In the ACLS Provider's Course all invasive monitoring techniques are considered supplemental material. More advanced providers should master these techniques, particularly when their professional work requires them.
Placement of an intra-arterial catheter allows the clinician to (1) continuously monitor arterial pressure accurately, (2) avoid the discomfort and injury from frequent arterial punctures, (3) sample arterial blood without disturbing the steady state, and (4) determine cardiac output using indocyanine green dye (this is becoming less necessary given modern noninvasive technology, such as blood pressure and oximetry devices). To use intra-arterial monitoring safely and effectively, the operator must be skilled in the technique, and the staff must be familiar with the catheter and transducer system so as to eliminate air bubbles, prevent clots and contamination, calibrate the system correctly, and avoid artifacts.
For patients who are in shock and have an elevated systemic vascular resistance there is often a significant difference between the pressure obtained by auscultatory or palpatory methods and pressures obtained by intra-arterial measurement.1 Central intra-arterial systolic pressure may be as much as 150 mm Hg higher than the pressure recorded with a sphygmomanometer. In hypotensive patients with normal or decreased systemic vascular resistance, there should be no discrepancy between pressure obtained with a cuff and intra-arterial pressure unless localized atherosclerosis is present.
The Korotkoff sounds heard over the brachial artery as the arm cuff is deflated are probably due to vibrations of the arterial wall set in motion by intermittent flow through the compressed segment. Absence of these sounds indicates that either flow is insufficient or the vessel wall itself has been altered so that sounds are not transmitted. Diastolic runoff is slowed with increased arterial constriction in hypotensive states. After release of pressure in the cuff at the onset of flow, there is a decreased pressure gradient. With a decreased gradient there is no intermittent turbulence-producing jet flow through the obstructed segment, and therefore no sounds are produced. The increased wall tension from vasoconstriction may also make the wall less likely to vibrate and produce sounds.1 In patients with increased vascular resistance, low cuff pressure does not necessarily indicate arterial hypotension. Failure to recognize this may lead to dangerous errors in therapy.
Any patient who requires titrated intravenous (IV) vasopressors or vasodilators for improved hemodynamics should have blood pressure recorded continuously. An intra-arterial line is vitally important if intense vasoconstriction is present.
A disparity of 5 to 20 mm Hg is probably within the expected range for direct and indirect pressure measurements. Directly recorded pressure may be slightly higher than indirectly recorded pressure for several reasons. As the arterial pressure pulse wave passes to the periphery, its form changes markedly. The pulse wave arrives later, the ascending limb becomes steeper, and the systolic pressure becomes higher, while the diastolic pressure is lower. The mean arterial pressure, however, is unchanged. The major factors responsible for changes in the arterial pulse contour are
There may also be a disparity in measurements if cuff size and placement are inappropriate. Finally, the transducer may be improperly calibrated or zeroed.
When indirect pressure is recorded as greater than direct pressure, either equipment malfunction or technical error is likely. Damping of the arterial waveform suggests a problem with the direct technique: air bubbles or blood in the line or the transducer dome, clotting at the catheter tip, mechanical occlusion of the catheter or the tubing, or loose or open connections. If the arterial waveform is normal, other causes must be excluded: improper cuff size and placement, failure to calibrate the sphygmomanometer and the transducer, or an error in electrically and mechanically zeroing the transducer.
When there is a disparity of 20 to 30 mm Hg between cuff pressure and intra-arterial pressure, all factors listed above may be responsible. In addition, the auscultatory method may lead to lower readings in the patient with severe vasoconstriction, such as in shock or hypothermia. Another possible source of error is that the cuff reads pressure from beat to beat, whereas the digital recording on the electronic monitor reads the highest pressure every 3 to 7 seconds. In the presence of occlusive peripheral disease, the pressure recorded in a peripheral artery, such as the radial or the dorsalis pedis, may be significantly lower than the cuff pressure taken more proximally.
When the disparity is greater than 30 mm Hg, the most common problem
is overshoot of the apparent systolic pressure (Fig 1) 
caused by
the resonance of the catheter system. This more commonly occurs when the
heart rate is rapid, when the rate of rise of pressure (dP/dt) is rapid,
and when the natural frequency of the catheter system is low. The longer
and more compliant the extension tubing and the lower the natural frequency,
the greater the error in measurement. This can be minimized by using stiff
extension tubing kept as short as possible.
