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Cardiovascular Sciences

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Arrhythmias * Are common and often benign, but can indicate underlying heart disease. They often occur intermittently and so can be difficult to diagnose. * Can present with palpitations, chest pain, presyncope/syncope, hypotension, pulmonary oedema. Some are asymptomatic e.g. AF. * History taking make sure include: * Precipitating factors, onset, nature (fast/slow, regular/irregular), duration, associated symptoms (chest pain, dyspnoea, collapse). * Causes: * CARDIAC: * MI. * CAD. * LV aneurysm. * Mitral valve disease. * Cardiomyopathy. * Pericarditis. * Myocarditis. * Aberrant conduction pathways. * NON-CARDIAC: * Caffeine. * Smoking. * Alcohol. * Pneumonia. * Drugs (β2 agonist, digoxin, L-dopa, tricyclics). * Metabolic imbalance (K, Ca, Mg, hypoxia, hypercapnia, acidosis, thyroid disease, phaeochromocytoma). * Tests: * Bloods: FBC, U&E, glucose, Ca, Mg, TSH. * ECG: look for signs of IHD, AF, short P-R interval, long QT interval, U waves. * If ECG normal consider doing 24 hour tape. * Echo: look for structural heart disease. * Others: exercise ECG, cardiac catheterisation etc. * Types of Arrhythmias: * Bradycardias: * If asymptomatic and rate >40bpm then no treatment. * Look for cause and stop any drugs that may be the cause or contributing. * If rate <40bpm and patient’s symptomatic give atropine (consider external pacemaker). * Sick Sinus Syndrome: * SAN dysfunction – causing bradycardia with possible arrest; or SAN block; or superventricular tachycardia alternating with bradycardia/asystole. * Superventricular Tachycardia (aka Narrow Complex): * Narrow complex tachycardia (HR >100bpm, narrow QRS). * Acute management: vagotonic manoeuvres, IV adenosine/verapamil, DC shock if compromised. * Atrial Fibrillation: * Often incidental finding, but can present with chest pain, palpitations, dyspnoea or presyncope. * Atrial rhythm 300-600bpm (no P waves on ECG). * AVN responds intermittently causing irregular contraction of ventricles. * Risk of embolic stroke – give warfarin. * Common causes: * Heart failure. * HT. * Cardiac ischaemia. * MI. * Mitral valve disease. * Pneumonia. * Hyperthyroidism. * Alcohol. * O/E – pulse is irregularly irregular, first heart sounds is of variable intensity. * Investigations: * ECG – absent P waves, irregular QRS complexes. * Bloods: FBC, U&Es, cardiac enzymes. * Echo – look for LA enlargement, mitral valve disease, poor LV function and other structural abnormalities. * Control ventricular rate with digoxin. * Maintenance: digoxin, verapamil, β-blocker or amiodarone. * Atrial Flutter = continuous atrial depolarisation producing a ‘saw-tooth’ appearance on the ECG (possibly with 2:1 block). Carotid sinus massage transiently blocks the AVN and so can unmask flutter waves. Try AF treatment or consider ablation if unsuccessful. * Ventricular Tachycardia: * Broad complex tachycardia (HR >100bpm, widened QRS). * Acute management = IV lignocaine/amiodarone. DC shock if compromised. * Wolf Parkinson White: * Caused by congenital accessory conduction pathway between atria and ventricles. * Resting ECG: * Short P-R interval. * Widened QRS – slurred upstroke a ‘delta’ wave. * 2 types of WPW: 1. WPW type A = positive delta wave in V1. 2. WPW type B = negative delta wave in V1. * Present with superventricular tachycardia.
Infective endocarditis
Infective Endocarditis:

