Troponins (I or T) Identifi cation of these in the blood is highly suggestive of myocardial injury, though the y can be raised in PE, renal failure, septicaemia and following tachyarrhythmias (but CK is seldom concurrently raised in these conditions). Detection is usually possible 6h after my ocardial injury and levels remain elevated for up to 14d. Troponins are also used as a prog nostic indicator in NSTEMI/UA (b p245) Enzyme found in all muscle and released in muscle ce ll lysis; not specifi c for cardiac muscle. Peaks within 24h post-MI and usually returns to normal within 48 \200\22372h, so useful in detecting further infarction in patients with p ain 3 \200\22314 days post MI (Fig. 7.1) Cardiac isomer of CK enzyme, so more specifi c tha n total CK. Rises and falls in similar fashion to total CK These were once used to retrospe ctively aid in the diagnosis of acute MI but have been superseded in recent years Creatine kinase (CK) CK-MB AST LDH x50 l e v e Troponin l e m y z n e m u r e S x5 x4 x3 x2 x1 CK-MB 1 2 3 4 Days 0 5 6 7 8 Fig. 7.1 Typical changes in cardiac markers following an acute myocardial infarction. _OHFP.indb 243 _OHFP.indb 243 30/05/2014 16:18 30/05/2014 16:18 244 CHAPTER 7 Cardiovascular 22STEMI (ST Elevation MI)1 (OHCM9 b p114) Worrying signs features of LV failure, cardiac dy srhythmia. Symptoms central, crushing, heavy chest pain ( \211 20min), radiating to left arm/jaw, shortness of breath, nausea, sweating, palpitations, anxiety. Risk factors smoking , obesity, DM, iBP, icholesterol, FH, previous IHD. Signs tachycardia, cool and sweaty ( \200\230clammy \200\231), 9LV failure or hypotension. Investigations ECG ST elevation (>1mm in 2 or more contiguous limb leads or >2mm in chest leads) or new LBBB; subsequent Q waves (commonly) T wave inversion (Fig. 7.2); CXR cardiomegaly, signs of LV failure; cardiac m arkers will be raised but treatment should not be withheld as ECG fi ndings and history alo ne are suffi cient to make the diagnosis. Acute treatment The goal is for rapid reperfusion by percutaneous coro- nary intervention (PCI) in those presenting within 12h of symptom on set so seek senior help. O2 (15l/min), aspirin (300mg), clopidogrel (300mg), diamorphine (2 .5 \200\2235mg IV), antiemetic (b p185), GTN (two puff s SL/5min until pain free; infusion if ongoing pain after 3 SL doses, provided not hypotensive, b p201). Where PCI is not avail able within 3h, consider fi brinolysis (b p536). B-blockade (eg bisoprolol 10mg/PO STAT) li mits infarct size and dmortality, but avoid use in COPD, hypoten- sion and overt failure. C areful glycaemic control (eg insulin sliding scale b p327) may improve outcomes.2 Secondary prophylaxis dmodifi able risk factors (smoking, obesity, DM, iBP, icholesterol), B-blockad e, statin, anti-platelets (aspirin indefi nitely, clopidogrel for 1 year), ACEi, symptom ma nagement (nitrates, Ca2+ channel antagonists). Complications dysrhythmias (AV block, bradyc ardia, VF/VT), LVF, valve prolapse, ventricular septal rupture, ventricular aneurysm format ion, pericarditis, Dressler \200\231s syndrome (OHAM3 b p32), recurrent pain. Normal Hours Days Weeks Months Fig. 7.2 Typical sequential ECG changes following an acute STEMI. Fig. 7.2 Typical sequenti al ECG changes following an acute STEMI. Care after myocardial infarction (OHCM9 b p114) \200 Bed rest for 48h with continuous ECG monitoring \200 Daily 12-lead ECG and thorough clinical examination of CVS/RS \200 Thromboembolism prophylaxis (b p406) \200 B-blocka de unless contraindicated \200 ACEi/angiotensin II receptor antagonist \200 Statin \200 Discuss modifi able risk factors and arrange cardiac rehabilitation \200 Primary PC I patients are at lower risk of complications and have shorter stays; thrombolysis patients will require risk stratifi cation and consideration for in-patient angiography. Consider electrophysiological studies in those with new dysrhythmias \200 Review in out-p atients at 5wk and 3mth for symptoms and to check lipids+BP 1 NICE guidelines available at (cid:27)guidance.nice.org.uk/CG167 2. Evidence low quality a nd confl icting. NICE review available at (cid:27)guidance.nice.org.uk/CG130 OHFP.indb 244 OHFP.indb 244 30/05/2014 16:18 30/05/2014 16:18 245 CHEST PAIN 22NSTEMI (Non-ST Elevation MI)1 (OHAM3 b p44) Diagnosis and intervention are often less \200\230dramatic \200\231 than for STEMI, requiring recognition of evolving ECG changes; ho wever, 1yr survival is poorer. Worrying signs features of LV failure, cardiac dysrhythmia. Symptoms, risk factors, and signs overlap with STEMI; patients typically tend to be older, with more co-morbidities. Investigations ECG ST depression, inverted T waves; subsequent ev olution of changes T wave inversion; CXR cardiomegaly, signs of LV failure; cardiac marke rs diff erentiate from UA by elevated troponin, taken according to local protocols (typical ly on