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Boards: Other Topics (Endocrine, CPR, Euthanasia, etc) > CPR > Flashcards

CPR Flashcards

1
Q

What are the three most common anesthetic complications?

A

hypoventilation (63%), hypothermia (53%), hypotension (38%)

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2
Q

Hemorrhage

A

Acute: hypovolemia, decreased d blood oxygen carrying capacity

Detectable at 10-20%, life-threatening circulatory failure if 30-40%

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3
Q

Clinical Signs of Hemorrhage

A

tachycardia, decreased pulse pressure/area under pulse arterial waveform, peripheral VC/pale MM

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4
Q

Treatment of Hemorrhage

A

Crystalloids 3x volume shed blood DT rapid extravasation of fluid
 Dilution will occur: further dilute HCT, concentration of clotting factors/platelets, decreased oxygen carrying capacity, although improved CO

Likely will need blood +/- components

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5
Q

Most common arrhythmias seen in canine patients under GA?

A

o VPCs warrant treatment if: R on T, multifocal, >180bpm, perfusion

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6
Q

Traumatic Myocarditis

A
  • Patient with traumatic myocarditis (trauma, HBC), arrhythmias, myocardial dysfunction peak ~ 24-48 hrs
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7
Q

RECOVER

A

Reassessment Campaign on Veterinary Resuscitation

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8
Q

Outcomes associated with CPR

A

100 patients undergo CPR: regardless of why experienced CPA, should get ROSC rate ~45%
 Cats generally 42-44%, dogs 28-35%

Once CPA occurs, will lose 50% of patients  best to prevent CPA

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9
Q

Survival to Discharge: Cause of CPA Matters

A

Perianesthetic 40-45% will survive to go home

ICU ~5-7%
o 20-90% of patients achieve ROSC in will die in PCA period

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10
Q

Risks Assoc with CPR

A

 Rib fx – 1.6%
 Muscle damage – 1.4%
 Chest pain – 11.7%

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11
Q

Circulation Detection

A

Dorsal pedal palpable if MAP >60mm Hg

Apex beat: 4-6th ICS, lower 1/3 chest or elbow caudal to level of costochondral junction

Pulses should be palpated even if heart beat ausculted: apneic patients with inadequate contractility to generate blood flow sufficient to produce palpable pulses may still require chest compressions

No longer recommended to check pulses in apneic patients

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12
Q

DDX absence of pulses

A

o Severe shock
o Marked decreased contractility
o Pericardial effusion with tamponade
o Severe pleural space dz

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13
Q

Most Important Step when CPA Identified?

A

START BLS!!

preserve organ function
 Promote circulation of RBCs  oxygen delivery to tissues
 Within 10’ of CPA, irreversible ischemic damage to tissues, decreases likelihood of successful ROSC

ALS techniques only applied once BLS perforated

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14
Q

At-Risk Patients for CPA

A

o 5 Hs: hypovolemia, hypoxia, hydrogen ions, hyperkalemia, hypoglycemia

o 5 Ts: toxins, tension pneumothorax, thromboembolism, tamponade, trauma

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15
Q

Main Cause of Canine, Feline CPA?

A

primary respiratory arrest more common with secondary cardiac arrest DT hypoxemia that develops from lack of ventilation

Horses: primary cardiac arrest

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16
Q

What are the most common arrest arrhythmias?

A

Pulseless electrical activity
Asystole

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17
Q

Doses of Emergency Drugs: epinephrine

A

High dose 0.1
Low dose 0.01mg/kg

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18
Q

Doses of emergency drugs: vasopressin

A

0.8U/kg

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19
Q

Doses of Emergency Drugs: Atropine

A

0.04-0.05mg/kg

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20
Q

Doses of Emergency Drugs: Amiodarone

A

5mg/kg

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21
Q

Doses of Emergency Drugs: Reversal Agents

A

Naloxone 10-40mcg/kg
Flumazenil 0.01mg/kg
Atipamezole 50mcg/kg

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22
Q

Defibrillation: monophasic, external

A

2-10J/kg

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23
Q

Defibrillation: monophasic, internal

A

0.2-1J/kg

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24
Q

Defibrillation: biphasic, external

A

2-4J/kg

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25
Q

Defibrillation: biphasic, internal

A

0.2-0.4J/kg

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26
Q

Components of BLS

A

Chest compressions
Ventilation

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27
Q

Components of ALS

A

–Monitoring
–Vascular Access
–Reversals
–Evaluation of ECG once monitoring

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28
Q

VF/Pulseless VT Algorithm

A

Continue BLS, charge defibrillator
Give one shock (or precordial thump)

