P wave Normally <0.12sec wide and <2.5mm tall. They are best seen in leads II and V 1 which are chosen for rhythm strips or monitoring. A tall peaked P wave in II may re \202 ect ri ght atrial hypertrophy; a widened bi \201 d P wave left atrial hypertrophy. P waves are ab sent in atrial \201 brillation (AF). PR interval Normally 0.12 \200\2230.2sec (<5 small squares). A short PR interval (abnormall y fast conduction between atria and ventricles) implies an accessory pathway (eg Wolf Parki nson White syndrome). A prolonged PR interval occurs in heart block ( \201 rst, second or third degree, see b Br adyarrhythmias, p.80). QRS width Normally 0.05 \200\2230.11sec (<3 small squares). Prolonge d QRS complexes may be due to: right bundle branch block (RBBB) (RsR or M shape in V 1 ), left bundle branch block (LBBB) (QS or W shape in V 1 with RsR or M shape in V 6 ), tricyc lic antidepressant poisoning ( b p.194), hypothermia, ventricular rhythms, and ectopics. Head \200\22390 aVR \200\223150 aVL \200\22330 Right Left 180 I 0 II +60 +120 III aVF +90 Feet Fig. 3.1 Diagram of the ECG frontal axis. 65 ELECTROCARDIOGRAM INTERPRETATION QRS amplitude The QRS amplitude can indicate left ventricular hypertrophy (LVH). Signs of L VH are: (S in V 2 + R in V 5 ) > 35mm; R in I > 15mm; R in aV L > 11mm. Q waves May be norm al in III, aV R , and V 1 , but are abnormal in other leads if > 0.04sec or > of the hei ght of the subsequent R wave. ST segment elevation is caused by: acute MI, pericarditis (concave up), ventricular aneurys m, Prinzmetal \200\231s angina, LVH, Brugada syndrome, hypertrophic cardiomyopathy, benign early repolarization. ST segment depression is caused by: ischaemia, digoxin, LVH with strain. QT interval = start of Q wave to end of T wave. QT c = QT \201\204 \210\232R \200\223R (Baz ett \200\231s formula). Normal QT c is <440msec. At rates of 60 \200\223100/min, QT should be <1/2 R \200\223R interval. A prolonged QT c predisposes to \200\230torsades de pointes \200\231 ( b Broad complex tachyarrhythmias, p.87) and is caused by acute MI, hypothermia, hypocalcaemia, drugs (quinidine, tricyclic antidepressants), certain congenital diseases (e g Romano \200\223Ward syndrome). T waves Abnormal if inverted in V 4 \200\2236 . Peaked T w aves are seen in early acute MI and hyperkalaemia ( b p.162). Flattened T waves (sometimes with prominent U waves) occur in hypokalaemia. R 1.0 PR segment ST segment m m 0 1 T 0.5 P P U 0 m m 1 P \200\223R interval Isoelectric line Q S QRS interval e g a t l o V ) V m Q \200\223T interval ( 0.0 0.2 0.4 Seconds 0.6 0.8 0.04 Fig. 3.2 66 CHAPTER 3 Medicine Chest pain Always take chest pain seriously. It may re \202 ect life-threatening illness. Triage patients with chest pain as \200\230urgent \200\231 and ensure that they are seen w ithin a few minutes. Ischaemic heart disease is understandably the \201 rst diagnosis to spring to mind in the middle-aged or elderly, but chest pain may have a variety of other di sease processes, many of which are also potentially life-threatening (Table 3.1 ). Table 3.1 The differential diagnosis of chest pain Common causes Less common causes Aortic dissection * Musculoskeletal (eg costochondritis) Acute coronary syndrome * Pneumothorax * Cholecystitis Herpes zoster Oesophageal rupture * Pancreatitis * Oesophagitis Pneumonia Pulmonary embolism * Vertebral collapse Obscure origin (eg precordial catch) Tabes dorsalis (very rare) Potentially rapidly fatal. Reaching the correct conclusion requires accurate interpretation of the history, examinatio n and investigations, bearing in mind recognized patterns of disease presentations. History Characterize the pain \200 Site (eg central, bilateral or unilateral). \200 Severity. \200 Time of onset and duration. \200 Character (eg \200\230stabbing \200\231, \200 \230tight/gripping \200\231, or \200\230dull/aching \200\231). \200 Radiation (eg to arm s and neck in myocardial ischaemia). \200 Precipitating and relieving factors (eg exercis e/rest/GTN spray). \200 Previous similar pains. Enquire about associated symptoms Breathl essness, nausea, and vomiting, sweating, cough, haemoptysis, palpitations, dizziness, loss of consciousness. Document past history, drug history, and allergies. Old notes and old ECG s are invaluable \200\224 request them at an early stage. Quickly consider contacting card iologists if acute coronary syndrome (ACS) is likely ( b ST segment elevation MI: treatment , p.76). Examination and resuscitation Evaluate Airway, Breathing, Circulation (ABC) and re suscitate (O 2 , venous access, IV analgesia) as appropriate. Listen to both lung \201 el ds and check for tension pneu- mothorax and severe left ventricular failure (LVF). Complete full examination. Investigations These depend upon the presentation and likely diagnosis, but an ECG and CXR are usually required. Remember that these may initially be normal in MI, PE and aortic dissection. Ensure that all patients receive ECG moni- toring in an area whe re a de \201 brillator is readily available. 