Dr Andy Potter GPwSI cardiology Milton Keynes Rhythm disturbances Dr Andy Potter GPwSI cardiology Milton Keynes

Community cardiovascular clinic Jan – Mar 2014 Jan – Mar 2017 % Increase Patients contacts 539 889 65% Monitors 204 415 103% Echocardiograms 206 403 95%

Community cardiovascular clinic Numbers referred to secondary care: 27 ( 3%)

Who do we see? 1. Palpitations thought to be caused by a significant rhythm disturbance 2. Syncope thought to be cardiac in origin 3. Perform prolonged rhythm monitoring (eg memory clinic)

What can we do 1. 24, 48, 72 hour ECG 2. Handheld monitor 3. Echocardiography

Palpitations – how to assess in primary care AF Long QT syndrome

Key messages 1. History and reassurance key in assessing palpitations 2. Don’t always trust automated ECG analysis software 3. Assume all need anticoagulation 4. Be aware of arrhythmogenc potential with polypharmacy 5. Manage ectopic beats with reassurance

Palpitations- how to assess in primary care Very common Worrying to the patient and doctor but usually benign (>90%) Good history and reassurance (where appropriate) is the key to management

Palpitations History Duration Trigger Frequency Associations Onset - time Exercise Stimulants FHx PMHx etc

Investigations Resting 12 lead ECG Bloods ?echo ?24 hour tape

24 hour tape 24, 48 and 72 hour and handheld monitor “Usefulness” (sensitivity and specificity) depends on patient selection Interpretation depends on pre-test probability Rate Rhythm Ectopics Symptom diary

Key message 1 History and reassurance key in assessing palpitations

AF Huge problem – disease of aging 5x risk of stroke Strokes are more severe with greater risk of dependence Emphasis (unless very symptomatic) should be on reducing risk of stroke

AF - diagnosis

AF – diagnosis

AF – symptomatic control Rate vs rhythm control Reverting to sinus rhythm from AF does not remove risk of stroke If asymptomatic, no need to treat. If slightly symptomatic, try rate control (beta-blockers, calcium channel blockers, digoxin) If more symptomatic, try rhythm control (=referral) Echo to rule out valve problems Bloods

NICE 2014 Offer rate control as the first-line strategy to people with atrial fibrillation, except in people: whose atrial fibrillation has a reversible cause who have heart failure thought to be primarily caused by atrial fibrillation with new-onset atrial fibrillation with atrial flutter whose condition is considered suitable for an ablation strategy to restore sinus rhythm for whom a rhythm control strategy would be more suitable based on clinical judgement.

NICE 2014 Consider pharmacological and/or electrical rhythm control for people with atrial fibrillation whose symptoms continue after heart rate has been controlled or for whom a rate-control strategy has not been successful.

Anticoagulation NICE/ESC guidelines “Why does the patient not need OAC” rather than “Does my patient need OAC” – i.e trying identify the truly low risk patients (<65, no RF for stroke) Warfarin reduces risk by 60% ASA by 20% With similar risks of bleeding Aspirin “placebo with bleeding”

CHA2DS2-VASc CCF HTN Age >75 (doubled) Diabetes Stroke (doubled) Vascular disease Age (65-74) Sex (female)

Score ≥ 1 = OAC Only truly low risk patients (<65, no risk factors “lone AF”) do not need OAC. If patient’s refuse/decline OAC ESC suggests ASA and clopidogrel (but caution over bleeding risk)

Bleeding- HAS-BLED HTN Abnormal liver/renal function Stroke Bleeding history/predisposition Liable INR ETOH Drugs >3 close consideration/monitoring

Warfarin Cheap Effective Even in trial situations TTR 60%

NOACs Oral direct thrombin inhibitors (dabigatran) Oral direct factor Xa inhibitors (rivaroxaban, apixaban)

NOACs All have their role Apixaban choice in MK (cost-effective) They do need monitoring (just not INR monitoring) Caution with renal impairment (3monthly U&Es) Dyspepsia is an issue

Summary Emphasis should be on anticoagulation Opt-in rather than opt-out Only low risk do not need OAC “Warfarin stopped as now in sinus rhythm” Rubbish!!!!!

key message 2 and 3 Don’t always trust automated ECG analysis software Assume all need anticoagulation

LONG QT syndrome Rare but potentially catastrophic Congenital LQTS Acquired QT prolongation

Acquired LQT Depolarisation/repolarisation Bazzett’s formula Depends on rate Always consider QT prolongation if the end of the T wave approaches the midpoint between the QRS complexes

