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Shock / CPR > CPR > Flashcards

CPR Flashcards

1
Q

What is the maximum time that should be spent on trying to rule out cardio-pulmonary arrest before starting CPR

A

10-15 sec

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2
Q

What are te two goals of chest compressions?

A
  • Restoration of pumonary CO2 elimination and O2 uptake
  • Delivery of O2 to tissues and restore organ function
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3
Q

What percentage of normal CO can be achieved with chest compressions

A

30%

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4
Q

During which phase of CPR does myocardial perfusion occur?

A

During the decompression phase of chest compressions

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5
Q

What is the coronary perfusion pressure

A

CPP = ADP - RADP

(ADP = aortic diastolic pressure, RADP = right atrial diastolic pressure)

** Higher CPP (primary determinant of myocardial blood flow) during CPR is associated with better success

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6
Q

Recommended rate and depth of chest compressions

A

100-120 per minute
1/3-1/2 width of the chest

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7
Q

How long does it take for coronary perfusion pressure to reach its maximum with chest compressions

A

60 sec

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8
Q

What should be the maximum time of interruption of compressions between each 2-minute cycle

A

2-5 sec

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9
Q

What is the inspiratory time, tidal volume, and max PIP recommended for ventilation in CPR

A

Short insp time of 1 sec to keep positive intrathoracic pressure to a minimum (with RR 10 brpm)
Vt 10 mL/kg
Max PIP 40 cmH2O

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10
Q

Why should hyperventilation be avoided during CPR?

A

Low arterial CO2 –> cerebral vasoconstriction –> decreased cerebral blood flow and O2 delivery

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11
Q

How to alternate ventilation and chest compressions during CPR in a patient who cannot be intubated

A

30 compressions - 2 mouth-to-snout breaths

Continue ratio of 30:2 for 2 minutes then switch operators

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12
Q

What is the predominant effect of epinephrine during CPR

A

Peripheral vasoconstriction by acting on receptors alpha-1 (which spares cerebral and coronary vasculatures)

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13
Q

What are the advantages of vasopressin over epinephrine?

A
  • Efficient in acidic environments where alpha1 can become unresponsive to epinephrine
  • Lacks inotropic and chronotropic beta1 effects that may worsen myocardial ischemia
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14
Q

What are the reversal agents and their doses

A
  • Opioids -> naloxone 0.04 mg/kg
  • Benzodiazepaines -> flumazenil 0.01 mg/kg
  • Alpha2-agonists -> atipamezole 0.1 mg/kg or yohimbine 0.1 mg/kg
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15
Q

What are the 3 phases of ischemia during Vfib

A
  • Electrical phase (first 4 min): minimal ischemia, continued availability of cellular energy stores
  • Circulatory phase (4-10 min): depletion in cellular ATP stores, reversible ischemic injury
  • Metabolic phase (> 10 min): irreversible ischemic damage
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16
Q

In a patient with Vfib as initial rhythm of CPR, when should defibrillation be performed

A
  • As soon as defibrillator ready if patient has been in Vfib for < 4 min (do compressions only during the time to get ready)
  • After a full 2-min cycle of compressions if patient is suspected to have been in Vfib for > 4 min
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17
Q

What is the defibrillation dose

A
  • Monophasic: 4-6 J/kg
  • Biphasic: 2-4 J/kg

Second dose should be increased by 50%, subsequent doses should NOT be further increased

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18
Q

What drugs can be considered in VF refractory to defibrillation, and what is one possible adverse effect of each?

A

Amiodarone 2.5-5mg/kg - anaphylaxis

Lidocaine 2mg/kg (although less effective than amiodarone) - possibly increase energy required for successful electrical defibrillation (one study)

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19
Q

What is the approach for open chest CPR

A

Left lateral thoracotomy between the 4th and 5th ribs. Use Finochietto retractors to access the chest.

20
Q

What is the survival to discharge rate following CPR

A

In general reported 6-7% (or 2-10%)
For peri-anesthetic: 47%
Cats reported 19% in one study

(ROSC rate 35-45%)

21
Q

What are the target PaCO2 and PaO2 in post-cardiac arrest

A

Dogs: PaCO2 32-43 mmHg, PaO2 80-100 mmHg (SpO2 94-98%)
Cats: PaCO2 26-36 mmHg, PaO2 80-100 mmHg (SpO2 94-98%)

(Subtract 5 mmHg to get EtCO2)

22
Q

What are the resuscitation endpoints in post-cardiac arrest

A

MAP 80-120 mmHg
ScvO2 > 70%
Lactate < 2.5 mmol/L

23
Q

How long does it take to deplete ATP stores in the cerebral cells during cardiac arrest

A

2-4 min

24
Q

What are beneficial effects of hypothermia in the post-cardiac arrest phase

A
  • Mitochondrial protection
  • Decreased cerebral metabolism
  • Decreased cellular calcium influx
  • Reduced neuronal excitotoxicity
  • Reduced production of ROS
  • Attenuated apoptosis
  • Control of seizure activity
25
Q

What is the temperature target in dogs and cats in the post-cardiac arrest phase

A
  • Initially core temperature of 32-34°C for 24-48h in patients remaining comatose following ROSC
  • Now mostly emphasize slow rewarming (0.25-0.5°C per hour) and aggressive management of hyperthermia
26
Q

What are adverse effects of targeted temperature management

A
  • Shivering -> increased metabolic rate, O2 consumption, HR, RR
  • Changes in acid-base status and electrolytes
  • Impaired drug metabolism
  • Decreased coagulation
  • Decreased immune function
27
Q

How long should be allowed before neurological prognostication after ROSC and what are 2 highly sensitive indicators of poor prognosis?

