Oleh: Ardhan Prahara Putra

Pembimbing: dr. Wiwi Jaya, Sp.An

LAB/SMF ANAESTHESIOLOGI DAN TERAPI INTENSIF FAKULTAS KEDOKTERAN UNIVERSITAS BRAWIJAYA RUMAH SAKIT UMUM DR.SAIFUL ANWAR MALANG 2011

ROSC CBF ICP STEMI NSTEMI AMI PCI ECG SSEP

: reperfusion of spontaneous circulatory : cerebral blood flow : intracranial pressure : ST-elevation myocardial infarction : Non ST-elevation myocardial infarction : acute myocardial infarction : percutaneous coronary intervention : electro-cardiography : somatosensory evoked potential

 Morbidity & Mortality remains though recent advances in resuscitation techniques

The International Liaison Committee on Resuscitation incorporates epidemiology, pathophysiology, treatment options and prognosticationfurther interventionsincrease good outcome

 The complex pathophysiological processes that occur following whole-body ischemia during cardiac arrest and the subsequent reperfusion response following successful resuscitation

 The immediate post-arrest phase occurs in the first 20 minutes following return of spontaneous circulation (ROSC) The early post- arrest phase occurs between 20 minutes and 6 to 12 hours after ROSC The intermediate phase is between 6 to 12 hours and 72 hours The recovery phase extends from 3 days and beyond

 Brain injury Myocardial dysfunction Systemic ischemia/reperfusion response Persistent precipitating pathology

 2/3 death cause out-of-hospital cardiac arrest patients

M A N I F E S T S

Persistent coma

Myoclonic status & Brainstem death

Complex mechanism
Free radical formation Disordered calcium homeostasis Activation of cell death signaling pathways Pathological protease cascades excitotoxicity

 Impaired cerebrovascular autoregulation + high CBF after ROSC cerebral edema BUT not significant increase of ICP Cerebral microvascular monitor: complexrarely performed Transcranial doppler ultrasound to detect:
Severe hyperemia Regional hypoperfusion

Other factors that affect cerebral function :

Pyrexia Seizure hyperglycemia

Caused by:
Myocardial stunningreversible reduction of contraction function Acute coronary syndrome
STEMI 30%

NSTEMI 25%
Unstable angina 38%

During cardiac arrest:

Blood flow ceases Halting oxygen delivery to tissue Halting removal of metabolic waste

CPRonly patially restore microcirculatory flow

Whole body ischemia reperfusion

Via immunological & coagulation pathways

Activate a systemic inflammatory response Activate coagulation pathways

If without activating endogenous fibrinolysis

Microvascular thrombosis

 To avoid further morbidity the cause of cardiac arrest must be addressed The cause of adult out-of-hospital cardiac arrest: AMI 50% Pulmonary emboli 10% The cause of in-hospital cardiac arrest patients: Systemic infection multi organ failure cardiac arrest

 Airway and ventilation Circulation Disability-optimizing neurological recovery

(admission to an Intensive Care Unit and involvement of several specialties)

 Intubate and ventilate patients after cardiac arrest no supported by specific research cerebral autoregulation impaired BUT cerebrovascular reactivity to CO2 seems to be preserved hipercarbi & subsequent vasodilation Hyperventilation cerebral ischemic targetting CO2 level

O2 cell essential

Must be in control

Oxydative stress
ischemiareperfusion response via the production of free radicals and mitochondrial damage

Neuronal damage

 In animal ventilate with 100% O2 (worse clinical and histopathalogical outcomes) ventilate with 96% O2 (better)

 half of cardiac arrest survivors caused by an acute coronary syndrome Early percutaneous coronary intervention (PCI) lower rates of death, reinfarction, congestive heart failure and cardiogenic shock than observed in those treated with conventional means ECG ST elevation (STEMI) angiography PCI History of chest pain & ST elevation poor predictors coronary lession angiography (considered postarrest care)

 Myocardial dysfunction is common after ROSC and is generally reversible and responsive to inotropes if fluid resuscitation alone is not effective

 optimize neurological recovery include seizure control, glucose control and control of temperature seizure control benzodiazepines, phenytoin, sodium valproate, propofol, or a barbiturate. Clonazepam is the treatment of choice for myoclonus Glucose control the upper value of the target range for blood glucose should be 144 mg/dL

 Hypothermia a part of standard treatment for cardiac arrest survivors who remain comatose post-ROSC 32 to 34C for 12 to 24 hours post-ROSC Complication: shivering,bradycardia,diuresis(hpovolemiaelectrolyte imbalance), insulin sensitivity & secretion hyperglicemia,impaired coagulation,impaired immune system risk of infection

 Remains complex Poor prognostication: absence of pupillary light reflexes, corneal reflex or motor response to painful stimuli at 72 hours post-ROSC, myoclonic status epilepticus Neurophysical test (SSEPs) = Bilateral absence of the N20 component with median nerve stimulation recorded on day 1 to 3 or later EEG & Radiology hasnt been developed

 Post-cardiac arrest syndrome occurs in four phases: immediate, early, intermediate and recovery Intervention in the early and intermediate phases well impact the outcome following cardiac arrest Post-cardiac arrest syndrome has four main components: post-cardiac arrest brain injury, post-cardiac arrest myocardial dysfunction, systemic ischemia reperfusion response, and persistent precipitating pathologies Optimal management critical team + several diffirent specialtists