduced
in the recumbent position, wheezing should worsen when lying
down. When accompanied by a prolonged expiratory phase,
wheezes signify the presence of airflow through a narrowed
tract that is often seen with asthma, allergies, or the toxic effects
associated with β-blockade. In some patients, the presence of
pulmonary edema may result in musical breath sounds similar
to wheezes, called cardiac asthma. When wheezing is detected
de novo in an older patient, a search for nonasthmatic causes,
including obstructing masses, pulmonary embolism, pulmonary
edema, aspiration pneumonitis, and foreign-body obstruction is
warranted.40 Decreased or absent breath sounds in a lung field
are consistent with atelectasis, pneumothorax, pleural effusions,
COPD, acute respiratory distress syndrome, or pleural thickening
(Audio 3.5).
Egophony (when a verbalized “e-e-e” is appreciated via
auscultation as an “a-a-a”) occurs in the presence of a pleural
effusion but can also be heard with lung consolidation and
pneumonia (Audio 3.6). Although not sensitive, egophony is
specific for a parapneumonic process.41 Lung consolidation can
be confirmed further by the presence of bronchophony (when
“clearer” voice sounds are heard over consolidated lung tissue).
Bronchial breath sounds (breath sounds that are louder than
normal; Audio 3.7) are also heard when consolidation of lung
tissue is present because solid tissue transmits sound better than
tissue filled with air (Audio 3.8). When bronchial breath sounds
are heard and accompany a dull area to percussion at the base
of the left scapula, it suggests the presence of a large pericardial
effusion (the Ewart sign).
Percussion of the chest can provide important information
about lung pathology (Videos 3.5 and 3.6). Expected percussion
sounds are summarized here (Video 3.7). Dullness to percussion
at the lung base suggests the presence of pleural effusion and,
rarely, lung consolidation. If the percussive dullness responds
to postural changes (i.e., diminution in the left lateral decubitus
position), a pleural effusion is likely present.42 Although left-sided
pleural effusions are common after chest surgery (e.g., coronary
artery bypass graft surgery after left internal mammary artery
dissection) and with pancreatitis or pancreatic cancer, bilateral
or right-sided effusions are more consistent with heart failure.
Pleural effusions may also occur with pneumonia, hypoalbuminemia (seen with nephrotic syndrome or cirrhosis), and nearly
all types of malignancy.
THORAX AND HEART EXAMINATION
The thorax should be appreciated by looking upward at the chest
from the foot of the bed. This view may reveal a pectus excavatum
(a congenital anterior chest wall deformity producing a concave,
or caved-in, appearance that suggests Marfan or Ehlers-Danlos
syndrome or right heart failure), pectus carinatum (an outward
“pigeon chest,” protrusion of the anterior chest wall associated
with decreased lung compliance, progressive emphysema, and
a predisposition to respiratory tract infections), and barrel chest
deformities (with increased anteroposterior chest diameters that
may be observed with obstructive forms of chronic pulmonary
disease, such as COPD, cystic fibrosis, and severe asthma).
When the examiner is positioned on the right side of the
patient, visi ble or palpable precordial pulsations may be appreciated owing to a thin body habitus or secondary to cardiac disease.
Pulsations in the second intercostal space to the left of the sternal
border suggest an elevated pulmonary artery pressure, whereas
pulsations seen in the fourth intercostal space at the left sternal
border are consistent with RV dysfunction or an acute ventricular
septal defect. Apical pulsations may be secondary to systemic
hypertension, LV hypertrophy, hemodynamically significant aortic
stenosis, or an LV aneurysm. With the examiner standing on
the right side of the patient, the LV apex or point of maximal
34 PART I Introduction
https://t.me/medicina_free
impulse (PMI) is palpated by placing the right hand transversely
across the precordium under the nipple and is perceived as an
upward pulsation during systole against the examiner’s hand
(Video 3.8). A normal PMI is depicted here (Video 3.9). An
enlarged apical impulse is variously described as an impulse
detected more than 2 cm to the left of the midclavicular line in
the fifth intercostal space or as greater than the size of a quarter
and palpable in at least two interspaces. Recognition may be
enhanced with the patient in the left lateral decubitus position
or when sitting up and leaning slightly forward.
Detection of LV enlargement is a function of age: it increases
steadily for men and women, occurring in 66% of men and 58%
of women in the 65- to 69-year age range and 82% of men and
79% of women older than 85 years.43 It has a sensitivity of approximately 65% and a specificity of 95%, with a negative predictive
value of 94% for LV systolic dysfunction.30 Although obesity
may limit the detection of the LV apical impulse, a displaced
impulse is effective in suggesting the diagnosis of heart failure,
even in patients with COPD.44 Fluid or air in the right pleural
cavity, a depressed sternum, and secondary retraction of the left
lung and pleura all can result in an apparent augmentation of
the LV impulse, however.45 LV enlargement is suggested further
by the presence of a sustained apical impulse (persisting more
than halfway between S1 and S2 during simultaneous auscultation
and palpation). A shifted PMI as seen with LV hypertrophy is
illustrated here (Video 3.10). If the LV apical impulse is detectable
at end-systole, a dyskinetic ventricle is most likely. If the apical
impulse seems to retract during systole, the presence of constrictive pericarditis or tricuspid regurgitation should be considered.
