Key Feature 3a: In an individual presenting with chronic or paroxysmal atrial fibrillation: Explore the need for anticoagulation based on the risk of stroke with the patient.
Skill: Patient Centered, Clinical Reasoning
Phase: Diagnosis, Treatment

Key Feature 3b: In an individual presenting with chronic or paroxysmal atrial fibrillation: Periodically reassess the need for anticoagulation.
Skill: Clinical Reasoning
Phase: Hypothesis generation, Follow-up

Key Feature 4: In patients with atrial fibrillation, when the decision has been made to use anticoagulation, institute the appropriate therapy and patient education, with a comprehensive follow-up plan.
Skill: Clinical Reasoning
Phase: Treatment, Follow-up

Key Feature 5: In a stable patient with atrial fibrillation, identify the need for rate control.
Skill: Clinical Reasoning
Phase: Hypothesis generation, Treatment

Key Feature 6: In a stable patient with atrial fibrillation, arrange for rhythm correction when appropriate.
Skill: Clinical Reasoning, Selectivity
Phase: Hypothesis generation, Treatment

In a patient with atrial fibrillation, whether or not they should be anticoagulated is based on the risk for stroke versus having a serious bleed. The CHADS2-VASc risk stratification score is the standard assessment tool to assess for the risk of stroke, while the HAS-BLED risk stratifications score is the equivalent to asses for the risk of a major bleed. In realtime, I use a medical calculator app (Canadian Cardiovascular Society) to determine the risk scores for the patient in front of me to help me make a decision. It's important to have a patient-centered conversation. Although the chances of having a major bleed may be higher for the patient than the risk of stroke based on their risk stratification scores, the majority of such patients may prefer to be anticoagulated given the proportional risk for decrease in quality of life should one versus the other occur. It is important to periodically reassess the need for anticoagulation as a patient's risk of stroke, risk of sustaining a major bleed, and goals of care may change over time. 

The Canadian Cardiovascular Society Atrial Fibrillation Guideline recommends the following for prevention of stroke and systemic embolism:

• Recommendation 1: Stratification of patients using a predictive index for stroke risk
• Recommendation 2: Oral anticoagulant therapy (OAC) for patients ≥ 65 years or CHADS2-VASc ≥ 1
• Recommendation 3: Acetylsalicylic acid (ASA) for patients with no risks besides arterial vascular disease
• Recommendation 4: No antithrombotic therapy for patients with no major risks​
• Recommendation 5: Most patients should receive non-vitamin K oral anticoagulant therapy (NOAC)
• Recommendation 6: Warfarin when mechanical valve, mitral stenosis, or renal dysfunction (15-30 mL/min)
• Recommendation 7: Patients who refuse OAC should receive ASA pus clopidogrel
• Recommendation 8: OAC therapy for highly selected patients with subclinical atrial fibrillation (AF)
• Recommendation 9: OAC for 3 weeks before and at least 4 weeks post cardioversion
• Recommendation 10: Annual renal function assessment
• Recommendation 11: Antithrombotic therapy should relate to creatinine clearance (CrCl)
• Recommendation 12: Left atrial appendage closure devices to be used only in research and exceptional cases
• Recommendation 13: Acute management of stroke patients as per American Heart Association (AHA)/American Stroke Association (ASA) guidelines (i.e., ACLS)
• Recommendation 14: Hemorrhage on OAC to be managed per American College of Chest Physicians (AACP) guidelines 
• Recommendation 15: Idarucizimab for emergency reversal of dabigatran's anticoagulant effect

In follow-up care of a patient who has been diagnosed with atrial fibrillation, be it paroxysmal, persistent, or permanent, the following issues should be reviewed:

1. Symptoms and functional status
2. Review of management for stroke risk
3. Review of management for either rhythm or rate control (see below)
4. Routine investigations may include repeat ECG and bloodwork to reassess kidney and liver functioning

