{"id":5612,"date":"2025-12-13T15:09:38","date_gmt":"2025-12-13T20:09:38","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&#038;p=5612"},"modified":"2025-12-13T17:53:48","modified_gmt":"2025-12-13T22:53:48","slug":"myocardial-infarction","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/myocardial-infarction\/","title":{"raw":"7p22  Myocardial Infarction","rendered":"7p22  Myocardial Infarction"},"content":{"raw":"<strong>Myocardial Infarctions and Vascular Complications<\/strong>\r\n<h1><strong>Myocardial Infarction (MI) \u2013 Pathophysiology &amp; Causes:<\/strong><\/h1>\r\n<strong>Causes:<\/strong>\r\n<ul>\r\n \t<li><strong>Total occlusion<\/strong>\u00a0of a coronary artery, most often due to\u00a0<strong>atherosclerotic plaque rupture<\/strong>.<\/li>\r\n \t<li><strong>Thrombus formation:<\/strong>\u00a0Clot forms at the plaque site or thrombi break off and lodge downstream.<\/li>\r\n \t<li><strong>Vasospasm:<\/strong>\u00a0Sudden constriction (though the exact cause is not fully understood).<\/li>\r\n<\/ul>\r\n<strong>Potential Triggers:<\/strong>\r\n<ul>\r\n \t<li><strong>Plaque rupture or hemorrhage.<\/strong><\/li>\r\n \t<li><strong>Thromboembolism:<\/strong>\u00a0Clot breaking free and occluding distal artery.<\/li>\r\n \t<li><strong>Vasospasm:<\/strong>\u00a0Sudden, intense constriction of the vessel.<\/li>\r\n<\/ul>\r\n<strong>Progression of Occlusion:<\/strong>\r\n<ul>\r\n \t<li>Partial occlusion causes\u00a0<strong>angina pectoris<\/strong>\u00a0(chest pain).<\/li>\r\n \t<li>Complete occlusion can lead to\u00a0<strong>myocardial infarction (MI)<\/strong>, commonly known as a heart attack.<\/li>\r\n<\/ul>\r\n<strong>Vascular Damage leads to Dysfunction:<\/strong>\r\n<ul>\r\n \t<li><strong>Endothelial cell dysfunction:<\/strong>\r\n<ul>\r\n \t<li>Reduced or lost\u00a0<strong>nitric oxide<\/strong>\u00a0(NO) production or sensitivity.<\/li>\r\n \t<li>Endothelial cells may produce less NO upon stimulation, or lose responsiveness to NO, leading to\u00a0<strong>excessive vasoconstriction<\/strong>\u00a0(spasm).<\/li>\r\n \t<li>Damaged blood vessels are also susceptible to both <strong>arteriosclerosis<\/strong> and <strong>atherosclerosis.<\/strong><\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<strong>Severity of MI:<\/strong>\r\n<ul>\r\n \t<li>Depends on:\r\n<ul>\r\n \t<li><strong>Size<\/strong>\u00a0of the infarct.<\/li>\r\n \t<li><strong>Location<\/strong>: Anterior wall, lateral wall, apex, etc.<\/li>\r\n \t<li><strong>Depth<\/strong>: How deep into the myocardium the infarct occurs.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\nDeeper infarcts and those in critical regions (e.g., LAD artery) cause more damage and worse prognosis.\r\n\r\n&nbsp;\r\n<h1><strong>Myocardial Infarction Signs and Symptoms:<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Chest Pain:<\/strong>\r\n<ul>\r\n \t<li>Described as\u00a0<strong>heaviness, pressure, burning<\/strong>\u00a0in the chest.<\/li>\r\n \t<li>Often\u00a0<strong>radiates<\/strong>\u00a0to the\u00a0<strong>left arm, shoulder, jaw, or neck<\/strong>.<\/li>\r\n \t<li>Usually\u00a0<strong>not relieved<\/strong>\u00a0by rest or nitroglycerin, distinguishing from angina.<\/li>\r\n \t<li><strong>In women:<\/strong>\u00a0Nausea and indigestion are common, and symptoms may be less recognizable, risking missed diagnosis.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Neurological Signs:<\/strong>\r\n<ul>\r\n \t<li>Reduced oxygen to the brain causes\u00a0<strong>anxiety, fear, confusion<\/strong>.<\/li>\r\n \t<li>Possible fainting or altered consciousness.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Progression:<\/strong>\r\n<ul>\r\n \t<li>ECG shows characteristic changes:\r\n<ul>\r\n \t<li><strong>Early:<\/strong>\u00a0Abnormal P wave and QRS complex indicate ischemia.<\/li>\r\n \t<li><strong>Later (hours\/days):<\/strong>\u00a0Elevated\u00a0<strong>ST segment<\/strong>,\u00a0<strong>T wave inversion<\/strong>,\u00a0<strong>minimal P wave<\/strong>.<\/li>\r\n \t<li><strong>Necrosis:<\/strong>\u00a0Shown by flattened QRS and abnormal T wave.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1>Diagnosis<\/h1>\r\n<ul>\r\n \t<li><strong>Blood Tests:<\/strong>\r\n<ul>\r\n \t<li>Elevated enzymes from necrotic heart cells:\r\n<ul>\r\n \t<li><strong>Creatine phosphokinase (CPK):<\/strong>\u00a0Released from damaged muscle.<\/li>\r\n \t<li><strong>Lactate dehydrogenase (LDH).<\/strong><\/li>\r\n \t<li><strong>Aspartate aminotransferase (AST):<\/strong>\u00a0Indicates tissue injury.