Are there any constant features ? For example \200\224 dizziness occurring: on standing is more likely to be postural hypotension \200 on exertion may have an ischae mic component \200 on turning the head may be due to vestibular problems, or carotid sinu s hypersensitivity (see b \200\230Carotid sinus syndrome \200\231, p.122) \200 in any si tuation or at any time is much more likely to be due to an arrhythmia A history of signi \201 cant injury (especially facial bruising) with a blackout increases the chances of \201 nding an arrhythmia, particularly a bradycardia re quiring pacing Always take a full drug history \200\224 antiarrhythmics can be pro- arrhythmogenic, drugs that cause bradyarrhythmias (commonly B -blockers, digoxin or rate li miting calcium channel blockers such as diltiazem), and antidepressants (especially the tri cyclics) that can predispose to arrhythmias. Medications containing ephedrine, thyroxine, c affeine and B -agonists can cause tachyarrhythmias ARRHYTHMIA: PRESENTATION 273 Examination \200 Should always include lying and standing BP, assessment of the baseline pulse character, rate and rhythm, full cardiovascular examination to look for evidence of s tructural cardiac disease (eg cardiomyopathy, heart failure, valvular lesions) all of which may predispose to arrhythmias General problems require a full general examination \200\224 it is rarely appropriate to e xamine a single system only in an elderly patient. A rectal examination, eg, may reveal a r ectal tumor causing anemia and hence palpitations It may also be appropriate to examine the vestibular system (see b \200\230HOW TO Examine the vestibular system \200\231, p.561) and central ner vous system Investigations \200 Blood tests \200\224 including FBC (anemia), UC + E (low potassium predisposes to arrhythmias), thyroid function, digoxin levels where relevant ECG \200\224 look for baseline rhythm and any evidence of conducting system disease (eg a bundle branch block, or any heart block). Measure the P-R and the Q-T interval. Also look f or LV hypertrophy (arrhythmias more likely) or ischaemia. A totally normal ECG diminishes t he possibility of clinically signi \201 cant arrhythmia CXR \200\224 look at cardiac size \200 Holter monitoring \200\224 a prolonged ECG recor ding. Usually a 24-hr period initially. Remember this is a very small snapshot, and of limited value especially i f symptoms are infrequent. Can be useful if the symptoms are experienced while the monitor is on, and the ECG trace shows normal sinus rhythm. If the suspicion of arrhythmias is high , then repeat the test, or arrange for trans-telephonic event recording or even an implanta ble loop recorder where the symptoms are severe enough (eg sudden syncope) 274 CHAPTER 10 Cardiovascular Arrhythmias: management Management of arrhythmias in older patients does not differ signi \201 cantly from management in other age groups, but consider the following. Precipitants \200 Always check for common precipitants in older patients: Electrolyte abnormalities (especially hypo or hyperkalaemia and hypocalcaemia) Anemia \200 MI \200 Antiarrhythmic toxicity (especially digoxin) \200 Sepsis \200 H ypothermia \200 Any other acute illness If the precipitant cannot be reversed quickly (eg sepsis) then the arrhythmia is likely to be recurrent. Consider cardiac monitoring if cardiovascular comprom ise or if arrhythmia recurrence is likely Effect of arrhythmia \200 Tachycardia may be less well tolerated than in younger patients causing signi \201 cant hypotension, angina, or heart failure Hypotension itself may be less well tolerated than in younger patients (risk of cerebral injury) and so prompt action is required Where there is heart failure because of an arrhythmia, \202 uids cannot be used for resus citation and so de \201 nitive action is required sooner rather than later. Begin by using standard treatment for acute heart failure (oxygen, intravenous diuretics, and opiates, et c.) while organizing cardioversion (usually electrical for speed) or rate limitation (appro priate for AF) Diagnosis \200 There is more likely to be underlying cardiac pathology \200\224 always c heck for ischaemia and structural heart disease even for apparently benign arrhythmias (eg SVT) Bundle branch block is common, and so there may be confusion between supraventricular and v entricular arrhythmias. There are numerous subtle ways of distinguishing between these but in an emergency: \200 If the patient is compromised, electrical cardioversion will treat both effectively If the patient is unwell, but stable, an amiodarone infusion will treat both effectively, a nd has the advantage of causing little myocardial depression ARRHYTHMIAS: MANAGEMENT 275 Treatment \200 Elderly patients are much more likely to be on an antiarrhythmic drug already. 