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pathophy
cardiovascular unit
| Question | Answer |
|---|---|
| active congestion | due to an increase of blood flow to an area due to dilation of arterioles |
| passive congestion | impaired drainage of blood to an area |
| edema | accumulation of fluids in the interstitual space or within body cavities |
| exudate | fluids high in protein |
| transudate | fluids low in proteins |
| hemorrhage | escape of blood from vascular system. can lead to vascular spasms, platelet plug, or coagulation. |
| 3 factors that affect ESV | preload, contractility, afterload |
| preload | ventricular stretching during diastole. directly proportional to EDV. affects ability to produce tension in muscle cells |
| Frank-Starling Principle | as EDV increases, stroke volume increases. the greater the stretch of myocardial fiber at the end of diastole, the greater the force of contraction. |
| contractility | changes in the developed force independent of changes in myocardial fiber length. causes ventricles to contract with more force. increases ejection fraction and decreases ESV. increase Ca levels. |
| afterload | increased by any factor that restricts arterial blood flow |
| EDV, preload and stroke volume AT REST | EDV is low, myocardium stretches less, stroke volume low |
| EDV, preload and stroke volume WITH EXERCISE | EDV increases, myocardium stretches more, stroke volume increases |
| Mean Arteriole Pressure | DBP+[(SBP-DBP)/3] normally 100 mmHg |
| FIBF: neural mechanism | sympathetic adregenic |
| FIBF: humoral mechanism | epinephrine, angiotensin II, ADH, histamines, bradykinin |
| FIBF: metabolic mechanism | potassium ions, hydrogen ions, oxygen, carbon dioxide, adenosine |
| FIBF: myogenic mechanism | mechanosensative smooth muscle in arterioles |
| FIBF: flow-mediated mechanism | mechanosensative endothelial cells |
| FIBF: angiogenic mechanism | new vessel growth |
| FIBF: rarefaction | decrease in the number of vessels |
| FIBF: remodeling | change in the size of blood vessels ex.-hypertrophy, hyperplasia |
| Putting it Together | blood flow is proportional to the pressure gradient, ex.-MAP and RAP |
| Putting it Together | blood flow is inversely proportional to resistance. SVR=(MAP-RAP)/CO |
| fatty streaks | non-obstructive patches on the endothelial surface; some accumulation of fat in smooth muscle and macrophages |
| fibrous plaques | obstructing plaque consisting of a central core of lipids and necrotic tissue. typically occur at bifurcations, curves, and narrowing. |
| stable plaques | have thick, fibrous plaques with more smooth muscle cells and fewer macrophages. associated with narrowing of the coronary lumen and produce ischemia and angina. |
| vulnerable plaques | have thin, fibrous caps. large lipid cores. fewer smooth muscle cells and more macrophages. do not narrow lumen. more likely to rupture and cause CAD. |
| thrombosis | formation of blood clots(thrombi) in vascular system |
| embolism | physical mass moving in blood stream |
| ischemia | inadequate blood supply to an area |
| infarction | cell death, localized necrosis resulting from obstruction of the blood supply |
| metabolic syndrome | abnormal abdominal obesity, elevated triglyceride levels, elevated BP, insulin resistance |
| atherosclerosis | a stage of arteriosclerosis involving fatty deposits (atheromas) inside the arterial walls. impaired function of endothelial cells, impaired vasodilation, loss of antithrombotic function, increased leukocyte adhesion |
| congestive heart failure | fluid in aveoli |
| papillary muscle dysfunction | AV valve insufficiency where blood regurgitates |
| cardiac rupture | the necrotic part bulges out |
| dysrythmias | normal PQRST wave is not accomplished. etopic beats, bizzare QRS. |
| P wave | atrial depolarization |
| QRS complex | ventricular depolarization |
| T wave | ventricular re-polarization |
| inferior wall: AVF, II, III | Right Coronary Artery |
| High lateral wall: I, AVL | Left circumflex |
| anterior wall: V2-V4 | Left anterior Descending |
| septal: V1-V2 | Left anterior Descending |
| anterior septal: V1-V4 | Left Anterior Descending |
