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1 Cardiology Teaching JOE SHAW MZYJS36@NOTTINGHAM.AC. UKCardiac Failure & Infective EndocarditisCardiac Failure & Infective Endocarditis u Learning Outcomes u Recap of cardiac physiology u Pathophysiology HF u Conditions that can lead to HF u Risk factors and Aetiology of IE u Clinical features, Investigations and management of both HF and IE u OSCE & SBA tips along the wayHeart Failure u Overview u Inability of the heart to maintain adequate cardiac output u“A problem with how your heart pumps” uCaused by abnormal cardiac structure or function u Most common causes: uIschaemic heart disease & Hypertensive heart disease u Associated with a high morbidity and mortality u Poor prognosis uApprox. 50% die within 5 yearsHeart Failure u Classification u Acute vs chronic u Right sided vs Left sided u Systolic (HFrEF) vs Diastolic (HFpEF) u High output vs Low outputBasic Physiology u Overview u Diastole vs Systole u Diastole uThe filling of the ventricles u Systole uThe contraction of the ventricles Basic Physiology u Cardiac Output u Heart failure = failure of cardiac output u “failure / inefficiency of the pump” u Cardiac Output = Stroke volume x Heart Rate u Stroke volume: u Preload u Stretching of the cardiomyocytes u Volume of blood in ventricles prior to contraction / systole u ↑ preload = ↑ CO u Contractility u Myocardial contractility u How hard it pumps u ↑ contractility = ↑ CO u Afterload u Pressure or load against which the ventricles must contract u Systemic Vascular Resistance u ↓ afterload = ↑ CO Pathophysiology u Overview u Heart failure occurs when there is a reduction in CO u This occurs when there is a pathophysiological change in either preload, contractility or afterload u That’s because -> ↓ stroke volume and hence, ↓ in CO u E.g. MI u Ischaemic damage to the cardiomyocytes u ↓ contractility = ↓ CO = HEART FAILURE u E.g. Hypertension u ↑ in afterload -> heart has to PUSH harder against high blood pressure u ↑ afterload = ↓ CO = HEART FAILURE u E.g. Restrictive cardiomyopathy u ↓ in preload as stiff ventricle walls impair diastolic filling of the ventricles u ↓ preload = ↓ CO = HEART FAILUREHeart Failure u Aetiology u u 1) Vascular u 3) Valvular uIHD (35-40%) uStenotic valves uHypertension (15-20%) uRegurgitant valves u 2) Muscular u 4) Electrical uDilated Cardiomyopathy (30%) uArrythmias uHypertrophic cardiomyopathy uCongenital heart disease Pathophysiology u Compensatory mechanisms u Increasing heart rate (sinus tachycardia) u S u m u CO = SV x HR m a ry u Activation of RAAS u ↓ C O c a u Due to renal hypoperfusion u se sR u ->W A A S t u Increased venous pressure through vasoconstriction and retention of sodium leads contributes to ater e e o be a oedema & water retention u ->W n ion,v ctiva u orsen sH asoco n te d u ↑ Afterload B a o re F sricton c ep t u Sympathetic nervous system activation u o s a c ↑ H ea r tv a te u Low cardiac output activates baroreceptors -> increases myocardial activity and heart rate trate t d b y ↓ o try o C O u Leads to Ventricular Hypertrophy & RAAS activation ↑ C O u -> ↓ Contractility Chronic Heart Failure u Clinical Featur- gradually worsened over months to years u Symptoms u Signs u SOB u Raised JVP u Cough: pink frothy sputum u Displaced Apex u Fatigue u Coarse Crackles u Wheeze u Ankle swelling u Paroxysmal nocturnal dyspnoeaHeart sounds S3/S4 u Orthopnoea u Hepatomegaly u Peripheral oedema u Ascites u Have a set of questions ? HF u “How many pillows do you sleep on?” u “Do you ever wake up at night feeling like you might be drowning?” u “Have you noticed your slippers are tighter than usual?” Chronic Heart Failure u Left vs Right heart failure Left= Lung uLeft u Right (cor pulmonale) Right