TOPIC26: ventricular arrhythmias Flashcards
what are ventricular arrhythmias? what causes them? (6)
rhythm disturbances below the AV node. Lack of response to IV adenosine (takes SVTs back to sinus rhythm)
causes:
- IHD/ HF
- electrolyte disturbances
- post MI
- hypotension/shock
- hypoxemia/hypercapnea
- stimulants eg drugs
Premature ventricular contractions
- isolated PVCs are common in normal hearts
- QRS wide and bizarre because ventricular depolarisation doesn’t follow the normal conduction pathways
- a retrograde P wave may sometimes be seen but it is more common to not see a P wave at all.
- it is usually followed by a long compensatory pause before the next beat appears.
- if the ratio is one normal sinus beat to one PVCs, the rhythm is called a bigeminy.
When do you worry about a PVC? (5)
- frequent PVCs.
- runs of consecutive OVCs, three or more in a row.
- multiform PVCS–> vary in the site of origin and hence their appearance.
- PVC falling on the T wave of the previous beat–> ‘R ON T PHENOMENON’ –> More likely to set off a VT
- any PVC occuring in the setting of an AMI
IV amiodarone is given
accelerated idioventricular rhythm
- a benign rhythm that is sometimes seen in ACUTE INFARCTION or during the early hours following REPERFUSION after an occluded coronary artery has been opened .
- a regular rhythm occuring at 50-100bpm and probably represents a ventricular escape focus that has accelerated insufficiently to drive the heart.
- rarely sustained, does not progress to VF and rarely requires treatment.
ventricular tacchycardia
- a run of three consecutive PVCs >30sec
- 120-200bpm and might be slightly irregular
- sustained VT is an emergency, preceeding cardiac arrest and requires immediate treatment
- morphology may be uniform with each complex appearing similar to the one before or it may be polymorphic changing appearance from beat to beat.
- AV dissociation, fusion and capture beats may be seen.
polymorphic VT
-more commonly associated with ACUTE CORONARY ISCHEMIA, INFARCTION, profound electrolyte disturbances and conditions causing prolongation of the QT interval.
Uniform VT
- more often seen in healed infarctions: the scarred myocardium provides the substrate for the reentrant VT
- The majority of pts developing VT after an MI get the arrhythmia within the first 48 hours and should be given IV lidocaine or amiodrone
VT in the normal heart (benign VT)
- Right ventricular outflow tract (RVOT) tacchycardia:
-automatic firing of cells in the RVOT giving a characteristic EKG pattern of LBBB with a strongly inferior axis
-paroxysm of palpitation may be related to exercise.
often adenosine sensitive
-controlled by verapamil, beta blockers, RFA is a potentially curative option. - Fascicular tacchycardia:
- a reentrant tachycardia emerging most commonly from the left posterior fascicle
- ECG typically show RBBB with superior axis
- often sensitive to IV verapamil but NOT adenosine.
VT with impaired LV function (hemodynamic alterations)
symptoms: palpitation, chest pain, dypnea, pulmonary edema.
etiology: impaired LV function can predispose to VT–> CAD,DCM,HCM
- VT is often due to reentry around areas of scarred or diseased myocardium.
- treat the underlying HF with beta-blockers, ACEi, diuretics, statins.
- prevent by use of ICD
- Acute management by: oxygen mask, IV amiodarone, lidocaine and if no response, DC shock
- Long term treatment:
- Beta blockers, amiodarone, RFA
Brugada syndrome
- form of idiopathic VT most commonly in men
- autosomal dominant condition with variable penetrance in the SCNA gene–> loss of function of the sodium channel
polymorphic VT–> torsade de pointes
- The cardiac action potential is generated by at least 10 distinct but finely balanced ionic currents ( Na, Ca, K)
- a functional abnormality in any of these, acquired or genetic can potentially lead to long QT syndrome
- VT with varying axis and amplitude, twisting of the points
- usually seen in pts with prolonged QT interval
Prolonged QT interval:
- congential: mutations in genes encoding cardiac ion channels
- electrolyte disturbances:
- hypocalcemia, hypomagnesaemia and hypokalemia. - AMI
- antiarrythmic drugs, anthistamines
- severe bradycardia: complete heart block, SA node disease, hypothyroidism and hypothermia.
- A PVC falling during the elongated T wave can initate TdP
- It may be short lived and terminate spontaneously but a prolonged episode needs immediate treatment with DC cardioversion.
- for recurrent bursts or following cardiac arrest, give IV magnesium bolus and infusion followed by urgent temporarily pacing if necessary.
management of Ventricular arrhythmias
- monitor
- give oxygen
- IV access
- ECG
- ABG
DDx- broad QRS ECG
- BBB
- WPW
- ventricular ectopy
- ventricular PM
- VT/VF/TdP
ventricular extra systole (ectopics)
risk of R on T phenomenon so treat with Amiodarone IV if frequent( more than 10/min)
