Cardio Conditions Flashcards
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1
Q
Abdominal Aortic Aneurysm
- Define
- Explain aetiology
- Explain the risk factors
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
A
- Localised enlargement of abdo aorta -> diameter >3cm or >50% normal diameter
- No specific identifiable causes.
- RF:
- Severe atherosclerotic damage to aortic wall
- FHx
- Smoking
- Male
- Age
- HTN
- Hyperlipidaemia
- Connective tissue disorders (Marfan’s)
- Inflammatory disorders (Behcet’s disease)
- Unruptured: No Syx, may have pain in groin/abdo/loin/back.
- Ruptured: Pain in abdo/back/loin, sudden or severe, syncope, shock
- Pulsatile, Lat expanding mass on bimanual palpitation of AA; abdo bruit; retriperitoneal haemorrhage = Grey-Turner’s sign
- Bloods -> FBC, clotting screen, renal/liver function and cross match if surgery planned; US to detect AAA, CT with contrast for rupture check, MRI angiography
2
Q
Aortic Regurgitation
- Define
- Explain aetiology
- Explain risk factors (joined with 2)
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
A
- Reflux of blood from the aorta into the LV during diastole, resulting in LV dilataton, so increased EDV and Increased SV, explaining high vol collapsing pulse
- Aortic valve leaflet abnormalities/damage:
- Bicuspid aortic valve
- Inf endocarditis
- Rheumatic Fever
- Trauma
- Aortic root/Asc. aorta dilatation:
- Systemic HTN
- Aortic dissection
- Aortitis
- Arthritides
- Connx tussue disease
- Pseudoxanthoma elasticum
- Osteogenesis imperfecta
- Chronic AR in late 50s; most frequent in >80s
- Syx related to aetiology
- Chronic: asymptomatic then pts develop HF Syx (exertional dyspnoea, orthopnoea, fatigue)
- Severe acute: sudden cardiovascular collapse
- Signs:
- Collapsing pulse
- Wide PP
- Thrusting/heaving displaced apex beat
- Early diastolic murmur
- Austin-Flint mid diastolic murmur (over apex)
- RARE Sx: Quincke (pulse nail bed), de Musset (nodding in time with pulse), Becker (pulse of retinal arteries and pupils), Muller (uvula pulse), Corrigan (pulse in neck), Traube (pistol shot on femoral artery), Duroziez (sys/dias bruit on femoral artery ausc.), Rosenbach (sys pulse of liver), Gerhard (sys pulse of spleen), Hill (popliteal cuff BP sys >60mmHg cf brachial)
- CXR (cardiomegaly, dilatation of asc aorta, sx of Pulm oedema), ECG (LV hypertrophy: deep S in V1/2, Tall R in V5/6, inverted T in I/aVL/V5/6, L axis dev), EchoCG (underlying path, monitor progression and see size), Cardiac catheter with angiography
3
Q
Aortic Dissection
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
A
- Condition where a tear in the aortic intima allows blood to surge into aortic wall, causing a split between the inner and outer tunica media, creating a false lumen. -> Type A = Ascending aorta, Type B = Descending aorta (distal to L SCA)
- Preceded by degen changes in smooth muscle of aortic media. RF/causes:
- HTN
- Aortic atherosclerosis
- Connx tissue disease
- Congenital cardiac abnormalities
- Aortitis
- Iatrogenic
- Trauma
- Cocaine
- (Can obstruct subclavian, carotid, coeliac and renal arteries leading to hypoperfusion)
- Most common in males 40-60y
- MAIN SYX: Sudden central tearing pain, may radiate to back between shoulder blades; other syx caused by obstruction of branches of aorta
- Carotid -> hemiparesis, dysphasia, blackout
- Coronary -> chest pain
- Subclavian -> ataxia, loss of consciousness
- Ant spinal -> paraplegia
- Coeliac axis -> severe abdo pain
- Renal -> anuria, renal failure
- Sx
- Murmur on back, desc to abdo
- HTN
- BP difference between arms >20mmHg
- Wide PP
- Hypotension =? tamponade
- Check for pulsus paradoxus (large decrease in sys BP during inspiration, indicating: Tamponade, pericarditis, chronic sleep apnoea, obstructive lung disease)
- Bloods: FBC, X match 10u of blood, U&E, clotting screen; CXR (widened mediastinum), ECG (normal unless LV hypertrophy/ inf MI signs), CT thorax, EchoCG, Cardiac cath and aortography
4
Q
Aortic Stenosis
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
A
- Narrowing of LV outflow at the level of the aortic valve
- 2ry to Rheumatic heart disease (Most common worldwide); calcification of congenital bicuspid aortic valve; calcification/degeneration of tricuspid valve in elderly
- Present in 3% of 75yr old; most in males and bicuspid aortic valve present earlier
- Initially asymptomatic, angina, syncope/dizziness on exercise and Syx of HF
- Narrow PP
- Slow rising pulse
- Thrill in aortic area
- Forceful sustained thrusting undiscplaced apex
- Ejection sys murmur, radiating to carotid artery
- 2nd heart sound may be softened or absent
- Bicuspid may produce ejection click
- ECG: LV hypertrophy shown (deep S in V1/2, tall R in V5/6, inverted T in 1/aVL/V5/6, L axis deviation) and LBBB; CXR (post-sternotic enlargement of asc aorta, calcification of aortic valve); EchoCG (assesses LV function); cardiac angiography (DDx from angina/MI
5
Q
Arterial Ulcer
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
A
- Localised area of damage and breakdown of skin due to inadequate arterial supply -> seen on feet of pts with severe atheromatous narrowing of leg arteries
- Caused by lack of blood flow to capillary beds of the lower extremities
- CHD
- Hx of stroke/TIA
- DM (!!!!)
- Peripheral arterial disease
- Obesity/immobility
- 22% of leg ucers and prevalence increases with age and obesity
- Distal -> dorsum of foot/between toes; punched out, often elliptical with clearly defined edges; base has grey, granulation tissue; NIGHT PAIN!
