In this Part 1 of our two-part series on acute heart failure, Anton is joined by Dr. Tarlan Hedayati and Dr. Bourke Tillman to answer such questions as: how does PoCUS compare with clinical assessment and CXR in diagnostic accuracy for acute heart failure? How do we best integrate PoCUS in the our assessment and management of the patient with acute heart failure? What is PPV HAVoC and how can we use it to optimize acute heart failure management goals? What should be our specific goals of management in the acute heart failure depending on the underlying cause? How does high flow nasal cannula (HFNC) compare to non-invasive positive pressure ventilation (NIPPV) in the management of acute heart failure? How should we interpret the C3PO trial in the context of the world’s literature on NIPPV in acute heart failure? How should we dose nitroglycerin to maximize its effects without dumping the blood pressure in patients with SCAPE and those without SCAPE? How should we best time and dose furosemide in the acute heart failure patient with renal insufficiency? Is there any role for morphine or ACEi in the ED management of acute heart failure? What are best anxiolytic medication choices in acute heart failure? Is there any role for second line diuretics in the management of acute heart failure in the ED? and many more…
Deep dive into value of BNP in ED management of heart failure: Journal Jam 12 BNP for Diagnosis of Acute CHF
Assessment of the patient suspected of acute heart failure with PoCUS helps to differentiate it from other causes of shortness of breath, is accurate for the diagnosis of acute heart failure and can help elucidate the underlying cause. B-lines are only the start. Follow the links for more info on each of the PoCUS aspects of assessment of the patients with acute heart failure.
POCUS Cases on LV Dysfunction with Rob Simard
POCUS Cases on IVC and volume assessment with Rob Simard
While medication non-compliance and dietary indiscretion are the most common causes of acute heart failure, there are several life-threatening causes that should be identified and addressed in the ED, the most time-sensitive being ACS:
PPV – positive pressure ventilation
Hypotension correction with vasopressors
Afterload reduction
Volume status (consider diuresis vs. intravascular volume repletion)
Cause (treat underlying cause)
Divide patients into two categories based on their hemodynamic status:
Identify and treat the underlying cause of acute heart failure in tandem
Escalation of oxygenation strategies is usually indicated in the dyspneic acute heart failure patient who continues to display an oxygen saturation <91%. Options include non-rebreather, high flow nasal cannula, non-invasive positive pressure ventilation (NIPPV) and endotracheal intubation.
Patients with pulmonary edema from acute heart failure who are tachypneic and in respiratory distress respond well to NIPPV because it helps to reduce cardiac preload (by increasing intrathoracic pressure) and afterload thus improving forward flow. It also improves atelectasis and gas exchange at the bases of the lungs which can improve hypoxia. NIPPV can reduce the work of breathing, decreasing intrathoracic muscle use, thereby reducing oxygen consumption.
Indications for NIPPV (Canadian Cardiovascular Society):
Contraindications NIPPV:
Failure of NIPPV (consider endotracheal intubation):
Tips to help patients tolerate NIPPV:
The Evidence for NIPPV in CHF: Controversy Surrounding the 3CPO Trial
Studies have shown significant mortality benefit (NNT 13) and avoidance of intubation (NNT 8) with the use of NIPPV in acute heart failure. Though not demonstrating a mortality benefit, other studies have shown that in comparison to standard oxygen delivery NIPPV showed a benefit in terms of self-reported dyspnea, tachycardia, acidosis, and hypercapnia, with no treatment related adverse events compared to standard oxygen delivery.
3CPO Trial (2008): A large multi-center RCT of C-PAP and B-PAP in the UK, that looked at 1069 patients in severe cardiogenic pulmonary edema. Patients were randomized to receive standard oxygen, C-PAP and B-PAP. Results demonstrated no significant difference between the 3 arms on the following parameters: 7-day mortality, 30-day mortality, intubation rates, admission to ICU.