<\/li>\r\n \t<li><strong>Troponins:<\/strong>\u00a0Highly specific for cardiac damage; elevated with necrosis.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Potassium:<\/strong>\u00a0Elevated due to cell rupture, risking dysrhythmias.<\/li>\r\n \t<li><strong>White blood cells:<\/strong>\u00a0Increase as part of inflammatory response.<\/li>\r\n \t<li><strong>CRP (C-reactive protein):<\/strong>\u00a0Marker of inflammation.<\/li>\r\n \t<li><strong>ESR (Erythrocyte Sedimentation Rate):<\/strong>\u00a0Increased during inflammation and tissue damage.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Additional Monitoring:<\/strong>\r\n<ul>\r\n \t<li><strong>Capillary wedge pressure:<\/strong>\u00a0Assesses left ventricle function and pressure.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>Possible Outcomes:<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Mortality:<\/strong>\r\n<ul>\r\n \t<li>About 25% die, mainly from\u00a0<strong>arrhythmias<\/strong>,\u00a0<strong>hypoxia<\/strong>, or\u00a0<strong>acidosis<\/strong>.<\/li>\r\n \t<li><strong>Cardiogenic shock:<\/strong>\u00a0Inadequate cardiac output leading to organ failure.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>If survived:<\/strong>\r\n<ul>\r\n \t<li>Can develop\u00a0<strong>acute or chronic congestive heart failure<\/strong>.<\/li>\r\n \t<li>Heart becomes less effective at contracting, leading to ongoing deterioration and possible death.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1>4 Possible Complications:<\/h1>\r\n<h1><strong>1.\u00a0 Cardiac Rupture:<\/strong><\/h1>\r\n<ul>\r\n \t<li>Typically occurs\u00a0<strong>3 to 7 days<\/strong>\u00a0post-MI.<\/li>\r\n \t<li>Necrotic, weakened heart tissue may rupture because the dead tissue breaks down.<\/li>\r\n \t<li><strong>Outcome:<\/strong>\u00a0Usually fatal due to sudden\u00a0<strong>hemorrhage<\/strong>\u00a0and\u00a0<strong>cardiac tamponade<\/strong>.<\/li>\r\n<\/ul>\r\n<h1><strong>2.\u00a0 Cardiac Tamponade:<\/strong><\/h1>\r\n<ul>\r\n \t<li>Damage near the heart can cause\u00a0<strong>exudate<\/strong>\u00a0or\u00a0<strong>blood<\/strong>\u00a0to fill the\u00a0<strong>pericardial sac<\/strong>.<\/li>\r\n \t<li><strong>Effects:<\/strong>\r\n<ul>\r\n \t<li>Increased pressure on the heart.<\/li>\r\n \t<li>Impaired filling during diastole.<\/li>\r\n \t<li>Reduced\u00a0<strong>stroke volume<\/strong>\u00a0and\u00a0<strong>cardiac output<\/strong>, leading to\u00a0<strong>shock<\/strong>.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Management:<\/strong>\r\n<ul>\r\n \t<li><strong>Pericardiocentesis:<\/strong>\u00a0Puncture the sac to aspirate fluid and relieve pressure.<\/li>\r\n \t<li>Critical to monitor for this complication as it can be fatal.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>3.\u00a0 Emboli &amp; Stroke:<\/strong><\/h1>\r\n<ul>\r\n \t<li>Damage tissue can lead to\u00a0<strong>clot formation<\/strong>\u2014<strong>thrombus<\/strong>.<\/li>\r\n \t<li><strong>Thrombus dislodgement:<\/strong>\r\n<ul>\r\n \t<li>Loose pieces (emboli) can travel.<\/li>\r\n \t<li><strong>Left ventricular MI:<\/strong>\u00a0Emboli may enter the\u00a0<strong>systemic circulation<\/strong>\u00a0(e.g., brain) causing\u00a0<strong>stroke<\/strong>.<\/li>\r\n \t<li><strong>Right ventricular MI:<\/strong>\u00a0Emboli may travel to\u00a0<strong>lungs<\/strong>\u00a0causing\u00a0<strong>pulmonary embolism<\/strong>.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Timing:<\/strong>\u00a0Usually occurs\u00a0<strong>3-7 days<\/strong>\u00a0after MI as thrombi dislodge.<\/li>\r\n<\/ul>\r\n<h1><strong>4.\u00a0 Acidosis &amp; Hypoxia:<\/strong><\/h1>\r\n<ul>\r\n \t<li>Ischemia causes tissues to revert to\u00a0<strong>anaerobic respiration<\/strong>.<\/li>\r\n \t<li>Produces\u00a0<strong>lactic acid<\/strong>, decreasing blood pH.<\/li>\r\n \t<li><strong>Acidosis (&lt;7.35):<\/strong>\r\n<ul>\r\n \t<li>Impairs cellular function, including the myocardium.<\/li>\r\n \t<li>Can cause\u00a0<strong>organ dysfunction<\/strong>\u00a0and\u00a0<strong>worse outcomes<\/strong>.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li>Emergency care aims to correct hypoxia and prevent acidosis progression.<\/li>\r\n<\/ul>\r\n<h1>Treatment:<\/h1>\r\n<strong>Emergency Response (Paramedics):<\/strong>\r\n<ol>\r\n \t<li><strong>Provide oxygen:<\/strong>\u00a0Ensures tissues, especially the brain and heart, receive adequate oxygen.<\/li>\r\n \t<li><strong>Pain relief:<\/strong>\r\n<ul>\r\n \t<li><strong>Analgesics<\/strong>\u00a0(e.g., opioids) to alleviate severe chest pain (\"elephant sitting on the chest\").