5 Postcardiac Arrest Care Flashcards

1
Q

What defines post-cardiac arrest care measures needed for each individual patient?

A
  1. Systemic response to ischemia and perfusion
  2. Anoxic brain injury
  3. Postresuscitation myocardial dysfunction
  4. Persistent precipitating pathologic conditions
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2
Q

What does immediate post-cardiac arrest care focus on?

A

Prevention of rearrest by ensuring optimal ventilation, oxygenation, and tissue perfusion, as well as identifying and correct reversible causes of cardiopulmonary arrest

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3
Q

Early hypoxemia and hyperoxemia after ROSC should be prevented by controlled reoxygenation by using what targets?

A
  1. SaO2/SpO2 94-98%
  2. PaO2 80-100mmHg
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4
Q

Hemodynamic optimization measures after ROSC, including IV fluids, pressors, inotropes and blood products, are used to reach what targets?

A
  1. MAP 80mmHg or higher
  2. ScvO2 70% or more
  3. Lactate of less than 2.5mmol/L
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5
Q

In patients that remain comatose, what range is the targeted temperature management, and for how long?

A
  1. 32-36*C (89.6-96.8F)
  2. 24-48 hours
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6
Q

List three neuroprotective strategies in post-ROSC care?

A
  1. Permissive hypothermia
  2. Slow rewarming (0.25-0.5*C / hr)
  3. Osmotic therapy
  4. Seizure prophylaxis
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7
Q

In veterinary medicine, approximately what % of dogs or cats with any ROSC are euthanized or die before hospital discharge?

A

79%

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8
Q

The first of two paradigms targets the pathophysiologic processes that occur in the post-resuscitation phase, which includes what 4 processes?

A
  1. ischemia and reperfusion (IR) injury
  2. PCA brain injury
  3. PCA myocardial dysfunction
  4. persistent precipitating pathologic conditions
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9
Q

The second paradigm of post-ROSC care, the focus is on

A

Preventing the recurrence of cardiac arrest and limitation of organ injury

Later care emphasizes treatment of the underlying disease processes, prognostication, and rehabilitation

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10
Q

In a recent observational study, ____% of the animals achieved any ROSC, and ___% of these animals rearrested within 20 minutes.

A

41%
15%

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11
Q

What vasopressor may be considered to maintain vascular tone and adequate blood pressure, since adrenal function may be insufficient after ROSC? This may be replaced with more targeted catecholamine use once a more refined understanding of the patient’s physiology is acquired.

A

Epinephrine 0.1-0.5ug/kg/min CRI

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12
Q

Positive inotropic support with what medication can help mitigate postischemic left ventricular systolic dysfunction and response to treatment can be assessed with repeat cardiovascular POC ultrasound

A

dobutamine 5-10ug/kg/min CRI

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13
Q

Once sustained ROSC has been achieved for 20 to 40 minutes, what is the priority of care?

A

Mitigation of further organ injury that arises as a consequence of I and the titration of supportive care adapted to the needs of the patient

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14
Q

List the main points of pathophysiology of systemic ischemia reperfusion response (6)

A
  1. SIRS
  2. Impaired vasoregulation
  3. Increased coagulation
  4. Adrenal suppression
  5. Impaired tissue oxygen delivery and utilization
  6. Impaired resistance to infection
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15
Q

List the clinical manifestations of systemic ischemia-reperfusion response (6)

A
  1. Ongoing tissue hypoxia-ischemia
  2. Hypotension
  3. Pyrexia (fever)
  4. Hyperglycemia
  5. Multiorgan failure
  6. Infection
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16
Q

List the potential treatments for systemic ischemia-reperfusion response (6)

A
  1. Early hemodynamic optimization
  2. Intravenous fluids
  3. Vasopressors
  4. Temperature control
  5. Glucose control
  6. Antibiotics for documented infection
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17
Q

List the pathophysiology points for post-cardiac arrest brain injury (3)

