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CVS-Alaa > ECG > Flashcards

ECG Flashcards

1
Q

Which lead is mostly used to detect p waves?

A

Lead 2,

V1 & V5 rythem

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2
Q

Define sinus bradycardia? Sinus Tachycardia?

A

Sinus rhythm with rate < 60/ minute is called Sinus bradycardia

Sinus rhythm with rate > 100/min is called Sinus tachycardia

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3
Q

define arryhthemia?

A

abnormal rate and/or rhythm of the heartbeat

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4
Q

Describe atrial fibrillation on an ECG?

And its effect of heart rate & pulse

causes?

A

Multiple atrial foci! its caotic!

Multiple vectors pointing at different places at different directions >> UNORGANIZED

NO P WAVES

just wavy baseline!

Narrow QRS complexes

Atrial quivers! does not contract!

Pulse and beart rate IRREGULARY irreugular

350-650 bpm

**anything that causes enlargment of the atrium>>associated with atrial fibrillation

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5
Q

define heart block

What r some causes of a heart block?

A

This occurs when the electrical impulses are partially or fully blocked between the atria and the ventricles.

  • MI>> most common
  • degenerative changes
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6
Q

what is the ventricular escape rythem?

A

/

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7
Q

how many types of heart block r there?

A

3

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8
Q

Describe 1st degree heart block

A

slight delay in the time it takes electrical pulses to move through the AV node.

First-degree heart block rarely causes any noticeable symptoms

  • P wave normal
  • delay in AV node is LONGER>> longer PR-interval

(5 small squares)

  • slower conduction in AV node
  • QRS is normal
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9
Q

what is Wenkebach phenomenon?

A

Mobitz 1 (Wenkebach phenomenon)

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10
Q

Describe briefly 2nd degree heart block

A

impulses from the atria are not conducted through to the ventricles.

eventually lead to a heartbeat being skipped

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11
Q

describe 2nd degree heart block type 1!

A

Mobitz 1 (Wenkebach phenomenon)

PR interval keeps getting longer and evetually it doesn’t make it to the ventricles! (they kept waiting and waiting for their turn until one eventually died)

until u get a ‘DROPPED BEAT” (when p wave is not filled by a QRS complex)

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12
Q

describe 2nd degree heart block type 2

A

-Mobitz 2

PR interval is NORMAL, it normal FAJ2A ykhtrb (sudden non-conduction of beat) Dropped QRS >>>>>>HIGH RISK OF PROGRESSING TO TYPE 3 COMPLETE BLOCK

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13
Q

difference btw mobitz 1 & mobitz 2 on an ecg

A

In mobitz 1= each time it conducts PR interval PROGRESSIVELY LONGER EACH TIME!

In mobitz 2= each time it does conduct> PR interval is the same! ( not delayed)

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14
Q

Describe 3rd degree heart block

A

COMPLETE BLOCK

***normal atrial depolarisation BUT none of atrial waves go to ventricles!

  • atrial and ventricles r dissociated
  • ventricular pacemaker takes over (ventricular escape rhythm)
  • SLOW HEART RATE 30-40 Bpm>>too low to maintain bp and perfusion
  • usulally wide QRS complexes
  • ECG= even though atria is working normal, none of those signals r going down to ventricles & ventricles struggle with escape beats at a very low rate! (30-40 bpm)*

even

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15
Q

what is the heart rate in 3rd degree heart block? explain why

A

30-40 bpm

so slow!!! bc atria and ventricles r completely dissociated and ventricles depolarise at their pwn rate which is slower!

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16
Q

in 3rd degree heart block, where is the block most likely to be?

A

AV node, bundle of his

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17
Q

what does idiopathic mean?

A

unknown cause

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18
Q

describe ventricular fibrillation and how it leads to cardiac arrest?

A
  • u get impulses from many ECTOPIC sites firing in ventricular muscle>this results from a ventricular flutter.
  • ventricles quiver, abnormal FAST ventricular depolarisation.
  • many ectopic firing mn kl mukan> cause ventricles to rapidly work> NO CO>> cardiac arrest> DEAD
  • kind of like rowing a boat, it rows best if everyone rows at the same time. but if each person rows 3ala kaifa, the row boat will move in cricles and evetually sink!*
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19
Q

how would ventricular fibrillation appear on a ecg?

how can we manage this?

A

the whole PQRST breaks down completely!

  • we need to De-fibrillate (give external stimulation)

its a high energy shock that will depolarize everything at once to allow the SA node to take control again!

(just like when the leader shouts on the rowers to start rowing properyl!)

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20
Q

how is ventricular fibrillation and atrial fibrillation different?

A

in atrial fibrillation, some beats got irregular. but some beats can be conducted to the ventricles, and ventricles depolarizes and contracts normally.

In ventricular fibrillation , ventricles quiver, abnormal FAST ventricular depolarisation.

-many ectopic firing mn kl mukan> cause ventricles to rapidly work> NO CO>> cardiac arrest> DEAD

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21
Q

what causes ectopic firing?

A

..

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22
Q

what can abnormal rythems arise from?

A
  1. abnormal conduction

2-abnormal impulses

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23
Q

what is meant by Supraventricular rythems?

A

rythems that may arise above the ventricles!

  • sinus node
  • atrium
  • Av node
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24
Q

label

A
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25
Q

it goes like this:

Atrial Tachycardia (120-250 bpm)

Atrial flutter (250-350 bpm)

Atrial Fibrillation (350-650 bpm)

A
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26
Q

what is meant by the “ventricular escape rythem?”

