Stack #186798
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| flow between two points within a tube is proportional to __ | pressure difference between the two points
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| ___ (right heart), ___ (left heart) ensure the valves open towards atria | chordae tendinae, papillary
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| hear murmur | leaky valves in heart resulting in backflow of blood
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| two semilunar valves are | pulmonary valve, aortic valve
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| left AV valve known as | bicuspid, or mitral
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| which myocardium (left or right) is thicker | left
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| is cardiac muscle striated? | yes
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| is cardiac muscle mono-nucleated? | yes
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| what is intercalated disks | gap junction in heart
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| what kind of junctions hold adjacent heart cells together at intercalated disks? | desmosome
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| left and right bundle branches in heart collectively called | bundle of His
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| examples of fast action potential and its characteristic | atrial, ventricular myocardium, purkinje finbers, bundle of His.
charac:fast depolarization
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| examples of slow action potential and its characteristic | SA, AV node
charac:slow depolarization
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| difference between fast and slow action potential | fast - quick depolaarization
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| what kind of action potential (fast or slow) has a plateau phase. and what is the plateau phase | plateau phase:slow repolarization
fast action potential.
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| channels in SA node | if(funny channel-sodium channel), ik, iCa(T-transient and L-latent channels).
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| in SA node what causes brings potential to threshold? | opening of if and iCa(T). both of which are closed after threshold is reached
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| in SA node what is responsible for the rapid depolarization phase? | opening of iCa(L)
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| in SA node what is responsible for repolarization phase | opening of ik and closing iCa(L)
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| why is there a delay in conduction between atria and ventricles. (ie. why does ventricle contract after atria) | to ensure that ventriclular filling is complete before ventricles contract.
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| channels involved in ventricular contractions | iNa, ik, iCa
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| what is responsible for fast depolarization in ventricular atria contractions? | iNa
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| what is responsible for the plateau phase | opening of iCa (L type) and closure of iK
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| what is responsible for the repol phase in vent/at contractions | opening of iK and closing of iCa(L)
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| notch in AP curve due to | iK (transient outward current)
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| electrical activity of the heart measured by | ECG - electrocardiogram
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| placement for leads for ECG recording | 1 right wrist, 1 left wrist and 1 left ankle
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| different waves in ECG | P wave-atrial depol
QRS wave-ventricular depol
T wave-ventricular repol
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| With patients with partial atrioventricular block, you would expect their ECG to be: | normal P waves. QRS, T waves do not always appear after P wave.
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| When would you expect to see QRS, T waves occuring independently of P waves? (P waves appearing normally) | full atrioventricular block
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| fast AP propagation would have long/short distance between P and QRS | short
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| myocytes receive nutrients from __ blood vessel | coronary artery
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| in ventricular and atrial muscles (not SA or AV) the depolarization phase followed by | plateau phase
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| why is if channels called a funny channel? what is so special about it | unlike other sodium channels which open up when the membrane potential is above threshold (positive) this channel is open when the potential is NEGATIVE.
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| AV node able to generate pacemaker potentials but it is driven to threshold by the action of SA node why??? | the inherent rate of AV node is slower than that of SA node. thus it is driven by SA node
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| some autorhythmic cells called ___ can take over the pacemaker job in case the SA is damaged. | ectopic pacemakers
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| atrial repol not on the ECG b/c | it occurs at the same time as the QRS wave
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| if you have a complete atrioventricular block, then would your ventricles be able to beat? | yes but not syncronous to atrial contraction, bc cells in the bundle of His would take over the pacemaker.
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| AV block cause and symptom | cause:AP not trasmitted to ventricles
symptom:contraction of ventricle not coordinated with atria
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| if impulse dies out in AV node, you have | AV blockage
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| reentry cause and symptom | cause:part of myocardium damaged, conduction finds a different route.