Key Feature 1: In a patient who presents with new onset atrial fibrillation, look for an underlying cause (ex: ischemic heart disease, acute myocardial infarction, congestive heart failure, cardiomyopathy, pulmonary embolus, hyperthyroidism, alcohol, etc.).
Skill: Clinical Reasoning
Phase: Hypothesis generation

In a patient who presents with new onset atrial fibrillation, either picked up because they are symptomatic (ex: palpitations, decreased exercise tolerance, dyspnea), as an incidental finding on physical examination (ex: irregularly irregular pulse), or on an ECG done for another reason (ex: presurgical baseline), it is important to look for an underlying cause. This is important so as to treat any underlying disease that has its own cluster of negative consequences, but also to identify any possible reversible reason for having atrial fibrillation. Atrial fibrillation increases the risk of stroke and peripheral embolisation, can decrease quality of life, and may increase the risk of death. Although these risks can be mitigated with medications, medications do not eliminate them altogether. 

Potential causes of reversible atrial fibrillation to assess for include: 

1. Associated alcohol or caffeine consumption
2. Associated exercise
3. Associated emotional stress
4. Hyperthyroidism

Note: Most patients will not have any identifiable reversible triggers

Important associated disease processes to look for include:

1. Cardiovascular disease
   
2. Cerebrovascular disease
   
3. Diabetes
4. Hypertension
   
5. COPD
   
6. Obstructive sleep apnea

Advanced Cardiac Life Support
Key Feature 1: Keep up to date with advanced cardiac life support (ACLS) recommendations (i.e., maintain your knowledge base). 
Skill: Professionalism
Phase: Treatment

Key Feature 2: Promptly defibrillate a patient with ventricular fibrillation (V fib), or pulseless or symptomatic ventricular tachycardia (V tach). 
Skill: Clinical Reasoning, Selectivity
Phase: Treatment

Key Feature 3: Diagnose serious arrhythmias (V tach, V fib, supraventricular tachycardia, atrial fibrillation, or second- or third-degree heart block), and treat according to ACLS protocols. 
Skill: Clinical Reasoning
Phase: Diagnosis, Treatment

Atrial Fibrillation
Key Feature 2a: In a patient presenting with atrial fibrillation: Look for hemodynamic instability.
Skill: Clinical Reasoning, Selectivity
Phase: Hypothesis generation

Key Feature 2b: In a patient presenting with atrial fibrillation: Intervene rapidly and appropriately to stabilize the patient.
Skill: Clinical Reasoning, Selectivity
Phase: Treatment

I am currently certified as an ACLS Provider. Expiring in April 2019, I will need to retake the course at some point in time prior to this expiry date so I can keep up to date and have some welcome practice.

If I encounter a patient who is unresponsive, I need to assess for a pulse straight away. If no pulse is definitively felt within the first 10 seconds (while simultaneously assessing for breathing), I need to activate the emergency response system. In the hospital this would be to call a "Code Blue." Once activated, I need to start CPR straight away. My priority is to perform high quality CPR until a defibrillator arrives and the cardiac rhythm is determined to be one of the following:

1. Ventricular fibrillation (VF) [a wide complex irregular rhythm] (first picture below)
2. Ventricular tachycardia (VT) [a wide complex regular rhythm] (second picture below) 
3. Asystole (flat line)
4. Pulseless electrical activity (any other cardiac rhythm occurring without a palpable pulse)

An automated external defibrillator would sense whether or not the rhythm is VF or VT automatically and simply directs the user to shock or not, while a manual defibrillator would require me to be able to read the rhythm strip and decide whether is represents VF or VT (shockable rhythms) or not (everything else being nonshockable). If a shockable rhythm is present, shocking that rhythm is the MOST IMPORTANT INTERVENTION I can do to save someone's life, so as soon as there is a defibrillator present, it is critical to have it set up ASAP and deliver a shock if the patient is in VF or VT. Other life-saving interventions include providing high-quality CPR, and using epinephrine (1 mg IV q3-5min) +/- adenosine (up to 2 times, first IV bolus of 300mg, second of 150 mg). 

