Anaesthesia and arrythmias

1. Cardiac Arrhythmias
and
their Management
Dr. Nandini Deshpande

2. Normal ECG

3. Arrhythmias
AHA defines an arrhythmia as:
The term "arrhythmia" refers to any change from the normal
sequence of electrical impulses.
The electrical impulses may happen too fast, too slowly, or erratically
– causing the heart to beat too fast, too slowly, or erratically.
When the heart doesn't beat properly, it can't pump blood effectively.
When the heart doesn't pump blood effectively, the lungs, brain and
all other organs can't work properly and may shut down or be
damaged.

4. Clinical Manifestations
Many arrhythmias go unnoticed by the patient and are picked up
incidentally on a routine physical examination or EKG.
Most Common manifestation is palpitation, an awareness of one's own
heartbeat.
More serious symptoms occur when the arrhythmia compromises the
heart's ability to pump blood effectively. Among these are light-
headedness and syncope.
Rapid arrhythmias can increase the oxygen demands of the
myocardium and cause angina (chest pain). The sudden onset of an
arrhythmia in a patient with underlying cardiac disease can also
precipitate congestive heart failure.
Sometimes, the first clinical manifestation of an arrhythmia is sudden
death.

5. Basic Types of Arrhythmias
The electrical activity follows the usual conduction pathways, but it is
too fast, too slow, or irregular. These are arrhythmias of sinus origin.
The electrical activity originates from a focus other than the sinus
node. These are called ectopic rhythms.
The electrical activity is trapped within an electrical racetrack whose
shape and boundaries are determined by various anatomic or
electrical myocardial configurations. These are called reentrant
arrhythmias.
The electrical activity follows anomalous accessory conduction
pathways that bypass the normal ones, called pre-excitation
syndromes.
The electrical activity originates in the sinus node and follows the
usual pathways but encounters unexpected blocks and delays. These
conduction blocks.

6. Arrhythmias of Sinus Origin

7. Sinus Tachycardia and Sinus Bradycardia
Normal sinus rhythm is the normal rhythm of the heart.
Depolarization originates spontaneously within the sinus node. The
rate is regular and between 60 and 100 beats per minute.
If the rhythm speeds up beyond 100, it is called sinus tachycardia;
if it slows down below 60, it is called sinus bradycardia.
Normal Variants: Strenuous exercise, for example, can accelerate the
heart rate well over 100 beats per minute, whereas resting heart
rates below 60 beats per minute are typical in well-conditioned
athletes.
Pathological: Sinus tachycardia can occur in patients with fever,
congestive heart failure, severe lung disease, or hyperthyroidism. Sinus
bradycardia can be caused by medications, eg beta-blockers, calcium
channel blockers, and opioids.

8. (A) Sinus tachycardia. Each beat is separated by two and one-half large
squares for a rate of 120 beats per minute.
(B) Sinus bradycardia. More than seven large squares separate each beat, and
the rate is 40 to 45 beats per minute.

9. Peri-operative Sinus bradycardia
Causes
Autonomic disturbance including
vasovagal stimulation.
Hypoxia
Hypothermia
Endotracheal suctioning
Increased intracranial pressure
Hypothyroidism
Drugs like B blockers, CCB’s

11. Peri-operative Sinus tachycardia[Narrow regular]
Causes
Pain
Fever
Hypercarbia
Hypovolemia
Inadequate anesthetic depth
Drugs like
sympathomimetics,
antimuscarinics
Correction of these conditions is
the first step in the treatment of
sinus tachyarrhythmia.
If required beta blockers may be
used after these factors have
been worked at.
Most commonly used agents are
esmolol and metoprolol.

12. Sinus Arrest, Asystole
Sinus arrest occurs when the sinus node stops firing. If nothing else
were to happen, the EKG would show a flat line without any electrical
activity, and the patient would die. Prolonged electrical inactivity is
called asystole.
Rx- ACLS protocol.

13. Ectopic Rhythms

14. Premature Atrial Complex (PAC)
These arise from ectopic pacemaking tissue within the atria.
 An abnormal (non-sinus) P wave is followed by a normal QRS complex.
 The abnormal P wave may be hidden in the preceding T wave.
•Multiple PACs, showing Bigeminy
•This hidden PAC gives a peaked
appearance to the T wave (circled).
•It is followed by a compensatory
pause.
•No QRS complex, indicating
blocked PAC.

