The Short Cases

The Short cases

 Cardiovascular examination  Vascular system examination  Respiratory system examination  Examination of precordium  GIT examination  Abdominal examination  Scrotal examination  Musculoskeletal examination – spine, knee, shoulder, elbow.  Nervous system examination o Cranial nerves o Peripheral nervous system o Higher mental function o Mental state examination  Examination of the hands  Examination of neck  Examination of the breast  Procedures o Control of epistaxis o Fundoscopy o Eye examination o Chest drain – needle and tube o Breaking bad news o Airway assessment o Urgent airway maneuvers – cricothyrotomy or transtracheal jet ventilation o Lumbar puncture o RSI o Defibrillation and cardioversion o Intraosseous access o Suprapubic catheter placement o CPR – single and two person Cardiovascular System examination (Includes general/peripheral examination and examination of precordium)

General appearance:  Notice any obvious clinical findings – ill vs. well looking, dyspnea ±, syndromic appearances – Down’s, Marfan’s, and Turner’s.  Notice any drips, infusions, drugs, puffers, mobilization aids, monitoring, and oxygen device.  Ask for vitals and temperature now  Clean hands with antiseptic solution provided (or own if carrying).  Place patient in preferred position

Syndrome Characteristics Associations Marfan’s Tall stature, thoracic kyphosis, pectus Cystic medial degeneration of valves and great excavatum, arachnodactyly, long limbs vessels → mitral/aortic valve prolapse, AR/MR, and high arched palate. Ectopia lentis. dilated aorta → aortic aneurysm/dissection. Disorder with fibrillin gene FBN1. ↑risk for spontaneous pneumothorax Down’s Microgenia (small chin), round face, Endocardial cushion defect → ASD (40%), VSD (trisomy 21) macroglossia, epicanthic fold of eye, up- (30%) slanting palpebral fissures, shorter limbs, single transverse palmar crease, hypotonia. Klinefelter’s Tall stature males, long extremities, ASD/VSD, PDA and some cases tetralogy of Fallot. (XXY) eunuchoid configuration and gynecomastia with atropic testes Turner’s (XO) Females, short-stature, lymphedema of Bicuspid aortic valve and coarctation of aorta. hands and feet, broad shield chest, low hairline, low set ears, obesity, shortened fifth finger, webbed neck Obesity Cushing’s, Pickwickian ↑ CAD/IHD risk syndromes Acromegaly Tall stature, spade hands, hypertelorism, Hypertension, cardiac hypertrophy, ↑ears/nose size cardiomyopathy and conduction defects

Initial position of patient: lying in bed semi-reclined at 45˚ angle with bed end raised or pillows

General examination: start peripherally at hands and moving centrally

Hands: Condition Findings Cardiovascular diseases Cyanosis Central – around lips, tip of Cyanotic heart disease – tetralogy of Fallot, nose/ears, tongue (usually with transposition of great vessels, tricuspid atresia, peripheral) – central CNS/CVS/Resp pulmonary stresia, critical pulmonary stenosis and cause late PDA. Eissenmenger syndrome→ reversal of L-to- Peripheral – fingers and extremities – R shunt in c/o ASD/VSD. CCF/PE/AMI/Shock inadequate circulation – all cause of Isolated peripheral – vasoconstriction d/t local and central + peripheral causes central causes Differential – lower extremity > upper – PDA/ coarctation Clubbing Stages – softening of nail bed, loss of CVS causes – chronic hypoxia, cyanotic heart disease, normal <165˚ angle, ↑convexity of SBE and atrial myxoma. nail fold, thickening of whole DIP Differential clubbing – PDA, Eissenmenger, (drumstick), wrist involvement coarctiation. Splinter Linear h’hages parallel to long axis of Trauma, infective endocarditis, vasculitis – RA, PAN, hemorrhages nail hematologic malignancy Osler’s nodes Red raised tender nodules on pulp of Infective endocarditis fingers, thenar/hypothenar eminences Janeway Non-tender erythematous Infective endocarditis lesions maculopapular lesions on palms, finger pulp Tendon Yellow orange deposits of lipids of Hand and arm – type II hyperlipidemia, xanthomata tendons elbows/knees – type III

