ALS - Adult Flashcards
(103 cards)
1
Q
First line treatment for polymorphic VT (Torsades de Pointes)
A
Magnesium Sulphate 2g/10 minutes
2
Q
Indication for beta blockers?
A
- Narrow-complex regular tachycardias, if uncontrolled by vagal manoeuvres/adenosine (alternative - calcium channel blockers)
- AF/atrial flutter rate - when ventricular function preserved
3
Q
Atenolol dose?
A
5mg/ 5 minutes
4
Q
Adenosine - action?
A
Slows transmission across AV node
5
Q
Adenosine - indications?
A
Praroxysmal SVT with re-entrant circuits that include the AV node.
6
Q
Benefit of adenosine if not a re-entrant narrow-complex tachycardia?
A
Will slow ventricular response so can see atrial rhythm.
7
Q
Adenosine - dose?
A
6mg
8
Q
2nd line to adenosine?
A
Verapamil
9
Q
WPW - give adenosine?
A
Promote accessory pathway conduction -> dangerous ventricular response and rarely AF, if supra ventricular arrhythmia
10
Q
Amiodarone - indications?
A
- Stable monomorphic VT, polymor- phic VT and wide-complex tachycardia of uncertain origin.
- Paroxysmal SVT uncontrolled by adenosine, vagal manoeuvres or AV nodal blockade
- To control rapid ventricular rate due to accessory pathway conduction in pre-excited atrial arrhythmias.
- Unsuccessful cardioversion
11
Q
What causes hypotension associated with amiodarone?
A
Vasoactive solvents - benzyl alcohol/polysorbate 80.
Use aqueous to reduce risk?
12
Q
Peripheral or central veins for amiodarone?
A
Thrombophlebitis if peripheral
13
Q
Unstable bradycardia 1st line?
A
Atropine 500 mcg IV
14
Q
Why are we bad at spotting deterioration to CA in hospital?
A
Patients often have slow and progressive physiological deterioration, involving hypox- aemia and hypotension that is unnoticed or poorly managed by ward staff. Essentially - infrequent, late or incomplete vital signs assess- ments; lack of knowledge of normal vital signs values; poor design of vital signs charts; poor sensitivity and specificity of ‘track and trigger’ systems; failure of staff to increase monitoring or escalate care, and staff workload
15
Q
When should we consider a DNACPR?
A
If unlikely to survive or does not wish to have CPR.
16
Q
What do the guidelines suggest to improve in hospital CA recognition and management?
A
Appropriate levels of care for critically ill. Early warning systems - frequent obs. Clear and usable charts for the above. Clearly identified response plan for critical illness. Education/training. Empower the call for help. Identify DNACPR pts early. Audit.
17
Q
Commonest cause of SCD?
A
Coronary artery disease.
Non- ischaemic cardiomyopathy and valvular disease account for most other SCD events in older people
18
Q
Commonest cause of SCD in young people?
A
Inherited abnormalities (e.g. Brugada syndrome, hypertrophic cardiomyopathy), congenital heart disease, myocarditis and substance abuse
19
Q
How do you manage children/young people with symptoms of arrhyhmogenic syncope?
A
Specialist cardiology assessment, which should include an ECG and in most cases an echocardiogram and exercise test
20
Q
Characteristics of arrhythmic syncope?
A
Syncope in the supine position, occurring dur- ing or after exercise, with no or only brief prodromal symptoms, repetitive episodes, or in individuals with a family history of sudden death.
21
Q
What factors increase the risk of syncope being arrhythmic?
A
Non-pleuritic chest pain, palpitations associated with syncope, seizures (when resistant to treatment, occurring at night or precipitated by exercise, syncope, or loud noise) and drowning in a competent swimmer should raise suspi- cion of increased risk
22
Q
Signs of LQTS?
A
A family history of syncope or SCD, palpitations as a symptom, supine syncope and syncope associated with exercise and emotional stress are more common in patients with long QT syndrome (LQTS).
23
Q
What are the common causes of inexplicable drowning in competent swimmers?
A
LQTS or catecholaminergic polymoprhic VT.
NB - association between LQTS and seizure phenotype.
24
Q
Predictors of arrhythmic syncope in older patients?
A
If there is NO nausea and vomiting before syncope and ECG abnormalities is an independent predictor of arrhythmic syncope.
25
Rules for termination of resuscitation prehospitally?