A

when the a pacemaker in the ventricles takes over!

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27
Q

how can u differentiate that this is not an escape rythem but an ectopic ventricular beat on a ecg?

A

Escape ryhthem will only start after a bit of a PAUSE!

whereas here it is starting where the next normal beat should become!

28
Q

Define Ventricular Tachycardia?

why is persistent VT so dangerous and must be treated ASAP?!

A

Run of more than 3 consecutive ventricular ectopics

bc it can eventually lead to

VENTRICULAR FIBRILLATION!

29
Q

how is sinus tachycardia different than ventricular tachycardia

A
30
Q

Describe how the heart moves in Ventricular fibrillation?

A

doe snot squeeze,

it quivers and squirms like a bag of worms

31
Q

Normally how is the ST segment shown on an ECG?

A

Usually the ST segemnt is FLAT bc the heart is completely depolarised and no current is moving throuhg the myocardium

32
Q

which region in the heart is most vunerable to ischemia? why?

A

Subendocardial region! cuz its the firthest away from blood supply

33
Q

In MI, describe the normal, ST elevation and ST depression on an ECG and in what type of infarct does each occur in?

A
34
Q

Transmural and non transmural infarct on an ECG

A
35
Q

when do u see ST depression?

A

During repolarisation of ventricles, the charges moving towards the sub- infarcted area AWAY from the electrode

(girl goes away from u and u r sepressed ;(

36
Q

if artery is only partly inculdued. sometimes, ECG changes can only be seen during excersize (exertion) and this is bc during exertion, ur heart rate speeds up, and diastole shortens and theres less blood during exertion

A

ok

37
Q

IN MI >>

Need to look at P-QRST in all 12 leads!!

A

ok chill

38
Q

in what cases would u see chnages in the ECG even at REST?

A

when u have Unsatble angina and NSTEMI (trasnmural infarct)

39
Q

when do u see ST segement Elevation?

A

In trasmural infarct

current is moving toward the Electrode

(from endocardium to epicardium)

This is an indication that there is a complete occlusion of the artery!

40
Q

what r pathalogical Q waves?

what is a normal Q wave

A

A normal Q wave is Septal depolarization in a fast and DOWNWARD motion

+ charges moves to - electrode= - deflection

** remember q waves sometimes dont show, and thats so normal ya

NOWW FOR PATHOLGY

Pathalogical Q waves Develop LATER in an MI

41
Q

_______________may be the permenent footprints of MI on the ECG pattern

A

Pathalogical Q waves.

cardiologist can know that patient had a previous MI by looking at his ECG

42
Q

how can u deterine from an ECG if it is partial thickness MI on full thickness MI?

A

if its partial >> No Q wave depression

If its full>> Pathalogical Q wave depression

43
Q

What r the earliest changes in an ECG for an MI??

A

ST elevation

44
Q

describe composition of ECG paper

A
45
Q

How many large sqaures make 1 second? small squares?

A
46
Q

how many large sqaures makes 1 minute?

A

300 Large sqaures|!

47
Q

How to calculate the Heart rate using ECG paper?

A
48
Q

how do u calculate irregular heart rate using ECG paper?

A
49
Q

calculate the PR, QRS & QT intervals

A
50
Q
A
51
Q
A
52
Q
A
53
Q
A
  1. SA Node depolarisation
  2. Atrial depolarisation
  3. conduction through AV node, but electrochemical actvity is so small that neddle does not flunctuate
  4. ventricular depolarisation
54
Q
A
55
Q
A
56
Q

What is the normal range for the PR interval?

A

0.12-0.2 seconds

57
Q

What causes the normal delay between the P wave and the QRS complex?

What might prolongation of this delay suggest?

A

Pause of electrical activity at the AV node

Prolonged delay suggests heart block because there is a block of electrical activity between the atria and ventricles

58
Q

What forms the inferior border of the heart and which coronary artery usually supplies this region?

A
59
Q

what is rate of ventricular depolarisation in 3rd degree heart block? why?

A

30-40 bpm>>so SLOW

bs ventricular pacemaker takes over and is extremely slow!

60
Q

which heart block presents with WIDE QRS complexes?

A

3rd degree (complete block)

Remeber alaa, theres SLOW ventricular depolarisation!>>wider qrs

61
Q

Describe how hyperkalemia would present on an ECG? how would it effect the heart activity

A

it will inactivate voltage gated Na channels>>heart will become Less excitable!

high T wave

long PR interval

depressed st segement

62
Q

how does hyper and hypokalemia effect RMP?

A
63
Q

how would hypokalemia appear on ecg?

A

Taiba hates bananas> (low T)

it rain, she opens her umbrella up HIGH

Sara & taiba fight over it (ST depression)

  • Low T wave
  • High U wave
  • Low ST segment
64
Q

Later changes with More adnvanced Hyperkalmeia may involve flattening________ wave, prolongation of the_______intervel and widening of the _______complex and Bradycardia/tacycardia

A

Later changes with More adnvanced Hyperkalmeia may involve flattening of the P wave, prolongation of the PR intervel and widening of the QRS complex and Bradycardia

65
Q

i am Irregularly irregular & ihave a wavy baseline.

Name moi

A

Atrial fibrillation

CVS-Alaa (21 decks)

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