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VET 415 > 44. CPR > Flashcards

44. CPR Flashcards

1
Q

ROSC

A

return of spontaneous circulation

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2
Q

Does cardiopulmonary arrest under anesthesia have a better survival outcome?

A

yes - often related to a drug reaction that’s reversible, monitoring and other necessary equipment readily available, as well as trained personnel

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3
Q

RECOVER Initiative

A

Reassessment Campaign in Veterinary Resuscitation

  • preparedness and prevention
  • basic life support
  • monitoring
  • advanced life support
  • post-cardiac arrest care
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4
Q

What type of communication works best when doing CPR in a team?

A

closed-loop communication between team leader and individuals

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5
Q

Basic life support

A
  • ABC (airway, breathing, compression/circulation)
  • recognition of arrest (unresponsive, absence of breathing, absence of palpable pulse/heart beat, ignore agonal breaths)
  • rapid!
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6
Q

Airway

A

place or VERIFY tracheal intubation –> 3 steps:

  • intubate airway (laryngoscope, lateral recumbency to allow simultaneous chest compressions)
  • inflate cuff
  • tie in endotracheal tube
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7
Q

What other options are there in the event of a difficult intubation?

A
  • mouth to snout ventilation (out of hospital)

- tight-fitting face mask (in hospital or for exotic species such as rabbit)

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8
Q

Breathing

A
  • ventilation rate 10 breaths/min
  • tidal volume ~10 ml/kg (just enough to see chest rise)
  • short inspiratory time of 1 second
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9
Q

Why do we aim for a short inspiratory time?

A

hemodynamic considerations - positive pressure in the lungs decreases venous return to the heart –> reduces CO

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10
Q

Chest compressions

A
  • 25-30% of normal CO (best-case scenario)
  • optimizing chest compressions is the most important aspect of CPR
  • should be initiated ASAP (airway and ventilation should not delay, i.e. intubate in lateral during chest compressions)
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11
Q

Compression rate

A

100-120 compressions/min

  • dogs and cats regardless of size
  • evidence rates up to 150/min beneficial
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12
Q

Cardiac pump (direct compression)

A
  • mimics normal cardiac function
  • intact valves cause unidirectional flow
  • compressions directly over heart
  • preferable for cats and small dogs < 10 kg
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13
Q

Thoracic pump (chest wall compression)

A
  • heart is passive conduit
  • increased intrathoracic pressure causes blood to move out of thorax
  • collapse of veins
  • compressions on wide part of thorax while staying in front of liver
  • preferable for most medium, large, and giant breed dogs
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14
Q

Circumferential technique

A
  • one-handed technique with hand wrapped around sternum over heart
  • cats and small dogs
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15
Q

Compression depth

A
  • 1/3 to 1/2 width of thorax (linear relationship between depth and MAP)
  • full elastic recoil of chest is key (important for restoration of negative intrathoracic pressure)
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16
Q

What is the proper stance for compressions?

A
  • straight up and down –> less force wasted
  • shoulders directly above with elbows locked
  • bend at hips to generate force
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17
Q

Direct cardiac massage

A
  • open-chest CPR
  • more effective than closed-chest
  • allows for direct visualization if heart starts beating again
  • rare
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18
Q

What are indications for direct cardiac massage?

A
  • already in the abdomen
  • already in the chest
  • ineffective closed-chest CPR
  • giant breed dog
  • pleural, pericardial, or rib cage disease
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19
Q

CPR cycles

A
  • 2 minutes of uninterrupted compressions, then rotate compressors (sooner if fatigued)
  • interruptions limited to 10-15 seconds (ideally 5-6 seconds)
  • ECG analysis during pauses
20
Q

What can we use to monitor efficacy of compressions?

A
  • pulse palpation
  • doppler flow probe
  • capnography (end-tidal CO2)
21
Q

End-tidal CO2

A
  • strong evidence to support routine use
  • sudden increase strong early indicator of ROSC
  • measure of circulation, not ventilation
  • limited data showing prognostic value (higher = better)
22
Q

What end-tidal CO2 values are we aiming for in dogs and cats while doing chest compressions?

A
  • dogs: >15 mm Hg

- cats: >20 mm Hg

23
Q

Can we do CPR in horses?

A

not in adult horses, but sometimes possible in young foals with spongy chests

24
Q

Advanced life support

A
  • drugs
  • ECGs
  • fluids
25
Q

Why vasopressors?

