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Hemodynamic Data
1
2
Lead 1
3
4
Lead 3
Lead 2 Lead 4
Figure 4-53 Standard limb leads and one precordial lead. (From Marriott
HLJ: Practical electrocardiography, ed 7, Baltimore, 1983, Williams and
Wilkins.)
MCL
AAL
MAL
PAL
A
1
3R
4R
E
Figure 4-54 Precordial points for chest leads. (From Marriott HLJ: Practi-
cal electrocardiography, ed 7, Baltimore, 1983, Williams and Wilkins.)
activity in the lateral wall of the heart; chest leads V1 and V2, reflect
electrical activity in the septal region of the heart; and V
reflect electrical activity in the anterior wall of the heart. Electrical
activity from the posterior wall of the heart is not directly recorded,
and ischemia, injury, and necrosis are reflected by depolarization and
repolarization abnormalities on the anterior surface of the heart (leads
V
to V3). In inferior-posterior myocardial infarction, ST segment,
1
T-wave changes, and Q waves are opposite in direction from an anterior myocardial infarction. During ischemia, instead of ST depression,
ST elevation occurs in leads V
2
3
4
5
6
7
and V4,
3
to V3. During acute injury, ST
1
R
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Hemodynamic Data 233
depression occurs; during infarction, a pathologic R wave rather than
a Q wave occurs in these leads.
Components of the
Electrocardiogram
Figures 4-55 and 4-56 show the components of the electrocardiogram.
P Wave
The sinus node normally is the pacemaker of the heart because the
cells of the sinus node possess the greatest spontaneous automaticity
(ability to initiate an impulse). As the electrical waves travel through
the atrium, a P wave is produced on the surface ECG, which represents
an electrical contraction (depolarization) of the atria. Mechanical contraction of the atria follows, which contributes to ventricular filling.
From the atria, the impulse travels through the AV node and the HisPurkinje system and results in electrical activation of the ventricle. The
P–R interval is the interval from the beginning of the P wave to the
onset of the QRS and reflects conduction time from the sinoatrial node
through the atria, AV node, and His-Purkinje system.
QRS Complex
After the P wave, the next tracing on the ECG usually is the QRS
complex, which represents ventricular depolarization. The electrical
activation of the ventricle results in myocardial contraction (systole).
5 mm
0.2 second
1 mm
P–R
segment
ST
segment
P
0.04
second
T
5 mm
0.5 mv
U
1 mm
0.1 mv
Q
P–R
interval
S
QRS
ST
interval
interval
Q–T
interval
ST Interval
0.14–0.16 sec
0.13–0.15 sec
0.12–0.14 sec
0.11–0.13 sec
0.10–0.11 sec
0.06–0.07 sec
Normal
Children
ranges
Calculation
of rate
Q–T intervalQRS IntervalP Interval Rate
Adults
0.18–0.20 sec
0.15–0.18 sec
0 1 2 3 3.5
Count number of R–R intervals (3.5) in 3 seconds
(15 time spaces of 0.2 second each)
Multiply 3.5 by 20 to give rate per minute
R–R
interval
0.07–0.10 sec 60
100
120
(70 in this case)
0.33–0.43 sec
70
0.31–0.41 sec
80
0.29–0.38 sec
90
0.28–0.36 sec
0.27–0.35 sec
0.25–0.32 sec
Figure 4-55 Components of the electrocardiogram (ECG) demonstrating
normal intervals. (Modified from the CIBA Collection of Medical Illustrations,
Vol. 5.)
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Hemodynamic Data
R
P
Electrocardiogram
Heart status
Diastole DiastoleSystole
Slow
Presystole
filling
Left ventricular pressure
IV
Heart sounds
Figure 4-56 Electrical and mechanical activity sequence of the heart.
(Modified from the CIBA Collection of Medical Illustrations, Vol. 5.)
S
Q
Isovolumic
contraction
a b c
components components
I II
Ejection
T
Isovolumic
relaxation
A P
Rapid
filling
III
U
Slow
filling
ST Segment and T Wave
The QRS is followed by the ST segment and T wave, which represent
repolarization of the ventricles and correspond to myocardial relaxation (diastole). The period from the end of the QRS complex to the
beginning of the T wave is called the ST segment. Depression or elevation of this segment from baseline may be produced by ischemia
(depression) or acute injury (elevation).
