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111 terms

CVP physiology - exam I

STUDY
PLAY
the major underlying cause of cardiovascular disease is due to
ischemia
a vasocontrictor and major secretory product of platelets, which potentiates release of granule contents
thromboxane A2
contents of platelets
- actin & myosin
- enzymes & calcium
- ADP & ATP
- thromboxane A2
- serotonin
- growth factor
initiates clotting
thromboplastin
prevents platelet aggregation and produces prostacyclin
endothelium
aspirin and ibuprofen block what
fatty acid cyclooxygenase
cyclooxygenase is an enzyme needed for what conversions
- ARA to thromboxane A2 in platelets
- ARA to prostacyclin in endothelium
- vasodilator
- inhibits platelet degranulation
prostacyclin
- vasoconstrictor
- potentiates platelet degranulation
thromboxane A2
acts as an anticoagulant by enhancing the action of antithrombin III
heparin
important for lysis of clots
plasmin
endogenous activators of plasminogen are found in
- tissue
- plasma
- urine
exogenous activators of plasminogen are found in
- streptokinase
- tPA (tissue plasminogen activator)
the ability to open up alternate routes of blood flow to compensate for a blocked vessel
collateralization
role of sympathetic nervous system in collateralization
- impede via vasoconstriction
- augment via release of NPY
blood coagulation initiated by chemical factors released by damaged tissues
extrinsic mechanism
blood coagulation requiring only components in blood and trauma to blood or exposure to collagen
intrinsic mechanism
depresses liver formation by blocking action of vitamin K
coumarin
a key step in clotting that requires thrombin
fibrinogen to fibrin
risk factors in heart disease
- increasing age
- male
- heredity
- tobacco smoke
- high blood cholesterol, pressure, and homocysteine
- physical inactivity
- obesity
- diabetes mellitus
high levels of this in the blood can be reduced by increasing intake of folic acid, B6, and B12
homocysteine
amino acid in the blood that may irritate blood vessels promoting atherosclerosis and can make blood more likely to clot
homocysteine
allows the heart to behave as a syncytium
intercalated discs
sharp increase at onset of depolarization
Na+
increased during the plateau
Ca++
increased during the resting polarized state
K+
increases at onset of depolarization and decreases during repolarization
Na+ and Ca++
decreases at onset of depolarization and increases during repolarization
K+
tetradotoxins block fast Na+ channels selectively changing what
a fast response into a slow response creating an increased time of depolarization
closed during resting membrane potential
- fast Na+ channels
- slow Ca++/Na+ channels
open during resting membrane potential
K+ channels
the inhibiting effects of digitalis on the Na+/K+ pump does what to the Na+/Ca++ pump? what happens to Ca++ inside the cell? what happens to contractile strength
- digitalis reduces Na+/K+ pump.
- Ca++ is built up inside of the cell
- contractile strength is increased because of all of the built up Ca++ inside the cell
refractory period where the cell is unable to re-stimulate and occurs during the plateau
absolute refractory period
refractory period that requires a supra-normal stimulus and occurs during repolarization
relative refractory period
delays the wave of depolarization from entering the ventricle
AV node
TRUE or FALSE
at resting heartrate diastole is greater than systole
TRUE
TRUE or FALSE
both the duration of systole and diastole shorten when cycle length shortens, but systole shortens to a greater extent
FALSE; diastole shortens at a greater extent
what is the position of the mitral and aortic valves during isovolumic contraction
MV - closed
AV - closed
what is the position of the mitral and aortic valves during ejection
MV - closed
AV - open
isovolumic contraction and ejection are part of systole or diastole
systole
what is the position of the mitral and aortic valves during isovolumic relaxation
MV - closed
AV - closed
what is the position of the mitral and aortic valves during rapid inflow to the LV (filling)
MV - open
AV- closed
what is the position of the mitral and aortic valves during diastasis
MV - open
AV - closed
what is the position of the mitral and aortic valves during atrial systole
MV- open
AV - closed
the volume in the ventricles at the end of filling is called
end diastolic volume (EDV)
the volume in the ventricles at the end of ejection
end systolic volume (ESV)
volume ejected by ventricles (EDV-ESV)
stroke volume (SV)
percentage of EDV ejected
ejection fraction
stretch on the wall prior to contraction
preload
the changing resistance that the heart has to pump against as blood is ejected
afterload
wave associated with atrial contraction
A wave
wave associated with ventricular contraction
C wave
wave associated with atrial filling
V wave
