Test 2: 28 ekg Flashcards

1
Q

how to get HR on 25 mm paper

A

(count RR interval over 30 boxes) x 10

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2
Q

what is HR- 25 mm/sec paper

A

30 boxes= 6 sec

17 QRS x 10= 170 bpm

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3
Q

anticholinergics will do what to HR

A

increase

used to treat hypotension

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4
Q

how to manage arrhythmia under anesthesia

A

identify

determine significance- impact on CO and potential for progression

continue to monitor or treat is needed- correct underlying cause if possible, administer anti-arrhythmics if needed

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5
Q
A

sinus arrhythmia

  • Normal variation of sinus rhythm → Related to changes in vagal tone associated with respiration
  • Common in dogs
  • Regularly irregular- varying R-R interval
  • No need to treat unless significant bradycardia
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6
Q
A

wandering pacemaker

  • Rate: low-normal
  • P for every QRS, QRS for every P
  • P wave morphology changes → Origin of sinus focus changes
  • Typically due to increased vagal ton
  • no need to treat unless significant
    bradycardia
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7
Q

what can cause sinus bradycardia

A

hypothermia
Drugs (opioids, alpha-2 agonists, deep inhalant anesthesia)
increased vagal tone
* Manipulation of eye (oculcardiac reflex), larynx/trachea, abdominal viscera

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8
Q

treat sinus brady?

A

Treat if hypotensive or excessively low impacting CO

  • Address underlying cause
  • Reverse alpha-2 agonist if hypertensive phase
  • Administer anti-cholinergic (atropine or glycopyrrolate)
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9
Q

how do anticholinergics work

A

Competitively antagonize the effects (parasympatholytic) of Ach at cholinergic postganglionic sites (muscarinic receptors)

work on cardiac M2 receptors to increase HR and increase BP

atropine, glycopyyrolate

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10
Q

what are two anticholinergics used during anesthesia

A

Atropine: faster onset, shorter acting- 1st choice for emergencies

Glycopyrrolate: slower onset, longer acting, doesn’t cross BBB or placenta

used to treat hypotension and slow HR

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11
Q
A

sinus arrest

  • Low heart rate,Irregular rhythm
  • Origin: Sinus node fails to depolarize→ pause
  • Prolonged sinus node arrest→ escape beat
  • atrial, AV junction or ventricular
  • Due to increased vagal tone
  • If prolonged or recurrent→↓CO,
  • treat: atropine, glycopyrrolate
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12
Q

how to treat

A

sinus arrest

  • If prolonged or recurrent→↓CO,
  • treat: atropine, glycopyrrolate
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13
Q

what are some causes of sinus tach

A

increased sympathetic tone

Causes:
* Pain
* Stress
* Hypovolemia
* Hyperthermia
* drugs (anticholinergics, beta-agonists)

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14
Q
A

APC

  • Normal heart rate (species/breed/age), Irregular Rhythm
  • APC(arrow)arrives early
  • Origin: ectopic atrial site
  • P wave different configuration but normal QRS configuration
  • normal P waves and QRS complexes are related
  • Common in anesthetized horses
  • No treatment required typically
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15
Q

treat?

A

APC

no treatment required typically

common in anesthetized horses

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16
Q

what?

A

supraventricular tachycardia

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17
Q

causes

A

Supraventricular Tachycardia
* High heart rate, regular rhythm, P may be lost in T wave
* Tachyarrhythmia that arises from atrial or atrioventricular (AV) nodal or
junctional tissue
* Potential Causes: primary cardiac disease, severe systemic disease, anesthetic drugs
* Treat underlying cause, beta- blockers, diltiazem, can try vagal maneuver

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18
Q

how to treat

A

supraventricular tachycardia

Treat underlying cause, beta- blockers, diltiazem, can try vagal maneuver

19
Q

what

A

Afib

  • Heart rate normal to high, Irregularly irregular rhythm with varying R – R intervals
  • Random, disorganized depolarization of atria with no coordinated atrial contraction
  • No normal P waves,“f”(fibrillation) waves, QRS morphology is normal
  • Ventricular rate will be normal to increased
20
Q

causes

A

Afib

  • Can be pre-existing or develop during anesthesia
  • Due to large atria +/- changes in vagal tone
    • Horses can be isolated
    • Cows can be related to GI disease
    • Canine typically due to heart disease → atrial dilation
21
Q

how to treat Afib

A

If pre-existing treat prior to anesthesia when possible

If develops during anesthesia treatment depends on hemodynamic consequences

  • Treat underlying cause when applicable
  • Can try lidocaine
  • Electrocardioversion
  • Rate control
22
Q
A

1st degree AV block

PR interval longer due to conduction delay through AV node

23
Q

treat 1st degree AV block?

