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  1. 1. Australasian Emergency Response Specialists Pty Ltd TASMANIA & PNGA.E.R.S Emergency Response & Specialist Training Services Advanced Cardiac Life Support Craig Stevens AREMT Instructor/Examiner Bachelor of Health Science Paramedic Version 1 June 2009
  2. 2. Scope of Training• The ACLS course provides participants the opportunity to learn and review the following key components of advanced cardiac care: – Arrhythmias – Pharmacological therapy – Electrical therapy – Patient assessment and management
  3. 3. CertificationA wallet size reference card and A4 certificates will be issued onsuccessful completion of this course.Valid for 2 years and then can be refreshed/recertified over a half –1 day session after that.
  4. 4. Introduction- Welcome!- The course you are about to participate in will be conducted over 2 days - Day 1 Theory and Practical Rehearsals - Day 2 Practical Stations & Examination- Internationally recognised certification, with credits for doctors and nurses in continuing education.
  5. 5. Cases- There are 10 cases studied and the morphology and management of these cases are covered in depth. - Acute Coronary Systems - Asystole - AED - Bradycardia - PEA - Narrow Complex tachycardia - Respiratory Arrest - Stroke - Ventricular Fibrillation - Wide Complex Tachycardia
  6. 6. Conduct of Course• Review of Cardiac Rhythms• Pharmacologic and Electrical Therapy• Patient Assessment and the Cardiac Patient• Skills Practice and Remediation• ACLS Practice Cases• ACLS Practice Written Test and Remediation• Final Skills Examination• Final Written Examination
  7. 7. Any Questions?
  8. 8. Chapter 1 – Review CardiacRhythms
  9. 9. Cardiac Electrical ConductionSystemRevision:
  10. 10. Cardiac Electrical ConductionSystemAs you recall the myocardium is different from every othermuscle.It has an ability to produce it’s own electrical activity by a processcall “automaticity”Specialised conduction system with impulses generated by pacemakerThe collection of nerve fibres sets theinherent rate of electrical discharge
  11. 11. Cardiac Electrical ConductionSystem“SA” Sino-Atrial NodePrimary pacemaker is the “SA” Sino AtrialNodeLocated in superior aspect of right atrium and discharges at 60 – 100beats per minuteOnce initiated the SA node, impulse travels through right and left atriaAtria depolarises cells, the discharge stimulates atria muscle tocontract
  12. 12. Cardiac Electrical Conduction System“AV” Atrio-Ventricular NodeImpulse travels from “SA” Node to the “AV”(Atrio-Ventricular Node)Located in wall of right atriumThe impulse from the “AV” Node is delayed slightly, before enteringventriclesThis allows the Atria and ventricles to beat independently whichprovides a double action pump“AV” Node discharges at a rate of 40 – 60 impulses per minute
  13. 13. Cardiac Electrical ConductionSystem“Bundle of His” and“Purkinje System”“Bundle of His” is located partially in thewalls of the right atrium and inter-ventricular septumAccommodates the “right and left bundle branches”, terminating at the“Purkinje Network”The cells depolarise and cause the ventricles to contract at the“Purkinje” level“Purkinje Network” discharges at a rate of 20 – 40 beats per minute
  14. 14. Cardiac Electrical ConductionSystemConduction FailureIf the “SA” Node is to fail the “AV”Node picks up the pace requirement,which fires at a delayed rate.If the “AV” Node fails to capture the“Bundle of His” and “Purkinje Network”will take over with a considerable lowerrate of contractilityIn both cases we see marked “Brady-cardia”
  15. 15. Any Questions?
  16. 16. ECG WaveformsEach event in the cardiac conduction system, produces a specific waveform that can be analysed on the ECG.
  17. 17. ECG Waveforms“P” wave is normally upright, first waveform, simultaneous depolarisation of the atria“P-R” segment is the time from “P” wave to commencement of “QRS” complex, which represents the delay in the “AV” nodeThe “PR” interval is from commencement of “P” wave to end of “QRS” represents the entire depolarisation of the atria and the delay of the “AV” nodeCollectively the “QRS” segment is the entire depolarisation of the ventricles
  18. 18. ECG WaveformsThe “Q” wave is the first negative deflection after the “P” wave, may or may not be presentThe “R” wave is the first positive deflection after the “P” waveThe “S” wave is the first negative deflection after the “R” wave
  19. 19. ECG WaveformsThe “S-T” segment represents time between ventricular depolarisation and repolarisationShould be “Iso-electric” (Neutral, baseline for ECG)The “T” wave represents repolarisation of the ventricles, (ready to fire)
  20. 20. Normal Sinus RhythmWe’ve look at the ECG representation, now let’s look at the “Sinus Rhythm”
  21. 21. Normal Sinus RhythmWe’ve look at the ECG representation, now let’s look at the “Sinus Rhythm”
  22. 22. Normal Sinus RhythmThe “Sinus Rhythm” indicates the “SA” node is the primary pacemaker site and all components are intact and functioning correctly.
  23. 23. ECG Markers of Acute CoronarySyndromeThe “ST” segment represents depolarisation and repolarisation, it should be “Isoelectric”. Which identifies that the myocardium is electrically “Neutral”
  24. 24. ECG Markers of Acute Coronary Syndrome (ACS) The “ST” segment “elevation” is commonly indicative of “Myocardial Injury”The “ST” segment “depression” is commonly indicative of “Myocardial Ischemia” These observations are only conclusive when seen in 2 or more leads, therefore “MCL’s” or a 12 lead needs to be used to confirm.
  25. 25. “T” Wave InversionThe “T” wave represents the repolarisation of the ventricles.Should be in the same direction as the “QRS” segment.Again these need to be observed in 2 or more leads to be conclusiveThose patients however presenting with signs and symptoms of “ACS” is clinically significant and to be treated as such until proven otherwise.
  26. 26. The “Q” WaveThe “Q” wave is the first negative deflection after the “P” wave.“Q” waves are insignificant in some leads, this is not a safe assumption however in someone presenting with chest pain, and showing them in multiple leads on a 12 lead ECG.A significant pathologic “Q” wave is one that is seen to be deeper than 1/3 of the “QRS” height or wider than 0.03 sec’s
  27. 27. The “Q” WavePathologic “Q” waves represent “dead myocardium” and are the ECG signature of a “Myocardial Infarction”.
  28. 28. Any Questions?
  29. 29. BradycardiaBradycardia is defined, “by a heart rate of less than 60 beats per minute”.Can result in a decreased cardiac output, which would make the patient clinically unstable.“Absolute” bradycardia refers to any heart rate less than 60 beats per minute “Relative” bradycardia is when the heart rate is faster than expected, (May be >60 bpm) and is accompanied by serious signs and symptoms. Eg: Hypotension, or Altered Mental Status
  30. 30. Sinus Bradycardia
  31. 31. Sinus Bradycardia “Sinus Bradycardia” Results from “excess vagal stimulation”, which slows “SA” node discharge Other causes include: - Disease - Damage to cardiac electrical conduction system - Certain drugs (Beta – blockers)***In well conditioned athletes sinus bradycardia may be present and a normal finding.
  32. 32. Idioventricular RhythmIdioventricular Rhythm occurs when a “ventricularfocus” acts as the primary pacemaker of the heart
  33. 33. Idioventricular RhythmOrigin:This is evident by the wide and bizarre appearance of the “QRS” complexes,and slow ventricular rate.Because atrial activity is absent there are no discernable “P” waves.Clinical Significance:In an absence of atrial contraction, minimal volumes of blood are ejected, intoventricles.Ventricular rate is slow, cardiac output significantly reduced.
