Stack #186798
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| flow between two points within a tube is proportional to __ | pressure difference between the two points | ||||
| ___ (right heart), ___ (left heart) ensure the valves open towards atria | chordae tendinae, papillary | ||||
| hear murmur | leaky valves in heart resulting in backflow of blood | ||||
| two semilunar valves are | pulmonary valve, aortic valve | ||||
| left AV valve known as | bicuspid, or mitral | ||||
| which myocardium (left or right) is thicker | left | ||||
| is cardiac muscle striated? | yes | ||||
| is cardiac muscle mono-nucleated? | yes | ||||
| what is intercalated disks | gap junction in heart | ||||
| what kind of junctions hold adjacent heart cells together at intercalated disks? | desmosome | ||||
| left and right bundle branches in heart collectively called | bundle of His | ||||
| examples of fast action potential and its characteristic | atrial, ventricular myocardium, purkinje finbers, bundle of His. charac:fast depolarization | ||||
| examples of slow action potential and its characteristic | SA, AV node charac:slow depolarization | ||||
| difference between fast and slow action potential | fast - quick depolaarization | ||||
| 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. | ||||
| channels in SA node | if(funny channel-sodium channel), ik, iCa(T-transient and L-latent channels). | ||||
| in SA node what causes brings potential to threshold? | opening of if and iCa(T). both of which are closed after threshold is reached | ||||
| in SA node what is responsible for the rapid depolarization phase? | opening of iCa(L) | ||||
| in SA node what is responsible for repolarization phase | opening of ik and closing iCa(L) | ||||
| 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. | ||||
| channels involved in ventricular contractions | iNa, ik, iCa | ||||
| what is responsible for fast depolarization in ventricular atria contractions? | iNa | ||||
| what is responsible for the plateau phase | opening of iCa (L type) and closure of iK | ||||
| what is responsible for the repol phase in vent/at contractions | opening of iK and closing of iCa(L) | ||||
| notch in AP curve due to | iK (transient outward current) | ||||
| electrical activity of the heart measured by | ECG - electrocardiogram | ||||
| placement for leads for ECG recording | 1 right wrist, 1 left wrist and 1 left ankle | ||||
| different waves in ECG | P wave-atrial depol QRS wave-ventricular depol T wave-ventricular repol | ||||
| 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. | ||||
| When would you expect to see QRS, T waves occuring independently of P waves? (P waves appearing normally) | full atrioventricular block | ||||
| fast AP propagation would have long/short distance between P and QRS | short | ||||
| myocytes receive nutrients from __ blood vessel | coronary artery | ||||
| in ventricular and atrial muscles (not SA or AV) the depolarization phase followed by | plateau phase | ||||
| 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. | ||||
| 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 | ||||
| some autorhythmic cells called ___ can take over the pacemaker job in case the SA is damaged. | ectopic pacemakers | ||||
| atrial repol not on the ECG b/c | it occurs at the same time as the QRS wave | ||||
| 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. | ||||
| AV block cause and symptom | cause:AP not trasmitted to ventricles symptom:contraction of ventricle not coordinated with atria | ||||
| if impulse dies out in AV node, you have | AV blockage | ||||
| 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 | ||||
| ventricular fibrillation cause and symptom | cause:uncoordinated stimulation and contraction of ventricles symptom:heart doesn't pump effectively | ||||
| arrhythmia cause and symptom | cause:irregular beating of heart(skipping a beat) symptom:inefficient pumping | ||||
| Ca2+ that binds to ryanodine receptor mostly from | iCa2+ (L type) | ||||
| refractory periods in heart, and its importance | only absolute refrac period. prevents tetanus | ||||
| Ca2+ moved into SR by what pump | Ca2+ atpase | ||||
| how is Ca2+ moved to ECM from cytosol | by Na+/Ca2+ exchanger. Na+ goes in (E released), Ca2+ goes out | ||||
| Ca2+ bind to what molecule to expose myosin head binding site on actin | troponin c | ||||
| what molecule blocks the binding site on actin | tropomyosin | ||||
| phospholamban | prevents Ca2+ from being released from SR and allows uptake of Ca2+ by SR | ||||
| __ prevents Ca2+ from being released from SR and allows uptake of Ca2+ by SR | phospholamban | ||||
| phospholamban | prevents Ca2+ from being released from SR and allows uptake of Ca2+ by SR | ||||
