Emergency Medicine Flashcards
Supraventricular Tachycardia (SVT) is any ____ complex tachycardia characterised by a heart rate of more than 100 bpm and a QRS width of less than ____ ms on an ECG.
Atrial Fibrillation (AF), AV Re-entry Tachycardia (AVRT) and AV Nodal Re-entry Tachycardia (AVNRT) are examples of SVTs.
Patients with adverse features should be given _____ .
These features can be remembered by the mnemonic HISS, which stands for:
______
narrow
120
Management of SVT in Stable patients with no adverse features.
- Determine if rhythm is regular or irregular.
Regular:
Irregular:
Regular Rhythm
1. Vagal Manouevres - Carotid sinus massage / Valsava manouervre
2. IV Adenosine (6mg) - (blocks conduction through av node)
Prior to administering Adenosine, patients must be warned that they might experience difficulty breathing, chest tightness and flushing.
It should then be given rapidly over 1-3 seconds, followed by a 20 ml IV Normal Saline bolus**.
If this fails, a second dose of Adenosine 12mg can be administered, followed by another 18mg.
If this fails also -** Beta blocker or Verapamil **
Irregular rhythm
Manage according to AF algorithm:
Rate control with Beta-blocker
Rhythm control: Digoxin / Amiodarone (if Heart failure)
If in AF>48hrs - Anticoagulate
https://www.resus.org.uk/sites/default/files/2021-04/Tachycardia%20Algorithm%202021.pdf
Drugs that potentiate the effect of adenosine and thus contraindicate the use of adenosine.
Dipyridamole (antiplatelet)
Carbamazepine
Adenosine cannot be given to ____ and thus ____ is used instead.
Asthmatics
Verapamil
Adenosine is known to regulate myocardial and coronary circulatory functions. Adenosine not only dilates coronary vessels, but attenuates beta-adrenergic receptor-mediated increases in myocardial contractility and depresses both sinoatrial and atrioventricular node activities.
Complications of SVT can include:
Syncope
Deep vein thrombosis
Embolism
Cardiac tamponade
Congestive cardiac failure
Myocardial infarction
Death
Which drug is most appropriate to prescribe in aspirin overdose?
Sodium bicarbonate and fluid resuscitation (helps to eliminate the salicylate)
Sodium bicarbonate increases plasma bicarbonate and buffers excess hydrogen ions, alkalinising the blood and urine and enhancing the elimination of aspirin.
Glucose is also important to treat hypoglycaemia.
** Haemofiltration ± mechanical ventilation should be considered in severe toxicity **
Clinical features of serotonin syndrome can be split into neurological and autonomic.
Neurological features:
Autonomic features:
Neurological:
- Altered mental state
- Tremor
- Ataxia
- Hyperreflexia.
Autonomic:
- Tachycardia
- Hypertension
- Diarrhoea
- Hyperthermia
NB - Distinct from *Neuroleptic malignant syndrome *which is caused by anti-psychotics or sudden reduction in dopaminergics (i.e parkinson’s).
Predominant neurological feature of NMS is also** rigidity **
Which antibiotic can cause prolongation of the QT interval, which can lead to a polymorphic VT, otherwise known as torsades de points?
Clarithromycin
Causes of a long QT interval which may predispose a patient to developing TDP include the following. This can be remembered by a useful mnemonic - TIIMMES:
Toxins: drugs including clarithromycin, anti-arrhythmics, anti-psychotics and tricyclic antidepressants
Inherited: congenital long QT syndromes such as Romano-Ward and Jervell and Lange-Nielson syndromes.
Ischaemia
Myocarditis
Mitral valve prolapse
Electrolyte abnormalities, such as hypokalaemia and hypocalcaemia
Subarachnoid Haemorrhage
TORSADES DE POINTES (VT) - PROLONGED QT INTERVAL
Management of Torsades de Pointes
In *unstable patients *with haemodynamic compromise, **DC cardioversion **can be done.
In stable patients, the choice of treatment is IV Magnesium Sulphate 2g over 1 to 2 minutes.
Management of tension pneumothorax?
This is with a large bore cannula/needle in the 2nd intercostal space, midclavicular line on the same side as the pneumothorax
This should be followed by chest drain insertion to reduce the risk of an immediate recurrence of the tension pneumothorax.
A tension pneumothorax occurs when air enters the pleural cavity through a one-way valve and cannot escape
Definition of Horners Syndrome and causes.
Horner’s syndrome is characterised by ptosis, meiosis with or without anhydrosis.
It is due to an interruption of the sympathetic nerve supply to the eye and can be classified into pre-ganglion causes, post ganglionic causes and central causes.
Causes:
Pancoast tumour (affecting sympathetic nerve supply)
Stroke
Carotid artery dissection (Red flag: neck pain)
Adult dose and route of adrenaline in anaphylaxis?
500ug MICROGRAMS
IM
Investigations and Management of pulmonary oedema due to Left Ventricular Failure.
Investigations
Bedside observations
Arterial blood gas
ECG
Troponin if concerned about a new cardiac event
Serum BNP
Chest X-ray
Management - POUR SOD
- Take an ABCDE approach
- Sit the patient up
- Administer oxygen
- Ensure IV access
- IV Furosemide (40mg stat)
- Consider non-invasive ventilation such as CPAP if failed medical therapy (usually in an intensive care setting)
- Consider further therapies in the intensive care setting such as invasive ventilation and inotropic support if the above fails
https://www.nice.org.uk/guidance/cg187/chapter/1-Recommendations
When taken as an overdose, the metabolism of paracetamol results in a buildup of a toxic substance called _____.
NAPQI (N-acetyl-p-benzoquinone-imine).
NAPQI is inactivated by glutathione. In an overdose, glutathione stores are rapidly depleted, and NAPQI is left un-metabolised. It can cause liver and kidney damage.
