cardiopulmonar post resucitacion

7/27/2019 Cardiopulmonar Post Resucitacion

1/4

Cardiopulmonaryresuscitation andpost-resuscitation careJonathan Mackenney

Jasmeet Soar

AbstractSurvival following cardiac arrest depends on early recognition and effec-

tive treatment with high-quality chest compressions with minimal inter-

ruption, ventilation, treatment of reversible causes, and defibrillation if

appropriate. Successfully resuscitated patients can develop a SIRS-like

post-cardiac arrest syndrome. Post-cardiac arrest care includes coronary

reperfusion, control of oxygenation and ventilation, circulatory support,

glucose control, treatment of seizures, and therapeutic hypothermia.

Prognostication in comatose survivors is challenging. Approximately

one-third of cardiac arrest survivors admitted to intensive care are dis-

charged home.

Keywords Asystole; cardiac arrest; cardiopulmonary resuscitation;

defibrillation; hypothermia; post-resuscitation care; pulseless electrical

activity; ventricular fibrillation

Royal College of Anaesthetists CPD Matrix: 1B03, 1B04, 3C00.

IntroductionThere are an estimated 50,000 cardiac arrests treated annually in

the UK. Of these, about 60% occur out-of-hospital. Post-cardiac

arrest patients who remain comatose after successful restoration

of a spontaneous circulation (ROSC) account for one in 17

intensive care unit (ICU) admissions in the UK. Ventricular

fibrillation (VF) or pulseless ventricular tachycardia (VT) is the

presenting rhythm in most out-of-hospital cardiac arrests. Early

defibrillation is the effective treatment for VF/VT and each

minute of delay decreases the chances of success by roughly

10%. Survival to hospital discharge after out-of-hospital cardiac

arrest is 8e10%. The incidence of in-hospital cardiac arrest is

about 1e5 per 1000 admissions. Survival is greatly increased if

the first rhythm recorded in cardiac arrest is shockable. In 80% of

in-hospital cardiac arrests, however, the first monitored rhythm

is asystole or pulseless electrical activity (PEA). Approximately

15e20% of patients suffering in-hospital cardiac arrests survive

to hospital discharge. One-third of cardiac arrests survivorsadmitted to ICU are discharged from hospital and survival rates

are improving. Most survivors have a good neurological

outcome.

The Chain of Survival

All four links in the Chain of Survival (Figure 1) must be strong

to improve survival from cardiac arrest.

Early recognition and call for help

Recognition of the importance of chest pain and alerting the

ambulance service can prevent out-of-hospital cardiac arrest. In

the hospital, early identification of patients at risk of cardiacarrest using an early warning scoring system, alerting the

resuscitation team or medical emergency team (MET), and

appropriate treatment may prevent cardiac arrest. Here, we cover

the issues following cardiac arrest.

Cardiopulmonary resuscitation

Diagnosis of cardiac arrest

Gasping (agonal breathing) after a sudden cardiac arrest (usually

VF/VT) is common and can cause a delay in starting CPR.

Rescuers should look for signs of life, including a pulse. If signs

of life are absent or the rescuer is unsure, CPR should be started.

In anaesthetized or intensive care unit (ICU) patients, the pres-ence of monitoring will also help to make the diagnosis but

should not cause delays in starting CPR. Chest compressions in

a low cardiac output state are unlikely to be harmful.

Chest compressions

Chest compressions generate blood flow by increasing intra-

thoracic pressure and compressing the heart directly. At best,

compressions achieve 25% of normal brain and myocardium

perfusion. A higher coronary perfusion pressure (CPP aortic

diastolic pressure e left ventricular end diastolic pressure) ach-

ieved during CPR is associated with improved ROSC. Each time

chest compressions stop, the CPP decreases rapidly. On resuming

Learning objectives

After reading this article, you should be able to:

C describe the recognition and treatment of cardiac arrest in

adults according to current guidelines, understanding the

importance of high-quality chest compressions and minimizing

interruptions to chest compressionsC describe a safe defibrillation technique that includes a brief

pause in chest compressions to confirm shockable rhythm,

charging during chest compressions, and a brief pause in

compressions for shock delivery

C list post-cardiac arrest care interventions including the use of

therapeutic hypothermiaC understand the difficulties of prognostication in comatose

survivors of cardiac arrest

Jonathan Mackenney MRCP is a CT2 in ACCS Emergency Medicine in the

Severn Deanery, UK. Conflict of interest: none declared.

Jasmeet Soar FRCA FFICM is a Consultant in Anaesthetics and Intensive

Care Medicine at Southmead Hospital, North Bristol NHS Trust, UK.

Conflicts of interest: none declared.

INTENSIVE CARE

ANAESTHESIA AND INTENSIVE CARE MEDICINE 14:1 15 2013 Elsevier Ltd. All rights reserved.
http://dx.doi.org/10.1016/j.mpaic.2012.11.009http://dx.doi.org/10.1016/j.mpaic.2012.11.009


2/4

chest compressions, it takes time to achieve the same CPP that

existed just before compressions were interrupted. Recent

evidence points to the need for deeper chest compressions at

a higher rate. The current recommended depth for chest

compressions in an adult is 5e

6 cm at a rate of 100e

120 perminute. The compression to ventilation ratio is 30:2.

Advanced life support (ALS)

The ALS algorithm gives a standardized approach to cardiac

arrest treatment (Figure 2).

Airway and ventilation

No specific airway and ventilation technique has been shown to

improve cardiac arrest outcomes. Tracheal intubation by trained

rescuers enables continuous chest compressions at 100e120 per

minute without pauses for ventilations. Tracheal tube placement

should be confirmed by auscultation of the chest during ventilation

and waveform capnography. During effective CPR, there should be

a carbon dioxide waveform. If no carbon dioxide is detected this

should immediately raise the possibility of oesophageal intubation.

Waveform capnography also provides a measure of CPR quality.

High-quality CPR will increase end-tidal carbon dioxide, and ROSC

is associatedwitha rapid increase in end-tidalcarbondioxideduring

CPR. The recommended ventilation rate is 10 per min as a higher

rate decreases the CPP. Compared with bag-mask ventilation, early

ventilation with a supraglottic device reduces the incidence of

gastric distension and regurgitation. If a supraglottic airway

(e.g. laryngeal mask airway, I-gel) has been inserted, attempt

continuous chest compressions without stopping for ventilations. If

excessive gas leakage results in inadequate ventilation of the

patients lungs, interrupt chest compressions to enable ventilation.

Defibrillation

Defibrillation creates a current across the myocardium to depo-

larize a critical mass of the cardiac muscle enabling natural

cardiac pacemaker tissue to resume control. Every 5-second

increase in the pre-shock pause (the interval between stopping

CPR and shock delivery) halves the chance of successful defi-

brillation. To minimize the pre-shock pause self-adhesive defi-

brillation pads should be applied without stopping CPR. Before

stopping chest compressions, the team should plan what to do if

defibrillation is appropriate including the importance of safety.

Identify who will assess the electrocardiogram (ECG), and in the

event of a shockable rhythm, identify who will charge the defi-

brillator and deliver the shock. Chest compressions should stop

briefly to analyse the ECG and confirm a shockable rhythm.

Chest compressions should then immediately resume whilst the

defibrillator is charged. All other rescuers are instructed to standclear and ensure no oxygen is flowing across the chest (leave

tracheal tubes or supraglottic devices attached to the breathing

circuit or bag device). Once the defibrillator is charged, the

rescuer performing chest compressions also stands clear. The

shock is delivered with no-one touching the patient. Chest

compressions then immediately resume for a further 2 minutes. If

there are delays due to difficulties in rhythm analysis or rescuers

still in contact with the patient, chest compressions should be

resumed whilst another plan is made.

Drugs

Drug use during CPR is supported by very little evidence.

Adrenaline (1 mg every 4e5 minutes) increases the CPP during

CPR and is associated with improved ROSC. Recent observational

studies suggest that adrenaline use may be associated with worse

survival and neurological function at 1 month. Amiodarone (300

mg) given to patients in ventricular fibrillation (VF) refractory to

defibrillation attempts has only been shown to improve short-

term survival. Drug administration and attempts at intravenous

access should not cause interruptions in chest compressions. The

intra-osseous route should be used if intravenous access is not

possible. The tracheal route is no longer recommended.

Reversible causes

Identify and treat reversible causes during CPR. These are

divided into two groups of four based upon their initial letter e

either H or T (Figure 2). Ultrasonography by trained rescuers

whilst minimizing interruptions in CPR can help identify

reversible causes (e.g. cardiac tamponade).

Post-cardiac arrest care

Resuscitation from cardiac arrest triggers a systemic inflamma-

tory response syndrome (SIRS). This post-cardiac arrest

syndrome consists of: (i) brain injury, (ii) myocardial dysfunc-

tion, (iii) systemic ischaemia/reperfusion response, and (iv) the

precipitating disease that caused the cardiac arrest. A bundle of

early post-cardiac arrest care using Airway, Breathing, Circula-

tion, Disability, Exposure approach improves survival. The

Figure 1 The chain of survival. CPR, cardiopulmonary resuscitation.

INTENSIVE CARE



3/4

decision to admit a comatose post-cardiac arrest patient to ICU

should be based predominantly on the patients status before the

cardiac arrest. To optimize their chances of survival, patients

resuscitated from cardiac arrest benefit from admission to

a designated cardiac arrest centre that offers both specialist ICU

and cardiac catheter facilities.

Airway and breathing

Considertracheal intubation, sedation and controlled ventilation in

comatose patients after ROSC. Adjust oxygenation and ventilation

to achieve normal arterial oxygen saturation (94e98%) and

normocapnia. Hypocapnia, hypoxia and hyperoxia are all poten-

tially harmful to the reperfused brain.

Circulation

Acute ST-segment elevation or new left bundle branch block on

a 12-lead ECG and a typical history of acute myocardial infarction

are indications for reperfusion therapy. Percutaneous coronary

intervention (PCI) performed by an experienced team within

90 minutes of first medical contact is the preferred technique for

reperfusion. CPR is not a contraindication to thrombolysis if PCI

is not available. About one-quarter of patients with primary

Resuscitation Council (UK)

ALS algorithm

CPR 30:2Attach defibrillator / monitor

Minimize interruptions

Shockable

(VF / Pulseless VT)

1 Shock

During CPR

Ensure high-quality CPR: rate, depth, recoil

Plan actions before interrupting CPR

Give oxygen

Consider advanced airway and capnography

Continuous chest compressions when advanced

airway in place

Vascular access (intravenous, intraosseous)

Give adrenaline every 35 minutes

Correct reversible causes

Reversible causes

Hypoxia

Hypovolaemia

Hypo- /hyperkalaemia /metabolicHypothermia

Thrombosis - coronary or pulmonary

Tamponade - cardiac

Toxins

Tension pneumothorax

Non-shockable

(PEA /Asystole)

Callresuscitation team

Unresponsive?

Not breathing or

only occasional gasps

Return ofspontaneous

circulation

Immediately resume

CPR for 2 minutesMinimize interruptions

Immediately resume

CPR for 2 minutesMinimize interruptions

Immediate post-cardiacarrest treatment

Use ABCDE approach

Controlled oxygenation and

ventilation

12-lead ECG

Treat precipitating cause

Temperature control /

therapeutic hypothermia

Assess

rhythm

Figure 2 Reproduced with permission from the Resuscitation Council (UK).

INTENSIVE CARE



4/4

cardiac arrest may have acute coronary artery occlusion despite

no preceding chest pain and no acute ST elevation on a 12-lead

ECG. Early PCI should therefore be considered for any cardiac

arrest patient in whom an acute coronary syndrome is suspected.

Haemodynamic instability caused by myocardial dysfunction is

common after cardiac arrest and often resolves within 48 hours.

Patients usually require large volumes of fluid, inotropes and

vasopressors to achieve haemodynamic stability. An intra-aorticballoon pump (IABP) can also provide mechanical assistance.

Aim to maintain serum potassium at 4.0e4.5 mmol/litre and

correct hypomagnesaemia. Patients resuscitated from VF cardiac

arrest outside the context of treated coronary artery disease

should be considered for an implantable cardioverter defibrillator

(ICD) before hospital discharge.

Disability and exposure

Cerebral hyperaemia immediately follows ROSC. This is followed

15e30 minutes later by global cerebral hypoperfusion. Normal

cerebral autoregulation is lost, leaving cerebral perfusion

dependent on mean arterial pressure (MAP). Hypotension can

worsen any neurological injury. After ROSC, attempt to maintainthe MAP at the patients usual level.

Mild hypothermia suppresses many of the chemical reactions

associated with reperfusion injury. Unconscious adult patients

with spontaneous circulation after cardiac arrest should be

cooled to 32e34C. Cooling should be started as soon as possible

and continued for at least 12e24 hours. Cooling can be rapidly

induced by infusing 30 ml/kg of cold (4C) crystalloid. There are

numerous techniques to maintain hypothermia (e.g. surface,

intravascular, intranasal cooling devices). Re-warm the patient

slowly (0.25C/hour) and avoid hyperthermia. The risk of a poor

neurological outcome increases for each degree of body

temperature over 37C.

Seizures and, or myoclonus occur in 5e

15% of consciouspatients after ROSC and 10e40% of comatose patients. Pro-

longed seizures are associated with a fourfold increase in

mortality and should be rapidly controlled. Treat with benzodi-

azepines, phenytoin, propofol, or a barbiturate. Clonazepam is

the treatment of choice for myoclonus. Alternative antimyoclonic

drugs include sodium valproate, levetiracetam and propofol.

Seizures or myoclonus are not always related to a poor prog-

nosis: 17% of these patients survive with good neurological

function. There have also been rare cases of good neurological

recovery despite status myoclonus. Continuous electroencepha-

lography monitoring should be used to detect seizures in patients

receiving neuromuscular blocking drugs.

Both a high and low blood glucose after ROSC is associatedwith a poor outcome. Aim to keep blood glucose between 4 and

10 mmol/litre.

Prognostication

Traditional markers of dismal prognosis at day 3 post-cardiac

arrest are less reliable than previously thought, due to the use

of therapeutic hypothermia. A significant proportion of coma-

tose, cooled patients with a motor response to pain no better than

extension at day 3 post-cardiac arrest later regain consciousness.

Even absent brainstem reflexes (pupillary response to light and

corneal reflexes) at day 3 can be unreliable. Hypothermia treat-

ment and use of sedation can delay recovery of motor responses

for 5e6 days after cardiac arrest. Reliable prognostication cannot

be achieved until 3 days after return to normothermia and has to

be multimodal. Prediction of a poor outcome should be based onat least two of the following: (i) incomplete recovery of brainstem

reflexes, (ii) myoclonus, (iii) an unreactive EEG, and (iv) absent

cortical somatosensory evoked potentials (SSEPs). Unfortunately

most ICUs do not have access to neurophysiology assessments.

Prognosis

In the UK, about one-third of ICU admissions after cardiac arrest

survive to hospital discharge. Survival rates are improving but

there is considerable variability between ICUs and regions. Most

cardiac arrest survivors return home and have a good quality of

life. Even those with good apparent survival can have neuro-

cognitive and psychiatric problems. A

FURTHER READING

Berdowski J, Berg RA, Tijssen JG, Koster RW. Global incidences of out-of-

hospital cardiac arrest and survival rates: systematic review of 67

prospective studies. Resuscitation 2010; 81: 1479e87.

Deakin CD, Nolan JP, Soar J, et al. European Resuscitation Council

Guidelines for Resuscitation 2010. Section 4. Adult advanced life

support. Resuscitation 2010; 81: 1305e52.

Meaney PA, Nadkarni VM, Kern KB, et al. Rhythms and outcomes of adult

in-hospital cardiac arrest. Crit Care Med 2010; 38: 101e8.

Nolan JP, Laver SR, Welch CA, et al. Outcome following admission to

UK intensive care units after cardiac arrest: a secondary analysis ofthe ICNARC Case Mix Programme Database. Anaesthesia 2007; 62:

1207e16.

Nolan J, Soar J, Eikeland H. The chain of survival. Resuscitation 2006; 71:

270e1.

Nolan JP, Soar J. Airway and ventilation techniques. Curr Opin Crit Care

2008; 14: 279e86.

Nolan JP, Soar J, Zideman DA, et al. European Resuscitation Council

Guidelines for Resuscitation 2010 section 1. Executive summary.

Resuscitation 2010; 81: 1219e76.

Oddo M, Rossetti AO. Predicting neurological outcome after cardiac

arrest. Curr Opin Crit Care 2011; 17: 254e9.

Zia A, Kern KB. Management of post cardiac arrest myocardial dysfunc-

tion. Curr Opin Crit Care 2011; 17: 241e

6.

USEFUL WEBSITES

European Resuscitation Council, www.erc.edu (accessed 5 May 2012).

International Liaison Committee on Resuscitation, http://www.ilcor.org

(accessed 5 May 2012).

Resuscitation Council UK, www.resus.org.uk (accessed 5 May 2012).

INTENSIVE CARE

http://www.erc.edu/http://www.ilcor.org/http://www.resus.org.uk/http://dx.doi.org/10.1016/j.mpaic.2012.11.009http://dx.doi.org/10.1016/j.mpaic.2012.11.009http://www.resus.org.uk/http://www.ilcor.org/http://www.erc.edu/

cardiopulmonar post resucitacion

Documents