The rule recommends termination when
there is no ROSC, no shocks are administered and EMS personnel do not witness the arrest.
Or 20 mins ALS, no ROSC, no reversible cause.
26
Rate of ventilation in an intubated patient?
10 breaths/minute
27
What is continuous Et CO2 monitoring useful for?
Quality indicator of CPR.
| Sign of ROSC if it increases.
28
How often do you rhythm check/give adrenaline?
- Rhythm check every 2 mins.
| - Adrenaline 1mg every 3-5 minutes. (in practice this is about once every two cycles, so after 2 shocks)
29
When do you give amiodarone and how much?
For Vf/pVT
300mg, after three shocks.
Can give another 150mg after 5 shocks.
30
What initial defibrillation shock levels are indicated in biphasic/pulsed biphasic shocks?
Biphasic: at least 150J.
| Pulsed biphasic: 120-150J.
31
Energy level for second and third shocks?
150-360J (biphasic)
32
How does the management of VT/VF differ in a witnessed arrest?
Three stacked shocks.
| Check for rhythm change/ROSC -> immediate chest compressions if has not worked.
33
When do you give adrenaline in a witnessed VT/VF arrest?
Do three shocks -> start compressions 2 minutes -> shock -> compressions 2 minutes -> shock -> then adrenaline.
34
When is the use of precordial thump appropriate? (And how deliver?)
Only when used without delay whilst awaiting the arrival of a defibrillator in a monitored VF/pVT arrest.
Using the ulnar edge of a tightly clenched fist, deliver a sharp impact to the lower half of the sternum from a height of about 20 cm, then retract the fist immediately to create an impulse-like stimulus
35
What are all drugs followed by?
20 ml flush of saline
36
Alternative to amiodarone?
Lidocaine 1mg/kg
37
PEA: define
Pulseless electrical activity - cardiac arrest in the presence of electrical activity (other than ventricular tach- yarrhythmia) that would normally be associated with a palpable pulse.
38
Pseudo-PEA?
Some mechanical myocardial contractions, but these are too weak to produce a detectable pulse or blood pressure.
39
4 Hs/4 Ts
Hypoxia
Hypotension
Hyperkalaemia/hypok/hyperm/hypom - metabolic disorders.
Hypothermia.
Thrombosis
Tension Pneumothorax
Tamponade (cardiac)
Toxins
40
What to check in asystole?
- Position of leads.
| P waves - can pace.
41
Treatment of hyperkalaemia, hypocalcaemia and CCB overdose?
Calcium chloride IV.
42
Most common rhythm in tension pneumothorax?
PEA
43
How would ultrasound be useful in CA?
To diagnose tamponade/other reversible causes e.g. PE/pneumothorax etc.
Also, to identify pseudo-PEA - low output cardiac states.
44
What might a pulse felt in the femoral triangle indicate?
Venous flow rather than arterial
45
Define end tidal carbon dioxide
Partial pressure of carbon dioxide at the end of an exhaled breath.
46
End tidal CO2 uses?
Tracheal tube placement, monitoring of ventilation rate, avoiding hyperventilation, monitoring compressions, identifying ROSC and prognosticating ROSC
47
eCPR?
Extracorporeal cardiopulmonary resuscitation- require vascular access and a circuit
with a pump and oxygenator and can provide a circulation of oxy-
genated blood to restore tissue perfusion.
48
Define monophasic and biphasic waveforms.
Biphasic defibrillators compensate for the wide variations in transthoracic impedance by electronically adjusting the waveform magnitude and duration to ensure optimal current delivery to the myocardium, irrespective of the patient’s size (impedance compensation
49
Levels of energy for biphasic waves?
First shock: 120J at least for RLB, and 150J for BTE. (ideally 150J)
Second and subsequent shocks: equivalent or escalating.
If pulsed: begin at 120-150
50
How does ICD affect electrode placement?
Place the electrode away from the device (at least 8cm) or use an alternative electrode position (anterior–lateral, anterior–posterior)
51
Define transthoracic impedence - when is it lowest?
Lowest at end-expiration.
52
Define PEEP - and how does asthma affect it?
Positive End Expiratory Pressure: (increases thoracic impedance). Asthma increases it (Auto-PEEP: gas trapping; might need higher defib levels)
53
Two types of biphasic waveforms?
Rectilinear biphasic (RLB) or biphasic truncated exponential (BTE)
54
What is a pulsed biphasic waveform?
