Chest Pain PDF

Week 2 Look at learn for other things to catch up on via this KCP A new slide will come with new updates via the answers. Has this been updated? Learning outcomes: 1. Describe the functional anatomy of the heart during the cardiac cycle 2...

Week 2 Look at learn for other things to catch up on via this KCP A new slide will come with new updates via the answers. Has this been updated? Learning outcomes: 1. Describe the functional anatomy of the heart during the cardiac cycle 2. Describe the blood supply of the heart and regions supplied by specific arteries 3. Understand the pathophysiology of atheroma 4. Describe common risk factors for atheroma 5. List common causes of chest pain and outline their common features 6. Ask patient questions that will help distinguish cardiac from non-cardiac causes of chest pain 7. Outline important features on clinical examination that can help identify the cause of chest pain 8. Describe what investigations will be useful in assessment of chest pain 9. Describe the features of a 12 lead ECG 10. Describe the features of an acute ST-elevation myocardial infarct 11. The role of blood tests in assessment of chest pain 12. Describe the cellular changes in myocardial ischaemia Pre-reading Coronary artery disease (CAD) is the commonest cause of angina and acute coronary syndrome and the leading cause of death worldwide Ischaemia is a condition that occurs when there is an inadequate blood supply to a part of the body, typically due to a blockage in the blood vessels Common risk factors for atherosclerosis: Age and sex Week 2 1  Genetics Smoking Hypertension Hypercholesterolaemia Diabetes melitus Haemostatic factors Physical activity Obesity Alcohol Diet Social deprivation What features of the history make ischaemic chest pain most likely and what features suggest an alternative cause? Chest pain that is accompanied by clinical evidence of increased intracardiac pressure (especially a raised jugular venous pressure) increases the likelihood of myocardial ischaemia or massive PE A large pneumothorax should be evident on clinical examination, with absent breath sounds and a hyper-resonant percussion note on the affected side. Aortic dissection Massive PE Oesophageal rupture Week 2 2  Angina is chest pain or discomfort that occurs when the heart muscle doesn't get enough oxygen-rich blood Acute Coronary Syndrome (ACS) is an umbrella term used to describe a range of conditions associated with sudden, reduced blood flow to the heart, typically due to blockage in the coronary arteries Coronary artery disease (CAD) is the commonest cause of angina and acute coronary syndrome and the leading cause of death worldwide Hazard ratio is the chances of something occurring in those exposed a certain factor against those not exposed Causes of elevated serum troponin other than acute coronary syndrome Cardiorespiratory causes Non-cardiorespiratory causes Pulmonary embolism Prolonged hypotension Acute pulmonary oedema Severe sepsis Tachyarrhythmias Severe burns Myocarditis/myopericarditis Stroke Aortic dissection Subarachnoid haemorrhage Week 2 3  Cardiorespiratory causes Non-cardiorespiratory causes Cardiac trauma End-stage renal failure Cardiac surgery/ablation Week 2 4 Week 2 5  This image shows a simplified diagram of a cardiac myocyte (heart muscle cell) with a focus on the process of excitation-contraction coupling, which involves calcium ions (Ca²⁺) and leads to muscle contraction. Here’s a breakdown of the numbered steps: 1. Depolarization via the T-tubule: The green line represents the action potential, an electrical signal traveling down the T-tubule, which is a structure within the myocyte. This depolarization activates DHP receptors (dihydropyridine receptors), which are voltage-sensitive L-type calcium channels located in the sarcolemma (muscle cell membrane). 2. Calcium influx: The activation of the DHP receptors leads to the opening of the calcium release channels in the sarcolemma, allowing a small influx of extracellular calcium (Ca²⁺) into the cell. 3. Calcium-induced calcium release (CICR): The small amount of Ca²⁺ entering the cell triggers the opening of Ryanodine receptors (RyR) located on the sarcoplasmic reticulum (SR), a specialized organelle that stores Ca²⁺. This leads to a large release of Ca²⁺ from the SR into the cytosol of the myocyte. 