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High Acuity > Electrical System of Heart > Flashcards

Electrical System of Heart Flashcards

1
Q

1st Type of Heart Cell and 4 Properties

A

Electrical/Pacemaker
Automaticity: property of cardiac cells to generate spontaneous action potentials; initiation

Excitability: the ability of a cardiac cell to generate an action potential at its membrane in response to depolarization and to transmit an impulse along the membrane.

Refractoriness: cannot fire another action potential even if a stimulus is received.

Conductivity: electrical signals travel through your heart. These signals cause different parts of your heart to expand and contract; transmission

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2
Q

2nd type of heart cell and 2 properties

A

Mechanical

  1. Contractibility: the ability of the cell to shorten/lengthen fibres
  2. Extensibility: the ability of the cell to stretch
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3
Q

Explain the hearts normal conduction pathway

A
  1. SA Node generates impulse and spreads from cell to cell from right to left atria
  2. Bachmann’s bundle: electrical connection between right and left atria
  3. 3 Internodal pathways transmit impulse from SA to AV node
  4. AV node slows impulse to allow for delay between atrial and ventricular contraction
  5. Bundle of his leaves AV and splits into purkinje fibres to supply rest of cardiac muscle
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4
Q

Intrinsic rates of SA, AV, and Purkinje Fibres

A

SA Node 60 – 100

AV Junction 40 – 60

Purkinje Fibres 20 – 40

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5
Q

What electrolytes are responsible for the electrophysiology of the heart?

A

Calcium, Magnesium, Potassium, Sodium

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6
Q

What is seen on the ECG of a patient with hypocalcemia or hypomagnesemia

A

Prolonged QT Interval

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7
Q

Phase 4, Phase 0, Phase, 1, Phase 2, and Phase 3 of Electrophysiology of the heart

A

Phase 4: resting, net negative

Phase 0: rapid depolarization - sodium influx and calcium channels open

Phase 1: fully depolarized - net positive

Phase 2: plateau - calcium entry and potassium diffussion slows

Phase 3: repolarization - calcium channels close and sodium is pumped out

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8
Q

Each small box on an ECG is

A

0.04 seconds

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9
Q

Each big box on an ECG is

A

0.2 seconds

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10
Q

Vertical and horizontal meanings of ECG

A

vertical: amount of depolarization

horizontal: time

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11
Q

P Wave normal length

A

0.08-0.11 seconds (2-3 boxes)

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12
Q

PR interval normal length

A

0.12-0.2 seconds (3-5 boxes)

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13
Q

QRS normal length

A

< 0.12 seconds

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14
Q

Normal ST segment

A

On isoelectric line

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15
Q

Normal T Wave

A

should begin in the same direction as the QRS

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16
Q

Normal QT interval

A

we use QTc (QT corrected interval because it is closely related to HR)
* Normal <0.41 seconds

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17
Q

P Wave represents

A

atrial depolarization and diastole - followed by atrial systole

0.08-0.11

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18
Q

PR Segment Represents

A

time that it takes for impulse to travel from atria to ventricle; period of delay

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19
Q

PR Interval represents

A

Inclusion of both the PR Segment (contraction + impulse travel time) and P Wave (atrial depolarization)

Total time depolarizing atria

0.12-0.2

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20
Q

QRS Complex represents

A

Ventricular depolarization + diastole followed by ventricular systole

< 0.12

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21
Q

J Point Represents

A

Junction of QRS Complex (ventricular depolarization) ends and ST segment (ventricular repolarization) begins

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22
Q

ST Segment Represents

A

early ventricular repolarization + ventricular contraction

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22
Q

T wave represents

A

ventricular repolarization + ventricular contraction ends (at end of T wave)

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23
Q

U Wave represents

A

late ventricular repolarization

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24
Q

QT Interval represents

A

Total time for ventricular depolarization and repolarization; dependent on HR. Interval increases with decreased HR, decreases with increased HR.

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25
Q

9 Step Method of ECG Analysis

A

Left to right:
P wave
- present?
- regular?
- P-P rate?
- PR interval?
QRS
- regular?
- R-R rate?
- Complex length?
Repolarization
- QTc Interval (refraction)
- ST Segment (ischemia/electrolyte changes)

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26
Q

If no P wave is present:

A

SA/AV not stimulating QRS or P wave hidden in other electric activity

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27
Q

You need to see a P wave to know

A

SA stimulated AV

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28
Q

Method to determine rate on ECG

A

1500 / no. of small boxes between each R wave

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29
Q

How do you calculate QRS Complex?

A

Normal < 0.12 (3 boxes)

of small boxes x 0.04 seconds

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30
Q

What does the QT Interval represent

A

The refractory period; beginning of Q to end of T

Cells are busy

Normal < 450 ms

31
Q

ST Segment and T Wave Changes are associated with

A
  • Myocardial ischemia/injury/infarction
  • Electrolyte changes
32
Q

How does hypokalemia change ECG?

