Cardiovascular - Comprehensive notes on cardio, everything that can be tested on by UCL in 4th PDF

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Summary

CardioVALVE DISEASE...............................................................................................................................................VALVE DISEASEAORTIC REGURGITATION............................................................................................................

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Cardiovascular

CONDITIONS

Cardio VALVE DISEASE............................................................................................................................................... 1 AORTIC REGURGITATION............................................................................................................................ 2 AORTIC STENOSIS....................................................................................................................................... 3 MITRAL REGURGITATION............................................................................................................................ 4 MITRAL STENOSIS....................................................................................................................................... 6 MITRAL VALVE PROLAPSE.......................................................................................................................... 7 TRICUSPID REGURGITATION...................................................................................................................... 8 INFECTIVE ENDOCARDITIS......................................................................................................................... 9 RHEUMATIC FEVER.................................................................................................................................... 12 ARRYTHMIAS.................................................................................................................................................. 13 HEART PACING........................................................................................................................................... 13 ATRIAL FIBRILLATION/FLUTTER................................................................................................................16 BRADYCARDIA............................................................................................................................................ 19 HEART BLOCK............................................................................................................................................ 20 SUPRAVENTRICULAR TACHYCARDIA......................................................................................................22 WOLFF-PARKINSON-WHITE SYNDROME.................................................................................................24 VENTRICULAR TACHYCARDIA..................................................................................................................26 VENTRICULAR FIBRILLATION.................................................................................................................... 28 HEART MUSCLE & PERICARDIUM...............................................................................................................30 PERICARDITIS............................................................................................................................................ 30 PERICARDIAL EFFUSION........................................................................................................................... 31 CONSTRICTIVE PERICARDITIS................................................................................................................. 31 TAMPONADE............................................................................................................................................... 32 MYOCARDITIS............................................................................................................................................. 33 ISCHEMIC HEART DISEASE.......................................................................................................................... 35 ATHEROSCOLEROSIS................................................................................................................................ 35 ANGINA........................................................................................................................................................ 37 ACUTE CORONARY SYNDROME..............................................................................................................38 CARDIAC ARREST...................................................................................................................................... 44 HYPERTENSION............................................................................................................................................. 47 HYPERTENSION......................................................................................................................................... 47 PULMONARY HYPERTENSION..................................................................................................................51 HEART FAILINGS........................................................................................................................................... 52 CARDIAC FAILURE (ACUTE AND CHRONIC)............................................................................................52 DIURETICS.................................................................................................................................................. 57 CARDIOMYOPATHY....................................................................................................................................... 59 DILATED CARDIOMYOPATHY.................................................................................................................... 59 HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY.............................................................................60 RESTRICTIVE CARDIOMYOPATHY............................................................................................................62 TAKOTSUBO CARDIOMYOPATHY (Broken Heart Syndrome)....................................................................63 OTHER............................................................................................................................................................. 64 SHOCK......................................................................................................................................................... 64 DIGOXIN OVERDOSE................................................................................................................................. 67 DVLA: CARDIOVASCULAR DISORDERS...................................................................................................69

