PPT Flashcards
What are the shockable rhythms?
🎶 DFIB for VFIB and pulseless VTACH 🎶
What are the non-shockable rhythms?
PEA & asystole
🎶 Don’t shock asystole you won’t get them back 🎶
Patient is unresponsive + not breathing - what to do?
Check for response, open airway and look, listen, feel for 10 seconds
Call resus team 2222 - state adult cardiac arrest + location
CPR 30:2 (100-120 compressions per min @ 5-6cm)
Attach defib/ monitor: once attached, pause for rhythm check
DON’T FORGET TO ATTACH OXYGEN, INSERT CANNULAE AND ATTACH SATS PROBE
- You will need to take blood to look for K+ derrangements that can cause cardiac arrest -
You’ve attended a cardiac arrest call and the ECG shows VF - what do you do?
VF is a shockable rhythm
1 shock followed by CPR for 2 mins
After 2 mins another rhythm check is performed
3 shocks have been given to a cardiac arrest patient - what drugs should be given at this point?
1mg adrenaline: 1:10,000 IV
3mg amiodarone IV
Done whilst continuing CPR
Give another 1mg adrenaline after alternate shocks
Give 150mg more amiodarone after a total of 5 shocks
Reversible causes of cardiac arrest
4 x H
- Hypoxia
- Hypovolaemia
- Hypokalaemia/ hyperkalaemia (important to take blood to assess this)
- Hypothermia
4 x T
- Thrombosis
- Tension pneumothorax
- Tamponade
- Toxins
How would management of a patient in cardiac arrest be different if they were in a non-shockable rhythm?
After a rhythm check is done that confirms the rhyhm is non-shockable
Continue CPR at 30:2
Amiodarone is NOT given in non-shockable rhythms
Adrenaline IS given (1mg 1:10,000 IV)
When is adrenaline normally synthesised?
Synthesised from noradrenaline in the adrenal medulla (chromaffin cells)
*Patients who have had their adrenal glands removed still produce adrenaline from sympathetic chains around the aorta*
Mechanism of action of adrenaline
Alpha and beta adrenoceptor agonist
With regards to cardiac arrest it increases coronary and cerebral perfusion via effects on the alpha receptors - causes vasoconstriction
Cautions of using adrenaline
- Ischaemic heart disease
- Cerebrovascular disease
- DM
- HTN: risk of cerebral haemorrhage
- Hyperthyroidism
- Hypokalaemia: adrenaline causes K+ to enter cells
- Ring blocks : do not use adrenaline, can cause necrosis
BUT remember the above do not apply to cardiac arrest… can’t do much harm if patient is in cardiac arrest
Most common cause of PEA?
Hypoxia secondary to respiratory failure
Explain how a PE causes PEA
Massive saddle PE
a) Prevents blood leave the right ventricle because it is blocking the way
b) The left side of the heart is receiving no blood from the lungs because of the PE
Meaning the blood is trying to pump but there’s nothing in it to pump
Why is there a risk of severe hypertension when beta blockers and adrenaline interact?
Adrenaline attempts to compete with the b-blocker and we end up with unopposed alpha effects and mainly vasoconstriction
Normally adrenaline would cause a bit of vasodilation - in the absence of a beta-blocker, a systemic dose of epinephrine does not have much effect on mean blood pressure because it has both alphaadrenergic effects (producing vasoconstriction) and beta-adrenergic effects (producing vasodilation).
