Lecture 9.1a - Ischemic Heart Disease Pathophysiology PDF
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Aston University
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Summary
This lecture covers the pathophysiology of ischemic heart disease, including various types of angina and infarctions. It details the underlying mechanisms, risk factors, and clinical presentations associated with these conditions.
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Ischemic heart disease: ◦Due to reduced oxygen supply ‣ Most commonly caused due to atherosclerotic plaques in the coronary vessels ‣ Embolus ‣ Vasospasms ◦Increased oxygen demand ‣ Tachycardia ‣ Left ventricular hypertrophy ‣ E...
Ischemic heart disease: ◦Due to reduced oxygen supply ‣ Most commonly caused due to atherosclerotic plaques in the coronary vessels ‣ Embolus ‣ Vasospasms ◦Increased oxygen demand ‣ Tachycardia ‣ Left ventricular hypertrophy ‣ Exertion ◦Risk factors for coronary atheroma (modifiable/non-modifiable): ‣ BMI > 30 ‣ Age > 65 years ‣ Diabetes mellitus ‣ Hypertension ‣ Ethanol ‣ Increased LDL/decreased HDL ‣ Relatives with CAD/family history ‣ Tobacco use Classifications: ◦Stable angina: ‣ Stable atherosclerotic plaque ‣ Pain develops when there is increased demand (exertion) ‣ The vessel is unable to dilate enough to allow adequate blood flow ‣ Subendocardial ischemia ◦Unstable angina: ‣ Plaque ruptures and thrombus forms around the plaque causing partial occlusion of the vessel ‣ Pain occurs at rest or progresses rapidly over a short period of time ‣ Subendocardial ischemia ◦Subendocardial infarction (NSTEMI): ‣ Ischemia for longer than 30 minutes lead to infarction (cell death) ‣ Pain occurs at rest or progresses rapidly over a short period of time ‣ Subendocardial infarction ◦Transmural infarction (STEMI): ‣ Complete occlusion of blood vessel lumen and infarct of the entire thickness of the myocardium ‣ Pain occurs at rest or progresses rapidly over a short period of time ‣ Transmural infarction Chest pain differential: Clinical features - ischemic cardiac chest pain: ◦Typical: ‣ Characterised as discomfort/pressure rather than pain (dull, crushing) ‣ Time duration > 2 mins ‣ Provoked by activity/exercise ‣ Radiation (arms, jaws) ‣ Does not change with respiration/position ‣ Associated with sweating/nausea ‣ Relieved by rest/nitroglycerin ◦Atypical: ‣ Pain that can be localised with one finger ‣ Constant pain lasting for a few days ‣ Fleeting pains lasting for a few seconds ‣ Pain reduced by movement/palpation ‣ NO PAIN (diabetes mellitus, elderly, post heart transplant) Pathophysiology and clinical features: ◦Right ventricular MI: ‣ Jugular venous distension ‣ Oedema (lower extremities) ‣ Hepatomegaly ‣ Ascites ‣ Hypotension ‣ Clear lungs ‣ Bradycardia/AV block ◦Left ventricular MI: ‣ Pulmonary oedema ‣ Shortness of breath ‣ Hypotension ‣ S4 heart sound ‣ Reflex tachycardia MI complications: ◦0 - 24 hours: ‣ Sudden cardiac death: VTAC -> Vfib -> sudden cardiac death ‣ Acute heart failure Hypotension -> shock Flash pulmonary oedema ◦24 hours - 3 days: ‣ Pericarditis Inflammation Frictional rub Pericardial effusion ◦3 - 14 days: ‣ Rupture syndromes Ventricular septal defect Free wall rupture -> cardiac tamponade Papillary muscle rupture - mitral regurgitation ◦14 days - months: ‣ LV aneurysms Risk of thrombus formation Pericarditis: ◦Inflammation of the pericardium often due to a viral illness ◦Causes retrosternal, sharp and localised chest pain ◦A pericardial rub may be heard on auscultation of the chest ◦Saddle-shaped ST elevations may be present in an ECG