If prolonged:
Amiodarone, lidocaine
epi, VP every other cycle
Increase defibrillation dose by 50%

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29
Q

Asystole/PEA Algorithm

A

-Low dose epi +/- VP every other BLS cycle
-Atropine every other BLS cycle

Prolonged >10’:
-High dose epi
-Bicarbonate therapy

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30
Q

Open Chest CPR Contraindications

A

contraindicated in small dogs <10kg, cats unless in sx DT size of chest cavity and difficulty assoc with cardiac massage in these patients

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31
Q

Importance of Good Compressions during CPR

A

o Only thing generating CO during arrest = compressions
o Ideal compressions: achieve 25-30% normal CO = without high-quality BLS, chances of ROSC minimal

Compression rate: 100-120/min, compression depth 1/3-1/2 width of thorax

Cycles = 2’

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32
Q

Consequences of compression rates >100-120bpm?

A

Higher compression rates decrease CO bc do not allow full elastic recoil of chest –> decrease return of blood to heart –> decrease CO

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33
Q

Why are cycles 2’?

A
  • Cycle = 2’ bc takes 1’ chest compressions for aortic BP to reach steady state that provides perfusion to heart/tissues
  • Cycles <2min decrease perfusion bc steady state not achieved or maintained
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34
Q

Consequences of chest compressions in small dogs, cats

A

possible to overwhelm chest: overt chest trauma, myocardial contusion

Larger patients: large amount of force to obtain effective compressions

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35
Q

Abdominal Compressions

A

 Must be coordinated with partner, alternate timing
 Can increase venous return, with possible increases in CO
 Medium sized dogs or greater

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36
Q

Normal Canine Cardiac Output?

A

100-200mL/kg/min

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37
Q

Normal Canine Stroke Volume?

A

1-2mL/kg

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38
Q

Cardiac Pump Theory

A

Direct compression of heart (LV/RV) generates blood flow

Key: forward flow of oxygenated blood to tissues accomplished via direct compression of heart
* Increased pressure in ventricles to close AV valves, prevent backflow of blood into atria
o Goal: provide maximum SV with each compression

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39
Q

How Heart Fills with Cardiac Pump Theory

A
  • Elastic recoil to chest, heart btw compressions creates negative pressure within heart to allow ventricular filling for next compression
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40
Q

Patient Populations for Cardiac Pump Theory

A

Cats, small dogs, larger keel-chested dogs
* High thoracic compliance
* Narrow, triangular shaped chests

Heart right up against rib case, able to compress ventricles directly to generate blood flow

One or two handed technique depending on patient size

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41
Q

Limitation of Cardiac Pump Theory

A

Older or obese animals with less compliant chests: chest may be too stiff to employ cardiac pump theory DT normal aging changes or SQ fat

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42
Q

Thoracic Pump Theory

A

Key: forward flow of oxygenated blood to tissues accomplished via indirect compression of aorta increasing intrathoracic pressure
* Should maximally compress thorax

Change in intrathoracic pressure causes blood flow

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43
Q

Heart During the Thoracic Pump Theory

A

Heart = passive conduit
o MV, TV not closed during chest compressions – blood flowing passively through heart
* Drive intrathoracic pressure high to push blood out

Maximal change in thoracic volume = hands over widest part of chest

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44
Q

Patient Population for Thoracic Pump Theory

A

Medium, large round-chested dogs; unable to directly compress heart

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45
Q

heart filling with thoracic pump theory

A

Recoil of chest btw compressions causes negative pressure within thorax = draws blood into cr/cd VC, heart

Blood drawn into lungs during recoil phase DT expansion of highly compliant pulmonary vessels

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46
Q

Key points of Two Handed Technique

A

o Hips patient height or higher = step stool, climb on table, move patient to floor
o Heels of hands stacked with elbows over hands, shoulders over elbows
o Bend from hips only
o Overlap hands with fingers interlocked, heel of upper hand directly over heart
o DO NOT LEAN - Must allow chest to recoil

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47
Q

Which are the two shockable rhythms?

