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MRCP > Emergency Medicine > Flashcards

Emergency Medicine Flashcards

1
Q

Indications for central venous line?

A
  • administration of emergency drugs
  • central venous pressure measurement
  • administration of IV fluids (when peripheral veins are collapsed or thrombosed)
  • transvenous cardiac pacing
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2
Q

why is internal jugular vein preferable to subclavian for central venous access?

A

subclavian vein cannulation has relatively high risk of pneumothorax, so IJV is preferable via ‘high’ approach

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3
Q

why is right internal jugular vein preferable to left in central venous access?

A

Right side reduces risk of thoracic duct damage

*if chest drain alr in situ, use same side for central venous cannulation

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4
Q

what technique is used for central venous access?

A

Seldinger technique

  1. needle in
  2. guidewire through needle, needle removed
  3. tapered dilator and plastic cannula in over guidewire and advance into vein
  4. guidewire and dilator removed
  5. cannula secured
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5
Q

complications of central venous access?

A

pneumothorax

haemothorax

arterial puncture

thoracic duct damage

air embolism

infection

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6
Q

SIRS?

A

2 or more of:

  • body temp >38 or <36
  • HR >90
  • RR >20 or PaCO2 <4.3
  • WCC > 12 or < 4 or >10% immature (band) forms
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7
Q

sepsis?

A

SIRS with evidence of hypoperfusion

e.g. lactate >3

or systolic BP <90 despite fluid resus

**require early ITU input, might need central venous/ arterial cath with IVI noradrenaline to maintain mean arterial pressure and IV fluid boluses to maintain CVP

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8
Q

what are the ITU therapeutic goals in septic patients?

A

CVP 8-12 mmHg

mean arterial pressure >65 mmHg

urine output >0.5mL/hr

Central venous saturation >65%

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9
Q

clinical signs of shock?

A

hypotension

tachycardia

altered consciousness

poor periphral perfusion

oliguria (UO <50mL/h)

tachypnoea

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10
Q

what are some hyperacute ECG changes in STEMI?
within minutes of infarction

A
  • increased ventricular activation time.

(interval between start of QRS to apex of R wave may be >0.045s- prolonged)

  • increased height of R wave (initially in inf leads in inf MI)
  • upward slowing ST segment
  • Tall, widened T waves
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11
Q

Leads affected in Right ventricular MI?

A

ST depression in V1

-> record ECG trace from lead V4R - ST elevation.

*usually occurs as part of an inferior MI

*treat RV failure with IVF to maintain adequate filling pressure

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12
Q

what does LAD artery supply?

A

anterior + septal cardiac areas

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13
Q

what does right coronary artery supply?

A

right ventricle

sino atrial node (in most)

inferior wall of left ventricule (in most)

ventricular septum (in most)

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14
Q

what does left dominance mean in coronary artery supply?

A

in 15%, inferior wall is supplied by circumflex branck of L coronary artery

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15
Q

in STEMI, when to consider giving gpIIb/IIIa inhibitor?

A

for patients undergoing PCI, consider IV gpIIb/IIIa receptor antagonist as adjuvant. be guided by local protocol

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16
Q

indications for PCI or thrombolysis?

A
  • ST elevation of >1 mm in 2 limb leads

or

  • ST elevation of >2 mm in 2 or more contiguous chest leads

or

  • LBBB in presence of typical history of acute MI
    (note: LBBB does not have to be new)
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17
Q

Contraindications to thrombolysis?

A

most are relative, discuss any w patient and cardiology

  • recent stroke, head injury, prev neurosurgery or cerebral tumour
  • recent GI bleed/ coagulopathy/ warfarin
  • severe HTN (BP>200/120), aortic dissection, pericarditis
  • major surgery recently
  • pregnancy
  • puncture of non compressible vessel e.g. subclavian vein, traumatic CPR, reduced GCS post arrest
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18
Q

thrombolytic agent?

A

1st line: alteplase (tissue plasminogen activator)

2nd: streptokinase

**always use alteplase if streptokinase was given >5 days ago or in ant MI in <75yo and <4h onset of symptoms, or if hypotensive

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19
Q

what is the recommended regimen for alteplase?

A

15mg IV bolus

followed by 0.75mg/kg (max 50mg) IVI for 30 min

then 0.5mg/kg (max 35mg) IVI over 60 min

*give LMWH e.g. enox 1mg/kg stat or heparin concomitantly through separate IV line, acoording to local protocol

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20
Q

what to consider during streptokinase administration?

