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systole and diastole basic defs
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
prolonged PR interval indicates...?
block at AV node
ST elevation indicates...?
full thickness infarct
1st degree, 2nd degree, and complete heart block
- 1st - if there's a minor disease in the AV node
- 2nd - more severe disease
- complete - SA and AV nodes aren't communicating
Q (can have a dot on top of it too) means what?
what influences it?
- Q = cardiac output = HR x SV
- influencing factors - HR, SV, contractility, preload, afterload, a-vO2 diff (amount of O2 used)
cardiac output (Q) normal range
5-20L/min (20 at max exercise)
Oxygen uptake (VO2) formula and values
- 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
myocardial oygenation (MVO2) is highly correlated w what?
- HR and RPP
- HR x SBP = RPP (rate pressure product)
amount of O2 body uses at rest, amount heart uses
- body - 20-30% of available oxygen
- heart - ~70% (much smaller reserve, so it's easier to infarct)
pulse pressure def
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.
preload basic def, why it's helpful
- 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)
Why would beta blockers be given to cardiac pts?
They decrease HR and contractility. This lowers the O2 demand and metabolic demands, so there's less risk of ischemia.
Frank Starling Mechanism
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
if there's not enough O2, muscles can't...?
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
fatty streaks in atherosclerosis
- subednothelial accumulations of large "foam cells" that are mostly derived from macrophages
- fatty streadks cause signals in endothelium to become disrupted
fibrous plaques in atherosclerosis
- 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
role of fibrous cap in fibrous plaques
seperates a necrotic core of cell debris, degenerated foam cells, cholesterol crystals, etc from the arterial lumen
5 types of complicated lesions seen in atherosclerosis
- plaques rupture
- weakening of vessel wall
details on calcification in atherosclerosis
usually of fibrous plaque --> pipelike rigidity of vessel wall --> increased fragility
more about "plaques rupture" in atherosclerosis
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.
more about hemorrhaging in atherosclerosis
hemorrhaging into fibrous cap form rupture of the cap or blood vessels that vascularize the plaque --> hematoma
more about weakening of vessel wall in atherosclerosis
- 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.
signaling (which becomes disrupted in endothelium as a result of fatty streaks)
- 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
Heather, just want to remind you that simply studying these cards isn't enough
In your notes you keep telling yourselve to visit her slides. You should probably do that before any exams.
When endothelial cells become injured or dysfunctional, atherosclerosis may occur. Stuff you'll see when you have injured endothelial cells:
- 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
4 major modifiable risk factors for heart disease
- tobaco smoking
- diabetes mellitus
about tobacco being a modifiable CRF
- 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
hypertension as a modifiable CRF
BP norm, high norm
Cholesterol healthy total
Desired LDL if no known heart disease, if heart disease
- 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)
dyslipidemias (a modifiable CRF)
- 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
diabetes as a modifiable CRF
the risk is related to what?
- risk is relative to glycosylation of lipoproteins or increased platelet adhesiveness
- risk is ~1.3x norm if there's good glucose control
desired trigliceride level (i'm not sure if this is for folks with DM or everyone)
esp w DM pts, look at pre and post exercise glucose
what are you looking for?
- if <100 before exercise, give a cracker
- if pre-exercise >260 check for urinary ketones
- if >300 ask pysician about exercise
exercise's impact on blood glucose
Usually exercise loweres blood glucose, but if it's already very high, exercise will raise it.
3 minor modifiable CRFs
- sedentary lifestyle
obesity as a minor modifiable CRF
- 20% above ideal wt will increase risk of heart disease, esp if it's around belly
- obesity is associated w HTN, DM, sedentary lifestyle
sedentary lifestyle is a minor modifiable CRF
recommended exercise time
expected positive results of exercise
- 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)
reasons stress is a minor modifiable CRF
- 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
3 major non-modifiable CRFs
- advanced age
- male gender
- family history of heart disease
caveat about old age being a major non-modifiable CRF
old folks respond to risk factor modification just like young'uns
most common manifestaion of ischemic heart disease
angina "strangling in the chest"
- comes on w exertion, stress, emotions, or a big meal
- subsides w rest
happens when? result of what?
- usually happens when at rest,
- result of coronary artery vasospasm rather than an increase in myocardial demand
unstable angina comes on when?
- comes after slight exertion or when at rest
- high freq of progression to MI
3 factors contributing to myocardial oxygen supply
- 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
3 major factors in myocardial oxygen demand
- 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
when vessel is stenosed _% it needs to be fully dilated to get blood thru
_% stenosed and the blood flow can't meet basal req.
endolthelial cell dysfunction leads to what 2 things?
- inappropriate vasoconstriction of coronary arteries
- loss of normal anithrombotic properties
i wrote to see slides...
endothelial cell dysfunction leads to imbalance of O2 suppy/demand how? 3 ways
- 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)
silent ischemia def, how it's id'd, common in who?
- 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
basic myocardial infarct def
condition of irreversible necrosis of heart muscle that results from prolonged ischemia
2 other names for a subendocardial MI
subendocardial = non ST elev = non Q wave
2 other names for a transmural MI
transmural = ST elev = Q wave
transmural aka ST elev aka Q wave MI
- spans thickness of myocardium
- results from prolonged total occlusion of an epicardial coronary arter
- causes a change in contractility
subendcardial aka non ST elev aka non Q wave MI
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
why is a subendocardial MI a non-ST wave MI?
bc the signal can still travel in a relatively normal way thru the outer layers of the heart
what's happening with the EKG in a "Q-wave MI?"
- the QRS complex is widened
- this doesn't reverse w time
Q wave vs non-Q wave MI comparing mortality and risk of another infarct
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)
EKG change after an MI
acute: ST segment elevation
EKG change after an MI
- ST segment elevation
- decreased R waves
- Q waves begin
(this is in a pic in the slides)
EKG change after an MI
- T waave inversion
- Q wave deeper
EKG change after an MI
- ST normalizes
- T wave inverted
EKG change after an MI
- ST and T normalize
- Q wave persists