Management of Arrhythmias Flashcards
What is the initial assessment of all patients with an arrhythmia?
- 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
What are the adverse features associated with an arrhythmia?
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
What additional medications can be given in SVT narrow complex?
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
What additional medications can be given in Tachycardia broad complex?
Amiodarone
What additional medications can be given in bradycardia?
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)
Summary of causes of bradycardia
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)
Different paths of the conduction system have different intrinsic rates of depolarisation…
- 60bmp = sinoatrial node
- 50bpm = atrioventricular node
- 40-50bpm = Bundle of His
- 30-40bpm = ventricular myocardium - the purkinje fibres that distribute depolarisation around the myocardium
What are the presenting symptoms related to bradycardia?
- Pre-syncope
- Syncope
- Nausea
- Breathlessness
- Weakness or fatigue
What are the different types of bradycardia?
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.
TREATMENT
BRADYCARDIA
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
How does atropine work?
- 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
How to pace…
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
What are the lateral leads?
I, aVL, V5, V6
What are the inferior leads?
II, III, aVF
What are the anterior leads?
V1, V2, V3, V4
Summary of causes of SVT…
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
What are the different types of SVT?
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
What are the presenting symptoms related to SVT?
- Palpitations
- Cardiac chest pain / tightness
- Pre-syncopal symptoms e.g. dizziness or SOB
- Onset often abrupt
- Episodes rare recurrent (paroxysmal)
TREATMENT
SVT
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
What does the CHAD 2 measure?
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
What does HAS-BLED measure?
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
What is VT?
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
Summary of causes of VT…
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
What are the different types of VT?
Ventricular
- Monomorphic VT
- Polymorphic VT
- Fasicular tachycardia
Supraventricular
- SVT with BBB
TREATMENT
VT
IF UNSTABLE
- Synchronised shock - up to 3 attempts
If NO adverse features + regular
- Hospital
- Amiodarone 300mg IV
How to cardiovert?
- 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
What parameters can we control with bag valve mask?
- Rate
- Volume
- Pressure release valves are the only ones that control pressure - higher ventilatory pressure in some conditions e.g. asthmatics
- pneumothorax
How to set up a ventilator?
- Pressure = 40
- Plug into oxygen port
- CVM
- Frequency = 12 (adults)
- Tidal volume = 900 (adults)
- Air mix - no mix (full O2|)
What are the different types of syncope?
- 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?
What are prodromal symptoms?
Predictors before syncope
- Feeling faint, or feeling like they were going to pass out
- Room spinning
- Those lasting few seconds suggest vasovagal syncope
What is important to note regarding syncope?
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
What examinations need to occur after syncope?
- 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
What is vasovagal (neurocardiogenic) syncope?
- 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
What is postural hypotension?
- 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
