VF

Question 1

def vf

Answer 1

Irregular, rapid ventricular activation with no cardiac output.

a life-threatening cardiac arrhythmia characterized by disorganized, high-frequency ventricular contractions that result in diminished cardiac output and hemodynamic collapse

Question 2

aetiology vf

Answer 2

underlying CVS disease

• most common - CAD
• prvious mI
• myocarditis
• cardiomyopathy
• severe CHF
• heart valve disease

congenital heart defects eg pulmonary atresia (characterized by right ventricular outflow obstruction, typically due to failure of pulmonary valve formation)

electrophysiologic disorders

• wolff-parkinson white syndrome
• long-QT syndrome - torsade de pointes

Question 3

path vf

Answer 3

normal electrical conduction can be disrupted by re-entry = chaotic circulating excitation of the myocardium - Vfib = simultaneous contractions at multiple foci = insufficient CO - haemodynamic collapse - loss of consciousness and sudden cardiac death

causes of reentry

• changes to the conduction pathway - unexcitable scar tissue as a result of past MI
• abnormal pattern of excitation
  
  • If the period of activation and recovery of myocardial cells becomes greater than the duration of an action potential (as in long-QT syndrome)
  • If excitation occurs outside of the normal pattern of activation (premature ventricular complex, PVC )

Question 4

vf epi

Answer 4

most commonly identified arrhythmia in cardiac arrest patients

incidence of VF parallels the incidence of ischaemic heart disease, with a peak incidence of VF occurring in people aged 45-75 years.

Question 5

sx vf

Answer 5

chest pain

palpitation

fatigue

SOB

dizziness

Question 6

ix vf

Answer 6

ecg

blood

ABG

coronary angiography

echo

nuclear imaging - detect previous MI

Question 7

ecg vf

Answer 7

comm0nly preceded by VT

erratic undulations, no clear QRS complexes

no p waves

chaotic, no pattern

arrhythmic, fibrillatory baseline, usually >300bpm

underlying conditions

Question 8

blood vf

Answer 8

electrolytes,

cardiac enzymes,

TSH (hyperthyroidism),

drug levels and toxicology screen (tricyclic antidepressants or cocaine, which can cause QT prolongation)

Question 9

vf mx

Answer 9

Use non-synchronized DC shock (there is no R wave to trigger defibrillation)

• Defibrillate once: 150–360 J biphasic, 360 J monophasic. (Ensure no one is touching patient or bed when defibrillating.)
• resume CPR for 2 mins then reassess rhythm
• adrenaline 1mg IV after 2nd defib and again every 3-5mins
• If ‘shockable rhythm’ persists after third shock, administer amiodarone 300mg IV bolus(or lidocaine)

Question 10

post resus vf care

Answer 10

ITU

control vital signs and acute metabolic imbalances

mild therapeutic hypothermia - helps neuro outcomes

anti-arrhythmics - usually IV amiodarone, IV lidocaine

treat underlying cause

ICD for pts w/o readily reversible or treatable cause and with high risk of recurrent, haemodynamically sig VF

Question 11

complications vf

Answer 11

• ultimately - loss of consciousness and death
• CNS ischemic injury
• myocardial injury
• post defib arrhythmias
• aspiration pneumonia
• defib injury to self or others
• injury from CPR and resus
• skin burns

Question 12

px vf

Answer 12

depends on time from onset and medical intervention (prognosis is poor without intervention by 4-6 minutes after onset of VF), and aetiology

If defibrillation is delivered promptly, survival rates as high as 75% have been reported

Death and disability after successful resuscitation correlate with the degree of central nervous system damage occurring during the event.

After resuscitation, the prognosis is largely dependent on haemodynamic stability, early neurological recovery and duration of the resuscitation.