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Managing Risk of Complications at Femoral Vascular Access Sites in

Percutaneous Coronary Intervention

Nakia Merriweather and Linda M. Sulzbach-Hoke
Crit Care Nurse 2012;32:16-29 doi: 10.4037/ccn2012123
2012 American Association of Critical-Care Nurses
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Cover Article

Managing Risk of
Complications at
Femoral Vascular
Access Sites in
Coronary Intervention
Nakia Merriweather, RN, MSN
Linda M. Sulzbach-Hoke, RN, PhD, CCNS, ACNS-BC, CCRN

Percutaneous coronary intervention for acute coronary syndrome or nonST- contribute to the occurrence of
elevation myocardial infarction requires the use of potent oral and intravenous anti-
femoral vascular access site compli-
platelet and antithrombin medications. Although these potent antithrombotic agents
cations (VASCs), including hematoma,
and regimens may increase the effectiveness of percutaneous coronary intervention,
retroperitoneal hemorrhage, pseudo-
they are also generally associated with an increased risk of vascular access complications
such as hematoma, retroperitoneal hematoma, pseudoaneurysm, arterial occlusion, aneurysm, arteriovenous fistula, arte-
and arteriovenous fistula, which in turn are associated with increased morbidity, mor- rial occlusion, femoral neuropathy,
tality, and costs. Risk factors predisposing patients to these complications are both and infection. This article specifically
modifiable (procedure technique, medications, hemostasis method) and nonmodifiable addresses patients undergoing PCI
(sex, age, body mass index, blood pressure, renal function). Patients risks can be for acute coronary syndrome or non
reduced by nurses who are knowledgeable about these risk factors and identify com- ST-segment-elevation myocardial
plications before they become problematic. (Critical Care Nurse. 2012;32[5]:16-30) infarction (NSTEMI) and discusses
how nurses can be instrumental in

CNEContinuing Nursing Education ercutaneous coronary optimizing patients outcomes.
intervention (PCI) has The reported incidence of VASCs
This article has been designated for CNE credit.
A closed-book, multiple-choice examination reduced morbidity and during PCI is from 5.4% to 20%,2-6
follows this article, which tests your knowledge mortality from cardio- depending on the definition and
of the following objectives:
vascular disease. In 2009, criteria used. VASCs remain an
1. Identify factors contributing to complications
related to vascular access sites an estimated 596000 PCI procedures important source of increased mor-
2. Describe the different types of anticoagulation were performed.1 Major advances in bidity,7-9 mortality,2,6,9-11 length of
used before, during, and after percutaneous
coronary intervention PCI have included increasingly com- stay,4,6 and cost.2,4 The economic ram-
3. Define the methods of attaining hemostasis plex antiplatelet and antithrombotic ifications of VASCs are significant.
in patients undergoing percutaneous coronary
intervention regimens used in conjunction with Jacobson et al4 reported that the cost
2012 American Association of Critical-Care Nurses
PCI. Unfortunately, although these of PCI when bleeding complications
doi: advances yield benefits, they also arose was more than double the

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costs of uncomplicated PCI ($25371
vs $12279).4 Interventions aimed at Table 1 Femoral puncture location and associated complicationsa
reducing the risk of adverse events Femoral puncture location: definition Complications
are likely to improve both financial Low stick: puncture below the femoral bifurcation Pseudoaneurysm
and clinical outcomes. Hematoma
Removing femoral sheaths and Arteriovenous fistula
managing related complications after High stick: puncturing the inferior epigastric artery Retroperitoneal hemorrhage
PCI are predominantly the responsi- Posterior wall puncture: puncture through the back Retroperitoneal hemorrhage
wall of the artery
bilities of nurses in many acute and
a Based on data from Turi,7 Ragosta,8 Baim and Simon,15 Kamineni and Butman,18 and Rashid and Bailey.19
critical care settings.3,5,12,13 Therefore,
it is essential for nurses to understand
the causes of and predisposing risk
factors for VASCs. These risk factors Exterior
can be categorized as modifiable iliac artery
and nonmodifiable.

Modifiable Risk Factors

The primary modifiable risk Common
factors for VASCs are femoral access; femoral artery
medications administered before, artery
during, and after the procedure; and Inguinal
Profunda ligament
hemostasis method. Although the
interventional cardiologist controls
the femoral access and medications
ordered, the hemostasis method is
controlled by the nurse unless a
vascular closure device is deployed.
Femoral Access femoral artery
Percutaneous entry through
the femoral artery and vein
Figure 1 Anatomical landmarks in relation to the femoral vessels.
approach for PCI is preferred
because of the large diameter of
those vessels,14 which improves the are often associated with the loca- catheter size17 (Table 1). To facilitate
speed and simplicity of the proce- tion of the femoral puncture,7,15,16 vessel entry and effective compres-
dure.15 VASCs at the femoral site the number of attempts,7,16 and sion, the puncture should be above
the femoral bifurcation but 1 or 2 cm
below the inguinal ligament,7,8,15,19
which extends from the anterior
Nakia Merriweather is a cardiology nurse in the echocardiography laboratory at the Hospital
of the University of Pennsylvania, Philadelphia. superior iliac spine to the pubic
Linda M. Sulzbach-Hoke is a clinical nurse specialist on a 48-bed progressive care unit at the tubercle (Figure 1). Many major
Hospital of the University of Pennsylvania, providing nursing care to adult cardiac patients. and potentially lethal VASCs are
Her research and several of her publications support evidence-based nursing practice, specifi- related to punctures either too high
cally in patients undergoing percutaneous coronary intervention.
or too low below the inguinal liga-
Corresponding author: Linda Hoke, Cardiac Intermediate Care Unit, Founders 10, Hospital of the University of ment.8 Table 2 describes the clini-
Pennsylvania, 3400 Spruce Street, Philadelphia PA 19104 (e-mail:
cal findings of VASCs and the
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Phone, (800) 899-1712 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, associated management. CriticalCareNurse Vol 32, No. 5, OCTOBER 2012 17