- Punched out appearance, hairlessness, pale skin, absent pulses, nail dystrophy, wasting of calf muscles
- Duplex US of lower limbs, ankle-brachial pressure index, percutaneous angiography, ECG, Fasting serum lipids/blood glucose and HbA1c, FBC
6
Q
Atrial fibrillation
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
- Generate Management (Mx) plan
- Identify possible complications
- Summarise prognosis
A
- Rapid, chaotic and ineffective atrial electrical conduction -> permanent, persistent and paroxysmal
- May be no identifiable cause, or 2ry causes lead to abnormal atrial electrical pathway, eg:
- Systemic: thyrotoxicosis, HTN, pneumonia, alcohol
- Heart: Mitral valve/Ischaemic heart/Rheumatic heart disease, cardiomyopathy, pericarditis, sick sinus syndrome, atrial myxoma
- Lung: Bronchial carcinoma and PE
- VERY common in elderly, may be paroxysmal
- Often asyx, palpitations, syncope, Syx of cause
- Irregularly irregular pulse, difference in apical beat vs radial pulse, check for thyroid/valvular disease
- ECG (uneven baseline, absent p waves, irreg intervals between QRS; atrial flutter = saw toothed appearance); Bloods (cardiac enzymes, TFT, lipid profile, U&E/Mg2+/Ca2+); EchoCG (mitral valve disease, left atrial dilatation, left ventricular dysfunction, structural abnormalities)
- Treat any reversible causes, then rhythm control and rate control:
- Rhythm: >48h onset = anticoagulate for 3-4wks before cardioversion; if <48h = cardioversion, chemical cardioversion (flecainide/amiodarone), contraindicated if IHD Hx; prophylaxis against AF = sotalol, amiodarone and flecainide
- Rate: Chronic = digoxin, verapamil, beta-blockers aiming for ventricular rate of 90
- Stroke risk stratification: Low risk can use aspirin; high risk require warfarin => based on CHADS-Vasc score, RF = previous thromboembolic event, >75yrs, HTN, DM, Vascular/Valvular disease, HF, impaired LV function
- Thromboembolism -> risk increased with left atrial enlargement/LV dysfunction; worsening of HF
- Chronic AF in a diseased heart doesn’t usually return to sinus rhythm
7
Q
Cardiac Arrest
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
- Generate a management plan
- Complications
- Prognosis
A
- Acute cessation of cardiac function
- REVERSIBLE causes: 4H and 4T
- Hypothermia, hypoxia, hypovolaemia, hypo/erkalaemia
- Toxin (other metabolic disorders), thromboembolic tamponade, tension pneumothorax
- N/A
- Sudden -> may be preceded by fatigue, fainting, blackouts, dizziness, vomiting aand chest pain
- Unconscious, not breathing, absent carotid pulses
- Cardiac monitor, bloods -> ABG, U&E, FBC, Xmatch, clotting, toxicology screen and blood glucose
- BLS, ALS (cardiac monitor and defib, assess rhythm = if pulseless V-tachy/V-fib then defib once, resume CPR and then shock again if still in pulseless V-T/V-F, admin adrenaline 1mg IV (after 2nd and every 3-5min) and if shockable rhythm persists after 3rd shock then amiodarone IV bolus 300mg; if puseless electrical activity/asystole then CPR for 2, reassess and admin adrenaline (1mg IV every 3-5min), atropine (3mg IV once) if asystole/PEA with 60bpm), Tx of reversible causes (warm hypothermia slowly, correction of electrolyte levels for hypo/erK, hypovol use IV colloids/crystalloids and blood products, tamponade = pericardiocentesis, tenion pneumothorax = aspiration/chest drain, TE = treat as PE/MI, toxins = antidote
- Irreversible brain damage due to hypoxia, death
- Resus is less successful if arrest happens outside hospital; increased duraton of inadequate/effective CO = poor prognosis
8
Q
Cardiac failure
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
- Generate managment plan
- ID complications
- Summarise prognosis
A
- Inability of the CO to meet the body’s demands despite normal venous pressure
- 2 types:
- Low output (reduced CO):
- LHF: IHD, HTN, cardiomyopathy, aortic valve diseases, mitral regurg
- RHF: 2ry to LHF (called congestive cardiac failure), infarction, cardiomyopathy, pulm HTN/embolus/valve disease, chronic lung disease, tricuspid regurg, constrictive pericarditis/pericardial tamponade
- Biventricular failure: arrhythmia, cardiomyopathy (dilated/restrictive), myocarditis, drug toxicity
- High output (increased demand): anaemia, beri beri, pregnancy, paget’s, hyperthyroidism, arteriovenous malformation
- Low output (reduced CO):
- 10% >65yr
- Syx:
- LHF: caused by pulm congestions -> dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, fatigue
- Acute LVF: dyspnoea, wheeze, cough, pink frothy sputum
- RHF: ankle oedema, fatigue, weight gain (oedema). reduced exercise tolerance, anorexia, nausea
- Sx
- LHF: tachycardia/pnoea, displaced apex beat, bilat basal crackles, s3 gallop (rapid ventricular filling), pansystolic murmur (functional mitral regurg)
- ALVF: tachypnoea/cardia, cyanosis, peripheral shut down, pulsus aternans (LV systolic impairment), s3 gallop, wheeze (cardiac asthma), fine crackles through lung
- RHF: raised JVP, hepatomegaly, ascites, ankle/sacral pitting oedema, Sx of functional tricuspid regurg
- Bloods -> FBC, U&E, LFT, CRP, Glucose, lipids, TFT, (ALVF: ABG, BNP^ and troponin); CXR -> Alveolar shadowing, Kerley B lines, _C_ardiomegaly, upper lobe _D_iversion, pleural _E_ffusion; ECG -> normal?, ischaemic changes or arrhythmia/LV hypertrophy; EchoCG -> assess ventricular contraction, sys function = LV ejection fraction <40%, diastolic = restrictive filling defect; swan-ganz catheter = measurement of right atrial, right ventricle, pulm artery/wedge and LV end-diastolic pressures
- For cardiac failure:
- ALVF:
- Tx of cardiogenic shock (severe CF with low BP) = inotropes (dobutamine)
- Tx of pulm oedema = sit up, 60-100% O2 (?CPAP), diamorphine (venodilator and anxiolytic), GTN infusion (venod), IV furosemide (venod and diuretic) -> monitor BP, RR, O2 sats, urine output and ECG
- Chronic LVF:
- Treat cause and exacerbating factors
- ACEi, beta blockers, loop diuretics, aldosterone antagonists, Ang receptor blockers, (hydralazine and nitrate), digoxin, N-3 polyunsat Fatty acids, cardiac resynch therapy (biventricular pacing and elegible for cardiac defib implanted)
- ALVF:
- Resp failure, cardiogenic shock and death
- 50% with cardiac failure die within 2yrs
9
Q
Cardiomyopathy
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
A
- Primary disease of myocardium -> dilated, hypertrophic or restrictive
- Majority idiopathic.