symptom:uncoordinated contraction of myocardium. a single myocardium may contract more than once during a single beating of a heart
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| ventricular fibrillation cause and symptom | cause:uncoordinated stimulation and contraction of ventricles
symptom:heart doesn't pump effectively
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| arrhythmia cause and symptom | cause:irregular beating of heart(skipping a beat)
symptom:inefficient pumping
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| Ca2+ that binds to ryanodine receptor mostly from | iCa2+ (L type)
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| refractory periods in heart, and its importance | only absolute refrac period. prevents tetanus
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| Ca2+ moved into SR by what pump | Ca2+ atpase
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| how is Ca2+ moved to ECM from cytosol | by Na+/Ca2+ exchanger. Na+ goes in (E released), Ca2+ goes out
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| Ca2+ bind to what molecule to expose myosin head binding site on actin | troponin c
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| what molecule blocks the binding site on actin | tropomyosin
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| phospholamban | prevents Ca2+ from being released from SR and allows uptake of Ca2+ by SR
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| __ prevents Ca2+ from being released from SR and allows uptake of Ca2+ by SR | phospholamban
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| phospholamban | prevents Ca2+ from being released from SR and allows uptake of Ca2+ by SR
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| contraction of atria, is this systole or diastole | systole
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| contraction of ventricle, is this systeole or diastole | systole
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| sound "lub" from | closing of AV valves
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| sound "dub" from | closing of semilunar
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| which parasympathetic nerve slows down HR. what neurotransmitter does it release and what it binds to? | vagus nerve, ACh, Muscarinic receptor on atria
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| __ neurotransmitter is released onto __ receptor on the heart by sympathetic nerves | NE, alpha-adrenergic
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| HR is | number of beats per minute
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| HR>100 beats called | tachycardia
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| HR<60 beats called | bradycardia
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| how does sympathetic speed up HR | 1.increase rate of slow depolarization phase
2.increase funny sodium channel current (quick depol)
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| how does parasympthetic speed up HR | 1.decrease rate of slow depolarization phase
2.decrease funny sodium channel current (slow depol)
3.hyperpolarization
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| sympathetic or parasympathetic has a steeper depolarization curve | sympathetic
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| tachycardia | HR>100
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| bradycardia | HR<60
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| which sympathetic hormone speeds up HR | E
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| stroke volume | volume at end of diastole - vol end of systole
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| how to lower the end systole volume to 0? | it is impossible, but it can be lowered
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| ways to increase stroke volume | 1. increase end diastolic volume via sympathetic
2. increase contractility via sympathetic
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| how does increasing end diastolic volume increase stroke volume? | stretch of ventricles aligns their actin and myosin optimally so they contract effectively.
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| increase contractility will increase or decrease end systolic volume | decrease
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| contractility(strength of contraction) quantified by | SV/EDV
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| sympathetic only causes rapid contraction/relaxation of heart. it doesn't effect force of contraction. T or F? | F. It also results in stronger contraction
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| Ca2+ flows into cytosol via ___ channel, and it binds to ___ on SR. | DHP(L type Ca2+), ryanodine
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| during sympathetic stimulation, more Ca2+ flows into cytosol. this is done by | GPCR receptor (NE, E agonists), cAMP, PKA activating DHP receptor
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| what increases contractility | 1sympathetic stimulation (NE, E)
2decrease afterload
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| effect of increasing end diastolic volume on HR | no effect
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| effect of parasympathetic on HR | slows down
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| effect of parasympathetic on stroke volume | no effect
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| cardiac output is | stroke volume * HR
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| what backup does a heart use in an anaerobic condition? | no backup. it doesn't have capacity for anaerobic metabolism
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| in atheletes you see low/high stroke volume and low/high heart rate | high, low
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| arterial pressure | pressure heart has to pump against
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| arterial pressure also known as | afterload
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| effect of high afterload on contractility | high afterload => sarcomeres cannot fully contract => reduced SV
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| aschemia | reduced O2 in myocytes
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| reduced O2 in myocytes called | aschemia
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| Frank Starling mechanism says | higher end diastolic volume => stronger contraction (NOT INCREAESD CONTRACTILITY)
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| effect of sympathetic on contractility and end diastolic volume | increase contractility, increase diastolic volume by contracting veins. (alpha adrenergic receptor)
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| effect of increasing end diastolic volume on contractility | no effect
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| how is contractility affected by end diastolic volume | NOT AFFECTED!!, because contractility is a force of contraction at ANY GIVEN EDV.
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| how does parasympathetic effect/doesn't effect stroke volume | doestn't effect, because no innervation to ventricles
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| in capillary __ membranes present. | only endothelial to allow exch of O2, glucose
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| major reservoir of blood is | elastic veins
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| how does blood continue to flow during diastole? | arteries expand during systole, and squeezes blood to return to normal form during diastole
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| mean arterial pressure (MAP) calc by | diastolic pressure + 1/3(systolic pressure-diastolic pressure)
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| effect of elasticity on mean arterial pressure | decreaseing elasticity increases MAP
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| calculation of systemic blood flow | pressure diff between aorta, vena cava / resistance
and pressure of vena cava is negligible
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| which artery used to measure BP | brachial artery
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| resistance of a tube depends on | 1.length of the tube (inc leng. increase R).
2.viscosity of liquid eta (increase R).
3.radius of the tube (inc rad, dec res)
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| what is the most important regulator for controlling the flow of blood | changing diameter
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| vasoconstriction/dilation mostly occurs in | arteriole
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| hormonal vasoconstrictors | 1.E
2.angiotensin II
3.vasopressin
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| hormonal vasodialator | 1.E
2.atrial natriuretic peptide
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| effect of parasympathetic on blood vessel | no effect
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| effect of sympathetic on blood vessel | constriction/dilation depending on what receptors used.
