VENTRICULAR RHYTHM

 Ventricles
- Least efficient pacemaker
- Generate impulses of 20 to 40
beats/min
- Ventricles may assume
responsibility for pacing the heart if
the SA node fails to discharge.
 Ventricular Depolarization is abnormal →
Ventricular Repolarization is also abnormal
→ changes in ST segments and T waves
 T waves → direction opposite that of the
QRS complex
 QRS deflection is negative → ST segment VENTRICULAR TACHYCARDIA
is usually depressed, and the T wave is  Three or more sequential PVCs occur at a
usually negative (i.e., inverted) rate of more than 100 beats/min
 P wave are usually not seen  Occur with or without pulses, and the
ACCELERATED IDIOVENTRICULAR RHYTHM patient may be stable or unstable with this
rhythm
 Three or more ventricular beats occur in a  Occur as short run that lasts less than 30
row at a rate of 41 to 100 beats/min seconds and spontaneously ends.
 Appears when the sinus rate slows and  Patients with heart disease, non-sustained
disappears when the sinus rate speeds up VT is often predictor or high risk for
 Last a few seconds to 1 minute sustained VT (ventricular tachycardia) or VF
(ventricular fibrillation).
CAUSES:
I. MONOMORPHIC VENTRICULAR
 Often seen during the first 12 hours of an TACHYCARDIA
acute myocardial infarction - QRS complexes of VT are of the same
 Common after successful reperfusion shape and amplitude
therapy or after interventional coronary - Monomorphic VT with a ventricular rate
artery procedures of 150 to 300 beats/min is called
 Acute myocarditis ventricular flutter by some
 Cocaine toxicity cardiologists
 Digitalis toxicity
 Dilated cardiomyopathy
 Hypertensive heart disease
 Subarachnoid haemorrhage
WHAT DO I DO ABOUT IT?
 No treatment → Rhythm is protective and
often transient spontaneously resolving on
its own
 Possible dizziness, light-headedness, or
other signs of hemodynamic compromise
may occur → loss of atrial kick
 Pulse oximeter and administer
supplemental oxygen
 IV access and obtain a 12-lead ECG CAUSES:
 IV atropine or atrial pacing
 Results of disorders of impulse formation,
such as abnormal automaticity or triggered
-Ica
 activity, or the result of disorders of  Occurs in the presence of a long QT interval
conduction such as re-entry (typically 0.45 second or more and often
 Acid base imbalance 0.50 second or more) is called torsade de
 Acute coronary syndromes pointes
 Cardiomyopathy  Congenital
 Cocaine abuse  Acquired (typically precipitated by
 Digitalis toxicity antiarrhythmic drug use or hypokalemia,
 Electrolyte imbalance (e.g., hypokalemia, which are typically associated with
hyperkalemia, hypomagnesemia) bradycardia)
 Mitral valve prolapse  Idiopathic (neither familial nor with an
 Trauma (e.g., myocardial contusion, identifiable acquired cause)
invasive cardiac procedures)
 Tricyclic antidepressant overdose
 Valvular heart disease
WHAT DO I DO ABOUT IT?
 Treatment is based on signs and symptoms
and the type of VT
 CPR and defibrillation are used to treat the
pulseless patient with VT
 Stable but symptomatic patients are treated
with oxygen (if indicated). IV access, and
ventricular antiarrhythmics to suppress the
rhythm.
 Unstable patients are treated with oxygen,
IV access and sedation
II. POLYMORPHIC VENTRICULAR
TACHYCARDIA
VENTRICULAR FIBRILLATION
- QRS complexes vary in shape and
amplitude from beat to beat and  Chaotic rhythm that begins in the ventricles
appear to twist from upright to  No organized ventricular depolarization
negative or negative to upright and  Ventricular muscle quivers, and as a result,
back, resembling a spindle. there is no effective myocardial contraction and
no pulse
 No normal-looking waveforms are visible
 VF with waves that are 3 or more mm high is
called coarse VF
 VF with low amplitude waves (i.e., less than 3
mm) is called fine Vf.

what CAUSES it?

-Ica
  When the cells repolarize the pacemaker with
the highest degree of automaticity should
assume responsibility for pacing the heart.

ASYSTOLE (CARDIAC STANDSTILL)

 Total absence of atrial and ventricular electrical
activity
 No atrial or ventricular rate or rhythm, no pulse,
and no cardiac output
 If atrial electrical activity is present the rhythm
is called P wave asystole or ventricular standstill

what CAUSES it?

Factors that increase the susceptibility of the
myocardium to fibrillate include the following:
 Acute coronary syndromes
 Dysrhythmias
 Electrolyte imbalance
 Environmental factors
 Hypertrophy
 Increased sympathetic nervous system
activity
 Proarrythmic effect of antiarrhythmics and
other medications
 Severe heart failure
 Vagal stimulation
WHAT DO I DO ABOUT IT?
 Unresponsive, apneic and pulseless
 Priorities of care in cardiac arrest as a result
of pulseless VT or VF are high-quality CPR
and defibrillation
DEFIBRILLATION
 Delivery of an electrical current across the heart
muscle over a very brief period to terminate an
abnormal heart rhythm
 Also called unsynchronized countershock or
asynchronous countershock because the
delivery of current has no relationship to the
cardiac cycle.
 Shock attempts to deliver a uniform electrical
current of sufficient intensity to depolarize
myocardial cells (including fibrillating cells) at
the same time
 Provides an opportunity for the hearts natural
pace makers to resume normal activity
-Ica