- Dilated: post-viral myocarditis, alcohol, drugs (cocaine, doxorubicin), familial, thyrotoxicosis, haemochromatosis, peripartum
- Hypertrophic: 50% are genetic
- Restrictive: amyloidosis, sarcoidosis, haemochromatosis
- Dilated/hypertrophic = 0.05-0.2%, restrictive is rarer
- Syx:
- Dilated: Syx of HF, arrhythmias, thromboembolism, FHx of sudden death
- Hypertrophic: No syx, syncope, angina, arrhythmias, FHx of sudden death
- Restrictive: Dypnoea, fatigue, arrhythmia, ankle/abdo swelling, FHx of sudden death
- Sx:
- Dilated: Raised JVP, displaced apex beat, functional mitral and tricuspid regurg, S3
- Hypertrophic: jerky carotid pulse, double apex beat, ejection systolic murmur
- Restrictive: raised JVP (Kussmaul sign), palpable apex beat, s3, ascites, ankle oedema, hepatomegaly
- CXR, ECG (ST changes, conduction defects, arrhythmia, hypertrophic - left axis deviation, signs of LV hypertrohpy, Q waves in inferior/lat leads; restrictive - low voltage complexes), EchoCG (Dil = dil ventricles with global hypokinesia; hypertrophic = in ventricle, assymetrical septal hypertrophy; restrictive = non-diil/hypertrophied ventricles, atrial enlargement, preserved sys function, diastolic dysfunction, granular/sparkling appearance of myocardium in amyloidosis), cardiac catheterisation, endomyocardial biopsy, pedigree/genetic analysis
10
Q
Constrictive pericarditis
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx) and Presenting signs (Sx) on examination
- Appropriate investigations
A
- Chronic inflammation of the pericardium with thickening and scarring; limits ability to function normally
- Underdx, common causes: idiopathic, virus, TB, mediastina irritation, post surgical, connective tissue disease
- Rare, all ages, TB has highest incidence, more common in males
- Gradual onset of S&S, early = very subtle; advanced = jaundice, cachexia, musclle wasting; RHF signs: dyspnoea, peripheral oedema, raised JVP, Kussmaul’s sign, pulsatile hepatomegaly
- CXR (calcification on pericardium), echoCG, MRI (thickness of pericardium), CT, pericardial biopsy (ifi infective cause)
11
Q
DVT
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
- Generate a Management plan
- Identify complications of DVT
- Summarise prognosis for pts with DVT
A
- Formation of thrombus within deep veins (Calf/thigh)
- Blood stasis in legs is more probable -> COCP, post surgery, prolonged immobility, obesity, pregnancy, dehydration, smoking, polycythaemia, thrombophilia, malignancy
- Very common, esp in hospitalised pts
- Swollen limb, might be painless
- Local erythema, warmth and swelling, measure leg circumference, varicosities, skin colour change, Homan’s sign (forced passive dorsiflexion of ankle causes deep calf pain), check for PE (RR, Sats O2, pulse)
- Doppler US, impedance plethysmography, bloods (d-dimer as -ve predictor and thrombophilia screen if indicated), if PE = ECG, CXR, ABG)
- 3 steps:
- Anticoagulation: Heparin whilst waiting for warfarin to increase INR to target range, DVT’s not above knee can be observed and anticoag for 3 months, DVT beyond knee need anticoag for 6 months; recurrent DVT need long term warfarin
- IVC filter: if anicoag contraindicated and risk of embolisation
- Prevention: graduated compression stockings, mobilisation prophylactic heparin
- PE, venous infarction (phlegmasia cerulea dolens), thrombophlebitis, chronic venous insufficiency
- Below knee = good prognosis, proximal = greater risk of embolisation
12
Q
Gangrene
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
A
- Tissue necrosis, either wet with superimposed infection, dry or gas gangrene
- Tissue ischaemia and infarction, physical trauma, thermal injury, gas gangrene caused by clostridia perfringens. RF: Diabetes, periperal vascular disease, leg ulcers, malignancy, immunosuppression, steroid use, puncture/surgical wounds
- Relatively common, gas gangrene is rare
- Pain, discolouration of affected area, often affects extremities or areas subject to high pressure
- Painful area (erythematous around gangrenous tissue), gangrenous tissue is black due to Hb break down products, wet gangrene associated with pus and strong odour, gas gangrene - spreading infection and destruction of tissues causes overlying oedema, discolouration and crepits
- Bloods (FBC, U&Es, glucose, CRP, blood culture), wound swab, pus/fluid aspirate, x-ray of affected area
13
Q
Necrotising fasciitis
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
A
- Life threatening infection which spreads rapidly across fascial planes
- Usually polymicrobial inc. strep, staph, bacterioides and coliforms; RF - diabetes, peripheral vascular disease, leg ulcers, malignnancy, immunosuppression, steroid use and puncture/surgical wounds
- Rare
- Pain is often severe and out of proportion to apparent physical signs, predisposing event
- Area of erythema and oedema, haemorrhagic blisters, sx of systemic inflammatory response and sepsis (high/low temp, tachypnoea, hypotension)
- Bloods (FBC, U&Es, glucose, CRP, blood culture), wound swab, pus/fluid aspirate, XR
14
Q
Heart Block
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
- Management plan
- Possible complications
- Summarise prognosis
A
- 3 types:
- !st degree: prolonged conduction through AV node
- 2nd degree:
- Mobitz Type I: progressive prolongation of AVN conduction culminating in one atrial impulse failing to be conducted through AVN
- Mobitz type II: intermittent/regular failure of conductions through the AVN, also defined by the number of normal onductions per failed one
- 3rd degree (complete): no relationship between atrial and ventricular contraction, with failure of AVN conduction leading to ventricular contraction generated by focus of depolarisation within the ventricle
- 250,000 pacemakers implanted every year, mostly for heart block
- MI/IHD most common, infection (RhF, endocarditis), Digoxin, metabolic (hyperK), infiltration of conducting system (sarcoidosis), degeneration of conducting system
- 1st and 2nd degree usually asymptomatic; 3rd and Mobitz TII may cause Stokes-Adams Attacks, also: dizziness, palpitations, chest pain and HF
- Normal, check for potential cause; complete HB: slow, large vol pulse, JVP may show cannon A waves (occur with simultaneous atria and ventricle contraction); mobitz II and 3rd - reduced CO (hypotension and HF)
- Investigations:
- ECG
- 1st = fixed prolonged PR interval