A

T wave inversion, ST depression, Prominent U Wave

33
Q

How does hyperkalemia change ECG?

A

Peaked T wave, P wave flattening, PR prolongation, Wide QRS complex

34
Q

How do you put all the information gathered together to interpret the rhythm?

A
  1. specify site of origin (sinus, atrial, ventricular)
  2. specify rate and bpm (ex sinus brady 38bpm)
  3. evaluate patient presentation (asymptomatic v symptomatic)
35
Q

Characteristics of SInus Rhythm

A
  • atrial/ventricular rate 60-100
  • rhythm: regular
  • P waves present, upright
  • 1P wave: 1 QRS
  • PR interval 0.12-2second
  • QRS < 0.12s
36
Q

Characteristics of Sinus Arrhythmia

A

Variation in rate regularity, otherwise normal

37
Q

Cause of sinus arrhythmia

A

changes in intrathoracic pressure during breathing

Common in athletes, children, can be normal

38
Q

Characteristics of Sinus Bradycardia

A
  • Rate < 60 beats per minute
  • Rhythm regular
  • 1:1 ratio
  • 1 P wave: 1 QRS complex
  • 1 Atrial complex: 1 Ventricular Complex
  • Originates in the SA Node
  • Causes: pathological, injury, medication, vagal stimulation
39
Q

Treatment of sinus bradycardia

A
  • Need to look at patient to determine if treatment is necessary
  • 0 signs of decreased CO = stable = determine cause (medications/beta blockers, hypothyroidism)
  • Signs of decreased CO = unstable = atropine to increase HR, acute transcutaneous pacemaker because SA node too slow; acts as SA node
40
Q

Characteristics of Sinus Tachycardia

A
  • Rate > 100 beats /minute (<180)
  • Rhythm regular
  • 1:1 ratio
  • 1 P wave:1 QRS
  • 1 Atrial Complex: 1 Ventricular Complex
  • Originates in the SA Node
41
Q

Treatment of Sinus Tachycardia

A

dependent on symptomatic (decreased CO)
* Always response of sympathetic stimulation – FIRST COMPENSATORY MECHANISM – always sign of another problem - (pain, fever, anxiety) therefore treat cause (antianalgesics, antipyretics, antianxiety); as well as beta blockers.
* Stimulation of vagal nerve; bear down like going to bathroom, increase intrathoracic pressure (blowing through straw)

42
Q

Description of Premature Atrial Contraction

A

Ectopic focus of atrial tissue fires an impulse before next SA node impulse is due

Normal QRS because random impulse made it to AV

43
Q

Causes + treatment of premature atrial contraction

A

stress, fatigue, anxiety, inflammation, infection, caffeine, nicotine, alcohol, certain drugs; usually benign.
Treatment is of cause.

44
Q

Characteristics of atrial flutter

A

Rate – ventricular rate regular or irregular
Saw-toothed/flutter waves
Ratio of P Waves:Ventricular Response – 2:1 or 3:1
SA re-entry circuit

45
Q

Treatment of atrial flutter

A
  • Medications: CCB or BB to slow SA node and hopefully reset (not likely – will ultimately need..)
  • Cardioversion: electrical stimulus to stop all activity and stop re-entry circuit
46
Q

Characteristics Atrial fibrillation

A
  • Rate – difficult to calculate – watch ventricular response
  • Rhythm – irregular
  • Ratio – Multiple p waves: irregular ventricular response
47
Q

What dysrhythmia has potential for clots and why?

A

Potential for clots (irreg rhythm) and HF = venous stasis

Atria contract very rapidly, unable to empty, discharging >400bpm

Unable to refill atrial chambers before contraction; Frank Starling Law

48
Q

Treatment of atrial fibrillation

A

anticoagulants, beta-blockers, calcium channels blockers, amiodarone, digoxin

cardioversion: halting of electrical activity

49
Q

Characteristics of supraventricular tachycardia

A
  • Rate 150-250
  • Regular rhythm – originates in or above AV node; somewhere in atria stimulated. AV re-entry circuit
  • Undistinguishable p waves
  • Normal QRS complex
50
Q

Treatment of SVT

A

Unstable: adenosine to stop all electrical activity (cardioversion in medication form – then SA node should begin to fire again)

51
Q

How do you determine difference between sinus tachy and SVT

A

Presence of P waves (not in SVT)

52
Q

What 4 things can cause ventricular rhythms?

A
  • SA node fails
  • Impulse from SA is blocked
  • Rate of SA is slower than ventricle
  • If there is an irritable site in the ventricle
53
Q

Rate associated with ventricular rhythms

A

20-40bpm

54
Q

What is PVC?