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Table 2 Vascular access site complications and management

Complication Description Clinical findings Management

Hematoma The most common vascular Swelling surrounding the puncture Apply pressure to site21
access site complication site (visible)21 Mark the area to evaluate for any
A collection of blood located in Area of hardening under the skin change in size21
5% to 23%20
the soft tissue21 surrounding the puncture site Provide hydration21
Occurs because of blood loss at (palpable)21 Monitor serial complete blood cell
the arterial and/or venous access Varies in size20 counts21
site or perforation of an artery Often associated with pain in the Maintain/prolong bed rest21
or vein22 groin area that can occur at rest or Interrupt anticoagulant and
May occur if the arterial puncture with leg movement22 antiplatelet medications if
is below the femoral bifurcation Can result in decrease in hemoglobin necessary21
so the femoral head is not and blood pressure and increase in Blood transfusion, if indicated21
available to assist with com- heart rate, depending on severity22 If severe, may require surgical
pression7,8,15,18 evacuation20
Many hematomas resolve within a
few weeks as the blood dissipates
and is absorbed into the tissue21
Retroperitoneal Bleeding that occurs behind the Moderate to severe back pain22 Provide hydration21
hemorrhage serous membrane lining the Ipsilateral flank pain20 Perform serial blood cell counts21
walls of the abdomen/pelvis21 Vague abdominal or back pain22 Maintain/prolong bed rest21
May occur if the arterial wall Ecchymosis and decrease in Interrupt anticoagulant and anti-
0.15% to 0.44%20
puncture is made above the hemoglobin and hematocrit are platelet medications if necessary20
inguinal ligament, resulting in late signs21 Blood transfusion, if indicated14
perforation of a suprainguinal Abdominal distention21 If severe, may require surgical
artery21 or penetration of the Often not associated with obvious evacuation20
posterior wall7,8,15 swelling21
Can be fatal if not recognized Hypotension and tachycardia20
early21 Diagnosed by computed tomography20
Pseudoaneurysm A communicating tract between Swelling at insertion site22 Maintain/prolong bed rest21
the tissue and, usually, one of Large, painful hematoma21 Small femoral pseudoaneurysms
the weaker walls of the femoral Ecchymosis22 should be monitored; they com-
0.5% to 9%20
artery, causing blood to escape Pulsatile mass22 monly close spontaneously after
from the artery into the sur- Bruit and/or thrill in the groin22 cessation of anticoagulant therapy20
rounding tissue14 Pseudoaneurysms can rupture, caus- Large femoral pseudoaneurysms
Possible causes include difficulty ing abrupt swelling and severe pain21 can be treated by ultrasound-
with arterial cannulation, inade- Suspect nerve compression when guided compression, surgical
quate compression after sheath pain is out of proportion to size of intervention, or ultrasound-guided
removal, and impaired hemo- hematoma21 thrombin injection21
stasis21 Nerve compression can result in
May occur if the arterial puncture limb weakness that takes weeks
is below the femoral bifurcation or months to resolve21
so the femoral head is not Diagnosed by ultrasound20
available to assist with com-
Arteriovenous fistula A direct communication between Can be asymptomatic14 Some arteriovenous fistulas
an artery and a vein that occurs Bruit and/or thrill at access site20 resolve spontaneously without
when the artery and vein are Swollen, tender extremity22 intervention21
0.2% to 2.1%20
punctured14 Distal arterial insufficiency and/or Some arteriovenous fistulas
The communication occurs once deep venous thrombosis can result require ultrasound-guided
the sheath is removed20 in limb ischemia21 compression or surgical repair20
Risk factors: Congestive heart failure20
Multiple access attempts7 Confirmed by ultrasound21
Punctures above or below
proper site level7
Impaired clotting21

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Table 2 Continued

Complication Description Clinical findings Management

Arterial occlusion Occlusion of an artery by a Classic symptoms include the 5 Ps: Treatment depends on size/type of
thromboembolism20 Pain22 embolus, location, and patients
Incidence: <0.8%20
Most common sources: mural Paralysis20 ability to tolerate ischemia in
thrombus originating in cardiac Parasthesias22 affected area20
chambers, vascular aneurysms, Pulselessness22 Small thromboemboli in well-
or vascular atherosclerotic Pallor22 perfused arterial areas may
plaques20 Doppler studies help localize the area20 undergo spontaneous lysis20
Thromboemboli can develop at Angiogram is required to identify Larger thromboemboli may require
sheath site or catheter tip; exact location of occlusion site20 thromboembolectomy, surgery,
embolization occurs during and/or thrombolytic agents20
sheath removal20 Distal embolic protection devices (ie,
Prevention or at least reduction filters) may be placed if necessary21
can be obtained by anticoagula-
tion, vasodilators, and nursing
Femoral neuropathy Nerve damage caused by injury Pain and/or tingling at femoral access Identification and treatment of the
of the femoral nerve(s) during site22 source23
Incidence: 0.21% 23
access and/or compression of Numbness at access site or further Treatment of symptoms23
nerves by a hematoma23 down the leg22 Physical therapy23
Leg weakness22
Difficulty moving affected leg23
Decreased patellar tendon reflex22
Infection Colonization by a pathogen Pain, erythema, swelling at access Treatment of symptoms (eg, pain)21
Causes: site14 Antibiotics20
Incidence: <0.1%20
Compromised technique14 Purulent drainage at access site20
Poor hygiene14 Fever14
Prolonged indwelling sheath Increased white blood cell count21
Femoral access closure device
(closure devices have been
linked with increased occur-
rence of infection)14

