Pain on defecation? Is blood mixed with stool, or just on surface? Is blood just on toilet paper, or also in the toilet bowl? 82 Tenesmus \200\223Visual loss Tenesmus is a sensation felt in the rectum of incomplete empty ing fol- lowing defecation, as if there was something else left behind that cannot be passe d. It is very common in irritable bowel syndrome but can be caused by a tumor. Terminal dri bbling Dribbling at the end of urination, often seen in con- junction with incontinence fol lowing incomplete urination; it is commonly associated with outlet obstruction. See prostat ism (p. 79). Tinnitus (p. 357) Tiredness See Fatigue (p. 75) Tremor is rhythmic oscillation of limbs, trunk, head, or tongue. Three types: 1 Resting tremor : Worst at rest; feature o f parkinsonism, but the tremor is more resistant to treatment than bradykinesia or rigidity . This is usually a slow tremor (frequency: 3 \200\2235 Hz) s n g i s d n a s m o t p m y S 2 Postural tremor : Made worse with certain positions (e.g., arms out- stretched). Typicall y, a rapid tremor (frequency: 8 \200\22312 Hz). May be exag- gerated physiological tremor ( e.g., anxiety, thyrotoxicosis, alcohol, drugs), metabolic (e.g., hepatic encephalopathy, CO 2 retention), due to brain damage (e.g., Wilson \200\231s disease, syphilis), or benign ess ential tremor (BET). This last is usually a familial (autosomal dominant) tremor of arms an d head presenting at any age. It is suppressed by alcohol and is rarely pro- gressive. Prop ranolol (40 \200\22380 mg/8 \200\22312 h PO) helps 30%. 3 Intention tremor: Made worse with movement; occurs in cerebellar disease (e.g., in MS). No effective drug has been found. 83 Trousseau \200\231s sign is elicited by inflating a BP cuff on an arm/leg to above systolic pressure. The hands and feet go into spasm (carpopedal spasm) in hypocalcemia. The metacar pophalangeal joints become flexed and the interphalangeal joints are extended. See Chvostek \200\231s sign (p. 72). Urinary changes Cloudy urine suggests pus (infection, UTI) but is often normal phosphate precipitation in an alkaline urine. Pneumaturia (bubbles in urine as it is passed) occurs with UTI due to gas-forming organisms or may signal an enterovesical (bowel-bladder) fistula from diverticulitis or neo- plastic diseases of the gut. Nocturia i s caused by bladder outlet obstruction (prostate enlargement), uncontrolled diabetes mellit us, UTI, and absorption of peripheral edema. Hematuria (red blood cells [RBCs] in urine) is due to neoplasia or glomerulonephritis until proven otherwise. Visual loss Get ophthalmic help. If sudden, ask: \212 \212 Is the eye painful/red (glaucoma; iritis)? Optic neuritis may be painful. What is each eye \200\231s acuity? Is there a contact lens problem (e.g., infection)? History of trauma, mig raine, TIA, MS, or diabetes; what is the blood sugar? Any detachment)? Is the cornea cloudy (corneal ulcer; glaucoma)? Is there a visual field problem/hemianopsia (stroke, space-occu pying lesion, glaucoma)? Formal field testing requires ophthalmic help. Any heart disease/b ruits (emboli)? Hyperlipidemia (xanthoma)? Is the BP raised or lowered? Measure it lying an d standing. Are there focal central nervous system (CNS) signs? Is there an afferent pupill ary defect (p. 81)? Tender temporal arteries steroids (p. 418). Any distant signs, such as HIV (causes retinitis), SLE, sarcoid, Beh et \200\231s disease, etc.? \212 \212 flashes/floaters (TIA, migraine, retinal artery occlusion, \212 \212 \212 \212 \212 \206\221 ESR points to giant cell arteritis: Urgent \212 \212 Voice and disturbance of speech \200\223Walking difficulty Voice and disturbance of speech (p. 66) may be noted by the patient or the doctor. Assess if difficulty is with articulatio n (dysarthria, e.g., from muscle problems), or of word command (dysphasia; always central). Vomiting Causes of nausea/vomiting include: Gastrointestinal Gastroenteritis Peptic ulceration Pyloric stenosis Intestinal obstruction Paralytic ileus Acute cholecystitis Acute pancreatitis CNS Meningitis/encephalitis Uremia Migraine Hypercalcemia \206\221 Intracranial pressure H yponatremia Brainstem lesions Motion sickness M ni re \200\231s disease Labyrinthitis Psychiatric disorder: \212 \212 \212 Metabolic/endocrine Pregnancy Diabetic ketoacidosis Addison \200\231s disease Drugs: \212 \212 \212 \212 \212 Alcohol Antibiotics Cytotoxics Digoxin Opiates Other Myocardial infarction Autonomic neuropathy UTI Self-induced Psychogenic Bulimia nervosa The history is very important: Ask about timing, relationship to meals, amount, and content (liquid, solid, bile, blood, \200\234coffee grounds \200\235). Associated symptoms and pr evious medical history often indicate the cause. Signs: Look for signs of dehydration. Exam ine the abdomen for distension, tender- ness, an abdominal mass, a succussion splash (pylor ic stenosis), or tinkling