Acutely decompensated CHF can be a highly dangerous condition and one that needs immediate management. Previous Resuscitation Leadership Academy (RLA) student Michelle Perkins comes on for her debut to discuss management of this condition.
Dr. Michelle Perkins is a rural emergency medicine physician working in Downeast Maine. She reminds us that chronic congestive heart failure (CHF) is divided into diastolic and systolic dysfunction. However, by the time patients reach us in the emergency department (ED), this is less helpful.
Acute decompensated CHF has a variety of causes such as ischemia, infection, and arrhythmia. Pulmonary edema is a back-up issue. The left ventricle (LV) can no longer handle the pulmonary venous return. Most likely one of three things has happened: increased preload, increased afterload, and decreased LV function but these can occur in combination.
It is critical to remember that the traditional teaching that patients in CHF are fluid-overloaded is not accurate for this situation. They are fluid-overloaded in their lungs but not total body. Amal Mattu describes this best in a small bucket and big bucket approach. The small bucket is the lungs which can be full without the whole body (the big bucket) being full. It is vital to understand this in order to understand the management.
Acute decompensated CHF has in most cases a very obvious presentation. These patients look sick and need to be recognized quickly. Often, their blood pressure is elevated in an emergent type fashion as discussed in the podcast just previous to this one. Ultrasound is especially helpful in the undifferentiated dyspnea patient as discussed two podcasts ago.
Labs are not a key point, especially in initial management. Most hospitalists will want Brain or B-Type Natriuretic Peptide (BNP) even though its use is limited in the ED. This was covered in 2009 in the Annals of Emergency Medicine and in a detailed review on emDocs. Given different underlying causes, routine labs and EKG along with imaging can all be done, but again this is a clinical diagnosis. Management is the more important initial step.
In its most severe for, Sympathetic Crashing Acute Pulmonary Edema (SCAPE), look no further than EmCrit for a crash course on this management. However, classic management has been taught under the mnemonic of LMNOP. This stands for Lasix, Morphine, Nitrates, Oxygen, and Position. This management has been cut down inprevious papers. As discussed above, these patients are not as described. They are not total-body fluid overloaded and Lasix is not beneficial in this case. Again, check out emDocs for more on why furosemide (Lasix) is not a good option in acute pulmonary edema. Basically though, this medicine does not work since patients are already "clamped down" and the fluid is not going to the kidneys (where this medicine works). When the kidneys do finally see this you risk dropping their blood pressure, raising creatinine, and now start the fight with IV fluids. Morphine also has risks that have been previously documented including with the ADHERE analysis. Essentially, the risk is respiratory depression along with its anti-platelet inhibition which could be a problem if these patients may go to a cath lab.
As the SCAPE podcast on EmCrit states, what you need to do is treat with nitroglycerin first. Also, non-invasive positive pressure ventilation (NIPPV) is key. This combination addresses most of what is going on with these patients. The combination will reduce preload, reduce afterload, and help with LV dysfunction in such patients. Decreasing preload will decrease RV output to an amount that the LV can handle which improves the fluid backup. Decreasing afterload also improves LV output. All of this has helped reduce the need for intubation in these sick patients.
When it comes to nitrates, the goal is to cause rapid and marked venodilation with the goals described above. Sublingual can be used first but drips are needed. When using this medication, it can be quickly titrated and reduced as needed. Initially, we are looking at drip rates often 100-200 mcg/min. The half-life is so short, that even if someone drops their pressure, you can shut off the drip and have the hypotension resolve without other intervention. If concerned about dosing, remember that the sublingual form is being given as 400 mcg at a time. If doses are being repeat every five minutes, this is equivalent of 80 mcg/minute of a drip.
Other medications such as ACE inhibitors could be used but not often needed initially. The same is true for Lasix but is often requested at some point during the management. This is something that again can be discussed with the hospitalist or admitting physician.
Finally, what about hypotensive patients? These are the ones that will require ionotropy or dysrhythmia management, if that is the underlying issue. Dobutamine is first line for an ionotrope, and consider adding a vasopressor if the blood pressure does not improve. These are the folks with primary pump failure, and really all you are doing is temporizing so the primary problem can be addressed (such as ischemia).
As mentioned in our last podcast, we have a couple of upcoming events in April. The first is SEMPA 360 located this year in Phoenix, Arizona and then the Podcasting Course in Lexington, Kentucky. If you are attending let us know as we would love to meet you.
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