CARDIOPULMONARY RESUSCITATION
BASIC LIFE SUPPORT
Recognition of cardiopulmonary arrest and maintenance of ventilation and circulation without equipment.
ADVANCED CARDIAC LIFE SUPPORT
1) Use of adjunctive equipment and special techniques for establishing and maintaining effective ventilation and circulation.2) ECG monitoring and arrhythmia recognition.
3) Establishment and maintenance of IV access.
4) Use of drug and electrical therapies.
PROLONGED LIFE SUPPORT
Post - resuscitative intensive care management.
BASIC LIFE SUPPORT
ABCs of CPR
Speed is the key to success.
Airway
1. Assessment : Determine unresponsiveness.
2. Call for help.
3. Position the pt. horizontal and supine on a flat hard surface.
4. Open airway with Head - Tilt / Chin - Lift Manoeuver or Jaw-Thrust Manoeuver.
5. Remove obstructions due to foreign body e.g. dentures, broken teeth, secretions, vomitus.
Breathing
1. Assessment : Determine breathlessness.
2. Perform rescue breathing:
Mouth- to- mouth : exhale into patient's lungs with a tidal volume of = 800-1000ml, each inspiration lasting 1-1.5 sec.
Mouth - to - mask: protects the resuscitator from contamination and a port is available for attaching O2.
Circulation
1. Assessment : Determine pulselessness.
2. Check carotid pulse. Pulse check should take 5-10sec.
3. If pulse present but no breathing , initiate rescue breathing - 2 breaths followed by 12 breaths/min.
4. If no pulse, begin external cardiac massage (ECM) after initiate 2 breaths.
5. ECM :
1. Compression rate : 80-100/min
2. Compression time should be at least 50% of each compression : relaxation cycle.
3. The ratio of ventilation to compression should be:
One operator - 2 to 15
Two operators - 1 to 5
ADVANCED CARDIAC LIFE SUPPORT
Adjuncts for oxygenation
Bag – valve – mask
Use a well-fitting mask and a self-inflating bag with a non-re breathing valve and O² supplement.
Oralpharyngeal airway
Use corret size and insert in the correct manner.
Endotracheal intubation
Intubate and vertilate with 100% O² as soon as practical.
Advantages :- isolates the airway and prevents aspirations.
- keeps it patient.
- Permits suctioning of the trachea.
- Ensure delivery of high concentration of O².
- Provides route for delivery of certain drugs.
Cardiac Monitoring & Arrhythmia Recognition
Establish ECG monitoring as soon as possible and identify arrhythmia and treat accordingly. ( see mx. Protocols for life threatening Arrhythmias).
Drug Therapy
Ideal intravenous access is a central vein e.g. internal jugular , subclavian or femoral vein because of significant delay of drug arrival at heart if peripheral veins are used.
Best peripheral access is antecubital vein. Follow injections of the drug with large volume of flush solution and elevate the extremity.
Adrenaline , atropine and lignocaine can be administered via the ETT (double the normal IV dose in 10 ml N/S).
- Adrenaline
Peripheral vasoconstriction which improves coronary and cerebral circulation. Makes VF more susceptible to countershock.
Dose : 1.0mg ( 1ml of 1:1,000 soln) every 5 min.
- Atropine
Parasympatholytic
Dose : Bradycardia – 0.5 mg bolus
Asystole : 1.0 mg ( repeat every 5 min )
- Dopamine
Low dose (dopaminergic effects) : 0.5 – 2.0 µg/ kg/ min – renal and mesenteric vasodilation.
Medium dose (predominantly β-effects ) : 2-10 µg/ kg/ min – increase myocardial contractility and cardiac output.
High dose (predominantly α-effects ): >10 µg / kg/ min – renal,mesenteric and peripheral vasoconstriction.
- Dobutamine
Predominantly β¹-effects. Increase cardiac output and peripheral vasodilation. Less tachycardia than dopamine.
Indication : cardiogenic shock.
Dose : similar to dopamine.
- Calcium Chloride and Sodium Bicarbonate
No longer recommended for the routine use in cardiac arrest except for the following specific indications:
☺Cacl²- hyperkalemia, hypocalcemia and calcium channel blocker toxicity.
☺NaHCO³ - hyperkalemia, severe metabolic acidosis, tricylic anti-depressant overdose and possibly prolonged resuscitation.
- Defibrillation & Cardioversion
Defibrillation is the emergency use of DC shock , without synchronization with the hearts electrical activity, to convert VF to sinus rhythm.
Cardioversion is the use of DC shock ( synchronized ) to convert certain atrial and ventricular tachyarrhythmias to sinus rhythm.
ADVANCED CARDIAC LIFE SUPPORT Key to survival is early access, early CPR , early defibrillation. Downtime = Access time i.e. time from observed collapse to call to + Arrival time i.e. dispatch to arrival at scene. + Arrival at scene until the 1st shock time. If downtime <6 minutes, survival = 28% If downtime >6 minutes, survival <5% |
DEFIBRILLATION
Rapid defibrillation is the major determinant of survival in cardiac arrest due to VENTRICULAR FIBRILLATION ( VF ).