A
  1. Impaired cerebrovascular autoregulation
  2. Cerebral edema (limited)
  3. Postischemic neurodegeneration
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18
Q

List the clinical manifestations for post-cardiac arrest brain injury (6)

A
  1. Delirium, stupor, coma
  2. Seizures
  3. Myoclonus
  4. Cognitive dysfunction
  5. Cortical blindness
  6. Brain death
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19
Q

List the potential treatments for post-cardiac arrest brain injury (6)

A
  1. Targeted temperature management
  2. Early hemodynamic optimization
  3. Airway protection and mechanical ventilation
  4. Seizure control
  5. Controlled reoxygenation (SaO2 94-98%)
  6. Supportive care
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20
Q

List the pathophysiology of persistent precipitating pathology (9)

A
  1. Infection (sepsis, pneumonia)
  2. Upper airway obstruction
  3. Cardiovascular disease (cardiomyopathy)
  4. Pulmonary disease (CHF, ARDS)
  5. Thromboembolic disease (PTE)
  6. CNS disease
  7. Toxicological (overdose, poisoning)
  8. Hypovolemia (hemorrhage, dehydration)
  9. MODS
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21
Q

List the clinical manifestations of persistent precipitating pathology (2)

A
  1. Specific to cause
  2. Complicated by concomitant PCA syndrome
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22
Q

List the potential treatments for persistent precipitating pathology (2)

A
  1. Disease specific
  2. Guided by patient condition and concomitant PCA syndrome
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23
Q

_______ shares many characteristics with severe sepsis, specifically in regard to inflammation, coagulation and endothelial injury

A

Sepsis-like syndrome (systemic response to ischemia and reperfusion)

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24
Q

In sepsis-like syndrome, the therapeutic concepts involve:

A
  1. early hemodynamic optimization
  2. glycemic control
  3. critical illness-related corticosteroid insufficiency (CIRCI)
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25
Q

Why is the MAP target higher in post-ROSC hemodynamic optimization than in septic patients?

A

Cerebrovascular autoregulation can be absent, and perivascular edema and intravascular clot formation can compromise PCA cerebral blood flow

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26
Q

________ commonly occurs after cardiac arrest in humans, dogs and cats and has been associated with worse outcomes.

A

Hyperglycemia

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27
Q

Hyperglycemia in dogs after ROSC may worsen

A

Ischemic brain injury

28
Q

In early ROSC, in an experimental research study in dogs, mild to moderate hyperglycemia combined with a total plasma insulin decrease of ____ was observed.

A

60%

29
Q

While implementing insulin administration to control severe hyperglycemia and avoid iatrogenic hypoglycemia is reasonable, however there has been no proven benefit to ________ __________ _______

A

tight glycemic control

30
Q

Due to the risk for infection, lack of proven benefit, risk of peptic ulcer and exacerbation of postischemic neurologic injury associated with the administration of this medication, routine administration of ________________ is not recommended despite concern for adrenal dysfunction.

A

Corticosteroids

Administration of low-dose hydrocortisone (1mg/kg IV followed by 1mg/kg IV q6hr or an IV CRI of 0.15mg/kg/hr) in dogs and cats with vasopressor-dependent shock after CPA, with or without documented CIRCI, may be considered

31
Q

In humans, ________ ________ after cardiac arrest is the single greatest concern and the most common single cause of death. In one study, this was the cause of death in 2/3rds of patients after out-of-hospital cardiac arrest and one-fifth after in-hospital cardiac arrest.

A

cerebral dysfunction

32
Q

PCA brain injury results from

A

global cerebral IR

33
Q

List 4 aspects of pathophysiology of cerebral IR injury:

A
  1. Most of the injury is sustained during reperfusion and not during ischemia, affording the clinician the opportunity to intervene after ROSC is achieved
  2. Cytosolic and mitochondrial calcium overload leads to the activation of proteases that may lead to neuronal death and production of reactive oxygen species (ROS)
  3. A burst of ROS occurs during reperfusion, leading to oxidative alterations of lipids, proteins, and nucleic acids, propagating injury of neuronal cell components and limiting the cells’ protective and repair mechanisms
  4. Hypothermia after ROSC is proven to reduce PCA cerebral dysfunction
34
Q

Much of the injury sustained after CPA evolves during what part of IR?

