CARDIAC

ARRYTHMIAS
By

Dr P.N. Karimi
Definition
 Cardiac arrhythmia is an abnormal
cardiac rhythm, usually involving a
change in rate or regularity

 Normal heart rate 60-100 beats per

minute

 Rhythm is monitored by ECG

Physiology of the Heart
 Heart has different types of cells divided into two

 Excitable cells : cardiomyocytes, pacemaker cells,

purkinje cells, smooth muscle cells
 These generate and conduct electrical stimuli and

cause muscles to contract

 Non excitable cells: fibroblasts, endothelial cells,

adipocytes
Physiology of the Heart…
 Various cells are capable of automaticity
 Overall rhythm is determined by cells
that do so fastest.
 SAN cell depolarize quickest controlling
the heart rhythm acting as the
pacemaker.
Physiology of the Heart…
 The SAN generate and conduct impulse
across the atria to the AV node then
down the Bundle of HIS, to the purkinje
fibre and the ventricles .This is known as
sinus rhythm.

 Once a conducting cell is stimulated it

passes impulse to adjacent cell and
enters refractory period( latent) where it
cannot be stimulated.
 ELECTRO- SA node
PHYSIOLOGY
ATRIA
OF

NORMAL AV node

CARDIAC His-Purkinje System

RHYTHM VENTRICLES
Heart Activity Regulation
 Sympathetic nervous system stimulate the
SAN
 Parasympathetic vagus nerve slows the SAN
 Therefore, parasympathetic vagus nerve
decreases conduction through AV node
 Excessive vagal stimulation causes
bradycardia which can occur in
 Abdominal surgery

 Very fit athletes

Etiology of Arrhythmias
 Abnormal impulse formation

 Abnormal impulse conduction

Aetiology…
 Death of pacemaker  Drugs e.g.
cells (MI) antiarrhythmics ,
 Cardiac tissue disorder inotropes, caffeine,
e.g. fibrosis, RHD
alcohol or bile salts
 Multisystem connective
tissue disorder e.g.
sarcoidosis
 Sympathetic or  Hypothyroidism,
parasympathetic
control changes e.g. hyperthyroidism,
stress, anxiety, hypokalemia,
exercise or smoking hyperkalemia
Risk Factors
 Cardiovascular  Surgery
disorders e.g heart  Stress, physical
failure, activity
hypertension, MI  Drinking alcohol,
 Old age smoking and
 Pregnancy coffee
Epidemiology
 Atrial arrhythmias are more common
than ventricular arrhythmias
 Atrial fibrillation is the commonest
chronic arrhythmia
Describing Arrhythmias
 There are described in relation to:
 Rate
 Origin
 Pattern

 Rate..
 Tachycardia (fast)
 Bradycardia (slow)
Describing Arrhythmias…
 Origin..
 Sinus-SAN
 Atrial- from atrial but not SAN
 Nodal- from AVN
 Supraventricular- above the ventricles,
usually but not necessarily AVN
 Ventricular- from the ventricular tissue
 Re-entrant retrograde conduction
Describing Arrhythmias…
 Pattern..
 Paroxysmal occurs in bursts
 Flutter- a fast, regular rhythm from a single
ectopic focus
 Fibrillations- a fast chaotic rhythm from
multiple foci
 Block- a delay in, or absence of, conduction
through the AV node
 Mobitz wenckebach- particular type of
second degree block
Describing Arrhythmias…
 Pattern..
 Ectopic and premature contractions- from a
focus other than the SAN
 Torsades de pointes- form of ventricular
tachycardia with complexes of varying
amplitude
 Electromechanical dissociation- electrical
impulses( recorded on ECG) do not lead to
mechanical activity (as detected by pulse)
Normal ECG
ECG Interpretation
 P wave
 atrial depolarization
 PR interval – time taken to conduct beat through the AVN. It is
lengthened by AV block
 QRS
 ventricular depolarization
 Narrow when ventricles are controlled from above
 Wide when they are not controlled from above
 T wave
 ventricular repolarization
 QT interval
 time between depolarization and repolarization of ventricles.
Affected by drugs e.g. TCAs, lithium, haloperidol ,antiarrthythmics
class 1a and 3, some antihistamines, and macrolides antibiotics
Signs & Symptoms of Cardiac
Arrhythmias

