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ACLS > Bradycardia and Tachycardia > Flashcards

Bradycardia and Tachycardia Flashcards

1
Q

Cornerstones of managing bradycardia?

A
  • Differentiate between signs and symptoms that are caused by the slow rate vs. those that are unrelated
  • Correctly diagnose the presence and type of AV block
  • Use atropine as the drug intervention of first choice
  • Decide when to initiate TCP
  • Decide when to start epinephrine or dopamine to maintain HR and BP
  • Known when to call expert consultation about complicated rhythm interpretation, drugs, or management decisions
  • Know the techniques and cautions for using TCP
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2
Q

Define the types of heart block.

A
  1. First degree - PR > 200ms (5 small squares)
  2. Second degree type I (Wenckebach) - progressive prolongation of the PR interval culminating in a non-conducted P wave - typically produces narrow QRS
  3. Second degree type II - intermittent non-conducted P waves without progressive prolongation of PR interval - typically produces wide QRS
  4. Third degree (complete) - absence of AV conduction - none of the SV impulses are conducted to the ventricles; perfusing rhythm is maintained by a junctional or escape rhythm
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3
Q

Sx concerning for bradycardia?

A

Chest discomfort or pain, SOB, decreased level of consciousness, weakness, fatigue, light-headedness, dizziness, presyncope or syncope

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4
Q

Signs concerning for bradycardia?

A

Hypotension, orthostatic hypotension, diaphoresis, pulmonary congestion on exam or CXR, frank congestive heart failure or PE, and bradycardia-related (escape) frequent premature ventricular complexes or VT

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5
Q

Bradycardia algorithm?

A
  1. Assess appropriateness for clinical condition. HR typically <50/min
  2. Identify and treat underlying cause (maintain patent airway/assist breathing if needed, O2 if hypoxemic, cardiac monitor to identify rhythm, monitor BP and O2, IV access, 12-lead EKG if available, don’t delay therapy)
  3. If persistent bradyarrhythmia causing hypotension, acutely AMS, signs of shock ischemic chest discomfort, or acute heart failure -> atropine
    [Otherwise can monitor and observe]
  4. If atropine is ineffective -> TCP or dopamine infusion or epinephrine infusion
  5. Consider expert consultation TVP
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6
Q

Atropine dosing?

A

First dose - 0.5 mg IV bolus
repeat Q3-5 minutes to a maximum of 3 mg

NOTE - atropine doses <0.5 mg may paradoxically slow the HR further

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7
Q

Dopamine IV infusion dosing?

A

Usual rate is 2-20 mcg/kg/min; titrate to patient response and taper slowly

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8
Q

Epinephrine IV infusion dosing?

A

2-10 mcg/min; titrate to patient response

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9
Q

When should atropine be avoided? What should be done instead?

A

Type II second degree or third degree AV block

Third degree AV block with a new wide QRS complex where the location of the block is likely to be in infranodal tissue such as in the bundle of His or more distal conduction systems

Use cautiously in the presene of ACS or MI (may worsen ischemia/infarct size)

TCP or beta-adrenergic support to prepare for TVP

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10
Q

How does atropine work?

A

Reverses cholinergic-mediated decreases in the HR and AV node conduction

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11
Q

When should TCP be considered?

A
  • Immediately in unstable patients with high-degree heart block when IV access is not available
  • Unstable patients who do not respond to atropine
  • Bradycardia w/symptomatic ventricular escape rhythms
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12
Q

What should be done after initiating pacing?

A

Confirm electrical and mechanical capture. Because HR is a major determinant of myocardial oxygen consumption, set the pacing rate to the lowest effective rate based on clinical assessment and symptom resolution

Reassess the patient for symptom improvement and hemodynamic stability; give analgesics and sedatives for pain control. (Give parenteral benzo for anxiety and muscle contractions, parenteral narcotic for analgesia)

Try to identify and correct the cause of bradycardia

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13
Q

Precautions for TCP?

A
  • Contraindicated in severe hypothermia, not recommended for asystole
  • Conscious patients require analgesia for discomfort unless delay for sedation will cause/contribute to deterioration
  • Do not assess the carotid pulse to confirm mechanical capture; electrical stimulation causes muscular jerking that may mimic the carotid pulse
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14
Q

Steps to perform TCP?

