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ALSchest compressions to ventilation is 30:2 -- continued while a defibrillator is chargedWitnessed VF/VT cardiac arrest, after the third shock adrenaline?1 mg+ 300 mg amiodarone if still VF?is given + chest compressions Adrenaine every 3-5 minutes 2nd dose Amiodarone after 5th shockA single shock for VF/pulseless VT?followed by 2 minutes of CPR, rather than a series of 3 shocks followed by 1 minute of CPRif the cardiac arrested is witnessed then 'up to three quick successive (stacked) shocks', rather than 1 shock followed by CPRasystole / pulseless-electrical activity:?adrenaline?1mg? + 2 minutes of CPR prior to reassessment of the rhythmatropine?is no longer recommended for routine use delivery of drugs via a tracheal tube is no longer recommendedfollowing successful resuscitation oxygen should be titrated to achieve saturations of 94-98%. This is to address the potential harm caused by hyperoxaemiaReversable causes (4H, 4T) (managed after adrenaline and chest compression)HypoxiaHypovolaemiaHyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disordersHypothermiaThrombosis (coronary or pulmonary)Tension pneumothoraxTamponade – cardiacToxinsHeart soundsS1S2S3 (Ventricular gallop rhythm)S4 (Atrial gallop rhythm)closure of MV and TV↓↓ long PRMRSevere MS↑↑ MS mild to moderateClosure of AV and PV ↓↓ ASSplitting during inspiration is normalDiastolic filling of the ventricle Early Diastole (Passive left ventricular filling)?CausesNormal < 30 Ys(Women up to 50 YsLVF ?Dilated Cardiomyopathy gallop rhythm "most specific and early signs"Constrictive Pericarditis(pericardial knock)MRAtrial contraction(late diastole) against Stiff ventricle = P wave on ECGCausesASHOCM Double apical impulse felt due to palpable S4HTN (noncompliant LV) = sign of diastolic HF?ValveSitePulmonary valveLeft 2 intercostal space, at the upper sternal borderAortic valveRight 2 intercostal space, at the upper sternal borderMitral valveLeft 5 intercostal space, just medial to mid clavicular lineTricuspid valveLeft 4 intercostal space, at the lower left sternal borderSites of auscultation Loud S2↑↑Pressure HTN (loud A2) or?PHT?(loud P2)↑↑Volume Hyperdynamic statesASD?without?PHTSoft S2AS and ARfixed split S2ASDwidely split S2deep inspirationRBBBpulmonary stenosissevere?MRReversed (paradoxical) split S2 (P2 A2)LBBBsevere aortic stenosisright ventricular pacingWPW type B?(causes early P2)PDA.MurmursEjection systolicASPSHOCMASD?F4Holosystolic (pansystolic)mitral/tricuspid regurgitation?(High-pitched and 'blowing')ventricular septal defect ('Harsh')Late systolicmitral valve prolapsecoarctation of aortaEarly diastolicAR?(high-pitched and 'blowing' in character)Graham-Steel murmur (pulmonary regurgitation, again high-pitched and 'blowing' inspiration)Mid-late diastolicmitral stenosis?('rumbling' in character)Austin-Flint murmur (severe aortic regurgitation 'rumbling')Continuous machine-like murmurPDA Jugular venous pulseAs well as providing information on right atrial pressure, the jugular vein waveform may provide clues to underlying valvular disease. A non-pulsatile JVP is seen in?superior vena caval obstruction. Kussmaul's sign describes a paradoxical rise in JVP during inspiration seen in?constrictive pericarditis.righttop'A' wave = atrial contractionlarge if atrial pressure e.g.?tricuspid stenosis, pulmonary stenosis,?pulmonary hypertensionabsent if in?atrial fibrillationCannon 'a' wavescaused by atrial contractions against a closed tricuspid valvecomplete heart block,?Atrial Flutter. ventricular tachycardia/ectopics, nodal rhythm, single chamber ventricular pacingRegular cannon wavesventricular tachycardia (with 1:1 ventricular-atrial conduction)atrio-ventricular nodal re-entry tachycardia (AVNRT)Irregular cannon wavecomplete heart block'C' waveclosure of tricuspid valvenot normally visible'x' descent fall in atrial pressure during ventricular systole↑↑ in constrictive pericarditis..'V' wavepassive filling of blood into the atrium against a closed tricuspid valvegiant v waves in tricuspid regurgitationEbestien Anomaly ( associated with TR) 'y' descent Opening of tricuspid valveSlow in tricuspid stenosis or cardiac tamponadeValsalva manoeuvrea forced expiration against a closed glottis ↑↑ intrathoracic pressure which in turn has a number of effects on CVS.Usesto terminate an episode of SVTnormalizing middle-ear pressuresStages of the Valsalva manoeuvre1. ↑↑intrathoracic pressure2. ↑↑ venous and right atrial pressure ↓↓ venous return3. ↓↓ cardiac output (Frank-Starling mechanism)4. When the pressure is released there is a further slight fall in cardiac output due to increased aortic volume5. Return of normal cardiac outputPulsesPulsus paradoxusgreater than the normal (10 mmHg) fall in systolic blood pressure during inspiration → faint or absent pulse in inspirationsevere asthma,?cardiac tamponadeSlow-rising/plateauaortic stenosisCollapsingaortic regurgitationpatent ductus arteriosushyperkinetic states?(anaemia, thyrotoxic, fever, exercise/pregnancy)Pulsus alternansregular alternation of the force of the arterial pulsesevere LVFBisferiens pulse'double pulse' - two systolic peaksmixed aortic valve disease'Jerky' pulsehypertrophic obstructive cardiomyopathy (may occasionally be associated with a bisferiens pulse)Absent radial pulse Takayasu's arteritisaortic dissection with subclavian involvement peripheral arterial embolustrauma and iatrogenic (post-cath).Takayasu's arteritis large vessel vasculitis. It typically causes occlusion of the aorta (obliterative arteritis affecting the aorta) and questions commonly refer to an absent limb pulse.It is more common in females and Asian peopleFeaturessystemic features of a vasculitis e.g. malaise, headacheunequal blood pressure in the upper limbscarotid bruitintermittent claudicationAR (around 20%)Associationsrenal artery stenosisManagementsteroidsCortication of the aorta most commonly at the site of insertion of the ductus arteriosusmales (despite association with Turner's syndromeleft subclavian artery Distal to the ductus arteriosus The commonest site systolic BP in the arms > the leg. Radio-femoral delayProximal left subclavian is involved, systolic BP in the right arm > left arm by more than 30 Infancy: heart failureAdult: hypertension (the most common)mid systolic murmur, maximal over backapical click from the aortic valvenotching of the inferior border of the ribs (due to collateral vessels) is not seen in young childrenClaudicating of the calf muscles.Hypertension (refractory) Associationsbicuspid aortic valveberry aneurysmsTurner's syndromeneurofibromatosisBicuspid aortic valve1-2% of the population, asymptomatic in childhoodthe majority AS or ARassociated with a left dominant coronary circulation (PDA arises from LCX instead of RCA) and Turner's syndrome5% of patients also have coarctation of the aortaComplicationsAS/ ARhigher risk for aortic dissection and aneurysm formation of the ascending aortaAortic dissectiontear in the?tunica intima?of the wall of the aortaAssociationshypertension: the most important risk factortraumabicuspid aortic valve ?six-foldcollagens: Marfan's syndrome, Ehlers-Danlos syndromeTurner's and Noonan's syndromepregnancysyphilisFeatures:chest pain: typically severe, radiates through to the back and 'tearing' in natureAR ( diastolic murmer)hypertensionInvolvement of specific arteries. coronary arteries → angina, spinal arteries →?paraplegia, distal aorta → limb ischaemiaNo or non-specific ECG changes. In a minority of patients,?ST-segment elevation may be seen in the inferior leads ClassificationStanford classificationtype A - ascending aorta, 2/3 of cases, surgical management, but BP controlled to a target systolic of 100-120 mmHg whilst awaiting intervention type B - descending aorta, distal to left subclavian origin, 1/3 of cases Conservative management → reduce blood pressure IV labetalol to prevent progression, Bed rest.DeBakey classificationtype I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distallytype II - originates in and is confined to the ascending aortatype III - originates in descending aorta, rarely extends proximally but will extend distallyManagementCT chest with IV contrast : size and extent of the false lumenChest X-ray: 20% of patients present with normal chest X-ray, Useful first line investigation → readily available and ruling out many other conditionWidened mediastinum, looking for a separation of the intimal calcification from the outer aortic soft tissue border by 10 mm → dissection.?Echocardiogram → identify disruption of the aortic root in a backwardsComplicationsbackward tear : aortic incompetence/regurgitation, inferior MI right coronary involvementforward tearunequal arm pulses and BPstrokerenal failureAortic regurgitationEarly diastolic murmur: Best heard during expiration ↑↑by the?handgrip manoeuvr, Associated with S3 heart sound when LV dysfunction present.wide pulse pressurecollapsing pulseQuincke's sign (nailbed pulsation)De Musset's sign (head bobbing)mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior MV cusps caused by the regurgitation streams. Causes Valve diseaserheumatic feverinfective endocarditisconnective tissue diseases e.g. RA/SLEbicuspid aortic valveAortic root diseaseaortic dissectionspondylarthropathies (e.g. ankylosing spondylitis)hypertensionsyphilisCollagen D: Marfan's, Ehler-Danlos syndrome Dilated cardiomyopathy is associated with the development of mitral regurgitation, not aortic regurgitationAortic stenosischest pain not a marker of severity , Dyspnea, syncope (systolic murmur radiating to carotid + syncope ) → ECHOAn?ejection systolic murmur?(ESM) is classically seen in aortic stenosis. ↓↓ Valsalva manoeuvre. Or after development of LVdyfnction Features of severe aortic stenosisNarrow pulse pressureSlow rising pulseDuration of murmurDelayed ESMsoft/absent S2 A2 componentS4 best indicateThrillLeft ventricular hypertrophy or failure (Apex displacement)(leads to ↓↓ESM) Causes of aortic stenosisdegenerative calcification (most common cause in older patients > 65 years)bicuspid aortic valve (most common cause in younger patients < 65 years)post-rheumatic diseaseWilliam's syndrome (supravalvular aortic stenosis)subvalvular: HOCM An exercise tolerance test would be contraindicated in a patient with suspected aortic stenosisManagementobserve → asymptomatic then valve replacement?symptomatic asymptomatic +?valvular gradient > 40 mmHg?+ features as ↓↓ EF an?angiogram?is often done prior to surgery so that the procedures can be combinedballoon valvuloplasty is limited to patients with critical aortic stenosis who are not fit for valve replacement Mitral regurgitation - pan-systolic murmur. Split second heart sound, Associated with S3 heart sound when left ventricular dysfunction present. Pulmonary regurgitation - decrescendo diastolic murmur. Best heard during inspiration. Often heard with a loud P2.Tricuspid regurgitation - pan-systolic murmur louder during inspiration. Usually difficult to auscultate. May be associated with S3 heart sound.Mitral stenosisRheumatic feverRarer Mucopolysaccharidoses, CarcinoidEndocardial fibroelastosisFeaturesmid-late diastolic murmur (best heard in expiration)loud S1,?opening snaplow volume pulseMalar flushAtrial fibrillationFeatures of severe MSlength of murmur increasesopening snap becomes closer to S2Chest x-rayleft atrial enlargement may be seenEchocardiographythe normal cross sectional area of the mitral valve is 4-6 sq cm. A 'tight' mitral stenosis implies a cross sectional area of < 1 sq cmPercutaneous valvotomy.The intervention of choice for severe mitral stenosisnarrow pulse pressureresistant cardiac failureContra-indications to valvotomymitral valve area >1.5 cm?Left atrial thrombus on ECHO> mild MRSevere valve calcificationSevere concomitant aortic valve diseaseSevere combined mixed tricuspid valve diseaseConcomitant coronary artery disease requiring bypass surgery.Symptoms are not resolved by valvotomy Surgical valve replacementOnly indicated where valvotomy is contraindicated or is unsuccessful.There is very limited opportunity to increase medical therapy population, with systolic blood pressure only just above 100, and a heart rate of 62 beats per minute.Prosthetic heart valvesThe most common valves which need replacing are the aortic and mitral valve. Biological (bioprosthetic) valvesMechanical valvesUsually bovine or porcine in originMajor disadvantage is structural deterioration and calcification over time. Most older patients ( > 65 years for aortic valves and > 70 years for mitral valves) Long-term anticoagulation not usually needed.Warfarin may be given for the first 3 months depending on patient factors. Low-dose aspirin is given long-term.The most common type now implanted is the bileaflet valve. Ball-and-cage valves are rarely used nowadaysMechanical valves have a low failure rateMajor disadvantage is the increased risk of thrombosis Long-term anticoagulation is needed.Aspirin is only given in additional indication, e.g. ischaemic heart disease.Target INRAortic: 3.0Mitral: 3.5Mitral valve prolapseCommon, occurring in around 5-10 % of the population. It is usually idiopathic but may be associated withCongenital heart disease: PDA, ASDCardiomyopathyTurner's syndromeMarfan's syndrome, Fragile XOsteogenesis imperfectaPseudoxanthoma elasticumEhlers-Danlos