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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3230_Библиотеки_им_академика_М_И_Перельмана
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CHAPTER 6 Cardiovascular symptoms
142
Bilateral ankle swelling
Think of increased pressure within the veins or lymphatic vessels or low
albumin in the vascular space, bilateral damage to veins, lymphatics, or
capillaries due to local inflammation.
Some differential diagnoses and typical outline evidence
Right ventricular
failure
due to
pulmonary
vascular disease
or CHF
Suggested by: jugular venous distension, edema, liver
enlargement and pulsation, right ventricular (RV)
heave. Onset over months, usually
Confirmed by: elevation of central venous pressure
(CVP) using a central venous catheter or elevation of
right arterial (RA) and RV pressures during right heart
catheterization, dilated RV on echocardiogram
Poor venous
return
due to abdominal
or pelvic masses,
post-phlebitic or
thrombotic
venous damage
Suggested by: onset over months. Worse on prolonged
standing or sitting, varicosities, venous eczema,
pigmentation or ulceration. Non-pitting edema if chronic
Confirmed by: clinically with Trendelenberg test
showing filling along extent of communicating valve
leaks or on venous Doppler ultrasound
Low albumin
states
caused by liver
failure, nephrotic
syndrome,
malnutrition, etc.
Suggested by: generalized edema often including face
after lying down. Onset usually over months
Confirmed by: low serum albumin
Bilateral
cellulitis
often associated
with diabetes
mellitus
Suggested by: warm, red, and tender legs, thrombo-
phlebitis and tracking, ulcers, etc. Onset over days
Confirmed by: positive blood cultures (usually
streptococcal or staphylococcal) (blood sugar i in
diabetes)
Inferior vena
cava (IVC)
obstruction
due to prolonged
immobility, carci-
noma, and oral
combined con-
traceptive use)
Suggested by: bilateral leg-swelling onset over hours,
associated risk factors (obesity, smoker, FH).
Symptoms of PE.
Confirmed by: CT abdomen, low flow on Doppler
ultrasound scan, or filling defect on venogram.
BILATERAL ANKLE SWELLING1
143
Bilateral
thromboses
Suggested by: onset over hours, risk factor of obesity,
history of immobility, carcinoma, oral contraceptive
use. Associated with PE. Leg(s) firm, warm, tender
Confirmed by: no flow on Doppler ultrasound scan
Impaired
lymphatic
drainage
Suggested by: firm, non-tender, non-pitting edema of
gradual onset over months to years
Confirmed by: obstruction to flow on lymphangiogram
(rarely done)
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Chapter 7
145
Cardiovascular signs
Thoughts on interpreting cardiovascular signs 146
Peripheral cyanosis 147
Central cyanosis 148
Tachycardia (pulse rate >100 bpm) 149
Bradycardia (<60 bpm) 150
Pulse irregular 151
Pulse amplitude high (bounding pulse) 152
Pulse amplitude low (thready pulse) 153
Blood pressure high (hypertension) 154
Blood pressure very low (hypotension) 156
Postural fall in blood pressure
(orthostatic hypotension) 157
BP/pulse difference between arms 158
BP/pulse difference between arm and legs 159
Prominent leg veins ± unilateral leg swelling 160
Unilateral leg and ankle swelling 162
Bilateral leg and ankle swelling 164
Raised jugular venous pressure 166
Abnormal apical impulse 168
Extra heart sounds 170
Diastolic murmur 171
Systolic murmur 172
Murmurs not entirely in systole or diastole 174
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CHAPTER 7 Cardiovascular signs
146
Thoughts on interpreting
cardiovascular signs
The findings are discussed in a sequence of the CV examination, thinking
of cardiac output, beginning with hand warmth, checking the radial pulse,
and measuring the BP. Continuing to think of cardiac output, examine the
carotids. Next think of venous return by inspecting the JVP. Finally, inspect,
palpate, percuss, and auscultate the heart. Examine the legs, and again
think of cardiac output (e.g., temperature of skin, peripheral pulses) and
venous return (e.g., pitting edema, leg veins, and liver enlargement).
PERIPHERAL CYANOSIS1
147
Peripheral cyanosis
This includes cyanosis of the hands but not the lips or tongue.
Main differential diagnoses and typical outline evidence
Raynaud’s
phenomenon
due to exposure of
hands to cold or
vibration
Suggested by: normal pulse and BP, history of blue
hands after exposure to cold, vibrating tools, etc.;
history of scleroderma
Confirmed by: hands and feet assume normal color in
warm room
Arterial
obstruction
due to atheroma
or small vessel
disease in
diabetics
Suggested by: absent or poor or asymmetric radial or
dorsalis pedis pulses. Absent hair and skin atrophy in
chronic cases
Confirmed by: Doppler ultrasound measure of low
blood flow and angiography
Hemorrhage
due to external or
internal
bleeding
Suggested by: pallor, sweating, low BP
, high pulse
rate, observable external bleeding or melena or
massive trauma expected to cause internal bleeding
Confirmed by: low Hb (although Hb is often normal
early after a bleed) and response to blood transfu-
sion or volume expansion and control of bleeding
Low cardiac
output
e.g., due to large
MI or severe
valvular disease
Suggested by: pallor, cold extremities, sweating, low
BP
Confirmed by: poor LV function on echocardiogram,
low cardiac output measured by a Swan-Ganz
catheter
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CHAPTER 7 Cardiovascular signs
148
Central cyanosis
This includes cyanosis of the lips, tongue, and hands.