  34. 34. Heart Blocks“First Degree AV Block”Origin:“First Degree AV” block is caused by an abnormal delay at the AV node whichprolongs the “P-R” interval > 0.20 secWhat can cause this cardiac rhythm:- Vagal stimulation- AV Nodal disease- Certain medications
  35. 35. Heart Blocks“First Degree AV Block”Clinical Significance:Unlike higher blocks, 1st degree AV block is less likely to be associatedwith BradycardiaHowever if Bradycardia is present cardiac output can fall1st degree AV block can be a variant in some people
  36. 36. Heart Blocks“Second Degree AV Block Type 1”Origin:2nd degree AV block Type I is caused by “AV” nodal disease or vagalstimulation.Each complex progressively delayed at AV node until a “QRS” segmentis lost, leaving sole “P” wave with no associated QRS segment.
  37. 37. Heart Blocks“Second Degree AV Block Type I”Clinical Significance:Depends on AV block (2:1, 3:1, 4:1 etc) this rhythm can either presentas a “normal” or “bradycardic” rate.If associated with Bradycardia, cardiac output may decrease.
  38. 38. Heart Blocks“Second Degree AV Block Type II”Origin:2nd degree AV Block Type II occurs when the AV node intermittentlyblocks some atrial complexes.Results in some “P” waves not followed by any “QRS” complexes.
  39. 39. Heart Blocks“Second Degree AV Block Type II”Clinical Significance:2ND Degree AV Block Type II results from more severe AV nodaldisease, excessive vagal toneFrequently associated with bradycardia and can decrease cardiacoutput
  40. 40. Heart Blocks“Third Degree AV Block”Origin:Occurs as a result of complete block at the “AV” node.Complete blockage at AV node, prevents any atrial conducted complexes to enter the ventriclesVentricles respond with escape complexes producing wide “QRS” complex.Also referred to as “CHB or Complete Heart Block”
  41. 41. Heart Blocks“Third Degree AV Block”Clinical Significance:Atrial and Ventricle contractions are dissociated cardiac output is significantly decreased and patient most always unstable.A ventricular pacemaker occurs at an intrinsic rate of 20 – 40 bpm with wide “QRS” complexes and severe bradycardia
  42. 42. Any Questions?
  43. 43. Tachycardia’s- Tachycardia is defined as,” heart rate that is > 100bpm”.- Varying types, narrow or broad complex tachycardia’s occur.- If heart beats too fast, ventricles may not adequately fill.- Decreases cardiac output, making clinically unstable patient.
  44. 44. Tachycardia’sNarrow QRS ComplexSinus TachycardiaOrigin:Sinus Tachycardia occurs when the SA node discharges faster than it’s inherent rate of 60 – 100 impulses per minute.This caused by, medication or required increased cardiac input. (Shock, fever, hypoxemia, exercise)
  45. 45. Tachycardia’s (Narrow Complex)Narrow QRS ComplexSinus TachycardiaClinical Significance:Can result in a decreased cardiac output secondary to inadequate ventricular filling.
  46. 46. Tachycardia’s (Narrow Complex)Supra Ventricular Tachycardia (SVT)SVT can manifest as:- Atrial tachycardia- Ectopic atrial tachycardia- Rapid atrial fibrillation or flutter- Junctional tachycardiaDefined as narrow complex tachycardia exceeds >150 bpm
  47. 47. Tachycardia’s (Narrow Complex)Supra Ventricular Tachycardia (SVT)Origin:Occurs when a supraventricular pacemaker initiates the impulse. Not necessarily the SA nodeSVT can be caused by medications or situations requiring increased cardiac output.(Shock, fever, hypoxemia, exercise or SA node disease).
  48. 48. Tachycardia’s (Narrow Complex)Supra Ventricular Tachycardia (SVT)Clinical Significance:SVT can result in a decreased cardiac output, secondary to inadequate ventricular filling,More than sinus tachycardia
  49. 49. Tachycardia’s (Narrow Complex)Atrial Fibrillation (AF)Origin:Result of multiple atrial pacemakers discharging chaotically.No discernible “P” waves, only fibrillatory waves between “QRS”No electrical pattern from Atria causes “irregularly irregular” ventricular rhythm, from the AV node area
  50. 50. Tachycardia’s (Narrow Complex)Atrial Fibrillation (AF)Clinical Significance:Frequently in patients with “Congestive Heart Failure” (CHF)Tendency to have blood stagnate, causing potential for, pulmonary, coronary or cerebral embolism.When >100bpm, cardiac output decreases, which is compounded by decreased atrial kick from small volumes of blood delivered to ventricles
  51. 51. Tachycardia’s (Narrow Complex)Atrial FlutterOrigin:Result of ectopic atrial pacemaker outside SA nodeCommonly lower atrium, near AV nodeSA node function suppressed by flutter“P” waves present as “flutter” waves, as abnormal atrial depolarisation occurs near AV node across atria in a retrograde direction
  52. 52. Tachycardia’s (Narrow Complex)Atrial FlutterClinical Significance:Occurs in “CHF” and in those with SA node diseaseComplications occur with inadequate ventricular filling especially when accompanied by rapid ventricular rateCardiac output significantly decreased
  53. 53. Tachycardia’s (Wide Complex)Monomorphic Ventricular Tachycardia (VT)Origin:Most common form of “VT”Complexes are all same shape, size and directionCaused by ectopic pacemaker in ventricle, overrides atrial activity“P” waves may be seen but usually buried in wide “QRS” complexes
  54. 54. Tachycardia’s (Wide Complex)Monomorphic Ventricular Tachycardia (VT)Clinical Significance:Can result from many underlying causesMost commonly significant:- “Coronary Artery Disease”- “QT” interval prolongation- Electrolyte imbalance, specifically potassium (K+)
  55. 55. Tachycardia’s (Wide Complex)Polymorphic Ventricular Tachycardia (VT)Origin:Complexes vary in size, shape and direction from complex to complexUsually occurs when “QT” interval of underlying rhythm prolongs, indicating severe delay in ventricular repolarisationVentricles become irritated and ectopic ventricular pacemaker overridesVariant known as “TdP” - “Torsades De Pointes” or “Twisting of Points”
  56. 56. Tachycardia’s (Wide Complex)Polymorphic Ventricular Tachycardia (VT)Clinical Significance:Prone to occur after administration of “Quinidine” or “Procainamide” both drugs prolong the “QT” intervalHypomagnesaemia (Low Magnesium) is also common causeAtria do not contract regularly or adequately to fill ventricles before they contractMarked reduction in cardiac outputHigh potential to deteriorate to “Ventricular Fibrillation”
  57. 57. Cardiac Arrest RhythmsVentricular Fibrillation (VF)/ Pulseless Ventricular TachycardiaOrigin:Multiple ectopic ventricular pacemakers, which depolarise in a random, chaotic fashion and spread throughout myocardiumLethal arrhythmiaUncontrolled quivering
  58. 58. Cardiac Arrest RhythmsVentricular Fibrillation (VF)/ Pulseless Ventricular TachycardiaClinical Significance:Does not produce a palpable pulseMost common rhythm in cardiac arrestImmediate defibrillation is criticalCoronary Artery Disease, leads to myocardial ischemia/infarction most common cause(Hypoxia, acidosis, early repolarisation, Eg: “R on T” phenomenon)
  59. 59. Cardiac Arrest RhythmsVentricular Fibrillation (VF)/ Pulseless Ventricular TachycardiaNote:“VT” covered earlier can be with cardiac output or pulselessIt can occur in patients in cardiac arrestNot as common as “VF”, but in witnessed arrest may be present before “VF”
  60. 60. Cardiac Arrest RhythmsAsystoleOrigin:All pacemaker sites fail to generate electrical impulseTotal absence of electrical and mechanical activityClinical Significance:Asystole does not produce a pulse,It is commonly the result of untreated ventricular fibrillation (VF)(Eg: Hypoxia, acidosis or electrolyte abnormalities)
  61. 61. Cardiac Arrest RhythmsPulseless Electrical Activity (PEA)“PEA” is not a particular cardiac rhythm, but rather any cardiac arrhythmia that does not produce a palpable pulse.The only rhythm that is not classed as “PEA” is “Pulseless VT”Can be caused by:- Hypoxia- Acidosis- Pericardial tamponade- Tension pneumothorax/haemothorax- Hypolvolaemia
  62. 62. SummaryIt is important to evaluate a cardiac rhythm of a patient with a cardiac- related chief complaint.Evaluation of the ECG of the patients signs and symptoms determines the most appropriate treatment protocols.More than one cardiac rhythm can be observed in a patient. The clinician needs to be versatile enough to change the course of management very quickly.It is important to analyse and interpret, however a systemic assessment is crucial in determining whether the cardiac rhythm is resulting in haemodynamic compromise.