Abnormal Rhythms
During sinus rhythm, there is usually a regular rhythm with a normal
sequence of activation. Premature beats are those that occur before
the next expected beat. PVCs arise from abnormal electrical activity
in the ventricles, and the configuration of a PVC is usually a wide,
bizarre QRS complex (Fig. 4-57, A). PVCs that occur from a single focus
are referred to as univocal PVCs. PVCs that arise from different areas
of the ventricles have different morphologies and are referred to as
multifocal PVCs. VT is defined as the occurrence of three or more PVCs
in a row (see Fig. 4-57, B). A PVC may result in a reduced pressure
pulse due to the abnormal activation sequence of the ventricle and a
lack of coordination between atrial and ventricular contraction.
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Premature contraction
A
Rate >120: Ventricular tachycardia
B
Ventricular fibrillation
Chaotic
ventricular
depolarization
QRS wider than normal and distorted in shape
Usually no P wave
Infarct
Slowed
conduction in
margin of
ischemic area
permits circular
course of
impulse and
reentry with
rapid repetitive
depolarization
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Hemodynamic Data 235
Rapid, bizarre, wide QRS complexes
C
Figure 4-57 A, Rhythm strip demonstrating a premature ventricular con-
traction (PVC). B, Rhythm strip demonstrating a run of monomorphic ven tricular tachycardia. C, Rhythm strip demonstrating ventricular fibrillation.
(Adapted from Scheidt S: Basic electrocardiography: abnormalities of electrocardiographic patterns. Clin Symp 36[6]:2–32, 1984.)
Coarse fibrillation Fine fibrillation
During sustained VT, blood pressure may drop dramatically. Ventricular fibrillation is the most disorganized and hemodynamically compromising arrhythmia that can occur (see Fig. 4-57, C). During ventricular
fibrillation, electrical activities are chaotic and uncoordinated so that
no effective ventricular contraction takes place. As a result, no pulse
or CO occurs, and clinical death results.
Typical Electrocardiographic
Changes Seen in the Cardiac
Catheterization Laboratory
Changes in the ST segment and T wave of the ECG may indicate a lack
of blood flow to the myocardium through the coronary arteries. This
lack of blood flow, referred to as ischemia, results in oxygen deprivation to the myocardium. If ischemia persists, tissue damage or death
(necrosis) may occur. Dead tissue is referred to as infarcted tissue. ECG
changes of ischemia and infarction are illustrated in Figures 4-58
and 4-59.
Ischemia can result in many different ECG changes. Ischemia
affecting the entire depth of the myocardium (transmural) is detected
as deep symmetric T-wave inversion. T-wave inversion can be seen in
many conditions unrelated to ischemia (intracranial trauma, pulmonary embolism, and myocardial contusion). Acute T-wave changes
occurring during anginal symptoms are specific for ischemia. Horizontal ST depression or downsloping ST segments are the hallmarks
of subendocardial ischemia or, in many cases, infarction. Reversible depression favors ischemia, however. Nonspecific ST and T-wave
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Hemodynamic Data
A C
ST
T
ST
T
Q
T
B D
Figure 4-58 Electrocardiogram (ECG) changes indicative of ischemia,
injury, and infarction (necrosis) of the myocardium. A, Normal ECG. B, Ischemia indicated by inversion of the T wave. C, Ischemia and current of injury
indicated by T-wave inversion and ST-segment elevation. The ST segment
may be elevated above or depressed below the baseline, depending on
whether the tracing is from a lead facing toward or away from the infarcted
area and depending on whether epicardial or endocardial injury occurs.
Epicardial injury causes ST elevation in leads facing the epicardium.
D, Ischemia, injury, and myocardial necrosis. The Q wave indicates necrosis
of the myocardium. (With permission from Urden L, Stacy K, Lough M:
Cardiovascular disorders. In Priorities in critical care nursing, St. Louis,
2008, Elsevier Inc.)
changes and normalization of T-wave abnormalities over findings on
a baseline ECG of a pain-free patient are also ECG findings consistent
with ischemia.