Acquired Long QT >460ms women >450ms men Bradycardia Drugs Metabolic Anorexia

Drugs Anti-psychotics Anti-depressants Macrolides

LQTS Awareness Monitor if concerned If abnormal – repeat and avoid certain medications

Key message 4 Be aware of arrhythmogenc potential with polypharmacy

ECTOPICS VERY common Almost always see on ECG monitoring Usually described as a missed beat, often at night/rest Almost always benign (slightly increased concern if very frequent or worsen on exercise) Management is reassurance

Key messages 1. History and reassurance key in assessing palpitations 2. Don’t always trust automated ECG analysis software 3. Assume all need anticoagulation 4. Be aware of arrhythmogenc potential with polypharmacy 5. Manage ectopic beats with reassurance

NHS Milton Keynes CCG GP PLT Thursday 25th May 2017

By Dr Assad Hamid GPWSI in Cardiology Syncope By Dr Assad Hamid GPWSI in Cardiology

Definition and Symptoms of Syncope The medical term for fainting is syncope. Syncope is a T-LOC due to transient global cerebral hypo perfusion characterized by rapid onset, short duration, and spontaneous complete recovery in usually less than 30 seconds Presyncope is a state of light-headedness, muscular weakness, blurred vision, and feeling faint (as opposed to a syncope, which is actually fainting). The following signs and symptoms may precede a fainting episode: A feeling of heaviness in the legs , Blurred vision, Confusion , Feeling warm or hot , Light-headedness, dizziness, a floating feeling, Nausea, Sweating, Vomiting Yawning.

Causes of syncope Neurally‐mediated (reflex) Or Neuro-cardiogenic Syncope due to Orthostatic hypotension Vasovagal syncope (common faint) Mediated by emotional distress, fear, pain, instrumentation, blood phobia, Mediated by orthostatic stress Situational syncope Cough, sneeze or gastrointestinal stimulation (swallow, defecation, visceral pain) micturition (post‐micturition) post‐exercise post‐prandial others ( laugh, brass instrument playing, weightlifting) Carotid sinus syncope Atypical forms ( without apparent triggers and/or atypical presentation ) Primary autonomic failure Pure Autonomic failure, Multi system Atrophy, Parkinson's disease with autonomic failure, Lewy body dementia Secondary Autonomic Failure Diabetes, Amyloidosis, Uraemia, Spinal cord injuries Drug Induced Orthostatic Hypotension Diuretics, vasodilators, Alcohol, Phenothiazine's, Antidepressants ( TCA’s) Volume Depletion Haemorrhage, Diarrhoea, vomiting etc.

Cont’d causes Structural cardiac or cardiopulmonary disease Cardiac arrhythmias as primary cause Sinus node dysfunction (including bradycardia/tachycardia syndrome) Atrioventricular conduction system disease Paroxysmal supraventricular and ventricular tachycardias Inherited syndromes (eg, long QT syndrome, Brugada syndrome) Implanted device (pacemaker, implantable cardioverter‐defibrillator) malfunction Drug‐induced arrhythmias Obstructive cardiac valvular disease Acute myocardial infarction/ischaemia Obstructive cardiomyopathy Atrial myxoma Acute aortic dissection Pericardial disease/tamponade Pulmonary embolus/pulmonary hypertension Cerebrovascular Vascular Subclavian steal syndromes

Causes of non‐syncopal attacks (commonly misdiagnosed as syncope) Disorders without any impairment of consciousness Disorders with partial or complete loss of consciousness but without cerebral hypoperfusion Falls Cataplexy Drop attacks Psychogenic pseudo‐syncope Transient ischaemic attacks (TIA) of carotid origin Metabolic disorders, including hypoglycaemia, hypoxia, hyperventilation with hypocapnia Epilepsy Intoxications Vertebro‐basilar TIA

Diagnosis of syncope The following questions should be answered: Was LOC complete? Was LOC transient with rapid onset and short duration? Did the patient recover spontaneously, completely and without sequelae? Did the patient lose postural tone? If the answers to these questions are positive, the episode has a high likelihood of being syncope. If the answer to one or more of these questions is negative, exclude other forms of LOC before proceeding with syncope evaluation.