Fever (of unknown origin) and new murmur = infective endocarditis until proven otherwise. * Classification: * Normal valves – infection presents acutely with heart failure (tricuspid valve is usually involved). * Abnormal valves – subacute course. Patient will have an abnormal valve e.g. aortic or mitral disease. * Causes: * Bacteria: * Streptococcus viridans – lives in the mouth (think about recent dental work). * Staphylococcus aureus/epidermis – found on the skin (think about IV drug use). * UTI, urinary catheterization, cystoscopy, IV cannulation can increase the risk of infective endocarditis. * Often no cause is found. * Clinical Features: * Signs of infection: * Fever (of unknown origin)/rigors/night sweats. * Malaise/weight loss. * Anaemia. * Clubbing. * Splenomegaly. * Cardiac lesions: * New murmur or change in a pre-existing murmur. * Immune complex deposition: * Vasculitis. * Microscopic haematuria. * Roth spots (retinal haemorrhages). * Splinter haemorrhages. * Osler’s nodes (painful pulp infarcts in fingers or toes). * Janeway lesions (painless palmar or plantar macules). * Diagnosis: * Duke criteria: (need 2 major OR 1major and 3 minors OR 5 minor). * MAJOR CRITERIA: * Positive blood culture – typical organism in 2 cultures. * Endocardium involvement – positive ECHO (vegetation, abscess etc.) or new valvular regurgitation. * MINOR CRITERIA: * Predisposition (cardiac lesion, IV drug use). * Fever >38deg. * Vascular/immunological signs. * Positive blood culture – doesn’t meet major criteria. * Positive ECHO that doesn’t meet major criteria. * Treatment = Antibiotics.
Hypertension
Hypertension:

* Is a risk factor for stroke and MI. * Difficult to define a high BP, but need to treat those with a BP >160/100mmHg; consider treating those with a BP >140/90mmHg if they’ve a risk of coronary events, have diabetes or signs of end organ damage. * ‘Malignant HT’: * Severe HT (>200/130mmHg). * Bilateral retinal haemorrhages and exudates. May see papilloedema. * Patients often have symptoms e.g. visual disturbances/headaches. * Need to find underlying cause e.g. phaeochromocytoma. * Management: * Controlled reduction of BP over days (NOT hours). * Need to avoid sudden drops in BP as cerebral autoregulation is poor and so stroke risk can be increased. * Bed rest, start loop diuretic ± thiazide. * Causes: * Essential HT: * Primary HT – cause unknown. * Accounts for 95% of cases. * Secondary HT: * Accounts for 5% of cases. * Causes include: * Renal disease e.g. glomerulonephritis, polyarteritis nodosa, polycystic kidneys, renovascular disease. * Endocrine e.g. Cushing’s, Conn’s, phaeochromocytoma, acromegaly, hyperparathyroidism. * Others – coarctation, pregnancy, steroids, MAOI, contraceptive pill. * Signs and Symptoms: * Usually asymptomatic unless malignant. * Always examine CVS and check for retinopathy. * Look for causes of secondary hypertension e.g. Cushing’s etc. * Look for end organ damage e.g. LV hypertrophy, retinopathy and proteinuria. * Long standing HT may cause proteinuria, added heart sounds (S4), heave/bruits and LVH. * Investigations: * Bloods: * FBC. * U&Es. * Creatinine. * Cholesterol. * Glucose. * Urine analysis. * ECG. * Specific tests for primary cause if secondary hypertension. * Treatment: * Lifestyle changes. * Drugs (remember ABCD): * Thiazide diuretics – first choice. * β-blockers – contraindicated in asthmatics and diabetics. * ACE-i – can be first choice in diabetics with microalbuminuria/proteinuria; or those with LVH. Contraindicated in renal artery stenosis and aortic stenosis. * Ca-channel antagonists.