bowel sounds (intestinal obstruction). See Table 4.5 for non-GI c auses of vomiting. Walking difficulty In the elderly, this is a common and nonspecific pres en- tation: The reason may be local (typically osteo- or rheumatoid arthritis, but remember fractured neck of femur), systemic (e.g., pneumonia, UTI, anemia, drugs, hypothyroidism, r enal failure, hypothermia), or even a manifestation of depression or bereavement. It is onl y rarely a manipulative strategy. More specific causes to consider are Parkinson \200\231s disease (p. 382), polymy- algia rheumatica (very treatable, p. 417), and various neuropathi es/myopa- thies. One of the key questions is \200\234Is there pain? \200\235 Another issue to address is whether there is muscle wasting and, if so, is it symmetrical? If there is a lso ataxia, the cause is not always alcohol: Other chemicals may be involved (cannabis, ars enic, thallium, mercury, or prescribed 84 Table 4.5 Non-GI causes of vomiting Never forget these, as they can be a sign of serious disease. The follow- ing mnemonic cove rs the most important nongastrointestinal causes of vomiting: ABCDEFGHI \212A cute renal f ailure/ A ddison \200\231s disease \212B rain (e.g., ^ ICP [p. 722]) \212C ardiac (myocar dial infarct) \212D iabetic ketoacidosis \212E ars (e.g., labyrinthitis, M ni re \200\231s disease) \212F oreign substances (alcohol, drugs [e.g., opiates]) \212G ravidit y (e.g., hyperemesis gravidarum) \212H ypercalcemia/ H yponatremia \212I nfection (e.g., UTI, meningitis) Walking difficulty \200\223Weight loss sedatives), or there may be a metastatic or nonmetas tatic manifestation of malignancy \200\224or a CNS primary or vascular lesion. Remember als o treatable conditions, such as pellagra (p. 245), \206\223 B12, and beriberi, and infecti ons such as encephalitis, myelitis, Lyme disease, brucel- losis, or rarities such as botuli sm (p. 581). Bilateral weak legs in an otherwise fit person suggests a cord lesion (p. 333) . If there is associated incontinence saddle anesthesia, prompt treatment for cord compr ession may be needed. Water brash refers to the excessive secretion of saliva, which sudden ly fills the mouth. It typically occurs after meals and may denote gastroe- sophageal reflu x disease. It is suggested that this is an exaggeration of the esophagosalivary reflex. It should not be confused with regurgitation (p. 209). Weight loss is a feature of chronic dis ease and depression and also of mal- nutrition, chronic infections, and infestations (e.g., TB, HIV/AIDS), malig- nancy, diabetes mellitus, and hyperthyroidism (typically in the pres ence of increased appetite). Severe generalized muscle wasting is also seen as part of a nu mber of degenerative neurological and muscle diseases and in cardiac failure (cardiac cache xia), although in the latter, right heart failure may not s n g i s d n a s m o t p m y S Table 4.6 Unexplained signs and symptoms: How to refer a patient for an opinion 85 When you don \200\231t know: Ask . If you find yourself wondering if you should ask: Ask. Frequently, you may require the help of a consultant. If so, during ward rounds, agree who should be asked for an opinion. You will be left with the job of making the arrangemen ts. This can be a daunting task, if you are very junior and have been asked to contact an i ntimidating consultant. Don \200\231t be intimidated: Perhaps this may be an opportunity to learn something new. A few simple points can help the process go smoothly. \212 \212 \212 \212 Have the patient \200\231s notes, observations, and drug charts at hand. Be familiar with t he history: You may be interrogated. Ask if it is a convenient time to talk. At the outset, state if you are just looking for advice or if you are asking if the patient could be seen . Make it clear exactly what the question is that you want addressed, \200\234We wonder wh y Mr. Smith \200\231s legs have become weak today \200 \200\235 This helps the listener to focus his or her thoughts while you describe the story and will save you wasting time if t he page operator has put you through to the wrong specialist. Give the patient \200\231s ag e and occupation, to give a snapshot of the person. Run through a brief history. Do not pre sent the case as if you are in formal rounds \200\224it will take ages to get to the point and the listener will get irritated. If you would like the patient to be seen, give warning if you know that the patient will be going off the ward for a test at a particular time. I f you are on the ward when the consultant arrives, offer to intro- duce him or her to the p atient. \212 \212 \212 \212 We thank Martin Zeidler for providing the first draft of this page. Weight loss \200\223Xanthomata make weight loss a major complaint. Do not forget anorexia n ervosa as a possible underlying cause of weight loss. Focus on treatable causes (e.g., diab etes is easy