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Stack #186798

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 metabolic activity 2.dec. O2, inc metabolites in interstitial fluid 3.arteriole dilation 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
Created by: honghee



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