- Priorities during cardiac arrest include CPR and early defibrillation.
- ACLS medications are used to improve survival chances.
- ACLS medications are administered during CPR for medication distribution.
- Without CPR, medications remain local.
- ACLS medications can be given ET/IV/IO.
- ACLS medications in stable patients are used to halt abnormal rhythms.
- ACLS medications vary depending on EKG rhythm & patient symptoms:
- PEA / Asystole = Epinephrine
- VF / Pulseless VT = Epinephrine & Amiodarone
- Unstable Bradycardia = Atropine
- Stable Tachycardia = Adenosine & Amiodarone
- ACLS Algorithms
- Is the patient unresponsive? Check for a pulse 5-10 seconds
- Activate emergency response
- Start CPR & attach monitor/defibrillator
- Rhythm shockable?
- (YES) VF / Pulseless VT
- (NO) Asystole / PEA
Questions to ask during a code blue:
- What is the cardiac rhythm?
- Does the patient have a pulse?
- Is the patient stable or unstable?
- Stable: No hypotension, NO AMS, NO shock, NO CP, NO HF is present
- Unstable: Hypotension, AMS, shock, CP or HF are present
- ACLS algorithms are AHA guidelines for managing cardiac emergencies
- These step-wise protocols follow certain sequences & steps
- VF / Pulseless VT
- Administer shock (biphasic 120-200 J, monophasic 360J)
- CPR 2 mins, epinephrine / consider advanced airway
- Admin shock (if still shockable rhythm), amiodarone 300 mg
- Asystole / PEA
- CPR 2 mins, epinephrine / consider advanced airway.
- Does unshockable rhythm remain? Continue CPR & epinephrine
- Stable Bradycardia = Monitor
- Unstable Bradycardia = Atropine
- Stable Tachycardia = Medications
- Wide QRS = Consider antiarrhythmic infusion (amiodarone) / expert consult
- Narrow QRS = Vagal maneuvers, adenosine, BB, CCB / expert consult
- Unstable Tachycardia = Cardioversion
- Stable Tachycardia = Medications
- Drug class: Adrenergic Agonist
- Dose: 1 mg every 3 – 5 minutes
- Action: Stimulates alpha- & beta- adrenergic receptors
- Alpha1 = Increases in blood pressure
- Beta1 = Increases cardiac output
- beta2 = Bronchi opens up, helping airway
- Side Effects: Restlessness, tremors, angina, hypertension
- Will raise BP / HR, which can cause myocardial ischemia & angina
- Use can cause myocardial dysfunction after ROSC
- Drug class: Antiarrhythmic
- Dose: 1st dose: 300 mg IV/IO bolus, 2nd dose: 150 mg IV/IO bolus
- Action: Blocks abnormal electrical activity to the heart
- Half-life lasts up to 40 days
- Side Effects: Pulmonary fibrosis, bradycardia, hypotension
- Rapid infusion may cause hypotension
- Do not administer other drugs that prolong QT interval
- Drug class: Anticholinergic
- Dose: 0.5 mg IV every 3 to 5 minutes (max 3 mg)
- Action: Blocks parasympathetic / Fight or flight
- Side Effects: Tachycardia, dry mouth, blurred vision, drowsiness
- Use with caution in myocardial ischemic patients
- Not effective with AV, type II HB & 3-degree CHBs
- Drug class: Antiarrhythmic
- Dose: 6 mg rapid IVP, follow with NS / 2nd dose 12 mg
- Action: Interrupts pathways / Restore sinus rhythms
- Half-life is < 10 seconds
- Side Effects: Flushing, chest pain, a brief period of asystole/bradycardia
- Use with caution with patients with asthma (may cause bronchospasm)
- When a patient has ROSC (return of spontaneous circulation), the following checklist should be completed:
- Optimize ventilation & oxygenation
- Maintain oxygen saturation > 94%
- Consider advanced airway / waveform capnography
- Do not hyperventilate
- Treat hypotension (SBP < 90 mm Hg)
- IV/IO bolus
- Vasopressor infusion
- Consider treatable causes
- 12-Lead EKG
Hello and welcome. Today we’re going to discuss ACLS medications and how they manage cardiovascular emergencies.