 Dizziness and fainting due to poor blood

supply to the brain
 Shortness of breath due to poor
oxygenation
 Weakness
 Angina- poor coronary circulation and or
increased cardiac workload arising from
tachycardia
 Palpitations- extra beats or absence of
beats
Diagnosis
 Patient history: Family history, PMH, SH
 Physical examination: pulse rate,
murmurs
 Electrocardiogram (ECG, EKG)
 Others: blood tests, chest x ray,
echocardiography and coronary
angiography
General Measures in Mgt
 Aims for treating:
 To restore a satisfactory circulation
 prevent future episodes
 avoid complications
 Consider 5 Cs
 cause
 coagulation
 control
 conversion
 cure
Treatment Modalities
 Non pharmacological management: reassurance,
patient education

 Pharmacologic therapy: Antiarrhythmic drugs,

antithrombotic and digoxin

 Electrical therapy

 Pacemakers

 Combination therapy
Electrical Therapy
 Electrical therapy is used for
 atrial flutter
 atrial fibrillation
 AV nodal disease where drugs are
unsuccessful.
 Hazards include
 oesophageal perforation
 Stroke
 pulmonary vein stenosis
Pacemakers and Implantable Defibrillators

 Pacemakers are inserted under the chest

wall. Wires are inserted through the
veins to the heart.

 Defibrillators are large, expensive and do

not last long
Types of Arrhythmias
 There are two major types of arrhythmias

 Bradyarrhythmias: Disturbance of heart's rhythm

resulting in rates less than 60 beats per minute:

 Tachyarrythmias: Disorders of heart rhythm

resulting in tachycardia i.e. a heart rate >100 bpm.

Aetiology
Abnormal impulse formation
Abnormal impulse conduction
Abnormal Impulse
Formation
Mechanisms
SA node dysfunction can be due to
 disorders of sympathetic system

 Ischaemia to the SA node

 Old age

 Athletes due to chronic vagal stimulation

 Diseases e.g. senile amyloidosis, hypothyroidism,

advanced liver disease/hypothermia, typhoid

fever and brucellosis.
 Drugs: CCB, Beta blockers, cardiac glycosides
Bundle
block
SAN Blockade
 First degree SA exit block causes prolonged

conduction from SA node to the atria

 In second degree SA exit block there is

intermittent failure

 Third degree SAN block causes complete

SAN block.
Abnormal AV Conduction
Mechanisms
 Athletes

 Imbalance between the sympathetic and

parasympathetic system
 Diseases: MI, coronary artery spasms, infections

(infectious mononucleosis, viral myocarditis), ARF

neoplasms, congenital disorders and inflammatory
disorders, degenerative disease (levi’s disease),
HTN, aortic or mitral valve disease
 Drugs: digitalis intoxication, beta blockers and

CCB
Abnormal AV Conduction
ctd
Abnormal AV Conduction
ctd
 AV blockade
 first degree block: all beats conducted through
AV node but with delay.

 second degree block: some but not all beats

conducted through AV node. It’s further
subdivided into mobitz type and wenckebach .

 Third degree block; no conduction of sinus or

atrial beats through the AV node. treatment is
needed.
Treatment of
Bradyarrythmias
 Identification and treatment of
underlying causes e.g. hypothyroidism,
jaundice and removal of underlying
agents.

 Immediate treatment is to decrease

vagal tone with IV atropine, decrease AV
block and increase SA rate
Atropine
 It’s an anticholinergic drug.
 A competitive blocker of ACH on cholinergic
receptors
 Dose: 300-600 micrograms Q 1 min (maximum
x6)
 OOA -1 min; DOA 5 min.
 Adverse effects: Dry mouth
 Atropine is most effective in sinus node
dysfunction or block at the level of the AVN.
 If atropine is ineffective, consider transcutaneous
or temporary transvenous pacing.
Isoprenaline &
Adrenaline
 Isoprenaline is required if both atropine and pacing fail
 Occasionally higher doses of isoprenaline may be
required, particularly in patients who have been
taking beta blockers.
 Adrenaline is preferred if systolic blood pressure is
very low (<80 mm Hg) as isoprenaline can sometimes
further reduce blood pressure.
 Isoprenaline : Dose: 10 to 20 micrograms IV, repeated
according to clinical response, followed by an infusion
at 1 to 4 micrograms/minute
 Adrenaline: Dose: 2 to 10 micrograms/minute IV
infusion, titrated according to clinical response
Summary of Heart block
and Mx
TACHYARRYTHMIAS
 Introduction
 Tachyarrhythmias are clinically important
because they can precipitate
cardiac arrest
cardiac failure
thromboembolic disease
syncopal events
Causes of Tachyarrhythmias