High sticks are significantly linked artery. Depending on the size of the near the bifurcation vessels to other
with retroperitoneal hemorrhage sheath used, these vessels may not be blood vessels. Various vein branches
resulting from the likelihood of large enough to accommodate the that run along or anterior to the
puncturing the inferior epigastric sheath. As a result, access below the bifurcation may be accessed during
artery.7,8,15,18,19 However, punctures femoral bifurcation is more likely to arterial puncture, resulting in an
below the proper access points do lead to a VASC.7,8,15,18 When the groin arteriovenous fistula.7,8,15,18
not eliminate the risk of retroperi- site is accessed under optimal condi- Repeat or multiple punctures of
toneal hemorrhage; penetration of tions, the femoral head can be used the artery increase the likelihood
the posterior wall of the artery dur- after sheath removal to achieve effec- that another artery or vein will be
ing femoral puncture can also cause tive compression of the site and pre- punctured, causing the development
retroperitoneal bleeding (Table 1).7,8,15 vent bleeding complications. With of VASCs.7 Increased sheath size
Low sticks can predispose patients low sticks, the femoral head is not increases the risk for vascular trauma
to pseudoaneurysm, hematoma, and available to assist with compression. and VASCs. Grossman and col-
arteriovenous fistula.7,8,15,18,19 When Instead, pressure is placed against leagues17 found that PCIs performed
the groin is accessed at or below the soft tissue, making effective hemosta- with 7F and 8F guides compared
level of the femoral bifurcation, the sis less probable. This can predispose with 6F guides were associated with
femoral sheath is put into vessels that patients to hematoma and pseudo- more use of contrast medium, renal
are smaller than the common femoral aneurysm.7,8,15,18 Finally, low sticks are complications, bleeding, VASCs, CriticalCareNurse Vol 32, No. 5, OCTOBER 2012 19

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transfusions, major adverse cardiac check the type and dosage of med- a modest excess of bleeding, the
events, and deaths. ication(s) prescribed, and monitor advantages of convenience should
the patients reactions to the med- be balanced.42,43
Medications ication(s) to reduce VASCs. Direct Thrombin Inhibitors. DTIs
As techniques for performing Unfractionated Heparin. The anti- may be used as an alternative to
PCI have progressed through the coagulant effect of UFH is mediated UFH and LMWH. DTIs exert their
years, so has the approach to anti- directly by inhibiting thrombin- effect by interacting directly with
coagulation before, during, and activated conversion of fibrinogen the thrombin molecule without the
after the procedure. Combinations to fibrin. UFH is used to prevent need for a cofactor. Unlike heparin,
of oral and intravenous antiplatelet thrombosis before and during PCI. DTIs do not rely on antithrombin to
and antithrombin therapy are uni- Heparin binds to thrombin, pre- provide anticoagulation but func-
versally used for patients with venting the conversion of fibrinogen tion by inhibiting thrombin that is
acute coronary syndrome, includ- to fibrin.38,39 During the PCI, heparin bound to fibrin or fibrin degrada-
ing unstable angina and NSTEMI, activity is monitored by measuring tion products.44 In addition, unlike
who are undergoing PCI. These activated clotting time, with a goal heparin, DTIs have an antiplatelet
agents (shown in Table 3) are criti- of maintaining times greater than effect.45,46
cal in reducing rates of mortality, 200 s.24 Activated clotting time indi- Their pharmacokinetic profile
adverse ischemic events (such as cates the effectiveness of high-dose precludes the need to measure acti-
recurrent myocardial infarction), heparin therapy by measuring the vated clotting times during the pro-
short- and long-term complications intrinsic clotting activity of the whole cedure or before sheath removal.
of PCI, and other major adverse blood. Activated clotting time lacks Additionally, it has been reported
cardiac events.35-37 correlation with results of other that the most commonly used DTI,
Antithrombins inhibit the coag- coagulation tests and is used to bivalirudin, is associated with lower
ulation factors that act in a com- demonstrate the inability to coagu- frequency of bleeding at the access
plex cascade to form fibrin strands late rather than to quantify the site (4%) than are UFH or LMWH
as part of the process of hemosta- ability to clot. (plus glycoprotein IIb/IIIa
sis. The antithrombins consist of Low Molecular Weight Heparin. inhibitors; 7%) in patients undergo-
unfractionated heparin (UFH), low LMWH, like UFH, exerts its antico- ing PCI (P<.001).47 DTIs offer many
molecular weight heparin (LMWH), agulant activity by activating anti- advantages over heparin, including
and direct thrombin inhibitors thrombin, which plays a role in the inhibition of both circulating
(DTIs; eg, bivalirudin, argatroban). restricting thrombus formation. and clot-bound thrombin; a more
Antiplatelet agents can prevent the Although it consists only of frag- predictable anticoagulant response;
formation of blood clots by inhibit- ments of UFH, it is just as effective inhibiting thrombin-induced platelet
ing the activation of platelets. In and has a half-life 2 to 4 times longer aggregation; and absence of induc-
so doing, these agents prevent than that of standard heparin.39 tion of immune-mediated thrombo-
blood clotting, usually in high-flow Because LMWH has little effect on cytopenia.44,48
areas of the circulation such as the measurements of activated clotting Glycoprotein IIb/IIIa Inhibitors.
arterial circulation. They have lit- time, it should not be used as a guide These inhibitors prevent the final
tle effect in inhibiting thrombosis to anticoagulation therapy.27 Sheath pathway of platelet aggregation by
in the venous circulation. The anti- removal when followed by manual attaching to fibrinogen and other
platelet agents include glycoprotein or mechanical compression may be proteins, blocking platelet aggrega-
IIb/IIIa inhibitors, adenosine performed 4 hours after the last intra- tion and preventing thrombosis.39
diphosphate inhibitors (eg, clopi- venous dose or 6 to 8 hours after the Three parenteral agentsabciximab,
dogrel and prasugrel), and aspirin. last subcutaneous dose.28 LMWH is eptifibatide, and tirofibanare cur-
It is the nurses responsibility to a safe and effective alternative to rently approved for clinical use by
know the mechanism of action of unfractionated heparin.27,28,40,41 the Food and Drug Administration.15
each medication, verify and double Although some studies have shown They are often used in conjunction