Pulse: Radial pulse: rate, rhythm, radio-femoral delay, character and volume, and condition of vessel wall Characteristic Disorder Causes Rate Bradycardia Drugs, CHB, athlete, hypothermia, hypothyroid, arrhythmia Tachycardia Drugs, fever, pregnancy, hypethyroid, CCF, SVT, anemia, hypovolemia, PE Rhythm Regularly irregular AV blocks, dropped beats, VPC, bigeminy Irregularly irregular Atrial fibrillation Radio-femoral Different strength of Coarctation of aorta, occlusion delay pulse Character Use brachial or carotid Collapsing (bounding) Aortic regurgitation Pulsus alternans Advanced CCF Pulsus paradoxus Severe asthma, constrictive cardiac conditions, sever COPD

Blood pressure: Abnormality Finding Causes Pulsus ↓BP >10mmhg with Constrictive pericarditis, effusion paradoxus inspiration Hypertension BP >145/90mmhg Classify as mild/moderate/severe Postural >15mmhg sys, >10mmhg Hypovolemia, anti-HT drugs esp. α adrenergic hypotension dias on standing blockers/TCA/diuretics, Addison’s, autonomic neuropathy e.g. DM

Face Abnormality Finding Causes Jaundice Yellow sclera, MM. Severe CCF, prosthetic valve RBC destruction Xanthalesma Cholesterol deposits around Type II or III hyperlipidemia eyes Malar flush Rosy cheeks with bluish tinge Pulmonary HT + ↓CO – severe MS High arched palate Marfan’s syndrome AR, MR, MVP Tongue/ears/nose Central cyanosis As above cyanosis

Neck Carotid pulse Character Finding Cause Anacrotic Small volume, slow uptake, Aortic stenosis notched wave on upstroke Plateau Slow upstroke with sustained Aortic stenosis plateau then fall Bisferiens Anacrotic and collapsing AS + AR Collapsing Slow upstroke rapid fall AR, hyperdynamic circ, PDA, AV fistula, severe atherosclerosis Small volume AS, pericardial effusion Alternans Alternating strong and weak Severe LVF

Jugular venous pulse (JVP)  Measured in 45˚ supine patient with sternal notch as zero point. Normal value is 3cm above sternal notch (5cm +3cm = 8cmH2O). Sternal notch to mid right atrium distance 5cm.  Two positive waves – o ‘a’ wave coincides with right atrial systole and first heart sound and precedes carotid pulsation o ‘v’ wavedue to atrial filling with tricuspid valve closed during ventricular systole  Two troughs/descents – o ‘x’ descent – between ‘a’ and ‘v’ waves caused due to atrial relaxation. May be interrupted by ‘c’ point (notch) due to transmitted carotid pulse. o ‘y’ descent – opening of tricuspid valve and rapid ventricular filling

Abnormality Finding Causes Raised JVP General rise in RVF, tricuspid stenosis/regurgitation, pericardial effusion, volume/height constrictive pericarditis, SVC obstruction, fluid overload. Dominant ‘a’ Tricuspid stenosis, pulmonary stenosis, pulmonary HT wave Cannon ‘a’ CHB, nodal tachycardia with retrograde atrial conduction, VT with waves AV dissociation Dominant ‘v’ Tricuspid regurgitation wave

The precordium Inspection  Scars – median sternotomy, lateral thoracotomy → CABG, valve replacements  Shape of chest – pectus excavatum, kyphoscoliosis, barrel chest  Pacemaker/defibrillator  Apex beat and abnormal pulsations

