Emergency Medicine Flashcards
Indications for central venous line?
- administration of emergency drugs
- central venous pressure measurement
- administration of IV fluids (when peripheral veins are collapsed or thrombosed)
- transvenous cardiac pacing
why is internal jugular vein preferable to subclavian for central venous access?
subclavian vein cannulation has relatively high risk of pneumothorax, so IJV is preferable via ‘high’ approach
why is right internal jugular vein preferable to left in central venous access?
Right side reduces risk of thoracic duct damage
*if chest drain alr in situ, use same side for central venous cannulation
what technique is used for central venous access?
Seldinger technique
- needle in
- guidewire through needle, needle removed
- tapered dilator and plastic cannula in over guidewire and advance into vein
- guidewire and dilator removed
- cannula secured
complications of central venous access?
pneumothorax
haemothorax
arterial puncture
thoracic duct damage
air embolism
infection
SIRS?
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
sepsis?
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
what are the ITU therapeutic goals in septic patients?
CVP 8-12 mmHg
mean arterial pressure >65 mmHg
urine output >0.5mL/hr
Central venous saturation >65%
clinical signs of shock?
hypotension
tachycardia
altered consciousness
poor periphral perfusion
oliguria (UO <50mL/h)
tachypnoea
what are some hyperacute ECG changes in STEMI?
within minutes of infarction
- 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
Leads affected in Right ventricular MI?
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
what does LAD artery supply?
anterior + septal cardiac areas
what does right coronary artery supply?
right ventricle
sino atrial node (in most)
inferior wall of left ventricule (in most)
ventricular septum (in most)
what does left dominance mean in coronary artery supply?
in 15%, inferior wall is supplied by circumflex branck of L coronary artery
in STEMI, when to consider giving gpIIb/IIIa inhibitor?
for patients undergoing PCI, consider IV gpIIb/IIIa receptor antagonist as adjuvant. be guided by local protocol
indications for PCI or thrombolysis?
- 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)
Contraindications to thrombolysis?
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
thrombolytic agent?
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
what is the recommended regimen for alteplase?
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
what to consider during streptokinase administration?
allergic reactions
+
hypotension may occur
management of cardiogenic shock secondary to MI?
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
infectious causes of pericarditis?
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
Common causes of acute pericarditis?
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
what drugs may cause acute pericarditis?
hydralazine
procainamide
methlydopa
minoxidil
investigations to request for in pericarditis apart from normal cardiac investigations?
ESR
blood cultures if evidence of sepsis or suspicion of bacterial cause
echo - pericardial effusion
ecg changes in acute pericarditis?
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)
management of dresslers syndrome?
requires cardiology specialist care
causes of bradycardia?
physiological e.g. athletes
drugs e.g. BB
hypothyroid, hypothermia, hypoxia
raised ICP
sick sinus syndrome
MI
hypovolaemia e.g. GI bleed, ectopic pregnancy
Left bundle branch divides into?
antero-superior
+
postero-superior
divisions
ie. the fascicles = these 2 divisions + right bundle branch
bifascicular block?
RBBB + left anterior hemiblock
-> left axis deviation and RBBB pattern on ECG
or
RBBB + left posterior hemiblock
-> right axis deviation and RBBB on ECG
trifascicular block?
bifascicular block + prolonged PR interval
-> represents impending progression to complete heart block
patient presenting to ED with malfunctioning pacemaker?
urgent specialist advice
external transcutaneous pacing will provide temporary support
a special magnet may be needed to inactivate an ICD which fires repeatedly
management of bradyarrhythmia with adverse feature?
ie. shock, syncope, MI, heart failure
atropine 500mcg IV
repeated up to maximum of 3mg
management of bradyarrhtyhmia with NO adverse features and no risk of asystole?
observe
management of bradyarrhythmia that has not responded to atropine?
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
management (treatment of choice) in bradyarrhythmias in pt who has not responded to atropine?
transvenous cardiac pacing
- through IJV or subclavian.
- correctly functioning ventricular pacemaker resilts in pacing spike followed by widened and bizarre QRS
management of SVT with BBB?
give adenosine as for regular SVT
management of refractory torsades de pointes?
may require overdrive pacing
If adenosine CI, what can u give in SVT?
IV Verapamil 2.5-5mg over 2 min
*avoid verapamil in HF, hypotension, concomitant BB, WPW
cardiac causes of acute AF?
IHD 33%
Heart failure 24%
hypertension 26%
valve disease 7%
pericarditis, sick sinus, cardiomyopathy, congenital heart disease, post cardiac surgery
mx of AF in WPW syndrome?