Intra-arterial pressure may be significantly higher than cuff pressure when a single end-hole catheter is in a narrow artery with high flow. When the catheter faces the flow, kinetic energy is converted to potential energy, falsely elevating the measured blood pressure.
The disparity between the direct and indirect pressure measurements can be minimized by the following procedures2,6:
1. Allow the transducer and amplifier to warm up for at least 10 minutes before starting to zero and calibrate the system.
2. Mechanically zero the transducer.
3. Purge all air from the pressure system.
4. Check all fittings for tightness.
5. Electrically zero and calibrate the system with a mercury manometer or a water column.7
6. Use stiff, noncompliant extension tubing of shortest possible length, and avoid use of more than one stopcock between catheter and transducer.
7. Avoid draining blood samples the full length of the plumbing system.
8. Maintain the catheter by continuous low-flow flushing so that clotting does not occur.
9. Place the extension tubing near the patient with care to prevent a pulsating line.
10. Recheck the mechanical and electrical zero position, and recalibrate the system if necessary when the level of the patient is changed.
11. Avoid making adjustments to the amplifier except at time of calibration.
12. Check the zero setting (both electrically and mechanically) and calibration at least once per shift.
A Doppler device and an arm cuff may be used to measure blood pressure noninvasively. The Doppler transducer, which should be an instrument with high frequency output (10 MHz), is placed over the radial artery at the wrist, and a blood pressure cuff of appropriate size is placed around the upper arm. The cuff is inflated until the Doppler signal disappears and then is slowly deflated until blood flow is again audible; this is the systolic pressure. Diastolic readings are not possible with this technique.
The Doppler signal can be heard clearly and recorded, even at low levels of systolic pressure, when the Korotkoff sounds are not audible and the pulse is not palpable. Doppler measurement of blood pressure over the radial artery correlates well with intra-arterial pressure in the radial artery even in patients with hypotension. With intense vasoconstriction, neither the Doppler nor the intravascular radial arterial pressure will reflect aortic pressure, and a more centrally placed line, such as one in the femoral or the axillary artery, may be required.
These devices have become increasingly available in emergency departments, critical care units, and even prehospital care settings. They often incorporate several features, including pulse oximetry and electrocardiographic (ECG) monitoring. Automatic indirect blood pressure determinations can be performed via automatic oscillometry, a technique that uses a double air bladder enclosed in a cuff to determine the arterial blood pressure of the extremity within the cuff. The cuff is positioned over an artery, and the proximal bladder is inflated to occlude blood flow while residual air volume is maintained in the distal bladder. The proximal bladder is deflated stepwise, and restoration of blood flow causes arterial wall oscillations that are sensed by the distal bladder. A microprocessor then assesses the transmitted signals and determines systolic blood pressure, diastolic blood pressure, and mean blood pressure.11 The accuracy of the data generated suffers from the same vagaries as do other nonautomatic blood pressure determinations. Cuff size and fit, extremes of blood pressure, and obesity may cause errors of measurement.12-15
Venus et al16 compared indirect automatic blood pressure determination vs blood pressure determination via direct radial arterial cannulation. In 109 determinations there were no significant differences in mean arterial blood pressure between the two techniques. However, the indirect determination underestimated systolic blood pressure by 9.2±16.4 mm Hg and overestimated diastolic blood pressure by 8.7±10.6 mm Hg. The investigators concluded that automatic indirect blood pressure monitoring was adequate for routine monitoring of mean arterial pressure, but for hemodynamic titration of vasoactive drugs, direct intra-arterial measurements should be considered.
In a study by Johnson and Kerr17 evaluating five automatic blood pressure monitors compared with measurements made from direct arterial line monitoring, the correlation coefficient ranged from .7 to more than .9. However, they concluded that in critically ill patients, especially those who were hypotensive and in whom peripheral recordings may themselves not correlate with central pressure, indirect monitorings were inadequate and direct monitoring necessary.
