1 / 109

Cardiopulmonary Resuscitation

Cardiopulmonary Resuscitation. Dr A. Anvaripour Cardiac Anesthesiologist . History of resuscitation back to 1966 Standards for the performance of CPR Most recent recommendations Guidelines 2005 New guidelines has undergone comprehensive evidence-based evaluation.

ina
Download Presentation

Cardiopulmonary Resuscitation

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Cardiopulmonary Resuscitation Dr A. Anvaripour Cardiac Anesthesiologist

  2. History of resuscitation back to 1966 • Standards for the performance of CPR • Most recent recommendations Guidelines 2005 • New guidelines has undergone comprehensive evidence-based evaluation

  3. Basic Life Support • Early recognition of medical emergencies • Emergency response system (e.g., dialing 911 in the United States) • BLS assessments : Airway, breathing, and circulation performed without equipment • BLS interventions: breathing/Heimlich maneuver/application-use of an automated external defibrillator (AED)/CPR

  4. Goal supporting the circulation until restoration of spontaneous circulation occurs after SCA

  5. For those performing BLS interventions Importance of prompt initiation and expert performance of these skills cannot be overemphasized

  6. Antegrade systemic arterial blood flow continues after cardiac arrest until the pressure gradient between the aorta and right heart structures reach equilibrium • Similar process occurs during cardiac arrest with antegrade pulmonary blood flow between the pulmonary artery and the left atrium

  7. Arterial-venous pressure gradients dissipateleft heart becomes less filled/the right heart becomes more filled/venous capacitance vessels become increasingly distended

  8. coronary perfusion and cerebral blood flow stop When arterial and venous pressure equilibrates (approximately 5 minutes after cardiac arrest)

  9. CPR is performed until return of spontaneous circulation occurs • CPR is far less efficient than the native circulation , it can provide coronary circulation and cerebral blood flow sufficient to afford full recovery in many case • Push hard and push fast • chest compressions performed at a rate of 100/min until generate a palpable carotid or femoral pulse are considered ideal.

  10. Chest compressions Must not frequently interrupted

  11. Current recommendations • Placing increased emphasis on limiting interruptions in chest compressions • single- and two-person CPR compression-ventilation ratios of 30 : 2

  12. “cardiac pump mechanism” • Blood is ejected • Actual compression heart between the sternum and the vertebral column • Reduction in left and right ventricular volume • Closure of the tricuspid and mitral valves • Ejection of blood into the arterial system

  13. Cough CPR • Forceful coughing sustain consciousness during ventricular fibrillation (VF) 100 seconds • Coughingarterial pressure pulseopens the aortic valve

  14. thoracic pump mechanism Increases in intrathoracic pressure generate forward blood flow

  15. cardiac pump and thoracic pump mechanisms exist during resuscitation

  16. Systemic, coronary, and cerebral blood flow during CPR is dependent on effective chest compressions • Modest increases in intrathoracic pressure will impair return of venous blood reducing the chance of spontaneous circulation • Cardiac output during effective CPR: 25% 30% • oxygen content in the lungs at the time of cardiac arrest usually sufficient for maintaining an acceptable arterial oxygen content during the first several minutes of CPR

  17. Result Breaths are less important than initiating chest compressions immediately after the onset of SCA

  18. Monitoring during CPR • palpation of the carotid or femoral • observation of pupillary size • Initial pupillary size and changes during CPR are of some prognostic value • 1978, Kalenda described the use of capnography as a guide to the effectiveness of external chest compressions

  19. Rapid decrease in Petco2 with the onset of arrest • Immediate increase with resuscitation • Noninvasive guide to advanced life support interventions during CPR

  20. Severe reductions in pulmonary blood flow acute failure of delivery of O2 to the lungs very low Petco2 • External chest compression & ventilaitonPetco2 increased to 1.9% ± 0.3%, • After successful defibrillation and 12 minutes of CPR  Petco2immediate increase to 4.9% ± 0.3%

  21. Result Close correlation was found between changes in cardiac output and Petco2

  22. Major determinants of Petco2 • CO2 production • Alveolar ventilation • Pulmonary blood flow.

  23. Breathing • Breathing is indicated for a nontracheally intubated cardiac arrest • two 1-second breaths are delivered after the 30th compression • Provide only enough force and volume to cause chest rise • Excessive ventilation gastric inflation • With tracheal tube 8 to 10 breaths per minute independent of chest compressions

  24. Scissors maneuver

  25. “Sniff“ position

  26. Macintosh laryngoscope in position

  27. Schematic view of the glottic opening during direct laryngoscopy

  28. Supraventricular Tachyarrhythmia • Atrial flutter • Atrial fibrillation • AV junctional tachycardia • Multifocal atrial tachycardia • Paroxysmal reentrant tachycardia

  29. hemodynamic compromise • Paroxysmal supraventricular tachycardia (PSVT) • Atrial fibrillation (or flutter) with rapid ventricular rates • Multifocal atrial tachycardia

  30. PSVT

  31. PSVT • With hemodynamic deterioration  cardioversion • 100 to 200 J if a monophasic defibrillator • 100 to 120 J with a biphasic defibrilator

  32. PSVT • Energy can be increased as needed if the arrhythmia is resistant to therapy

  33. hemodynamically stable psvt • vagal maneuvers (Valsalva ) before initiating pharmacologic interventions • terminate about 20% to 25% • Adenosine (very effective in terminating PSVT)

  34. adenosin • slows sinoatrial and AV nodal conduction • prolongs refractoriness • diagnostic usefulness with uncertain origin

  35. After injection of 6 mg adenosin

  36. short half-life (<5 seconds) and short lived side effects • Flushing • Dyspnea • chest pain

  37. tachyarrhythmia may recur  necessitate the use of another drug

  38. verapamil PSVT does not respond to adenosine or if it recurs contraindicated in WPW syndrome

  39. Af/af • Rate-related hemodynamic compromise  cardioversion • 100 to 200 J with monophasic • 100 J to 120 J with biphasic • Escalation of energy doses for the second and subsequent doses is indicated

  40. AF/Af • hemodynamically stable patients  pharmacologic • Ibutilidemost rapid onset in restoring sinus rhythm • Prolongs the action potential dration / effective refractory • 1 mg given over a 10-minute • second dose can be administered 10 minutes after the first, if necessary

  41. Conversion to sinus rhythm is more frequent with atrial flutter than with atrial fibrillation (63% versus 31%)

  42. Ibutilide side effects • Prolongation of the QT interval • PVT (polymorphic v tach)

  43. options for the treatment of supraventricular arrhythmias drugs • Diltiazem • Verapamil • β-blocking medications • Procainamide • Amiodaron

  44. Multifocal (multiform) atrial tachycardia

  45. Often misdiagnosed as atrial fibrillation • Increased automaticity in multiple atrial foci • At least three morphologically different P waves in the same lead with ventricular rate more rapid than 100/min • occurring in patients with COPD, especially during exacerbations, and ICU management

More Related