A client presents to the emergency department complaining of sudden onset of palpitations and chest pain. After assessment, the nurse notes the client to be diaphoretic, skin is cool to touch, BP is 80/40 mm Hg. Resp 26 and Sats of 89% [see image]. The nurse anticipates an order for which of the following interventions?

A) Spironolactone:
Spironolactone is a potassium-sparing diuretic commonly used in the treatment of heart failure. Unlike other diuretics, spironolactone works by antagonizing aldosterone, a hormone that promotes sodium and water retention and potassium excretion. By blocking aldosterone's action, spironolactone prevents the kidneys from excreting potassium, thus increasing potassium levels in the blood (hyperkalemia). Additionally, spironolactone can lead to hyponatremia (low sodium levels), as it also causes the kidneys to retain sodium and water, diluting sodium levels in the blood.

B) Furosemide:
Furosemide, a loop diuretic, is typically used in heart failure to remove excess fluid. It works by inhibiting the reabsorption of sodium, chloride, and potassium in the loop of Henle, which increases urine output. While furosemide can cause hypokalemia (low potassium levels) due to the increased excretion of potassium, it does not typically cause hyperkalemia.

C) Hydrochlorothiazide:
Hydrochlorothiazide is a thiazide diuretic, which works by inhibiting sodium and chloride reabsorption in the distal convoluted tubule of the kidney, leading to increased urine production. Thiazide diuretics can cause hypokalemia (low potassium levels) and hyponatremia (low sodium levels) due to the enhanced excretion of both electrolytes.

D) Metolazone:
Metolazone is also a thiazide-like diuretic that works similarly to hydrochlorothiazide. It can cause hypokalemia and hyponatremia, but like hydrochlorothiazide, it does not typically cause hyperkalemia. Metolazone is more potent than hydrochlorothiazide but still does not carry the risk of hyperkalemia like spironolactone does.

A. Synchronized cardioversion: Synchronized cardioversion is indicated for unstable supraventricular tachycardia (SVT), especially when the client shows signs of hemodynamic instability, such as hypotension, altered mental status, or chest pain. This intervention delivers a timed shock to restore normal rhythm, prioritizing the client's immediate stabilization.

B. Adenosine infusion over 30 minutes: Adenosine is typically administered as a rapid intravenous push to terminate SVT by temporarily blocking atrioventricular nodal conduction. However, this client is unstable, and synchronized cardioversion is the preferred intervention in cases of hemodynamic compromise.

C. Immediate defibrillation: Defibrillation is used for life-threatening arrhythmias like ventricular fibrillation or pulseless ventricular tachycardia. In this case, the rhythm is SVT, and the client is not in cardiac arrest, so defibrillation is inappropriate.

D. Vagal maneuvers: Vagal maneuvers, such as carotid sinus massage or the Valsalva maneuver, are first-line interventions for stable SVT. However, in unstable clients with severe symptoms or hemodynamic compromise, these measures are insufficient, and synchronized cardioversion is urgently required.