<\/li>\r\n \t<li>Reduces\u00a0<strong>stress<\/strong>\u00a0and\u00a0<strong>sympathetic nervous system<\/strong>\u00a0activation, which can decrease the heart\u2019s workload.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Anticoagulant and thrombolytic therapy:<\/strong>\r\n<ul>\r\n \t<li><strong>Anticoagulants:<\/strong>\u00a0Prevent further clot formation.<\/li>\r\n \t<li><strong>Thrombolytics:<\/strong>\u00a0Break up existing clots, especially if embolism caused the MI.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ol>\r\n<h1><strong>Additional Treatments:<\/strong><\/h1>\r\n<ol>\r\n \t<li><strong>Treat dysrhythmias and hypertension:<\/strong>\r\n<ul>\r\n \t<li>Use medications like\u00a0<strong>digoxin<\/strong>\u00a0(for contractility),\u00a0<strong>beta blockers<\/strong>,\u00a0<strong>calcium channel blockers<\/strong>,\u00a0<strong>alpha blockers<\/strong>.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Address heart failure:<\/strong>\r\n<ul>\r\n \t<li>Use medications to reduce load, manage blood pressure, and normalize heart rate.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ol>\r\n<h1><strong>Surgical Intervention Procedures:<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Coronary interventions:<\/strong>\r\n<ul>\r\n \t<li><strong>Catheter-based delivery:<\/strong>\u00a0Thrombolytics, balloons, and stents.\r\n<ul>\r\n \t<li><strong>Angioplasty:<\/strong>\u00a0Balloon inserted via catheter to open blocked arteries; sometimes followed by placement of a\u00a0<strong>stent<\/strong>.<\/li>\r\n \t<li><strong>Laser therapy:<\/strong>\u00a0To remove or reduce plaque.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Bypass surgery (CABG):<\/strong>\u00a0Creating new pathways around blocked arteries.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Plaque removal:<\/strong>\u00a0Can be performed via laser, balloon, or stent insertion depending on location.<\/li>\r\n<\/ul>\r\n<strong>Tools:<\/strong>\r\n<ul>\r\n \t<li><strong>Defibrillators:<\/strong>\u00a0Automated external defibrillators (AEDs) are accessible in public places and gyms; easy for laypersons to operate.<\/li>\r\n<\/ul>\r\n<h1><strong>Other Organ Systems Affected by Vascular Occlusion:<\/strong><\/h1>\r\n<ol>\r\n \t<li><strong>Brain (Stroke):<\/strong>\r\n<ul>\r\n \t<li><strong>TIA (Transient Ischemic Attack):<\/strong>\u00a0A mini-stroke caused by partial occlusion of cerebral arteries.<\/li>\r\n \t<li><strong>Full occlusion:<\/strong>\u00a0Leads to\u00a0<strong>cerebrovascular accident<\/strong>\u00a0or\u00a0<strong>stroke<\/strong>\u00a0\u2014 an ischemic stroke.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Peripheral arteries (Aneurysm and Peripheral Vascular Disease):<\/strong>\r\n<ul>\r\n \t<li>Damage and narrowing of arteries (e.g., in the aorta) cause <strong>aneurysm<\/strong> formation:\r\n<ul>\r\n \t<li>Bulging of arterial wall due to damage and calcium deposits.<\/li>\r\n \t<li><strong>Brittle<\/strong>\u00a0and\u00a0<strong>susceptible to rupture<\/strong>.<\/li>\r\n \t<li>Rupture of the aorta is often\u00a0<strong>fatal<\/strong>\u00a0due to massive internal bleeding.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Other arteries (e.g., iliac arteries):<\/strong>\r\n<ul>\r\n \t<li>Can develop\u00a0<strong>peripheral vascular disease<\/strong>.<\/li>\r\n \t<li>Usually affects\u00a0<strong>legs and feet<\/strong>.<\/li>\r\n \t<li><strong>Occlusion<\/strong>\u00a0leads to\u00a0<strong>ischemia<\/strong>, tissue death,\u00a0<strong>gangrene<\/strong>, and possibly\u00a0<strong>amputation<\/strong>.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ol>\r\n<h1><strong>Signs and Symptoms of Peripheral Vascular Disease:<\/strong><\/h1>\r\n<ul>\r\n \t<li style=\"list-style-type: none\">\r\n<ul>\r\n \t<li><strong>Muscle pain and fatigue:<\/strong>\r\n<ul>\r\n \t<li>Occurs during activity (exercise) when muscles demand more oxygen.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Nerve symptoms:<\/strong>\r\n<ul>\r\n \t<li>Tingling, numbness, burning sensations due to oxygen deprivation.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Pulse weakness or absence:<\/strong>\r\n<ul>\r\n \t<li>Reduced blood flow results in weak or absent pulses in affected limbs.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Physical signs:<\/strong>\r\n<ul>\r\n \t<li><strong>Cyanosis:<\/strong>\u00a0Bluish skin.<\/li>\r\n \t<li><strong>Paleness:<\/strong>\u00a0Reduced blood flow.