A
  1. Place pacing electrodes on the chest according to package instructions
  2. Turn the pacer on
  3. Set the demand rate to ~60/min (can be adjusted up or down once pacing is established)
  4. Set current milliamperes output 2 mA above the dose at which consistent capture is observed (safety margin)
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15
Q

Place TCP electrodes in anticipation of clinical deterioration in patients with acute MI associated with what rhythms?

A
  1. Symptomatic sinus node dysfunction with severe and symptomatic sinus bradycardia
  2. Asymptomatic Mobitz type II second-degree AV block
  3. Asymptomatic third-degree AV block
  4. Newly acquired left, right, or alternating bundle branch block or bifascicular block in the setting of AMI
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16
Q

Adult tachycardia with a pulse algorithm?

A
  1. Assess appropriateness for clinical condition; HR typically 150+ if tachyarrhythmia
  2. Identify and treat underlying cause (maintain patent airway, assist breathing as necessary, O2 if hypoxemic, cardiac monitor to identify rhythm, monitor BP and oximetry)
  3. Persistent tachyarrhythmia causing hypotension, acutely AMS, signs of shock, ischemic chest discomfort, acute heart failure?
  4. If yes -> synchronized cardioversion (consider sedation; if regular narrow complex, consider adenosine)
  5. If no -> assess QRS.
  6. If wide (0.12+ seconds) -> IV access, 12-lead EKG, consider adenosine if regular and monomorphic; consider antiarrhythmic infusion, consider expert consultation
  7. If not wide -> IV access, 12-lead EKG, vagal maneuvers, adenosine (if regular), beta-blocker or CCB, consider expert consultation
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17
Q

Synchronized cardioversion initial recommended doses?

A

Narrow regular: 50-100 J
Narrow irregular: 120-200 J biphasic or 200 monophasic
Wide regular - 100 J (if no response, increase the dose in a stepwise fashion)
Wide irregular (polymorphic, like torsades) - defibrillation dose, NOT synchronized

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18
Q

Adenosine dose?

A

6 mg rapid IV push over 1 second + NS flush (first dose) + elevate arm immediately
12 mg if required (second dose) if it does not convert within 1-2 minutes

19
Q

Options for antiarrhythmic infusions for stable wide QRS tachcyardia?

A

Procainamide
Amiodarone
Sotalol

20
Q

Procainamide dose?

A

20-50 mg/min IV until arrhythmia suppressed, hypotension ensues, QRS duration increases >50%, or max dose 17 mg/kg given

Maintenance infusion: 1-4 mg/min

Avoid if prolonged QT or CHF

21
Q

Amiodarone dose?

A

First dose: 150 mg IV over 10 minutes
Repeat as needed if VT recurs
Follow by maintenance infusion of 1 mg/min for first 6 hours

22
Q

Sotalol dose?

A 
100 mg (1.5 mg/kg) IV over 5 minutes
Avoid if prolonged QT
23
Q

You may not always be able to distinguish between supraventricular and ventricular rhythms. Mose wide-complex (broad-complex) tachycardias are ___ in origin, especially if the patient has underlying heart disease or is older.

A

Ventricular

24
Q

If the patient has a wide-complex tachycardia and is unstable, assume it is ___ until proven otherwise. The amount of energy required for cardioversion is determined by…

A

VT; morphologic characteristics

25
Q

When to use synchronized shocks?

A

Unstable SVT
Unstable AFib
Unstable AFlutter
Unstable regular monomorphic tachycardia w/pulses

26
Q

When to use unsynchronized shocks?

A

Pulseless
Pre-arrest clinical deterioration (severe shock, polymorphic VT)
Unsure whether monomorphic or polymorphic VT is present in unstable patient

27
Q

Cardioversion is unlikely to be effective for treatment of junctional tachycardia or ectopic or multifocal atrial tachycardia - why?

A

Because these rhythms have an automatic focus arising from cells that are spontaneously depolarizing at a rapid rate; delivery of shock generally cannot stop these rhythms and may actually increase ther ate

28
Q

Steps to perform synchronized cardioversion?

A
  1. Sedate all conscious patients unless unstable or deteriorating rapidly
  2. Turn on the defibrillator
  3. Attach the monitor leads to the patient (white to right, red to ribs, what’s left over to the left shoulder) and ensure proper display of the patient’s rhythm. Position adhesive electrode (conductor pads) on the patient
  4. Press the sync control button to engage the synchronization mode
  5. Look for markers on the R wave indicating sync mode
  6. Adjust monitor gain if necessary until sync markers occur with each R wave
  7. Select the appropriate energy level
  8. Announce to team members - charging defibrillator, stand clear
  9. Press the charge button
  10. Clear the patient when defibrillator is charged
  11. Press shock button
  12. Check the monitor. if tachycarid persists, increase the energy level (joules) according to the electrical cardioversion algo
  13. Activate the sync mode after delivery of each synchronized shock. Most defibrillators default back to unsynchronized mode after delivery to allow for immediate shock if cardioversion produces V
29
Q

Classify tachycardias based on QRS or regularity.