A

The reperfusion phase

35
Q

Cerebral adenosine triphosphate (ATP) stores are depleted within

A

2 to 4 minutes

36
Q

ATP stores in the GI and myocardium are depleted after how long?

A

20-40 minutes

37
Q

Once ATP is depleted, what is rapidly lost?

A

Cellular membrane potentials

38
Q

Clinically, any cardiac electrical activity as detected by ECG provides evidence that the _________ ____________ __________ has not yet subsided or has been reestablished during reperfusion.

A

Global myocardial membrane potential

39
Q

In the loss of the cellular membrane potential, what three electrolytes enter the cells, shortly followed by cellular edema and membrane disruption.

A

Large amounts of sodium, chloride, and calcium

40
Q

It is believed that the combined influences of increased exposure to ________, ____________ _______, and ______ _________ lead to mitochondrial injury, finally leading to more ROS production upon reperfusion and to apoptosis and necrosis.

A

Calcium
Oxidative stress
Energy depletion

41
Q

Excessive production of ROS in the presence of exhausted protective mechanisms results in elaboration of ______________, namely _________ and _________, which in turn cause cell membrane damage, lipid peroxidation, DNA damage, and protein alterations

A

highly reactive free radicals
hydroxyl radicals
peroxynitrate

42
Q

Much evidence suggests that arterial hyperoxemia soon after ROSC increases (4)

A

Oxidative brain injury
Increases neurodegeneration
Worsens functional neurologic outcome
Negatively effects overall survival

43
Q

Mechanistically, the protective effect of hypothermia from global IR injury is well established and has been shown to occur via many pathways, including (6)

A
  1. Mitochondrial protection
  2. Decreased cerebral metabolism
  3. Impediment of cellular calcium influx
  4. Reduced neuronal excitotoxicity, reduced elaboration of ROS
  5. Attenuated apoptosis
  6. Control of seizure activity
44
Q

List 5 benefits of hypothermia during CPA and post-CPA care

A
  1. mild hypothermia reduces anoxic brain injury
  2. hypothermia during arrest has the most profound and long-lasting effect
  3. after reperfusion, any delay in hypothermia reduces the beneficial effect
  4. long duration of hypothermia improves the protective effect
  5. long duration of hypothermia can “rescue” the loss of effect dur to delayed onset of cooling
45
Q

A rewarming rate of _____ to _____ *F per hour should be targeted

A

0.45-0.9*F

46
Q

In reality, for targeted temperature management, most small animal PCA patients will be hypothermic when they achieve ROSC, so the goal is:

A

Prevention of rapid rewarming rather than induction of hypothermia

47
Q

The TTM target refers to the core temperature, so what is the best means to monitor it?

A

Esophageal thermocouple is preferred over a rectal probe

48
Q

Cooling induces increased muscle tone and shivering, which in turn leads to

A

Increased oxygen consumption, metabolic rate, and respiratory and heart rates
Requires sedation - Cooling without it may abolish the protective effect of TTM.
Sometimes requires endotracheal intubation and ventilation
Changes in metabolism, acid-base status, electrolytes, ECG, drug elimination, coagulation, immune function

49
Q

How much should the clinician be concerned with physiologic disturbances related to TTM?

A

Probably not too much. Adverse effects associated with PCA hypothermia in humans with OHCA were found to be on par with normothermic care and did not affect mortality

However, in dogs/cats, where sepsis and coagulopathy are more common, the side effect profile may be more pronounced and the benefit of TTM should be carefully weighed against the risk and a higher temperature (35C) as opposed to lower (33C) temperature target may be indicated

50
Q

In humans, the occurrence of seizures during the first ____ ____ after CPA is associated with worse outcome.

