Cardiovascular Disorders Flashcards
Most major cause of cardiac disease
Atherosclerosis
More minor causes include hypertensive heart disease, congenital heart disease, bacterial endocarditis, rheumatic carditis, cardiomyopathies
Congenital heart disease
• ~25,000 babies/year born with heart defects
• Symptoms evident at birth or early childhood
Defects may be:
• Minor: asymptomatic or only minor clinical symptoms
• Major: associated with major clinical problems or may be lethal
Etiology of congenital heart disease
• Causes mostly unknown (most common)
• Exogenous: viruses, alcohol
• Endogenous: chromosomal abnormalities (Down’s
syndrome)
• Congenital heart defects form before the 10th week of pregnancy
Ventricular septal defect (congenital)
• Left ventricular pressure > Right ventricular pressure
• Blood flows from left ventricle to right ventricle
• Left to right shunt
• Overburdens the right ventricle
• Right ventricle hypertrophy
• Pulmonary hypertension
• Reverse → cyanosis
Atrial septal defect (congenital)
• Usually due to incomplete closure of the foramen ovale
• Defective formation of adjacent connective tissue part of the interatrial septum
• Endocardial cushion defect: Affects mitral and tricuspid valves
• Left to right shunt
• Minor functional consequences
Teratology of Fallot
• Complex congenital defect of heart and
major vessels
4 typical lesions:
1. Stenosis (narrowing) of pulmonary artery
2. Ventricular septal defect
3. Dextroposition of the aorta
4. Hypertrophy of the right ventricle
• “Blue babies” cyanosis
Atherosclerosis
• Systemic disease of arteries
• Simultaneous hardening and softening of the
arteries
• Localized – 4 major locations
A. Coronary heart disease
B. Cerebrovascular disease
C. Atherosclerosis of aorta
D. Peripheral vascular disease
Unmodifiable risk factors of atherosclerosis
Age, gender, hereditary
Modifiable risk factors of atherosclerosis
Lipid metabolism-related (diet, obesity, hyperlipidemia, diabetes mellitus)
Hypertension
Clotting factors
Cigarette smoking
Risky behaviours
Protective factors against atherosclerosis
Exercise, estrogen
Pathogenesis of atherosclerosis
- Endothelial cell injury
• Metabolic derangements
• Physical force - Influx of lipids
• Deposition of blood platelets and lipoproteins - Proliferation of smooth muscle cells → foam cells
• Accumulation of lipids in vessel wall
• Accumulation of macrophages - Atheromas
• Consists of lipid-rich soft interior
• Firm fibrous cap (collagen fibers
Complications of atheromas
Thrombus formation
• Pressure of the internal fatty material may rupture the surface cap
• Large arteries transform into scar
• Small arteries (cerebral) complete occlusion, infarction
• Calcification → hardening
• Atherosclerotic aorta tends to dilate → aneurysm
Atherosclerosis and the aorta
• Almost all persons older than 50 years have some atherosclerosis of the aorta
• Lesions vary from mild to severe and may be focal or diffuse
1. Fatty streaks (sites of plaque form)
2. Atheroma
3. Calcification
4. Aneurysms
Aneurysm
• Dilations of the aortic lumen associated with changes in the wall
• Clinically silent
• Major danger: rupture leading to death by exsanguination
Saccular aneurysm: bulge on one side
Fusiform aneurysm: bulge on all sides
Dissecting aneurysm: blood flows between layers of the wall due to tear
Peripheral vascular disease
Arteries and veins
Atherosclerosis of renal arteries:
• hypoperfusion → failure → renin → hypertension
• Reduced urine output
• irreversible (end stage) kidney failure
Atherosclerosis of the intestinal arteries
• Ischemia, embolism, infarction
Atherosclerosis of extremities
• ischemic occlusion (lower limbs)
• Dry gangrene: necrotic tissue, black, mummified
• Wet gangrene: infected
Coronary heart disease
Pathogenic mechanism: myocardial ischemia
Clinical presentation depends on:
1. Extent of occlusion
(10-25% leads to asymptomatic or angina pectoris, 50-70% may lead to angina pectoris or congestive heart failure, 100% may lead to congestive heart failure or myocardial infarct)
2. Rate of onset
3. Anatomical location of the occlusion
4. Additional complications (i.e., hypertension)
Angina pectoris (clinical feature of coronary heart disease)
• Myocardium that is inadequately perfused
• Functions normally until more demand (exercise)
• Ischemia causes pain
• Alleviated by nitroglycerin (dilates coronary arteries)
Congestive heart disease (clinical presentation of coronary heart disease)
• Pump failure due to hypoxia
• Right back flow causes congestion in peripheral organs and extremities
• Left side insufficient output causes pulmonary edema, pleural effusions, dyspnea, hypoperfusion of organs
Myocardial infarction
• Rapid occlusion of coronary artery = infarct
• Sudden death occurs in ~25% of cases
Consequences of arrhythmia
• Ventricular fibrillation
• Heart block
• Asystole (cardiac arrest)
Right coronary artery obstruction: posterior septum between LV and RV
Left anterior descending artery: anterior on the side of the LV
Left circumflex artery: lateral on the side of the LV
Diagnosis of myocardial infarction
- complaints of chest pain, shortness of breath, fainting
- enzymatic diagnosis (Troponin T or I being the best, most specific indicator)
Treatment of myocardial infarction
• Angioplasty – catheter into coronary arteries to dilate them
• Coronary artery bypass – surgery to restore arterial blood flood to ischemic area
• Transplant – damaged heart cannot be repaired but can be replace
Complications of myocardial infarction
- Endocardial mural thrombus
- Ventricular rupture (Hematopericardium: Blood fills the pericardial sac → cardiac tamponade 5-7 days afterwards)
- Cardiac tamponade (Fluid in sac surrounding heart)
- ventricular aneurysm
Arterial Pressure
Pressure generated by left ventricle or the ejectionof blood
Normotensive: 120 mmHg during systole and 80 mmHg during diastole
Hypertensive: >160 mmHg systole and >90 mmHg diastole
• required antihypertensive treatment
Hypotensive: <90 mmHg during systole and <60 mmHg during diastole