<\/li>\r\n \t<li><strong>Dry skin, less hair growth, thickened nails<\/strong>\u00a0(clues of chronic ischemia).<\/li>\r\n \t<li><strong>Slow healing of wounds<\/strong>\u00a0due to poor tissue maintenance.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>Prevention and Management of Arterial Disease:<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Prevention is key:<\/strong>\r\n<ul>\r\n \t<li>Maintain a\u00a0<strong>healthy diet<\/strong>\u00a0low in saturated fats, trans fats, cholesterol, and salt.<\/li>\r\n \t<li>Engage in regular\u00a0<strong>exercise<\/strong>\u00a0to help control weight and improve vascular health.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Control Diabetes:<\/strong>\r\n<ul>\r\n \t<li>Adherence to medications and blood glucose management to prevent vascular damage.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Weight Management:<\/strong>\r\n<ul>\r\n \t<li>Avoid obesity as it contributes to high lipid levels and increased cardiovascular risk.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Lipid Control:<\/strong>\r\n<ul>\r\n \t<li>Use\u00a0<strong>anticoagulants<\/strong>\u00a0and\u00a0<strong>platelet inhibitors<\/strong>\u00a0if at risk for thrombosis or thromboembolism.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Lifestyle Changes:<\/strong>\r\n<ul>\r\n \t<li><strong>Stop smoking<\/strong>: Significantly reduces the formation of atherosclerotic plaques.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Leg Care:<\/strong>\r\n<ul>\r\n \t<li>Maintain dependent positions (legs below the heart) to improve perfusion.<\/li>\r\n \t<li>Proper foot hygiene and wound care to prevent infections.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Interventional Procedures:<\/strong>\r\n<ul>\r\n \t<li><strong>Vasodilators:<\/strong>\u00a0Medications to improve blood flow.<\/li>\r\n \t<li>Surgical options include:\r\n<ul>\r\n \t<li><strong>Coronary artery bypass grafting (CABG):<\/strong>\u00a0Restores blood flow around blocked arteries.<\/li>\r\n \t<li><strong>Angioplasty:<\/strong>\u00a0Balloon dilatation to open narrowed vessels.<\/li>\r\n \t<li><strong>Endarterectomy:<\/strong>\u00a0Surgical removal of plaque from vessels.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>Lifestyle Adjustments:<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Exercise regularly.<\/strong><\/li>\r\n \t<li><strong>Healthy diet.<\/strong><\/li>\r\n \t<li><strong>Stress reduction.<\/strong><\/li>\r\n<\/ul>\r\n<h1><strong>Summary:<\/strong><\/h1>\r\n<strong>Occlusions<\/strong> in arteries can cause localized tissue ischemia in the heart, brain, or limbs, leading to serious conditions such as MI, stroke, aneurysm rupture, or limb gangrene. Recognizing symptoms like pain during activity, skin changes, and slow wound healing is vital to early diagnosis and intervention, preventing catastrophic outcomes.\r\n\r\nPrevention of <strong>artery disease<\/strong> involves lifestyle modifications, proper disease management, and surgical interventions when necessary. Myocardial infarctions are typically caused by plaque rupture and <strong>thrombus formation,<\/strong> with <strong>vasospasm<\/strong> also contributing. Damaged endothelium reduces NO availability, leading to increased <strong>constriction<\/strong> and risk of infarction. The extent of myocardial damage depends on the size and location of the occlusion.\r\n\r\nMyocardial infarction presents with characteristic chest pain, ECG changes, and elevated cardiac enzymes indicating cell death. Early diagnosis and treatment are crucial to prevent fatal arrhythmias, shock, or heart failure. Post-infarction, the heart\u2019s compromised ability can cause long-term dysfunction, emphasizing the importance of timely intervention.\r\n\r\nComplications after MI include <strong>heart wall rupture<\/strong>, <strong>pericardial tamponade<\/strong>, and <strong>emboli formation<\/strong> leading to stroke or pulmonary embolism. Acidosis from tissue hypoxia further exacerbates organ failure risks. Rapid intervention and close monitoring are essential to prevent these potentially fatal outcomes.\r\n\r\nTreatment of MI involves rapid oxygenation, pain management, clot dissolution, and mechanical intervention with angioplasty, stents, or bypass surgery. Long-term management includes lifestyle changes and medications to support the heart and prevent recurrent events. Early intervention and use of devices like defibrillators can save lives","rendered":"<p><strong>Myocardial Infarctions and Vascular Complications<\/strong><\/p>\n<h1><strong>Myocardial Infarction (MI) \u2013 Pathophysiology &amp; Causes:<\/strong><\/h1>\n<p><strong>Causes:<\/strong><\/p>\n<ul>\n<li><strong>Total occlusion<\/strong>\u00a0of a coronary artery, most often due to\u00a0<strong>atherosclerotic plaque rupture<\/strong>.