VALVE DISEASE AORTIC REGURGITATION Define

Cardiovascular

CONDITIONS

Reflux of blood from the aorta into the left ventricle during diastole. Also known as aortic insufficiency Aetiology/risk factors Acute  Aortic valve leaflet damage  Infection  Infective endocarditis  Trauma (blunt trauma or rapid declaration)  Aortic root/ascending aorta dilatation  Aortic dissection Chronic  Infection  Rheumatic fever, syphilis  Bicuspid aortic valve  instead of tricuspid  Aortic root/ascending aorta dilatation  HTN, Aortitis, aortic aneurysm, Arthritides (RA, seronegative arthritides), Connective tissue disease (Marfan's, Ehlers-Danlos), Pseudoxanthoma elasticum, Osteogenesis imperfecta Pathophysiology  Reflux of blood into the left ventricle results in left ventricular dilatation  This means greater flow into aorta so increased LV end diastolic volume and increased stroke volume  The combination of increased stroke volume and low end-diastolic aortic pressure may explain the high-volume collapsing pulse, collapsing pulse and wide pulse pressure. Epidemiology  Chronic AR often begins in the late 50s  It is most frequently seen in patients > 80 yrs Symptoms and signs  Chronic AR  initially asymptomatic, then symptoms of Heart Failure (exertional dyspnoea, orthopnoea, fatigue, collapse), occasionally angina  Severe acute AR  sudden cardiovascular collapse o Left ventricle cannot adapt to rapid increase in end-diastolic volume  Collapsing ‘water-hammer’ high-volume pulse and wide pulse pressure o This hyperdynamic state can also be seen in  hyperthyroid, anaemia, dehydration, pregnancy  Thrusting and heaving disp laced apex beat  Early diastolic murmur at L sternal edge/aortic valve region o Better heard with patient sitting forward with breath held in expiration  An ejection systolic murmur may also be heard because of increased flow across the valve (due to increased stroke volume)  Austin Flint mid-diastolic murmur  over the apex, from turbulent reflux hitting anterior cusp of mitral valve and causing a physiological mitral stenosis o Suggests severe AF Rare Signs  Quincke’s sign  visible pulsations on nail bed  De Musset’s sign  head nodding with each heart beat  Duroziez’s sign in the groin, a finger compressing femoral artery 2cm proximal to stethoscope gives systolic murmur and 2cm distal, gives diastolic murmur o Get systolic and diastolic bruit  Traube’s sign  ‘pistol shot’ (loud systolic and diastolic sounds) sound over femoral arteries  Becker's Sign  visible pulsation of the pupils and retinal arteries

Cardiovascular

CONDITIONS

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Muller's Sign  visible pulsation of the uvula Corrigan's Sign  visible pulsation carotid arteries in the neck Rosenbach's Sign  systolic pulsations of the liver Gerhard's Sign  systolic pulsations of the spleen Hill's Sign  popliteal cuff systolic pressure exceeding brachial pressure by > 60 mm Hg Investigation  Echocardiogram  shows underlying cause (bicuspid valve, aortic root dilation) + effects of regurgitation (LV dilatation, fluttering of mitral valve anterior leaflet). o Doppler echocardiography can detect AR and assess severity  ECG  LV hypertrophy (deep S wave in V1-2, tall R wave in V5-6, inverted T waves in I, aVL, V56 and L axis deviation)  CXR  cardiomegaly, dilation of ascending aorta, signs of pulmonary oedema with L HF Management 1. Surgical aortic valve replacement / TAVI (transcatheter aortic valve implantation - if not for surgery) o TAVI  catheter with a balloon is put into the femoral or carotid artery and passed to the aortic valve, balloon is then inflated to make room for the new valve.  If metallic, anticoagulation 2. If not for surgery or TAVI  reduce systolic BP  vasodilator (nifedpine) or ACEi Complication Congestive heart failure, arrhythmias, infective endocarditis, sudden death, MI Prognosis Depends on underlying aetiology  acute AR caused by aortic dissection or infective endocarditis is fatal if not urgently treated Chronic AR is well tolerated for many years without symptoms

AORTIC STENOSIS Define Narrowing of the left ventricular outflow at the level of the aortic valve. MOST COMMON TYPE Aetiology/risk factors  Causes: o Stenosis can be secondary to rheumatic heart disease  Most common worldwide o Senile calcification  calcification of a tricuspid aortic valve  occurs in elderly  Most common cause in UK o Calcification of a congenital bicuspid aortic valve  Most common cause in younger people  Aortic sclerosis  senile de tricuspid aortic valve (does not radiate and normal pulse)  Aortic stenosis + GAVE (gastric antral vascular ectasia = Heydes Sydrome Pathophysiology Narrowed aortic valve causes high velocity, high pressure blood flow leading to LVH and post stenotic dilation of aorta Epidemiology