to diagnose; TB can be very hard). For example, the CXR may look like cancer, so you may forget to send bronchoscopy samples for acid-fast bacillus (AFB) stain and TB cu l- ture (to the detriment not just of the patient, but the entire ward). Wheeze (p. 57) Whi spered pectoriloquy refers to the increased transmission of a patient \200\231s whispers he ard when auscultating over consolidated lung. It is a manifestation of increased vocal reso nance. ( Vocal resonance is sound vibration of the patient \200\231s spoken or whispered vo ice transmitted to the stethoscope.) Tactile fremitus is the sound vibration of the spoken or whis- pered voice transmitted via the lung fields and detected by palpation over the bac k. Xanthomata are localized deposits of fat under the skin surface, com- monly occurring ov er joints, tendons, hands, and feet. They are a sign of hyperlipidemia (p. 109). Xanthelasm a palpebra is a xanthoma on the eyelid. Knowing when to refer a patient for an expert opini on is equally important as making the diagnosis yourself. See Table 4.6 for guidelines. 86 This page intentionally left blank Cardiovascular medicine Stuart D. Russell , M.D. e n i c i d e m Contents Cardiovascular health 89 Cardiovascular symptoms 90 Investigations r a l u c s a v o d r a ECG: A methodical approach 92 ECG: Abnormalities 94 ECG: Additional points 95 Exercise ECG testing 99 Ambulatory ECG monitoring 100 Cardiac catheterization 101 Echocardiography 104 N uclear cardiology and other cardiac scans 107 i Drugs and the heart Hyperlipidemia 108 Atherosclerosis and statins 111 Other cardiovascular drugs 112 C 5 Diseases and conditions 88 Acute coronary syndromes 113 Management of ACS 114 Complications of MI 116 Angina pectoris 117 Arrhythmias 118 Narrow complex tachycardia 121 Atrial fibrillation and flutter 123 Wide complex tachycardia 125 Pacemakers 127 Heart failure: Basic concepts 128 Heart failure: Ma nagement 130 How to start ACE-inhibitors 131 Hypertension 132 Hypertension: Management 134 Rheumatic fever 137 Mitral valve disease 138 Aortic valve disease 139 Right-heart valve dis ease 140 Cardiac surgery 140 Infective endocarditis 141 Prevention of endocarditis 143 Dise ases of heart muscle 144 The heart in various, mostly rare, systemic diseases 145 Pericardi al diseases 146 Congenital heart disease 148 Driving and the heart 149 Cardiovascular health Maintaining good cardiovascular health is important to all patients. Table 5.1 discusses the most important parameters of heart health. e n i c i d e m Table 5.1 Cardiovascular health r a l u c s a v o d r a C Ischemic heart disease (IHD), even though decreasing in incidence, is still the most common cause of death worldwide. Encouraging cardiovas- cular health is not only about preventing IHD. The activities associated with improving cardiovascular health have many beneficial s ide effects as well. Exercise will improve cardiovascular health (blood pressure [BP] , high-density lipoprotein [HDL] ^ ) but can also prevent osteopo- rosis, improve glucose tol erance, and promote weight loss. People who improve and maintain their fitness live longer: Age-adjusted mortality from all causes is reduced by >40% . Avoiding obesity helps too, bu t there is no evidence that losing weight will lengthen life. However, the risk of diabetes (DM) will diminish if weight loss can be achieved. Smoking is the major modifiable risk fa ctor for cardiovascular mortal- ity. You can help people quit, and quitting does undo much of the harm of smoking. Simple advice works . Most smokers want to give up. Just because sm oking advice does not always work, do not stop giving it. Ask about smoking during every vi sit \200\224especially those concerned with smoking-related diseases. \212 \212 \212 i Ensure advice is congruent with the patient \200\231s beliefs about smoking. Concentrate on the benefits of giving up. Invite the patient to choose a date (when there will be few str essors) on which he or she will become a nonsmoker. You may suggest the birthday of a loved one or an anniversary so that they stop as a \200\234gift. \200\235 Suggest throwing away all accessories (cigarettes, pipes, ashtrays, light- ers, matches) in advance; inform frie nds of the new change; practice saying \200\234no \200\235 to their offers of \200\234jus t one cigarette. \200\235 89 \212 \212Nicotine gum , chewed intermittently to limit nicotine release: Ten 2 mg sticks may be needed/day. Transdermal nicotine patches may be easier. Written advice offers no added ben efit to advice from nurses. Always offer follow-up. \212Bupropion may improve the success rate in those who want to quit to 30% at 1 yr vs. 16 % with patches and 15.6% for placebo (patches + bupropion: 35.5%): Consider if the above fa ils. Dose: 150 mg/d PO (while still smoking; quit within 2 wks); dose may be twice daily fr om day 7; stop after 7 wks. Warn of side