Management of Paracetamol overdose:
If ingestion less than 1 hour ago + dose >150mg/kg: Activated charcoal
If ingestion <4 hours ago: Wait until 4 hours to take a level and treat with N-acetylcysteine based on level using** nomogram**
If ingestion 4-15 hours ago: Take immediate level and treat based on level
If staggered overdose ( which is defined as being an overdose taken over > 1 hour) or ingestion >15 hours ago: Start N-acetylcysteine immediately
Obtain following bloods:
FBC
Urea and Electrolytes
INR
Venous gas
If a patient presents after 16 hours, there is *uncertainty about timing * or has a staggered overdose then NAC should be started regardless of the nomogram.
NAC is associated with anaphylactoid reactions. These are not true anaphylactic reactions and can usually be managed by stopping the infusion temporarily and then restarting at a lower rate.
Consider need for transfer to liver unit if blood tests are worsening
Management Flow chart:
https://emj.bmj.com/content/19/3/202
Emergency Management of PE:
Massive PE and HD unstable - ______
Acute PE and stable - _____
Recurrent PE or Anticoagulation resistant - _____
Unstable: Thrombolysis - (Streptokinase/Alteplase - seek senior input)
Stable: LMWH or UFH infusion (5 days - and INR >2 on 2 consecutive days) -** bridge with NOAC or Warfarin **
NB - Provoked PE - 3 months DOAC and check INR. Unprovoked PE - 6 months DOAC and check INR
(Side note: remember warfarin takes time to titrate INR but also can be reversed quickly with Vit.K)
Recurrent or treatment resistant: Inferior Vena Cava Filter
NICE visual summary:
https://www.nice.org.uk/guidance/ng158/resources/visual-summary-pdf-11193380893
ECG interpretation method
Details - patient/time/previous ECG’s
Rate - Rhythm strip X 6
Rhythm - count boxes between each QRS wave (use ruler and dots if neccessary)
P wave - Present before every QRS? Yes - sinus NO? - AF etc.
PR interval - <200ms or 5 boxes (each box 40ms or 0.04 secs). NO? - heart block. Primary secondary etc.
QRS wave - < 3 boxes or 120ms/0.12 seconds. NO? - Bundle Branch BLock (BBB). - William Marrow (V1 and V6)
ST segments - Compare with isoelectric line after the complex.
(ST elevation is caused by a lack of blood supply to the muscle. The potassium channels responsible for depolarization are ATP dependent and thus cannot open when there is a lack of blood)
T waves - inverted or flattened more than twice in each segment?
Axis - look at leads 1 and 3
If lead 3 is greater in amplitude than lead 1 - consider axis deviation
If leads arriving - right axis deviation
If leads leaving - left axis deviation
Everything else is normal.
Other stuff - QT/QTc Interval / P wave morphology / Ventricular hypertrophy / Strain (amplitude of QRS - can be nromal in a skinny person)
Important St.Johns wort interactions to be aware of
Anti-depressants
Warfarin
Oestrogen and Progesterone
Causes of Hyperkalaemia?
3 causes:
- Reduced excretion from kidneys
- Release from cells
- Acidosis
- Reduced excretion from kidneys:
AKI
and
Addison’s
DRUGs that reduce K+ excretion from the kidneys : **KBANK **:
K+ containing laxatives (movicol/fybogel)
Beta Blockers
ACE inhibitors
NSAIDs
Potassium Sparing Diuretics (i.e aldosterone antagonists - spironolactone/eplerenone etc.) but also diuretics in general
Heparin (which inhibits aldosterone release)
and
Ciclosporin/Tacrolimus (immunosuppressants)
- Cellular Release:
Rhabdomyolysis
Digoxin Toxicity (NB - Can be precipitated by hypokalemaia) - “Reverse tick sign” on ECG
Tumour Lysis Syndrome
Massive Haemolysis
- Acidosis:
DKA or any other metabolic acidosis
Hyperkalaemia is a potentially life threatening electrolyte abnormality.
Treat K+ >___ mmol/L or any hyperkalaemia with ECG changes with the following;
Give 10ml of 10% _____ (or chloride) over 10 mins - this is cardioprotective
Intravenous ____ (10u soluble insulin) in 25g ____ (50mL of 50% or 125ml of 20% glucose) - insulin causes intracellular K+ shift and glucose to required to prevent hypoglycaemia
Nebulised salbutamol - also causes intracellular K+ shift
Treatment with sodium bicarbonate is controversial
Other aspects of management:
Check contributing drugs (e.g. ACE inhibitors, spironolactone)
Once initial measures completed, recheck urea and electrolytes and ECG and glucose
Urinary potassium
Hyperkalaemia is a potentially life threatening electrolyte abnormality.
Treat K+ >6.5mmol/L or any with ECG changes with the following;
Give 10ml of 10% calcium gluconate (or chloride) over 10 mins - this is cardioprotective
Intravenous insulin (10u soluble insulin) in 25g glucose (50mL of 50% or 125ml of 20% glucose) - insulin causes intracellular K+ shift and glucose to required to prevent hypoglycaemia
Nebulised salbutamol - also causes intracellular K+ shift
Treatment with sodium bicarbonate is controversial
Other aspects of management:
Check contributing drugs (e.g. ACE inhibitors, spironolactone)
Once initial measures completed, recheck urea and electrolytes and ECG and glucose
Urinary potassium
Causes of Hyponatraemia?
Remember to classify into:
Hypovolaemic (In the elderly dehydration is a very common cause especially in patients with dementia)
Euvolaemic (SIADH / Hypothyroidism)
Hypervolaemic
and drugs:
Thiazide diuretics > Loop Diuretics > K+ sparing diuretics
Hyponatraemia Management
