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Pathophysiology > EKG > Flashcards

EKG Flashcards

1
Q

The flow of which 3 ions in and around the myocardial cells creates this electrical current?

A

Na+, K+ and Ca+

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2
Q

what do the 12 leads represent?

A

12 different viewpoints, each representing a different axis through the heart

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3
Q

normal P wave axis in adults vs kids (in degrees)

A

The normal P wave axis lies between 0 degrees to plus 70 degrees in adults (0 to plus 90 in children)

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4
Q

A wave of de-polarization moving toward a positive electrode will record what kind of wave?

A

a positive deflection (a P wave or QRS complex)

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5
Q

beats generating in the SA node should generate what kind of waves in lead II?

A

Beats originating in the SA node should generate an upright P wave Lead II

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6
Q

2 types of cardiac muscle cells

A

Contractile cells : which constitute the majority of the atrial and ventricular tissue. These cells are responsible for generating cardiac pressures.

Conducting cells.:Responsible for the spontaneous generation of electrical impulses (action potentials), and rapidly spreading the action potentials over the entire myocardium.

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7
Q

what is the normal pace of the SA node?

A

60-100 bpm - has the fasted firing rate

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8
Q

what is the SA nodes influence on other cardiac conducting cells?

A

normally overdrive suppresses other cells with intrinsic automaticity (the ability to spontaneously generate an action potential)
atrial cells, AV junction and ventricular conducting system

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9
Q

what are the atria internodal tracts

A

The action potential spreads from the SA node to the left and right atria via the atrial internodal tracts. Simultaneously, the action potential is conducted to the AV node

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10
Q

what does the AV node do- 2 fxns? what do increases in its conducting velocity do?

A
  1. slow conduction- insures that the ventricles have sufficient time to fill with blood before they are activated and contract.
  2. protects the ventricles from rapid atrial rates because of its slow conducting velocity and prolonged refractory period.
    Increases =decrease ventricular filling and decrease stroke volume and cardiac output. (and vice versa)
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11
Q

what does the bundle of his connect?

A

connects the AV node to the 2 bundle branches.

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12
Q

what are included in the “AV junction”? what is the inherent firing rates of its cells?

A

AV node and the bundle of His

junctional pacemaker cells: 40 - 60 beats per minute.

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13
Q

what makes up the ventricular conducting system? what is its firing rate?

A

Right and left bundle branches and Purkinje system. Ventricular cells: 30 - 45 beats per minute.

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14
Q

what is an “ectopic pacemaker”?

A

Failure of the SA node to generate an impulse (sinus pause) will allow a lower pacemaker (atria, AV junction or ventricular) to escape overdrive suppression and become the heart’s pacemaker at its inherent firing rate;
AV junction 40 -60, ventricular 30-45.

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15
Q

what is “altered automaticity”? what 3 kinds of events increase this automaticity?

A

Pacemaker cells other than the SA node may also become the hearts pacemaker.
MI, increase sympathetic tone, hypokalemia.

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16
Q

escape or premature beats: what are they like if the originate above the bundle branches (unless…)? what if they originate in the ventricles?

A

originate above the bundle branches (atrium or A-V junction) are narrow complex
*unless there is an accompanying bundle branch block.

originating in the ventricles will be wide complex

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17
Q

wide vs narrow complex

A

narrow: QRS <0.12 seconds
wide: QRS equal to or >0.12 seconds

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18
Q

PJC- premature junctional (AV jxn) complexes: what will be the result?

A

captures the atria (retrograde) and the ventricles (antegrade).
The retrograde P wave may appear before, during, or after the QRS complex; if before, the PR interval is usually short (i.e., < 0.12 s)
inverse wave before the QRS = before jxn. (bundle of his) - at AV node
inverse after QRS = after jxn (bundle of his)

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19
Q

escape junctional beats: what are they? wide vs narrow?