If VF recurs after transiently converting, use whatever energy level that has previously been successful for defibrillation.
DRUGS
- Lignocaine
Anti-arrhythmic drug of choice for the management of ventricular ectopy, ventricular tachycardia ( VT ) and ventricular fibrillation (VF).
It is recommended in VT & VF that persists after defibrillation and adrenaline.
Dose : 1 mg/kg followed by 0.5 mg/kg/ every 8-10 min if needed to a total dose of 3mg/kg.
- Sodium Bicarbonate
ABG changes during cardiac arrest.
Metabolic acidosis : lactic acidosis from anaerobic metabolism. During the initial 10 min of CPR , only minor increases of blood lactate occur. Thus , metabolic acidosis is only significant if the arrest has been present for some time. Respiratory acidosis : inadequate ventilation leads to hypercarbia and respiratory acidosis. This is the major acid-base abnormality during CPR. Respiratory acidosis has a greater negative inotropic effect on myocardial contractility than metabolic acidosis. Effective ventilation and perfusion are the mainstay of management of acidosis.
Adverse effects of NaHCO
HCO³ + Hͭͭͭ ͭ ß-----à CO² + H²O
- CO² rapidly diffuses into cells causing intracellular acidosis.
- Hypernatraemia
- Hyperosmolity
- Shift oxy-haemoglobin dissociation curve to the left
- Induces rebound extracellular alkalosis
- Inactivate simultaneously administered catecholamines
- reduces extracellular ionised calcium
- reduces extracellular potassium
- induces or exacerbates congestive cardiac failure
- does not improve the ability to defibrillate
- precipitates in intravenous lines if given with calcium salts
- veno-irritant
Therefore NaHCO³ is not administered routinely during CPR
Used in following situations:
- pre-existing metabolic acidosis
- hyperkalemia
- tricyclic anti-depressant overdose
- protracted arrest or after prolonged resuscitation – 1 mmol/kg initially, then 0.5 mmol/kg not more frequently than every 10 min.
3.Calcium Chloride
Ca²ͭ increases myocardial contractility . High levels of Ca²ͭ in blood may induce reperfusion injury and may adversely affect neurologic outcome of the patient.
Indications : Hyperkalemia, Hypocalcemia, Calcium channel blocker toxicity.
CPR ALGORITHMS
VENTRICULAR FIBRILLATION ( VF ) / PULSELESS
VENTRICULAR TACHYCARDIA ( VT ) ALGORITHM
Ø ABCs Ø Perform CPR until defibrillator attached Ø VF / VT present on defibrillator |
↓
Defibrillate up to 3 times if needed for persistent VF/ VT ( 200J. 200-300J. 360J ) |
↓
Rhythm after the first 3 shocks ? |
↓
↓ ↓ ↓ ↓
Persistent or recurrent Return of spontaneous respiration PEA Asystole
VF / VT go to Fig2 go to Fig3
↓ ↓
* continue CPR * Assess vital signs
* Intubate * Support airway
* Obtain IV * Provide medications appropriate
For blood pressure, Heart rate
And rhythm
↓
Epinephrine 1 mg IV push, repeat Every 3-5 min |
↓
Defibrillate 360J Within 30-60 s |
↓
Administer medication of probable benefit in persistent or recurrent VF/VT |
↓
|
PULSELESS ELECTRICAL ACTIVITY (PEA) ALGORITHM
(Figure 2)
Includes - Electromechanical dissociation (EMD)
- Pseudo – EMD
- Idioventricular rhythms
- Ventricular ascape rhythms
- Bradyasystolic rhythms
- Postdefibrillation idioventricular rhythms
| * Continue CPR Assess blood flow using Doppler ultrasound, end-tidal CO², * Intubate at once echocardiography, or arterial line * Obtain IV access |
↓
| Consider possible causes * Hypovolemia (volume infusion) * Drug overdoses such atricyclics,digitalis, * Hypoxia (ventilation) β-blockers, calcium channel blockers * Cardiac tamponade (pericardiocentesis) * Hyperkalemia * Tension pneumothorax * Acidosis * Hypothermia * Massive acute myocardial infarction * Massive pulmonary embolism ( surgery , thrombolytics) |
↓
| Epinephrine 1 mg IV push repeat every 3-5 min |
↓
|
ASYSTOLE TREATMENT ALGORITHM
( Figure 3)
|
↓
| Consider possible causes
|
↓
| Consider immediate Transcutaneous pacing (TCP) |
↓
| Epinephrine 1 mg IV push , repeate every 3-5 min |
↓
| Atropine 1 mg IV repeat every 3-5 min up to a total of 0.03-0.04 mg /kg |
↓
| Consider termination of efforts |
BRADYCARDIA ALGORITHM
(Figure 4 )
| * Assess ABCs * Assess vital signs * Secure airway * Review history * Administer oxygen * Perform physical examination * Start IV * Order 12 lead ECG * Attach monitor , pulse oximeter, * Order portable CXR And aoutomatic blood pressure |