<\/li>\n<li><strong>Thrombus formation:<\/strong>\u00a0Clot forms at the plaque site or thrombi break off and lodge downstream.<\/li>\n<li><strong>Vasospasm:<\/strong>\u00a0Sudden constriction (though the exact cause is not fully understood).<\/li>\n<\/ul>\n<p><strong>Potential Triggers:<\/strong><\/p>\n<ul>\n<li><strong>Plaque rupture or hemorrhage.<\/strong><\/li>\n<li><strong>Thromboembolism:<\/strong>\u00a0Clot breaking free and occluding distal artery.<\/li>\n<li><strong>Vasospasm:<\/strong>\u00a0Sudden, intense constriction of the vessel.<\/li>\n<\/ul>\n<p><strong>Progression of Occlusion:<\/strong><\/p>\n<ul>\n<li>Partial occlusion causes\u00a0<strong>angina pectoris<\/strong>\u00a0(chest pain).<\/li>\n<li>Complete occlusion can lead to\u00a0<strong>myocardial infarction (MI)<\/strong>, commonly known as a heart attack.<\/li>\n<\/ul>\n<p><strong>Vascular Damage leads to Dysfunction:<\/strong><\/p>\n<ul>\n<li><strong>Endothelial cell dysfunction:<\/strong>\n<ul>\n<li>Reduced or lost\u00a0<strong>nitric oxide<\/strong>\u00a0(NO) production or sensitivity.<\/li>\n<li>Endothelial cells may produce less NO upon stimulation, or lose responsiveness to NO, leading to\u00a0<strong>excessive vasoconstriction<\/strong>\u00a0(spasm).<\/li>\n<li>Damaged blood vessels are also susceptible to both <strong>arteriosclerosis<\/strong> and <strong>atherosclerosis.<\/strong><\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<p><strong>Severity of MI:<\/strong><\/p>\n<ul>\n<li>Depends on:\n<ul>\n<li><strong>Size<\/strong>\u00a0of the infarct.<\/li>\n<li><strong>Location<\/strong>: Anterior wall, lateral wall, apex, etc.<\/li>\n<li><strong>Depth<\/strong>: How deep into the myocardium the infarct occurs.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<p>Deeper infarcts and those in critical regions (e.g., LAD artery) cause more damage and worse prognosis.<\/p>\n<p>&nbsp;<\/p>\n<h1><strong>Myocardial Infarction Signs and Symptoms:<\/strong><\/h1>\n<ul>\n<li><strong>Chest Pain:<\/strong>\n<ul>\n<li>Described as\u00a0<strong>heaviness, pressure, burning<\/strong>\u00a0in the chest.<\/li>\n<li>Often\u00a0<strong>radiates<\/strong>\u00a0to the\u00a0<strong>left arm, shoulder, jaw, or neck<\/strong>.<\/li>\n<li>Usually\u00a0<strong>not relieved<\/strong>\u00a0by rest or nitroglycerin, distinguishing from angina.<\/li>\n<li><strong>In women:<\/strong>\u00a0Nausea and indigestion are common, and symptoms may be less recognizable, risking missed diagnosis.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Neurological Signs:<\/strong>\n<ul>\n<li>Reduced oxygen to the brain causes\u00a0<strong>anxiety, fear, confusion<\/strong>.<\/li>\n<li>Possible fainting or altered consciousness.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Progression:<\/strong>\n<ul>\n<li>ECG shows characteristic changes:\n<ul>\n<li><strong>Early:<\/strong>\u00a0Abnormal P wave and QRS complex indicate ischemia.<\/li>\n<li><strong>Later (hours\/days):<\/strong>\u00a0Elevated\u00a0<strong>ST segment<\/strong>,\u00a0<strong>T wave inversion<\/strong>,\u00a0<strong>minimal P wave<\/strong>.<\/li>\n<li><strong>Necrosis:<\/strong>\u00a0Shown by flattened QRS and abnormal T wave.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1>Diagnosis<\/h1>\n<ul>\n<li><strong>Blood Tests:<\/strong>\n<ul>\n<li>Elevated enzymes from necrotic heart cells:\n<ul>\n<li><strong>Creatine phosphokinase (CPK):<\/strong>\u00a0Released from damaged muscle.<\/li>\n<li><strong>Lactate dehydrogenase (LDH).<\/strong><\/li>\n<li><strong>Aspartate aminotransferase (AST):<\/strong>\u00a0Indicates tissue injury.<\/li>\n<li><strong>Troponins:<\/strong>\u00a0Highly specific for cardiac damage; elevated with necrosis.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Potassium:<\/strong>\u00a0Elevated due to cell rupture, risking dysrhythmias.<\/li>\n<li><strong>White blood cells:<\/strong>\u00a0Increase as part of inflammatory response.<\/li>\n<li><strong>CRP (C-reactive protein):<\/strong>\u00a0Marker of inflammation.<\/li>\n<li><strong>ESR (Erythrocyte Sedimentation Rate):<\/strong>\u00a0Increased during inflammation and tissue damage.