ACLS medications are used in cardiopulmonary arrest or other cardiac emergencies. Some situations cause temporary injury or insult, while other events cause permanent cellular death. Therefore, time is tissue.
ACLS medications are used to improve cardiac performance due to recent cardiac injury or defect. These medications are used to optimize cardiac output, improve blood pressure, and end lethal dysrhythmias (3 punch combo). When you think of ACLS medications I want you to think about four words, restart, restore, improve and support (RRIS). In nursing school, you were probably told that cardiac output equals stroke volume times heart rate. Well, disturbances to these elements will cause cardiovascular compromise. HR issues include bradycardia and tachycardia. Cardiac arrest has no heart rate so therefore, no cardiac output.
Before we get into ACLS medications, we must start with the most important question, what is the rhythm? The rhythm and the patient’s symptoms will determine the type of ACLS medication used. So with that in mind, what is the rhythm being displayed here? Ventricular tachycardia, that is correct. Once we determine the rhythm, we must see if there is a pulse present. What you do is determined by rhythm & patient presentation (pulse vs no pulse – stable vs unstable).
After determining the cardiac rhythm, it is now time to find out whether the patient is stable or unstable. Stable patients have normal blood pressures, no change in mentation, no displays of shock, no chest pain and no symptoms of heart failure. Unstable patients have one or all signs of instability shown in the chart here. Most of the time, stable patients can be monitored or provided medication, while unstable patients require more aggressive treatments such as cardioversion or pacemaker.
Let’s look at the main meds used in each of the major algorithms. Then, we’ll dive into the actual meds themselves. Here, we have ventricular fibrillation and pulseless ventricular tachycardia. Ventricular fibrillation and pulseless ventricular tachycardia are rhythms where your patient will NOT have a pulse. The 2 ACLS medications used in this scenario is epinephrine and amiodarone. I remember this by thinking, VF/VT = AE. Amiodarone, epinephrine.
Now, let move on to asystole/PEA situations. These rhythms lack a pulse, the patient is pulseless. Unlike ventricular fibrillation and pulseless ventricular tachycardia where the electrical activity is chaotic, here you might just see a line (like on TV) and no, shock isn’t required here. The focus here is epinephrine. No other ACLS drug is used besides epinephrine. Just think APE (Asystole/PEA/Epi = APE).
Bradycardia is a cardiac emergency has 2 tracks. First, you must first determine whether the patient is stable or unstable. If the patient is stable, we merely monitor and observe. My heart resting heart rate is 45 bpm. I show no signs of instability, so what would you do in my case? That is right, you would monitor and observe. Now, if the patient is unstable, like we mentioned, we would use ACLS medications. In this case, atropine first. Followed by infusions of dopamine or epinephrine. Again, symptoms will determine our action or inaction.
Now, tachycardia is another cardiac emergency that is managed based on patient symptoms. In the tachycardia, a stable patient has time for medications – chemical cardioversion. Depending on the width of the QRS interval, amiodarone or adenosine can be used. If the patient is unstable, we move right to synchronized “electrical” cardioversion. Remember CO = SV x HR? Elevated heart rate cause perfusion and blood flow issues d/t decreased filling times. The faster it beats, the less time there is to fill the tank. We are attempting to fix this.
Now let’s review the ACLS drug, epinephrine. This drug is an adrenergic agonist and stimulates both alpha and beta receptors. When alpha-1 receptors are stimulated, there is an increase in blood pressure. When alpha-2 receptors are stimulated, there is an increase in cardiac output. And lastly, when beta-2 receptors are stimulated, the bronchi of the lungs open up, helping breathing. When you think of epinephrine, think of adrenaline and the potential side effects of this drug entering your body. This drug is to be used with caution in patients with cardiovascular dysfunction as the receptor stimulation could cause further cardiac damage d/t patient’s already myocardial fragile state.