SyndromeWPWLong-QT syndromepolycystic kidney diseaseFeaturesAtypical chest pain or palpitationsMid-systolic click (occurs later if patient squatting)Late systolic murmur (longer if patient standing)Complications: mitral regurgitation, arrhythmias (including long QT), emboli, sudden deathAtrial septal defects (ASDs)Most likely adulthood congenital heart, significant mortality, 50% of patients die at 50 years.ejection systolic murmur, fixed splitting of S2embolism may pass from venous system to left side of heart causing a stroke Ostium secundum (70% of ASDs)"commonest"associated with Holt-Oram syndrome (tri-phalangeal thumbs)ECG: RBBB with RADOstium primumpresent earlier than ostium secundum defectsassociated with abnormal AV valvesECG: RBBB with LAD, prolonged PR intervalVentricular septal defectthe most common cause of congenital heart disease close spontaneously in around 50% of cases. Associated with chromosomal disorders (Down's syndrome, Edward's syndrome, Patau syndrome) and single gene disorders such as Non-congenital causes include post myocardial infarctionFeaturesclassically a pan-systolic murmur which is louder in smaller defectsComplicationsAR a poorly supported right coronary cusp resulting in cusp prolapsedinfective endocarditisEisenmenger's complexright heart failurePulmonary hypertension: pregnancy is contraindicated in women with pulmonary hypertension as it carries a 30-50% risk of mortalityAtrial myxoma Most common?primary cardiac tumour. ↑↑ in female75% occur in?left atrium, most commonly attached to the?fossa ovalisFeaturessystemic: dyspnoea, fatigue, weight loss,?pyrexia of unknown origin, clubbingemboliatrial fibrillationmid-diastolic murmur, 'tumour plop'echo:?pedunculated heterogeneous mass?typically attached to the fossa ovalis region of the interatrial septumTricuspid regurgitationSignspan-systolic murmurprominent/giant V waves in JVPpulsatile hepatomegalyleft parasternal heave (RV)CausesEbstein's anomalycarcinoid syndromEright ventricular infarctionpulmonary hypertension (COPD, MS) Causes functional tricuspid regurgitation rheumatic heart diseaseinfective endocarditis (especially intravenous drug users) TR + new pan-systolic murmur + large V waves + pulmonary emboli.Investigating palpitationscauses includearrhythmiasstressincreased awareness of normal heart beat / extrasystolesFirst-line investigations include:12-lead ECG: miss episodic arrhythmias. However, other abnormalities linked to the underlying arrhythmia (a prolonged QT interval or PR interval, or changes suggesting recent myocardial ischaemia) thyroid function tests: thyrotoxicosis may precipitate atrial fibrillation and other arrhythmiasurea and electrolytes: looking for disturbances such as a low potassiumfull blood countCapturing episodic arrhythmiasFirst-line investigations are often normal in patients complaining of palpitations. The next step is to exclude an episode arrhythmia.The most common investigation is Holter monitoringportable battery operated devicecontinuously records ECG from 2-3 leadsusually done for 24 hours but may be used for longer if symptoms are less than dailypatients keep a diary to record any symptomatic palpitations. This can later be compared to the rhythm strip at the time of the symptomsat the end of the monitoring (heart rate, arrhythmias and changes in ECG waveform)If no abnormality is found on the Holter monitor, and symptoms continue:external loop recorderimplantable loop recorderSupraventricular tachycardiaWhilst strictly speaking the term supraventricular tachycardia (SVT) refers to any tachycardia that is not ventricular in origin the term is generally used in the context of paroxysmal SVT. Episodes are characterised by the sudden onset of a narrow complex tachycardia, typically an atrioventricular nodal re-entry tachycardia (AVNRT). Other causes include atrioventricular re-entry tachycardias (AVRT) and junctional tachycardias.Acute managementvagal manoeuvres: e.g. Valsalva manoeuvre, carotid sinus massageintravenous adenosine?6mg → 12mg → 12mg: contraindicated in asthmatics - verapamil is a preferable optionelectrical cardioversionPrevention of episodesbeta-blockersradio-frequency ablationAmiodarone is contra-indicated due to the risk of teratogenicity and neonatal goitres. Adenosine and Verapamil can cause decreased uterine blood flow, particularly in higher doses, thus are often avoided. Flecainide can be used, but is initiated in specialist care due to the association with foetal toxicity and hyperbilirubinaemia. Metoprolol, although can cause intra-uterine growth restriction, is seen as the safest as toxicity is usually associated with higher doses in treatment of gestational hypertension.Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, 5% of patients over aged 70-75 , 10% of patients aged 80-85 years. most important aspect is reducing the increased risk of stroke which is present in these patients.Types first detected episode?(whether symptomatic or self-terminating)paroxysmal AF?: ≥ 2 episodes of AF, terminate spontaneously Such episodes < 7 days (typically < 24 hours). persistent AF : not self-terminating, > 7 dayspermanent AF?: continuous AF cannot be cardioverted or if attempts to do so are deemed inappropriate. Symptoms palpitations, dyspnoea, chest pain, irregularly irregular pulseAn ECG is essential to make the diagnosis Management Onset < 48 hoursHeparinizeCardioversion Pharmacology (amiodarone SHD, flecainide or amiodarone in those without structural heart disease Less effective agents ( BB "Sotalol", CCB, Digoxin, disopyramide, procainamide)DC unstable, especially if HTN patient with hypotension.Onset > 48 hoursAnticoagulation 3 weeks prior to cardioversion orTrans-oesophageal echo (TOE) to exclude (LAA) thrombus Heparinised and cardioverted immediatelyAnticoagulation for at least 4 weeks after DC rate control preferred > 65Y, IHD ? BB?or a?rate-limiting CCB?(e.g. diltiazem) is used first-line. If one drug not control the rate → combination therapy with any 2 of the following: BB, diltiazem, digoxin (AF+ HF) Rhythm control tried first if < 65 years - Symptomatic - First presentation - Lone AF or AF secondary to a corrected precipitant (e.g. Alcohol) - Congestive heart failure - Failure of rate control to control symptoms or heart rate. Time of switching from AF to sinus rhythm presents the highest risk for embolism leading to stroke. A stable patient ( AF + obvious cause (alcohol) may revert to sinus rhythm without specific antiarrhythmic treatment Just rehydration If ↑↑cardioversion failure (e.g. Previous failure or AF recurrence) at least 4 weeks amiodarone or sotalol electrical cardioversion Catheter Ablation Electrical activity between the pulmonary veins and left atrium (RFA or Cryo-ablation) Anticoagulation 4 weeks before and during the procedure Lifelong anticoagulation according CHA2DS2VASCComplications cardiac tamponade, stroke, pulmonary valve stenosisSuccess rate 50% of patients early recurrence (within 3 months), often resolves spontaneously Long term 3 years, around 55% of patients single procedure remain in sinus rhythm. 80% patient multiple procedures are in sinus rhythm Risk factorPointsCCongestive heart failure1HHypertension (or treated hypertension)1A2Age >= 75 years2Age 65-74 years1DDiabetes1S2Prior Stroke or TIA2VVascular disease (including IHD and PAD)1SSex (female)1 Reducing stroke risk(coagulation) CHA2DS2-VASc?score anticoagulation strategy.? warfarin and the novel oral anticoagulants (NOACs). Target INR 2-3TIA → in the absence of cerebral infarction or haemorrhage, Anticoagulation should begin as soon as possible ischaemic stroke → waiting two weeks before anticoagulationScoreAnticoagulation0No treatment1Males: Consider anticoagulationFemales: No treatment (score of 1 is only reached due to their gender)2 or moreOffer anticoagulation is commenced to reduce the risk of haemorrhagic transformation Risk factorPointsHHypertension, uncontrolled, systolic BP > 160 mmHg1AAbnormal renal function (dialysis or creatinine > 200)Abnormal liver function (cirrhosis, bilirubin > 2 times normal, ALT/AST/ALP > 3 times normal1 for any renal ↓↓1 for any liver ↓↓SStroke, history of1BBleeding, history of bleeding or tendency to bleed1LLabile INRs (unstable/high INRs, time in therapeutic range < 60%)1EElderly (> 65 years)1DDrugs Predisposing to Bleeding (Antiplatelet agents, NSAIDs)Alcohol Use (>8 drinks/week)1 for drugs1 for alcoholThere are no formal rules on how we act on the HAS-BLED score of >= 3 → 'high risk' of bleeding, ICH, hospitalisation, Hb decrease >2 g/L, and/or transfusion.Do not withhold anticoagulation solely because of the risk of falls (NICE CG180). There is no other reason to consider withdrawing anticoagulation here Combination antiplatelet and anticoagulant therapy 2ry prevention of stable CAD + indication for an anticoagulant (CHAD-VASC)anticoagulant monotherapy is given without the addition of antiplatelets Post-ACS /PCI interventiontriple therapy (2 antiplatelets + 1 anticoagulant) for 1-6 months dual therapy (1 antiplatelet + 1 anticoagulant) for 12 monthsvariation from patient to patient however given that the stroke risk in atrial fibrillation varies according to risk factors. Venous thromboembolism (VTE)if a patient on antiplatelets develops a VTE anticoagulants for 3-6 monthsHAS-BLED score should be calculated. Low risk of bleeding continue antiplatelets. Intermediate or high risk of bleeding consideration should be given to stopping the antiplateletsAtrial flutter'sawtooth' appearanceatrial rate 300/min, dependent on the degree of AV block is 2:1 block the ventricular rate will be 150/min(DD by rate)flutter waves may be visible following carotid sinus massage or adenosineManagementis similar AF, although medication less effectiveAtrial flutter is more sensitive to cardioversion however so lower energy levels may be usedRFA of the tricuspid valve isthmus is curative for most patientsMultifocal atrial tachycardia (MAT)Irregular cardiac rhythm least three different sites in the atria morphologically distinctive P waves. It is more common in elderly patients with chronic lung disease, for example COPDManagementcorrection of hypoxia and electrolyte disturbancesRate-limiting CCB 1st-lineCardioversion and digoxin are not useful in the management of MATWolff-Parkinson WhiteCaused by a congenital accessory conducting pathway between the atria and ventricles leading to a atrioventricular re-entry tachycardia (AVRT). As the accessory pathway does not slow conduction AF can degenerate rapidly to VFPossible ECG features include:short PR intervalwide QRS complexes with a slurred upstroke - 'delta wave'left axis deviation if right-sided accessory pathwayin the majority of cases, or in a question without qualification, WPW left axis deviationright axis deviation if left-sided accessory pathwayDifferentiating between type A and type Btype A (left-sided pathway): RightAxis dominant R wave in V1type B (right-sided pathway): no dominant R wave in V1rare type C WPW, WPW in which the delta waves are upright in leads V1-V4 but negative in leads V5-V6Associations of WPWHOCMMitral valve prolapseEbstein's anomalyThyrotoxicosisSecundum ASDManagementdefinitive treatment: radiofrequency ablation of the accessory pathwaymedical therapy: sotalol should be avoided if coexistent AF ↑↑refractory period at the AV node ↑↑ rate of transmission through the accessory pathway, increasing the ventricular rate VFAmiodarone Flecainide?DC cardioversionVerapamil exerts the most reliable and long-lasting effect on AV node refractoriness and therefore is the most contra-indicated?Broad complex tachycardiaFeatures suggesting VT rather than SVT with aberrant conductionAV dissociationfusion or capture beatspositive QRS concordance in chest leadsQRS > 160 msmarked left axis deviationhistory of IHDlack of response to adenosine or carotid sinus massageIrregular broad-complex tachycardia is it is most likelyAF + LBBB aberrant conduction pathway such as WBWManagement Haemodynamically stable patient Amiodarone.Diltiazem, bisoprolol and adenosine are all contraindicated in irregular broad complex tachycardia enhance the aberrant pathway VFMg for torsades de pointes (polymorphic VT) Complete heart blockSyncoperight coronary artery (RCA) infarction AVN is supplied by the posterior interventricular artery, 90% of patientsheart failureregular bradycardia (30-50 bpm)wide pulse pressureJVP: cannon waves in neckvariable intensity of S1 1st degree heart blockPR interval > 0.2 seconds 2nd degree heart blocktype 1 (Mobitz I, Wenckebach): progressive prolongation of the PR interval until a dropped beat occurstype 2 (Mobitz II): PR interval is constant but the P wave is often not followed by a QRS complex 3rd degree (complete) heart blockthere is no association between the P waves and QRS complexesdigoxindown-sloping ST depression ('reverse tick')flattened/inverted T wavesshort QT intervalarrhythmias e.g.?AV block,?bradycardia↑↑Ca+'bones, stones, groans and psychic moans'corneal calcificationshortened QT interval (Ca+ channels opened for shorter time ↓↓ phase 2 (the plateau phase) prolonged PR, widened QRS and ST elevation.severe cases (un ttt ↑↑ Ca+) ?Osborne (J) waves, VF hypertensionhypokalaemiaEx: Bartter's disease (Kidney disorder associated with excess loss amounts of salt and water .ECG abnormalities begin to appear when K+ falls < 2.7mmol/L.prolong PR intervalST depressionsmall or absent T waves (occasionally inversion)U waves (due to reduced efflux of K+ delayed ventricular repolarisation "T &U" waves )long QTMenomic U have no Pot and no T, but a long PR and a long QT*hyperkalaemia can rarely cause a prolonged PR interval, but this is a much less common association than hypokalaemia.hypothermiaBradycardiafirst degree heart blockAtrial and ventricular arrhythmias'J' wave - small hump at the end of the QRS complexlong QT intervalJ waves are seen in hypothermia whilst delta waves are associated with WPW WPWDelta wave due to early ventricular activation?ECG changes are considered normal variants in an athlete:sinus bradycardiajunctional rhythmfirst degree heart blockWenckebach phenomenonCauses of a?prolonged PR intervalidiopathicIHDdigoxin toxicityhypokalaemia*rheumatic feveraortic root pathology?e.g. abscess secondary to endocarditisLyme diseasesarcoidosismyotonic dystrophyA?short PR interval?is seen in Wolff-Parkinson-White syndromeCauses of ST elevationmyocardial infarctionpericarditis/myocarditisnormal variant - 'high take-off'left ventricular aneurysmPrinzmetal's angina (coronary artery spasm)Takotsubo cardiomyopathyrare: subarachnoid haemorrhageCauses of ST depressionsecondary to abnormal QRS (LVH, LBBB, RBBB)ischaemiadigoxinhypokalaemiasyndrome XCauses of left axis deviation (LAD)left anterior hemiblockleft bundle branch blockinferior MIWPW* -?right-sided accessory pathway↑↑ K+congenital:?ostium primum ASD, tricuspid atresiaminor LAD in obese peopleCauses of LBBBIHDHTNAScardiomyopathyrare: idiopathic fibrosis, digoxin toxicity, ↑↑ K+Left anterior hemiblock (Electricity)left axis deviationAortic stenosis (structural Conduction)left bundle branch block Causes of right axis deviation (RAD)RVHleft posterior hemiblocklateral MIchronic lung disease →?cor pulmonalepulmonary embolismostium secundum ASDWPW * -?left-sided accessory pathwaynormal in infant < 1 years oldminor RAD in tall peopleOne of the most common ways to remember the difference between LBBB and RBBB is WiLLiaM MaRRoW?in LBBB there is a 'W' in V1 and a 'M' in V6in RBBB there is a 'M' in V1 and a 'W' in V6Causes of RBBBnormal variant - more common with increasing ageright ventricular hypertrophychronically increased right ventricular pressure - e.g. cor pulmonalepulmonary embolismmyocardial infarctionatrial septal defect (ostium secundum)cardiomyopathy or myocarditisLong QT syndromeInherited condition associated with delayed repolarization of the ventricles ventricular tachycardia/torsade de pointes?and sudden death. The commonest variants (LQT1 & LQT2) Defects in alpha subunit of the slow delayed rectifier?K+ channel.QT interval (between the start of the Q wave and the end of the T wave ) Normal corrected QT interval < 430 ms in males and 450 ms in females.Drugs prolong the QT interval ?blockage of potassium channels ?overload of myocardial cells with positively charged ions during ventricular repolarisationCongenitalDrugsOtherJervell-Lange-Nielsen syndrome?(Deafness abnormal potassium channel)Romano-Ward syndrome(no deafness)Antiarrhythmics :Amiodarone,?sotalol, class 1a drugsTricyclic antidepressants, SSRI (especially?citalopram)Antipsychotics : Risperidone, HaloperidolMethadone (OPIOD)ChloroquineTerfenadine non-sedating antihistamine, especially if taking P450 enzyme inhibitor, e.g. Patient with a cold takes terfenadine and erythromycin at the same timeErythromycinOndanestron↓↓ Ca+ ,↓↓ K+ , ↓↓Mg+acute myocardial infarctionmyocarditishypothermiasubarachnoid haemorrhage ischaemic strokeMalnutritionFeaturesmay be picked up on routine ECG or following family screeningLong QT1 - usually associated with exertional syncope, often swimmingLong QT2 - often associated with syncope occurring following emotional stress, exercise or auditory stimuliLong QT3 - events often occur at night or at restVT, Torsade de pointes, sudden cardiac deathManagementavoid drugs which prolong the QT interval and other precipitants if appropriate (e.g. Strenuous exercise)beta-blockers sotalol may exacerbate long QT syndromeimplantable cardioverter defibrillators in high risk casesVentricular tachycardiaBroad-complex tachycardia originating from a ventricular ectopic focus precipitate ventricular fibrillation and requires urgent treatment.↓↓ K+ is the most important cause of VT clinically followed by ↓↓Mg++. Severe ↑↑ K+ may cause VT in certain circumstances SHD, but it is not as common a cause as hypomagnesaemiaFusion and capture beats strongly suggests a diagnosis of Ventricular tachycardia (VT)Two main types of VTmonomorphic VT: most commonly caused by myocardial infarctionpolymorphic VT: A subtype of polymorphic VT is torsades de pointes which is precipitated by prolongation of the QT interval. The causes of a long QT interval are listed belowManagementIf Unstable (systolic BP < 90 mmHg, chest pain, heart failure) DC. In the absence of such signs antiarrhythmics may be used. If these fail, then electrical cardioversion may be needed with synchronised DC shocksDrug therapyAmiodarone: ideally administered through a central line.Lidocaine: use with caution in severe LV impairment.ProcainamideVerapamil should NOT be used in VT class IV antiarrhythmic which only acts on nodal tissue May precipitate VFAdenosine is sometimes given in this situation as a 'trial' if there is a strong suspicion the underlying rhythm is a SVT with aberrant conductionIf drug therapy failselectrophysiological study (EPS)implant able cardioverter-defibrillator (ICD) - this is particularly indicated in patients with significantly impaired LV functionTorsades de pointes('twisting of the points') is a form of polymorphic ventricular tachycardia associated with a long QT interval. It may deteriorate into VF SCD Potent blocking of K channels ↑↑↑of cardiac re-polarisation development of membrane oscillations (early after-depolarisation) due to calcium/sodium re-entry.Early after-depolarisation, when propagated may trigger torsade de pointespredisposing factors to drug-induced torsade de pointes include Bradycardia,Electrolyte imbalanceFemale sex genetic polymorphisms in various ion channel constituentsTtt 2gm IV Mg++Brugada syndrome Sudden cardiac death/ prevalence of 1:5,000-10,000/ common in Asians.a large number of variants existAD fashion 20-40% caused by a?mutation in the SCN5A gene sudden cardiac Na encodes the myocardial Na channel proteinECG changesconvex ST segment elevation > 2mm in > 1 of V1-V3 followed by a negative T wavepartial RBBBmore apparent after flecainide or ajmaline investigation of choice in suspected cases implantable cardioverter-defibrillatorCASQ2 gene Ca+ binding protein catecholaminergic polymorphic ventricular tachycardia (CPVT).KCNQ1 and KCNH2 K+ channels long-QT syndrome (Romano-Ward) or short-QT syndrome RYR2 gene cardiac ryanodine receptor catecholaminergic polymorphic ventricular tachycardia (CPVT) and arrhythmogenic right ventricular dysplasiaPeri-arrest rhythms: bradycardiaThe management of bradycardia depends on:Signs indicating haemodynamic compromise - 'adverse signs'Identifying the potential risk of AsystoleAdverse signsShock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousnessSyncopeMIHFManagementAtropine (500mcg IV)?is the first line treatment in this situation.If there is an unsatisfactory response the following interventions may be used:Atropine, up to maximum of 3mgTranscutaneous pacingIsoprenaline/Adrenaline infusion titrated to responseSpecialist consideration of Transvenous pacing if there is no response to the above measures.Potential risk of Asystole ( Indications for Transvenous pacing)Even if there is a satisfactory response to atropine specialist help is indicated to consider the need for Transvenous pacing: if CHB with broad complex QRSRecent asystoleMobitz type II AV blockVentricular pause > 3 secondsCHB + a narrow complex QRS carries the least risk of asystole as the atrioventricular junctional pacemaker may provide an haemodynamically acceptable and stable heart rate. Peri-arrest rhythms: tachycardiaManagement of broad-complex tachycardia, narrow complex tachycardia and Atrial fibrillation have one unified treatment algorithmUnstable (any adverse signs) -- Synchronised DC shock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, clammy extremities, confusion or impaired consciousnesssyncopemyocardial ischaemiaheart failureStable HemodynamicBroad-complex tachycardia RegularVentricular tachycardia (unless previously confirmed SVT with bundle branch block) Loading dose of Amiodarone 24 h infusion IrregularPolymorphic VT (e.g. Torsade de pointes) - IV magnesium.AF with bundle branch block - treat as for narrow complex tachycardiaNarrow-complex tachycardia RegularVagal Maneuvers carotid sinus massageIf this is unsuccessful IV adenosine6mg at first followed by 12mg if no response then further 12mg If unsuccessful consider diagnosis of Atrial flutter and control rate (Beta-blockers) Irregularprobable Atrial fibrillationif onset < 48 hr consider electrical or chemical cardioversionrate control (e.g. Beta-blocker or digoxin) and anticoagulationCardiac catherisation and O2 levelDiagnosis & notesRARVPALALVAortaNormal70%70%70%100%100%100% (ASD) O2 in LA mixes with the deoxygenated blood RA intermediate ↑↑ O2 RA85%85%85%100%100%100% (VSD) O2 in LV mixes with the deoxygenated blood RV, intermediate ↑↑O2 RV onwards. The RA blood remains deoxygenated70%85%85%100%100%100%(PDA) aorta PA This results in only the PA having intermediate ↑↑ O2 PA70%70%85%100%100%100%VSD with Eisenmenger's70%70%70%100%85%85%PDA with Eisenmenger's70%70%70%100%100%85%ASD with Eisenmenger's70%70%70%85%85%85%Pulmonary capillary wedge pressureIs measured using a balloon tipped Swan-Ganz catheter inserted into the pulmonary artery. The pressure measured is similar to that of the left atrium (normally 6-12 mmHg).One of the main uses determining whether PO is caused by either heart failure or ARDS.In many modern ITU departments PCWP measurement has been replaced by non-invasive techniques.Cardiac imagingNuclear imagingradiotracers which are extracted by normal myocardium. Examples include:Thallium'MIBI' or cardiac/Single Photon Emission Computed Tomography (SPECT) scans Technetium (99mTc) sestamibi ( radioisotope technetium-99m + methoxyisobutyl isonitrile (MIBI) ) Myocardial perfusion and myocardial viability. rest & stress (exercise or adenosine / dipyridamole ) areas of ischaemia can classified as reversible or fixed Positron Emission Tomography (PET) scans Fluorodeoxyglucose (FDG) MUGAMulti Gated Acquisition Scan (radionuclide angiography)radionuclide (technetium-99m) is injected IVthe patient is placed under a gamma cameramay be performed as a stress testcan accurately measure LV EF. (before and after cardiotoxic drugs)Cardiac Computed Tomography (CT)calcium score: amount of calcium atherosclerotic plaque calcium is related to the risk of future ischaemic eventsContrast enhanced CT: allows visualisation of the coronary artery lumenhigh negative predictive value for ischaemic heart disease.Cardiac MRIgold standard structural images of the heart. congenital heart disease, ventricular mass and cardiomyopathy.Myocardial perfusion can also be assessed by gadolinium. limited data on the extent of coronary artery disease.Exercise tolerance tests (ETT, also exercise ECG) Indications:suspected angina - guidelines do not support the use of ETTs for all patientssensitivity of around 80% and a specificity of 70% for IHD.risk stratifying following a myocardial infarctionassessing exercise tolerancerisk stratifying of hypertrophic cardiomyopathyHeart rate:maximum predicted heart rate = 220 - patient's agethe target heart rate is at least 85% of maximum (interpretation of a test as low-risk or negative)Contraindications?myocardial infarction < 7 days.unstable anginauncontrolled hypertension (systolic BP > 180 mmHg) or hypotension (systolic BP < 90 mmHg)ASLBBB: ECG very difficult to interpretStop if:?exhaustion / patient request'severe', 'limiting' chest pain> 3mm ST depression> 2mm ST elevation.Stop if rapid ST elevation and painsystolic blood pressure > 230 mmHgsystolic blood pressure falling > 20 mmHgheart rate falling > 20% of starting rateattainment of maximum predicted heart ratearrhythmia developsExercise: physiological changesBlood pressuresystolic ↑, diastolic ↓leads to ↑↑ pulse pressurein healthy young people the increase in MABP is only slightCardiac output↑ in cardiac output may be 3-5 foldDue to venous constriction, vasodilation ,↑ myocardial contractibility, & maintenance of right atrial pressure by ↑↑in venous returnheart rate up to 3-fold increasestroke volume up to 1.5-fold increaseSystemic vascular resistance falls in exercise due to vasodilatation in active skeletal muscles.Blood pressure measurement Reasons for inaccurate values:Wrong cuff size: too small: overestimation of BP. Too large: underestimation of BPThe arm should be horizontal at the level of the heart. Below heart level: overestimation of BP. Above heart level: underestimation of BPPosture: the sitting position is considered standard.Arm support: if the arm is unsupported this may raise the diastolic blood pressure (as the arm is performing isometric exercise)Blood pressure in both arms when considering a diagnosis of hypertension.?difference in readings between arms > 20 mmHg repeat