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Table 3 Dosing of anticoagulant and antiplatelet agents used in percutaneous coronary intervention (PCI)
Drug Dosing Comments
Anticoagulant agents
Bivalirudin (Angiomax) Loading dose: 0.75 mg/kg intravenous bolus (wait 30 With addition of 600 mg clopidogrel, can be
minutes if patient received unfractionated heparin) administered with or without unfractionated
Maintenance dose: 1.75 mg/kg per hour infusion during heparin for antithrombotic treatment in PCI
PCI24 and acute coronary syndrome24
Enoxaparin Loading dose: 30 mg intravenous bolus No anticoagulation monitoring available27
Maintenance dose: 1 mg/kg subcutaneous every 12 hours Risk for heparin-induced thrombocytopenia26
If patient received initial anticoagulant therapy <8 hours Only partial reversal with administration of
before PCI: no additional therapy protamine sulfate26
If last subcutaneous dose >8 hours ago: 0.3 mg/kg intra-
venous bolus25,26
Creatinine clearance <30 mL/min: 1 mg/kg every
24 hours26
Unfractionated heparin Loading dose: 70-100 IU/kg intravenous bolus; if target Monitor by using activated partial thromboplas-
values for activated clotting time are not achieved, tin time or activated clotting time at bedside26,29
administer additional heparin boluses 2000 to 5000 IU28 Reverse with protamine sulfate26
Loading dose on glycoprotein IIb/IIIa inhibitor: 60 U/kg Risk for heparin-induced thrombocytopenia29
intravenous bolus28
Administer for target activated clotting time of 200-250
seconds (target activated clotting time may vary by
method of measurement)24
Dosing must take into account whether patient received
initial medical therapy
Intravenous antiplatelet agents
Abciximab (ReoPro) Loading dose: 0.25 mg/kg intravenous bolus Administer with aspirin and heparin30
Maintenance dose: 0.125 g/kg per minute (maximum, Platelet aggregation returns to normal 24-48
10 g/min) infusion during percutaneous coronary inter- hours after discontinuation26
vention and for 12 hours after PCI 30
Monitor activated clotting time, activated partial
thromboplastin time, hemoglobin, platelet
count when given with heparin30
Eptifibatide (Integrilin) Loading dose: 180 g/kg intravenous bolus Administer with aspirin and heparin31
Maintenance dose: 2 g/kg per minute during PCI; continue Platelet aggregation returns to normal 4-8
18-24 hours after PCI hours after discontinuation26
Creatinine clearance <50 mL/min: Reduce both loading Monitor activated clotting time, activated partial
and maintenance dose infusion rate by 50%24 thromboplastin time, hemoglobin, platelet
count when given with heparin31
Tirofiban (Aggrastat) Loading dose: 0.4 g/kg per minute intravenous for 30 Administer with aspirin and heparin32
minutes Platelet aggregation returns to normal 4-8
Maintenance dose: 0.1 g/kg per minute infusion during hours after discontinuation26
percutaneous coronary intervention and continued for Monitor activated clotting time, activated partial
18-24 hours after PCI thromboplastin time, hemoglobin, platelet
Creatinine clearance <30 mL/min: Reduce both loading count when given with heparin32
and maintenance dose infusion rate by 50%24
Oral antiplatelet agents
Aspirin Daily dose: 162-325 mg daily orally (patients at high risk Administer as soon as possible after hospital
of bleeding may receive 75-162 mg/d)25,26 admission (if patient has not already taken
Clopidogrel (Plavix) Loading dose: 300-600 mg orally Administer to patients not able to take aspirin
Maintenance dose: 75 mg/d, ideally up to 1 year24 because of hypersensitivity or significant
gastrointestinal intolerance26
Use in conjunction with aspirin33
Antiplatelet effects are irreversible34
Takes several days to achieve maximum effective-
ness without a loading dose34
Variability in patients responsiveness to the drug33
Prasugrel Loading dose: 60 mg orally Antiplatelet effects are irreversible26
Maintenance dose: 10 mg daily for 12 months after Little variation noted in patients response34
stenting24 CriticalCareNurse Vol 32, No. 5, OCTOBER 2012 21

