SA¹ú¼Ê´«Ã½

By Megan A. Mason MPH, NRP, FFII

It is mid-afternoon on a beautiful summer day when your crew is dispatched for an elderly female down with an unknown medical problem. Upon arrival, you find an elderly female in her back yard, conscious, with an altered mental status. The patient’s daughter reports the patient was working outside all day. As your partner begins her assessment, you ask the patient’s daughter to retrieve the patient’s medications. Your partner reports vital signs of:

• BP: 90/60
• Pulse: 60 and weak
• Respirations: 14
• SpO2: 98% on room air
• Lungs: clear
• Glucose: 134mg/dl
• Skin warm and dry
• Responsive to verbal stimuli and attempting to answer questions appropriately

You quickly instruct your partner to perform a 12-lead EKG, which shows sinus rhythm. At this time, the daughter reappears with the patient’s medications, which you quickly review, while also obtaining a medical history, which includes hypertension and high cholesterol. You notice that the patient is on metoprolol, which you remember is a beta blocker. You vaguely remember someone in medic school saying that beta blockers can slow the heart rate, but what exactly is a beta blocker, and is this why your patient’s heart rate is lower than expected?

| More: Become an EKG detective

Common beta blockers

Beta blockers, also known as beta-adrenergic blocking agents, are a class of medications commonly used to treat cardiovascular conditions, including angina, aortic dissection, heart failure, coronary artery disease, hypertrophic obstructive cardiomyopathy, portal hypertension, cardiac arrhythmias (SVT, atrial fibrillation, etc.), myocardial infarction, hypertension and migraines [2, 3].

Less commonly, they may also be used off label to treat hyperthyroidism, anxiety, tremors, and glaucoma [2, 3]. Some beta blockers work mainly on the heart, while others affect both the heart and blood vessels [8]. Common beta blockers include [3, 8]:

• Acebutolol
• Atenolol (Tenormin)
• Bisoprolol (Cardicor or Emcor)
• Carvedilol
• Labetalol (Trandate)
• Metoprolol Tartrate/Succinate (Kapspargo Sprinkle, Lopressor, Toprol-XL)
• Nadolol (Corgard)
• Nebivolol (Bystolic)
• Propanolol (Inderal or Angilol, InnoPran XL)
• Sotalol

Beta receptors

To understand beta blockers, it is necessary to first understand the role of beta receptors.

There are three types of beta receptors: beta-1 (B1), beta-2 (B2) and beta-3 (B3) [5]. Beta-1 receptors are the primary focus of beta blockers, and are located in the heart, kidneys and fat cells [1]. Beta-1 receptors are adrenergic receptors primarily responsible for sympathetic nervous system signaling, in conjunction with alpha-1 and alpha-2 receptors [1, 5]. Beta-1 receptors are G-protein coupled receptors that are activated by the catecholamines norepinephrine (noradrenaline) and epinephrine (adrenaline) [1, 4]. Activation of cardiac beta-1 receptors increases sinoatrial (SA) nodal, atrioventricular (AV) nodal, and ventricular muscular firing, thus increasing heart rate and contractility, and thereby increasing stroke volume and cardiac output, and also activate the release of renin in the kidneys [1, 2].

Beta-2 receptors are located in multiple organ systems, and control various aspects of metabolic activity, while also inducing smooth muscle relaxation [5]. B2 receptors relax smooth muscles in the lungs, improving breathing, relax cardiovascular smooth muscle lowering blood pressure, activate the conversion of glycogen to glucose in the liver, and increase the heart’s pumping force and rate [2]. B2 receptors may also cause muscle tremors [2].

Beta-3 receptors induce breakdown of fat cells, and are found primarily in fat cells and the bladder [2, 5]. Activation of B3 receptors causes fat cells to break down, relaxation and increase in bladder capacity, and tremors, limiting potential medical applications for B3 receptor-targeted medications [2].

Beta blocker roles

There are three generations of beta blockers, which differ based on their selectivity, and thus elicit different responses [4]. First-generation beta blockers (sotalol and propranolol) are nonselective antagonists for beta-1 and beta-2 receptors, while second-generation beta blockers (atenolol, metoprolol and labetalol) are dose dependent for B-1 and B-2 receptors [4]. Third-generation beta blockers (carvedilol and nebivolol) inhibit B1 receptors on cardiomyocytes and function as cardiac vasodilators [4]. Beta blockers decrease heart rate and strength, cardiac output, activity of the renin-angiotensin system (kidneys) and blood pressure, while third-generation beta blockers decrease peripheral vascular resistance, and reduce cardiac remodeling, and endothelial and cardiac dysfunction [4].

Certain beta blockers have unique properties, including [2]:

• Carvedilol and labetalol, which block some alpha receptors, further lowering heart rate and blood pressure
• Nebivolol, which increases vasodilation and further lowers blood pressure

Beta blocker risks and contraindications

Beta blockers, while a front-line treatment for many cardiovascular conditions, are not without their risks. Because beta blockers block the activation of beta receptors, they are not used in certain conditions. Beta blockers that affect both the heart and lungs are generally not used in patients with severe asthma, as they may trigger severe asthma attacks [8].