A

3 days

51
Q

Is intracranial hypertension common or uncommon after CPA in small animals?

A

Uncommon

In dogs, hypertonic fluid administration after 14minutes of anoxic brain injury decreased cerebral edema but did not affect survival or functional neurologic outcome.

52
Q

In dogs after 12.5minutes of untreated ventricular fibrillation, more than _____% of the brain remained below baseline blood flow 1 to 4 hours after resuscitation

A

50%

53
Q

Experimental evidence suggests that the CO2 responsiveness of cerebral arteries is disturbed for the first several hours after prolonged ischemia such that:

A

arterial vasodilation in response to increasing PaCO2 is abolished

54
Q

Complete neurologic examinations should be undertaken directly after ROSC and initially every ______

A

2-4 hours

55
Q

Any signs of normal neurological function after early ROSC (ie spontaneous ventilation, gag reflex, pupillary light reflex) support

A

a favorable prognosis despite the lack of evidence in veterinary literature

56
Q

What is a poor predictor of functional outcome during the first 72 hours after RSOC?

A

Neurological examination alone

57
Q

For neurologic assessment, what are the findings from the five modes of examination? Which are supportive of poor prognosis?

A
  1. clinical examination
  2. EEG
  3. somatosensory evoked potential (SSEP)
  4. imaging
  5. circulating markers

Poor neurologic outcome predicted:
Clinical exam after 72hr shows absence of response to noxious stimuli and bilaterally absent PLRs and corneal reflexes
Absence of SSEP in an unconscious patient
Both together are highly sensitive indicators of poor prognosis

58
Q

If SSEP or PLR are not available, a set of less sensitive signs to determine prognosis should be considered, but not until ____ after the 72hr assessment.

A

24hours

59
Q

If SSEP or PLR are not available, some less sensitive signs to evaluate may include:

A
  1. High levels of circulating neurospecificity enolase, a commonly used biomarker of neuronal injury after CPA
  2. Diffuse anoxic injury on brain computed tomography/magnetic resonance imaging
  3. unreactive burst-suppression or status epilepticus on EEG
  4. status myoclonus

The presence of at least 2 of these less reliable factors suggest poor outcome is highly likely

60
Q

How long should you allow following ROSC to make a euthanasia decision if cost is not a factor?

A

Because adult animals and humans with CPA-related anoxic brain injury recover along a similar timeline, allowing 24-72 hours prior to making a euthanasia decision is reasonable.

61
Q

Experimental and limited clinical evidence in dogs and cats demonstrates the significant potential for neurological recovery, provided adequate supportive care. One study documented that neurologic abnormalities after ROSC resolved in _____% of CPA survivors before hospital discharge.

A

90%

62
Q

________ __________ results from cellular processes associated with cellular IR comparable to those evolving in the nervous system. The severity of this depends on the duration and extent of the ischemia of these related cells as well as the conditions under which reperfusion occurs (presence or absence of hypothermia and hyperoxia)

A

Myocardial dysfunction

63
Q

__________ ___________ (or __________) may occur subsequent to endothelial cell activation and swelling, neutrophil-endothelial cell interactions, activation of coagulation and platelet aggregation

A

Microvascular obstruction (plugging)

64
Q

What is myocardial no-reflow?

A

A lack of capillary blood flow during PCA

65
Q

Myocardial dysfunction is reversible and typically resolves within 48 hours. This reversibility in the absence of cell necrosis is the basis for the term:

A

myocardial stunning

66
Q

What is the best way to diagnose and monitor for progression and resolution of MD during the PCA phase are best accomplished noninvasively by:

A

serial echocardiography

67
Q

What medication administration at typical doses used in dogs and cats was shown to effectively improve left ventricular function and cardiac output in humans and swine?

A

Dobutamine