Palpation  Apex beat – only palpable in 50%, in mid-clavicular line in 5th ICS, lateral and inferior displacement indicates enlargement (chest wall deformity, pleural or pulmonary disease) Type Finding Cause Pressure loaded Heaving, hyperdynamic Systolic overload Thrusting Displaced, diffuse, non-sustained Advanced MR, dilated CMpathy Dyskinetic Uncoordinated, diffuse LV dysfunction Double Two distinct impulses HOCM Absent None Thick chest wall, emphysema, effusion, shock, dextrocardia  Parasternal impulse – RV enlargement, severe LA enlargement, palpable P2 in c/o pulmonary HT  Thrills – palpable murmurs

Percussion – usually not conducted for CVS

Auscultation Auscultation sites – mitral – 4th ICS medial to mid-clavicular line, tricuspid – 5th ICS L parasternal, pulmonary – 2nd ICS L parasternal, aortic – 2nd ICS R parasternal, axilla and carotids. Normal heart sounds  S1 – two components – mitral and tricuspid valve closure indicates beginning of ventricular systole  S2 – softer, shorter and slightly higher pitch marks the end of systole, composed of sounds arising from aortic and pulmonary valve closure. Normally split in 70% adults due to low pressure RV closure occurs later in pulmonary valve best appreciated in pulmonary area. Abnormalities of heart sounds Abnormality Mechanism Causes Loud first HS Mitral or tricuspid valve wide open at end Mitral stenosis, tachycardia or shortened AV of diastole and forceful shutting at conduction time beginning of systole Soft first HS Prolonged diastolic filling time or delayed 1st HB, LBBB or mitral regurgitation onset of systole or failure of cusps to close fully Loud A2 Forceful aortic valve closure Hypertension, congenital AS Loud P2 Forceful pulmonary valve closure Pulmonary HT Soft S2 Failure of aortic valves to close Aortic regurgitation Splitting S1 Delayed cardiac conduction RBBB Splitting S2 Normal, increased if conduction delay RBBB, pulmonic stenosis(delayed ejection), VSD (↑RV load), mitral regurgitation (early AV closure d/t rapid filling) Reversed P2 occurs first d/t delayed LV LBBB, PDA, severe AS, coarctation of aorta splitting S2 depolarization, emptying or load

Extra heart sounds Sound Mechanism Causes S3 Low-pitched mid-diastolic, triple rhythm Physiologic in children/young, pathologic – reduced – gallop rhythm – tautening of ventricular compliance, increased atrial pressure. LV S3 – mitral/tricuspid muscles at end of rapid left sternal edge, louder in expiration d/t ↑CO, LVF and diastolic filling dilatation, AR/MR/VSD/PDA RV S3 – left sternal edge louder in inspiration – RVF/constrictive pericarditis S4 Late diastolic sound pitched higher than LV S4 – AS/acute MR, HT/IHD or advanced age, S3 d/t high pressure atrial wave sometimes only sing in angina reflecting from non-compliant RV S4 – pulmonary HT or pulmonary stenosis ventricular wall

Additional heart sounds Sound Mechanism Causes Opening snap High pitched sound at variable distance from S2 d/t sudden Mitral stenosis opening of mitral valve followed by diastolic murmur Ejection systolic Early systolic high-pitched sound heard over aortic or Congenital click pulmonary and LSB due abnormal valve doming in early aortic/pulmonary stenosis systole Non-ejection High-pitched sound during systole due to prolapse of ASD or Ebstein’s anomaly systolic click redundant mitral valve leaflet during systole

