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NURS 2500 > CLASS 22 - Cardiac Arrhythmias + Exemplars > Flashcards

CLASS 22 - Cardiac Arrhythmias + Exemplars Flashcards

1
Q

What does it mean to be chronotropic ?

A

Affects the heart rate and rhythm by affecting the electrical conduction system of the heart

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2
Q

What does it mean to be inotropic?

A

Changes the force of the heart’s contractions. Can be +ve or -ve inotropes.

Positive inotropes strengthen the force of the heartbeat, negative inotropes weaken the force of the heartbeat.

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3
Q

What initiates the Cardiac Conduction System?

A

The SA node.

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4
Q

Why is the SA node considered to be the pacemaker of the heart?

A

the cells of the SA node spontaneously depolarize FASTER than other cardiac cells and create electrical impulses, therefore setting the normal rhythm and rate of the heart.

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5
Q

once the SA node creates an electrical impulse, where does it travel?

A

travels through atria and reaches the AV node.

then travels to the ventricles by the bundle of His and the Purkinje fibers

synchronized so that all ventricles contract at the same time

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6
Q

what is overdrive suppression?

A

SA node depolarizes first and resets all other cells

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7
Q

what is an ectopic rhythm?

A

occurs if another cardiac cell initates contraction resulting in premature atrial conraction

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8
Q

describe the effects of the SNS and PSNS on the SA Rate

A

SNS: increases SA rate

PSNS: slows SA rate via vagus nerve

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9
Q

what is the only electrical pathway from the atra to the ventricles?

A

AV node

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10
Q

what is the PR interval?

A

AV node conduction

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11
Q

what is a normal sinus rhythm (NSR)?

A

temr used to decribe a normal ECG rate and rhythm generated in the SA node

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12
Q

what are the effects of potassium balances on the ECG?

A

potassium has effects on the myocardium’s resting potential and ability to repolarize

potassium imbalances tend to slow impulse conduction through the AV node and myocytes.

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13
Q

what are the effects of hypokalemia on the ECG?

  • PR
  • ST
  • U
  • QT
A 
prolonged PR
depressed ST
low or inverted T
appearance of U
increased in QT
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14
Q

what are the effects of hyperkalemia on the ECG?

A

diminished or absent P
widening of QRS
peaked T
unexcitable cells

progresses to VT or VF and cardiac arrest

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15
Q

what are ‘U’ waves thought to represent?

A

repolarization of purkinje fibers

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16
Q

compare cardiac arrhythmias and dysrhythmias

A

arrhythmias are alterations in cardiac rhythm, where dysrhythmias imply loss of rhythm

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17
Q

when are cardiac arrhythmias / dysrhythmias harmful?

A

when the interfere with the heart’s pumping ability.

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18
Q

what do cardiac arrhythmias / dysrhythmias indicate ?

A

may indicate alterations in automaticity, excitability, conductivity, or refraction due to ischemia and infarction, electrolyte imbalances, drug effects, or defects in condiction.

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19
Q

what is sinus bradycardia?

where is it often seen?

A

defined as sinus rhythm with a resting rate less than 60 per minute

seen in trained athletes or during sleep, but may occur during myocardial infarction, respiratory depression, hypothyroidism, or drug toxicity.

can also be a compensation for an underlying disorder.

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20
Q

what is sinus tachycardia?

A

sinus rhythm with a resting rate over 100 per minute

seen with exercise or fever, but may occur with CHF, MI, hyperthyroidims, drug toxicity, and hypovolemia

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21
Q

why are sinus tachy - and bradycardia not often treated directly?

A

bc they usually occur secondary or as a compensation for another underlying disorder.

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22
Q

describe increased automaticity as a mechanism of arrhythmias.

A

increase in the natural depolarization rate of nodal cells

occurs commonly in response to SNS activation, can lead to uncontrolled electrical activity

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23
Q

decribe triggered activity as a mechanism of arrhythmias

A

occurs whn ischemia or fibrosis are present, or during heart failure.

following a normal AP, myocytes can sometimes depolarize spontaneously. These are called early or delayed afterpolarizations. (EAD or DAD) commonly causes ectopic or premature beats.

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24
Q

how does re-entrant activation occur?

A

in the presence of a one-way block, the stip of muscle is excited at only one location (instead of 2)

impulses spreading from this area meet no impulses coming from the left, and therefore can trael far enough to simulate branch 1 of the Purkinje fiber . This stimulation passes back up the fiber, past the region of one-way block, and then stimulates branch 2, causing reentrant activation.

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25
Q

what are premature atrial contractions (PAC)?

A

Premature atrial beats that originate within the atria but outside of the sinus node (ectopic beat)

26
Q

what are the potential causes of PACs?

A

stimulants such as tobacco, emotion, or coffee

hypoxia/ischemia, electrolyte imbalances, or other cardiac conditions

27
Q

what are the key ECG features of Premature Atrial Contractions?

A

underlying NSR

P-P interval shortened on premature beat

P-wave may look different

narrow QRS

28
Q

what are the key findings of PAC on assessment?

A

primarily regular pulse

ooccasional early or irregular beat

otherwise asymptomatic

29
Q

what is paroxysmal supraventricular tachycardia (PSVT)?

A

Re-entry at AV node

30
Q

what are the ECG features of PSVT?

A

narrow QRS

P hidden / distorted

rate of 170-250

starts and stops abruptly or “bursts”

31
Q

what are some mechanisms for long-term control of PSVT?

A

Calcium channel blockers

beta blockers

ablation therapy

if unstable: adenosine IV bolus

32
Q

what is atrial flutter?