  63. 63. Any Questions?
  64. 64. Pharmacologic and ElectricalTherapyIntroductionThis chapter reviews the most common pharmacologic and electrical interventions used in ACLS to treat patients with a variety of cardiovascular and respiratory system emergencies.
  65. 65. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyAspirin (Acetylsalicylic Acid, ASA)Therapeutic Effects- Blocks formation of thromboxane A2,- Inhibiting platelet aggregation and vasoconstriction- Reduces mortality from acute myocardial infarction, reduces reinfarction and nonfatal strokeIndications- S & S suggestive of ACS such as chest pain or discomfort- ECG changes consistent with ACS, - ST Depression/Elevation - T wave inversion
  66. 66. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyAspirin (Acetylsalicylic Acid, ASA)Contra-Indications- Known hypersensitivity- Bleeding disorders- Concomitant use of anti-coagulants- Active ulcer, or recent GI BleedAdult Dose- 160 – 325mg of chewable aspirin ASAP after onset of chest pain- To achieve peak therapeutic plasma levels, instruct patient to chew tablet before swallowing
  67. 67. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyFibrinolytic Therapy (Thrombolytics)Therapeutic Effects- Alteplase (Activase, tPA), Anistreplase (Eminase), Reteplase (Retavase), Streptekinase, Tenectaplase- Produce similar therapeutic effect, which is the conversion of plasminogen to plasmin.- Plasmin destroys fibrin and fibrinogen matrix of thrombus, destroying clot obstructing the artery and re-establishing distal blood flow
  68. 68. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyFibrinolytic Therapy (Thrombolytics)Indications:- Acute Myocardial Infarction (AMI) in adults - ST segment elevation > or equal to 1mm in 2 or more contiguous leads - In S & S of AMI, no > than 12 hours from duration of onset (chest pain)- Acute Ischaemic Stroke - Sudden onset focal neurologic deficit (slurred speech, facial droop) or alterations in mental status - Absence of intracerebral/subarachnoid haemorrhage (rule out if required) - S & S not rapidly improving (TIA) - S & S no > 3 hours in duration
  69. 69. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyFibrinolytic Therapy (Thrombolytics)Contra-Indications:- Active bleeding within 21 days, menses excluded- History of intra-cerebral, intracranial, or intra-spinal event within 3 months - Stroke - Arteriovenous (AV) malformation - Neoplasm - Aneurism - Trauma or surgery - Major trauma or surgery in last 14 days - Aortic dissection - Severe uncontrolled hypertension - Severe bleeding disorders
  70. 70. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyFibrinolytic Therapy (Thrombolytics)Contra-Indications:- History of intra-cerebral, intracranial, or intra-spinal event within 3 months cont….. - History of prolonged CPR with evidence of thoracic trauma - Lumbar puncture within 7 days - Recent arterial puncture or non-compressible site - Aspirin or heparin administered in last 24 hours after acute ischaemic stroke
  71. 71. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyFibrinolytic Therapy (Thrombolytics)Adult Dose:- Variable depending on fibrinolytic agent used
  72. 72. Any Questions?
  73. 73. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyMorphine Sulphate (MSO4)Therapeutic Effects:- Narcotic analgesic that promotes, through it’s vasodilatory effects, systemic venous pooling, reducing pre-load (venous return) as well as systemic vascular resistance (after load)- Reduces myocardial oxygen demand, and consumption- Reduces chest pain and anxiety
  74. 74. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyMorphine Sulphate (MSO4)Indications:- Chest pain in ACS that is not responsive totally to GTN- Cardiogenic pulmonary oedema, (BP > 90mmHg)Contra-Indications:- Hypersensitivity to Morphine or opiate based medications- Signs of CNS depression (Eg: respiratory depression, hypotension, bradycardia)
  75. 75. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyMorphine Sulphate (MSO4)Adult Dose:- 2 – 4mg via slow IV push, over 1 – 5 minutes,- May be repeated every 5 – 30 minutes, to acquire the desired effect - Should signs of CNS depression occur, including respiratory depression, - Naloxone (Narcan) 0.4mg – 2.0mg should be administered IV or IMI to reverse effects
  76. 76. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyGlyceryl TrinitrateTherapeutic Effects:- Smooth muscle relaxant, producing systemic venous pooling of blood through it’s vasodilatory effects- Reducing pre-load (venous return) as well as systemic vascular resistance (after load)- Reduces myocardial oxygen demand, and consumption
  77. 77. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyGlyceryl TrinitrateIndications:- Chest pain suspected of cardiac in origin- Cardiogenic pulmonary oedema to left sided CHFContra-Indications:- Systolic BP <90mmHg- Severe Bradycardia <50 bpm or Tachycardia >100bpm- Use of “Viagra” in last 24 hours- Or “Cialis” in last 48 hours
  78. 78. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyGlyceryl TrinitrateAdult Dose:- Tablet - 0.4mg sublingually - If not had before or > 65 y/o give half tablet first- Spray - 0.4mg (1 spray) given every 5 minutes, up to maximum of 3 sprays- IV Infusion - 10-20mcg, titrated for effect, - Frequently monitor BP to maintain >90mmHg
  79. 79. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyOxygen (O2)Therapeutic effect:- Increases haemoglobin saturation- Enhances tissue oxygenation, provided that adequate ventilation and circulation are maintained- Increase oxygen surface tension in blood
  80. 80. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyOxygen (O2)Indications:- Any suspected, cardiovascular, cerebrovascular or respiratory system emergency - Chest pain - Stroke - Altered mental status - SOB - Anyone where it is felt it is needed!Contra-Indications:- None when given in emergency situations
  81. 81. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyOxygen (O2)Dose/Method of Administration:- Mild hypoxia with adequate breathing - Nasal cannula @ 4lpm- Severe hypoxia with adequate breathing - Non re-breathing mask @ 15lpm- Inadequate breathing or apnoea - Bag valve mask resuscitator (BVM) and reservoir bag @ 15lpm
  82. 82. Any Questions?
  83. 83. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyAnti-ArrhythmicsIntroduction:Used to treat a variety of arrhythmia’s both supraventricular (narrow) and ventricular (wide) in origin. - Adenosine - Amiodarone - Lidocaine/Lignocaine - Magnesium Sulphate - Procainamide
  84. 84. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyAdenosineTherapeutic Effects:- Natural occurring endogenous nucleoside that is rapidly metabolised. - Slows discharge rate of SA node and the conduction through the AV node - Restoring sinus rhythm in SVTIndications:- Narrow QRS supraventricular tachycardia’s - SVT to slow the rate to determine underlying rhythm
  85. 85. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyAdenosineContra-Indications:- Toxin induced tachycardia’s (sepsis, crush injury)- 2nd or 3rd degree AV block- Atrial fibrillation or flutter- Wide QRS VT
  86. 86. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyAdenosineAdult Dose:- Initial Dose: - 6mg rapid (1-3 seconds) IV push, with extremity elevated, followed by 20ml IV saline flush- Repeat Dose: - 12mg rapid IV push, 1-2 minutes after initial dose, further 12mg dose may be repeated, 1-2 minutes later - Up to a maximum of 30mg
  87. 87. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyAmiodarone:Therapeutic Effects:- Diverse anti-arrhythmic, blocks sodium, calcium and potassium, and inhibits sympathetic nervous system stimulation.- Suppressing SA node discharge, reducing heart rate- Slows conduction through AV node- Effective in slowing conduction in accessory pathways in WPW syndrome.