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Additional Monitoring:<\/strong>\n<ul>\n<li><strong>Capillary wedge pressure:<\/strong>\u00a0Assesses left ventricle function and pressure.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>Possible Outcomes:<\/strong><\/h1>\n<ul>\n<li><strong>Mortality:<\/strong>\n<ul>\n<li>About 25% die, mainly from\u00a0<strong>arrhythmias<\/strong>,\u00a0<strong>hypoxia<\/strong>, or\u00a0<strong>acidosis<\/strong>.<\/li>\n<li><strong>Cardiogenic shock:<\/strong>\u00a0Inadequate cardiac output leading to organ failure.<\/li>\n<\/ul>\n<\/li>\n<li><strong>If survived:<\/strong>\n<ul>\n<li>Can develop\u00a0<strong>acute or chronic congestive heart failure<\/strong>.<\/li>\n<li>Heart becomes less effective at contracting, leading to ongoing deterioration and possible death.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1>4 Possible Complications:<\/h1>\n<h1><strong>1.\u00a0 Cardiac Rupture:<\/strong><\/h1>\n<ul>\n<li>Typically occurs\u00a0<strong>3 to 7 days<\/strong>\u00a0post-MI.<\/li>\n<li>Necrotic, weakened heart tissue may rupture because the dead tissue breaks down.<\/li>\n<li><strong>Outcome:<\/strong>\u00a0Usually fatal due to sudden\u00a0<strong>hemorrhage<\/strong>\u00a0and\u00a0<strong>cardiac tamponade<\/strong>.<\/li>\n<\/ul>\n<h1><strong>2.\u00a0 Cardiac Tamponade:<\/strong><\/h1>\n<ul>\n<li>Damage near the heart can cause\u00a0<strong>exudate<\/strong>\u00a0or\u00a0<strong>blood<\/strong>\u00a0to fill the\u00a0<strong>pericardial sac<\/strong>.<\/li>\n<li><strong>Effects:<\/strong>\n<ul>\n<li>Increased pressure on the heart.<\/li>\n<li>Impaired filling during diastole.<\/li>\n<li>Reduced\u00a0<strong>stroke volume<\/strong>\u00a0and\u00a0<strong>cardiac output<\/strong>, leading to\u00a0<strong>shock<\/strong>.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Management:<\/strong>\n<ul>\n<li><strong>Pericardiocentesis:<\/strong>\u00a0Puncture the sac to aspirate fluid and relieve pressure.<\/li>\n<li>Critical to monitor for this complication as it can be fatal.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>3.\u00a0 Emboli &amp; Stroke:<\/strong><\/h1>\n<ul>\n<li>Damage tissue can lead to\u00a0<strong>clot formation<\/strong>\u2014<strong>thrombus<\/strong>.<\/li>\n<li><strong>Thrombus dislodgement:<\/strong>\n<ul>\n<li>Loose pieces (emboli) can travel.<\/li>\n<li><strong>Left ventricular MI:<\/strong>\u00a0Emboli may enter the\u00a0<strong>systemic circulation<\/strong>\u00a0(e.g., brain) causing\u00a0<strong>stroke<\/strong>.<\/li>\n<li><strong>Right ventricular MI:<\/strong>\u00a0Emboli may travel to\u00a0<strong>lungs<\/strong>\u00a0causing\u00a0<strong>pulmonary embolism<\/strong>.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Timing:<\/strong>\u00a0Usually occurs\u00a0<strong>3-7 days<\/strong>\u00a0after MI as thrombi dislodge.<\/li>\n<\/ul>\n<h1><strong>4.\u00a0 Acidosis &amp; Hypoxia:<\/strong><\/h1>\n<ul>\n<li>Ischemia causes tissues to revert to\u00a0<strong>anaerobic respiration<\/strong>.<\/li>\n<li>Produces\u00a0<strong>lactic acid<\/strong>, decreasing blood pH.<\/li>\n<li><strong>Acidosis (&lt;7.35):<\/strong>\n<ul>\n<li>Impairs cellular function, including the myocardium.<\/li>\n<li>Can cause\u00a0<strong>organ dysfunction<\/strong>\u00a0and\u00a0<strong>worse outcomes<\/strong>.<\/li>\n<\/ul>\n<\/li>\n<li>Emergency care aims to correct hypoxia and prevent acidosis progression.<\/li>\n<\/ul>\n<h1>Treatment:<\/h1>\n<p><strong>Emergency Response (Paramedics):<\/strong><\/p>\n<ol>\n<li><strong>Provide oxygen:<\/strong>\u00a0Ensures tissues, especially the brain and heart, receive adequate oxygen.<\/li>\n<li><strong>Pain relief:<\/strong>\n<ul>\n<li><strong>Analgesics<\/strong>\u00a0(e.g., opioids) to alleviate severe chest pain (&#8220;elephant sitting on the chest&#8221;).<\/li>\n<li>Reduces\u00a0<strong>stress<\/strong>\u00a0and\u00a0<strong>sympathetic nervous system<\/strong>\u00a0activation, which can decrease the heart\u2019s workload.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Anticoagulant and thrombolytic therapy:<\/strong>\n<ul>\n<li><strong>Anticoagulants:<\/strong>\u00a0Prevent further clot formation.<\/li>\n<li><strong>Thrombolytics:<\/strong>\u00a0Break up existing clots, especially if embolism caused the MI.<\/li>\n<\/ul>\n<\/li>\n<\/ol>\n<h1><strong>Additional Treatments:<\/strong><\/h1>\n<ol>\n<li><strong>Treat dysrhythmias and hypertension:<\/strong>\n<ul>\n<li>Use medications like\u00a0<strong>digoxin<\/strong>\u00a0(for contractility),\u00a0<strong>beta blockers<\/strong>,\u00a0<strong>calcium channel blockers<\/strong>,\u00a0<strong>alpha blockers<\/strong>.