A

24-72h

Bilateral absent PLRS & absence of somatosensory evoked potential (SSEP)

28
Q

What is the “no-reflow” phenomenon

A

Absence of organ reperfusion following ROSC due to microvascular obstruction (endothelial cell swelling, activation of coagulation, decreased deformability and adhesion of RBC)

29
Q

What is the prevalence of serious adverse events caused by chest compressions in human patients who were no in cardiac arrest

A

Less than 2% (possible rib fractures, tracheal bleeding, rhabdomyolysis)

30
Q

What is the only situation where ventilation should be initiated before compressions in CPR

A

In an unwitnessed cardio-pulmonary arrest not suspected cardiac in origin where only 1 rescuer is present

/!\ assessment should still start with the airway (ABC) even if resuscitation usually starts with the compressions (CAB). In multiple-rescuer situation, compressions are started, the airway is assessed and intubation is performed during compressions

31
Q

What is the ETCO2 target in CPR

A

15 mmHg (18 mmHg in 2024 guidelines)

32
Q

In patients with invasive blood pressure in place at the time of CPR, what is the therapeutic target for IBP

A

DBP of at least 30 mmHg

33
Q

How to differentiate pulseless VT from PEA during CPR

A

HR > 200 bpm (only criteria - not based on complex morphology as long as it is repeating complexes, ie not Vfib or asystole)

34
Q

What is the coronary perfusion pressure during CPR

A

During CPR, COPP = diastolic aortic pressure - right atrial end-diastolic pressure (because ventricular pressure very low)

  • in alive patient COPP = diastolic aortic pressure - left ventricular end-diastolic pressure
35
Q

What coronary perfusion pressure is required to achieve ROSC

A

30-40 mmHg

36
Q

What are the 4 processes that contribute to tissue injury in patients in the post-cardiac arrest period

A
  • Ischemic injury
  • Reperfusion injury
  • Myocardial dysfunction
  • Precipitating disease
37
Q

3 components of RECOVER PCA algorithm

A
  • Respiratory optimization
  • Hemodynamic optimization
  • Neuroprotection
38
Q

3 components of PCA neuroprotection

A
  • Hypothermia (or at least do not warm faster than 1°C/h and avoid hyperthermia)
  • Hyperosmolar therapy
  • Seizure prophylaxis / treatment
39
Q

What has been noted in the literature regarding high dose epinephrine and what are the possible mechanisms?

A

High dose epinephrine has been associated with a higher rate of ROSC, but a lower rate of survival to discharge. It should therefore be used as a Hail Mary and avoided in patients who already have a high chance of ROSC.

  • Vasoconstriction +++ (alpha1) leading to severe acidosis
  • Increased ventricular arrhythmias (beta1 –> increased HR and contractility –> increased O2 demand –> more ischemia)
  • hyperglycemias from beta effects –> worsening neuro outcome
40
Q

True or false: mild hypotension during the first 30-60 minutes in the PCA period can be beneficial.

A

False! It is hypertension that can be beneficial for a short period of time –> explains why the range of BP is more liberal in the PCA algorithm (tolerates up to 200mmHg)

Rational: cerebrovascular autoregulation can be absent, and perivascular oedema and intravascular clot formation may compromise PCA cerebral blood flow

41
Q

Explain the cardiac pump theory and the thoracic pump theory.

A

Cardiac pump theory (keel chested dogs, small dogs, cats)
- Direct compression of the ventricles increases ventricular pressure –> pulmonic and aortic valves open allowing blood flow. During chest recoil in between compressions –> negative intrathoracic pressure draws venous blood into the ventricles

Thoracic pump theory (round chested dogs)
- Compressions over the widest part of the chest –> Overall increase in intrathoracic pressure during compressions forces blood from the lungs into the R ventricle + squeeze blood out of the aorta and into the systemic circulation. During recoil, blood sucked back into the lungs and from the rest of the body back to the right side of the heart —> Heart acts as a conduit - not physiologic blood flow

42
Q

How does defibrillation terminate the arrhythmia at the cellular level?

A

The application of an asynchronous electrical current causes simultaneous depolarization of the cardiac myocytes to force them into their refractory period. Once the malignant rhythm is terminated, the underlying pacemaker rhythm takes over.

43
Q

Why are corticosteroids not routinely recommended in the PCA patient, when CIRCI may occur?

A
  • Evidence of benefit is lacking
  • Risk for infection
  • Risk for GI ulceration
  • exacerbation of post-ischemic neurological injury
44
Q

True or false: most of the brain injury in CPA is sustained due to ischemia.

A

False: ost of the injury is sustained during reperfusion.

45
Q

What is the role of calcium in brain injury in the PCA period that explains why mild hypocalcemia should be tolerated?

A

ATP is depleted –> loss of cellular membrane potential –> large influx of Na+, Ca2+, Cl- –> cellular edema and membrane disruption –> mitochondrial dysfunction (with contribution of oxidative stress and energy depletion) –> more ROS –> apoptosis and necrosis

  • tolerate hypocalcemia + avoid hyperoxemia!
46
Q

What is myocardial stunning?

A

Reversible myocardial dysfunction in the absence of cell necrosis.

Shock / CPR (5 decks)

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