Valve disease

* First heart sound (S1): * Represents closure of mitral and tricuspid valves. * Second heart sound (S2): * Represents closure of aortic and pulmonary valves. * Can be physiologically split on breathing. * Third heart sound (S3): * Rare. * Occurs after S2 – is low pitched and best heard with the bell. * Is pathological over the age of 30 years. * Occurs in a dilated left ventricle causing rapid ventricular filling (mitral regurgitation or VSD); or poor LV function (post-MI or dilated cardiomyopathy). * When auscultating think ‘Kentucky’ for the rhythm. * Fourth heart sound (S4): * Occurs just before S1. * Always pathological – represents atrial contraction against a stiff, non-compliant ventricle. * Several cause e.g. hypertensive heart disease, aortic stenosis. * When auscultating thing ‘Tennessee’ for the rhythm.

Cardiac murmurs
Consider any murmur in terms of character, timing, loudness, area where loudest, radiation and accentuating manoeuvres.
When in doubt, rely on echocardiography.

* Character and Timing: * There are four types of murmur: 1. Ejection systolic: a. Crescendo-decrescendo in nature. b. Common in children and high output states (tachycardia, pregnancy). c. Causes = aortic stenosis, aortic sclerosis, pulmonary stenosis and hypertrophic cardiomyopathy. 2. Pansystolic: d. Uniform intensity and merges with S2. e. Occurs in mitral or tricuspid regurgitation or VSD. 3. Early diastolic: f. High pitched. g. Usually indicates aortic regurgitation (rarely occurs in pulmonary regurgitation). 4. Mid-diastolic: h. Low pitched and rumbling. i. Occurs in mitral stenosis, rheumatic fever and aortic regurgitation. * Intensity: * Graded as so: * 1 = very soft, only heard after listening for a while. * 2 = soft, but detectable immediately. * 3 = clearly audible, no palpable thrill. * 4 = clearly audible, palpable thrill. * 5 = audible with stethoscope partially touching the skin. * 6 = can be heard without placing a stethoscope on the skin. * Systolic murmurs are louder than diastolic (only graded 1-4).

* Area where loudest: * Mitral murmurs tend to be louder over the apex and radiating into the axila. * Aortic murmurs = right 2nd intercostal space. * Pulmonary murmurs = left 2nd intercostal space. * Tricuspid murmurs = left sternal edge. * Radiation: * Aortic stenosis classically radiates to the carotids. * Mitral regurgitation classically radiates to the axilla. * Accentuating manoeuvres: * Leaning forward – aortic regurgitation. * Leaning to left lateral position – mitral stenosis. * Expiration – left sided murmurs. * Inspiration – right sided murmurs.

Common Heart Murmurs:

Aortic Stenosis: * Causes: * Senile dysfunction is the commonest, can also be congenital (bicuspid valve, William’s syndrome). * Symptoms: * Angina. * Dyspnoea. * Syncope/faints. * Systemic emboli if infective endocarditis. * Congestive cardiac failure. * Signs: * Slow rising pulse with narrow pulse pressure (feel for diminished and delayed carotid upstroke). * Heaving, un-displaced apex beat. * LV heave. * Aortic thrill. * On auscultation: * Ejection systolic murmur – heard best in the right 2nd intercostal space. * As stenosis worsens – A2 is increasingly delayed. Commonly a quiet S2 is heard. * Tests: * ECG – look for LV hypertrophy with strain pattern, left anterior hemiblock, poor R wave progression, LBBB or complete AV block. * CXR – LV hypertrophy, calcified aortic valve, post-stenotic dilation of ascending aorta. * Echo – diagnostic. * Don’t forget differential is hypertrophic cardiomyopathy. * Management: * Symptomatic patients have a poor prognosis. * Prompt valve replacement.