An artery suitable for placing an indwelling catheter for continuous monitoring of intra-arterial pressures should have the following characteristics:
The axillary artery is large and has excellent collateral flow, so that thrombosis should not lead to any serious sequelae. It can be used to monitor central arterial pressure. However, embolism of air or thrombus that forms about the catheter tip may produce ischemic injury to the brain or the hand.
The femoral artery also can be used. The femoral pulse still may be palpable when the radial pulses are lost in patients with marked hypotension. It also reflects intra-aortic pressure better than peripheral arteries do.1 Caution is advised in the presence of occlusive arterial disease.
The radial artery can be used for cannulation. It is usually safe for use if careful attention is directed toward demonstrating adequate ulnar collateral flow before cannulation. Even though thrombosis of the radial artery at the catheter site is common (as noted later), ischemic injury of the hand is rare if there is adequate ulnar collateral flow. (See "Modified Allen Test.")
The dorsal pedal arteries are without significant cannulation hazards if collateral flow is demonstrated to the remainder of the foot through the posterior tibial artery. Cannulation of the brachial artery is not recommended because of the potential for thrombosis and ischemia of the lower arm and hand.18 Alternative sites such as the radial, femoral, or axillary artery should be chosen.
The major complications of arterial cannulation are ischemia and necrosis secondary to either thrombosis or embolism. Ischemia is manifested by pain (either at rest or when using the involved extremity), pallor, and paresthesias. Necrosis is manifested by obvious tissue death. Whether ischemia or necrosis distal to the area of obstruction occurs depends on the presence of collateral flow and the rate of recanalization. Other complications include hemorrhage, infection, vasovagal syncope, aneurysms, and arteriovenous fistula — the complications that may occur with cannulation of any artery. Complications following cannulation of specific arteries will be discussed as a separate topic in the sections pertaining to each artery.
The longer the cannula is in place, the greater the incidence of thrombosis. Radial artery cannulas left in place longer than 48 hours markedly increase the incidence of thrombosis.19-22 Yet cannulation of the femoral artery with a long, thin catheter for up to 16 days was not associated with any thrombotic complications in one published series of studies.23,24 The larger the size of the cannula relative to the diameter of the arterial lumen, the greater the incidence of thrombosis. This may relate both to the fact that the larger cannula relative to vessel size may produce more intimal damage and that the larger cannula in a small vessel occupies most of the lumen and in itself obstructs the flow. A large 18-gauge catheter in a small vessel would occupy most of the lumen, whereas a smaller 20-gauge catheter in a large vessel might occupy only 15% to 20% of the lumen.25 A 20-gauge catheter produces the lowest incidence of thrombosis in the radial artery.25-27
One study indicated that the incidence of dysfunction of the catheter as manifested by damping of the arterial waveform was the same with 18-gauge and 20-gauge catheters. However, the dysfunction was invariably due to thrombosis with the larger catheter; with the smaller catheter it was usually due to kinking.25 The shape of the cannula and the material from which the cannula is made also influence the incidence of thrombosis. Nontapered catheters induce a lower incidence of thrombus formation compared with tapered catheters,26,28 and catheters made of Teflon have been shown to invoke the lowest incidence of thrombosis.25,27 Repeated attempts at puncturing the radial artery not only may lead to thrombosis in the absence of an indwelling catheter but also may increase the incidence of thrombosis with an indwelling catheter.20,28 Hypotension and low cardiac output, the use of vasopressors, peripheral arteriosclerotic occlusive disease, diabetes mellitus, Raynaud's disease, hypothermia, autoimmune diseases with vasculitis, and excessive and prolonged pressure on the artery to control bleeding after catheter removal predispose to thrombosis and the ischemic sequelae of thrombosis.20,29
Intermittent flushing of the catheter increases the risk of thrombosis.
A continuous flush system should be used to ensure catheter patency, prevent
thrombosis, and minimize the incidence of embolism. Several systems are
now available that provide continuous flow at 3.0 mL/h when the system is
pressurized to 300 mm Hg. A valve can be opened that provides a flush at
1.5 mL/s.30
With the flush valve closed, the resistance in the system is so high that
the pressure measured within the system does not differ by more than 2%
from the pressure at the tip of the catheter.30,31 However, since air will pass easily
through the flow system, it must be removed from the bag before pressurization.
