Computer generated transcript

Warning!
The following transcript was generated automatically from the content and has not been checked or corrected manually.

MENTI: 2480 7154 Shruti Rajendra sr1220@ic.ac.uk B a s e d o f f s l i d e s f r o m : A k a s h S r i n i v a s a n Cardiac Shortness of Breath MedEd Y3 Written Exam Lectures 2025SESSION STRUCTURE ✓ Heart Failure ✓Cardiomyopathy ✓Constrictive pericarditis ✓MyocarditisSHORTNESS OF BREATH Poor removal of CO 2 Poor delivery of oxygen SHORTNESS OF BREATH 1. Not enough oxygen reaching the lungs Breathing issues • Eg. asthma, COPD, anaphylaxis SHORTNESS OF BREATH 2. Not enough oxygen getting into the blood V/Q mismatch • Eg. PE, pulmonary oedema, pulmonary fibrosis SHORTNESS OF BREATH 3. Not enough oxygen reaching the rest of the body Heart issues (or anaemia, shock etc) SBA 1 Menti: JB is a 34-year-old male, with a history of infective endocarditis, complaining that he’s tired all the time and struggles to run as far as he used to. He also says that his ankles and face feel more swollen than before. On examination, he has a raised JVP, breathing rate and heart rate. You also hear a pansystolic murmur on auscultation. What is the most likely diagnosis? A. Left heart failure secondary to mitral regurgitation B. Left heart failure secondary to cocaine abuse C. Right heart failure secondary to tricuspid regurgitation D. Myocardial infarction E. High output heart failureHEART FAILURE Definition: The failure of the heart to maintain the cardiac output (CO) required to meet the body’s demands Not enough oxygen reaches the rest of the body High Output Acute Left State or or or Chronic Right Low Output State HF: CLASSIFICATION Chronic • Long term condition in which the heart fails to maintain an adequate circulation for the needs of the body Acute • Rapid onset symptoms and signs of heart failure, requiring urgent management • Caused by acute coronary syndrome OR decompensation of chronic heart failureHF: CLASSIFICATION • Left Heart Failure (LHF) • Right Heart Failure (RHF) • LHF + RHF = Congestive Heart Failure (CHF)HF: CLASSIFICATION • Low Output State: Heart fails to pump in response to normal exertion, which means there is low cardiac output • High Output State: Cardiac output is normal but there are higher metabolic needs (eg. pregnancy, anaemia, hyperthyroidism)CHRONIC LEFT HF: AETIOLOGY Valvular • Aortic stenosis • Aortic regurgitation • Mitral regurgitation Muscular • Ischaemia (IHD) • Cardiomyopathy • Myocarditis • Arrhythmias (AF) Systemic • Hypertension • Amyloidosis • Drugs (eg. cocaine, chemo)CHRONIC RIGHT HF: AETIOLOGY Lungs • Pulmonary hypertension (cor pulmonale) • PE • disease, cystic fibrosis) interstitial lung Valvular • Tricuspid regurgitation • Pulmonary valve disease LHF can lead to CHF CHRONIC HIGHT OUTPUT HF: AETIOLOGY Conditions that require a higher cardiac output= strain on the heart NAP MEALS • Nutritional (B1/thiamine deficiency) • Anaemia • Pregnancy • Malignancy • Endocrine • AV malformations • Liver cirrhosis • SepsisHF: SIGNS AND SYMPTOMS What happens if fluid is congested backwards? LHF: fluid accumulates in lungs → respiratory symptoms RHF: fluid accumulates in the peripheries → swelling signs LHF: SYMPTOMS Respiratory Problems OSCETIPS: • Dyspnoea: 1) Assess SOB: “How far are you able to walk • Paroxysmal nocturnal before getting breathless? How many flights of dyspnoea (PND) stairs?” • Exertional dyspnoea 2) Assess orthopnoea: “Have you noticed • Orthopnoea anything making the SOB worse?What about lying down, as opposed standing up?” • Nocturnal cough (+/- pink 3) Assess PND: ”Do you ever wake up at night frothy sputum) gasping for air? How many pillows do you sleep with at night? Has this changed recently?” • FatigueLHF: SIGNS Heart Lungs ➢↑HR, ↑RR ➢ Fine end-inspiratory ➢Irregularly irregular crackles at lung bases heartbeat (pulmonary oedema) ➢Pulsus alternans ➢ Wheeze (cardiac ➢Displaced apex beat asthma) ➢S3 Gallop rhythm ➢S4 in severe HF ➢Murmur (AS, MR,AR) RHF: SIGNS AND SYMPTOMS Symptoms Signs • Fatigue • Face: face swelling • Reduced • Neck: ↑ JVP exercise • Heart/Chest:TR tolerance murmur, ↑ HR, ↑ RR • Anorexia • Abdomen: ascites, • Nausea hepatomegaly • Nocturia • Other: ankle and sacral pitting oedemaHF: SIGNS & SYMPTOMS SUMMARY SBA 1 JB is a 34-year-old male, with a history of infective endocarditis, complaining that he’s tired all the time and struggles to run as far as he used to. He also says that his ankles and face feel more swollen than before. On examination, he has a raised JVP, breathing rate and heart rate. You also hear apansystolic murmur on auscultation. What is the most likely diagnosis? A. Left heart failure secondary to mitral regurgitation B. Left heart failure secondary to cocaine abuse C. Right heart failure secondary to tricuspid regurgitation D. Myocardial infarction E. High output heart failureSBA 1 A. Left heart failure secondary to mitral regurgitation No breathlessness symptoms – LHF unlikely B. Left heart failure secondary to cocaine abuse No breathlessness symptoms – LHF unlikely C. Right heart failure secondary to tricuspid regurgitation Signs of RHF, pansystolic murmur, infective endocarditis D. Myocardial infarction This would present more acutely with crushing chest pain E. High output heart failure No mentioned condition like anaemia or hyperthyroidism HF: INVESTIGATIONS HF can be diagnosed Bedside: ECG clinically using the Framingham’s criteria, but there are useful Bloods: FBC, U&Es, investigations to perform. LFTs,TFTs, BNP Imaging: CXR,TTE HF: INVESTIGATIONS BNP is SENSITIVE but NOT SPECIFIC ↓ BNP ↑BNP HF unlikely TTE HF: INVESTIGATIONS T ransthoracic echocardiogram (TTE) coupled with doppler = DIAGNOSTIC 1. Used to visualise the structure and function of the heart → may show the cause of HF 2. Can calculate ejection fraction (EF): % of the blood present in the LV that gets pumped during systole (normal = 50-70%) EF < 40%: HF with reduced ejection fraction EF > 50%: HF with preserved ejection fraction (HFrEF) – previously called systolic HF (HFpEF) – previously called diastolic HF Indicates inability of the ventricle to Indicates inability of the ventricle to relax and contract normally fill normally HF: INVESTIGATIONS Chest X-Ray Alveolar oedema B-lines (Kerley) Cardiomegaly Dilated upper lobe vessels + Diverted upper lobe pleural effusion)ative HF: DIAGNOSIS Clinical diagnosis can be made using the Framingham Criteria 2+ majors OR 1 major and 2 minors Major: Minor • Paroxysmal nocturnal dyspnoea • Bilateral ankle oedema • Bibasal crepitations • Dyspnoea on ordinary exertion • S3 gallop • Cardiomegaly • Tachycardia rd • Increased central venous pressure • Decrease in vital capacity by 1/3 • Weight loss • Nocturnal cough • Neck vein distension • Hepatomegaly • Acute pulmonary oedema • Hepatojugular reflux • Pleural effusion HF: MANAGEMENT For Chronic HF: 1. Treat the underlying cause 2. Treat the exacerbating factors 3. Lifestyle modifications: smoking cessation, diet (reduce salt), exercise 4. Drugs (ABD): ACE inhibitors, beta-blockers, diuretics HF: MANAGEMENT ACE inhibitors: give to all patients with LV dysfunction • Eg. enalapril, perindopril, ramipril • Can switch toARB if not tolerable (eg. due to cough) Beta-blockers: reduce O dem2nd on the heart • Eg. bisoprolol, carvedilol Diuretics: use if evidence of fluid retention • Loop diuretics (eg. furosemide) • Aldosterone antagonists (eg. spironolactone) Hydralazine + nitrates – considered inAfro-Caribbean patients Digoxin – positive inotrope; improves symptoms but not mortality Cardiac resynchronisation therapy – aims to improve timings of contraction of atria and ventricles HF: MANAGEMENT ForAcute HF: MEDICAL EMERGENCY -ABC DMONS 1. Sit patient upright 2. 60-100% oxygen • Diuretics • Morphine 3. IV Diamorphine 2.5-5 mg • Oxygen • Nitrates 4. GTN infusion • Sit-up 5. IV Furosemide 40-80 mg HF: COMPLICATIONS AND PROGNOSIS Complications: Prognosis: • Respiratory failure • Very poor, worse than most malignancies • Renal failure – due to • 50% of severe HF patients hypoperfusion die within 2 years • Acute exacerbations • Acute HF in-hospital • Death mortality = 2-20% Menti: SBA 2 After measuring BNP levels and performing echocardiography on JB, a diagnosis of heart failure is confirmed.ou perform a chest X-ray as well. What would you expect to see on the CXR? A. Reduced cardio-thoracic ratio B. Lower lobe diversion C. Sharp costophrenic angles D. Kerley C lines E.Alveolar oedema SBA 2 After measuring BNP levels and performing echocardiography on JB, a diagnosis of heart failure is confirmed.ou perform a chest X-ray as well. What would you expect to see on the CXR? A. Reduced cardio-thoracic ratio B. Lower lobe diversion C. Sharp costophrenic angles D. Kerley C lines E.Alveolar oedemaSBA 2 A. Reduced cardio-thoracic ratio Cardiomegaly so cardio-thoracic ratio is increased B. Lower lobe diversion Upper lobe diversion C. Sharp costophrenic angles Pleural effusion results in blunt costophrenic angles D. Kerley C lines Kerley B lines E.Alveolar oedema Left heart failure causes pulmonary oedemaHEART FAILURE: Summary slide Aetiology: Examination: Investigations: Cardiac output ✶ Swelling – RHF Bloods: FBC, U&Es, LFTs,TFTs, BNP insufficient to meet body’s demands Peripheral oedema, ✶ LHF – valve disease (eg. AS),P, ascites muscular issues (eg. MI), CXR: pulmonary oedema, cardiomegaly systemic disease (eg. HTN) ✶ RHF – lung disease (eg. PE), leading to CHF(eg. T✶ Crackles – LHF ✶ High Output – anaemia, Echo: BEST INVESTIGATION hyperthyroidism, pregnancy History: Management: Complications: ✶ DYSPNOEA – LHF ✶ Chronic HF: treat cause, treat exacerbating factors, ✶ Respiratory failure lifestyle measures, drugs (ACEi most important) Orthopnoea (SOB when ✶ Renal failure lying flat) ✶ Acute HF: DMONS – diuretics, morphine, oxygen, Paroxysmal nocturnal ✶ Acute exacerbations dyspnoea nitrates, sit up ✶ VAGUE ✶ Surgical: Heart transplant BAD PROGNOSIS SYMPTOMS – RHF CARDIOMYOPATHY Definition: A group of diseases in which the myocardium becomes structurally and functionally abnormal • In the absence of coronary artery disease, valvular disease and congenital heart disease • It can affect young people Primary: Secondary: confined to the part of a systemic myocardium diseaseCARDIOMYOPATHY: TYPES Dilated – ventricle dilated, thin walls, reduced ventricular pressure Hypertrophic – muscle hypertrophies inwards, more rigid, obstruction etc Restrictive –the same amount of muscle but it is rigid and does not pump as well as normal CARDIOMYOPATHY: PRESENTATION History Examination Investigations • Symptoms of HF: • Signs of HF: • No single diagnostic test ➢SOB on ➢Respiratory for all types exertion crackles • ECHO – main test; used ➢Fainting ➢Murmurs