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
what to examine for in hypertensive patients?
examine for retinal changes / papilloedema
evidence of hypertensive encephalopathy
investigations for hypertensive patients?
Urinalysis
U+E
CXR
ECG
features of hypertensive encephalopathy?
headache
N+v
confusion
retinal changes. e.g papilloedema
fits
focal neurology
reduced GCS
first line management of malignant HTN?
IV sodium nitroprusside/ labetalol/ GTN
*labetalol if aortic dissection/ phaeo
** BB CI in HTN caused by cocaine, amphetamine/ sympathomimetic
Examination findings in Aortic regurgitation?
- 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
investigation of choice for aortic dissection?
CT angiography
if haemodynamically unstable, trans-oesophageal echo in theatre
normal anion gap?
12-16
most common cause of high anion gap metabolic acidosis?
lactic acidosis
causes of lactic acidosis?
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
causes of normal anion gap metabolic acidosis?
chronic diarrhoea
pancreatic/ intestinal fistula
acetazolamide
renal tubular acidosis
diagnostic criteria for exudative pleural effusion?
- 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
sign of berry aneurysm rupture involving posterior communicating artery?
oculomotor nerve palsy
investigations in subarachnoid haemorrhage?
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
what score is used in determining severity of subarachnoid haemorrhage?
Hunt and Hess score
1- 5
5: coma, decerebrate posturing
management of subarachnoid haemorrhage?
- 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
management of wound botulism?
botulinum anti-toxin
benzylpenicillin + metronidazole
+/- respiratory support
when may glucagon not be suitable for use in hypoglycaemia?
in patients with liver failure, chronic alcoholism or due to sulphonylurea drugs
- as there may be little liver glycogen stores available for mobilization
management of persistence of altered conscious level despite treatment for hypoglycaemia?
- 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
what medication may be helpful in recurrent hypoglycaemia due to overdose of a sulphonylurea?
octreotide
what is HHS characterized by?
- high glucose levels (usually >30)
- high blood osmolality
- lack of urinary ketones
common causes of DKA/ HHS?
Infection
Infarction: MI, stroke, GI, peripheral vasculature
Insufficient insulin
Intercurrent illness
what respiratory signs may you get in DKA?
hyperventilation
- due to respiratory compensation for metabolic acidosis
+ Kussmaul respiration (deep rapid breathing)
+ smell of acetone on breath
causes of hypernatraemia?
hypovolaemic: DI, diarrhoea, vomiting, diuretics
hypertonic saline
sodium bicarb administration
cushings syndrome
treatment of hyperNa?
0.9% NS to correct any hypovolaemia
once euvolaemic: 0.45% saline or 5% dextrose
formula to calculate free water deficit (in L)?
0.6 x weight (kg) x (serum Na/140 -1)
* replace this over 48h (in addition to normal maintenance fluids)
management of addisonian crisis?
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
precipitants of a thyroid storm?
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
Investigations of thyrotoxic storm?
- 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
managment of thyroid storm?
- 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
what medication should you omit in patient with thyrotoxic storm?
aspirin
- asprin can exacerbate the clinical problem by displacing thyroxine from thyroid binding globulin
management of pulmonary oedema secondary to chronic renal failure?
most are virtually anuric, so diuretics are ineffective
*DIALYSIS without delay
high flow O2
IV/ SL buccal nitrates
causes of hyperK?
- 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)
investigations of acute porphyria?
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
Management of acute porphyria?
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
management of DIC?
tx underlying cause
Obtain expert advice about replacement therapy
- platelets, FFP, prothrombin complex concentrate, heparin and blood (esp if pt is actively bleeding)
Homan’s sign?
calf pain on dorsiflexion
- positive in DVT
complications of status epilepticus?
hyperthermia
acidosis (raised lactate)
hypotension
respiratory failure
rhabdomyolysis
aspiration
what features of DKA would indicate early referral to ITU?
- pH <7.1
- Severe DKA: Ketones > 6, Bicarb <5
- hypokalaemia: <3.5
GCS <12
- Syst BP <90
- Significant comorbidity
- Pregnancy
what factors predispose a patient to delirium?
age>65
dementia
multiple comorbidities
visual and hearing impairment
polypharmacy
recent surgery
drug and alcohol dependence
what are the causes of dementia?
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
what treatment is available for treatment of alzheimers?
should be initiated by specialist
mild-mod: Donepezil (acetylcholinesterase inhibitor)
mod-severe: memantine (NMDA receptor antagonist)
what markers suggest severe attack of IBD?
>6 bloody stools / day
syst features; tachycardia, fever
Hb<10
Albumin<30
Toxic dilatation
