exam 1 High Acuity Cardiac lecture

Card Set Information

exam 1 High Acuity Cardiac lecture
2010-06-24 16:30:28
High Acuity exam ekg abg

high acuity exam 1
Show Answers:

  1. Closed ICU
    patient care is provided by a dedicated ICU team that includes a CC physician
  2. Open ICU
    care is provided by a team with doctors who have responsibilities outside of the ICU
  3. SBAR
    • Method of communication among professionals. Required info.
    • S--Situation
    • B--Background
    • A--Assessment
    • R--Recommendation

    Important when contacting a physician for a patients needs
  4. characteristics of critically ill patients
    resiliency, vulnerability, stability, complexity, predictability, resource availability, participation in care, participation in decision making
  5. Role of sedation in Critical illness
    Reduces anxiety, reduces agitation, helps provide amnesia

    Important to provide adequate pain control FIRST
  6. What is a "sedation vacation"?
    Titration down of sedation medications once every 24 hours before the doctor rounds so they can perform an appropriate assessment.
  7. do you want a family to see a Code BLUE?
    Yes. It gives families insight that all was done that could be done for the family member.
  8. how long should a PR interval be?
    5 little blocks or 0.20
  9. how long should a QRS complex be?
    3 little blocks or 0.12
  10. How long should a QT interval be?
    10 little blocks or 0.40
  11. Steps to analyzing a rhythm strip
    • 1. Are QRS's present?
    • 2. Are the R-R intervals regular? (Sinus or not?)
    • 3. What is the rate? Is it normal, tachy or brady?
    • 4. Are P-waves present before each QRS? (absence of P waves indicates Heart block)
    • 5. Measure the PR interval
    • 6. Measure the QRS complex and the QT interval
    • 7. Look for ST changes.
  12. what does the P wave indicate?
    atrial depolarization from the SA node
  13. Types of rhythms that originate in the SA node
    • Sinus Rhythm
    • Sinus Brady
    • Sinus Tachy
  14. Rhythms that originate in The Atria
    • Atrial flutter (saw tooth)
    • Atrial fibrillation
    • SVT
    • Premature atrial complexes
  15. Rhythms originating in AV Node
    Junctional Rhythm
  16. Rhythms that originate in ventricle
    • Ventricular fibrillation
    • Vtach
    • Asystole
    • Torsades de pointes
    • Pacemaker rhythms
    • PVC's
    • Idioventricular rhythms
  17. Hypokalemia effect on heart rhythms
    PRI increases, T wave is flat, QT interval lengthens, Brady-dysrhythmias, conduction blocks, PVC's
  18. HYPERkalemia and the heart
    Tall peaked T wave, QT shortens, if not treated b/c asystole
  19. HYPERcalcemia and the heart
    QT intervals shortens
  20. HYPOcalcemia and the heart
    QT interval lengthens
  21. HYPERmagnesemia and the heart
    PRI prolongs, QRS widens, tall peaked T waves, Bradycardia
  22. First degree heart block
    PRI less than 5 blocks
  23. second degree AV block, Type I Wenckebach
    Gradual lengthening of the PR interval until a QRS complex is dropped

    Causes: Surgery near valves, inferior or posterior MI, Dig toxicity.
  24. second degree AV block, Type II Mobitz
    Every other p wave not conducted through the AV node

    Caused by: Inferior MI

    • manifestations: Possibly none, hypotension, S/S of decr perfusion
    • May deteriorate to complete HB
  25. 3rd degree AV block--Complete heart block
    Asynchronous contraction of the atria and the ventricles

    • Caused by Acute MI
    • Manifestations are shock and loss of consciousness
  26. Junctional rhythms
    SA node sin't firing and the rhythm originates in the AV node. P wave is inverted, absent or behind QRS complex.

    Caused by: vagal stimulation, hypoxia, SA node ischemia, Dig toxicity.
  27. Ventricular rhythms
    • Origin of depolarization is in the ventricles
    • May be fast or slow
    • QRS is bizarre

    • Wide QRS= Vtach
    • Narrow QRS=SVT
  28. Idioventricular Rhythm
    Regular rhythm, rate of 20-40

    Caused by severe hypoxia or MI
  29. accelerated idioventricular rhythm
    Looks like IVR except can be regular or irregular with a rate of 40-100.

    Caused by AMI, reperfusion
  30. Ventricular Tachycardia
    • Rapid rhythmic contraction of the ventricles
    • No P waves
    • Wide bizarre complexes
    • Caused by Heart disease, hypokalemia, hypoxia
  31. Torsades de Pointes
    Oscillating ventricular rhythm, rate >200

    Caused by Prolonged QT interval of >0.40, quinidine or procainamide, heart disease, hypokalemia, hypoxia
  32. Ventricular fibrillation
    • Uncoordinated electrical activity
    • NO cardiac output

    Caused by heart disease, hypokalemia, hypoxia


  33. Pulseless Electrical Activity (PEA)

    5 H's and 5 T's
    • 5 H's
    • Hypovolemia, hypothermia, hydrogen ion (acidosis), hypoxia, hyperkalemia

    • 5 T's
    • Tablets (OD), Tamponade, Tension pneumo, Thrombosis in ACS or Thrombosis in Pulmonary.
  34. AVPU measures what?

