Post-resusitation care Flashcards

1
Q

Following ROSC what is the next goal of patient care?

A

To return the patient to normal cerebral function

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2
Q

Where does post-resuscitation care start?

A

Where ROSC is achieved, immediately after

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3
Q

Once a patient is stabalised after ROSC where should they be transferred ?

A

To the most appropriate high-acuity area i.e. ICU or CCU

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4
Q

What 4 things does the post cardiac arrest syndrome comprise of ?

A
  1. Post cardiac arrest brain injury
  2. Post cardiac arrest myocardial dysfunction
  3. Systemic ischaemia/reperfusion response
  4. Persistent precipitating pathology.
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5
Q

What does post-cardiac arrest brain injury manifest as ?

A

Comas, seizures, myoclonus, varying degrees of neurocongitive dysfunction and brain death

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6
Q

Significant myocardial dysfunction post cardiac arrest is common how long does it take to improve?

A

Usually starts to recover by 2-3 days although full recovery may take longer.

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7
Q

What does the whole body ischaemia/reperfusion of a cardiac arrest cause ?

A
  • Activates immune and coagulation pathways contributing to multi-organ failure and increasing risk of infection.
  • It has many features in common with sepsis such as intravascular volume depletion, vasodilatation, endothelial injury and microcirculatory abnormalities.
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8
Q

Following ROSC an ABCDE approach should be taken.

What do you do for A&B?

A
  • If not already occured during CPR and patient is comatosed then carry out tracheal intubation.
  • If patient has normal cerebral function then deliver oxygen via a face mask.
  • Target sats are 94-98% or 88-92%.
  • Insert NGT to decompress the stomach
  • ABG
  • CXR
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9
Q

What does hypoxaemia & hypercarbia post ROSC increase the likelihood of ?

A

Of a further cardiac arrest & may contribute to secondary brain injury.

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10
Q

After ROSC what will the PaCO2 levels often be ?

What are you aiming to achieve in post-resus care for PaCO2 levels ?

A
  • Raised - due to intra-arrest hypoventilation and poor tissue perfusion, causing a mixed resp/metabolic acidosis.
  • Aim for normocarbia. This is because hypercarbia causes vasoconstriction and possibly cerebral ischaemia. Whilst hypocarbia increases cerebral blood flow and ICP.
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11
Q

If a tracheal tube is inserted too far where is it more likely to go down?

A

The right main bronchus, therefore failing to ventilate the left lung.

Right main bronchus is shorter, wider and more verticle ==> easier for tube to pass into.

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12
Q

Following ROSC an ABCDE approach should be taken.

What do you do for C?

A
  • Record a new 12-lead ECG
  • Continuous cardiac monitoring.
  • Arterial line for BP monitoring.
  • Measure urine output.
  • Central venous catheter.
  • Consider fluids, diuretics and vasodilators or vasopressors/inotropes.
  • If suspected ACS as cause d/w cardiology and consider PCI or fibrinolysis.
  • ECHO
  • Bloods.
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13
Q

Is hyperoxaemia bad post ROSC?

A

Yes it causes oxidative stress and harms post ischaemic neurones.

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14
Q

Following ROSC an ABCDE approach should be taken.

What do you do for D&E?

A
  • Exclude other precipitating causes e.g. massive blood loss, resp failure, PE, drug overdose, SAH.
  • Consider CTPA & CTH
  • Record GCS
  • Consider targeted temperature management (TTM) if patient remains comatosed (32-36degrees).
  • Maintain tight BM control - aim 4-10.
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15
Q

Following post ROSC A-E assessment, what should you also obtain?

A

A comprehensive history from staff & family +/- patient if possible.

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16
Q

Go over the GCS

A
17
Q

On an ABG what is often seen post ROSC?

A
  • Mixed resp/metabolic acidosis.
  • Metabolic acidosis due to tissue hypoperfusion causing low bicarb, and a high lactate.
  • Resp acidosis due to hypoventilation and poor tissue perfusion driving up PaCO2.
18
Q

What is the most effective way of correcting post cardiac arrest acidaemia ?

A

Address the underlying cause e.g. poor perfusion give inotropes and fluids not bicarbonate.

Bicarbonate may paradoxically increase intracellular acidosis so is only given in association with hyperkalaemia and TCA overdose.

19
Q

Why should all patients get an ECHO post cardiac arrest, regardles if ACS is suspected or not ?

A

To ax degree of myocardial dysfunction. This often requires transient inotropic support.

20
Q

What is the 1st line for supporting a patients BP post cardiac arrest and why?

