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EBME 202 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

list the steps of how electrical activation spreads throughout the heart.

A

SA node -> AV node -> bundle of his (AV bundle -> left and right bundle branches) -> purkinje fibers -> ventricular muslce

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2
Q

lead 1

A

aVL - aVR

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3
Q

lead 2

A

aVF - aVR

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4
Q

lead 3

A

aVF - aVL

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5
Q

aVR

A

right arm

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6
Q

aVL

A

left arm

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7
Q

aVF

A

left leg

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8
Q

which lead has the greatest magnitude and why?

A

lead 2 because it has the greatest alignment with the mean depolarizing vector

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9
Q

what variable does blood flow rate depend most strongly on and how?

A

it depends most strongly on the radius of the vessel. increasing radius increases the blood flow as the ratio between resistance R and radius r is R = 1/r^4. increasing radius will decrease resistance of flow.

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10
Q

what are the next two most important variables that blood flow rate depends on?

A

pressure and length of vessel

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11
Q

what are the 2 major classifications of arrythmias

A

impulse conduction and impulse formation

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12
Q

how does a heart attack contribute to future arrythmias?

A

it interferes with the normal conduction patterns

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13
Q

release of endothelin by the vessels of the small intestine

A

-local vasoconstriction
-blood flow impacted
-decrease
-local to small intestine

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14
Q

low concentration of oxygen and nutrients available to vascular smooth muslce in a vessel (oxygen demand theory)

A

-vasodilation
-blood flow primarily imapcted
-increase
-local to vessel (smooth muscle)

oxygen deman theory and adenosine

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15
Q

release of adenosine by the leg muscles

A

-vasodilation
-blood flow primarily impacted
-increase
-local at leg

oxygen demand theory and adenosine

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16
Q

sympathetic stimulation of the small arteries and arterioles

A

-vasoconstriction
-blood pressure primarily impacted
-increase
-systemic (all blood vessels)

systemic & sympathetic and epinephrine & nonepinephrine

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17
Q

release of epinephrine and nonepinephrine from the adrenal glands into the blood stream

A

-vasocinstriction
-blood pressure
-increase
-systemic (all blood vessels)

systemic & sympathetic and epinephrine & nonepinephrine

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18
Q

explain what muscles drive inspiration and expiration during normal quiet bretahing vs heavy breathing. if any breathing actions occur with no muscle involvement, explain what factor drives the action instead.

A

during normal quiet breathing, almost all work is done by the diaphragm. inspiration is driven by the lower surface of the diaphragm pushing downwards and expiration is driven by relaxation and elastic recoil of the diaphragm. during heavy breathing, the diapgrahm is still in motion but the use of the intercostal muscles helps drive pulmonary ventilation. the internal intercostals help with expiration and depressing the ribs. the external intercostals help with inspiration and expanding the ribs. the abdominal muscles are also used to help push organs downward to help the lungs inflate more.

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19
Q

how does muscle contraction lead to changes in lung volume when no muscles directly attach to the lungs?

A

pleural pressure is developed by the lymphatic system which removes excess pleural fluid. muscle contraction increases this pleural negative pressure ad the lungs expand, the lung volume increases as the lungs are supported by the slippers pleural fluid in the pleural space.

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20
Q

what is the difference between external and internal respiration? from where and to where do oxygen and carbon dioxide move in each process?

A

inspiration: gas exchange between blood and body cells in the tissue capilaries. O2 moves from blood to the body cells and CO2 moves from cells and interstitial fluid to the blood.
expiration: gas exchange between air and alveoli. O2 moves from the alveoli to the blood and CO2 moves from the blood to the alveolar air.

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21
Q

what is one specific change in the blood that leads to the Bohr effect (direction and specific quantity)

A

increase in [H+] ions whihc moves to reaction to be more acidic.

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22
Q

what is the outcome of the Bohr effect on oxygen exchange at the lungs and tissues?

A

at the lungs: O2 transfer into blood improves
at the tissues: O2 release into tissues improves

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23
Q

in what specific structures are the peripheral chemoreceptors ocated?

A

aortic and carotic bodies

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24
Q

what chemical factors can the peripheral chemoreceptors measure in the blood?

A

H+, CO2, and O2

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25
Q

signals from chemoreceptors are sent to the brainstem. what is the outcome of the effect mediated by the vasomotor center? what is the outcome of the effect of mediated by the brainstems respiratory center?

A

-increase blood pressure
-increase breathing rate

26
Q

normal breathing is primarily regulated by central chemoreceptors. what is the only stimulus that can directly excite the central chemoreceptors?

A

an increase in [H+] ions.

27
Q

list the four steps of the cardiac cycle and describe what each chamber and valves are doing.