15. Premature Atrial Complex (PAC)
Causes
1. Anxiety.
2. Sympathomimetics.
3. Beta-agonists.
4. Excess caffeine.
5. Hypokalemia.
6. Hypomagnesaemia.
7. Digoxin toxicity.
8. Myocardial ischemia
Clinical Significance :
Frequent PACs may cause palpitations
and a sense of the heart “skipping a
beat”.
In patients with underlying
predispositions (e.g LA enlargement,
IHD, WPW), it may be the trigger for
the onset of a re-entrant
tachyarrhythmia — e.g. AF, flutter,
AVNRT or AVRT.
Usually no treatment is required.
May use Beta blockers or Calcium
Channel blockers.

16. Premature Ventricular Complex (PVC)
Causes
 Anxiety
 Sympathomimetics
 Beta-agonists
 Excess caffeine
 Hypokalemia
 Hypomagnesaemia
 Digoxin toxicity
 Myocardial
ischemia
Multifocal PVCs
Ventricular Bigeminy

17. When to worry about PVCs?
PVCs posing an increased risk for triggering ventricular tachycardia:
 Frequent PVCs.
 Runs of consecutive PVCs, especially three or more in a row.
 Multiform PVCs, in which the PVCs vary in their site of origin and hence in
their appearance.
 PVCs falling on the T wave of the previous beat, called the “R-on-T”
phenomenon.
Although PVCs meeting one or several of these criteria are associated with an
increased risk for developing a life-threatening arrhythmia, there is no evidence
that suppressing these PVCs with antiarrhythmic medication reduces mortality in
any setting.

18. PAC PVC
Abnormal p waves Normal p waves
Normal QRS complex Abnormal QRS complex
Problems in the atria Problems in the ventricles
No compensatory pause Compensatory pause is present
Rarely life threatening Life threatening if progresses to VT

19. AV Nodal Reentrant Tachycardia [Narrow
regular]
 AVNRT is a very common arrhythmia. Its onset is sudden, usually initiated
by a premature supraventricular beat , and its termination is just as abrupt.
 AVNRT is an absolutely regular rhythm, with a rate between 150 and 250
bpm.
 It is most often driven by a reentrant circuit looping within the AV node.
Retrograde P waves may sometimes be seen in leads II or III, or we may see
a pseudo-R′ disturbance in V1 lead. QRS complex is usually narrow.
 It can occur in perfectly normal hearts. Persons with AVNRT typically
present with palpitations, shortness of breath, dizziness, or syncope. Not
uncommonly, alcohol, coffee, or just sheer excitement can elicit this
rhythm.

21. SINUS TACHYCARDIA AVNR TACHYCARDIA
HR- 100-150/bpm HR-150-250/bpm
P waves and QRS both present,
regular RR interval
P waves not present, regular RR
interval
Gradual onset Abrupt onset
Physiological as well as
pathological
Always pathological

22. Atrial Flutter [Narrow regular]
It may occur in normal hearts .
The atrial activation in atrial flutter is absolutely regular but is at a rate of 250 to
350 bpm, generated by a reentrant circuit that usually runs around the tricuspid
valve.
Discrete P waves may not be seen. Instead saw-toothed pattern may be seen.
The AV node cannot handle the extraordinary number of atrial impulses
bombarding it, some impulses just bump into a refractory node. This phenomenon is
called AV block.

23. Atrial Flutter - associations
1. Hypertension
2. Obesity
3. Diabetes mellitus
4. Electrolyte imbalances
5. Alcohol intoxication
6. Drug abuse, particularly cocaine and amphetamines
7. Pulmonary disease (e.g., chronic obstructive pulmonary disease and pulmonary
embolism)
8. Thyrotoxicosis
9. Various underlying cardiac conditions, both congenital (e.g., atrial septal defect)
and acquired (e.g., rheumatic valvular disease, coronary artery disease, and
congestive heart failure)

24. Atrial Fibrillation [Narrow irregular]
In atrial fibrillation, atrial activity is completely chaotic, and the AV node may be
bombarded with more than 500 impulses per minute!
Multiple tiny reentrant circuits whirl around in totally unpredictable fashion.
No true P waves can be seen.
The AV node allows only occasional impulses to pass through at variable intervals,
generating an irregularly irregular ventricular rate.
This irregularly irregular appearance of QRS complexes in the absence of discrete
P waves is the key to identifying atrial fibrillation. Associations similar to flutter.

