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Human Function > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

What do intercalated disks contain? For what purpose

A
  • gap junctions: provide electrical continuity bw cardiac myocytes –> allows heart to function as an electrical unit and each muscle fiber to contract in coordinated fashion.
  • desmosomes: anchor fibers together
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2
Q

Does cardiac muscle have greater or fewer mitochondria? Why?

A
  • Greater
  • Allows for continuous aerobic respiration via ox phos
  • uses whatever fuel available (switches metabolic pathways)
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3
Q

Does the heart use motor-unit contraction or organ contraction?

A

Organ contraction

-Heart contracts as a unit or not at all ( no ‘motor-unit’)

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4
Q

Is the ARP long or short in cardiac muscle?

Why?

A
  • Long

- it prevents tetanus

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5
Q

What is the mech of contraction of myocardial fibers

A
  • depol by opening voltage-gated fast Na+ channels
  • transmission of depol down T-tubules causing Ca2+ release (80% of Ca comes from the SR via Ca induced Ca release)
  • Calcium spark and decr K+ permeability (prolongs depol – plateau)
  • Excitation contraction coupling via troponin binding leads to sliding of filaments.
  • Repolarization (relaxation) occurs due to Ca2+ transport out of the cytoplasm and K+ perm incr.
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6
Q

Difference bw ventricular myocyte AP and SA node AP

A 
ventricular:
 -has phase 0,1,2,3,4
-Has plateau period
-solid phase 4
SA:
- has phase 4,0,3.  
-phase 4 (resting pot) is not stable (it's continuously depolarizing), known as funny current.
-phase 0 is not as fast bc of opening of Ca channels
-NO refractory period
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7
Q

What is the funny current due to?

Where do we see this?

A
  • Due to slow Na channels opening

- We see this in autorhythmic cells (SA node)

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8
Q

Rank in terms of AP length? (shortest to longest)

  • Purkinje fibers
  • Atria
  • Ventricles
A

1-Atria
2- Ventricles
3- Purkinje

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9
Q

What is the P wave?

A

Depolarization of both atria (contraction)

-Impulses originate at SA node and spread through both atria

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10
Q

What is the QRS complex?

A
  • Ventricles depolarize and contract

- Normal duration 80-120 ms

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11
Q

Why is the QRS complex larger than the P-wave?

A

Ventricles have a greater muscle mass

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12
Q

What is the T-wave?

A

-Repolarization begins at apex of heart and spreads upwards through ventricles
(Represents electrical recovery of ventricles?

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13
Q

What is the PR interval?

A
  • Conduction time from atria to the ventricles (through the bundle of his)
  • Helps distinguish arrhythmias
  • Signal must pass through AV node, so any block that would show elongation of PR –> 1st degree block
  • -Normal duration 120-200 ms
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14
Q

What is the ST interval?

A
  • Hearts electrical activity immediately after ventricles contract
  • Even with baseline bc no electrical activity flows
  • Normal duration:
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15
Q

Where is the ARP located in the EKG?

A

From middle of QRS complex to middle of T-wave

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16
Q

What are the inflow valves?

A

Atrioventricular valves:

-tricuspid and bicuspid (mitral)

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17
Q

What are the outflow valves?

A

Semilunar valves?

-Aortic and pulmonary

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18
Q

What are the phases of the cardiac cycle?

A
  • diastasis (middle of phase 1)
  • Isovolumetric contraction (phase 2)
  • Ejection or outflow (phase 3)
  • Isovolumetric relaxation (phase 4)
  • Rapid ventricular filling (early phase 1)
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19
Q

ESV is in which phase of cardiac cycle?

A

end of phase 3- isovolumetric relaxation

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20
Q

EDV is in which phase of the cardiac cycle?

A

End of phase 1 (late diastole)– both sets of chambers are relaxed and ventricles fill passively

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21
Q

What is CO?

A

volume of blood pumped per ventricle per minute

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22
Q

What is SV

A

volume of blood pumped by a ventricle per beat

-it’s the diff bw EDV and ESV

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23
Q

What is EDV?

A

vol of blood in ventricles at end of diastole

-pre-load

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24
Q

What is the cardiac cycle

A

seq of mechanical and electrical events that repeat with every heart beat

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25
Q

What is SV determined by?

A

EDV
TPR
FOC

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26
Q

What is TPR?

A

-Impedance to flow in the arteries (afterload)

part of determination for SV

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27
Q

What influences EDV?

A
  • Venous return
  • Bp
  • Venous pressure
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28
Q

What is the preload?

A

Amount of tension in the ventricular myocardium before it begins to contract?
(from EDV)

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29
Q

What is the Frank-Starling Law?

A

-Strength of ventricular contraction varies directly with EDV
-SV is proportional to EDV (as EDV incr, myocardium is stretched more, causing greater contraction and SV)
(Ventricles pump out all the blood that enters them)
-Describes an intrinsic property of the myocardium

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30
Q

What is contractility?

A

-FOC at any given EDV (or pre-load)

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31
Q

What is the after-load?

What does an incr in afterload do to SV?

A

Pressure in the arteries just outside the semilunar valves (pressure in the aorta and pulmonary artery)
-Any incr in afterload reduces stroke vol

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32
Q

List positive inotropic agents

A

Cause contraction (incr Ca)

  • Adrenergic agonists (epi)
  • cardiac glycosides
  • High extra cellular Ca
  • Low extracellular Na
  • Incr HR
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33
Q

List negative inotropic agents

A

Cause relaxation (decr Ca)

  • Ca channel blockers
  • Low extracellular Ca
  • High extracellular Na
34
Q

Why is Cardiac muscle resistant to developing tetanus? Compare to skeletal?