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with UFH or a DTI. The adjunct use benefit. Clinical practices with these as 30 minutes after administration.64
of a glycoprotein IIb/IIIa inhibitor and other antithrombotic agents Prasugrel is superior to clopidogrel
during PCI is effective and associ- continue to evolve. in preventing ischemic events in
ated with improved in-hospital sur- Clopidogrel. This oral antiplatelet patients with acute coronary syn-
vival rates.49-52 However, the optimal agent specifically inhibits the P2Y12 drome undergoing PCI, even
timing of initiation of glycoprotein adenosine diphosphate receptor on though there is an associated
IIb/IIIa inhibitor therapy in patients the platelet surface, preventing acti- greater risk of bleeding.24,35,57,65 Pra-
with unstable angina or NSTEMI vation of the glycoprotein IIb/IIIa sugrel therapy should be individual-
(ie, whether to administer therapy receptor complex, thereby reducing ized and targeted toward those
before or after PCI) and the optimal platelet aggregation.39,57 Platelets patients with stents or patients
application of this therapy have not blocked by clopidogrel are affected with decreased platelet inhibition
been determined.24,53 The 2011 for the remainder of their lifespan by clopidogrel.57 Patients with a his-
guidelines on PCI from the Ameri- (~7-10 days).39 Clopidogrel reduces tory of cerebrovascular events have
can College of Cardiology Founda- the frequency of ischemic complica- experienced significant harm from
tion/American Heart Association tions after PCI and improves postin- administration of prasugrel.35 Pra-
(ACC/AHA) support early adminis- tervention outcomes.24,58 sugrel has a black box warning, not
tration of glycoprotein IIb/IIIa Clopidogrel resistance (ie, to be used in patients with previous
before catheterization for patients decreased inhibition of platelet func- stroke or transient ischemic attack
with unstable angina or NSTEMI tion after administration of clopido- because of its greater tendency to
undergoing PCI who are judged grel) may occur in 30% of patients cause intensive inhibition of platelet
clinically to be at high risk of and may relate to factors such as aggregation in general and the find-
thrombotic events relative to bleed- bioavailability, noncompliance, ings of increased levels of bleeding
ing risk.24 The guidelines further underdosing, lower absorption, compared with clopidogrel.66
note that much of the research drug interference, or single nucleotide Aspirin. Aspirin inhibits the
evaluating use of these agents for polymorphisms.24,57,59 Poor response cyclo-oxygenase enzyme, which
patients with STEMI was performed to oral antiplatelet agents increases stops prostaglandin synthesis and
in the era before routine dual oral the risk of thrombotic events, includ- release, and inhibits prostaglandin
antiplatelet therapy and was evalu- ing myocardial infarction,60 particu- synthetase action, which prevents
ated largely by placebo-controlled larly after coronary angioplasty.61 formation of thromboxane A2, thus
comparisons.24 The authors of a recent meta-analysis inhibiting platelet aggregation.39
More recently, 3 trials were done suspect that the cause of clopidogrel Long-term aspirin therapy is recom-
to evaluate glycoprotein IIb/IIIa resistance is an interaction with gly- mended for patients who undergo
antagonists as adjuncts to oral anti- coprotein IIb/IIIa inhibitors and the any revascularization procedure,
platelet therapy in patients with use of different cutoffs to identify including PCI.
primary PCI.54-56 The results bring nonresponders.62
into question whether glycoprotein Prasugrel. This novel third- Hemostasis Methods
IIb/IIIa antagonists provide addi- generation rapid-acting thienopyri- Currently, 3 main techniques are
tional benefit to STEMI patients dine is a more potent blocker of the used to achieve hemostasis at the
who received dual antiplatelet ther- platelet P2Y12 receptor than is clopi- femoral access site after PCI: manual
apy before catheterization. The dogrel,57,63 and no resistance has been compression, mechanical compres-
ACC/AHA guidelines judge that reported.57 The 60-mg loading dose sion, and vascular closure devices.
routine use of glycoprotein IIb/IIIa achieves faster, more consistent, and Manual Compression. Manual
antagonists for such patients cannot greater inhibition of adenosine compression has been the gold
be recommended, although some diphosphateinduced platelet aggre- standard for obtaining hemostasis
patients (eg, those with a large throm- gation than does 600 mg clopidogrel. at the vascular access site for years,
bus burden or who received inade- Prasugrel produces a significantly but this standard has changed as new
quate thienopyridine loading) may greater effect than clopidogrel as early devices have come on the market.

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The artery punctured is superior and
medial to the skin puncture site, so
External compression
pressure is applied as the sheath is
Pulsatile flow
removed by placing the index and
middle fingers 1 to 2 cm above the External pressure
on arterial puncture Sheath removal
site where the sheath enters the skin (proximal to skin incision)
and applying pressure as the sheath is
removed (Figure 2).67 Hemostasis is
achieved by compressing the femoral
artery against the femoral head.
Manual compression for some
practitioners is not an option
because it requires strength and the
ability to hold a good compression
for 15 to 20 minutes.6,21 If hand and B
arm fatigue develops during the Sheath removed
procedure, the amount of pressure Constriction around wound
applied to the femoral artery may Skin incision
vary, causing VASCs.3 Hematoma
Mechanical Compression.
Mechanical compression involves the
application of constant pressure on Puncture tract
Arterial puncture
the artery to obtain hemostasis and
allows hands-free catheter removal so
that nurses can monitor the patient.3
There are 2 main types of compres-
sion: The C-clamp (CompressAR,
Advanced Vascular Dynamics) and
pneumatic (FemoStop, Radi Medical
Systems AB, St Jude Medical, Inc). Figure 2 (A) Once the sheath is removed, external compression is applied 1 to
The C-clamp consists of a flat metal 2 cm above the puncture site. (B) Effective compression was not maintained,
causing a hematoma to develop.
plate, placed under the mattress at
the patients hip to stabilize the
device, and a C-clamp arm. A dis- the C-clamp arm or adjusting the Vascular Closure Devices. These
posable translucent pad is attached pressure with the pump. Mechanical devices first appeared in the 1990s
to the tip of the C-clamp arm (Fig- compression does not cause hand as means of reducing time on bed
ure 3). The FemoStop device uses a and/or arm fatigue and is just as rest and improving both hemostasis
small pneumatic clear pressure dome, effective as manual compression in and patients comfort. A variety of
a belt placed around the patients obtaining hemostasis.3,5,68 The translu- devices seek to mechanically close
hips, and a pump with a manometer cent pad or clear dome provides easy the arterial puncture site during
making it possible to adjust pressure visualization of the puncture site sheath removal in the catheterization
to an optimal level (Figure 4). As while the pressure is slowly released. laboratory in fully anticoagulated
with manual compression, the It is important to remember that patients and shorten the time to
translucent pad or clear dome is both manual and mechanical com- hemostasis and ambulation.15 Three
placed 1 to 2 cm above the site where pression can be ineffective in obtain- main types of vascular closure devices
the sheath enters the skin and pres- ing hemostasis in patients who can be categorized by the mecha-
sure is applied by pressing down on received low sticks.7 nism of hemostasis, including CriticalCareNurse Vol 32, No. 5, OCTOBER 2012 23

