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ECG Cases 28 Approach to Atrial Fibrillation
In this ECG Cases blog we assess 10 patients who presented with potential atrial fibrillation or atrial flutter. What is the diagnosis and best management? Written by Jesse McLaren; peer Reviewed and edited by Anton Helman, February 2022 10 patients presented with possible atrial fibrillation/flutter. What’s the diagnosis and the management? Case 1: 70yo, no prior atrial fibrillation, feeling weak for one day, normal vitals. Old then new ECG
Case 2: 70yo, history of atrial fibrillation taking anticoagulants, fall at home and found two days later. HR 150, BP 120/70 RR 20 oxygen saturation 96% temp 36.6
Case 3: 65yo, no history of atrial fibrillation, with 5 days shortness of breath on exertion and pleuritic chest pain. HR 115 BP 130/80 RR 20 oxygen saturation 95% temp 36.5
Case 4: 30yo two months postpartum with palpitations for 6 hours. HR 115 BP 110/80 RR 18 oxygen saturation 100% temp 36.4
Case 5: 80yo, history or CAD, with 2 hours chest pressure. HR 140 BP 120/75 RR 16 oxygen saturation 95% temp 36.4. Old then new ECG
Case 6: 70yo with two days on/off chest pain, suddenly worse over an hour. HR 120 BP 110/80 RR 20 oxygen saturation 96% temp 37 Old then new ECG
Case 7: 75yo, history of atrial fibrillation but not taking anticoagulants, with 10 hours of chest pain. HR 110, BP 120/80 RR 20, oxygen saturation 92%. Old then new ECG.
Case 8: 60yo history of diabetes, hypertension and atrial fibrillation, on beta-blocker and DOAC, with palpitations. HR 120, BP130 RR 18 oxygen saturation 95% temp 37.2
Case 9: 65yo history of CAD, CVA and paroxysmal atrial fibrillation, takes DOAC daily, with 7 hours of chest pressure. HR 120 BP 120/80. Old then new ECG
Case 10: 65yo history of hypertension and diabetes, with 4 hours palpitations. HR 150 BP130/80 R16 sat 99% T36.0
Approach to ECG interpretation of Atrial fibrillationAtrial fibrillation/flutter is the most common dysrhythmia we treat in the emergency department, and there is a lot of room for quality improvement. As a recent study found, atrial fibrillation has high rates of overtreatment and undertreatment: a third of patients with atrial fibrillation secondary to an underlying medical condition received rate control rather than treatment of the underlying cause, while 40% of those with primary atrial fibrillation did not receive sufficient rate control to achieve a normal heart rate on discharge; and 10% with stroke risk factors were not discharge on anticoagulation.[1] This highlights the importance of standardization to improve the quality of care of patients with atrial fibrillation, as summarized in the CAEP AF best practices checklist.[2] As EM atrial fibrillation expert Dr. Ian Stiell has demonstrated, implementation of this checklist has been associated with increased rhythm control and reduced length of stay without any increase in adverse events.[3] AFIB mnemonicThe approach to atrial fibrillation involves a series of questions summarized by the mnemonic AFIB:
Question 1: is it atrial fibrillation? Before treating atrial fibrillation, the first step is ECG rhythm interpretation: is it actually atrial fibrillation or is it another dysrhythmia or simply artifact? Automated ECG interpretation is inaccurate in general, and has a high rate of error when it comes to atrial fibrillation. This includes overdiagnosis (applying the label of AF to what is actually sinus dysrhythmia, sinus tachycardia with premature atrial contraction, and/or baseline artifact) and underdiagnosis (applying the label of sinus tachycardia or SVT to what is actually AF, especially flutter).[4] Question 2: if it is atrial fibrillation and there is rapid ventricular response, is it fast from a secondary cause? This is important for diagnosis, management and prognosis. As EM atrial fibrillation expert Dr. Clare Atzema has found, patients with atrial fibrillation and an alternate primary diagnosis have three times the mortality rate compared with primary atrial fibrillation.