remains > 20 mmHg recorded from the arm with the higher reading.HypertensionSecondary causesprimary hyperaldosteronism (including Conn's syndrome) ?5-10% single most common causeRenal disease accounts for a large percentage glomerulonephritispyelonephritisadult polycystic kidney diseaserenal artery stenosisEndocrine disorders phaeochromocytomaCushing's syndromeLiddle's syndromecongenital adrenal hyperplasia (11-beta hydroxylase deficiency)acromegalyDrug causes:steroidsmonoamine oxidase inhibitors (anti-depressant) (ex: Phenelzine used post surgerythe combined oral contraceptive pillNSAIDsleflunomideOther causes include:pregnancycoarctation of the aortaIsolated systolic hypertensioncommon in the elderly, affecting around 50% of people older than 70 years old. NICE guidelines which recommends treating ISH in the same stepwise fashion as standard hypertension.if the first reading is > 140/90 mmHg second reading during the consultation The lower reading of the two determine managementambulatory blood pressure monitoring (ABPM) and home blood pressure monitoring (HBPM) to any patient with a blood pressure >= 140/90 mmHg to confirm the diagnosis of hypertension & exclude 'white coat hypertension patients whose blood pressure climbs 20 mmHg whenever they enter a clinical settingAmbulatory blood pressure monitoring (ABPM)at least 2 measurements per hour during the person's usual waking hours (for example, between 08:00 and 22:00)use the average value of at least 14 measurementsIf ABPM is not tolerated or declined HBPM should be offered.Home blood pressure monitoring (HBPM)for each BP recording, two consecutive measurements need to be taken, at least 1 minute apart and with the person seatedBP should be recorded twice daily, ideally in the morning and eveningBP should be recorded for at least 4 days, ideally for 7 daysdiscard the measurements taken on the first day and use the average value of all the remaining measurementsIf the blood pressure is >= 180/110 mmHg:immediate treatment if there are signs of papilloedema or retinal haemorrhages same day assessment by a specialistreferral if a phaeochromocytoma is suspected (labile or postural hypotension, headache, palpitations, pallor and diaphoresis)StageCriteriaStage 1 hypertensionClinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHgStage 2 hypertension(20)/10(15)/10Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHgSevere hypertension20)/10Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 110 mmHg Interpreting the resultsABPM/HBPM >= 135/85 mmHg (i.e. stage 1 hypertension)treat if < 80 years of age AND any of the following apply; target organ damage, established cardiovascular disease, renal disease, diabetes or a 10-year cardiovascular risk equivalent to 10% or greaterin 2019, NICE made a further recommendation, suggesting that we should?'consider antihypertensive drug treatment in addition to lifestyle advice for adults aged under 60 with stage 1 hypertension and an estimated 10-year risk below 10%. '. This seems to be due to evidence that QRISK may underestimate the lifetime probability of developing cardiovascular diseaseABPM/HBPM >= 150/95 mmHg (i.e. stage 2 hypertension)offer drug treatment regardless of ageManagementlowering the threshold for treating stage 1 hypertension in patients < 80 years from 20% to 10%Lifestyle advice should not be forgotten and is frequently tested in exams:a low salt diet is recommended, aiming for less than 6g/day, ideally 3g/day. The average adult in the UK consumes around 8-12g/day of salt. A recent BMJ paper* showed that lowering salt intake can have a significant effect on blood pressure. For example, reducing salt intake by 6g/day can lower systolic blood pressure by 10mmHgcaffeine intake should be reducedthe other general bits of advice remain: stop smoking, drink less alcohol, eat a balanced diet rich in fruit and vegetables, exercise more, lose weightABPM/HBPM >=?135/85 mmHg?(i.e. stage 1 hypertension)treat if < 80 years + ( target organ damage or CVD or CKD or DM or a 10-year cardiovascular risk ≥10% )Antihypertensive drug + lifestyle (< 60 + estimated 10-year risk < 10%. QRISK may underestimate the lifetime probability of developing cardiovascular diseaseABPM/HBPM >=?150/95 mmHg?(i.e. stage 2 hypertension)offer drug treatment regardless of ageFor patients < 40 years consider specialist referral to exclude secondary causes. Clinic BPABPM / HBPMAge < 80 years140/90 mmHg135/85 mmHgAge > 80 years150/90 mmHg145/85 mmHg Blood pressure targetsStep 1 patients < 55-years-old?or type 2 DM:? (ACE-i or?ARB):?(A)patients >= 55-years-old?or of?Afro-Caribbean origin:?CCB (C) Step 2 (A + C) or (A + D)if ?ACE-i or?ARB addCCB OR Thiazide-like?Diuretic chlortalidone (12.5–25.0 mg OD) or indapamide (1.5 mg modified or 2.5 mg OD)?they are prefered to a conventional thiazide diuretic (bendroflumethiazide or hydrochlorothiazide) (choose it if the correct answer is thiazide and they are the only applied thiazide)contraindicated history of gout if already taking a?CCB add an?ACE-i or?ARBAfro-Caribbean patients taking CCB, if they require a second agent consider ARB blocker in preference to ACE-I Step 3 (A + C + D) Step 4 first, check for: confirm elevated clinic BP with ABPM or HBPM, postural hypotension, adherenceadd low-dose spironolactone if < K 4.5 > alpha blocker or BBOR specialist advice. Malignant hypertensionsevere hypertension (e.g. >200/130 mmHg)occurs in both essential and secondary typesFibrinoid necrosis of bl.vessels Retinal Hge, exudates, and proteinuria, haematuria due to renal damage (benign nephrosclerosis).Cerebral oedema → EncephalopathyFeaturesClassically: severe headaches, nausea/vomiting, visual disturbanceChest pain and dyspnoea common presenting symptomsPapilloedemasevere encephalopathy (e.g. seizures)Management↓↓ diastolic no lower than 100mmHg within 12-24 hrsbed restmost patients: oral therapy e.g. AtenololIf severe/encephalopathy/ Papilloedema IV Sodium Nitroprusside / LabetololHypertension +Heart failure The echocardiogram shows a degree of left ventricular impairment. It is important an ACE inhibitor is started in such patients. This will help to both control her blood pressure and also slow the deterioration in her cardiac function.Even though bendroflumethiazide is no longer the recommend thiazide of choice, and thiazides now come 'third' in the A + C + D guidelines, NICE do not recommend stopping treatment in patients who are already taking the drug.A beta-blocker should also be added in the near future given the left ventricular impairment.Centrally acting Anti-hypertensives include:methyldopa: hypertension during pregnancymoxonidine: essential hypertension when conventional antihypertensives have failed clonidine: +++ alpha-2 adrenoceptors in the vasomotor centre New drugsDirect renin inhibitors e.g. Aliskiren (branded as Rasilez) blocks the conversion of angiotensinogen to angiotensin I↓↓ blood pressure to a similar ACEI & ARBSno mortality data yet, occasional diarrhea, only patients intolerant to established antihypertensive drugs HTN and D.M Tight blood pressure control (targets < 130/85 mmHg) slightly reduced rate of stroke only not other outcomes.Type 1 diabetes135/85 mmHg? 130/80 mmHg (albuminuria or 2 or more features of metabolic syndrome)Avoid use of BB in uncomplicated HTN, particularly when given with thiazides, ↑↑ insulin resistance ↓↓ (insulin secretion & autonomic response to hypoglycaemia)Type 2 diabetics < 140/90 mmHg, the same as for patients without diabetes.Hydralazine'older' antihypertensives and is not commonly used. It is still sometimes used for hypertension in pregnancy and for severe hypertension.Mechanism of actionincreases cGMP leading to smooth muscle relaxation (Artioles> veins)Contraindicationssystemic lupus erythematousischaemic heart disease/cerebrovascular diseaseAdverse effectstachycardiapalpitationsflushingfluid retentionheadachedrug-induced lupusNitroprusside is degraded into nitric oxide after its administration and the nitric oxide activates the enzyme guanylate cyclase which catalyzes the conversion of GTP to cyclic GMP. Nitroprusside is the preferred drug in a hypertensive emergencyHypertension in pregnancyPre-existing hypertensionPregnancy-induced hypertension?(PIH, also known as gestational hypertension)Pre-eclampsia< 20 weeks gestationhypertension before pregnancy or ↑blood pressure > 140/90 No proteinuria, no oedema?3-5% of pregnancies and is more common in older womensecond half of pregnancy after 20 weeks)No proteinuria, no oedema?Occurs in around 5-7% of pregnanciesResolves following birth (after 1 month). ↑↑ risk of future pre-eclampsia or hypertension after 20 weeks)proteinuria (> 0.3g / 24 hours)Oedema may occur but is now less commonly used as a criteriaOccurs in around 5% of pregnancies↓↓ risk of hypertensive disorders developing in the first place. Women who are at high risk of developing pre-eclampsia should take aspirin 75mg od from 12 weeks until the birth of the baby. hypertensive disease during previous pregnancieschronic kidney diseaseautoimmune disorders such as SLE or antiphospholipid syndrometype 1 or 2 diabetes mellitusIn normal pregnancy:blood pressure usually ↓↓ in the 1st trimester (particularly the diastolic) until 20-24 weeks (end of 2nd )after this time the blood pressure usually ↑↑ to pre-pregnancy levels by termHypertension in pregnancy in usually defined as:Systolic > 140 mmHg or diastolic > 90 mmHgor an increase above booking readings > 30 mmHg systolic or > 15 mmHg diastolicPre-eclampsiaAfter 20 weeks gestation ( pregnancy-induced hypertension + proteinuria (> 0.3g / 24 hours) + Oedema) used to be third element of the classic triad but is now often not included in the definition as it is not specificThere is some evidence to suggest that pre-eclampsia is actually less common in smokersIt predisposes to the following problemsfetal: prematurity, intrauterine growth retardationeclampsiahaemorrhage: placental abruption, intra-abdominal, intra-cerebralcardiac failureHigh risk factors (mother)Moderate risk factors (pregnancy)Hypertensive disease in a previous pregnancyChronic hypertensionChronic kidney diseaseAutoimmune disease: SLE or antiphospholipid syndromeType 1 or type 2 diabetes1st pregnancy≥ 40 years Pregnancy interval of > 10 yearsBMI ≥ 35 kg/m? at first visitfamily history of pre-eclampsiamultiple pregnancy multi-organ failureFeatures of severe pre-eclampsiaHypertension: typically > 170/110 mmHg Proteinuria: dipstick ++/+++headachevisual disturbancepapilloedemaRUQ/epigastric painHyperreflexiaPlatelet count < 100 * 106/l, abnormal liver enzymes or HELLP syndrome ManagementTreating blood pressure > 160/110 mmHg although many clinicians have a lower thresholdOral labetalol first-line, Nifedipine and hydralazine may also be usedDelivery of the baby is the most important and definitive management.Eclampsia Development of seizures in association pre-eclampsia > 20 weeks gestationpregnancy-induced hypertensionproteinuriaMg+ sulphate?is used to both prevent seizures in patients with severe pre-eclampsia and treat seizures once they developGiven once a decision to deliver has been madeEclampsia IV bolus of 4g over 5-10 minutes then infusion of 1g / hourUrine output, reflexes, RR and O2 sat?should be monitored during treatmentrespiratory ↓↓ can occur:?Ca++ gluconate 1st-line for Mg+ sulphate induced respiratory ↓↓treatment should continue for 24 hours after last seizure or delivery (around 40% of seizures occur post-partum)Other aspects of treating severe pre-eclampsia/eclampsia fluid restriction to avoid fluid overload (Pulmonary and cerebral oedema)StatinsInhibit the action of HMG-CoA reductase, ↓↓ (intrinsic) hepatic cholesterol synthesis.Adverse effectsMyopathy: myalgia, myositis, rhabdomyolysis and asymptomatic ↑↑ CK (Not routinely assessed before ttt) Risks factors: ↑↑ age, female, ↓↓BMI and multisystem disease (D.M). ↑↑ lipophilic statins (Simvastatin, Atorvastatin) > hydrophilic statins (Rosuvastatin, Pravastatin, Fluvastatin).liver impairment: LFTs at baseline 3 Ms 12 Ms. Discontinued ↑↑transaminase and persist at 3 times the upper limit of N reference range Continue and repeat LFTs for 1 month if ↑ but < 3 times May ↑↑ the risk of ICH who've previously had a stroke. Not seen in primary prevention Avoid statins with a history ICHContraindicationsMacrolides (Erythromycin, clarithromycin) are an important interaction (stopped until patients complete the course)(- -) CYP3A4 enzyme systemWhilst ciprofloxacin is a 'P450 inhibitor' it affects a different enzyme system and does not produce a clinically significant interactionGrapefruit juice ↓↓of the cytochrome P450 enzyme CYP3A4 - ↑↑ Statin serum level.Pregnancy and also 3 months before attempting pregnancyWho should receive a statin?all people with established cardiovascular disease (stroke, TIA, ischaemic heart disease, peripheral arterial disease)with a 10-year cardiovascular risk >= 10%Patients with type 2 D.M assessed using QRISK2 like other patients determine Statin.