1. ACLS Recertification Review
No notes for this case.
2010 Guidelines 1

2. C A B Focus: High Quality CPR
C = Compressions: check for responsiveness, call for help all while looking for effective breathing. If unresponsive and not breathing, check for a pulse. No pulse = begin chest compressions
A = Airway: open the airway
B = Breathing: provide two positive-pressure ventilations. Each breath administered over 1 second

3. High Quality CPR Push fast – at least 100 compressions per minute
Push deep – 2 inches for an adult
Allow full chest recoil
30:2 if no advanced airway is in place
8-10 breaths per minute with advanced airway
Each breath delivered over 1 second

4. Monitoring During CPR End tidal CO2 Below 10 mm Hg – ROSC unlikely
Abrupt increase good indicator of ROSC
Coronary perfusion pressure
Aortic diastolic pressure – right atrial diastolic pressure
↑ CPP >15 mm Hg needed for ROSC

5. AED Use AED is only placed on patients who are in cardiac arrest
Use the AED as soon as it is available
Minimize interrupting compressions while you apply the AED pads
If the AED does not promptly analyze the rhythm begin chest compressions
The AED’s hands free pads allow for a more rapid defibrillation than manual paddles

6. Waveform Capnography
Most reliable method for confirming placement and monitoring dislodgement
Quality monitoring of CPR

7. Qualitative End-Tidal CO2 Detector
What should the operator’s next action be? 1
Use caution when securing an endotracheal tube as it is possible to obstruct venous return from the brain if the device passes circumferentially around the patient’s neck

8. Res-Q-Pod Impedance Threshold Device (ITD)
Connects to the endotracheal tube (theoretically can be used with pocket mask or BVM)
Enhances circulation, not ventilations

9. Res-Q-Pod Only to be used on a patient in cardiac arrest
Connected directly to the endotracheal tube
If you are using an end tidal CO2 monitor/detector the monitor/detector should be connected in-line between the BVM and the ITD

10. Res-Q-Pod
How it works
During chest recoil the heart usually refills with blood while at the same time some air is drawn into the lungs
Any air drawn into the lungs lessens the quantity of blood refilling the heart (preload)
The Res-Q-Pod does not allow any air to be drawn into the endotracheal tube during chest recoil which allows for additional preload

11. Causes: H’s and T’s Hypoxia (CNS events)
Hypokalemia/hyperkalemia (and other electrolytes)
Hypothermia
Hypovolemia (tank/anaphylaxis, gravid)
Hydrogen Ion (Acidosis)

12. Causes: H’s and T’s (cont’d)
Tamponade (cardiac)
Thrombosis, pulmonary
Thrombosis, cardiac
Toxins (ODs, drugs, etc)
Tension pneumothorax

13. Adult BLS Algorithm

14. High Quality CPR Push fast – at least 100 compressions per minute
Push deep – 2 inches for an adult
Allow full chest recoil
30:2 if no advanced airway is in place
8-10 breaths per minute with advanced airway
Each breath delivered over 1 second
If end tidal CO2 <10 mm HG, improve CPR

15. Monitoring During CPR End tidal CO2 Below 10 mm Hg – ROSC unlikely
Abrupt increase good indicator of ROSC
Coronary perfusion pressure
Aortic diastolic pressure – right atrial diastolic pressure
↑ CPP >15 mm Hg needed for ROSC

16. Waveform Capnography
Most reliable method for confirming placement and monitoring dislodgement
Quality monitoring of CPR
Post resuscitation goal is mmHg

17. Ventricular Fibrillation
Characteristics of VF
Organized QRS complexes and absent P waves
Wavy, chaotic, inconsistent baseline
Irregular rhythm
VF may occur spontaneously or be preceded by VT.

18. Ventricular Tachycardia
Characteristics of VT
Wide, bizarre QRS complexes
Regular rhythm and mostly uniform in shape
Absent P waves
Ventricular rate is 150 bpm. How is the patient tolerating this rhythm?
Does this produce a pulse? Cases 8 and 9 discuss patients with VT rhythms that are associated with a pulse.

19. Asystole / PEA?
Any rhythm (bradycardia, sinus, tachycardia) is PEA if no pulse is present. Immediate treatment includes initiation of CPR and administration of epinephrine

20. Asystole
Verify that the flat line seen on the ECG monitor is indeed “true asystole” (an electri-cally silent heart) and not some other rhythm (eg, fine ventricular fibrillation) masquerading as a flat line or an operator error that creates a flat line (ie, “asystole”) on the monitor screen when in fact another rhythm is present.