  88. 88. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyAmiodarone:Indications:- “V”-Fib and Pulseless VT that is refractory to defibrillation- Polymorphic “V”-Tach and wide complex tachycardia of unknown origin- Stable “V”-Tach when cardioversion is unsuccessful- Adjunct to synchronised cardioversion in supraventricular tachycardia’s (Atrial Fibrillation)- Termination of atrial tachycardia- Rate control in atrial fibrillation and atrial flutter, when other therapies have proven unsuccessful
  89. 89. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyAmiodarone:Contra-Indications:- Known hypersensitivity- Sinus node disease with significant bradycardia- 2nd and 3rd degree AV block
  90. 90. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyAmiodarone:Adult Dose:- V Fib and Pulseless V Tach - 300mg diluted in 20-30ml of D5W via rapid IV push - May repeat 150mg diluted in 20-30ml of D5W via rapid IV push 3-5 min intervals- Stable V Tach, SVT and Atrial flutter/fibrillation - 150mg diluted in 20-30ml of D5W via rapid IV push over 10 minutes - May be repeated every 10 minutes as required- 24 hour maintenance infusion - 360mg via IV infusion over first 6 hours (1mg/min) - 540mg over remaining 18 hours via IV infusion (0.5mg/min) - Up to a maximum of 2.2 grams in 24 hours
  91. 91. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyLidocaine / XylocardTherapeutic Effects: - Blocks influx of sodium through fast channels of myocardium, decreasing irritability in ischaemic areas - Increases V-Fib threshold, - Lidocaine decreases defibrillation thresholdIndications: - V-Fib and Pulseless VT refractory to defibrillation - Stable wide complex tachycardia’s (e.g. V-Tach, wide complex tachycardia’s of uncertain origin)
  92. 92. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyLidocaine / XylocardContra-Indications: - Known hypersensitivity to Lidocaine or any “cain” based medications (e.g. Marcain etc) - Sinus bradycardia - AV Blocks
  93. 93. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyLidocaine / XylocardAdult Dose:- V-Fib and Pulseless V-Tach - 1-1.5mg/kg via rapid IV push - May be repeated at 0.5-0.75mg/kg every 5-10mins, to a maximum of 3mg/kg- Stable V-Tach and wide complex tachycardia of unknown origin - 1-1.5mg/kg via rapid IV push - May be repeated at 0.5-0.75mg/kg every 5-10mins, to a maximum of 3mg/kg- Maintenance Infusion - 1-4mg per minute, titrated to desired effect
  94. 94. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyMagnesium SulphateTherapeutic Effects: - Classified as an electrolyte, possesses an anti-arrhythmic type property - Slows SA node impulse rate, and suppresses automaticity in partially depolarised cells - Has CNS depressant properties- Indications: - Torsade de Pointes (TdP) with pulse - Cardiac arrest only if Torsades or Hypomagnesaemia is present
  95. 95. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyMagnesium SulphateContra-Indications: - CNS depression - Hypomagnesaemia - HypocalcaemiaAdult Dose:- Torsades with Pulse - Loading dose of 1 -2 g mixed in 50-100ml of D5W given over 5-60 min - Follow by 0.5-1g/hr IV, titrated to control Torsades de Pointes- Cardiac Arrest (From Hypomagnesaemia or Torsades) - 1-2g (2-4ml of 50% solution) diluted in 10ml of D5W given IV over 5- 20mins
  96. 96. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyProcainamide (Pronestyl)Therapeutic Effects: - Slows conduction of the atria, ventricles and “HIS” bundle, - Prolonging P-R and Q-T intervals and refractory period of AV node - Slows refractory period within the atriaIndications: - Recurrent V-Fib or Pulseless V-Tach - Stable SVT uncontrolled by vagal manoeuvres or adenosine - Atrial fibrillation with rapid ventricular rate in WPW
  97. 97. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyProcainamide (Pronestyl)Contra-Indications: - Known hypersensitivity to procainamide or similar medications - 3rd degree AV block (without artificial pacemaker) - Digitalis toxicity (may exacerbate AV conduction depression) - Pre-existing QRS and Q-T interval prolongation
  98. 98. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyProcainamide (Pronestyl)Adult Dose:- Recurrent V-Fib and Pulseless V-Tach - 20mg/min via IV infusion - In urgent situations, up to 50mg/min may be administered, - Use of procainamide in cardiac arrest is limited by need for slow IV infusion and uncertain efficacy- SVT, AF, and wide complex tachycardia of unknown origin - 20mg/min via IV infusion- Maintenance Infusion - 1-4mg/min titrated to desired effect
  99. 99. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyProcainamide (Pronestyl)Adult Dose:- Stop procainamide infusion if: - Arrhythmia suppression - Hypotension develops - QRS complex widens > 50% of it’s pre-treatment width - Maximum dose of 17mg/kg has been given
  100. 100. Any Questions?