[5] This is where the CAEP atrial fibrillation checklist starts: aggressively treat secondary causes (eg sepsis, GI bleed, PE, CHF, ACS, alcohol withdrawal), and avoid aggressive rate control in these patients. One conundrum often arises with atrial fibrillation and ACS. As Dr. Atzema notes, 20% of patients with rapid AF experience chest pain, “but in the majority this is demand-related and not due to a rupture of an atherosclerotic plaque…The ECG findings before and subsequent to rate or rhythm control should be incorporated into the assessment.”[6] This also relates to the pattern of ischemic changes. Diffuse ST depression with reciprocal ST elevation in aVR is a non-specific sign of subendocardial ischemia that can be secondary to rapid atrial fibrillation—from secondary causes (like GI bleed or sepsis) or primary atrial fibrillation—and can be reassessed after treatment. Whereas rate controlled atrial fibrillation with regional and reciprocal ST/T changes is more concerning for acute coronary occlusion. While this is usually from plaque rupture, patients with atrial fibrillation are also at risk for coronary embolism, especially in those who are not anticoagulated.[7] Automated interpretation is also unreliable in this step, not only because of the limits of STEMI criteria to identify Occlusion MI, but also because they can apply the label “STEMI” to what is simply atrial flutter with fluctuating baseline. Question 3: if it is atrial fibrillation with a rapid ventricular response without a secondary cause, what is the intervention? Patients who are unstable as a result of acute primary atrial fibrillation require cardioversion, but as the checklist notes this is rare except for cases of atrial fibrillation with pre-excitation like WPW, and should prompt consideration of secondary causes. Stable patients with primary atrial fibrillation have the option of rhythm or rate control based on current anticoagulation, risk factors, and duration of symptoms. According to the checklist, it is safe to cardiovert if:
As the RAFF2 trial found, both drug-shock (procainamide 15mg/kg followed by cardioversion if necessary for the 50% that don’t cardiovert with procainamide) and shock-only were highly effective at rhythm control.[8] Rate control for patients for whom cardioversion is unsafe includes calcium channel blockers or beta-blockers, and digoxin if hypotension or acute heart failure. Question 4: does the patient need an anticoagulant started in the ED? According to the checklist, anticoagulation is indicated (DOACs preferred over warfarin) if there are any CHADS-65 risk factors. EM thrombosis expert Dr. Kerstin de Wit has summarized contraindications to anticoagulation in the “McMaster checklist,” which is included in the CAEP best practices document. This includes absolute contraindications such as active serious bleeding, relative contraindications such as liver cirrhosis and renal failure (note that DOAC dose adjustments for patients with stable chronic kidney disease is often acceptable – speak with your pharmacist/hematologist). Back to the casesCase 1: artifact, no treatment needed
Impression: baseline artifact. Repeat ECG less artifact with visible P waves. Had negative workup
Case 2: atrial fibrillation with rapid ventricular response secondary to hypovolemia, treated with fluid resuscitation
Impression: atrial fibrillation secondary to hypovolemia. POCUS revealed hyperdynamic left ventricle and no free fluid in the abdomen to suggest bleeding from a fall while on anticoagulation. After fluid resuscitation the heart rate slowed down and rate-related LBBB resolved. Septic workup was negative, and the patient was admitted for dehydration.