The solution for continuous irrigation should have heparin added; a concentration
of 2 to 4 U/mL appears adequate. Opening the flush valve and then rapidly
closing it generates a square wave on the arterial waveform that indicates
that no clot or bubbles are present in the system (Fig 2A).
If clots, bubbles, or loose connections are present,
the square wave response will be damped significantly32
(Fig 2B).
Embolism from small clots that form around the tip of the catheter or from air and particulate matter introduced into the system may occur. Emboli are more common when intermittent flushing of the catheter is done by hand. If hand flushing is required, a few milliliters of blood should be withdrawn through the stopcock to clear the system of air or clot before flushing. A continuous flush system that eliminates the need for intermittent flushing minimizes the problem of embolism.26,30
If any connection in the arterial line between the patient and the transducer opens or becomes disconnected, rapid exsanguination of the patient may follow unless the situation is promptly recognized. A bleeding diathesis, due either to anticoagulation or a disease process, increases the incidence of hemorrhage from the puncture site. Bleeding may occur around the catheter if a needle larger than the catheter is used to introduce the catheter, or it may occur after catheter removal. Hypertension, especially with a rapid rise of the systolic upstroke (dP/dt) within the artery, may also increase the incidence of bleeding. Hematoma following removal of an arterial catheter is common, although it may not appear for 1 to 2 days after removal of the cannula, and may persist for 7 to 10 days. The incidence and size of the hematoma can be minimized with the application of pressure to the cannulation site for 10 minutes after withdrawal of the catheter.29,30
The most obvious risk factor for catheter-related infection appears to be the length of time the catheter resides in the vessel. Most infections are caused by arterial catheters left in place for more than 72 hours.33 Arterial catheters inserted by cutdown involve an increased incidence of infection compared with catheters inserted percutaneously.33 Infection also depends on bacterial exposure during placement of the catheter and the frequency of catheter-stopcock manipulation as well as a variety of host-related factors.
Hypotension with bradycardia may occur during arterial puncture and can be reversed promptly with atropine.34
The femoral artery (Fig 3)
is the continuation of the external iliac artery
and traverses beneath the inguinal ligament in the leg. If a line is drawn
from the anterosuperior iliac spine to the symphysis pubis, the femoral
artery generally passes through the midpoint of that line at the level of
the inguinal ligament. Lateral to the femoral artery is the femoral nerve,
and medial to the artery within the femoral sheath is the femoral vein.35
See Figs 10 and
11, chapter 6.
Thrombosis. The larger the catheter used, the greater the incidence of thrombosis. When the femoral artery is used for cardiac catheterization via the Seldinger technique, thrombosis after catheterization may be as high as 1% to 4%.36-40 Although rare with 19- or 20-gauge catheters,23,24 thrombosis of the femoral artery may occur in the presence of peripheral vascular disease, after repeated attempts at insertion of catheters into the artery, or after prolonged, excessive pressure to control bleeding after catheter removal.
Embolism. A thrombus that forms about the catheter in the femoral artery may embolize to the lower leg and the foot, producing gangrene.41 To detect emboli early, the pulses of the femoral, popliteal, posterior tibial, and dorsalis pedis arteries should be checked frequently, ideally with a Doppler flowmeter. If there is evidence of loss of pulses or diminution in peripheral pulses, the femoral artery catheter must be removed.
Hematoma and Hemorrhage. Hematoma is common after removal of the femoral arterial catheter but can be minimized by maintaining pressure over the femoral artery for approximately 10 minutes after removal of the catheter. However, the femoral pulse must not be completely obliterated by pressure since this will predispose the patient to thrombosis.39,42 Above the inguinal ligament, the femoral artery joins the external iliac artery, which slopes abruptly backward as it ascends. If the artery is punctured above the inguinal ligament, it becomes difficult to tamponade the vessel to control bleeding. Since the posterior wall of the artery is commonly punctured during insertion, this occurrence may lead to unrecognized retroperitoneal hemorrhage.40,43
Arteriovenous Fistula: A fistula between the femoral artery and the femoral vein may be produced, especially with larger catheters such as are used for cardiac catheterization and angiography.37,40 A false aneurysm ("pseudoaneurysm") may also follow femoral arterial catheterization.