  101. 101. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyCalcium Channel BlockersIntroduction:- Calcium Channel Blockers are used in the treatment of stable narrow complex tachycardias- As well as the rate control in atrial fibrillation and atrial flutter
  102. 102. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyDiltiazem (Cardizem)Therapeutic Effects:- Blocks movement of calcium ions, across cell membranes of myocardium and smooth muscle- Results in decreased myocardial contractility (negative inotropy)- Slowing of conduction through AV node (negative dromotropy)- Dilation of coronary arteries and peripheral vasculature, decreasing myocardial oxygen demand
  103. 103. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyDiltiazem (Cardizem)Indications: - Control of ventricular rate in atrial fibrillation and atrial flutter - Adjunct to adenosine to treat stable narrow complex tachycardia’sContra-Indications: - Wide complex tachycardia’s of unknown origin - Poison or drug induced tachycardia’s - Rapid AF and atrial flutter in WPW - Sinus node disease - AV block (without an artificial pacemaker) - Concurrent use of beta blocking agents (e.g. Atenolol, Inderal) - May precipitate significant hypotension
  104. 104. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyDiltiazem (Cardizem)Adult Dose:- IV Bolus: - 15-20mg (0.25mg/kg) IV over 2 minutes - May be repeated 15 minutes later, at 20-25mg (0.35mg/kg) over 2 minutes- Maintenance Infusion: - 5-15mg/hour titrated to desired effect
  105. 105. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyVerapamil (Calan, Isoptin)Therapeutic Effects:- Blocks movement of calcium ions across cell membranes and smooth muscle of vasculature- Results in decreased myocardial contractility,- Slowing AV conduction through AV node and dilation of coronary arteries and peripheral vasculature- Decreases myocardial oxygen demand
  106. 106. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyDiltiazem (Cardizem)Indications: - Control of ventricular rate in atrial fibrillation and atrial flutter and ectopic atrial tachycardia - Adjunct to adenosine to treat stable narrow complex tachycardia’sContra-Indications: - Wide complex tachycardia’s of unknown origin - Poison or drug induced tachycardia’s - Rapid AF and atrial flutter in WPW - Sinus node disease - AV block (without an artificial pacemaker) - Concurrent use of beta blocking agents (e.g. Atenolol, Inderal) - May precipitate significant hypotension
  107. 107. Pharmacologic and ElectricalTherapyAcute Coronary Syndrome – PharmacologyVerapamil (Calan, Isoptin)Adult Dose:- 2.5-5mg via IV push over 2 minutes - May be repeated 5-10mg via IV push every 15-30 mins - Maximum dose 20mg- Alternative dosing regime - 5mg via IV push every 15 minutes - Maximum dose 30mg
  108. 108. Pharmacologic and ElectricalTherapyElectrical TherapyIntroduction- Electrical therapy is frequently used- Where serious S & S as a result of patients cardiac rhythm- Patients with heart beat too fast or too slow, chaotic or pulseless- Need prompt electrical therapy to stabilise their condition
  109. 109. Pharmacologic and ElectricalTherapyDefibrillation:Therapeutic Effects:- Unsynchronised delivery of energy into myocardium- To stop chaotic electrical activity by literally freezing the heart in animation- So an organised SA or AV pacemaker can dominate and restore a perfusing rhythm
  110. 110. Pharmacologic and ElectricalTherapyDefibrillation:Indications: - V-Fib and Pulseless V-Tach - Unstable polymorphic V-TachContra-Indications: - Asystole - Routine defibrillation of asystole is not recommended, because it may result in failure to identify and treat underlying cause of asystole - Regular cardiac rhythm with a pulse - Other health care providers being in physical contact with the patient - Ensure no one is in contact with patient at time of defibrillation
  111. 111. Pharmacologic and ElectricalTherapyDefibrillation:Adult Energy Settings:- V-Fib or Pulseless V-Tach - 360J (or biphasic equivalent) for first and subsequent shocks - Follow each shock immediately with CPR - Reassess after 2 minutes CPR - If first defibrillation unsuccessful, defibrillate one time, as needed, after every 2 minutes of CPR- Unstable polymorphic V-Tach - 360J (or biphasic equivalent) repeated as needed - Be prepared to perform CPR if patient becomes pulseless
  112. 112. Pharmacologic and ElectricalTherapySynchronised CardioversionTherapeutic Effects:- Timed delivery of energy into myocardium- To correct rapid, regular cardiac rhythms, in patients who are unstable as a result of cardiac rhythm- An internal “synchroniser” times the shock to deliver when it senses the “R” wave- Avoids the shock during the refractory period (down slope of the “T” wave) which may precipitate V-Fib
  113. 113. Pharmacologic and ElectricalTherapySynchronised CardioversionIndications: - Perfusing narrow and wide QRS complex tachycardia’s, >150bpm with serious S & S linked to tachycardia - Monomorphic V-Tach, SVT, AF, Atrial FlutterContra-Indications: - V-Fib or pulseless VT (Requires Defibrillation) - Poison or drug induced tachycardia - Treat underlying problem with an antidote if available - The serious symptoms are associated with poison or drug not tachycardia - Other health care providers being in physical contact with the patient - Ensure no one is in contact with patient at time of defibrillation
  114. 114. Pharmacologic and ElectricalTherapyDefibrillation:Adult Energy Settings:- Monomorphic V-Tach and AF - Start with 100J (or biphasic equivalent) - Repeat at 200J, 300J, 360J respectively if the rhythm is not corrected- SVT and Atrial Flutter - Start with 50J, (or biphasic equivalent) - Repeat at 100J, 200J, 300J, 360J respectively if the rhythm is not corrected
  115. 115. Pharmacologic and ElectricalTherapyTranscutaneous Cardiac Pacing:Therapeutic Effects:- Uses an artificial electrical impulse to increase electrical discharge rate of slow inherent pace maker in the heart- Preferred initial cardiac pacing method in emergency cardiac care because it is quickly initiated and relatively safe
  116. 116. Pharmacologic and ElectricalTherapyTranscutaneous Cardiac Pacing (TCP):Indications:- Symptomatic bradycardia, where S & S are related to bradycardia, non reactive to atropine or if unavailable- Rhythms that may require TCP: - AV Blocks (Especially 2nd and 3rd degree) - Bradycardia with ventricular escape beats (PVC’s)Contra-Indications:- Severe hypothermia- Prolonged brady-asystolic cardiac arrest
  117. 117. Pharmacologic and ElectricalTherapyDefibrillation:Adult Energy Settings:- Set pacing rate at 80bpm- Symptomatic Bradycardia - Increase output (mA) from minimum setting until consistent capture is achieved - Is evidenced by a widening QRS and broad “T” wave after each pacing spike. - Then increase by 2 mA as a safety margin to ensure positive capture
  118. 118. Any Questions?
  119. 119. Pharmacologic and ElectricalTherapyParasympatholytics:Introduction:- Referred to as parasympathetic blockers, vagolytic and anticholinergic drugs- Parasympatholytics block the parasympathetic nervous system, via the vagus nerve- Used to treat symptomatic bradycardia’s (absolute or relative) caused by increased vagal tone
  120. 120. Pharmacologic and ElectricalTherapyParasympatholytics:Atropine SulphateIndications:- Symptomatic bradycardia (absolute or relative)- Asystole- Bradycardic pulseless electrical activity (PEA)Contra-Indications:- Glaucoma (causes pupillary dilation)- May not be effective in treating bradycardia associated with 2nd degree type II and 3rd degree AV blocks- Tachycardia- Denervated (transplanted) hearts, use TCPM and catecholamines instead
  121. 121. Pharmacologic and ElectricalTherapySympathomimeticsIntroduction:- Mimic the effects of the sympathetic nervous system- Increasing heart rate and blood pressure- Synthetically produced- Equivalent to endogenous bases that occurs in human body naturally
  122. 122. Pharmacologic and ElectricalTherapySympathomimetics:Epinephrine (Adrenaline):Therapeutic Effects:- Naturally occurring catecholamine, contains natural occurring Alpha and Beta adrenergic effects- Alpha effects result in vasoconstriction, increasing blood pressure- Beta1 effects result in increased heart rate (positive chronotropy) and increased myocardial contractility (positive inotropy)- Beta2 effects cause relaxation of bronchial smooth muscle, (bronchodilation)
  123. 123. Pharmacologic and ElectricalTherapySympathomimetics:Epinephrine (Adrenaline):Indications:- Cardiac Arrest - V-Fib or Pulseless V-Tach- Symptomatic Bradycardia - After atropine and pacing- Severe hypotension - Treat with fluid boluses first- Anaphylactic Shock - Combined with fluid bolus, corticosteroids and antihistamines
  124. 124. Pharmacologic and ElectricalTherapySympathomimetics:Epinephrine (Adrenaline):Contra- Indications:- Tachycardia- Hypertension- Do not mix with alkaline solutions, (e.g. sodium bicarbonate) deactivation will occur, as will, with all catecholamines.
  125. 125. Pharmacologic and ElectricalTherapySympathomimetics:Epinephrine (Adrenaline):Adult Dose:- Cardiac Arrest: - 1mg (10ml of 1:10,000) every 3-5mins, followed by 20ml flush of normal saline - No maximum dose when administered for persistent cardiac arrest- Symptomatic bradycardia or severe hypotension - 2-10mcg per minute - Add 1mg Adrenaline (1ml of 1:1000) to 500ml normal saline and infuse at 1- 5mL/min
  126. 126. Pharmacologic and ElectricalTherapySympathomimetics:Dopamine (Intropin):Therapeutic Effects:- Naturally occurring catecholamine,- Physiological effects vary with increasing doses- At medium or “cardiac doses” (5-10mcg/kg/min), dopamine acts directly on beta receptors- Causing increased myocardial contractility, (increased inotropy), and increased SA nodal discharge and increased heart rate (positive chronotropy)- Doses > 10mcg/kg/min (vasopressor dose) stimulate Alpha receptors, increasing systemic vascular resistance (vasoconstriction)- Dosing depends on patients condition
  127. 127. Pharmacologic and ElectricalTherapySympathomimetics:Dopamine (Intropin):Indications:- Symptomatic Bradycardia: - After atropine, pacing and adrenaline- Hypotension (Systolic <70-100mmHg) with S & S of shock - Consider fluid boluses first, dopamine should not be given when hypovolaemic
  128. 128. Pharmacologic and ElectricalTherapySympathomimetics:Dopamine (Intropin):Contra-Indications:- Known hypersensitivity- Hypolvolaemia- Tachydysrhythmia’s or V-Fib- Pheochromocytoma (Adrenal tumor producing adrenaline)- Concurrent use of MOAI’s- Do not mix with alkaline solutions, (e.g. sodium bicarbonate) deactivation will occur, as will, with all catecholamines.