Cardiac murmurs – MSMD, MRMS, ASMS, ARMD Timing Type Mechanism Associated Causes features Systolic Pansystolic Ventricle leaks to MR heard best MR, TR and VSD lower pressure over apex radiating chamber or vessel to axilla, louder begins at S1 and with isometric continues until handgrip. pressure equalizes S2. Ejection (mid) S1-murmur peaks mid- AS murmur AS, PS, HOCM, pulmonary systolic systole –S2. Turbulent radiates into flow of ASD flow across aortic/ carotid arteries. pulmonary valve or HOCM murmur ↑flow through normal louder with sized valves valsalva, squatting to standing and softer with isometric handgrip. Late systolic Appreciable gap b/w MVP, MR S1 and murmur Diastolic Early diastolic Immediately after S2 AR, PR high-pitched d/t regurgitant flow through leaking aortic/pulm valves Mid-diastolic Short or extend up to MS, TS, atrial myxoma, S2, lower pitched d/t Austin-Flint murmur of AR impaired during and Carey Coombs of ventricular filling rheumatic fever Continuous S1 to S2 to S1 Flow throughout PDA, AV fistula, venous murmurs cardiac cycle hum, mammary soufflé of pregnancy Pericardial Superficial Varies with resp Pericarditis friction rub scratching and posture, sound louder when sitting up and breathing out Mediastinal Crunchy sound Hamman’s sign Post cardiac surgery, crunch with systolic pneumomediastinum or and diastolic post-pericardial effusion components drainage

Dynamic maneuvers  Respiration – o Inspiration → ↑ venous return → ↑blood flow to right side → right sided murmurs louder; no effect on left sided murmurs o Expiration → opposite effects → R murmurs softer; no effect on L murmurs or louder.  Deep expiration in leaning forward position – AR murmur may become discernible (otherwise absent), pericardial rub best heard.  Valsalva maneuver – forceful expiration against closed glottis → ↑HR, ↓BP and ↓stroke volume → louder HOCM systolic murmur  Standing to squatting → ↑stroke volume and arterial pressure → ↑ intensity of most murmurs except HOCM which gets softer.  Squatting to standing → opposite effect to above  Isometric handgrip for 20-30s → ↑ arterial resistance, ↑BP and heart size→ AS becomes softer, HOCM becomes softer and MVP murmur is delayed due to ↑ventricular volume

The neck → carotid bruit and conducted murmur of AS The lung bases → late or pan-inspiratory crackles – CCF The back → murmur of coarctation of aorta best heard over upper back, pitting over sacrum. The abdomen →  enlarged tender liver in RVF;  pulsatile liver due to transmission of RV systolic pressure wave to hepatic veins in tricuspid regurgitation  hepatojugular reflux – increase in JVP waveforms s/o RVF  pulsation of abdominal aorta to the left of midline – expansile pulsations in AAA The lower limbs → peripheral edema, Achilles tendon xanthomata, toe clubbing (isolated or with finger clubbing)

Peripheral vascular examination Inspection  atrophic skin and loss of hair, colour changes of the feet (blue or red)  muscle wasting or asymmetry  surgical scars  ulcers at the lower end of the tibia Palpation  temperature  palpate both femoral arteries for equality, then auscultate them for bruit  palpate popliteal pulse – supine and if not felt in prone position  palpate posterior tibial under medial malleolus and dorsalis pedis on forefoot on both sides  reduced capillary return by compressing toenails  Buerger’s test – elevate legs to 45˚ (rapid pallor), then place them dependent over the edge of the bed (cyanosis if arterial blood supply compromised). Special maneuvers  Buerger’s test – red coloration of extremity >than normal suggestive of ischemia  Brodie-Trendelenburg test – empty superficial veins by milking then place tumb over saphenofemoral junction (2cm below and lateral to pubic tubercle), get patient to stand up with thumb in place → if superficial veins fill up incompetence below saphenofemoral junction.