| contraction of atria, is this systole or diastole | systole | ||||
| contraction of ventricle, is this systeole or diastole | systole | ||||
| sound "lub" from | closing of AV valves | ||||
| sound "dub" from | closing of semilunar | ||||
| which parasympathetic nerve slows down HR. what neurotransmitter does it release and what it binds to? | vagus nerve, ACh, Muscarinic receptor on atria | ||||
| __ neurotransmitter is released onto __ receptor on the heart by sympathetic nerves | NE, alpha-adrenergic | ||||
| HR is | number of beats per minute | ||||
| HR>100 beats called | tachycardia | ||||
| HR<60 beats called | bradycardia | ||||
| how does sympathetic speed up HR | 1.increase rate of slow depolarization phase 2.increase funny sodium channel current (quick depol) | ||||
| how does parasympthetic speed up HR | 1.decrease rate of slow depolarization phase 2.decrease funny sodium channel current (slow depol) 3.hyperpolarization | ||||
| sympathetic or parasympathetic has a steeper depolarization curve | sympathetic | ||||
| tachycardia | HR>100 | ||||
| bradycardia | HR<60 | ||||
| which sympathetic hormone speeds up HR | E | ||||
| stroke volume | volume at end of diastole - vol end of systole | ||||
| how to lower the end systole volume to 0? | it is impossible, but it can be lowered | ||||
| ways to increase stroke volume | 1. increase end diastolic volume via sympathetic 2. increase contractility via sympathetic | ||||
| how does increasing end diastolic volume increase stroke volume? | stretch of ventricles aligns their actin and myosin optimally so they contract effectively. | ||||
| increase contractility will increase or decrease end systolic volume | decrease | ||||
| contractility(strength of contraction) quantified by | SV/EDV | ||||
| 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 | ||||
| Ca2+ flows into cytosol via ___ channel, and it binds to ___ on SR. | DHP(L type Ca2+), ryanodine | ||||
| during sympathetic stimulation, more Ca2+ flows into cytosol. this is done by | GPCR receptor (NE, E agonists), cAMP, PKA activating DHP receptor | ||||
| what increases contractility | 1sympathetic stimulation (NE, E) 2decrease afterload | ||||
| effect of increasing end diastolic volume on HR | no effect | ||||
| effect of parasympathetic on HR | slows down | ||||
| effect of parasympathetic on stroke volume | no effect | ||||
| cardiac output is | stroke volume * HR | ||||
| what backup does a heart use in an anaerobic condition? | no backup. it doesn't have capacity for anaerobic metabolism | ||||
| in atheletes you see low/high stroke volume and low/high heart rate | high, low | ||||
| arterial pressure | pressure heart has to pump against | ||||
| arterial pressure also known as | afterload | ||||
| effect of high afterload on contractility | high afterload => sarcomeres cannot fully contract => reduced SV | ||||
| aschemia | reduced O2 in myocytes | ||||
| reduced O2 in myocytes called | aschemia | ||||
| Frank Starling mechanism says | higher end diastolic volume => stronger contraction (NOT INCREAESD CONTRACTILITY) | ||||
| effect of sympathetic on contractility and end diastolic volume | increase contractility, increase diastolic volume by contracting veins. (alpha adrenergic receptor) | ||||
| effect of increasing end diastolic volume on contractility | no effect | ||||
| how is contractility affected by end diastolic volume | NOT AFFECTED!!, because contractility is a force of contraction at ANY GIVEN EDV. | ||||
| how does parasympathetic effect/doesn't effect stroke volume | doestn't effect, because no innervation to ventricles | ||||
| in capillary __ membranes present. | only endothelial to allow exch of O2, glucose | ||||
| major reservoir of blood is | elastic veins | ||||
| how does blood continue to flow during diastole? | arteries expand during systole, and squeezes blood to return to normal form during diastole | ||||
| mean arterial pressure (MAP) calc by | diastolic pressure + 1/3(systolic pressure-diastolic pressure) | ||||
| effect of elasticity on mean arterial pressure | decreaseing elasticity increases MAP | ||||
| calculation of systemic blood flow | pressure diff between aorta, vena cava / resistance and pressure of vena cava is negligible | ||||
| which artery used to measure BP | brachial artery | ||||
| 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) | ||||
| what is the most important regulator for controlling the flow of blood | changing diameter | ||||
| vasoconstriction/dilation mostly occurs in | arteriole | ||||
| hormonal vasoconstrictors | 1.E 2.angiotensin II 3.vasopressin | ||||
| hormonal vasodialator | 1.E 2.atrial natriuretic peptide | ||||