All auscultatory fields should be palpated with the fingertips
to detect a thrill (required for the diagnosis of a grade IV/VI
murmur). In addition, the presence of a palpable P2 (an upward
pulsation during diastole in the pulmonic position) suggests the
presence of either secondary (acute pulmonary embolism, chronic
mitral regurgitation, or stenosis) or primary pulmonary hypertension. When a pulsation is palpable in the aortic position during
systole, it suggests either hypertrophic cardiomyopathy or severe
aortic stenosis. Its presence over the left sternal border in the
fourth intercostal space, especially in the setting of an acute MI,
raises the possibility of a ventricular septal defect. A presystolic
impulse (correlating with the a wave and equivalent to an audible
) suggests ventricular noncompliance and may be present with
S
4
myocardial ischemia or infarction, with LV hypertrophy secondary
to hypertension, aortic stenosis, acute mitral regurgitation, or
hypertrophic cardiomyopathy.
Auscultation of the Heart
Cardiac auscultation in the CICU setting allows for the detection
of common holosystolic (mitral regurgitation and ventricular
septal defect), systolic ejection (aortic stenosis or hypertrophic
cardiomyopathy), and diastolic (aortic insufficiency and mitral
stenosis) murmurs that can precipitate or exacerbate a decompensation in the CICU or the presence of abnormal heart sounds
(S1, S2, S3, S4) indicating underlying pathology (Table 3.4). While
rapid assessment can often be lifesaving, it should not replace
a more systematic investigation when acute stabilization has
occurred.
TABLE 3.4 Clinical Auscultation of S
, and S
S
3
Heart Sound Consider
S
1
Accentuated Atrial fibrillation, mitral stenosis
Soft Immobile mitral valves, MR, or severe AI
S
2
Accentuated (P2) Pulmonary hypertension; (A2) systemic
Soft (A
-P2 Splitting
A
2
Wide Severe MR, RBBB, atrial septal defect (secondary),
Paradoxical Severe TR, WPW, LBBB, severe hypertension, or AS
Fixed Large atrial septal defect, severe RV failure
S
3
Present Heart failure, HOCM, thyrotoxicosis, AV fistula, sepsis,
S
4
Present Ischemic or infarcted LV, hypertrophic, dilated, or
AI, Aortic insufficiency; AS, aortic stenosis; AV, atrioventricular;
HOCM, hypertrophic obstructive cardiomyopathy; LBBB, left bundle
branch block; MR, mitral regurgitation; RBBB, right bundle branch
block; TR, tricuspid regurgitation; WPW, Wolff-Parkinson-White.
S1, S2, S3, and S
4
hypertension; aortic dilation
) AI, sepsis, AV fistula
2
pulmonary hypertension
hyperthermia
restrictive cardiomyopathy
4
, S2,
1
An understanding of the cardiac events of systole and diastole
is required before performing auscultation (Video 3.11).
S1, best appreciated as a high-pitched and split sound at the
cardiac apex, is produced at the time of mitral (M1) and tricuspid
(T1) valve closure and occurs before the upstroke of the peripheral
pulse (Audio 3.9). An accentuated S1 is present when the mitral
or tricuspid valves are widely separated in diastole (e.g., with
atrial fibrillation, with a shortened PR interval, or in the presence
of an obstructing myxoma) or with mitral or tricuspid valves
that are difficult to open (e.g., mitral or tricuspid stenosis when
the valves have become calcified). When a stenotic valve becomes
nearly immobile, however, the intensity of S
decreases. A soft
1
S1 may be present when the valves are already nearly closed at
the onset of systole, as occurs with moderate to severe aortic
insufficiency, with advanced heart failure, with a prolonged
PR interval or when the mitral valves are incompetent (from
papillary muscle dysfunction, ventricular dilation, or myxomatous
degeneration).
S2, which occurs at the time of closure of the semilunar aortic
(A2) and pulmonary (P2) valves, is probably caused by the
deceleration of blood in the root of the pulmonary artery and
aorta at end-systole. It is best appreciated in the second intercostal
space, midclavicular line (pulmonic position) using the diaphragm
of the stethoscope (Audio 3.10). Normally, the intensity of A2
exceeds the intensity of P2. A soft A2 can occur in the setting of
incompetent aortic valves (e.g., aortic insufficiency), a decrease
Соседние файлы в папке Библиотека им академика М.И. Перельмана