ECG findings of acute infarction occur in a stepwise temporal
fashion. The earliest phase of infarction is associated with tall upright
T waves that are referred to as hyperacute T waves. These T-wave
changes are usually followed shortly by the development of ST-segment
elevation in the region where myocardial damage is occurring. Conversely, reciprocal ST-segment depression can be noted in the ECG
leads recording from the opposing surface of the heart. In an acute
inferior myocardial infarction, ST-segment elevation is present in inferior leads (II, III, and aV
simultaneously in anterior leads (I, aV
onset of myocardial infarction, Q waves appear as a result of damage
that occurs throughout all layers of the myocardium, resulting in a
transmural or Q-wave myocardial infarction. Myocardial necrosis
results in an electrically silent segment that fails to contribute to the
normal electrical forces of the heart during cardiac depolarization. An
ECG lead recording over a segment of infarcted myocardium detects
electrical forces moving away from the dead region, resulting in a
negative Q wave. Infarctions that are confined to the subendocardial
region do not result in Q-wave formation and are termed non–Q-wave
or non–ST elevation myocardial infarctions.
), whereas ST-segment depression is recorded
F
, V, and V2). Within hours of the
L
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Hemodynamic Data 237
I
II
III
Figure 4-59 Fif teen-lead electrocardiogram (ECG) with inferior, lateral,
posterior, and right ventricular acute myocardial infarction (AMI). The standard 12-lead ECG reveals the typical ST segment elevation (STE) in the
inferior and lateral leads as well as ST segment depression (STD) with
prominent R wave in the right precordial leads. Posterior AMI is indicated
by both the right precordial STD with prominent R wave and the STE in
posterior leads V8 and V9. Note that the degree of STE is less pronounced
than that seen in the inferior leads because of a relatively longer distance
from the posterior epicardium to surface leads. The right ventricular infarction is noted in this case using the simplified approach with only RV4, which
demonstrates STE of relatively small magnitude. (With permission from
Marx et al: Acute coronary syndrome. In Rosen’s emergency medicine:
concepts and clinical practice, ed 8, Philadelphia, 2014, Elsevier Inc.)
aV
aV
aV
R
L
F
V
1
V
1
V
1
V
4
RV
4
V
5
V
6
V
8
V
9
Before a cardiac catheterization is performed, obtain a baseline
12-lead ECG; the ECG can be used for comparison if symptoms develop
during the procedure. During the catheterization, monitor one to three
ECG leads continuously to evaluate for rhythm disturbances or ST
segment and T-wave changes that may indicate alterations in myocardial blood supply. During coronary angioplasty, balloon inflation temporarily interrupts blood supply to the downstream myocardium. This
interruption may result in reversible ischemia and transient ST-segment
and T-wave changes. Persistent ST-segment elevation or depression
may indicate ongoing ischemia or acute myocardial injury. Other situations encountered in the cardiac catheterization laboratory that may
result in ST-segment or T-wave changes include injection of contrast
media into a coronary artery, occlusion of an artery with a diagnostic
catheter (engaging the ostium of the left main [LM] artery or RCA),
improper or incomplete deflation of an angioplasty balloon catheter,
dissection of a coronary artery, coronary artery spasm, and blockage
of a side branch by the balloon catheter or thrombus.
Rhythm disturbances are encountered commonly during cardiac
catheterization. During right-sided heart catheterization, atrial arrhythmias and PVCs can result from catheter irritation. Catheter trauma to
the right bundle branch can occur while attempting to float a catheter
into the RVOT. Although this situation often results in transient right
bundle-branch block, complete heart block can be induced if preexisting left bundle-branch block is present. In this situation, the operator must be prepared to pace the RV until the right bundle recovers
its function. PVCs and VT can be induced by LV irritation from the
ventriculography catheter or during contrast media injection. Bradycardia, sinus arrest, VT, and ventricular fibrillation can result from
contrast media injection of the coronary arteries (especially the
RCA). Catheter-induced coronary spasm can result in ventricular fibrillation caused by impaired coronar y blood flow. The treatment of
catheter-induced arrhythmias is straightforward; removing the catheter from the LV cavity or the coronary artery ostium is often enough
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Hemodynamic Data
to terminate the arrhythmia. VT or fibrillation that persists requires
immediate resuscitation. If arrhythmias persist, investigate other
underlying causes, including ischemia or electrolyte abnormalities.
Prophylactic use of antiarrhythmic drugs to suppress arrhythmias
during cardiac catheterization is not recommended. Coronar y spasm
during cardiac catheterization may be reversed by intracoronary infusion of nitroglycerin. Bradycardia and sinus node dysfunction can
typically be reversed with vigorous coughing or the administration of
atropine (see Chapter 3). Knowledge of and experience with the defibrillator in the cardiac catheterization laboratory are crucial (see
Chapter 8).