  129. 129. Pharmacologic and ElectricalTherapySympathomimetics:Dopamine (Intropin):Adult Dose:- As IV Infusion - Mix 400mg-800mg of dopamine in 250ml of normal saline, D5W, or Hartmann’s and titrate on patients clinical response- Symptomatic bradycardia - 2-10mcg/kg/min- Profound hypotension (Non-hypovolaemic) - 10-20mcg/kg/min
  130. 130. Pharmacologic and ElectricalTherapySympathomimetics:Vasopressin (Pitressin Synthetic):Introduction:- Is an Anti-Diuretic Hormone (ADH) produced in the pituitary gland- Binds to specific receptors, specifically vasopressin (V) receptors- 2 receptors V1(V1a and V1b) and V2.- V1a produces potent vasoconstriction- V2 produces vasodilation- Vasopressin possesses a greater vasoconstrictive effect, especially in an acidotic or hypoxic environment (e.g. Cardiac Arrest)- Does not increase myocardial oxygen consumption
  131. 131. Pharmacologic and ElectricalTherapySympathomimetics:Vasopressin (Pitressin Synthetic):Indications:- Used to replace the first and second dose of adrenaline for patients in cardiac arrest from V-Fib/pulseless V-Tach, asystole and PEAContra-Indications:- Known sensitivity to vasopressin- Acute Coronary Syndrome - Vasopressin may exacerbate hypertension because of it’s vasoconstrictive effects
  132. 132. Pharmacologic and ElectricalTherapySympathomimetics:Vasopressin (Pitressin Synthetic):Adult Dose:- 40 units via IV push as a one off dose - Wait approximately 10 minutes after vasopressin administration before initiating/resuming adrenaline therapy
  133. 133. Any Questions?
  134. 134. Assessment of Non-CardiacArrest PatientsIntroduction:- Appropriate and prompt assessment and treatment of the patient experiencing difficulties because of a cardiovascular or respiratory related condition is imperative.
  135. 135. Assessment of Non-CardiacArrest PatientsIntroduction:- You must perform a careful and systematic assessment aimed at identifying serious S&S linked to the patient, or their cardiac rhythm.
  136. 136. Assessment of Non-CardiacArrest PatientsUniversal Treatment of the NON-Cardiac Arrest Patient- Certain interventions must be performed on all non cardiac arrest patients, presenting with cardiovascular or respiratory related S&S. - Oxygen - IVT - Pulse Oximetry - 12 lead if available - Cardiac monitoring
  137. 137. Assessment of Non-CardiacArrest PatientsSummary:- Patient presenting with S&S of Non cardiac related cardiovascular or respiratory system emergencies needs a systematic assessment.- Your findings will dictate the most appropriate treatment- All patients require: - Supplementary oxygen therapy - Cardiac monitoring - Intravenous therapy- The goal in managing these patients is preventing them from going into cardiac arrest.
  138. 138. Assessment and treatment ofCardiac Arrest PatientsIntroduction:- Successful management of a patient in cardiac arrest requires a careful and systematic assessment, immediate identification of their cardiac rhythm and selection of the appropriate treatment.
  139. 139. Assessment and treatment ofCardiac Arrest PatientsAssessing the Underlying causes of Cardiac Arrest- Careful assessment needs to occur: - Pm Hx – Past Medical History - Hx - History - Events leading to incident- Management: - Defibrillation, adrenaline and other pharmacological adjuncts will not be effective until the underlying cause is identified and rectified.- We use the 6 H’s and T’s to assess the underlying causes.
  140. 140. Assessment and treatment ofCardiac Arrest PatientsUniversal Treatment of Cardiac Arrest- Certain interventions must be carried out in all cases of cardiac arrest regardless of the presenting cardiac rhythm. - CPR - Endotracheal intubation - Vascular Access - Vasopressors - Circulation of cardiac drugs - Identify and Correct underlying causes
  141. 141. Assessment and treatment ofCardiac Arrest PatientsPost Cardiac Arrest Treatment- If a pulse and perfusing rhythm are successfully restored, you must perform certain interventions to prevent the recurrence of cardiac arrest.- If the patient re-arrests, the chances of a second successful resuscitation are much lower- Prevention of recurrent cardiac arrest can be maximised by performing appropriate management
  142. 142. Assessment of Non-CardiacArrest PatientsSummary:- You must focus on identifying and correcting the underlying cause of cardiac arrest.- Failure will significantly decrease the likelihood of successful resuscitation- Interventions must be performed regardless of underlying rhythm- Interventions are aimed at maintaining effective ventilation and circulation until the abnormal rhythm can be corrected
  143. 143. Any Questions?
  144. 144. Case Review 1 - ACSIntroduction:- Looks at a patient presenting with Acute Coronary Syndrome.- Term used to describe unstable angina pectoris “Angina” or an acute myocardial infarction (AMI).- Most patients present with chest pain, discomfort, SOB, diaphoresis, dyspnoea- Advised to air on side of caution and suspect AMI
  145. 145. Case Review 1 - ACSSigns & Symptoms:
  146. 146. Case Review 1 - ACSImmediate Treatment & Management:- In first 10 mins an immediate assessment and treatment regime must occur- Diagnosing patients problem, provide adequate treatment- Mnemonic – “MONA” - Morphine - Oxygen - Nitro-glycerine (GTN) - Aspirin
  147. 147. Immediate Treatment & Management:
  148. 148. Case Review 1 - ACSTargeted History for Fibrinolytic Therapy:- In conjunction with 12 lead ECG- Perform brief targeted history and physical examination targeted on eligibility- If administered within 12 hours of onset of symptoms, “clot busters” can significantly reduce size of infarct, preserving myocardium- The indications or “inclusion criteria” for therapy must be carefully matched to contraindications “exclusion criteria”, if they are administered to wrong patient, they can be lethal.
  149. 149. Case Review 1 - ACSTargeted History for Fibrinolytic Therapy:- Inclusion criteria:
  150. 150. Case Review 1 - ACSOther Perfusion Strategies:- Depending on condition and haemodynamic status- Other strategies may include: - Percutaneous Coronary Interventions (PCI) - (e.g. Coronary angioplasty with or without stent) - Coronary Artery Bypass Grafting (CABG) (GAGS)
  151. 151. Case Review 1 - ACSTargeted History for Fibrinolytic Therapy:- Exclusion criteria:
  152. 152. Case Review 1 - ACSSummary:- Patient who presents with S & S of ACS, requires immediate assessment within 10 minutes of presentation - 12 lead ECG - Cardiac serum markers - Targeted history - Emphasis on fibrinolytic therapy suitability- Immediate management aimed at oxygenation and ventilation with pharmacologic interventions to reduce pain and anxiety- The adage “time is myocardium” definitely applies and should be remembered and taken seriously in patients with ACS presentation
  153. 153. Any Questions?