2Check the medication carefully before administering any therapy. See Box 10.1 for common p itfalls. \200 Electrical cardioversion is well tolerated by most older patients, usually effective and less likely to cause side effects than many medications. It should be conside red early where there is signi \201 cant compromise. Anesthetic support is required, which can take some time to arrange, so prompt referral is recommended. It is less useful in acu te sepsis where the arrhythmia is likely to recur, and it is hard to establish whether comp romise is caused by the sepsis or the arrhythmia. \200 Implantable cardiovertor de \201 brillators are life-saving for malignant ventricular arrhythmias (VT and VF) in patients wi th low ejection fractions. However they are very expensive, can cause debility and pain and do not allow a natural death (they must be turned off during palliative care). There is re luctance to use them in older, frail patients in whom non-arrhythmic deaths are common. Box 10.1 Common pitfalls with anti-arrhythmic medication Adenosine \200 Its action is prolonged by dipyridamole (commonly prescribed with aspirin in stroke), so avoid using together Exacerbates asthma and is antagonized by theophylline, so avoid in asthmatic people Amiodarone \200 Risk of ventricular arrhythmias when used with disopyramide, procainamide and quinidine, so avoid concomitant use \200 Increases plasma half-life of \202 ecainide, so reduce dose Atropine \200 Can precipitate glaucoma, so avoid in patien ts with this condition Flecainide \200 Contraindicated when there is IHD, heart failure a nd haemodynamic compromise Probably best avoided in most older patients, who may well have occult cardiac disease Verapamil \200 Do not use intravenously in a patient already on a B -blocker (high risk of asystole and hypotension) General guidance Most antiarrhythmic medication used concomitantly increases the risk of my ocardial depression and arrhythmias. This effect is more pronounced in older patients. Caut ion when using more than one, and consider using sequentially rather than additively if one alone is ineffective. 276 CHAPTER 10 Cardiovascular Atrial \201 brillation Common arrhythmia, becoming more common with age (risk doubles wit h each additional decade of age, rising to 7 % in > 85 year olds). Often associated with ot her disease (eg hypertension, coronary artery disease, mitral valve disease, thyrotoxicosis ) but also occurs in 1 \200\2232 % of otherwise healthy elderly people. Unlike other arrhyt hmias, it is often chronic. Disorganized atrial activity with variable conduction to the ventricles leads to an irregul arly irregular pulse rate and volume. Up to a third of older patients with AF will have AV nodal disease that limits the rate to less than 100bpm, often making it asymptomatic. It is therefore often noted incidentally during routine examination \200\224 but should never b e ignored. Assessment Should include examination for hypertension and valve disease, blood tests for t hyroid disease and an ECG to con \201 rm the diagnosis (may be sinus rhythm with ectopics) . Paroxysmal AF may cause intermittent symp- toms and should be looked for with Holter moni toring. Complications AF causes an increase in morbidity and mortality, even if there is no underly ing cardiac disease. \200 Pulse > 120 often causes palpitations, light-headedness, or syn cope \200 Rapid rate may also cause dyspnoea, angina, or heart failure \200 General mal aise may also result from a chronically suboptimal cardiac output AF is often associated with periods of AV conduction delay ( \200\230pauses \200\231) and if > 3sec these may cause syncope The main complication is stroke from cardiac emboli Atrial \202 utter \200 Rapid, regular atrial activity (usually 300/min) \200 Characte ristic saw tooth appearance on ECG (revealed by carotid sinus massage if rate high) Rate depends on degree of AV block (150bpm if 2:1 block, 75bpm if 4:1 block etc.) 2Always think of atrial \202 utter when the pulse rate is 150 \200 Commonly associated with COPD or IHD \200 Similar embolic risk to AF, and as the patient will often \202 ip in and out of \202 utter and \201 brillation they should be managed in the same way \200 Treat with rate control and stroke prophylaxis. This rhythm is usually amenable to ca rdioversion, but if there are signi \201 cant comorbidities, structural heart disease or v alve disease, then sinus rhythm is unlikely to be sustained ATRIAL FIBRILLATION: RATE/RHYTHM CONTROL 277 Atrial \201 brillation: rate/rhythm control Acute AF \200 Treat underlying condition, e g sepsis, ischaemia, heart failure \200 If compromised, consider electrical cardioversion \200 Otherwise, control rate (usually with B -blocker or rate-limiting calcium channel blocker such as verapamil if no contraindication, eg heart failure; digoxin if resi stant) May resolve once precipitant has been dealed with \200 Remember stroke prophylaxis Chronic AF \200 Guidelines suggest rate control with B -blockade (eg bisoprolol) or calcium channel blockers (eg diltiazem, verapamil) In practice, many frail old patients will tolerate digoxin better, and this remains the \201 rst choice of many geriatricians (see b \200\230HOW TO Use digoxin \200\231, p. 281) Where chemical cardioversion is considered on symptomatic grounds give amiodarone (initiall y 200mg tds for a week, then 200mg bd for a week, then 200mg od thereafter. May be able to drop dose further to 100mg a day, or even every other day). 