presentation and 12h after worst pain). Acute treatment O2 (15l/min), aspirin (300mg) , clopidogrel (300mg), diamorphine (2.5 \200\2235mg IV), antiemetic (b p185), GTN (two puff s SL/5min until pain free; infusion if ongoing pain after 3 SL doses, pro- vided not hypot ensive, b p201) Anticoagulation with fondaparinux (b p407).2 B-blockade (eg bisoprolol 10mg STAT) but beware use in patients with COPD, hypotension or overt failure. Risk stratify (s ee below) and involve CCU+cardiologist early for high-risk patients for consideration of pr ompt catheterisation and glycoprotein IIb/IIIa inhibitors. Secondary prophylaxis and compli cations are broadly the same as in STEMI, though complications are less common. Risk strati \201 cation in ACS Estimation of the risk of death in ACS allows individualize d assessment of the risks and benefi ts of interventions and careful targeting of resources to those patients who stand to benefi t the most. A number of validated scoring algorithms have been developed from major clinical trial data. These include the pioneering Thromboly sis In Myocardial Infarction (TIMI) risk score3 still widely used in many hospitals. Howeve r, many such trials had restricted entry criteria, leading to under-representation of patie nts with renal or heart failure. The Global Registry of Acute Coronary Events (GRACE) algor ithms were developed from a multinational registry (94 hospitals, 14 countries, and 22,645 patients) involving patients with all subtypes of ACS (STEMI, NSTEMI, and UA).4 Risk scores may be cal- culated on admission (to predict in hospital and 6mth mortality) or on dischar ge (to predict 6mth mortality). A free online calculator is available at (cid:27)www.outcom es-umassmed.org/grace High-risk patients will need a CCU bed, and consideration for glycopr o- tein IIb/IIIa inhibitors and urgent catheterisation (within 96h). Low/intermediate-risk require observation to ensure pain free, then fur - ther stratifi cation using exercise ECG , coronary calcium scoring or stress imaging (echo or perfusion imaging) to determine need for catheterisation. 3 Antman, E.M. et al. JAMA 2000 284:835 available free online at (cid: 27)jama.ama-assn.org/cgi/ content/full/284/7/835 See also the excellent collection of resources available free at (ci d:27)www. timi.org 4 Granger, C.B. et al. Arch Intern Med 2003 163:2345 available free online at (cid:27)archi nte.ama- assn.org/cgi/content/full/163/19/2345 1 NICE guidelines available at (cid:27)guidance.nice.org.uk/CG94 2 Use unfractionated heparin infusion if angiography is planned within 24h, or if signifi c ant bleeding risk (consider in frail elderly, active/recent bleeding complications, signifi can t renal impairment or those with extreme low body mass). _OHFP.indb 245 _OHFP.indb 245 30/05/2014 16:18 30/05/2014 16:18 246 CHAPTER 7 Cardiovascular 22Unstable angina (OHAM3 b p44) Diagnosis is based upon typical history in the presence of ECG changes, but without subsequent elevation of cardiac markers. Worrying signs features o f LV failure, cardiac dysrhythmia. Symptoms, risk factors, and signs overlap with other for ms of ACS; typically episodes of angina occurring on minimal provocation or at rest, with p oor response to GTN; more frequent and more severe than patient \200\231s \200\230usual \200\231 angina; few symptoms or signs between episodes of pain. Investigations ECG ST depr ession, fl at or inverted T waves with dynamic changes over time, signs of previous MI; car diac markers not elevated. Acute treatment as for NSTEMI (b p245); analgesia (morphine, GTN ), antiplatelet agents (aspirin, clopidogrel), limit ischaemia (B-blockade) and disrupt thr ombus (fondaparinux). Risk stratify, further management and secondary prophylaxis as for NS TEMI (b p245). Stable angina1 (OHCM9 b p110) Frequently encountered in primary care, retros ternal chest discomfort occurring predictably upon exertion and relieved by rest and nitrat es. Symptoms central, heavy chest pain (lasting <20min) radiating to left arm and jaw, prec ipitated by exertion and relieved by rest or rapidly by GTN (<5min), shortness of breath, n ausea, sweating, palpitations. Risk factors common for IHD; see ACS above; severe aortic st enosis. Signs tachycardia, cool and sweaty ( \200\230clammy \200\231), pallor. Normal after episode. Investigations ECG transient ST depression during pain; fl at or inverted T waves ; signs of previous MI; cardiac markers are not elevated (if elevated this is NSTEMI). If d iagnostic uncertainty, further assessment should be guided by assessment of the likelihood of IHD based upon age, sex, presence of risk factors and nature of pain.2 Acute treatment p ain relief with rest and GTN is characteristic. If pain lasting >20min, investigate and tre at as for NSTEMI/UA. Primary prophylaxis assessment and reduction of modifi able risk facto rs (smoking, obesity, DM, BP, cholesterol), statin, anti-platelets, ACEi, symptom managemen t (nitrates, B-blockade, Ca2+ channel antagonists, nicorandil). Angina with normal coronaries? Throughout your career, you will encounter numerous patients with atypical chest pain who require basic investigations to exclude serious pathology and subsequent reassurance. However, some patients experience convincing ischaemic heart pain, despite angiographically normal coronary arteries. Consider: \200 Prinzmetal \200\231s a ngina: spontaneous coronary artery vasospasm \200 Cocaine-induced vasospasm: give GTN b enzodiazepines; can lead to MI \200 \200\230Microvascular angina \200\231 eg coronary sy ndrome X in postmenopausal women with evidence of perfusion defi cits on dynamic imaging. 1 NICE guidelines available at (cid:27)guidance.nice.org.uk/CG126 2 See NICE guidelines at (cid:27)guidance.nice.org.uk/CG95 for risk stratifi cation table and a discussion of approp riate tests. In short, if the likelihood of angina is >90%, treat without further investiga tion; if likelihood 60 \200\22390%, consider coronary angiography; if likelihood 30 \200 \22360% or unsuitable for angiog- raphy, off er functional imaging (stress echo or perfusio n imaging); if likelihood 10 \200\22330%, perform CT coronary calcium scoring dynamic and p roceed to CT coronary angiography if score >0; if likelihood <10%, reconsider other causes. Exercise ECG, though widely available, is limited by lower sensitivity and specifi city th an other tests, and should not be a 1st-line test in patients without known IHD. OHFP.indb 246 OHFP.indb 246 30/05/2014 16:18 30/05/2014 16:18 247 CHEST PAIN 3Aortic dissection (OHCM9 b p656 or OHAM3 b p142) Symptoms sudden onset severe chest pain, anterior or interscapular, tearing in nature, dizziness, breathlessness, sweating, neurolog ical defi cits. Risk factors smoking, obesity, DM, iBP, icholesterol, FH, previous IHD. Sig ns unequal radial pulses, tachycardia, hypotension/hypertension, dif- ference in brachial p ressures of \211 15mmHg, aortic regurgitation, pleural eff usion (L>R), neurological defi cits from carotid artery dissection. Investigations ECG may be normal or show LV strain/isc haemia (b p572); CXR classically widened mediastinum >8cm (rarely seen), irregularity of ao rtic knuckle and small left pleural eff usion can develop from blood tracking down; echo ma y show aortic root leak, aortic valve regurgitation or pericardial eff usion. Also consider MRI/CT/conventional angiography. Acute treatment seek senior help. If hypotensive, treat a s shock (b p476). O2 (15l/min), two large-bore cannulae, X-match 6 units, analgesia (IV opi oids). If hypertensive aim to keep systolic BP <100mmHg (b p265). Further treatment surgery (for type A: involves the ascending aorta) or conservative management (for type B: involve s descending aorta only). Musculoskeletal chest pain Symptoms localized chest wall pain, wo rse on movement and/or breathing, recent trauma or exertion (eg lifting). Signs focal tende rness, erythema, absence of other signs in CVS or RS. Investigations only investigate if yo u cannot satisfy yourself of the diagnosis on clinical grounds; ECG normal (no ischaemia/MI ); CXR normal (no pneumothorax); D-dimer normal and low probability PE (b p278). Acute trea tment reassurance and simple analgesia (b p86). Chronic treatment should settle within 2wk, prevention from further injury (no more heavy lifting for a few weeks), adequate regular a nalgesia to allow activities of daily living to be carried out and to allow deep inspiratio n and coughing (to prevent chest infection), stop smoking. Pericarditis (OHAM3 b p150) Symp toms pleuritic chest pain, worse on lying fl at and deep inspiration, relieved by sitting f orwards, recent viral illnesses. Signs may be no abnormalities, pericardial rub. Investig ations ECG saddle-shaped ST segments in most leads (see Fig. 7.3); blds iWCC and infl ammat ory markers, iviral titres; echo pericardial eff usion. Acute treatment reassurance and analgesia; paracetamol, NSAIDs. Chronic treatment should settle within 2 \200\2234wk; recu rrence common. Fig. 7.3 Typical saddle-shaped ST segment seen in pericarditis. _OHFP.indb 247 _OHFP.indb 247 30/05/2014 16:18 30/05/2014 16:18 248 CHAPTER 7 Cardiovascular Tachyarrhythmia emergency Check airway is patent; consider maneuvers/adjuncts If no respiratory eff ort \200\223 CAL L ARREST TEAM Airway Breathing Circulation If no palpable pulse \200\223 CALL ARREST TEAM 22Call for senior help early if patient \200\230unstable \200\231 (Fig. 7.4): Signs of an unstable patient include: \200 Reduced conscious level \200 Systolic BP <90 mmHg Chest pain \200 Heart failure Sit patient up unless hypotensive, then lay fl at with legs elevated \200 15l/min O2 if S OB or sats <94% \200 Monitor pulse oximeter, BP, defi brillator ECG leads if unwell \200 Request full set of observations