Cardiovascular

CONDITIONS

 More common in males, more common in elderly (3% of 75 yr olds)  Those with bicuspid aortic valve present earlier Symptoms and signs  May be asymptomatic initially o Symptoms appear when aortic area 12 hours apart  Evidence of endocardial involvement  echocardiogram positive for IE (vegetation or valvular regurgitation) or new murmur or leakage around prosthetic valve (if present) o Minor  all must be positive for definite diagnosis  Risk factors  Predisposing heart condition or IV drug use  Fever >38  Vascular phenomena  Janeway lesions, splinter haemorrhages, conjunctival haemorrhages, intracranial haemorrhage, arterial emboli  Immunological phenomena  Osler’s nodes, Roth’s spots, positive rheumatoid factor, glomerulonephritis  Microbiological evidence  positive blood cultures or serological evidence of active infection with organism consistent with IE BUT findings not meeting major criteria o Or 1 major and 3 minor Management Antibiotics  Antibiotics  6 weeks  Broad spectrum antibiotics  IV amoxicillin + IV gentamicin  then tailor to.. o Streptococci + Enterococci  beta lactam (amoxicillin) + gentamicin o Staphylococci  flucloxacillin + gentamicin  If MRSA vancomycin is used o Fungal  surgery and antifungals o Prosthetic valve endocarditis: vancomycin, gentamicin + rifampacin Valve replacement done if…

Cardiovascular

CONDITIONS

Urgent valve replacement if poor response to antibiotics or degeneration or heart block Heart failure  o Severe acute MR or AR causing refractory pulmonary oedema or cardiogenic shock  Uncontrolled infection o Locally uncontrolled  abscess, fistula, enlarging vegetation, perforation o Infection caused by fungi or resistant organism o Persisting positive blood culture  Prevention of embolism o Presence of large vegetations >3cm o Persisting vegetations after embolic event NOTE  surgery is best delayed to allow effective antibiotic treatment if the patient’s condition allows Complications  Heart abscesses can cause heart block as they disrupt conduction fibres causes changes  Congestive heart failure, complete heart block  Systemic embolization, TIA  AKI  Vertebral osteomyelitis Prognosis  Fatal if untreated  15-30% mortality even with treatment  

RHEUMATIC FEVER Define An inflammatory multisystem disorder, occurring following group A -haemolytic streptococci (GAS) infection  strep pyogenes Aetiology/risk factors  The pathogenic mechanisms remain incompletely understood

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Molecular mimicry is thought to play an important role in the initiation of the tissue injury  antibodies directed against GAS antigens cross-react with host antigens

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Streptococcal pharyngeal infection (pharyngitis) is required  occurs 2-4 weeks later

o o

Or scarlet fever Genetic susceptibility may be present

Epidemiology  Peak incidence  between 5 and 15years. More common in the Far East, Middle East, eastern Europe and South America.

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The mean incidence is 19/100 000. Despite decrease incidence over time in the West, the incidence rates remain relatively high in

non-Western countries. Symptoms and signs  Fever, malaise, anorexia.  Joints  Painful, swollen, decreased movement / function.  Cardiac  Breathlessness, chest pain, palpitation Duckett Jones criteria  Positive diagnosis if at least two major criteria, or one major plus two minor