Main differential diagnoses and typical outline evidence
Right-to-left
cardiac shunt
due to congenital
heart disease, e.g.,
tetralogy of Fallot,
Eisenmenger’s
syndrome, tricuspid
atresia, Ebstein’s
anomaly,
pulmonary AV
fistula,
transposition of the
great vessels
Suggested by: breathlessness, clubbing, systolic or
continuous murmur, right ventricular heave
Confirmed by: echocardiogram and cardiac
catheterization
Right-to-left
pulmonary shunt
due to decreased
perfusion of lung
tissue from
extensive collapse
or consolidation or
alveolar filling
Suggested by: breathlessness, poor chest movement,
dullness to percussion and absent breath sounds
over a large area of the chest
Confirmed by: chest X-ray and bronchoscopy
Hemoglobin
abnormalities
due to congenital
NADH diaphorase,
Hb M disease, or
acquired methemo-
globinemia or
sulfhemoglobinemia
Suggested by: no clubbing, no murmurs, normal
chest movement, no chest signs. History from
childhood or exposure to toxic drugs, e.g., aniline
dyes
Confirmed by: Hb electrophoresis
TACHYCARDIA (PULSE RATE >100BPM)1
149
Tachycardia (pulse rate >100bpm)
Main differential diagnoses and typical outline evidence
Fever Suggested by: warm skin, erythema, sweats,
temperature >38*C
Confirmed by: elevated temperature, fever pattern
Hemorrhage Suggested by: signs of blood loss, pallor, sweats,
low BP, poor peripheral perfusion
Confirmed by: low Hb (can be normal in initial
stages), low central venous pressure
Hypoxia Suggested by: cyanosis, respiratory distress
Confirmed by: pulse oximetry or dPaO
2
Thyrotoxicosis Suggested by: sweating, fine tremor, weight loss, lid
lag, frequent bowel movements, sweats, weight loss
Confirmed by: iFT4, ± iFT3 and dTSH
Severe anemia Suggested by: subconjunctival and nail-bed pallor,
tiredness, poor exercise tolerance
Confirmed by: dHb (and indices)
Heart failure (LVF,
RHF, CHF)
associated
with ischemic
heart disease,
myocarditis, etc.
Suggested by: third heart sound, fine crackles at
bases, raised JVP
Confirmed by: CXR showing large heart, pulmonary
congestion; poor LV function on echocardiogram,
low cardiac output measured by a Swan-Ganz
catheter
Pulmonary
embolus (PE)
Suggested by: history of sudden breathlessness, cyano-
sis, raised JVP, loud P2. ECG: right axis deviation
Confirmed by: V/Q scan
showing mismatched de-
fects, pulmonary angiography of spinal CT showing
filling defect in pulmonary artery
Drugs
e.g.,
amphetamines,
B-agonists,
anticholinergic
agents, cocaine
Suggested by: drug history
Confirmed by: normal pulse rate if drug stopped
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CHAPTER 7 Cardiovascular signs
150
Bradycardia (<60 bpm)
Main differential diagnoses and typical outline evidence
Athletic heart
(nonpathologic)
Suggested by: young and fit, asymptomatic
Confirmed by: above clinical findings. Normal
chronotropic response to exercise. Normal
echocardiogram
Drugs Suggested by: history e.g., beta blockers
Confirmed by: improvement when drug withdrawn
Sinoatrial
disease
Suggested by: elderly, ischemic heart disease
Confirmed by: ECG: Slow atrial rate with sinus P
waves or abnormal
P waves
Ventricular or
supraventricular
ectopy or
bigeminy
Suggested by: known ischemic heart disease
Confirmed by: comparison of pulse rate to ECG:
premature ectopic beats may not generate a pulse if
early enough to not allow sufficient ventricular filling
Myocardial
infarction (MI)
Suggested by: central, crushing chest pain (can be
atypical pain)
Confirmed by: ECG: Q waves, raised
ST segments,
and inverted T waves. iCPK-MB
or troponin.
Bradycardia is most frequently seen with inferior MI
Hypothyroidism Suggested by: constipation, weight gain, dry skin, dry
hair, slow-relaxing reflexes, other symptoms and
signs of hypothyroidism
Confirmed by: iTSH, dT4
Hypothermia Suggested by: history of exposure to cold
temperature and immobility
Confirmed by: Core temperature <35*C
PULSE IRREGULAR1
151
Pulse irregular
Main differential diagnoses and typical outline evidence
Atrial fibrillation
caused by
ischemic
heart disease,
thyrotoxicosis, etc.
Suggested by: irregularly irregular pulse
Confirmed by: ECG
showing no P waves, and
irregularly irregular normal QRS complexes
Atrial flutter
with variable
heart block
caused by
ischemic
heart disease, etc.
Suggested by: irregularly irregular pulse
Confirmed by: ECG
showing “saw tooth” F waves,
and irregularly irregular normal QRS
complexes
Atrial or
ventricular
ectopics
caused by
ischemic
heart disease, etc.
Suggested by: pulse with early or dropped beats,
compensatory pause with ventricular ectopy
Confirmed by: ECG
showing underlying sinus rhythm
with early QRS
complexes. Atrial ectopic beats
have a narrow or wide QRS and are preceded by an
early P wave. Ventricular ectopic beats have a wide
QRS, are not preceded by an early P wave, and
usually are followed by a compensatory pause.
Wenkebach
heart block
caused by
ischemic
heart disease, etc.
Suggested by: regular rate with periodic slightly
longer pauses
Confirmed by: ECG
showing AV conduction with
progressive prolongation of
P-R interval with
normal QRS complex followed by a P wave not
followed by a QRS complex. The next P-R interval
is abruptly shorter.
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