Beta-Blockers

Cuts myocardial oxygen consumption in muscle fighting for supply — started orally within 24 h in hemodynamically stable patients, with the clearest benefit when LVEF is reduced. Contraindicated in cocaine-associated ACS or suspected vasospasm.

A genuinely different kind of answer: treat the body, not the thought. "Although beta-blockers are typically used to treat high blood pressure and other cardiac conditions, they can also be used to help relieve the physical symptoms of anxiety, such as rapid heartbeat, shaking, trembling, and flushing. These medications, when taken for a short period of time, can help people keep their physical symptoms under control. Beta-blockers can also be used as-needed to reduce acute anxiety or as a preventive intervention for predictable forms of performance anxieties — for example, some students who experience severe test anxiety that impairs their exam performance may take prescribed beta-blockers before their exams." Why the class earns a place here is what it does not do: it treats the peripheral symptoms without touching cognition or sedation, which is what makes an as-needed dose before a predictable performance situation workable. The cautions are short and have an awkward overlap with this population: common effects are "fatigue, hypotension, dizziness, weakness, and cold hands," and beta-blockers "are typically avoided in clients with asthma or diabetes" — and asthma and COPD are named comorbidities of panic disorder, so the patient most likely to want a beta-blocker for their heart racing may be the patient who should not have one.

The first drug in acute aortic syndrome (ACC/AHA 2022 Class 1): IV esmolol, labetalol, or metoprolol cuts heart rate and contractility together, lowering dP/dt and shear stress on the flap — titrated to HR 60–80 and SBP < 120 with an arterial line. It goes before any vasodilator so the vasodilator’s drop in pressure cannot trigger reflex tachycardia. Contraindications to respect: acute aortic regurgitation (the tachycardia is maintaining cardiac output), heart block, bradycardia. After dissection the class is lifelong to reduce late aortic events, and in Marfan or thoracic aneurysm a beta-blocker (or an ARB) at maximally tolerated dose slows aortic dilation. The trap: for abdominal aneurysm, beta-blockers do not slow growth or prevent rupture — there they are only a BP and cardiac-risk drug.

HCM first-line — a negative inotrope, titrated until the resting heart rate is suppressed; "Beta-blockade failure should not be declared until suppression of the resting heart rate is demonstrated." In DCM carvedilol, bisoprolol or long-acting metoprolol are part of the HFrEF regimen; in stable takotsubo a cardioselective beta-blocker (with an ACE inhibitor) is used for about 3 to 6 months; in RCM it may lengthen filling time.

Must be nonselective (propranolol, nadolol, carvedilol — carvedilol preferred): the target is portal pressure, not blood pressure — lower cardiac output means less splanchnic flow and a lower HVPG. Primary prophylaxis cuts first-bleed risk from ≈ 25% to 15%; after a bleed, the beta-blocker is the modality that reduces mortality (banding alone does not).

Lower heart rate, contractility, and BP — oxygen demand falls. Beta-blockers are first-line for angina symptom control, with calcium channel blockers used when a beta-blocker is contraindicated, not tolerated, or insufficient. Titrate to a resting HR of 55–60 if symptoms persist; avoid in vasospastic (Prinzmetal) angina, where CCBs are first-line and beta-blockers can worsen spasm.

First-line rate control in afib (chronic goal < 110 bpm) and long-term suppression of recurrent SVT. The flip side: beta-blockers sit on the ledger’s cause list for bradycardia — assess the HR before every dose and notify the provider if it is < 60 bpm.

Pillar 2: blunts the sympathetic arm of the compensation cycle. Only three are evidence-based in HFrEF — carvedilol, bisoprolol, metoprolol succinate — started low and titrated slowly.

Not first-line for uncomplicated hypertension in any current major guideline — reserved for compelling indications (HFrEF, post-MI, AF rate control). The exception where they lead: aortic dissection, where IV esmolol is first-line crisis therapy.

The symptom bridge while definitive therapy takes weeks: the misery of hyperthyroidism is largely β-adrenergic (palpitations, tremor, anxiety), so beta-blockade brings rapid relief without changing hormone levels. Atenolol is preferred for daily control; propranolol is preferred in storm because it additionally inhibits 5′-monodeiodinase, blocking peripheral T4→T3 conversion (esmolol IV in the ICU; a cardioselective agent if reactive airway disease; verapamil if beta-blockers can’t be used).

Prevention: metoprolol or propranolol, especially in hypertensive non-smokers. Avoid starting them as initial therapy over 60 or in smokers, and use caution with asthma, bradycardia, erectile dysfunction and peripheral vascular disease.

Only after alpha-blockade — never first. "At least 3 to 4 days after starting α-blockade, β-blockade with propranolol, atenolol, or metoprolol should be initiated to manage tachycardia." Given first, a beta-blocker removes beta-2 vasodilation and leaves "unopposed alpha-adrenergic receptor-mediated vasoconstriction, which can lead to a life-threatening crisis." Labetalol is not preferred — its α:β ratio of 1:7 means it can still provoke unopposed alpha stimulation. Non-selective beta-blockers are also on the list of crisis triggers. In pregnancy beta-blockers are used only if needed (intrauterine growth restriction).

[RAY] A cause, not a treatment. "Drugs, such as antimigraine medications, interferon alpha and beta, cyclosporine, and nonselective beta blockers, can cause secondary Raynaud phenomenon"; NIAMS adds that blood-pressure medicines may make Raynaud's worse. Review the medication list.

[Raynaud’s] Caution. "nonselective beta blockers" can cause secondary Raynaud’s, and StatPearls advises that "switching to an alternative medication should be attempted if possible, as β-blockers may exacerbate Raynaud symptoms." Flag the order for the prescriber — do not stop it yourself.

In mitral stenosis beta-blockers are first-line rate control: a stenotic mitral valve passes blood only in diastole, so slowing the heart prolongs diastolic filling and lowers the transmitral gradient with exertion; they also control the ventricular rate once AF arrives. In aortic stenosis the same drug is used cautiously — the fixed obstruction limits the compensation a slowed, weakened ventricle can mount. In acute AR they are avoided outright: blocking the compensatory tachycardia lengthens diastole and lets more blood regurgitate. In secondary MR and rheumatic heart failure they are part of guideline-directed HF therapy as tolerated.

Lower BP by blocking angiotensin conversion. Classic dry cough & angioedema risk.

Lower LDL cholesterol via HMG-CoA reductase inhibition. Monitor for myopathy.

Injectable antibodies that protect the liver’s LDL receptors, cutting LDL cholesterol by about half and lowering cardiovascular events. Given subcutaneously every 2–4 weeks.

PPAR-α agonists that mainly lower triglycerides — used with diet for severe hypertriglyceridemia — with muscle, gallbladder, liver and kidney risks, highest for gemfibrozil combined with a statin.

Non-absorbed resins that trap bile acids in the gut, forcing the liver to use cholesterol and pull LDL from the blood. Constipation, drug binding and rising triglycerides are the issues to manage.

Six non-statin drugs with six targets: ezetimibe (intestinal cholesterol absorption), bempedoic acid (liver cholesterol synthesis), inclisiran (PCSK9 mRNA), niacin and icosapent ethyl (triglyceride-rich lipoproteins) and lomitapide (MTP, for homozygous FH only).