A

allergic reactions

+

hypotension may occur

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21
Q

management of cardiogenic shock secondary to MI?

A

treat the MI

contact ITU and cardiologist

echo to exclude conditions requiring urgent surgical repair e.g. MR from pap muscle rupture, aortic dissection, Ventricular septum rupture, cardiac tamp or massive PE

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22
Q

infectious causes of pericarditis?

A

viral

e.g Coxsackie A9, B1-4, EBV, CMV, mumps, Varicella, HIV, rubella, Parvo B19

bacterial

e.g. pneumococcus, meningococcus, chlamydia, gonorrhoea, haemophilus

TB

esp in HIV pts

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23
Q

Common causes of acute pericarditis?

A

viral/ bacterial/ TB

post MI

Locally invasive carcinoma e.g. breast/ lung

rheumatic fever

uraemia

SLE

post radiotherapy/ cardiac surgery

drugs e.g. hydralazine, procainamide

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24
Q

what drugs may cause acute pericarditis?

A

hydralazine

procainamide

methlydopa

minoxidil

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25
Q

investigations to request for in pericarditis apart from normal cardiac investigations?

A

ESR

blood cultures if evidence of sepsis or suspicion of bacterial cause

echo - pericardial effusion

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26
Q

ecg changes in acute pericarditis?

A

widespread saddle shape st elevation

  • in at least 2 limb leads and all chest leads

*ST elevation is concave up unlike MI

PR depression (reflecting atrial inflammation)

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27
Q

management of dresslers syndrome?

A

requires cardiology specialist care

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28
Q

causes of bradycardia?

A

physiological e.g. athletes

drugs e.g. BB

hypothyroid, hypothermia, hypoxia

raised ICP

sick sinus syndrome

MI

hypovolaemia e.g. GI bleed, ectopic pregnancy

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29
Q

Left bundle branch divides into?

A

antero-superior

+

postero-superior

divisions

ie. the fascicles = these 2 divisions + right bundle branch

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30
Q

bifascicular block?

A

RBBB + left anterior hemiblock

-> left axis deviation and RBBB pattern on ECG

or

RBBB + left posterior hemiblock

-> right axis deviation and RBBB on ECG

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31
Q

trifascicular block?

A

bifascicular block + prolonged PR interval

-> represents impending progression to complete heart block

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32
Q

patient presenting to ED with malfunctioning pacemaker?

A

urgent specialist advice

external transcutaneous pacing will provide temporary support

a special magnet may be needed to inactivate an ICD which fires repeatedly

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33
Q

management of bradyarrhythmia with adverse feature?

ie. shock, syncope, MI, heart failure

A

atropine 500mcg IV

repeated up to maximum of 3mg

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34
Q

management of bradyarrhtyhmia with NO adverse features and no risk of asystole?

A

observe

35
Q

management of bradyarrhythmia that has not responded to atropine?

A

adrenaline

  • as temporizing measure prior to transvenous pacing
  • controlled infusion at 2-10mcg/min

OR

transcutaneous pacing

  • available on most defibrillators
    • IV opioid / sedation if pt finds external pacing very uncomfortable

** these are both interim measures

36
Q

management (treatment of choice) in bradyarrhythmias in pt who has not responded to atropine?

A

transvenous cardiac pacing

  • through IJV or subclavian.
  • correctly functioning ventricular pacemaker resilts in pacing spike followed by widened and bizarre QRS
37
Q

management of SVT with BBB?

A

give adenosine as for regular SVT

38
Q

management of refractory torsades de pointes?

A

may require overdrive pacing

39
Q

If adenosine CI, what can u give in SVT?

A

IV Verapamil 2.5-5mg over 2 min

*avoid verapamil in HF, hypotension, concomitant BB, WPW

40
Q

cardiac causes of acute AF?

A

IHD 33%

Heart failure 24%

hypertension 26%

valve disease 7%

pericarditis, sick sinus, cardiomyopathy, congenital heart disease, post cardiac surgery

41
Q

mx of AF in WPW syndrome?

A

do not give AV blocking drugs e.g dig, verapamil, adenosine, as can result in acceleration of conduction through accessory pathway -> cardiovasc collapse or VF

*seek expert help

42
Q

what to examine for in hypertensive patients?

A

examine for retinal changes / papilloedema

evidence of hypertensive encephalopathy

43
Q

investigations for hypertensive patients?

