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PATASS III > Management of Arrhythmias > Flashcards

Management of Arrhythmias Flashcards

1
Q

What is the initial assessment of all patients with an arrhythmia?

A
  • Assessment - ABCDE
    - D - tone, cognition (GCS)
  • ECG - to identify anything more sinister - identifing underlying rhythm - may change management
  • BP
  • IV access
  • Identify + treat reversible causes (e.g. electrolyte abnormalities)
  • Adverse features
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2
Q

What are the adverse features associated with an arrhythmia?

A

SHOCK - hypoperfusion of body’s tissues

  • Confusion / agitated pts
  • Cap Refill changes
  • Hypotension <90 systolic
  • Pallor
  • Sweating
  • Cold
  • Clammy extremities
  • Impaired consciousness

SYNCOPE
- Transient loss of consciousness due to global reduction in blood flow to the brain

Myocardial Ischemia

  • ECG changes e.g. ischeamia
  • Ischaemic chest pain

HEART FAILURE

  • Hx
  • Raised JVP
  • Peripheral oedema - expose
  • Pulmonary oedema - listen to chest
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3
Q

What additional medications can be given in SVT narrow complex?

A

Adenosine

  • Reduces frequency of spontaneous depolarisation =breaks the re-entry circuit allowing normal depolarisations from SA node to resume control of HR (cardioversion)
  • Half-life ten seconds -readily taken up by cells

Amiodarone
- reduces ventricular rate

Valsalvour maeniuvor
- Increases tone of vagus nerve = slows HR

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4
Q

What additional medications can be given in Tachycardia broad complex?

A

Amiodarone

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5
Q

What additional medications can be given in bradycardia?

A

Atropine
- Reverses effects of vagal overdrive

Adrenaline

  • Potent agonist of alpha & beta adrenoceptors
  • Vasoconstriction of vessels supplying skin, mucosa + abdominal viscera (alpha 1)
  • Increases HR, force of contraction + myocardial excitability (beta 1)
  • Vasodilation of vessels supplying heart + muscles (beta 2)
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6
Q

Summary of causes of bradycardia

A

Physiological/ autonomic causes

  • Athletics - physiological
  • Vasovagal - autonomic

Cardiac

  • MI - affects septal area = causes bradycardia
  • Ischemic heart disease / atherosclerosis
  • Congenital heart disease e.g. septal deviations can cause bradycardia
  • Six sinus rhythm - stops beating regularly = bradycardia
  • Cardiac surgery e.g. transplants

Infection
- Endocarditis

Drugs

  • Beta blockers, calcium channel blockers (BP meds) - AV blocking agents
  • Dixogin - cardiac glycosides
  • Organophosphates - cholinergic agents
  • Clonidine - antihypertensives
  • Quinidine - antiarrhymic
  • Amitriptyline - antipsychotics

Endocrine

  • Hypothyroidism
  • Hypothermia

Metabolic

  • Hypokalaemia/hyperkalemia
  • Hypomagnesium

Trauma
- Head injury (cushings triad)

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7
Q

Different paths of the conduction system have different intrinsic rates of depolarisation…

A
  • 60bmp = sinoatrial node
  • 50bpm = atrioventricular node
  • 40-50bpm = Bundle of His
  • 30-40bpm = ventricular myocardium - the purkinje fibres that distribute depolarisation around the myocardium
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8
Q

What are the presenting symptoms related to bradycardia?

A
  • Pre-syncope
  • Syncope
  • Nausea
  • Breathlessness
  • Weakness or fatigue
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9
Q

What are the different types of bradycardia?