Valvular heart disease Mitral stenosis Normal area of mitral valve is 4-6 cm2, reduction of area to <50% causes significant obstruction to LV filling and LA pressures will have to rise for blood to flow to LV. Symptoms – dyspnea, orthopnea, PND, hemoptysis, ascites, edema and fatigue General signs – tachypnea, mitral facies and peripheral cyanosis in severe cases CV signs  Reduced pulse volume due to reduced CO  AF may be present  JVP normal or reduced in volume, loss of ‘a’ wave if in AF  Palpation – tapping apex beat, RV heave and palpable P2 if pulmonary HT, diastolic thrill rarely.  Auscultation – loud S1, loud P2 (if PHT), opening snap, low pitched rumbling diastolic murmur best heard with bell on mitral area in left lateral position  Severe mitral stenosis – small pulse pressure, soft S1, early OS, long diastolic murmur, diastolic thrill at apex with signs of PHT Causes  Rheumatic heart disease  Congenital parachute valve

Mitral regurgitation A regurgitant mitral valve allows part of the LV stroke volume to return into LA, imposing a load on both LA/LV. Symptoms – dyspnea, fatigue General signs – tachypnea CV signs  Pulse – normal or sharp upstroke, AF common  Apex beat displaced, diffuse and hyperdynamic, palpable systolic thrill and parasternal impulse d/t dilated LA (>than MS)  Auscultation – soft or absent S1, LV S3 d/t rapid LV filling during diastole. Pansystolic murmur maximal at apex and radiating to axilla  Severe mitral regurgitation – small volume pulse, enlarged LV, loud S3, soft S1, early A2, early diastolic rumble, signs of Pulmonary HT and LVF Causes  MVP  Degenerative changes associated with age  Rheumatic heart disease  Papillary muscle dysfunction due to LVF or ischemia  Cardiomyopathy – hypertrophic, dilated or restrictive  Connective tissue disease – Marfan’s, RA, Ankylosing spondylitis  Congenital – AV canal defect

Mitral valve prolapse MVP may cause a systolic murmur or click or both at apex, presence of murmur indicates MR. CV signs  Auscultation – systolic clicks at variable times of systole with associate murmur commencing with the click and extending to rest of systole  Dynamic maneuvers – increases and comes earlier with valsalva maneuver and becomes softer and delayed with isometric handgrip. Causes  Myxomatous degeneration with age – common  Associated with ASD, HOCM or Marfan’s syndrome

Aortic stenosis Normal area of aortic valve is >2cm2. Significant narrowing restricts LV outflow imposing pressure load on LV. Symptoms: exertional CP (without CAD in 50% of patients), exertional syncope and dyspnea. General signs – none CV signs  Pulse – plateau or anacrotic , ‘pulsus parvus et tardus’ – small volume and late peaking.  Palpation – hyperdynamic, displaced apex beat, systolic thrill at base of heart.  Auscultation – narrowly split or reversed S2, harsh midsystolic ejection murmur, maximal over aortic area extending into carotid arteries. Loudest with patient sitting up and full expiration. Associate AR may be commonly present. Ejection systolic click sometimes present.  Severe AS – (valve area <1cm2, pressure gradient >50mmhg) plateau pulse, thrill in aortic area, soft or absent A2, signs of CCF (late). Causes  Degenerative calcific AS (common)  Calcific change in young patients – usually bicuspid aortic valve.  Rheumatic heart disease.  Other – supra-valvular fibrous diaphragm, sub-valvular diaphragm or fibrous ridge, dynamic outflow tract obstruction in HOCM.

Aortic regurgitation Incompetent aortic valve allows regurgitation of blood from aorta to LV during diastole during the period that aortic pressure > LV diastolic pressure Symptoms – late in disease, exertional dyspnea, fatigue, palpitations and exertional angina. General signs – Marfan’s syndrome, Ankylosing spondylitis and other CT diseases may be obvious. CV signs  Pulse – ‘water hammer pulse’, collapsing, wide pulse pressure. Bisferiens pulse in severe cases.  Prominent carotid pulsations – ‘Corrigan’s signs’ head-bobbing.  Palpation – apex beat displaced and hyperkinetic, diastolic thrill at LSB when patient sits up and breathes out.  Auscultation – Soft A2, decrescendo high-pitched diastolic murmur immediately after S2, extending variable time into diastole, loudest at 3rd and 4th ICS; systolic murmur usually present due to associated AS. Austin Flint murmur – low-pitched rumbling mid-diastolic and presystolic murmur at apex (regurgitant jet from aortic valve making mitral valve shudder) – differentiate from MS as S1 not loud and no opening snap.  Severe AR – collapsing pulse, wide pulse pressure, long decrescendo diastolic murmur, LV S3, soft A2, Austin Flint murmur, LVF. Causes  Chronic – rheumatic, congenital (bicuspid, VSD), Ankylosing spondylitis, aortic root dilatation (Marfan’s, CT disease, syphilis), dissecting aneurysm  Acute – valvular – endocarditis, aortic root – Marfan’s, dissecting aneurysm of aortic root.