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Figure 6 AngioSeal, Bioabsorbable
Active Closure System With an
Intra-Arterial Anchor.
Figure 3 CompressAR C-Clamp.
Courtesy of Radi Medical Systems AB, St Jude
Courtesy of Advanced Vascular Dynamics, Portland, Oregon.
Medical, Inc., St Paul, Minnesota. Permission
to reproduce these images granted by St Jude
Medical, Inc.

Figure 4 FemoStop. Pneumatic

Courtesy of Radi Medical Systems AB, St Jude
Medical, Inc, St Paul, Minnesota. Permission Figure 5 Perclose Proglide 6F
to reproduce these images granted by St Jude Suture-Mediated Closure System.
Medical, Inc.
Courtesy of Abbott Vascular, Redwood City,
California. 2010 Abbott Laboratories. All
rights reserved. Figure 7 StarClose Vascular Closure
sutures, collagenlike plugs, and sta- System, Extraluminal Nitinol Clip.
ples/clips (Figures 5-7).14,19,69 Suture- Courtesy of Abbott Vascular, Redwood City,
mediated closure devices tie off the are used to seal off the puncture site California. 2010 Abbott Laboratories. All rights
femoral artery with sutures. Colla- in the artery. Hemostasis is usually
gen plugs seal the puncture site by obtained shortly after deployment,
stimulating platelet aggregation and allowing the patient to get out of C-clamp and manual compression,
the release of coagulation factors, bed and ambulate faster.14,15,69-72 all provide low and comparable
which results in the formation of a Vascular closure devices, when complication risks following sheath
clot. Extravascular clips or staples compared with the mechanical removal in the era of antiplatelet

24 CriticalCareNurse Vol 32, No. 5, OCTOBER 2012

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and antithrombotic therapies.3,72 reached higher acuity by the time of 16783 patients who underwent
Appropriate selection of patients by they arrive at the cardiac catheteri- PCI. The patients were grouped
the physician is important, and the zation laboratory, thereby contribut- according to 6 BMI groups: under-
device should be placed only after ing to their level of complications.28,78 weight (BMI, <18.5), normal
confirmation of the vascular anatomy weight (BMI, 18.5-24.9), overweight
and the absence of significant local Advanced Age (BMI, 25-29.9), class I obesity (BMI,
peripheral arterial disease. In cases in Advanced age, generally more 30-34.9), class II obesity (BMI, 35-
which vascular closure devices are not than 70 years of age, is directly 39.9), and class III obesity (BMI, 40).
effective, manual compression must linked to increased incidence of The incidence of major bleeding
be applied to accomplish hemostasis. VASCs.3,7,11,28,37,73-76,79 Results of a retro- varied significantly throughout the
spective study of the incidence, pre- BMI spectrum: from underweight
Nonmodifiable Risk Factors dictors, and prognostic impact of (5.6%) to normal-weight (2.5%) to
Nonmodifiable risk factors for periprocedural bleeding and trans- overweight (1.9%) to class I obese
VASC are characteristics of patients fusion in 10974 patients undergo- (1.6%) to class II obese (2.1%) to class
that cannot be changed in the PCI ing PCI indicated that age was among III obese (1.9%) patients (P<.001).
setting. These include sex, advanced the strongest predictors of major Compared with normal-weight
age, body mass index (BMI), hyper- bleeding.80 It is generally agreed patients, the risk of major bleeding
tension, and renal dysfunction. Each that with increasing age, patients was higher in underweight patients
of these factors alone, and especially are at increased risk of bleeding com- (odds ratio, 2.29 [95% CI, 1.56-3.38])
in combination, can affect the likeli- plications, possibly related to local and lower in class I obese patients
hood that a patient will experience a vascular changes or more advanced (odds ratio, 0.65 [95% CI, 0.47-0.90]).
VASC after a procedure. vascular disease.81
Sex Body Mass Index Hypertension may increase
An estimated 34% of the almost Researchers have identified a patients risk for a VASC develop-
600000 PCIs in the United States lower BMI (calculated as weight in ing.3,12,37,74,79 In a study of 413 patients
annually are performed in women, kilograms divided by height in undergoing PCI, it was reported that
and being female has been clearly meters squared) as a risk factor for patients with a higher systolic blood
identified as a risk factor for vascular complications in several pressure (135 vs 129 mm Hg; df=410,
VASCs.7,11,28,73-76 Compared with men, studies.7,74,76,82 Mehta et al83 studied P=.02) were significantly more likely
women undergoing PCI are older 2325 patients with acute myocardial to have complications than were
and have a higher incidence of infarction who received primary patients with lower blood pressures.3
hypertension, diabetes mellitus, PCI and reported that although In a larger study of 13819 patients,
hypercholesterolemia, and comorbid obese patients (those with BMI 30) Manoukian et al74 found that the
disease.28 A nationwide study of had more cardiovascular risk factors 644 patients (4.7%) who experienced
199690 patients showed that women at baseline, they had fewer VASCs, major bleeding were more likely to
presented for PCI with unstable shorter hospital stays, and fewer have hypertension than were patients
angina and/or NSTEMI more often deaths in the hospital and at 12 without major bleeding. Although
than men did and had a significantly months than did patients with a elevated blood pressure during PCI
higher frequency of VASCs.77 These normal BMI. This difference may and sheath removal may increase
women were older than their male have been because the obese patients the risk of VASCs, no evidence-based
counterparts, although they had were a mean of 6 years younger than blood pressure guidelines for PCI
fewer high-risk angiographic features the patients with normal BMI or patients are currently available.
and higher ejection fractions. How- because obesity is related to impaired
ever, women have been observed to fibrinolysis and increased platelet Renal Dysfunction
have atypical and sometimes ambigu- aggregation.83 Delhaye et al84 further Renal dysfunction, defined as
ous symptoms, which may have examined the role of BMI in records creatinine clearance less than CriticalCareNurse Vol 32, No. 5, OCTOBER 2012 25