| Low Lateral Wall: V5-V6 | Left Anterior Descending |
| Posterior Wall: V1-V2 | Left Circumflex. Reciprocal changes. Large R waves, ST segment depression=MI |
| OLD MI | prominant Q wave |
| Left Heart Failure | causes pulmonary congestion |
| Right Heart Failure | causes systemic venous congestion. ex.-edema |
| 1st degree dysrhythmia | abnormally long AV nodal conduction |
| 2nd degree dysrhythmia | AV node conduction, some block. ex.-PQRS P PQRS PQRS P P P |
| 3rd degree dysrhythmia | no AV node conduction. P wave with no QRS, heart rate is slow. |
| CAD mods: antihypertensives | Beta blockers that increase renin secretion, Ca channel blockers |
| CAD mods: antihyperlipidemics | (lipid transports) statins=muscle weakness |
| CAD mods: anti-platelet aggregation | preserve some blood flow. ex.-aspirin, GPIIb/IIIa inhibitors |
| CAD mods: angioplasty | replacing stents; catheter based |
| Vavular Heart Disease (VAD) pathogenesis | rheumatic fever, infective endocarditis, inborn defects of CT, dysfunction of papillary muscles, cogenital malformation. |
| Mitral Valve Stenosis | impedes blood flow between LA and LV. LA hypertrophy and dilation can occur. pulmonary congestion leading to increased pulmonary arterial pressure. chronic disease results in right heart failure. |
| aortic stenosis | impedes outflow during ventricular contraction. slightly irregular or high BP |
| echocardiogram | measures doppler blood flow |
| perfusion imaging | hot and cold analysis, timed; with dye |
| compensatory mechanisms | in heart failure increased sympathetic drive, and prelaod through activation on the renin angtiostem system |
| treatment for compensatory mechanisms | reduction in preload(diuretics) and afterload(vasodilators such as ACE inhibitors; more NE icr. HR and needs heart needs more O2)). increase contractility(digitalis glycosides) |
| Peripheral Vascular Disease | can be occlusive or aneurysmal, with microvascular and macrovascular |
| collateral blood flow | development of alternative routes of blood flow in response to chronic obstruction, enlargment of existing vessels and development of new network of smaller vessels |
| cystic medial necrosis | a degenerative change in the medial layer of vessels, leads to aneurysms, aortic dissection, or spontaneous |
| Marfan Syndrome | inherited CT disorder, leads to aortic rupture with or without aneurysm. normally affects taller individuals |
| Bueger's Disease | chronic occlusive disease of small and middle sized arteries and veins. inflammation ->healing->thrombosis->occlusion->temporal arteries |
| arteritis | inflammation of arterial wall due to an autoimmune attack of the internal elastic lamina-usually in ppl over age of 50 (eosinophils, and t-lymphocytes) (common in temporal artery and common carotid) BLINDNESS(so corticosteriod therapy reccomended) |
| vasospatic disease | associated with temporary occlusion due to inappropriate contractions of the vasculature-not due to obstruction |
| Reynauds Syndrome | vasospasm of small cutaneous and subcutaneous arteries and arterioles |
| Prinzmetals Angina | vasospasm of coronary arteries |
| fibromuscular dysplasia | abnormalities in fibrous CT, not atherosclerotic or inflammatory. results in "string of beads appearance." SURGERY |
| occlusive artery disease | most common- aortic illiac, femoral popiteal, popiteal tibial. bifurcations branching, abrupt curvature, vascular narrowing=turbulance(atherogenesis). THROMBOSIS and EMBOLISM= main concern |
| intermittent claudication | ischemic pain in lower limbs. hips(aorticilliac disease) thigh(femoral and illiac) calf(popiteal) |
| 6 P's of acute arteriole occlusion | Pain. Palor(color). Parathesia(tingling). Pulselessness. Poikilothermia(body temp). Paralysis. |
| aneurysmal disease | degeneration and weakening of the medial layer. abdominal aorta is most common site. asymptomatic |
| hypertension | 140/90. asymptomatic, etiology unknown. altered renal excretion of Na and H20, altered baroreceptors and SNS function, elevated renin release. |
Created by:
megshock1020
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