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
everything thats happening one one side in ventricular ejection...
is happening on the other side
26
Eventually, in vent. eject., pressure in the the ventricles
exceeds that of | the big artery
27
when pressure in the the ventricles exceeds that of | the big artery (in vent eject.)
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
28
As the ventricles starts to relax,
the pressure decreases and as soon as the pressure in the aorta is higher than in the ventricles the aortic/pulmonary valves close
29
Diastole
a putting asunder, separation, expansion, dilation (ventricles relax)
30
isovolumetric ventricular relaxation
o Atria relaxed o Ventricles contract o AV valves closed o Aortic/Pulmonary valves closed
31
why is isovolumetric ventricular relaxation iso?
Relaxation of the ventricles but the volume is still ‘ISO’ because both of the valves are closed
32
effect on ventricle pressure and volume/pressure in atria during isovolumetric ventricular relaxation
The ventricle pressure decreases and the volume and the pressure in the atria increases
33
in isovolumetric ventricular relaxation, Once the volume in the ventricles is lower than the volume in the atria,
the intraventricular AV valve opens
34
Atria Relaxed
§ Ventricles contract § AV valves open § Aortic/Pulmonary valves closed
35
Atrial contraction
``` § 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
A decrease in the radius by 10% leads to
a 60% increase in resistance
37
An increase in the radius by 10%
to a 70% decrease in resistance
38
Resistance is controlled by
the smooth muscle in the walls of the arteries and arterioles by contracting and relaxing
39
The smooth muscle is affected by
Neural o Hormonal o Local (metabolic) o Endothelialàdiffuseoversmoothmuscle
40
Most of the blood vessels are under the control of
SNS
41
Receptors found along the vessels
alpha-adrenergic receptor
42
What do alpha-adrenergic receptors do?
Produces a 2nd messenger cascade which leads to the | constriction of smooth muscle
43
alpha-agonist
The site of alpha-agonist will bind to alpha-adrenergic receptor and produce constriction o TPR increases therefore, MAP increases
44
When are alpha-agonist used
o Used when the BP is too low
45
Where are adrenal glands found?
on top of the kidney
46
in the sympathetic control of adrenal glands, what are E and NE acting as?
both alpha and beta agonist
47
neurotransmitter in in the sympathetic control of adrenal glands,
• ACh is the neurotransmitter
48
axons in the sympathetic control of adrenal glands,
• There are no post-ganglionic axonsàthey are modified ganglion cells whose function is to synthesize
49
baroreceptor
operates on the time scale of | seconds within the bodyàe.g. when you stand up
50
kidneys have the intrinsic property to
produce urine by extracting water | from blood
51
what do diuretics treat
high blood pressure (hypertension)
52
The Renin-Angiotensin-Aldosterone (RAA) System: all acting to...
alter the BP to keep it at a constant level
53
RAA System: stimulus
Stimulus is a fall in renal artery or arteriole due to decrease in BP
54
RAA System: what makes up the renin
Arterioles and kidney make up the renin and dump it into the circulation if the BP decreases
55
what is renin
Renin is an enzyme that attacks angiotensinogen that’s made in the liver and converts it to angiotensin-1
56
During exercise: total peripheral resistance
Decreases, resistance in heart muscle and skeletal muscles and skin decreases more than resistance in other vascular beds increases
57
During exercise:mean arterial pressure
Increases, cardiac output increases more than total peripheral resistance decreases MAP = CO * TPR
58
During exercise: pulse pressure
increases, stroke volume and velocity of ejection of the stroke volume increase
59
During exercise: end diastolic volume
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
During exercise: blood flow to heart with skeletal muscle
Increases, active hyperemia occurs in both vascular beds, mediated by local metabolic factors
61
During exercise: blood flow to skin
Increases, sympathetic activation of skin blood vessels is inhibited reflexively by the increase in body temp
62
During exercise: blood flow to viscera
Decreases, sympathetic activation of blood vessels in the abdominal organs and kidneys is increased
63
During exercise: blood flow to brain
Increases slightly, auto regulation of brain arterioles maintains constant flow despite the increased mean arterial pressure
64
effects: AT-2-Receptor Blockers (ARBs)
Prevents angiotensin from functioning and thus decreases MAP
65
effects: ACE inhibitors
Makes less angitotensin-2 which therefore decreases MAP
66
effects: Renin Inhibitors
Inhibits renin to decrease the conversion of angiotensinogen to angiotensin-1 which therefore decreases MAP
67
During exercise: cardio output
Increases, heart rate and stroke volume both increased, the former to a much greater extent. CO = HR * SV
68
During exercise: heart rate
Increases, sympathetic stimulation of the SA node increases, and parasympathetic stimulation decreases
69
During exercise: stroke volume
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