A

Pulseless VT
Ventricular fibrillation

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48
Q

Which recumbency is preferred for CPR per RECOVER guidelines?

A

Lateral

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49
Q

Pulseless Ventricular Tachycardia

A

Contractions very fast, no time for ventricular filling

regular, repeated electrical activity with ventricles contracting in coordinated fashion but very fast rate (>200bpm) without palpable pulses

50
Q

Ventricular Fibrillation

A
  • Both ventricles quivering in, out of sync: no effective ctx of heart
  • Aberrant, uncoordinated mechanical activity of muscle cells of ventricles
  • Ineffective mechanical activity, no forward flow of blood
  • ECG: random, irregular activity
51
Q

What are the two non-stockable rhythms?

A
  1. Asystole
  2. Pulseless electrical activity
52
Q

Asystole

A
  • Complete cessation of electrical, mechanical heart activity
  • ECG: flatline
53
Q

Pulseless Electrical Activity

A
  • No effective mechanical activity of the heart, no palpable pulses
  • ECG: continue to show [normal] electrical activity but no mechanical activity of heart
54
Q

Consequences of Hypovenilation

A

Dilation of peripheral blood vessels, pooling of blood in periphery = decreased perfusion to core organs (brain, heart, lungs)

Cerebral vasculature extremely sensitive to [CO2] in arterial blood

Cerebral vasodilation secondary to hypoventilation can lead to increased ICP, further decreasing cerebral perfusion

55
Q

Consequences of Hyperventilation

A
  • Cerebral VC: increased resistance to blood flow to brain, compromising CPP
  • Excessive PPV leads to increased mean intrathoracic pressure = compression of VC, decreased preload to heart = decreased CO
  • Low PaCO2 decreases ventilatory drive, decreases likelihood that patients spontaneously ventilate if ROSC achieved
56
Q

Ventilation Parameters

A

 Do not interrupt compressions for intubation or breaths
 10bpm, 1s duration, ~10mL/kg VT
 Goal: minimize time thoracic pressure possible, opposing venous return

57
Q

Mouth to Snout Breathing

A

 30:2 compression:breath ratio
 Close mouth
 Extend neck to align snout with spine, open airway as completely as possible
 Blow firmly into nares to inflate chest until normal chest excursion accomplished, inspiratory time <1s

58
Q

Limitations of Mouth to Snout breathing

A

cannot be performed simultaneously with chest compression
* When chest compressed, increased intrathoracic pressure prevents air from entering lungs
* Air diverted into esophagus, stomach

59
Q

Components of ALS

A

o Vascular Access
o Drugs
ALWAYS: vasopressors, reversals
MAYBE: atropine, bicarbonate, electrolytes
o Defibrillation

60
Q

Drug Administration During CPR

A

ETT
IV - use most central catheter
IO

Without CO, need large volume of flush to push drugs in: 5-15mL in dogs, 3-5mL in cats

61
Q

ETT Drug Administration

A

o Absorption is variable, use 2-3x standard dose except epi
o NAVEL: naloxone, atropine, vasopressin, epi (high dose), lidocaine
o Place red rubber tube down ET tube, give drug, flush

62
Q

Vasopressor Therapy in ALS

A

o All cases of CPA, impt to shunt blood to central circulation
o Every other BLS cycle ~4’
o Epi = vasopressin: can give one or other every other cycle or together (equivalent in 2012 guidelines)

63
Q

Epinephrine

A

 a1 activity: VC
 a1 activity: increased contractility, HR,
* Leads to myocardial oxygen demand, maybe bad in PCA
 Receptors inactive with acidemia
* Dead = acidemia due to CO2, lactate
 Low dose 0.01mg/kg = 0.1mL/10kg
High dose 0.1mg/kg – last resort, after 2-3 rounds with low dose = high ROSC, lower survival to discharge UNLESS giving via ET

64
Q

Reversal Agents during CPR

A

o Atipamezole IV for 2s, flumazenil for benzos, naloxone for opioids
o TURN OFF THE VAPORIZER AND FLUSH SYSTEM!!!