27. Ventricular Tachycardia[Wide regular]
A run of three or more consecutive PVCs is called ventricular tachycardia. The rate
is usually between 120 and 200 beats.
Sustained VT — lasting more than 30 seconds—or VT associated with
hemodynamic instability are emergencies, presaging cardiac arrest and requiring
immediate treatment.
Polymorphic ventricular tachycardia is more commonly associated with acute
coronary ischemia, infarction, profound electrolyte disturbances, and conditions
causing prolongation of the QT interval. Uniform ventricular tachycardia is more
often seen with healed infarctions.

28. Ventricular Tachycardia
MECHANISMS
 Enhanced automaticity (ectopic
activity)
 Enhanced trigger activity
 Re-entry
Drugs that cause QT Prolongation
Clarithromycin
Erythromycin
Metaclopramide
Haloperidol
TCA Methadone
Droperidol
Electrolytes
• Hypokalaemia
Hyperkalaemia
• Hypomagnesaemia
Hypocalcaemia
Hypothermia
Structural heart disease
• LV dysfunction
• Coronary artery disease
• MI
• HOCM

30. Ventricular Tachycardia Supraventricular
Tachycardia
Clinical Clues
Clinical history Diseased heart Usually healthy heart
Carotid massage No response May terminate
Cannon A waves May be present Not seen
EKG Clues
AV dissociation May be seen Not seen
Fusion beats May be seen Not seen
Initial QRS
deflection
May differ from normal QRS
complex
Same as normal QRS complex

31. Ventricular Fibrillation[Wide irregular]
Ventricular fibrillation is a preterminal event seen solely in dying hearts.
The EKG tracing jerks about spasmodically, there are no true QRS complexes.
In VF, the heart generates no cardiac output, and cardiopulmonary resuscitation and
electrical defibrillation must be performed.
Common precipitants of ventricular fibrillation include
 Myocardial ischemia/infarction
 Heart failure
 Hypoxemia or hypercapnea
 Hypotension or shock
 Electrolyte imbalances
 Overdoses of stimulants, especially when used in combination.
In many cases, ventricular fibrillation is preceded by ventricular tachycardia

34. Conduction Blocks

35. First degree AV Blocks
 The depolarisation at AV node is held
up for longer than the usual.
 PR interval is longer than 0.2 seconds.
 Every QRS complex is preceded by a
single P wave.
 It can also be an early sign of
degenerative disease of the conduction
system or a manifestation of
myocarditis or drug toxicity.
 By itself, it does not require treatment.
 .

36. Second degree AV Blocks
Wenckebach Block
Almost always due to a block within the AV node.
The delay is variable increasing with each ensuing impulse.
Each successive atrial impulse encounters a longer delay in the AV node
until one impulse (usually every third or fourth) fails to make it through.
Progressive lengthening of the PR interval is seen and then a dropped beat is seen.
The sequence repeats itself, over and over, and often with impressive regularity.

37. Second degree AV Blocks
Mobitz Type II Block- Usually due to a block below the AV node.
The EKG shows two or more normal beats with normal PR intervals and a dropped
beat. The cycle is then repeated.
The ratio of conducted beats to nonconducted beats is may or not be constant.
Mobitz type II block is far more serious that type1, often signifying serious heart
disease and capable of progressing suddenly to third-degree heart block.
Mobitz type II heart block requires insertion of a pacemaker.

38. Third degree AV Blocks
No atrial impulses at all make it through to activate the ventricles. For this reason,
it is often called complete heart block / AV dissociation.
The site of the block can be either at the AV node or lower. The ventricles generate
an escape rhythm. The atria continue to contract atria at 60 to 100 bpm and
ventricles at 30 to 45 bpm.
May be seen in MI / degenerative diseases / Lyme’s – reversible.

39. Management of Blocks
• 1st degree
– nothing unless symptomatic and other causes of symptoms
excluded
• 2nd degree (Mobitz type I)
– nothing unless symptomatic and other causes of symptoms
excluded
• 2nd degree (Mobitz type II)
– pacemaker
• 3rd degree –
pacemaker