A

Urinalysis

U+E

CXR

ECG

44
Q

features of hypertensive encephalopathy?

A

headache

N+v

confusion

retinal changes. e.g papilloedema

fits

focal neurology

reduced GCS

45
Q

first line management of malignant HTN?

A

IV sodium nitroprusside/ labetalol/ GTN

*labetalol if aortic dissection/ phaeo

** BB CI in HTN caused by cocaine, amphetamine/ sympathomimetic

46
Q

Examination findings in Aortic regurgitation?

A
  • AR murmur 30%
  • Asymmetry of absence of peripheral pulses
  • HTN
  • hypotension with features of tamponade or neurological signs in assoc w pain e.g. spinal /carotid art involvement
47
Q

investigation of choice for aortic dissection?

A

CT angiography

if haemodynamically unstable, trans-oesophageal echo in theatre

48
Q

normal anion gap?

A

12-16

49
Q

most common cause of high anion gap metabolic acidosis?

A

lactic acidosis

50
Q

causes of lactic acidosis?

A

trauma w major haemorrhage, septic shock

tissue hypoxia (CO / cyanide poisoning)

hepatic / renal failure

ethylene glycol or methanol poisoning

cocaine/ amphetamines

salicylate poisoning

metformin

strenuous exercise

isoniazid

51
Q

causes of normal anion gap metabolic acidosis?

A

chronic diarrhoea

pancreatic/ intestinal fistula

acetazolamide

renal tubular acidosis

52
Q

diagnostic criteria for exudative pleural effusion?

A
  • pleural fluid:serum protein >0.5
  • fluid:serum LDH >0.6

or fluid LDH >2/3 the upper limits of normal value for serum LDH

53
Q

sign of berry aneurysm rupture involving posterior communicating artery?

A

oculomotor nerve palsy

54
Q

investigations in subarachnoid haemorrhage?

A

Airway + Breathing: if unconscious, open airway. ITU involvement for ?intubation + ventilation

  • send for bloods, clotting, U+E
  • CXR: neurogenic pulmonary oedema
  • ECG: ischaemic changes
  • emergency CT head
  • LP >12 h
  • early neurosurgical involvement
55
Q

what score is used in determining severity of subarachnoid haemorrhage?

A

Hunt and Hess score

1- 5

5: coma, decerebrate posturing

56
Q

management of subarachnoid haemorrhage?

A
  • SpO2 94-98%
  • analgesia + antiemetic
  • may require intubation - will allow control of pCO2 (aim normocapnia)
  • catheter + art line
  • contact neurosurgery
  • nimodipine to prevent vasospasm
  • IV mannitol if evidence of raised ICP
57
Q

management of wound botulism?

A

botulinum anti-toxin

benzylpenicillin + metronidazole

+/- respiratory support

58
Q

when may glucagon not be suitable for use in hypoglycaemia?

A

in patients with liver failure, chronic alcoholism or due to sulphonylurea drugs

  • as there may be little liver glycogen stores available for mobilization
59
Q

management of persistence of altered conscious level despite treatment for hypoglycaemia?

A
  • might suggest another underlying pathology e.g. stroke, or due to cerebral oedema (due to hypo)
  • maintain plasma glucose at 7-11
  • contact ITU
  • consider mannitol +/- dex
  • Urgent CT head
  • explore other causes of altered consciousness
60
Q

what medication may be helpful in recurrent hypoglycaemia due to overdose of a sulphonylurea?

A

octreotide

61
Q

what is HHS characterized by?

A
  • high glucose levels (usually >30)
  • high blood osmolality
  • lack of urinary ketones
62
Q

common causes of DKA/ HHS?

A

Infection

Infarction: MI, stroke, GI, peripheral vasculature

Insufficient insulin

Intercurrent illness

63
Q

what respiratory signs may you get in DKA?

A

hyperventilation

  • due to respiratory compensation for metabolic acidosis

+ Kussmaul respiration (deep rapid breathing)

+ smell of acetone on breath

64
Q

causes of hypernatraemia?

A

hypovolaemic: DI, diarrhoea, vomiting, diuretics

hypertonic saline

sodium bicarb administration

cushings syndrome

65
Q

treatment of hyperNa?

A

0.9% NS to correct any hypovolaemia

once euvolaemic: 0.45% saline or 5% dextrose

66
Q

formula to calculate free water deficit (in L)?

A

0.6 x weight (kg) x (serum Na/140 -1)

* replace this over 48h (in addition to normal maintenance fluids)

67
Q

management of addisonian crisis?