67 ANGINA Angina Angina is de \201 ned as discomfort in the chest, arm, neck, or adjacent areas due to myocardial ischaemia. It can be brought on by exertion, cold weather and emotion. It occ urs when coronary artery blood \202 ow fails to meet the O 2 demand of the myocardium (eg during exercise, coronary artery spasm or anemia). Ischaemia may produce ST depression or inversion, which resolves on recovery. First presentation of angina Patients may come to the ED with angina as a \201 rst presen tation of ischaemic heart disease (IHD). Always consider the possibility of MI. In particul ar, suspect myocardial cell death with any pain lasting > 10min (even if relieved by glycer yl trinitrate (GTN)). A normal examination, normal ECG and normal baseline cardiac markers do not exclude MI. If in any doubt, admit the patient . If considering discharge, discuss w ith senior ED/medical staff. Atypical cardiac chest pain Patients with acute MI are occasionally sent home from the ED i nadvertently. Cardiac chest pain may be poorly localized, and may present with musculoskele tal features or gastrointestinal (GI) upset. In particular, patients with acute coronary sy ndromes commonly have chest wall tenderness. Some patients understandably play down symptom s in order to avoid admission to hospital. If the clinical history is suspicious of cardiac pain (especially in a patient with risk factors, such as family history of IHD, hypertensi on, smoking), then refer for admission. Do not be fooled by a normal ECG, normal examinatio n, or the fact that the patient is <30 years old. Remember that oesophageal pain may improv e with GTN and true cardiac pain may appear to improve with antacids. The decision whether or not to refer the patient for admission and investigation depends upon an assessment of t he risk of MI. In general, exclude an MI where chest pain lasting > 15min has some features of IHD. Also refer patients who look unwell, even if the chest pain lasts <15min. 68 CHAPTER 3 Medicine Acute coronary syndromes Coronary artery plaque rupture can result in a variety of ischaemi c conditions which fall under the overall term of \200\230acute coronary syndrome \200\231 and include unstable angina, non-ST segment elevation MI (NSTEMI) and ST segment elevation MI (STEMI). Patients labeled as having acute coronary syndrome, but without initial ST ele vation, comprise a relatively heterogenous group \200\224 some later proving (on the basis of elevated blood troponin levels) to have suffered an NSTEMI. The patient presenting with unstable angina or NSTEMI Unstable angina can occur as worsenin g angina or a single episode of \200\230crescendo \200\231 angina, with a high risk of inf arction. Features include angina at rest, i frequency, i duration, and severity of pain (in cluding response to GTN). It may be dif \201 cult to distinguish between unstable angina a nd NSTEMI in the ED. \200 Provide O 2 to maintain SpO 2 94 \200\22398 % and attach cardia c monitor. \200 Administer IV opioid analgesia ( antiemetic) as required. \200 Give aspirin 300mg PO and clopidogrel 300mg PO. \200 Start low molecular weight heparin (LMWH) , eg dalteparin 120units/ kg SC every 12hr (max 10,000U) or enoxaparin 1mg/kg SC every 12hr . Synthetic pentasaccharide fondaparinux 2.5mg SC may be used instead. Follow local guideli nes. If pain is unrelieved, commence GTN intravenous infusion (IVI; start at 0.6mg/hr and i as necessary), provided systolic BP is > 90mmHg. Glycoprotein IIb/IIIa inhibitors (eg epti \201 batide and tiro \201 ban) are going out of favor for patients at risk of NSTEMI or high TIMI risk score (see Table 3.2 ). If high risk of NSTEMI, haemodynamically stable and no contraindications, consider atenolol (5mg IV slowly over 5mins repeated once after 15mins), according to local policy. Contrain dications include: hypotension, bradycardia, second or third degree heart block, heart fail ure and severe reactive airways disease. Refer for admission, repeat ECGs and blood troponin testing 12hr after pain onset. Discuss with cardiology all patients at high risk of NSTEMI or with TIMI score > 3. They ma y bene \201 t from early revascularization procedures. 