Tricuspid stenosis TS is very rare valvular disorder in isolation usually a result of rheumatic heart disease. Murmur similar to MS except best heard on tricuspid area and louder on inspiration. TR and MS are usually associated d/t RHD. Abdominal examination may show presystolic liver pulsation.

Tricuspid regurgitation CV signs  JVP – large v waves and elevated if RVF present  Palpation – RV heave  Auscultation – pansystolic murmur maximal at tricuspid area, increases on inspiration, but diagnosis more likely on peripheral signs.  Abdomen – large pulsatile and tender liver usually present. Ascites, edema and pleural effusions may be present.  Legs – dilated veins

Causes  Functional in RVF  Rheumatic valve disease rarely affects TV alone usually associated MV disease present  Right sided endocarditis in IVDU  Tricuspid valve prolapse, RV papillary muscle infarction, blunt steering wheel trauma  Congenital – Ebstein’s anomaly

Pulmonary stenosis  General signs – peripheral cyanosis d/t low CO  Pulse – reduced d/t reduced CO  JVP – giant a waves d/t RA hypertrophy may be elevated.  Palpation – RV heave, thrill over pulmonary area.  Auscultation – ejection click, harsh, loud ejection systolic murmur best heard in pulmonic area, ↑ with inspiration or only heard then, and not radiating to carotids.  Abdomen – presystolic pulsation of liver may be present  Severe PS – signs of RVF and loud murmur with absence of click. Causes  Congenital  Carcinoid rarely

Pulmonary regurgitation  Rare clinical condition, rarely pathological primarily usually a result of PHT.

Hypertrophic cardiomyopathy There is abnormal hypertrophy in the LV or RV outflow tract or both. Obstruction occurs towards the end of systole when the hypertrophied area contracts. Systolic displacement of mitral valve into LV outflow tract also occurs → MR + further outflow obstruction. Different types may involve the mid-ventricle or apex.  Symptoms – dyspnea, angina, syncope or sudden death CV signs  Pulse – sharp rising and jerky  JVP – prominent a wave d/t forceful atrial contraction against a non-complaint RV  Palpation – double or triple apical impulse d/t presystolic expansion of the ventricle caused by atrial contraction.  Auscultation – systolic murmur at LSB and apex d/t obstruction of flow and a pansystolic murmur at apex d/t MR and S4.  Dynamic maneuvers - ↑with valsalva, standing, and by isotonic exercise; ↓with squatting and isometric exercise.  Causes – AD sarcomere or troponin gene mutation, idiopathic and Friedreich’s ataxia Dilated cardiomyopathy Cardiac muscle abnormality causing global reduction in cardiac function (CAD excluded by definition). The signs are those of CCF including MR/TR. Ventricular arrhythmias are common. Causes  Idiopathic and familial  Alcohol and drugs e.g. doxorubicin  Post-viral  Myotonic dystrophy  Hemochromatosis

Restrictive cardiomyopathy It causes signs similar to constrictive pericarditis with Kussmaul’s sign more common and palpable apex beat. Causes  Idiopathic  Endomyocaridal fibrosis, infiltrative disease (amyloid), granulomas (sarcoid)

