Cardiovascular System Flashcards

Question

What are the categories of heart disease and failure and provide examples?

Answer 1

Ischemic Heart Disease  a) Angina Pectoris  b) Myocardial Infarction  c) Chronic Ischaemic Heart Disease Congestive Heart Failure   a) Forward Failure  b) Backward Failure Congenital Heart Disease  a) Left-to-Right Shunts  b) Right-to-Left Shunts  c) Obstructive Anomalies

Answer 2

- Ischemic heart disease = coronary heart disease - Most common form of heart disease in Australia - Acute vs. chronic ischemia - Coronary Atherosclerosis (> 90% of cases) - High Mortality & Morbidity Four basic forms  - Angina pectoris  - Myocardial infarction  - Chronic ischemia leading to chronic heart failure (CHF)  - Sudden death from arrhythmia - Risk factors: Hypertension, Hypercholesterolemia, Diabetes, Smoking, Life style, Diet, Genetic

Answer 3

- Myocardial infarction = "heart attack" - Death of cardiac muscle from ischemia - 90% caused by thrombosed artery (disruption of atherosclerotic plaque à thrombus) -> total occlusion                   - Severe crushing chest pain often accompanied by sweating, nausea, vomiting & dyspnea Generally lasts for several hours Complications:  - Cardiogenic shock  - Cardiac failure  - Arrhythmias  - Mural thrombosis  - Rupture or death 

Answer 4

Transmural infarction (common)  - Ischemic necrosis involving full or nearly full ventricular wall thickness in the distribution of a single coronary artery.   - Cause: Coronary atherosclerosis, acute plaque change, superimposed thrombosis   Subendocardial infarct  - Necrosis usually limited to the inner one third or at most one half of the ventricular wall (localised or sometimes circumferential)  - Subendocardium not well perfused so susceptible to ischemic infarct from hypotension in presence of non-critical stenosis   - Cause: Acute coronary thrombosis, hypotension etc.

Answer 5

Early Acute MI (1-3hrs):  - 1-3hrs: Wavy myocardial fibres but no inflammatory cells  - 2-3hrs: Staining defect in myocardial fibre cytoplasm with tetrazolium or basic fuchsin dye  Early Acute MI (4-12hrs) : - Coagulation necrosis with loss of cross striations, contraction bands, edema, hemorrhage, and early neutrophilic infiltrate Acute MI (18-24hrs) : - Continuing coagulation necrosis, pyknosis of nuclei, and marginal contraction bands   - nuclei often not present  - extensive hemorrhage at the border of the infarction -> grossly apparent hyperemic border 3-7 Days:  - Macrophage and mononuclear infiltration begins, fibrovascular response begins   - still some neutrophilic infiltrate but increasingly more macrophages and monocytes  - prominent necrosis and hemorrhage  - beginning of fibrosis  7-21 Days:  - Fibrovascular response with prominent granulation tissue containing capillaries and fibroblasts   - healing of a myocardial infarction (mainly repair)  - ingrowth of capillaries along with fibroblasts and macrophages filled with hemosiderin  - granulation tissue peaks around 1-2 weeks  - Cardiac troponin markers may still be present in the blood up to weeks following the initial ischemic event >21 Days/3 Weeks:  - healing (repair) is well under way - more extensive collagen deposition in the region of myocardium that was infarcted >2months:  - remote myocardial infarction is evidenced by a collagenous scar (partially re-organized)  - some residual surviving myocardial fibers (red)  - Note: This scar tissue is non-functional  - reduction in ejection fraction is related to the extent of scarring

Answer 6

Symptoms i.e. chest pain ECG pattern – ST elevation, new Q waves in silent infarction Cardiac biomarkers:   - raised cardiac troponin (cardiac protein)  - MB subtype of the enzyme creatine kinase (CK-MB = cardiac isoenzyme)   - Cardiac troponins T and I are released within 4–6 hours of an attack of MI and remain elevated for up to 2 weeks

Answer 7

- Diminished out volume of either ventricle  - Left-sided or right sided heart failure  - Forward failure: diminished cardiac output  - Backward failure: damming back of blood in the venous system Often loss of contractility of the myocardium  - Systolic failure: - Loss of pumping strength  - Backup of blood behind weakened ventricle  - Atherosclerosis leading to chronic ischemia  - Diastolic failure : - Reduced ability of ventricle to fill  - Constriction of trapping of ventricle  - Abnormal retention of water and sodium

Answer 8

- Diminished pumping ability of left ventricle - Results in an inadequate supply of of blood oxygen to cells - Back up of blood in pulmonary vasculature - Pulmonary edema - Peripheral edema

Answer 9

Pulmonary Edema: - A condition caused by excess fluid in the lungs - When the heart is not able to pump efficiently, blood can back up into the veins that take blood through the lungs. - As the pressure in these blood vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs. Peripheral Edema: - Edema in tissues perfused by the peripheral vascular system, usually in the lower limbs. - The heart's lower chambers stop pumping blood well. As a result, small blood vessels leak fluid into nearby tissues

Answer 10

- Clinical symptoms come from mixing of blood - Mixing due to shunts Present at birth  - Genetic factors are rare  - Environmental (developmental) are common  - Maternal infections  - Fetal alcohol syndrome Types: - Left-to-Right shunts - Right-to-Left shunts - Obstructive Anomalies

Answer 11

Left-to-Right Shunts: - Atrial Septal Defect (ASD): left atrium -> right atrium - Ventricular Septal Defect (VSD): left ventricle -> right ventricle - Patent Ductus Arteriosus (PDA): a persistent opening between the aorta and the pulmonary artery Right-to-Left Shunts: Tetralogy of Fallot  - Transposition of the great arteries = aorta arises from the right ventricle and the pulmonary artery arises from the left ventricle  - Often presents with cyanosis early in life 