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Address heart failure:<\/strong>\n<ul>\n<li>Use medications to reduce load, manage blood pressure, and normalize heart rate.<\/li>\n<\/ul>\n<\/li>\n<\/ol>\n<h1><strong>Surgical Intervention Procedures:<\/strong><\/h1>\n<ul>\n<li><strong>Coronary interventions:<\/strong>\n<ul>\n<li><strong>Catheter-based delivery:<\/strong>\u00a0Thrombolytics, balloons, and stents.\n<ul>\n<li><strong>Angioplasty:<\/strong>\u00a0Balloon inserted via catheter to open blocked arteries; sometimes followed by placement of a\u00a0<strong>stent<\/strong>.<\/li>\n<li><strong>Laser therapy:<\/strong>\u00a0To remove or reduce plaque.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Bypass surgery (CABG):<\/strong>\u00a0Creating new pathways around blocked arteries.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Plaque removal:<\/strong>\u00a0Can be performed via laser, balloon, or stent insertion depending on location.<\/li>\n<\/ul>\n<p><strong>Tools:<\/strong><\/p>\n<ul>\n<li><strong>Defibrillators:<\/strong>\u00a0Automated external defibrillators (AEDs) are accessible in public places and gyms; easy for laypersons to operate.<\/li>\n<\/ul>\n<h1><strong>Other Organ Systems Affected by Vascular Occlusion:<\/strong><\/h1>\n<ol>\n<li><strong>Brain (Stroke):<\/strong>\n<ul>\n<li><strong>TIA (Transient Ischemic Attack):<\/strong>\u00a0A mini-stroke caused by partial occlusion of cerebral arteries.<\/li>\n<li><strong>Full occlusion:<\/strong>\u00a0Leads to\u00a0<strong>cerebrovascular accident<\/strong>\u00a0or\u00a0<strong>stroke<\/strong>\u00a0\u2014 an ischemic stroke.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Peripheral arteries (Aneurysm and Peripheral Vascular Disease):<\/strong>\n<ul>\n<li>Damage and narrowing of arteries (e.g., in the aorta) cause <strong>aneurysm<\/strong> formation:\n<ul>\n<li>Bulging of arterial wall due to damage and calcium deposits.<\/li>\n<li><strong>Brittle<\/strong>\u00a0and\u00a0<strong>susceptible to rupture<\/strong>.<\/li>\n<li>Rupture of the aorta is often\u00a0<strong>fatal<\/strong>\u00a0due to massive internal bleeding.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Other arteries (e.g., iliac arteries):<\/strong>\n<ul>\n<li>Can develop\u00a0<strong>peripheral vascular disease<\/strong>.<\/li>\n<li>Usually affects\u00a0<strong>legs and feet<\/strong>.<\/li>\n<li><strong>Occlusion<\/strong>\u00a0leads to\u00a0<strong>ischemia<\/strong>, tissue death,\u00a0<strong>gangrene<\/strong>, and possibly\u00a0<strong>amputation<\/strong>.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<\/li>\n<\/ol>\n<h1><strong>Signs and Symptoms of Peripheral Vascular Disease:<\/strong><\/h1>\n<ul>\n<li style=\"list-style-type: none\">\n<ul>\n<li><strong>Muscle pain and fatigue:<\/strong>\n<ul>\n<li>Occurs during activity (exercise) when muscles demand more oxygen.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Nerve symptoms:<\/strong>\n<ul>\n<li>Tingling, numbness, burning sensations due to oxygen deprivation.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Pulse weakness or absence:<\/strong>\n<ul>\n<li>Reduced blood flow results in weak or absent pulses in affected limbs.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Physical signs:<\/strong>\n<ul>\n<li><strong>Cyanosis:<\/strong>\u00a0Bluish skin.<\/li>\n<li><strong>Paleness:<\/strong>\u00a0Reduced blood flow.<\/li>\n<li><strong>Dry skin, less hair growth, thickened nails<\/strong>\u00a0(clues of chronic ischemia).<\/li>\n<li><strong>Slow healing of wounds<\/strong>\u00a0due to poor tissue maintenance.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>Prevention and Management of Arterial Disease:<\/strong><\/h1>\n<ul>\n<li><strong>Prevention is key:<\/strong>\n<ul>\n<li>Maintain a\u00a0<strong>healthy diet<\/strong>\u00a0low in saturated fats, trans fats, cholesterol, and salt.<\/li>\n<li>Engage in regular\u00a0<strong>exercise<\/strong>\u00a0to help control weight and improve vascular health.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Control Diabetes:<\/strong>\n<ul>\n<li>Adherence to medications and blood glucose management to prevent vascular damage.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Weight Management:<\/strong>\n<ul>\n<li>Avoid obesity as it contributes to high lipid levels and increased cardiovascular risk.