(should not automatically prescribed)Patients with type 1 D.M > 10 years OR aged > 40 OR NephropathyAt night (Last thing in evening) majority of cholesterol synthesis (Simvastatin which has a shorter half-life than other Statins)Prevention of CVDAtorvastatin 20mg 1ry prevention fasting lipid profile monitoring to assess response (↑↑dose if non-HDL not ↓↓for >= 40%)Atorvastatin 80mg 2ry preventionHyperlipidaemia: xanthomat Palmar xanthoma remnant hyperlipidaemia less commonly be seen in familial hypercholesterolaemiaEruptive xanthoma ↑↑ triglyceride levels multiple red/yellow vesicles on the extensor surfaces (e.g. elbows, knees) Causes familial hypertriglyceridaemia lipoprotein lipase deficiencyTendon xanthoma, tuberous xanthoma, xanthelasmafamilial hypercholesterolaemiaremnant hyperlipidaemiaXanthelasma are also seen without lipid abnormalitiesManagement of xanthelasma surgical excision, topical trichloroacetic acid, laser therapy, electrodesiccationCoronary circulationArterial supply of the heartleft aortic sinus → left coronary artery (LCA)right aortic sinus → right coronary artery (RCA)LCA → LAD + circumflexRCA → posterior descendingRCA supplies SA node in 60%, AV node in 90%Venous drainage of the heartcoronary sinus drains into the right atriumThe?coronary arteries fill during diastoleWellens' syndrome is an ECG manifestation of critical proximal (LAD) stenosis in unstable angina. symmetrical deep (>2 mm), T wave inversions in the anterior precordial leads ECG changesCoronary arteryAnteroseptalV1-V4Left anterior descendingInferiorII, III, aVFRight coronaryAnterolateralV4-6, I, aVLLeft anterior descending or left circumflexLateralI, aVL +/- V5-6Left circumflexPosteriorTall R waves V1-2Usually left circumflex, also right coronarynew (LBBB)?may point towards a diagnosis of ACS.CAD BB or CCB?first-line based on 'co-morbidities, contraindicationsmaximum tolerated dose?(atenolol 100 od) still symptomatic - add ( BB/ CCB) and vice versa S/E bronchospasm, cold peripheries, Fatigue, sleep disturbances, including nightmares, erectile dysfunctionCI uncontrolled HF, Asthma, SSS, concurrent verapamil use: may precipitate severe bradycardia Cannot tolerate the addition CCB or BB then consider -- long-acting nitrate/ ivabradine ↓↓ HR It acts on the?If?(I = current, F =funny') ion current (highly expressed in the SAN delays depolarisation in SAN ↓↓ cardiac pacemaker activity.metabolised by oxidation through cytochrome P450 3A4 (CYP3A4) only drugs that induce (e.g rifampicin) or inhibit (e.g erythromycin, itraconazole) CYP3A4 affect the plasma concentration. Taking the potent CYP3A4 inhibitor ↑↑ ivabradine visual side effects Adverse effectsvisual effects: particular?luminous phenomena (phosphenes and green luminescence) are common ?15%bright spots appearing in their field of vision. Less commonly blurred vision . ?by inhibition of a channel similar to the If channel found in the retina called the Ih channel. The h = hyperpolarisation-activated, these channels were formerly called IQ channels, Q = queer, again for their unusual characteristicsheadachebradycardia,?heart blocknicorandil ? a vasodilatory drug used to treat angina (if CCB and BB could not be used). It is a?potassium-channel activator with vasodilation is through?activation of guanylyl cyclase which results in increase cGMP.S/E Headache, flushing, anal ulceration CI left ventricular failure Ranolazine inhibit late Na influx, decrease diastolic stiffnes and allows relaxation ↑contractility and perfusion (Caution with liver & kidney ↓; ↑ QT) ( ↓ dose with CYP 3A ↓ (verapamil, Dpltiazem) If a patient is taking both a BB and a CCB then only add a third drug whilst a patient is awaiting assessment for PCI or CABG (stop Apixaban, dabigtran or rivaroxiban 24h before)Aspirin OR clopidogril is most likely to improve his long-term prognosis in stable angina (excertional chest pain) (angina pectoris)?. VS. The benefit of ACE inhibitors and beta-blockers are significant in patients who've had a myocardial infarction but modest in those with stable angina Statin.Nitrates Sublingual glyceryl trinitrate (acute attack).isosorbide mononitrate? starting dose? 10 mg 2/day2nd dose of after 8 hours rather than after 12 hours allows blood-nitrate levels to fall for 4 hours and maintains effectiveness Modified release isosorbide mononitrate (no tolerance)Annual influenza and pneumovax vaccine ≥ 65 or 19 -64 ( smoker, CVD, pulmon, renal, liver, alcoholism, aplenia, transplant, DMCABG improves sympotoms and survival (LM ≥ 50% , 3VD, 2VD≥ 70% + proximal LAD+ DM or ↓EF)If?(I = current, F =funny') ion current?mixed Na and K+ channels found in spontaneously active regions of the heart such as SAN and are triggered by hyperpolarisation. Activated funny channels allow an influx of positive ions, triggering depolarisation and are therefore responsible for the spontaneous activity of cardiac myocytesSyndrome XFeaturesangina-like chest pain on exertionST depression on exercise stress testbut?normal coronary arteries on angiographyManagementnitrates may be beneficial.ACSReferralcurrent or chest pain in the last 12 hours + an abnormal ECG emergency admissionchest pain 12-72 hours ago: refer to hospital same-day for assessmentchest pain > 72 hours ago: perform full assessment with ECG and troponin deciding upon further actionsymptoms consistent with (typical chest pain/atypical angina OR ECG changes):1st line:?CT coronary angiography2nd line: non-invasive functional imaging (looking for reversible myocardial ischaemia)myocardial perfusion scintigraphy with single photon emission computed tomography (MPS with SPECT) orstress echocardiography orfirst-pass contrast-enhanced magnetic resonance (MR) perfusion orMR imaging for stress-induced wall motion abnormalities3rd line: invasive coronary angiography?STEMIPoor prognostic factors (AMERICA) Timi scoring ( high score -- early invasive)INo clinical signs heart failure6% IILung crackles, S317%IIIFrank pulmonary oedema38%IVCardiogenic shock81%agemarkers elevated initial cardiac ECG ST segment deviation Risk factors > 3 /development of heart failure most important factor post MI can be up to 10x more likely to die than those that do not have an MI / Reduced systolic blood pressureCK-MB (Role of 2)2-6 hours16-20 hours2-3 daysTrop T (role of 4)4-6 hours onset12-24 hours peak7-14 days resolve Ischemia (peripheral vascular disease/ Angina past 24h) Cardiac arrest on admissionCreatinine (initial serum concentration)CA stenosis (=/> 50%)Killip class* 30 days mortalityCardiac EnzymesMyoglobin 1-2 h , CKMB,CK, Trep T, AST, LDHTreponin T binds with tropomyocin protein which regulates actin. It associates with actin in muscle fibres and regulates muscle contraction by regulating the binding of myosinCardiac muscle thin filaments ( Treponin + Tropomyosin + Actin) Thick filaments (Myosin)?Sgarbossa criteria?diagnosing MI for patients with?existing?LBBBOriginal Sgarbossa CriteriaConcordant ST elevation?> 1mm?in leads with a positive QRS complex (score 5)Concordant ST depression?> 1 mm?in V1-V3 (score 3)Excessively discordant ST elevation?> 5 mm?in leads with a -ve QRS complex (score 2).Modified Sgarbossa Criteria:≥ 1 lead with ≥1 mm of concordant ST elevation≥ 1 lead of V1-V3(-ve QRS) with ≥ 1 mm of concordant ST depression≥ 1 lead anywhere with ≥ 1 mm STE and proportionally excessive discordant STE, as defined by ≥ 25% of the depth of the preceding S-wave.Management? Prinzmetal angina - treatment = dihydropyridine calcium channel blocker= Amlodipineprimary PCI to patients who present within 12 hours of onset of symptoms, within 90 min Primary PCI is the most treatment given with recent operation and associated risk of bleeding.if it can be delivered to non-pci within 120 minutes of the time when fibrinolysis, less than 12h). tenecteplase is easier to administer and has been shown to have non-inferior efficacy to alteplase with a similar adverse effect profileoxygen saturations are < 94%Sublingual glyceryl trinitrate ( CI: Sildinafil, vardinafil < 24h, tadalafil < 48h, Severe AS, HOCM, RV infarction, SBP < 90 or 30 below baseline morphine + metoclopramide. Aspirin 300mg (unless contraindicated)clopidogrel (Ticagrel / prasurgel ) -- (P2Y12 adenosine diphosphate receptor antagonist ) --------- CathStatin Beta- blocker ACEI/ Aldesteron EF < 40Bivalirudin direct thrombin inhibitor + (aspirin + clopidogrel) + heparin (low-molecular weight or unfractionatedDose-adjusted insulin infusion with regular monitoring of blood glucose levels to glucose below 11.0 mmol intensive insulin therapy (an intravenous infusion of insulin and glucose with or without potassium, sometimes referred to as 'DIGAMI') regimes are not recommended routinelyRight ventricular MI occurs in 30-50% of the cases of inferior MIIV fluids should be administered in controlled quantities in monitored 250ml boluses in hypotension with RV MI to improve RV preload and cardiac throughput. Volume loading has much evidence supporting the increase in cardiac output generated by small doses of IV fluids, particularly in those who are volume deplete.Inotropes if suboptimal response to fluid resuscitation in hypotensive patients. Dobutamine drug of choice improve RV stroke volumeEarly and late complications of myocardial infarction (MI).Cardiac arrest most commonly due to ventricular fibrillation and is the most common cause of death following a MICardiogenic shock inotropic support and/or an intra-aortic balloon pump.Chronic heart failure Loop diuretics such as furosemide ACEI and BBTachyarrhythmia Ventricular fibrillation, ventricular tachycardia.Bradyarrhythmias inferior myocardial infarctions.Pericarditis in the first 48 hours following a transmural MI is common?10% of patientsDressler's syndrome?tends to occur around?2-6 weeks?following a MI. autoimmune reaction against antigenic proteins formed as the myocardium recovers. fever,?pleuritic pain, pericardial effusion and a raised ESR. treated with NSAIDs.Left ventricular aneurysmpersistent ST elevation?and left ventricular failure. Thrombus may form increasing the risk of stroke. Patients are therefore anticoagulated.Left ventricular free wall rupture3% of MIs and occurs around 1-2 weeks afterwardsacute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds). Urgent pericardiocentesis and thoracotomy Ventricular septal defectfirst week and is seen in 1-2% of patients. acute heart failure associated with a pan-systolic murmur. An echocardiogram is diagnostic and will exclude acute mitral regurgitation which presents in a similar fashion. Urgent surgry.Acute mitral regurgitationMore common with infero-posterior infarction and may be due to?ischaemia or rupture of the papillary muscle. Acute hypotension and?pulmonary oedema?. An early-to-mid systolic murmur.treated with vasodilator therapy but often require emergency surgical repair.The best predictor of mortality post-STEMI Above average exercise capacity performed before discharge.MedicationMechanism of actionAspirin 300Antiplatelet - inhibits the production of thromboxane A2ClopidogrelprasugrelTicagrelorTiclopidineThienopyridinesAntiplatelet - inhibits ADP binding to its platelet receptor, (PPIs) may make less effective?( meprazole and esomeprazole !!!!. Other PPIs such as lansoprazole √Prasugrel ___>PCI ( 60 mg loading then 10/day CI if history of stroke, TIA, active bleedingTicagrelor (berlique) : 180 loading then 90/ day , dysnea 15% ↓↓↓enzyme adenosine deaminase convert to clopidogril EnoxaparinFondaparinuxArextra"""Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xaangiography is likely within 24 hours creatinine is > 265 ?mol/l unfractionated heparin( 1/2 life = 60 mg )1 mg protamine sulfate for 100 u heparinFondaparinux if not having angiography within the next 24 hours, not high risk of bleedingBivalirudinDabigatran"NOAC"Reversible direct thrombin inhibitorAbciximab, Eptifibatide,TirofibanGlycoprotein IIb/IIIa receptor antagonistsintermediate or higher risk (predicted 6-month mortality above 3.0%) who undergo angiography within 96 hours of hospital admissionAbciximab thrombocytopenia 1.6 --- stopped± heparin if PLT < 100,000 OR > 50%dropRivaroxaban"Xarelto"direct factor X inhibitorNSTEMI MedicationEarly invasiveTIMI risk score ≥ 3Grace score ≥ 3% 6 month mortality score to guide treatmentRefractory anginaUnstableHigh risk stress testEF< 40PCI/ CABG 6 months agoLowest (<1.5%)Low (1.5-3.0%)Intermediate (3-6%)High (6-9%)Highest(>9%)Aspirin 12 monthsAspirin + Clopidogrel for 12 months & outpatient perfusion/stress imagingGlycoprotein inhibitor & angiography within 96 hoursGlycoprotein inhibitor & angiography within 96 hoursGlycoprotein inhibitorangiography within 96 hoursGRACE score 2ry prevention of MI Diet: Mediterranean style diet(fish,2-5 fruit, veg, bread), cholesterol( <200mg/D), sea food 1-2/ week, switch butter and cheese for plant oil based product, not recommend omega-3 supplements or eating oily fishExercise: advise 20-30 mins a day moderate intensity 5-7 / week until patients are 'slightly breathless'Sexual activity may resume 4 weeks after an uncomplicated MI. Reassure patients that sex does not increase their likelihood of a further MI. PDE5 inhibitors (e.g, sildenafil) may be used 6 months after a MI. and avoided in patient prescribed either nitrates or nicorandilBB For 3Ys normal LV after ACSCarvidilol, bioprolol, metoprolol succinate (ustained release) EF< 40 (HF or MI)Dual antiplatelet therapy (DAPT). Clopidogrel was previously. Now ticagrelor and prasugrel. post ACS (medically managed): add ticagrelor to aspirin, stop after 12 monthspost PCI: add prasugrel or ticagrelor to aspirin, stop the second antiplatelet after 12 monthsthis 12 month period may be altered for people at a high-risk of bleeding or those who at high-risk of further ischaemic eventsAldosterone antagonistsMI + HF + ↓EF (e.g. eplerenone) 3-14 days of the MI, preferably after ACE inhibitor therapyLoop diuretic is not indicated unless there is evidence of fluid overload.Surgery Elective: 30 days if BES , 6 m-1y if DES, 1 year if PCI after ACS Urgent : stop P2Y12 5 days prior and continue ASACoronary angiogramVentricular arrhythmia secondary to irritation of the myocardium. catheter must be pulled back immediately to restore normal sinus rhythm. transient complication of the procedure rather than a patient factor. If all other cardiac investigations are normal and the patient is medically fit, then it would be safe for her to be discharged.Cholesterol embolisation vascular surgery or?angiography, aneurysm repair , severe atherosclerosis, large arteries aorta, eosinophilia 70%, renal disease, purpura, livedo reticularis ?arterial thromboembolism would not be associated with eosinophiliaPercutaneous coronary interventionStents are implanted in around 95% of patients - it is now rare for just balloon angioplasty to be performed Following stent insertion migration and proliferation of smooth muscle cells and fibroblasts Covered by endothelium Until this happens there is an increased risk of platelet aggregation leading to thrombosis.Two main complications may occurStent thrombosis: 1-2% of patients, most commonly 1st monthPlatelet aggregation .presents with acute MIRestenosis:Around 5-20% of patients, most commonly 3-6 months.Excessive tissue proliferation around stent. Presents with the recurrence of angina symptoms. Risk factors include D.M, Renal impairment and Stents in venous bypass graftsTypes of stentBare-metal stent (BMS)Drug-eluting stents (DES): Stent coated with Paclitaxel or Rapamycin.