and ECG \200 Take brief history if possible/check note s/ask ward staff \200 Examine patient: condensed CVS, RS, abdo exam \200 Establish l ikely causes and rule out serious causes \200 Initiate further treatment, see (cid:9) p24 9 \200 Venous access, take bloods: FBC, U+E, D-dimer, cardiac markers, TFT Consider requesting urgent CXR, portable if too unwell \200 Call for senior help \200 R eassess, starting with A, B, C \200 Life-threatening causes Ventricular tachycardia (VT) or ventricular fi brillation (VF) \200 Torsades de pointes \200 Supraventricular tachycardia with haemodynamic compromise \200 Fast atrial fi brill ation/fl utter with haemodynamic compromise \200 Sinus tachycardia secondary to shock, including PE \200 iatrogenic (drugs) OHFP.indb 248 OHFP.indb 248 30/05/2014 16:18 30/05/2014 16:18 _ _ O O H H F F P P i i n n d d b b 2 2 4 4 9 9 Assess using the ABCDE approach \200 Give oxygen if appropriate and obtain IV access \200 Monitor ECG, BP, SpO2, record 12-lead ECG \200 Identify and treat reversible causes (eg electrolyte abnormalities) Adverse features? Yes/Unstable Synchronized DC Shock Up to 3 attempts Shock \200 Syncope \200 Myocardial ischaemia \200 Heart failure Amiodarone 300 mg IV over 10 \200\22320 min and repeat shock; followed by: \200 Amiodaron e 900 mg over 24 h No/Stable Broad Narrow Is QRS narrow (<0.12 s)? Broad QRS Is rhythm regular? Narrow QRS Is rhythm regular? Irregular Regular Regular Irregular T A C H Y A R R H Y T H M A Use vagal maneuvers \200 Adenosine 6 mg rapid IV bolus; if unsuccessful give 12 mg; if un successful give further 12 mg. Irregular Narrow Complex Tachycardia Probable atrial \201brillation Control rate with: \200 B-Blocker or diltiazem \200 Co nsider digoxin or amiodarone if evidence of heart failure Seek expert help Monitor ECG continuously Sinus rhythm restored? If ventricular tachycardia (or uncertain rhythm): \200 Amiodarone 300 mg IV over 20 \200 \22360 min; Yes No Possibilities include: \200 AF with bundle branch block treat as for narrow complex \200 Pre-excited AF \200 Polymorphic VT Seek expert help I Probable re-entry paroxysmal SVT: \200 Record 12-lead ECG in sinus \200 If recurs, give adenosine again & then 900 mg over 24 h consider amiodarone E M E R G E N C Y If previously confirmed SVT with bundle branch block: \200 Give adenosine as for regular narrow complex tachycardia rhythm (eg torsade de pointes - give magnesium 2 g over 10 min) Possible atrial \202utter \200 Control rate (eg B-Blocker) consider choice of anti-arrhythmic prophylaxis Fig. 7.4 Adult tachycardia (with a pulse) algorithm; 2010 guidelines. Reproduced with the k ind permission of the Resuscitation Council (UK). 2 4 9 3 3 0 0 / / 0 0 5 5 / / 2 2 0 0 1 1 4 4 1 1 6 6 1 1 8 8 : : 250 CHAPTER 7 Cardiovascular Tachyarrhythmias Worrying features dGCS, dBP (sys <90mmHg), chest pain, heart failure. Think about common sinus tachycardia, fast ventricular rate in AF, supraventricular tachyca rdia (SVT), atrial fl utter; uncommon ventricular tachycardia (VT), re-entrant tachycardia (eg Wolff \200\223Parkinson \200\223White); non-cardiac causes beware an appropriate tachy cardic response to eg sepsis or shock, in those with pre-existing conduction defects. Ask about onset, associated symptoms (chest pain, shortness of breath, dizziness, palpitati ons, facial fl ushing, headache), previous episodes; PMH cardiac problems (IHD, valvular le sions, hypertension), thyroid disease, DM; DH cardiac drugs, levothyroxine, salbutamol, ant icholinergics, caf- feine, nicotine, allergies; SH smoking, alcohol, recreational drug use. \200 AF risk factors iBP, coronary artery and valvular heart disease, pulmonary embolism , pneumonia, thyrotoxicosis, alcohol, sepsis. \200 Sinus tachycardia risk factors shock ( hypovolaemic, cardiogenic, septic, anaphylactic, spinal), pain/anxiety, fever, drugs (levothyroxine, salbutamol, antic holinergics, caff eine, nicotine, cocaine). Obs pulse (check apical pulse since radial can underestimate), BP, cap refi ll, RR, O2 sats , GCS, temp. Look for any \200\230worrying features \200\231 classify arrhythmia as \200 \230unstable \200\231; see Fig. 7.4 algorithm (b p249). Investigations ECG P waves before each QRS imply sinus rhythm, irregular QRS without clear P waves implies AF, saw-tooth baseline implies atrial fl utter, rate of \211 140 (narrow c omplexes) suggests SVT (including fl utter with block), broad regular complexes suggests VT (always check for a pulse) (Tables 7.4 and 7.5); blds FBC, U+E, TFT, CRP, D-dimer (if PE s uspected), cardiac markers, others as indicated by suspicion (eg X-match if hemorrhage); AB G and CXR only once treatment has been initiated or if results are likely to alter manageme nt; urgent echo only if large PE, acute valvular lesion, very poor LV or pericardial eff us ion is suspected. Treatment In all patients \200 Airway, Breathing (with