Cardiopathophys

• SA node: right atrium
• av node: at atrial ventricular junction
• bund. of his: at atrial ventricular junction
• bundle branches: at intraventricular septum
• perkinje fibers: in ventricles

• sequential transmission through the heart muscle
• ventricle- each contract as one unit
• enough force is generated to pump blood out

• systemic resistance> pulmonic
• left ventricle pressure> right ventricle pressure
• aortic resistance> pulmonary resistance

can be generated within the ventricles or the atria which can lead to chaotic contractions and eventually afib or vfib

• less dangerous bc the way the pump is pumped into the ventricles
• most of the blood accumulates in the ventricles in diastole in a passive manner
• so if afib person can live

• more dnagerous
• no way of pumping blood out bc chaotic action potentials leading to chaotic contractions and eventually blood is not able to get out. 
• heart cannot sustain without its own blood supply and energy and the heart muscle will die

• stroke vol x heartrate
• av = 70x70= 4.9L

• should be equal between r and l ventricle
• even though theres more resistance on left side, it has higher perssure to keep up

• parasymp: decreases hr
• symp: increases heartrate and therefore stroke volume
• venous return: increases end diastolic volume which increases stroke volume and therefore CO

acetylcholine, secreted by the parasymp ns

adrenaline/aka epinephirine secreted from symp ns

• coronary blood vessels: supply blood to the heart
• pump: heart failure- muscle not able to function
• heart wall: pericardium, myocardium, endocardium abnormaliites
• conduciton system: rhtym disorders
• shock: usually result of these other problems
• perfusion probs

left heart failure

• atherosclerosis
• cad
• myo ischemia
• MI
• hypertension

• occlusion of blood vessels
• lumen has decreased volume which causes problems with blood flow and additional injury leads to ischemia

• childhood
• its an inflammatory disease

• elevated LDL
• free rads
• diabetes mellitus
• infections (herpes, chlamydia)
• high bp

all of these cause injury to the endothelial cell and lead to artherosclerosis

• endothelial cells are supposed to be smooth wall lining the blood vessels
• with things like smoking/HTN/toxins/immune problems you might induce injury to endothelial cells causing inflammation and production of selectins to make other cells stick to the cells

• as cells get injured LDL attracts to proteins and then they migrate into the tunica intima
• once they migrate below the intima they accumulate underneath the endothelial cells causing a fatty streak
• once the LDL gets inside it has a tendency to get oxidized, and once this happens, the macrophages migrate to the area underneath the endothelial cells and start phagocytosing the oxidized LDL and that will create a foam cell
• so now you have macrophages loaded up with fat making these foam cells
• foam cells start producing cytokines

chemicals that will activate smooth muscle cells and fiborblasts so eventually there will be a fiber formation around the lipid pool to give rise to the lesion which is infact enclosed by a fibrous capsule- called a fibrous PLAQUE

lesion from foam cell covered by fibrous tissue

oxidized LDL makes endothelial cells more activated so monocytes become macrophages and enter the intima to take up the LDL where they will then become foam cells

endothelial injury: attracts LDL towards it which will migrate into the itima and underneath

fatty streak: once LDL are accumulated in the intima

• fibrous plaque: once macrophages are loaded with fat and foam cells they activate cytokines and fibroblasts deposit fibers around the fatty area. an area around the fatty streak where fibroblasts have been activated and formed a cap
• Complicated lesion: when fibrous plaque eventually breaks off and fat starts coming out causing a thrombus or embolus

• prevent expression of cell adhesion molecules
• prevent macrophage adhesion
• prevent LDL oxidation
• prevent formation of foam cells
• promote cholesterol efflux

• needed for brain function
• parent molecule for a lot of hormones including sex hormones and cortisol

• lipids plus proteins
• relative density based on classification
• chylomicron
• VLDL
• IDL
• LDL
• HDL

• largest, lowest in density
• triaclyglycerols highest by weight
• ratio of lipid to protein is high

• very low density lipoprotein
• 2nd highest in tracylglycerols by weight

• intermediate density lipoprotein
• >30nm

• low density lipoprotein
• highest in cholesteryl esters as % by weight
• 20-22nm

• high density lipoprotein
• high protein/lipid ratio
• 9-15nM

• proinflammatory: chilomicrons, vldl, and ldl
• antiinflammatory: HDL

• we eat, fat gets into intestinal ep cells and thats how we get the combo of the cholesterol, cholesterol esters, phospholipids, tryglicerides and apoproteins
• these make particles cale chylomicrons which are transported to liver and in the liver they are chopped into VLDL which is modified to LDL
• ldl made in liver and can be placed in blood or taken up by liver cells or cells that need fat

• as a small protein rich particle by the liver and intestine
• it will go aroudn the blood and pick up cholesterol back to liver

• from cells
• by receptor mediated endocytosis