Aortic sclerosis is senile degeneration of the valve. There is an ejection systolic murmur, no carotid radiation, and normal pulse (character and volume) and S2

Aortic Regurgitation:

* Causes: * Congenital, rheumatic fever, infective endocarditis, rheumatoid arthritis, SLE. * Aortic root disease caused by: hypertension, trauma, aortic dissection, seronegative arthritic conditions (ankylosing spondylitis etc), Marfan’s etc. * Symptoms: * Dyspnoea. * Palpitations. * Cardiac failure. * Signs: * Collapsing pulse with wide pulse pressure. * Displaced hyper-dynamic apex beat. * On auscultation: * High pitched early diastolic murmur – heard best in expiration with patient sitting forward. * Associated signs: * Corrigan’s sign – carotid pulsation. * de Musset’s sign – head nodding. * Quincke’s sign – capillary pulsations in nail beds. * Duroziez’s sign – femoral diastolic murmur as blood flows backwards in diastole. * Traube’s sign – pistol shot sound over femoral arteries. * In severe aortic stenosis may hear an Austin flint murmur. * Tests: * ECG – look for LV hypertrophy. * CXR – cardiomegaly, dilated ascending aorta, pulmonary oedema. * Echo – diagnostic. * Management: * Surgery – if increasing symptoms, cardiac enlargement, ECG deterioration (T wave inversion in lateral leads).

Mitral Stenosis:

* Causes: * Rheumatic, congenital, malignant carcinoid, prosthetic valve. * Symptoms: * Dyspnoea. * Fatigue. * Palpitations. * Chest pain. * Systemic emboli. * Haemoptysis. * Signs: * Malar flush. * Low-volume pulse. * AF is common. * Tapping un-displaced apex beat (palpable S1). * On auscultation: * Loud S1. * Opening snap. * Rumbling mid-diastolic murmur (heard best in expiration with the patient lying on their left side). * Possible Graham Steell murmur. * If more severe – longer diastolic murmur and the opening snap is closer to S2. * Tests: * ECG – look for AF, RVH, progressive right axis deviation. * CXR – LA enlargement, pulmonary oedema, mitral valve calcification. * Echo – diagnostic. * Management: * AF – digoxin (need control rate <90bpm, use beta-blocker if digoxin not enough). * Anticoagulate – warfarin. * Diuretic to decreased preload/pulmonary venous congestion. * Complications: * Pulmonary hypertension. * Emboli. * Pressure from large LA on local structures e.g. left recurrent laryngeal nerve causing hoarseness, bronchial constriction.

Mitral Regurgitation:

* Causes: * Functional (LV dilation), annular calcification (elderly), rheumatic fever, infective endocarditis, mitral valve prolapse, ruptured chordae tendinae, papillary muscle dysfunction/rupture, connective tissue disorders, cardiomyopathy, congenital. * Symptoms: * Dyspnoea. * Fatigue. * Palpitations. * Infective endocarditis. * Signs: * AF. * Displaced hyper-dynamic apex. * RV heave. * On auscultation: * Soft S1. * Split S2 – loud P2 (pulmonary hypertension). * Pansystolic murmur at apex radiating to axilla. * The more severe, the larger the LV. * Tests: * ECG – look for AF, LV hypertrophy. * CXR – enlarged LA and LV, mitral valve calcification, pulmonary oedema. * Echo – assess LV function. * Management: * If fast AF – digoxin. * Anticoagulation if: fast AF; history of embolism; prosthetic valve; additional mitral stenosis. * Diuretics improve symptoms. * Surgery if no improvement.

Mitral valve prolapse aka Barlow syndrome aka click murmur syndrome
The most common valvular abnormality
A mid-systolic click followed by a late systolic murmur is heard at the apex as the thickened mitral valve leaflet is displaced into the left atrium during systole.

Austin flint murmur
A low pitched, mid-diastolic rumble at the apex, classically MV displacement as well as aortic turbulence due to regurg = Austin flint murmur. It occurs in severe aortic regurgitation. It is due to the fluttering of the anterior mitral valve cusp caused by regurgitant flow

Constant machinery murmur
Produced by a patent ductus arteriosus. Patient is clubbed and cyanosed

Graham Steell murmur
Heard best at the left sternal edge, second intercostal space during inspiration. High pitched early diastolic murmur plus pulmonary hypertension. It is caused by pulmonary regurgitation which is secondary to pulmonary hypertension, which is caused by mitral stenosis.
Carey Coombs murmur
A short, mid-diastolic rumble heard best at the apex due to turbulent blood flow over a thickened mitral valve, most often due to rheumatic fever. Due to thickened mitral valve leaflets.

