Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Resuscitation 2015 > Post ROSC Care > Flashcards

Post ROSC Care Flashcards

1
Q

Targeted temperature?

A

36 degrees (not 32-34 anymore)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why is hyperventilation dangerous?

A

Hypocapnia - cerebral ischaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is included in post cardiac arrest syndrome?

A

Post-cardiac arrest brain injury, myocardial dysfunction, the systemic ischaemia/reperfusion response and the persistent precipitating pathology.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What accounts for most of the deaths within the first few days and then after?

A

Cardiovascular failure - first three days. Brain injury - thereafter. 2/3rd of IHCA, 25% of OOHCA survive to die in ICU.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Features of post-cardiac arrest that are similar to sepsis?

A

Intravascular volume depletion, vasodilation, endothelial injury and microcirculatory abnormalities.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Post -ROSC oxygen therapy - what and why?

A

Titrate to 94-98%. Hyperaemia possibly increases neurological injury/post MI harm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Position of tracheal tube?

A

Above carina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Effects of hypocarbia?

A

Cerebral vasoconstriction and decreased cerebral blood flow.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Ideal tidal volume/positive end expiratory pressure?

A
  • TV: 68ml/kg of IDEAL BW

- PEEP: 4-8cm H2O

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What might a continuous infusion of a neuromuscular blockade result in?

A
  • Masking of seizures.

- Interfere with clinical examination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

PCI in a post-ROSC pt without STE or LBBB?

A

Possibly - controversial but bear in mind likely cardiac cause in patient and the lack of sensitivity/specificity in usual markers - ECG/biomarkers/examination etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

ROSC patient - no obvious cardiac cause -action?

A

Hospital - CT to identify early respiratory or neurological cause. If trauma/haemorrhage - whole body CT.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Haemodynamic management?

A
  • Early echocardiography to detect/quantify degree of myocardial dysfunction
  • Often, transient, inotrope support - dobutamine. However if SIRS -> vasoplegia and severe vasodilation, give noradrenaline, with or without dobutamine, and fluid.
  • Other things: monitoring including arterial line for continuous BP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

BP target post-ROSC?

A

Aim for adequate urine output as a measure of end-organ perfusion.
(1ml/kg/hour)
And normal/decreasing plasma lactate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What can impair lactate clearance and increase urine output?

A

Hypothermia -> central diuresis and reduced BMR.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Would you treat a bradycardia of < or equal to 40bpm

A

No probably not - protective, especially against diastolic dysfunction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Explain mechanism behind hyperkalaemia, then hypokalaemia post-ROSC.

A

Hyperkalaemia straight away (decreased clearance/respiration etc?). Endogenous catecholamine release and correction of metabolic/respiratory acidosis -> pushes K into cells -> hypokalaemia.
Maintain between 4.0-4.5mmol/l

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

When might you consider an ICD?

A
  • Ischaemic patients with significant LV dysfunction, who have been resuscitated from a ventricular arrhythmia that occurred later than 24–48 h after a primary coronary event.
  • At risk of SCD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What happens to cerebral perfusion post-ROSC?

A
  • Short period of multifocal cerebral no-flow.
  • Global cerebral hyperaemia (15-30 mins)
  • Cerebral hypoperfusion (up to 24 hours)
    NB after asphyxia - transient oedema can occur, without pressure change.
    Worth mentioning - auto regulation of cerebral blood flow impaired (absent/right shift)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How common are seizures post ROSC?

A

1/3rd who remain comatose post ROSC (Myoclonus, then tonic-clonic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How do you treat seizures post ROSC?

a. Which drugs?
b. Which drugs post anoxic injury?
c. Which drugs in post-anoxic myoclonus?

A

a. Sodium valproate, levetiracetam, phenytoin, benzodi- azepines, propofol, or a barbiturate.
b - to suppress: propofol
c. tx: clonazepam, sodium valproate and levetiracetam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Blood glucose targets post ROSC?

A

< or equal to 10mmol/l and avoid hypo.

