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Chest Pain and Syncope Xavier Machado 4th yea, Cardiovascular Sciences BSc xmd21@ic.ac.ukStructure Best way to learn, in my opinion, is through understanding Memory will help, but understanding will get you those last few marks to get awards Definition Epidemiology Pathophysiology Background Classification Aetiology Overview Investigations Diagnosis Clinical Features Criteria ManagementContent Theres a lot, will be difficult to focus on everything in amount of depth I want If thers anything you want more teaching on/notes, email me For this talk I have used BMJ best pract, NICE (CKS), StatPearls and my own notes Ischaemic Heart Disease Cardiac Arrest Arrhythmias Stable Angina Atrial Fibrillation Unstable Angina Atrial Flutter ACS NSTEMI WPW SVT STEMI VT + VF Syncope Heart blockContent There’s a lot, will be difficult to focus on everything in amount of depth I want If thers anything you want more teaching on/notes, email me Presentations Cardiorespiratory arrest Chest pain Palpitations Blackouts and faints (use that red Oxford book) Decreased/loss of consciousnessConcept Heart has two main functions: 1 Pump Circulation, functional 2 Battery Conduction, electrophysiology Stuff can go wrong with either one and covers most conditionsConcept Heart has two main functions: 1 Pump Circulation, functional 2 Battery Conduction, electrophysiologyIschaemic Heart Disease Definition Inadequate blood supply (circulation) to a local area due to blockage of the Ischaemic blood vessels supplying the area Ischaemic AKA coronary heart disease (CHD) Heart Disease arteries that supply blood to the heart muscle (myocardium)ry) (Stable) Angina Unstable Angina Ischaemic Heart NSTEMI Disease Acute Coronary Syndrome STEMIIschaemic Heart Disease Background Describes the gradual build up of fatty plaques within the walls of the coronary arteries Two main problems Gradual Narrowing -> less blood -> less 1 oxygen -> tissue demand not met -> myocardial damage -> angina Gradual build up of plaque -> plaque 2 instability increases -> sudden plaque rupture -> sudden occlusion of artery (thrombosis/embolism)Ischaemic Heart Disease Background Atherosclerosis By far most common way to develop ischaemic heart disease Hopefully there is another lecture dedicated to talking about this in more depth Risk Factors: Unmodifiable: age, male, family history Remember these 5 CV risk factors Modifiable: Smoking, DM, HT , dyslipidaemia, obesity Endothelial dysfunction Smooth muscle (smoking, hypertension) proliferation -> fibrous capsule over fatty plaque Pro-inflammatory state Foam cells Fatty infilitration Monocytes -> (LDL particles) macrophagesStable Angina Definition Symptom of myocardial ischaemia Characterised by chest discomfort that is provoked with exertion and relieved at rest Epidemiology Aetiology Ischaemic heart disease Coronary disease is leading Supply-demand mismatch cause of morbidity and mortality worldwide Other is non-atherosclerotic; beyond 1c S: substernal chest. O: sudden (may have Stable Angina had before) C: heaviness/tightness R: neck/jaw/left arm. A: dyspnoea, fatigue, Diagnosis nausea. T: n/a E: provoked with exercise/ relieved by rest S: high 5+ Approach Look at symptoms + risk factors Determine if symptoms are stable or not (could be ACS ⚠) History Angina - pretty obvious What is angina? Use SOCRA TES in OSCE Often a triad: Physical Exam 1 Substernal chest discomfort Signs of HF, HCM or risk factors (prev surgery) Provoked by exercise Investigations 3 Relieved with rest Bedside: ECG (Q-wave) Imaging: echo, CXR, coronary angiography Bloods: FBC (haemoglobin); renal function; lipid panel; HbA1c; tropsStable Angina Diagnosis S: substernal chest O: sudden (may have had before) C: heaviness/tightness R: neck/jaw/left arm A: dyspnoea, fatigue, nausea Q-Wave > 40 ms (1 mm) wide T: n/a > 2 mm deep > 25% of depth of E: provoked with exercise/relieved by rest QRS complex S: high 5+ Seen in leads V1-3 Sign of previous ischaemiaStable Angina Management Goals Improve QoL through symptomatic relief and activity increase Improve outcomes by reducing complications (MI + death) Treatment algorithm Education and lifestyle modification Cardiac rehabilitation, physical a, diet, weight management, smoking Low-dose aspirin / clopidogrel High-dose statins Consider revascularisiation (PCI/CABG) Can get B-blockers, sublingual GTN sprayAcute Coronary Syndrome Definition Refers to spectrum of acute myocardial ischaemia and/or infarction Divided into three clinical categories: unstable angina, STEMI, NSTEMI Classification Unstable angina: anginal symptoms at rest; no trop rise; no ST elevation NSTEMI: anginal symptoms at rest; trop rise; no ST elevation STEMI: anginal symptoms at rest; ST elevationAcute Coronary SyndromeAcute Coronary Syndrome Anatomy Two coronary arteries branch from the root of the aorta: Right coronary