Cardiac Arrest

ALLOW the chest to fully recoil between compressions.

Subsequent shock energy should be equal to or GREATER than previous shock energy

1. Airway - secure a patent airway
2. Breathing - ensure ventilation with oxygen but avoid hyperventilation.
3. Circulation - administer vigorous chest compressions.
4. Circulation - obtain IV access and administer fluid boluses if potentially
hypovolemic.
5. Circulation - administer epinephrine as a vasopressor to improve
coronary perfusion. Administer atropine if bradycardic.
6. The students need to be reminded of the importance of resuscitating the
patient and trying to determine the underlying etiology for the PEA at the
simultaneously.

Beneficial mainly due to alpha stimulation - increases systemic vascular resistance and improves coronary and cerebral blood flow. Value of beta stimulation is controversial - increases myocardial electrical activity and strength of contraction, but also increases myocardial oxygen requirements and automaticity.

ECG criteria for Torsades de Pointes: heart rate is fast and the rhythm is irregular. The QRS complex is wide and the direction of polarity is changing. Torsades de Pointes is a variant form of VT in which the polarity periodically changes from positive to negative. P waves are not apparent. The relationship between the P waves and QRS complexes is not defined since the P waves are not identifiable. TREATMENT: Always assess the ABCs first. It is important to distinguish Torsade de Pointes from VT since the treatment is different. Torsade de Pointes is associated with a long QT interval. Agents such as quinine and procainamide can prolong the QT interval and worsen the arrhythmia. Torsades is an unstable rhythm and decays rapidly to VT. Torsades is associated with electrolyte abnormalities, drug overdose or other toxins. Magnesium may be beneficial for Torsade de Pointes associated with long QT syndrome. If the patient has become unstable, use defibrillation rather than synchronized cardioversion for polymorphic VT since it will be difficult to sync to the irregular waveform (start with 200J). Low energy level shocks can cause VT. Apply CPR and the remainder of the pulseless arrest algorithm.

5 H's and 5 T's

Parasympatholytic - reverses bradycardia due to excessively high
vagal tone
• Competitive blockade of acetylcholine at muscarinic receptors.
• Increases sinus node automaticity and AV conduction.

1. Treatment of sustained ventricular tachycardia depends on the
hemodynamic status.
2. Treat pulseless ventricular tachycardia the same as ventricular
fibrillation.
3. For unstable ventricular tachycardia, prepare for immediate
synchronized cardioversion. Start at 100 Joules and increase to 200,
300, 360 Joules.

epinephrine is contra-indicated in patients on beta-blockers.

Treat bradycardia if there are serious signs or symptoms due to the
bradycardia.
1. Assess patient; observe if no signs or symptoms.
2. Atropine 0.5-1.0 mg IV if signs or symptoms, repeat every 3-5 minutes if
continued signs or symptoms. Note that the denervated, transplanted
heart will not respond to atropine.
3. Consider pacemaker if available.
4. Infuse dopamine 2-10 mcg/kg per min or epinephrine 2-10 mcg/min if
continued signs or symptoms.
5. If no serious symptoms, but Mobitz II or Third degree heart block:
a. Prepare for transvenous pacer.
b. Use TCP (TransCutaneous Pacemaker) as a potential bridge device.

1. the heart rate is very rapid and the rhythm is not regular.
2. the QRS complex is absent.
3. P waves are absent.
4. There are no P waves or QRS complexes so there is no relationship between them.
5. In V fib, areas of the ventricles are depolarizing and repolarizing in a completely disorganized fashion. All pumping function of the ventricles is lost.
6. The ECG may show voltage fluctuations. The amplitude of these waves is descrived by the terms "coarse" and "fine".
7. If it is unclear if the rhythm is v fib or asystole, treat as if it is V fib since it is the much more successfully treated arrhythmia.

Recommended dose: 1 mg IV push every 3-5 min.
Intermediate dose: 2-5 mg IV push every 3-5 min.
Escalating dose: 1 mg, 3 mg, 5 mg IV push 3 min apart.
High dose: 0.1 mg/kg IV push every 3-5 min.
Epinephrine can be delivered via the endotracheal tube. Increase dose to 2-2.5 mg per ETT.

1. The heart rate is slow to normal. The rhythm is not regular since some
QRS complexes are missing.
2. The QRS complex is narrow.
3. The P waves are upright.
4. There are more P waves than QRS complexes. The PR interval
progressively lengthens until a QRS complex is dropped. The shortest
PR interval follows the dropped beat.
5. Second degree type I AV block is also known as Mobitz Type I or
Wenkebach. The conduction block occurs in the AV node. The PR
interval progressively lengthens until the impulse is not conducted to the
ventricles.
6. Second degree type I AV block is most commonly associated with right
coronary artery occlusion with inferior wall infarctions. This block
generally has a good prognosis.

1. The heart rate is slow to normal and the rhythm is regular.
2. The QRS complex is often wide.
3. There are usually more P waves than QRS complexes. There is usually
atrial and ventricular regularity, but they are independent of each other. P
waves march through QRS complexes.
4. Third degree AV block is complete heart block. The atria beat at their
rate while the ventricular rate is determined by a junctional or ventricular
pacemaker. P waves "march through" or are unrelated to QRS
complexes.

1. The heart rate is slow to normal and the rhythm is not regular. QRS
complexes are missing.
2. There are more P waves than QRS complexes. The PR interval is fixed
and usually has normal duration.
3. Second degree type II AV block is also known as Mobitz Type II. The
conduction block is infranodal. The PR interval is fixed duration until the
impulse is not conducted to the ventricles.
4. Second degree type II AV block is most commonly associated with
anterior wall infarctions. This block has a propensity to progress to third
degree AV block.