Suggested Readings
Baim DS: Grossman’s cardiac catheterization, angiography, and intervention, ed 7, Phila-
delphia, 2006, Lippincott Williams & Wilkins.
Brown L, Kahl F, Link K, et al: Anatomic landmarks for use when measuring intracardiac
pressure with fluid-filled catheters. Am J Cardiol 86:121–124, 200 0.
Chatterjee K: The Swan-Ganz catheter s: past, present, and future: a viewpoint. Circulation
119:147–152, 2009.
Cui W, Dai W, Zhang G: A new simplified method for calculating mean mit ral pres sure
gradient. Cath Cardiovasc Interv 70:754–757, 2007.
Doorey AJ, Gakhal M, Pasquale MJ: Utilization of a pre ssure sensor guide wire to measure
bileaflet mechanical valve gradients: hemodynamic and echocardiographic
sequelae. Cath Cardiovasc Interv 67:535–540, 2006.
Folland ED, Parisi AF, Carbone C: Is peripheral arter ial pressure a satisfactory substitute
for ascending aortic pressure when measuring aortic valve gradients? J Am Coll
Cardiol 4:1207–1212, 1984.
Ford LE, Feldman T, Chiu YC, et al: Hemodynamic resistance as a measure of functional
impairment in aortic valvular stenosis. Circ Res 66:1–7, 1990.
Goldstein JA, Harada A, Yagi Y, et al: Hemodynamic importance of systolic ventricular
interaction, augmented right atrial contractilit y and atrioventricular synchrony in
acute right ventricular dysfunction. J Am Coll Cardiol 16:181–189, 1990.
Gorlin R, Gorlin SG: Hydraulic formula for calculation of stenotic mitral valve, other
cardiac valves, and central circulator y shunt s. Am Heart J 41:1–29, 1951.
Grayburn PA: Asses sment of low-gradient aortic stenosis with dobutamine. Circulation
113:604–606, 20 06.
Hakki AH, Iskandr ian AS, Bemis CE, et al: A simplified valve formula for the calculation
of stenotic cardiac valve areas. Circulation 63:1050, 1981.
Hurrell DG, Nishimura RA, Higano ST, et al: Value of dy namic re spirator y changes in lef t
and right ventr icular pressures for the diagnosis of constrictive pericarditis. Circulation 93:2007–2013, 1996.
Kern MJ, editor: Hemodynamic rounds: interpretation of cardiac pathophysiology from
pressure waveform analysis, ed 3, New York, 2009, Wiley-Liss.
Kern MJ, Aguirre F V: Interpretation of cardiac pathophysiology from pressure waveform
analysis: pericardial compressive hemodynamics, Part I. Cathet Cardiovasc Diagn
25:336–342, 1992.
Kern MJ, Aguirre F V: Interpretation of cardiac pathophysiology from pressure waveform
analysis: pericardial compres sive hemodynamics, Part II. Cathet Cardiovasc Diagn
26:34– 40, 1992.
Kern MJ, Aguirre F V: Interpretation of cardiac pathophysiology from pressure waveform
analysis: pericardial compre ssive hemodynamics, Part III. Cathet Cardiovasc Diagn
26:152–158, 1992.
Nichols WW, O’Rourke MF, editors: Measuring principles of arterial waves. In McDonald’s
blood flow in arteries: theoretical, experimental and clinical practices, ed 3, Philadelphia, 1990, Lea & Febiger, pp 143–161.
Nishimura RA, Otto CM, Bonow RO, et al: 2014 AHA/ACC guideline for the management
of patients with valvular heart disease: a report of the American College of Cardiology/
American Hear t Association Task Force on practice guidelines. J Am Coll Cardiol
63(22):e57, 2014.
Omran H, Schmidt H, Hackenbroch M, et al: Silent and apparent cerebral embolism after
retrograde catheterisation of the aortic valve in valvular stenosis: a prospective,
randomised study. Lancet 361:1241–1246, 2003.
Parham W, Shafei AE, Rajjoub H, et al: Retrograde left ventricular hemodynamic assess-
ment across bileaflet prosthetic aortic valves: the use of a high-fidelity pressure
sensor angioplasty guide wire. Cath Cardiova sc Interv 59:509–513, 2003.
Reddy PS, Curtiss EI, Uretsky BF: Spectrum of hemodynamic changes in cardiac tampon-
ade. Am J Cardiol 66:1487–1491, 1990.