artery Left coronary artery RCA curves around the right side and under the heart and supplies: right atrium, right ventricle, inferior aspect of left ventricle, posterior septal area LCA becomes the circumflex artery and the left anterior descending arter. Circumflex artery curves around the top, left and back of the heart and supplies: left atrium and posterior aspect of left ventricle LAD travels down the middle of the heart and supplies: anterior aspect of the left ventricle, anterior aspect of the septumAcute Coronary Syndrome AnatomyAcute Coronary Syndrome Why is this important? this to an artery.G and see changes, we can relate Leads of an ECG correlate to different areas of heart due to placement of leads Won’t go into the why/how right now If we see ECG changes in certain leads, correlated to area of heart, and arteryAcute Coronary Syndrome Approach Anginal chest pain (refer to previous slide) This is of course the case in stable angina, but for this to be ACS symptoms should continue at rest for more than 15 minutes. N.b. a silent myocardial infarction is when someone does not experience typical chest pain during ACS. Patients with diabetes are at particular risk of silent MIs. So are women and the elderly. STEMI: anginal chest pain + ECG changes (ST elevation; new LBBB) NSTEMI: anginal chest pain + raised troponin + normal ECG/ST depression or TWI Unstable angina: anginal chest pain + normal troponinAcute Coronary Syndrome History Socrates that is similar to stable angina, just doesn’t go away with rest Key points: pain radiating to jaw or arms, N+V , sweating, feeling of impending doom, shortness of breath Exam Look for risk factors, pleuritic rub, sweating (sympathetic drive - why?) Investigations Bedside: ECG Bloods: high-sensitivity troponin (within 60 mins), FBC, U+Es, LFT s, glucose, CRP , lipids, coagulation profile Imaging: CXR (rule out other causes) NICE states anyone coming in with functional damage to the heart. Coronary angio -> see what is going on Acute Coronary Syndrome Investigations STEMI NSTEMI ST segment ECG changes ST-segment elevation depression New left bundle branch block T wave inversion Pathological Q-waves suggest a deep infarction involving full thickness of the heart muscle, and typically appear 6 or or a prior infarcthe onset of symptoms; Bloods: repeated tests of troponin is cardiac and skeletal muscle. A rise inonin: troponin indicates NSTEMI but is non- specificAcute Coronary Syndrome InvestigationsAcute Coronary Syndrome Management Often in SBAs it is easy to diagnose/identify ACS. The difficulty comes in the management. Immediate management: MONA MONA is pretty general for ACS; however it is very outdated. I found it helpful for exams as a base, but do not rely on this Morphine Oxygen (as long as sats < 90%) Nitrates (symptomatic relief) Anti-coagulation (aspirin 300mg) [sometimes c is added = clopidogrel] Secondary Prevention (DABS) Dual antiplatelet therapy (aspirin 75mg OD + clopidogrel - 12 months) ACE inhibitors (titrated as high as possib+ Aldosterone antogonastis (eplerenone titrated to 50mg OD) Beta-blockers Statins And also control risk factorsAcute Coronary Syndrome Management NSTEMI/Unstable Angina BA TMAN Base the decision on >3% do itre Aspirin 300mg stat Ticagrelor 180mg stat Morphine Antithrombin therapy (fondaprinaux) NitratesAcute Coronary Syndrome Management STEMIAcute Coronary Syndrome ComplicationsAcute Coronary Syndrome Classification of MI Type 1: traditional MI due to acute coronary event Type 2: ischaemia secondary to increased demand or reduced supply of oxygen (severe anaemia, tachycardia, hypotension) Type 3: sudden cardiac death or cardiac arrest suggestive of an ischaemic event Type 4: MI associated with procedures such as PCI, coronary stenting, CABG Y ou could remember these with the “ACDC” mnemonic: •Type 1: A – ACS-type MI •Type 2: C – Can’t cope MI •Type 3: D – Dead by MI •Type 4: C – Caused by us MIConcept Heart has two main functions: 1 Pump Circulation, functional 2 Battery Conduction, electrophysiologyConcept Heart has two main functions: 1 Pump Circulation, functional 2 Battery Conduction, electrophysiologyArrhythmias Definition Arrhythmia is an abnormal rhythm of the heart A disturbance in the rate of cardiac muscle contractions The only normal rhythm of the heart is termed “normal sinus rhythm” Background Impulse is generated in sinoatrial (SA) node Conducted through and slowed down while passing through the atrioventricular (AV) node Conducted by bundle of His to the left and right bundle branches then into the Purkinje fibresArrhythmias Classification Site Supraventricula, atrial, ventricular Mechanism Fibrillation, automati, re-entry Rate Brady/tachy ECG appearance e.g. long QT syndrome Acute/chronic e.g. Persistent AF Life-threatening? e.g. Ventricular FibrillationArrhythmias Classification Supraventricular T achycardias Ventricular