cardiac 2

systole - period during wich contraction of heart occurs

diastole - period during which the heart is relaxed and filling with blood, and the period when the coronary arteries are filling

block at AV node

full thickness infarct

• 1st - if there's a minor disease in the AV node
• 2nd - more severe disease
• complete - SA and AV nodes aren't communicating

atrial depol

vent. depol

vent repol

• Q = cardiac output = HR x SV
• influencing factors - HR, SV, contractility, preload, afterload, a-vO2 diff (amount of O2 used)

5-20L/min (20 at max exercise)

• VO2 =  HR x SV x a-vO2 diff
• <14 ml/kg -- get on transplant list
• 15 ml/kg -- min for functional activity
• 35-38 ml/kg -- ok for middle aged folk
• 102 ml/kg -- total bad ass

• HR and RPP
• HR x SBP = RPP (rate pressure product)

• body - 20-30% of available oxygen
• heart - ~70% (much smaller reserve, so it's easier to infarct)

SBP minus DBP

• effects that change the heart rate.
• Chronotropic drugs may change the heart rate by affecting the nerves controlling the heart, or by changing the rhythm produced by the sinoatrial node.
• Positive chronotropes increase heart rate; negative chronotropes decrease heart rate.

• alters the force or energy of muscular contractions.
• Negatively inotropic agents weaken the force of muscular contractions. Positively inotropic agents increase the strength of muscular contraction.

• amount of tension on a muscle before it contracts
• this maximizes the blood pushed out by maximizing cross bridges (so more blood in --> more blood out)

They decrease HR and contractility. This lowers the O2 demand and metabolic demands, so there's less risk of ischemia.

 stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end diastolic volume)

• the force against which the heart must contract in order to move the blood
• this is diff for L ventand R vent bc they're pusing blood to diff places that have diff pressures

release calcium, so they can't fully relax or fully contract

• a disease of muscular arteries in which the inner layer becomes thickened by fatty deposits and fibrous tissue
• frequently involves coronary + cerebral vessels

• subednothelial accumulations of large "foam cells" that are mostly derived from macrophages
• fatty streadks cause signals in endothelium to become disrupted

• more advanced lesions than fatty streaks
• the source of clinical manifestations of the disease
• most changees occur in the intimal layer
• looks gray and waxy, and elevates into the lumen causing some occlusion
• create a fibrous cap

seperates a necrotic core of cell debris, degenerated foam cells, cholesterol crystals, etc from the arterial lumen

• calcification
• plaques rupture
• hemorrhage
• fragmentation
• weakening of vessel wall

usually of fibrous plaque --> pipelike rigidity of vessel wall --> increased fragility

this exposes thrombogenic material to circulating blood --> platelets build up --> thrombosis (clot)

a stationary blood clot along the wall of a blood vessel, frequently causing vascular obstruction. Some authorities differentiate thrombus formation from simple coagulation or clot formation.

hemorrhaging into fibrous cap form rupture of the cap or blood vessels that vascularize the plaque --> hematoma

• embolization of fragments of disrupted atheroma to distal sites --> stroke
• weakenting of vessel wall --> aneruism --> rupture --> tamponade + MI

A deposit or degenerative accumulation of lipid-containing plaques on the innermost layer of the wall of an artery.

• plaque builidup and swelling limits the signaling, and healthy signaling (hormone release and other communication?) results in  vessels relaxing, blood passing w/o adhering, prevents smooth muscle migration, etc.
• endothelial cells scred vasoactive substances that directly modulate the contraction of the smooth muscle cells in the medial layer - so if they're in trouble, smooth muscle contraction is too

In your notes you keep telling yourselve to visit her slides. You should probably do that before any exams.

