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PCS V > Exam 1 - CPCR 2.0 > Flashcards

Exam 1 - CPCR 2.0 Flashcards

1
Q

T/F: currently, survival to discharge following cardiopulmonary arrest (CPA) in veterinary species is <6% if not associated with anesthesia; survival for anesthetic-related CPA approaches 50%

A

true

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2
Q

what is the most common underlying cause in veterinary medicine leading to CPA?

A

multi-organ dysfunction causing high vagal tone - leads to arrest

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3
Q

what is the most common etiology resulting in arrest? what are some other etiologies?

A

hypoxemia

anemia, arrhythmias, cerebral trauma, & anaphylaxis

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4
Q

what common signs are associated with arrest?

A

agonal breathing & apnea followed by collapse

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5
Q

why does respiratory arrest carry a better prognosis than cardiopulmonary arrest? which is more commonly encountered?

A

the heart continues beating for a short period of time following to the development of apnea

cardiopulmonary arrest is more common

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6
Q

what is the mechanism of cardiopulmonary arrest?

A

cessation of cardiac contractions

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7
Q

what is the most commonly encountered rhythm in patients with CPA?

A

asystole

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8
Q

what is asystole?

A

no electrical or mechanical activity of the heart

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9
Q

what is pulseless electrical activity?

A

occurs when there is still electrical activity in the heart but these impulses don’t stimulate contractions - complexes generated can appear as sinus beats or escape rhythms

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10
Q

when is ventricular fibrillation seen in veterinary patients?

A

rare - association with CPR, cardiac disease, or anesthesia

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11
Q

how can you differentiate between ventricular tachycardia & pulseless electrical activity?

A

if the heart rate is greater than 180 bpm - v tach

if the heart rate is less than 180 - PEA

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12
Q

what is the pathogenesis of CPA at 20 seconds, 5 minutes, & 30 minutes?

A

20 seconds - electrical activity within the brain is compromised due to lack of oxygen for high energy metabolism

5 minutes - complete depletion of ATP stores within the body

30 minutes - irreversible histological changes within cells are identified

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13
Q

what is phase I of ventricular fibrillation?

A

first 4 minutes - little to no ischemic damage to myocardial cells

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14
Q

why is phase I (electrical phase) of ventricular fibrillation most successful for defibrillation?

A

little to no ischemic damage to myocardial cells

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15
Q

what is phase II of ventricular fibrillation?

A

circulatory phase - next 6 minutes, reversible damage occurs within the cardiac myocytes

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16
Q

why is CPR recommended during phase II of ventricular fibrillation?

A

provide oxygen to the patient prior to defibrillation - if no CPR, patients suffer increased damage & are likely to fibrillate again even if successful the first time

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17
Q

what is phase III of ventricular fibrillation?

A

metabolic phase - fibrillation that has occurred greater than 10 minutes

irreversible ischemic damage to the myocardium & defibrillation is typically unsuccessful

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18
Q

the fundamentals of CPR focus on what 2 things?

A

improving perfusion to the heart & brain

identifying/addressing the underlying cause of the arrest

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19
Q

what is needed on a CPR team?

A

leader, compressors, ventilator, drug administrator, recorder/timer, & someone to obtain a history

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20
Q

what are the 2 most important pieces of equipment that should be immediately attached to a coding patient?

A

ECG & ETCO2

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21
Q

why is an ECG important for a coding patient?

A

essential for rhythm diagnosis between compressors & helps determine next therapeutic course of action

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22
Q

what therapy is indicated for non-shockable rhythms? what about shockable rhythms?

A

non-shockable: epinephrine & compressions

shockable: defibrillation & compressions

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23
Q

what are the non-shockable rhythms?

A

asystole & PEA

24
Q

what ETCO2 measurement is considered to correlate with effective compressions? what if this isn’t achieved?

A

15 mmHg

efficiency of compressions should be evaluated for proper rate, depth, compression point, & posture

25
Q

T/F: while not all patients will achieve an EtCO2 of >15 mmHg during CPR (which conveys a poor prognosis for recovery), every attempt should be made to ensure that this low value is not from inadequate compressions

A

true

26
Q

how should compression be performed?

A

rate of 100-120 bpm, compressing the chest 1/3 to 1/2 of the total width allowing for complete recoil

27
Q

what do incomplete or rapid compressions cause?

A

decreased ventricular filling & decreased cardiac output

28
Q

T/F: efficacy of compressions decrease after 2 minutes regardless of perceived fatigue

A

true - switch every 2 minutes

29
Q

optimal compressions generate approximately ___% of normal cardiac output when performed appropriately?