A
  1. isovolumetric contraction: ventricles contract, AV and aortic pulmonary valves are closed. high pressure in ventricles (systole).
  2. ventricular contraction: ventricles eject blood from the heart, the aortic and pulmonary vales are open and contract blood. high pressure in ventricles (systole).
  3. isovolumetric relaxation: ventricles relax and all valves are closed. low pressure in ventricles (diastole).
  4. ventricular filling: blood rushes to venticles as the AV valves relax and open. low pressure in ventricles (diastole).
28
Q

what would happen to the lead II ECG waveform if the electrodes were accidentally places on top of the head and the bellybutton?

A

there would be a decrease in magnitude because the pplacement in in a straight vector downwards which does not align with the mean vector which goes from top left to bottom right for lead II.

29
Q

why are arrythmias more likely with high heart rates?

A

the wavelengths are shorter which leads to re-entry.

30
Q

if a mutation of the potassium channels in the cardiac muscle cells caused them to open earlier than normal, how would this affect the duration of the cardiac action potential?

A

the duration would be shorter as the ions run out faster.

31
Q

an ectopic foci is an example of what category/type of arrythmia?

A

impulse formation/automaticity

32
Q

angiogenesis

A

the formation of new blood vessels for long term local control of blood flow.

33
Q

what is a type of vasodilator and what does it do?

A

adenosine. it controls local blood flow.

34
Q

what is autoregulation?

A

regulatory mechanism that allows blood flow to remain constant despite variations in arterial pressure.

35
Q

myogenic:

A

reactive vascular constriction

36
Q

metabolic:

A

high blood pressure = high blood flow = increase vasoconstriction

37
Q

what is the primary mechanism of long-term local control of blood flow?

A

local control is specific to certain tissues in recieving oxygen and nutrient from blood flow. systemic control is focused on the whole body, it is mainly regulated by sympathetic nervous system.

38
Q

where is nitric oxide produced?

A

edothelium of blood vessels

39
Q

what triggers nitric oxide production?

A

high shear stress

40
Q

what does nitric oxide do?

A

acts as a local vasodilator

41
Q

what does nonepinephrine do and where is it released?

A

regulates circulation and is released by the autonomic nervous system.

42
Q

what is the effect of nonepinephrine on the arterioles?

A

vasoconstriction

43
Q

how will nonepineprine release affect systemic blood pressure?

A

will increase

44
Q

in what form is the majority of oxygen transported from the lungs to the tissues?

A

in molecular form (O2), binded to hemoglobin. ~97%

45
Q

in what form is the majority of carbon dioxide transported from the tissues to the lungs?

A

as bicarbonate ions in the plasma. ~70%

46
Q

what is the only direct stimulus that can activate the central chemoreceptors?

A

H+ ions

47
Q

why cant the H+ stimulus enter the brain?

A

H+ ions cannot cross the blood brain barrier- the highly selective semipermeable membrane that limits diffusion of solutes into/and out of the blood in the CNS.

48
Q

explain how the H+ stimulus gets to the central chemoreceptors even though it cannot enter the brain itself.

A

CO2 can readily pass through the blood brain barrier and reacts with H2O to form carbonic acid which then dissociate into H+ and bicarbonate. THis makes the blood acidic.

49
Q

what component of the lungs is the primary site of gas exchange?

A

the alveoli

50
Q

what muscles contract to produce expiration

A

the internal intercostal muscles

51
Q

what is pleural pressure, where is it, and why is it important for breathing?

A

pleural pressure is the pressure within the pleural space and the lungs. it is important because it acts as a suction to the lymphatic system by creating negative pressure which holds the lungs against the interior rib cage.

52
Q

from where and to where does the carbon dioxide move during external respiration?

A

it moves from the blood and into the alveoli to be expired.

53
Q

if you breathed a normal breath into a spirometer right now, what is the name of the pulmonary volume or capacity that would be measured?

A

tidal volume

54
Q

what is the reason why alveolar air does not have the same composition as atmospheric air?

A

the alveoli are the primary site of gas exchange so the levels of CO2 and O2 are constantly changing, so the composition is different to atmospheric air.

55
Q

which is the source of the cardiac vector (or dipole)?

A

ion flow in a common direction

56
Q

what ion is responsible for the plateau phase in the cardiac action potential?

A

calcium

57
Q

what happens to the cardiac action potential duration as the heart rate increases?

A

the duration decreases

58
Q

what structure allows impulse conduction between cardiac muscle cells?

A

gap junctions between cardiac muscle cells allow the ion currents to flow.

59
Q

name the 2 categories of arrythmias and give and example of each.

A

-abnormal signal generation: early afterdepolarization-abnormal signal conduction: re-entry

60
Q

how do you stop ventricular fibrilation?

A

a defibrilator will send an electrode impulse that will wipe out the disordered signal/the cardiac pathway, which allows the SA node to restart an ordered heart beat.

EBME 202 (3 decks)

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