what happens when the LV pressure is greater than the aortic pressure
the aortic valve opens
what happens when the aortic pressure is greater than the LV pressure
the aortic valve closes
valves that are
- thin and filmy
- contain chorda tendineae and papillary muscles
AV valves (bicuspid, tricuspid)
valves that are
- strong in construction
- lack chorda tendineae and papillary muscles
semilunar valves (aortic & pulmonary)
acts as check lines to prevent prolapse of a valve
chorda tendineae
increases tension on chorda tendineae
papillary muscle
valve that does not open fully is referred to as
stenotic
valve that does not close fully is referred to as
insufficient/leaky
when a valve creates a vibrational noise
murmur
heart murmurs in systole are caused by
- aortic & pulmonary stenosis
- mitral & tricuspid insufficiency
heart murmurs in diastole are caused by
- aortic & pulmonary insufficiency
- mitral & tricuspid stenosis
heart murmurs in both diastole and systole are caused by
- patent ductus arteriosis
- combined valvular defect
a valve that is both insufficient and stenotic is said to have
combined valvular defect
(P)(r)/2 =
wall tension (law of laplace)
law of laplace states
wall tension = Pr/2
- In two chambers operating at the same pressure but with different chamber radii, the larger the chamber will have to generate more tension; consuming more energy & oxygen
anything that affects heart rate
chronotropic
anything that affects conduction velocity
dromotropic
anything that affects strength of contraction
inotropic
ability to increase strength of contractino independent of a length change
homeometric autoregulation
increased stroke volume maintained as EDV decreases
flow induced homeometric autoregulation
increase in aortic BP will increase force of contraction
pressure induced homeometric autoregulation
increased heart rate will increase force
rate induced homeometric autoregulation
direct stretch on the SA node will affect that heart rate in what way
increase heart rate; increases Ca and Na permeability
sympathetics control the heart in what ways
increase:
- heart rate
- strength of contraction
- conduction velocity
parasympathetics control the heart in what ways
decrease:
- heart rate
- strength of contraction
- conduction velocity
what happens when ANS effects on the heart are blocked
- heart rate increases
- strength of contraction decreases
ACh from the parasympathetics inhibits what
Norepinephrine
NPY and norepinephrine from sympathetics inhibit what
ACh
TRUE or FALSE
thyroid hormones are both positive inotropics and chronotropics
TRUE
effects of elevated K+ lead to
- dilation and flaccidity or cardiac muscle
- decreasing resting membrane potential
effects of elevated Ca++ lead to
spastic contraction
effect of body temperature on heart
- for every degree F the temp. increases, the heartrate increases by 10 BPM
- contractile strength increases temporarily
- decrease in body temp. decreases heartrate and contractile strength
energy substrates for cardiac cells
- fatty acids (70%)
- glucose
- glycerol
- lactate
- pyruvate
- amino acids
the energy produced by the heart is split up between heat production and work, what are the aspects of work
- pressurization of blood (99%)
- acceleration of blood (1%)
greater than 100 BPM
tachycardia
less than 50 BPM
bradycardia
p wave
atrial depolarization
QRS complex
ventricular depolarization
T wave
ventricular repolarization
atrial repolarization is buried in the
QRS complex
when the wave of depolarization is moving toward the + electrode
positive deflection
when the wave of of depolarization is moving toward the - electrode
negative deflection
when the wave of of repolarization is moving toward the + electrode
negative deflection
when the wave of repolarization is moving toward the - electrode
positive deflection
lead I is perpendicular to
AvF
lead II is perpendicular to
AvL
lead III is perpendicular to
AvR
prolonged QT interval has what implications
increased incidence of sudden cardiac death
what the longest and shortest cycle length (RR) vary by more than .16 seconds
sinus arrhythmia
depolarization wave from atria to ventricle is delayed excessively
1st degree AV block
the wave of depolarization is occasionally blocked form entering the ventricle
2nd degree AV block
the atria and ventricles are beating independently, all depolarization waves from the atria to ventricles are blocked
3rd degree AV block
no relationship between P waves and QRS complexes
3rd degree AV block
PR interval is greater than .2 seconds
1st degree AV block
dropped beat p wave with no associated QRS complex
2nd degree AV block
when the QRS and T waves point in opposite directions
inverted T wave, implies ischemia
released only when myocardial necrosis occurs
cardiac troponins T and I
what do the SA node, AV node, and purkinje cells have in common
the all contract weakly and have few fibrils