BiteMedicine (Atrial Fibrillation and Limb Ischaemia) slides

CardiovascularLecture 3

Dr Azeem Alam, MBBS BSc (Hons)Surgical AFPGuy’s and St. Thomas’ Hospital

Email: [email protected]: www.bitemedicine.comFacebook: https://www.facebook.com/biteemedicineInstagram: @bitemedicine Content reviewed on 01/04/2020.

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Learning objectives• 1 cardiology topic: Atrial fibrillation

• 1 vascular topic: Limb ischaemia

• Case-based discussion(s) to identify the top differentials and why

• Theory to cover pathophysiology, diagnostic criteria, investigations and

management

• Quiz (Mentimeter and multi-step SBAs)2www.bitemedicine.com Instagram: @bitemedicine Facebook: /biteemedicine

Case 1History

A 67-year-old male barrister presents to your cardiology clinic with a 3-week history of palpitations and shortness of breath. He has been anxious about work, which is causing him to drink 3 pints of lager in the evening to relax.

He has a history of hypertension and asthma, for which he takes enalapril and salbutamol. On examination, he is anxious with an irregularly irregular pulse.

Observations

HR 130, BP 140/95, RR 21, SpO2 96%, Temp 37.4

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Pathophysiology• Chaotic irregularly irregular atrial rhythm

• Type of SVT

• Sinoatrial node impulses overwhelmed

• Classification• First episode• Paroxysmal: recurrent episodes that terminate spontaneously in <7 days• Persistent: recurrent episodes that last >7 days• Permanent: continuous atrial fibrillation that is also refractory to treatment


Pathophysiology: PIRATES

PIRATESPulmonary: PE and COPD

Ischaemic heart disease

Rheumatic heart disease (or valvular abnormalities)

Anaemia, Alcohol, Advancing age

Thyroid disease

Electrolyte disturbance, Elevated BP

Sepsis and Sleep apnoea

Pathophysiology


Structural abnormalities

RAAS activation

Atrial dilatation and fibrosis

Examples include heart failure and valvular abnormalities

Activation of the RAAS causes an increased left atrial pressure

Difference in refractory periods causes electrical re-entry and ectopic foci

Triggering event

Pre-excitation of the atria

Overview


[2]


Differentials


Atrial fibrillation Atrial flutter Wolff-Parkinson-White syndrome

Clinical features

• Palpitations • Irregular pulse

• Difficult to differentiate from AF

• Young age (20s)• Precipitated by

exercise

ECG • Irregular rhythm• No P waves• QRS <120 ms• Variable rate

• Saw-tooth• QRS regularity

variable• QRS <120 ms• ~300 bpm

• Short PR interval• Delta wave on QRS • QRS >120 ms

ECG: Atrial fibrillation


[3]

ECG: Atrial flutter


[4]

ECG: Wolf-Parkinson-White syndrome


[5]


InvestigationsBedside• ECG: irregular rhythm with no p waves. If rate >100 this is known as AF with rapid

ventricular response (‘fast AF’)

Bloods• Inflammatory markers: infection can cause AF • U&Es: hyper/hypokalaemia • Magnesium: hypomagnesemia • TFTs: hyperthyroidism • Troponin: if chest pain is present, important to assess for myocardial ischaemia

Imaging• CXR: fast AF can present with heart failure and pulmonary oedema • ECHO: can assess ejection fraction as well as evidence of an atrial thrombus

Specialist tests• 24-hour or 5-day ECG: useful for people in paroxysmal AF



ManagementManagement• Treat the underlying cause, if possible• Two options: rate control and rhythm control

Onset < 48 hours• Rate control or rhythm control

Onset > 48 hours or unknown onset• Rate control • Consider rhythm control after 3 weeks


Management: Rate control

• First line: beta-blocker or rate-limiting calcium channel blocker (CCB)• E.g. bisoprolol or verapamil• Digoxin is first line in patients with AF and co-existing heart failure

• Second line: combination therapy • E.g. Add digoxin to either bisoprolol or diltiazem (avoid combining a beta-blocker

with a non-dihydropyridine CCB)


Management: Rhythm control• Electrical DC cardioversion (120-150 J)

• Pharmacological cardioversion • E.g. flecainide or amiodarone• Amiodarone preferred if evidence of structural heart disease• Key indications: after electrical cardioversion for adverse features

or onset > 48 hours after rate control


Adverse features

Shock Syncope

Myocardial ischaemia Heart failure

Management: Summary


Onset < 48 hours

Rate or rhythm control

Onset > 48 hours or unknown

Rate control and anticoagulation for

3 weeks (min.)