21. Learning Objectives (cont’d)
Recognize that asystole usually represents a confirmation of death rather than a “rhythm” to be treated. Describe the criteria that clinicians should follow for stopping resuscitative efforts.

22. ACLS Cardiac Arrest Circular Algorithm
In order to minimize interruptions in chest compressions the defibrillator should be charged while compressions continue. The use of hands-free pads allows for a more rapid defibrillation.

23. Post Cardiac Arrest Care

24. VF/Pulseless VT: Return of Spontaneous Circulation
Maintain open, protected airway
Optimize ventilation and oxygenation
Stabilize airway devices during transport; avoid dislodgment
Monitor ventilation (end tidal CO2) and oxygenation (O2)
Monitor rhythm; give rhythm-appropriate medications
If defibrillation occurred after use of antiarrhythmic agent, then continue maintenance infusion of same agent

25. Post Resuscitation Titrate Oxygen
Oxygen sat goals of 94-99% (closer to 94% is better)
Assure moderate blood oxygen levels
Very high blood oxygen is associated with release of free radicals and brain injury
Patients who are intubated and require suctioning should be suctioned for no longer than 10 seconds while the catheter is withdrawn

26. Therapeutic Hypothermia
“It’s Really Cool”

27. Therapeutic Hypothermia
Only considered for ROSC patients who do not follow commands
Appropriate for non-responsive patients who will be going to the cardiac cath lab
No upper age limit cutoff for hypothermia
Presenting cardiac arrest rhythm does not matter as it pertains to appropriate utilization of hypothermia

28. Therapeutic Hypothermia
77 patients who were randomly assigned to hypothermia (33 degrees C) vs. normothermia
21/43 treated with hypothermia
49% survived and had a good outcome
9 of the 34 treated with normothermia
26% survived and had a good outcome (P=0.046).
Benard, S.A., et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N. Engl J Med Feb 21;346(8):

29. Therapeutic Hypothermia
273 patients randomized to hypothermia vs. normothermia
Neurologic outcome
75/136 patients in the hypothermia group had a favorable neurologic outcome
54 of 137 in the normothermia group had a favorable neurologic outcome
Mortality at six months
Hypothermia - 56 of 137 (41%)
Normothermia - 76 of 138 (55%)
Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest.N. Engl J Med Feb 21;346(8): Erratum in: N Engl J Med 2002 May 30;346(22):1756

30. Asystole
Active search for “do not attempt resuscitation” (DNAR) orders/status
Explicit criteria for stopping
Death certification in the field
Prohibition on transporting failed ACLS with CPR

31. Asystole/PEA Family presence at resuscitation efforts
Survivor support plans
More formal death notification
After multiple doses of epinephrine combined with high quality CPR and a fluid bolus, consideration for terminating the resuscitation is appropriate
Family Presence at Resuscitation Attempts
Allowing, even encouraging, family presence at resuscitation attempts is an emerging clinical practice. Post hoc interviews with family members and survivors confirm a positive and prolonged effect of this experience. Everyone needs to “say goodbye” and obtain closure on the death of a loved one. There are obvious limits to this practice. Variable levels of staff resistance must be overcome. There is, however, an impressive body of evidence documenting a strong therapeutic effect of these programs.
Allowing family members to be present at resuscitation attempts is a good thing.
EMS systems need to provide 24/7 on-call coverage by trained bereavement personnel. These personnel may be available from a community-wide chaplains’ panel, designated healthcare personnel, shift supervisors, or even ride-along staff with specifically assigned roles to help with survivors.
Furthermore, there needs to be in place a procedure for legal death certification and clear directions and support for handling a person who has died at home.

32. Bradycardias 1. Discuss Unstable vs stable bradycardia
Signs and symptoms of unstable bradycardia
Intervention agents and sequences to use
Recognition criteria for heart blocks: 1st, 2nd (types I and II), and 3rd degree
Pathology of conduction system in heart blocks
Some Examples to Consider Using
Clinical Information: a man is having an acute myocardial infarction. He has severe chest pain, HR = 40; BP = 80/55.
Comment: It is important to decide the sequence of chest pain, bradycardia, and hypotension. Chest pain before bradycardia suggests that the AMI is causing the bradycardia and hypotension.
If the person gets dizzy, lightheaded, and weak, and then gets the chest pain, the sequence may be vaso-vagal event = bradycardia = low cardiac perfusion = drop in pressure = ischemic myocardium = ischemic pain begins.

