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153 Cards in this Set
- Front
- Back
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cardiac output of left heart (1) cardiac output of right heart
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1 = equals
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arteries deliver (1) blood to (2)
arteries are (3) walled with (4) and (5). they are under (6) pressure |
1 = oxygenated
2 = tissues 3 = thick walled 4 = elastic tissue 5 = smooth muscle 6 = high pressure |
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blood volume contained in arteries is called (1)
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1 = stressed volume
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place of highest resistance in CV system?
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arterioles
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alpha1 adrenergic R. are found on arterioles of ? (3)
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skin
splanchnic renal |
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b2 adrenergic R. are found on arterioles of? (1)
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skeletal muscle
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capillaries have the highest (1) and consist of (2) and (3).
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1 = cross sectional area/SA
2 = single layer of endothelial cells 3 = basal lamina |
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veins are (1) walled with (2) pressure.
veins contains highest (3) and this blood volume is known as (4) |
1 = thin walled
2 = low pressure 3 = blood volume 4 = unstressed volume |
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formula for velocity of blood flow
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V = Q / A
Q = blood flow A = cross section area V = velocity |
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formula for blood flow
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Q = P / R
P = pressure gradient R = resistance |
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formula for cardiac output
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CO = MAP - RAP / TPR
MAP = mean arterial pressure RAP = right atrial pressure TPR = total peripheral resistance |
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Poiseuille's equation for resistance
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R = 8 n l / (pi) r^4
n = viscosity l = length r = radius |
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parallel resistance is in (1) circulation and thus, the total resistance is (2) than individual resistance's
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1 = systemic
2 = less |
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parallel resistance:
pressure (1) resistance (2) blood flow (3) |
1 = stays the same
2 = decreases 3 = increases |
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series resistance is in (2) circulation, and thus, the total resistance is the (2) of individual resistance's.
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1 = organ circulation
2 = sum of individual R |
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series resistance:
pressure (1) resistance (2) blood flow (3) |
1 = decreases
2 = increases 3 = stays the same |
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Reynold's number
- predicts? (1) - increased Reynolds number = ? (2) |
1 = whether blood flow is laminar or turbulent
2 = greater tendency for turbulence |
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Formula for Reynold's number
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Re = v p d / n
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Reynold's number is increased by:
(1) blood viscosity (2) blood velocity |
1 = decreased
2 = incresed |
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where is velocity of blood flow the highest?
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at the centre of the vessel
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where is shear the highest? (1)
where is shear the lowest? (2) |
1 = at the wall where difference in blood velocity is the greatest
2 = centre |
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capacitance aka (1)
- describes? (2) |
1 = compliance
2 = distensibility of blood vessels |
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formula for capacitance
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C = V / P
how volume changes in response to change in pressure |
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Veins have a (1) capacitance than arteries
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1 = higher
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capacitance of arteries (1) with age
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1 = decreases
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systolic pressure is the (1) arterial pressure during cardiac cycle; measured when heart (2)
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1 = highest
2 = contracts |
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diastolic pressure is the (1) arterial pressure during cardiac cycle; measured when heart (2)
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1 - lowest
2 - relaxes |
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pulse pressure
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difference between systolic and diastolic pressures
PP = SV / compliance |
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what is the most important determinant of pulse pressure?
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stroke volume
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formula for Mean Arterial Pressure
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diastolic pressure + 1/3 of PP
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P wave
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atrial depolarization
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PR interval
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initial depolarization of ventricle
signals rate of impulse conduction in AV node |
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PR interval is increased by stimulation with (1) and decreased by stimulation with (2)
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1 = PNS
2 = SNS |
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QRS complex
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depolarization of ventricles
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QT interval
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entire period of depolarization and repolarization of ventricles
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ST segment
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isoelectric
period when ventricles are depolarized |
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T wave
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ventricular repolarization
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RMP of cardiac cells is determined by (1) conductance
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K+
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ventricles, atria and Purkinje RMP = (1)
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RMP = - 90 mV
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Phase 0 ventricles
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transient increase in Na+ conductance (upstroke)
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Phase 1 ventricular AP
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initial repolarization
- outward K+ current - decrease in Na+ conductance |
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Phase 2 ventricular AP
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plateau
transient increase in Ca2+ conductance (equal to K+ leaving) |
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Phase 3 ventricular AP
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outward K+ current
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Phase 4 ventricular AP
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RMP
- inward and outward currents are equal |
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cardiac pacemaker is located in (1)
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sinoatrial node
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does the SA node have a RMP?