Restof heb ody u SOB u Raised JVP u Cough: pink frothy sputum u Peripheral pitting oedema u Fatigue u Ascites u Wheeze u Enlarged liver & spleen u Paroxysmal nocturnal dyspnoeu Anorexia u Orthopnoea u Weight gain u Restlessness u Tachycardia u Cyanosis Chronic Heart Failure u Investigations u Bedside u Bloods u Imaging u Special tests u CXR u Coronary angiogram u Baseline obs u FBC, U&Es, LFTs, u ECG u Troponin -> ?MI recentu ECHO u Cardiac catheterization u Cardiac MRI u 24hr ECG u Urinalysis u Lipids / HbA1c u Lung function tests u ? DM / renal diseaseu CVD health / DM u TFTs u BNP u Cardiomyopathy screen dget! s ve no bu st aton SCE’sha g &inve u O ed fndin u U nl iInvestigations u ECG changes u Tachycardia u Atrial Fibrillation u Left Axis deviation (LVH) u Prolonged PR interval (AV block) u Wide QRS complexes (ventricular dyssynchrony)Investigations u BNP u Should be measured in all patients who present with ?HF u B-type natriuretic peptide (BNP) is a hormone released by left ventricular myocardium in response to strain u Can also be raised in u Left ventricular hypertrophy u Tachycardia •>2000 ng/L •refer urgently for specialist assessment and transthoracic u Liver cirrhosis echocardiography within 2 weeks •400-2000ng/L u Diabetes •refer routinely for specialist assessment and transthoracic echocardiography within 6 weeks u Acute or chronic renal disease •<400 ng/L •heart failure unlikely •Used primarily to rule out HFInvestigations u CXR u A -> E u A – Alveolar oedema u Bat wing / perihilar opacification u B – Kerley B lines u Interstitial oedema u C – Cardiomegaly u D – Dilated upper lobe vessels u E – Effusions u Pleural effusions -> blunted costophrenic angles Chronic Heart Failure u Classification u “Iwo ud thro wa ntto ug h h eirE en quie a u Structural classification h ey are H C HO resu bo utthisp u “ FrEF orHIF ltsto ind a tin ’sL u Based on LVEF Iw ou ldc pEF ” ou tw heth V EF sc om lassfy h s e r u HFrEF = <40% LVEF i fora ble a p ate ntC n p hysica trest but a ssIIa sth u HFpEF = >50% LVEF la ctiiy ” has m arke e pa ten t d lm ta io ns u Symptomatic / functional u New York Heart Associations classification system (NYHA) Chronic Heart Failure uManagement – supportive 1) Life style u 3) Optimise co-morbidities u Fluid and salt restriction u Hypertension u 5) Cardiac u Regular exercise u Diabetes Rehabilitation u Smoking cessation Program u AF / CAD u Reduced alcohol intake u u u u 2) Vaccination u 4) Medication r/v u Identify meds which can u All patients offered yearly worsen HF influenza and one-off pneumococcal disease u E.g. CCBs, Lithium, NSAIDs, prolonging medications u uCardiac Rehabilitation uOverview uHolistic approach to cardiac healthcare uCombines “Bio-psycho-social” principle uOSCE catch phrase – examiners love it Chronic Heart Failure uManagement – medical (<40% LVEF / HFrEF) u 2ndline therapy uBAD – Beta blockers, ACEi and Diuretics u 1) Aldosterone antagonist e.g Spironolactone u u ↓ RAAS activation u Diuretics u Added to ACEi and Beta-blocker u E.g. Furosemide 20mg OD Look out for hyperkalaemia if paired with ACEi u All patients are prescribed a diuretic to relieve symptoms of fluid overload e.g. furosemide u 3rd line therapy u Works by reducing cardiac afterload -> improving stroke volume1) Ivabradine u No long-term reduction in mortality associated u 2) Sacubitril-valsartan u 1 line therapy u 3) Digoxin u 1) ACE inhibitor e.g Ramipril 1.25mg OD u 4) Hydralazine + nitrate u ↓ RAAS activation so ↓ afterload u 5) SGLT2 inhibitors u 2) Beta blockers e.g. Bisoprolol 1.25mg OD u 5) Cardiac resynchronization therapy u ↓ sympathetic activation & improve LVEF Different clinical scenarios dictate different 3 line NICE advise starting one drug at a time therapies -> passmed