Consider rhythmcontrol

Adverse features

Rhythm control: electrical

cardioversion

Rhythm control: pharmacological

cardioversion

CHA₂DS₂-VASc vs HASBLED

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HAS-BLED

H Hypertension

A Abnormal renal function Abnormal liver function

S Stroke history

B Prior major bleeding / predisposition to bleeding

L Labile INR

E Elderly: >65 years of age

D Drugs predisposed to bleeding

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CHA2DS2-VASc

C Congestive heart failure

H Hypertension

A2 Age: 65-74, >75

D Diabetes

S2 Stroke / TIA /thromboembolism history

V Vascular disease e.g. prior MI, PVD

S Female sex

Management: Anticoagulation• AF is associated with an increased risk of thromboemboli

• CHA₂DS₂-VASc: • Consider anticoagulation in males with a score of 1• Offer anticoagulation to people with a score of ≥2

• HASBLED: • Consider alternative to anticoagulation if ≥3

• Options for anticoagulation: • Heparin: for new-onset AF whilst awaiting full assessment• DOAC: preferred long-term• Warfarin: an alternative to DOACs but preferred in valvular AF


Summary 1 – Atrial Fibrillation• Atrial fibrillation is unsynchronised atrial electrical conduction, resulting in

mechanically ineffective pumping of blood into the ventricles

• ECG confirms the diagnosis, followed by investigations to find and correct the underlying cause

• Haemodynamically-stable patients generally require rate control with a beta-blocker or a calcium channel blocker

• Haemodynamically unstable patients require DC cardioversion

• AF increases the risk of thromboembolic events; calculate the CHA₂DS₂-VAScand HASBLED scores to determine whether to initiate anticoagulation



Case 2History

A 75-year-old lady presents to A&E with a 3-day history of worsening, persistent pain in the left leg and a burning sensation in the left foot.

On examination, the left leg is purple, tender and cold. There is guttering of superficial veins throughout the left leg. Only the femoral pulse is palpable on the left. There is a sensory loss of the toes.

Observations

HR 80, BP 110/70, RR 20, SpO2 95%, Temp 36.525www.bitemedicine.com Instagram: @bitemedicine Facebook: /biteemedicine


PathophysiologyAcute limb ischaemia (ALI)• Embolisation followed by thrombosis are the

most common causes • Nerves are first affected, followed by muscles

and then skin (necrosis)• Irreversible damage within 6 hours

Chronic and critical limb ischaemia (CLI)• Narrowing of the peripheral arteries • CLI is an advanced form of peripheral arterial

disease


[6]

Pathophysiology• Acute limb ischaemia

• Sudden reduction in limb perfusion• Threatened limb viability (6 Ps)

• Critical limb ischaemia• Rest or night pain for >2 weeks• Often associated with ulcers or gangrene

• Intermittent claudication• Pain on exertion


Acute limb ischaemiaPain

Paralysis

ParaesthesiaPulselessness

Pallor

Perishingly cold


InvestigationsALI: do not delay surgery by performing extensive investigations in a threatened limb

Bedside• Ankle-brachial pressure index (ABPI)• ECG: very important in ALI

Bloods: particularly for ALI• U&Es: assess for rhabdomyolysis and required prior to CT• Creatine kinase: elevated in rhabdomyolysis

Imaging• Arterial duplex ultrasound• CT angiogram: vital pre-operatively and perform urgently

in ALI


[7]

Investigations


[8]

ABPI result Interpretation>1.4 Abnormally calcified (false negative)0.9-1.09 Normal

0.5-0.9 Peripheral arterial disease

<0.5 Critical limb ischaemia: rest pain, ulceration, gangrene


Management (acute limb ischaemia)


Category Sensory MotorI: Viable Present Present

IIA: Threatened (salvageable)

Partial loss (toes) Present

IIB: Threatened (salvageable)

Partial loss (more than toes)

Partial paralysis

III: Irreversible (major tissue loss or permanent nerve damage)

Profound loss Profound paralysis

Management (acute limb ischaemia)• IV fluids and analgesia• IV unfractionated heparin: initial management

Thrombolysis or thrombectomy• I (viable): perform within 6-24 hours• IIA (threatened): perform <6 hours

Percutaneous/open thromboembolectomy or bypass• IIB (threatened): perform <6 hours

Amputation• III (irreversible)


[9]

Management (critical limb ischaemia)


[10]

Conservative (20%)• MDT referral and analgesia

Revascularisation• Endovascular angioplasty or stenting (40%)• Bypass surgery (25%)

Amputation (15%)• Offered if revascularisation has failed or is inappropriate


Long-term management• Reduce cardiovascular risk: smoking cessation, supervised exercise programme, diet,

manage co-morbidities

• Antiplatelet therapy: clopidogrel 75mg is preferred in arterial disease

• Statin: atorvastatin 80mg


Summary 2 – Acute limb ischaemia

• Acute limb ischaemia (ALI) describes a sudden decrease in perfusion, usually due to an embolus

• Patients usually present with acute limb pain, however the history can differ between causes

• Key risk factors include AF (embolic) and PVD (thrombotic)

• The Rutherford classification may be used to guide the management of ALI

• The gold-standard investigation for suspected ALI is a CT angiogram

• Initial management is with IV heparin, followed by endovascular or open surgical intervention


Summary 2 – Critical limb ischaemia

• Critical limb ischaemia (CLI) involves rest or night pain for greater than 2 weeks, with or without tissue loss, and occurs secondary to severe peripheral vascular disease

• Risk factors for arterial disease include smoking, diabetes, hypertension and hypercholesterolaemia

• An arterial duplex is the first-line investigation, whilst a contrast-enhanced CT angiogram is more detailed and used pre-operatively

• Management includes: conservative options, revascularisation or amputation

• Long-term management is vital



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DOI:10.15347/wjm/2014.010. ISSN 2002-4436. / CC BY (https://creativecommons.org/licenses/by/3.0)10. CC BY-SA (https://creativecommons.org/licenses/by-sa/3.0)

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BiteMedicine (Atrial Fibrillation and Limb Ischaemia) slides