33. Bradycardias 2. Discuss Significance of bradycardia in AMI patients
Significance of RV infarction plus bradycardia
Atropine pharmacology: why atropine helps some heart blocks and not others
Set up, start, troubleshoot transcutaneous pacing

34. Drugs to Learn
The actions, indications, administration, and precautions for these drugs and therapies:
Atropine
Dopamine
Epinephrine
Transcutaneous pacing

35. Adult Bradycardia

36. Hierarchy of Care Treat the patient, not the rhythm
Bradycardia is commonly associated with hypoxia
Any bradycardic patient should be evaluated for signs/symptoms of hypoxia and treated with positive pressure ventilations as needed.
Positive pressure ventilations may correct a bradycardia in a hypoxic patient

37. What Is This Rhythm?
Third-degree AV block at the level of the AV node (supra-nodal or supraventricular level)
Atrial rhythm is irregular due to sinus arrhythmia at a rate of bpm.
The atrial rate = bpm; ventricular rate = 44 bpm. There is no constant P-R interval. The narrow QRS complex indicates that the block is occurring above the ventricles (supraventricular) at an upper level of the AV node.
The pathology is usually
(a) increased parasympathetic tone, which can result from drug effects such as digoxin, or -blockers; or
(b) damage to the AV node
Third-degree AV block with a narrow junctional escape rhythm is usually transient and is associated with a favorable prognosis.

38. AV Block Third-degree AV block
Characteristic variable P-R interval with regular R-R interval.
Emphasize that one must look at similar QRS complexes to assess the regularity of the R-R interval (to ensure that ectopics, etc, do not cause confusion).

39. What Is This Rhythm?
Third-degree AV block at the infra-nodal (bundle branch) level
The wide QRS indicates that the block is occurring at the ventricular level.
There is no relation between the atrial and ventricular rhythm. Ventricular rhythm is regular and very slow (38 bpm).
The QRS is wide because block is at the bundle branch level, usually involving both bundle branches. The ventricular pacemaker is downstream from that level.
Damage to both bundle branches indicates extensive conduction system disease below the AV node. This is most often caused by extensive anterior myocardial infarction.
The ventricular escape pacemaker is slow (< 40 bpm) unstable and may lead to episodes of ventricular asystole.
New third-degree AV block demands urgent pacing, likely with TCP.
Emphasize that this is why TCP should be readied while atropine is tried.

40. Treatment? Third-degree AV block at the supra-nodal level
Third-degree AV block with a narrow junctional escape rhythm is usually transient and associated with a favorable prognosis.

41. What Is This Rhythm? Third-degree AV block with ventricular asystole
Patient has acute anterior myocardial infarction.
He developed right bundle branch block (see wide-QRS complex on left side of strip).
Complete heart block abruptly developed: only P waves seen on right side of strip.
P waves are not followed by a ventricular escape focus, resulting in ventricular asystole.
Comment on lidocaine issue here (escape rhythms are less likely with lidocaine).

42. Treatment?
Third-degree AV block at the infra-nodal (bundle branch) level
The ventricular escape pacemaker is slow (<40 bpm) unstable and may lead to episodes of ventricular asystole.
New third-degree AV block demands urgent pacing, likely with TCP.
Emphasize that this is why TCP should be readied while atropine is tried.
Transcutaneous pacing
The advantage of TCP over catecholamine infusion is significant.
A transvenous pacemaker often takes too long to place.
The key focus is on the unstable patient and the value of TCP as a bridge while transvenous pacing is organized.
Note the use of pacing to allow the use of lidocaine in stable second-degree AV block with PVC or runs of VT.
This is a good place to reinforce this contraindication to lidocaine for ventricular escape rhythms.
Standby pacing (pads applied but not in pacing mode) is the reason for understanding intranodal AV blocks.

