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Adult lll > Dysrhythmia Interpretation > Flashcards

Dysrhythmia Interpretation Flashcards

1
Q

Automaticity

A

creates an electrical impulse

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2
Q

Excitability

A

ability to respond to outside stimulus

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3
Q

Conductivity

A

receives an impulse and conducts it to an adjacent cell

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4
Q

Contractility

A

shortening of fibers in response to impulses

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5
Q

Polarized

A

resting membrane potential (movement of ions across a membrane)

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6
Q

Depolarization

A

Sodium goes in, Potassium goes out

electrical activation of cell caused by influx of sodium into cell while potassium exits

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7
Q

Repolarization

A

Potassium back in, Sodium back out

return of cell to resting state caused by re-entry of potassium into cell while sodium exits

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8
Q

Effective or absolute refractory period

A

Refractory Period

- phase in which cells are incapable of depolarizing

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9
Q

Relative Refractory period

A

phase in which cells require stronger-than-normal stimulus to depolarize

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10
Q

Pacemaker Sites

A

SA node, AV node, Bundle of HIS, Purkinje Fibers

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11
Q

Cardiac Cycle

A

Atrial depolarization (blood drains into ventricles) -> atrial contraction (atrial kick) -> AV node (impulse delayed ventricles fill) -> impulse moves through the common Bundle of HIS (divides into left and right branches) -> purkinje fibers (ventricular contraction)

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12
Q

Electrocardiogram (EKG)

A

looking at electrical activity of the heart viewed as “leads”

picked up by sensors placed on the skin (electrodes)

waves on the ECG correlate with the electrical activity conducted to the atria and ventricles

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13
Q

P wave

A

atrial depolarization

looking at where it leaves the baseline and returns back
want to know if there is a P wave present

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14
Q

QRS Complex

A

should be

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15
Q

T Wave

A

ventricular depolarization

Follows QRS complex and is usually in the same direction; coming back to resting state

*Atrial depolarization also occurs but is not visible on the EKG because it occurs at the same time at QRS

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16
Q

PR Interval

A

0.12 to 0.20 seconds

measured from beginning of P waves to the beginning of the QRS complex

represents time needed for sinus node stimulation, atrial depolarization and conduction through the AV node before ventricular depolarization

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17
Q

ST Segment

A

represents early ventricular depolarization

End of QRS complex to the beginning of the T wave
normally isoelectric

18
Q

QT Interval

A

total time for ventricular depolarization and depolarization

Beginning of the QRS complex to the end of the T wave
varies w/ HR, gender, age and lead

Prolonged: can lead to lethal dysrhythmia Torsades de points

19
Q

Sinus Tachycardia Intervention

A

Assessment; worry about perfusion
Want to address underlying causes: fever, pain, hypoxia, CHF, hypovolemia, dehydration, anxiety, drugs

continue to monitor

20
Q

Six Second Method/Rule of 10

A

number of complete QRS complexes in 6 seconds of strip multiply by 10 and get the heart rate

ex: 9 QRS complex X 10 seconds = 90HR

21
Q

Normal Sinus Rhythm

A 
Rate: 60-100bpm
Rhythm: atrial and ventricular regular
P Waves: uniform, upright, one preceding each QRS
PR Interval: 0.12-0.2 seconds
QRS: 0.10 seconds or less
22
Q

Sinus Tachycardia

A 
Rate: usually 100-160bpm
Rhythm: atrial and ventricular regular
P waves: uniform, upright, one preceding each QRS
PR Interval: 0.12-0.2 seconds
QRS: 0.10 seconds or less
23
Q

Sinus Bradycardia

A 
Rate: less than 60 bpm
Rhythm: atrial and ventricular regular
P waves: uniform, upright, one preceding each QRS
PR interval: 0.12-0.2 seconds
QRS: 0.10 seconds or less
24
Q

Vagal Stimulation

A

bearing down, coughing, sneezing

25
Q

Atrial Dysrhythmias

A

impulse originates from somewhere other than the SA node in the atria
premature atrial depolarization

ex: SVT, AFIB, Aflutter

26
Q

Supraventricular Tachycardia aka SVT

A

varied group of dysrhytmias that originates above the AV node with a heart rate greater than 150

can include: ST, atrial tachycardia (afib/aflutter); AV nodal reentrant tachycardia, AV reentrant tachycardia

27
Q

Atrial Tachycardia

A

an SVT
originates usually from an irritable site in the atria and overrides the SA node
looks similar to ST but P waves differ in shape

going very fast, don’t really know what it is; don’t know underlying rhythm

28
Q

Atrial Tachycardia Interventions

A

assess pt, ABS, oxygen, IV access, vagal maneuvers

Adenosine, calcium channel blockers and beta blockers to slow ventricular rate, consider cardioversion if rhythm is resistant to drugs; cardioversion seldom stops AT’s
ablation

29
Q

Atrial Fibrillation

A

involves several reentry circuits within the atria; the four pulmonary veins that drain into the left atria are a trigger site

Assess, ABS, **Research is finding that staying out of Afib may be an unattainable goal!

