Index
Module 11 • Cardiology
Cardiovascular Critical Care I
65%
Data Tables
Cardiovascular Critical Care I
Sajni V. Patel ~3 min read Module 11 of 20
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Cardiovascular Critical Care I

2Once other causes of symptomatic congestion and/or low perfusion at rest have been ruled out and

a diagnosis of decompensated HF is deemed likely, the following should be considered: If volume

overloaded, provide intravenous diuretics at least equal to the patient’s home oral dose (or alternatively

up to 2–2.5 times the patient’s home dose may be used) (N Engl J Med. 2011;364(9):797-805). For

patients who are diuretic naive on admission, a starting dose of 20–80 mg of furosemide (or equivalent)

is reasonable.

Monitor for clinical improvement in symptoms and adequate urine output.

Proactive evaluation of urine output adequacy should be used to facilitate optimization/escalation

of diuretic regimen.

Increase in loop diuretic dose and/or addition of sequential nephron blockade (i.e., metolazone)

may be considered as needed to achieve the desired urine output and fluid balance. Recent evidence

also suggests that SGLT2 inhibitors and acetazolamide may also help improve response to diuretic

therapy (Circulation 2022;146:289-98; N Engl J Med 2022;387:1185-95). Administration of the loop

diuretic as a continuous infusion can also be considered.

d.For patients unresponsive to diuretic escalation as above or those with end-stage renal disease,

hemodialysis and isolated ultrafiltration can be used for fluid removal.

3

Evaluate for use of vasodilator therapy.

If normotensive or hypertensive (e.g., SBP greater than 100 mm Hg) in the presence of acute

pulmonary edema (despite diuretic therapy):

Continuous infusion intravenous vasodilators (e.g., nitroglycerin or nitroprusside) should be

considered.

ii.

If the presence of high afterload is confirmed (systemic vascular resistance [SVR] greater

than 1200 dynes/s/cm5), then nitroprusside may be warranted more than other vasodilators.

However, careful attention to patient selection is important because nitroprusside elimination

is dependent on both hepatic metabolism and renal clearance. Note that nitroprusside is

converted to nitric oxide and cyanide, with subsequent conversion to thiocyanate. Signs of

potential toxicity include metabolic acidosis and mental status changes. In addition, patients

receiving nitroprusside should have an arterial line for close blood pressure monitoring and

typically a Swan-Ganz catheter in place.

iii.

Pulmonary vasodilators may be required in patients with evidence of pulmonary arterial

hypertension: inhaled nitric oxide, epoprostenol, or alternatively phosphodiesterase type 5

inhibitors (sildenafil). Inhaled nitric oxide and epoprostenol may also be considered as short-

term adjuncts in patients with right ventricular dysfunction and pulmonary hypertension in the

perioperative setting. The delivery system and high cost associated with inhaled nitric oxide is

a limitation relative to other options.

If hypotensive (e.g., SBP of 100 mm Hg or less): Can consider vasodilators, but with caution

4

Monitor for clinical improvement of symptoms and adequate urine output.

Proactive evaluation of urine output adequacy should be used to facilitate optimization/escalation

of diuretic regimen. An optimized diuretic dose should produce 100–150 mL/hour of urine output

at 6 hours or 50–70 mEq/L of urine sodium at 2 hours.

5

Evaluate for use of inotrope therapy

If inadequate response on escalation of diuretics (and vasodilators, if appropriate), inotrope therapy

should be considered, accounting for any concurrent physiologic considerations (e.g., right HF,

pulmonary hypertension, ischemia, or valvular disease)

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