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| vasopressin is | hormonal vasoconstrictor
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| atrial natriuretic peptide is | hormonal vasodilator produced by heart
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| neural vasodilator | neurons that release NO
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| local vasoconstrictors | internal blood pressure (myogenic response) - important for afferent arteriole of kidney, respond to stretching of tissue by causing constraction
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| active hyperemia | 1.inc metabolic activity
2.dec. O2, inc metabolites in interstitial fluid
3.arteriole dilation
4.inc. blood flow to organ
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| flow autoregulation | 1.dec arterial pressure in organ
2.dec blood flow to organ
3.dec O2, inc metabolites, dec vessel wall stretching in organ
4.arteriole dilation
5.increased blood flow
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| active hypermia causes | arteriolar dilation
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| flow autoregulation causes | arteriolar dilation
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| increase in metabolic activity of organ results in | active hyperemia
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| decreased in arterial pressure in organ results in | flow autoregulation
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| NE (neurotransmitter or hormone) binds to __ | neurotrans, alpha adrenergic
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| E (neurotrans or hormone) binds to __ | hormone, alpha and beta adrenergic
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| NO produced from endothelium also called | endothelium derived relaxing factor
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| endothelium dervied relaxing factor (EDRF) is | NO
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| blood flow to heart mainly regulated by | local metabolic factors
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| blood flow to skeletal muscle mainly regulated by | local metabolic factor
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| sympathetic nerve to GI tract causes vasodilation or vasoconstriction | vasoconstriction
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| blood flow to kidney mainly regulated by | flow autoregulation
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| blood flow to brain mainly regulated by | flow autoregulation
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| blood flow to skin mainly regulated by | sympathetic nerve
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| ___ controls amount of blood entering capillary | precapillary sphincters
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| arteraial venus shunt known as, function | metaarteriole, shunt blood directly to venuole from arteriole
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| local control of blood by | CO2, H+, Adenosine, K+, Eicosanoid, Bradykinin, NO, osmolarity
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| distinguishing feature about capillaries near skin surface | have more meta-arterioles
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| blood travels the slowest through __ | capillary
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| highest resistance in __ | arteriole
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| basic mechanisms to move molec out of capillary | 1.diffusion-lipid soluble through PM, fenestrate
2.bulk flow-diffusion of fluids, and gasses
3.vesicle transport
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| movement of stuff out of blood called | filteration
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| movement of stuff into blood called | absorption
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| filteration is | movement of stuff out of blood
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| absorption is | movement of stuff into blood
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| hydrostatic pressure is | force pushing fluid out of the compartment
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| force pushing fluid out of the compartment is | hydrostatic pressure
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| opposing force of hydrostatic pressure is | oncotic pressure (pi)
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| osmotic pressure due to only protein is | oncotic pressure
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| oncotic pressure (pi) is | osmotic pressure due to only protein (pressure drawing fluid into the compartment)
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| oncotic pressure caused by | big molecules (proteins) that cannot cross the membrane
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| net filtration pressure is | net hydrostatic pressure - net oncotic pressure
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| as blood move further from the heart hydrostatic pressure __ | decreases
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| as blood move further form the heart oncotic pressure __ | remains constant
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| a positive net filteration pressure indicates | favors filteration. ie. stuff flows out of blood
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| if stuff flows into blood (ie. absorption) then a net filteration pressure is | negative
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| at arterial end of capillary the net filtration pressure is | positive
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| at venuole end of capillary the net filtration is | negative
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| the hydrostatic pressure P, of venuole end of capillary in comparison to arterial end of capillary is | smaller
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| the oncotic pressure Pi, of venuole end of capillary in comparison to arterial end of capillary is | same
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| effect of vasodilation on hydrostatic pressure | increases P
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| effect of vasoconstriction on hydrostatic presure | decrease P
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| how does vasodilation increase hydrostatic presure | vasodilation occurs in arterioles hence the blood flow to capillaries is increased in case of vasodilation. and increased blood flow = increased hydrostatic pressure
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| effect of vasoconstriction @ capillaries on BP in artery and capillary | inc .art, dec. capillary
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| in regulating the end diastolic volume, sympathetic stimulus binds to alpha1-adrenergic receptor. how does affect the EDV?? | allows vasoconstriction of veins so more blood can be returned to the heart
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| two things that help blood return back to the heart | 1.valves in vein
2.muscle squeeze
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| end diastolic volume is increased by | sympathetic stimulus (binds to alpha-ad receptor) causing veins to contract
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| how many layers of cells are in lymphatic system | 1, only endothelial
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| where is lymphatic fluid taken to | veins
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Created by:
honghee
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