A

-Long ARP

35
Q

A recording of the SA node AP exhibits a sudden incr in slope of phase. How would you explain this? Permeability to which ion is increasing or decreasing?

A
  • increase in symp tone

- Incr Na influx

36
Q

During which phase of the ventricular AP would you expect permeability to K to be the highest?

A

3

37
Q

How would incr symp activity affect the relationship bw ventricular EDV and SV

A

-Incr EDV which increases SV

38
Q

What is bl flow driven by?

A

a const pressure head across variable resistances

39
Q

What is the link bw HR and SV?

A

Symp innervation and epi from adrenal medulla cause incr HR and also cause incr contractility which incr SV

40
Q

Which side is the volume resevoir?

A

Venous side

41
Q

Which side is the pressure resevoir

A

Arterial side

42
Q

What influences venous return?

A
  • Bl vol
  • Venous pressure
  • Urine vol (affects bl vol)
  • Vasoconstriction by symps
  • Skeletal muscle pumps (affects venous pressure)
  • Pressure drop during inhalation
43
Q

What is delta P equal to?

A

F * R

44
Q

What does resistance across a circulatory bed result from?

A

serial arrangements of resistances

45
Q

What does TPR result from

A

parallel arrangement of all the circulatory beds in the body

46
Q

Relationship bw R and flow?

A

as R increases, F decr

47
Q

What are 3 parameters that determine resistance for fluid flowing through a vessel?

A

L- longer vessel, greater R
viscosity - thicker fluid, incr R ??
r- incr r, decr R

48
Q

What is the velocity of blood flow affected by?

-Where is bl flow the slowest and fastest?

A

TOTAL cross-sectional area

  • Slowest in the capillaries
  • Fastest in the aorta
49
Q

Which blood vessels play the most impt role in the regulation of blood flow to a tissue and blood pressure

A

Arterioles

50
Q

As blood travels from the aorta to the capillaries what increases?

A

R

bc the radius is decr

51
Q

As a subjects age increase, his/her arterial compliance _____

A

decr

52
Q

As symp tone incr, TPR _____

A

incr

-bc vasoconstriction

53
Q

As blood moves from the arteries to the capillaries, bp _______

A

decr

-highest pressure right when it exits the heart and decr from there

54
Q

As blood flow from the arteries to the capillaries, velocity of flow ______

A

decr

-bc R incr bc r decr

55
Q

As you go from arteries to capillaries, the fluid pressure exerted by blood on the vessel walls _______

A

decr

56
Q

As HR decr. diastolic pressure will _____

A

decr

57
Q

The majority of the blood volume is contained within the _______

A

veins

volume resevoir

58
Q

What factor is most sig in affecting TPR?

A

radius bc r^4

59
Q

Brief incr in bp will cause symp ton on the blood vessels to_______

A

decr

60
Q

Where is the biggest pressure drop?

A

-arterioles

(greatest site of vasoconstriction)– incr R so decr P

61
Q

Which circ has a higher P, pulmonary or systemic?

A

systemic

62
Q

C =

A

compliance

delta V / delta P

63
Q

What is the major cause of non-linear pressure-flow relationship in vascular beds?

A

elastic properties of the vessels

-if it’s linear, it’s rigid

64
Q

What are the 3 types of capillaries

A

continuous
fenestrated
sinusoidal

65
Q

continuous capillaries

A
  • most comon
  • have inter endothelial junctions (in BBB tight junctions instead)
  • numerous exocytotic vesicles
  • NO fenestrae
  • Continuous with few wall interruptions
66
Q

Fenestrated capillaries

A
  • Endothelial cells are thin and perforated

- Has fenestrations

67
Q

Sinusoidal capillaries

A
  • Type of fenestrated capillary
  • Also called discontinuous
  • VERY leaky –> extremely large fenestrae and have actual gaps bw adj endothelial cells
68
Q

What travels through cap wall by diffusion?

A

O2, Co2, lipid-soluble molecules

69
Q

What travels through cap wall by bulk flow?

A

H20, electrolytes, small molecules

70
Q

What travels through cap wall by vesicular transport?

A

macro-molecules

71
Q

What travels through cap wall by active transport?

A

ions, small molecules

72
Q

What is Kf in the NDF equation?

A

water permeability of cap wall (hydrolic flux)

73
Q

When NDF is greater that 0 what is favored?

A

filtration

74
Q

What is Pc?

A

capillary hydrostatic pressure

  • higher at arteriolar end than venule end BUT more affected by changes in venous end
  • forces fluid OUTWARD
75
Q

What is Pif?

A

IF hydrostatic pressure

  • Normally neg (due to pumping action of lymphatics)
  • opposes filtration
  • Inward force
76
Q

What is Pi p/c

A

Plasma colloid osmotic pressure (oncotic)

  • Plasma proteins are major determinant (albumin is most abundant plasma protein and generates about 70% of osmotic pressure)
  • forces fluid inward
77
Q

What is Pi if?

A

IF colloid osmotic pressure (oncotic)

  • Caused by small amt interstitial proteins (in proteoglycans that leak into IF space (so little loss, so little protein in IF –> why Pi if is low)
  • Favors filtration
  • Forces fluid outward
78
Q

As you move from the arterial end of a capillary bed to the venous end, the capillary hydrostatic pressure will ______

A

decr (bc it’s higher at arteriolar end)

79
Q

Liver dysfunction would cause capillary osmotic pressure to _____

A

decr

80
Q

Dehydration causes capillary osmotic pressure to ______

A

incr

81
Q

(T/F) Capillary surface area does not influence the amt of substance which diffuses down a conc gradient

A

F

82
Q

(T/F) Transport of small solutes across the capillary wall cannot be described in terms of physical laws

A

F- small pore effect (small polar molecules can cross wall by water-filled pores)

Human Function (5 decks)

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