effects (se): Seizures (risk <1:1,000), insomnia, headache. Contraindicated (CI) in epilepsy, cirrhosis, preg- nancy/lactation, bipolar depre ssion, eating disorders, central nervous system (CNS) tumors, on antimalarials etc., alcoho l or benzodiazepine withdrawal. Lipids and BP (pp. 108, 132) are the other major modifiable risk factors. Nonmodifiable ris k factors include sex and family history. Apply preventive measures such as healthy eating (see p. 203) early in life to maximize impact, when there are more years to save and before bad habits get ingrained. For more on risk factors and their impact, see the American Hear t Association Heart Disease and Stroke Statistics 2012 update. Cardiovascular symptoms Chest pain Cardiac-sounding chest pain may have no serious cause, b ut always think \200\234Could this be an myocardial infarction (MI), dissecting aortic ane urysm, pericarditis, or pulmonary embolism? \200\235 Nature of pain: Constricting suggests angina, esophageal spasm, or anxiety; a sharp pain may be from the pleura or pericardium, e specially if exacerbated by inspiration. A prolonged (>0.5 h), dull, central crushing pain or pressure suggests MI. Stabbing, short lasting (<30 sec), or pain in continually varying location is less likely to be cardiac. Radiation: To shoulder, either or both arms, or neck /jaw suggests cardiac ischemia. The pain of aortic dissection is classically instantaneous, tearing, and interscapular, but may be retrosternal. Epigastric pain may be cardiac. Preci pitants: Pain associated with cold, exercise, palpitations, or emotion suggest cardiac pain or anxiety; if brought on by food, lying flat, hot drinks, or alcohol, consider esophageal spasm (but meals can cause angina). Relieving factors: If pain is relieved within minutes by rest or nitroglycerin, suspect angina. Nitroglycerin can relieve esophageal spasm, but u sually more slowly. If antacids help, suspect GI causes. Pericarditis pain improves on lean ing forward. Associations: Dyspnea occurs with cardiac pain, pulmonary embolism, pleurisy, or anxiety. MI may cause nausea, vomiting, or sweating. In addi- tion to coronary artery di sease, angina may be caused by aortic stenosis (AS), hypertrophic obstructive cardiomyopath y (HOCM), or paroxysmal supraventricular tachycardia (SVT) and be exacerbated by anemia. Ch est pain with tenderness suggests self-limiting costochondritis (Tietze \200\231s syn- drom e). See Table 5.2 for tips on how to decipher a patient \200\231s description of cardiac se nsations. Differential diagnosis of chest pain: Pleuritic pain (i.e., exacerbated by inspir a- tion) implies inflammation of the pleura secondary to pulmonary infec- tion, inflammatio n, or infarction. The patient may \200\234catch his breath. \200\235 Musculoskeletal pain: Exacerbated by pressure on the affected area. Fractured rib: Pain on respiration, exacerba ted by gentle pressure on the sternum. Subdiaphragmatic pathology may also mimic cardiac pa in. Acutely ill patients: \212 \212 90 Admit to hospital. Check pulse, BP in both arms, jugular venous pressure (JVP), heart sound s, and examine the legs for deep vein thrombosis (DVT). Give O Insert an IV line. Relieve p ain (e.g., morphine 5 \200\22310 mg IV slowly + an antiemetic). Place on cardiac monitor; d o 12-lead electrocardiogram (ECG). \212 \212 \212 \212 \212Obtain chest x-ray (CXR). \212Obtain Arterial blood gas (ABG) . Famous traps: Aortic dissection (a tearing or ripping sensation, often midscap- ular). Ma ke sure you check all pulses and bilateral BP; herpes zoster (p. 557), ruptured esophagus, cardiac tamponade (shock with JVP ^ ), opiate addiction. Dyspnea may be from left ventricul ar failure (LVF), pulmonary embolism, any respiratory cause, or anxiety. Severity: Emergenc y presentations. Ask about shortness of breath at rest or on exertion, orthopnea, paroxysma l nocturnal dyspnea (PND), exercise tolerance, and coping with daily tasks. Associations: S pecific symptoms associated with heart failure are ortho- pnea (ask about number of pillows used at night or if sitting in a recliner), paroxysmal nocturnal dyspnea (waking up at nig ht gasping for breath), and peripheral edema. Pulmonary embolism is associated with acute o nset of dyspnea and pleuritic chest pain; ask about risk factors for DVT. 2 by face mask. Palpitation(s) may be due to premature ventricular contractions, atrial fibrillation (AF), SVT and ventricular tachycardia (VT), thyrotoxicosis, anxi- ety, and rarely pheochromocytom a. History: Ask about previous episodes, precipitating/relieving factors, duration of sympt oms, associated chest pain, dyspnea, or dizziness. Did the patient check her pulse? Syncope may reflect cardiac or CNS events. Vasovagal \200\234faints \200\235 are com- mon (pulse , pupils dilated). The history from an observer is invaluable in diagnosis. Prodromal sy mptoms: Chest pain, palpitations, or