Acyanotic congenital heart disease Ventricular septal disease (VSD) CV signs  Palpation – hyperkinetic displaced apex and thrill at LSB  Auscultation – harsh systolic murmur maximal and almost confined to lower LSB with S3, S4; louder on expiration. Murmur may be louder with smaller defects and viv. Causes  Congenital  Acquired – post AMI

Atrial septal defect (ASD)  Two main types – ostium secundum (90%) not involving the AV valve and ostium primum (10%) involving the AV valves. CV signs  Palpation – normal or RV enlargement  Auscultation – fixed splitting of S2, no murmurs directly but ↑flow through right side may produce a low- pitched diastolic tricuspid flow murmur and sometimes a pulmonary systolic ejection murmur, both louder on inspiration.  Ostium primum defects may be associated with MR/TR or other signs if VSD present.

Patent ductus arteriosus PDA is a persistent embryonic vessel connecting the aorta to the pulmonary artery. The shunt is usually from the aorta to the pulmonary artery unless PHT has occurred. CV signs  Pulse – collapsing pulse with rapid upstroke and low diastolic pressure d/t ejection of large volume of blood into empty aorta in systole and rapid decompression of the aorta.  Palpation – hyperkinetic apex beat  Auscultation – moderate sized shunt →single S2, significant sized shunt → reversed splitting of S2 d/t delayed A2 as a result of ↑load on LV. Continuous loud machinery murmur, maximal at 1st LICS and other flow murmurs may be heard. Coarctation of aorta This is a congenital narrowing of the aorta usually just distal to the origin of the left subclavian artery. There is an association with bicuspid aortic valve and Turner’s syndrome. CV signs  Upper body better developed than lower; radiofemoral delay with weak femoral pulses; HT in arms but not legs  Midsystolic murmur audible over precordium and back d/t blood flow across the coarct and the collateral chest vessels

Cyanotic congenital heart disease Causes  Eisenmenger’s syndrome – pulmonary HT and right to left shunt  Tetralogy of Fallot  Ebstein’s anomaly  Truncus arteriosus  Transposition of great vessels  Tricuspid atresia  Total anomalous pulmonary venous drainage

Tetralogy of Fallot Four features due to a single developmental anomaly: 1. Ventricular septal defect 2. RV outflow obstruction d/t pulmonic stenosis or infundibular level 3. Over-riding of aorta due to VSD → cyanosis 4. RV hypertrophy d/t outflow obstruction CV signs  Central cyanosis – without pulmonary HT d/t venous mixing at ventricular level, over-riding aorta receives both RV and LV blood  Clubbing and polycythemia  RV enlargement → LSB parasternal impulse; systolic thrill d/t pulmonary valve or RV outflow obstruction  Pulmonary ejection systolic murmur with normal S2  Repaired TOF with correction of RV outflow obstruction may leave severe PR leading to exertional dyspnea. Repair may also lead to arrhythmia due to RV damage from operative scars → palpitations and syncope.  Signs of repaired TOF – median sternotomy scar, long diastolic murmur of PR, RV enlargement and later signs of TR → giant v waves and pulsatile liver. The Neurological examination

Biographical information  Name, age, place of birth, handedness, occupation and level of education General examination  Level of consciousness  Examination for neck stiffness  Assessment of higher centres, speech and abnormal movements The cranial nerves  Cranial nerves II to XII Upper limbs  Motor system – inspection, tone, power, reflexes, coordination  Sensory system – pinprick, proprioception, vibration sense and light touch Lower limbs  As for upper limbs but including assessment of walking (gait) Skull and spine for local disease Carotid arteries for bruits

General signs  Consciousness – levels of consciousness – alert, verbally arousable, painful stimuli or unarousable  Neck stiffness – causes →infections of the meninges, cervical spondylosis, cervical fusion, Parkinson’s disease, raised ICP. Higher centres and speech  Handedness – 94% of right-handed and 50% of left-handed people have dominant left hemisphere. Dominant hemisphere controls language and mathematical function Orientation