Transport and Perfusion: Electrical Conduction - ECG (Week 4) Flashcards

1
Q

four terms that describe the heart’s electrical properties?

A

1) Automaticity: Ability to initiate an impulse spontaneously and continuously.
2) Contractility: Ability to respond mechanically to an impulse.
3) Conductivity: Ability to transmit an impulse along a membrane in an orderly manner.
4) Excitability: Ability to be electrically stimulated.

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2
Q

What is Automaticity:

A

Ability to initiate an impulse spontaneously and continuously.

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3
Q

Contractility:

A

Ability to respond mechanically to an impuls

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4
Q

Conductivity:

A

Ability to transmit an impulse along a membrane in an orderly manner.

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5
Q

Excitability:

A

Ability to be electrically stimulated.

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6
Q

What does the autonomic system control in impulse formation?

A

1) The rate of impulse formation.
2) The speed of impulse conduction.
3) The strength of myocardial contraction.

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7
Q

What nerve in the parasympathetic system is responsible for the resting state?

A

The Vagus nerve

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8
Q

The intracellular region of the heart contains Sodium or potassium?

A

Potassium

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9
Q

The outside/ intersitial are of the heart contains Sodium or Potassium?

A

Sodium

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10
Q

What causes depolarization of the heart?

A

Upon stimulation, however, a flood of Na+ cations flow across the semipermeable cardiac cell’s membrane, making it more positive. The change in voltage that occurs with this flood of Na+ ions cause depolarization,

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11
Q

What causes repolarization?

A

Wen sodium comes out of the cell and potassium comes inside the cell. Voltage pumps return to normal

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12
Q

monitor oscilloscope.

A

The device that converts ECG voltage measurements to the visual representation, “rhythm-strips,”

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13
Q

What are artifacts?

A

Momentary disturbances in ECG pattern (pg 45 in Ryan’s notes)

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14
Q

Telemetry monitoring

A

monitoring of a client’s heartrate and rhythm to determine problems such as dysrhythmias, ischemia, or infarction. It can be performed by a telemetry technician or through computerized, automated, devices that are programmed to identify, and alarm to, specific problem-patterns.

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15
Q

Normal sinus rhythm

A

rhythm that originates in the SA node and follows the normal conduction pattern of the cardiac cycle.

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16
Q

isometric line.

A

A flat line extending through an ECG pattern i

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17
Q

isoelectric line.

A

A flat line within the ECG pattern, such as from the bottom of the P-wave to the Q-point

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18
Q

What are the automaticity Rate for the SA Node, AV Node, and the Purkinje Fibres??

A

Automaticity Rates
SA Node: 60-100 bpm
AV Node: 40-60 bpm Purkinje Fibres: 20-40 bpm

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19
Q

ectopic impulse.

A

an impulse that originates from a source outside of the normal cardiac conduction system.

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20
Q

What causes a premature beat?

A

When cardiac tissue damage occurs, i.e. ischemia/necrosis, the damaged tissues do not conduct the nervous impulse as quickly; it serves as a “conduction block.” Because of this delayed conduction, cardiac tissues adjacent to the block, that have already contracted, may repolarize out of their refractory period back to their excitable state.

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21
Q

How do you asses a cardiac ECG Rhythm? (9 steps)

A

1) Evaluate atrial and ventricular rhythms. (Regular or irregular?)
2) Determine the atrial and ventricular rates.
3) Assess the presence and configuration of P waves.
4) Calculate the duration of the PR interval.
5) Calculate the QRS duration.
6) Calculate the QT interval.
7) Assess for ST interval or T wave changes.
8) Interpret the rhythm. (i.e. atrial fib?)
9) Determine the clinical significance. (Is the client stable or unstable?)
10)
Determine course of treatment.

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22
Q

4 noninvasive ways to assess cardiac rhythms?

A

1) Holter monitering.
2) Event recorder monitoring.
3) Exercise treadmill (stress-) testing.
4) Signal averaged ECGs.