to visualise structure and ➢Fatigue see how the ventricle is ➢S3, S4 pumping • Suddensteath often 1 OSCETIP: • Can also do bloods, BNP, presentation CXR, ECG, cardiac • Family history sudden, unexplained cardiac deatherisation, stress test at a young age (eg. under 50). DILATED CARDIOMYOPATHY Pathophysiology Ventricles enlarge and become dilated. Walls thin and weaken → cannot contract effectively Law of Laplace: increased radius leads to reduced ventricular pressure Risk Factors Alcohol, post-viral, haemochromatosis, genetic Presentation Signs and symptoms of HF Displaced apex beat, TR/MR murmur, S3 Investigations Globular heart on CXR Dilated ventricle on Echo HYPERTROPHIC CARDIOMYOPATHY Pathophysiology • Muscle thickens inwards • Increased stiffness of the muscle affects pumping • Thickened muscle disrupts electrical conduction and causes arrythmia • Hypertrophic Obstructive Cardiomyopathy (HOCM) = thickened ventricle obstructs the outflow of blood • 50% is familial (autosomal dominant) HOCM: PRESENTATION Symptoms Usually asymptomatic Sudden cardiac death is often the 1 presentation Angina, dyspnoea on exertion, palpitations, syncope LVH by voltage criteria: Signs Ejection systolic murmur Jerky carotid pulse ➢ Deep S inV1/2 ➢ Tall R inV5/6 Double apex beat but NOT DISPLACED ➢ S inV1 + R inV5 orV6 ≥ S4 7 large squares Investigations • ECG: Q waves, left axis deviation, signs of left ventricular hypertrophy • Echo: ventricular hypertrophy (asymmetrical septal hypertrophy RESTRICTIVE CARDIOMYOPATHY Pathophysiology • Ventricles become abnormally rigid and lose flexibility • Impaired ventricular filling during diastole • backing up of bloodeduced blood flow + Causes Symptoms • Sarcoidosis, amyloidosis, Asymptomatic or HF symptoms haemochromatosis (the infiltrative ”osis” diseases) Signs • Familial RHF signs: raised JVP, S3, ascites and • Idiopathic oedema, hepatomegaly Rarer than dilated or hypertrophic Kussmaul’s sign = paradoxical rise in JVP cardiomyopathy during inspirationOTHER CARDIOMYOPATHIES Arrhythmogenic RightVentricular Cardiomyopathy • Progressive fatty and fibrous replacement of the ventricular myocardium • Inherited (autosomal dominant) Takotsubo Cardiomyopathy • Sudden temporary weakening of heart muscle after a significant stressor • ”Broken heart syndrome”CARDIOMYOPATHY: Summary slide Definition: Causes: History: Examination: Myocardium is structurally ✶ Dilated – alcohol, ✶ Dilated – similar to HF ✶ Dilated – displaced apex, and functionally abnormal post-viral TR/MR murmur ✶ Dilated – enlarged ✶ Hypertrophic – ✶ Hypertrophic – ejection ventricles familial ✶ Hypertrophic – angina, systolic murmur, jerky carotid SOB, FH of sudden death pulse ✶ Hypertrophic – muscle thickens inwards ✶ Restrictive – sarcoidosis, ✶ Restrictive – similar to ✶ Restrictive – RHF signs, ✶ Restrictive – ventricles amyloidosis, hepatomegaly, Kussmaul’s become rigid haemochromatosis HF sign Investigations: Management: CXR: globular heart (dilated) No cure, manage symptoms and alleviate exacerbating factors with lifestyle changes and medication (eg. stop alcohol, treat ECG: Q waves and signs of left ventricular hypertension) hypertrophy (hypertrophic) Septal myomectomy for HOCM → remove part of the thickened Echo: dilated ventricle (dilated), asymmetrical septum septal hypertrophy (hypertrophic) Manage heartbeat and arrhythmias (ie. pacemaker, ICD) CONSTRICTIVE PERICARDITIS Definition Chronic inflammation of the pericardium (outer sac) with thickening and scarring Causes • Idiopathic • Infectious (TB, bacterial, viral) • Acute pericarditis • Cardiac