2Remember that amiodarone interacts with warfarin and regular moni- toring of INR will be n eeded if the two are used together \200\224 as is often the case. Also can cause thyroid a bnormalities, and this should be monitored with TFTs (see b \200\230Amiodarone \200\231, p .138). Dronedarone is a newer agent that is simpler to use than amiodarone, but cannot be u sed in severe heart failure and safety in permanent AF is unclear. \200 Electrical cardio version for chronic AF should only be attempted after a period of anticoagulation (minimum 3 weeks). It is more likely to succeed (and less likely to recur) where there are fewer of the following present: \200 Structural heart d isease (hypertrophy, atrial enlargement, valvular heart disease etc.) Comorbidity (especially hypertension, heart failure) \200 Increasing age Recent evidence suggests that an older patient with several of the factors listed is better off being treated with rate control and anticoagulation only, without attempting cardiover sion \200 Consider atrial catheter ablation if refractory to treatment, to destroy or isolate abnormal electrical impulses Paroxysmal AF \200 Equal embolic risk, so consider anticoagulation as for chronic AF \200 Remember that digoxin does not prevent AF \200 Amiodarone, dronedarone, or B -block ers (eg bisoprolol) are useful to prevent paroxysms of AF Ablation therapy may be useful in those with normal-sized atria and few comorbidities, although the recurrence rate is probably higher than in younger patients 278 CHAPTER 10 Cardiovascular Atrial \201 brillation: stroke prevention This is a complex and often emotive issue. Many older people will have very strong views about stroke ( \200\230I \200\231d rather die tha n ever have a stroke \200\231) or warfarin (many know it as rat poison, or have known someo ne who had a bleed while on warfarin). As we are dealing with population risks and bene \201 ts, it is impossible to accurately predict for a single individual what will happen to them if they do, or do not take preventative therapy. Conveying this concept is dif \201 cult, but because the decision is complex, involvement of the patient becomes key. This tak es time and patience. It is important to have a simple way of explaining the facts as they are known, perhaps wri ting them down for clarity, then allowing time for them to sink in before coming to a \201 nal decision. There is no enormous urgency \200\224 the stroke risks quoted are per a nnum, and it is worth giving the patient time to think things over if required. Address eac h of the following questions. What is the risk of stroke in this patient with AF? Overall, the risk is about \201 ve ti mes greater than a person with similar health and age who does not have AF. Paroxysmal AF c arries the same embolic risk. This risk may be more accurately quanti \201 ed by the following: High risk (6 \200\22312 % chance of stroke per year) \200 > 65 with cardiovascular risk f actors (hypertension, diabetes) \200 Previous stroke or TIA \200 Cardiac disease (MI, h eart failure) \200 Echo abnormalities (poor LV function on echo, atrial clot) \200 Thyr oid disease Medium risk (3 \200\2235 % chance of stroke per year) \200 > 65 but with none of the high-risk characteristics \200 <65 with cardiovascular risk factors (hypertension , diabetes) Low risk (less than 1 % chance of stroke per year) \200 < 65 with no addition al high risk factors Risk prediction tools \200 CHADS2 aims to predict risk of stroke in AF using clinical features (congestive heart failure, hypertension, age > 75, diabetes and previous stroke) Validated and widely used (see b \200\230Further reading \200\231, p.279, for details) Recently modi \201 ed to include female sex, age > 65, and a history of vascular disease (CHA2DS2-VASc), which may be more discriminatory at low risk 2In clinical practice, most frailer older patients will have a risk of stroke that warrants consideration of anticoagulation. ATRIAL FIBRILLATION: STROKE PREVENTION 279 What is the risk of therapy? \200 Warfarin when taken correctly and monitored carefully h as around 1 % per year risk of major bleeding in primary prevention of stroke, and 2.5 % ri sk in secondary prevention Newer, direct thrombin inhibitors, eg dabigatran require less monitoring and are likely to be used more in