A

prolonged PR intervals from conduction delay through AV node

May be due to ↑vagal tone or anesthetic drugs

  • No adverse hemodynamic effects, no treatment required
24
Q
A

2nd degree AV block- Mobitz 1

dropped beat- P wave not followed by QRS
P-R interval becomes progressively prolonged

normal in athletic horses with high vagal tone
common after use of ⍺2 agonist in the horse or dog

25
Q

what does 2nd degree AV block Mobitz 1 look like

A
  • P-R interval becomes progressively prolonged
  • Eventually results in complete block and a lack of QRS complex (“dropped beat”)
26
Q

what does 2nd degree AV block, mobitz type II look like

A

Consistent P-R interval with occasional complete conduction block (dropped beat)

27
Q

treat 2nd degree AV block?

A
  • Only required if causing↓ BP/MAP or CO
  • Reduce inhalants / anesthetic drugs
  • Anticholinergics
  • Reversal agents (caused by ⍺2 agonist)
  • Chronotropic agents
28
Q

what

A

3rd degree AV block- atria and ventricles are contracting independent of each other

Complete failure of conduction between atria and ventricles
* normal P waves
* Ventricular escape rhythm is slow and regular, QRS configuration
depends upon location of ectopic pacemaker
* P waves and QRS complexes are dissociated

Slow ventricular rate causes marked reduction in cardiac output

29
Q

how to treat

A

3rd degree AV block: atria and ventricles contracting at different rates

Treatment:
* pacemaker is the definitive treatment
* Dobutamine (β agonist), Isoproteronol can be attempted → try to increase ventricle contraction

30
Q

what

A

VPC

wide and bizzare QRS
early beat with no P wave

31
Q

causes

A

VPC

Potential Causes: Myocarditis, hypoxemia, electrolyte and acid-base
abnormalities, disease states (GDV, equine colic), and some drugs
(barbiturates)
* Can be catecholamine induced
* May have pulse deficits

32
Q

treat?

A

VPC- wide and bizzare

May have pulse deficits
* Treat with lidocaine if progressive or multiform

33
Q

what

A

AV dissociation
often called accelerated idioventricular rhythm (AIVR)

Atria and ventricles depolarize independently
* P waves and QRS complexes are not
associated
* Regular rhythm; atrial rate is normal/slow; ventricular increased compared to the normal ventricular escape rate

34
Q

causes

A

AV dissociation- P and QRS independent of eachother but ventricular pace is faster then 3rd degree AV block

often called accelerated idioventricular
rhythm (AIVR)

Associated with GI disease (dog, horse), anesthesia (cats)

35
Q

how to treat

A

Associated with GI disease (dog, horse), anesthesia (cats)
* Treat underlying disease
* Increase sinus rate if slow and causing hemodynamic effects (cats usually)

AV dissociation- P and QRS independent of eachother but ventricular pace is faster then 3rd degree AV block

often called accelerated idioventricular
rhythm (AIVR)

slower then Vtach

36
Q

what

A

V tach

> 4 VPCs in a row, fast rate, no p-waves, wide QRS

Can progress to ventricular fibrillation

37
Q

how to treat

A

Vtach

Can progress to ventricular fibrillation

Treat with lidocaine or amiodarone

May require electrical conversion if pulseless

38
Q

what

A

V fib

No discernable complexes, random depolarization of ventricle with no contractions

39
Q

treat?

A

V fib

Defibrillation is treatment of
choice
* Amiodarone +/- Mg (torsades) can be
attempted in addition if not responsive to defibrillation
* Can try precordial thump if no defibrillator available

40
Q

what happens with pulseless electrical activity

A

EKG looks weird normal

no pulseox
CO2 drops on capnograph
no pulse on doppler or A line or by palpation

Need CPR
* start compressions and ventilation
* Administer Epinephrine
* Treat underlying cause of arrest

41
Q

how to treat

A

asystole

CPR
* Chest compressions & ventilation
* Epinephrine
* Correct underlying cause if possible

42
Q

what can happen to EKG with hyperkalemia

A
  • tall T wave
  • Shortened QT interval
  • Prolonged PR interval & Widened QRS
  • Decreased amplitude & Widened P wave
  • Absence of P waves & Bradycardia with sinoventricular rhythm
  • Sine Wave, Ventricular Fibrillation, Ventricular Asystole
43
Q

how to treat hyperkalemia

A

Direct antagonism of the membrane actions
* Administration of calcium

Increased K entry into cells
* Glucose and insulin
* Sodium bicarbonate
* Beta-2 Agonists

Promote excretion or removal of potassium
* Diuresis, diuretics
* Dialysis