B-blockers mean adrenaline causes excessive vasoconstriction leading to severe HTN
Mechanism of action of amiodarone
Class III antiarrhythmic - blocks K+ channels
- Used to disrupt irregular electrical activity by prolonging the duration of the cardiac action potential
Multiple anti-arrhythmic actions across all four groups
- Prolongs cardiac action potential and delays refractory period
- Inhibits K+ channels involved in repolarisation
Challenges of amiodarone
- Poorly orally absorbed
- Large volume of distribution
- Extremely long half life: takes many weeks to reach steady state so it is given in different doses over a number of weeks, once stopped takes a long time to be eliminated
Side effects of amiodarone
Most term side effects are long term
- Gastrointestinal disturbances – constipation, nausea, vomiting, taste disturbance
- Corneal microdeposits – reversible on withdrawal of treatment, associated with night glare, if vision impaired or optic neuritis/neuropathy develops amiodarone must be stopped to prevent blindness
- Hypothyroidism – prevents conversion of T4 to T3 resulting in hypothyroidism requiring replacement with thyroxine
- Hyperthyroidism – high iodine content, can cause a destructive thyroiditis leading to release of preformed thyroid hormones and refractory thyrotoxicosis
- Skin reactions – photosensitive skin rashes and blue-grey discolouration
- Hepatotoxicity – severe LFT abnormalities or clinical signs of liver disease require discontinuation of treatment
- Progressive pneumonitis and lung fibrosis – should be suspected if new onset SOB or cough
Proarrhythmic effects
Peripheral neuropathy/myopathy – reversible with withdrawal of treatment
Short term
- Bradycardia
- Heart block
>> Again in cardiac arrest, we don’t worry about side effects because patient already dead <<
What monitoring would you arrange for a patient commencing amiodarone?
TFT and LFT should be checked before treatment and every 6 months
Check potassium levels and chest x-ray before treatment
With IV use ECG monitoring must be available
Amiodarone contra-indications
- Severe cardiac conduction disturbances (unless pacemaker fitted)
- Thyroid dysfunction
- Iodine sensitivity
- Severe respiratory failure – amiodarone causes fibrosis
- Circulatory collapse
Amiodarone side effects
What do we do BEFORE we give a carotid sinus massage?
Listen for a bruit
Does the patient have a plaque that we could dislodge?
What is the first way to try and terminate a supraventricular tachycardia?
Vagal manoeuvres
- Carotid sinus massage: works on the baroreceptors at the bifurcation of the common carotid artery which control BP and HR by measuring degree of stretch in the vessels. Results in reduction in HR and BP >> performed by applying pressure over the carotid pulse for 5-10 seconds >> continuous ECG nonitoring
- Valsalva manoeuvre: forced exhalation against a closed airway, performed for 15-20 seconds causing fluctuations in HR and BP due to altering venous return
How does adenosine work?
IV adenosine has potent effects on the SA node inducing sinus bradycardia and slows impulse conduction through the AV node with no effect on conduction through the ventricles
Used for emergency management of SVT for rapid conversion back to sinus rhythm
Works on adenosine receptor - binding promotes opening of adenosine sensitive K+ channels and increased K+ efflux out of myocardial cells - cells become hyperpolarised and slows the rate of the pacemaker potential
Bolus of adenosine lasts 20-30 seconds
How many doses of adenosine are given before giving for senior help?
3
Adenosine contraindications
- Asthma/COPD
- Decompensated heart failure
- Long QT syndrome/AV block/sick sinus syndrome
- Severe hypotension
- Many cautions associated with cardiac disease
Adenosine side effects
- Side effects are common but last less than 1 minute.
- Arrhythmias, chest discomfort/pain, dizziness, dyspnoea, flushing, headache, hypotension, apprehension, sweating, metallic taste, blurred vision, nausea/vomiting, cardiac arrest, apnoea, loss of consciousness
- Important when giving adenosine: give it QUICKLY! It has such a short half life that it can dissipate before it hits the AV node
Patient has tachycardia, they are stable - what is the first thing to consider?
Is the QRS broad or narrow?
What is pre-excited AF?
Pre-excitation refers to early activation of the ventricles due to impulses bypassing the AV node via an accessory pathway
Management for a regular, narrow complex tachycardia
- Vagal manoeuvres
- Adenosine 6mg rapid IV bolus followed by flush into central vein
> If no effect give 12mg
> If no effect give 12mg
If sinus rhythm not achieved seek expert help
Vagal manoeuvres or adenosine will terminate almost all AVNRT or AVRT within seconds. Termination of a regular narrow-complex tachycardia in these ways identifies it as being AVNRT or AVRT. Failure to terminate a regular narrow-complex tachycardia with adenosine suggests an atrial tachycardia such as atrial flutter (unless the adenosine has been injected too slowly or into a small peripheral vein).