4. Calcium binding to troponin: The released Ca²⁺ binds to Troponin C (TN-C), a component of the troponin complex (which also includes TN-T and TN-I) on the actin filaments of the muscle. This causes a conformational change in the troponin-tropomyosin complex (TM), exposing the binding sites for myosin on the actin filament, which allows muscle contraction to occur. 5. Calcium reuptake via SERCA: After contraction, Ca²⁺ is actively pumped back into the SR by the SERCA (Sarcoplasmic/Endoplasmic Reticulum Calcium Week 2 6  ATPase) pump, lowering the cytosolic Ca²⁺ concentration and leading to muscle relaxation. This cycle of calcium release and reuptake is central to the contraction and relaxation of the heart muscle. Investigations used to diagnose a myocardial infarct: Electrodiagram Serum troponin The P-wave reflects atrial depolarization (activation). The PR interval is the distance between the onset of the P-wave to the onset of the QRS complex. The PR interval ECG is assessed in order to determine whether impulse conduction from the atria to the ventricles is normal. The QRS complex represents the depolarization (activation) of the ventricles. It is always referred to as the “QRS complex” although it may not always display all three waves. Since the electrical vector generated by the left ventricle is many times larger than the vector ECG generated by the right ventricle, the QRS complex is actually a reflection of left ventricular depolarization. The ST segment corresponds to the plateau phase (phase 2) of the action potential. If the first wave is negative then it is referred to as Q-wave. If the first wave is not negative, then the QRS complex does not possess a Q-wave, regardless of the appearance of the QRS complex. Week 2 7  ECG leads Comparing normal ECG and an ECG re. cardiac myoinfarction: Abnormal has a higher ST elevation ST elevation in leads 1 ,2 and aVL ,leads V2-V6. The ST segment is of particular interest in the setting of acute myocardial ischemia because ischemia causes deviation of the ST segment (ST segment deviation). There are two types of ST segment deviations. ST segment depression implies that the ST segment is displaced, such that it is below the level of the PR segment. Week 2 8  ST segment elevation implies that the ST segment is displaced, such that it is above the level of the PR segment. What differences can be seen compared to the normal ECG? Main points is T wave inversion in leads I, II, aVL and V4-V6 showing LV ischaemic changes (if acute) Myocardial infarction is the term used when there is evidence of myocardial necrosis.Myocardial ischemia occurs due to reduced blood flow. Cardiac myocyte is a specialised striated muscle cell. Gap junctions and movement of ions is what triggers contraction in unison. Chemical and physical interactions between the actin and myosin cause the sarcomere length to shorten, and therefore the myocyte to contract.When the action potential reaches the cell ,calcium enters and binds to troponin-C (TN-C), which serves as a binding site for Week 2 9  Ca++. When Ca++ binds to TN-C, there is a conformational change in the troponin complex such that TN-I moves away from the myosin binding site on the actin, making it assessable to the myosin head resulting in a contraction. When Ca++ is removed from the TN-C, the troponin complex resumes its inactivated position, inhibiting myosin-actin binding. TN-I is important in clinical practice because it is used as a diagnostic marker for myocardial infarction (it is released into the circulation when myocytes die) Cardiac myocyte-What happens when the cell does not have enough oxygen? TN-I is important in clinical practice because it is used as a diagnostic marker for myocardial infarction (it is released into the circulation when myocytes die) Week 2 10  Troponins in MI Week 2 11  Troponin assays Week 2 12  Summary: Ischaemic heart disease is a common problem Many modifiable risk factors Myocardial infarct causes chest pain, but there are many causes Careful history needed Key investigations are: ECG-disruption of normal electrical signals caused by ion movement Highly sensitive troponin assay-released due to disruption of cell structure Q&A: If a patient had a fitbit that showed an irregular / too fast heart rate, WWYD? Take a history ECG Trust what the patient says & not numbers Week 2 13  we don’t know how reliable numbers are ECG can diagnose ischaemia as well as electrical activity Week 2 14