| effect of parasympathetic on blood vessel | no effect | ||||
| effect of sympathetic on blood vessel | constriction/dilation depending on what receptors used. | ||||
| vasopressin is | hormonal vasoconstrictor | ||||
| atrial natriuretic peptide is | hormonal vasodilator produced by heart | ||||
| neural vasodilator | neurons that release NO | ||||
| local vasoconstrictors | internal blood pressure (myogenic response) - important for afferent arteriole of kidney, respond to stretching of tissue by causing constraction | ||||
| active hyperemia | 1.inc metabolic activity 2.dec. O2, inc metabolites in interstitial fluid 3.arteriole dilation 4.inc. blood flow to organ | ||||
| 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 | ||||
| active hypermia causes | arteriolar dilation | ||||
| flow autoregulation causes | arteriolar dilation | ||||
| increase in metabolic activity of organ results in | active hyperemia | ||||
| decreased in arterial pressure in organ results in | flow autoregulation | ||||
| NE (neurotransmitter or hormone) binds to __ | neurotrans, alpha adrenergic | ||||
| E (neurotrans or hormone) binds to __ | hormone, alpha and beta adrenergic | ||||
| NO produced from endothelium also called | endothelium derived relaxing factor | ||||
| endothelium dervied relaxing factor (EDRF) is | NO | ||||
| blood flow to heart mainly regulated by | local metabolic factors | ||||
| blood flow to skeletal muscle mainly regulated by | local metabolic factor | ||||
| sympathetic nerve to GI tract causes vasodilation or vasoconstriction | vasoconstriction | ||||
| blood flow to kidney mainly regulated by | flow autoregulation | ||||
| blood flow to brain mainly regulated by | flow autoregulation | ||||
| blood flow to skin mainly regulated by | sympathetic nerve | ||||
| ___ controls amount of blood entering capillary | precapillary sphincters | ||||
| arteraial venus shunt known as, function | metaarteriole, shunt blood directly to venuole from arteriole | ||||
| local control of blood by | CO2, H+, Adenosine, K+, Eicosanoid, Bradykinin, NO, osmolarity | ||||
| distinguishing feature about capillaries near skin surface | have more meta-arterioles | ||||
| blood travels the slowest through __ | capillary | ||||
| highest resistance in __ | arteriole | ||||
| 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 | ||||
| movement of stuff out of blood called | filteration | ||||
| movement of stuff into blood called | absorption | ||||
| filteration is | movement of stuff out of blood | ||||
| absorption is | movement of stuff into blood | ||||
| hydrostatic pressure is | force pushing fluid out of the compartment | ||||
| force pushing fluid out of the compartment is | hydrostatic pressure | ||||
| opposing force of hydrostatic pressure is | oncotic pressure (pi) | ||||
| osmotic pressure due to only protein is | oncotic pressure | ||||
| oncotic pressure (pi) is | osmotic pressure due to only protein (pressure drawing fluid into the compartment) | ||||
| oncotic pressure caused by | big molecules (proteins) that cannot cross the membrane | ||||
| net filtration pressure is | net hydrostatic pressure - net oncotic pressure | ||||
| as blood move further from the heart hydrostatic pressure __ | decreases | ||||
| as blood move further form the heart oncotic pressure __ | remains constant | ||||
| a positive net filteration pressure indicates | favors filteration. ie. stuff flows out of blood | ||||
| if stuff flows into blood (ie. absorption) then a net filteration pressure is | negative | ||||
| at arterial end of capillary the net filtration pressure is | positive | ||||
| at venuole end of capillary the net filtration is | negative | ||||
| the hydrostatic pressure P, of venuole end of capillary in comparison to arterial end of capillary is | smaller | ||||
| the oncotic pressure Pi, of venuole end of capillary in comparison to arterial end of capillary is | same | ||||
| effect of vasodilation on hydrostatic pressure | increases P | ||||
| effect of vasoconstriction on hydrostatic presure | decrease P | ||||
| 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 | ||||
| effect of vasoconstriction @ capillaries on BP in artery and capillary | inc .art, dec. capillary | ||||
| 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 | ||||
| two things that help blood return back to the heart | 1.valves in vein 2.muscle squeeze | ||||
| end diastolic volume is increased by | sympathetic stimulus (binds to alpha-ad receptor) causing veins to contract | ||||
| how many layers of cells are in lymphatic system | 1, only endothelial | ||||
| where is lymphatic fluid taken to | veins |
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Created by:
honghee
on 2008-12-12