Congenital Defect:
non-oxygenated blood away from the pulmonary circuit and into the systemic circulation reducing the oxygen saturation of the aterial blood causing immediate cyanosis
cynosis
bluish discoloration of the skin due to accumilation of reduced hemoglogin in capillary beds and seen most readily around lips and nail beds
Congenital Defects:
divert oxygenated blood from the systemic circulation depriving the systemic tissues of oxygen excess blood flowing throught the pulmonary circulation produces a pulmonary hypertension
Congenital Defects:
physical barriers to blood flow and generally do not cause cyanosis
Atherosclerosis
a slow progressive disease of the large elastic and large and medium sized muscular arteries characterized by the formation of atherosclerotic plaques
Non-alterable factors of Atherosclerosis
age (increase with age) sex (male, until menopause) race (caucasion) genetic predisposition
Major risk factors for atherosclerosis
smoking hyperlipidemia hypertension diabetes mellitus
Minor risk factors for atherosclerosis
physical activity stress behavior patterens obesity long term oral contraceptive use
chylomicrons
primarily transports dietary triglycerides in the body for 2 hours after you eat
beta lipoproteins
low density lipoprotein LDL bad cholesterol
pre-beta lipoprotein
very low density lipoprotein VLDL triglycerides- to the liver
alpha lipoprotein
high denisty lipoprotein more cholestrole than triglycerides good cholesterol
Receptor pathway
Liver cells have specific cell surface receptors that bind to LDL, and removes it by excreting it through the bile
Phagocytic (receptor independent) pathway
cells of macrphages contain modified LDL, can not excrete through the bile, so the HDL helps to excrete it through the bile
xanthomas
form when high levels of phagocitic cells for cholesterol little bumps on the skin, expression of hyperlipidemia
Sign of hyperlipidemia: Familial hyperlipidemia
excessive caloric intake, excessive dietary cholesterol, and saturated fatty acids
Fatty streaks
fatty yellow streaks on the inner surface of vessels they are the fist sign of atherosclerosis
Atherosclerotic plaques
multifocal asymmetric elevations of the vessel linning will induce thrombosis
fibrous plaques
hard formed by larde amount of collagen
atheromatous
soft made with abundant lipid material
LDL/ HDL ratio
> 4:1 high <1:4:1 border <3:1 good
Ischemis Heart Disease
results from an imbalance between the metabolic demand of the heart for oxygen and the amount available decrease Oxygen in the heart
Reasons for low availability of Oxygen to the heart (ischemic heart disease) is
decrease coronary flow (atherosclerosis) increased metabolic demand (tachycardia{infections/ exersice} pregnacies) decreased saturated hemoglobin (anemia, hemoglobinopathy, carboxyhemoglobin, right to left shunts)
Types of Ischemic Heart Disease
angina pectoris myocardial infarction sudden cardiac death
ischemic Heart Disease
symptoms : Chest discomfort or neck, left jaw, left shoulder, left armStable : predicable, like when you work out or do physical labor and you know you will have chest painUnstable : first time you have the attack
Ischemic Heart Disease
60% deaths related to IHD exclusion of blood flow due to the athersclerosis and thrombus ( most common location is left anterior descending coronary artery) risk is dependent on the material of the plaque not the size
Complications of myocardial infarcts
cardiac arrhythmias 90% left ventricualr dysfunction mural thrombosis/ embolization ruputre ventricular aneurysm
Laboratory result for myocardial infarction
CPK- during the first 24 hours Troponin- serum when muscle necrosis Myoglobin- serum LDH which persist for 7-12 days
Modes for interventino for myocardial infarction
thrombolytic theraby- clot busting drug angioplasty- balloon/ stent coronary bypass- for sever cases
Ischemic heart disease
death quickly after the even
Chronic Ischemic Heart Disease
slow diffuse myocarial atrophy, spotty loss of myocardial cells, diffuse fibrosis, and possible scarring from previous infarcts
stenosis in vascular disease
failure of a vlave to open obstruction of forward flow
insufficiency of vascular disease
inability of a valve to close allows backward flow
Rheumatic Heart Disease
inflammatory disease streptococci (strep throat) more common in children Main sympotms (migratory polyarthritis and carditis)
pericarditis
friction rub bread and butter appearance
myocarditis
inflammation of the myocardium may lead to arrhythmias
endocarditis
this is the most crippling and destructive aspect of the disease occurs in the heart valves (primarily the MV)
Rheumatic Heart Disease
cardiac failure mural thrombosis and embolication bacterial (infective) endocarditis
Calcific Aortic Stenosis
no fusion of the valves obstructs the flow through the valves most often seen in elderly patients and may be a result of wear and tear
Mitral Valve Prolapse
more frequent in your women enlarged mitral leaflets most patients are asymptomatic (severe is chordal rupture)
Infective Endocarditis
vegetations thrombi with embedded bacteria
Infective Endocarditis
Staph seen in IV drug users or severe alcholoics usually no underlying heart problems high virulence bulky vegitation acute onset high mortality
Infective Endocarditis
hearts usually have some underlying heart disease usually occurs in the mitral valve and aortic valve streptococcus viridans low virulence insidious onset better prognoses
Myocardial Heart Disease
(blood pressure >140/90) cardiac volume output and the peripheral arteriolar resistance in the absence of any other abnormality that might produce left ventricular hypertrophy (i.e. valve disease) this is the identifying hallmark of hypertension heart failure, stroke, renovascular disease and or vascular complications
Myocardial Heart Disease
most common in infants, pregnant women and immonosuppressed patients viral heart becomes flabby and soft usually resolves in 6-8 weeks
Myocardial Heart Disease
Dialated (congestive) --dialation and hypertrophy of all the chamber of the heart Hypertrophic (obstructive) --usually a family history --disproportional hypertrophy of the interventricular septum with myofiber disarray --aortic outflow obstruction and mitral insufficiency --angina, syncope, dyspnea --obstruction of the left ventricular outflow tract Restructive/ infiltrative --restriction of ventricular filling --stiffening of the muscle, not allowing it to dialte or contract
Pericardial Disease
Acute -irriation of the pericardium -(serous, fibrinous, suppurative, hemorrahgic) -prevent venous blood from reentering therefor decrease cardiac output (caridac tamponade) Chronic -adhesive or constructive (harden)
Vascular Disease
Abdominal- result from atherosclerotic weaking, leave until >5cm Thoracic- more symptomatic -Cystic medial necrosis- majority of the aneurysms (no known etiology) -syphilis- near the arch or ascending aorta
Vascular disease
tearing of the inner liner of the aorta (transverse tear) hypertension is frequenlty an associated condition retrograde dissection, rupture into the pericardial cavity and cardiac tamponade
Vascular Disease
atherosclerotic plaque often as a complication of diabetes eventual ulceration and gangrenous necrosis of the sking and underlying tissues
Vascular Disease
appartent with increasing age, especially females gravitational effects valve insufficiency stasis dermatitis and chronic ulcerations (because not enough oxygen in the tissue)