O2), Circulation (HR, BP and capil lary refi ll) \200 IV access (two large-bore cannula in both antecubital fossa) \200 Ob tain ECG or view trace on defi brillator to decide on rhythm \200 If hypotensive or dizzy lay fl at with legs up \200\223 Call senior help \200 If semi-conscious lay in recovery position \200\223 Call senior/ARREST TEAM. Speci \201 c arrhythmias \200 Sinus tachyca rdia establish cause of sinus tachycardia, ?shock (b p476) \200 AF is the patient normall y in AF or is this new onset? (b p252) \200 SVT usually time to call for help and get dru gs ready (b p253) \200 VT no pulse: 3call ARREST TEAM and start BLS/ALS (b p226) \200 V T with pulse: if haemodynamically stable, attempt chemical cardioversion (eg amiodarone b p184); if fails or if unstable, will need DC cardioversion ( b p532), under anesthetic unless unconscious. OHFP.indb 250 OHFP.indb 250 30/05/2014 16:18 30/05/2014 16:18 251 TACHYARRHYTHMIAS Table 7.4 ECG features of tachyarrhythmias Rate Regular P waves Broad/narrow Narrow (unless BBB)1 Sinus tachycardia >100 (cid:57) (cid:57) Narrow (unless BBB)1 (cid:57)or (cid:56) Narrow (unless BBB)1 >100 Fast AF (cid:56) (cid:56) \211 140 SVT (cid:57) \211 150 Broad VT (with pulse) (cid:57) (cid:56) As for \200\230VT with pulse \200\231; always perform a pulse-check (carotid) Chaotic irre gular electrical activity; never has a pulse VT (pulseless) VF ECG, lead II view (rhythm strip) Sinus tachycardia Fast AF SVT VT with or without a pulse VF Torsades de pointes Fig. 7.5 Typical appearance of various tachyarrhythmias. 1 An electrical impulse arising above the atrioventricular node, but then conducted into th e ventricles through a diseased conduction pathway (as in BBB) will result in a broad compl ex tachycardia which can be hard to diff erentiate from VT. Concordance , in which the QRS direction in all precordial leads is consistent, and occasional narrow complex capture beats suggest VT, but the diagnosis is often not straightforward. If in doubt, treat as VT . _OHFP.indb 251 _OHFP.indb 251 30/05/2014 16:18 30/05/2014 16:18 252 CHAPTER 7 Cardiovascular Atrial \201 brillation (AF)1 (OHAM3 b p72) Worrying signs heart failure, hypotension, dGC S or chest pain. Symptoms palpitations, shortness of breath, dizziness chest pains. Risk factors previous AF, iBP, IHD, valvular heart disease, PE, pneumonia, thyrotoxicosis, alcoh ol (acute excess, chronic use or withdrawal), dilated cardiomyopathy, iage, acute illness. Signs irregularly irregular pulse, hypotension if cardiovascular compromise, signs of concu rrent/precipitant disease (pneumonia, thyrotoxicosis). Investigations ECG absent P waves, i rregularly irregular QRS complexes; blds FBC (iWCC), U+E, TFT, alcohol, D-dimer (PE), tro ponin (if concern that ischaemic episode responsible); CXR heart size, pulmonary oedema, pn eumonia; echo LV dilatation/impairment, valvular lesion. Treatment \200 Haemodynamic comp romise seek immediate senior help. Treat shock (b p476); O2, IV access, DC cardioversion; if unsuccessful, amiodarone IV further cardiov ersion. Chronic AF very unlikely to cause compromise: do not shock, but consider other caus es of compromise, eg sepsis Haemodynamically stable treatment options include: Conservative: if AF is likely new in onset and patient has obvious underlying precipitant (eg electrolyte disturbance, sepsis) then appropriate treatment of p recipitant may be all that is required to resolve AF so long as patient remains monitored a nd stable Rate control: control of tachycardia reduces myocardial metabolic demands. Eff ective means include B-blockade (b p188) or a rate- limiting calcium-channel blocker (diltiazem is bett er tolerated than verapamil). Digoxin can be added in where these are insuffi cient, but sh ould not be used as a fi rst-line therapy except in the sedentary elderly (b p196); this ap proach is especially useful in those who are unlikely to revert to sinus rhythm (older pati ents, established AF, dilated left atrium, mitral valve disease) Rhythm control: younger patients and those with new presentations of AF, may be suitable for attempted cardioversion. If the patient is not kno wn to have IHD, use PO/IV fl ecainide, otherwise use IV amiodarone (given via a central lin e). DC cardioversion under sedation may also be used. Maintenance of sinus rhythm after suc cessful cardioversion, or less rapid cardioversion, may be achieved using B-blockade, escal ated to sotalol, fl ecainide or amiodarone if this is not tolerated or fails (do not use so talol or fl ecainide in those with structural heart disease). These agents also help mainta in sinus rhythm in paroxysmal AF Anticoagulation In all patients in whom a rate control strategy is adopted, consider oral anticoagulation therapy (b p406) versus use of aspirin 75mg/24h PO, based upon a stroke risk assessment.2 Full anticoagulation should be achieved for 4wk befor e and after any form of planned cardioversion, unless onset of AF is defi nitely within pre vious 48h, or trans-oesophageal echo demonstrates no thrombus in left atrium. Complications thromboembolic disease (eg ischaemic stroke). Drug side- eff ects (amiodarone, warfarin, B -blockers, digoxin etc). 