Intra-cardiac Extra-cardiac
causes causes
 Ischaemic heart  Drugs

disease
 Alcohol
 Valvular heart
 Stimulants e.g.
caffeine
disease  Stress
 Heart failure
 Hyperthyroidism
 Cardiomyopathy
 Infections/Sepsis
 Congenital heart  Metabolic e.g.
disease hyperkalaemia
 Signs and Symptoms of
Tachyarrhythmias

Symptoms Signs
 Asymptomatic  Rapid pulse

 Irregular pulse
 Palpitations
 Low blood pressure
 Shortness of
 Signs of acute heart
breath
failure including:
 Chest pain (due to
tachypnoea,
rate related respiratory crackles
ischemia) on auscultation,
 Syncope or pre- raised JVP, peripheral
syncope oedema
Classification of
Tachyarrhythmias
 Tachyarrhythmias are classified based on
whether they have broad or narrow QRS
complexes on the ECG.

 Broad: QRS >0.12s (or more than 3 small

squares on the standard ECG).
 Narrow: QRS ≤0.12s.

 Broad QRS complexes are slower ventricular

depolarizations that arise from the
ventricles.
Classification of Tachyarrhythmias…

 Narrow complexes are ventricular

depolarizations initiated from above
the ventricles (supraventricular).

 Exception: a supraventricular
depolarization conducted through a
diseased AV node will produce wide QRS
complexes despite the rhythm being
supraventricular in origin.
Classification of Tachyarrhythmias…

Narrow Complex
Broad Complex
Tachyarrhythmias
Tachyarrhythmias
(Supraventricular
(Ventricular Tachycardias)
Tachycardias)  Sinus Tachycardia
 Ventricular  Atrial Tachycardia

Fibrillation  Atrial Fibrillation

 Torsades de
 Atrial Flutter

Pointes  Reentrant Tachycardias

(AVNRT and AVRT)

Sinus Tachycardia
 This is the commonest cause of
arrhythmias
 HR -100bpm with a normal ECG
 May be beneficial (appropriate) for
increasing CO
 Can be inappropriate
 Managed by giving rate control drugs
e.g. Beta blockers
Appropriate Vs Inappropriate Sinus
Tachycardia
Atrial Tachycardia
 Rare arrhythmias
 Usually regular and narrow complex ECG
 Due to impulse spread from ectopic
atrial focus
 HR- 250bpm
 Can be paroxysmal, classically seen in
digoxin toxicity and congenital heart
diseases
Management
Rate control drugs
beta blockers

Cardioselective CCB
e.g verapamil

Cardioversion if
persisent and
recurrent
Atrioventricular Nodal Reentrant
Tachycardia (AVNRT)

 AVNRT is the commonest junctional

arrhythmia.
 It occurs due the presence of a second
conduction pathway in (or near) the AV node
 One pathway conducts quickly and
repolarises slowly, whilst the other
conducts slowly and repolarises quickly
 Ectopic atrial beats can cause short circuit
 Ectopic beat uses slower conducting pathway
because the fast one is still repolarising
AVNRT…
 Impulse reenters AV node in the opposite
direction through the fast conducting pathway
 Short circuit creates normal ventricular
depolarisation and retrograde ATRIAL
DEPOLARISATION
 Results in regular, narrow complex
 Rate: 120-240bpm
 P wave buried within the QRS, visible, its
inverted
 AVNRT are paroxysmal and self limiting
 Acute AVNRT Mgt
1st line prophylaxis for frequent and
symptomatic
 Beta blockers