Ventricular septal defect
Harsh pan-systolic murmur loudest at lower left sternal edge. Inaudible at the apex. Apex is not displaced

Atrial septal defect
Fixed splitting of the second heart sound
Aortic aneurysm * True aneurysms – abnormal dilations of arteries. * False aneurysms – collections of blood around the vessel wall, can occur after trauma. * Common sites: * Aorta. * Iliac. * Femoral. * Popliteal. * Usual cause = atheroma, but can be caused by connective tissue disorders (Marfan’s, Ehler-Danlos) and infections (endocarditis, tertiary syphilis). * Thoracic Aorta Dissection: * Blood causes a splitting of the aortic media – causing sudden tearing chest pain that radiates to the back. * As the dissection progresses branches of the aorta become occluded giving rise to specific symptoms depending on the branch. For example: hemiplegia (carotid), unequal arm pulses/BP (arch), paraplegia (anterior spinal artery) and anuria (renal). * Ruptured AAA: * Signs/symptoms: * Intermittent or continuous abdominal pain, can radiate to the back, iliac fossae or groin. * Collapse. * Expansile abdominal mass. * Unruptured AAA: * Often symptomless, but can cause abdominal/back pain. * Needs monitoring to measure diameter.

Stroke: * Types – ischaemic or haemorrhagic. * Causes: * Thrombosis-in-situ. * Heart emboli (AF, MI). * Atherothrombolism e.g. from carotids. * CNS bleed (Increased BP, trauma, aneurysm rupture). * Risk factors: * Increased BP. * Smoking. * Diabetes. * Heart disease (valvular, ischaemic, AF). * PVD. * Past TIA. * The contraceptive pill in those who smoke. * Excess alcohol. * Clotting abnormalities e.g. increased plasma fibrinogen. * Signs: * Sudden onset, or step-wise progression over hours. Signs depend on area affected. * Cerebral hemisphere infarcts: * Contralateral hemiplegia - initially flaccid, but becomes spastic (is an UMN lesion). * Contralateral sensory loss. * Homonymous hemianopia. * Dysphasia. * Brainstem infarct: * Wide range of effects including quadriplegia, disturbances of gaze/vision and locked in syndrome. * Lacunar infarct: * Small infarcts around the basal ganglia, internal capsule thalamus and pons. * Can cause pure motor, pure sensory, mixed motor/sensory signs; or ataxia. * Have intact cognition and consciousness. * Investigations: * Look for: * Long-standing hypertension – retinopathy, enlarged heart on CXR. BP is often raised, acutely, in early stroke. * Cardiac source of emboli: * AF – look at ECG, CXR, echo. * Post-MI – mural thrombus best seen on echo. * Carotid artery stenosis. * Hypoglycaemia, hyperglycaemia and hyperlipidaemia. * Giant cell arteritis e.g. is ESR is increased (treat with steroids). * Syphilis. * Thrombocytopenia, polycythaemia and other bleeding disorders. * To do: * Pulse and BP. * Bloods – FBC, U&Es, clotting, ESR, lipids, glucose. * ECG, carotid doppler, consider echo. * Imaging – CXR, CT head. * Differentials: * CNS tumour. * Subdural bleed. * Migraine. * Hypoglycaemia. * Possible drug overdose.