Too slow (< 60 bpm )↓
| Bradycardia, either absolute (<60 bpm) or relative |
↓
| Serious symptoms or signs |
↓
↓ ↓
No Yes
↓ ↓
| Type II second-degree AV heart block? Third-degree AV heart block |
↓_________________________↓ ↓
Observe * Prepare for transvenous pacer Intervention sequence
* Use TCP as a bridge device * Atropine 0.5-1.0mg
* TCP if available
* Dopamine5- 20µg/kg/min
* Epinephrine 2- 10
µg/kg/min
* Isoprenaline
TACHYCARDIA ALGORITHM
( Figure 5)
| * Assess ABCs * Assess vital signs * Secure airway * Review history * Administer oxygen * Perform physical examination * Start IV * Order 12-Lead ECG * Attach monitor, pulse oximeter * order portable CXR And automatic, blood pressure |
↓
→Yes→
| Unstable with serious symptoms or signs | If ventricular rate >150/min
|
↓_____________________________________________________________
↓
| Atrial fibrillation Atrial flutter | Paroxysmal Supraventricular Tachycardia (PSVT) | Wide-complex tachycardia of uncertain type | Ventricular tachycardia (VT) |
↓ ↓ ↓ ↓
| Consider *Diltiazem *β-blockers *Verapamil *digoxin * Procainamide * Quinidine * Anticoagulants | Vagal maneuvers | Lidocaine 1-1.5 mg iv push | Lidocaine 1-1.5 mg IV push |
↓ ↓ ↓
| Adenosine 6 mg Rapid IV push over 1-3ṣ | Lidocaine 0.5-0.7 , 5 mg IV push , max. total 3mg/kg | Lidocaine 0.5-0.7 , 5 mg IV push. Max. total 3mg/kg |
1-2 min ↓ ↓ ↓
| Adenosine 12mg, Rapid IV push over 1-3ṣ ( may repeat once in 1-2 min) | Adenosine 6 mg Rapid IV push over 1-3ṣ |
↓ ↓ 1-2 min
| Complex width? | Adenosine 12mg, Rapid IV push over 1-3ṣ ( may repeat once in 1-2 min) |
↓
___________________________________
↓ ↓
Narrow Wide
↓ ↓
Blood Pressure? Lidocaine 1-1.5 mg IV push
↓ ↓
↓ ↓
↓ Procainamide 20-30mg/min,
←← ↓ max. total 17mg/kg →→↓
| Verapramil 2.5-5mg IV |
↓
| Verapramil 5-10mg IV |
↓
| Consider
|
↓→→→→→→→→→→Synchronised cardioversion←←←←←←←↕
ELECTRICAL CARDIOVERSION
( Figure 6)
| Tachycardia With serious symptoms and signs |
↓
| If ventricular rate is >150/min, prepare for Immediate cardioversion. May give brief trial of medications bassed on specific arrythmias. Immediate cardioversion is generally not needed for rates < 150/min. |
↓
| Check
|
↓
| Sedate whenever possible |
↓
| Synchronised cardioversion VT } PSVT } 100 J, 200 J, 300 J, 360 J Atrial Fibrillatio } Atrial fluter } |
CEREBRAL PROTECTION ( POST – CPR )
Significant proportion of survivors of cardiac arrest suffer severe neurological deficits. Most patients who ultimately recover full neurological function awaken and improve dramatically in the first 48 hours following resuscitation. If the patients remain totally unresponsive, with no evidence of cognitive or motor recovery after 3 days, the chance of recovering meaningful cerebral function is almost nil.
Measures to improve cerebral outcome
- Improving cerebral perfusion during CPR.
- Ameliorating the injurious changes that occur at the time of reperfusion and reoxygenation of the brain.
Biochemical Consequences of Cardiac Arrest
- Cerebra oxygen stores become depleted within 15 s of total circulatory arrest.
- Cerebral glucose stores are exhausted within 5 min.
- When oxygen is depleted, anaerobic glycolysis continues while glucose and / or glycogen are available, resulting in the production of lactic acid sufficient to reduce intracellular pH from 7 to approximately 6.4 if normoglycemia is present before arrest.
- Lactate production is greater, and tissue pH is lower, if hyperglycemia is present at the time of arrest.
Therapeutic Measures
- Measures for improving Cerebral Blood Flow during CPR.
- Rapidly restore spontaneous circulation e.g. by early defibrillation.
- Adrenaline improves CBF and myocardial blood flow.
- Measures used in post-resuscitation period.
1. Continuous observation, monitoring and provision of supportive care.
2. prime importance – maintenance of adequate Cerebral Perfusion Pressure (CPP) ; i.e. CPP = MAP – ICP
Therefore > avoid systemic hypotension , control raised ICP
- Value of hyperventilation in post-cardiac arrest is as yet unproven. The major advantage of controlled ventilation may be the provision of adequate oxygenation and prevention of hypercarbia.
- Treat vigorously conditions that increase the brains oxygen requirements e.g. seizures and hyperthermia.
- Avoid hyperglycemia.
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