A

a delayed beat originating not from the atrium but from an ectopic focus somewhere in the AV junction.
when the rate of depolarization of the SA node falls below the rate of the atrioventricular node.
narrow- above bifurcation, wide- below bifurcation

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20
Q

normal sinus rhythm: rate, rhythm, p wave positive in what lead, P:QRS ratio, PR interval, QRS complex length

A
  1. 60 - 100 beats per minute
  2. Regular (may vary some with respiration) - speed up a bit with inspiration
  3. P wave positive in lead 2
  4. 1 P wave before each QRS complex
  5. PR interval 0.12 - 0.20 seconds
  6. QRS complex less than 0.12 seconds
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21
Q

Sinus tachy: Dx

A

Same as sinus rhythm except rate between 100 - 160 at rest.

narrow complex tachycardia: QRS duration is < 0.12 seconds (narrow= super ventricular in origin)

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22
Q

sinus tachy: Txt

A
  • Identify underlying cause, such as volume depletion, CHF or hyperthyroidism and treat appropriately.
  • if hyperthyroidism: beta blockers or calcium channel blockers. (Verapamil or Diltiazem)
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23
Q

PSVT: paroxysmal super ventricular tachy

(aka wandering atrial pacemaker): what is it often caused by? Dx?

A

a reentry circuit w/in the AV node, precipitated by a PAC:
Regular narrow complex tachycardia between 150- 250 beats per minute.
Usually no P waves seen.

24
Q

Txt GOAL for PSVT, then 3 step approach (each step done if the previous doesnt work)?
what about for unstable pts or pts refractory ot AV nodal blocking agents?

A

GOAL: blocking conduction through the AV node which terminates the re-entry circuit.

  1. vagal maneuvers which increase PSNS tone to the AV node.
  2. adenosine
  3. CCBs or beta blockers.
    * unstable patients or patients refractory to AV nodal blocking agents: cardioversion
25
Q

Rate: 100-160bpm
QRS <0.12
all other aspects WNL
Dx and txt?

A

sinus Tachycardia
Txt the underlying cause (CHF, vol. depletion, hyperthyroid)
*hyperthyroid: use CCBs or BB

26
Q

what CCBs do we use?

A

verapamil or diltiazam

27
Q 
Rate: 150-250 bpm
QRS <0.12 
possibly no p waves 
all other aspects WNL 
Dx and txt?
A 
PSVT: paroxysmal ventricular tachycardia 
txt: 1. vagal maneuvers 
2. adenosine
3. CCBs or BB 
unstable/refractory: Cardiovert!
28
Q

GOAL of txt for PSVT?

A

block conduction through the AV node to stop re-entry (precipitated by PAC).

29
Q

what are the vagal maneuvers we use? why do we do this ?

A

carotid sinus massage
Valsalva maneuver
purpose: increase parasympathetic tone in AV node.

30
Q 
Rate: 250-350 bpm 
QRS <0.12 
rhythm: regular or irregular 
ventricular rate is a multiple of atrial 
no flat baseline 
all other aspects WNL 
Dx and txt?
A

Atrial flutter: “flutter waves “ - no baseline

txt: CCBs or BBs
unstable: cardiovert!

31
Q

GOAL of txt for atrial flutter?

A

control ventricular rate by slowing conduction through AV node… to increase refractory period so that there are fewer impulses from A –> V

32
Q 
Rate: atrial  >350 bpm, ventricle: irregular  
QRS <0.12 
rhythm: irregular
irregular baseline 
no p waves
all other aspects WNL 
Dx and txt?
A

Atrial fibrillation

txt: CCBs or BBs
unstable: Cardiovert
* same as Aflutter

chronic: digoxin

33
Q

QRS > 0.12
*if rate increased significantly, p waves maybe buried in Twaves
all other aspects WNL
Dx and txt?

A

*may appear like ventricular tachycardia BUT
its Bundle Branch Block
txt: pacemaker

34
Q

PVC vs escaped ventricular beats

A

PVCs: premature -before next expected beat
- can be suppressed w/ little clinical consequence
escaped ventricular beat: after a LONG pause
-suppression could be fatal (this escaped beat may be life saving)

35
Q 
rate: 120-250 bpm
QRS > 0.12 
no Pwaves 
ST segment and T wave slope in opposite direction of QRS deflection 
all other aspects WNL 
Dx and txt?
A

ventricular tachycardia
txt:
1. stable mono/polymorphic - 1st line anti-arrythmics or
(only for monomorphic)- synchronized cardiovert
2. unstable monomorphic- synch cardiovert
3. pulseless mono/polymorphic - Defib
(*ACLS cardiac arrest protocol - pulseless VT/VFib )

36
Q

what are the anti-arrythmics we use? what do we use them for?

A

amiodarone, procainaminde, sotalol

- for ventricular tachycardias

37
Q

what type of drug is adenosine?