A
  1. Narrow QRS complex (SVT) tachycardias:
    - Sinus tachycardia
    - AFib
    - AFlutter
    - AV nodal reentry
  2. Wide QRS complex tachycardias
    - Monomorphic VT
    - Polymorphic VT
    - SVT w/aberrancy

Regular or irregular

30
Q

What is sinus tachycardia? Compare to reentry SVT.

A

HR >100, generated by sinus node discharge. Does not exceed 220/min, is age-related. Usually does not exceed 120-130/min; has gradual onset and termination, caused by external influences on the heart; regular rhythm

Abrupt onset and termination

31
Q

Why might beta-blockers cause clinical deterioration?

A

If CO falls when a compensatory tachycardia is blocked

32
Q

You may not always be able to distinguish between SV (aberrant) and ventricular wide-complex rhythms. If you are unsure, be aware that most wide-complex (broad-complex) tachycardias are ___ in origin.

A

Ventricular

33
Q

A regular wide-complex tachycardia is presumed to be ___ or ___.

A

VT or SVT w/aberrancy

34
Q

An irregular wide-complex tachycardia may be what?

A

AFib w/aberrancy
Pre-excited AFIb
Polymorphic VT/torsades

Expert consultation

35
Q

Avoid AV nodal blocking agents such as adenosine, CCBs, digoxin, and possibly beta-blockers in patients with ___ - why?

A

Pre-excitation AFib; may cause a paradoxical increase in the ventricular response

36
Q

Considerations for use of adenosine.

A
  • Safe and effective in pregnancy
  • Larger doses may be required if taking theophylline, caffeine, theobromine
  • Initial dose should be reduced to 3 mg if taking dipyridamole or carbamazepine, also if transplanted heart or if administering via central line
  • Avoid in asthma or COPD (can cause bronchospasm)
37
Q

If the rhythm converts w/adenosine, it is probably ___.

A

Re-entry SVT

38
Q

How should recurrence be treated?

A

Adenosine or a longer-acting AV nodal blocking agent such as non-dihydropyridine CCBs (verapamil and diltiazem) or beta-blockers

Obtain expert consultation

39
Q

If the rhythm does not convert w/adenosine, what might the cause be?

A

AFlutter
Ectopic atrial tachycardia
Junctional tachycardia

Expert consultation

40
Q

Key parts of post-ROSC care?

A

Optimize hemodynamic and ventilation status (advanced airway if unconscious, elevate HOB to 30 degrees to reduce incidence of cerebral edema, aspiration, vent-associated pneumonia; titrate O2 to lowest level required to achieve 94-99% O2; frequency assess vitals, monitor for recurrent arrhythmia w/continuous ECG monitoring; if hypotensive, fluid boluses +/- pressors)
Initiate TTM for any patient who is comatose and unresponsive to verbal commands after ROSC
Dx and Rx precipitating cause (EKG, coronary angiography if suspected cardiac etiology of arrest + ST elevation)
Provide immediate coronary reperfusion w/PCI
Provide neuro care and prognostication

41
Q

Post-arrest care algo:

A
  1. ROSC
  2. Optimize ventilation and oxygenation (O2 94+, consider advanced airway/waveform cap, do not hyperventilate - 10 breaths/min, titrate to PETCO2 of 35-40)
  3. Rx hypotension - IV/IO bolus of 1-2 L NS or LR, pressors, treatable causes
  4. 12-lead EKG
  5. If STEMI or high suspicion of AMI -> coronary reperfusion (then eval for TTM)
  6. If no STEMI/high suspicion, evaluate if they can follow commands
  7. If no, TTM, then advanced critical care
42
Q

Pressor doses?

A

Epi IV infusion - 0.1-0.5 mcg/kg per minute
Dop IV infusion - 5-10 mcg/kg/min
NE IV infusion - 0.1-0.5 mcg/kg/min

43
Q

TTM?

A

32-36 C for at least 24 hours

ACLS (6 decks)

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