Additionally, because beta blockers prevent increased heart rates, they may block some of the signs of hypoglycemia in diabetics, and may also prevent the increase in heart rate commonly associated with shock patients [8].

Beta blockers may also aggravate Raynaud’s syndrome, some types of arrhythmias and are not used in patients with chronically low blood pressure or heart rate because they may further lower these [2].

Beta blockers may also interact with other medications, such as antidepressants, nitrates, baclofen, prostate medications (e.g., tamsulosin) and Parkinson’s medications (e.g., levodopa), potentially causing a decrease in blood pressure [2, 3]. Other contraindications for beta block use include [4]:

• Second- and third-degree heart block
• Overt cardiac failure
• Cardiogenic shock
• Sick sinus syndrome (except when permanent pacemaker present)
• Severe hepatic impairment
• Severe hypersensitivity

Beta blockers also have several side effects, including [2]:

• Bradycardia
• Hypotension
• Arrhythmias
• Fatigue
• Dizziness
• Nausea
• Insomnia and changes in sleep
• Dry mouth and eyes
• Sexual and erectile dysfunction (rare)

Beta blocker overdose

Symptoms of a beta blocker overdose commonly occur within 1-2 hours, although the toxicity of sotalol is greatest up to 20 hours [7]. Hypotension may be one of the first signs of a beta blocker overdose, and may be coupled with hypoglycemia and altered mental status [7]. Hypoglycemia is especially common in pediatric beta blocker overdoses [6]. Certain beta blockers, such as sotalol, may cause QTc prolongation [7]. Other symptoms of an overdose include [6]:

• Dyspnea/Wheezing (in asthmatics)
• Blurred or double vision
• Irregular heart rhythm
• Lightheadedness
• Hypotension (sometimes extreme)
• Rapid or slow heartbeat
• Heart failure (shortness of breath and swelling of the legs)
• Weakness
• Nervousness
• Excessive sweating
• Drowsiness
• Confusion
• Convulsions
• Fever
• Coma

As with any overdose, providers should obtain a complete history, including any co-ingested medications. Medications such as calcium channel blockers may cause profound hypotension and cardiotoxicity, while tricyclic antidepressants and antipsychotics may potentiate (increase) the effects of beta blockers [7]. Additionally, different beta blockers have different half-lives, ranging from several minutes to several hours, and thus it is necessary to determine exactly what medications were ingested [7].

Vital signs and EKG should be monitored continuously, and 12-lead EKGs should be done at frequent intervals.

As certain beta blockers may cause CNS depression, airway management is crucial, and in some cases, it may be necessary to intubate the patient [7]. Minor respiratory complications, such as bronchospasm, may be treated with supplemental oxygen and albuterol [7].

Benzodiazepines may be used if seizures occur [7]. Glucagon is considered a first-line treatment for beta blocker overdose, although the evidence of its effectiveness is unclear, and should be administered according to local protocol [7].

Atropine may be required in cases of bradycardia.

Sodium bicarbonate and magnesium sulfate may be administered in cases of QRS widening and QTc prolongation respectively, however, providers should always follow their local treatment protocols and consult with their medical command physician if necessary for treatment guidance [7].

Additionally, the national poison control hotline may be contacted for further information and guidance.

Case resolution

You load the patient into the ambulance for transport. While en route to the hospital, you begin a fluid bolus with normal saline and reassess the patient’s vital signs and EKG. The patient’s blood pressure improves to 110/72 with a fluid bolus and she becomes more coherent. Her heart rate remains in the range of 60-64 bpm, and her 12-lead EKG continues to show normal sinus rhythm.

She tells you that she was working outside and did not have much fluid intake during that time. She feels tired, but otherwise denies chest pain, shortness of breath and other symptoms. You arrive at the hospital and transfer care to the emergency department team for evaluation.

Afterwards, you see your medical command physician in the hallway and stop to chat. You ask him about the patient’s heart rate, and why it was so low. He confirms your suspicions that the properties of the beta blocker were likely causing her heart rate to remain low. On a later call, you see the patient’s daughter, who tells you that there were no major findings, other than mild dehydration, and the patient will be discharged shortly.

Another job well done!

REFERENCES

1. Alhayek S, Preuss CV. Beta 1 Receptors. [Updated 2023 Aug 14]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from:
2. Beta-blockers. (2022, January 18). Cleveland Clinic.
3. Beta blockers. (2022, December 2). NHS UK.
4. Celic, I. (2022, November 17). Beta blockers. Cardiology Advisor.
5. Farzam K, Jan A. Beta Blockers. [Updated 2023 Aug 22]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from:
6. Icahn School of Medicine at Mount Sinai. (2024). Beta-blockers overdose. Mount Sinai.
7. Khalid MM, Galuska MA, Hamilton RJ. Beta-Blocker Toxicity. [Updated 2023 Jul 28]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from:
8. Mayo Clinic Staff. (2023, August 22). Beta blockers. Mayo Clinic.