Post ROSC Care Flashcards
Targeted temperature?
36 degrees (not 32-34 anymore)
Why is hyperventilation dangerous?
Hypocapnia - cerebral ischaemia
What is included in post cardiac arrest syndrome?
Post-cardiac arrest brain injury, myocardial dysfunction, the systemic ischaemia/reperfusion response and the persistent precipitating pathology.
What accounts for most of the deaths within the first few days and then after?
Cardiovascular failure - first three days. Brain injury - thereafter. 2/3rd of IHCA, 25% of OOHCA survive to die in ICU.
Features of post-cardiac arrest that are similar to sepsis?
Intravascular volume depletion, vasodilation, endothelial injury and microcirculatory abnormalities.
Post -ROSC oxygen therapy - what and why?
Titrate to 94-98%. Hyperaemia possibly increases neurological injury/post MI harm.
Position of tracheal tube?
Above carina
Effects of hypocarbia?
Cerebral vasoconstriction and decreased cerebral blood flow.
Ideal tidal volume/positive end expiratory pressure?
- TV: 68ml/kg of IDEAL BW
- PEEP: 4-8cm H2O
What might a continuous infusion of a neuromuscular blockade result in?
- Masking of seizures.
- Interfere with clinical examination
PCI in a post-ROSC pt without STE or LBBB?
Possibly - controversial but bear in mind likely cardiac cause in patient and the lack of sensitivity/specificity in usual markers - ECG/biomarkers/examination etc.
ROSC patient - no obvious cardiac cause -action?
Hospital - CT to identify early respiratory or neurological cause. If trauma/haemorrhage - whole body CT.
Haemodynamic management?
- 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
BP target post-ROSC?
Aim for adequate urine output as a measure of end-organ perfusion.
(1ml/kg/hour)
And normal/decreasing plasma lactate
What can impair lactate clearance and increase urine output?
Hypothermia -> central diuresis and reduced BMR.
Would you treat a bradycardia of < or equal to 40bpm
No probably not - protective, especially against diastolic dysfunction.
Explain mechanism behind hyperkalaemia, then hypokalaemia post-ROSC.
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
When might you consider an ICD?
- 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
What happens to cerebral perfusion post-ROSC?
- 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 common are seizures post ROSC?
1/3rd who remain comatose post ROSC (Myoclonus, then tonic-clonic)
How do you treat seizures post ROSC?
a. Which drugs?
b. Which drugs post anoxic injury?
c. Which drugs in post-anoxic myoclonus?
a. Sodium valproate, levetiracetam, phenytoin, benzodi- azepines, propofol, or a barbiturate.
b - to suppress: propofol
c. tx: clonazepam, sodium valproate and levetiracetam
Blood glucose targets post ROSC?
< or equal to 10mmol/l and avoid hypo.
Avoid strict control as it risks hypo.
Temperature control after cardiac arrest - natural history?
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 much is CMRoxygen reduced by each degree drop?
(Cerebral metabolic rate for oxygen) drops by 6%/degree.
What are some of the cellular processes affected by cooling?
- 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.
What are the treatment recommendations for targeted temperature management for OHCA?
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)
-
What are the targeted temperature management recommendations for IHCA?
IHCA with any initial rhythm who remain unresponsive after ROSC (weak recommendation, very low-quality evidence)
How long should targeted temperature management be in place for?
At least 24 hours.
What confounding factor around quicker cooling affected trials?
More severely neurologically damaged patients lost thermoregulation more quickly and therefore cooled quickly -> had worse outcome.
When to control temperature?
No rapid infusions pre-hospitally.
Three phases of targeted temperature management?
Induction, maintenance and rewarming.
How to reduce core temperature by 1.0-1.5 degrees?
30ml/kg of 4 degree saline or Hartmann’s
What can be given to reduce shivering?
- Sedation and neuromuscular blockade.
- Magnesium sulphate.
Rate of rewarming?
0.25-0.5 degrees/hour
Physiological effects of mild induced hypothermia?
- 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)
Contraindications of targeted temperature management at 33 degrees?
- Severe systemic infection.
- pre-existing medical coagulopathy (not fibrinolytic therapy)
Suggested mechanism from animal data behind improved contractile function in mild induced hypothermia?
Increased calcium sensitivity.
What drug is currently under evaluation for use with mild-induced hypothermia?
Xenon
Why is minimising the risk of a falsely pessimistic outcome post-CA so important?
Majority of deaths are due to WLST; if a poor neurological outcome is predicted.
Some problems with prognostication studies?
- 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.
What two clinical sings predict poor outcome with close to 0% FPR?
- Bilateral absence of pupillary light reflex at 72 hr post ROSC.
- Bilaterally absent corneal reflex.
What is the effect of the NM blockade on examining?
Affects motor response -> to pain/stimulation.
Criteria for when myoclonus is associated with a poor outcome.
If a status myoclonus starts within 48 hours post ROSC in TTM and non-TTM patients. Not the best predictor
What is an SSEP?
Short-latency somatosensory evoked potentials.
What does bilateral absence of N20 SSEP waves suggest?
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.
What are the limitations of EEG reactivity?
Lack of standardisation as concerns the stimulation modality and modest interrater agreement.
Name some more predictors of poor outcome and details.
- 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,
Name some biomarkers released following injury to neurons and glial cells. Detail.
NSE: Neuron-specific enolase. Sep in non-TTM pts. sat days 24-72 post ROSC.
S-100B, less well-documented.
Advantages and limitations of biomarkers as prognostic markers?
- 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.
How does a global anoxic ischaemic injury present on CT/MRI?
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.
MRI advantages over CT (NB can over-complicate)
Better spatial definition and a high sensitivity for identifying ischaemic brain injury
Talk through prognostication strategy algorithm.
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.
Other than sedatives/nm blockade, what other confounding factors are there?
Hypothermia, severe hypotension, hypoglycaemia, and metabolic and respiratory derangements
Common neurological sequela in cardiac arrest survivors?
Cognitive impairments (1/2 survivors): memory most common, then attention and executive functioning.
Emotional/ mental health problems.
Fatigue.
Controlled organ donation vs uncontrolled?
Controlled: planned withdrawal of treatment following non-survivable injuries and illnesses.
Uncontrolled: unsuccessful CPR
What can exacerbate brain injury post arrest?
Microcirculatory failure, impaired autoregulation, hypotension, hypercarbia, hypoxaemia, hyperoxaemia, pyrexia, hypoglycaemia, hyperglycaemia and seizures.
What happens in hyperxaemia?
Oxidative stress and harms post-ischaemic neurones.
myocardial injury, recurrent myocardial infarction and major cardiac arrhythmia
Indications for a CT?
ROSC patient - no obvious cardiac cause
What are the Richmond/Ramsay scales?
Sedation scales - ?look up
How does post-cardiac arrest brain injury manifest?
Coma, seizures, myoclonus, varying degrees of neurocognitive dysfunction and brain death.