The axillary artery (Fig 5) 
is a continuation of the subclavian artery as it
leaves the root of the neck at the lateral border of the first rib to enter
the axilla. As the axillary artery leaves the axilla at the lower border
of the teres major muscle, it enters the arm as the brachial artery. The
axillary artery, vein, and the three cords of the brachial plexus form a
neurovascular bundle within the axillary sheath. Because of the extensive
collateral circulation that exists between the thyrocervical trunk of the
subclavian artery and the subscapular artery, which is a branch of the distal
axillary artery, ligation or thrombosis of the axillary artery usually will
not lead to compromise of flow to the distal arm.44,45 Since the axillary is a large
artery (almost the size of the femoral artery) and is close to the aorta,
pulsation and pressure are maintained even in the presence of peripheral
vascular collapse with marked peripheral vasoconstriction.
Thrombosis. Because of extensive collateral circulation, thrombosis of the axillary artery should not lead to any ischemic or necrotic sequelae. Moreover, with 19- or 20-gauge catheters, thrombosis is rare.24,45-47
Embolism. Although thrombosis of the axillary artery may not lead directly to injury to the distal arm, it is still possible that a thrombus that forms about the catheter tip may embolize to the radial or ulnar circulation. In the absence of adequate collateral flow through the superficial palmar arch, this could produce ischemic injury to the hand.
Since the right axillary artery arises from the right brachiocephalic trunk in direct communication with the common carotid artery, it is quite possible that air, clot, or particulate matter may embolize to the brain during flushing. It may be safer to use the left axillary artery rather than the right, but in either instance, flushing should be performed gently, with minimum volume and with careful attention to prevent the introduction of air or clot into the system. Irrigation with a continuous flow system should be used.
Neurological Complications. During attempts at axillary arterial puncture, direct injury to the cords of the brachial plexus may occur, or an axillary sheath hematoma may lead to nerve compression and injury.46 The axillary artery, therefore, should not be used for intra-arterial monitoring in patients with bleeding diatheses.
The brachial artery (Fig 7)
extends into
the arm as a continuation of the axillary artery. It passes down the upper
inner arm just under the medial edge of the biceps muscle. In the antecubital
fossa, just above the elbow crease, it is easily palpable medial to the
biceps tendon and lateral to the median nerve. In the lower part of the
antecubital fossa, the brachial artery divides into the radial artery and
the ulnar artery. There are anastomoses around the elbow from the inferior
ulnar collateral artery above to branches of the ulnar artery below.44
However, if collateral circulation is inadequate, obstruction of the brachial
artery may be catastrophic, leading to loss of the forearm and hand. Therefore,
this site should not be used unless other options have greater contraindications.
Thrombosis and Embolism. Barnes et al48 reported brachial artery catheterization in 1000 patients with no objective ischemia of the distal arm.48 However, the duration of catheter placement was not described. The same group reported that of 54 patients who had brachial artery catheterization for 1 to 3 days with an 18-gauge Teflon catheter connected to a continuous flush system, 2 patients had evidence of ulnar artery obstruction and 1 had evidence of radial artery obstruction. Nevertheless, neither of the 2 patients had any symptoms or signs of ischemia of the hand. Another group reported a study of 25 patients in whom an 18-gauge polyethylene catheter was inserted in the brachial artery for an average of 11.5 hours.18 Angiography, both before catheter removal and 6 months later, revealed a high incidence of early and late vascular abnormalities: 14 of the 25 subjects had absent peripheral pulses and vascular abnormalities after removal of the catheter. Of 11 patients who were studied 6 months later, 4 had evidence of vascular irregularities and narrowing of the brachial artery at the puncture site. They had, nonetheless, regained peripheral pulses.