They noted earlier resolution of respiratory distress and metabolic acidosis in the C-PAP/B-PAP arm. It should be recognized that patients who failed standard oxygen therapy were able to use NIPPV. This means that the sickest patients in the standard arm may have received the intervention but were still counted in the standard arm.
In a subsequent meta-analysis of the use of NIPPV in acute cardiogenic pulmonary edema that included the 3CPO, the evidence gathered supported the use of NIPPV for patients in acute pulmonary edema. They were unable to detect a significant difference between C-PAP and B-PAP when they were compared directly. They found that NIPPV reduced mortality, reduced the need for intubation and ICU admission in patients who fail high flow oxygen, and improved the patient’s subjective symptoms.
Bottom Line: Despite controversy stemming from 3CPO trial, the best evidence to date suggests that NIPPV reduces mortality, need for intubation and ICU admission rates, but only in patients who fail high flow oxygen.
A small observational study in 2019 compared HFNC to intubation in patients with acute CHF and found that they had similar outcomes. 87% of patients who were in the HFNC group recovered from progressive hypoxemia without the need for endotracheal intubation. HFNC acts to decrease physiologic dead space in the upper airway, increase the delivery of FiO2 and may provide a small amount of PEEP. It should be considered in patients who are not tolerating B-PAP/C-PAP to stave off intubation. However, it is not recommended as a first line oxygenation strategy in acute heart failure patients who fail a nonrebreather.
Bottom Line: in those patients who are failing a nonrebreather, NIPPV is considered first line, and if it fails, consider HFNC to prevent the need for endotracheal intubation.
Nitroglycerin is the first line medication in patients with acute heart failure who are not in cardiogenic shock as it reduced afterload and preload and redistributes fluid from the pulmonary system rapidly. It has been shown to improve hemodynamic status, respiratory distress, reduces intubation rates and ICU admissions, however it has not been shown to improve mortality. Canadian Cardiovascular Society suggests IV nitroglycerin in patients with SBP >100.
Our experts’ approach to administering nitroglycerin:
Start with 3 sprays or tabs sublingual (400ug x3 =1200ug), apply NIPPV (when indicated), and start a nitroglycerin infusion (50-100 ug/min, and titrate to 100-200ug/min)
Common pitfall: not giving enough nitroglycerin when we start an infusion; remember that 1 spray of nitroglycerin is ~ 400 ug sublingual, so starting a nitro infusion at 5 ug/min akin to a homeopathic dose! Rather, nitroglycerin infusions should be started at 50-100 ug/min depending on the patient’s blood pressure.
Update 2024: An open-label randomized control trial including 54 patients with sympathetic crashing acute pulmonary edema (SCAPE) found that patients receiving high-dose nitroglycerin (600-1000mcg IV bolus followed by 100mcg/min) compared to conventional low-dose nitroglycerin (no bolus, 20-40mcg/min) had higher symptom resolution at 6 hours (65.4% vs 11.5%; P<0.001) and 12 hours (88.5% vs 19.5%; P<0.001), shorter hospital stay (12 hours vs 72 hours), less frequent MACE (3.8% vs 26.9%; P=0.02), and lower intubation rate (3.8% vs 19.2%; P=0.08). Abstract
Based on the following protocol, a 2021 study suggests that in patients with SCAPE high dose NTG (600 – 1000mcg) bolus and NTG drip (100ug/min) and NIPPV is a safe strategy that may help to reduce the rate of endotracheal intubation and ICU admission.
Source: REBEL EM adapted from JEM https://www.frankenthalerfoundation.org
Indications for diuretics in acute heart failure: For patients with total body volume overload (eg. history of medication non-compliance and fluid restriction non-compliance with pedal edema, JVD, bibasilar crackles, plump IVC on PoCUS), removal of excess fluid via diuresis is likely to improve perfusion of the heart and kidneys by decreasing venous congestion and improving forward flow (Forward flow = MAP – CVP). Is is important to realize, however, that many patient with acute heart failure do not have true