A

**Noradrenaline +/- dobutamine **
This is because despite dobutamine being the most established med for cardiac dysfunction, post arrest there is vasoplegia and severe vasodilatation. => low SVR is the main issue.

21
Q

If post ROSC tx with fluid resus, inotropes and vasopressors is inadequate to maintain someones BP what can be considered?

A

Intra-aortic balloon pump (IABP).

22
Q

What is the target BP post ROSC?

A
  • Decided on a patient to patient basis usually MAP >65.
  • Target adequate UO >0.5ml/kg/hr & normal or decreasing lactate values i.e. adequate tissue perfusion.
23
Q

What often happens to potassium levels post cardiac arrest?

A
  • Immediately after there is a period of hyperkalaemia and then subsequent catecholamine release and correction of resp/metabolic acidosis causes hypokalaemia.
  • There may need to supplement K+ maintain levels 4.0-4.5.
24
Q

What can hypokalaemia predispose to post ROSC?

A

Ventricular arrythmias.

25
Q

What should all patients whom were in a shockable rhythm on presentation of cardiac arrest and the cause was not ACS be referred/considered for ?

A

ICD.

26
Q
A
27
Q

What happens to cerebral blow flow after ROSC?

A
  • Initially cerebral hyperemia occurs between 5 and 30 min after resuscitation.
  • Following hyperemia, cerebral hypoperfusion occurs from 30 min to 6 h after resuscitation
  • Maintain MAP near normal
28
Q

Patients after often sedated following ROSC what is often given and for how long?

A
  • Usually a combo of opiates and hypnotics e.g. propofol, alfentanil, remifentanil.
  • Usually for a min of 24hrs.
29
Q

How often are seizures reported post ROSC and what are they usually a sign of ?

A
  • 20-30% of the time.
  • They are usually a sign of severe hypoxic-ischaemic brain injury.
30
Q

What is the most common type of seizure post ROSC?

A

Myoclonus
https://www.youtube.com/watch?v=8J2aKLK0dpo

Note - other seizures e.g. tonic-clonic do occur.

31
Q

What investigation will help diagnose seizures post ROSC?

A

EEG

32
Q

What is the 1st line options for treating post ROSC seizures?

A

1st line = levetiracetam (Keppra) &/or sodium valproate.

33
Q

Why should you induce hypothermia post ROSC and how do you do this ?

A

Hypothermia is neuroprotective and improves outcomes. It reduces excitatory amino acids and free radicals, blocks intracellular consequences of excitotoxin exposure (high calcium and glutamate) and reduces inflammatory response.

34
Q

Targeted temperature management is recomended for patients following ROSC if comatosed, what is the target temp and duration it should be continued for ?

A
  • Aim temp 32-36 degrees.
  • Cont >24hrs min.
35
Q

Target temperature management involves induction, maintenance and rewarming

What are methods of inducing, maintaining and re-warming?

A
  • Inducing TTM - can give 30ml/kg saline or hartmanns, simple ice packs or wet towels, cooling blankets, extracorporeal circuluation, or neuromuscular blockade and sedation
  • Maintaing - external or internal cooling devises are used
  • Rewarming - aim for about 0.25-0.5 degrees per hour
36
Q

If initial cooling is facilitated by neuromuscular bblockeade and sedation, what can be given for this?

A
  • NMBA’s usually Succinylcholine or Rocuronium
  • Also reg antipyretic agents (to prevent shivering) e.g. NSAID’s, Mg2+ sulphate etc.
37
Q

What are the physiological effects of hypothermia ?

A
  • Shivering - may inhibit cooling methods, hence antipyretics used.
  • Increased SVR and can cause arrythmias usually bradycardia
  • Diuresis amd electrolyte abnormalities (hypokalaemia/hypomagnesaemia/hypophosphataemia/hypocalcaemia)
  • Decreased insulin sensitivity and hence hyperglycaemia
  • Impaired coagulation/increased bleeding
  • Impairs immune system and increase infection rates.
  • Reduced clearance of sedative drugs and NMBA’s
38
Q

Prognositication is not reliable until after 72 hour from cardiac arrest

What can be measured to help prognose?

A

Combination of:
* **GCS + clinical exam **
* Neurophysiological studies - SSEP’s & EEG
* Biochemical markers - Neuron-specific enolase (NSE) high levels are associated with ischemic brain injury and poor outcome after cardiac arrest.
* Imaging - CTH and MRI.

39
Q

Go over the summary of the post-resus ALS algorithm

A