Avoid strict control as it risks hypo.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Temperature control after cardiac arrest - natural history?

A

Period of hypothermia is common in first 48 hours. Sep after mild induced hypothermia. Both associated worse outcomes. (?maybe elevated temp is evidence of a more damaged brain)
Regardless: treat with antipyretics and consider cooling.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How much is CMRoxygen reduced by each degree drop?

A

(Cerebral metabolic rate for oxygen) drops by 6%/degree.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are some of the cellular processes affected by cooling?

A
  • Supresses pathways leading to apoptosis/other cell death.
  • Blocks intracellular consequences of excitoxin exposure (high calcium and glutamate concentrations) -> reduces inflammatory response.
  • Decreases CMRo2 -> in turn reduces release of excitatory amino acids/free radicals.
26
Q

What are the treatment recommendations for targeted temperature management for OHCA?

A

Maintain between 32 and 36 degrees for adults after OHCA if:
- initial shockable rhythm who remain unresponsive after ROSC (strong recommendation, low-quality evidence).
- initial non-shockable rhythm and unresponsive post-ROSC (weak recommendation, very low-quality evidence)
-

27
Q

What are the targeted temperature management recommendations for IHCA?

A

IHCA with any initial rhythm who remain unresponsive after ROSC (weak recommendation, very low-quality evidence)

28
Q

How long should targeted temperature management be in place for?

A

At least 24 hours.

29
Q

What confounding factor around quicker cooling affected trials?

A

More severely neurologically damaged patients lost thermoregulation more quickly and therefore cooled quickly -> had worse outcome.

30
Q

When to control temperature?

A

No rapid infusions pre-hospitally.

31
Q

Three phases of targeted temperature management?

A

Induction, maintenance and rewarming.

32
Q

How to reduce core temperature by 1.0-1.5 degrees?

A

30ml/kg of 4 degree saline or Hartmann’s

33
Q

What can be given to reduce shivering?

A
  • Sedation and neuromuscular blockade.

- Magnesium sulphate.

34
Q

Rate of rewarming?

A

0.25-0.5 degrees/hour

35
Q

Physiological effects of mild induced hypothermia?

A
  • Increases systemic vascular resistance -> bradycardia (improves outcomes by reducing diastolic dysfunction).
  • Diuresis -> electrolyte abnormalities.
  • Decreases insulin sensitivity and secretion - > hyperglycaemia tx.
  • Impairs coagulation: ? clinical effect negligible.
  • Impairs immune system and increases infection rates.
  • ? increases serum amylase concentration.
  • Reduced clearance of sedative drugs/neuromuscular blockers (by up to 30% at 34 degrees)
36
Q

Contraindications of targeted temperature management at 33 degrees?

A
  • Severe systemic infection.

- pre-existing medical coagulopathy (not fibrinolytic therapy)

37
Q

Suggested mechanism from animal data behind improved contractile function in mild induced hypothermia?

A

Increased calcium sensitivity.

38
Q

What drug is currently under evaluation for use with mild-induced hypothermia?

A

Xenon

39
Q

Why is minimising the risk of a falsely pessimistic outcome post-CA so important?

A

Majority of deaths are due to WLST; if a poor neurological outcome is predicted.

40
Q

Some problems with prognostication studies?

A
  • Most studies include so few patients that even if the FPR is 0%, the upper limit of the 95% CI is often high.
  • Self-fulfilling prophecy - not blinded physicians.
  • TTm, sedatives or neuromuscular blockade interfere with clinical examination and therefore prognostication indices.
41
Q

What two clinical sings predict poor outcome with close to 0% FPR?

A
  • Bilateral absence of pupillary light reflex at 72 hr post ROSC.
  • Bilaterally absent corneal reflex.
42
Q

What is the effect of the NM blockade on examining?

A

Affects motor response -> to pain/stimulation.

43
Q

Criteria for when myoclonus is associated with a poor outcome.

A

If a status myoclonus starts within 48 hours post ROSC in TTM and non-TTM patients. Not the best predictor

44
Q

What is an SSEP?