dyspnea point to a cardiac cause (e.g., arrhythmia). A ura, headache, dysarthria, limb weak- ness indicate CNS causes. During the episode : Was th ere a pulse? Was there limb jerking, tongue biting, or urinary incontinence? NB : Hypoxia f rom lack of cerebral perfusion may cause seizures. Recovery: Was this rapid (arrhyth- mia) or prolonged and associated with postictal drowsiness (seizure)? e n i c i d e m r a l u c s a v o d r a C i Table 5.2 How patients communicate ischemic cardiac sensations In emergency departments, we are always hearing questions such as \200\234Is your pain sha rp or dull? \200\235 followed by an equivocal answer. The doctor goes on \200\234Sharp lik e a knife \200\224or dull and crushing? \200\235 The doctor is getting irritated because th e patient must know the answer, but is not saying it. Instead of asking the questions that we relate to cardiac chest pain (chest heaviness associated with dyspnea and radiation to t he jaw and left arm), allow the patient to tell his story. Patients often avoid using the w ord \200\234pain \200\235 to describe ischemia: \200\234Heaviness, \200\235 \200\234tigh tening, \200\235 \200\234pressure, \200\235 \200\234burning, \200\235 or \200\234a lump in the throat \200\235 (angina means to choke) may be used. They may say \200\234sharp \200\235 to communicate severity and not character. So be as vague in your questioning as y our patient is in his answers. \200\234Tell me some more about what you are feeling (long pause) as if someone was doing what to you? \200\235 \200\234Sitting on me, \200\235 or \200\234like a hotness \200\235 might be the response (suggesting cardiac ischemia). D o not ask \200\234Does it go into your left arm. \200\235 Try \200\234Is there anything e lse about it? \200\235 (pause) \200\234Does it go anywhere? \200\235 Note your patie nt \200\231s exact words. Note also nonverbal clues: The clenched fist placed over the ster num is a telling feature of cardiac pain (Levine sign positive). A good history, taking acc ount of these features, is the best way to strat- ify patients likely to have cardiac pain. If the history is nonspecific, there are no risk factors for cardiovascular diseases, and ECG and plasma tro- ponin T (p. 114) are normal (<0.2 mcg/L) 6 \200\22312 h after the onset of pain, discharge will probably be OK. But when in doubt, get help. Features making cardi ac pain unlikely: \212 \212 \212 \212 \212 Do not feel that you must diagnose every pa in. Chest pain with no cause is common. Extensive testing, including cardiac catheterizatio n and rul- ing out depression, may not find the cause. Do not reject these patients: Explai n your findings to them. Some have a \200\234chronic pain syndrome \200\235 that responds to a tricyclic (e.g., imipramine 50 mg at night 1 ; this dose does not imply any depression ). It is similar to postherpetic neuralgia. 91 Stabbing, shooting pain Pain lasting <30 sec, however intense Well-localized, left submamma ry pain ( \200\234In my heart, doctor \200\235) Pains of continually varying location Youth 1 Cannon RO, Quyyumi AA, Mincemoyer R, et al . Imipramine in patients with chest pain despi te normal coronary angiograms. N Engl J Med . 1994 May 19;330(20):1411 \200\2231147. ECG: A methodical approach First confirm the patient \200\231s name and age, and the ECG da te. Then: \212Rate: At usual speed (25 mm/sec) each \200\234big square \200\235 is 0.2 se c; each \200\234small square \200\235 is 0.04 sec. To calculate the rate, divide 300 by th e number of big squares per R \200\223R interval (p. 93). \212Rhythm: If the cycles are not clearly regular, use the \200\234card method \200\235: Lay a card along the ECG, marking positions of three successive R waves. Slide the card to and fro to check that all intervals are equal. If not, note if dif- ferent rates are multip les of each other (i.e., varying block)or if it is 100% irregular (AF or ventricular fibril lation [VF]). Sinus rhythm is characterized by a P wave (upright in II, III, and aVF; inver ted in aVR) followed by a QRS complex. AF has no discernible P waves, and the QRS complexes are irregularly irregular. Atrial flutter usually has a \200\234sawtooth \200\235 baselin e of atrial depolarization ( 300/min) and regular QRS complexes. Nodal rhythm has a normal QRS complex, but P waves are absent or occur just before or within the QRS complex. Ventric ular rhythm has QRS complexes of >0.12 sec with P waves following them. Axis: The mean frontal axis is the sum of all the ventricular forces during ventricular dep olarization. The axis lies at 90 degrees to the isoelectric complex (i.e., the one in which positive and negative deflections are equal). Normal axis is between \200\22330 and +90 . As a simple rule of thumb, if the complexes in leads I and II are both \200\234positiv e, \200\235 the axis is normal. Left axis deviation (LAD) is \200\22330 