Sagrista- Sauleda J, Angel J, Sambola A, et al: Low-pressure cardiac tamponade: clinical
and hemodynamic profile. Circulation 114:945 –952, 2006.
5
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Peripheral Arterial
Disease and Angiography
ANDREW JOHN KLEIN • SUBHASH BANERJEE •
DOUGLAS EMMET DRACHMAN
Peripheral arterial disease (PAD) encompasses a wide spectrum of
systemic diseases including atherosclerosis, aneurysms, and vasculitis. The term peripheral arterial disease is most often used to describe
the result of atherosclerosis in the arteries of the lower extremity,
upper extremity, renal, mesenteric, and carotid arterial beds. Patients
with PAD are at significant risk of cardiovascular morbidity and mortality, primarily due to stroke (from cerebrovascular atherosclerosis)
and myocardial infarction (from coronary atherosclerosis). Therefore,
the foundation of PAD treatment is risk factor reduction and modification of atherosclerosis and concomitant comorbidities that can
increase cardiovascular morbidity and mortality, including tobacco
use, hypertension (HTN), dyslipidemia, and diabetes. The prevalence
of PAD increases with age. Of U.S. individuals aged 40 to 59 years, 3%
will develop PAD; in those aged 60 to 69 years, 8% will be affected;
and in those above age 70, 19% will develop PAD.
Symptoms of PAD of the lower extremities are related to the
demand-supply mismatch of blood secondary to arterial vessel
obstruction/occlusion (Table 5-1). Similar to angina of the coronary
vessels, pain in the legs with exertion is called claudication. Present
in 10% to 30% of patients with PAD, classic intermittent claudication is
described as exertion-induced calf, thigh, or leg pain that abates with
rest. Of the 10% to 30% of patients with PAD, some have atypical symptoms of claudication, perhaps due to altered sensation or neuropathy
from diabetes. Patients with PAD have a marked impairment in their
quality of life. Fortunately, only 1% to 4% of patients with PAD will
progress with impaired vascular extremity flow, resulting in rest pain
and/or ulcerations and tissue loss. This condition is called critical limb
ischemia (CLI). CLI patients are at highest risk for amputation unless
they receive revascularization. Patients with CLI may describe a pain,
ache, or numbness in the leg at rest, worsened with elevation of the
leg, and relieved with dependent positioning, such as dangling the leg
off the edge of the bed. CLI patients have poor outcomes, with an
estimated 25% chance of death at 1 year mainly due to cardiovascular
causes. The three risk factors that exponentially increase the risk for
CLI are ongoing tobacco abuse, diabetes, and advancing age.
Patients being evaluated for or who have cardiovascular disease
should also undergo a complete review of systems for all forms of PAD
including the following:
•
Impaired ambulation due to cramping, fatigue, aching, numbness,
or pain (Document the patient’s primary site(s) of discomfort,
usually in the buttock, thigh, calf, or foot, along with the relationship
of such discomfort to rest or exertion.)
•
Poorly healing or nonhealing wounds of the legs or feet
• Pain at rest, localized to the lower leg or foot, which is associated
with upright or recumbent positions
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Table 5 -1
Peripheral Arterial Disease and Angiography
Clinical Presentation of Patients with Peripheral Arterial
Disease
Clinical Presentation of Peripheral Artery Disease
Asymptomatic No obvious symptomatic complaint (but usually
Classic claudication Lower- extremity symptoms are confined to the
“Atypical” leg pain Lower- extremity discomfort that is exertional
Critical limb ischemia Ischemic rest pain, nonhealing wound, or
Acute limb ischemia The “six Ps,” defined by the clinical symptoms
presents with a functional impairment)
muscles with a consistent (reproducible)
onset with exercise and relief with rest
but does not consistently resolve with rest,
consistently limited exercise at a
reproducible distance, nor meets all “Rose
questionnaire” criteria
gangrene
and signs that suggest potential limb
jeopardy: pain, pulselessness, pallor,
paresthesias, paralysis, and poikilothermia
Box 5 -1 Physical Examination Findings of Peripheral Artery
Disease
Limb examination includes the following:
• Absent or diminished femoral or pedal pulses (esp ecially after exercising
the limb)
• Arterial bruits
• Hair loss
• Poor nail growth (brittle nails)
• Dry, scaly, atrophic skin
• Dependent r ubor
• Pallor with leg elevation after 1 minute at 60 degrees (normal color
should return in 10 to 15 seconds; longer than 40 seconds indicates
severe ischemia)
• Ischemic tissue ulceration (punched- out, painful, with lit tle bleeding),
gangrene
• Abdominal pain provoked by eating and associated with weight
loss
•
Family history of a first-degree relative with an abdominal aortic
aneurysm (AAA)
Physical examination for PAD may disclose the following (see Box 5-1):
•
Diminished or absent pulses (All should be assessed with Doppler
if needed.)