↓↓ Local tissue growth reduces restenosis rates.↑↑Stent thrombosis rates as the process of stent endothelisation is slowed.Longer duration of clopidogrel therapyFollowing insertion the most important factor in preventing stent thrombosis is antiplatelet therapy Aspirin should be continued indefinitely. The length of clopidogrel treatment depends on the type of stent, reason for insertion and consultant preferencePeripheral arterial diseaseStrongly linked to smoking. Patients who still smoke should be given help to?quit smoking.Co morbidities should be treated, includingHypertensionD.MobesityEstablished cardiovascular disease all patients should be taking?Statin (Atorvastatin 80 mg) Clopidogrel? 1st - line in patients with peripheral arterial disease in preference to aspirin.Exercise training?has been shown to have significant benefits. Supervised exercise programme for all patients with (PAD) prior to other interventions.Severe PAD or critical limb ischaemia may be treated by:AngioplastyStentingBypass surgeryAmputationReserved for Critical limb Ischaemia are not suitable for other interventions such as angioplasty or bypass surgery.Drugs licensed (PAD) include:Naftidrofuryl oxalate: 5-HT2 receptor antagonist which causes?vasodilator, may for patients with a poor quality of lifeCilostazol: phosphodiesterase III inhibitor with both antiplatelet and vasodilator effects - not recommended by NICEPericarditis one of the differentials of any patient presenting with chest pain. Featureschest pain: pleuritic. relieved by sitting forwardsnon-productive cough, dyspnoea and flu-like symptomspericardial rub, tachypnoea, tachycardiaCausesviral infections (Coxsackie)tuberculosisuraemia?(causes 'fibrinous' pericarditis)traumapost-myocardial infarction, Dressler's syndromeconnective tissue diseasehypothyroidismmalignancyInvestigationsECG changesglobal/widespread, as opposed to the 'territories' seen in ischaemic events, 'saddle-shaped' ST elevationPR depression: most specific ECG marker all patients with suspected acute pericarditis should have transthoracic echocardiographyA modest rise in troponin is seen in around one-third of patientsManagementtreat the cause, uraemic pericarditis. Haemodialysis is urgently requireda combination of NSAIDs and colchicine first-line for acute idiopathic or viral pericarditisMyocarditisUsually young patient with an acute history chest pain, dyspnoeaCausesViral Coxsackie B, HIVBacteria Diphtheria, ClostridiaSpirochaetes Lyme diseaseProtozoa Chagas' disease, ToxoplasmosisAutoimmuneDrugs DoxorubicinInvestigationsraised inflammatory markers in 99%ECG: ST/T wave changes including ST-segment elevation and T wave inversionComplicationsheart failurearrhythmia, possibly leading to sudden deathdilated cardiomyopathy: usually a late complicationChronic heart failure: diagnosisNYHA Class Ino symptomsno limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitationsNYHA Class IImild symptomsslight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoeaNYHA Class IIImoderate symptomsmarked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptomsNYHA Class IVsevere symptomsunable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activityall patients should have an N-terminal pro-B-type natriuretic peptide (NTproBNP) blood test first-line.if levels are 'high' 2 weeks specialist assessment + TTE if levels are 'raised' 6 weeks specialist assessment + TTE.Very high levels are associated with a poor prognosis.BNPNTproBNPHigh levels> 400 pg/ml (116 pmol/litre)> 2000 pg/ml (236 pmol/litre)Raised levels100-400 pg/ml (29-116 pmol/litre)400-2000 pg/ml (47-236 pmol/litre)Normal levels< 100 pg/ml (29 pmol/litre)< 400 pg/ml (47 pmol/litre)B-type natriuretic peptide Hormone produced mainly by the?left ventricular myocardium?by strain.Increase BNP levelsDecrease BNP levelsLV dysfunction, Heart failure "most common"Age > 70Left ventricular hypertrophyRight ventricular overloadIschaemiaTachycardiaHypoxaemia (including pulmonary embolism)COPDSepsisDiabetesGFR < 60 ml/minLiver cirrhosisACEI, ARBSDiureticsAldosterone antagonistsObesityBeta-blockersEffects of BNPvasodilatordiuretic and natriuretic↓↓ sympathetic tone and the renin-angiotensin-aldosterone systemClinical uses of BNPDiagnosing acute dyspnoea Low concentration of BNP(< 100pg/ml) heart failure unlikely good negative predictive value rather than positive predictive value Raised levels further investigation to confirm the diagnosisPrognosis in chronic heart failure useful marker of prognosisGuiding treatment in patients with chronic heart failureeffective treatment lowers BNP levelsScreening for cardiac dysfunctionnot currently recommended for population screeningManagementdrugs that improve mortality in chronic heart failure (ACEI, BB, spironolactone, hydralazine with nitrates)ACEI and BB have no effect on mortality in HF with?preserved?ejection fraction?first-line ?ACE-inhibitor?and a?beta-blocker only (Bisoprolol, Carvedilol, & Nebivolol). one drug should be started at a timesecond-line either an?aldosterone antagonist, ARBS or a hydralazine + nitrateif symptoms persist?CRT?or?digoxin (NO mortality reduction , should be considered HF+AF)OR?Ivabradine. the criteria includepatient is already on suitable therapy (ACEI, BB+ aldosterone antagonist),HR > 75/min EF < 35%Diuretics? for fluid overload (no long-term reduction in mortality) offer?annual influenza vaccineoffer ?pneumococcal vaccine ( only 1 dose unless asplenia, splenic dysfunction or CKD booster every 5 years)sacubitril-valsartan? neprilysin inhibitor (neprilysin = membrane bound endopeptidase, found in tissues + ↑ concentrations in kidney inactivate ANP & BNP)this drug ?inhibit the breakdown of natriuretic peptides. HF with ↓↓EF who are symptomatic on ACEI or ARBs initiated following ACEi or ARB wash-out period reduce mortality, reduce hospitalisations and improve symptoms in comparison to enalapril.Cardiac resynchronisation therapyfor patients with heart failure EF < 35% and (wide QRS > 120) ,LBBB asynchronous contraction biventricular pacing (synchronous contraction) improved symptoms (exercise tolerance) and ↓↓ hospitalisation in NYHA class III patientsExercise trainingimproves symptoms but not hospitalisation/mortalityLoop diureticsFurosemide and bumetanide loop diuretics inhibit a transmembrane cotransporter protein (Na-K-Cl cotransporter (NKCC)) in the thick ascending limb of the loop of Henle ↓↓ the absorption of NaCl loss of water, NaCl, K+, Ca++ and H+ There are two variants of NKCC loop diuretics act on NKCC2, which is more prevalent in the kidneys.DD. Thiazide ↓↓of the Na+Cl- transporter in distal convoluted tubuleDD. Amiloride and Triamterene ↓↓of Na channels in collecting tubules Indicationsheart failure: both acute (usually intravenously) and chronic (usually orally)resistant hypertension, particularly in patients with renal impairmentAdverse effectshypotensionhyponatraemiahypokalaemia,?hypomagnesaemiahypocalcaemiahypochloraemic alkalosishyperglycaemia (less common than with thiazides)Hyper urecimia. ototoxicityrenal impairment?(from dehydration + direct toxic effect)Thiazide diuretic↓↓ Na reabsorption beginning (proximal part) of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive Na+-Cl??symporter.K+ is lost by sodium-potassium exchanger if ↑↑↑ Na+ reaching the collecting ducts. Another cause of ↓↓ K+ is activation of the renin-angiotensin-aldosterone system secondary to hypovolaemiaTreatment of mild heart failure although loop diuretics are better for reducing overload. The main use of bendroflumethiazide was in the management of hypertension Recent guidelines recommend other thiazide-like diuretics such as indapamide and mon adverse effectsDehydrationpostural hypotensionhyponatraemia,?hypokalaemia,?hypercalcaemia, hypocalciuria and ?metabolic alkalosis conserve Ca++ by ↓↓ its excretion by kidneysWhereas loop diuretics (such as furosemide) ↑↑ Ca++ excretion and ↓↓ serum Ca++ levels.goutimpaired glucose toleranceimpotenceRare adverse effectsthrombocytopaeniaagranulocytosisphotosensitivity?rashpancreatitis Dilated cardiomyopathy (DCM) the?most common form of cardiomyopathy, accounting for 90% of cases.Causes:Idiopathic: the most common causeMyocarditis: e.g.Parvovirus B-19 and human herpes 6 most common, Coxsackie previously, CMV,EBV, HIV, diphtheria,?Chagas diseaseMay present with flu like symptoms, ↓ EF complicated with stroke (cardioembolic) (ECHO)IHDperipartumHTNiatrogenic: e.g.?Doxorubicinsubstance abuse: e.g.?alcohol,?cocaineinherited: either a familial genetic predisposition to DCM or a specific syndrome e.g.?Duchenne muscular dystrophy1/3 DCM genetic predispositiona large number of heterogeneous defects have been identifiedthe majority AD although other patterns of inheritance are seeninfiltrative e.g. haemochromatosis, sarcoidosis + these causes may also lead to restrictive cardiomyopathynutritional e.g.?wet beriberi (thiamine deficiency)↓↓Selenium (as it is anti-oxidant prevent the oxidative modification of lipids protect against CVS)Path physiologydilated heart systolic dysfunctionall 4 chambers are dilated, but the left ventricle more so than right ventricleEccentric hypertrophy (sarcomeres added in series) is seenFeaturesclassic findings of heart failuresystolic murmur: stretching of the valves may result in mitral and tricuspid regurgitationS3'balloon' appearance of the heart on the chest x-rayHypertrophic obstructive cardiomyopathy (HOCM)Prevalence is 1 in 500. The most common cause of?sudden cardiac death in the young.AD?(sibling of affected patient have 50% chance to be affected) genes encoding (sarcomere protein) (contractile proteins) β-myosin heavy chain protein (15-25%)? or myosin-binding protein C 15-25% LVH (myofibrillar hypertrophy with chaotic and disorganized fashion myocytes ('disarray') and fibrosis on biopsy ?diastolic dysfunction decreased cardiac outputAlso Mutations to other proteins ( alpha-tropomyosin and troponin T) Features?Family history of sudden death consider hypertrophic obstructive cardiomyopathyoften asymptomaticexertional dyspnoeaanginaSyncope typically following exercise Due to subaortic hypertrophy of the ventricular septum functional aortic stenosissudden death?(most commonly due to?ventricular arrhythmias), arrhythmias, heart failurejerky pulse, large 'a' waves, double apex beatejection systolic murmur ↑ with Valsalva manoeuvre & ↓on squatting may impair mitral valve closure, thus causing regurgitationAssociationsFriedreich's ataxiaWPWEcho findings?- mnemonic – MR- SAM -ASHmitral regurgitation (MR)systolic anterior motion (SAM) of the anterior mitral valve leafletasymmetric hypertrophy (ASH)ECGleft ventricular hypertrophynon-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seendeep Q wavesAF may occasionally be seenManagementAmiodaroneBeta-blockers or verapamil for symptomsCardioverter defibrillatorDual chamber pacemakerEndocarditis prophylaxis*Drugs to avoidnitratesACE-inhibitorsInotropesVerapamil avoided with coexistent WPW VT or VFPoor prognostic factorsSyncope not chest painfamily history of sudden deathyoung age at presentationnon-sustained ventricular tachycardia on 24 or 48-hour Holter monitoringabnormal (↓↓) blood pressure changes on exerciseAn increased septal wall thickness > 30mmventricular wall thickness Specific genetic mutations (such as in myosin binding protein C and troponin T)Arrhythmogenic right ventricular cardiomyopathy (ARVC) Syncope or sudden cardiac death and palpitation. 