65
Q

Atropine

A

No more than every other BLS cycle

 Bc more dogs, cats die from vagal arrests, more useful than in people?
 Induced PEA in dogs: higher ROSC with atropine + epi

66
Q

Calcium Gluconate

A

o Calcium Gluconate 1mL/kg SLOWLY IV if iCa <1.0, K >6-7
 Essential for muscle ctx

67
Q

Steroids per 2012 Guidelines

A

no benefit, likely harmful in hypoperfused patients

68
Q

NaBicarb 1mEq/kg

A

 Generates CO2, can worsen acidemia
 Not routinely used, consider if prolonged CPR effort (>10’)

69
Q

Intravenous Fluid Therapy

A

Detrimental in euvolemic patients: harder to pump circulation

Beneficial if known/suspected hypovolemia?
 Blood loss, severe dehydration
 TFAST to eval cardiac contractility

70
Q

Coronary Perfusion Pressure

A

Diastolic blood pressure (DBP) – right atrial pressure (RAP)
 Heart only gets blood during diastole, opposed by right atrial pressure

71
Q

ECG with ALS

A

o Can only interpret during compressor change
o Non-shockable: asystole, PEA – 95% of CPR rhythms
o Shockable: vfib (course or fine) 5%, pulseless ventricular tachycardia <1%

72
Q

Defibrillation

A

Goal = large current to depolarize all cells at once

Induce asystole, hopefully then SA node returns to normal activity

If used for non-shockable rhythms, will injure myocytes
 Use least amt of energy possible

MUST PLACE IN DORSAL

73
Q

Maximum Dose of Energy Used for Defibrillation?

A

10J/kg

74
Q

MOA Defibrillator

A

Capacitor serves as “collection bucket” of continuous low current provided by wall outlet or battery: able to store then release when needed to provide brief, large electrical current

When potential difference applied across capacitor, excess positive charges on one side of plate, negative accumulate in other

To charge capacitor: charging system applies high voltage (via set up transformer) across capacitor based on energy level selected by operator

For capacitor to discharge, electrons need path to flow from one plate of capacitor to other: uses paddles and heart to accomplish

75
Q

Hand Paddles

A

Opposite sides of thorax ~ over costochondral junction directly over heart

Allows maximal amt of current to pass directly through ventricles, increasing likelihood of successful defibrillation

Sufficient electrode gel or paste applied to paddles to ensure electrical contact - NO ALCOHOL

76
Q

Posterior Hand Paddles

A

 Flat paddle replacement for one hand of paddles
 Can increase efficacy/safety of defibrillation by minimizing interruption to compressions, eliminating need to place in dorsal
 Essentially placed under patient thorax
 Traditional hand paddle used on up thorax

77
Q

Pediatric Paddles

A

 Consider for smaller patients
 Directs more current through the heart

78
Q

Monophasic Current

A

current only goes in one direction

  • Inducer that slows current: lower peak, spread over longer period of time
79
Q

Biphasic Current

A

current starts in forward direction, changes direction, goes in reverse direction
* Forward current stops before capacitor finished discharging (return to baseline)

Switching Interval
Truncation

80
Q

Biphasic Current: Switching Interval

A

provides adequate time for forward current to properly switch off before reverse currents put on
o Otherwise, all four current switches would be on at same time
o Creation of short circuit: current returns back across switches, does not go through heart, dissipates as heat

81
Q

Biphasic Current: Truncation

A

o If do nothing: gradual decrease returns to baseline gradually – problematic bc can induce fibrillation

o Truncation: cuts off tail end of biphasic waveform

82
Q

What are the three phases of electrical defibrillator timing?

A
  1. Electrical Phase
  2. Circulatory Phase
  3. Metabolic Phase

Affects optimal timing for first electrical defibrillation attempt

83
Q

Electrical Phase of Defibrillation

A
  • 0-4min no circulation
  • Minimal ischemia
84
Q

Circulatory Phase of Defibrillation

A
  • 4-10min
  • Energy depletion, potentially reversible cell injury – insufficient oxygen
85
Q

Metabolic Phase of Defibrillation

A
  • > 10min
  • Advanced ischemia, cellular injury
86
Q

Witnessed or Monitored Arrest for Shockable Rhythm

A

<4min CPA: minimal ischemic injury

Heart capable of re-establishing perfusing rhythm quickly if VF/PVT terminated immediately

Perform BLS long enough to charge defibrillator: shock, 1 cycle BLS then check ECG

87
Q

Unwitnessed CPA for Shockable Rhythm

A

> 4min
Complete full 2’ cycle BLS before defibrillation

Likely that entered circulatory or metabolic phase so full BLS cycle provides perfusion to heart, restoration of ATP stores and thus increasing likelihood of successful defibrillation

