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PHGY210 > cardio 2 > Flashcards

cardio 2 Flashcards

1
Q

Normal Sinus Rhythm:

A

~60bpm

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2
Q

if sinus bradycardia…

A

Doesn’t mean something is wrong à physiological arrythmia

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3
Q

rate for sinus bradycardia

A

less than 60 bpm

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4
Q

Rate for sinus tachycardia

A

> 100bpm

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5
Q

What happens with sinus tachycardia

A

fever heart rate increases

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6
Q

what happens w/ sinus arrhythmia

A

on inspiration rate increases, on expiration rate decreases

Goes away as you age

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7
Q

what is 2:1 AV block

A

AP doesn’t get down the ventricle

Block of conduction or propagation in AV node

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8
Q

why is 2:1 av block problematic?

A

Problematic because heart rate is 1⁄2 (60 bpm à 30 bpm)

  • Cardiac output and blood flow is 1⁄2
  • Need pacemaker cells
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9
Q

Every ____ action potential is blocked on its way from travelling from the atrium to the ventricles (in 2:1 av block)

A

second

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10
Q

where is the 2:1 av blocked?

A

Blocked either in the Purkinje fibers, bundle of his, bundle branches or in the AV node

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11
Q

rate of ventricle in 2:1 av block

A

For every 2nd activation of the atrium there is only 1 activation of the ventricle which can
gradually worsen
The rate of the ventricle is 1⁄2

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12
Q

What is a complete Av block

A

Only P waves, no QRS Complexes & no AP reaches the ventricle
There is one transient wave because it comes back but if it stays you are in complete AV block because you have no cardiac output

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13
Q

treatment for complete AV block

A

electronic pacemaker

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14
Q

in complete AV block, what happens after P wave

A

After the P-wave there is a little dip which corresponds to the atrium repolarization
If you look carefully enough 1/12 leads will show atrial repolarization but it occurs at the same time as the QRS wave so you can only see it during complete AV block

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15
Q

can you get complete av block with qrs complexes

A

You can still get complete AV block with QRS complexes except this time the QRS complexes are
not related in time
- Independent pacemakers
- Normally the SA node is the pacemaker in the heart because other pacemaker areas in your heart usually don’t manifest because they are suppressed

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16
Q

why are other pacemaker areas suppressed in complete Av

A

The reason they are suppressed is because they get the input from the SA node
at about once/second.

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17
Q

what is the subsidiary pacemaker

A

During Complete AV block there are some cells in the ventricle that are no longer
subject to this input so the QRS complexes are generated in the ventricles
i.e. they aren’t getting into the ventricles via the His-Purkinje fibers; instead they are getting in via the ventricular muscle, the Purkinje fibers
and one of the bundle branches

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18
Q

if theres a complete av block with no subsidiary pacemaker

A

just p waves

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19
Q

The rate of subsidiary pacemakers are much _____ than the SA node and sometimes they are
so ____ that the person dies anyways

A

slower, slow

heart rate, cardiac output and BP too low

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20
Q

systole

A

ventricles contracting (to draw together/contract)

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21
Q

Isovolumetric ventricular contraction:

A

o AV valves closed
o Aortic and Pulmonary valves closed
o Atria relaxed
o Ventricles contract

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22
Q

Ventricular ejection

A 
o Blood flows out of ventricle
o AV valves closed
o Aortic and Pulmonary valves open
o Atria relaxed
o Ventricles contract
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23
Q

What happens to the AV valve when pressure(ventricles) > pressure(atria)

A

the AV valve will close which is the start of

ventricular systole

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24
Q

Once contraction of the ventricle starts (vent. eject.)…

A

the volume starts to increase, called isovolumetric contraction,
volume of the ventricle is constant because both valves are closed -> ‘iso’

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25
Q

everything thats happening one one side in ventricular ejection…

A

is happening on the other side

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26
Q

Eventually, in vent. eject., pressure in the the ventricles

A

exceeds that of

the big artery

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27
Q

when pressure in the the ventricles exceeds that of

the big artery (in vent eject.)

A

the aortic valves are open and the pressure

of blood in the ventricle will be higher than the pressure of blood in the aorta -> phase of ejection

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28
Q

As the ventricles starts to relax,

A

the pressure decreases and as soon as the pressure in the aorta is
higher than in the ventricles the aortic/pulmonary valves close

29
Q

Diastole

A

a putting asunder, separation, expansion, dilation (ventricles relax)

30
Q

isovolumetric ventricular relaxation

A

o Atria relaxed
o Ventricles contract
o AV valves closed
o Aortic/Pulmonary valves closed

31
Q

why is isovolumetric ventricular relaxation iso?