• permiability of endoltheilial layer may increase
• may lose their antithrombitic properties
• reduced secretion of vasokilaters, impairing the smooth muscle relaxation in the media layer
• secrete increased amounts of mitogenic substances (platelet derived growth factors) that recruit smooth muscle cells into the intima
• secrete chemotactic factors that attrace other key cells toward intima

• tobaco smoking
• hypertension
• dyslipidemias
• diabetes mellitus

• relative to nosmokers, smokers are 1.35-2.4 times more likely to get heart disease (1.43-3.5x more likely for heavy smokers)
• tobacco smoking decreases circulating HDL
• gives inappropriate stim of symp nervous system

• see slides! I can't get them at the lib.
• Norm: (120-129)/(80-84)
• Hi Norm (130-139)/(85-89)
• healthy total <200mg/dl
• LDL < 130 if no known heart disiease
• LDL < 100 if known heart disease
• HDL > 35 or 40 (exercise will raise it)

• abnormal circulating libid levels
• countries w low saturated fat intake and low serum cholesterol levels have low incidence of heart idsease
• < 10% of diet should be saturated fat

• risk is relative to glycosylation of lipoproteins or increased platelet adhesiveness
• risk is ~1.3x norm if there's good glucose control

<150

• if <100 before exercise, give a cracker
• if pre-exercise >260 check for urinary ketones
• if >300 ask pysician about exercise

Usually exercise loweres blood glucose, but if it's already very high, exercise will raise it.

• obesity
• sedentary lifestyle
• stress

• 20% above ideal wt will increase risk of heart disease, esp if it's around belly
• obesity is associated w HTN, DM, sedentary lifestyle

• it's recommended you exercise 30 minutes at mod intensity 5-7 days/week 
• exercise raises HDL, lowers BP, helps normalized blood glucose, increases fibrinolysis, decreases plately aggregability (so yr less likely to have a clot)

• stress raises plately activation bc of increased leveles of chatecholemines
• platelet secreted proteins are noted in persons undergoing emotional stress
• depression is also a CRF

• advanced age
• male gender
• family history of heart disease

old folks respond to risk factor modification just like young'uns

angina "strangling in the chest"

• comes on w exertion, stress, emotions, or a big meal
• subsides w rest

• usually happens when at rest,
• result of coronary artery vasospasm rather than an increase in myocardial demand

• comes after slight exertion or when at rest
• high freq of progression to MI

• diastolic perfusion pressure
• coronary vascular resistance (from external compression or intrinsic regulation from local metabolites, endothelial factors, neural innervation)
• oxygent carrying capacity - enoug hemogobin around to carry the O2

• wall tension - more wall tension + pressure in chamber stresses cross bridges --> increased O2 demand
• HR - the higher the HR the more the heart needs O2
• contractility - the harder it has to contract to move blood, the greater the O2 demand

• 70%
• 90%

• inappropriate vasoconstriction of coronary arteries
• loss of normal anithrombotic properties

i wrote to see slides...

• decreased aortic perfusion pressure
• severe decrease in blood oxygen carrying capacity
• profound increase in myocardial O2 demand (such as in marked increase in wall stress)

• episodes of ischiemia in absense of symptoms (ie anginga)
• seen in EKG changes
• common in diabetics - they have neuropathies so might not feel angina, may only have the "short of breath" symptom

• patients with typical symptoms of angina pectoris who have no evidence of significant atherosclerotic coronary stenosis
• may be due to inadequate vasodialator reserve

pt has typical symptoms of angina but no CAD, but shows evidence of CAD on ETT (exercise tolerance test)

it's thought that vessels may not be dilating properly during periods of increased myocardial O2 demand

condition of irreversible necrosis of heart muscle that results from prolonged ischemia

subendocardial = non ST elev = non Q wave

transmural = ST elev = Q wave

• spans thickness of myocardium
• results from prolonged total occlusion of an epicardial coronary arter
• causes a change in contractility

exclusively involve the innermost layers of the myocardium (that area is at greatest risk for ischemia as wall tension increases bc blood supply to here must travel furthest

bc the signal can still travel in a relatively normal way thru the outer layers of the heart

• the QRS complex is widened
• this doesn't reverse w time

Q wave MI: higher risk of mortality, lower risk of another infarct (bc pt's dead?)

non Q wave MI: lower risk if immediate death, higher risk of another MI (that's bc it's usually a smaller infarct and multi vessel)

acute: ST segment elevation

• ST segment elevation
• decreased R waves
• Q waves begin

(this is in a pic in the slides)

• T waave inversion
• Q wave deeper

• ST normalizes
• T wave inverted

• ST and T normalize
• Q wave persists