A

20%

30
Q

where are compressions performed in small dogs & cats?

A

directly over the heart in line with the cardiac pump theory

31
Q

what is the cardiac pump theory?

A

ventricles of the heart are compressed mimicking a contraction - compressions directly over the heart for small dogs/cats

32
Q

where are compressions performed in large breed dogs?

A

compressions are performed at the highest point of the chest to increase intrathoracic pressure & causes the great vessels (vena cava & aorta) to collapse - thoracic pump theory

33
Q

what is the thoracic pump theory?

A

compressions are performed at the highest point of the chest to increase intrathoracic pressure which causes the great vessels (vena cava & aorta) to collapse

recoil causes the vessels to expand again & triggers the movement of blood with the heart acting as a conduit for blood instead of the mechanism of movement

34
Q

where are compressions performed in barrel-chested dogs (bulldogs)?

A

dorsal recumbency

35
Q

what is the respiration rate used for CPR?

A

one breath every 10 seconds with an inspiratory time of 1 second & pressure of 10-15 cmH2O

36
Q

how does hyperventilation negatively affect the coding patient?

A

it maintains positive intrathoracic pressures which compresses the major vessels impeding venous return

37
Q

how does hypoventilation negatively affect the coding patient?

A

allows for the accumulation of carbon dioxide which results in cerebral vasodilation, increased intracranial pressure, and decreased cerebral perfusion

38
Q

what kind of drug is epinephrine?

A

non-selective sympathomimetic - alpha & beta adrenergic stimulation

39
Q

giving epinephrine results in what?

A

increased systemic vascular resistance, heart rate, & force of contraction

40
Q

what is the primary purpose of giving epinephrine to a coding patient?

A

increase systemic vascular resistance to shunt blood back to the core organs

41
Q

what is the recommended dose of epi given for the first two administrations given every other cycle?

A

0.01mg/kg

42
Q

when is high dose epi used? why is it not the first choice?

A

when low dose epi has failed

it will achieve a higher ROSC, but is also associated with higher rates of neurologic impairment & mortality

43
Q

what are your shockable rhythms?

A

pulseless ventricular tachycardia & ventricular fibrillation

44
Q

what is the mechanism of vasopressin?

A

acts on V1 receptors in peripheral vasculature to increase systemic vascular resistance without increasing myocardial oxygen demand

45
Q

what is the mechanism of action of atropine?

A

parasympatholytic - decreases vagal tone

46
Q

what is the dose used for atropine for a coding patient?

A

0.04 mg/kg administered every other cycle opposite of epi - low dose epi -> 2 minutes later -> 1 dose atropine -> 2 minutes later -> low dose epi

47
Q

what drugs can a patient receive through an ET tube? how does the dosing change?

A

epinephrine, atropine, vasopressin, lidocaine, & naloxone

double the doses - give through a red rubber as close to the carina as possible to improve absorption

48
Q

T/F: asystole & PEA respond well to defibrillation

A

false

49
Q

how is a defibrillator used?

A

patient in dorsal recumbency, paddles covered in electrode transducer gel, placed on lateral adjacent thoracic walls directly over the heart

no one in direct contact with table & patient after the paddles are in place, operator yells clear, everyone says clear back, patient is shocked

50
Q

what is assessed after defibrillating your patient?

A

another round of compressions is performed & rhythm analysis performed at the next compressor change

51
Q

T/F: in cases of shockable rhythms, epinephrine is typically not administered; instead defibrillation is performed every cycle that a shockable rhythm is diagnosed until the patient converts to a perfusing or non-shockable rhythm.

A

true

52
Q

why should iv fluids only be given to hypovolemic patients as a part of CPR?

A

giving fluids to normovolemic/hypervolemic patients will increase right atrial pressure & decrease venous return

53
Q

when is open chest CPR indicated?

A

pleural space/pericardial disease, thoracic trauma, giant breed dogs, concurrent surgery, & prolonged CPR (> 10 minutes)

54
Q

why is open chest CPR not commonly performed?

A

significant morbidity and cost following this procedure with no change in survival to discharge

55
Q

how is open chest CPR performed?

A

patient placed in lateral recumbency (left preferred) & 6th ICS is clipped/prepped while external compressions continue - sterile gloves are worn & chest cavity is entered & internal massage starts

56
Q

in cases of open chest CPR for pericardial effusion, what should be done?

A

pericardium should be torn to allow the fluid to evacuate

57
Q

how often should compressors switch in internal CPR?

A

every 2 minutes

PCS V (8 decks)

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