A

Relaxation of the ventricles but the volume is still ‘ISO’ because both
of the valves are closed

32
Q

effect on ventricle pressure and volume/pressure in atria during isovolumetric ventricular relaxation

A

The ventricle pressure decreases and the volume and the pressure in
the atria increases

33
Q

in isovolumetric ventricular relaxation, Once the volume in the ventricles is lower than the volume in the
atria,

A

the intraventricular AV valve opens

34
Q

Atria Relaxed

A

§ Ventricles contract
§ AV valves open
§ Aortic/Pulmonary valves closed

35
Q

Atrial contraction

A 
§ Atria Relaxed
§ Ventricles contract
§ AV valves open
§ Aortic/pulmonary valves closed
§ SA node è P-wave, expels more blood into the ventricles
§ Systole/diastole = ventricles
36
Q

A decrease in the radius by 10% leads to

A

a 60% increase in resistance

37
Q

An increase in the radius by 10%

A

to a 70% decrease in resistance

38
Q

Resistance is controlled by

A

the smooth muscle in the walls of the arteries and arterioles by
contracting and relaxing

39
Q

The smooth muscle is affected by

A

Neural
o Hormonal
o Local (metabolic)
o Endothelialàdiffuseoversmoothmuscle

40
Q

Most of the blood vessels are under the control of

A

SNS

41
Q

Receptors found along the vessels

A

alpha-adrenergic receptor

42
Q

What do alpha-adrenergic receptors do?

A

Produces a 2nd messenger cascade which leads to the

constriction of smooth muscle

43
Q

alpha-agonist

A

The site of alpha-agonist will bind to alpha-adrenergic receptor
and produce constriction
o TPR increases therefore, MAP increases

44
Q

When are alpha-agonist used

A

o Used when the BP is too low

45
Q

Where are adrenal glands found?

A

on top of the kidney

46
Q

in the sympathetic control of adrenal glands, what are E and NE acting as?

A

both alpha and beta agonist

47
Q

neurotransmitter in in the sympathetic control of adrenal glands,

A

• ACh is the neurotransmitter

48
Q

axons in the sympathetic control of adrenal glands,

A

• There are no post-ganglionic axonsàthey are modified ganglion cells whose function is to synthesize

49
Q

baroreceptor

A

operates on the time scale of

seconds within the bodyàe.g. when you stand up

50
Q

kidneys have the intrinsic property to

A

produce urine by extracting water

from blood

51
Q

what do diuretics treat

A

high blood pressure (hypertension)

52
Q

The Renin-Angiotensin-Aldosterone (RAA) System: all acting to…

A

alter the BP to keep it at a constant level

53
Q

RAA System: stimulus

A

Stimulus is a fall in renal artery or arteriole due to decrease in BP

54
Q

RAA System: what makes up the renin

A

Arterioles and kidney make up the renin and dump it into the circulation if
the BP decreases

55
Q

what is renin

A

Renin is an enzyme that attacks angiotensinogen that’s made in the liver
and converts it to angiotensin-1

56
Q

During exercise: total peripheral resistance

A

Decreases, resistance in heart muscle and skeletal muscles and skin decreases more than resistance in other vascular beds increases

57
Q

During exercise:mean arterial pressure

A

Increases, cardiac output increases more than total peripheral resistance decreases MAP = CO * TPR

58
Q

During exercise: pulse pressure

A

increases, stroke volume and velocity of ejection of the stroke volume increase

59
Q

During exercise: end diastolic volume

A

Increases, filling time is decreased by the high heart rate, but the factors favouring venous return – venoconstriction, skeletal muscle pump, and increased inspiratory movements – more than compensate for it.

60
Q

During exercise: blood flow to heart with skeletal muscle

A

Increases, active hyperemia occurs in both vascular beds, mediated by local metabolic factors

61
Q

During exercise: blood flow to skin

A

Increases, sympathetic activation of skin blood vessels is inhibited reflexively by the increase in body temp

62
Q

During exercise: blood flow to viscera

A

Decreases, sympathetic activation of blood vessels in the abdominal organs and kidneys is increased

63
Q

During exercise: blood flow to brain

A

Increases slightly, auto regulation of brain arterioles maintains constant flow despite the increased mean arterial pressure

64
Q

effects: AT-2-Receptor Blockers (ARBs)

A

Prevents angiotensin from functioning and thus decreases MAP

65
Q

effects: ACE inhibitors

A

Makes less angitotensin-2 which therefore decreases MAP

66
Q

effects: Renin Inhibitors

A

Inhibits renin to decrease the conversion of angiotensinogen to angiotensin-1 which therefore
decreases MAP

67
Q

During exercise: cardio output

A

Increases, heart rate and stroke volume both increased, the former to a much greater extent. CO = HR * SV

68
Q

During exercise: heart rate

A

Increases, sympathetic stimulation of the SA node increases, and parasympathetic stimulation decreases

69
Q

During exercise: stroke volume

A

Increases, contractility increases due to increased sympathetic stimulation of the ventricular myocardium; increased ventricular end-diastolic volume also contributes to increased stroke volume by the frank Starling mechanism

PHGY210 (6 decks)

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