Calcium Channel Blocking Agents

Calcium channel blockers (calcium ion antagonists) have a variety of effects. These agents decrease
sinoatrial node automaticity and atrioventricular node conduction, resulting in a slower heart rate and a
decrease in the strength of myocardial contraction (negative inotropic effect). These effects decrease the
workload of the heart. Calcium channel blockers also relax the blood vessels, causing a decrease in
blood pressure and an increase in coronary artery perfusion. Calcium channel blockers increase
myocardial oxygen supply by dilating the smooth muscle wall of the coronary arterioles; they decrease
myocardial oxygen demand by reducing systemic arterial pressure and the workload of the left ventricle.
The calcium channel blockers most commonly used are amlodipine (Norvasc) and diltiazem (Cardizem,
Tiazac).
They may be used by patients who cannot take beta-blockers, who develop significant side effects from
beta-blockers or nitrates, or who still have pain despite beta-blocker and nitroglycerin therapy. Calcium
channel blockers are also used to prevent and treat vasospasm, which may occur after a PCI. First-
generation calcium channel blockers such as nifedipine (Procardia) should be avoided or used with
caution in people with heart failure because they decrease myocardial contractility. Amlodipine and
felodipine (Plendil) are the calcium channel blockers of choice for patients with heart failure. Hypotension
may occur after the IV administration of any of the calcium channel blockers. Other side effects may
include atrioventricular block, bradycardia, constipation, and gastric distress.
Antiplatelet and Anticoagulant Medications
Antiplatelet medications are administered to prevent platelet aggregation and subsequent thrombosis,
which impedes blood flow.
Aspirin. Aspirin prevents platelet aggregation and reduces the incidence of MI and death in patients with
CAD. A 160- to 325-mg dose of aspirin should be given to the patient with angina as soon as the
diagnosis is made (eg, in the emergency department or physician’s office) and then continued with 81 to
325 mg daily. Patients should be advised to continue aspirin even if they concurrently take other
analgesics such as acetaminophen (Tylenol). Because aspirin may cause gastrointestinal upset and
bleeding, the use of H2-blockers (eg, famotidine [Pepcid]) or proton pump inhibitors (eg, omeprazole
[Prilosec]) should be considered to allow continued aspirin therapy.
Clopidogrel. Clopidogrel (Plavix) is given in addition to aspirin in patients at high risk for MI. Patients are
given more than one platelet inhibitor because the medications act on different pathways to block platelet
activation (Housholder-Hughes, 2006). Unlike aspirin, this medication takes a few days to achieve
antiplatelet effects.

Heparin. IV unfractionated heparin prevents the formation of new blood clots. Treating patients with
unstable angina with heparin reduces the occurrence of MI. If the patient’s signs and symptoms indicate a
significant risk for a cardiac event, the patient is hospitalized and may be given an IV bolus of heparin and
started on a continuous infusion. The amount of heparin administered is based on the results of the
activated partial thromboplastin time (aPTT). Heparin therapy is usually considered therapeutic when the
aPTT is 2 to 2.5 times the normal aPTT value.
A subcutaneous injection of low-molecular-weight heparin (LMWH; enoxaparin [Lovenox] or dalteparin
[Fragmin]) may be used instead of IV unfractionated heparin to treat patients with unstable angina or
non–ST-segment elevation MIs (Antman, Hand, Armstrong, et al., 2007). LMWHs provide effective and
stable anticoagulation, potentially reducing the risk of rebound ischemic events, and eliminate the need to
monitor aPTT results. LMWHs may be beneficial before and during PCIs and for ST-segment elevation
MIs.
Because unfractionated heparin and LMWH increase the risk of bleeding, the patient is monitored for
signs and symptoms of external and internal bleeding, such as low blood pressure, increased heart rate,
and decreased serum hemoglobin and hematocrit. The patient receiving heparin is placed on bleeding
precautions, which include:
• Applying pressure to the site of any needle puncture for a longer time than usual
• Avoiding intramuscular (IM) injections
• Avoiding tissue injury and bruising from trauma or use of constrictive devices (eg, continuous use of an
automatic blood pressure cuff)
A decrease in platelet count or evidence of thrombosis may indicate heparin-induced thrombocytopenia
(HIT), an antibody-mediated reaction to heparin that may result in thrombosis (Cooney, 2006). Patients
who have received heparin within the past 3 months and those who have been receiving unfractionated
heparin for 5 to 15 days are at high risk for HIT (see Chapter 33 for further discussion of HIT).
Glycoprotein IIb/IIIa Agents. IV administration of glycoprotein (GP) IIb/IIIa agents (abciximab [ReoPro],
tirofiban [Aggrastat], eptifibatide [Integrilin]) is indicated for hospitalized patients with unstable angina
and
as adjunct therapy for PCI. These agents prevent platelet aggregation by blocking the GP IIb/IIIa
receptors on the platelets, preventing adhesion of fibrinogen and other factors that crosslink platelets to
each other and thus form platelet clots. As with heparin, bleeding is the major side effect, and bleeding
precautions should be initiated.
Oxygen Administration
Oxygen therapy is usually initiated at the onset of chest pain in an attempt to increase the amount of
oxygen delivered to the myocardium and to decrease pain. The therapeutic effectiveness of oxygen is
determined by observing the rate and rhythm of respirations. Blood oxygen saturation is monitored by
pulse oximetry; the normal oxygen saturation (SpO2) level is greater than 93%.
NURSING PROCESS
THE PATIENT WITH ANGINA PECTORIS
Assessment
The nurse gathers information about the patient’s symptoms and activities, especially those that precede
and precipitate attacks of angina pectoris. Appropriate questions are listed in Chart 28-4. The answers to
these questions form the basis for designing an effective program of treatment and prevention. In addition
to assessing angina pectoris or its equivalent, the nurse also assesses the patient’s risk factors for CAD,
the patient’s response to angina, the patient’s and family’s understanding of the diagnosis, and
adherence to the current treatment plan.
Diagnosis
Nursing Diagnoses
Based on the assessment data, major nursing diagnoses may include:
• Ineffective cardiac tissue perfusion secondary to CAD as evidenced by chest pain or other prodromal
symptoms
• Death anxiety related to cardiac symptoms
• Deficient knowledge about the underlying disease and methods for avoiding complications
• Noncompliance, ineffective management of therapeutic regimen related to failure to accept necessary
lifestyle changes
Collaborative Problems/Potential Complications
Potential complications that may develop include the following, which are discussed in the chapters
indicated:
• ACS and/or MI (described later in this chapter)
• Dysrhythmias and cardiac arrest (see Chapters 27 and 30)
• Heart failure (see Chapter 30)