Downloaded from at Mobile User on May 6, 2013
60 mL/min,11 has been consistently
identified as a major risk factor for Sex __________
bleeding in patients undergoing Age __________
PCI.11,12,37,74,76,81 The underlying mech- Weight __________
anism for such an association has BMI __________
been postulated to be advanced age, Assessment of groin sites prior to procedure
as well as the presence of more Right Left
severe atherosclerosis and multiple Palpable femoral pulse Y/N Palpable femoral pulse Y/N
comorbid conditions.76 Patients with Quality of pulse ___________ Quality of pulse _________
renal dysfunction who are undergo- Bruit Y/N Bruit Y/N
ing PCI are at increased risk of exces- Thrill Y/N Thrill Y/N
sive dosing of anticoagulant and Assessment of dorsalis pedis and posterior tibial pulses
antiplatelet medications such as UFH Right Left
and glycoprotein IIb/IIIa inhibitors, Palpable dorsalis pedis pulse Y/N Palpable dorsalis pedis pulse Y/N
considering that most of these med- Quality of pulse _________ Quality of pulse ________
ications are eliminated via the kid- Dorsalis pedis pulse by Doppler Y/N Dorsalis pedis pulse by Doppler Y/N
neys (Table 3). Palpable posterior tibial pulse Y/N Palpable posterior tibial pulse Y/N
Quality of pulse _________ Quality of pulse _________
Implications for Nursing Posterior tibial pulse by Doppler Y/N Posterior tibial pulse by Doppler Y/N
The main goals of patient care Anticoagulant and/or antiplatelet used and dosage
after PCI include maintenance of Pre-procedure ____________
hemostasis at the puncture site and Intra-procedure ____________
assessment for VASCs. Achieving Post-procedure ____________
these goals requires diligent assess- Catheter size used ____________
ment of patients with frequent mon- Location of catheter ____________
itoring of vital signs, puncture site, High stick Y/N
and pulse check. Duration of bed Low stick Y/N
rest and time to ambulation depend Hemostasis method ____________
on the method of arterial closure Successful Y/N
and the patients overall clinical Assessment of groin sites post-procedure
condition. Figure 8 is an assessment Right Left
worksheet for units or individual Palpable femoral pulse Y/N Palpable femoral pulse Y/N
nurses to use as a reference when Quality of pulse ____________ Quality of pulse ____________
getting report from the catheteriza- Bruit Y/N Bruit Y/N
tion laboratory or assessment checks Thrill Y/N Thrill Y/N
on the unit. The worksheet assists Assessment of dorsalis pedis pulse
nurses in determining the patients Right Left
baseline assessment so that any Quality of pulse Y/N Quality of pulse Y/N
Dorsalis pedis pulse by Doppler ________ Dorsalis pedis pulse by Doppler ________
Palpable posterior tibial pulse Y/N Palpable posterior tibial pulse Y/N
Quality of pulse ____________ Quality of pulse ____________
To learn more about percutaneous coro-
nary intervention, read Trait Anger, Hos- Posterior tibial pulse by Doppler Y/N Posterior tibial pulse by Doppler Y/N
tility, Serum Homocysteine, and Recurrent
Cardiac Events After Percutaneous Coro-
nary Interventions by Song et al in the Figure 8 Worksheet to guide nurses in asking the right questions when getting
American Journal of Critical Care, 2009;18: report from the catheterization laboratory.
554-561. Available at