69 ACUTE CORONARY SYNDROMES Table 3.2 TIMI risk score: increasing score predicts mortality or adverse event Risk factor Points Age > 65 1 3 + risk factors for coronary artery disease 1 Family history of IHD, hypertension, hypercholesterolemia, diabetes, or smoker Known coronary artery disease with stenosis \211 50 % 1 Aspirin use in last 7 days 1 Recent episode of angina prior to this event 1 Raised troponin levels (or other cardiac marker) 1 ST segment deviation \211 0.5mm on ECG 1 Normal lead II (Fig. 3.3 ) R T P ST S Fig. 3.3 Ischaemic changes in lead II (Fig. 3.4 ) R P T ST S Fig. 3.4 Prinzmetal \200\231s or \200\230variant \200\231 angina Angina associated with ST elevatio n may be due to coronary artery vasos- pasm. This may occur with or without a \201 xed co ronary abnormality and may be indistinguishable from an acute MI until changes resolve rapi dly with GTN as pain is relieved. 70 CHAPTER 3 Medicine ST segment elevation MI IHD is the leading cause of death in the Western world. Mortality f rom acute MI is believed to be 45 % , with 70 % of these deaths occurring before reaching m edical care. Contributory risk factors for MI include smoking, hypertension, age, male sex, diabetes, hyperlipidaemia, and family history. MI pathology MI mostly affects the left ventricle. It usually results from sudden occlusion of a coronary artery or one of its branches by thrombosis over a pre- existing atheromatou s plaque. Patients with IHD are at risk of sustaining an MI if additional stresses are plac ed upon their already critically impaired myocardial circulation (eg a high level of carbox yhaemoglobin (COHb) following smoke inhalation). MI may also occur in vasculitic processes, eg cranial arteritis ( b p.132) and Kawasaki disease. MI diagnosis The diagnosis of acute MI requires 2 out of the following 3 features: \200 A history of cardiac-type ischaemic chest pain. \200 Evolutionary changes on serial ECGs. \200 A rise in serum cardiac markers. Note that 50 \200\22360 % of patients will not have a diagnostic ECG on arrival and up to 17 % will have an entirely normal initial ECG. Late presentation does not improve diagnostic accuracy of the ECG. History The classic presentation is of sudden onset, severe, constant central chest pain, w hich radiates to the arms, neck, or jaw. This may be similar to previous angina pectoris, b ut is much more severe and unrelieved by GTN. The pain is usually accompanied by one or mor e associated symptoms: sweating, nausea, vomiting, breathlessness. Atypical presentation is common. Have a high level of suspicion. Many patients describe aty pical pain, some attributing it to indigestion (be wary of new onset \200\230dyspeptic \200\231 pain). Up to a third of patients with acute MI do not report any chest pain. These patients tend to be older, are more likely to be female, have a history of diabetes or hea rt failure, and have a higher mortality. These patients may present with: \200 LVF. \200 Collapse or syncope (often with associa ted injuries eg head injury). \200 Confusion. \200 Stroke. \200 An incidental ECG \201 nding at a later date. In a patient who presents with possible MI, enquire about past medical history (IHD, hypertension, diabetes, hyperlipidaemia) and contraindications to thr ombolysis. Ask about drug history, including drugs of abuse (particularly cocaine b p.215). 71 ST SEGMENT ELEVATION MI Examination Examination and initial resuscitation (maintain SpO 2 in normal range, IV cannu la, analgesia) go hand in hand. The patient may be pale, sweaty, and distressed. Examinatio n is usually normal unless complications have super- vened (eg arrhythmias, LVF). Direct in itial examination towards searching for these complications and excluding alternative diagn oses: \200 Check pulse, BP and monitor trace (?arrhythmia or cardiogenic shock). \200 L isten to the heart (?murmurs or 3rd heart sound). \200 Listen to the lung \201 elds (?L VF, pneumonia, pneumothorax). \200 Check peripheral pulses (?aortic dissection). \200 C heck legs for evidence of deep vein thrombosis (?PE). \200 Palpate for abdominal tenderne ss or masses (?cholecystitis, pancreatitis, perforated peptic ulcer, ruptured aortic aneurysm). Investigations The diagnosis of ST segment elevation myocardial infarction within the \201 rst few hours is based upon history and ECG changes (serum cardiac markers may take se veral hours to rise \200\224 see below). \200 Record an ECG as soon as possible, ideally within a few minutes of arrival at hospital. Sometimes patients arrive at hospital with EC Gs of diagnostic quality already recorded by paramedics. If the initial ECG is normal, but symptoms are suspicious, repeat the ECG every 15min and re-evaluate. Request old notes (these may contain previous ECGs for comparison). \200 Ensure continuou s cardiac monitoring and pulse oximetry. \200 Monitor BP and respiratory rate. \200 Obt ain venous access and send blood for cardiac markers, U&E, glucose, FBC, lipids. Obtain a CXR if there is suspicion of LVF or aortic dissection. Cardiac markers Troponins are now universally used. Troponin T (cTnT) and Troponin I (cTnI) are proteins virtually exclusive