stroke prevention How effective is therapy at reducing risk? \200 Warfarin reduces stroke risk in AF by aro und 60 \200\22370 % \200 Aspirin (300mg) reduces risk by around 20 \200\22325 % What are the recommendations? \200 Where there are no contraindications, any patient with a stroke risk estimated at greater than 4 % per year should have anticoagulation (ie the h igh-risk and most of the moderate-risk groups, see b \200\230What is the risk of stroke in this patient with AF? \200\231, p.278) Those with a risk of 1 \200\2234 % should have aspirin \200 Those with a risk <1 % should have no treatment Other options There is limited trial evidence that occlusion of the left atrial appendage u sing a percutaneous device is equivalent to warfarin in the prevention of stroke (see b \200\230Further reading \200\231, p. 279). This may be an option for high- risk patients in whom anticoagulation is not feasible. Further reading Gage BF , Waterman AD , Shannon W , et al . ( 2001 ). Validation of clinica l classi \201 cation schemes for predicting stroke: results from the National Registry of Atrial Fibrillation . JAMA 285 : 2864 \200\223 70 . Holmes DR , Reddy VY , Turi ZG , et al . ( 2009 ). PROTECT-AF trial . Lancet 374 : 534 \200\223 42 . 280 CHAPTER 10 Cardiovascular HOW TO Discuss warfarin for AF Your patient is an 86-year-old woman with hypertension, IHD, and mild heart failure. She cu rrently takes aspirin, atenolol, bendro \202 umethiazide, furosemide, and ramipril. She ha s newly diagnosed AF, which is rate con- trolled because of the atenolol. You wish to discuss starting warfarin with her. The conversation may go as follows: Doctor: \200\230You have a condition called atrial \201 brillation \200 \224 where the heart beat is irregular. It is not causing you any problems at the moment, i t is common and it is not a dangerous heart condition. However, there is a risk that this i rregular beat could send a clot to the brain and cause a stroke and I would like to conside r a treatment to reduce the risk of this happening. \200\231 Patient: \200\230A stroke? I \200\231m going to have a stroke? \200\231 Doctor: \200\230If we took 100 people in your s ituation, then in a year about 10 of them would have a stroke \200\224 but 90 would not \200\231 Patient: \200\230I would hate to have a stroke. What can you do? \200\231 Doctor: \200\230We can thin your blood with a drug called warfarin \200\231 Patient: \200\230I \200\231ve heard of that \200\224 isn \200\231t it very dangerous? \200\231 Doctor: \200 \230You would need to have regular blood tests to make sure the dosage was right. If those 100 people all took warfarin, then one of them would have a serious problem with bleeding \200\231 Patient: \200\230But it will stop me from having a stroke? \200\231 Doctor: \200 \230Going back to those 100 people \200\224 if they all take the warfarin, then only three or four will have a stroke instead of the original 10. The risk is reduced by about 2/3. \200\231 Patient: \200\230Which three or four people? \200\231 Doctor: \200\230There is n o way of predicting who will bene \201 t from treatment and who will have a problem. What we do know is that overall, the risk is lower with warfarin, and so we do recommend treatme nt for someone like you. \200\231 Patient: \200\230Do I have to? \200\231 Doctor: \200 \230No, of course not. It is your decision. I will give you an information lea \202 et \200\224 why don \200\231t you go away and think it over \200\224 we will talk again \200 \231. ATRIAL FIBRILLATION: STROKE PREVENTION 281 HOW TO Use digoxin Indications \200 Rate control of AF \200 Mild positive inotrope sometimes used in heart failure Not useful for \200 Paroxysmal AF prevention \200 Exercise induced fast AF Loa ding with digoxin 1mg in divided doses over 24hr. This dose is always required, regardless of renal function \200\224 modify maintenance doses only in renal impairment. Example: Day 1 \200\224 8am digoxin 500micrograms po, 8pm digoxin 500 micrograms po. Day 2 \200\224 8am digoxin at maintenance dose Deciding a maintenance dose \200 Main determinant is renal function \200\224 digoxin is excreted this way, so use low dose with renal impairment Consider also body mass \200\224 eg start with 62.5micrograms for a small elderly woman \200\224 the dose can always be increased if there is inadequate rate control Dosage is determined clinically, but serum levels can be used to assess toxicity or concordance Digoxin toxicity \200 Hypokalaemia predisposes to this, so always monitor potassium and supplement if needed. Target [K] > 4.0mM Symptoms include confusion, nausea, vomiting, arrhythmias (especially nodal bradycardia and ventricular ectopics) and yellow or green visual haloes ECG may show ST depression and inverted T wave in V5 and V6 (reversed tick) Treat by stopping medication, rehydrating and correcting hypokalaemia