ROSCAND POST RESUSCITATION CARE

LAKMAL NANDADEWA

ROSC OPENS THE DOORS TO CONTINUUM OF RESUSCITATION

MAIN GOALS TO INSTITUTE MEASSURES THAT ENSURE A HIGHER LIKELYHOOD OF NEUROLOGICALLY INTACT SURVIVAL

PROMPT IDENTIFICATION AND TREATMENT OF THE CAUSE OF CARDIAC ARREST -4Ts AND 4Hs

ESTABLISH DEFINITIVE AIRWAY MAMAGEMENT TO MAINTAIN NORMOCAPNIC VENTILATION,PREVENT HYPEROXIA

TO ESTABLISH AND MAINTAIN A STABLE CARDIAC RHYUTHM

TO ACHIEVE A NORMAL HAEMODYNAMIC FUNCTION-JUDICIOUS IV FLUIDS/VASOPRESSORS/INOTROPES

TTM,GLYCAEMIC CONTROL,SEIZURE MANAGEMENT,NEUROPROGNOSTICATION

TRANSFER THE PATIENT TO THE MOST APPROPRIATE HIGH-CARE AREA –ICU,CCU FOR CONTINUED MONITORING AND TREATMENT

POST CARDIAC ARREST SYNDROME

PATHOPHYSIOLOGY

1.Persistant precipitating pathology

coronary thrombus,hypoxia,PE,sepsis

2.Anoxic brain injury

Reperfusion after a period of cerebral hypoxia------formation of free radicals--------activation of cell death signalling pathways --------disturbance of cerebral microvascular haemostasis despite of adequate CPP and CBF is established

Aggravated by hyperthermia, hyper/hypoglycaemia, hyperoxia/hypoxia

Symptoms-coma, seizure, myoclonus, neurocognitive dysfunction and brain death

3.Post cardiac arrest myocardial dysfunction

Hypokinesia of the cardiac myocytes leads to significant drop in LVEF----first 24-48hrs post ROSC despite preserved coronary blood flow

Manifests as tachycardia, hypotension, poor cardiac output and elevated LVEDP

4.Systemic ischaemia/reperfusion responseWhole body hypoxia and ischaemia-------post ROSC reperfusion-----systemic inflammation, endothelial activation immunologic and coagulation cascade activation, ------increased risk of multiorgan system dysfunction

Manifests as fever , altered oxygen consumption, increased susceptibility to infection

POST CARDIAC ARREST BRAIN INJURY

POST CARDIAC ARREST BRAIN INJURY

POST CARDIAC ARREST MYOCARDIAL DYSFUNCTION

SYSTEMIC ISCHAEMIA/REPERFUSION SYNDROME

AIRWAY , VENTILATION AND OXYGENATION(ANZCOR)

Ensure clear airway, adequate ventilation and oxygenation

All comatose patients –definitive airway, ventilation and sedation

Blood oxygen saturation of 94%98%-ABG/pulse oximetry

Aim for normocapnia and avoid hyperventilation-End tidal CO2and waveform capnography

Avoid prolonged periods of hyperoxia-excessive oxidative stress may harm various organs, neuronal damage and irreversible changes within alveolar spaces ,associates with decreased survival to hospital discharge

Avoid hypocapnia .Aim arterial PaCO2 35-45mmHg and end tidal CO2 at 30-40mmHg

Initial vent settings should begin with 6-8ml/kg for TV and RR at 10-12 breaths/min

Look listen and feel

Consider collapse/consolidation, tension pneumothorax, Bronchial intubation, pulmonary oedema, aspiration and fractured ribs

THE EXACT STUDY

Reduction of oxygen after cardiac arrest (EXACT)

Compelling evidence that 100% oxygen (“hyperoxia”) during reperfusion(i.e. post arrest) may be harmful to the brain and the heart:

•Animal studies

•Observational human studies

•The AVOID trial

Multicenter retrospective cohort study

120 US hospitals 2001-2005

Non-traumatic cardiac arrest within 24 hours of ICU admission

Association between PaO2 of 1st ABG in ICU and in-hospital mortality

• Hyperoxia mortality rate 63%

• Hypoxia mortality rate 57%

• Normoxia mortality rate 45%

THE EXACT STUDY

Proposed Phase 3 study started in 2016 conducts in Victoria, Adelaide and Perth

Post OHCA with pulse oximeter>94%

Paramedics randomise to •2L/min O2(=50%) or •10L/min 02(=100%)

ED/Cath lab continue target of 100% or 94% oxygen saturation

ICU adjust to “normal”

HAEMODYNAMIC MANAGEMENT

Aim for a blood pressure equal to patients usual BP or at least a SBP >100mmHgor a MAP of >65mmHg

Targets for other haemodynamic parameters can vary among patients based on their specific comorbidities

Hypotensive patients –Vasopressors/inotropes(small IV increments of Adrenaline 50-100mcg)/infusion

Insufficient evidence to support or refute the routine use of IV fluids-cold 0.9%NACL/lactated ringers appears to be well tolerated in TTM

ECHO should be performed at 24-48Hrs following ROSC to monitor EF and rule out regional wall motion abnormalities

Mechanical circulatory support may be beneficial-IABP,ECMO

TARGETED TEMPERATURE MANAGEMENT

Maintain a constant, target temperature of 32–36oC for 24 h and rewarm slowly 0.25oC h-1

TTM is recommended for adults after out-of-hospital cardiac arrest with an initial shockable rhythm who remain unresponsive after ROSC