- Mobitz I = progressively prolonged PR interval, culminating in P wave not followed by QRS
- Mobitz II = intermittent P wave not followed by QRS
- 3rd = no relation between P and QRS, if QRS initiated in bundle of hig then narrow complex, distally has wide complex
- CXR: cardiac enlargement, pulm oedema
- Bloods: TFT, digoxin level, cardiac enzymes, troponin
- EchoCG: wall motion abnormalities, aortic valve disease and vegetations
- ECG
- Chronic block: permanent pacemaker in complete, Advance mobitz II and symptomatic Mobitz I; Acute: associated with clinical deterioration = IV atropine, with temp external pacemaker
- Asystole, cardiac arrest, HF and complications of pacemaker inserted
- Mobitz II and 3rd block usually indicate serious underlying cardiac disease
15
Q
Hypertension
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
- Management plan
- Complications
- Prognosis
A
- Systolic >140 and/or diastolic >90 on 3 separate occasions. Malignant is >200/130
- 1ry: essential or idiopathic, responsible for 90% of cases
- 2ry:
- Renal: renal artery stenosis, chronic glomerulonephritis, chronic pyelonephritis, PCKD, chronic renal failure
- Endocrine: DM, hyperthyroidism, Cushing’s syndrome, Conn’s syndrome, hyperparathyroidism, phaeochromocytoma, CAH, acromegaly
- Cardiovascular: coarctation of aorta, increased intravascular volume
- Drugs: sympahomimetics, corticosteroids, COCP
- Pregnancy: pre-eclampsia
- 2ry:
- Very common, 10-20% of adults in western world
- Often asymptomatic, syx of complication/cause; accelerated malignant HTN: scotomas, blurred vision, headache, seizures, nausea and vomiting, acute HF
- BP measured on 2-3 different occasions, radiofemoral delay (coarctation of aorta distal to LSCA), renal artery bruit (renal artery stenosis), fundoscopy to detect hypertensive retinopathy (silver wiring and/arteriovenous nipping/flame haemorrhages and cotton wool exudates/papilloedema
- Bloods (U&E, glucose, lipids), urine dipstick (blood and proteins), ECG (LV hypertrophy/ischaemia), ambulatory BP monitorig
- x
- Conservative: stop smoking, lose weight, reduce alcohol intake, reduce dietary Na
- Investigate 2ry causes
- Medical if >160/100, multiple drug therapy needed: ACEi/ARB (<55, DM, HF and LV dysfunction), CCBs (>55, black) then beta blockers (younger pts, may increase HF risk and with thiazide increases DM risk), alpha blocker (pts with prostate disease)
- Target BP: <140/90 in non-diabetic, diabetic = <130/80, diabetes with proteinuria = <125/75)
- Severe HTN management (dias >140) = atenolol and nifedipine
- Acute malignant HTN: IV BB (emolol), labetalol, hydralazine Na nitroprusside. NB: lower BP slowly to prevent cerebral infarction
- HF, coronary artery disease, Cerebrovascular accidents, peripheral vascular disease, emboli, HTN retinopathy, renal failure, HTN encephalopathy, posterior reversible encephalopathy syndrome, malignant HTN
- Good prognosis if well controlled, uncontrolled = increased mortality. Tx reduces renal damage, stroke and HF
16
Q
Infective endocarditis
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
- Managment plan
- Complications
- Prognosis
A
- Infection of intracardiac endocardial structures
- Common organisms: strep (40% - S. viridans and S bovis), staph (35% - S aureus and S epidermidis), Enterococci (20% - E faecalis), others = haemophilus, actinobacillus, cardiobacterium, coxialla burnetii histoplasma -> form vegetations of platelets, fibrin and infective organisms which destroy valve leaflets and invade myocardium. RF: abnormal valves, prosthetic heart valves, turbulent blood flow, recent dental work/poor dental hygiene
- 16-22 people per 1 million per year
- Fever with sweats/chills/rigors, malaise, athralgia, myalgia, confusion, skin lesions, recent dental surgery/IV drug use
- Pyrexia, tachycardia, signs of anaemia, clubbing, new regurgitant mumur/muffled heart sounds (M>A>T>P), splenomegaly, vasculitic lesions (Roth spots on retina, petechiae on pharyngeal//conjunctival muscosa, janeway lesions, osler’s nodes and splinterhaemorrhages
- x
- Bloods: FBC (high neutrophils, normocytic anaemia), high ESR/CRP, U&Es - also tend to be Rheumatoid factor positive
- Urinalysis: microscopic hameaturia, proteinuria
- Blood culture: microscopy and sensitivities
- EchoCG: Transthoracic/transoesophageal
- Duke’s classification: Dx infective endocarditis based on findings of investigations and S&S
- ABx for 4-6wks. On clinical suspicion: benzylpenicillin, gentamicin; strep continue with benzylpenicillin and gentamicin; staph: flucloxacillin/vancomycin and gentamicin; enterococci: Ampicillin, gentamicin; Culture -ve: vancomycin and gentamicin. Surgery for urgent valve replacement needed if poor response to ABx
- Valve incompetence, intracardiac fistulae/abcesses, Aneurysm, HF, Renal failure, glomerulonephritis, arterial emboli from vegetations can move to brain, kidneys, lungs and spleen
- FATAL if untreated, 15-30% mortality with Tx
17
Q
Ischaemic heart disease
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
- Management plan
- Complications
- Prognosis
A
- Decreased blood supply to the heart muscle resulting in chest pain -> may present as stable angina or acute coronary syndrome (ACS). ACS subdivided into: unstable angina (chest pain at rest due to ischaemia without cardiac injury), NSTEMI, STEMI (STE with transmural infarction)
- Angina pectoris = myocardial O2 demand exceeds O2 supply, due to atherosclerosis or (rare) coronary artery spasm (cocaine induced), arteritis and emboli. RF: male, DM, FHx, HTN, Hyperlipidaemia, smoking
- Common >2%, more common in males
- ACS: acute onset chest pain, central/heavy/tight/crushing pain, radiates to arms/neck/jaw/epigastrum, occurs at rest, more severe/frequent than stable angina, SOB, sweating, N&V, silent infarcts occur in elderly and diabetics. Stable angina: chest pain brought on by exertion and relieved by rest
- Stable angina: RF signs; ACS: may be no clinical signs, pale, sweating, low-grade pyrexia, check both radial pulses (aortic dissection DDx), arrhythmias, disturbances of BP, new heart murmurs, sx of complications (acute HF, cardiogenic shock)
- x
- Bloods:
- FBC
- U&E
- CRP
- Glucose
- Lipid profile
- Cardiac enzymes (troponins, CK-MB)
- Amylase
- TFT
- AST/LDH (raised 24-48h post-MI respectively)
- ECG: Unstable angina/NSTEMI (ST depression/T wave inversion), STEMI (hyperacute T waves, ST elevation (>1mm limb, >2mm chest), new onset LBBB, T wave inversion and pathological Q waves); Tall R wave and ST depression in V1-3
