Makindo Medical Notes.com

Related Subjects: |Atrial Flutter |Atrial Fibrillation |AF and Anticoagulation |AF and Rate Control |AF and Rhythm Control and Cardioversion |AF ECG |DC cardioversion |Wolff-Parkinson White syndrome (WPW) |Supraventricular Tachycardia (SVT) |Ventricular Tachycardia |Ventricular Fibrillation |Resuscitation - Adult Tachycardia Algorithm |Resuscitation - Advanced Life Support

Quick Guide

About

• With AF there is uncoordinated chaotic atrial activation
• This leads to atrial mechanical dysfunction
• Major risk of cardioembolism causing ischaemic stroke
• Most patients need anticoagulation

Aetiology

• Atrial fibrosis, loss of atrial muscle mass.
• Increased automaticity or multiple re-entrant wavelets.
• Atrial rate AF is 400-600/min but it is the ventricular response that matters.
• Ventricular rate limited at AV node to a max of approximately 200/min
• An accessory bundle (WPW) can allow faster rates to conduct causing VF.

ECG

Physiology

• Haemodynamics: High heart rate shortens diastole and limits LV filling and coronary perfusion.
• LV filling already compromised by loss of atrial systole.
• Rate control with drugs, treat failure and DC shock if needed.
• Impaired LV function or mitral stenosis makes things much worse.

Clinical

• Asymptomatic. Palpitations, dyspnoea, chest discomfort.
• Cardioembolic stroke, mesenteric emboli, limb emboli, dyspnoea.
• Fatigue and worsening heart failure, syncope, dizziness.
• Low BP with fast/slow AF, irregularly irregular pulse. Pulse deficit.
• Murmurs suggesting valve disease, signs of thyroid disease, hypertension.

Clinical Effect of AF

• Death: Usually doubled in incidence < 48 hrs and is reduced by antithrombotic therapy
• Stroke: Increase in Ischaemic and haemorrhagic stroke and more severe
• Admissions: Increased risk of hospital admission
• Quality of life: Wide variation from no impact to severe
• LV function: Wide variation from a tachycardiomyopathy to no effect on LV

Causes of atrial fibrillation

• Ischaemic, valvular, rheumatic, hypertensive heart disease, cardiomyopathy,
• Post cardiac surgery, thyrotoxicosis, alcohol acute binge or chronic, sick sinus syndrome
• Congenital heart disease, pulmonary embolism, pneumonia, sarcoidosis
• Amyloidosis, haemochromatosis, lone AF (idiopathic), pericarditis, myocarditis.

Atrial fibrillation can come in several different forms as shown in the table below.

Valvular Atrial Fibrillation

• Valvular heart disease tends to infer the presence of rheumatic mitral stenosis which is the most common lesion associated with thromboembolism, irrespective of the coexistence of mitral regurgitation.
• Atrial fibrillation develops as MS progresses and increases the risk of thromboembolism up to 18 times. Thrombi associated with mitral stenosis can be found on the atrial wall or in the left atrial appendage.
• Risks of embolic stroke in these patients is related to age and low cardiac output, but not left atrial size, mitral calcification, or severity of mitral stenosis. The association of mitral regurgitation with thromboembolism correlates with the coexistence of mitral stenosis.
• Oral anticoagulation reduces the risk of stroke in patients with rheumatic mitral stenosis, particularly those with coexistent atrial fibrillation. The risk-benefit ratio in those without atrial fibrillation is not known. Of those patients who have had one event, early recurrent embolism has been reported in up to two thirds and aggressive anticoagulation instituted with Warfarin.
• The newer agents such as Dabigatran have not been licensed for use in this group of patients and either Warfarin or LMWH is needed long term.

Non-Valvular Atrial Fibrillation

• This is defined above as those with AF but no rheumatic mitral stenosis, no mechanical or bioprosthetic heart valve or mitral valve repair and this definition is used in the AHA/ACC guidelines listed below.
• For these patients the CHA2DS2-Vasc score is recommended for assessment of stroke risk.
• There are some patients with AF who are at very low risk of cardioembolism. Where the stroke risk is less than 1% Warfarin is not advocated and aspirin is possibly a reasonable choice. In an attempt to improve risk assessment, the CHADS2 score has been very helpful and has been improved upon with the CHADS2-Vasc score [Lip GY et al. 2010, Olesen JB 2011].
• The score is useful for assessing risk, giving a more personalised risk assessment to patients and communicating risk and beneficial strategies. However, the risk of anticoagulation related bleeds must balance the reduction in embolic episodes. The HAS-BLED score has been shown to be useful.

Investigations

• Bloods: FBC low Hb, high WCC with sepsis, U&E, Mg, Ca, K, TFT - thyrotoxicosis, LFTs, alcohol, haemochromatosis.
• CXR: cardiomegaly, pulmonary oedema, infection, post cardiac surgery effusion.
• Troponin: Elevated with ACS or myocarditis and minor rise with DC shock.
• ECG: absent p waves no organised atrial activity, fibrillatory waves that vary in amplitude, shape, and timing, QRS complexes which are irregularly irregular. Aberrantly conducted AF wide complex and fast but irregular. Pre-excited AF: QRS 160-300/min and slurred up or downstroke of delta waves seen giving wide complex appearance but very irregular; the irregularity means that it is not VT. Dangerous if it conducts to ventricles at 1:1 and can precipitate VT/VF. This depends on the character of the accessory pathway. If there are RR intervals <260 ms this is considered unsafe and needs inpatient cardiology review for ablation. If unstable simply DC cardiovert.
• Capturing PAF: 24 h tape in those with suspected asymptomatic episodes or symptomatic episodes less than 24 h apart. Use an event recorder ECG in those with symptomatic episodes more than 24 h apart. Some may use 7-day tape.
• Transthoracic echocardiogram: assess LV function, valve disease, LA size. Anticoagulation rarely depends on the echo.
• Trans oesophageal echocardiogram: closer inspection of valves, mitral disease, ASD, endocarditis, LA appendage thrombus may be seen and can help assess the risk of thromboembolism.
• Coronary angiography: if IHD suspected.