 CCB

 Digoxin

 Ablation therapy
AVRT (Wolff-white
Syndrome)
 Atrioventricular reentrant tachycardia
(AVRT) is the 2nd commonest junctional
tachycardia.
 It occurs as the result of an additional
pathway through the AV junction called
the Bundle of Kent.
 Normal sino-atrial impulses are
preferentially conducted through this
pathway, rather than the AV node
because it conducts faster.
 This state is known as pre-excitation
AVRT…
 Short circuit is established by ectopic atrial
beat
 Impulse is forced to pass through the SA
node as bundle of kent is repolarising
 After ventricles depolarize, impulse passes
retrogradely through the bundle of kent
which has repolarised
 Cycle continues
 Result in narrow, complex tachycardia
 Rate 140-240 bpm
AVRT…
 Atrial depolarizes soon after the
ventricles P-R interval is short, P wave is
buried within QRS
 They are paroxysmal and self limiting

 Management
 Symptomatic patient – pathway ablation
 Tachyarrhythmias- guidelines as AVNRT
Atrial Fibrillation (AF)
 Most common arrythmia:10% over 80 yrs
 Atria chaotically fibrillate instead of
contracting in a synchronized manner
 Rate 350-600bpm
 Usually results in irregular- irregular
ventricular rhythm
 Morbidity due to thromboembolic disease
 Unmanaged 5% stroke risk
AF…
 fibrillating atria are unable to empty all
blood to the ventricles, leading to stasis
and thrombus formation within the atria
 Emboli can break off travel to distant
organs through the systemic circulation
causing cerebral infarction, bowel
infarction, limb ischaemia
 AF can be paroxysmal and 2/3 terminate
within 24hrs.
AF Classification
 AF Management

 Depends on stable or unstable

 Treat underlying causes
 Infections, blood loss, MI, thyrotoxicosis
Cardioversion
Initial thromboembolism risk stratification

and treatment is part of initial

management
Pharmacological: fleicainide and
amiodarone
 AF Management ctd

Cardioversion
 Depend with the time of onset

 Less effective but no sedation and

anaesthesia is required
 Electrical: attempted 12 months after onset

 Prior anticoagulation is required as

procedure increases risk of thromboembolic

disease
 The Longer the atrial fibrillation the greater

the risk of coagulation

 AF Management ctd
 4 weeks of oral anticoagulation (INR >2.0) required in those
presenting >48 hours of onset (or uncertain timing) or,
 Stat dose of heparin required in those presenting <48 hours
since onset.
 All patients must remain anticoagulated for 4 weeks following
cardioversion therapy.
 Consider also that cardioversion will be contraindicated in
many patient with AF because:
 They have been in AF for over 1 year and/or
 Their AF is likely to recur e.g. due to underlying structural
heart disease or extra cardiac precipitants like thyrotoxicosis
and/or
 Cardioversion has previously failed a number of times
and/or
 Anticoagulation is contraindicated.
Long Term Mgt

Control rate and rhythm

Rate control

beta blackers

CCB(verapamil, il,
diltiazem)

Rhythm control

sotalol

amiodarone

fleicainide
AF Anticoagulation
 Atrial Flutter

 Narrow complex
 The flutter waves result from an ectopic atrial beat that
causes a reentrant circuit to be set up with the atria.
 The impulse can indefinitely circle through the atria at a
rate of approximately 300 times per minute.
 It is usually the right atrium which is involved with an
anticlockwise circuit.
 As with AF, atrial flutter commonly occurs in the context
of ischaemic heart disease and flutter can easily
degenerate into AF.
 Rate 100-150bpm
Management of Atrial
Flutter
 Immediate rhythm control or DC shock
 External pacing
 60%underlying pulmonary or cardiac
disease- treated will reverse the
arrhythmia
 Cardioversion: more sensitive to
electrical cardioversion than
pharmacological
 Long Term Mgt

• rhythm control agents and

catheter ablation.
• Ablation involves making
lesions to interrupt the
reentrant circuit within the
atrium.
• Ablation is far more
successful than the
pharmacological methods.
With success rates of 80-
90% compared with 30-40%,
respectively.
 BROAD COMPLEXES
( Ventricular tachycardias)

 A broad complex regular tachycardia

of a rate >120bpm.
 Requires 3 or more successive
ventricular (broad complex) beats for
diagnosis.
 VT arise due to mini electrical circuits
around edges of infarcted myocardium.
 VT may arise as an escape rhythm due
to bradycardia
VT mgt
The patient may
need an implantable
defibrillator or
pacing if the rhythm
is related to a
bradycardia. The
arrhythmic focus can
be ablated in the
electrophysiology
lab.
Polymorphic VT( Torsades de
Pointes)

