Closed ICU
patient care is provided by a dedicated ICU team that includes a CC physician
Open ICU
care is provided by a team with doctors who have responsibilities outside of the ICU
SBAR
Method of communication among professionals. Required info.S--SituationB--BackgroundA--AssessmentR--RecommendationImportant when contacting a physician for a patients needs
characteristics of critically ill patients
resiliency, vulnerability, stability, complexity, predictability, resource availability, participation in care, participation in decision making
Role of sedation in Critical illness
Reduces anxiety, reduces agitation, helps provide amnesiaImportant to provide adequate pain control FIRST
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.
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.
how long should a PR interval be?
5 little blocks or 0.20
how long should a QRS complex be?
3 little blocks or 0.12
How long should a QT interval be?
10 little blocks or 0.40
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 interval6. Measure the QRS complex and the QT interval7. Look for ST changes.
what does the P wave indicate?
atrial depolarization from the SA node
Types of rhythms that originate in the SA node
Sinus RhythmSinus BradySinus Tachy
Rhythms that originate in The Atria
Atrial flutter (saw tooth)Atrial fibrillationSVTPremature atrial complexes
Rhythms originating in AV Node
Junctional Rhythm
Rhythms that originate in ventricle
Ventricular fibrillationVtachAsystoleTorsades de pointesPacemaker rhythmsPVC'sIdioventricular rhythms
Hypokalemia effect on heart rhythms
PRI increases, T wave is flat, QT interval lengthens, Brady-dysrhythmias, conduction blocks, PVC's
HYPERkalemia and the heart
Tall peaked T wave, QT shortens, if not treated b/c asystole
HYPERcalcemia and the heart
QT intervals shortens
HYPOcalcemia and the heart
QT interval lengthens
HYPERmagnesemia and the heart
PRI prolongs, QRS widens, tall peaked T waves, Bradycardia
First degree heart block
PRI less than 5 blocks
second degree AV block, Type I Wenckebach
Gradual lengthening of the PR interval until a QRS complex is droppedCauses: Surgery near valves, inferior or posterior MI, Dig toxicity.
second degree AV block, Type II Mobitz
Every other p wave not conducted through the AV nodeCaused by: Inferior MImanifestations: Possibly none, hypotension, S/S of decr perfusionMay deteriorate to complete HB
3rd degree AV block--Complete heart block
Asynchronous contraction of the atria and the ventriclesCaused by Acute MIManifestations are shock and loss of consciousness
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.
Ventricular rhythms
Origin of depolarization is in the ventriclesMay be fast or slowQRS is bizarreWide QRS= VtachNarrow QRS=SVT
Idioventricular Rhythm
Regular rhythm, rate of 20-40Caused by severe hypoxia or MI
accelerated idioventricular rhythm
Looks like IVR except can be regular or irregular with a rate of 40-100. Caused by AMI, reperfusion
Ventricular Tachycardia
Rapid rhythmic contraction of the ventriclesNo P wavesWide bizarre complexesCaused by Heart disease, hypokalemia, hypoxia
Torsades de Pointes
Oscillating ventricular rhythm, rate >200Caused by Prolonged QT interval of >0.40, quinidine or procainamide, heart disease, hypokalemia, hypoxia
Ventricular fibrillation
Uncoordinated electrical activityNO cardiac outputCaused by heart disease, hypokalemia, hypoxiaTREATMENT: DEFIB!VFIB=DEFIB
Pulseless Electrical Activity (PEA)5 H's and 5 T's
5 H'sHypovolemia, hypothermia, hydrogen ion (acidosis), hypoxia, hyperkalemia5 T'sTablets (OD), Tamponade, Tension pneumo, Thrombosis in ACS or Thrombosis in Pulmonary.
AVPU measures what?
ResponsivenessA--AlertV--VoiceP--PainU--Unresponsive
if found to be unresponsive, then what do we look for--
ABC's
If responsive, next steps in assessment
OIMFO--oxygenI--IV accessM--MonitorF--Fluids
Slow Narrow QRS complexes interventions
1. OIMF2. Assess QRS width3. 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
Slow WIDE QRS complexes interventions >0.10
1. Go directly to TCP2. Dopamine 5-20 per minute3. Epinepherine 2-10 mcg4. Prepare for Transcutaneous pacingDo not give atropine!
Fast rhythms with QRS <0.12 interventions
OIMF then assess for stability.If unstable, synchronized cardioversion
Synchronized Cardioversion
Low dose electrical therapy delivered on the QRS complex.Oh Say It Isn't SoOh O2 with sat monitorSay SuctionIt functional IVIsn't equipment for intubationSo sedation plus analgesia
What do you premedicate with for cardioversion?
Sedation and analgesia--Sedatives: Versed, fast acting barbituates, etomidate, ketamineAnalgesia: Fentanyl, morphine, merperidine
cardioversion process
100, 200, 300, 360. Shock once each time and check for rhythm. when reaches 360 shock and then shock again.
Stable Regular Narrow QRS Complex tachycardia interventions
ID the rhythm then:VACVagal maneuvers, Adenosine (very fast--6-6-12)Cardiazem
Fast IRREGULAR narrow QRS complex rhythms
Control the RATE first with cardiazem or beta blocker
How do you control a rhythm???
If less than 48 hours use cardioversion and AmiodaroneIf more than 48 hours, anticoags for 3 weeks THEN cardioversion
STABLE ventricular tachycardia treatment
OIMF, Amiodarone or lidocaine IV, cardioversion if unresolved.
Torsades treatment
Mag Sulfate 2G IV
UNSTABLE ventricular tachycardia
Go immediately to cardioversion, premedicate whenever possible with Versed
Ventricular Fibrillation/Pulseless V-Tachy
DEFIBRILLATE! Vfib-DfibSCREAMS--shock 360 (monophasic) or 200 (biphasic) onceC--CPRR--Check rhythm in 2 minutesE--Epi 1 mg IV push, repeat every 3-5 mins or Vasopressin 40 U IV, single doseAM--Antiarrhythmic meds (Amiodarone or lidocaine)
Asystole or Agonal rhythm interventions
Check another leadGive 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
Defibrillation
The therapeutic use of electrical current to deliver large amounts over a very brief period of time. Used for V Fib
Synchronized Cardioversion
Uses a lower dosage of electrical current for termination of V tach, SVT and atrial rhythms with rapid ventricular responses.
Phases of cardiac cycle affected by medications
Phase 0--Fast influx of Na causing rapid depolarizationPhase 1--inactivation of Na channels causes early repolarizationPhase 2--slow influx of Ca that prolongs contraction of cardiac musclePhase 3--Calcium channel closes, potassium channels open causing rapid repolarizationPhase 4--resting membrane potential
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 potentialLidocaine blocks fast Na channels and accelerates phase 3 shortening the action potential.
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
Class 3 Potassium channel blockers
slows phase 3 depolarizationAmiodarone for atrial or ventricularIbutilide for supraventricular rhythms
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)
Other cardiac drugs
Adenosine--Blocks conduction thru the AV node converts SVT to NSRAtropine--Blocks the effects of Ach in the atria, SA and AV nodes nullifying the influence of the vagus nerve BradycardiaEpinephrine--Stimulates the alpha and beta receptors in the heart given when dead.