The current rapidly oscillates between baseline and a positive value before inverting in a negative pat- tern.
55
Refractory VF vs refibrillation
Refractory VF: ‘fibrillation that persists after one or more shocks’
Refibrillation: recurrence of fibrillation, after initial termination.
56
Define cardioversion
Shock synchronised to occur with the R wave, rather than the T wave. Why? Can induce VF if shock in relative refractory period.
57
Define pacing and what responds to it
Block at or below the His-Purkinje level.
| Symptomatic bradycardia refractory to anti-cholinergic drugs/other2nd line tx
58
What energy levels do ICDs discharge at?
40J, 80J if subcutaneous.
59
What causes laryngeal airway obstruction?
Oedema from burns, inflammation, anaphylaxis.
60
What causes obstruction below the level of the larynx?
Excessive bronchial secretions, mucosal oedema, bronchospasm, pulmonary oedema or aspiration of gastric contents.
61
Stridor vs wheeze
Inspiratory stridor: obstruction at laryngeal level or above.
Expiratory wheeze: lowe airway problem
62
See-saw breathing?
Paradoxical chest/abdo: complete obstruction with respiratory effort.
63
What % O2 is delivered by a BVM?
21%
64
What % O2 is delivered by a BVM and 10litres o2?
85%
65
What % O2 is delivered by rescue breaths?
16%?
66
Gastric inflation - causes?
If the tidal volume or inspiratory flow is excessive -> increased airway pressure
67
Gastric inflation - causes?
If the tidal volume or inspiratory flow is excessive -> increased airway pressure.
Malalignment of head/neck and obstructed airway.
Incompetent oesophageal sphincter (all patients in cardiac arrest)/.
High airway inflation pressure.
68
Clinical assessment of tube placement?
Primary assessment includes observation of
chest expansion bilaterally, auscultation over the lung fields bilat-
erally in the axillae (breath sounds should be equal and adequate)
and over the epigastrium (breath sounds should not be heard).
Clinical signs of correct tube placement (condensation in the tube,
chest rise, breath sounds on auscultation of lungs, and inability to
hear gas entering the stomach) are not reliable.
69
Indications for surgical cricothyroidotomy
Extensive facial trauma or laryngeal obstruction caused by oedema or foreign material.
70
Vasopressin - what and mechanism
Naturally occurring antidiuretic hormone -> powerful vasoconstrictor -> stimulation of smooth muscle V1 receptors.
No chronotropic or ionotropic effects on the heart.
71
Amiodarone - moi?
Increases duration of action potential and refractory period in myocardium.
Effects: mild negative inotropic action and causes peripheral vasodilation through non-competitive alpha- blocking effects.
72
Amiodarone - indications?
refractory VF/pVT.
| Haemodynamically stable VT and other resistant tachyarrhythmias.
73
What causes hypotension with amiodarone?
More due to the solvent (polysorbate 80 and alcohol).
| Use PM101 - which uses a cyclodestrin instead
74
What are the adverse effects of amiodarone?
Hypotension and bradycardia.
If give concurrent with QT prolonging drugs -> arrhythmogenic.
Thrombophlebitis.
(prolonged oral use - abnormalities of thyroid function, corneal microdeposits, peripheral neuropathy, and pul- monary/hepatic infiltrates)
75
What is the alternative to amiodarone? MOI? Dosing?
Lidocaine.
Increases the myocyte refractory period. It decreases ventricular automaticity, and its local anaesthetic action suppresses ventricular ectopic activity.
Good for depolarisation arrhythmias (ischaemia, digitalis toxicity), but not rrhythmias occurring in normally polarised cells (e.g. atrial fibrillation/flutter).
100mg, followed by 50mg if necessary.
76
Lidocaine toxicity?
Paraesthesia, drowsiness, confusion and muscular twitching progressing to convulsions.
Can depress myocardial function, but less than amiodarone.
77
Normal magnesium range?
0.8-1.0 mmol/l.
78
How does hypomagnesaemia and hypokalaemia affect digoxin?
Increase myocardial digoxin uptake -? become toxic even at therapeutic levels.
79
What dose of Mg?
2g of 50% magnesium sulphate
80
Indications for calcium chloride?
Hyperkalaemia
Hypocalcaemia
Overdose of CCB.
(10ml 10% calcium chloride)
81
Indications for sodium bicarbonate?
