Treatment of Noncardiogenic Pulmonary Edema
Question# 827
My question pertains to the use of nitroglycerin in pulmonary edema. Our directive specifies the use of nitro solely for cardiogenic pulmonary edema. I recently had a patient who deteriorated and did not respond to CPAP to the point of borderline respiratory failure. On our assessment, this patient was experiencing pulmonary edema due to chronic kidney disease, and not due to cardiac causes (this was later all but confirmed at hospital). On arrival to hospital, the patient promptly was switched to BiPAP and was administered several doses of nitro (both through spray and patch). The patient improved significantly, and I believe nitroglycerin would have been a benefit to the patient en route to hospital. Is there a reason our directive limits us to cardiogenic pulmonary edema? In this situation it was difficult to complete a BHP but would a BHP be recommended for nitro administration? Is there room for our own clinical judgment in these situations?
Answer:
Pulmonary edema occurs as a consequence of excess fluid into the alveoli as a result of a deficiency in Starling’s forces, and is generally categorized as cardiogenic or noncardiogenic.
In cardiogenic pulmonary edema, the abnormal fluid movement into the lungs is caused by high pulmonary pressures, leading to potentially fatal acute respiratory failure. Usually, this is often the result of acute decompensated heart failure, but other conditions can cause this as well, such as primary fluid overload, severe hypertension, renal artery stenosis, and severe renal disease.
In contrast, noncardiogenic pulmonary edema “is a distinct clinical syndrome associated with diffuse filling of the alveolar spaces in the absence of elevated pulmonary capillary wedge pressure”. The major causes of noncardiogenic pulmonary edema are the acute respiratory distress syndrome (ARDS) and, less often, high altitude and neurogenic pulmonary edema. Other less common causes include pulmonary edema due to opioid overdose, pulmonary embolism, eclampsia, transfusion-related acute lung injury and acute kidney injury
Despite the differing underlying pathologies, the distinction is not often possible and can require a focused history, physical examination, echocardiography, laboratory analysis, and more invasive investigations – many of which can not be performed prehospitally.
In terms of treatment, we often see “flash” cardiogenic pulmonary edema prehospitally. Often, this the edema is caused by a hypertensive emergency (sudden rise in left-sided intracardiac filling pressures), acute ischemia, a new onset tachyarrhythmia, or obstructive valvular disease. As you’ve seen, this condition responds well to BiPAP, and venous and arterial vasodilators, such as the nitroglycerine we administer. Nitroglycerin effectively reduces preload in cases of acute pulmonary edema and at higher doses, it also moderately decreases afterload. Based on the current literature, there is no consistently demonstrated significant clinical benefits of using Nitroglycerin in the management of non-cardiogenic pulmonary edema.
Treating the noncardiogenic causes of pulmonary edema requires us to treat the underlying cause, which as mentioned, is very hard to diagnose prehospitally. Having said that, providing supportive measures such as non-invasive ventilation (CPAP) can still treat symptoms and underlying SOB and crackles, until further assessment and management can be started in the emergency department
If you feel that the patient in front of you can benefit from a treatment outside of the ALS PCS, we encourage you to patch to a base hospital physician to engage in these patient-centred discussions.
In cardiogenic pulmonary edema, the abnormal fluid movement into the lungs is caused by high pulmonary pressures, leading to potentially fatal acute respiratory failure. Usually, this is often the result of acute decompensated heart failure, but other conditions can cause this as well, such as primary fluid overload, severe hypertension, renal artery stenosis, and severe renal disease.
In contrast, noncardiogenic pulmonary edema “is a distinct clinical syndrome associated with diffuse filling of the alveolar spaces in the absence of elevated pulmonary capillary wedge pressure”. The major causes of noncardiogenic pulmonary edema are the acute respiratory distress syndrome (ARDS) and, less often, high altitude and neurogenic pulmonary edema. Other less common causes include pulmonary edema due to opioid overdose, pulmonary embolism, eclampsia, transfusion-related acute lung injury and acute kidney injury
Despite the differing underlying pathologies, the distinction is not often possible and can require a focused history, physical examination, echocardiography, laboratory analysis, and more invasive investigations – many of which can not be performed prehospitally.
In terms of treatment, we often see “flash” cardiogenic pulmonary edema prehospitally. Often, this the edema is caused by a hypertensive emergency (sudden rise in left-sided intracardiac filling pressures), acute ischemia, a new onset tachyarrhythmia, or obstructive valvular disease. As you’ve seen, this condition responds well to BiPAP, and venous and arterial vasodilators, such as the nitroglycerine we administer. Nitroglycerin effectively reduces preload in cases of acute pulmonary edema and at higher doses, it also moderately decreases afterload. Based on the current literature, there is no consistently demonstrated significant clinical benefits of using Nitroglycerin in the management of non-cardiogenic pulmonary edema.
Treating the noncardiogenic causes of pulmonary edema requires us to treat the underlying cause, which as mentioned, is very hard to diagnose prehospitally. Having said that, providing supportive measures such as non-invasive ventilation (CPAP) can still treat symptoms and underlying SOB and crackles, until further assessment and management can be started in the emergency department
If you feel that the patient in front of you can benefit from a treatment outside of the ALS PCS, we encourage you to patch to a base hospital physician to engage in these patient-centred discussions.
References
ALS PCS
UpToDate – Noncardiogenic Pulmonary Edema
UpToDate – Pathophysiology of Cardiogenic Pulmonary Edema
Published
29 July 2024
ALSPCS Version
5.3
Views
516
Please reference the MOST RECENT ALS PCS for updates and changes to these directives.