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23
Q

Electrophysiology (EPS) testing

A

invasive means of assessing cardiac rhythms, and involves the insertion of multiple catheters to the right side of the heart via the femoral vein. Performing this procedure can cause serious dysrhythmias

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24
Q

Sinus Bradycardia or Absolute Bradycardia

A

when the SA node fires at a rate of less than 60 beats per minutes

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25
Q

relative bradycardia

A

When the client is experiencing a HR that is less than their norm and is causing symptoms, and can be more than 60 bpm

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26
Q

what are the symptoms of bradycardia?

A

pale, cool skin, hypotension, angina, dizziness or syncope, confusion or disorientation, and
shortness of breath.

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27
Q

How do you treat Sinus bradycardia?

A
  • anticholinergic medications.
  • Atropine is used as first-line pharmacotherapy for bradycardia
  • Pacemaker may be require
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28
Q

Sinus Tachycardia

A
  • rate (>100bpm)
  • can be absolute or relative as well.
  • can occurs by either
    (1) parasympathetic (vagus) nerve inhibition or
    (2) sympathetic nervous system excitation.
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29
Q

Symptoms of Sinus Tachycardia

A

dizziness, dyspnea, and hypotension. The increased oxygen demands of the heart may cause angina.

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30
Q

How to treat Sinus Tachycardia

A
  • If the cause is hypovolemia, fluid administration may suffice to correct the HR. If the cause is pain, analgesics can correct the rate.
  • Beta-blockers may be used to slow the HR if the cause is identified as excessive SNS stimulation or consumption of exogenous stimulants (epi/norepi).
  • Adenosine is used to correct tachycardia. It is an antiarrhythmic agent that works like a “chemical defibrillation.” It causes the heart to momentarily “stall-out,” in hopes that, when it re-engages, the rhythm will correct itself.
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31
Q

How does premature atrial contraction occur?

A

Occurs when an ectopic current originates in atrial tissues other than the SA node.

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32
Q

What can cause Premature atrial contractions?

A

from emotional stress, fatigue, or the use of drugs such as caffeine, alcohol, and nicotine. A PAC can also occur from hypoxia, electrolyte imbalances, and disease states such as hyperthyroidism, COPD, and CAD.

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33
Q

Paroxysmal Supraventricular Tachycardia

A

dysrhythmia originating from an ectopic focus between the AV node and the bundle of HIS. It occurs because of electrical re-entry of current into already contracted tissues after the absolute refractory period has passes.

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34
Q

How to diagnose Paroxysmal Supraventricular Tachycardia

A

HR must be 100-300 bpm. On the ECG, the P wave will often be absent as it is masked by the preceding T wave.

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35
Q

Wolff-Parkinson-White syndrome

A

he development of additionally nerve pathways in the heart. It can lead to PSVT.

36
Q

What is a Atrial flutter?

A
  • ectopic current originating in the right atrium.
  • Impulses travel in circular course in atria
  • Has a recurring P wave.
  • the atrial and ventricular rates are regular (consistent)
  • Associated with slower ventricular response.
37
Q

What diseases are associated with a atrial flutter?

A

1) CAD
2) Hypertension
3) Cor Pulmonale
4) Mitral valve disorders 5) Pulmonary embolus

6) Chronic lung disease
7) Cardiomyopathy
8) Hyperthyroidism
9) Use of drugs such as digoxin and epinephrine.

38
Q

How to Treat an atrial Flutter?

A
  • beta-blockers and calcium channelblockers are used.
  • Cardioversion, which is a broad term meaning “return to regular rhythm” is performed using electricity or drugs (adenosine).
  • anti-dysrhythmic medications may be used.
39
Q

What is Cardioversion?

A

broad term meaning “return to regular rhythm” is performed using electricity or drugs (adenosine).

40
Q

What can Atrial flutters cause?