2nd most common cause of SCD in the young after HOCMPathophysiologyinherited in an AD with variable expressionMyocardium is replaced by fatty and fibro-fatty tissue50% of patients have a mutation of one of the several genes which encode components of desmosome.InvestigationECG abnormalities in V1-3, typically T wave inversion. An?epsilon wave?is found in about 50% terminal notch in the QRS complexECHO often subtle in the early stages but may show an enlarged, hypokinetic RV with a thin free wallMRI is useful to show fibrofatty tissueManagementdrugs: sotalol is the most widely used antiarrhythmiccatheter ablation to prevent ventricular tachycardiaICDNaxos diseasean autosomal recessive variant of ARVCa triad of ARVC + palmoplantar keratosis, + woolly hairCatecholaminergic polymorphic ventricular tachycardia (CPVT)Inherited cardiac disease associated with sudden cardiac death, AD fashion and prevalence of 1:10,000.the most common cause is a mutation RYR2 gene ↓↓ ryanodine receptor (RYR2) (myocardial sarcoplasmic reticulum)symptoms generally develop < 20 yearsexercise or emotion induced polymorphic ventricular tachycardia syncopeTreated by BB & ICDImplantable cardiac defibrillators1ry ICM (40 days after MI) (90 days after PCI)EF < 35% (NYHA 2,3) EF < 30 NIHA 1 MI with non-sustained VT on 24 hr monitoring, inducible VT EPSlong QT syndrome, Brugada syndromhypertrophic obstructive cardiomyopathy2ry with previous VT,VF with unknown or untreatable causePacemakers: temporaryIndications symptomatic/haemodynamically unstable bradycardia, not responding to atropinepost-ANTERIOR MI: type 2 or complete heart blockpost-INFERIOR MI complete heart block is common and can be managed conservatively if asymptomatic and haemodynamically stabletrifascicular block prior to surgeryEisenmenger's syndrome an uncorrected left-to-right shunt remodeling of the pulmonary microvasculature PHT VSDASDPDAFeaturesoriginal murmur may disappearcyanosisclubbingright ventricular failure?↑↑ JVPsystolic murmur and a loud S2 Haemoptysis, embolismManagementheart-lung transplantation is requiredCardiac tamponadeaccumulation of pericardial fluid under pressure.?Beck's triadhypotensionraised JVPmuffled heart soundsOther features:dyspnoeatachycardiaan absent Y descent on the JVP - this is due to the limited right ventricular fillingpulsus paradoxus?- an abnormally large drop in BP during inspirationKussmaul's sign - much debate about thisECG:?electrical alternansurgent pericardiocentesisThe key differences between constrictive pericarditis and cardiac tamponade are summarised in the table below: Common features between 2 types ↓↓(blood pressure, heart sounds) , ↑↑ (JVP, HR)Cardiac tamponadeConstrictive pericarditisJVPAbsent Y descentX + Y presentPulsus paradoxusPresentAbsentKussmaul's signRarePresentCharacteristic featuresPericardial calcification on CXRRestrictive cardiomyopathyCausesamyloidosis (e.g. secondary to myeloma) - most common cause in UKhaemochromatosispost-radiation fibrosisLoffler's syndrome: endomyocardial fibrosis with a prominent eosinophilic infiltrateendocardial fibroelastosis: thick fibroelastic tissue forms in the endocardium; most commonly seen in young childrensarcoidosissclerodermaPathophysiologyprimarily characterized by decreased compliance of the ventricular endomyocardiumcauses predominately diastolic dysfunctionFeaturessimilar to constrictive pericarditislow-voltage ECGFeatures suggesting restrictive cardiomyopathy rather than constrictive pericarditisprominent apical pulseabsence of pericardial calcification on CXRthe heart may be enlargedECG abnormalities e.g. bundle branch block, Q wavesInvestigationsechocardiographycardiac MRI Rheumatic feverRheumatic fever develops following an immunological reaction to recent (2-6 weeks ago)?Streptococcus pyogenes?infection.?PathogenesisStreptococcus pyogenes?infection → (++) immune system leading to antigen presentation to T cellsB and T cells produce IgG and IgM antibodies and CD4+ T cells are activatedCross-reactive immune response (a form of type II hypersensitivity) thought to be mediated by?molecular mimicryCell wall of?Strept. Pyogenes?(M protein, a virulence factor & highly antigenic) Abs against M protein cross-react with myosin and smooth Ms.arteriesleads to the clinical features of rheumatic feverAschoff bodies? Granulomatous Nodules found in rheumatic heart feverAnitschkow cells Enlarged Macrophages + Ovoid, Wavy, Rod-like NucleusOther DD.Councilman bodies hepatitis C, yellow feverMallory bodies alcoholism (hepatocytes)Call-Exner bodies Granulosa cell tumourSchiller-Duval bodies yolk-sac tumourDiagnosis is based on evidence of recent streptococcal infection accompanied by:2 major criteria1 major with 2 minor criteriaEvidence of recent streptococcal infectionraised or rising streptococci antibodies,positive throat swabpositive rapid group A streptococcal antigen testMajor criteriaerythema marginatumSydenham's chorea: this is often a?late featurepolyarthritiscarditis and valvulitis (eg, pancarditis)*subcutaneous nodulesMinor criteriaraised ESR or CRPpyrexiaarthralgia (not if arthritis a major criteria)prolonged PR interval*The latest iteration of the Jones criteria (published in 2015) state that rheumatic carditis cannot be based on pericarditis or myocarditis alone and that there must be evidence of endocarditis (the clinical correlate of which is valvulitis which manifests as a regurgitant murmur).Infective endocarditisThe strongest risk factor for developing infective endocarditis is a?previous episode?of endocarditis. Types of patients are affected:Previously normal valves (50%, typically acute presentation)the mitral valve is most commonly affectedRheumatic valve disease (30%)Prosthetic valvesCongenital heart defectsintravenous drug users (IVDUs, e.g. typically causing?tricuspid?lesion)others:?recent piercingsCausesStaph aureus?is the most common cause of infective endocarditis (↑↑ acute presentation and?IVDUs), lung cavitations?Strept. viridans?α-hemolytic?2nd commonest 20% of cases. no longer the commenest, except in developing countries.? The most viridians Streptococcus mitis?and?Streptococcus sanguinis. Found in the mouth and in particular dental plaque linked with?poor dental hygiene?or dental procedure Strept.s bovis??colorectal cancer, elderly and immunocompromised (subtype?Streptococcus gallolyticus?is most linked).? most appropriate investigation after culture is colonoscopy Prosthetic valve < 2 months after surgery coagulase -ve Staphylococci (Staph epidermidis, colonize indwelling lines) Perioperative contamination. >2 months? cause returns to normal (Staphylococcus aurous?"most common")non-infective: systemic lupus erythematosus (Libman-Sacks), malignancy: marantic endocarditisCulture negative causesprior antibiotic therapyCoxiella burnetii ?(an abattoir, cattle/sheep or inhaled from infected dust)BartonellaBrucella most common bacteria contracted from contact with animals (sheep and goats). unprocessed animal products in endemic countries of the Mediterranean and middle East such as Syria, Iraq, Turkey, Greece and Tunisia. Infection is characterised by a malodorous 'wet-hay smell.'HACEK:? Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella) Lives on dental gums and are more common in intravenous drug users.Modified Duke criteriaInfective endocarditis diagnosed ifpathological criteria positive, or2 major criteria, or1 major and 3 minor criteria, or5 minor criteriaPathological criteria+Ve histology or microbiology obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments or intracardiac abscess content)Major criteriaPositive blood culturesTwo +Ve blood cultures typical organisms consistent with infective endocarditis (Streptococcus viridans?and HACEK group)persistent bacteraemia 2 blood cultures > 12 hours apart or ≥ 3 positive blood cultures less specific (Staph aureus?and?Staph epidermidis)positive serology for?Coxiella burnetii,?Bartonella?species or?Chlamydia psittaci, positive molecular assays for specific gene targets Evidence of endocardial involvementpositive echocardiogram (oscillating structures, abscess formation, new valvular regurgitation or dehiscence of prosthetic valves), ornew valvular regurgitationMinor criteriapredisposing heart condition or intravenous drug usemicrobiological evidence does not meet major criteriafever > 38?Cvascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpuraimmunological phenomena: glomerulonephritis, Osler's nodes, Roth spotsPoor prognostic factorsStaphylococcus aureus?infection (see below)prosthetic valve (especially 'early', acquired during surgery)culture negative endocarditis↓↓ complement levelsMortality according to organismstaphylococci -?30%bowel organisms - 15%streptococci -?5% streptococcal infection carries a good prognosisScenarioSuggested antibiotic therapyInitial blind therapynormally the antibiotic course is 6 weeks.Native valveamoxicillin + low-dose gentamicinpenicillin allergic, MRSA or severe sepsis vancomycin + low-dose gentamicin Prosthetic valvevancomycin + rifampicin + low-dose gentamicinNative valve staphylococciFlucloxacillinPenicillin allergic or MRS vancomycin + rifampicinProsthetic valve staphylococciFlucloxacillin + rifampicin + low-dose gentamicinPenicillin allergic or MRSA vancomycin + rifampicin + low-dose gentamicinfully-sensitive streptococci (e.g. viridans)Benzylpenicillin?Penicillin allergic vancomycin + low-dose gentamicinless sensitive streptococciBenzylpenicillin + low-dose gentamicinPenicillin allergic vancomycin + low-dose gentamicinIndications for surgery (Urgent)severe valvular incompetenceaortic abscess (often indicated by a lengthening PR interval)infections resistant to antibiotics/fungal infections (+/- perivalvular abscess, fistulae, perforation)Acute cardiac failure?refractory to standard medical treatmentrecurrent emboli after antibiotic therapyPregnancyInfective endocarditis: prophylaxisProcedures do not require prophylaxis:dental proceduresupper and lower gastrointestinal tract proceduresupper and lower respiratory tract; this includes ear, nose and throat procedures and bronchoscopygenitourinary tract; urological, gynaecological and obstetric procedures and childbirthThe guidelines do however suggestany episodes of infection in people at risk of infective endocarditis should be investigated and treated promptly to reduce the risk of endocarditis developingif a person at risk of infective endocarditis is receiving antimicrobial therapy because they are undergoing a gastrointestinal or genitourinary procedure at a site where there is a suspected infection they should be given an antibiotic that covers organisms that cause infective endocarditisEuropean Society of Cardiology guidelines which still advocate antibiotic prophylaxis for high-risk patients who are undergoing dental procedures. Antibiotic prohylaxis is not routinely recommended in the UK for dental and other procedures NICE GuidancePulmonary arterial hypertensionDefined as a resting mean pulmonary artery pressure of >= 25 mmHg. Endothelin thought to play a key role in pathogenesis of PAH. It is more common in females and typically presents between the ages of 30-50 years.Around 10% of cases are inherited in an AD fashion.Right ventricular failure is the most common cause of death in patients with primary pulmonary hypertension.Pulmonary hypertension may of course develop secondary to chronic lung diseases such as COPD – PAH is diagnosed in the absence of this although certain factors increase the risk,HIV, cocaine Anorexigens(e.g. fenfluramine). Featuresprogressive exertional dyspnoea is the classical presentationExertional syncope, exertional chest pain and peripheral oedemaCyanosisRV heave, loud P2, raised JVP with prominent 'a' waves, tricuspid regurgitationDiagnosis Cardiac catheterisation is the single most important investigation all patients need to have right heart pressures measured. Echocardiography may strongly point towards a diagnosis of pulmonary hypertension A ventilation/perfusion scan can help to look for causes of pulmonary artery hypertension such as chronic pulmonary embolismManagementTreating any underlying conditions( anticoagulants or oxygen)Acute vasodilator testing?is central such as intravenous Epoprostenol or inhaled nitric oxide.+Ve response to acute vasodilator testing?(a minority of patients) oral?calcium channel blockers–Ve response to acute vasodilator testing?(the vast majority of patients)?improve symptoms, delay disease progression and improve survival.Prostacyclin analogues PGI2? vasodilatory effects and↓↓ platelet aggregation Treprostinil, IloprostEndothelin receptor antagonists ↓↓ pulmonary vascular resistance ↓↓ RV strain (RV failure) Ambrisentan (S\E peripheral oedema, sinusitis, flushing and nasal congestion) Bosentan,?Phosphodiesterase (PED5) inhibitors ↑↑cGMP in pulmonary vessels (relaxing vascular smooth muscle and ↓↓PA pressure) SildenafilPatients with progressive symptoms should be considered for a heart-lung transplant.Pulmonary embolism(around 10%) present with triad of pleuritic chest pain, dyspnoea and haemoptysis.PE is difficult to diagnose can present with any cardiorespiratory symptom/sign depending on its location and size.The relative frequency of common clinical signs is shown below:Tachypnea (respiratory rate >20/min) - 96%Crackles - 58%Tachycardia?