1 NICE guidelines available at (cid:27)guidance.nice.org.uk/CG36 2 eg CHADS2 risk score \200\2241 point each for presence of CHF, HTN, Age>75, DM; 2 points i f prior TIA or stroke. A cumulative score of 2 predicts a 4% annual stroke risk, and is gen er- ally taken as a cut off for starting oral anticoagulation therapy. Gage, B.F. et al. JA MA 2001 285:2864 available free at (cid:27)jama.ama-assn.org/cgi/content/full/285/22/2864 OHFP.indb 252 OHFP.indb 252 30/05/2014 16:18 30/05/2014 16:18 253 TACHYARRHYTHMIAS Atrial \202 utter (OHAM3 b p78) \200\230Saw tooth \200\231 fl utter waves refl ecting at rial activity with ventricular response rate characteristically around 150bpm. Management i s similar to AF, but cardioversion rates much lower. May require ablation. Supraventricular tachycardia (SVT) (OHAM3 b p68) Worrying signs heart failure, hypotension, dGCS or chest p ain. Symptoms palpitations, shortness of breath, dizziness chest pains. Risk factors prev ious SVT, structural cardiac anomaly, alcohol, iT4. Signs tachycardia, anxiety, hypotension if haemodynamic compromise. Investigations ECG narrow complex tachycardia (unless concurre nt BBB) with P waves (which may merge into QRS and so be diffi cult to see), regular QRS co mplexes, rate usually \211 140; further investigations only required if diagnosis in quest ion, otherwise initiate treatment as below. Acute treatment O2, large-bore IV access (antec ubital fossa). Monitor rhythm on defi brillator: \200 Vagal maneuvers (b p531) \200 Che mical (b p531) Chronic treatment if recurrent, seek cardiology advice as may require electr ophysiological testing of cardiac conduction pathways. Complications hypotension, ischaemia , heart failure in individuals with existing cardiac disease, deterioration into more sinis ter arrhythmia. Wolff \200\223Parkinson \200\223White syndrome (WPW) (OHAM3 b p80) Etiolog y This is a re-entrant tachy- cardia which results from an accessory conduction pathway bet ween the atria and the ventricles (bundle of Kent). It classically appears as a short PR in terval and a D/delta wave (shown by arrow in Fig. 7.6). Treatment Avoid digoxin and verapam il. Refer to a cardiologist for consideration of electrophysiology studies and abla- tion o f accessory pathway. Fig. 7.6 D wave in WPW. Table 7.5 Anti-dysrhythmics commonly used in tachyarrhythmias 3These drugs should only be used after discussion with a senior Amiodarone (should be given via a central vein, but can be given peripherally in an emergen cy) Loading dose 300mg/over 60min IVI via central line followed by 900mg/over 24h IVI via centr al line OR 200mg/8h PO for 1wk then 200mg/12h PO for 1wk then Maintenance dose 200mg/24h PO 5mg/over 2min IV; further 0.5 \200\2231mg doses every 5min until target rate achieved (tot al maximum 20mg) OR 40 \200\223120mg/8h PO 2mg/kg/over 10min IV (maximum 150mg) OR 100 \200 \223200mg/12h PO Verapamil (avoid if pt on B-blockers) Flecainide (avoid if pt has IHD) Patient must be in a monitored bed during administration of these agents. _OHFP.indb 253 _OHFP.indb 253 30/05/2014 16:18 30/05/2014 16:18 254 CHAPTER 7 Cardiovascular Ventricular tachycardia (VT) (OHAM3 b p62) Worrying signs heart failure, hypotension, dGCS, chest pain or absent pulse (pulseless VT). Symptoms palpitations, dizziness, shortness of breath chest pain, arrest. Risk factors IHD, trauma, hypoxia, acidosis, long QT. Signs tachycardia, anxiety, pallor, h ypotension, dGCS, shock. Investigations ECG broad complex tachycardia, absence of P waves, rate usually >150; blds check urgent U+E (especially K+) and Mg2+; other investigations sho uld be directed by clinical situation though cardioversion is main priority at this stage. Acute treatment \200\223 call senior help \200 3Pulseless VT: Call ARREST TEAM, commence BLS/ALS (b p228) after pre-cordial thump (if witnessed and monitored arrest) \200 VT with a pulse: O2, lar ge-bore IV cannula in antecubital fossa; restoration of sinus rhythm with either drugs (eg sotalol, amiodarone) or DC cardioversion (under sedation unless unconscious) Possible SVT with bundle branch block or VT: treat as VT. Chronic treatment may need drug t herapy to maintain sinus rhythm, elec- trophysiological studies/ablation or implantable car dioverter/defi brillator (OHAM3 b p62). Complications may deteriorate into VF or other dysrhythmia. Torsades de pointes (OHAM3 b p6 4) Looks like VF but has a rotating axis (b p251). Develops on background of iQT interval. Give Mg2+ sulfate 2g/IV (8mmol) over 15min (dilute in small volume eg 50ml of 0.9% saline) overdrive pacing. Table 7.6 Causes