surgery and radiation Investigations Signs and Symptoms • CXR: pericardial calcification Similar to restrictive cardiomyopathy • Echo: increased pericardial thickness – differentiate • RHF presentation (raised JVP, oedema) from restrictive cardiomyopathy • Kussmaul’s sign • Cardiac CT/MRICONSTRICTIVE PERICARDITIS: Summary slide Examination: Definition: Causes: History: Chronic • Idiopathic inflammation • RHF presentation of the • Infectious (TB, bacterial, Similar to restrictive (raised JVP, oedema) pericardium viral) cardiomyopathy and (outer sac) with • Acute pericarditis heart failure • Kussmaul’s sign thickening and scarring • Cardiac surgery and radiation Investigations: Management: • CXR: pericardial calcification Conservative: reduce activity, reduce salt intake etc • Echo: increased pericardial thickness – differentiate from Medical: anti-inflammatory agents, colchicine restrictive cardiomyopathy • Cardiac CT/MRI Surgical: pericardiectomy MYOCARDITIS Definition Inflammation of the myocardium Inflammatory cardiomyopathy Causes • Infectious • Drugs – cocaine • Metals • Radiation • Coxsackie B virus – most common cause in Europe Signs and Symptoms Investigations • Flu-like prodrome • ECG: non-specific ST and T wave changes • Chest pain – worse when lying down • Cardiac biomarkers: CK and troponin • SOB • Endomyocardial biopsy: diagnostic but • Palpitations not routinely performedMYOCARDITIS: Summary slide Definition: Causes: History and Examination: Causes • Infectious •Flu-like prodrome Inflammation of the • Drugs – cocaine myocardium • Metals •Chest pain (worse when lying down) • Radiation Inflammatory Coxsackie B virus is •SOB cardiomyopathy the most common cause of myocarditis in Europe •Palpitations Investigations: Management: • ECG: non-specific ST and T wave changes Supportive care – viral; usually self-limiting • Cardiac biomarkers: CK and troponin • Endomyocardial biopsy: diagnostic Heart failure management in severe cases but not routinely performed VALVULAR DISEASE Stenosis = narrowing of valve → difficult for blood to pass through Regurgitation = valve does not close tightly → blood is able to flow backwards Both of these can happen to all 4 heart valves Direction of blood flow through the heart must be known in order to predict consequences of each valve defect. Main Causes ofValvular Disease: ✶ Infective endocarditis – especially mitral and aortic valve ✶ Rheumatic fever – especially mitral valve disease ✶ Calcification – especially aortic stenosis ✶ Myocardial infarction – papillary muscle rupture → aortic regurgitation ✶ Congenital causes VALVULAR DISEASE Murmurs • During SYSTOLE, the pulmonary and aortic valves are open. If stenosis of these valves is affecting the flow of blood, there will be a SYSTOLIC murmur. • During DIASTOLE, the pulmonary and aortic valves are closed. If insufficiency/regurgitation of these valves is enabling backflow of blood, there will be a DIASTOLIC murmur. The opposite is true for the mitral and tricuspid valves because these are closed during systole and open during diastole. Tricuspid Tricuspid Pulmonary Pulmonary Aortic Aortic Mitral Mitral Regurgitation Stenosis Regurgitation Stenosis Regurgitation Stenosis Regurgitation Stenosis Pansystolic Mid/late Early diastolic Ejection Early diastolic Ejection Pansystolic Mid/late diastolic systolic systolic diastolic VALVULAR DISEASE Investigations • Simple tests – to investigate the cause (eg. bloods and blood cultures) • ECG – mitral valve disease often presents with atrial fibrillation • Chest X-ray – heart size and shape may change as a