exam 1 High Acuity Cardiac lecture
Card Set Information
exam 1 High Acuity Cardiac lecture
High Acuity exam ekg abg
high acuity exam 1
patient care is provided by a dedicated ICU team that includes a CC physician
care is provided by a team with doctors who have responsibilities outside of the ICU
Method of communication among professionals. Required info.
Important 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 amnesia
Important 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
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 interval
6. Measure the QRS complex and the QT interval
7. 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
Rhythms that originate in The Atria
Atrial flutter (saw tooth)
Premature atrial complexes
Rhythms originating in AV Node
Rhythms that originate in ventricle
Torsades de pointes
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 dropped
Causes: 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 node
Caused by: Inferior MI
: Possibly none, hypotension, S/S of decr perfusion
May deteriorate to complete HB
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
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.
Origin of depolarization is in the ventricles
May be fast or slow
QRS is bizarre
Wide QRS= Vtach
Regular rhythm, rate of 20-40
Caused 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
Rapid rhythmic contraction of the ventricles
No P waves
Wide bizarre complexes
Caused by Heart disease, hypokalemia, hypoxia
Torsades de Pointes
Oscillating ventricular rhythm, rate >200
Caused by Prolonged QT interval of >0.40, quinidine or procainamide, heart disease, hypokalemia, hypoxia
Uncoordinated electrical activity
NO cardiac output
Caused by heart disease, hypokalemia, hypoxia
Pulseless Electrical Activity (PEA)
5 H's and 5 T's
Hypovolemia, hypothermia, hydrogen ion (acidosis), hypoxia, hyperkalemia
Tablets (OD), Tamponade, Tension pneumo, Thrombosis in ACS or Thrombosis in Pulmonary.
AVPU measures what?
if found to be unresponsive, then what do we look for--
If responsive, next steps in assessment
Slow Narrow QRS complexes interventions
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
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!
Fast rhythms with QRS <0.12 interventions
OIMF then assess for stability.
If unstable, synchronized cardioversion
Low dose electrical therapy delivered on the QRS complex.
Oh Say It Isn't So
Oh O2 with sat monitor
It functional IV
Isn't equipment for intubation
So sedation plus analgesia
What do you premedicate with for cardioversion?
Sedation and analgesia--
Sedatives: Versed, fast acting barbituates, etomidate, ketamine
Analgesia: Fentanyl, morphine, merperidine
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:
Adenosine (very fast--6-6-12)
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 Amiodarone
If more than 48 hours, anticoags for 3 weeks THEN cardioversion
STABLE ventricular tachycardia treatment
OIMF, Amiodarone or lidocaine IV, cardioversion if unresolved.
Mag Sulfate 2G IV
UNSTABLE ventricular tachycardia
Go immediately to cardioversion, premedicate whenever possible with Versed
Ventricular Fibrillation/Pulseless V-Tachy
S--shock 360 (monophasic) or 200 (biphasic) once
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)
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
The therapeutic use of electrical current to deliver large amounts over a very brief period of time. Used for V Fib
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 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
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.
Class 2 drugs--Beta Blockers
compete with endogenous catecholamines for receptor sites causing the depression of spontaneous depolarization leading to delayed impulse conduction.
Class 3 Potassium channel blockers
slows phase 3 depolarization
Amiodarone for atrial or ventricular
Ibutilide 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 NSR
Atropine--Blocks the effects of Ach in the atria, SA and AV nodes nullifying the influence of the vagus nerve
Epinephrine--Stimulates the alpha and beta receptors in the heart
given when dead.