A
-decreased cardiac 
output
-heart failure.
-hypotension
-thrombus formation
41
Q

Atrial Fibrillation

A
  • more chaotic and originates from several atrial points.
  • may occur intermittently or chronically.
  • common dysrhythmia in North America, and affects 0.7% of adults.
42
Q

Atrial fibrillation is associated with what 9 underlying diseases

A

) CAD

2) Cardiomyopathy
3) Hypertension
4) Heart Failure
5) Alcohol
6) Caffeine
7) Stress
8) Electrolyte disturbances 9) Cardiac Surgery.

43
Q

Beats per minute in atrial flutter vs. Atrial fibrillation

A

Atrial Flutter- 250-300 bpm

Atrial Fibrillation 350-600

44
Q

What objective measure classifies rapid ventricular response? (think hr)

A

> 100 bpm

45
Q

What objective measure classifies slow or controlled, ventricular response

A

<100 bpm

46
Q

Junctional Dysrhythmias

A
  • Occurs when the SA node fails and the AV node takes over (40-60bpm).
  • SO It starts in the AV node
47
Q

Junctional Dysrhythmias bpm

A

40-60 bpm.

48
Q

Accelerated Junctional Rhythym

A

61-100 bpm

49
Q

Junctional tachycardia rhythym

A

101-150 bpm

50
Q

How to treat junctional dysrhyhmia

A
  • Digoxin
  • Beta-blockers
  • Calcium Channel Blockers
51
Q

First Degree AV Block

A
  • nerve impulse is not conducted normally through the AV node.
    -still allows conduction to pass through the AV node, but it is delayed.
    -he P-R interval is extended >0.2sec (greater than 1 big box).
    -
52
Q

T/F First Degree AV Blocks show clinical symptoms

A

FALSE

53
Q

Second-Degree AV Blocks, Type 1 AKA “Mobitz I” Blocks

A

increasing lengths of the P-R interval and intermittently absent QRS complexes

54
Q

Second-Degree AV Blocks, Type 1 AKA “Mobitz I” Blocks

TYPE I are d/t what?

A
  • the result of ischemia or infarction.

- well-tolerated by the person and transient;

55
Q

Second-Degree AV Blocks, Type II AKA “Mobitz II” Blocks

A
  • the ventricles will still sometimes fire, which is why the person does not immediately die.
  • usually lead to 3rd degree blocks
56
Q

What can
Second-Degree AV Blocks, Type II AKA “Mobitz II” Blocks
lead to?

A

Result in decreased CO, hypotension, and often an MI.

57
Q

How do you treat Second-Degree AV Blocks?

A

PACEMAKERS!

58
Q

Third Degree AV Block

A
  • AV node completely fails to conduct the P-impulse. The ventricles receive no impulse and only fire because of AV (40-60bpm) or Purkinje (20-40bpm) pacemaker automaticity.
  • Atria Ventricles receive no impulse
59
Q

Third degree AV blocks are associated with:

A

1) CAD
2) Myocarditis
3) Cardiomyopathy
4) Medications such as beta blockers, calcium channel blockers, and digoxin.

60
Q

Premature Ventricular Contractions (PVC)

A
  • originate from ectopic currents originating in the ventricles
  • usually benign except in pre-existing heart disease
61
Q

ventricular bigeminy

A

ventricular contractions will occur on every other beat.

62
Q

PVCs are associated with:

A

1) Use of stimulants (epinephrine, caffeine, nicotin) or digoxin.
2) Electrolyte imbalances.
3) Hypoxia
4) Fever
5) Exercise
6) Emotional stress

63
Q

Ventricular Tachycardia

A
  • when we see 3 or more PVCs in a row
  • Considered life-threatening because of decreased CO and the possibility of deterioration to ventricular tachycardia to ventricular fibrillation (lethal)
64
Q

What is the rate in ventricular tachycardia,

A

150-250bpm maybe

65
Q

T OR F PVC’s can be benign

A

TRUE! usually benign except in pre-existing heart disease

66
Q

Ventricular Fibrillation

A

a severe derangement of the hearts rhythm and is characterized by random ECGs
-Ventricles are constantly quivering

67
Q

What does ventricular fibrillation cause?