43. Transcutaneous Pacing
Some Pearls and Perils to share about treating symptomatic bradycardia:
Why does capture sometimes fail?
A large percentage of awake patients experience enough discomfort to require medications.
Give small doses of a narcotic and/or benzodiazepines.
Clinically assess the patient continuously: capture will cease if the ventricles fibrillate.
A pacing shock on a T wave may induce VF, but this is extremely rare.
PVCs are frequently not sensed by pacemakers.
Catecholamine infusions
Dopamine infusion
Use if unresponsive to atropine and TCP is unavailable or ineffective
Transvenous pacing as soon as possible
Same doses as for cardiogenic shock
Epinephrine infusion
For profound shock
Doses of 2 to 10 g/kg per min stimulate 1 receptors; milder  (vasoconstrictor) effects.
Increased rate () and systemic resistance () can increase myocardial workload and ischemia.
Catecholamines can precipitate coronary vasoconstriction.
Extravasation can cause tissue ischemia and sloughing.
Effects profoundly increased in patients on MAO inhibitors or with pheochromocytoma.
Dopamine = short half-life; with rapid discontinuation, bradycardia and hypotension can return.
Double the concentration if the initial low-dose infusion (1 to 4 g/min) is inadequate
AV block diagnoses
Reinforce how often patients can be stable without spending time analyzing the exact site and nature of the block.
Patients requiring repeated atropine, TCP, or catecholamine infusions will require transvenous pacing as quickly as possible.
Always start making arrangements for transvenous pacing for stable patients with new infra-nodal blocks.

44. Transcutaneous Pacing: “Capture” vs “No Capture”
25 Feb Lead I Size HR=41
Bradycardia: no pacing
Bradycardia: No Pacing
Pacing Spike
25 Feb Lead I Size HR= mA
Pacing below threshold:
no capture
Capture:
Spike + broad QRS
QRS: opposite polarity
It is critical that ACLS provider candidates understand the difference between pacing artifact, pacing without QRS capture, and pacing with QRS capture.
Also note electrical capture vs mechanical capture. If pacing produces the spike and broad QRS complexes seen in the third rhythm strip (electrical capture), you must check to see whether the paced beats are producing a detectable pulse and blood pressure.
Pacing Below Threshold (35 mA): No Capture
25 Feb Lead I Size HR= mA
Pacing above threshold:
with capture
Pacing Above Threshold (60 mA): With Capture (Pacing-PulseMarker )

45. Tachycardias At the end of this lesson be able to
Recognize stable vs. unstable tachycardia
Recognize when that instability is due to the tachycardia
Rapidly identify the specific rhythm
Follow algorithms for tachycardias and cardioversion
Properly perform synchronized cardioversion
Provide post-cardioversion treatment and monitoring

46. Know How to
Operate defibrillator/monitor to both defibrillate and cardiovert
Monitor rhythm through pads or paddles
Define “defibrillation” vs “cardioversion”
Switch to defibrillator/monitor mode or cardioversion mode
Attach monitor leads in modified lead II configuration
Recognize when device is in active synchronization mode
Switch from synchronized cardioversion to unsynchronized defibrillation
Understand major elements of post-cardioversion care: oxygen, IV access, monitoring, antiarrhythmics

47. Step 1 Is patient stable or unstable?
Patient has serious signs or symptoms? Look for
Chest pain (ischemic? possible ACS?)
Shortness of breath (lungs getting ‘wet’? possible CHF?)
Low blood pressure (orthostatic? dizzy? lightheaded?)
Decreased level of consciousness (poor cerebral perfusion?)
Clinical shock (cool and clammy? peripheral vasoconstriction?
Are the signs and symptoms due to the rapid heart rate?
An initial assessment should be done quickly to determine whether the condition is stable.
In the absence of serious signs or symptoms, vagal maneuvers and drug therapy should be tried first.
Patients with serious signs or symptoms related to the tachycardia should be managed according to the algorithm for unstable tachycardia (see Case 8).

48. Step 2
Identify arrhythmia; classify patient into 1 of 3 tachycardia categories:
1. Sinus tachycardia
2. Narrow-complex supraventricular tachycardia
3. Wide-complex tachycardia,
Make sure that everyone in the small groups has in hand the 2000 ECC Handbook or an equivalent source of the 3 tachycardia algorithms and the table on atrial fibrillation/flutter.

49. Sinus Tachycardia
Paroxysmal Supraventricular Tachycardia

50. Paroxysmal Supraventricular Tachycardia
Review the key characteristics of PSVT.
Stable patients in SVT should have a 12 lead ECG performed prior to the administration of medications. The first line treatment for stable SVT patients is a vagal maneuver. Unstable patients should be immediately cardioverted

51. 1. Atrial Fibrillation/Flutter
Notice this technique of asking a clinical question on one slide and then providing the answer on the next one. 
The questions at the end of most of the slides are not rhetorical: pause long enough before advancing to let the students know you expect an answer from them––not from the next slide.
Your evaluation of atrial fibrillation/flutter should focus on 4 clinical features.
What are they?