to cardiac myocytes. They are highly speci \201 c and se nsitive, but are only maximally accurate after 12hr. Troponin T and I cannot be used to rul e out MI in the \201 rst few hours. In addition, cardiac cells may release troponin into the blood when cardiac muscle is damaged by pericarditis, pulmonary embolism with a large c lot burden, or sepsis. Renal failure reduces excretion of troponin. Chest pain assessment units These units are becoming established in some EDs. A combination of ECGs, ST segment monitoring, cardiac markers, and exercise testing is used to allow dis charge of low to moderate risk patients within 6 \200\22312hr. However, simply excluding an acute coronary syndrome is only part of the assessment of chest pain. 72 CHAPTER 3 Medicine Myocardial infarction: ECG changes 1 Infarction of cardiac muscle results in ECG changes th at evolve over hours, days, and weeks in a relatively predictable fashion. Hyperacute changes Frequently ignored, although often subtle, some or all of the following may be observed within minutes of infarction: \200 i Ventricular activation time , since the infarcting myocardium is slower to conduct electrical impulses. The interval between th e start of the QRS and apex of the R wave may be prolonged > 0.045sec. i Height of R wave may be seen initially in inferior leads in inferior MI. \200 Upward-sl oping ST segment \200\224 having lost normal upward concavity, the ST segment straightens, then slopes upwards, before becoming ele- vated. Tall, widened T waves. Evolving acute changes In isolation, none of these changes are speci \201 c to MI. In comb ination, and with an appropriate history, they can diagnose MI: \200 ST elevation : the m ost important ECG change. ST segments become concave down and are signi \201 cant if eleva ted > 1mm in 2 limb leads, or > 2mm in 2 adjacent chest leads. Reciprocal ST depression may occur on the \200\230opposite side \200\231 of the heart. \200 Pathological Q waves (de \201 ned on b p.65) re \202 ect electrically inert necroti c myocardium. ECG leads over a large transmural infarct show deep QS waves. Leads directed towards the periphery of a large infarct or over a smaller infarct may show a QR complex or a loss of R wave amplitude . T wave inversion : typically deeply inverted, symmetrical and pointed. \200 Conduction pr oblems may develop. LBBB in a patient with acute cardiac chest pain makes interpretation of the ECG very dif \201 cult. LBBB does not have to be new to be signi \201 cant. Do not d elay intervention in patients with a good clinical history of MI in order to obtain old ECG s. Sgarbossa criteria for diagnosing ACS in the presence of LBBB \200 ST segment elevation > 1mm in leads with positive QRS complexes. \200 ST segment depression in leads V1, V2, or V3. \200 ST segment elevation > 5mm in lead with negative QRS complexes. If all 3 are pr esent, MI is likely. Chronic changes In the months following an MI, ECG changes resolve to a variable extent. ST segments become isoelectric, unless a ventricular aneurysm develops. T waves gradually bec ome + ve again. Q waves usually remain, indicating MI at some time in the past. 73 MYOCARDIAL INFARCTION: ECG CHANGES 1 Electrocardiogram changes following myocardial infarction (Fig. 3.5 ) Normal Hours Days Weeks Months Fig. 3.5 Electrocardiograms after myocardial infarction (Figs 3.6 and 3.7 ) I aVR V4 V1 II V2 V5 aVL V6 V3 aVF III Fig. 3.6 Acute inferolateral infarction with \200\230reciprocal \200\231 ST changes in I, aVL, and V 2 \200\223V 3 . V1 I aVR V4 V2 V5 II aVL III aVF V6 V3 Fig. 3.7 Acute anteroseptal infarction with minimal \200\230reciprocal \200\231 STchanges in III and aVF. 74 CHAPTER 3 Medicine Myocardial infarction: ECG changes 2 Localization of myocardial infarction MI usually affec ts the left ventricle (LV), occasionally the right ventricle (RV), but virtually never the atria. The part of myocardium affected is implied by which leads show changes (Table 3.3 ). Table 3.3 ECG leads Location of MI V 1 \200\2233 Anteroseptal V 5 \200\2236 , aV L Anterolateral V 2 \200\2234 Anterior V 1 \200\2236 Extensive anterior I, II, aV L , V 6 Lateral II, III, aV F Inferior V 1 , V 4 R Right ventricle Posterior myocardial infarction Posterior MI nearly always occurs as part of inferior (post ero-inferior) or lateral (postero-lateral) MI. No conventional electrode views the poste- r ior heart, since intervening tissues result in an attenuated signal. ECG diagnosis of true posterior MI may be made from the use of V 7 \200\2239 and from reciprocal changes seen in leads V 1 \200\2233 : tall, slightly widened R (reciprocal of Q), concave up ST depression (reciprocal of ST elevation), upright tall widened T (reciprocal of inverted T). Right ventricular infarct This occurs most often as part