key: cord-0848785-4u3fgg9h
authors: Gyory, Michael; Abdallah, Samantha; Lagina, Anthony; Levy, Phillip D.; Twiner, Michael J.
title: Ultra‐high dose intravenous nitroglycerin in an ESRD patient with acutely decompensated heart failure
date: 2021-03-02
journal: J Am Coll Emerg Physicians Open
DOI: 10.1002/emp2.12387
sha: 615204f89c69f5e7da457c59de14b6583a33392f
doc_id: 848785
cord_uid: 4u3fgg9h

Acute cardiogenic pulmonary edema is a highly unstable and potentially lethal condition that is most commonly associated with markedly elevated blood pressure (BP). Use of nitrates, diuretics, and non‐invasive positive pressure ventilatory support are the mainstays of early intervention and stabilization. Use of high‐dose bolus intravenous nitroglycerin, which causes both preload and afterload reduction, has shown significant promise in studies to date, reducing the need for endotracheal intubation (ETI) and intensive care unit admission. To date, the highest recorded total dose of nitroglycerin used during the initial stabilization of acute pulmonary edema has been 20 mg. Here, we describe a patient with end‐stage renal disease who developed acute cardiogenic pulmonary edema and received a total of 59 mg nitroglycerin (56 mg push dose intravenous + 3 mg intravenous drip) over 41 minutes leading to successful stabilization and avoidance of ETI, facilitating rapid initiation of emergent hemodialysis.

Mainstay therapy for acute heart failure (AHF) consists of vasodilators and diuretics. Vasodilators, such as nitroglycerin (NTG), provide both preload and afterload reduction, which is beneficial in AHF, especially for those who present with markedly elevated blood pressure (BP). 1 The mortality rate for severe AHF may be as high as 15% during the initial treatment period and 35% by 1 year. 2 Unfortunately, standard vasodilatory therapy does not reduce mortality or hospital readmission in these patients. 3 6 Existing data suggest a substantial improvement in symptoms and better in-hospital outcomes for patients with AHF, with minimal adverse effects. A subsequent chest x-ray showed no acute cardiopulmonary process.

Initial workup was significant for a serum creatinine of 6.89 mg/dL and a blood urea nitrogen of 46 mg/dL (estimated [glomerular filtration rate] GFR = 10 mL/min/1.73 m 2 ). A venous blood gas revealed hypoxic hypercapnic respiratory acidosis (pH = 7.31, PCO 2 = 54, pO 2 = 28, HCO 3 = 27) and a high sensitivity cardiac specific troponin (hs-cTnl) of 113 ng/L (Beckman Coulter assay; reference range: 3 ng/L detection limit and ≥18 ng/L suggestive of myocardial injury). A coronavirus swab was negative.

After the initial sublingual and intravenous bolus NTG, the patient was given 40 mg of intravenous furosemide for diuresis. There was an initial improvement in the patient's BP to 160/100 mm Hg and respiratory rate to the low 20s. He was started on a 5 µg/minutes (0.3 mg/hours) continuous NTG infusion, which was gradually scaled up to 20 µg/minutes based on the patient's symptoms (see Figure 1 for a time course of vital signs and treatments). At this time, the patient was stable enough to be given his home anti-hypertensive medications orally (80 mg valsartan, 10 mg amlodipine, and 25 mg metoprolol) and was transitioned from 15 L/minutes nonrebreather to 6 L/minutes nasal cannula. However, shortly thereafter, he developed worsening tachypnea and BP increased substantially to 249/147 mm Hg. He was placed on bilevel positive airway pressure (BiPAP) and intravenous push doses of NTG were administered in rapid succession starting with 2 2-mg doses followed by a 4-mg dose and an 8-mg dose. Endotracheal intubation was considered as he was tachypneic to the 40 seconds. Two additional 16-mg intravenous push doses of NTG followed by another 8 mg were given, and he experienced significant improvement in his symptoms. He was given another dose of intravenous furosemide (40 mg) and the NTG drip was increased to 100 µg/minutes. At this stage, his BP had improved to the 140s/90s with a respiratory rate in the 20 seconds. He was admitted to the ICU for further management, including bronchodilators and emergent hemodialysis.

It has previously been demonstrated that high-dose bolus intravenous NTG for acute, cardiogenic pulmonary edema is associated with lower rates of ICU admission and ETI 4 and shorter lengths of stay in the hospital. Based on published reports, most patients are rapidly stabilized on lower doses of (ie, 1-2 mg NTG) 5 with the highest reported total dose given over a short time period of 20 mg. 4 In summary, when it comes to use of bolus intravenous NTG for AHF with acute hypertensive cardiogenic pulmonary edema, our case shows that early aggressive dosing coupled with on-going maintenance of BP reduction was both safe and effective for this single patient.

The pathophysiology of hypertensive acute heart failure

Treatment of severe decompensated heart failure with high-dose intravenous nitroglycerin: a feasibility and outcome analysis

Lack of evidence for intravenous vasodilators in ED patients with acute heart failure: a systematic review

Use of nitroglycerin by bolus prevents intensive care unit admission in patients with acute hypertensive heart failure

Role of high-dose intravenous nitrates in hypertensive acute heart failure

Impact of a high-dose nitrate strategy on cardiac stress in acute heart failure: a pilot study

High-dose nitroglycerine infusion for the management of sympathetic crashing acute pulmonary edema (SCAPE): a case series

Ultra-high dose intravenous nitroglycerin in an ESRD patient with acutely decompensated heart failure

The authors wish to thank our ED pharmacist Colin Cox and nurses Brian Brennan and Darryl Parado for their help in this case.