• Torsades de Pointes ( twisting of the

points) is a variant of VT with a
characteristic undulating baseline
around which the broad complexes arise.
• The rhythm is less regular than
monomorphic VT.
• It is associated with long QT syndrome
and sudden cardiac death.
• Long QT syndrome can be congenital or
acquired.
Risk factors for QT
prolongation
 anaesthetics  antipsychotics
 antiarrhythmics  hypokalaemia and
 tricyclics hypomagnesaemia
 (some)  hypothyrodism
antihistamines  female gender
 antimalarials  structural heart
 antibiotics disease
(especially  bradycardia
macrolides and
fluoroquinolones)
Ventricular Fibrillation
 A chaotic broad complex tachycardia
which often occurs as a result of
ischaemia and is immediately life
threatening.
 Management: the patient may need an
implantable defibrillator, though if VF
occurs within 48 hours of an MI no
treatment for the arrhythmia is
necessary.
ANTI – ARRYTHMIC DRUGS
Classification
 Anti-arrhythmic drugs can be classified
in two ways
 Clinically
 Vaughan williams classification:
Depending on action potentials
Clinical classification:
 Those that act on supraventricular arrhythmias,

eg adenosine, verapamil, cardiac glycosides and

beta blockers.

 Those that act on both supraventricular and

ventricular arrhythmias, eg amiodarone, beta
blockers, disopyramide, flecainide, and
propafenone.

 Those that act on ventricular arrhythmias, eg

lidocaine and moricizine
 Vaughan William’s Classification:
Phases of Action Potential
Phase Dominant ion Drug class effect
movement
O Na+ inward 1A block ++
1B block +
1C block+++

1 Ca2+ inward IV block

2 K+ inward III Marked slowing

3 Na+ inward, K+ I, II,IV Slows

outward
Phases of Action Potential…..
Phase 1 Phase 2
>Limited depolarization >Plateau Stage
>Inactivation of fast >Cell less permeable to Phase 3
Na+ channels→ Na+ Na+ >Rapid repolarization
ion conc equalizes >Ca++ influx through >Na+ gates closed
>↑ K+ efflux & Cl- influx slow Ca++ channels
>K+ efflux
>K+ begins to leave cell
>Inactivation of slow
Ca++ channels

Phase 0
>Rapid depolarization
>Opening fast Na+ Phase 4
>Resting Membrane
channels→ Na+ rushes Potential
in →depolarization
>High K+ efflux
>Ca++ influx
Vaughan williams classification

CLASS I: Sodium Channel Blocking Drugs

 IA - lengthen AP duration
- Intermediate interaction with Na+ channels
- Quinidine, Procainamide, Disopyramide
 IB - shorten AP duration
- rapid interaction with Na+ channels
- Lidocaine, Mexiletene, Tocainide,
Phenytoin
 IC - no effect or minimal AP duration
- slow interaction with Na+ channels
- Flecainide, Propafenone, Moricizine
Class II: Beta-blocking Agents
 Increase AV nodal conduction
 Increase PR interval
 Prolong AV refractoriness
 Reduce adrenergic activity
 Propranolol, Esmolol, Metoprolol,
Sotalol
Class III: Potassium Channel Blockers

 Prolong effective refractory period

by prolonging Action Potential
 Amiodarone - Ibutilide
 Bretylium - Dofetilide
 Sotalol
Class IV: Calcium Channel Blockers
 Blockscardiac calcium currents
→ slow conduction
→ increase refractory period
*esp. in Ca++ dependent tissues (i.e. AV
node)

 Verapamil, Diltiazem, Bepridil

CLASS I: SODIUM CHANNEL BLOCKERS

CLASS IA: QUINIDINE

 Pharmacokinetics:
 Oral → rapid GI absorption
 80% plasma protein binding
 20% excreted unchanged in the urine →
enhanced by acidity
 t½ = 6 hours
 Parenteral → hypotension
 Dosage: 0.2 to 0.6 gm 2-4X a day
Quinidine….
 Therapeutic Uses:
– Atrial flutter & fibrillation
– Ventricular tachycardia
– IV treatment of malaria

 Drug Interaction:
– Increases digoxin plasma levels
Quinidine MOA
 Depress pacemaker rate