A

death is vasodilating

26
Q

MPP

A

myocardial perfusion pressure

  • prime determinant of ROSC
  • want to use vasopressors to increase aortic diastolic pressure while not driving up right atrial pressure

MPP = ADP - RAP

27
Q

Epinephrine

A
  • used for alpha-1 agonism (vasoconstrictor effects)
  • beta-1 activity may be detrimental
  • low dose for routine use (0.01 mg/kg IV q 3-5 min), every other BLS cycle
  • high dose (0.1 mg/kg) not recommended
28
Q

Vasopressin

A
  • peripheral vasoconstrictor through V1 receptor
  • remains responsive in acidic pH (advantage because death causes metabolic acidosis)
  • no inotropic or chronotropic effects (i.e. wouldn’t increase myocardial workload in the event of ROSC)
  • not inferior to epinephrine –> can be given as an alternative or in combination
  • 0.8 unit/kg IV q 3-5 min
  • single manufacturer –> very expensive –> not routinely used in vet CPR
29
Q

Atropine

A
  • many studies show no benefit, and high doses may be harmful (0.1, 0.2, 0.4 mg/kg)
  • standard dose (0.04 mg/kg IV) given once isn’t detrimental
  • likely helpful with asystole and PEA due to high vagal tone in dogs/cats
30
Q

ECG

A

need to stop compressions to evaluate (no more than 10-15 seconds) –> watching for:

  • asystole
  • ventricular fibrillation
  • PEA (pulseless electrical activity)
31
Q

Asystole

A
  • absent electrical activity

- treat with improved chest compression and epinephrine

32
Q

Ventricular fibrillation

A
  • chaotic uncoordinated electrical activity (course, undefined undulations of baseline)
  • groups of random myocardial cells
  • coordinated mechanical activity not present
  • treat with electrical defibrillation
33
Q

Electrical defibrillation

A
  • simultaneous depolarization of all cells at once –> allows a pacemaker to drive rhythm (hopefully)
  • treatment of choice for pulseless ventricular tachycardia or ventricular fibrillation
34
Q

Guidelines for electrical defibrillation

A
  • continue compressions until charged
  • use copious coupling gel
  • paddles on each side of the heart (if giant breed, can place on same side)
  • end exhalation
  • safety first (no contact with animal, table, equipment, etc.)
  • immediately start a 2-minute compression cycle afterward (don’t sequentially shock multiple times)
35
Q

When should you defibrillate a patient before starting chest compressions?

A

CPA due to ventricular fibrillation of less than 4 minutes duration

36
Q

Precordial thump

A
  • “mechanical” defibrillation
  • minimal evidence of efficacy
  • only recommended if electrical defibrillation unavailable
37
Q

PEA

A

pulseless electrical activity

  • electrical activity within the heart without meaningful contraction (i.e. ECG has some squiggles but BP reading is flat-lined)
  • heart has more energy substrate than in asystole
  • treat with more good-quality chest compressions (improve myocardial oxygen delivery)
38
Q

What are 2 pro’s of fluid therapy during CPR?

A
  • if hypovolemic, will increase aortic pressure > right atrial pressure (remember: MPP = ADP - RAP)
  • death is vasodilating, so some fluids are indicated
39
Q

What is a con of fluid therapy during CPR?

A

if not hypovolemic, will increase right atrial pressure > aortic pressure (remember: MPP = ADP - RAP)

40
Q

Fluid therapy for ER patient

A

1/2 to full shock dose of LRS

41
Q

Fluid therapy for ICU patient

A

only flush behind each drug administered

  • cat - 6 ml
  • small dog - 12 ml
  • large dog - 20-30 ml
42
Q

When to finish?

A
  • underlying disease process
  • effective chest compressions –> ~30+ minutes
  • ineffective chest compressions (i.e. low to no EtCO2) –> ~20 minutes
  • could become a triage situation
43
Q

PCA (post-cardiac arrest) care

A
  • can be very extensive depending on level of injury that occurred during CPA or underlying disease processes
  • CPA leads to MODS (multi-organ dysfunction syndrome), anoxic brain injury, or I-R (ischemia-reperfusion) syndrome
44
Q

Oxygenation considerations

A

hypoxemia and hyperoxemia are bad

  • hypoxemia leads to poor DO2
  • high O2 levels (PaO2 >300 mm Hg) lead to increased ROS
  • worse neurologic outcome
  • titrate SpO2 = 94-98% (normoxemic range)
45
Q

KEY POINTS!

A
  • slow ventilation rates
  • start high-quality chest compressions ASAP
  • full 2-minute cycles of chest compressions (10-15 second interruptions max)
  • change compressors every 2 minutes (sooner if tired!)

VET 415 (4 decks)

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