Neurological Complications. Subfascial bleeding after percutaneous puncture of the artery has been reported49 in patients on anticoagulant therapy and may lead to median nerve neuropathy and Volkman's contracture. Increasing pain, swelling, or minimal evidence of neuropathy in the area of distribution of the median nerve (such as paresthesias or weakness) are indications for both immediate reversal of anticoagulation treatment and fasciotomy. To prevent this complication, the brachial artery should not be used for cannulation in patients with bleeding diatheses.
The radial artery (Fig 9),
a branch
of the brachial artery, extends down the anterior radial aspect of the forearm
where, after sending a branch to the palm, it disappears deep to the abductor
pollicis longus tendon just beyond the distal end of the radius. From there
it continues across the floor of the anatomical snuffbox into the dorsum
of the hand. At the wrist the radial artery is palpable in a longitudinal
groove formed by the tendon of the flexor carpi radialis medially and the
distal radius laterally. The ulnar artery, the other major branch of the
brachial artery, extends down the ulnar aspect of the forearm to the wrist,
where it is sheltered by the tendon of the flexor carpi ulnaris. At the
wrist the ulnar artery is palpable just lateral to this tendon. The superficial
palmar arch is formed from a continuation of the ulnar artery into the hand;
both the deep palmar arch and the dorsal arch are a continuation of the
radial artery. Mozersky et al50 studied 140 hands using a Doppler
flow probe and found that the superficial palmar arch was predominantly
supplied by the ulnar artery in only 88% of the cases; 12% of the hands
had either poor collateral flow or an incomplete palmar arch with no collateral
circulation whatsoever.
Since radial artery cannulation is commonly associated with radial artery thrombosis, continued viability of the hand in such a situation depends on collateral flow via the superficial arch from the ulnar artery. If collateral flow is incomplete or absent, ischemic injury to the hand will follow radial artery thrombosis. It is therefore essential before cannulating a radial artery that the presence of collateral flow be demonstrated.51 Four methods for determining the presence of collateral circulation are described.
The Modified Allen Test.52 The modified Allen test (Fig 10)
differs from Allen's
original description53 in 1929 and is performed as follows:
Modified Allen Test With Doppler Plethysmography.50,54 A Doppler instrument can be used to detect patency of the ulnar and radial artery by placing the probe over the artery to be examined. The normal arterial velocity signal is multiphasic, with a prominent systolic component and one or more diastolic sounds. If the artery examined is obstructed, velocity distal to the obstruction is attenuated, with a resultant decrease in the systolic component and loss of the normal diastolic sounds.
The continuity of the palmar arch may be assessed by noting the response of the arterial velocity in either the radial or ulnar artery during a period of compression of the opposite artery. Normally the arterial velocity signal is increased in response to compression of the opposite artery at the wrist. If there is a lack of continuity between the radial and ulnar circulations in the hand, arterial compression will not result in an increase in velocity in the opposite artery. A similar response would result if the artery being compressed were congenitally absent or occluded by disease.
Doppler Assessment of the Superficial Palmar
Arch (Fig 11).
Method Using Plethysmography.55
Equipment Needed
Technique (Fig
12)
Thrombosis. Thrombosis is common, occurring in some series in more than 50% of radial artery cannulations.17,21,23-28,34,56-58 Although the incidence of thrombosis is high, ischemic and necrotic complications are much less common, occurring in fewer than 1% of patients with radial artery cannulas. However, one study group reported persistent ischemic symptoms in the hands of 50% of patients with radial arterial thrombosis.22 Patients with vasospastic (Raynaud's) disease and those with inadequate ulnar arches frequently exhibit ischemic and necrotic signs and symptoms following cannulation of radial arteries.20,21,51 If there are frequent small emboli issuing from the site of catheter insertion to the distal vessels of the digits, they may lead to ischemic and necrotic symptoms even in the presence of an intact palmar collateral circulation. Thrombosis may occur several days following catheter removal. Although thrombosis of the radial artery is frequent, patients whose progress has been followed for several months generally show evidence of recanalization.19,21,51
To prevent complications that might follow thrombosis of the radial artery, it is important not only to demonstrate adequate ulnar collateral circulation before insertion of the radial catheter but also to monitor the radial artery daily at the site of insertion with a Doppler instrument. Decreased or absent velocity signals may be due either to the catheter's obstructing flow in the radial artery or, more commonly, to the presence of a thrombus at the site of catheterization. If the Doppler signal is lost or ischemic changes appear, the cannula should be removed.