Shocking ischemic heart depleted of ATP unlikely to retire perfusing rhythm, creates additional myocardial injury

88
Q

Other Features of Defibrillation

A

Lots of gel, NO ALCOHOL = burns, fire

Roll into dorsal, tape into place if two regular paddles

Avoid contact with pet, table: can kill someone but usually just knocks them out, can induce fibrillation in person
 Person shocking responsible for group safety

89
Q

After Electrical Defibrillation

A

–Restart BLS: resume chest compressions immediately after each defibrillating attempt, interpret ECG after 2’ cycle

–If VT/PVT persists: increase dose by 50%

–Repeat every BLS cycle

90
Q

Precordial Thump

A

large forceful single manual compression to chest if no defibrillator
o Delivers only 5-10J of energy to heart
o Strike chest directly over heart

Med to large dogs: strike chest with as much force as possible

Small dogs, cats: careful not to overly traumatize heart

91
Q

Post Cardiac Arrest Syndrome

A

Consequences to dying - brain injury, acute kidney disease, myocardial damage, severe vasodilation and coagulopathy, secondary to low blood flow and subsequent ischemia-reperfusion injury

Second arrest common in first 24hr after resuscitation

92
Q

4 Main Features of Post Cardiac Arrest Syndrome

A
  1. Systemic ischemia, repercussion response: SIRS potenital, MODS
  2. Brain injury: seizures, altered mentation, death
  3. Myocardial injury, dysfunction: decreased CO, arrhythmias, hypotension, ongoing organ perfusion
  4. Persistant precipitating pathology: need to address why happened in the first place
93
Q

Goal Parameters for Post Arrest Patient

A

BP normal to hypertensive with systolic >100, MAP 80-120 (settle for 60)
* Injured brain/organs cannot autoregulate perfusion well
* Must maintain normal perfusion from them

Central venous oxygen >70%

Lactate <2.5mmol/L – will take time to come down

Urine output >1mL/kg/hr
* <0.5mL/kg/hr suggestive of renal injury

94
Q

Oxygenation in the Post Arrest Patient

A

 Do not hyperoxygenate  creation of more free radicals, particularly injurious to brain
 May have pulmonary contusions from compressions

95
Q

Cardiovascular Rhythm in the Post Arrest Patient

A

 Caution treating
 Sinus tachycardia may take a while to resolve: do not chase # for several hours

96
Q

Ventilation in the Post Arrest Patient

A

 Often hypercapnic from some period of time bc large build up from ischemic tissues that has to be cleared
* Hypovolemic, decreased vascular resistance

Goal = normocapnia
May take awhile to start ventilating well on own, may be painful when expanding chest
 +/- MV for short period of time

97
Q

Blood Glucose in Post Arrest patient

A

Blood glucose >80mg/dL
 Typically high initially from catecholamine surge
 If persistently high, consider insulin to maintain <180mg/dL, may worsen brain injury if persistently high

98
Q

Permissive Hypothermia in the Post Arrest Patient

A

Practically withhold warming after arrest but warm if hypotensive, shivering

True hypothermia = core temp ~90F
* Mild hypothermia (~97F) seems to be safe target
* True target, speed of rewarming not established

Shivering increases myocardial oxygen consumption!

99
Q

Advantages of Permissive Hypothermia

A
  • Decreased cerebral O2 requirements, brain metabolic demand, excitatory NTs, inflammatory cytokines, and free radicals
100
Q

Other Brain Protective Strategies

A

Elevate head 15-30*: do not kink neck, elevate front half of animal

Brain will slowly come back online: return of ventilation efforts, facial nerve responses

101
Q

Impedance Threshold Device

A

Connected to ET tube, controls air entry into lungs - requires certain inspiratory threshold

Decompression phase of CPR: patients upper airway pressure decreases = closure of valve
* Recoil, valve opens

Enhancing negative intrathoracic pressure during recoil

Can augment venous return, increase CO; improves coronary perfusion pressure, aortic pressure

102
Q

Negatives assoc with ITD

A

Cause pulmonary edema (increased transthoracic pressure (between intrathoracic and alveolar pressures), may favor leaky capillaries

