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Accreditation:

• Describe the clotting cascade.
• Describe the classification system for anti-arrhythmics.
• State 2 suggested therapies for treatment for deep vein thrombosis.

Simple Case Study? Amiodarone and Lovenox.

Frances C. is a 93 yr. old woman admitted to the Hospital repair of fractured right hip. She fell when attempting to pivot transfer to the commode in her home. She did not suffer from syncope, loss of consciousness, or dizziness before she fell. She simply lost her balance. She was being treated with Bactrim DS for a UTI. Her dementia included treatment with Aricept 5 mg daily. Her medications taken prior to admission also included synthroid for hypothyroidism.

She underwent an (R) ORIF. However, post-operatively developed atrial fibrillation with rapid ventricular response of 160-170, significant increased JVP, was unable to sustain blood pressure, and was transferred to the Coronary Care Unit to stabilize the cardiac arrhythmia. She remained in the CCU for 3 days. She was then transferred to the medical unit.

Her CCU course initially included Amiodarone drip. The family did not want her intubated or cardioverted. Therefore, the medical course included Amiodarone. The chest X-rays indicated pulmonary edema, which resolved with diuresis. DVT prophylaxis was initiated with Lovenox 30 mg. sc. bid. Her cardiac arrhythmia converted with the Amiodarone, the drip was decreased and discontinued after 48 hours, and she was started on oral Amiodarone. All blood chemistries and EKGs ruled out an MI.

Her current medical course now includes; Amiodarone 400 mg. po tid, Lovenox 30 mg. sc bid. The pain medications ordered were Vicodin one tablet po q4h prn pain, Tylenol 650 mg. p.o. q4h prn pain/fever. Her TSH levels are low, and she is no longer on synthroid for her hypothyroidism. She is allergic to penicillin. Aricept and Bactrim were not continued during her hospital course.

Her surgical course includes Physical Therapy, and eventual transfer to rehabilitation facility with long-term care possible. Unfortunately, she is refusing to participate in the physical therapy, and refusing to stand due to the pain in her hip. It requires two people to stand her, assist her with pivot transfer, and to cue her to sit down. She is out of bed most of the day in a chair. 

Pharmacology Discussion

Persistent tachycardias lead to tachycardia-induced cardiomyopathy, most often demonstrable in the case of sustained ectopic or reentrant supraventricular tachycardia. However, a persistently high and poorly controlled ventricular rate in the case of atrial fibrillation may induce CHF with a greater morbidity or mortality.

The issue here was whether AF was the result of CHF or the converse. In patients with CHF, atrial transport may contribute up to 30% of total cardiac output. The loss of forward output after the onset of AF could result in rapid and severe de-compensation because of a faster ventricular rate. This may be associated with two important consequences, thrombo-embolism and worsening heart failure.

Amiodarone Class III Antiarrhythmic drug, adrenergic blocker

The classification system for anti-arrhythmics is based on each drug’s electro-physiological effects on the heart. The entire electrical cycle begins in a resting state in which the electrical charge inside the cardiac cell membrane is negative. In the next phase, depolarization, a series of “fast channels” open up in the membrane, allowing positively charged sodium ions to rush into the cell, changing the charge within the membrane to positive. That is followed by an influx of calcium ions through the membrane’s slow channels. Repolarization begins when the sodium ions leave the cell. When the cell is once again in its resting state, it’s ready to begin the next cycle.

Anti-arrhythmics work by altering various steps in this electrical cycle, by blocking the autonomic nervous system, or both.

Class I anti-arrhythmics make cardiac cell membranes less permeable to incoming sodium ions. That, in turn, slows down depolarization, stabilizing the cell. These drugs alter repolarization.

Class II depress depolarization. They do so by blocking the beta-receptors in the parasympathetic nervous system. This means they can also lengthen atrio-ventricular conduction, slow the heart rate, and reduce contractility.

Class III drugs affect electro-physiology in several ways. Depending on the Class III drug, it can inhibit potassium and sodium channels, or even act as beta-blockers. The mechanisms of Class III drugs prolong repolarization, markedly prolong the refractory period, and lengthen QT interval.

Amiodarone is a Class III drug. Amiodarone is used to both treat and prevent ventricular tachycardia. Because of its extremely long half-life, the oral form takes a very long time to begin working – three weeks in some cases. Making patients aware of that fact may help improve compliance. Amiodarone’ s long half-life also necessitates loading doses to obtain steady-state blood levels in a reasonable amount of time.

The long half-life, accompanied by its slow elimination, also explains why the drug’s potent anti-arrhythmic effects persist for weeks or event months after it’s discontinued. It is necessary to explain this to patients, too, and tell them to call the MD if they have any palpitations or strange sensations in their hearts.

Despite the fact that the drug is eliminated mainly through the liver and stool, patients with hepatic insufficiency do not require dosage adjustments.

IV Amiodarone, indicated for acute therapy to stabilize recurrent ventricular fibrillation or V-tach, offers onset of action within two hours. As with the oral form, dosages do not need to be adjusted for renal or hepatic problems. However, since the drug may worsen heart failure, closely monitor elderly patients and those with severe left ventricular dysfunction.

Most patients will require IV therapy for 48-96 hours.