of an inferior MI. In the presence of changes of acute MI in the inferior leads, ST elevation in V 1 suggests right ventricul ar involvement. In this case, record an ECG trace from lead V 4 R. The diagnosis of RV infa rct helps determine treatment of ensuing cardiac failure. Treat RV failure with IV \202 u ids to maintain adequate \201 lling pressure and exercise caution if considering use of n itrates. Blood supply to the heart and coronary artery dominance The left anterior descending artery supplies the anterior and septal cardiac areas (Fig. 3.9). The circum \202 ex branch supp lies the anterolateral aspect of the heart. The right coronary artery supplies the right ve ntricle. In most people the right coronary artery also supplies the sino-atrial node, the i nferior wall of the left ventricle and the ventricular septum. In 15 % of individuals, the inferior wall is supplied by the circum \202 ex branch of the left coronary artery (left d ominance). 75 MYOCARDIAL INFARCTION: ECG CHANGES 2 I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 Fig. 3.8 ECG of subendocardial infarct. Ascending aorta Left main stem Circumflex coronary artery Right coronary artery Diagonal branches (of the LAD) Left anterior descending artery Posterior descending artery Septal branches (of the LAD) Fig. 3.9 76 CHAPTER 3 Medicine STEMI: treatment Speed is crucial \200\224 time is muscle. Ambulance control may alert the ED in advance of a patient with cardiac-type chest pain. Work ef \201 ciently as a team t o ensure treatment is not delayed. \200 Give O 2 to maintain SpO 2 94 \200\22398 % and at tach cardiac monitor. \200 Obtain IV access and take samples for U&E, glucose, FBC, cardi ac markers. Provide small increments of IV opioid analgesia titrated to effect. \200 Ensure the patie nt has had 300mg aspirin and 300mg clopidogrel PO. \200 Contact cardiology for primary pe rcutaneous coronary intervention (PCI). Arrange transportation to the cath lab. For patients undergoing PCI, consider IV glycoprotein IIb/IIIa receptor antagonist as an adjuvant. Be guided by local protocol. If PCI is not available, consider thrombolysis and monitor carefully. Start LMWH, heparin, or fondaparinux, according to local protocols. If pain continues, give IVI GTN (start at 0.6mg/hr and i as necessary), provided systolic BP is > 90mmHg. Consider atenolol (5mg slowly IV over 5min, repeated once after 15min), or metoprolol, unle ss contraindicated (eg uncontrolled heart failure, hypotension, bradyarrhythmias, COPD). Indications for PCI or thrombolysis \200 ST elevation of > 1mm in 2 limb leads, or \200 ST elevation of (cid:2)2mm in 2 or more contiguous chest leads, or \200 LBBB in the pres ence of a typical history of acute MI (NB: LBBB does not have to be new). Primary angioplasty for ST segment elevation MI Primary percutaneous coronary intervention (coronary angioplasty and stenting) is the treatment of choice for STEMI. Compared with thr om- bolysis, PCI administered within 12hr of symptom onset results in lower mortality and r e-infarction rates. The sooner it is performed, the greater the bene \201 ts. Thrombolysis If PCI cannot be performed within 90min of diagnosis, thrombolytic therapy is an alternative. The bene \201 ts reduce markedly with time delay, so if PCI is not availab le, do not delay the administration of a thrombolytic agent. Rural areas with long hospital transfers may have a protocol for ambulance administered thrombolysis, aided by telemedici ne advice from the ED or cardiology. Patients presenting > 12hr after symptom onset will no t bene \201 t from thrombolysis. Strokes, intracranial hemorrhage and major bleeds are more common in patients given thrombo lysis. Intracranial bleeding is more common in older patients, those with hypertension on a dmission and those given tPA. Prior to administering thrombolysis, always explain the bene \201 ts and risks to the patient. Obtain verbal consent to give the medication and record this in the notes. 77 STEMI: TREATMENT Contraindications to thrombolysis Most are relative, but discuss any contraindications with the patient and cardiology: \200 Head injury, recent stroke, previous neurosurgery or ce rebral tumor. \200 Recent GI or GU bleeding, menstruation, or coagulopathy/warfarin. \200 Severe hypertension (eg systolic BP > 200mmHg, diastolic BP > 120mmHg), aortic dissection or pericarditis. Puncture of non-compressible vessel (eg subclavian vein), traumatic CPR, d GCS post-arrest. Major surgery within recent weeks. \200 Pregnancy. Choice of thrombolytic agents Tissue plasminogen activator (tPA), rather than streptokinase , is the agent of choice. Always use tPA if streptokinase was given > 5 days ago or in ante rior MI in a patient <75 years old and <4hr of onset of symptoms, or if hypotensive (systol