 Depress conduction & excitability

 Slows repolarization & lengthens AP duration

→ due to K+ channel blockade with reduction of

repolarizing outward current → reduce
maximum reentry frequency → slows
tachycardia
 (+) alpha adrenergic blocking properties →

vasodilatation & reflex ↑ SA node rate

 Toxicity:
– Antimuscarinic actions → inh. vagal effects
– Quinidine syncope (lightheadedness, fainting)
– Ppt. arrhythmia or asystole
– Depress contractility & ↓ BP
– Widening QRS duration
– Diarrhea, nausea, vomiting
– Cinchonism ( dizziness, tinnitus)
– Rare: rashes, fever, hepatitis,
thrombocytopenia,etc
CLASS IA: PROCAINAMIDE

PHARMACOKINETICS:
 Oral,IV, IM
 N-acetylprocainamide (NAPA) → major
metabolite
 Metabolism: hepatic
 Elimination: renal
 t½ = 3 to 4 hrs.
CLASS IA: PROCAINAMIDE……

 Dosage:
Loading IV – 12 mg/kg at 0.3 mg/kg/min or
less rapidly
Maintenance – 2 to 5 mg/min
 Therapeutic Use:
2nd DOC in most CCU for the treatment of
sustained ventricular arrhythmias
associated with MI
CLASS IA: DISOPYRAMIDE

 Dosage: 150 mg TID up to 1 gm/day

 Therapeutic Use: Ventricular
arrhythmias
 Toxicity:

- negative inotropic action (HF without

prior myocardial dysfunction)
- Urinary retention, dry mouth, blurred
vision, constipation, worsening
glaucoma
CLASS IA: AMIODARONE
 Pharmacokinetics:
> t½ = 13 to 103 days
> effective plasma conc: 1-2 μg/ml
 Dosage: - Loading – 0.8 to 1.2 g daily
- Maintenance – 200 to 400 mg
daily
 Drug Interaction: reduce clearance of warfarin,
theophylline, quinidine, procainamide,
flecainide
 Therapeutic Use: Supraventricular &
CLASS IA: AMIODARONE…
 Toxicity:
- fatal pulmonary fibrosis
- yellowish-brown microcrystals corneal deposits
- photodermatitis
- grayish blue discoloration
- paresthesias, tremor, ataxia & headaches
- hypo - / hyperthyroidism
- Symptomatic bradycardia or heart block
- Ppt. heart failure
- Constipation, hepatocellular necrosis, inflam’n,
fibrosis, hypotension
CLASS IB: LIDOCAINE…
 Pharmacokinetics:
- Extensive first-pass hepatic
metabolism
- t½ = 1 to 2 hrs
 Dosages: loading- 150 to 200 mg
maintenance- 2-4 mg
 Drug Interaction:
propranolol, cimetidine – reduce
clearance
 Therapeutic Use:
DOC for suppression of recurrences
CLASS IB: LIDOCAINE…

 Toxicity:
 Ppt. SA nodal standstill or worsen
impaired conduction
 Exacerbates ventricular arrhythmias
 Hypotension in HF
 Neurologic: paraesthesias, tremor,
nausea, lightheadedness, hearing
disturbances, slurred speech, convulsions
Class II: Beta Adrenoceptor Blockers
 “membrane stabilizing effect”
 Exert Na+ channel blocking effect at high doses
 Acebutolol, metoprolol, propranolol, labetalol,
pindolol
 “intrinsic sympathetic activity”
 Less antiarrhythmic effect
 Acebutolol, celiprolol, carteolol, labetalol,
pindolol
 Therapeutic indications:
 Supraventricular & ventricular arrhythmias
 hypertension
CLASS II: BETA ADRENOCEPTOR BLOCKERS…

Specific agents:
 Propranolol – (+) MSA
 Acebutolol – as effective as quinidine
in suppressing
ventricular ectopic beats
 Esmolol - short acting hence used
primarily for intra-operative &
other acute
arrhythmias
 Sotalol – has K+ channel blocking
actions (class III)
CLASS IV: CALCIUM CHANNEL BLOCKERS

VERAPAMIL
 Blocks both activated & inactivated calcium

channels
 Prolongs AV nodal conduction & effective

refractory period
 Suppress both early & delayed after

depolarizations
 May antagonize slow responses in severely

depolarized tissues
 Peripheral vasodilatation → HTN &

vasospastic disorders