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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

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