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NO!
unstable resting potential |
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Phase 0 SA node AP
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upstroke of AP
increase in Ca2+ conductance |
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Phase 3 SA node AP
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repolarization
increased K+ conductance |
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Phase 4 SA node AP
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slow depolarization
inward Na+ current (gradual) - I f |
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upstroke of the AP in AV is a result of (1) ?
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1 = inward Ca2+ current
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where is cardiac conduction velocity the highest?
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Purkinje system
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where is cardiac conduction velocity the slowest?
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AV node --> allows time for ventricular filling
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the (1) the inward current, the (2) the conduction velocity
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1 = larger
2 = faster |
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negative chronotropic effect
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decreases HR by decreasing firing rate at SA node
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positive chronotropic effect
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increases HR by increasing firing rate at SA node
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negative dromotropic effect
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decreases conduction velocity through AV node --> increases PR interval
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positive dromotropic effect
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increases conduction velocity through AV node --> decreases PR interval
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PNS vagal innervation is found in these 3 areas (1) but not in (2)
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1 = SA node, atria, AV node
2 = ventricles |
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PNS vagal stimulation in heart uses (1) nt. and acts on (2) receptors
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1 = Ach
2 = muscarinic |
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PNS stimulation produces a (1) chronotropic effects and a (2) dromotropic effect
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1 = negative
2 = negative |
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How does PNS decrease HR?
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decreases rate of Phase 4 depol. due to decreased inward Na+ current
decreases slope of prepotential |
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How does PNS decrease conduction velocity?
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decreased inward Ca2+ current and increased outward K+ current at AV node
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SNS effects on heart use (1) nt. and act on (2) receptors
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1 = NE
2 = B1 adrenergic R. |
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SNS produces a (1) chronotropic effect and a (2) dromotropic effect
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1 = positive
2 = positive |
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How does SNS decrease HR? (chronotropic effect)
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increases the rate of Phase 4 depol. due to increased inward Na+ current
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How does SNS decrease conduction velocity? (dromotropic effect)
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increased inward Ca2+ current in AV node (upstroke)
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intercalated discs occur at (1) and maintain (2)
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1 = ends of cells
2 = cell to cell adhesion |
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gap junctions are present at (1) and provide a (2) between cells forming a (3)
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1 = intercalated discs
2 = low resistance path 3 = electrical syncitium |
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(1) are more numerous in cardiac muscle than in skeletal muscle
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mitochondria
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T tubules are (1) and they carry (2) to (3).
T tubules are well developed in (4) |
1 = continuous with cell membrane
2 = AP 3 = cell interior 4 = ventricles |
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Sarcoplasmic reticulum is the site of (1) and (2)
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1 = storage of Ca2+
2 = release of Ca2+ into cytoplasm |
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Steps in Excitation-Contraction coupling:
(1) (2) (3) (4) (5) (6) |
1 - AP spread from cell mb to T tubule
2 - inward Ca2+ current from ECF via L-type Ca2+ channels (DHP receptors) 3 - Ca2+ induced Ca2+ release from SR (ryanodine R.) 4 - intracellular Ca2+ increases 5 - Ca2+ binds troponin C, tropomyosin moves 6 - actin/myosin bind, sliding filament theory 7 - Ca2+ ATPase pump, relaxation |
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magnitude of tension in cardiac muscle is proportional to (1)
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intracellular Ca2+ conc.
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inotropism
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intrinsic ability of cardiac muscle to develop force at a given muscle length --> contractility
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inotropism is related to (1) and can be estimated by (2)
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1 = intracellular Ca2+ conc.
2 = ejection fraction |
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ejection fraction
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stroke volume / end-diastolic volume (normally 55%)
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positive inotropic agents
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increase in contractility
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negative inotropic agents
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decrease in contractility
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how does increased HR cause increased contractility?
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increased HR = increased AP = more Ca2+ entering from ECF = more Ca2+ released from SR = greater tension during contraction
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how does SNS cause increased contractility? (2 mechanisms)
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1 = increases inward Ca2+ current during plateau
2 = increases activity of Ca2+ pump of SR, more Ca2+ accumulates in SR and thus more Ca2+ available for subsequent beats |
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phospholamban
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mediates upregulation of Ca2+ ATPase pump on SR by phosphorylation
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how do cardiac glycosides increase contractility of heart?
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- inhibit Na+/K+ ATPase
- intracellular Na+ accumulates and there is no longer Na+ gradient - Na+ Ca2+ exchanger relies on Na+ gradient, therefore, more Ca2+ remains in cell |
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example of cardiac glycosides
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digitalis
ouibain |
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how does PNS stimulation decrease contractility of heart?