ic BP <90mmHg). Alteplase (recombinant tPA (rtPA)) is most effective given by an accelerated regimen, eg 15 mg IV bolus, followed by 0.75mg/kg (max 50mg) IVI for 30min, then 0.5mg/kg (max 35mg) IVI o ver 60min. Give LMWH (eg enoxaparin 1mg/kg stat) or heparin concomitantly through a separat e IV line (5000unit IV bolus, then 1000units/hr IV), according to local protocols. Reteplase (modi \201 ed tPA) can be given as two IV boluses of 10units each exactly 30min apart. Give LMWH/heparin as for alteplase. Tenecteplase (modi \201 ed tPA) is given as a single IV bolus over 10sec. Dose according t o weight (<60kg = 30mg; 60 \200\22369kg = 35mg; 70 \200\22379kg = 40mg; 80 \200\22389kg = 4 5mg; > 90kg = 50mg). Give LMWH/heparin as for alteplase. Streptokinase Given as 1.5mega-units by continuous IVI over 1hr. Strepto- kinase is allerge nic (may require slow IV chlorphenamine 10mg and IV hydrocortisone 100mg) and frequently ca uses hypotension ( d IVI rate and tilt the bed head down \200\224 treatment rarely needs t o be discontinued). After a recent streptococcal infection, streptokinase may be ineffectiv e due to the antibodies produced. Further management Arrhythmias Occur commonly after MI. Occasional ventricular ectopics or transient AF (lasting <30sec) require no treatment. Watch for sudden VT/VF and treat as in b Cardiac arrest, p.46. Hypokalaemia Treat if K + <4mmol/L. Pulmonary oedema Treat as descr ibed on b p.101. Cardiogenic shock d cardiac output with tissue hypoxia, which does not imp rove with correction of intravascular volume. Mortality is 50 \200\22380 % . Contact ICU an d cardiologist. Echocardiography may be required to exclude conditions requiring urgent sur gical repair (mitral regurgitation from papillary muscle rupture, aortic dissection, ventri cular septum rupture, cardiac tamponade from ventricular wall rupture) or massive PE. If th ese are excluded, emergency coronary intervention may i survival. 78 CHAPTER 3 Medicine Pericarditis Acute in \202 ammation of the pericardium characteristically produces chest p ain, low grade fever, and a pericardial friction rub. Pericarditis and myocarditis commonly co-exist. Causes \200 Myocardial infarction (including Dressler \200\231s syndrome \200\224 see b p.79). \200 Viral (Coxsackie A9, B1-4, Echo 8, mumps, EBV, CMV, varicella, HIV, rubella, Parvo B19). Bacterial (pneumococcus, meningococcus, Chlamydia , gonorrhea, Haemophilus ). Tuberculosis (TB; especially in patients with HIV) \200\224 see b p.232. \200 Locally in vasive carcinoma (eg bronchus or breast). \200 Rheumatic fever \200\224 see b Acute arth ritis, p.497. \200 Uraemia. \200 Collagen vascular disease (SLE, polyarteritis nodosa, rheumatoid arthritis). After cardiac surgery or radiotherapy. \200 Drugs (hydralazine, procainamide, methyldopa, minoxidil). Diagnosis Classical features of acute pericarditis are pericardial pain, a friction rub and concordant ST elevation on ECG. The characteristic combination of clinical presentation an d ECG changes often results in a de \201 nite diagnosis. Chest pain is typically sharp, central, retrosternal, and worse on deep inspiration, change in position, exercise, and swallowing. A large pericardial effusion may cause dysphagia by compressing the esophagus. A pericardial friction rub is often intermittent, positional, and elusive. It tends to be l ouder during inspiration, and may be heard in both systole and diastole. Low grade fever is common. Appropriate investigations include: ECG, chest X-ray, FBC, erythrocyte sedimentation rate ( ESR), C-reactive protein (CRP), U&E, and troponin. Obtain blood cultures if there is eviden ce of sepsis or suspicion of a bacterial cause (eg spread of intrathoracic infection). A pe ricardial effusion is most quickly and easily demonstrated by echocardiography or FAST scan ning: clinical evidence of cardiac tamponade is rare. ECG changes In acute pericarditis ECG changes result from associated epicardial in \202 am - mation (see Fig. 3.10 ). Sinus tachycardia is usual, but AF, atrial \202 utter or atria l ectopics may occur. ST elevation is concave up (unlike MI, b p.72), and present in at lea st 2 limb leads and all chest leads (most marked in V 3 \200\2236 ). T waves are initially prominent, upright, and peaked, becoming \202 attened or inverted over several days. PR d epression (re \202 ecting atrial in \202 ammation) may occur in the same leads as ST elev ation (this PR \200\223ST discordance is characteristic). Pathological Q waves are not pres ent. Pericardial effusion causes d QRS amplitude in all leads. Electrical alternans is diag nostic, but rare. 79 PERICARDITIS Management Refer to the medical team for echocardiography and treatment. The appropriate tr eatment depends on the underlying cause. Idiopathic pericarditis or viral