to \200\22390 . Causes: Left anterior hemiblock, inferior MI, VT from LV focus, Wolff \200\223Parkinson \200\223White (WPW) syndrome (some types). Right axis deviation (RAD) is +90 to +180 . C auses: Right ventricular hypertrophy (RVH), PE, anterolateral MI, left posterior hemiblock (rare), WPW syndrome (some types). \212P wave: Normally precedes each QRS complex. Absent p wave : AF, sinoa- trial block, junctional (AV nodal) rhythm. Dissociation between P waves and QRS complexes indicates complete heart block. p mitrale: Bifid P wave in lead II and b iphasic P wave in lead V 1 indicate left atrial hypertro- phy. p pulmonale : Peaked P wave (>2.5 mm in lead II) indicates right atrial hypertrophy. Pseudo-P-pulmonale is seen in K + . 92 \212P \200\223R interval: Measure from start of P wave to start of QRS. Normal range : 0.1 2 \200\2230.2 sec (3 \200\2235 small squares). A prolonged P \200\223R interval implies del ayed atrioventricular (AV) conduction (first-degree heart block). A short P \200\223R inter val implies unusually fast AV conduction down an accessory pathway (e.g., WPW [ECG, p. 124] ). In second-degree block, some P waves aren \200\231t followed by a QRS. If the PR interva l increases with each cycle until there is a P wave not followed by a QRS, this is Mobitz t ype I (Wenckebach) AV block. If the PR interval is constant and a P wave is not followed by a QRS, this is Mobitz type II AV block. In third-degree block, the P waves and QRS waves a re independent of each other. \212QRS complex: Normal duration : <0.12 sec. If \211 0.12 sec, suggests ventricu- lar c onduction defects (e.g., a bundle branch block [p. 95]). Large QRS complexes suggest ventri cular hypertrophy (p. 96). Normal Q wave is <0.04 sec wide and <2 mm deep. Pathological q w aves may occur within a few hours of an acute MI. \212QT interval: Measure from start of QRS to end of T wave. It varies with rate. Calculat e corrected QT interval (QTC) by dividing the measured QT interval by the square root of th e cycle length, i.e., QT c = (QT)/( \226 R \200\223 R). Normal QT c : 0.38 \200\2230.43 s ec. Prolonged qt interval : Acute myocardial isch- emia, myocarditis, bradycardia (e.g., AV block), head injury, hypothermia, electrolyte imbalance (K + , Ca 2+ , Mg 2+ ), c ongenital (Romano \200\223Ward and Jervell \200\223Lange \200\223Nielson syndromes), sotalo l, quinidine, antihistamines, mac- rolides (e.g., erythromycin), amiodarone, phenothiazines , tricyclics. \212ST segment: Usually isoelectric. Planar elevation (>1 mm) or depres- sion (>0.5 mm) us ually implies infarction (p. 97) or ischemia (p. 100), respectively. e n i c i d e m \212T wave: Abnormal if inverted in I, II, and V 4 \200\223V 6 . It is peaked in hyper- kalemia (ECG 13 [p. 672]) and flattened in hypokalemia. \212U wave: May be prominent in hypokalemia but can also be normal \212J wave: Associated with hypothermia r a l u c s a v o d r a C Figure 5.1 ECG nomenclature (ventricular activation time, VAT) i 93 Calculating the R \200\223R interval To calculate the rate, divide 300 by the number of big squares per R \200\223R interval if the standard ECG speed of 25 mm/sec is used (elsewhere , 50 mm/sec may be used: Don \200\231t be confused!) R \200\223R duration(s) 0.2 Big squares 1 Rate (per min) 300 0.4 0.6 0.8 1.0 1.2 1.4 2 3 4 5 6 7 150 100 75 60 50 43 Figure 5.2 Determining the ecg axis \212 The axis lies at 90 to the isoelectric complex (the one in which positive and negative de flections are equal in size). If the complexes in I and II are both predominantly positive, the axis is normal. \212 Causes of lad Left anterior hemiblock Inferior MI VT from LV focus WPW syndrome (some); p. 124 Causes of rad RVH Pulmonary embolism Anterolateral MI Left posterior hemiblock (rare) 94 Left ventricular hypertrophy WPW syndrome (some) ECG: Abnormalities Sinus tachycardia: Rate >100. Anxiety, exercise, pain, fever, sepsis, hy po- volemia, heart failure, pulmonary embolism, pregnancy, thyrotoxicosis, beriberi, CO 2 r etention, autonomic neuropathy, sympathomimetics; e.g., caffeine, adrenaline, and nicotine (may produce abrupt changes in sinus rate, and other arrhythmias). Sinus bradycardia: Rate <60. Physical fitness, vasovagal attacks, sick sinus syndrome, acute MI (esp. inferior), dr ugs ( -blockers, digoxin, amiodarone, verapamil), hypothyroidism, hypothermia, intracran ial pressure (ICP) ^ , cholestasis. AF (ECG p. 120): Common causes : IHD thyrotoxicosis, hy pertension. First- and second-degree heart block: Normal variant, athletes, sick sinus syn- drome, IHD, acute carditis, drugs (digoxin, -blockers). Complete heart block: Idiopathi c (fibrosis), congenital, IHD, aortic valve cal- cification, cardiac surgery/trauma, digoxi n toxicity, infiltration (abscesses, granulomas, tumors, parasites). ST elevation: Normal v ariant (high take-off), acute MI, Prinzmetal \200\231s angina, acute pericarditis (saddle-s haped), left ventricular aneurysm. ST depression: Normal variant (upward sloping), digoxin (downward slop- ing), ischemic (horizontal): Angina, acute posterior MI. T inversion: In V 1 \200\223V 3 : Normal (African Americans and children), right bundle branch block (RBBB), pulmonary embolism. In V 2 \200\223V 5 : Subendocardial MI, HOCM, subarachnoid hemorrhage , lithium. In V 4 \200\223V 6 and AVL : Ischemia, left ventricular hypertrophy (LVH), asso ciated with left bundle branch block (LBBB). NB: ST and T wave changes are often nonspecific, and must be interpreted in the light of th e clinical context. MI (ECG p. 97): \212 e n i c i d e m Within hours, the T wave may become peaked and the ST segment may begin to rise. Within 24 h, the T wave inverts as ST segment elevation begins to resolve. ST elevation rarely persis ts, unless a left ventricular aneurysm develops. T wave inversion may or may not persist. W ithin a few days, pathological Q waves begin to form. Q waves usually persist, but may reso lve in 10%. \212 r a l u c s a v o d r a C \212 The leads affected reflect the site of the infarct: Inferior (II, III, a VF), anteroseptal (V 1 \200\2234 ), anterolateral (V 4 \200\2236 , I, aVL), posterior (tall R and ST in V 1 \200\2232 ). \200\234Non-Q wave infarcts \200\235 (formerly called subendocardial infarc ts) may have ST and T changes without Q waves. Pulmonary embolism: Sinus tachycardia is mos t common. There may be RAD, RBBB (p. 97), right ventricular strain pattern V 1 \200\2233 , or AF. Rarely, the classic \200\234S i Q iii T iii \200\235 pattern occurs: Deep S waves in I, pathological Q waves in III, inverted T waves in III. Metabolic abnormalities: Digoxi n effect: ST depression and inverted T wave in V 5 \200\2236 . In digoxin toxicity, any arr hythmia may occur (ventricular ectopy and nodal bradycardia are common). Hyperkalemia: Tall , tented T wave, widened QRS, absent P waves, \200\234sine wave \200\235 appearance (ECG 1 3, p. 672). Hypokalemia : Small T waves, prominent U waves. Hypercalcemia: Short QT interva l. Hypocalcemia : Long QT interval, small T waves. i 95 ECG: Additional points Figure 5.3 Where to place the chest leads V 1 : Right sternal edge, fourth intercostal space V 2 : Left sternal edge, fourth intercostal space V 3 : Half-way between V 2 and V 4 V 4 : The patient \200\231s apex beat All subsequent leads are in the same horizontal plane as V 4 V 5 : Anterior axillary line V 6 : Mid-axillary line (V 7 : Posterior axillary line) Finish 12-lead ECGs with a long rhythm strip in lead II. Disorders of ventricular conduction Bundle branch block ( see ECGs 1 and 2) Delayed conduct ion is evidenced by prolongation of QRS >0.12 sec. Abnormal conduction patterns lasting <0. 12 sec are incomplete blocks. The area that would have been reached by the blocked bundle d epolarizes slowly and late. Taking V 1 as an example, right ventricular depolarization is n ormally +ve and left ventricular depo- larization is normally \200\223ve. In RBBB, the following pattern is seen: QRS >0.12 sec, \200\234RSR \200\235 pattern in V 1 , dominant R in V 1 , inverted T waves in V 1 \200\223V 3 or V 4 , deep wide S wave in V 6 . Causes: Normal variant (isolated RBBB), pulmonary embolism, cor pulmonale. In LBBB, the following pattern is seen: QRS >0.12 sec, \200\234M \200\235 pattern in V 5 , no septal Q waves, inverted T waves in I, aVL, V 5 \200\223V 6 . Causes: IHD, hypertension, cardio-my opathy, idiopathic fibrosis. NB: If there is LBBB, no comment can be made on the ST segment or T wave. Bifascicular block is the combination of RBBB and left bundle hemi- block, mani fest as an axis deviation (e.g., LAD in the case of left anterior hemiblock). Trifascicular block is the combination of bifascicular block and first-degree heart block. Ventricular h ypertrophy There is no single marker of ventricular hyper- trophy: Electrical axis, voltage , and ST wave changes should all be taken into consideration. Relying on a single marker su ch as voltage may be unre- liable as a thin chest wall may result in large voltage, whereas a thick chest wall may mask it. Suspect LVH if the R wave in V 6 >25 mm or the sum of the S wave in V 1 and the R wave in V 6 is >35 mm (ECG 8, p. 136). Suspect RVH if dominant R wa ve in V 1 , T wave inversion in V 1 \200\223V 3 or V 4 , deep S wave in V 6 , RAD. Other c auses of dominant r wave in V1 : RBBB, posterior MI, some types of WPW syndrome (p. 124). C auses of low-voltage QRS complex : QRS <5 mm in all limb leads. Hypothyroidism, chronic obs tructive pulmonary disease (COPD), hema- tocrit ^ (intra-cardiac blood resistivity is relat ed to hematocrit), changes in chest wall impedance (e.g., in renal failure, subcutaneous em physema but not obesity), pulmonary embolism, bundle branch block, carcinoid heart disease, myocarditis, cardiac amyloid, Adriamycin cardiotoxicity, and other heart muscle diseases, pericardial effusion, pericarditis. 