Adult tachycardia ALS algorithm revision
What is a fluid challenge?
Consists of 500ml of 0.9% NaCl or 500ml Hartmann’s given over 15mins
Called a challenge because it is a way to see whether the patient with haemodynamic compromise will benefit from further fluid replacement
What do U waves on an ECG represent?
Thought to represent repolarisation of Purkinje fibres
Prominent U waves (>1-2mm) = hypokalaemia
Hypokalaemia is shown as what on an ECG?
Prominent U waves and flattening of T wave
What is given to patients with bradycardia + adverse features?
Atropine - 500mcg IV
Repeat to a maximum of 3mg
Options for patients with bradycardia (other than atropine)
Transcutaneous pacing
Isoprenaline
Adrenaline
Dopamine
Aminophylline
What is given if a bradycardia is due to beta-blockers or calcium channel blockers?
Glucagon
Glucagon increases HR and contractility via a mechanism separate to catecholamines
How does atropine work?
Muscarinic antagonist
Muscarinic receptors are key within the parasympathetic NS
Blocking the muscarinic receptors reduces the effect of the vagus nerve and therefore increases SA node firing and increases HR
Side effects of atropine
Anticholinergic at the muscarinic receptor
- 👁 Eyes (pupillary dilatation): blurred vision, mydriasis, angle closure glaucoma
- 💩 GI tract (decreased motility/secretions/tone): constipation, abdominal distension, nausea, vomiting, dysphagia
- 🫁 🫀CVS (increased HR, contractility, BP): tachycardia, palpitations, angina, hypertension, arrhythmias
- 💦 Secretions (decreased sweat/salivary gland secretion): dry mouth, anhidrosis, thirst, increased body temperature
- 💦🌕 Urinary tract (decreased detrusor function and increased sphincter tone): urinary retention,
- 🧠 CNS: confusion, hallucination
Just think of everything that would happen when sympathetic NS is activated
Contraindications of atropine
- GI: obstruction, paralytic ileus, pyloric stenosis, severe ulcerative colitis, toxic megacolon
- Urinary tract: bladder outflow obstruction, prostatic enlargement, retention
- Myasthenia gravis: atropine has anticholinergic effects and we need all the ACh we can get
Atropine + phenylepherine = ?
Severe HTN
Phenylepherine is an alpha-1 antagonist
Where is IM adrenaline given in anaphylaxis?
Anterolateral aspect of the middle third of the thigh
Mechanism of action of LAs
Block the Na+ gated ion channels that depolarise the neuron
LAs progressively interrupt Na+ channel mediated depolarisation until nerve conduction stops - when >90% Na+ channels blocked
Fibre type relating to sensitivity to local anaesthetics
How many nodes of Ranvier must be blocked for LA to have an effect?
3 consecutive nodes - if not, conduction can jump and bypass the blockade
The closer the pHa of local anaesthetic to physiological pH means what?
Faster onset
Amide LAs generally have a faster onset compared to esters
What is pKa?
pKa is the pH at which the ionised and non-ionised forms are equal
•LAs in solution exist in equilibrium between basic uncharged (non-ionised) form (LA), which is lipid soluble and a charged (ionised) form (LAH+), which is water soluble
Implications of pKa relating to local anaesthetic
•LAs with high pKa will be more ionised at physiological pH so their speed of onset of anaesthesia will be slower
High pKa = needs a higher pH to dissociate from H+ ions
More ionised = attached to H+ ions
More ionised = more water soluble
More ionised = slower onset but more effective because a higher pKa means more re-ionisation within the cell meaning the drug cannot then leave the neuron
Explain why, based on pH, LAs do not work as well in infected or injured tissue
Infected/ inflamed tissue = lower pH
Lower pH = more LA is ionised meaning it cannot enter neurons
Less LA in neurons = less effective
Why is plasma 1/2 life of ester-linked LAs short?