Clinical features suggestive of specific causes of syncope Neurally‐mediated syncope Syncope caused by orthostatic hypotension Absence of cardiac disease Long history of syncope After sudden unexpected unpleasant sight, sound, smell or pain Prolonged standing or crowded, hot places Nausea, vomiting associated with syncope During or in the absorptive state after a meal With head rotation, pressure on carotid sinus (as in tumours, shaving, tight collars) After exertion After standing up Temporal relationship with start of medication leading to hypotension or changes of dosage Prolonged standing especially in crowded, hot places Presence of autonomic neuropathy or parkinsonism After exertion

Cont’d clinical features Cardiac syncope Cerebrovascular syncope Presence of severe structural heart disease During exertion, or supine Preceded by palpitation or accompanied by chest pain Family history of sudden death With arm exercise Differences in blood pressure or pulse in the two arms

Suspected Epilepsy A bitten tongue. Head-turning to one side during TLoC. No memory of abnormal behaviour that was witnessed before, during or after TLoC by someone else. Unusual posturing. Prolonged limb-jerking (note that brief seizure-like activity can often occur during uncomplicated faints). Confusion following the event. Prodromal déjà vu, or jamais vu

DIAGNOSTIC YIELD AND PREVALENCE OF CAUSES OF SYNCOPE The EGSYS study which is based on strict adherence to the Guidelines on Syncope of the European society of cardiology showed : A definite diagnosis was established in 98% (unexplained in 2%): Neurally‐mediated syncope accounted for 66% of diagnoses, orthostatic hypotension 10%, primary arrhythmias 11%, structural cardiac or cardiopulmonary disease 5%, and non‐syncopal attacks 6% . The initial evaluation established a diagnosis in 50% of cases

Evaluation of the patient Careful history taking including of any prodromal symptoms and preceding events also if there was any loss of sphincter control and tongue bite, palpitations, chest pains, association with food, exercise, alcohol intake Examination Detailed cardiovascular examination including Lying , Sitting and standing ( after 3 min) blood pressure with Systolic drop of >20 mm and Diastolic drop of > 10mm of Hg or reproduction of symptoms, listening for any heart murmurs, checking and comparing radial and femoral pulses, listening for any carotid bruits and infra/supra clavicular bruits, checking for any signs of dehydration, pallor, cyanosis. Complete neurological exam and checking for any signs of infection. ECG mainly looking for any arrhythmia, ischaemia, heart block, short PR interval, Prolonged QT interval. Blood test to look for Anaemia, electrolyte imbalance and renal and metabolic function including blood sugar levels.

ECG abnormalities suggesting cardiac cause Conduction abnormality (for example, complete right or left bundle branch block or any degree of heart block) Inappropriate persistent bradycardia. Any ventricular arrhythmia (including ventricular ectopic beats). Long QT (corrected QT > 450 ms) and short QT (corrected QT < 350 ms) intervals. Brugada syndrome. Ventricular pre-excitation (part of Wolff-Parkinson-White syndrome) – Short PR interval less than 0.2 sec or Delta wave Left or right ventricular hypertrophy. any ST segment or T wave abnormalities. Pathological Q waves. Atrial arrhythmia (sustained) including atrial flutter, fibrillation, Atrial tachycardia Paced rhythm.

EGSYS Score and Urgent Cardiology referral Palpitations before syncope ( +4 ) Abnormal ECG and/or heart disease ( +3 ) Syncope during effort ( +3) Syncope while supine ( +2 ) Autonomic Prodrome ( -1) Predisposing/precipitating factors ( -1) Refer if score  ≥ 3

Referral and further tests No need for referral if simple vasovagal faint with features suggestive of uncomplicated faint or Typical history with 3 P’s of Posture, provoking factors and Prodromal symptoms or typical history of situational syncope with normal examination, normal ECG and no alternative diagnosis If confirmed Orthostatic Hypotension with history and examination and no alternative diagnosis possibility then again no need for referral unless unsure of management and needs specialist input. Urgent Cardiology referral if An ECG abnormality as discussed earlier Heart failure (history or physical signs). TLoC during exertion. Family history of sudden cardiac death in people aged younger than 40 years and/or an inherited cardiac condition. New or unexplained breathlessness. A heart murmur. Consider referring within 24 hours for cardiovascular assessment, as above, anyone aged older than 65 years who has experienced TLoC without prodromal symptoms. Investigations can include Holter Monitoring , Echocardiogram, ETT, Cardiac MRI, Coronary angiogram, Implantable loop recorder ( ILR ) , Telemetery, tilt Table testing and carotid sinus Massage Neurology referral if Suspected Epilepsy, TIA/Stroke, History of head injury or concussion etc. Investigations may include CT/MRI brain, EEG ( has been shown to be of little benefit in diagnosing syncope ) Psychiatric referral – if after careful history, examination and tests Pseudo seizures are diagnosed especially if patient < 40 years of age with past history of some form of psychiatric illness and absence of cardiovascular disease . There are usually multiple episodes during the day/week with prolonged periods of LOC, do not be distracted with injuries as one study showed some form of injury in >50 % of patients with Pseudo Seizures.