96 Figure 5.4 ECG 1: Left bundle branch block. Note the W pattern in V 1 and the M pattern in V 6 V 4 aVR V 1 I aVL 11 V 2 V 5 111 aVF V 3 V 6 11 e n i c i d e m Figure 5.5 ECG 2: Right bundle branch block. Note the M pattern in V 1 and the W pattern in V 5 V 4 aVR V 1 I r a l u c s a v o d r a C V 2 aVL 11 V 5 111 aVF V 3 V 6 i 11 Figure 5.6 ECG 3: Acute inferolateral myocardial infarc- tion. Note the marked ST elevation in the inferior leads (II, III, aVF), but also in V 5 and V 6 , indicating lateral involve - ment as well. There is also \200\234reciprocal change \200\235; i.e., ST-segment depress ion in leads I and aVL. The latter is often seen with a large myocardial infarction. 97 V4 aVR V1 I aVL V2 V5 11 111 aVF V3 V6 11 Figure 5.7 ECG 4: Acute anterior myocardial infarction. Note the marked ST segment elevatio n and evolving Q waves in leads V 1 \200\223V 4 . aVR V1 V4 I V5 aVL V2 11 111 aVF V3 V6 Figure 5.8 ECG 5: Complete heart block. Note the dis- sociation between the P waves and the QRS complexes. QRS complexes are relatively narrow, indicating that there is a ventricular rhythm originating from the conducting pathway. 98 aVR V1 V4 I aVL V2 V5 11 111 aVF V3 V6 11 e n i c i d e m Figure 5.9 ECG 6: Ventricular tachycardia. Note the broad complexes. aVR V1 V4 I r a l u c s a v o d r a C V5 aVL V2 11 i 111 aVF V3 V6 11 Figure 5.10 ECG 7: Dual-chamber pacemaker. Note the pacing spikes that occur before some of the P waves, and the QRS complexes. 99 aVR V1 V4 I aVL V2 V5 11 111 aVF V3 V6 Exercise ECG testing The patient undergoes a graduated treadmill exercise test with continu ous 12-lead ECG and BP monitoring. There are numerous treadmill protocols; the \200\234Bru ce protocol \200\235 is the most widely used. Indications: \212 \212 \212 To help confirm a suspected diagnosis of IHD To assess cardiac function and exercise tolera nce To develop prognosis following MI; often done predischarge (if +ve, worse outcome) \212 To evaluate response to treatment (drugs, angioplasty, coronary artery bypass grafting [CAB G]) To assess exercise-induced arrhythmias \212 Contraindications: \212 Unstable angina \212 Recent Q wave MI (<5 d) \212 Severe A S Uncontrolled arrhythmia, hypertension (systemic or pulmonary), or heart \212 failure Be cautious about arranging tests that will be hard to perform or interpret. These patients should have some type of imaging in addition to a stress test: \212 \212 \212 Stop the test if: \212 Complete heart block, LBBB Pacemaker patients Osteoarthritis, COPD, stroke, or other limita tions to exercise Chest pain or dyspnea occurs. You want to make sure that the patient has a maximal test and would consider not stopping for minor chest pain without ECG changes. The patient feels fa int, exhausted, or is in danger of falling. ST segment elevation/depression >2 mm is presen t(with or without chest pain). Atrial or ventricular arrhythmia (not just ectopy) is presen t. Fall in BP or excessive rise in BP (systolic >230 mm Hg)occurs. AV block or LBBB develop s. Maximal or 90% maximal heart rate for age is achieved. \212 \212 \212 \212 \212 \212 Interpreting the test: A +ve test only allows one to assess the pro bability that the patient has IHD. 75% of patients with significant coronary artery disease have a +ve test, but so do 5% of people with normal arteries (the false-positive rate is e ven higher in middle-aged women, e.g., 20%). The more +ve the result, the higher the predic tive accuracy. Down-sloping ST depression is much more significant than up-sloping; e.g., 1 mm J-point depression with down-sloping ST segment is 99% predictive of 2 \200\2233 vessel disease. Morbidity: 24 in 100,000. Mortality: 10 in 100,000. 100 Ambulatory ECG monitoring Continuous ECG monitoring for 24 h may be used to evaluate for pa roxys- mal arrhythmias. However, >70% of patients will not have symptoms during the period of monitoring. 20% will have a normal ECG during symptoms and only up to 10% will have an arrhythmia coinciding with symptoms. Give these patients an event recorder they can activat e themselves dur- ing a symptomatic episode. These episodes can then be transmitted via a t elephone for evaluation. Recorders may also be programmed to detect ST segment depression, either symptomatic (to prove angina), or to reveal \200\234silent \200\235 ischemia (predi ctive of reinfarction or death soon after MI). e n i c i d e m Figure 5.11 (a) r a l u c s a v o d r a C i Each complex is taken from sample ECGs (lead V 5 ) recorded at 1-min in- tervals during exe rcise ( top line ) and recovery ( bottom line ). At maximum ST depression, the ST segment i s almost horizontal. This is a positive exercise test. (b) 101 This is an exercise ECG in the same format. It is negative because al- though the J point i s depressed, the ensuing ST segment is steeply up sloping.