Life-threatening poisoning can be treated with digoxin-speci \201 c antibody fragments 282 CHAPTER 10 Cardiovascular Bradycardia and conduction disorders As the heart ages the function of the cardiac pacemake r (the SA node) and the conducting system (bundle of His and Purkinje \201 bres) tends to decline, due to: \200 Declining numbers of cells in the SA node \200 Increasing preval ence of disease (atheroma, amyloid and hypertension) \200 Degeneration with \201 brosis and fat in \201 ltration This is not inevitable, but around 50 % of older patients will h ave some ECG evidence of conduction delay (prolonged PR and QT interval, left axis deviatio n, etc.) and be prone to symptomatic bradycardia and conduction disorders. Causes \200 Medication \200\224 digoxin, amiodarone, B -blockers (including some eye drops), calcium channel blockers, donepezil, tricyclic antidepressants \200 Sick sinus sy ndrome \200\224 isolated sinus node dysfunction, very common in older patients, with uncer tain cause (theories include vascular insuf \201 ciency or amyloid in \201 ltration, but often no cause is found) IHD \200 Structural heart disease \200\224 eg hypertrophic cardiomyopathy \200 Systemi c disease \200\224 hypothyroidism, liver failure, hypothermia, hypoxia, hypercapnia, cereb ral disease (eg stroke, raised intracranial pressure, hemorrhage) Presentation \200 Often picked up incidentally on an ECG \200 When symptomatic bradycar dia causes low output syndromes ranging from fatigue, dizziness, dyspnoea and presyncope, s yncope and falls, angina to heart failure and shock May be intermittent (with paroxysmal bradyarrhythmias), chronic (with stable arrhythmias) or occur acutely (usually post-MI) Management Not every bradycardic patient needs an urgent pacemaker \200\224 the local card iology service will help if in doubt. For every problem, consider: Is the patient acutely compromised? \200 If so, then urgent treatment is required in orde r to minimize cerebral injury. For shock, lie the patient down, and elevate the legs. Use i v \202 uids and/or try to increase the heart rate using atropine (0.6mg iv, repeated up t o total dose of 3mg), an isoprenaline infusion, or temporary pacing (external pads are quic k and often well tolerated; if the situation persists, insert a temporary pacing wire) If the patient is stable and has no reversible factors then they can wait for the next available permanent pacing list BRADYCARDIA AND CONDUCTION DISORDERS 283 Tailor your treatment to each individual \200\224 if the cause of the bradycardia is a catastrophic intracerebral event, then putting the patient through a tempo rary wire is not sensible \200\224 try external paddles to increase the heart rate and see if this has a positive impact on consciousness level while a CT scan is organized. Convers ely, an acute inferior MI may cause signi \201 cant short-term problems with bradycardia y et little longer-term cardiac damage Are there any symptoms? \200 If so, are they attributable to the bradycardia? Is the cond ition likely to resolve? Reversible bradyarrhythmia commonly occurs after acute inferior MI, in which case support t he patient during the acute episode as needed (non-invasively if feasible) How frequent are the symptoms? \200 Continuous \200\224 temporary wire may be needed bef ore permanent pacing \200 Exertional \200\224 consider bed rest pending permanent pacing instead of a temporary wire (reduces risk of infection and makes insertion of permanent wi re easier) Infrequent \200\224 elective permanent pacemaker can be organized \200 No symptoms \200 \224 no action is required unless there is a high risk of future asystole. Asystole is a major risk with second-degree heart block type II where ther e is also bundle branch block and complete heart block even if asymptomatic and a pacemaker is required for these Are there any reversible factors? \200 Check medication. Digoxin (especially with toxicit y), amiodarone, B -blockers and calcium channel blockers can all cause or exacerbate bradycardia Check thyroid function \200 Acutely, hypothermia can also cause bradycardia which reverse s when patient normothermic again 284 CHAPTER 10 Cardiovascular Permanent pacemakers Indications \200 Over 85 % are used for patients > 64 years old \200 50 % are for sick sinus syndrome and AV block \200 Increasingly used for vasodepressor carotid sinus hypers ensitivity \200 Occasionally used for recurrent syncope where no cause is found \200 Us ed with AV node ablation with refractory AF \200 Resynchronization therapy for heart fail ure Pacemakers \200 Dual chamber pacemakers are more expensive but tend to produce a better cardiac output and less AF than single chamber ones Permanent pacing should be programmed to minimize paced beats allowing the intrinsic rhythm to get through as much as possible \200 In LV dysfunction, pacing may need to include