Management and Treatment The principal goals of treatment for patients with syncope are to prolong survival, limit physical injuries, and prevent recurrences. Knowledge of the cause of syncope has a key role in selection of treatment. Reflex syncope Non-pharmacological ‘physical’ treatments and avoidance of trigger factors . Isometric physical counter pressure manoeuvres ( PCMs ) of the legs (leg crossing), or of the arms (hand grip and arm tensing), are able to induce a significant BP increase during the phase of impending reflex syncope that allows the patient to avoid or delay losing consciousness  Tilt training The prescription of progressively prolonged periods of enforced upright posture (so-called ‘tilt training’) may reduce syncope recurrence Pharmacological therapy Many drugs have been tested but with disappointing results for reflex syncope including β-blockers, disopyramide, scopolamine, theophylline, ephedrine, etilefrine, midodrine, clonidine, and serotonin reuptake inhibitors. Cardiac Pacing plays a small role in therapy for reflex syncope, unless severe spontaneous bradycardia is detected during prolonged monitoring. Vasovagal syncope All patients should be taught PCMs, which now form the cornerstone of therapy together with education and reassurance. Driving follow the DVLA guidance , advice all patients to stop driving until the cause of syncope has been ascertained and for non simple faints until after specialist assessment and advice or once treatment has started and patient has no further attacks or has reduced risk.

Cont’d Situational syncope Treatment strategies are similar to VVS and have been covered. Treatment of most forms of situational syncope relies heavily on avoiding or ameliorating the triggering event and may be attenuated by maintenance of central volume, protected posture, and slower changes in posture. Carotid sinus syndrome Dual chamber Cardiac pacing appears to be beneficial in CSS when bradycardia has been documented also avoiding tight collars, ties, electric shaver. Orthostatic hypotension and orthostatic intolerance syndromes The principal treatment strategy in drug-induced ANF is elimination of the offending agent. Expansion of extracellular volume is an important goal to drink 2-3 litres of water daily, salt up to 10 grams NACL for non hypertensive patients . Rapid cool water ingestion for post-prandial hypotension. Sleeping with the head of the bed elevated (10°) prevents nocturnal polyuria, maintains a more favourable distribution of body fluids, and ameliorates nocturnal hypotension. Gravitational venous pooling in older patients can be treated with abdominal binders or compression stockings. In contrast to reflex syncope, the use of the α-agonist, midodrine, (5–20 mg, three times daily) is a useful addition to the first-line treatment in patients with chronic ANF. Fludrocortisone (0.1–0.3 mg once daily) less frequently used treatments, alone or in combination, include desmopressin in patients with nocturnal polyuria, octeotride in post-prandial hypotension, erythropoietin in anaemia, pyridostigmine, use of walking-sticks, frequent small meals, and judicious exercise of leg and abdominal muscles, especially swimming. Cardiac Syncope – Specific treatments as per diagnosis including antiarrhythmic medication, ICD, Pacemakers, radiofrequency ablation, surgery for Atrial Myxoma HOCM etc.

Summary and Questions Careful history taking including of the eye witness and detailed examination including CVS with sitting /standing Bp, ECG, blood test, leads to diagnosis in > 50 % of cases. If you suspect a cardiac cause like an arrhythmia or Structural heart disease then your can refer to a community cardiologist for most cases. But if serious ventricular arrhythmia suspected , or there is a history of Ischaemic heart disease /MI or family history of SCD then urgent hospital admission or referral to hospital cardiology department is recommended. If the history is suggestive of a neurological cause like Epilepsy or there is history of head injury /concussion then urgent neurology referral is recommended. For simple vasovagal fainting with clear trigger and no sinister findings on examination and tests no referral is required. Manage as discussed before. If the cause of syncope is not clear from history and examination then the patient will possibly need both cardiology and Neurology input and more extensive testing likely insertion of ILR. Consider referral to a Psychiatrist/Psychotherapist for confirmed and persistent Psuedoseziures.

Refreshment Break