Not recommended for patients <5 kg or cats

103
Q

Contraindications of ITD

A

congestive heart failure, DCM, pulmonary hypertension, aortic stenosis, flail chest, chest pain, and shortness of breath

104
Q

Lidocaine as Anti-Arrhythmic - Literature

A

Increases energy requirements to successfully electrically defibrillate dogs, humans, pigs

Decreases defibrillation threshold with biphasic defibrillation

Successful defibrillation at lower energies in patients with prolonged VF

105
Q

Incidence of Perianesthetic Respiratory Problems

A

Resp problems implicated in up to 50% of canine, 66% of feline anesthetic related deaths

106
Q

Causes of Unexpected Hypoxia

A

Endobronchial intubation, mucus occluded tube, kinking or cuff induced occlusion of ETT, presences of pleural fluid or undiagnosed pneumothorax

Hypoxia can be from airway obstruction secondary to laryngospasm

107
Q

Acute Pneumothorax

A

defect in pleura that allows air leakage into pleural space causing partial or total lung lobe collapse but air does not continue expanding

108
Q

Types of Pneumothorax

A

Spontaneous/simple
* Primary: without underlying lung disease
* Secondary: underlying lung disease

Traumatic: any kind of trauma

Iatrogenic: baro or volutrauma

109
Q

Tension Pneumothorax

A

pleural injury acts as one way valve that allows air to enter pleural space during inspiration, unable to escape during expiration

Patient can tolerate volume of pleural air that 2.5-3.5x FRC (~45 ml/kg)

110
Q

Consequences of Pneumothorax

A

maximal expansion of chest, inspiratory muscles can’t work

lung collapses, IttP increases  vena cava collapses, even aorta = CV collapse

111
Q

Clinical Signs of Pneumothorax

A

 Rapid shallow breathing
 Activation of accessory respiratory muscles, gasping inspiration
 May be hyper-resonant on percussion
 Diminished breath sounds, tachycardia, hypotension

112
Q

Treatment Pneumothorax

A

If no intervention: cyanosis then arrest

Tx: thoracocentesis +/- chest tube placement
o Open pneumothorax, start IPPV until defect can be fixed – require gentle expansion of lung, no aggressive ventilation

113
Q

Bronchospasm

A

o Drug reaction, physical intervention
o Cats, sheep = particularly sensitive
o Fluid instillation during broncho-alveolar lavage can initiate bronchospasm, often associated with oxygen responsive hypoxia

114
Q

Clinical Signs of Bronchospasm

A

 Difficulty maintain acceptable hemoglobin saturation, tachypnea, tachycardia, and increasing airway pressures (if being ventilated), shark fin wave form on capnograph, wheezing may be auscultated

115
Q

Treatment of Bronchospasm

A

 Bronchodilator: albuterol, terbutaline SQ or IV, atropine
 Aspiration of ruminal or stomach contents, consider pulmonary lavage
* Non-ruminants = controversial

Most inhalants, ketamine = bronchodilation
Desflurane: airway irritation

116
Q

Volutrauma, Barotrauma

A

Even brief periods of lung overinflation: air leak, extraalveolar air accumulation
 Increases in endothelial, epithelial permeability = edema, severe ultrastructural damage

Can lead to fulminant pulmonary edema with tracheal flooding, severe hypoxemia, death

High airway pressures depend on species, comorbidities: lower in amphibians, ruminants

117
Q

Tracheal Tears - Cats

A

dorsal, longitudinal trachealis muscle most common in cats
 2-5 cm, most commonly at level of thoracic inlet
 Interval from anesthesia and diagnosis = 4 hours to 14 day

RF: dentals (83% of cases), stylet, multiple positions

118
Q

Dx, Tx Tracheal Tears

A

pneumomediastinum on AXR

1/2 of cats improve with conservative treatment
 Oxygen therapy and cage rest
 Progressive dyspnea is an indication for surgical intervention

119
Q

Procedures Associated with Higher Risk for Asp Pneumonia

A

upper airway surgery, neurosurgery, laparotomy, thoracotomy, endoscopy

120
Q

Closed APL Valve

A

volutrauma, pneumothorax, or failure of venous return = cardiac arrest

121
Q

Tipped Vaporizer

A

Precision vaporizers tip, or even move > 45 degrees = super high vaporizer output

Boards: Other Topics (Endocrine, CPR, Euthanasia, etc) (8 decks)

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