Cardiovascular Alterations - PDF
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2025
Dr. Shazam Bacchus
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Summary
This presentation by Dr. Shazam Bacchus from Spring 2025 covers various cardiovascular alterations including angina, myocardial infarction, and coronary artery disease. The presentation details topics from the structure of the heart to diagnostic studies and treatment options. The presentation offers an overview of the cardiovascular system and related clinical cases.
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Cardiovascular Alterations Dr. Shazam Bacchus Spring 2025 Hypertensive crisis Angina MI Cardiomyopathy Interventional studies Arterial Venous Normal Structure (1 of 2) Heart Mediastinal space Covered by pericardium Composed of three layer...
Cardiovascular Alterations Dr. Shazam Bacchus Spring 2025 Hypertensive crisis Angina MI Cardiomyopathy Interventional studies Arterial Venous Normal Structure (1 of 2) Heart Mediastinal space Covered by pericardium Composed of three layers Epicardium Myocardium Endocardium Normal Structure (2 of 2) Right side is low pressure Left side is high pressure Flow of blood Cardiac valves Autonomic Control Sympathetic nervous system Norepinephrine Parasympathetic nervous system Acetylcholine Chemoreceptors Baroreceptors Cardiac Function Coronary circulation Conduction system Hemodynamics Heart sounds S1, S2, S3, and S4 Heart murmur Turbulent blood flow through valves Heart Murmur Caused by a turbulence of blood flow through the valves Rumbling, blowing, harsh, or musical in sound Identify location, sound, loudness, and intensity and whether other heart sounds are heard Coronary Artery Disease (CAD) Progressive narrowing of coronary arteries by atherosclerosis Coronary heart disease Atherosclerotic heart disease Pathophysiology of CAD (1 of 3) Injury to epithelial cells in intima Platelet aggregation Migration of monocytes Lipoproteins enter intima Fatty streak Monocytes develop into macrophages Lipid-rich "foam cells” develop Atheroma Pathophysiology of CAD (2 of 3) Damage to intima Liberates platelet-derived growth factor Proliferation of smooth muscle cells Fibrous cap forms From connective tissue and low-density lipoprotein (LDL) Fibrous cap often ruptures Thrombus Clotting cascade initiated Pathophysiology of CAD (3 of 3) Adhesion: platelets bind to receptors Activation: platelets change shape and activate receptors Release: thromboxane A2 and serotonin Activate glycoprotein IIb/IIIa receptors Aggregation: platelets clump together Drugs administered to stop the process Aspirin Glycoprotein IIb/IIIa inhibitors Risk Factors Nonmodifiable factors Modifiable Age Smoking Men > 45 years Inactivity Women > 55 years Overweight Family history Cholesterol High LDL Low levels of HDL Diabetes Hypertension History Risk factors Prior hospitalizations Shortness of breath, chest pain Medications Erectile dysfunction meds if considering nitroglycerin Psychosocial history Include stressors Diagnostic Studies (1 of 3) 12-lead electrocardiogram (ECG) Holter monitor Exercise tolerance test (stress test) Exercise to increase demand on heart Stressed via drugs (e.g., adenosine) if patient cannot tolerate exercise Monitoring vital signs, ECG Pharmacological stress testing Nuclear stress testing Chest x-ray Diagnostic Studies (2 of 3) Echocardiography Ultrasound to visualize cardiac structures Transesophageal echocardiography Multigated blood pool study (MUGA scan) Diagnostic Studies (3 of 3) Positron emission tomography (PET scan) Cardiac magnetic resonance imaging Cardiac Catheterization and Arteriography Electrophysiology study Catheter (right or left) Heart pressures (similar to PA catheter) Cardiac output Arteriography Visualize blood vessels Post-catheterization Care Bed rest; head of bed no higher than 30 degrees Monitor bleeding; newer collagen agents for hemostasis may be used Monitor pulses Antiplatelet drugs after the procedure (usually after interventions such as PCI) May be discharged in 6 to 8 hours; depends on diagnosis and procedures done in catheterization laboratory Laboratory Tests CBC Hemoglobin Hematocrit Sodium Potassium Calcium Magnesium Cardiac Enzymes Troponin I and T As early as 1 hour after injury Normal values less than 0.5 mcg/L for Troponin I Normal values less than 0.1 mcg/L for Troponin T Cholesterol in CAD Categories HDL is considered good LDL is considered bad LDL Target Levels (NIH) No CHD and fewer than two risk factors o 160 mg/dL No CHD and two or more risk factors o 130 mg/dL CAD o