A

Sinus Brady

  • HR <60, P wave before every QRS complex. PR interval constant
  • Causes
    • Hypothermia e.g. elderly
    • Drugs e.g. beta blockers
    • Head injury - bushings response - caused by brain stem compression

Sinus Arrest

  • often intermittent
  • Absence of P waves and pauses 3 sec +

Junctional bradycardia

  • 40-60 bmp + narrow complex
  • regular rhythm initiated in AV nodal tissue and occurs when SA nodal pacemaker fails

Atrioventricular blocks

  • Occurs when atrial depolarisation fails to reach the ventricles because of a block involving the AV node or the His-Purkinje system.
  • If block is at the AV nodal level complexes will be narrow.
  • If block is lower down in the His-Purkinje system complexes will be wide.
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10
Q

TREATMENT

BRADYCARDIA

A

IF ADVERSE EFFECTS
- Atropine 500mcg IV

If NO adverse effects…

  • Hospital
  • Monitor
  • Risk of asystole?
    • recent asystole
    • Mobitz 2 AV block
    • Complete HB with broad QRS
    • Ventricular pauses >3 sec
IF NO SATISFACTORY RESPONSE FROM ATROPINE OR RISK OF ASYSTOLE...
- Atropine 500mcg - up to 3mg
- Transcutaneous Pacing 
OR
- Adrenaline
- Dopamine
- Glucagon
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11
Q

How does atropine work?

A
  • Blocks action of acetylcholine at the musclarinic receptors = blocks the action of the vagus nerve on the SA & AV nodes
  • Doses below 0.5 mg may paradoxically worsen bradycardia - dose of 3mg complete blocks the vagus nerve
  • Half-life of 2-3 hours
  • Side effects; dry mouth, blurred vision & resting tachycardia
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12
Q

How to pace…

A

Provides electricity to myocardial - overrode abnormal rhythm

  • Attach 3 lead + defib
  • Switch to pace mode
  • Freq = 75-80/ min - Don’t want to over increase heart load = can worsen heart failure
  • Increase intensity until captures with every QRS
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13
Q

What are the lateral leads?

A

I, aVL, V5, V6

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14
Q

What are the inferior leads?

A

II, III, aVF

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15
Q

What are the anterior leads?

A

V1, V2, V3, V4

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16
Q

Summary of causes of SVT…

A

Idiopathic/paroxysmal

Congenital e.g. in WP.W.

Cardiac

  • Old age
  • Ischemic heart disease

Endocrine
- Hyperthyroidism

Drugs

  • Sympathetics = Cocaine
  • Alcohol - cardio toxic
  • Caffeine
  • Digoxin

Infections

  • Pericarditis
  • PE - vascular
  • Sepsis
17
Q

What are the different types of SVT?

A

Atrial tachycardia

  • > 100bmp norm 150-200
  • P waves present before QRS - but shape may be abnormal
  • R-P baseline isoelectric (distinguishes from AF)
  • Arises from atrial tissue other than SAN.

Junctional Tachycardia

  • Re-entry - can be subdivided into nodal or non-nodal
    • AV Nodal re-entry (within AV node, P waves berried in QRS)
    • AV re-entry (extra citation not from SA node
  • A re-entry circuit consists of two pathways the normal fast conducting pathway, plus another area of conducting tissue allowing impulses to pass only at a slower rate the slow pathway.
  • Slower pathway has a shorter refractory period. Impulses from the atria down the slower pathway meet refractory tissue & stop

Atrial flutter
- saw tooth pattern

AF
- from an ectopic focus or foci in the atria

18
Q

What are the presenting symptoms related to SVT?

A
  • Palpitations
  • Cardiac chest pain / tightness
  • Pre-syncopal symptoms e.g. dizziness or SOB
  • Onset often abrupt
  • Episodes rare recurrent (paroxysmal)
19
Q

TREATMENT

SVT

A

IF UNSTABLE + adverse features
- Synchronised shock - up to 3 attempts

If NO adverse features + rhythm REGULAR

  • Vagal manoevers
  • Adenosine

If NO adverse features + rhythm IRREGULAR
- Possible AF - BB

20
Q

What does the CHAD 2 measure?

A

Risk of developing a stroke

Congestive heart failure - 1
Hypertension - 1
> 75 y/o - 2
Diabetes - 1
Stroke or TIA - 2 
Vascular disease - 1 
65 - 74 y/o - 1
Females - 1

max points 9

21
Q

What does HAS-BLED measure?

A

Risk of bleeding

H- hypertension - 1
A - Abnormal liver or renal function - 1 or 2
S - Stroke - 1
B- Bleeding - 1
L - Labile INR - 1
E - Elderly (age >65) - 1
D - Drugs or alcohol - 1 or 2

3+ high risk of bleeding

22
Q

What is VT?