A

fleeting

re-entry

ischemic

usually resolves or converts to afiv

33
Q

what are the key findings of atrial flutter on assessment?

A

flutter in chest

weak pulse
low BP
sluggish cap refill
cyanosis
pale syncope
low uring output
34
Q

what is an AFIB?

A

multiple uncontrolled re-entry circuits

35
Q

what is a junctional escape beat / rhythm ?

A

sa node failed or is blocked at the AV node

36
Q

what is heart block?

A

conduction block / delay in the AV node or bundle branches

37
Q

what are the potential causes of heart block?

A

ischemia, infarction, increased PSNS tone, fibrosis, inflammation, surgery, drug toxicity, potassium imbalance, aortic valve disease, dilated myopathy

often associated with bradycardia and sometimes palpitations, can be temporary or permanent, may be drug induced from CCBs.

38
Q

What is first degree heart block?

2nd degree?

3rd degree?

A

1st: PR interval delayed
2nd: PR interval delay + dropped QRS
3rd: dissociated P-wave and QRS complex.

39
Q

what should we assess for when looking for heart block?

A

bradycardia, hypotension, if IHD may induce angina

signs and symptoms of low CO

40
Q

how can we treat heart block ?

A

treatment depends on if it is temporary or permanent

treat underlying cause

  • ischemia
  • discontinue SNS / calcium blocking drug
  • add or block PSNS (vagal)stimulation

pacemaker temporarily to keep pt safe while treating for underlying cause, then re-evaluate need for permanent pacemaker

41
Q

what is the typical cause of first-degree AV block ?

A

digitalis (digoxin), iscnemia, increased potassium, beta blockers, ccbs

42
Q

what is the typical cause of type 1 second degree AV block?

A

caused by digoxin, BBs

occurs w myocardial ischemia or infarction, but caused by increased PSNS activity

43
Q

what is the typical cause of type 2 second degree AV block?

A

digitalis toxicity

often deteriorates to third degree Heart Block

44
Q

what is third degree heart block?

A

COMPLETE heart block and AV dissociation

45
Q

identify the 7 cardiac interventions and devices

A

pacemaker

cardiac resynchronization therapy (CRT)

ICD (implantable cardioverter defibrillator)

Cardioversion

Defibrillation

AED Automated External Defibrillator

CPR (cardiopulmonary resuscitation)

46
Q

What is the refractory period?

A

time when the heart is unresponsive to further electrical stimulation.

prolonging the refractory period can terminate an arrhythmia

47
Q

describe the vaughan williams classification of anti-dysrhythmic drugs.

A

CLASS I - Na Channel Blockers

CLASS II - Beta Blockers

CLASS III - K Channel Blockers

CLASS IV - CCBs

CLASS V - other

48
Q

What are the 8 potential side effects of Anti-Arrhythmic drugs?

A

ALL anti-arrhythmics can cause arrhythmias

  • hypersensitivity rxns
  • nausea
  • vomiting
  • diarrhea
  • dizziness
  • blurred vision
  • headache
49
Q

Describe the function of Sodium channel blockers (Class I).

A

Membrane stabilizing drugs

suppress automaticity

further classified as Ia, Ib, and Ic

50
Q

Describe the MOA of Procainamide as a class Ia sodium channel blocker

A

block sodium (FAST) channels

delay repolarization

increased Action Potential Depolarization

Used for atrial fibrillation, premature atrial contractions, premature ventricular contractions, ventricular tachycardia, Wolff-Parkinson-White syndrome

51
Q

Describe the MOA of Lidocaine as a class Ib sodium channel blocker

A

Block sodium channels

accelerate repolarization and minimally decrease APD

Used for ventricular dysrhythmias only

52
Q

provide 3 examples of Beta Blockers (class II)

  • the LOLS
A

atenolol

esmolol

metoprolol

53
Q

what is the MOA of beta blockers?

A

reduce / block SNS stimulation, thus reducing transmission of impulses in the heart’s conduction system

depress phase 4 depolarization

general myocardial depressants for both supraventricular and ventricular dysrhythmias

also used as anti-anginal and anti-hypertensive drugs

prevent or terminate tachyarrhythmias

54
Q

provide an example of class III anti-arrhythmic drugs (potassium channel blockers)

A

Amiodarone

55
Q

what is the MOA of Amiodarone?

A

inhibit K+ channels

prolong repolarization in phase 3

used for dysrhythmias that are difficult to treat, life threatening ventricular tachycardia, PSVT, ATRIAL FIBRILLATION OR FLUTTER

Long term use can lead to “amiodarone lung” - fibrosis

56
Q

provide 2 examples of cardiac calcium channel blockers (class IV)

A

verapamil

diltiazem

57
Q

what is the MOA of cardiac calcium channel blockers ?

A

inhibit slow-channel (calcium-dependent) pathways

decrease rate of spontaneous depolarization, which reduces the rate of pacemaker firing

slows conduction velocity within the AV node, lengthens the AV nodal EFP (effective refractory period)

used for PSVT,

58
Q

describe digoxin as a class IV antidysrhythmic

A

used in AFIB, promoes rate control and increased contractility

last line in HF, has many side effects, impacts K level and is impacted by K level

59
Q

describe adenosine as a class IV antidysrhythmic

A

inhibits AV node activity

used to terminate PSVTs that involve the AV node

used diagnostically to distinguish VT from PVST w aberrant conduction

60
Q

describe magnesium sulfate (IV) as a class IV antidysrhythmic

A

bring serum magnesium to normal levels

membrane stabilizer

reduce likelihood of ventricular arrhythmias

NURS 2500 (22 decks)

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