Page 568 - Cardiac Nursing

ara
7-5
44
Apt
p53
54.
0
qxd
54.
44
8:2
9 A
9/2
009
M
g
e 5
P
P
9/0
K34
0-c
23_
K34
L L LWB K34 0-c 23_ p53 7-5 54. qxd 0 9/0 9/2 009 0 0 8:2 9 A M P a a g e 5 44 Apt ara
LWBK340-c23_23_p537-554.qxd 09/09/2009 08:29 AM Page 544 Aptara
LWB
544 PA R T I V / Pathophysiology and Management of Heart Disease
Use of Vascular Closure Devices Antithrombotic Therapy 3
Vascular closure devices (VCDs) for rapid hemostasis after
femoral sheath removal became available in the early 1990s. The Class I recommendations:
use of the VCD evolved to allow early sheath removal and hemo- 1. UFH should be administered to patients undergoing PCI.
stasis of femoral access sites, increased patient comfort, decreased (Level of evidence: C)
compression time by hospital staff, and early ambulation. Despite 2. For patients with heparin-induced thrombocytopenia, it is rec-
advances in VCD technique, improved patient comfort, and ear- ommended that bivalirudin or argatroban (direct thrombin in-
lier ambulation, VCDs have not been routinely adapted. Their hibitors) be used to replace heparin. (Level of evidence: B)
limited use reflects concerns about complications, device cost, and
lack of evidence-based superiority over manual compression. 44 Class IIa recommendations:
The most commonly used closure devices with active hemostasis 1. Bivalirudin may be used as an alternative to UFH and GP
components include collagen plugs (Angio-Seal, St. Jude Medical, IIb/IIIa inhibitors in low-risk patients undergoing elective PCI.
St. Paul, MN), suture devices (Perclose, Abbott Vascular, Red- 2. LMWH is an alternative to UFH in patients with unstable
wood City, CA), and surgical staples/clips (StarClose, Abbott Vas- angina/NSTEMI undergoing PCI. Enoxaparin can be used
cular, Redwood City, CA). The use of arterial closure devices re- without crossover to another agent. Fondaparinux should not
quires specific training by the cardiologist and the catheterization be used as the sole anticoagulant during PCI but should be
staff. coupled with UFH or bivalirudin. 4
Patients undergoing PCI who are treated with LMWH
(enoxaparin) require no additional dosing if the last dose of
ANTICOAGULATION OPTIONS enoxaparin was given less than 8 hours before PCI. If the last dose
FOR PCI was administered more than 8 hours previously, an IV bolus is
given per protocol. 47,48 LMWH is less frequently used in the
Arterial injury at the PCI site and indwelling angioplasty equip- catheterization laboratory with PCI and sheath management be-
ment serve as potent stimuli for thrombus formation during PCI. cause of the longer half-life and the inability to monitor ACT or
Anticoagulation and antiplatelet agents are administered routinely PTT to establish anticoagulation status. The direct thrombin in-
to reduce the risk of an acute thrombotic complication. See Table hibitor, bivalirudin, prolongs the ACT allowing monitoring of the
22-2, Applying Classification of Recommendations and Level of dose during PCI similar to UFH.
Evidence, in the previous chapter.
GP IIb/IIIa Receptor Inhibitors 3
Oral Antiplatelet Therapy 3 The GP IIb/IIIa receptor inhibitors are a class of drugs used intra-
Class I recommendations: venously before and during interventional cardiology procedures
and ACS. The final common pathway to platelet aggregation and
1. Patients already on ASA should take 75 to 325 mg before the coronary thrombus involves the activation of the platelet GP
PCI. (Level of evidence: A) IIb/IIIa receptor. The GP IIb/IIIa receptor inhibitors act by occu-
2. Patients not already on chronic ASA should be pretreated with pying the receptors, preventing fibrinogen from binding and
ASA 75 to 325 mg at least 2 hours before and preferably 24 thereby preventing platelet aggregation. There are three GP
hours before PCI is performed. (Level of evidence: C) IIb/IIIa receptor antagonists available for intravenous use to block
3. After the PCI, in patients with neither ASA resistance, platelet aggregation: abciximab, tirofiban, and eptifibatide. GP
allergy, or risk of increased bleeding, ASA 75 to 325 mg daily IIb/IIIa receptor antagonists diminish ischemic complications as-
should be given for at least 1 month for BMS, 3 months sociated with PCI (Chapter 20). 3,46–52
for SES, and 6 months for PES. Then all patients should
take daily chronic ASA 75 to 162 mg indefinitely. (Level of Class I recommendations:
evidence: B) 1. In patients with unstable angina or NSTEMI undergoing
4. A loading dose of clopidogrel should be administered before PCI without clopidogrel administration, a GP IIb/IIIa recep-
PCI. (Level of evidence: A) The recommended dose of clopi- tor inhibitor (abciximab, tirofiban, and eptifibatide) should
dogrel dose of 300 mg at least 6 hours before PCI has the best be given. (Level of evidence: A)
evidence of efficacy. (Level of evidence: B)
5. After PCI, patients should be given clopidogrel 75 mg daily for
at least 1 month after BMS, 3 months after SES, 6 months af-
ter PES, and ideally up to 12 months. (Level of evidence: C) COMPLICATIONS ASSOCIATED
WITH PCI
Recent clinical studies evaluated a 600 mg loading dose of
clopidogrel given 2 hours before PCI. This dose was found to be Chest Pain or Discomfort Post-PCI
safe, and provide faster and greater platelet inhibition than the
lower dose. 45,46 Risk of thrombocytopenia with clopidogrel re- Persistent or recurrent chest pain/discomfort after PCI requires
quires surveillance of platelet counts before and after PCI. Patients immediate evaluation. It may be caused by acute or threatened clo-
who are allergic to clopidogrel should be given ticlopidine. When sure, MI, loss of coronary artery side branch, distal embolization,
using ticlopidine, there is a risk of neutropenia requiring moni- vessel perforation, vascular spasm, or may be residual chest pain as-
toring a complete blood count with differential before and then sociated with vessel dilatation and stretch. Obtaining full details of
again 7 to 10 days after PCI. the PCI and patient information including presenting symptoms,