Questions of the Week for 10/24/2023

Author: Christian Gerhart

A patient presents with palpitations and has the following EKG. Vital signs are HR 140, BP 90/55, RR 25, O2 sat 95% on RA, T: 37C. What would be your initial steps in management.

EKG from Life in the Fast Lane

  • This rhythm is a wide complex tachycardia with clear pacing spikes before every ventricular beat, consistent with pacemaker mediated tachycardia. This is treated with a magnet over the pacemaker site. This patient should also have defibrillator pads placed while obtaining IV access. The magnet triggers the pacemaker to switch to an asynchronous mode where the ventricle is paced at a backup rate (AOO, DOO, or VOO) and should terminate the arrhythmia. An electrophysiology consult is essential in these cases.

You have a patient who needs a transvenous pacemaker for cardiogenic shock secondary to complete heart block. What mode should the pacer be floated in? 

  • It is generally recommended to float a transvenous pacemaker in either VVI (V paced, V sensed and V inhibited) or asynchronous mode (DOO or VOO). On our pacer boxes, you can place it in asynchronous mode by pressing the red “DOO” button at the top of the box. This mode means the atria and ventricle will be paced and there will be no sensing or inhibiting. However, when floating a transvenous pacer in the ED, a single lead is used and placed in the ventricle and so practically the mode is VOO.

A hiker has recently ascended to an altitude of 6000 meters. They begin to experience headache and vomiting. Their neurologic exam is notable for ataxia. What is the diagnosis and treatment? 

  • This is high altitude cerebral edema (HACE). Descent from altitude is the definitive treatment, however, 10 mg of PO or IV dexamethasone can be given as a temporizing measure while supplemental oxygen is provided. Acetazolamide is sometimes used as a prophylactic measure but is not generally effective after disease onset.

What underlying pathophysiology leads to acute mountain sickness and high-altitude cerebral edema? 

  • Hypoxic cerebral vasodilation

What differentiates the neurologic symptoms of type II decompression sickness and an arterial air embolism? 

  • Arterial air emboli are sudden onset and lead to stroke-like presentations, whereas type II decompression illness is subacute and causes spinal cord symptoms.

A patient presents with shortness of breath. A bedside ultrasound demonstrates a large pericardial effusion. What clinical and ultrasonographic features should you look for to determine if the patient has tamponade? 

  • Pericardial tamponade is primarily a clinical diagnosis, but ultrasound can aid us in making decisions. Signs of poor perfusion and unstable vitals in the setting of a pericardial effusion are signs of clinical tamponade. Ultrasonographic findings of RV diastolic collapse, RA systolic collapse and a dilated, non-collapsible IVC can be seen in tamponade and are sometimes seen before clinical decompensation. Larger pericardial effusions are more likely to cause tamponade, however even small effusions, if the accumulation is rapid, can lead to tamponade.

Potassium management in DKA is crucial. What is the minimum potassium level before insulin should be given? 

  • 3.3 meq/L. Remember that it is generally recommended that the potassium should actually be repleted if it is less than 5.3 meq/L while on an insulin infusion. It is usually easiest to shoot for a potassium between 4 to 5 meq/L. A good rule of thumb is that the patient should receive 20 to 30 meq of potassium for every liter of IV fluid.

A patient with insulin-dependent diabetes and end stage renal disease on MWF hemodialysis presents with DKA. How would you change your management for this patient? 

  • Remember that ESRD is an exclusion for SQUID! These patients are very complex and there is not great evidence for management. That being said, it is probably prudent to be more cautious with fluids, potassium repletion and insulin dosing. ESRD patients do not have an osmotic diuresis like those with normal kidneys and therefore do not have as significant of a fluid deficit. They are also less likely to have as much potassium wasting. Finally, insulin will take longer to be cleared in renal failure. Consider starting your insulin infusion at 0.05 units/kg rather than the usual 0.1 unit/kg we usually use in DKA. Weaning the infusion is more complicated as ESRD patients have a chronically elevated anion gap and it can be challenging to determine when their DKA has resolved. Consider trending their beta-hydroxybutyrate level in addition to BMPs.

A patient presents with an insulin pump and is found to have DKA. What kind of insulin is administered through an insulin pump? How should the pump be managed in the setting of DKA?  

  • Insulin pumps administer a continuous infusion of rapid acting insulin, which is usually an aspart or lispro formulation. Remember that disconnecting their pump can lead to relatively rapid development DKA as this is their main source of insulin. However, in the setting of DKA, most authors and professional societies recommend deactivating or removing the subcutaneous insulin pump and placing the patient on an IV insulin infusion during the episode of DKA. The decision to remove or keep the insulin pump on can be challenging and depends on numerous patient factors as well as the specific disease process. A discussion with endocrinology can be helpful for guidance in many scenarios.

References: 

 

  1. Mulpuru SK, Madhavan M, McLeod CJ, Cha YM, Friedman PA. Cardiac Pacemakers: Function, Troubleshooting, and Management: Part 1 of a 2-Part Series. J Am Coll Cardiol. 2017;69(2):189-210. doi:10.1016/j.jacc.2016.10.061 

  2. Davis C, Hackett P. Advances in the Prevention and Treatment of High Altitude Illness. Emerg Med Clin North Am. 2017;35(2):241-260. doi:10.1016/j.emc.2017.01.002 

  3. Alerhand S, Adrian RJ, Long B, Avila J. Pericardial tamponade: A comprehensive emergency medicine and echocardiography review. Am J Emerg Med. 2022;58:159-174. doi:10.1016/j.ajem.2022.05.001 

  4. Long B, Willis GC, Lentz S, Koyfman A, Gottlieb M. Evaluation and Management of the Critically Ill Adult With Diabetic Ketoacidosis. J Emerg Med. 2020;59(3):371-383. doi:10.1016/j.jemermed.2020.06.059 

  5. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes Care. 2009;32(7):1335-1343. doi:10.2337/dc09-9032 

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