- CXR -> sx of HF
- Exercise ECG
- Radionuclide myocardial perfusion imaging
- EchoCG - LV Ejection fraction
- Pharmacological stress testing: dipyrimadole, adenosine, dobutamine with Echo/rMPI to detect ischaemic myocardium
- Cardiac catheterisation/angiography
- Coronary calcium scoring (CT scan)
- Bloods:
- x
- Stable angina:
- Minimise cardiac risk factors -> aspirin 75mg a day
- Immediate Syx relief = GTN spray
- Long term = beta blockers (not in acute HF, cardiogenic shock, bradycardia, heart block, asthma), CCB, nitrates
- Percutaneous coronary intervention
- Coronary artery bypass graft
- Unstable angina/NSTEMI (MONABASH)
- Coronary care unit -> O2, IV access, monitor vital signs and serial ECG
- GTN, morphine, metoclopramide (nausea), aspirin (300mg initially then 75mg indefinitely), clopidogrel (300mg initially then 75mg for at least 1 yr), LMWH (enoxaparin), beta blocker, insulin infusion if >11mmol/L, GlpIIb/IIIa inhibitors considered if undergoing PCI
- STEMI: same as above except clopidogrel = 600mg if PCI, 300mg if thrombolysis and <75, 75mg if thrombolysis and >75 annd 75mg daily for 1yr+; PCI: IV heparin and GlpIIb/IIIa inhibitor, Bivalirudin. 1ry PCI <90 min, thrombolysis within 12h of chest pain, rescue PCI if continued chest pain/STE after thrombolysis; 2ry prevention: aspirin and clopidogrel, beta blockers, ACEi, statins and control risk factors; no driving for 1 month after MI, CABG in pts with left main stem/3 vessel disease
- Stable angina:
- Increased risk of MI/other vascular disease, cardiac injury can lead to F and arrhythmia: DARTHVADE = death, arrhythmia, rupture (myocardium), tamponade, HF, valve disease, aneurysm, dressler’s syndrome, embolism. (cardiogenic shock, heart block, pericarditis, thromboembolism, ventricular wall rupture, valvular regurg, ventricular aneurysms)
- TIMI score = high score = high risk of cardiac events within 30d of MI; Killip classification = class I no evidence of HF, II mild to mod HF, III over pulm oedema, IV cardiogenic shock
18
Q
Mitral Regurgitation
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
A
- Retrograde flow of blood from left ventricle to left atrium during systole
- Caused by mitral valve damage/dysfunction caused by: Rheumatic heart disease (most common), infective endocarditis, mitral valve prolapse, papillary muscle rupture/dysfunction, chordal rupture and floppy mitral valve associated with connective tissue disease
- Affects 5% of adults; prolapse common in young females
- Acute MR = syx of LV failure; chronic MR: asyx or exertional dyspnoea, palpitations in AF, fatigue; mitral valve prolapse = asyx or atypical chest pain/palpitations
- Pulse irregularly irregular if in AF, lat displaced apex beat with thrusting due to LV dilatation; pansystolic murmur (loudest at apex, radiating to axilla, soft S1, S3 due to to rapid ventricular filling in early diastole; sx of LV failure in acute MR; mitral valve prolapse - mid sys click, late sys murmur and click moves towards S1 when standng and away when lying down
- ECG: normal/AF. p mitrale (left atrial hypertrophy); CXR: acute MR shows LV failure, chronic MR shows LA enlargement, cardiomegaly and mitral valve calcification; EchoCG: every 6-12months in mod-severe MR, assessment of LV EF and end-systolic dimension
19
Q
Mitral stenosis
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
A
- Mitral valve narrowing causing obstruction to blood flow from LA to LV
- Rheumatic heart disease = main cause; Rare: congenital, SLE, RhA, endocarditis, atrial myxoma
- Declining as RhF is more rare
- Asyx, fatigue, SOB on exertion, orthopnoea, palpitations (AF), Rare syx: cough, haemoptysis, hoarseness due to compression of left recurrent laryngeal nerve by enlarged LA
- Peripheral cyanosis, malar flush, irregularly irregular pulse in AF, apex beat undisplaced and tapping, parasternal heave (RV hypertrophy 2ry to pulm HTN), loud S1 with opening snap, mid diastolic murmur, evidence of pulm oedema on auscultation
- ECG: normal, p mitrale (broad p wave with bunny ears), AF, RV hypertrophy evidence if severe pulm HTN; CXR: LA enlargement, cardiac enlargement, pulm congestion, mitral valve calcification; echoCG: assess functional and structural impairments, transoesophageal echoCG; Cardiac catheterisation: severity of HF
20
Q
Myocarditis
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
A
- Acute inflammation and necrosis of cardiac muscle
- Usually idiopathic, Viruses: coxsackie B, EBV, CMV, adenovirus, influenza; bacteria: post strep, TB, diptheria; fungal: candidiasis; protozoal: trypanosomiasis; helminths: trichinosis; Non-infective: systemic = SLE, sarcoidosis, polymyositis, hypersensitivity mypcarditis = sulphonamides; chemotherapy agents (doxorubicin, streptomycin); cocaine, heavy metals, radiation
- Difficult to measure accurately
- Prodromal flu-like illness with fever, malaise, fatigue and lethargy, SOB (Pleural effusion), palpitations, sharp chest pain
- Sx of pericarditis and complications
- Bloods: FBC (^WCC if infective), U&E, ESP/CRP raised, cardiac enzyme may be raised, tests to ID cause (serology); ECG: non specific T wave and ST changes, saddle shaped ST elevation with pericarditis; CXR: normal/cardiomegaly; pericardial fluid drainage: glucose, protein, cytology, culture and sensitivity; EchoCG: assess sys and dias function, wall motion abnormalities, pericardial effusions; myocardial biopsy is rarely required
21
Q
Pericarditis
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
- Management plan
- Complications
- Prognosis
A
- Inflammation of the pericardium -> acute, subacute or chronic
- Idiopathic, infective (coxsackie B, echovirus, mumps, strep, fungi staph, TB), connective tissue disease (SLE, sarcoidosis), post MI (24-72h), Dressler’s syndrome, malignancy (lung, breast, lymphoma, leukaemia, melanoma), radiotherapy thoracic surgery, Hydralzine/isoniazid
- Uncommon, <1/100 hospital admissions, more common in males
- Chest pain (sharp and central, radiates to neck and shoulders, worse on deep inspiration/coughing, relieved by sitting forwards), dyspnoea, nausea
- Fever, pericardial friction rub (lower left sternal edge, leaning forwards at expiration), heart sounds faint due to pericardial effusion; cardiac tamponade: Beck’s triad = raised JVP, low BP, muffled heart sounds, tachycardia, pulsus paradoxus.