52. Atrial Flutter: Atrial Rate = 250 bpm, Ventricular Rate = 125 bpm
Stress that approximately 80% of wide-complex tachyarrhythmias are VT. Also discuss typical postcardioversion medication therapy of VT, including lidocaine, procainamide, and bretylium. Review the appropriate doses and IV infusion rates.

53. Ventricular Tachycardia
Pose the question in the header with a brief case: a 55 year-old-male with substernal chest pain, some nausea, mild SOB, improved with nitroglycerin x 3; nondiagnostic changes on 12-lead ECG.
The setting (ie, a patient with ischemic pain and an acute coronary syndrome) makes VT more likely than PSVT with aberrant conduction.
Briefly review the drug sequence for VT (Figure 9, page 19). Remind the students who were tempted to diagnose PSVT with aberrancy that adenosine is not part of the VT algorithm. Discuss the possibilities of harm that could occur if VT is treated with adenosine and a calcium channel blocker (eg, verapamil; see page 18, Narrow-Complex Tachycardia).
Continue the scenario, assuming correct identification of the arrhythmia as VT; include a deterioration in clinical status, and initiate a discussion of the appropriate next step in management.
Emphasize the need for immediate cardioversion (without further pharmacologic interventions) when the tachycardia becomes unstable.
Emphasize that the participant must
Proceed to synchronized cardioversion if vagal maneuvers and drug therapy fail or the patient becomes unstable
Synchronize before each attempt at cardioversion
Know the appropriate drug sequences and doses for each arrhythmia
Know the appropriate energy levels for cardioversion of each arrhythmia

54. Adult Tachycardia

55. Wide Complex Tachycardia
Adenosine is recommended for undifferentiated regular monomorphic wide complex tachycardia
Do not use Adenosine for irregular or polymorphic wide complex tachycardias, as it may cause degeneration of the arrythmia to VF

56. Electrical Cardioversion
Immediate electrical cardioversion is indicated for a patient with serious signs and symptoms related to the tachycardia.
During defibrillation/cardioversion supplemental oxygen should be removed from the patient in order to ensure it is not blowing over the patient’s chest
Is the patient stable or unstable?
How do you define “unstable”?
“Hemodynamically unstable” is defined by the following signs and symptoms: chest pain, shortness of breath, decreased level of consciousness, low blood pressure, shock, pulmonary congestion, congestive heart failure, and AMI.

57. Synchronized Cardioversion
Procedure
1. Attach monitor leads to patient
2. Apply conductive material to paddles if not using hands-free defibrillation pads 3. Turn on defibrillator
Review the procedure for synchronized cardioversion. Demonstrate the procedure on equipment that is comparable to equipment used by the participants. Many EMS systems have “hands-free” defibrillation.

58. Synchronized Cardioversion
Procedure (cont’d)
4. Turn on synchronization mode
5. Verify synchronization signal on monitor screen
6. Select energy level
7. Place defibrillator paddles on chest and apply pressure (if necessary)
8. Charge defibrillator

59. Synchronized Cardioversion
Procedure (cont’d)
9. “CLEAR!”
Check yourself
Check patient
Check bed/stretcher
10. Press both buttons until discharge occurs

60. Synchronized Cardioversion
Energy selection
Narrow regular: joules
Narrow irregular: joules biphasic
Narrow irregular: 200 joules monophasis
Wide regular: 100 joules
Wide irregular: standard defibrillation dose-not synchronized
Solicit participant responses.
Complications may include deterioration to VF, embolization of a thrombus, etc.
If the rhythm deteriorates to VF, instruct the participants to rapidly assess cardiovascular status and proceed to immediate defibrillation.

61. Stroke Care 8 D’s of Stroke Care
Detection – Rapid recognition of symptoms
Dispatch – Early activation of EMS (call 911)
Delivery – Rapid EMS identification, management & transport
Door – Appropriate triage to a stroke center
Data – Rapid triage, evaluation, and management in the ED
Decision – Stroke expertise and therapy selection
Drug – Fibrinolytic therapy, intra-arterial strategies
Dispostion – Rapid admission to stroke/critical care unit
If resources are not available (no neurologist, no CT, etc.) patients arriving via EMS should be diverted to a nearby stroke center

62. Rapid Response Teams (RRT)
Many hospitals have developed these teams in order to identify and treat early clinical deterioration
Designed in an attempt to “rescue” a patient before they decompensate and code