They are rapidly broked down by plasma cholinesterase
Outline the typical sequence used in GA
Pre-medication
Induction
Muscle relaxation + intubation
Maintenance of anaesthesia
Analgesia
Reversal
Stages of GA
Stage 1 - analgesia: consciousness retained
Stage 2 - excitation: excitation with delirium, respiration rapid and irregular, frequent eye movements, increased pupil diameter, amnesia
Stage 3 - loss of consciousness: split into 4 planes
Plane 1: decreased eye movements and pupil constriction
Plane 2: loss of corneal reflex
Plane 3 and 4: increasing loss of pharyngeal reflex, progressive decrease in thoracic breathing and muscle tone
Stage 4 - medullary depression: loss of spontaneous respiration and progressive depression of cardiovascular reflexes, no eye movement, requires CV support
How does inhalational anaesthesia work?
Not precisely known…
Idea is that when inhalational agents dissolve in the lipid bilayer the ion channel distorts and impairs synaptic transmission
How do etodimate, propofol and thiopental work?
Enhance activity at GABA-A receptors
Potent sedatives but weak muscle relaxants
How do sevoflurane, isoflurane and desflurane work?
Enhance activity at GABA-A receptors
Enhance activity at glycine receptors
Inhibit NMDA glutamate receptors
Potent sedatives and potent muscle relaxants
What is minimum alveolar concentration?
Measure of potency
Minimum alveolar concentration at which 50% of the population will fail to respond to a single noxious stimuli e.g. frst surgical incision
Used to compare potency of inhaled anaesthetics
Example NO MAC = 104% - meaning there needs to be a 104% conc. in the alveoli to cause anaesthesia… in other words it never will
Discuss blood gas coefficients
Measure of inhaled anaesthetic within the blood
The lower the blood:gas coefficient the faster the induction and the faster the recovery e.g. NO and desflurane
The higher the blood:gas coefficient the slower the induction and slower the recovery e.g. isoflurane and halothane
Nitrous oxide
Gaseous anaesthetic not potent enough to be used alone
Used in combination with other drugs to allow a reduction in dose of other drugs
Used for anaesthetic maintenance
Also used in sub-anaesthetic concentrations for analgesia - ENTONOX (50:50 NO:oxygen)
Why are isoflurane and desflurane not used for induction of anaesthesia?
Unpleasant and cause patients to hold their breath
Unwanted effects of inhaled anaesthetics
Types of IV anaesthetics
Etomidate
Ketamine: rarely used for this purpose
Propofol
Thiopental
IV anaesthetics are given for induction and then replaced by inhaled anaesthetics for longer-term maintenance
What is thiopental?
Barbiturate
Rapidly diffuses into CNS due to lipid solubility and mainly in un-ionised state at body pH
Metabolised in the liver
Up to 30% can remain in the body at 24hrs causing a hangover effect
Propofol
Does not accumulate
Continuous infusion can be used for total IV anaesthesia or for sedation of adults in ICU
Has largely replaced thiopental as the main induction agent
More rapid recovery and less hangover effect than occurs with thiopental
Metabolised by 1st order kinetics
Etomidate
Rapid onset following IV injection
Duration is 6-10mins with minimal hangover
Less effect on CV system (causes less hypotension) so is preferred in shocked patients
Not used for continuous infusion because causes adrenal toxicity
Which GA is preferred in shocked patients?
Etomidate - causes less hypotension
Which GA is toxic to adrenals?
Etomidate
How do neuromuscular blockers work?
Block transmission through NMJ at nicotonic receptors thus decrease skeletal muscle tone
Examples of neuromuscular blockers
Non-depolarising = CUR not deep, curm down
- Atracurium
- Cisatracurium
- Mivacurium
- Pancuronium
- Rocuronium
- Vecuronium
Depolarising = its deep, it sux
•Suxamethonium
Suxamethonium lasting a very prolonged period of time… why?
Suxamethonium is hydrolysed by pseudocholinesterase
Some patients are genetically deficient in pseudocholinesterase meaning they cannot break suxamethonium down
How can neuromuscular block be reversed?
Anticholinesterases e.g. neostigmine
Atropine is given before neostigmine to prevent bradycardia/ excessive salivation caused by stimulation of muscarinic receptors
