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Fifth Year Medicine > Emergencies > Flashcards

Emergencies Flashcards

1
Q

If a patient has a very high heart rate but is in sinus rhythm (sinus tachycardia) how should they be managed?

A

Don’t try to cardiovert- it’s not an arrhythmia

If necessary b blockers

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2
Q

Name the four kinds of atrial tachyarrhythmias:

HR >100, narrow QRS

A
  1. Atrial fibrillation: no P waves
  2. Atrial flutter: saw tooth baseline (often re-entrant circuit)
  3. Atrial tachycardia: abnormal P waves
  4. Multifocal atrial tachycardia: >3 P wave morphologies
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3
Q

What is the first step in any treatment of narrow complex tachycardia?

A

Decide if compromised or not
If compromised: DC cardiovert
If not: determine underlying rhythm (vagal manouvres, adenosine)

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4
Q

When would you not use vagal manoeuvres for a narrow complex tachycardia to unmask the atrial rhythm?

A

Caution if suspected carotid bruit, digoxin toxicity or acute ischaemia

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5
Q

Patient has narrow complex tachycardia, is not compromised, vagal manoeuvres haven’t worked. Next step?

A

Adenosine 6mg bolus
Then 12mg, 12mg

Verapamil if this fails

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6
Q

CI to giving adenosine to unmask atrial rhythms in narrow complex tachycardia?

A

Relative: asthma
2nd degree heart block
Sinoatrial disease (if patient doesn’t have a pacemaker)

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7
Q

Which drugs potentiate and antagonise adenosine (used for unmasking AV rhythms in narrow complex tachycardias)?

A

Potentiate: dipyridamole (anti-platelet aggregation)
Antagonise: theophylline (asthma)

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8
Q

Supraventricular tachycardia emergency: adenosine fails. What next?

A

Verapamil 5mg IV over 2 minutes

Not if on a beta-blocker

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9
Q

What are the different types of AF and their definitions?

A

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)

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10
Q

What types of head pathology would cause a headache that is worse on leaning forward or in the morning or when coughing?

A

Raised ICP

Venous thrombosis

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11
Q

Which tropical disease might present with a headache?

A

Malaria

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12
Q

Which drugs given for hypertension can cause headaches as a side effect?

A

Those that dilate vessels namely:
Nitrates
Calcium channel antagonists

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13
Q

Aside from meningitis, which other major neuro problem may cause a patient to present with signs of meningism (neck stiffness, photophobia)?

A

Subarachnoid haemorrhage

Causes: rupture of saccular aneurysms, AV malformations, unknown 15%

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14
Q

Patient is breathless and you can hear crepitations, name 4 possible causes?

A

Heart failure
Pneumonia
Bronchiectasis
Fibrosis

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15
Q

In a normal individual what kind of 02 sats would warrant an ABG?

A

<94%

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16
Q

Name 5 basic groups of investigations you’d consider for breathlessness

A
  1. Basic obs
  2. ABG (if low sats, concern about sepsis/drugs/acidosis)
  3. ECG (PE, pulmonary oedema- MI)
  4. CXR
  5. Bloods (FBC- anaemia, U+Es- pulmonary renal syndrome, drug screen- salicylates)
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17
Q

What is the GCS scoring for voice?

A 
5- Orientated
4- Confused
3- Inappropriate speech
2- Incomprehensible sounds
1- None
18
Q

How does flexion or extension of the arm (decorticate vs decerebrate) indicate the level of damage in the brain?

A

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

19
Q

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?

A

Apneustic breathing
Indicates damage in the pons where centres are located that inhibit the inspiratory phase
Grave prognostic

20
Q

If someone semi-conscious has mid-position non-reactive pupils (3-5mm) where would the lesion be likely to be?

A

Midbrain- where the Edinger-westphal nuclei are located that control pupillary reflexes to light

21
Q

If semi-conscious patient has unilateral dilated unreactive pupil, where is the lesion?

A

3rd nerve compression which innervates sphincter pupillae to constrict the iris

=no constriction

22
Q

What is the difference in eye signs when there is damage to the pons compared to the midbrain in terms of pupil size?

A

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

23
Q

What test will suggest that the brainstem is intact from the medulla (7th CN) to the midbrain (3rd CN)?