It’s very difficult to clinically distinguish between haemorrhagic and ischaemic strokes. But pointers to haemorrhagic strokes = meningism, severe headache and coma within hours. Pointers to ischaemic strokes = carotid bruit, AF, past TIA.
Peripheral vascular disease
Limb Embolism and Ischaemia:

Chronic ischaemia:

* Always due to atherosclerosis. * Main feature is intermittent claudication, which is a cramping pain in the calf, thigh or buttock after walking. * Critical ischaemia: * Ulceration. * Gangrene. * Foot pain at rest (often a burning pain at night relieved by hanging the leg out of the bed). * Signs: * Absent pulses. * Cold, white leg. * Atrophic skin. * Punched out ulcers – often painful. * Postural colour change. * REMEMBER the 6 P’s: * Pain. * Pallor. * Paraesthesia. * Paralysis. * Pulselessness. * Perishing with cold. * Tests: * Are they diabetic? Good control? * Look for arteritis – measure ESR and CRP. * FBC – look for anaemia and infection. * U&Es – check renal function. * Lipids – dyslipidaemia? * Syphilis serology. * Clotting/group and save if operating. * ECG – cardiac ischaemia? * Ankle-brachial pressure index (Doppler) – normal is 1, claudication 0.9-0.6, rest pain is 0.3-0.6, impending gangrene is <0.3. * Do a duplex to assess extent and location of stenosis and quality of distal vessels (‘run off’). * Management: * Conservative treatments – stop smoking, lose weight, increase exercise, treat pre-existing conditions e.g. diabetes, hypertension and hyperlipidaemia. * Surgical treatments: * Percutaneous transluminal angioplasty – for short stenoses in large arteries. Inflate a balloon and leave a stent to maintain patency. * Amputation – may relieve intractable pain and prevent death from sepsis/gangrene.

Acute ischaemia:

* Causes: thrombosis in-situ, emboli, graft/angioplasty occlusion or trauma. * Signs/symptoms: * 6 P’s: * Pain. * Pallor. * Paraesthesia. * Paralysis. * Pulselessness. * Perishing with cold. * Fixed mottling implies irreversibility. * Emboli commonly arise from the heart (infarcts, AF) or an aneurysm (aorta, femoral or popliteal). * Management: * Is an emergency – may require urgent surgery. * Anticoagulate with heparin.

Deep vein thrombosis
Deep Vein Thrombosis (DVT):

* Differentials diagnoses – cellulitis (can co-exist), ruptured Baker’s cyst (can also co-exist). * 10 Questions to ask a patient with swollen legs: 1. Are both legs affected? 2. Are they pregnant? 3. Are they mobile? 4. Any recent trauma? 5. Any pitting? 6. Any pain? 7. Any skin changes? 8. Any oedema elsewhere? 9. Any past history of DVT, cellulitis? 10. What drugs are they on? * Risk factors: * Old age. * Pregnancy. * Synthetic oestrogen (contraceptive pill). * Surgery (especially pelvic/orthopaedic). * Previous DVT. * Malignancy. * Obesity. * Immobility. * Thrombophilia. * Pretest Clinical Probability Scoring for DVT: * Active cancer (1pt). * Paralysis, paresis or recent plaster immobilisation of leg (1pt). * Major surgery or recently bed-ridden for >3days in last 4weeks (1pt). * Local tenderness along distribution of deep venous system (1pt). * Entire leg swollen (1pt). * Calf swelling >3cm compared to asymptomatic leg (measure 10cm below tibial tuberosity) (1pt). * Pitting oedema – most noticeable in affected leg (1pt). * Collateral superficial veins (non-varicose) (1pt). * Alternative diagnosis as likely or more likely than that of DVT (-2pts). * Signs: * Calf may be warm, tender or swollen. * Mild fever. * Pitting oedema (Homans’ sign – increased resistance/pain on forced foot dorsiflexion – DON’T perform as it may dislodge the thrombus). * Investigations: * Bloods – FBE, U&Es, CRP, clotting, D-dimer. * D-dimer is sensitive but not specific for DVT as it can be raised in infection, pregnancy, malignancy and post-operatively. * A negative D-dimer in someone with few risk factors can rule out DVT. * Ultrasound scan. * Prevention: * If having surgery: * Stop contraceptive pill 4 weeks pre-op. * Mobilise early. * Heparin infusion. * TED stockings. * Treatment: * Heparin (LMWH) and warfarin. * Stop heparin when INR is 2-3.