pericarditis in young patients is usually benign and self- limiting, responding to symptomatic treatment (high dose NSAID PPI cover). Occasionally, it follows a relapsing course before \200\230burning itself out \200\231. Dressler \200\231s syndrome (autoimmune pericarditis effusion 2 \200\22314 weeks after 3 % of MIs) requires cardiology specialist care. Pericardial effusion may occur with any type of pericarditis. It is relatively common in ac ute bacterial, tuberculous, and malignant pericarditis. Acute tamponade may occur following cardiac rupture with MI, aortic dissection, or after cardiac surgery. Summon senior help a nd arrange immediate echocardiography for patients with signs of tamponade, with pericardio centesis under ultrasound guidance, and then a de \201 nitive drainage procedure. Emergenc y \200\230blind \200\231 pericardiocentesis is described on b p.343. aVR aVL aVF I II III V2 V3 V4 V5 V6 V1 Fig. 3.10 ECG of pericarditis. 80 CHAPTER 3 Medicine Bradyarrhythmias Bradycardia is a ventricular rate of <60/min in the adult. It usually re \202 ects in \202 uences on or disease of the sino-atrial (SA) node, or atrioventricular ( AV) block. Intraventricular conduction disturbances may progress to AV block. Sinus bradyca rdia may be physiological (eg athletes), due to drugs ( B -blockers), or pathological (hypo thyroidism, hypothermia, hypoxia, iICP, sick sinus syndrome, MI, myocardial ischaemia). Bra dycardia also occurs in up to 1/3 of patients with hypovolaemia (eg GI bleed, ectopic pregn ancy). Sick sinus syndrome (or \200\230sinus node disease \200\231) is usually the result of isch aemia or degeneration of SA node. It is characterized by sinus pauses ( > 2sec) or sinus ar rest. Junctional or other escape beats may occur and occasionally a tachyarrhythmia may eme rge ( \200\230tachy-brady \200\231 syndrome). Patients may present with dizziness, collapse , loss of consciousness or palpitations. A continuous 24hr ECG tape may demonstrate arrhyth mias. AV block may be caused by IHD, drugs (eg excess digoxin) or cardiac surgery. First degree A V block Conduction from atria to ventricles occurs every time, but is delayed. The PR inter val is > 0.2sec (5 small squares on standard ECG) (Fig. 3.11 ). Second degree AV block Only a proportion of P waves are conducted to the ventricles. There are two types: \200 Mobitz type I block (Wenckebach) : the PR interval becomes increasing ly lengthened until a P wave fails to conduct (Fig. 3.12 ). Mobitz type II block : failure to conduct P waves may occur regularly (eg 3:1) or irregular ly, but the PR interval remains constant (Fig. 3.13 ). Third degree (complete) heart block Atrial activity is not conducted to ventricles. With a proximal block (eg at the AV node), a proximal escape pacemaker in the AV node or bundle of His may take over, producing narrow QRS complexes at a rate of 8 50/min. With distal AV bl ock, a more distal escape pacemaker results in broad bizarre complexes at a rate of 8 30/mi n. Ventricular asystole may occur if the escape pacemaker stops discharging, unless a subsi diary pacemaker takes over (Fig. 3.14 ). Intraventricular conduction disturbances The intraventricular conducting system commences a s the bundle of His and divides into right and left bundle branches \200\224 the latter su bdivides further into antero-superior and postero-superior divisions. These two divisions a nd the right bundle branch are referred to as the \200\230fascicles \200\231. Blockage of 2 out of 3 fascicles = bifascicular block . \200 RBBB + left anterior hemiblock causes le ft axis deviation and RBBB pattern on ECG. RBBB + left posterior hemiblock causes right axis deviation and RBBB pattern on ECG. Trifascicular block is present when bifasciular block is accompanied by a prolonged PR inte rval. Note that true blockage of all 3 fascicles would cause complete heart block, so \200 \230trifascicular block \200\231 represents impending progression to complete heart block. 81 BRADYARRHYTHMIAS Fig. 3.11 ECG of \201 rst degree heart block. Fig. 3.12 ECG of Mobitz type I AV block. Fig. 3.13 ECG of Mobitz type II AV block. Fig. 3.14 ECG of complete AV block. 