of prolonged QT interval QTc = QT/ (RR interval) \200\223 this allows correction of the QT interval for heart rate and is usually calculated automatically on an ECG trace. Normal QTc values are gender-spec ifi c; values <430ms (4) and <450ms (5) are considered normal; values >450ms (4) and >470ms (5) are abnormal; values in between these are borderline. There is a dose-response relatio nship between risk of cardiac death and prolongation of QTc.1 Congenital Romano \200\223Ward syndrome (AD), Jervell, Lange \200\223 Nielsen syndrome (AR, associated with deafness) Anti-dysrhythmics (amiodarone, sotalol, quinidine), Psychoactives (thiorida zine, haloperidol, fl uoxetine), Antihistamines (terfenadine, loratadine), Antimicrobials ( erythromycin, clarithromycin, fl uconazole) i/dK+, dMg2+, dCa2+ Complete heart block, sinus bradycardia Ischaemia, myocarditis Subarachnoid hemorrhage Drugs Electrolyte disturbance Severe bradycardia IHD Intracranial bleed 1 Straus, M. et al. J Am Coll Cardiol. 2006 47:362 available free online. OHFP.indb 254 OHFP.indb 254 30/05/2014 16:18 30/05/2014 16:18 255 TACHYARRHYTHMIAS _OHFP.indb 255 _OHFP.indb 255 30/05/2014 16:18 30/05/2014 16:18 256 CHAPTER 7 Cardiovascular Bradyarrhythmia emergency Check airway is patent; consider maneuvers/adjuncts If no respiratory eff ort \200\223 CAL L ARREST TEAM If no palpable pulse \200\223 CALL ARREST TEAM Airway Breathing Circulation 3Call for senior help early if patient has \200\230adverse features \200\231 (Fig. 7.7): Adverse features include: \200 Systolic BP <90mmHg \200 Syncope Ischaemic chest pain \200 Heart failure Sit patient up unless hypotensive/dizzy, then lay fl at with legs elevated \200 15l/min O 2 if SOB or sats <94% \200 Monitor pulse oximeter, BP, defi brillator \200\231s ECG leads if very unwell \200 Request full set of observations and ECG with long rhythm strip \200 Take brief history if possible/check notes/ask ward staff \200 Examine patient: con densed CVS, RS, abdo exam \200 Establish likely causes and rule out serious causes \200 Consider IV atropine, 500micrograms, repeat at 2 \200\2233min intervals (max 3mg) Initiate further treatment, including transcutaneous pacing, see following pages Venous access, take bloods: FBC, U+E, LFT, cardiac markers, TFT Consider requesting urgent CXR, portable if too unwell \200 Call for senior help. \200 Reassess, starting with A, B, C \200 Life-threatening causes Complete (3rd degree) heart block ( following MI) \200 M bitz type II \200 Pauses >3s on ECG \200 Hypoxia in children OHFP.indb 256 OHFP.indb 256 30/05/2014 16:18 30/05/2014 16:18 257 BRADYARRHYTHMIA EMERGENCY Assess using the ABCDE approach \200 Give oxygen if appropriate and obtain IV access \200 Monitor ECG, BP, SpO2, record 12-lead ECG \200 Identify and treat reversible causes (eg electrolyte abnormalities) Adverse features? Shock \200 Syncope \200 Myocardial ischaemia \200 Heart failure YES NO Atropine 500 mcg IV YES Satisfactory response? NO Interim measures: \200 Atropine 500 mcg IV repeat to maximum of 3 mg \200 Isoprenaline 5 mcg min \210\2221 IV \200 Adrenaline 2 \200\22310 mcg min \210\2221 IV \200 Alternati ve drugs* OR \200 Transcutaneous pacing Risk of asystole? Recent asystole \200 M bitz II AV block \200 Complete heart block with broad QRS \200 Ventricular pause >3s YES NO Seek expert help Arrange transvenous pacing Observe Alternatives include: \200 Aminophylline \200 Dopamine \200 Glucagon (if beta-blocker or calcium-channel blocker overdose) \200 Glycopyrrolate can be used instead of atropine Fig. 7.7 Adult bradycardia algorithm; 2010 guidelines. Reproduced with the kind permission of the Resuscitation Council (UK). _OHFP.indb 257 _OHFP.indb 257 30/05/2014 16:18 30/05/2014 16:18 258 CHAPTER 7 Cardiovascular Bradyarrhythmias Worrying features systolic BP <90mmHg, HR <40bpm, heart failure, ventricular arrhythmia. Think about sinus bradycardia MI (typically inferior MI) drugs (including digoxin toxicity) , vasovagal, dT4, hypothermia, Cushing \200\231s refl ex (bradycardia and hypertension 2 to iICP), sleep, anorexia nervosa, physical fi tness; complete or 3rd-degree atrioventricul ar (AV) heart block. Ask about dizziness, postural dizziness, fi ts/faints, weight change, visual disturbance, n ausea, vomiting; PMH cardiac disease (IHD/AF), thyroid disease/surgery, DM, head injury or intracranial pathology, glaucoma, eating disorder; DH cardiac medications (B-blockers, Ca2+ antagonists, amiodarone, digoxin), eye drops (B-blockers); SH exercise tolerance. \200 I HD risk factors iBP, icholesterol, FH, smoking, obesity, DM, previous angina/MI. Obs HR, BP, postural BP, RR, sats, temp, GCS. Look for pulse rate/rhythm/volume, pallor, shortness of breath, dGCS, drowsy, iJVP (cannon waves in 3rd-degree AV block), signs of cardiac failure (iJVP, pulmonary oedema, swollen an kles), features of iICP (papilloedema, focal neurology \200\223 b p360). Investigations ECG sinus bradycardia or complete heart block (see Table 7.7 and Fig. 7.8), evidence of ischaemia or infarction (b p572) or of digoxin toxicity (see opposite); blds FB C, U+E, glucose, Ca2+, Mg2+, TFT, cardiac markers, digoxin level, coagulation (if consideri ng pacing-wire); CXR unlikely to be helpful in the immediate setting, but may reveal heart size and evidence of pulmonary oedema; head CT useful if you suspect raised intracranial pr essure, though patient will be in extremis (about to cone, b p338) if iICP causing bradycar dia (speak to on-call neurosur- geon). Treatment \200 Airway, Breathing (with O2) and monitor Circulation \200 If either dGCS or dBP (<90mmHg systolic), 3call senior help/ ARREST TEAM IV cannula and take bloods \200 Consider giving IV atropine if systolic BP <90mmHg (500mi crograms at 2 \200\2233min intervals to a maximum of 3mg) Check ECG to exclude myocardial infarction and to identify heart block or extreme sinus bra dycardia or very slow atrial fi brillation. OHFP.indb 258 OHFP.indb 258 30/05/2014 16:18 30/05/2014 16:18 259 BRADYARRHYTHMIAS Table 7.7 ECG features of bradyarrhythmias and types of heart block Sinus bradycardia 1st-degree AV block M bitz I (Wenkebach) M bitz II P waves precede each QRS, rate <60 P \200\223R interval >5 small squares (>0.2s) P \200\223R interval lengthens from beat to beat, until failure of AV conduction, then patt ern restarts Intermittent P waves fail to conduct to ventricles, but P \200\223R interval d oes not lengthen, unlike M bitz type I; typically 2:1 (P waves:QRS complexes): Ratios of 3 :1 and above are considered high-grade AV block Complete dissociation between P waves and Q RS complexes, which will be broad as a result Down-sloping ST segment (reversed tick), inve rted T waves; often present even when drug is at non-toxic levels No P waves; irregularly i rregular rhythm 3rd-degree AV block Digoxin eff ect/ toxicity Rate controlled AF ECG, lead II (rhythm strip) view; arrows indicate P wave Sinus bradycardia 1st-degree AV block M bitz type I M bitz II with 3:1 AV block 3rd-degree (complete) AV block Digoxin effect/ toxicity Fig. 7.8 Typical appearances of various bradyarrhythmias and types of heart block. _OHFP.indb 259 _OHFP.indb 259 30/05/2014 16:18 30/05/2014 16:18 260 CHAPTER 7 Cardiovascular Sinus bradycardia (OHAM3 b p82) Worrying signs features of heart failure, hypotension, dGCS . Symptoms asymptomatic, dizziness ( on standing), recurrent falls, palpitations, shortnes s of breath, symptoms of iICP, hypothermia or dT4. Signs orthostatic dBP, hypothermia, evid ence of iICP (b p360). Investigations ECG QRS complex will be preceded by a P wave, rate <6 0, QRS will be narrow unless BBB; exclude ischaemia/infarction; blds FBC, U+E, Ca2+, Mg2+, TFT, cardiac markers, coagulation (if considering pacing- wire); CXR unlikely to be helpful in immediate resuscitation phase. Acute treatment if symptomatic (dizzy or GCS <15) or sys tolic <90mmHg, monitor heart rate on defi brillator, lay fl at with legs elevated (as long as iICP not suspected). O2, secure IV access and take bloods. If worrying signs present, 3C all senior help/ARREST TEAM. Titrate 500micro- grams atropine IV every 2 \200\2233min (to a maximum of 3mg) followed by a large fl ush, until HR improves. Identify and correct precip itant. Consider external pacing/pacing-wire via central line (b p534); a rhythmical precord ial thump (percussion pacing) can be used in extremis when an external pacing machine is no t immediately available. Chronic treatment consider 24h tape; frequent symptomatic episodes of bradycardia or pauses are sign of sick sinus syndrome (b p261) and may need a permanent pacemaker (OHCM9 b p126). Complications severe bradycardia and high vagal tone can deterio rate into asystole so prompt treatment is required. Remember to talk con- tinually to the p atient and/or check for a pulse since pulseless electrical activity (PEA) is common and the ECG trace may not change. Vasovagal attacks Sudden refl ex bradycardia from unopposed parasympathetic inhibition upon heart rate is com mon. Often brief loss of consciousness, preceded by eg light- headedness, visual disturbanc e, nausea or sweating. Recovery of consciousness is prompt \200\223 consider other diagnos es if not. Typical precipitants are listed. Fear and pain (including needles) Post-micturition (especially in older men) Nausea and vom iting Dilatation of anal sphincter and cervix (during surgery) Pulling of extra-ocular musc les/pressure on eye (during ophthalmic surgery) iIntra-abdominal pressure (during laparosco pic surgery, straining on the toilet) Drugs which can precipitate bradycardia B-blockers Digoxin Ca2+ antagonists Verapamil and diltiazem slow heart rate Amiodarone A-ag onists Reports of bradycardia even from B-blocking eye drops Rhythm likely to be AF, but may be si nus if reverted