Management

• ABC, O₂ is hypoxic. Fast AF and compromised. AF and fast AF can be a response to an infective, inflammatory or metabolic/toxic cause. Treatment must balance to focus on treating the underlying cause as well as using rate control drugs. Look for causality.
• If fast AF is causing compromise: Low BP, LVF, angina then consider rate control with Amiodarone or Digoxin but if that fails then consider DC cardioversion which may be done without anticoagulation but start treatment dose LMWH [NICE 2014].
• Consider Rhythm control and cardioversion if the arrhythmia is less than 48 h. If AF duration > 48 h and not anticoagulated then needs TOE/TEE to exclude atrial thrombus.
• DC Cardioversion should be anticoagulated 3-4 weeks before DC cardioversion. If unwell and needs DCC take expert advice. Anticoagulate post-procedure for at least 4 weeks. Long term if AF continues.
• Pharmacological Cardioversion should be anticoagulated 3-4 weeks before chemical cardioversion. If not needs TOE/TEE to exclude atrial thrombus. Give Flecainide 1-2 mg/kg over 10 minutes or Amiodarone 300 mg IV bolus then 900 mg over 24 hrs. Anticoagulate post-procedure for at least 4 weeks. Long term if AF continues.
• ABC, high flow oxygen as needed. IV fluids cautiously if at all in LVF or fluid overloaded. Start treatment dose LMWH in all with AF and not anticoagulated with no contraindications. Look for and treat any cause: chest infection, thyrotoxicosis, ACS, PE, sepsis, MI/ACS, pulmonary oedema, PE, alcohol excess or withdrawal.
• AF and well: ventricular rate 60-120/min and haemodynamically well. Determine and manage the cause. Anticoagulate (as above). Decide rhythm vs rate control strategy as defined below.

Rate control

• Consider oral beta-blocker or rate limiting CCB. Digoxin may be considered if sedentary lifestyle. Avoid Amiodarone long term as side effects significant.

Specific scenarios

• Pre-excited AF and WPW syndrome: use IV Procainamide or IV Amiodarone or Sotalol or Flecainide and if unstable then immediate DC cardioversion. Avoid digoxin, beta-blockers and Verapamil or Diltiazem in pre-excited AF. They may increase the risk of VF. Assess for anticoagulation.
• Prevention and management of postoperative AF: cardiothoracic surgery reduce postoperative AF by offering either amiodarone, a standard beta-blocker (not sotalol), a rate-limiting calcium antagonist. DO NOT offer digoxin. Continue any pre-existing beta-blockade. Postop offer a rhythm-based strategy. For postop AF, use appropriate antithrombotic therapy and correct identifiable precipitants (U&E, low SpO₂) [NICE 2014].
• Atrial flutter: needs rate control and risk assessed and anticoagulation. Consider Beta blockade or diltiazem or digoxin for rate control. Cardioversion should be considered with the same assessment and anticoagulation as for AF.
• Anticoagulation: For AF, atrial flutter or PAF. Determine CHA2DS2VaSc score and HAS-BLED score and assess risk/benefits of anticoagulation. Control hypertension, review the need for Aspirin or NSAIDs, stop/reduce alcohol. Do not avoid anticoagulation purely on the risk of falls. Quantify risk and intervene to reduce falls where possible. Anticoagulate CHA2DS2VaSc > 1 in men and >2 in women. If non-valvular AF (those with severe MS or AS or with a metal valve must have warfarin or LMWH) then consider Warfarin or a DOAC (Apixaban, Dabigatran or Rivaroxaban, etc.). A high CHA2DS2VaSc score needs urgent commencement on LMWH or a DOAC or Warfarin. If anticoagulation is contraindicated or not acceptable then consider cardiology referral for Left atrial appendage occlusion.
• Bridging anticoagulation: interruptions in anticoagulation can increase embolic risk. It is common to give LMWH bridging in the perioperative period but this may lead to the risk of bleeding. A recent study has looked at this. The study excluded those with mechanical heart valves, stroke/ TIA/systemic embolization within 12 weeks, major bleeding within 6 weeks, renal insufficiency, low platelets or planned cardiac, brain or spinal surgery. The conclusion was that bridging is not warranted for most AF patients with CHA2DS2VaSc scores of <4, for low-risk procedures. This study must be interpreted along with local expert guidance balancing the risk of peri-procedure bleeding and embolic risk [N Engl J Med 2015;373(9):823].

Surgery/Ablation

• A surgical procedure (maze operation) controls AF in more than 90% of selected patients.
• Catheter ablation eliminates or reduces the frequency of recurrent AF in more than 60% of patients, but the risk of recurrent AF is 30% to 50%

Left atrial appendage occlusion

• Anticoagulation is the standard treatment of choice to reduce the risk and size of cardioembolic stroke. When anticoagulants are contraindicated due to excessive bleeding risk then Percutaneous Left atrial appendage occlusion may be considered.
• Patients selected should be those patients with AF with high stroke risk and contraindications for Oral Anticoagulation. An excellent review can be found here. It is an evolving field and perhaps best if those undergoing the procedure do so as part of an RCT.

References and further reading

• Management of Atrial fibrillation 2016 ESC Clinical Practice Guidelines
• 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: Executive Summary
• Atrial fibrillation: management Clinical guideline [CG180] Published date: June 2014 Last updated: August 2014
• Canadian Cardiovascular guidelines on AF 2010