- Constrictive pericarditis: Kussmaul’s sign, pulsus paradoxus, hepatomegaly, ascites, oedema, pericardial knock, AF
- ECG - saddle STE; Echo - pericardial effusion and cardiac function; Bloods - FBC, U&Es, ESR/CRP, cardiac enzymes (normal), blood cultures/ASO titres/ANA/RhF for cause; CXR - normal, may be globular
- Acute: cardiac tamponade = pericardiocentesis; Medical = underlying cause and NSAIDs for pain and fever relief; Recurrent = low dose steroids, immunosuppressants, colchicine; surgical = pericardiectomy (constrictive)
- Pericardial effusion, cardiac tamponade, cardiac arrhythmias
- Viral cases = good; malignant = poor
22
Q
Peripheral Vascular Disease
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
A
- Occurs due to atherosclerosis causing stenosis of arteries via a multifactorial process involving modifiable and non-modifiable risk factors
- Atheroscerosis -> types of PVD = intermittent claudication (calf pain on exercise); critical limb ischaemia (pain at rest = most severe), acute limb ischaemia (sudden decrease in arterial perfusion in limb), arterial ulcers, gangrene. RF -> smoking, diabetes, HTN, hyperlipidaemia, physical inactivity, obesity
- 55-70 = 4-12% affected, above 70 = 15-20% affected; more common in males and increases with age
- x
- Intermittent claudication: cramping pain in calf, thigh, buttock after walking a given diseance, relieved by rest -> calf = femoral disease, buttock = iliac disease
- Critical limb ischaemia: ulcers, gangrene, rest pain and night pain (relieved by dangling leg over side of bed)
- Leriche syndrome (aortoiliac occlusive disease): buttock claudication, impotence, absent/weak distal pulses
- Fontaine classification of PVD: asyx -> intermittent claudication -> rest pain -> ulceration/gangrene
- Acute limb ischaemia = Pain, Pale, Pulseless, Paralysis, Paraesthesia, Perishingly cold; other syx: atrophic skin, hairless, punched out ulcers, colour change when raising leg
- Full CV risk assessment = BP, FBC, FBG, lipid levels, ECG, thrombophilia (<50yrs); Colour duplex US showing site and degree of stenosis; MRI/CT (extent and location of stenosis); Ankle brachial pressure index -> marker of CVD, <0.8 = do not apply a pressure bandage as it worsens ischaemia
23
Q
Pulmonary hypertension
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
A
- Increase in mean pulm arterial pressure which can be caused by/associated with a wide variety of conditions
- Idiopathic, problems with smaller branches of the pulm arteries, LV failure, lung disease, thromboses/emboli in lungs
- Idiopathic pulm HTN = rare, common in severe resp and cardiac disease
- Progressive SOB, weakness/tiredness, exertional dizziness and syncope, angina and tachyarrhythmia; late stage - oedema and ascites
- RV heave, loud pulm S2, murmur (pulm regurg), tricuspid regurg, raised JVP, peripheral oedema, ascites
- CXR - exclude other lung diseases; ECG RV hypertrophy and strain; pulm function tests; LFTs (liver damage => portal HTN); lung biopsy (interstitial lung disease); echo assess RV function; right heart catheterisation - directly measure pulm pressure and confirm diagnosis
24
Q
Supraventricular tachycardia
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
- Management plan
- Complications
- prognosis
A
- Regular narrow-complex tachycardia with no p waves and supraventricular origin -> atrioventricular nodal reentry tachycardia (AVNRT) and atrioventricular rentry tachycardia (AVRT)
- AVNRT = localised reentry circuit forms around the AVN; AVRT = re-entry circuit forms between the atria and ventricles due to the presenc eof accessory pathway (Bundle of Kent); RF: nicotine, alcohol, caffeine, previous MI, digoxin toxocity
- Very common, 2x more common in females
- Present with syncope; Syx vary depending on rate and duration of SVT, palpitations, light-headedness, abrupt onset and termination of Syx, fatigue, chest discomfort, dyspnoea, syncope
- AVNRT - normal except tachycardia; wolff-parkinson-white = tachycardia, 2ry cardiomyopathy (s3 gallop, RV heave, displaced apex beat)
- x
- ECG: differentiating AVNRT and AVRT - once the SVt has been terminated and normal rhythm are reestablished = AVNRT appears normal, AVRT delta waves (slurred upstroke of QRS); 24h ECG monitoring
- Cardiac enzymes: check for MI features
- Electrolytes - arrhythmia
- TFTs - arrhythmia
- Digoxin level
- Echo - structural heart disease
- If haemodynamically unstable -> DC cardioversion; if stable -> vagal maneouvres (Valsalva/carotid massage) and chemical cardioversion (adenosine 6mg bolus, verapmil 2.5-5mg (atenolol/amiodarone as alternatives)). If unresponsive to above or >250bpm or low BP/HF/low consciousness then sedate snd synch DC cardioversion and amiodarone.
- Ongoing Mx: AVNRT = radiofrequency ablation of slow pathway, beta blockers (alternative: fleicanide, propafenone, verapmil); AVRT = radiofrequency ablation; Sinus tachy = exclude 2ry cause and beta blocker/ rate limiting CCB
- Haemodynamic collapse, DVT, systemic embolism, cardiac tamponade
- Dependent on presence of underlying structural heart disease; if structurally normal heart = good prognosis; pre-excitation = small risk of sudden death
25
Q
Tricuspid Regurgitation
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
A
- Backflow of blood from RV to RA during systole
- Congenital = Ebstein’s anomaly, cleft valve in ostium primum; functional = RV dilation (pulm HTN) or valve prolapse; Rheumatic heart disease; infective endocarditis; carcinoid syndrome, trauma, cirrhosis, iatrogenic
- Differs based on cause -> infective endocarditis is the most common cause
- Fatigue, SOB, palpitations, headaches, nausea, anorexia, epigastric pain (worse on exercise), jaundice, lower limb swelling
- Pulse = irregularly irregular; inspection = raised JVP with giant V waves and maybe giant A waves; palpation = parasternal heave; auscultation = pansystolic murmur @ lower left sternal edge, louder on inspiration (carvallo sign), loud P2 component of S2; chest exam = pleural effusion, pulm HTN; abdo exam = palpable liver (tender, smooth, pulsatile), ascites; legs = pitting oedema
- Bloods: FBC, LFT, Cardiac enzymes and blood cultures; ECG: P pulmonale (right atrial hypertrophy); CXR: RHS enlargement of cardiac shadow; Echo: extent of regurg estimated using doppler US (may show valve prolapse and RV dilation); Right heart catheterisation: useful for assessing pulm artery pressure
26
Q
Varicose Veins
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
- Managment plan
- Complications
- Prognosis
A
- Veins that become prominently elongated, dilated and tortuous (commonly the superficial veins of the lower limbs)
- 1ry = genetic/developmental weakness in the vein wall, resulting in increased elasticity, dilatation and valvular incompetence; 2ry = venous outflow obstruction: pregnancy, pelvic malignancy, ovarian cysts, ascites, lymphadenopathy, retroperitoneal fibrosis OR due to valve damage OR high flow; RF= age, female, FHx, caucasian, obesity
- Common, increases with age, 10-15% of men, 20-25% of women
- Cosmetic appearance, aching in legs, aching is worse towards end of day after standing for long period, swelling, itching, bleeding, infection, ulceration
- Inspect whilst standing; Palpation = feel fascial defects along the veins, cough impulse felt over saphenofemoral junction (tap test also), palpation of thrill or auscultaton of bruit would suggest AV fistula; Trendelenburg test (leg elevated, veins emptied -> hand over saphenofemoral junction, then leg lowered to fill veins and observed before and after release of SFJ); Rectal/Pelvic examination if 2ry causes;
- Venous insuffieciency: varicose eczema, haemosiderin staining, atrophie blance, lipodermatosclerosis, oedema, ulceration
- Duplex US -> sites of incompetence/reflux, allows exclusion of DVT
- Conservative = exercise, elevation of legs at rest and support stockings; venous telangectasia and reticular veins = laser sclerotherapy, microinjection sclerotherapy; surgical = saphenofemoral ligation, stripping of the long saphenous vein, avulsion of varicosities
- Venous pigmentation, eczema, lipodermatosclerosis, superficial thrombophlebitis, venous ulceration; complications of Tx = sclerotherapy = skin staining/local scarring; surgery = haemorrhage, infection, recurrence, paraesthesia, peroneal nerve injury
- Slowly progressive, high recurrence rates
27
Q
Vasovagal syncope
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
A
- Loss of consciousness due to a transient drop of blood flow in the brain caused by excessive vagal discharge
- Very common cause of fainting -> precipitated by emotions (fear, severe pain, phobia), orthostatic stress (prolonged standing/hot weather)
- Very common; syncope affects 40% of people
- Loss of consciousness lasting a short time; vagal syx (sweating, dizziness, light headedness) before passing out; some twitching of limbs during blackout; recovery is very quick
- No signs
- Check for other causes: ECG for arrhythmia; Echo for outflow obstruction; lying/standing BP for orthostatic hypotension; FBG for DM/hypoglycaemia
28
Q
Venous ulcers
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
- Management plan
- Complications
- Prognosis
A
- Large, shallow sometimes painful ulcers found superior to the medial malleoli, caused by incompetent valves in lower limbs leading to venous stasis and ulceration
- Incompetent valves in lower limbs, leading to venous stasis and increased venous pressure -> ulceration. RF = obesity, immobility, recurrent DVt, varicose veins, previous surgery/injury to leg, age
- Very common, increases with age
- Large, shallow, relatively painless ulcer with irregular margin situated above medial malleolus; Hx: varicose veins, DVT, phlebitis, fracture/trauma/surgery, FHx, venous insufficiency = swelling, itching, aching
- Stasis eczema, lipodermatosclerosis (inverted champagne bottle sign if severe), haemosiderin deposition (dark)
- ABPI, exclude arterial ulcer and if <0.8 do not apply pressure bandage; measure surface of ulcer; swabs for microbiology, biopsy (Marjolin’s ulcer)
- Graduated compression (exclude diabetes, neuropathy and PVD before attempt), debridement and cleaning, ABx if infected, topical steroids (surrounding dermatitis)
- Recurrence and infection
- Good and better if mobile with few comorbidities
29
Q
Ventricular fibrillation
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx) and signs (Sx) on examination
- Appropriate investigations
- Management
- Complications
- Prognosis
A
- Irregular broad comlex tachycardia that can cause cardiac arrest and sudden cardiac death
- Ventricular fibres contract randomly causing complete failure of ventricular function; most cases occur with underlying heart disease; RF = CAD, AF, hypoxia, ischaemia, pre-excitation syndrome
- Most common arrhythmia in cardiac arrest pts; incidence similar to ischaemic heart disease
- Hx of chest pain, fatigue and palpitations; pre-exsisting conditions = CAD, cardiomyopathy, valvular heart disease, long QT syndrome, Wolff-Parkinson-White syndrome, brugada syndrome
- ECG, cardiac enzyme (recent ischaemic event); electrolytes - arrhythmias and VF; drug levels and toxicology screen - anti-arrhythmics and cocaine can cause arrhythmia; TFTs - hyperthyroidism can cause tachyarrhythmias, coronary angiography (after VF survival check coronary arteries)
- Urgent defib and cardioversion, surviving pts need full assessment of LV function, myocardial perfusion and electrophysiological stability; implantable cardioverter defib; empirical beta blockers and some may be treated with radiofrequency ablation
- Ischaemic brain injury due to loss of CO; myocardial injury; post-defib arrhythmias, aspiration pneumonia, skin burns, death
- Early defib essential (4-6min) -> anoxic encephalopathy is major outcome of VF
30
Q
Ventricular Tachycardia
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx)
- Presenting signs (Sx) on examination
- Appropriate investigations
- Managemnt
- Complications
- Prognosis
A
- Regular broad complex tachycardia originating from ventricular ectopic focus -> >120bpm
- Electrical impulses arise from ventricular ectopic focus; RF = CHD, Structural heart disease, electrolyte deficiencies (hypok/Ca/Mg), use of stimulant drugs (caffeine/cocaine)
- Fairly common, shockable rhythms in cardiac arrest patients; incidence peaks in middle decades of life
- Syx of IHD/haemodynamic compromise due to poor perfusion; chest pain, palpitations, dyspnoea, syncope
- Depend on degree of haemodynamic instability = resp distress, bibasal crackles, raised JVP, hypotension, anxiety, agitation, lethargy, coma
- ECG -> VT vs SVT with aberrant conduction -> rate >100bpm, borad QRS complexes, AV dissociation; electrolytes, drug levels (digoxin toxicity), cardiac enzyme (ischaemic event)
- ABC approach; Pulse? NO = ALS; unstable VT = reduced cardiac output so defib, correct lectrolyte abnormalities and amiodarone; stable VT = no haemodynamic compromise, correct electrolyte abnormalities, Amiodarone, synchronised DC shock; implantable cardioverter defib if sustained VT causiing syncope, systained Vt with EF <35%, previous cardiac arrest due to VT/VF, MI complicated by non-sustaned VT
- Congestive cardiac failure, cardiogenic shock, VT may deteriorate to VF
- Good if rapid treatment, long term prognosis depends on underlying cause
31
Q
Wolff-Parkinson-White Syndrome
- Define
- Explain aetiology/risk factors
- Summarise epidemiology
- Presenting symptoms (Syx) and signs (Sx) on examination
- Appropriate investigations
A
- Congenital abnormality which can result in SVT that use an accessory pathway -> preexcitation syndrome
- Bundle of kent is likely to be congenital; associated = congenital cardiac defects, ebstein’s anomaly, mitral valve prolapse, cardiomyopathies
- Common, (most of all ventricular pre-excitation syndromes), found in all ages, more common in young, prevalence decreases with age
- SVT in early childhood; often asyx, palpitations, light-headedness, syncope; paroxysml SVT followed by period of polyuria (atrial dilatation and ANP release), sudden death if SVT deteriorates into VF; clinical features of associated cardiac defects
- ECG may be normal if conduction speed matched bundle of His = short PR interval, borad QRS complex, slurred upstroke producing delta wave; pt may be in SVT (AVRT), bloods check for other causes of arrhythmia, echo for structural heart defects
32
Q
Syx and Sx
AAA
A
- Unruptured: No Syx, may have pain in groin/abdo/loin/back.
