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Closed ICU
patient care is provided by a dedicated ICU team that includes a CC physician
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Open ICU
care is provided by a team with doctors who have responsibilities outside of the ICU
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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
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characteristics of critically ill patients
resiliency, vulnerability, stability, complexity, predictability, resource availability, participation in care, participation in decision making
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Role of sedation in Critical illness
Reduces anxiety, reduces agitation, helps provide amnesia
Important to provide adequate pain control FIRST
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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.
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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.
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how long should a PR interval be?
5 little blocks or 0.20
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how long should a QRS complex be?
3 little blocks or 0.12
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How long should a QT interval be?
10 little blocks or 0.40
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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.
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what does the P wave indicate?
atrial depolarization from the SA node
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Types of rhythms that originate in the SA node
- Sinus Rhythm
- Sinus Brady
- Sinus Tachy
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Rhythms that originate in The Atria
- Atrial flutter (saw tooth)
- Atrial fibrillation
- SVT
- Premature atrial complexes
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Rhythms originating in AV Node
Junctional Rhythm
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Rhythms that originate in ventricle
- Ventricular fibrillation
- Vtach
- Asystole
- Torsades de pointes
- Pacemaker rhythms
- PVC's
- Idioventricular rhythms
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Hypokalemia effect on heart rhythms
PRI increases, T wave is flat, QT interval lengthens, Brady-dysrhythmias, conduction blocks, PVC's
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HYPERkalemia and the heart
Tall peaked T wave, QT shortens, if not treated b/c asystole
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HYPERcalcemia and the heart
QT intervals shortens
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HYPOcalcemia and the heart
QT interval lengthens
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HYPERmagnesemia and the heart
PRI prolongs, QRS widens, tall peaked T waves, Bradycardia
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First degree heart block
PRI less than 5 blocks
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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.
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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
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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
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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.
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Ventricular rhythms
- Origin of depolarization is in the ventricles
- May be fast or slow
- QRS is bizarre
- Wide QRS= Vtach
- Narrow QRS=SVT
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Idioventricular Rhythm
Regular rhythm, rate of 20-40
Caused by severe hypoxia or MI
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accelerated idioventricular rhythm
Looks like IVR except can be regular or irregular with a rate of 40-100.
Caused by AMI, reperfusion
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Ventricular Tachycardia
- Rapid rhythmic contraction of the ventricles
- No P waves
- Wide bizarre complexes
- Caused by Heart disease, hypokalemia, hypoxia
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Torsades de Pointes
Oscillating ventricular rhythm, rate >200
Caused by Prolonged QT interval of >0.40, quinidine or procainamide, heart disease, hypokalemia, hypoxia
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Ventricular fibrillation
- Uncoordinated electrical activity
- NO cardiac output
Caused by heart disease, hypokalemia, hypoxia
TREATMENT: DEFIB!
VFIB=DEFIB
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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.
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AVPU measures what?
Responsiveness
- A--Alert
- V--Voice
- P--Pain
- U--Unresponsive
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if found to be unresponsive, then what do we look for--
ABC's
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If responsive, next steps in assessment
OIMF
- O--oxygen
- I--IV access
- M--Monitor
- F--Fluids
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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
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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!
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Fast rhythms with QRS <0.12 interventions
OIMF then assess for stability.
If unstable, synchronized cardioversion
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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
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What do you premedicate with for cardioversion?
Sedation and analgesia--
Sedatives: Versed, fast acting barbituates, etomidate, ketamine
Analgesia: Fentanyl, morphine, merperidine
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cardioversion process
100, 200, 300, 360. Shock once each time and check for rhythm. when reaches 360 shock and then shock again.
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Stable Regular Narrow QRS Complex tachycardia interventions
ID the rhythm then:
- VAC
- Vagal maneuvers,
- Adenosine (very fast--6-6-12)
- Cardiazem
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Fast IRREGULAR narrow QRS complex rhythms
Control the RATE first with cardiazem or beta blocker
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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
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STABLE ventricular tachycardia treatment
OIMF, Amiodarone or lidocaine IV, cardioversion if unresolved.
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Torsades treatment
Mag Sulfate 2G IV
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UNSTABLE ventricular tachycardia
Go immediately to cardioversion, premedicate whenever possible with Versed
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Ventricular Fibrillation/Pulseless V-Tachy
DEFIBRILLATE! Vfib-Dfib
SCREAM
- 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)
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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
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Defibrillation
The therapeutic use of electrical current to deliver large amounts over a very brief period of time. Used for V Fib
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Synchronized Cardioversion
Uses a lower dosage of electrical current for termination of V tach, SVT and atrial rhythms with rapid ventricular responses.
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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
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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.
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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
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Class 3 Potassium channel blockers
slows phase 3 depolarization
Amiodarone for atrial or ventricular
Ibutilide for supraventricular rhythms
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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)
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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.
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