mu ltisite pacing as RV pacing can worsen dyssynchrony and exacerbate LV failure \200 Cardiac resynchronization t herapy (biventricular pacing) may reduce heart failure symptoms in patients with reduced LV function, especially if they have wide QRS complexes Insertion \200 Relatively simple procedure, done while awake, which is usually well toler ated by even very frail patients, with often dramatic improvements in quality of life \200 \224 consider in most where indicated although such patients may need reassuring that it wo n \200\231t prolong their life or stop them dying Technical problems can occur with insertion if the patient cannot lie still and \202 at Usually straightforward, but rare complications during insertion include arrhythmias (commonly AF) and rarely perforation of the right ventricle Later problems include sepsis and failure of pacemaker output \200 Regular follow-up is r equired to check the pacemaker function and battery reserve Further reading NICE . Bradycardia; dual chamber pacemaker guidance ( 2005 ) online: M www. nice.org.uk/ta88 . This page intentionally left blank 286 CHAPTER 10 Cardiovascular Common arrhythmias and conduction abnormalities See Table 10.4 . Table 10.4 Common arrhythmias and conduction abnormalities Condition Clinical features Treatment Sinus bradycardia Intrinsic SA nodal disease Treat only if symptomatic (rarely causes problem) Pulse rate <60 Check thyroid function Common incidental \201 nding Drugs are common cause Acute onset associated with inferior MI and raised intracranial pressure Consider hypothyroidism Benign Supraventricular ectopics Narrow complex QRS without a P wave, followed by a compensatory pause Reassure the patient No action required Patient may be aware of this, and describe an \200\230early beat \200\231 with a gap after wards Sinoatrial block Intermittent inability of SA node to depolarize atrium Usually asymptomatic Treat only if symptoms ECG shows pauses that are multiples of the PR interval Slow AF Combination of AF and SA nodal disease very common Anticoagulation for stroke prevention Symptomatic pauses frequent High index of suspicion for pauses if suggestive symptoms \200\224 check with Holter monit or and treat with pacemaker Treat symptoms Sick sinus syndrome Sinoatrial node dysfunction (degenerative or due to IHD) causing a bradycardia \200\224 in cludes sinus bradycardia and slow AF Often associated with other conduction problems Usually requires pacemaker for bradycardia and rate limiting drugs to control tachyarrhythm ias Tachy-brady syndrome Combination of slow underlying rate (sinus bradycardia of slow AF) with tendency for runs o f SVT that often terminate with a long pause Symptoms due to both slow and fast pulse COMMON ARRHYTHMIAS AND CONDUCTION ABNORMALITIES 287 Table 10.4 (Contd.) Condition Clinical features Treatment First degree heart block PR > 0.22sec Benign if isolated, but always check for coexisting second or third degree block No action required PR interval increases progressively until a QRS is dropped Often occurs transiently post MI Second degree heart block, Mobitz type I (Wenckebach) Usually appropriate to monitor until resolves Often symptomatic Fixed PR interval, but conduction to the ventricles does not occur on every beat. Usually i n a \201 xed pattern (conducting every second, third or fourth beat) Second degree heart block, Mobitz type II High risk of progression to complete heart block Usually requires elective pacing Often associated with bundle branch block Usually symptomatic although if rate > 50 may only be on exertion Complete dissociation of atrial and ventricular activity. P waves visible, but not conducte d. QRS originates at ventricular pacemaker (escape rhythm). If this is in the AV node then the rate is around 60 and the QRS morphology narrow. If it is more distal then the rate ten ds to be around 40 with wide QRS complexes Complete heart block (third degree) If chronic, limit activity until permanent pacing arranged If acute (eg post MI) likely to resolve When associated with hypotension, angina or heart failure at rest, may need temporary pacin g wire Bundle branch block Widened QRS due to delayed conduction. Acutely, LBBB may indicate acute infarct Not related to rate, so asymptomatic If found incidentally tell the patient (aids future emergency treatment) and consider givin g a copy of the ECG to the patient RBBB is a common \201 nding in healthy elderly and is usually benign, but if acute consid er acute pulmonary embolism LBBB is associated with hypertension and IHD Trifascicular block High risk of intermittent complete heart block. Pacemaker is required Prolonged PR, RBBB, and left anterior or posterior fascicular block (causing left axis devi ation) 288 CHAPTER 10 Cardiovascular Heart failure: assessment Heart failure is very common, occurring in 1 in 10 of the > 65s a nd accounting