A
  • no CO occurs,

- unresponsive and pulseless state. If not treated immediately, the person will die.

68
Q

How to treat ventricular fibrillation

A

-CPR immediately

69
Q

Asystole

A

systole occurs when there is a total absence of ventricular electrical activity. On the ECG, occasional P waves may be seen. The client is pulseless and likely going to die.

70
Q

How to treat asystole

A

CPR and HR-increasing drugs may be administered.

71
Q

Pulseless Electrical Activity

A

patient may have a relatively normal ECG, but the heart is simply not firing.

72
Q

What causes pulseless electrical activity?

A

hypovolemia and hypoxia, MI, tension pneumothorax, hypothermia, drug overdose, metabolic acidosis, hyperkalemia, and pulmonary embolus.

73
Q

Sudden Cardiac Death

AND what is it usually d/t

A

a blanket term referring to death from a cardiac cause. Usually, it is due to ventricular dysrhythmias
such as tachycardia or fibrillation.

74
Q

Prodysrhythmia

A

the use of anti-dysrhythmic medications can cause other types of dysrhythmia.

75
Q

P Wave

A

Atrial Depolarizaton (contraction); begins with firing of the SA node

76
Q

PR Interval

and normal range

A

represents travel from SA to AV to His-Purkinje, just before ventricle contraction0.12-0.20 sec

77
Q

QRS Complex

and normal range

A

ventricular depolarization (contraction) and atrial repolarization 0.06 –0.10 sec

78
Q

T wave

A

ventricular repolarization, tall and peaked, ?high K

79
Q

On an electrocardiogram what does the vertical line indicate vs. the horizontal line

A

Vertical is voltage and horizontal is time line

80
Q

Clinical associations with Sinus Tachycardia

A
Associated with physiological stressors
•Exercise 
•Fever
•Hypotension 
•Hypovolemia, anemia •Myocardial ischemia
•Hypoxia, hypoglycemia 
•HF
•Anxiety &amp; fear
•Meds such as epi, atropine, caffeine, OTC cold remedies with pseudoephedrin
81
Q

Clinical associations with Sinus Bradycardia

A
  • Occurs in response to•Carotid sinus massage (by MD only)
  • Hypothermia
  • Increased vagal tone
  • Administration of parasympathomimeticdrugsClinical Association
  • Occurs in disease states •Hypothyroidism
  • Increased intracranial pressure
  • Obstructive jaundice
  • Inferior wall M
82
Q

How to treat atrial fibrillation?

A

Primary goal is to slow ventricular response by increasing AV block
•Emergent electrical cardioversion
•Diltiazem, digoxin, and -adrenergic blockers used to control ventricular rate
•Anti-arrhythmic drugs used to convert atrial flutter to sinus rhythm or maintain sinus rhythm
•Radio frequency catheter ablation used as curative therapy

83
Q

Premature Ventricular Contractions (PVC) can lead to?

A

PVCs may reduce CO and precipitate angina and heart failure

84
Q

Cardioversion

Indications:

A

Is used for symptomatic dysrhythmias on an emergent basis (eg. patients with decreased LOC, hypotension, chest pain, signs of decreased cardiac output
-an emergent or non-emergent basi

85
Q

Defibrillation

A

-Most effective method of terminating ventricular fibrillation
•Ideally performed within 15-20 seconds of onset of arrhythmia but CPR will teach after 5 cycles (2 minutes) of CPR prior to AED use
•Passage of direct current electrical shock through heart to depolarize cells
•Intent is to allow SA node to resume ro

86
Q

Implantable Cardioverter-Defibrillator

A
  • Defibrillator
  • Implanted subcutaneously usually over pt’s non dom side
  • Indicated: with dysrhytmias
87
Q

Pace maker

A

Electronic device used to pace heart when normal conduction is damaged