82 CHAPTER 3 Medicine Treatment of bradyarrhythmias The emergency treatment of bradycardia depends upon two impor tant factors: the clinical condition of the patient and the risk of asystole. Give O 2 , in sert an IV cannula and follow the 2010 European Resuscitation Council Guidelines shown oppo site ( www.resus.org.uk ). Atropine is the \201 rst-line drug. The standard dose is 500mcg IV, which may be repeated to a total of 3mg. Further doses are not effective and may result in toxic effects (eg psy chosis, urinary retention). Adrenaline (epinephrine) can be used as a temporizing measure prior to transvenous pacing i f an external pacemaker is not available. Give by controlled infusion at 2 \200\22310mcg/mi n, titrating up according to response (6mg adrenaline in 500mL 0.9 % saline infused at 10 \200\22350mL/hr). External transcutaneous pacing is available on most de \201 brillators. It allows a pacing current to be passed between 2 adhesive electrodes placed over the front of the chest and the back. Select external demand pacing mode at a rate of 70/min, then gradually i the paci ng current from zero until capture is shown on the monitor. Clinically, capture results in a palpable peripheral pulse at the paced rate and clinical improvement in the patient \200 \231s condition. Provide small doses of IV opioid sedation if the patient \201 nds ext ernal pacing very uncomfortable. Transvenous cardiac pacing is the treatment of choice for bradycardic patients who are at r isk of asystole. The technique should only be performed by an experienced doctor. The prefe rred route of access is the internal jugular or subclavian vein. However, if thrombolysis h as recently been given or is contemplated, or if the patient is taking anticoagulants, use the right femoral vein instead. Obtain a CXR to exclude complications. A correctly function ing ventricular pacemaker results in a pacing spike followed by a widened and bizarre QRS ( Fig. 3.15 ). Fig. 3.15 Paced rhythm. Permanent pacemakers and implantable de \201 brillators Increasingly sophisticated implant able devices are being used to manage arrhythmias. Occasionally, a patient will present to the ED with a malfunctioning pacemaker. Get urgent specialist advice. External trans- cutan eous pacing will provide temporary support whilst the problem is resolved. A special magnet may be needed to inactivate an implantable de \201 brillator which \201 res repeatedly. 83 TREATMENT OF BRADYARRHYTHMIAS Algorithm for the management of bradycardia (Fig. 3.16 ) See www.resus.org.uk 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 (e.g. electrolyte abnormalities) Adverse features? Shock \200 Syncope \200 Myocardial ischaemia \200 Heart failure NO YES Atropine 500 mcg IV YES Satisfactory response? NO Interim measures: Risk of asystole? Atropine 500 mcg IV repeat to maximum of 3 mg \200 Isoprenaline 5 mcg min \200\2231 IV \200 Adrenaline 2 \200\22310 mcg min \200\2231 IV \200 Alternative drugs* OR \200 Tran scutaneous pacing Recent asystole \200 Mobitz 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 Glycopyrronium bromide can be used instead of atropine Fig. 3.16 Algorithm for the management of bradycardia. 8 4 T a c h y c a r d i a C H A P T E R 3 M e d i c i n e 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 (e.g. electrolyte abnormalities) a l g o r i t h m \200\223 w i t h 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: No/Stable Amiodarone 900 mg over 24 h p u l s e Broad Narrow Is QRS narrow (< 0.12s)? Narrow QRS Is rhythm regular? Broad QRS Is rhythm regular? Regular Irregular Regular Irregular Use vagal maneuvers \200 Adenosine 6 mg rapid IV bolus; if unsuccessful give 12 mg; if un successful give further 12 mg \200 Monitor ECG continuously Irregular narrow complex tachycardia Probable atrial fibrillation Control rate with: \200 -Blocker or diltiazem \200 Consi der digoxin or amiodarone if evidence of heart failure Seek expert help ! Sinus rhythm restored? If ventricular tachycardia (or uncertain rhythm): Possibilities include: \200 AF with bundle branch block treat as for narrow complex \200 Pre-excited AF consider amiodarone \200 Polymorphic VT (e.g. torsade de pointes - give magnesium 2 g over 10 min) No Seek expert help Amiodarone 300 mg IV over 20 \200\22360 min; then 900 mg over 24 h If previously confirmed Yes ! T A C H Y C A R D A SVT with bundle branch block: \200 Give adenosine as for regular narrow complex tachycard ia Probable re-entry paroxysmal SVT: \200 Record 12-lead ECG in sinus rhythm \200 If recur s, give adenosine again and consider choice of anti-arrhythmic prophylaxis Possible atrial flutter \200 Control rate (e.g. -Blocker) I A L G O R Fig. 3.17 Tachycardia algorithm with pulse (www.resus.org.uk). I T H M 8 5 86 CHAPTER 3 Medicine Tachyarrhythmias The single Resuscitation Council 2010 tachycardia algorithm (Fig. 3.17 ) ( see www.resus.org.uk ) is based on the fact that, irrespective of the exact underlying card iac rhythm, many of the initial management principles in the peri-arrest setting are the sa me: \200 Rapidly assess ABC. \200 Monitor cardiac rhythm and record a 12-lead ECG. \200 Provide O 2 . \200 Identify and treat reversible causes. \200 Assess for evidence of instability (signs of shock, syncope, signs of heart failure, or myocardial ischaemia) \200\224 these indicate the need for urgent intervention, initially in the form of synchro nized cardioversion.