Beta-adrenergic blocking agents, commonly known as beta-blockers, are frequently used in conjunction with anticoagulants to treat acute coronary syndrome. The indications for beta-blocker use include but are not limited to hypertension, migraine headaches, angina, arrhythmias and tremors.
Beta-blockers reduce morbidity and mortality associated with hypertension, myocardial infarction and congestive heart failure. They are contraindicated in patients with decompensated heart failure.
These agents work by reducing the heart's workload acting on the sympathetic nervous system. Beta-receptor activation results in increased heart rate and increased force of the heartbeat. Beta-blockers inhibit this action, thereby easing cardiac stress by slowing down the heart rate and decreasing the myocardial contractile force. This is one reason beta-blockers are utilized to reduce blood pressure in patients who have had a myocardial event or congestive heart failure.
Mechanism of Action
Beta-blockers work by blocking the action of epinephrine and norepinephrine on beta-adrenergic receptors in the body. This in turn stimulates the sympathetic nervous system by acting on the receptors. Beta blockers are divided into beta 1 receptors and beta 2 receptors. Beta 1 receptors are found mainly in the heart and beta 2 receptors are located in the lungs, muscles and arterioles. Additionally, beta-blockers inhibit the release of renin in the kidney, which leads to constriction of blood vessels, and ultimately provides blood pressure control.
Three classes of beta-blocking agents are available:
Nonselective beta-blockers block beta 1 and beta 2 receptors. Examples are propranolol and atenolol. Nonselective agents produce noncardiac effects such as bronchoconstriction or vasoconstriction and should be avoided in patients with asthma and chronic obstructive pulmonary disease.
Selective beta-blockers inhibit beta 1 receptors selectively and are cardioprotective. Examples include metoprolol and bisoprolol.
Nonselective beta-blockers and vasodilators due to a blockade block beta 1 and beta 2 receptors nonselectively, plus alfa 1.
Beta-blockers may be available for oral or parental use. Tables 1 & 2 show commonly used beta-blockers available in an oral and parenteral forms.
Drug Interactions & Side Effects
Nurses caring for patients receiving beta-blockers need to be aware of the numerous drug interactions and potential side effects associated with this class of medications. Beta-blockers may interact with many medications including but not limited to:
calcium channel blockers;
monoamine oxidase (MAO) inhibitors;
oral hypoglycemic agents; and
The presence of these medical conditions may require special consideration when using beta-blockers:
diabetes mellitus; and
Side effects that may be associated with beta-blockers include:
masking of hypoglycemia signs and symptoms;
cold hands and feet;
shortness of breath;
lower extremity edema;
Also, beta-blockers should not be abruptly stopped. Dosage should be tapered and gradually discontinued to allow beta-adrenergic receptors to return to predrug density and sensitivity. Symptoms associated with abrupt cessation include chest pain, arrhythmias, headache, diaphoresis, tremors and shortness of breath.
To have an understanding of anticoagulation therapy, one must understand the concept of hemostasis, coagulation cascade and thromboembolic events.
Blood is meant to flow continuously, transporting vital nutrients and oxygen to every cell of the body. When an injury occurs to a blood vessel, a natural defense mechanism called hemostasis should occur. Hemostasis is a balance between coagulation and bleeding. The formation of blood clots under normal circumstances is essential, and without the coagulation process, to maintain normal homeostasis a person would bleed to death from a relatively minor wound.
Normally, platelets are suspended in plasma and circulate freely, not adhering to the endothelial cells that line blood vessels. However, when a blood vessel is damaged, the clotting process is initiated.
When injured, the normally smooth endothelium of blood vessels exposes collagen. The collagen attracts platelets. This exposed endothelium also attracts antithrombin III, a naturally occurring coagulation inhibitor. The blood vessel vasoconstricts surrounding the disrupted area; hence, clotting factors are pooled.
In response, the platelets, which normally are round and flat, become activated. They swell and change shape into a spherical formation, become sticky and adhere to the injured vessel lining. The activated platelets also release a variety of biochemicals including clotting factors V and VII as well as additional coagulation components. The platelets aggregate to form an unstable platelet plug and initiate the stabilization process referred as the coagulation cascade.
The coagulation cascade is a complex series of enzymatic processes that takes place during hemostasis. The clotting cascade can be initiated by either of two distinct pathways: the intrinsic or extrinsic pathway. The intrinsic pathway is activated when there is trauma within the lumen of blood vessels, which encompasses direct damage to the red blood cells or platelets. The intrinsic pathway requires only elements found within, or intrinsic to, the vascular system. When factor XII comes into contact with damaged endothelial cells, the endothelial basement membrane activates the intrinsic pathway. Activated factor XII then activates factor XI. Factors VIII and IX are the final components of the intrinsic pathway. Factor IX requires vitamin K for its synthesis.
The extrinsic pathway is activated when there is tissue injury. It requires a substance, which is extrinsic to, or not normally circulating in, the vessel and involves the activation of only one factor, factor VII. This factor requires vitamin K for its synthesis. A substance known as tissue thromboplastin is released when there is tissue trauma. Exposure to tissue thromboplastin activates factor VII.
Regardless of whether the extrinsic or intrinsic pathway starts coagulation, completion of the process follows a final common pathway and is required for normal hemostasis. This common pathway begins with the final component of the intrinsic pathway or the final component of the extrinsic pathway. Either end product activates factor X and is dependent on vitamin K. Activated factor X, along with factor V, calcium and phospholipids activate prothrombin to thrombin. In the next step of the sequence, thrombin converts fibrinogen into fibrin and the end product is clot formation.