for 5 % of admissions to medical wards and 1 \200\2232 % of all health- care costs. Overall prevalence is 3 \200\22320 cases per 1000 population, but this doubles with each decade after 45 years. Becoming more common as population ages and survival from coron ary events improves. Pathology \200 Poor LV function (systolic or diastolic) decreases cardiac output, resulting in increased pulmonary pressures and oedema Sympathetic nervous system activated (increased pulse, myocardial contractility, peripheral vasoconstriction, and catecholamines) Renin \200\223angiotensin system activated (increases salt and water retention) \200 Vaso pressin and natriuretic peptides increase Causes Usually due to CHD (especially in Caucasians \200\224 CHD risk factors are markers for heart failure) and hypertension (especially African Caribbeans). Other causes include v alve disease, arrhythmias, pericardial disease, pul- monary hypertension (eg with COPD or m ultiple pulmonary embolisms), high output states (look especially for anemia, thyroid disea se and Paget \200\231s disease) and cardiomyopathy (check alcohol history). Diagnosis Heart failure is a complex clinical diagnosis, with no universally agreed diag- n ostic criteria. Often dif \201 cult to diagnose accurately, particularly in older patients with increased comorbidity and symptoms. Many older people are put on a diuretic for presu med heart failure, but diuretic use as a marker of heart failure is 73 % sensitive but only 41 % speci \201 c. This predisposes to postural symptoms, and adds to polypharmacy. Symptoms Ask are these symptoms cardiac and what is the underlying disease causing them? Ex ertional dyspnoea is 100 % sensitive for heart failure (ie every case has it), but only 17 % speci \201 c (ie many other causes of exertional dyspnoea exist \200\224 the main one b eing respiratory). Fatigue and ankle swelling are also very common in heart failure but occ ur in many other diseases too. Orthopnoea and paroxysmal nocturnal dyspnoea are much more s peci \201 c, but occurring late in the disease are not sensitive. Signs Again, early signs are sensitive, but not speci \201 c (eg tachycardia, pulmo- nary crepitations, peripheral oedema). Later signs are more speci \201 c, but not sensitive (eg elevated JVP \200\224 98 % speci \201 c, 17 % sensitive; gallop rhythm \200\224 99 % sp eci \201 c and 24 % sensitive) 2Overall, clinical features tend to be sensitive OR speci \201 c, but not both. The multiple pathology of older patients poses a particular challenge in diagnosis. Clinical suspicion should then be supported by investigation before embarkin g on a trial of treatment. HEART FAILURE: ASSESSMENT 289 HOW TO Investigate a patient with suspected heart failure Use investigations to support a clinical diagnosis and establish cause. \200 ECG \200 \224 abnormal in over 90 % of cases (Q waves, T wave/ST segment changes, LVH, bundle branch block, AF). Consider Holter monitor if paroxysmal symptoms CXR \200\224 look for cardiac enlargement (although this is absent with acute onset eg pos t MI or PE), upper lobe blood diversion, \202 uid in the horizontal \201 ssure, Kerley B lines, bat wing pulmonary oedema, pleural effusions (usually bilateral; R > L if unilater al), any other cause for breathlessness 2Combination of a normal CXR and ECG makes heart failure very unlikely indeed. \200 Blood tests \200\224 FBC (? anemic), biochemistry (? renal function, sodium low in severe heart failure), glucose and lipids (CHD risk factors), liver function (? congestion), thyroid function. BNP if available (see Box 10.2 ) Echocardiography \200\224 echo should be done for all with suspected heart failure (NICE g uidelines) to help con \201 rm diagnosis, establish cause and grade disease severity. Look s for LV function (systolic and diastolic \200\224see b \200\230Diastolic heart failure \200\231, p.296), estimates ejection fraction, looks for evidence of valve disease, cardiom yopathy, regional wall abnormalities from IHD, pericardial disease, intracardiac shunts, LV aneurysms or cardiac thrombus. Open access echo (ie direct GP referral) has improved the n umber of patients who have an echo, but the results are only as good as the echo technician and there can be problems with interpreting results (eg diastolic problems). Overall, only 25 % of those referred for echo have LV systolic dysfunction Pulmonary function tests \200\224 may help distinguish cardiac from respiratory breathlessness (peak expiratory \202 ow rate (PEFR) and forced expiratory vol ume in one second (FEV 1 ) reduced in heart failure, but less than in COPD). Remember many patients have both 290 CHAPTER 10 Cardiovascular Box 10.2 B-type natriuretic peptide (BNP) Three types of natriuretic peptide known, with effects on heart, kidneys and the nervous sy stem. B-type is found mainly in the heart and increases with pressure