  154. 154. Case Review 2 - AsystoleIntroduction:- Asystole represents the absence of both cardiac electrical and mechanical activity on a cardiac monitor- Unfortunately asystole is rarely associated with a positive outcome
  155. 155. Case Review 2 - AsystoleTreatment:- Must be assessed in 2 or more leads, as it may be asystole in appearance in one lead and fine V-Fib in another- CPR- Airway management- Medications- Assessment as to why the patient is presenting in this way
  156. 156. Case Review 2 - AsystoleTreatment:
  157. 157. Case Review 2 - AsystoleSummary:- It should be considered to be the only true arrhythmia because it represents a total absence of any electrical or mechanical activity of the heart- Unfortunately is associated with a poor prognosis- There are potentially reversible causes of asystole, therefore systematic assessment, and appropriate interventions will maximise chances of successful resuscitation
  158. 158. Any Questions?
  159. 159. Case Review 3 – AutomatedExternal DefibrillationIntroduction:- Most cardiac patients present with ventricular fibrillation (V-Fib) as the initial dysrhythmia- V-Fib does not produce a pulse, therefore blood is not circulated- Pulseless V-Tach is less common but as lethal as V-Fib- The single most effective treatment for V-Fib is defibrillation- V-Fib is a transient rhythm and rapidly deteriorates- The AED can provide rapid defibrillation and does not require an ACLS operator to perform treatment
  160. 160. Case Review 3 – AutomatedExternal DefibrillationAssessment and Initial Treatment:- A careful and systematic assessment is required for a patient in cardiac arrest- If arrest was witnessed by you, begin CPR and apply AED immediately.- If not witnessed perform 2 minutes of CPR prior to applying AED- A return of spontaneous circulation (ROSC) occurs more often in V- Fib or Pulseless V-Tach if 1 ½ - 3 minutes of CPR is conducted prior to defibrillation
  161. 161. Case Review 3 – AutomatedExternal DefibrillationCardiac Rhythm Analysis and Defibrillation:- As soon as AED is available it must be attached- For each minute in V-Fib and Pulseless V-Tach defibrillation is delayed, the chance of survival is reduced by 10%- If indicated the AED will deliver a single shock, after which CPR should be continued- After 2 minutes the AED will assess the patient’s rhythm and ask you to check pulse, reanalyse and deliver a shock if indicated
  162. 162. Case Review 3 – AutomatedExternal DefibrillationSummary:- A rapid assessment is required in order to confirm the presence of cardiac arrest and begin the appropriate treatment ASAP.
  163. 163. Any Questions?
  164. 164. Case Review 4 – BradycardiaIntroduction:- A careful and systematic approach must occur to determine whether serious S & S linked to bradycardia are present- Bradycardia can take many forms - Sinus bradycardia - 1st, 2nd degree and complete heart blocks- However the important concept to remember is that regardless of the rhythm the rate is too slow and if the patient is symptomatic it must be treated.
  165. 165. Case Review 4 – BradycardiaAbsolute and Relative Bradycardia:- Absolute bradycardia exists when the ventricular rate is less than 60 beats per minute, such occurs in sinus bradycardia- Relative bradycardia exists when the patient’s heart rate is faster than one would expect for his/her condition yet the patient is unstable.- E.G. A patient who has a heart rate of 65bpm, but a BP of 80/50mmHg may be experiencing “relative” bradycardia because the pulse relative to BP is too slow
  166. 166. Case Review 4 – BradycardiaTreatment of Bradycardia:- Treatment depends on the presence or absence of serious S & S.- The asymptomatic patient may require little more than close monitoring,- However the unstable patient requires interventions aimed at increasing the heart rate and improving perfusion.
  167. 167. Case Review 4 – BradycardiaTreatment of Bradycardia:- Treatment depends on the presence or absence of serious S & S.- The asymptomatic patient may require little more than close monitoring,- However the unstable patient requires interventions aimed at increasing the heart rate and improving perfusion.
  168. 168. Case Review 4 – BradycardiaSummary:- A patient who is asymptomatic requires no more than observation- However the patient presenting with serious S & S of inadequate perfusion linked to bradycardia need immediate interventions- Aimed at increasing the heart rate and preventing cardio-vascular collapse- Remember even though th4 patient may have a heart rate of 60- 70bpm, if the blood pressure is poor, the cardiac rate is bradycardic and needs intervention rapidly- “Absolute” or “relative” bradycardia needs rapid intervention to ensure adequate oxygenation and perfusion
  169. 169. Any Questions?
  170. 170. Case Review 5 – Narrow ComplexTachycardiaIntroduction:- The term “Narrow Complex Tachycardia” refers to a rhythm in which the QRS complex is less than 0.12 seconds or 3 small boxes on the ECG,- The ventricular rate is equal or > 100bpm- SVT indicates that the origin of the cardiac rhythm is above (supra) the ventricles- SVT manifests as many other rhythms, atrial tachycardia, atrial fibrillation, or flutter with rapid ventricular rate (RVR) and Junctional tachycardia
  171. 171. Case Review 5 – Narrow ComplexTachycardiaTreatment:- Careful and systematic assessment must be performed so that the most appropriate treatment can be provided to the patient.- If the patient is not experiencing serious S & S linked to tachycardia,- Initial treatment involves interventions aimed at decreasing the ventricular rate and identifying the underlying cardiac rhythm- If serious S & S are present synchronised cardioversion must be performed without delay.
  172. 172. Case Review 5 – Narrow ComplexTachycardiaSummary:- Patient’s with narrow complex tachycardia requires careful and systematic assessment- All patient’s require: - Supplemental oxygen - IVT - Cardiac monitoring - 12 lead if available- If the patient is stable, initial treatment is aimed at decreasing the heart rate with a combination of vagal manoeuvres and pharmacologic interventions- Unstable patient’s require immediate synchronised cardioversion, which in the conscious patient should be preceded with a sedative agent
  173. 173. Any Questions?
  174. 174. Case Review 6 – Pulseless Electrical Activity(PEA)Introduction:- Patients with Pulseless Electrical Activity (PEA) , is characterised by a rhythm on the cardiac monitor when the patient does not have a cardiac output- Any rhythm can be seen with PEA- Only exception is V-Fib and Pulseless V-Tach, both of which were previously mentioned as requiring immediate defibrillation
  175. 175. Case Review 6 – Pulseless Electrical Activity(PEA)Treatment:- In addition to managing cardiac arrest, management focus is on identifying the underlying cause- Common causes of cardiac arrest, their clinical signs, their respective treatments are in Table 3-14- As a general rule, any rhythm that is slow indicates Hypoxia- Any rhythm fast indicate Hypolvolaemia
  176. 176. Case Review 6 – Pulseless Electrical Activity(PEA)Summary:- PEA is a phenomenon that could be overlooked if you do not perform a careful assessment- Treatment of PEA involves treating cardiac arrest with: - CPR - Airway management - IV Therapy - And medications- Ultimate goal is to rapidly identify and treat underlying cause(s)
  177. 177. Any Questions?