30
Q

Rhythm Conversion for Afib

A

convert the afib to sinus with using pharmacological or electrical cardioversion (rhythm control) and anti coagulate if the person has been in Afib for greater than 3days

patient may require long term drug therapy to maintain sinus rhythm (amiodarone, dofetilide, ilbutilide)

31
Q

Rate Control for Afib

A

control the VENTRICULAR response rate using antidysrhythmic drugs and anticoagulation

ex: calcium channel blockers, beta blockers, digoxin

may leave pt in a fib and control ventricular to slow number of impulses that contract the ventricles

32
Q

Atrial flutter intervention and Tx

A

assess pt; ABC

causes: reentry circular pathway

Tx: electrical cardioversion, atrial overdrive pacing, pharmacological cardioverson: ibutilide; radiofrequency catheter ablation

always check BP

33
Q

Premature Ventricular Complexes intervention and tx

A

assess pt, ABC

Assess underlying problem: hypoxia, digitalis toxicity, acid-bace imbalance, MI, electrolyte imbalance, HF, AMI, increased sympathetic tone, stimulants
**Seen with low K

Tx: O2, IV therapy, correct underlying imbalance

34
Q

Ventricular Tachycardia intervention and causes

A

Assess pt and ABCs

Causes: ACS; cardiomyopathy, tricyclic overdose; digoxin toxicity, valvular heart disease, cocaine abuse, MVP, acid-base imbalances, trauma

35
Q

Ventricular Tachycardia Tx

A

pulseless VT: Defibrillate!!!**
Unstable VT w/ a HR of 150 or more: oxygen, IV access, ventricular antiarrhythmics, sedation (if wake and time permits) electrical therapy
stable VT w/ HR less than 150 and a BP: use drugs such as amiodarone, beta blockers, lidocaine, or overdrive pacing

determine cause
pt’s who have had sustained VT are at risk of sudden cardiac death
therapy is aimed at preventing a recurrence

36
Q

Ventricular Fibrillation Intervention and Causes and TX

A

Assess pt and ABCs

Causes: VT is the most common precursor of Vfib!!
increases sympathetic nervous system activity; vagal stimulation; electrolyte imbalance; antiarrhythmics and other meds; electrocution; ACS; HF

Tx: CPR, defibrillation, meds, supportive measures (airway, correct imbalances)

37
Q

Asystole intervention and causes

A

Check second lead; O2, IV, consider pacing, meds, termination

underlying causes: (H&Ts)
H’s: hypovolemia, hypoxia, H+ (acidosis), hypokalemia, hyperkalemia, hypotherma
T’s: toxins, tamponade (cardiac), tension pneumothorax, thrombosis (pulmonary, coronary)

38
Q

Pulseless Electrical Activity causes

A

H and T’s

H’s: hypovolemia, hypoxia, H+ (acidosis), Hypokalemia, hyperkalemia, hypothermia
T’s: toxins, tamponade (cardiac), tension pneumothorax, thrombosis (pulmonary, coronary)

start giving them fluid back if hypovolemia like 18 gauge run them in

39
Q

1st degree AV block

A

assess pt and continue to monitor for increase block

causes: may be normal; ischemia or injury to AV node; rheumatic heart disease; hyperkalemia, AMI; increased vagal tone

40
Q

2nd Degree AVB Type 1 Mobitz Type 1, Wenkebach

A

intervention: assess and continue to monitor for increased block
caused by a conduction delay within the AV node
patients are usually asymptomatic

if symptomatic: give O2, IV, Atropine, transcutaneous pacing

41
Q

2nd Degree AVB Type ll, Mobitz Type ll

A

Intervention: assess and continue to monitor for increased block

caused by a conduction delay lower in the conduction system: bundle of HIS, bundle branches

treatment depends on ventricular response rate; if response is slow prepare for pacing

atropine will increase discharge from SA node but fewer impulses are conducted through the AV node further decreasing the ventricular rate

42
Q

3rd Degree AVB

A

assess and monitor
ventricular response will determine pt presentation

O2, IV, atropine, transcutaneous pacemaker

may require a permanent pacemaker depending on cause of rhythm

Adult lll (9 decks)

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