Why are calcium channel blockers (CCB) contra-indicated in congestive heart failure, while beta-blockers aren't?
I understand that CCB may worsen the situation with a significant drop in cardiac output (CO), since they're negative inotropes and can further deteriorate the cardiac function.... but don't beta-blockers ultimately do the same thing? They're negative chronotropes, so they will also cause a decrease in CO. Why can they be used in heart failure while CCB cannot?
Thanks in advance.
It's a good question! Your thought process is correct.
Fundamentally while both (assuming you mean cardioselective CCBs) are negative chronotropes (also both ionotropes btw), diltiazem/verapamil are stronger with longer durations than even the standard Toprol XL (succinate) and they carry a Black Box warning for HF (i.e. the data says they exacerbate the issue more than BB). Where this becomes clinically relevant is atrial arrhythmias like AFib/Flutter which often are associated with structural heart disease. The first step if a patient presents in AF with RVR is to try IV BB if they're hemodynamically stable and then add a oral BB. Afterwards, you generally escalate to a Calcium Channel blocker like Diltiazem XR if you're on orals of a CCB gtt if IV metop didn't work after two chances and their BP is still OK. You don't do that in a patient with reduced EF or history of ICM with mEF. Rhythm control should be reserved to cases where patient's are anticoagulated for a while or with cardiology OB because you generally don't know for sure if this is paroxysmal or not because most people don't have event monitors. The amiodarone will also need to be weaned and cardiologists generally like to manage this.
Amlodipine/Nifedipine (non-cardioselective) are fine in most cases including rEF, BUT keep in mind if you're trying to optimize guideline directed therapy on a new patient with HF with reduced EF the goal should be to add on as many agents as the patient can tolerate BP-wise for afterload reduction, ventricular remodeling, improved cardiac energetics, decreased stress (Angiotensin modulators, Beta Blockers, MRAs, SGLT2i, etc.) most of these drop BP in some way. Non-selective CCBs and Thiazides drop BP as well, but don't have the cardiac benefits. This is what is meant when attendings say they "we have more room (BP, HR), let's add XYZ GDMT". You can create more room oftentimes by throwing out the Amlodipine and HCTZ their PCP probably had them on before their heart failed.
Bonus Info Re: HF in general:
1.) Diastolic HF vs. HFpEF. While Diastolic HF sounds like a more physiologically precise term and the ICD code promotes use of this as opposed to HFpEF, it really creates a misconception. Take a patient with EF 65-70%, moderate LVH, presenting with SBP-170s with some HF symptoms. Many clinicians would surmise this being Diastolic HF because 1) patient has HF symptoms (current reasoning) 2) patient fits picture of pathological hypertrophy which would caused increased LV EDP which is an oversimplified approach. Unless you do an LV gram or RHC giving you the hemodynamics though you can't prove that point. HFpEF is actually being studied and there are more mechanisms at play other than impaired diastole. Therefore, while less fulfilling, it is probably best to adhere to the less precise, but at least not incorrect, HFrEF and HFpEF nomenclature. I hate the terms too.
2.) When administered IVF in heart failure, I've heard people make the distinction between low EF and LVH when thinking how much fluid to give them. There's not hard rule and I've seen patients with normal ECHOs with mild LVH get edematous/edema from minimal fluids while patients with HFrEF seem compensated superficially on exam at least despite fluids left running for days. In other words, what factors predispose someone to edema from fluids seems a bit unpredictable simply from my clinical experience. The most reliable factor seems to be age.
Hope that helps!