v useful u u u 1 line therapy u 1) ACE inhibitor e.g Ramipril u 2) Beta blockers e.g. Bisoprolol NICE advise starting one drug at a time Chronic Heart Failure Acute Heart Failure uOverview u u Acute heart failure may present as new-onset or an acute decompensation of chronic heart failure u High mortality rate u Leading cause of hospital admission in people aged 65< in the UK u Rapid onset or worsening of the signs and symptoms of heart failure uPathophysiology u Acute failure of the heart to pump blood u Causes : u 1) Congestion u Due to pulmonary hypertension -> pulmonary oedema u 2) Hypoperfusion u End organ hypoperfusion due to reduced cardiac outputAcute Heart Failure u uCauses u New-onset AHF u Acute myocardial dysfunction e.g. MI -> ischaemia u Acute valve dysfunction u Arrythmias u Acute decompensation of CHF u Infection u Acute myocardial dysfunction -> MI u Uncontrolled hypertension u Arrythmias u Worsening valve disease u Change in drug regimen – med r/v Acute Heart Failure u Management Sit up O2 • 15L non-rebreathe mask u A to E assessment Diuretics • e.g. IV furosemide 20-50mg u SOD A CIN Alert cardiology CPAP Inotropic support Nitrates (IV)Heart Failure Key Tips u u Chronic Heart Failure Acute Heart Failure u Caused by reduced cardiac output An acute, life-threatening drop in cardiac output u Most common causes are IHD and HTN Sit up u Symptoms of SOB, fatigue, peripheral oedema O2 • 15L non-rebreathe mask u Key Ix -> ECG, BNP, ECHO u CXR -> A to E Diuretics • e.g. IV furosemide 20-50mg u Mx -> BAD -> Beta-blockers, ACEis, Diuretics Alert cardiology CPAP Inotropic support Nitrates (IV)u EndocarditisEndocarditis u uOverview uAn infective vegetation on a heart valve u“pyrexia with a new or changing murmur” uMost commonly affected valve is the: umitral valve uLife threatening condition – very difficult to fight injection due to location uMortality rate 40% worldwide uCan presents as an acute, rapidly progressive infection uGlobally becoming more prevalent and associated with significant morbidity and mortalityEndocarditis equen cy: uPathophysiology uFr u1) Bacteraemia uMital uPathogens enter the blood stream o ri rti uA d mital&ao uVia dental infections, IVDU, intra-operative uCom bie u2) Attach to the valves s i uTrcu uPathogens will then attach to exposed endothelium on dPulgonaralves uDamage present due to valvulopathies or prosthesis u u3) Pathogens form a vegetation uThrough deposition of platelets and fibrin u4) Poor immune response uEndocardium is poorly vascularized meaning very difficult to clear infection u5) Embolisation uCausing cerebral infarcts, pulmonary infarcts or pulmonary abscesses u6) Circulating Immune complexes kidneys and eyess can also begin circulating and deposit in organs such as the skin, Endocarditis uRisk factors u uPatient uCardiac uAge uStructural heart disease u>60 >50% uValvular heart disease uMale > Female uRheumatic valve disease uIVDU uCongenital heart disease uDirect injection of skin flora intorosthetic heart valves circulation uPrevious IE uTricuspid valve uDamaged valves = predisposed uDentition / poor oral hygiene uEndocarditis uAetiology u uMainly caused by bacterial infections that enter blood stream and attach to the heart valves u1) Staph Aureus uMost common cause uEspecially common in IVDU’s u2) Strep Viridans uAssociated with poor dental hygiene or following dental procedure u3) Staph Epidermis uMost common following prosthetic valve surgery uOnly for 1st 2 months post surgery u4) Strep Bovis uColorectal cancer -> Bovis and Bowel Endocarditis uClinical features u uIE most commonly associated with fever (90%) and Cardiac murmurs (85%) -> pyrexia with a new or changing murmur M AJO R PEN M u r u Symptoms uSigns m ur A nae mia u Fever (90%) uCardiac Murmur (85%) Jane w uHeart failure O a yLe ions u Malaise slerNo des uRaised JVP, bilateral crackles h spo u Anorexia ts u Weight loss uSplinter haemorrhages uPetechiae P ye ia u Abdominal pain Em bo i uJaneway lesions Na uSplenic abscess uOsler Nodes h l- u Cardiac symptoms aem orrhag e uRoth spots s uSOB, chest pain, palpitations uSplenomegaly uClinical features uOsler’s Nodes – Osler’s Ow u Janeway Lesions Endocarditis uSplinter Haemorrhages uRoth Spots Endocarditis uEmbolic Phenomenon u u Around 25% of patients with IE will have evidence of emboli u Hands and feet uOsler nodes and Janeway lesions u Ophthalmological uRoth Spots u Neurological uCerebral abscess, embolic stroke, intracerebral haemorrhage u Septic Emboli uSplenic, renal, pulmonary abscess, septic arthritis, vertebral osteomyelitis u Immune reactions uGlomerulonephritis, synovitis Endocarditis u u Major Criteria uDiagnosis u Positive Blood cultures uModified Duke’s Criteria u 2 blood cultures showing typical organisms associated with IE uIE can be diagnosed with uPathological criteria positive, or u Persistent bacteraemia from 2 cultures taken >12 hrs u2 Major criteria, or u Positive Echo u1 major and 3 minor criteria, or u New valvular regurgitation u5 minor criteria u Minor Criteria u Pathological Criteria u Predisposing heart condition or IVDU u Positive histological or microbiology of pathological u Micro evidence does not meet major criteria material obtained at autopsy or cardiac surgery u Fever >38*C u Vascular phenomena e.g. Janeway lesions, petechia u Immunological phenomena e.g. Roth spots, GlomerulonephritisEndocarditis u u uInvestigations uImaging uBedside uTransthoracic Echocardiogram uBaseline Obs u1 line Ix uUrine dip (glomerulonephritis) uTransoesophageal echo uECG uCXR uBloods uCT chest uFBC, U&Es, LFTs, CRP/ESR uPre-operative uVBG ? Sepsis 6 uBlood cultures u3 sets of blood cultures to be taken 30 mins apart Endocarditis uManagement uRefer uRefer to cardiology and contact microbiology • Surgical uReferral to ‘Endocarditis team’ • 50% of cases will require surgery to repair or u Involve cardiologist, cardiothoracic surgeon, replace the affected valve microbiologist and specialist nurse uIndications for surgery: u E.g. “I would escalate to cardiology, inform microbiology and contact the local endocarditis team” u Cardiac failure uMDT approach u Uncontrolled infection u Prevention of embolism uMedical uProlonged course of Broad Spectrum IV Abx uIV 2/52s then switch to oral uRefer to local guidelines & liaise with micro Endocarditis uComplications uLocalised uSystemic uValve destruction uSeptic emboli uHeart failure uE.g. Stroke, splenic infarction, abscess’ uSecondary to valve regurgitation uImmune complex deposition u Arrythmias and conduction disorderuE.g. glomerulonephritis uMyocardial infarction uSepticaemia uPericarditis uDeath uAortic root abscess Infective Endocarditis Key Tips u Consider in pyrexia of unknown origin +/- new murmur u IVDU, dental operations and structural valvulopathy increase risk st u 1 line Ix = Blood cultures u Diagnosis made using Duke’s Criteria u 1 Pathological, 2 Major, 1 Major 3 minor, 5 minor u Treatment with prolonged Abx +/- surgery u Complications include heart failure, embolic events and death Useful sources uHeart failure • Endocarditis u • https://app.pulsenotes.com/medicine/ca https://app.pulsenotes.com/medicine/cardiology/n rdiology/notes/infective-endocarditis otes/heart-failure • https://geekymedics.com/infective- uhttps://www.youtube.com/watch?v=ypYI_lmLD7g endocarditis/ uhttps://www.youtube.com/watch?v=q2t9sFITAIY • https://www.youtube.com/watch?v=10R uhttps://www.youtube.com/watch?v=ItKGeEbzAis aKBTTyeo u u Thank you! Any Questions? mzyjs36@nottingham.ac.uk