A

IV access

bloods: cortisol, ACTH, blood cultures, urine cultures

if hypotensive -> o.9% NS

STAT IV hydrocort 100mg

Check blood glucose -> Dextrose IV if hypoglycaemic

if infection -> IV abx

68
Q

precipitants of a thyroid storm?

A

usually a physiological stressor:

  • premature/ inappropriate cessation of anti-thyroid medication
  • recent surgery/ radio iodine treatment
  • intercurrent infection
  • trauma
  • emotional stress
  • DKA/ HHS
  • thyroxine OD
  • preeclampsia
69
Q

Investigations of thyrotoxic storm?

A
  • U+E, blood glucose, Ca (HyperCa occurs in ~10%)
  • FBC, infection markers, coag
  • Septic screen: MSU, blood cultures, sputum
  • TFTs
  • CXR: congestive heart failure/ infection
  • ECG: AF, arrhythmias
70
Q

managment of thyroid storm?

A
  • airway +/- oxygen
  • IV access + IV saline
  • if vomiting: NG tube
  • if sedation require: small amts diazepam/ haloperidol
  • IV 100mg Hydrocortisone/ PO dex 4mg QDS
  • Abx if infection suspected

if hyperthermic: cooling measures

  • Propranolol + Carbimazole +/- Iodine
71
Q

what medication should you omit in patient with thyrotoxic storm?

A

aspirin

  • asprin can exacerbate the clinical problem by displacing thyroxine from thyroid binding globulin
72
Q

management of pulmonary oedema secondary to chronic renal failure?

A

most are virtually anuric, so diuretics are ineffective

*DIALYSIS without delay

high flow O2

IV/ SL buccal nitrates

73
Q

causes of hyperK?

A
  • spurious: haemolysed sample/ taken from limb with IVI containing K
  • Decreased renal excretion: AKI, CKD, K+ sparing diuretics e.g. spironolactone
  • Cell injury: rhabdo, tumour lysis, burns, massive/ incompatible blood transfusion
  • K+ cellular shifts: DKA, acidosis from any cause, drugs e.g. BB
  • Hypoaldosteronism: Addisons, Drug induced (NSAIDs, ACEi)
74
Q

investigations of acute porphyria?

A

fresh urine sample (protected from light) to test for amino laevulinic acid and porphobilinogen

  • in an attack, urine goes dark red or brown when exposed to light - due to polymerization of porphobilinogen
75
Q

Management of acute porphyria?

A

treat supportively

  • may need ITU
  • maintain carbohydrate intake (PO/IV)

pracetamol +/- morphine for pain

management of status epilepticus: IV diazepam first line

Seek specialist advice: haem arginate might help pts with acute crises

76
Q

management of DIC?

A

tx underlying cause

Obtain expert advice about replacement therapy

  • platelets, FFP, prothrombin complex concentrate, heparin and blood (esp if pt is actively bleeding)
77
Q

Homan’s sign?

A

calf pain on dorsiflexion

  • positive in DVT
78
Q

complications of status epilepticus?

A

hyperthermia

acidosis (raised lactate)

hypotension

respiratory failure

rhabdomyolysis

aspiration

79
Q

what features of DKA would indicate early referral to ITU?

A
  • pH <7.1
  • Severe DKA: Ketones > 6, Bicarb <5
  • hypokalaemia: <3.5

GCS <12

  • Syst BP <90
  • Significant comorbidity
  • Pregnancy
80
Q

what factors predispose a patient to delirium?

A

age>65

dementia

multiple comorbidities

visual and hearing impairment

polypharmacy

recent surgery

drug and alcohol dependence

81
Q

what are the causes of dementia?

A

Primary:

neurodegenerative: alzheimers, Parkinsons/ LBD, CJD, frontotemporal
other: vascular

Secondary:

infections: Syphilis, HIV

Vascular: Cerebrovascular disease

Neoplastic

Inflammatory

Metabolic* usually reversible: B12/ folate, WIlsons disease, hypothyroidism

82
Q

what treatment is available for treatment of alzheimers?

A

should be initiated by specialist

mild-mod: Donepezil (acetylcholinesterase inhibitor)

mod-severe: memantine (NMDA receptor antagonist)

83
Q

what markers suggest severe attack of IBD?

A

>6 bloody stools / day

syst features; tachycardia, fever

Hb<10

Albumin<30

Toxic dilatation

MRCP (21 decks)

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