exam 1 High Acuity Cardiac lecture

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.
• S--Situation
• B--Background
• A--Assessment
• R--Recommendation

Important when contacting a physician for a patients needs

resiliency, vulnerability, stability, complexity, predictability, resource availability, participation in care, participation in decision making

Reduces anxiety, reduces agitation, helps provide amnesia

Important to provide adequate pain control FIRST

Titration down of sedation medications once every 24 hours before the doctor rounds so they can perform an appropriate assessment.

Yes. It gives families insight that all was done that could be done for the family member.

5 little blocks or 0.20

3 little blocks or 0.12

10 little blocks or 0.40

• 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.

atrial depolarization from the SA node

• Sinus Rhythm
• Sinus Brady
• Sinus Tachy

• Atrial flutter (saw tooth)
• Atrial fibrillation
• SVT
• Premature atrial complexes

Junctional Rhythm

• Ventricular fibrillation
• Vtach
• Asystole
• Torsades de pointes
• Pacemaker rhythms
• PVC's
• Idioventricular rhythms

PRI increases, T wave is flat, QT interval lengthens, Brady-dysrhythmias, conduction blocks, PVC's

Tall peaked T wave, QT shortens, if not treated b/c asystole

QT intervals shortens

QT interval lengthens

PRI prolongs, QRS widens, tall peaked T waves, Bradycardia

PRI less than 5 blocks

Gradual lengthening of the PR interval until a QRS complex is dropped

Causes: Surgery near valves, inferior or posterior MI, Dig toxicity.

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

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
• Narrow QRS=SVT

Regular rhythm, rate of 20-40

Caused by severe hypoxia or MI

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

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

TREATMENT: DEFIB!

VFIB=DEFIB

• 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.

Responsiveness

• A--Alert
• V--Voice
• P--Pain
• U--Unresponsive

ABC's

OIMF

• O--oxygen
• I--IV access
• M--Monitor
• F--Fluids

• 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

• 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!

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
• Say Suction
• It functional IV
• Isn't equipment for intubation
• So sedation plus analgesia

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.

ID the rhythm then:

• VAC
• Vagal maneuvers,
• Adenosine (very fast--6-6-12)
• Cardiazem

Control the RATE first with cardiazem or beta blocker

If less than 48 hours use cardioversion and Amiodarone

If more than 48 hours, anticoags for 3 weeks THEN cardioversion

OIMF, Amiodarone or lidocaine IV, cardioversion if unresolved.

Mag Sulfate 2G IV

Go immediately to cardioversion, premedicate whenever possible with Versed

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)

• 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.

• 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

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.

compete with endogenous catecholamines for receptor sites causing the depression of spontaneous depolarization leading to delayed impulse conduction.

esmolol, metoprolol

slows phase 3 depolarization

Amiodarone for atrial or ventricular

Ibutilide for supraventricular rhythms

inhibit the influx of Ca in phase 2 prolonging depolarization in the atria, SA and AV nodes.

Examples: Verapamil, Cardiazem (Diltiazem)

• 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.