overload of the heart , acting as a biochemical marker for heart failure. BNP concentration correlates with the s everity of heart disease \200\224 very high levels carry a poor prognosis. In addition a n egative value makes a diagnosis of heart failure extremely unlikely (negative predictive va lue of 96 % ). Problems \200 What is a high level? Different assays produce different numbers, and there is a continuum of results making a diagnostic cut-off necessary \200 What is the gold st andard for diagnosis in order to evaluate the test? (Echo has limitations) BNP level does not help distinguish systolic from diastolic heart failure Drug treatment can affect levels, eg reduced by ACE inhibitors \200 False positives can b e caused by COPD, PE, age > 70, diabetes, LVH, previous MI, tachycardia, renal impairment, and liver cirrhosis Cost-effectiveness unknown \200 Limited clinical trial evidence \200 Signi \201 cance of a high level in an asymptomatic patient is unclear and it is not currently recommended for screening Currently not widely available in the UK 2Overall, a \200\230negative \200\231 (ie very lo w) result in a breathless patient makes heart failure very unlikely, and other causes shoul d be sought. NICE recommends measuring BNP in patients with suspected heart failure without previous MI in order to help preselect patients for echocardiog- raphy and specialist revi ew. ACUTE HEART FAILURE 291 Acute heart failure Treatment \200 Immediate treatment with oxygen, intravenous loop diur etic, and nitrates given iv or sublingually (if adequate BP), opiate, and antiemetic Address cause (eg acute MI, arrhythmia) \200 Stop any exacerbating medications (NSAIDs, B -blockers) \200 Consider thromboprophylaxis (eg low molecular weight heparin) \200 Con sider ventilatory support (begin with non-invasive positive pressure ventilation which can be done in a non \200\223ITU setting and does not present problems of weaning) After improvement is seen begin to plan ongoing treatment \200\224 write up regular loop d iuretic and usually ACE on the drug chart and make plans for further assessment Monitor electrolytes, BP, and weight Prognosis Patients with acute heart failure look extremely unwell yet can often make appare ntly \200\230miraculous \200\231 recoveries as the precipitant is dealed with. Remember th at it is the pre-morbid state and the nature of the acute injury, never age alone, that sho uld determine how aggressively to manage the acute condition. Rapid AF and heart failure \200 A common combination in older patients \200 It is rarel y clear which came \201 rst \200 Treat both simultaneously \200 Digoxin may slow AF i n this situation without depressing the myocardium (may occur with amiodarone). Load 1mg of digoxin over 24hr in divided doses \200\224 eg 500 micrograms iv or po repeated at 12hr, followed by the maintenance dose Always look for a precipitant \200\224 sepsis, MI, PE, etc. 292 CHAPTER 10 Cardiovascular Chronic heart failure 2Begin by reviewing basis for diagnosis as it means a poor prognosis and a commitment to a large number of medications. A multidisciplinary approach is preferable, involving the patient in monitoring where possible (eg daily weighing). Best done by those with an interest, and with facilities for ongoing follow-up, eg DHs (par ticularly suited to the frailer elderly), heart failure clinics, by heart failure specialis t nurses or GPs with special interest. Lifestyle Address cardiovascular risk actors, reduce alcohol intake, increase aerobic exerc ise (ideally as part of a rehabilitation program). Medication Large evidence base for a large number of drugs (see Box 10.3 ). It may be tempt ing to limit the number of drugs in older patients, justi \201 ed by concerns about side e ffects, but if the diagnosis is secure then all classes should be at least attempted. It is probably better to prescribe a low dose of an ACE with a B -blocker, rather than a maximum dose of ACE when the BP may be insuf \201 cient to introduce the B -blocker. Treating cause \200 AF should be slowed and anticoagulation started (cardioversion unlikely to succeed once LV dysfunction) Hypertension should be treated until disease progression drops cardiac output and hence BP Valvular disease should be assessed for surgical correction where appropriate (especially aortic valve disease \200\224 discuss with patient early after ons et of heart failure) Treat anemia and thyroid disease Vaccination Offer in \202 uenza vaccination annually and pneumococcal vaccination (once on ly). Monitoring Should include: \200 Clinical assessment of symptoms and functional capacity ( how far can they walk without stopping etc.) Blood pressure, including postural measurements \200 Fluid status (weigh regularly. Estim ate dry weight, record it and use this to titrate future management. Examine for JVP, oedema, and lung crepitations)