  178. 178. Case Review 7 – Respiratory ArrestIntroduction:- You must perform a rapid assessment and management regime in patients with respiratory arrest- Including patients with respiratory arrest as a result of a foreign body airway obstruction (FBAO)- Immediate positive pressure ventilations must be provided, while maintaining airway patency- Failure to recognise and immediately treat leads to cardiopulmonary arrest and death within minutes
  179. 179. Case Review 7 – Respiratory ArrestAssessment:- Ensure airway is open and patent, clear of secretions, or obstructions- In the non-injured patient, head tilt, chin lift manoeuvre or in the patient with suspected spinal injury, the jaw thrust manoeuvre- Critical the patient’s airway remains clear at all times- Vomitus and other secretions in the airway require immediate oropharyngeal suctioning- Assess for spontaneous breathing, evident by rise and fall of the chest and sounds of air exiting the chest, via nose and mouth
  180. 180. Case Review 7 – Respiratory ArrestManagement:- Maintain patent airway, with a combination of manual positioning of head and insertion of basic airway adjunct, OPA or NPA- Positive pressure ventilations are then provided with a bag valve mask (BVM) or a pocket mask at 10 -12 breaths per minute- In order to deliver high concentrations of oxygen, you must ensure supplemental oxygen is attached
  181. 181. Case Review 7 – Respiratory ArrestForeign Body Airway Obstruction (FBAO):- May be food, can obstruct airway and prevent patient from moving air- Recognised in initial attempts to ventilate, you meet resistance and/or do not see the chest rise and fall- This needs to be rectified immediately- Reposition patients head- Attempt to re-ventilate, If both breaths do not produce visible chest rise and fall,- Perform chest compressions in an attempt to clear obstruction- If compressions fail to dislodge airway obstruction, visualise vocal chords with a laryngoscope (direct laryngoscopy) and remove the obstruction with Magill Forceps
  182. 182. Case Review 7 – Respiratory ArrestEndotracheal Intubation:- In an adult patient Endotracheal intubation it is seen to be the “gold standard” for airway management- Patients in respiratory or cardiac arrest usually require prolonged ventilatory support and are at extremely high risk for regurgitation and aspiration of stomach contents- The airway should be protected with an endotracheal tube
  183. 183. Case Review 7 – Respiratory ArrestAlternate airway management:- Alternate airway management tools include: - LMA – Laryngeal mask Airway - Oesophageal Combitube
  184. 184. Case Review 7 – Respiratory ArrestSummary:- Ensure airway is open and clear of obstructions- Confirm absence of breathing, then ventilate with BVM for 2 breaths- If initial ventilations unsuccessful, airway obstruction likely- Clear obstruction, manually or by laryngoscopy- Once airway is patent, continue positive pressure ventilation 10 – 12 breath per minute- To secure airway, endotracheal intubation should be performed
  185. 185. Case Review 8 – StrokeIntroduction:- An ischaemic stroke is the result of a blocked cerebral artery- Common causes include formation of local thrombus or a thrombus that breaks free (embolus) and travels to brain from another part of the body- Less common causes cerebral arterial vasospasm, and generalised hypoperfusion (shock)- All areas distal of the blocked artery are deprived of oxygen resulting in varying degree’s of neurological impairment, ranging from: - Limited mobility - To total debilitation
  186. 186. Case Review 8 – StrokeStroke Survival and Recovery:- The goal is to begin therapy no longer than 60 minutes after the arrival at the hospital door and within 3 hours of the initial onset- This requires both pre-hospital and hospital providers to avoid delays- Pivotal points represent survival and recovery
  187. 187. Case Review 8 – StrokeAssessment:- After appropriate management of ABC’s a rapid assessment of patient and a brief targeted history helps identify patient’s potential for stroke enabling prompt treatment- Warning signs of acute ischaemic stroke: - Confusion - Slurred speech - Unilateral facial droop - Unilateral weakness or paralysis- Particularly important to determine when symptoms began- If patient meets inclusion criteria fibrinolytic therapy can begin- This must be accomplished within 3 hours of onset of symptoms
  188. 188. Case Review 8 – StrokeCincinnati Pre-Hospital Stroke Scale:- Allows identification of possible stroke- Three tests, any abnormality in any one – STROKE suspected
  189. 189. Case Review 8 – StrokeTreatment:- Mainly supportive and focuses on protecting the airway and delivering supplemental oxygen- Monitoring ECG and providing IV therapy- Promptly transporting patient to facility that specialises in stroke care where fibrinolytic therapy can be initiated
  190. 190. Case Review 8 – StrokeFibrinolytic Therapy for Acute Ischaemic Stroke:- If within 3 hours of onset, and meets inclusion criteria- Fit the following criteria, therapy can commence
  191. 191. Case Review 8 – StrokeSummary:- Can be a catastrophic event that can leave the patient with permanent disabilities ranging from mild neurologic deficits to complete incapacitation- All patients require supplemental oxygen, IV therapy, cardiac monitoring- After assessment act quickly to identify as a candidate for therapy and transfer for this critical intervention
  192. 192. Any Questions?
  193. 193. Case Review 9 – Ventricular FibrillationIntroduction:- It is important to reiterate that for every minute in V-Fib and Pulseless V-Tach persists the survivability is reduced by 10%- The single most important treatment is immediate defibrillation, monophasic or biphasic
  194. 194. Case Review 9 – Ventricular FibrillationTreatment of V-Fib or Pulseless V-Tach:- The clinician must be prepared to change the treatment on the basis of the patient’s clinical response to therapy.- Remember to circulate all drugs with effective CPR for 2 minutes followed by defibrillation in V-Fib or pulseless V-Tach persists- Following defibrillation, immediately resume CPR and reassess in 2 minutes
  195. 195. Case Review 9 – Ventricular FibrillationSummary:- V-Fib is most common initial dysrhythmia in cardiac arrest and if not promptly treated will deteriorate to asystole- Successful management requires rapid assessment to confirm cardiac arrest- If witnessed begin CPR ASAP- If not witnessed perform CPR for 2 minutes and then apply cardiac monitor and defibrillate- Intubation, IVT and pharmacological interventions are mandatory- Patient should be defibrillated with once off 360J or biphasic equivalent then CPR for 2 minutes, reassess and defibrillate as required
  196. 196. Any Questions?
  197. 197. Case Review 10 – Wide Complex Tachycardia’sIntroduction:- A wide complex tachycardia refers to a rhythm in which QRS complexes are greater than 0.12 seconds in width and ventricular rate is > 100bpm- Approximately 90% of wide complex tachycardia’s are ventricular tachycardia, indicating rhythm originated from an ectopic pacemaker in the ventricles
  198. 198. Case Review 10 – Wide Complex Tachycardia’sIntroduction:
  199. 199. Case Review 10 – Wide Complex Tachycardia’sTreatment of Wide Complex Tachycardia’s:- Careful and systematic assessment- If patient not experiencing serious S & S, pharmacologic intervention, aimed at decreasing ventricular irritability, reducing tachycardia- If serious symptoms linked to tachycardia, synchronised cardioversion needed without delay- High risk of deterioration to V-Fib, be prepared to defibrillate if patient becomes pulseless
  200. 200. Case Review 10 – Wide Complex Tachycardia’sAntiarrhythmic Maintenance Infusions:- If terminated pharmacologically begin a maintenance infusion of anti-arrhythmic agent that aided in the conversion- If synchronised cardioversion was used with no pharmacological agent, give anti-arrhythmic bolus and commence maintenance infusion- Important to maintain therapeutic blood levels of anti-arrhythmic agent because this will prevent the recurrence of the wide complex tachycardia
  201. 201. Case Review 10 – Wide Complex Tachycardia’sSummary:- If a patient presents with a wide complex tachycardia you must assume it is ventricular tachycardia until proven otherwise- Continuous monitoring of the patient- V-Tach can rapidly deteriorate to V-Fib- Must have: - Supplemental oxygen - Cardiac monitoring - IVT - 12 lead if available- Treatment is based on being unstable or stable in origin, therefore systematic and careful assessment needs to occur, rapidly to identify S & S associated with wide complex tachycardia
  202. 202. QUESTIONS?That now concludes the theory component of the “ADVANCED CARDIAC LIFE SUPPORT” Course.
  203. 203. Thank you for your participation on behalf of the…….Australasian Emergency Response Specialists Pty Ltd TASMANIA & PNG “FAILURE TO PREPARE IS TO PREPARE TO FAIL”