Spasm has been implicated as a cause of obstruction to flow in the hand and may occur both during cannulation and following removal of the cannula.1,59 However, Crossland and Neviaser51 reported that all instances of impaired circulation to the hand following radial artery cannulations were due to thrombosis rather than to spasm. Following catheter removal, if flow does not return to the hand after 1 hour, the artery should be explored for probable thrombectomy.51,60 The radial pulse may still be palpable distal to a complete occlusion. In one series with a complete occlusion, the distal pulse was palpable in 64% of the research subjects, and 10% had a radial pulse equal to the opposite radial pulses.27
Embolism. Embolism, both distally and cephalad, occurs less commonly than thrombosis. Although distal emboli may be demonstrated with angiography in as many as 25% of patients after radial artery cannulation, objective and symptomatic digital ischemia is uncommon.19,26,51,61 Whereas thrombosis with inadequate collateral flow to the hand is manifested by a pale or cold hand, emboli commonly produce cold and purple spots on the digits. These symptoms usually clear within approximately 1 week but may lead to digital gangrene, necessitating the amputation of fingers or, rarely, the entire hand.
Vigorous flushing with large volumes of flushing solution, especially when trying to correct a partially obstructed catheter with a damped arterial tracing, may allow the flushing solution to reach the central circulation and lead to either air or small-clot embolism in the brain. Lowenstein et al61 showed that it took only 7 mL of fluid vigorously flushed as a bolus into a radial catheter to reach the central circulation of the aortic arch. The volume of flushed solution correlated with arm length and patient height. If intermittent flushing is performed, it is recommended that meticulous care be used to avoid introducing any air bubbles into the system and that no more than 2 mL of solution be flushed at any one time, and then at a relatively slow rate. Since a continuous flow system delivers approximately 1.5 mL/s when the flush valve is open, flushes should be restricted to 2 seconds or less.30,61,62
Necrosis of Overlying Skin. Necrosis of the skin proximal to the site of insertion may also occur. The blood supply to the skin of the distal forearm arises directly from small branches of the radial artery without any collateral circulation. If the tip of the catheter interferes with these small branches, ischemia to the overlying skin may follow.63,64 If temporarily localized blanching of the skin appears with intermittent flushing, the tip of the catheter should be repositioned until blanching no longer occurs. The following steps should be used to decrease the incidence of skin necrosis:
Aneurysm. Mathieu et al65 reported an aneurysm of the radial artery in a patient cannulated with an 18-gauge catheter. The catheter, which was inserted after repeated attempts at puncture, remained in place for 10 days; 18 days after removal of the catheter, an aneurysm of the radial artery was noted. It was repaired without sequelae.
The dorsalis pedis artery (Fig
13)
extends subcutaneously as a continuation
of the anterior tibial artery down the dorsum of the foot parallel and lateral
to the extensor hallucis longus tendon. The lateral plantar artery, which
is the terminal branch of the posterior tibial artery, is the other major
artery supplying the foot. In most persons it supplies collateral flow via
the main arterial arch of the foot, which is analogous to the palmar arch
of the hand. However, in approximately 12% of the population, the dorsalis
pedis artery is absent, usually bilaterally.66-69
Before cannulating the dorsalis pedis artery, it must be determined that adequate collateral flow to the distal foot is present. The foot should be warm, and immersion in water may be necessary. The simple procedure, which is analogous to the Allen test, follows:
A Doppler flowmeter may also be used to assess flow in both the dorsalis pedis artery and the posterior tibial artery.70
Thrombosis.70 Thrombosis may occur in approximately 7% of those arteries cannulated. It can be recognized during cannulation by noting blanching of the great and second toes lasting longer than 15 seconds with compression of the posterior tibial artery. Occlusion can be confirmed with the Doppler technique by demonstrating retrograde flow distal to the site of cannula insertion in the dorsalis pedis artery and with loss of the signal upon occlusion of the posterior tibial artery.
Forward to Section 13.4