Now let’s review the ACLS drug, epinephrine. This drug is an adrenergic agonist and stimulates both alpha and beta receptors. When alpha-1 receptors are stimulated, there is an increase in blood pressure. When alpha-2 receptors are stimulated, there is an increase in cardiac output, for example, an increase in heart rate. And lastly, when beta-2 receptors are stimulated, the bronchi of the lungs open up, helping breathing. When you think of epinephrine, think of adrenaline and the potential side effects of this drug entering your body. This drug is to be used with caution in patients with cardiovascular dysfunction (such as AMI or heart failure) as the receptor stimulation could cause further cardiac damage d/t patient’s already myocardial fragile state.
Atropine is a drug used in unstable bradycardia with a pulse. This drug is an anticholinergic and blocks the parasympathetic system (rest & digest) and induces the flight-or-fight (stress) response. So when you think of atropine, think of the drug activating your fight-or-flight response, in an attempt to increase your heart rate. But due to its anticholinergic properties, it causes other issues such as dry mouth, blurred vision and drowsiness. This drug only works on lower tier heart blocks. Other aggressive heart blocks will require a pacemaker. Please check out our ECG course regarding heart blocks and how they vary.
Amiodarone is an antiarrhythmic which means that the drug is used to block abnormal cardiac electrical activity aka “chemical” cardioversion. The goal of this drug is to convert the rhythm and restore NSR. In cardiac emergencies, amiodarone is given various doses, often resulting in a patient being on an intravenous drip. Amiodarone can cause bradycardia and hypotension in some patients. One unique thing about amiodarone is it’s very long half-life of up to 40 days. One key concept again with using amiodarone is its potential for bradycardia and hypotension.
Adenosine like amiodarone is an antiarrhythmic drug. Its goal is to block abnormal electrical activity and restore NSR. When you think of adenosine, think of restarting your computer. Your patient’s heart rate is going to slow way down. Let’s say from 150 to 50 to 30, the patient might complain of feeling weird. When you look at the monitor, you might even see asystole for a few brief seconds, followed by NSR. Antiarrhythmics are drugs used to “chemically” cardiovert dysrhythmias. The side effects of chest pain and flushing are due to the slowing down of the heart rate which alters cardiac output. This drug also has a side effect of bronchospasms, so this drug should be used with caution in patients with asthma.
So, you got your patient back, you have a blood pressure, you have a pulse and now it’s time to do your ROSC checklist. ROCS stands for return of spontaneous circulation. The goal with ROSC is to restore proper heart function & perfusion. Immediate post-cardiac arrest care includes optimizing ventilation, treating hypotension (maybe some of the drugs that we gave), and if your patient is unresponsive (induced hypothermia) or had a STEMI (cath lab). The heart has taken a hit from this acute event, now it’s time to find out the why and provide support.
Nursing concepts for ACLS medications include EKG rhythms and pharmacology.
Let’s recap & review the rhythm and their corresponding drugs… VF / Pulseless VT? Epi and amiodarone (think adrenaline & antiarrhythmic = AA). Asystole / PEA? Epi all day. It rhymes (a little). Symptomatic bradycardia? Atropine. And lastly, Stable tachycardia? Adenosine and amiodarone (Double AA). If there is no pulse, what med would you pull out of the code cart? That is right! Epi all day!
Here are some key points to take away from the ACLS meds presentation:
1. We must know the EKG rhythm. Does your patient have a pulse? 2. Is your patient stable or unstable? Will you monitor or will medications be needed? 3. If ACLS medications are needed, what are the doses / types of drugs needed? 4. Responses – What is the expected outcome of you administering these drugs? Lastly, the evaluation. If your patient who had a cardiac arrest event and is now in ROSC, what happens next. The goal isn’t simply to memorize these drugs, the goal is to understand the sequence of events that are needed, why they’re needed and how they affect your patient. It’s a few drugs and few rhythms, don’t overthink it. You can do this!
Don’t forget to check our the lecture on parasympathetic vs sympathetic pathways, along with the ECG lessons to further understand the drug actions mentioned in this presentation. Now, go out and be your best self today and as always, Happy Nursing!