9-15th August Flashcards
(113 cards)
1
Q
How much does a large square represent on an ECG?
A
0.2 seconds
2
Q
View of the heart from each lead?
A
- V1 and V2 septal view of the heart
- V3 and V4 anterior view of the heart
- V5 and V6 lateral view of the heart
- Lead I: lateral view
- Lead II and III: inferior views
- aVR and aVL lateral view
- aVF: inferior view
3
Q
What is the normal HR?
A
Between 60-100bpm
4
Q
How to calculate HR?
A
- 300/number of large squares R-R interval
- if irregular, count number QRS complexes x6 [as trace normally 10s long]
5
Q
Cardiac axis
A
- lead II normally most positive
- lead I left axis deviation
- lead III right axis deviation
6
Q
How long should PE interval be?
A
120-200ms [2-5 large squares]
7
Q
What is a heart block?
A
Prolonged PR interval over 0.2s
8
Q
Types of heart block?
A
- Prolonged PR interval over 0.2s suggests first-degree heart block [AV block]
o Second-degree heart block [type 1] also known as Mobitz type 1 AV block, or Wenckebach phenomenon: progressive prolongation PR interval until atrial impulse not conducted and QRS complex dropped
o Second-degree heart block [type 2]: Mobitz type 2 AV block. Consistent PR interval duration with intermittently dropped QRS complexes due to failure of conduction. Intermittent dropped QRS complexes typically follows a repeating cycle of every 3rd or 4th P wave
o Third-degree heart block: no electrical communication between the atria and ventricles due to a complete failure of conduction.
9
Q
Cause of shortened PR interval?
A
o P-wave originate somewhere closer to the AV node and so conduction takes less time
o Atrial impulse getting to the ventricle by a faster shortcut instead of conducting slowly across the atrial wall. There is an accessory pathway and can be associated with a delta wave. Delta wave found in Wolff Parkinson White syndrome and includes a slurred upstroke of the QRS complex.
10
Q
Classify a broad vs narrow QRS complex
A
- Width can be narrow [<0.12 seconds] or broad [>0.12]:
o Narrow: well-organised and syndronised ventricular depolarisation
o Broad: abnormal depolarisation for example if ventricular ectopic
11
Q
Height in QRS complexes
A
- Height can be small or tall:
o Small: less than 5mm in limb leads, or 10mm in chest leads
o Tall: imply ventricular hypertrophy
12
Q
Morphology of a QRS complex
A
-Morphology:
o Delta wave in WPW [though also needs tachyarrhythmias and Delta wave for Dx]
13
Q
Summarise QRS findings on an ECG
A
Width can be narrow [<0.12 seconds] or broad [>0.12]:
o Narrow: well-organised and syndronised ventricular depolarisation
o Broad: abnormal depolarisation for example if ventricular ectopic
Height can be small or tall:
o Small: less than 5mm in limb leads, or 10mm in chest leads
o Tall: imply ventricular hypertrophy
Morphology:
o Delta wave in WPW [though also needs tachyarrhythmias and Delta wave for Dx]
14
Q
Q-wave pathology
A
- Isolated Q waves can be normal
- Pathological Q wave is >25% the size of the R wave that follows it or >2mm in height and >40ms in width. Evidence of previous MI.
15
Q
ST segment abnormalities
A
- Part of the ECG between the end of the S wave and the start of the T wave
- Healthy, it should be isoelectric line
- ST-elevation is significant when it is greater than 1mm [1 small square] in 2 or more contiguous limb leads or over 2mm in 2 or more chest leads -> commonly caused by acute MI
- ST depression of over 0.5mm in 2 or more contiguous leads indicated myocardial ischaemia
16
Q
What are tall T waves associated with?
A
- Tall T waves is over 5mm in the limb leads AND over 10mm in the chest
- Associated with hyperkalaemia [“tall tented T waves”] and hyperacute STEMI
17
Q
What would inverted T waves represent?
A
o Normally inverted in V1 and inversion in lead III is a normal variant
o Sign of variety of conditions including ischaemia, bundle branch bocks [V4-V6 in LBBB, V1-V3 in RBBB], PE, LVH [lateral leads], hypertrophic cardiomyopathy [widespread], general illness
o Around 50% ITU patients have some evidence of T wave inversion
18
Q
Cause of biphasic and flattened T waves
A
- Biphasic T waves indicated ischaemia and hypokalaemia
- Flattened T waves -> may represent ischaemia or electrolyte imbalance-
19
Q
What do U-waves represent?
A
U waves are not a common finding.
The U wave is a > 0.5mm deflection after the T wave best seen in V2 or V3.
These become larger the slower the bradycardia – classically U waves are seen in various electrolyte imbalances, hypothermia and secondary to antiarrhythmic therapy (such as digoxin, procainamide or amiodarone).
20
Q
First-degree heart-block pathology
A
Impulse that conducts from atria to the ventricles through the AVN is delayed and travels slower than normal
21
Q
Common causes of AVN block
A
AV node disease Enahnced vagal tone [e.g. athletes] Myocarditis Acute MI Electrolyte disturbances Medications
22
Q
Which medications can cause 1st degree heart block?
