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54 Cards in this Set
- Front
- Back
lattice work of dividing and recombining cardiac myocytes
- some cytoplasm continuous - atrial and ventricular are separated from each other |
syncytiums
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undulating double membranes which connect cardiac myocytes along longitudinal axis
- gap junctions for electrical synapses for AP conduction |
intercalated discs
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similarities and differences between skeletal and cardiac muscle?
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- cardiac have more mitochondria
- sarcomere organization is similar - both striated - cardiac m needs both extracellular and SR Ca for contraction |
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Steps in excitation-contraction coupling
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1. AP from contractile cell
2. plateau phase - Ca2+ rushes into cells (L-type) 3. Ca2+ induced Ca2+ release from SR 4. intracellular Ca2+ level rise - Ca2+ inds to troponinC 5. troponin pushes tropomyosin to expose myosin binding site on actin |
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magnitude of tension produced by cross-bridge cycling is proportional to...
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intracellular Ca2+ level
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relaxation mechanism Ca 2+ is removed in what 2 ways?
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1. Ca2+ pumped into SR by Ca2+ ATPase
2. Ca2+ is moved back into ECF via Ca2+ ATPase AND Ca2+ exchanged for Na+ (secondary) |
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SANS effect on inotropism (contractility)
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- increased peak tension
- increased rate of tension - shortened contraction time - increased Ca entry - E and NE on B1 |
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PANS effect on inotropism (contractililty)
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- ATRIA ONLY
- Ach on M2 - decreased Ca2+ entry |
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positive inotropism factors
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* increased HR - more Ca build up
* cardiac glycosides - inhibit Na/K ATPase, leaves more Ca in cell |
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negative inotropism factors
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* Beta 1 blockers
* Ca2+ channel blockers * heart failure * acidosis * hypoxia * hypercapnia |
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why does the F-S relationship work with optimal myocyte length for producing tension?
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cardiac muscle is relatively stiff
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what is preload?
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ventricular end-diastolic pressure
- amount of blood that has filled the L ventricle at the end of diastole right before contraction |
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what is afterload?
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aortic pressure
-force against which left ventricle must eject blood -left ventricle must exceed aortic pressure to open valve |
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Stroke volume =
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SV = EDV - ESV
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ejection fraction =
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EF = SV/EDV
- fraction of EDV that is ejected by the ventricle - 55-80% |
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CO =
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CO = SV x HR
- volume of blood ejected from ventricle/min |
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L ventricular contraction; mitral and aortic valves are closed
- volume constant - increasing pressure (eventually opens aortic valve) |
isovolumetric contraction
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after building pressure in L ventricle exceeds aortic pressure
-aortic valve opens -pressure rises until most blood leaves ventricle -pressure falls, aortic valve closes |
ventricular ejection
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left ventricle relaxes
-mitral and aortic valves closed - volume constant - pressure drops |
isovolumetric relaxation
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pressure drops below atrial
- mitral valve opens - volume increases - pressure increases slightly - when pressure exceeds atrial, mitral valve closes |
ventricular filling
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what does increased preload do?
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F-S
- increased EDV - increased contractility - increased stroke volume |
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what does increased afterload do?
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- harder for left ventricle to eject blood
- decreases stroke volume - increases ESV |
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what does increased contractility do?
positive ionotropism |
increased SV
decreased ESV |
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CO =
related to oxygen consumption Fick's |
CO = total O2 consumption/ [O2]pv - [O2]pa
Pulmonary vein can be sampled by peripheral artery |
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3 assumptions of using Fick principle
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1. CO of R heart = CO of L heart
2. rate of O2 consumption = amount of O2 leaving lungs - amount of O2 coming back 3. can also be used for measuring blood flow in individual organ systems |
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when does atrial systole occur?
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during the end of ventricular diastole - most of the blood has already flowed into ventricles since AV valve is open before atrial contraction
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EKG are electrical events and will _______ mechanical events
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EKG events precede mechanical events
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1st heart sound
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1. closure of AV valves
- normal - possibly split, mitral closes first |
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2nd heart sound
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2. closure of semilunar valves
- normal - possibly split, aortic closes first |
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3rd heart sound
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rapid flow of blood from atria to ventricles
- normal in children - adults - indicates CHF |
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4th heart sound
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atrial contraction
- occurs with high atrial pressure or ventricular hypertrophy - sound of blood filling against a stiffened ventrical - atrial kick |
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what does the cardiac function curve represent?
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Right atrial pressure determines CO
- directly related - F-S until stretched too much |
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How does the cardiac function curve move?
what causes it? |
ROTATIONS
upward - SANS, LVH, positive ionotropism downward - PANS, increased TPR (CO decreased) , negative ionotropism |
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what does the vascular function curve represent?
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- inverse relationship between venous return and right atrial pressure
- decrease in pressure causes greater pressure gradient driving blood flow, greater VR |
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what is the plateau in the vascular function curve?
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- VR increases to a point as RAP decreases
- levels off low pressure will cause collapse of veins in the chest |
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venoconstriction does what to MSP?
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venoconstriction causes increased MSP
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How does the vascular function curve move?
What causes shift? |
SHIFTS RIGHT - increased blood volume & venoconstriction (decreased compliance)
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what causes the vascular function curve to rotate?
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ROTATES UPWARD - decreased TPR
ROTATES DOWNWARD - increased TPR - MSP is unchanged in rotation! |
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how do inotropic effect CV function curve?
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+ rotate cardiac function curve upward
- rotate cardiac function curve downward |
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Arterial pressure is _____________________ in major arteries
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approximately equal
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equation for arterial pressure
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Pa = CO x TPR
- variables are dependent |
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if Pa moves above or below ____ set point, changes are made in TPR, CO, or both
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100 mm Hg
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where are the baroreceptors located and which nerves do they follow?
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aortic arch - vagus
carotid sinus - glossopharyngeal |
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where do the baroreceptors project to?
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NTS - medulla
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3 cardiovascular motor centers that the NTS directs messages to
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vasoconstrictor - increases SANS, vasoconstriction
cardiac accelerator - increases SANS, HR and contract cardiac decelerator - increases PANS, HR (ATRIA ONLY) |
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during a hemorrhage, decreased arterial pressure causes what?
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decreased arterial pressure, decreased baroreceptor stretch & firing rate, decreased PANS, increased SANS
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what stimulates renin release?
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decreased perfusion of renal arteries
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what does renin do?
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renin converts angiotensinogen to angiotensin 1
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what does angiotensin II do?
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- constrict arterioles
- thirst - ADH release - Na+ reabsorption - aldosterone synthesis and release |
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what does aldosterone do?
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Na+ reabsorption
- raise blood volume - raise BP - takes hours to days |
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what are central chemoreceptors stimulated by?
where? response? |
Medulla
- brain ischemia, increased CO2 - massive vasoconstriction in many vascular beds to increase BF to brain |
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what are the peripheral chemoreceptors stimulated by?
where? response? |
aortic and carotid bodies
- low PaO2 > 70 mm Hg - vasoconstriction in many vascular beds |
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what is ADH?
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from posterior pituitary
- stimulated by increased plasma osmolarity - low blood volume and pressure - causes vasoconstriction and increases water reabsorption |
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what is ANP?
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from atria
- stimulated bu increased atrial pressure - causes vasodilation and increased water excretion |