Pulmonary Embolism * Causes: * Usually arise from a venous thrombosis in the legs or pelvis. * Rare causes: * Right ventricular thrombus (post-MI). * Septic emboli (right-sided endocarditis). * Fat. * Air. * Risk factors (Any cause of immobility or hypercoagulability): * Recent surgery. * Recent stroke or MI. * Disseminated malignancy. * Thrombophilia (antiphospholipid syndrome). * Prolonged bed rest. * Pregnancy; post-partum; the pill; HRT. * ALWAYS ASK ABOUT RISK FACTORS and FAMILY HISTORY! * Symptoms: * Acute breathlessness. * Pleuritic chest pain. * Haemoptysis. * Dizziness/syncope. * Signs: * Pyrexia. * Cyanosis. * Tachypnoea. * Tachycardia. * Hypotension. * Raised JVP. * Pleural rub/pleural effusion. * LOOK for signs of cause e.g. swollen leg, recent surgery. * Investigations: * CXR – often normal; can show dilated pulmonary artery, linear atelectasis, diminished vascular markings. * ECG – may be normal, or show tachycardia, RBBB. * ABG – may show low PaO2 and PaCO2, increased pH. * Bloods – U&Es, FBC, clotting, D-dimer. * V/Q scan or CTPA (V/Q less radiation). * Management: * Anticoagulate with low molecular weight heparin (e.g. dalteparin) and start warfarin. * Stop heparin when INR >2, but continue warfarin for 3 months (aim for INR 2-3). * Prevention: * Give heparin to all immobile patients. * Prescribe TED stockings – encourage early mobilization. * Women to stop HRT and the pill pre-operatively. * Patients with a family history of thromboembolism should be investigated for thrombophilia.

Varicose veins
Varicose Veins:

* Cause: * Incompetent valves between the deep and superficial veins. * Therefore allowing backflow of blood from deep veins back into the superficial veins. * Incompetent valves can be caused by: * Venous hypertension: * Prolonged standing. * Pregnancy – occlusion by the fetus. * Ovarian tumour. * Previous DVT. * Symptoms: * Patient complaining of ‘ugly legs’. * May also mention: * Pain. * Cramps. * Tingling. * Heaviness and tingling legs. * Signs: * Oedema. * Eczema. * Ulcers. * Haemosiderin skin staining. * Haemorrhage. * Phlebitis. * Method of Examination: (Start with patient standing) 1. Any signs of poor skin nutrition, ulcers? Inspect the legs from anterior thigh to medial calf (long saphenous); and back of the calf (short saphenous). Palpate veins for tenderness and hardness. 2. Feel for cough impulse at the sapheno-femoral junction – if present indicates incompetence. The percussion test: tap the top of a vein and feel how far down its length you can feel the repercussions (valves prevent transmission). 3. Doppler ultrasound – listen to flow in incompetent valves. * Saphena varix: * A dilation in the saphenous vein at its confluence with the femoral vein. * One of the many causes of a lump in the groin. * It can be mistaken for an inguinal/femoral hernia due to its cough impulse. But, on closer inspection, it may have a bluish tinge and it disappears when the patient lies down.

Cardiac arrest

* Do not stop CPR for >10s except to defibrillate. * Shockable rhythm – give amiodarone 300mg IV with first dose of adrenaline. Alternatives for amiodarone are lidocaine or procainamide. * Asystole/PEA – give adrenaline 1mg immediately, if there are P waves – may need pacing. * Treat acidosis with good ventilation, sodium bicarbonate may worsen intracellular acidosis and precipitate arrhythmias so only use in severe acidosis.

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