(heart rate >100/min) - 44% (Well's criteria for diagnosing a PE use tachycardia rather than tachypnoea)Fever (temperature >37.8°C) - 43% Low-grade pyrexia is common in pulmonary embolism.Type 1 respiratory failure in a tachycardic, tachypnoeic with an absence of chest signs points pulmonary embolismShould have a history taken, examination performed and a chest x-ray to exclude other pathology.Pulmonary embolism rule-out criteria (PERC) If no +Ve criteria pre-test probability is <15% (PERC Rule criteria are satisfied) If any +Ve criteria (PERC rule cannot be used to rule out PE).Age ≥ 50, HR 100. O2sat room air < 95%, Unilateral leg swelling, HemoptysisRecent surgery or trauma (Surgery or trauma ≤4 weeks ago requiring treatment with general anesthesia)Prior PE or DVTHormone use Oral contraceptives, hormone replacement or estrogenic hormones use in males or female patientif your suspicion of PE > 15 straight to the 2-level PE Wells score, without doing a PERCClinical featurePointsClinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins)3An alternative diagnosis is less likely than PE3Heart rate > 100 beats per minute1.5Immobilisation for more than 3 days or surgery in the previous 4 weeks1.5Previous DVT/PE1.5Haemoptysis1Malignancy (on treatment, treated in the last 6 months, or palliative)1Clinical probability simplified scores≤ 4 points PE unlikely D-dimer test negative alternative diagnosis> 4 points PE likely Immediate computed tomography pulmonary angiogram (CTPA).If there is a delay in getting the CTPA interim therapeutic anticoagulation until the scan is performed low-molecular weight heparinNICE 2020 intrim anticoagulant that will be long term direct oral anticoagulant (DOAC) apixaban or rivaroxabanIf the patient has an allergy to contrast media or renal impairment a V/Q scan should be used instead of a CTPA.CTPA or V/Q scan?CTPA advantages than V/Q the initial lung imaging modality of choice speed, easier to perform out-of-hours, ↓↓ further imaging may give an alternative diagnosis if PE is excludedif the CTPA is negative then patients do not need further investigations or treatment for PEV/Q scanning m initially if facilities exist, x-ray is normal, no significant symptomatic concurrent cardiopulmonary disease. V/Q scanning is also the investigation of choice if there is?renal impairment(doesn't require the use of contrast unlike CTPA)D-dimers sensitivity = 95-98%, but poor specificityECGa large S lead I, a large Q lead III and an inverted T lead III - 'S1Q3T3' ( in no more than 20% of patients)right bundle branch block and right axis deviation are also associated with PEsinus tachycardia?may also be seenChest x-raya chest x-ray is?recommended for all patients?to exclude other pathologyhowever, it is typically?normal in PEpossible findings include a?wedge-shaped opacificationV/Q scansensitivity of around 75% and specificity of 97%other causes of mismatch in V/Q include old pulmonary embolisms, AV malformations, vasculitis, previous radiotherapyCOPD gives matched defectsCTPAperipheral emboli affecting subsegmental arteries may be missedPulmonary angiographyThe gold standardsignificant complication rate compared to other investigationsManagementdirect oral anticoagulants (DOACs) as first-line treatment for most people with VTEDOACs in patients with active cancer, as opposed to LMWH previously recommended.Patient has cancer and suffered multiple DVTs in a short space of time, despite being fully anti-coagulated. ↑↑ INR to 3–4 for long term high-intensity oral anticoagulant therapy orSwitching to LMWH.'IVC filters for patients with recurrent proximal DVT or PE despite adequate anticoagulation treatment only after considering alternative treatments outpatient treatment in low-risk pulmonary embolism (PE) patientsroutine cancer screening is no longer recommended following a VTE diagnosisOutpatient treatment in low-risk PE patientsDVT and PE with low-risk outpatients. Pulmonary Embolism Severity Index (PESI) score used for assessment.key requirements haemodynamic stability, lack of comorbidities and support at homeAnticogulant therapyChoice of anticoagulant2020 guidelines was the increased use of DOACsapixaban or rivaroxaban (both DOACs) should be offered first-line following the diagnosis of a PEonce a diagnosis is suspected, with this continued if the diagnosis is confirmedif neither apixaban or rivaroxaban are suitable LMWH + dabigatran or edoxaban OR LMWH + vitamin K antagonist (warfarin)if the patient has active cancernew guidelines now recommend using a DOAC, unless this is contraindicatedif renal impairment is severe (e.g. < 15/min) unfractionated heparin or LMWH followed by a VKAif antiphospholipid syndrome (specifically 'triple positive' in the guidance) LMWH followed by a VKA should be usedLength of anticoagulationall patients should have anticoagulation for at least 3 monthscontinuing anticoagulation after this period is partly determined by whether the VTE was provoked or unprovokedA provoked VTE (obvious precipitating event) immobilisation major surgery transient and no longer at increased risk initial 3 months OR (3 to 6 months for people with active cancer)unprovoked VTE No obvious precipitating event (e.g. mild thrombophilia) making the patient more at risk from further clots Typically continued for up to 3 further months (i.e. 6 months in total)3-6 months anticoagulant is based upon balancing a person's risk of VTE recurrence and their risk of bleedingthe HAS-BLED score can be used to help assess the risk of bleedingNICE state: 'Explain to people with unprovoked DVT or PE and a low bleeding risk that the benefits of continuing anticoagulation treatment are likely to outweigh the risks.?'. The implication of this is that in the absence of a bleeding risk factors, patients are generally better off continuing anticoagulation for a total of 6 monthsPE with haemodynamic instabilityThrombolysis is now recommended as the first-line treatment for massive PE other invasive approaches should be considered where appropriate facilities exist Repeat pulmonary embolismsDespite adequate anticoagulation, ?inferior vena cava (IVC) filters stopping clots formed in the deep veins of the leg from moving to the pulmonary arteries. Paradoxical embolisationRight-sided (Venous) thrombus (DVT) left-sided (Arterial) embolism (stroke) pass from the right-to-left side of the heartcardiac lesions may cause patent foramen ovale around 20% of the population May be association between migraine and PFO improvement in migraine after closure of the PFOASD a much less common causeTOE superior views of the atrial septum is preferred to TEE for detecting PFOStroke management is controversial (antiplatelet, anticoagulant or PFO closure)Pregnancy: DVT/PE investigationFor patients with a suspected deep vein thrombosis (DVT):Compression duplex ultrasound should be undertaken where there is clinical suspicion of DVTFor patients with a suspected pulmonary embolism (PE):ECG and chest x-ray should be performed in all patientsSymptoms and signs of DVT compression duplex ultrasound should be performed. If compression U\S confirms DVT no further investigation and treatment for VTE should continue May provide indirect evidence of a pulmonary embolism. As both conditions require anticoagulation this may negate the need for further radiation exposure.The decision to perform a V/Q or CTPA should be taken at a local level after discussion with the patient and radiologistComparing CTPA to V/Q scanning in pregnancyCTPAV/Q scanningSlightly ↑↑the lifetime risk of?maternal breast cancer?(↑↑ up to 13.6%, background risk of 1/200 for study population).Pregnancy makes breast tissue particularly sensitive to the effects of radiationSlightly ↑↑ risk of?childhood cancer?compared with CTPA (1/50,000 versus less than 1/1,000,000)D-dimer is of limited use in the investigation of thromboembolism as it often raised in pregnancy.Warfarinoral anticoagulant (--) Epoxide reductase? (--) reduction of Vit. K to active hydroquinone form( cofactor in the carboxylation of clotting?factor II, VII, IX and X and protein C.IndicationsDVT target INR = 2.5 if recurrent 3.5AF target INR = 2.5Mechanical valves MV higher INR than AVINR (international normalised ration), the ratio PT ?for the patient over the normal PT . Warfarin has a long half-life and achieving a stable INR may take several days. There a variety of loading regimes and computer software is now often used to alter the dose.Factors that may potentiate warfarinLiver diseaseP450 enzyme inhibitors, e.g.: amiodarone, ciprofloxacincranberry juiceDrugs which displace warfarin from plasma albumin, e.g. NSAIDsInhibit platelet function: NSAIDsSide-effectshaemorrhageTeratogenic but safe in breastfeeding mothersskin necrosis: when warfarin is first started biosynthesis of protein C is ↓↓. This results in a temporary procoagulant state after initially starting warfarin, normally avoided by concurrent heparin administration. Thrombosis may occur in venules leading to skin necrosispurple toesStoppage before interventional Dentistry in warfarinised patientsIf history of stable INR check INR 72 hours before procedure, proceed if INR < 4.0If history of an unstable INR checked within 24 hours of the dental procedure.Patients on warfarin having emergency surgery:can wait for 6-8 hours give 5 mg vitamin K IVcan't wait (Aortic Aneurysm) 25-50 units/kg four-factor prothrombin complexManagement of high INR Emphasised the preference of prothrombin complex concentrate over FFP in major bleeding FFP can take time to defrost prothrombin complex concentrate should be considered in cases of intracranial haemorrhageSituationManagementMajor bleedingStop warfarinGive intravenous vitamin K 5mgProthrombin complex concentrate - if not available then FFP*INR > 8.0Minor bleedingStop warfarinGive intravenous vitamin K 1-3mgRepeat dose of vitamin K if INR still too high after 24 hoursRestart warfarin when INR < 5.0INR > 8.0No bleedingStop warfarinGive vitamin K 1-5mg by mouth, using the intravenous preparation orallyRepeat dose of vitamin K if INR still too high after 24 hoursRestart when INR < 5.0INR 5.0-8.0Minor bleedingStop warfarinGive intravenous vitamin K 1-3mgRestart when INR < 5.0INR 5.0-8.0No bleedingWithhold 1 or 2 doses of warfarinReduce subsequent maintenance doseINR > 8.0 (no bleeding) - stop warfarin, give oral vitamin K 1-5mg, repeat dose of vitamin K if INR high after 24 hours, restart when INR < 5.0The BNF recommends a dose of between 1 to 5mg of vitamin K in this situation.DVLA RulesHTN drive unless treatment causes unacceptable side effects, no need to notify DVLA. Disqualifies as Group 2 driving if resting BP consistently ≥180 systolic and/or ≤100 diastolic angina stop driving if symptoms occur at rest/at the wheelAngioplasty (elective) 1 week off drivingCABG 1 month off drivingACS 1 month off driving, 1 week if successfully treated by PCIpacemaker 1 week off driving ICD 1 month (prophylactic) Having an ICD results in a 6 months (2ry prevention) permenant cessation for group 2 successful catheter ablation for an arrhythmia- 2 days off drivingaortic aneurysm of 6cm or more - notify DVLA. Licensing will be permitted subject to annual review. An aortic diameter of 6.5 cm or more disqualifies patients from driving heart transplant: DVLA do not need to be notified Symptomatic heart failure will lead to revocation of a Group 2 licence, regardless of whether the symptoms lead to incapacity. If a patient on treatment becomes asymptomatic, then they may be relicensed only if their LVEF is >= 40%.For Group 1 entitlements, the DVLA does not need to be informed of symptomatic heart failure if it does not lead to distracting or incapacitating symptoms.Scoring systemsScoring systemNotesCHA2DS2-VAScUsed to determine the need to anticoagulate a patient in atrial fibrillationABCD2Prognostic score for risk stratifying patients who've had a suspected TIANYHAHeart failure severity scaleDAS28Measure of disease activity in rheumatoid arthritisChild-Pugh classificationA scoring system used to assess the severity of liver cirrhosisWells scoreHelps estimate the risk of a patient having a deep vein thrombosisMMSEMini-mental state examination - used to assess cognitive impairmentHADHospital Anxiety and Depression (HAD) scale - assesses severity of anxiety and depression symptomsPHQ-9Patient Health Questionnaire - assesses severity of depression symptomsGAD-7Used as a screening tool and severity measure for generalised anxiety disorderEdinburgh Postnatal Depression ScoreUsed to screen for postnatal depressionSCOFFQuestionnaire used to detect eating disorders and aid treatmentAUDITAlcohol screening toolCAGEAlcohol screening toolFAST*Alcohol screening toolCURB-65Used to assess the prognosis of a patient with pneumoniaEpworth Sleepiness ScaleUsed in the assessment of suspected obstructive sleep apnoeaIPSSInternational prostate symptom scoreGleason scoreIndicates prognosis in prostate cancerAPGARAssesses the health of a newborn immediately after birthBishop scoreUsed to help assess the whether induction of labour will be requiredWaterlow scoreAssesses the risk of a patient developing a pressure soreFRAXRisk assessment tool developed by WHO which calculates a patients 10-year risk of developing an osteoporosis related fractureRanson criteriaAcute pancreatitisMUSTMalnutrition*FAST is also mnemonic to help patients/relatives identify the symptoms of a strokeNext question? ................
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