Case 3: Atrial fibrillation secondary to pulmonary embolism, treated with anticoagulation
Impression: atrial fibrillation with pleuritic chest pain and shortness of breath. D-dimer positive and CT chest revealed pulmonary embolism. Started on low molecular weight heparin and admitted. Remained in atrial fibrillation, and discharged on beta-blocker and DOAC. Case 4: atrial fibrillation secondary to postpartum thyroiditis, treated with propranolol
Impression: atrial fibrillation postpartum. Had negative D-dimer, undetectable TSH was admitted with hyperthyroidism. Had normal echo, high T3/T4, and diagnosed with postpartum thyroiditis. Started on propranolol for rate control, no anticoagulation due to lack of CHADS-65 risk factors. Case 5: primary atrial fibrillation with rapid ventricular response and rate-related subendocardial ischemia, unnecessary cath lab activation
Impression: atrial fibrillation with rapid ventricular response and rate-related subendocardial ischemia. Cath lab was activated prior to rate control. No obstructive lesions, troponin negative, and ST changes resolved after spontaneous conversion.
Case 6: atrial fibrillation with inferoposterior MI, treated with reperfusion
Impression: atrial fibrillation with inferoposterior MI. This could be from Occlusion MI, or Non-Occlusive MI with demand ischemia from rapid atrial fibrillation. Cath lab activated: 99% circumflex occlusion, first trop I was 3,000 (normal <26) and peak 43,000. Post-stent had spontaneous conversion, resolution of anterior ST depression, ongoing inferior Q waves. Discharged on DOAC in addition to antiplatelets.
Case 7: atrial fibrillation with first diagonal occlusion from coronary embolism, treated with reperfusion
Impression: first diagonal occlusion in patient with AF without anticoagulation. Cath lab activated: 100% first diagonal occlusion from coronary embolism. First troponin 25,000 and peak 48,000. Discharge ECG had resolution of ST changes and deeper reperfusion T wave inversion. Started on DOAC and antiplatelet.
Case 8: primary persistent atrial flutter, treated with rate control
Impression: atrial flutter. Negative workup and rate controlled with beta-blocker
Case 9: primary paroxysmal atrial fibrillation, cardioverted with procainamide
Impression: primary paroxysmal atrial fibrillation. History of CVA but on DOAC and has not missed any doses. Cardioverted with procainamide, negative workup and discharged.
Case 10: primary atrial flutter, electrically cardioverted
Impression: atrial flutter, no obvious secondary causes. Procainamide slowed down the ventricular response but did not cardiovert, so the patient received electrical cardioversion and was discharged on DOAC.
Early vs delayed cardioversion EM Quick Hit with Paul Dorion Atrial fibrillation anticoagulation EM Quick Hit with Clare Atzema Take home points on ECG approach to atrial fibrillation
References for ECG Cases 28: ECG approach to atrial fibrillation
Share your interesting ECG cases with us! Dr. Jesse McLaren (@ECGcases), is an Emergency Physician in Toronto with a special interest in emergency cardiology quality improvement and education. He is an Assistant Professor at the University of Toronto. Related PostsWhat is atrial fibrillation with rapid ventricular response?What is Afib with RVR? Some cases of Afib involve atrial fibrillation with rapid ventricular response (RVR). This is when the rapid contractions of the atria make the ventricles beat too quickly. If the ventricles beat too fast, they can't receive enough blood. So they can't meet the body's need for oxygenated blood.
How do you treat atrial fibrillation with rapid ventricular response?Drugs called beta-blockers. They control your heart rate. Your doctor will get them to you in your vein (they'll call this intravenously) if you have AFib with RVR.. Esmolol (Brevibloc). Metoprolol (Lopressor, Toprol). Propranolol (Inderal, Innopran). Is AFib with RVR life threatening?AFib with RVR can be life-threatening. Patients who have AFib have a 1.5- to 1.9-fold higher risk of death, due to the increased risk of blood clots (thromboembolism) and stroke. AFib with RVR (atrial fibrillation with a rapid ventricular rate) can be life-threatening.
What is the difference between rapid AFib and AFib with RVR?That is what happens during AFib with RVR, the overall pulse rate is very rapid, over 100 beats per minute. On the other hand, AFib with controlled ventricular rate is defined as AFib where the overall pulse is not rapid, usually betweem 60-100 beats per minute.
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