Amiodarone (Cordarone) is a class III anti-arrythmic drug that possesses some of the characteristics of all four anti-arrhythmic drug classes. It was initially used to treat ventricular arrhythmias, but over the last several years has been used mainly for atrial arrhythmias. Possible side effects include low blood pressure, liver damage, cardiac rhythm irregularities (including asystole and cardiac arrest), and nausea. It is a very effective drug in the right circumstances, but should not be used lightly.

Amiodarone has several potential side effects that need to be followed by the prescribing physician. Liver function tests are usually done on a regular basis. Due to the possibility of pulmonary fibrosis (1%), pulmonary function tests and diffusing capacity are done once to twice a year (a baseline when starting the drug is usually done). EKGs were done to check the electrical intervals to see that they were not progressing in the wrong direction. She was maintained on continuous telemetry while on the medical unit.

Lovenox – used as DVT prophylaxis

            AF may be associated with thrombo-embolism and worsening heart failure, both of which lead to reduced survival.

Unlike many life-threatening conditions, deep vein thrombosis (DVT) can strike silently. The emboli associated with DVT cause up to 25% of all hospital deaths, and in nearly all of those cases, the thrombi originate in the deep leg veins (Church, 2000). A clot large enough to totally occlude the pulmonary artery can quickly cause cardiac arrest. Because the lethal potential of DVT and PE and the difficulty diagnosing them, thorough assessment and prevention are key to caring for patients at risk for these conditions.

Clot formation occurs when the body initiates either the intrinsic or the extrinsic pathway. When a blood vessel is lacerated or crushed from an outside source, the body initiates the extrinsic pathway to achieve hemostasis. The vessel contracts to slow blood loss, and platelets adhere to the area and combine with collagen to form a temporary plug or clot over the area. When platelets combine with collagen, they stimulate platelet aggregation and thromboplastin release, which activates the clotting cascade. Forces that initiate the intrinsic pathway include venous stasis, diseases associated with hypercoagulability, and internal vessel disruption or injury. In the intrinsic pathway, internal forces in the body expose the blood to collagen fibers underlying the endothelium in the blood vessels. This exposure activates clotting factors, which likewise initiate the clotting cascade.

Whether intrinsic or extrinsic, the pathway results in prothrombin activator. In the presence of calcium, this activator converts prothrombin to thrombin, and then to fibrin, which forms the basis of the clot. When the vessel has adequately healed, the body stops continuous clot formation and begins to dissolve the clot. To do so, it initiates a feedback system, which consists of endothelial cell enzymes, circulating heparin, and substances within the clot that break it down and maintain hemostasis. Secreted by mast cells, heparin prevents the conversion of fibrinogen to fibrin, preventing further clot formation.

Enoxaparin and heparin both interfere with normal clotting but they do so by inhibiting different steps in the cascade. Enoxaparin disrupts the process mainly by blocking the conversion of factor X to its activated form. Heparin combines with a naturally occurring substance called anti-thrombin III, the function of which is to partially block the effects of thrombin. Heparin increases this effect at least a thousand fold, and that in turn greatly slows down the conversion of fibrinogen to fibrin. Unfortunately, heparin’s powerful effects on thrombin also greatly increase the risk of bleeding. That’s much less of a concern with low molecular weigh heparins like enoxaparin, which studies show are just as effective as heparin in several clinical situations (Majerus, 2000).

Clot formation and lysis involve an intricate balance. When the balance is disrupted, life-threatening DVT can be the result. Clinicians look at three major factors, called Virchow’s triad that can upset this balance.

1.      Venous stasis. Three forces can cause venous stasis: decreased velocity of flood flow through the vessels, venous dilation and pooling, and venous obstruction. Decreased velocity is usually caused by immobility, as was the case for Frances C. Normally, when a person ambulates, the foot’s plantar plexus compresses. This action, combined with the contraction of calf muscles, propels blood from the lower extremities back the heart. Since she was immobile, blood return was slowed. Immobility also causes venous pooling, which results in venous dilation and congestion. Venous stasis inhibits the blood stream’s ability to carry away locally activated clotting factors, so their concentration rises and potentiates continued clot formation.

2.      Vessel wall injury. General anesthesia can decrease vascular tone, disrupting the endothelial lining.

3.      Clotting abnormalities. Various factors can increase blood coagulability, including aging. Surgery, trauma, burns, MI, and infusion of plasma or clotting factors also activate blood coagulation. All post operative patients experience some change in fibrinolytic activity, which varies with the extent of the surgery.

Prevention and prophylaxis for DVT   Mobilization is the simplest and best way to decrease a patient’s risk of DVT and PE. Since Frances C. was immobile in the CCU, and then refused to bear weight on her leg once transferred to the medical unit, she was at increased risk. PT was working with the patient, nursing staff attempted to get her OOB, however, her pain and fear of falling, combined with her limited mental capacity to understand made this all but impossible. Therefore, the medical team initiated the prophylaxis use of Lovenox.

Lovenox (enoxaparin sodium) is an antithrombotic agent known as a low-molecular-weight heparin. Lovenox (enoxaparin sodium) injection is approved for the extended prevention of deep-vein thrombosis (DVT) following hip replacement surgery.

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