Grand Rounds Recap 5.29.19

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Morbidity & Mortality Conference WITH DR. SHAW

Atrial Fibrillation with Rapid Ventricular Response (A-fib with RVR) in Heart Failure

Afib management can be difficult in the setting of acute illness as it may be a sign they are compensating for some other illness (severe anemia, sepsis, cardiogenic shock, etc.), and decreasing the heart rate may lead to further decompensation. Beta blockers in chronic heart failure have a level Ia recommendation for their use, but they can be harmful in decompensated heart failure. Nonetheless, in patients on chronic beta-blockers, withdrawal of the beta-blocker during an acute decompensation leads to higher in-hospital mortality.1 However, in patients in a-fib with RVR and decompensated heart failure, beta-blockers should be avoided due to removal of the catecholamine surge that may be sustaining cardiac output. Instead, the treatment should be focused on optimizing volume status, diuresis, and treating the underlying cause of heart failure if possible. Digoxin may be a reasonable alternative in this setting because it is a positive inotrope. Amiodarone and electrical cardioversion can also be considered with appropriate anticoagulation when indicated.

Thyroid Storm

Thyroid storm typically presents with acute onset of hyperpyrexia, altered mental status, gastrointestinal symptoms, and cardiac symptoms. The most common reason for this is poor medication compliance in patients with Grave’s disease. It carries a mortality of 11%, and death is usually due to high-output heart failure and subsequent cardiogenic shock.2 The treatment involves beta-blockers, propothyouracil/methimazole, steroids, and iodine.

Paget Schroetter Disease

This is a unique form of thoracic outlet syndrome that is due to repetitive arm movements leading to a venous upper extremity clot. This results in varying degrees of venous thoracic outlet syndrome. Exam findings can screen for subtle findings of concomitant arterial impingement- Adson’s test, Eden’s test, Wright’s test. Anticoagulation is generally sufficient for management, and vascular surgery follow-up is indicated. If arterial insufficiency is identified on provocative testing, angiography and vascular surgery consultation should be obtained in the emergency department.

Hyperglycemia Control in the ED

When given intravenously, regular insulin’s onset is about 15 minutes and its peak effect is at about 30 minutes. If given subcutaneously, its peak effect is 2.5-5 hours. Subcutaneous lispro peaks at about two hours and is present for approximately five hours. When deciding between subcutaneous lispro versus regular insulin in a hyperglycemic patient who is tolerating PO, lispro is generally preferred because it causes less hypoglycemia generally. In mild DKA cases, subcutaneous regular insulin is preferred to lispro because it has a more gradual effect and is longer acting. Be cautious of dose stacking and remember its longer duration of action. The target glucose necessary to appropriately discharge a patient is really unknown and is somewhat controversial. One study showed that there is not a standard glucose level at which patients stop spilling glucose into the urine.3

Wolff Parkinson White Syndrome (WPW)

The classic EKG features include a shortened PR interval and a widening of the QRS due to the delta wave. The pathophysiology involves an accessory pathway called the Bundle of Kent. Patients with WPW who present in a-fib with RVR should not receive AV nodal blocking agents because it may cause uncontrolled conduction down the accessory pathway. This should be treated with procainamide in stable patients and electrical cardioversion in unstable patients.

Tumor Lysis Syndrome

Massive cell lysis causes hyperphosphatemia, hyperuricemia, and hypocalcemia. The mainstay of treatment is fluid resuscitation and rasburicase which rapidly corrects hyperuricemia. Dialysis may be indicated depending on the clinical circumstances.

  1. Prins K, Neill J, Tyler J, Eckman P, et al. Effects of beta-blocker withdrawal in acute decompensated heart failure: a systematic review and meta-analysis. JACC Heart Fail, 2015; 3(8): 647-653.

  2. Akamizu T, Satoh T, Isozaki O, Suzuki A, et al. Diagnostic criteria, clinical features, and incidence of thyroid storm based on nationwide surveys. Thyroid, 2012; 22(7): 661-679.

  3. Rave K, Nosek L, Posner J, Heise T. Renal glucose excretion as a function of blood glucose concentration in subjects with with type 2 diabetes- results of a hyperglycaemic glucose camp study. Nephrol Dial Transplant, 2006; 21(8): 2166-2171.

tPA and Stroke  WITH DR. ADEOYE

There has been and still is significant debate surrounding the utility of intravenous tPA for acute strokes. Looking at the timeline of major tPA trials is helpful in understanding the controversy. ECASS I was published in 1995 and was negative. NINDS was also published in 1995 and was positive. Shortly thereafter, tPA was FDA approved. ECASS II in 1998 was negative, as was ATLANTIS in 1999. Based on this, it is not unreasonable to conclude the tPA seems bad given the ratio of three negative studies versus one positive. It is important to look at the details of these studies, however. ECASS I used a larger dose of tPA and had a median time to treatment of 4 hours and 24 minutes. ECASS II ‘s median time to treatment was 5 hours, and ATLANTIS was 4 hours 36 minutes. On the other hand, in the NINDS trial, the median time to treatment was 1 hour and 30 minutes. This is the crucial difference.

One example of this important time to tPA difference is highlighted by studies conducted at Cleveland Clinic. In the first study of 70 patients who received tPA (no specific timing requirements), they found higher rates of intracranial hemorrhage (ICH) than reported in many of the trials (15%).1 When these authors looked at ICH rates three years later when patients could only receive tPA within three hours of symptoms onset, rates of ICH had decreased substantially and were very similar to what was reported in NINDS.2 The utility of tPA is very dependent on finding the right patient population because it definitely is not appropriate for everyone but may be beneficial for some, and as imaging and systems improve, so have the improvement in patient oriented outcomes.

  1. Katzan I, Furlan A, Lloyd L, Frank J, et al. Use of tissue-type plasminogen activator for acute ischemic stroke- the Cleveland area experience. JAMA, 2000; 283(9): 1151-1158.

  2. Katzan I, Hammer M, Furlan A, Hixson E, et al. Quality improvement and tissue-type plasminogen activator for acute ischemic stroke: a Cleveland update. Stroke, 2003; 34(3): 799-800.