A
  • Result of increased irritability of ventricular cells. Firing prior to stimulation from SA or AV
  • Was not stimulated SA/AV therefore no visible P wave
55
Q

Characteristics of PVC

A

WIDE QRS WITH NO P

Early ventricular (QRS) complexes followed by compensatory pause

R-T phenomenon - Depolarization occurring before repolarization has fully occurred

56
Q

Possible patterns of PVC

A

Couplet/Triplet: 2 or 3 in a row

Bigeminy/Trigeminy: every second QRS is PVC or every third QRS is PVC

Unifocal: look the same
Multifocal: look different

57
Q

Characteristics of VTach

A

3 or more consecutive PVCs occurring at a rapid rate

Rate: 100-200 bpm – up to 300

No p-waves (dissociated atrial rate)

May or may not have pulse

Sustained v not

> 0.12s

58
Q

Treatment of sustained v not sustained v tach

A

o Stable: short spurts/non-sustained: IV amiodarone/antiarrhythmic/cardioversion
o Unstable (usually quick deterioration): as soon as loose pulse – start CPR, defibrillation and IV Epinephrine (treated same as in VFib)

59
Q

Description of VFib

A
  • Electrical chaos in ventricles
  • Chaotic multifocal firing of ectopic origin in ventricles
  • Life-threatening; faster decompensation than VTach
  • Coarse vs fine
60
Q

Treatment of VFib

A
  • CPR, defibrillation, IV Epinephrine
61
Q

Asystole description

A
  • Cardiac standstill
  • Complete cessation of electrical impulses (atrial & ventricular)
  • If atrial activity present, called “ventricular standstill”
  • No rate, rhythm, CO, or pulse
  • Ventricular fibrillation can mimic asystole
  • Terminal rhythm; if CPR, defib, and epi did not work
62
Q

What is PEA

A

Any organized rhythm present on ECG without ability to palpate central pulse

63
Q

Explain treatment of symptomatic bradycardia

A

< 60BPM with S+S
1. Identify and treat underlying cause
- airway, oxygen, cardiac monitor, IV, 12 lead
2. Persistent and symptomatic?
- atropine, dopamine, epinephrine
- consider trancutaneous pacing

64
Q

Explain treatment of symptomatic tachycardia

A

<150
1. Identify and treat underlying cause
- airway, oxygen, cardiac monitor, IV, 12 lead
2. Persistent and symptomatic?
No: Wide QRS? > No: vagal stim, adenosine, CCB, BB.
Yes: cardioversion, adenosine

65
Q

Function of adenosine, amiodarone and atropine

A

Adenosine: stops heart
Atropine: speeds heart
Amiodorane: AFib

66
Q

Causes of lethal arrhythmias

A

Hypoxia
Hypothermia
Hydrogen ions (Acidosis)
Hypovolemia
Hyper/hypokalemia

Toxins
Tamponade
Trauma
Thrombosis
Tension Pneumo

67
Q

Explain cardiac arrest algorithm for VF/pVT

A
  1. help
  2. CPR
  3. IV/BVM
  4. search for and treat causes (Hs and Ts)
  5. Assess rhythm - if vF/pVT SHOCK
  6. 2 min CPR
  7. Assess rhythm - if vF/pVT SHOCK
  8. 2 min CPR + Epi q3-5min
  9. Assess rhythm - if vF/pVT shock
  10. 2 min CPR - amiodorane or lidocaine
68
Q

Explain cardiac arrest algorithm for asystole/PEA

A
  1. Epinephrine ASAP
  2. CRP q2min epi q3-5min
  3. Assess rhythm - if shockable move to that algorithm, if not CPR, treat reversible cause
  4. determine appropriateness of resuscitation
69
Q

Unstable Angina Description, ECG and Trops

A

Plaque rupture, thrombus formation around plaque causing partial occlusion of vessel, anginal pain at rest

ECG can be normal, inverted T waves, ST depression

Normal troponin

70
Q

NSTEMI description, ECG and troponin

A

Plaque rupture, partial occlusion resulting in injury and infarct

ECG can be normal inverted T waves, ST depression

Elevated troponin

71
Q

STEMI description, ECG and troponin

A

Complete occlusion, resulting in injury and infarct

ECG ST elevation

Elevated troponin

72
Q

ST elevation in V3-V4 shows infarct in

A

LAD, anterior position

73
Q

ST elevation in V5, V6, I, of avL shows infarct in

A

left circumflex (LAD or RCA) lateral position

74
Q

ST elevation in leads II, III, or aVF shows infarct in

A

RCA, inferior position

75
Q

ST elevation in leads V7-V9 show infarct in

A

RCA, circumflex, posterior position

76
Q

ST elevation in V1 or V2 show infarct in

A

LAD, septal position

High Acuity (20 decks)

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