A

Short-latency somatosensory evoked potentials.

45
Q

What does bilateral absence of N20 SSEP waves suggest?

A

Predicts death or vegetative state with 0-3% FPR as early as 24 hour post ROSC-> following 48 hours in TTM-treated and non-TTM treated patients.

46
Q

What are the limitations of EEG reactivity?

A

Lack of standardisation as concerns the stimulation modality and modest interrater agreement.

47
Q

Name some more predictors of poor outcome and details.

A
  • Absence of EEG reactivity - esp TTM pts? less reliable evidence.
  • Status epilepticus, in TTM puts after rewarming.
  • ## Burst-suppression: more than 50% of the EEG record consisting of periods of EEG voltage <10 􏰁V, with alternating bursts. Usually a transient finding,
48
Q

Name some biomarkers released following injury to neurons and glial cells. Detail.

A

NSE: Neuron-specific enolase. Sep in non-TTM pts. sat days 24-72 post ROSC.
S-100B, less well-documented.

49
Q

Advantages and limitations of biomarkers as prognostic markers?

A
  • Advantages: quantitive results and independence from sedative effects.
  • Limitations: difficult to define threshold with certainty - serum concentrations of biomarkers are per se continuous variables, which limits their applicability for predicting a dichoto- mous outcome, especially when a threshold for 0% FPR is desirable.
50
Q

How does a global anoxic ischaemic injury present on CT/MRI?

A

CT - cerebral oedema: reduction in the depth of cerebral sulci (sulcal effacement) and an attenuation of the grey matter/white matter (GM/WM) interface, due to a decreased density of the GM.

MRI: hyperintensity in cortical areas or basal ganglia on diffusion weighted imaging (DWI) sequences.

51
Q

MRI advantages over CT (NB can over-complicate)

A

Better spatial definition and a high sensitivity for identifying ischaemic brain injury

52
Q

Talk through prognostication strategy algorithm.

A

ROSC
Days 1-2: TTM -> rewarming
Days 3-5: Exclude confounders (residual sedation etc) If pt still unconscious at more than or 72 hr post ROSC:
- Pupillary/corneal relfex?
- Bilaterally absent N20 SSEP waves?
If any: poor outcome very likely.
If none - wait 24hr and re-evaluate.
Other poor outcome predictors:
- Status myoclonus at or more than 48 hours post ROSC
- High NSE levels
- Unreactive burst-suppresion or status epilepticus on EEG.
- Diffuse anoxic brian injury on CT/MRI.

Other notes: daily clinical examination, extensive monitoring.

53
Q

Other than sedatives/nm blockade, what other confounding factors are there?

A

Hypothermia, severe hypotension, hypoglycaemia, and metabolic and respiratory derangements

54
Q

Common neurological sequela in cardiac arrest survivors?

A

Cognitive impairments (1/2 survivors): memory most common, then attention and executive functioning.
Emotional/ mental health problems.
Fatigue.

55
Q

Controlled organ donation vs uncontrolled?

A

Controlled: planned withdrawal of treatment following non-survivable injuries and illnesses.
Uncontrolled: unsuccessful CPR

56
Q

What can exacerbate brain injury post arrest?

A

Microcirculatory failure, impaired autoregulation, hypotension, hypercarbia, hypoxaemia, hyperoxaemia, pyrexia, hypoglycaemia, hyperglycaemia and seizures.

57
Q

What happens in hyperxaemia?

A

Oxidative stress and harms post-ischaemic neurones.

myocardial injury, recurrent myocardial infarction and major cardiac arrhythmia

58
Q

Indications for a CT?

A

ROSC patient - no obvious cardiac cause

59
Q

What are the Richmond/Ramsay scales?

A

Sedation scales - ?look up

60
Q

How does post-cardiac arrest brain injury manifest?

A

Coma, seizures, myoclonus, varying degrees of neurocognitive dysfunction and brain death.

Resuscitation 2015 (31 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions