Flashcards in ALS Introductuon Deck (35):
1) Test for the patient’s response
1) Open their airway and check for normal breathing. Take care not to confuse normal breathing with agonal breathing.
2) Simultaneously with breathing assessment, check for other signs of life, e.g. coughing or movement - this should include checking for the carotid pulse.
3) Use any monitoring attached to the patient to assist in the decision making process.
This is slow, sighing respirations and is common in the early stages after cardiac arrest. It should not be confused with signs of life.
Diagnose cardiac arrest
unresponsive and either not breathing or only having occasional gasps
2) Calling for help
1) Send a member of staff to call 2222
2) Give location, nature of emergency and response required. (Send cardiac arrest team)
3) Starting CPR
1) 30 chest compressions
2) 2 ventilations
3) Attach the defibrillator/monitor as soon as it is available.
4) Give high flow oxygen
Good CPR (5)
1) Alternate 30 high quality chest compressions with 2 ventilations.
2) Compressions at centre of the chest, to a depth of 5-6 cm at a rate of approximately 100-120 min-1.
3) Allow the chest to fully re-expand between compressions and avoid residual pressure on the chest between compressions. Even brief interruptions in chest compressions are harmful and should be avoided.
4) Once the airway is secured switch to continuous chest compressions with asynchronous ventilation.
5) To avoid fatigue switch the CPR provider every 2 minutes.
4) Assess rhythm (3)
1) Attach defibrillator
2) Briefly pause to assess the underlying rhythm. Avoid interruptions in CPR of greater than 10 seconds duration.
3) Once you have determined if a shockable or non-shockable rhythm is present, re-start CPR
Ventricular fibrillation (coarse/fine)
Ventricular tachycardia (Monomorphic/Polymorphic)
VF see ECG
Characterised by bizarre irregular waveform with no recognisable QRS complexes. There is no pattern to the frequency or amplitude giving the appearance of uncoordinated electrical activity.
The amplitude (or size) of the ECG trace can lead to VF being described as either coarse or fine. Very fine VF rarely responds to a shock and will eventually degenerate into asystole. If you are uncertain whether there is fine VF or asystole, treat as asystole and continue CPR.
Be aware that movement or electrical interference can on occasion give rise to an ECG that could look like VF.
Monomorphic VT is a characterised by broad QRS complexes, rapid rate and constant QRS morphology.
Polymorphic VT is characterised by a cyclical increasing and decreasing waveform amplitude.
If the patient is in cardiac arrest, treat both rhythms as if they are VF
3a) Preparing for shock
Once a shockable rhythm is identified, restart CPR and prepare the team to deliver a shock. It is important to minimise the hands off time both before and after delivering a shock
Charge the defibrillator during CPR. Ensure all other team members are clear of the patient during charging.
Once defibrillator is charged, the team and CPR provider stand clear of the chest and the shock is delivered without pausing to recheck the rhythm.
As soon as the shock is delivered, restart CPR immediately and continue for a further 2 minutes.
Throughout the shock sequence minimise interruptions in chest compressions
to be told
3c) After 2 mins of CPR post shock
If after 2 minutes of high quality CPR, VF/VT persists give a second shock and restart CPR for a further 2 minutes. (Start preparing adrenaline 1 mg IV and amiodarone 300 mg IV.)
If VF/VT still persists then give a third shock and restart CPR.
After the third shock give adrenaline 1 mg IV and amiodarone 300 mg IV.
3d) After the third shock
After the third shock give adrenaline 1 mg IV and amiodarone 300 mg IV.
Asystole is characterised by absent ventricular activity. Occasionally atrial activity may persist. Unlike true asystole, isolated P wave activity may respond to pacing.
If a completely straight line is seen check the defibrillator setting is correct and leads/pads are appropriately attached.
Asystole is treated by providing CPR for 2mins
Identification and treatment of reverisble causes and administering 1mg IV adrenaline.
Repeat doses may be given every 3-5 minutes.
Pulseless electrical activity (PEA) is defined as organised cardiac electrical activity in the absence of any palpable pulses.
These patients often have some mechanical myocardial contractions but they are too weak to produce a detectable pulse or blood pressure.