Cardiovascular

CONDITIONS

criteria are present. Major criteria (pneumonic JONES)  (Joints) Arthritis, synovitis  Migratory or fleeting polyarthritis with swelling, redness and tenderness of large joints.  (heart is O) Carditis  New murmur (e.g. Carey Coombs murmur (mid-diastolic murmur due to mitral valvulitis), mitral regurgitation or aortic regurgitation), pericarditis, endocarditis, myocarditis, pericardial effusion or rub, cardiomegaly, cardiac failure, ECG changes o Mitral valve is most commonly effected  Subcutaneous Nodules  Small firm painless subcutaneous nodules seen on extensor surfaces, joints and tendons.  Erythema marginatum (20% cases)  Transient pink erythematous rash with raised edges, seen on trunk and proximal limbs. They may form crescent- or ring-shaped patches  Chorea (Sydenham’s)  Rapid, involuntary, irregular movements with flowing or dancing quality. May be accompanied by slurred speech. More common in females. Minor criteria:  Pyrexia  Increased inflammatory markers  ESR, CRP or WCC  Arthralgia (only if arthritis is not present as major criteria)  pain in joints  Increased PR and QT intervals on ECG  only if carditis not present as major criteria  Previous rheumatic fever Investigation  Jones criteria  evidence of recent strep infection and 2 major criteria / 1 major + 2 minor  Blood  FBC (increase WCC), ESR/CRP (increased), blood cultures  Evidence of recent strep infection  1 of the following o Increased or rising antistreptolysin O titre (antigen test for group A streptococci) o A positive rapid GAS carbohydrate antigen test o Positive throat swap for GAS  ECG  Saddle-shaped ST elevation and PR segment depression or prolongation (features of pericarditis), arrhythmias.  Echocardiogram  Pericardial effusion, myocardial thickening or dysfunction, valvular dysfunction. Management 1. Antibiotic therapy  benzylpenicillin or phenoxymethylpenicillin or erythromycin base  With arthritis  NSAIDs (aspirin or ibuprofen)  With heart failure  diuretic (furosemide) or ACE inhibitors (enalapril)  With AF  digoxin or amiodarone  With valve leaflet rupture  valve replacement  Severe chorea  anticonvulsants (carbamazepine) NOTE  Rheumatic fever is often recurrent and may cause progressive cardiac damage – secondary antibiotic prevention is important and this may be for up to 10 years in mild heart murmurs (or until 25 years of age), or lifelong for severe heart murmurs/post-surgery. Complications Typically affect mitral valve causing stenosis (can be mixed mitral and aortic). Women are move likely to develop this mitral stenosis Prognosis Acute fever could last up to 3 months if untreated.

Cardiovascular

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ARRYTHMIAS HEART PACING Defibrillation  Treatment for immediately life-threatening arrhythmias with which the patient does not have a pulse, ie ventricular fibrillation (VF) or ventricular tachycardia (VT)  This uses much higher joules for shocks and can be done at any point in the cardiac cycle  GOAL  to terminate disorganised electrical activity Transcutaneous (External) pacing  Temporary means of pacing a patient’s heart during medical emergencies that aren’t as serious as when a defib is needed  typically in bradycardia  GOAL  control the heart rate and/or rhythm DC cardioversion  convert an arrhythmia back to sinus rhythm  patient has a pulse but can be unstable or chemical cardioversion has failed   GOAL  to reset the hearts intrinsic firing rate  The shock must be properly timed, so it does not occur during the vulnerable period (such as T wave)  This is typically an elective procedure where the patient is sedated  Indications  mainly decompensated AF but also supraventricular and ventricular tachycardia  Need to do transoesophageal echocardiogram prior to check no clots in left ventricular appendage (unless new onset AF (100 bpm) with a supraventricular origin. (If its irregular narrow complex = AF) It is usually paroxysmal, and episodes may occur regularly or very infrequently. Aetiology/risk factors  Idiopathic  Hyperthyroidism  Excess alcohol consumption, excess caffeine, cocaine, methamphetamines  Structural abnormality  accessory pathway (AVNRT, AVRT), Previous MI Types  AVNRT (atrioventricular nodal re-entry tachycardia)  is the most common form of SVT and is due to the presence of an extra functionally and anatomically distinct conducting pathways in (or close to) the AVN, which has a fast-conducting and slow-conducting branch o A localised re-entry circuit forms which bypass the actual AV node o Impulse goes down the slow pathway  anterograde conduction o The fast pathway conducts impulses upwards into the atrium  retrograde conduction  Looping round the AVN o Stimulation of atrium occurs at same time as ventricles

Cardiovascular

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AVRT (atrioventricular re-entry tachycardia)  is due to the presence of an accessory bypass pathway that bridges the normal insulation between the atria and ventricles, and lies outside the AVN somewhere else in the heart o A re-entry circuit forms between the atria and ventricles due to the presence of an accessory pathway o Wolff-Parkinson-White syndrome is the most well-known type of AVRT  due to an accessory pathway called the Bundle of Kent o Signa...