A

VT is defined as three or more ventricular extra systoles in succession at a rate of more than 120 beats/minute.

Broad complex tachycardia + Ischemic heart disease = ventricular tachycardia

Arrhythmias that are NOT CONSTANT are called paroxysmal

23
Q

Summary of causes of VT…

A

Cardiac
- Ischemic heart disease - MI (anterior specifically)

Infection

  • Myocarditis
  • Pericarditis

Drugs (drugs that prolong QT interval)

  • Amitriptyline
  • Digoxin

Metabolic
- Hypo & hyperkalemia

Trauma
- Head injury

Vascular
- Subarachnoid haemorrhage

24
Q

What are the different types of VT?

A

Ventricular

  • Monomorphic VT
  • Polymorphic VT
  • Fasicular tachycardia

Supraventricular
- SVT with BBB

25
Q

TREATMENT

VT

A

IF UNSTABLE
- Synchronised shock - up to 3 attempts

If NO adverse features + regular

  • Hospital
  • Amiodarone 300mg IV
26
Q

How to cardiovert?

A
  • Pads
  • Manual mode
  • Sync - want to shock on R waves, synchronised to when depolarising at ventricles
  • Sedate pt
  • Narrow complex - 100- 150 J
  • Broad complex - 150-200J
  • Charge and shock as normal
  • Max 3 shocks
27
Q

What parameters can we control with bag valve mask?

A
  • Rate
  • Volume
  • Pressure release valves are the only ones that control pressure - higher ventilatory pressure in some conditions e.g. asthmatics
  • pneumothorax
28
Q

How to set up a ventilator?

A
  • Pressure = 40
  • Plug into oxygen port
  • CVM
  • Frequency = 12 (adults)
  • Tidal volume = 900 (adults)
  • Air mix - no mix (full O2|)
29
Q

What are the different types of syncope?

A
  • Lying down/seated, with absent or brief prodromal symptoms (?cardiac)
  • Within 2 min of standing (?postural hypotension)
  • Stressor (pain or emotional upset) with longer prodromes & associated pallor, sweating, nausea or vomiting (?vasovagal/arrhythmia)
  • Head rotation or movement (?carotic sinus sensitivity)
  • Visit to the toilet (?micturition or defecation syncope)
  • Coughing (?cough syncope)
  • Exertion (?cardiac arrhythmia) hot/cold?
30
Q

What are prodromal symptoms?

A

Predictors before syncope

  • Feeling faint, or feeling like they were going to pass out
  • Room spinning
  • Those lasting few seconds suggest vasovagal syncope
31
Q

What is important to note regarding syncope?

A

What happened during syncope?

  • Falls/trauma
  • Few seconds of mild tonic-clonic activity may be caused by syncope ‘anoxic jerks’
  • Absence seizures minis syncope

What happened after syncope?

  • Long period of confusion occurs after generalised seizures
  • Neurological deficits e.g. hemiparesis may occur after a seizure (Todd’s palsy) or may represent a TIA/stroke
32
Q

What examinations need to occur after syncope?

A
  • Neurological + cardiac assessment - include GCS, cranial nerves, limb tone, power + reflexes
  • Carotid bruits, valvular disease, outflow obstruction or evidence of HF
  • Postural BP
  • Abdo pain may indicate bleeding or AAA
  • Rectal examination
  • Tongue biting or incontinence suggests seizure - absence doesn’t rule it out
33
Q

What is vasovagal (neurocardiogenic) syncope?

A
  • May be precipitated by stressful event, lack of food or drink
  • Usually proceeded by pallor, sweating, nausea & dizziness (may be short or non-existent in elderly)

Cause
- vagal parasympathetic outflow causes bradycardia = when CO falls, sympathetic driven tachycardia & vasoconstriction fails to rectify situation = transient loss of cerebral perfusion. when pt collapses, venous return increases & CO is restored

34
Q

What is postural hypotension?

A
  • Normally moving from lying to standing causes a reflex rise in HR + BP to maintain cerebral perfusion.
  • Drugs (vasodilators) + autonomic dysfunction (diabetes, Parkinson’s disease) may interfere with this response

PATASS III (16 decks)

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