TTM is suggested for those unresponsive after non-shockable/in-hospital cardiac arrest

Exclusions: severe sepsis, pre-existing coagulopathy

TARGETED TEMPERATURE MANAGEMENT

Induction

30 ml kg-1 4oC IV fluid with monitoring (in-hospital)

+/- external cooling

Maintenance - external cooling

ice packs, wet towels

cooling blankets or pads

water circulating gel-coated pads

Maintenance - internal cooling

intravascular heat exchanger

cardiopulmonary bypass

Complications---sepsis, bradyarrhythmia, coagulopathy, shivering, decreased clearance of drugs ,electrolyte imbalances, Hyperglycaemia

GLYCAEMIC CONTROL, SEIZURE MANAGEMENT

BSL-6-10mmol/l

Seizure incidence -3-44%,no routine seizure prophylaxis recommended by NAZCOR but to treat if occurs and maintain therapy

CORONARY ARTERY DISEASE –MAJORITY

ASAP following ROSC-12 –lead ECG

Recommendation –ANZCOR guideline 11.7

STEMI/new LBBB –immediate angiography and PCI

Typical history without STE-Urgent angio+/- PCI

Fibrinolytic if primary PCI is not feasible in an appropriate time frame(within 90 mins of first medical contact –Resus council UK)

TTM is recommended in combination with primary PCI-should be started preferably prior to PCI

ACUTE PULMONARY EMBOLISM

Accounts for about 2-10% of cases

Fibrinolysis following cardiac arrest in suspected /diagnosed PE might be beneficial-Several studies showed no significant increase in survival to hospital discharge . Increased bleeding risk specially who had CPR

Surgical embolectomy for suspected /diagnosed after ROSC following cardiac arrest-Mortality is high and should be avoided in patients who have received CPR

Percutaneous mechanical thromboembolectomy may be beneficial and may be considered in patients sustaining cardiac arrest from PE who are not candidates for fibrinolysis

CARDIOTOXIC AGENTS, METABOLIC DISTURBANCES, SEPSIS

TCA, cardiac glycosides etc

Intralipids to enhance elimination may be considered and in massive overdoses HD to be considered

Hyper / hypokalaemia, hypercalcaemia should be promptly addressed

Sepsis-one of the common causes of circulatory collapse –Cultures, antibiotics

Resuscitation related injuries always to be assessed and appropriately manage post ROSC

TRANSFER OF THE PATIENT

discuss with admitting team

cannulae, drains, tubes secured

suction

oxygen supply

monitoring

documentation

reassess before leaving

talk to the patient’s family

PROGNOSTICATION , ORGAN DONATION

Brain injury is a result of initial ischaemic injury followed by reperfusion injury

Features- coma, seizures, myoclonus ,neurocognitive dysfunction ,memory deficits, persistent vegetative state and finally brain death

Absence of both pupillary light and corneal reflex at or after 72 hrs predicts poor outcome in who are comatose and no TTM,myoclonus ,low GCS,absence of vestibule ocular reflex are less reliable

Patients who had TTM prognostication should be performed 72 hrs post cardiac arrest and DNR orders/withdrawal of care should be avoided for 72 hrs following ROSC

Clinical examination, blood markers ,neurophysiological studies (Somatosensory evoked potentials /SEEPs,EEG,TCDs)imaging are used

ANZCOR recommends all patients who had ROSC post CPR and subsequently progress to death should be evaluated for organ donation

Pacing

TargetedTemperatureManagement

IABP

Defibrillator

Inotropes

Ventilation

Enteral nutrition

Insulin

REHABILITATION

REFERENCES

Deakin CD, Morrison LJ, Morley PT, Callaway CW, Kerber RE, Kronick SL, et al. Part 8: Advanced life support: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Resuscitation. [doi: DOI: 10.1016/j.resuscitation.2010.08.027]. 2010;81(1, Supplement 1):e93-e174.

Nolan JP, Neumar RW, Adrie C, Aibiki M, Berg RA, Bottiger BW, et al. Post-cardiac arrest syndrome: epidemiology, pathophysiology, treatment, and prognostication. A Scientific Statement from the International Liaison Committee on Resuscitation; the American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; the Council on Stroke. Resuscitation. 2008 Dec;79(3):350-79.

Soar J, Callaway C, Aibiki M, Böttiger BW, Brooks SC, Deakin CD, Donnino MW, Drajer S, Kloeck W, Morley PT, Morrison LJ, Neumar RW, Nicholson TC, Nolan JP, Okada K, O’Neil BJ, Paiva EF, Parr MJ, Wang TL, Witt J, on behalf of the Advanced Life Support Chapter Collaborators. Part 4: Advanced life support. 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Resuscitation 2015;95:e71–e1203

Consensus on Science and Treatment Recommendations Part 4: Advanced life support. Resuscitation 2005;67(2-3):213-47.

Randomized clinical study of thiopental loading in comatose survivors of car-diac arrest. Brain Resuscitation Clinical Trial I Study Group. N Engl J Med1986;314:397–403.234.

Longstreth Jr WT, Fahrenbruch CE, Olsufka M, Walsh TR, Copass MK, CobbLA. Randomized clinical trial of magnesium, diazepam, or both after out-of-hospital cardiac arrest. Neurology 2002;59:506–14.235.

SMJ-post resuscitation care

ANZCOR guideline 11.7 and 12.7

BMJ-therapeutic hypothermia for comatose survivors in OHCA