    • A--Alert
    • V--Voice
    • P--Pain
    • U--Unresponsive
  35. if found to be unresponsive, then what do we look for--
  36. If responsive, next steps in assessment

    • O--oxygen
    • I--IV access
    • M--Monitor
    • F--Fluids
  37. Slow Narrow QRS complexes interventions
    • 1. OIMF
    • 2. Assess QRS width
    • 3. If <0.10 intervention sequence
    • a. Atropine 0.5 to 1.0 mg IVP (up to 3 doses)
    • b. Transcutaneous pacing
    • c. Dopamine 5 to 20 per minute
    • d. Epinepherine 2-10 mcg
  38. Slow WIDE QRS complexes interventions >0.10
    • 1. Go directly to TCP
    • 2. Dopamine 5-20 per minute
    • 3. Epinepherine 2-10 mcg
    • 4. Prepare for Transcutaneous pacing
    • Do not give atropine!
  39. Fast rhythms with QRS <0.12 interventions
    OIMF then assess for stability.

    If unstable, synchronized cardioversion
  40. Synchronized Cardioversion
    • Low dose electrical therapy delivered on the QRS complex.
    • Oh Say It Isn't So

    • Oh O2 with sat monitor
    • Say Suction
    • It functional IV
    • Isn't equipment for intubation
    • So sedation plus analgesia
  41. What do you premedicate with for cardioversion?
    Sedation and analgesia--

    Sedatives: Versed, fast acting barbituates, etomidate, ketamine

    Analgesia: Fentanyl, morphine, merperidine
  42. cardioversion process
    100, 200, 300, 360. Shock once each time and check for rhythm. when reaches 360 shock and then shock again.
  43. Stable Regular Narrow QRS Complex tachycardia interventions
    ID the rhythm then:

    • VAC
    • Vagal maneuvers,
    • Adenosine (very fast--6-6-12)
    • Cardiazem
  44. Fast IRREGULAR narrow QRS complex rhythms
    Control the RATE first with cardiazem or beta blocker
  45. How do you control a rhythm???
    If less than 48 hours use cardioversion and Amiodarone

    If more than 48 hours, anticoags for 3 weeks THEN cardioversion
  46. STABLE ventricular tachycardia treatment
    OIMF, Amiodarone or lidocaine IV, cardioversion if unresolved.
  47. Torsades treatment
    Mag Sulfate 2G IV
  48. UNSTABLE ventricular tachycardia
    Go immediately to cardioversion, premedicate whenever possible with Versed
  49. Ventricular Fibrillation/Pulseless V-Tachy


    • S--shock 360 (monophasic) or 200 (biphasic) once
    • C--CPR
    • R--Check rhythm in 2 minutes
    • E--Epi 1 mg IV push, repeat every 3-5 mins or Vasopressin 40 U IV, single dose
    • AM--Antiarrhythmic meds (Amiodarone or lidocaine)
  50. Asystole or Agonal rhythm interventions
    • Check another lead
    • Give Epinepherine 1 mg IV push, repeat every 3-5 minutes OR vasopressin 40 U IV single dose, Atropine 1 mg IVP repeated every 305 mins PRN to a total dose of 0.04 mg/kg
  51. Defibrillation
    The therapeutic use of electrical current to deliver large amounts over a very brief period of time. Used for V Fib
  52. Synchronized Cardioversion
    Uses a lower dosage of electrical current for termination of V tach, SVT and atrial rhythms with rapid ventricular responses.
  53. Phases of cardiac cycle affected by medications
    • Phase 0--Fast influx of Na causing rapid depolarization
    • Phase 1--inactivation of Na channels causes early repolarization
    • Phase 2--slow influx of Ca that prolongs contraction of cardiac muscle
    • Phase 3--Calcium channel closes, potassium channels open causing rapid repolarization
    • Phase 4--resting membrane potential
  54. Class 1 drugs
    Slows the rapid influx of Na prolonging the absolute refractory period therefore decreasing premature depolarizations and depressing automaticity.

    Quinidine and procainamide block fast Na channels and phase 3 prolonging action potential

    Lidocaine blocks fast Na channels and accelerates phase 3 shortening the action potential.
  55. Class 2 drugs--Beta Blockers
    compete with endogenous catecholamines for receptor sites causing the depression of spontaneous depolarization leading to delayed impulse conduction.

    esmolol, metoprolol
  56. Class 3--
  57. Class 3 Potassium channel blockers
    slows phase 3 depolarization

    Amiodarone for atrial or ventricular

    Ibutilide for supraventricular rhythms
  58. Class 4 Ca channel blockers
    inhibit the influx of Ca in phase 2 prolonging depolarization in the atria, SA and AV nodes.

    Examples: Verapamil, Cardiazem (Diltiazem)
  59. Other cardiac drugs
    • Adenosine--Blocks conduction thru the AV node
    • converts SVT to NSR

    • Atropine--Blocks the effects of Ach in the atria, SA and AV nodes nullifying the influence of the vagus nerve
    • Bradycardia

    • Epinephrine--Stimulates the alpha and beta receptors in the heart
    • given when dead.