Terms in this set (116)

For atrial fibrillation patients at low perioperative risk for thromboembolism (CHADS2 score ≤2 and no additional risk factors [mechanical valve, history of stroke or transient ischemic attack]), no bridging anticoagulation is needed.
For this patient with a CHADS2 score of 2 (hypertension and diabetes mellitus), no periprocedural bridging is needed.

Periprocedural management of anticoagulation in the setting of atrial fibrillation depends on the patient's risk of developing a thromboembolism and having an adverse bleeding event. The CHADS2 score is one commonly used risk stratification tool for the perioperative period. The assessment of low, moderate, and high risk, however, is different in the perioperative period versus long-term use. For those with CHADS2 scores of 0-2, who are at lowest perioperative risk, it is best to simply discontinue warfarin approximately 5 days before the procedure with no bridging agent. Alternatively, low-dose subcutaneous low-molecular-weight heparin (LMWH) can be used as a "bridge" to provide adequate anticoagulation when the INR is not in the therapeutic range. Therapeutic-dose subcutaneous LMWH or intravenous unfractionated heparin (UFH) is not recommended. Warfarin can then often be restarted 12 to 24 hours after the procedure if there is no active bleeding.

For atrial fibrillation patients with moderate risk features (CHADS2 score of 3 or 4), a history of remote transient ischemic attack or stroke, or a mechanical aortic valve, management is individualized and bridging with therapeutic-dose LMWH or therapeutic dose intravenous UFH may be reasonable.

For those with high-risk features (CHADS2 score of 5 or 6), a recent transient ischemic attack or stroke, a mechanical mitral valve, or rheumatic valvular disease, bridging anticoagulation with therapeutic-dose subcutaneous LMWH or therapeutic-dose intravenous UFH should be provided.
No Pressors! period!

In patients with left ventricular outflow tract obstruction associated with hypertrophic cardiomyopathy, inotropic agents may precipitate hemodynamic collapse and are contraindicated.

The most appropriate treatment for this patient with progressively worsening hypotension is volume resuscitation, stopping dopamine, and starting phenylephrine. Echocardiogram shows findings of hypertrophic cardiomyopathy (HCM) with prolonged systolic anterior motion of the mitral valve consistent with a hemodynamically significant left ventricular outflow tract obstruction. The severity of obstruction is more severe with small ventricular volumes, low afterload, and increased contractility. Patients with HCM may present with hemodynamic collapse secondary to acute severe left ventricular outflow tract obstruction. This may occur spontaneously or be precipitated by inotropic agents (dopamine, dobutamine), withdrawal of negative inotropic agents (β-blockers, calcium channel blockers), volume depletion, vasodilators, sustained atrial arrhythmias, or sinus tachycardia. In this patient, hypotension following a motor vehicle accident was treated with dopamine, precipitating left ventricular outflow obstruction and worsening his hypotension. Phenylephrine is an α-agonist and raises afterload by peripheral vasoconstriction. Stopping dopamine and starting phenylephrine is the most appropriate treatment to reduce or ameliorate the left ventricular obstruction, and thereby raise systemic blood pressure. Intravenous β-blockers, such as esmolol, may be useful in the treatment of severe left ventricular outflow obstruction.
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