A

misc drug class- used as anti-arrythmic for PSVT (paroxysmal vent. tachy)

38
Q

what is “high energy unsynchronized shock” also known as

A

Defib

39
Q

monomorphic vs polymorphic ventricular tachycardia

A

monomorphic: QRS complexes w/ SAME morphology in given lead
polymorphic: QRS comples w/ DIFFERENT morphologies in given lead

40
Q

what is polymorphic VT with prolonged QT also known as? txt (stabls vs unstable/pulseless)

A

Torsades de Pointes
stable - IV magnesium
unstable/pulsemless- Defib

41
Q

what 3 electrolyte disturbances can cause torsades?

A

hypoCa+
hypoK+
hypoMg+

42
Q

rhythm strips looks like “chaotic electrical activity w/ no defined waveforms”
Dx and txt

A

ventricular fibrillation
1. “cardiac arrest protocol”: ACLS Defib for VFib/ pulseless VT
if not responding to shock…
2. epinephrine + amiodarone

43
Q

what are the “chronotrophic agents”? what does that mean?

A

epinephrine + dopamine

- change HR

44
Q

Rate <60 bpm
QRS < 0.12
all other aspects WNL
Dx and txt?

A

Dx: Sinus bradycardia
Txt (ONLY IF SYMPTOMATIC)
1. atropine
2. transcutaneous pacing OR epinephrine OR dopamine

45
Q

what kind of drug is atropine ? what is the significance?

A

anti-cholinergic:
AV node richly supplies by SNS
- so anti-cholinergic can help for blocks higher than this but not lower blocks

46
Q

no QRS
may see p-waves or just a flat line
Dx and txt?

A

Dx: asystole
txt: CPR w/ epi

47
Q

organized rhythm OTHER than VT w/out a pulse

dx and txt?

A

Dx: PEA (pulseless electrical activity)
txt: CPR w/ epi

48
Q

what two general things can cause PEA (kinda weeds)

A

hypovolemia or hypoxia

49
Q

QRS < 0.12
PR interval: prolonged
all other things WNL
Dx and txt?

A

Dx: 1st degree heart block

txt: ONLY IF SYMPTOMATIC
acute:
1. atropine
2. transcutaneous pacing OR epinephrine OR dopamine
* same as sinus bradycardia
chronic: pacemaker

50
Q

when would 1st or 2nd, or 3rd degree heart block have a wide complex QRS?

A

if there is a bundle branch block

51
Q

QRS < 0.12
PR interval: progressively prolonged until QRS dropped
rhythm: atrial- regular, ventricle- irregular
Dx and txt?

A

Dx: 2nd degree heart block: mobitz type 1 or wenckebach

txt: ONLY IF SYMPTOMATIC
1. atropine
2. transcutaneous pacing OR epinephrine OR dopamine
* same as sinus bradycardia

52
Q

what 4 things do we txt the same as sinus bradycardia?

A

-acute 1st degree heart block
-2nd degree heart block mobitz type 1/wenckebach
-2nd degree heart block mobitx type 2
(BUT more likely go right to transcutaneous pacing/epi/dopa)
-3rd degree heart block
(BUT more likely need pacemaker)

53
Q

what is transcutaneous pacing?

A 
Transcutaneous Pacing (TCP) is a temporary means of pacing a patient's heart during an emergency and stabilizing the patient until a more permanent means of pacing is achieved. It is accomplished by delivering pulses of electric current through the patient's chest, stimulating the heart to contract
*mostly for bradycardia + heart blocks
54
Q

what can digoxin treat?

A

chronic Afib

also for CHF

55
Q 
QRS< 0.12 
rhythm: atrial- regular, ventricle- regular (but multiple of atrial rate) 
more p-waves than QRS complexes 
all other things normal 
Dx and txt?
A

Dx: 2nd degree heart block mobitz type 2

txt:
1. atropine BUT prepare for…
2. transcutaneous pacing OR epinephrine OR dopamine

(can quickly become 3rd degree HB)

56
Q 
QRS <0.12 
PR: interval varies 
more p waves than QRS 
ventricle rate <60 bpm 
Dx and txt
A

Dx: 3rd degree heart block

txt:
1. atropine
2. transcutaneous pacing OR epinephrine OR dopamine
* same as sinus bradycardia

*usually get pacemaker

57
Q

what is happening in a 3rd degree heart block?

A

no electricity getting from atria to ventricles

- beating independent of each other

Pathophysiology (28 decks)

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