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decreases the force of contraction in atria by decreasing inward Ca2+ current during plateau of AP
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preload
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end diastolic volume
- related to right atrial pressure |
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when venous return (1), EDV (2) and (3) the ventricular muscle fibers
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1 = increases
2 = increases 3 = lengthens/stretches |
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afterload for LV is (1) and for RV is (2); increase in pressure in any of these areas, causes an (3) in afterload
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1 = aortic pressure
2 = pulmonary artery pressure 3 = increase |
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sarcomere length determines the maximum (1) and maximum (2)
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1 = cross-bridges between actin/myosin
2 = force of contraction/tension |
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velocity of contraction at a fixed muscle length is MAX when afterload is (1) and is (2) by increases in afterload
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1 = zero
2 = decreased |
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Frank Starling Relationship
increases in (1) cause an increase in (2) which produces an increase in (3) |
1 = end diastolic volume
2= ventricular fibre length 3 = tension |
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Frank Starling
the greater the venous return, the greater the (1) |
1 = cardiac output
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changes in contractility shift the Frank-Starling curve (1) for increased contractility, and (2) for decreased contractility
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1 = upward
2 = downward |
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Frank Starling
- increases in contractility cause an (1) in CO for any level of (2) - decreases in contractility cause an (3) in CO for any level of (4) |
1 = increase
2= EDV 3 = decrease 4 = EDV |
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increased preload = increased (1) = increased (2) = increase in (3) as marked by (4) on pressure-volume loop
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1 = EDV
2 = venous return 3 = stroke volume 4 = increased width |
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increased afterload = increased (1) = decreased (2) reflected as decreased in (3) on pressure volume loop
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1 = aortic pressure
2 = decrease stroke volume 3 = width |
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decrease in stroke volume = (1) in ESV
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increase
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increased contractility = increased (1) = (2) stroke volume = decreased (3)
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1 = greater tension
2 = increased SV 3 = ESV |
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mean system pressure = (1) axis intercept on vascular function curve
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x axis
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mean systolic pressure (1) right atrial pressure when there is (2) in CV system
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1 = equals
2 = no flow |
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when TPR is decreased for a given RAP, there is an (1) in venous return
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increased venous return
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when TPR is increased for a given RAP, there is a (2) in venous return
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decreased venous return
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increases in blood volume/ decreases in compliance = (1) mean systemic pressure = (2) CO and (3) RA pressure
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1 = increased
2 = increased CO 3 = increased RA |
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stroke volume
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volume ejected from ventricle on each beat
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formula for stroke volume
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EDV - ESV
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formula for cardiac output (2)
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CO = HR x SV
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ejection fraction
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fraction of EDV ejected in each stroke volume --> related to contractility, normally 55%
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formula for ejection fraction
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EF = SV / EDV
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stroke work
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aortic pressure x strove volume
--> the work the heart performs on each beat |
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cardiac O2 consumption is increased by: (4)
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increased afterload
increased size of heart increased contractility increased heart rate |
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Fick Principle for Measuring CO
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CO = O2 consumption / (O2 pul. vein - O2 pul. artery)
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What is responsible for first heart sound?
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closure of AV valves
- during isovolumetric contraction |
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What is responsible for the 4th heart sound?
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- filling of ventricle by atrial systole
- not heard in adults |
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What is responsible for the 2nd heart sound?
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closure of aortic valve
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What is responsible for the 3rd heart sound? Is this sound normal?
