Emergencies Flashcards
(42 cards)
If a patient has a very high heart rate but is in sinus rhythm (sinus tachycardia) how should they be managed?
Don’t try to cardiovert- it’s not an arrhythmia
If necessary b blockers
Name the four kinds of atrial tachyarrhythmias:
HR >100, narrow QRS
- Atrial fibrillation: no P waves
- Atrial flutter: saw tooth baseline (often re-entrant circuit)
- Atrial tachycardia: abnormal P waves
- Multifocal atrial tachycardia: >3 P wave morphologies
What is the first step in any treatment of narrow complex tachycardia?
Decide if compromised or not
If compromised: DC cardiovert
If not: determine underlying rhythm (vagal manouvres, adenosine)
When would you not use vagal manoeuvres for a narrow complex tachycardia to unmask the atrial rhythm?
Caution if suspected carotid bruit, digoxin toxicity or acute ischaemia
Patient has narrow complex tachycardia, is not compromised, vagal manoeuvres haven’t worked. Next step?
Adenosine 6mg bolus
Then 12mg, 12mg
Verapamil if this fails
CI to giving adenosine to unmask atrial rhythms in narrow complex tachycardia?
Relative: asthma
2nd degree heart block
Sinoatrial disease (if patient doesn’t have a pacemaker)
Which drugs potentiate and antagonise adenosine (used for unmasking AV rhythms in narrow complex tachycardias)?
Potentiate: dipyridamole (anti-platelet aggregation)
Antagonise: theophylline (asthma)
Supraventricular tachycardia emergency: adenosine fails. What next?
Verapamil 5mg IV over 2 minutes
Not if on a beta-blocker
What are the different types of AF and their definitions?
Paroxysmal: terminates within 7 days, intermittent
Persistent: doesn’t terminate within 7 days
Permanent: long standing, no longer pursuing rhythm control
(Classification doesn’t apply to AF caused secondarily to MI etc)
What types of head pathology would cause a headache that is worse on leaning forward or in the morning or when coughing?
Raised ICP
Venous thrombosis
Which tropical disease might present with a headache?
Malaria
Which drugs given for hypertension can cause headaches as a side effect?
Those that dilate vessels namely:
Nitrates
Calcium channel antagonists
Aside from meningitis, which other major neuro problem may cause a patient to present with signs of meningism (neck stiffness, photophobia)?
Subarachnoid haemorrhage
Causes: rupture of saccular aneurysms, AV malformations, unknown 15%
Patient is breathless and you can hear crepitations, name 4 possible causes?
Heart failure
Pneumonia
Bronchiectasis
Fibrosis
In a normal individual what kind of 02 sats would warrant an ABG?
<94%
Name 5 basic groups of investigations you’d consider for breathlessness
- Basic obs
- ABG (if low sats, concern about sepsis/drugs/acidosis)
- ECG (PE, pulmonary oedema- MI)
- CXR
- Bloods (FBC- anaemia, U+Es- pulmonary renal syndrome, drug screen- salicylates)
What is the GCS scoring for voice?
5- Orientated 4- Confused 3- Inappropriate speech 2- Incomprehensible sounds 1- None
How does flexion or extension of the arm (decorticate vs decerebrate) indicate the level of damage in the brain?
Flexion- above the red nuclei in the midbrain
(Brainstem= midbrain, below it is the pons, then the medulla with the respiratory centres)
Extension- adducted and internally rotated -below the red nuclei
A semi-conscious patient is breathing in really deeply on inspiration then not exhaling properly before inhaling again. What type of breathing is this and where would the damage be?
Apneustic breathing
Indicates damage in the pons where centres are located that inhibit the inspiratory phase
Grave prognostic
If someone semi-conscious has mid-position non-reactive pupils (3-5mm) where would the lesion be likely to be?
Midbrain- where the Edinger-westphal nuclei are located that control pupillary reflexes to light
If semi-conscious patient has unilateral dilated unreactive pupil, where is the lesion?
3rd nerve compression which innervates sphincter pupillae to constrict the iris
=no constriction
What is the difference in eye signs when there is damage to the pons compared to the midbrain in terms of pupil size?
Damage at the pons interrupts sympathetic fibres leading to ‘pin-point pontine pupils’ that are small but reactive (midbrain intact)
Damage to the midbrain affects the Edinger-Westphal nucleus coordinating the light reflexes so the pupils are unresponsive and fixed in mid-position bilaterally
What test will suggest that the brainstem is intact from the medulla (7th CN) to the midbrain (3rd CN)?
Vestibulo-ocular test
Doll’s eye head manoeuvres- turn head, normal if eyes remain fixed on original point
Ice water calorics- put cold water in ear, normal if eye deviates to cold side and nystagmus to opposite side
Why does damage to the mid-brain cause fixed mid-position pupils when damage to cranial nerve 3 causes dilated unilateral pupils?
Light reflex= CN2 > midbrain (dorsal tectum then edinger-westphal nucleus) > CN3
If CN3 is damaged, sympathetic input is unopposed
If midbrain is damaged, sympathetic + parasympathetic pathways are affected