Life threatening hyperkalaemia,
CA -> hyperkalaemia
Tricyclic overdose
(50 mmol/l or 1mmol/kg - Severe tissue damage may be caused by subcutaneous extravasation of concentrated sodium bicarbonate. The solution is incompatible with calcium salts as it causes the precipitation of calcium carbonate.)
82
Indications for fibrinolysis
PE suspected cause of CA. Continue CPR for 60-90 mins?
83
Adverse signs associated with peri-arrest arrhythmias?
Shock, syncope, heart failure, myocardial ischaemia,
84
What is fist pacing?
Serial rhythmic blows with the closed fist over the left lower edge of the sternum to pace the heart at a phys- iological rate of 50–70 bpm. Can be used if atropine is ineffective and transcutaneous pacing not immediatelyavailable.
85
What can cause the effect of adenosine to be exaggerated?
Dipyridamole or carbamazepine. Or denervated hearts.
86
Max dose amiodarone?
2g/day
87
Which beta-blocker is used in CA and why?
The intravenous dose of atenolol (beta1 ) is 5 mg given over
5 min, repeated if necessary after 10 min. Metoprolol (beta1 ) is
given in doses of 2–5mg at 5-min intervals to a total of 15mg.
Propranolol (beta and beta effects), 100 g kg−1 , is given slowly 12
in three equal doses at 2–3-min intervals.
Intravenous esmolol is a short-acting (half-life of 2–9min) beta-1 selective blocker - Iv loading dose 500 ug/kg, then infusion dose.
88
What was the PaRAMeDIC trial about?
Prehospital Randomised Assessment of a Mechanical Compression Device - LUCAS or control.
89
The CIRC trial?
Circulation Improving Resuscitation Care trial - Auto-Pulse.
90
What is ACD-CPR
Active compression-decompression CPR.
Hand-held device equipped with a suction cup to lift the anterior chest actively during decompression. Decreasing intrathoracic pressure during the decompression phase increases venous return to the heart and increases cardiac output and subsequent coronary and cerebral perfusion pressures dur- ing the compression phase.
91
ITD?
Impedance threshold device: valve that limits air entry into lungs during chest recoil between chest compressions; this decreases intrathoracic pressure and increases venous return to the heart.
Not recommended routinely.
92
Unstable patient with tachycardia?
Synchronised DC shock (up to 3)
| -> Amiodarone 300mg IV -> repeat shock -> amiodarone 900mg over 24 hours
93
Stable patient with tachycardia and broad, regular QRS?
VT: amiodarone 300mg -> 900mg.
| If previously
94
Stable patient with tachycardia and broad, irregular QRS?
```
Polymorphic VT (torsades des pointes- 2g magesium).
Or AF with bundle branch block: treat as for narrow complex (rate control with b blocker/dilitazem. If hf -> digoxin/amiodarone)
```
95
Stable patient with tachycardia and narrow, regular QRS?
Vagal manoeuvres -> 6mg adenosine, then 12, the 12 if unuccessful.
If not restored, consider atrial flutter - beta blocker.
96
Stable patient with tachycardia and narrow, irregular QRS?
Irregular Narrow Complex Tachycardia - ate control with b blocker/dilitazem. If hf -> digoxin/amiodarone.
If more than 48 hours - anticoagulant.
97
Bradycardia and adverse signs?
500mcg atropine IV.
| If not satisfactory response or risk of asystole then repeat dose OR pace.
98
Risk of systole in bradycardia?
Recent asystole
Mobitz II AV block
Complete
99
Risk of systole in bradycardia?
Recent asystole
Mobitz II AV block
Complete heart block with broad QRS
Ventricular pause of more than 3seconds.
100
Alternatives to atropine 500mcg IV dose?
Isoprenaline 5mcg IV
Adrenaline 2-10 mcg IV
Also: aminophylline, dopamine, glucagon (if betablocker/CCB overdose) or glycopyrolate.
101
Indications for calcium channel blockers and which?
- Stable regular narrow-complex tachycardias uncontrolled or unconverted by adenosine or vagal manoeuvres;
- To control ventricular rate in patients with AF or atrial flutter and preserved ventricular function.
Diltiazem and verapamil.
102
MOI of CCBs?
Slow conduction and increase refractoriness in the AV node.
103
Danger of giving a calcium channel blocker to ventricular tachycardia rather than atrial tachycardia?
Cardiovascular collapse.