•
Bruits (carotid, supraclavicular, abdominal, and femoral)
• Muscle atrophy
• Dependent rubor and elevation pallor of the feet
• Signs of CLI: Hair loss, smooth/shiny skin, dystrophic nails, cool-
ness, pallor, or cyanosis of the foot
•
Pulsatile abdominal and/or popliteal masses (aneurysms)
It is important to differentiate between other processes with
similar symptoms, such as degenerative disc disease or spinal stenosis
(pseudoclaudication). In some instances, patients may describe pain
that persists while standing still or that is relieved while continuing to
walk or leaning forward. These symptoms are less characteristic of
PAD and indicative of pseudoclaudication. Diabetic neuropathy,
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deconditioning, and muscular strain may be difficult to distinguish
from PAD.
5 —
Peripheral Arterial Disease and Angiography 241
Noninvasive Diagnostic Testing
As recommended in the guidelines, the most useful and cost-effective
test to diagnose PAD is the ankle-brachial index (ABI). The study is
performed by applying a blood pressure (BP) cuff to the calf, then
measuring BP at the ankle using a continuous-wave Doppler probe:
Record as the ankle pressure the highest of the dorsalis pedis or posterior tibial artery (PTA) pressures. The process is then repeated with
the cuff on the biceps and the Doppler on the brachial artery, quantifying the brachial pressure. The ABI is then calculated by dividing the
ankle pressure by the higher of the two brachial pressures. A normal
ABI is between 0.9 and 1.3. An ABI after exercise is very useful for
those patients who have classic symptoms of claudication and/or
decreased common femoral pulses and a normal ABI at rest. Resting
ABI may be insensitive for detecting mild aortoiliac disease and is not
designed to define the degree of functional limitation. In some patients
(e.g., those with end-stage renal disease [ESRD] or diabetes mellitus
[DM]) with secondary to medial calcification, infrapopliteal vessels
can become noncompressible. This limits the ABI result and leads to
an ABI >1.3. In these cases, a toe-brachial index (TBI) can be used.
Severity of the ABI has been linked to overall mortality in a U-shaped
distribution, with increasing mortality associated with ABIs <1.0 and
>1.3. An abnormal ABI in patients with established coronary artery
disease (CAD) and DM is associated with an incremental risk of
adverse cardiovascular outcomes.
Another technique performed in the vascular laboratory is to
obtain segmental limb pressures (SLPs) that assess BP at the thigh,
calf, ankle, transmetatarsal, and digit. Identifying the location in the
leg where BP abruptly diminishes relative the brachial pressure determines the “level” of arterial obstruction. Additionally, an arterial pressure gradient of >
Analogous and often obtained simultaneously, pulse volume recordings (PVRs) can also aid in determination of disease burden and
location. SLPs record a pressure and PVRs record a waveform at
the same anatomic levels. Analyzing the amplitude of the waveform
and contour provides insight into the presence and severity of
obstruction.
The natural history of PAD with respect to limb morbidity and
patient morbidity/mortality varies among patients with and without
claudication. Most patients with claudication (~75%) will have constant stable symptoms for the next 5 years, approximately 20% will
report progressive worsening of symptoms, and few (2% to 4%) will
require amputation. In contrast, morbidity/mortality is much greater.
A PAD patient that develops claudication after age 55 has a 5-year
mortality rate of 25% to 30%, with the majority (75%) of these deaths
attributed to cardiovascular causes. Another 20% of these patients will
suffer a nonfatal cardiovascular event.
The two most common classification schemes for PAD are Rutherford and Fontaine classifications (Tables 5-2 and 5-3).
20 mm Hg implies significant obstructive disease.
Noninvasive Imaging for
Anatomic Assessment
There are four possible methods for prerevascularization anatomic
delineation, each with their own advantages and disadvantages.
These include (1) duplex ultrasound, (2) computed tomography angiography (CTA), (3) magnetic resonance angiography (MRA), and
(4) invasive digital subtraction angiography (DSA).
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