A

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

24
Q

Why does damage to the mid-brain cause fixed mid-position pupils when damage to cranial nerve 3 causes dilated unilateral pupils?

A

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

25
Q

Name 3 causes of bleeding that could result in shock (systemic hypoperfusion)

A
  1. Upper GI bleed
  2. Ruptured AAA
  3. Trauma
26
Q

Name 4 causes of cardiogenic pump failure?

A
  1. ACS- ischaemia
  2. Arrhythmia
  3. Acute valve failure
  4. Aortic dissection
27
Q

Why might a patient be in shock but not be tachycardic?

A

If they are on beta-blockers or have spinal/neurogenic shock

(Neurogenic- damage to sympathetics
Spinal- wipe out of all reflexes temporarily)

28
Q

A patient is presenting with shock, you give a fluid bolus of 20mL/kg, what two parameters would prompt you to call ICU if they haven’t improved?

A

Lactate >4 on ABG

Systolic BP <90mmHg

29
Q

What proportions of blood loss are associated with the 4 different classes of shock?

A
  1. <750mL or 15%
  2. 750-1500mL or 15-30%
  3. 1500-2000L or 30-40%
  4. > 2000L or 40%
30
Q

What heart rate is associated with different classes of shock?

A
  1. <100
  2. 100-120
  3. 120-140
  4. > 140
31
Q

If a patient has low BP, what class of shock are they in at least?

A

Class 3 = low BP

Class 4 = undetectable BP (call cardiac arrest team)

32
Q

Why does a narrow pulse pressure occur in shock?

A

Cardiac output reduces

33
Q

If 2 or more of the following 4 criteria are fulfilled, the patient is defined to have SIRS (systemic inflammatory response syndrome):

A

Temperature < 36 or > 38
WCC < 4 or > 12, or >10% immature forms
HR > 90
RR > 20 or PaCO2 < 4.3kPa

34
Q

What’s the difference between severe sepsis and septic shock?

A

Severe sepsis = evidence of tissue hypoperfusion: altered mental state, lactic acidosis, oliguria

Septic shock = change in blood pressure + severe sepsis
(Under 90mmHg or MAP under 60mmHg)

35
Q

What type of hypersensitivity reaction is anaphylaxis?

A

Type 1- IgE mediated (atopy)

Others:
Type 2- antibodies against cell antigen (Goodpasture’s, rheumatic heart disease)
Type 3- antibodies against soluble antigen- immune complex (SLE, rheumatoid)
Type 4- memory cell mediated antibody (contact dermatitis, chronic transplant rejection)
Type 5- receptor mediated (Graves, myasthenia gravis(

36
Q

If 2 or more of the following 4 criteria are fulfilled, the patient is defined to have SIRS (systemic inflammatory response syndrome):

A

Temperature < 36 or > 38
WCC < 4 or > 12, or >10% immature forms
HR > 90
RR > 20 or PaCO2 < 4.3kPa

37
Q

What’s the difference between severe sepsis and septic shock?

A

Severe sepsis = evidence of tissue hypoperfusion: altered mental state, lactic acidosis, oliguria

Septic shock = change in blood pressure + severe sepsis
(Under 90mmHg or MAP under 60mmHg)

38
Q

What type of hypersensitivity reaction is anaphylaxis?

A

Type 1- IgE mediated (atopy)

Others:
Type 2- antibodies against cell antigen (Goodpasture’s, rheumatic heart disease)
Type 3- antibodies against soluble antigen- immune complex (SLE, rheumatoid)
Type 4- memory cell mediated antibody (contact dermatitis, chronic transplant rejection)
Type 5- receptor mediated (Graves, myasthenia gravis(

39
Q

Why might CRP not be very helpful for someone in A+E with a ?infection that started in the last day or so?

A

CRP lags behind by a day

40
Q

How soon after chemotherapy is someone likely to become neutropenic?

A

5-12 days

41
Q

Someone on longterm steroids comes in with ?infection. Along with antibiotics what else do they need?

A

An increase in the steroid as ‘sick day rules’ apply.

42
Q

In someone with abnormal LFTs and cancer, if you suspect a hepatitis and are getting an USS, what else needs to be requested on the USS?

A

Doppler of the hepatic portal vein to see if patient has clotted off the liver vein, causing damage

Think about paracetamol overdose in hospital especially if low weight

Fifth Year Medicine (32 decks)

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