There may also be the circumstance in which I encounter a patient with a slow heart rate (bradyarrhythmia, <50 bpm) or a rapid heart rate (tachycardia, >100 bpm, usually >150 bpm to cause serious symptoms or signs), and I must determine if their heart rate is life-threatening and in need of electrical intervention. Let's start with the patient who has a bradyarrhythmia. 

Bradyarrhythmia
For an unwell patient with a bradyarrhythmia, my first step is to consider the ABCs: Airway, Breathing (supplemental oxygen if hypoxemic), Circulation (cardiac monitoring to identify rhythm, monitors for BP and oximetry, obtain IV access, and get a 12-lead ECG). Urgent intervention is warranted if the patient has any of the following serious features (even if the 12-lead ECG has not yet been obtained so as to accurately characterise the rhythm):

1. Acutely altered mental status
2. Signs of shock or hypotension (see "SHOCR" mnemonic from this blog post)
3. Ischemic chest discomfort or acute heart failure

If urgent intervention is needed, the first line treatment is atropine 0.5 mg bolus IV, which can be repeated every 3-5 minutes up to a maximum of 3 mg. If administration of atropine is ineffective, second line therapy is transcutaneous pacing, dopamine infusion, or an epinephrine infusion. I would definitely be calling an expert for help. As soon as the ECG is available my goal is to determine if the bradyarrhythmia is secondary to a type 2 second-degree or third-degree AV block, since these types of rhythms will not respond to atropine and instead I should proceed directly to transcutaneous pacing or beta adrenergic infusion rather than trialing more atropine. These second-line therapies are temporising measures to help keep the patient from arresting in preparation for transvenous pacing. It's also important to use atropine cautiously in the presence of acute coronary ischemia or myocardial infarction as it can worsen ischemia or increase the size of the infarct.

If I need to perform transcutaneous pacing, here are the steps to so so:

1. Sedate the patient, time-permitting (you're basically repeatedly electrocuting your patient, ouchie)
   1. Parenteral benzodiazepine for anxiety and muscle contractions (ex: midazolam 1 mg IV slowly q2-3min up to 5 mg)
   2. Parenteral narcotic for analgesia (ex: fentanyl 50-100 mcg IV q1-2h PRN)
2. Place pacing electrodes on the chest according to package instructions
3. Turn the pacer on
4. Set the demand rate to approximately 60/min (can be adjusted up or down based on patient clinical response once pacing is established)
5. Set the current milliamperes output 2 mA above the dose at which consistent capture is observed (safety margin)
6. Use a chronotropic infusion once available (dopamine or epinephrine)
7. Obtain expert consultation for transvenous pacing

If the patient is only mildly symptomatic from poor perfusion secondary to the bradyarrhythmia, it is still important to address the arrhythmia, but there is a bit more time. The ECG can be examined and we can look for a correctable etiology for the bradyarrhythmia.

Types of bradyarrhythmias (from the ACLS Provider Manual). Generally speaking, the more progressive the block, from sinus to complete AV block, the more clinically significant the ramifications. Also note that sinus bradycardia may in fact be physiologic (Muhammad Ali reportedly had a heart rate in the 30s because he was so in shape - quite the anomaly!)

Tachyarrhythmia
​For an unwell patient with a tachyarrhythmia, like with a bradyarrhythmia (or anytime a patient appears unwell), my first step is to consider the ABCs: Airway, Breathing (supplemental oxygen if hypoxemic), Circulation (cardiac monitoring to identify rhythm, monitors for BP and oximetry, obtain IV access, and get a 12-lead ECG). Urgent intervention is warranted if the patient has any of the following serious features (even if the 12-lead ECG has not yet been obtained so as to accurately characterise the rhythm), and these are the same as the serious features to look for with a bradyarrhythmia

1. Acutely altered mental status
2. Signs of shock or hypotension 
3. Ischemic chest discomfort or acute heart failure

If urgent intervention is needed, the patient needs to receive synchronised cardioversion. 

