cardiovascular - lecture 6 Flashcards

1
Q

(T or F) The left bundle branch is blocked. This will lead to a long QRS, and no Q wave

A

true
septum activated early by left bundle branch = gives Q
LEFT ventricle will contract more slowly as his system cannot trigger synchronous contraction

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2
Q

(T or F) The left bundle branch block can result in a change of direction of the R wave.

A

Tricky! Both True and False. True – in that the left ventricle isn’t going to contract synchronously (endo-epi), and this could result in a change of the waves direction relative to the electrodes. But also false, as we defined the R wave as a positive deflection. Terrible question

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3
Q

(T or F) A repolarization wave deflecting in the same direction as an activation wave on the same lead means that the direction of the repolarization wave changed

A

True! If that didn’t happen, the direction would reverse as the charge at the two electrodes has switched.

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4
Q

(T or F) The sinus node beats twice in a row, 50 milliseconds apart. We therefore see two P waves.

A

False! The sinus node doesn’t have enough cells in it to cause a deflection in the ECG. To do so, it would have to trigger the atria. But the atrial action potential duration is 150 ms, and it wouldn’t be possible to do that so quickly.

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5
Q

describe p-r segment

A

end of p to start of q
time delay between atrial and ventricular activation
defines as reference line for ecg

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6
Q

what is p-r interval

A

start of p to start of q
mostly a measure of av transit time
long intervals = av block

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7
Q

what is s-t segment

A

end of s to start of t
time between ventricular depolar and repolar
if elevated not 0v = then some tissue have abnormal aps - typical of an infarction

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8
Q

what is q-t interval

A

start of q to end of t
proportional to ap duration
long qt - problem with repolarization
can lead to arrythmias

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9
Q

what is qrs interval

A

start q to end of s
longer than 100ms = slow excitation, possible problems in his purkinje (bundle branch block) or slow conduction in cardiac muscle (ischemia)
can be long = when have block in left or right bundles
if ventricles activate at diff times = longer

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10
Q

describe excitation contraction coupling

A

calcium channels from sr and outside cell
binds toponin
ryanodine receptors sense calcium
pulseless electrical conduction = when not coupled = damaged
voltage response followed by mechanical response, calcium doesnt cause motion directly. 8 ms delay between voltage transient and ca transient on avg
Mechanical activity always lags electrical activity and can have complete dissociation (no mechanical activity).

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11
Q

what is a normal vs abnormal rhythym

A

Normal sinus rhythm about 70 BPM
Abnormally slow rhythm: bradycardia < 60 bpm
Abnormally fast rhythm: tachycardia > 100 bpm

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12
Q

describe bradycardia and tachycardia

A

can be physiologically healthy processes
for trained athletes = resting hr as low as 40bpm
exercising bring heart rate above 100bpm
respiratory sinus arrhythmia = sinus rate increases as you breath in and slows as you breath out - response decreases as you age

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13
Q

what is pathological sinus tachycardia

A

at rest and heart rate >100bpm
if heart being driven by activity in sinus node = bad in this case

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14
Q

what is av block

A

2:1 av block
no qrs in middle of 2 normal beats
septum not contracting
bc av blocked - av node and down his bundle and bundle branches = both would have to be blocked
treatment = pacemaker cause could lead to complete block (blocks all qrs)

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15
Q

what is pvc

A

premature ventricular complexes/contraction

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16
Q

describe premature complex

A

strange deflection before ventricle contracts
bead out of sync with heart
common

17
Q

describe ectopic pacemaker

A

from outside

18
Q

describe ventricular parasystole

A

usually benign

19
Q

describe ventricular tachycardia

A

leads to fibrillation = crazy, 300 bpm, v dangerous
bp drops to 0 = dead
fatal if not treated in minutes
defibrillator = causes all cells to beat at once
AED= automated external defibrillator

20
Q

describe how to treat atrial fibrillation

A

not as useful as ventricles
treatment by pulmonary vein isolation
paroxysmal atrial contractions
premature atrial contraction = pac, wont feel when and might have trouble climbing stairs
leads to irregular contraction of ventricles
treatment = surgery, originates in pulmonary veins = burn them to stop it

21
Q

describe tachycardia mapping - sock array

A

figure out when waves activate
rapid waves spinning around
circular fashion
surgery to remove scar so will not propagate around
circus movement reentry around anatomical obstacle

22
Q

descrive reentrant ventricular tachycardia

A

dangerously low bp due to inadequate filling
can transition to ventricular fibrillation
if hits itself = many waves
if spiral wave breaks up = fibrillations

23
Q

describe George Mines, discovery of reentry

A

chunk of cardiac tissue with hole in middle
slight inexcitable then becomes excitable - could be reason for tachy arrhythmias if abnormally fast rhythym
stimulate –> set up - propagates one dir and not next, sufficient time to recover –> around and around, uninterrupted
reentry responsible for tachycardias in ppl
need refractory period
increase refractory time by 50%
even longer refractory period for cell next to initiation site

24
Q

when can cell fire ap

A

excitable polarized –> excited depolarized
cell can only fire ap once it recovers (becomes polarized)
inexcitable time = refractory time