- Ruptured: Pain in abdo/back/loin, sudden or severe, syncope, shock
- Pulsatile, Lat expanding mass on bimanual palpitation of AA; abdo bruit; retriperitoneal haemorrhage = Grey-Turner’s sign
33
Q
Investigations
AAA
A
- Bloods -> FBC, clotting screen, renal/liver function and cross match if surgery planned;
- US to detect AAA,
- CT with contrast for rupture check,
- MRI angiography
34
Q
Definition
AAA
A
Localised enlargement of abdo aorta -> diameter >3cm or >50% normal diameter
35
Q
Definition
Aortic Regurg
A
Reflux of blood from the aorta into the LV during diastole, resulting in LV dilataton, so increased EDV and Increased SV, explaining high vol collapsing pulse
36
Q
Sx and Syx
Aortic regurg
A
- Syx related to aetiology
- Chronic: asymptomatic then pts develop HF Syx (exertional dyspnoea, orthopnoea, fatigue)
- Severe acute: sudden cardiovascular collapse
- Signs:
- Collapsing pulse
- Wide PP
- Thrusting/heaving displaced apex beat
- Early diastolic murmur
- Austin-Flint mid diastolic murmur (over apex)
- RARE Sx: Quincke (pulse nail bed), de Musset (nodding in time with pulse), Becker (pulse of retinal arteries and pupils), Muller (uvula pulse), Corrigan (pulse in neck), Traube (pistol shot on femoral artery), Duroziez (sys/dias bruit on femoral artery ausc.), Rosenbach (sys pulse of liver), Gerhard (sys pulse of spleen), Hill (popliteal cuff BP sys >60mmHg cf brachial)
37
Q
Investigations
Aortic regurg
A
- CXR (cardiomegaly, dilatation of asc aorta, sx of Pulm oedema),
- ECG (LV hypertrophy: deep S in V1/2, Tall R in V5/6, inverted T in I/aVL/V5/6, L axis dev),
- EchoCG (underlying path, monitor progression and see size),
- Cardiac catheter with angiography
38
Q
Definition
Aortic dissection
A
Condition where a tear in the aortic intima allows blood to surge into aortic wall, causing a split between the inner and outer tunica media, creating a false lumen. -> Type A = Ascending aorta, Type B = Descending aorta (distal to L SCA)
39
Q
S&S
Aortic dissection
A
- MAIN SYX: Sudden central tearing pain, may radiate to back between shoulder blades; other syx caused by obstruction of branches of aorta
- Carotid -> hemiparesis, dysphasia, blackout
- Coronary -> chest pain
- Subclavian -> ataxia, loss of consciousness
- Ant spinal -> paraplegia
- Coeliac axis -> severe abdo pain
- Renal -> anuria, renal failure
- Sx
- Murmur on back, desc to abdo
- HTN
- BP difference between arms >20mmHg
- Wide PP
- Hypotension =? tamponade
- Check for pulsus paradoxus (large decrease in sys BP during inspiration, indicating: Tamponade, pericarditis, chronic sleep apnoea, obstructive lung disease)
40
Q
Investigations
Aortic dissection
A
- Bloods: FBC, X match 10u of blood, U&E, clotting screen;
- CXR (widened mediastinum),
- ECG (normal unless LV hypertrophy/ inf MI signs),
- CT thorax
- EchoCG,
- Cardiac cath and aortography
41
Q
Definition
Aortic stenosis
A
Narrowing of LV outflow at the level of the aortic valve
42
Q
S+S
Aortic stenosis
A
- Initially asymptomatic, angina, syncope/dizziness on exercise and Syx of HF
- Narrow PP
- Slow rising pulse
- Thrill in aortic area
- Forceful sustained thrusting undiscplaced apex
- Ejection sys murmur, radiating to carotid artery
- 2nd heart sound may be softened or absent
- Bicuspid may produce ejection click
43
Q
Investigations
aortic stenosis
A
- ECG: LV hypertrophy shown (deep S in V1/2, tall R in V5/6, inverted T in 1/aVL/V5/6, L axis deviation) and LBBB
- CXR (post-sternotic enlargement of asc aorta, calcification of aortic valve);
- EchoCG (assesses LV function);
- cardiac angiography (DDx from angina/MI
44
Q
Definition
Aterial Ulcer
A
Localised area of damage and breakdown of skin due to inadequate arterial supply -> seen on feet of pts with severe atheromatous narrowing of leg arteries
45
Q
S+S
Arterial ulcer
A
- Distal -> dorsum of foot/between toes; punched out, often elliptical with clearly defined edges; base has grey, granulation tissue; NIGHT PAIN!
- Punched out appearance, hairlessness, pale skin, absent pulses, nail dystrophy, wasting of calf muscles
46
Q
Investigations
Arterial Ulcer
A
- Duplex US of lower limbs,
- ankle-brachial pressure index,
- percutaneous angiography,
- ECG,
- Fasting serum lipids/blood glucose and HbA1c,
- FBC
47
Q
Definition
AF
A
Rapid, chaotic and ineffective atrial electrical conduction -> permanent, persistent and paroxysmal
48
Q
S+S
AF
A
- Often asyx, palpitations, syncope, Syx of cause
- Irregularly irregular pulse, difference in apical beat vs radial pulse, check for thyroid/valvular disease
49
Q
Investigations
AF
A
- ECG (uneven baseline, absent p waves, irreg intervals between QRS; atrial flutter = saw toothed appearance);
- Bloods (cardiac enzymes, TFT, lipid profile, U&E/Mg2+/Ca2+);
- EchoCG (mitral valve disease, left atrial dilatation, left ventricular dysfunction, structural abnormalities)
50
Q
Treatment
AF
A
- Treat any reversible causes, then rhythm control and rate control:
- Rhythm: >48h onset = anticoagulate for 3-4wks before cardioversion; if <48h = cardioversion, chemical cardioversion (flecainide/amiodarone), contraindicated if IHD Hx; prophylaxis against AF = sotalol, amiodarone and flecainide
- Rate: Chronic = digoxin, verapamil, beta-blockers aiming for ventricular rate of 90
- Stroke risk stratification: Low risk can use aspirin; high risk require warfarin => based on CHADS-Vasc score, RF = previous thromboembolic event, >75yrs, HTN, DM, Vascular/Valvular disease, HF, impaired LV function
51
Q
Definition
Cardiac Arrest
A
- Acute cessation of cardiac function
- REVERSIBLE causes: 4H and 4T
- Hypothermia, hypoxia, hypovolaemia, hypo/erkalaemia
- Toxin (other metabolic disorders), thromboembolic tamponade, tension pneumothorax
52
Q
S+S
Cardiac Arrest
A
- Sudden -> may be preceded by fatigue, fainting, blackouts, dizziness, vomiting aand chest pain
- Unconscious, not breathing, absent carotid pulses
53
Q
Treatment
Cardiac arrest
A
- BLS,
- ALS - cardiac monitor and defib,
- assess rhythm = if pulseless V-tachy/V-fib then defib once, resume CPR and then shock again
- if still in pulseless V-T/V-F, admin adrenaline 1mg IV (after 2nd and every 3-5min)
- if shockable rhythm persists after 3rd shock then amiodarone IV bolus 300mg;
- if puseless electrical activity/asystole then CPR for 2, reassess and admin adrenaline (1mg IV every 3-5min), atropine (3mg IV once) if asystole/PEA with 60bpm),
- Tx of reversible causes;
- warm hypothermia slowly,
- correction of electrolyte levels for hypo/erK,
- hypovol use IV colloids/crystalloids and blood products,
- tamponade = pericardiocentesis,
- tenion pneumothorax = aspiration/chest drain,
- TE = treat as PE/MI,
- toxins = antidote