26 CriticalCareNurse Vol 32, No. 5, OCTOBER 2012

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procedural or medication-related complications are essential to mini- 12. Dumont CJ, Keeling AW, Bourguignon C,
Sarembock IJ, Turner M. Predictors of vas-
complications can be promptly noted mize the substantial morbidity, cular complications post diagnostic cardiac
catheterization and percutaneous coronary
and addressed. mortality, and hospital costs associ- interventions. Dimens Crit Care Nurs. 2006;
Never before has it been so clini- ated with them. CCN 25:137-142.
13. Jones T, McCutcheon H. Effectiveness of
cally important to understand the mechanical compression devices in attain-
ing hemostasis after femoral sheath removal.
predictors and effect of VASCs in Am J Crit Care. 2002;11:155-162.
Now that youve read the article, create or contribute
PCI, acute coronary syndrome, and to an online discussion about this topic using eLetters. 14. Hamel WJ. Femoral artery closure after car-
Just visit and click Submit a diac catheterization. Crit Care Nurse. 2009;
STEMI.37 Patients are increasingly response in either the full-text or PDF view of the 29:39-46.
treated with higher complexity regi- article. 15. Baim DS, Simon D. Percutaneous approach,
including trans-setal and apical puncture.
mens containing greater numbers Acknowledgments In: Baim DS, ed. Grossmans Cardiac
Editorial assistance was provided by Rina Kleege, Catheterization, Angiography, and Interven-
of more potent oral and intravenous MS, of AdelphiEden Health Communications. This
tion. 7th ed. Philadelphia, PA: Lippincott
antiplatelet and antithrombin med- assistance was funded by Merck Sharp & Dohme Williams & Wilkins; 2006.
Corp, a subsidiary of Merck & Co, Inc, White- 16. Tu TM, Tremmel JA. Management of
ications for longer periods. These house Station, New Jersey. femoral arterial access: to close or hold
pressure? Endovascular Today. 2007;38-42.
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CNE Test Test ID C1253: Managing Risk of Complications at Femoral Vascular Access Sites in Percutaneous Coronary Intervention
Learning objectives: 1. Identify factors contributing to complications related to vascular access sites 2. Describe the different types of anticoagulation used
before, during, and after percutaneous coronary intervention 3. Define the methods of attaining hemostasis in patients undergoing percutaneous coronary

1. Which of the following is the gold standard for achieving hemostasis at 8. Which of the following is true regarding manual compression for obtaining
the femoral access site after percutaneous coronary intervention (PCI)? hemostasis at the vascular access site?
a. Mechanical compression c. Manual pressure a. Hemostasis is achieved by placing the ring and middle fingers 2 to 4 cm below the
b. Vascular closure device d. Sand bag pressure access site.
b. Hemostasis is achieved by applying pressure to the site immediately after the sheath
2. Which of the following is true regarding the use of low molecular weight has been removed.
heparin (LMWH) in PCI patients? c. Manual compression requires firm compression for 15 to 20 minutes.
a. LMWH has little effect on measurements of activated clotting time. d. Hemostasis is achieved by compressing the femoral artery against the femoral neck.
b. LMWH is not as effective as unfractionated heparin and has a half-life 1 to 2
times longer than standard heparin. 9. Which of the follow is true regarding the risk of VASCs in obese patients?
c. LMWH exerts its anticoagulant activity by deactivating antithrombin. a. Obese patients have a longer length of stay than patients with normal BMI.
d. Sheath removal followed by manual compression may be performed 6 hours b. Obese patients are typically 6 years younger than patients undergoing PCI with
after the last intravenous dose of LMWH. normal BMI.
c. Obesity can decrease platelet aggregation.
3. Which of the following is true about direct thrombin inhibitors (DTIs)? d. Obese patients have a greater risk of VASCs than patients with normal BMI.
a. DTIs inhibit thrombin-activated conversion of fibrinogen to fibrin.
b. DTIs interact directly with thrombin molecules without the need for a cofactor. 10. Key implications for nursing care of patients after PCI include which of the
c. DTIs activate antithrombin, which plays a role in restricting thrombus formation. following?
d. DTIs inhibit the cyclo-oxygenase enzyme, which stops prostaglandin synthesis a. Maintenance of hemostasis at the puncture site
and release. b. Assessment for VASCs
c. Assessment of the patients risk factors for VASCs including modifiable and
4. Which of the following is true about clopidogrel? nonmodifiable risks
a. Clopidogrel resistance can occur in up to 30% of patients. d. All of the above
b. Clopidogrel is a third-generation rapid-acting thienopyridine.
c. The American College of Cardiology supports early administration of 11. Which of the following is the reported incidence of VASCs during PCI?
clopidogrel before catheterization for patients with unstable angina. a. 20%-30%
d. Clopidogrel is an oral antiplatelet agent that prevents the final pathway of b. 2%-15%
platelet aggregation by attaching to fibrinogen and other proteins, blocking c. 5.4%-20%
platelet aggregation. d. 0%-40%

5. Femoral vascular access sites (VASCs) are often associated with all the 12. Low percutaneos entry through the femoral artery and vein approach for PCI
following except which one? can predispose the patient to which of the following?
a. High femoral sticks a. Retroperitoneal hemorrhage of the inferior epigastric area
b. Number of attempts b. Accidental puncture of another artery
c. Catheter size c. Pseudoaneurysm, hematoma, and arteriovenous fistula
d. Use of contrast media during the procedure d. Inguinal ligament injury

6. Which of the following hemostasis methods does not allow the patient to 13. The American College of Cardiology Foundation/American Heart Associ-
get out of bed and ambulate faster? aiong/Society of Cardiovascular Angiography and Interventions support early
a. Suture mediated closure c. Extravascular clips administration of which medication for patients at high risk for thromobotic
b. Collagen plug d. FemStop events related to bleeding?
a. Prasugrel
7. Which of the following is not a nonmodifiable risk factor? b. Aspirin
a. Low body mass index (BMI) c. Advanced age c. Glycoprotein IIb/IIIA
b. Hypertension d. Ethnicity d. Unfractionated heparin

Test answers: Mark only one box for your answer to each question. You may photocopy this form.
1. a 2. a 3. a 4. a 5. a 6. a 7. a 8. a 9. a 10. a 11. a 12. a 13. a
b b b b b b b b b b b b b
c c c c c c c c c c c c c
d d d d d d d d d d d d d
Test ID: C1253 Form expires: October 1, 2014 Contact hours: 1.0 Fee: AACN members, $0; nonmembers, $10 Passing score: 10 correct (77%) Synergy CERP: Category A
Test writer: Tina Cronin, APRN, MSN, CCRN, CCNS, CNRN
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