In the presence of pulseless electrical activity, in skilled hands, ultrasound can be useful for the detection of potentially reversible causes of cardiac arrest (e.g. cardiac tamponade, pulmonary embolism, ischaemia (regional wall motion abnormality), aortic dissection, hypovolaemia, pneumothorax). The integration of ultrasound into advanced life support requires considerable training if interruptions to chest compressions are to be minimised. A sub-xiphoid probe position is recommended. Placement of the probe just before chest compressions are paused for a planned rhythm assessment enables a well-trained operator to obtain views within 10 seconds. The Focused Echocardiography Extended Life Support Course (FEEL-UK) provides a valuable introduction to echocardiography in this setting.
Return of spontaneous
Controlled oxygenation and ventilation
12 lead ECG
Treat precipitation causes
supraglottic airway device e.g. LMA, i-gel
Do not attempt intubation unless trained and competent to do so
Once airway secured, if possible, do not interrupt chest compressions for ventilation
Ventilate the lungs at 10 breaths min-1 and avoid hyperventilation
Capnograph: may be used to confirm tube placement and monitor the quality of CPR. A rapid rise in ETCO2 may be an early sign of ROSC (return of spont circ)
Although the time taken for drugs to reach the central circulation is longer for peripheral rather than centrally administered drugs, the risk of complications from inserting a central line during CPR is high.
Unless the patient has a pre-existing, patent central line, peripheral venous access is the route of choice for administering drugs in cardiac arrest. Follow all injections of drugs with at least a 20ml bolus of fluid and elevate the limb if possible.
IO access if no IV access in 2 mins
Causes of cardiac arrest
Ensuring the airway is patent. Ventilate the lungs using high flow supplemental oxygen.
Although it has been common practice to hyperventilate a patient in cardiac arrest based on the premise that this will blow off excess CO2, this practice should be avoided as hyperventilation reduces coronary perfusion pressure and worsens outcome
Clues to hypovolaemia may come from the patient history, review of observation charts or clinical examination. Evidence of hypovolaemia may be obvious such as internal or external haemorrhage, blood in drains or more subtle, such as severe sepsis or anaphylaxis.
If hypovolaemia is suspected, rapidly infuse intravenous fluids
Rapid measurement of potassium and glucose.
Review the patient’s latest laboratory results.
Immediate treatment of hyperkalaemia is administration of calcium chloride followed by insulin/dextrose infusion.
Low potassium/magnesium levels may be treated with electrolyte infusions.
Hypothermia is rare as a cause of cardiac arrest if the patient is an in-patient.
Measure core temperature with a low reading thermometer.
Treatment of the hypothermic patient in cardiac arrest will require active re-warming techniques.
Cardiopulmonary bypass may be considered if facilities are immediately available or if active re-warming strategies fail
In the intubated patient check tube position as intubation of the right main bronchus can complicate the diagnosis of tension pneumothorax.
Clinical signs of a tension pneumothorax comprise decreased breath sounds and hyper-resonant percussion note on the side of the pneumothorax. The mediastinum will be shifted to the contralateral side which gives rise to the clinical sign of tracheal deviation away from the side of the pneumothorax.
Treat with needle decompression. Be aware that chest wall thickness may exceed standard cannula lengths. If this is suspected perform a thoracostomy
Cardiac tamponade is difficult to diagnose without echocardiography as many of the features on clinical examination are difficult or impossible to elicit during cardiac arrest.
Tamponde should be considered after penetrating chest trauma or after cardiac surgery.
Treatment is with either needle pericardiocentesis or resuscitative thoracotomy
Drug toxicity is relatively rare unless there is evidence of deliberate overdose.
For in-patients, a review of the patient’s drug chart may be helpful.
There is no evidence to support the routine thrombolysis of a suspected acute myocardial infarction. If PE is suspected then fibrinolytic therapy can be considered.
Following fibrinolysis during CPR for acute pulmonary embolism, survival and good neurological outcome have been reported in cases requiring in excess of 60 min of CPR. If a fibrinolytic drug is given in these circumstances, consider performing CPR for at least 60–90 min before termination of resuscitation attempts.
A successful resuscitation attempt is one which allows the patient to go home from hospital with no neurological deficit or other functional impairment. Far from being the end of a resuscitation attempt, the return of spontaneous circulation marks the start of the post resuscitation care phase. Careful assessment using the ABCDE approach and application of a post resuscitation care bundle which includes controlled oxygenation and ventilation, identification and treatment of precipitating cause, and consideration of therapeutic hypothermia.