Tachycardias Atrial Fibrillation Ventricularachycardia Atrial Flutter (Sustained or non-sustained) Atrial achycardia Ventricular Fibrillation AVNRT Torsades de Pointes AVRTAtrial Fibrillation Definition A supraventricular tachycardia with inappropriate electrical activity and ineffective atrial contraction Background Classification First-detected episode Episodes of AF that terminate spontaneously Paroxysmal Recurrent Comes back after cardioversion Persistent Not self-terminating; >7 days Permanent Cannot be cardiovertedAtrial Fibrillation Background Epidemiology Doubles with advancing decades (10-15% at 80) Elderly mainly affected M > F Most common sustained cardiac arrhythmia in adults worldwide Prevalence about 2-4% Aetiology Largely unknown Pulmonary veins origin? Triggers: SMITH -> Sepsis, mitral valve pathol, IHD, thyrotoxicosis, HTAtrial Fibrillation Background Pathophysiology Electrical activity becomes disorganised (the how is questioned) Atria contracts uncoordinated: rapid and irregular Overrides the SAN Passes to ventricles: irregularly irregular ventricular contraction n.b. this can also stagnate blood in atria, forming a thrombus. May travel to brain and cause ischaemic strokeAtrial Fibrillation Diagnosis Approach Often asymptomatic and first presentation is a stroke CHADs-VASc is super important: tool for assessing whether a patient with AF needs anticoagulation (to mitigate risk of ischaemic stroke) Results: 0: No anti-coagulation 1: Consider if men 2+: Offer anti-coagulation One should balance this with the ORBIT score: assessing risk of major bleeding Older age (>=75); Renal Impairment (GFR < 60); Bleeding previously: Iron (aneamia); Taking anti-plateletsAtrial Fibrillation Diagnosis Investigations Features Irregularly irregular pulse ECG → irregularly irregular narrow Palpitations tachycardia with no discernable p- waves Clots Chest pain Bloods, asess stroke risk, echo SOB/fatigueAtrial Fibrillation Management The following on rate vs rhythm is often changing, complex. Most patients nothing works = ablation, plus a DOAC. Remember this if anything. WhenAtrial Flutter Definition A supraventricular tachycardia with inappropriate electrical activity and ineffective atrial contraction Notice basically the same as atrial fibrillation. Difference: sawtooth pattern on ECG. Faster (>300bpm). More regular .Supraventricular T achycardia Definition Refers to when abnormal electrical signals from above the ventricles cause a fast heart rate Pathophysiology SVT cased by electrical signals re-entering the atria from the ventricles. It goes again through the atria and AVN, causing another ventricular contraction Self-perpetuating electrical loop. Causes a narrow-complex (<120ms) tachycardia (>100bpm) Types Atrioventricular nodal re-entrant tachycardia (AVNRT) Atrioventricular nodal re-entrant tachycardia (AVRT) Atrial tachycardiaSupraventricular achycardiaSupraventricular T achycardia Diagnosis Investigations Features ECG Palpitations Chest pain U+Es TFTs Syncope/pre-syncope Digoxin level SOB Cardiac enzymesSupraventricular Tachycardia ManagementW olff-Parkinson-White Definition Congential accessory pathway that conducts electrical signals between atria and ventricles May be called “Bundle of Kent” Similar to a AVRT Pathophysiology Creates its own conduction pathway between atria and ventricles Prone to dysrhythmiasW olff-Parkinson-White Diagnosis Features SAME AS SVT s Investigations ECG Palpitations U+Es Chest pain TFTs Syncope/pre-syncope Digoxin level SOB Cardiac enzymesWolff-Parkinson-WhiteHeart BlockHeart BlockHeart BlockVentricular achycardiaVentricular achycardiaAdvanced Life Support TreeVentricular FibrillationVentricular FibrillationSyncope For this section, the Oxford red handbook (forgot the name) is very good Definition Form of loss of consciousness Aetiology Hypoperfusion of the brain Classification Primitive reflex; HR slows, BP drops, reducing Reflex cerebral perfusion Cardiac Reduction in cardiac output Orthostatic Hypotension on sitting or standing Cerebovascular Structural causes, non-cardiacSyncope Since this is a presentation, we will treat it as a case Questions to ask: Before Warning? No warning = cardiac Precipitating factors? Postural triggers = orthostatic/ vasovagal. If sitting = cardiac Recent head trauma? ?subdural haemorrhage During How long? Seconds or minutes = VVS/cardiac Bite tongue? Move limbs? Incontinent? Tongue-biting = epileptic After Recovery time? Slow = epileptic. Fast = other than neurologicalSyncope Since this is a presentation, we will treat it as a case Questions to ask:Syncope Investigations Bloods - CBG, FBC, U+Es ECG - arrhythmia Echo - if structural heart defects are suspected CT/MRI - if neurological cause suspected Management Highly dependent on causeThank Y ou Any Questions? Feel free to email me too xmd21@ic.ac.ukQR code Please take time to fill out, helps me and MedEd