result of valvular disease (eg. aortic regurgitation causing left ventricular dilatation) • ECHO – key test for visualising the heart valves and blood flow across the diseased valves Management • Valve replacement – can be done via open surgery or through the transcatheter approach • Replacement valves can be metallic (increased risk of clots afterwards; requires warfarin) or animal tissue (risk of tissue rejection and degeneration) Menti: SBA 3 Aston was a 33-year-old male who suddenly collapsed on stage. Although the doctors attempted “love CPR”, the patient died, and the post-mortem revealed a hypertrophic heart. What was the most likely cause of death? A. Obstructed flow of blood from the heart B.Arrhythmia C. Reduced pumping of blood due to stiff myocardium D. Stroke E. Sub-arachnoid haemorrhage SBA 3 Aston was a 33-year-old male who suddenly collapsed on stage. Although the doctors attempted “love CPR”, the patient died, and the post-mortem revealed a hypertrophic heart. What was the most likely cause of death? A. Obstructed flow of blood from the heart B. Arrhythmia C. Reduced pumping of blood due to stiff myocardium D. Stroke E. Sub-arachnoid haemorrhageSBA 3 A. Obstructed flow of blood from the heart Likely to experience warning symptoms beforehand B. Arrhythmia Most likely cause of death from HOCM, hypertrophic muscle affects electrical circuits C. Reduced pumping of blood due to stiff myocardium Likely to experience warning symptoms beforehand D. Stroke Heart issue rather than brain issue, ventricular arrhythmia (not AF) E. Sub-arachnoid haemorrhage Heart issue rather than brain issue Menti: SBA 4 Oritsé presents with breathlessness and he says that he experienced a fever recently. His CK and troponin are elevated, so a presumptive diagnosis of myocarditis is made. What other signs or symptoms would be consistent with this diagnosis? A. Kussmaul’s sign B.Ankle oedema C.Ascites D. Jaundice E. Chest pain SBA 4 Oritsé presents with breathlessness and he says that he experienced a fever recently. His CK and troponin are elevated, so a presumptive diagnosis of myocarditis is made. What other signs or symptoms would be consistent with this diagnosis? A. Kussmaul’s sign B.Ankle oedema C.Ascites D. Jaundice E. Chest painSBA 4 A. Kussmaul’s sign B.Ankle oedema C.Ascites D. Jaundice All of these are subacute/chronic signs of heart failure, restrictive cardiomyopathy, constrictive pericarditis etc. E. Chest pain Only option which fits with the acute picture of myocarditis Menti: SBA 5 Marvin presents with a 4-month history of increasing breathlessness and ankle swelling. On examination, he has ascites and Kussmaul’s sign is elicited. What would be the most useful diagnostic investigation? A. Echocardiography B. ECG C. Endomyocardial biopsy D.Abdominal X-ray E. CK SBA 5 Marvin presents with a 4-month history of increasing breathlessness and ankle swelling. On examination, he has ascites and Kussmaul’s sign is elicited. What would be the most useful diagnostic investigation? A. Echocardiography B. ECG C. Endomyocardial biopsy D.Abdominal X-ray E. CK SBA 5 A. Echocardiography Allows differentiation between restrictive cardiomyopathy and constrictive pericarditis B. ECG Non-specific signs – not the most useful C. Endomyocardial biopsy Pericardial biopsy might be useful – but highly invasive D.Abdominal X-ray Chest X-ray would be useful to look for pericardial calcifications, but these are not specific to constrictive pericarditis E. CK May be mildly elevated in both constrictive pericarditis and restrictive cardiomyopathy – not that helpful