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Lipid Control:<\/strong>\n<ul>\n<li>Use\u00a0<strong>anticoagulants<\/strong>\u00a0and\u00a0<strong>platelet inhibitors<\/strong>\u00a0if at risk for thrombosis or thromboembolism.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Lifestyle Changes:<\/strong>\n<ul>\n<li><strong>Stop smoking<\/strong>: Significantly reduces the formation of atherosclerotic plaques.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Leg Care:<\/strong>\n<ul>\n<li>Maintain dependent positions (legs below the heart) to improve perfusion.<\/li>\n<li>Proper foot hygiene and wound care to prevent infections.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Interventional Procedures:<\/strong>\n<ul>\n<li><strong>Vasodilators:<\/strong>\u00a0Medications to improve blood flow.<\/li>\n<li>Surgical options include:\n<ul>\n<li><strong>Coronary artery bypass grafting (CABG):<\/strong>\u00a0Restores blood flow around blocked arteries.<\/li>\n<li><strong>Angioplasty:<\/strong>\u00a0Balloon dilatation to open narrowed vessels.<\/li>\n<li><strong>Endarterectomy:<\/strong>\u00a0Surgical removal of plaque from vessels.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>Lifestyle Adjustments:<\/strong><\/h1>\n<ul>\n<li><strong>Exercise regularly.<\/strong><\/li>\n<li><strong>Healthy diet.<\/strong><\/li>\n<li><strong>Stress reduction.<\/strong><\/li>\n<\/ul>\n<h1><strong>Summary:<\/strong><\/h1>\n<p><strong>Occlusions<\/strong> in arteries can cause localized tissue ischemia in the heart, brain, or limbs, leading to serious conditions such as MI, stroke, aneurysm rupture, or limb gangrene. Recognizing symptoms like pain during activity, skin changes, and slow wound healing is vital to early diagnosis and intervention, preventing catastrophic outcomes.<\/p>\n<p>Prevention of <strong>artery disease<\/strong> involves lifestyle modifications, proper disease management, and surgical interventions when necessary. Myocardial infarctions are typically caused by plaque rupture and <strong>thrombus formation,<\/strong> with <strong>vasospasm<\/strong> also contributing. Damaged endothelium reduces NO availability, leading to increased <strong>constriction<\/strong> and risk of infarction. The extent of myocardial damage depends on the size and location of the occlusion.<\/p>\n<p>Myocardial infarction presents with characteristic chest pain, ECG changes, and elevated cardiac enzymes indicating cell death. Early diagnosis and treatment are crucial to prevent fatal arrhythmias, shock, or heart failure. Post-infarction, the heart\u2019s compromised ability can cause long-term dysfunction, emphasizing the importance of timely intervention.<\/p>\n<p>Complications after MI include <strong>heart wall rupture<\/strong>, <strong>pericardial tamponade<\/strong>, and <strong>emboli formation<\/strong> leading to stroke or pulmonary embolism. Acidosis from tissue hypoxia further exacerbates organ failure risks. Rapid intervention and close monitoring are essential to prevent these potentially fatal outcomes.<\/p>\n<p>Treatment of MI involves rapid oxygenation, pain management, clot dissolution, and mechanical intervention with angioplasty, stents, or bypass surgery. Long-term management includes lifestyle changes and medications to support the heart and prevent recurrent events. Early intervention and use of devices like defibrillators can save lives<\/p>\n","protected":false},"author":1370,"menu_order":28,"template":"","meta":{"pb_show_title":"on","pb_short_title":"","pb_subtitle":"","pb_authors":["zoe-soon"],"pb_section_license":"cc-by-nc-sa"},"chapter-type":[],"contributor":[60],"license":[57],"class_list":["post-5612","chapter","type-chapter","status-web-only","hentry","contributor-zoe-soon","license-cc-by-nc-sa"],"part":55,"_links":{"self":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/5612","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/users\/1370"}],"version-history":[{"count":8,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/5612\/revisions"}],"predecessor-version":[{"id":5621,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/5612\/revisions\/5621"}],"part":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/parts\/55"}],"metadata":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/5612\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/media?parent=5612"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapter-type?post=5612"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/contributor?post=5612"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/license?post=5612"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}