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rapid flow of blood from atria to ventricles
- normal in children - disease in adults |
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diastasis
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- blood continues to enter ventricles but at a slower rate
- longest phase of cardiac cycle |
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baroreceptor reflex
- (1) term regulation of BP - depends on fast (2) |
1 = short term / minute to minute
2 = neural mechanisms |
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baroreceptors
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bifurcation of common carotid arteries --> walls of carotid sinus
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baroreceptors in the aortic arch respond to (1) but not (2) in arterial pressure
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1 = increases
2 = decreases |
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Baroreceptor Reflex
- decreased (2) decreases the firing rate of (3) nerve results in decreased (4) outflow to heart and increased (5) outflow to heart and blood vessels |
2 = stretch/ low BP
3 = carotid sinus nerve aka. Hering's nerve (CN IX) 4 = PNS 5 = SNS |
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Baroreceptor reflex
- increased heart rate is due to decreased (1) and increased (2) stimulation to the (3) of heart |
1 = PNS
2 = SNS 3 = SA node |
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baroreceptor reflex
- increased contractility and SV is a result of increased (1) tone to heart; this leads to an increase in (2) |
1 = SNS tone
2 = increased CO |
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baroreceptor reflex
- SNS stimulation causes an (1) in vasoconstriction of (2) and (3) |
1 = increase
2 = arterioles (increases TPR) 3 = veins (decreases unstressed volume, increases venous return) |
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increase in intrathoracic pressure (1) venous return
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decreases
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Renin-Angiotensin-Aldosterone System
- a (1) hormonal mechanism - is a (2) term regulation |
1 - slow hormonal
2 = long term reg. of change in blood volume |
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RAS reflex
- decreased arterial pressure causes a (1) in renal perfusion pressure, which causes release of (2) |
1 = decrease
2 = renin |
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Renin catalyzes conversion of (1) to (2)
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1 = angiotensinogen
2 = angiotensin I |
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angiotensin-converting enzyme catalyzes conversion (1) to (2)
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1 = angiotensin 1
2 - angiotensin II (biologically active) |
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ACE inhibitors are used to treat?
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high blood pressure
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What are the FOUR functions of angiotensin II?
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1 = aldosterone release
2 = Na+ H+ exchange 3 = thirst 4 = vasoconstriction |
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chemoreceptors in vasomotor centre detect changes in ?
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pCO2
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Cushing reaction
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increased intracranial pressure compresses cerebral blood vessels, leading to cerebral ischemia and elevated PCO2
--> vasomotor centre responds by increase SNS outflow and a profound increase in MAP |
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chemoreceptors in carotid and aortic bodies respond to ?
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PO2
- very sensitive to decreases in PO2 |
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ADH is involved in regulation of blood pressure in response to (1); Two main effects of ADH are (2) and (3)
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1 = hemorrhage (large loss of blood volume)
2= vasoconstrictor (increased TPR) on V1 R 3 = increases H20 absorption by renal distal tubule on V2 R |
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atrial natriuretic peptide
- released in response to (1) - causes (2), (3) and decreased (4) |
1 = increased blood volume, increased atrial pressure
2 = relaxation of smooth muscle 3 = vasodilation 4 = TPR |
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Starling Equation
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J = Kf [ (Pc - Pi) - (Oc - Oi) ]
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Capillary Hydrostatic Pressure (Pc) favors (1) and is determined by (2) and (3) pressures
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1 = filtration
2 = arterial pressure 3 = venous pressure (more so) |
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Capillary Oncotic pressure favors (1) and is determined by (2) in blood
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1 = reabsorption
2 = protein conc. |
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protein conc. in blood is increased by (1) and decreased by (2), (3), and (4).
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1 = dehydration
2 = protein malnutrition 3 = nephrotic syndrome 4 = liver failure |
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Factors that INCREASE filtration (4)
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1 = increased Pc
2 = decreased Pi 3 = decreased protein conc. in blood 4 = increased interstitial fluid protein conc. (inadequate lymphatic function) |
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Edema as a result of Increased Pc can be caused by? (6)
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arteriolar dilation
venous constriction increased venous pressure heart failure extracellular volume expansion standing |
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Edema as a result of decreased capillary oncotic pressure can be due to? (4)
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decreased plasma protein conc.
liver disease protein malnutrition nephrotic syndrome |
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edema as a result of increased filtration can be due to? (2)
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burn
inflammation |
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autoregulation
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blood flow to an organ remains constant over a wide range of perfusion pressures
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active hyperemia
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blood flow to an organ is proportional to its metabolic activity
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reactive hyperemia
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increase in blood flow to an organ that occurs after a period of occlusion of flow
--> the longer the period of occlusion, the greater the increase |
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Myogenic hypothesis
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- smooth muscle contracts when it is stretched
- explains autoregulation due to vasoconstriction |
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Metabolic Hypothesis
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tissue supply of O2 is matched to tissue demand for O2
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metabolically active tissue releases (1) which include (5)
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1 = vasodilator metabolites
2 = CO2, H+, K+, adenosine, lactate |
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histamine causes arteriolar (1) and venous (2) which causes increased (3) and thus (4) filtration leading to local (5)
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1 = dilation
2 = constriction 3 = Pc 4 = filtration 5 = local edema |
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bradykinin has same action as ?
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histamine
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serotonin causes arteriolar (1); implicated in (2)
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1 = constriction
2 = migraines |
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E series prostaglandins
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vasodilator
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F series prostaglandins
TXA2 |
vasoconstrictors
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