Page 569 - Cardiac Nursing

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C HAPTER 2 3 / Interventional Cardiology Techniques: Percutaneous Coronary Intervention 545
procedure type, results, and procedural complications is valuable vations have shown increased incidence of adverse long-term
in evaluating the chest pain symptoms. events, while isolated troponin elevation has conflicting prognostic
Anatomic improvement after a PCI correlates with elimination significance. Treatment with GP IIb/IIIa receptor inhibitors, distal
of angina symptoms. Persistent chest pain or recurrent chest pain protection devices, and statin therapy are recommended to prevent
should be monitored and reported to the cardiologist if there is a microembolization in high-risk patients. 54
change in intensity. Residual chest discomfort should be transient Loss of a side branch of a major coronary artery occurs when a
and dissipate in severity over several hours of PCI. If ongoing stent is placed across the side branch and poststent dilatation oc-
angina persists, an ECG should be obtained for comparison and cludes the branch. The occlusion can be transient or result in stent-
if new or suspicious ECG changes are present, the patient must re- induced occlusion of the branch (“stent jail”) and result in my-
turn to the catheterization laboratory for repeat coronary angiog- ocardial ischemia. Treatment options for side-branch occlusions
raphy and possible intervention. include placing a guidewire into the “jailed” side branch and dilat-
ing the lesion through the stent struts with an angioplasty balloon.
Abrupt Vessel Closure
ST-Elevation MI
Coronary artery plaque disruption or dissection is caused by a
controlled injury resulting from balloon dilatation with PTCA or STEMI, as documented by ECG changes (including new Q
atherectomy device. However, large progressive dissections may waves, new LBBB pattern) or cardiac enzyme elevation greater
interfere with blood flow; cause compression of the true lumen by than three times upper level of normal occurs in less than 1% of
the dissection flap; cause superimposed thrombus formation, patients after PCI. STEMI is usually due to an ACS, abrupt ves-
platelet adhesion, or vessel spasm; and lead to a total occlusion of sel closure, acute stent thrombosis, or loss of a major side branch
the treated artery—a phenomenon known as abrupt closure. Ves- originating within or in close proximity to the lesion being
sel wall damage activates the GP IIb/IIIa receptor on the platelet treated. Patients are treated as per protocol for MI (Chapter 22).
surface causing platelet aggregation and thrombosis formation.
Abrupt or acute vessel closure causes acute myocardial ischemia Coronary Vessel Perforation
with chest pain and ECG changes. If the coronary artery is not
successfully reopened percutaneously, the event may progress to Perforation or frank rupture of a coronary artery may lead to rapid
MI, require emergency CABG surgery, and/or lead to death. With hemodynamic collapse and cardiac tamponade. Perforation is an in-
the use of stents and GP IIb/IIIa receptor inhibitors, the incidence frequent event with PTCA, occurring in less than 0.6% of PCIs but
of abrupt closure and the need for emergency bypass surgery has up to 2.0% with directional and rotational atherectomy. 55 Mecha-
been reduced to less than 0.5% of patients. 53 nisms of perforation with a guidewire include forceful advance-
ment, crossing of a chronic total occlusion, passage of a device over
Acute Stent Thrombosis a wire that is extra luminal or into a septal branch. Anticoagulation
during PCI complicates the management of wire perforation. Ves-
Acute stent thrombosis is a potential catastrophic complication re- sel perforation may also occur with an oversized balloon or stent,
sulting in acute closure of the coronary vessel. The metallic sur- atherectomy devices, or high postdilatation pressures.
face of the stent contributes to the thrombogenic potential seen Management of coronary perforation includes pain manage-
with BMS and DES. Risks associated with acute stent thrombosis ment, close hemodynamic monitoring, and early echocardiogra-
include stenting in ACS, inadequate deployment of the stent, or phy. The administration of intravenous fluids and vasopressor
propagation of thrombus from inadequate anticoagulation or an- agents may be required. Cessation of GP IIb/IIIa receptor in-
tiplatelet therapies. Use of the current antiplatelet regimen before hibitors and reversal of anticoagulation with protamine is recom-
and after the procedure has reduced the incidence of acute stent mended only with frank rupture and hemopericardium. Balloon
thrombosis. Intravascular ultrasound (IVUS) has provided an inflation at the perforation site can occlude the perforation and
evaluation tool to assess stent expansion and full apposition of the prevent further extravasation of blood. The polytetrafluoroethyl-
stent struts to the vessel wall preventing inflow and outflow ob- ene membrane-covered stent graft is the most effective device for
struction in the coronary artery leading to thrombus formation. urgent management of perforation to tack up the perforation and
Acute stent thrombosis rates have decreased to less than 0.5% prevent further extravasation into the pericardium. Patients with
with current treatment regimens. 53 limited pericardial blood can be managed conservatively and fol-
lowed with echocardiogram surveillance. If there is a significant leak
Non-ST-Elevation MI into the pericardial space resulting in hemopericardium and poten-
tial cardiac tamponade, pericardiocentesis is required. If unable to
Elevation of cardiac enzymes occurs after uncomplicated PCI in up manage the bleeding in the catheterization laboratory, emergency
to 38% of patients, with isolated serum troponin elevation in 20% cardiac surgery may be necessary. 56
of patients. The most common causes are distal microembolization
or loss of small coronary artery side branches. Distal embolization Vascular Spasm
of friable plaque or thrombus can be released into the microcircu-
lation during PCI and atherectomy procedures. Release of a large Vascular spasm at the site or distal to the treated site is a potential
burden of embolic debris into the coronary circulation with rota- cause of acute chest pain or ischemia during or after PCI. Vascular
tional atherectomy, an ACS, or during treatment of a saphenous spasm is most common with atherectomy devices, particularly the
vein graft creates a “no-flow” phenomenon with transient occlu- high-speed rotational atherectomy device. It may occur at the treated
sion of the distal coronary vessel, causing myocardial necrosis and site, in the proximal vessel secondary to guide catheter-related injury,
elevation of CK-MB and/or troponin. Patients with CK-MB ele- or in the distal vessels. Vascular spasm is usually transient, can cause