Steps to perform synchronised cardioversion:

1. Sedate all conscious patients (as per TCP) unless unstable or deteriorating rapidly
   1. Parenteral benzodiazepine for anxiety and muscle contractions
   2. Parenteral narcotic for analgesia
2. Turn on the defibrillator (monophonic or biphasic)
3. Attach monitor leads to the patient ("white to right, red to ribs, what's left over to the left shoulder" - see below) and ensure proper display of the patient's rhythm. Position adhesive electrode (conductor) pads on the patient.
4. Press the sync control button to engage the synchronisation mode
5. Look for markers on the R wave indicating sync mode
6. Adjust monitor gain if necessary until sync markers occur with each R wave
7. Select the appropriate energy level. Deliver monophasic* synchronised shocks in the following sequence:
   1. Unstable atrial fibrillation: 200 J initial dose
   2. Unstable monomorphic VT: 100 J initial dose
   3. Other unstable SVT/atrial flutter: 50-100 J initial dose
   4. Polymorphic VT (irregular form and rate) and unstable (treat as VF with high-energy shock) defibrillation doses
   5. *Biphasic synchronised shocks should be given at a dose of 120 to 200 J, with escalation as needed. Consult the device manufacturer for specific recommendation​s
8. Announce to team members: "Charging defibrillator - stand clear!"
9. Press the charge button
10. Clear the patient when the defibrillator is charged
    1. Make sure you are clear of contact with the patient, the stretcher, or other equipment, visually check to ensure that no one is touching the patient or stretcher, and be sure oxygen is not flowing across the patient's chest
    2. When pressing the shock button, face the patient, not the machine
11. Press the shock button(s)
12. Check the monitor. If tachycardia persists, increase the energy level according to the Electrical Cardioversion Algorithm
13. Activate the sync mode after delivery of each synchronised shock (Most defibrillators default back to the unsynchronised mode after delivery of a synchronised shock. This default allows an immediate shock if cardioversion produces VF.)

If the patient is only mildly symptomatic from poor perfusion secondary to the tachyarrhythmia, like with bradyarrhythmias, it is still important to address the arrhythmia, but there is a bit more time. The ECG can be examined and we can look to see whether or not the QRS complexes are wide (≥0.12 sec). 

For the wide-complex tachyarrhythmia: If it is monomorphic, consult an expert. If it is polymorphic, treat with immediate unsynchronised cardioversion (notice the description is the same as for VF, which requires defibrillation in a patient without a pulse - the only difference here is that unsynchronised cardioversion sends less energy with each shock than a defibrillation dose) and consult an expert.

For the narrow-complex tachyarrhythmia:

1. Attempt vagal manoeuvres (Valsalva or carotid sinus massage), which terminate about 25% of supraventricular tachycardias. If this doesn't work,
2. Give adenosine: First dose 6 mg rapid IV push in large (ex: antecubital) being over 1 second followed by 20 mL NS flush and elevate arm immediately. Second dose 12 mg rapid IV push with flush as first dose to be given if SVT has not converted within 1-2 min of giving first dose.

So, that is my ultrabasic and never-done-in-real-life approach to managing bradyarrhythmias and tachyarrhythmias. By having this approach, hopefully if I see one being treated I can figure out what's up.

SUMMARY: If a patient is found to have bradycardia (<50) or tachycardia (>150) and is also having symptoms of decreased perfusion, heed the ABCs. If they have any of the following signs or symptoms:

1. Altered mental status
2. Hypotension or signs of shock
3. Ischemic chest discomfort or acute heart failure

...Then there's a good chance they may need electricity

• Transcutaneous pacing in the setting of life-threatening bradycardia (if the rhythm is a type 2 second-degree AV block or third-degree AV  block, otherwise atropine may do the trick)
• Synchronised cardioversion in the setting of life-threatening tachycardia
• Defibrillation if they go into cardiac arrest