A
CCB Beta-blockers Cardiac glycosides Cholinesterase inhibitors Digitalis
23
Q
When do tall T-waves typically present?
A
Typically in the hyper-acute period [3-30 minutes after onset]. In reality, rarely seen as ECG recordings typically later with ST elevation being more comonly noted.
24
Q
Which leads have inverted T waves?
A
aVR and V1 T waves
25
Types of ECG rhythms
Sinus = regular rhythm
Regular irregular = ectopic
Irregularly irregular = AF
26
Rates of the nodes?
SAN has rate 70/80
AVN rate of 60s
Purkinje rate of 50s
Myocytes rate of 30
27
RBBB definition on ECG
- QRS duration > 120ms
- RSR’ pattern in V1-3 (“M-shaped” QRS complex)
- Wide, slurred S wave in lateral leads (I, aVL, V5-6)
28
LBBB definition
- QRS duration > 120ms
- Dominant S wave in V1
- Broad monophasic R wave in lateral leads (I, aVL, V5-6)
- Absence of Q waves in lateral leads
- Prolonged R wave peak time > 60ms in leads V5-6
29
Tx in ACS
Tx in ACS
- GTN spray -> reduce pre-load and afterload
- PCI referral [some CI to this, and thrombolysis]
- Problem in patients with arrhythmias cause deaths in patients [VT can lead to this], or cardiogenic shock
30
Monomorphic VT
Looks like scribbles
31
Polymorphic VT
Scirbbles with dip in middle
| Tx with magnesium
32
Normal ranges on an ABG
```
pH: 7.35 – 7.45
PaCO2: 4.7 – 6.0 kPa || 35.2 – 45 mmHg
PaO2: 11 – 13 kPa || 82.5 – 97.5 mmHg
HCO3–: 22 – 26 mEq/L
Base excess (BE): -2 to +2 mmol/L
```
33
Definition of hypoxia
<10kPa
34
Definition of severe hypoxia
<8kPa
35
Definition of type 1 respiratory failure
Hypoxaemia [<8kPa] with normocapnia [<6kPa]
36
Why does type 1 respiratory failure occur?
It occurs as a result of ventilation/perfusion (V/Q) mismatch; the volume of air flowing in and out of the lungs is not matched with the flow of blood to the lung tissue. As a result of the VQ mismatch, PaO2 falls and PaCO2 rises. The rise in PaCO2 rapidly triggers an increase in a patient’s overall alveolar ventilation, which corrects the PaCO2 but not the PaO2 due to the different shape of the CO2 and O2 dissociation curves. The end result is hypoxaemia (PaO2 < 8 kPa /60mmHg) with normocapnia (PaCO2 < 6.0 kPa / 45mmHg).¹
37
Examples of VQ mismatch
* Reduced ventilation and normal perfusion (e.g. pulmonary oedema, bronchoconstriction)
* Reduced perfusion with normal ventilation (e.g. pulmonary embolism)
38
Define type 2 respiratory failure
Type 2 respiratory failure involves hypoxaemia (PaO2 is <8 kPa / 60mmHg) with hypercapnia (PaCO2 >6.0 kPa / 45mmHg). It occurs as a result of alveolar hypoventilation, which prevents the patient from being able to adequately oxygenate and eliminate CO2 from their blood.
39
When can hypoventilation occur?
Hypoventilation can occur for a number of reasons including:
• Increased resistance as a result of airway obstruction (e.g. COPD).
• Reduced compliance of the lung tissue/chest wall (e.g. pneumonia, rib fractures, obesity).
• Reduced strength of the respiratory muscles (e.g. Guillain-Barré, motor neurone disease).
• Drugs acting on the respiratory centre reducing overall ventilation (e.g. opiates)
40
What suggests acidosis is caused by respiratory, what suggests it's caused by metabolic problems?
Caused by either CO2 [respiratory] or HCO3- [metabolic].
41
Go through pH, CO2 and HCO3- values in patient with: respriatory acidosis, respriatory alkalosis, and each of these with metaoblic compensation
see table
42
Underlying biochemistry with ABGs
CO2 + H20 <=> H2CO3 <=> HCO3- + H+
43
pH, HCO3- and CO2 in metaoblic acidosis, alkalosis, with and without respiratory compensation
see table
44
What do base excess levels represent?
correlates to high level of HCO3-
45
Rate of compensation in respiratory versus metabolic disorders
Respiratory
- quickyl due to increased/decreased alveolar ventilation
Metaoblic
- takes few days to occur, so can assume the respriatory derangement has been ongoing for a couple of days if not more
46
Clear and simple: respriatory acidosis
low pH, high CO2
47
Causes respiratory acidosis
Respiratory depression [e.g.] opiates, Guillain-Barre paralysis, asthma
48
Clear and simple: respriatory alkalosis
high pH, low CO2
49
Causes of respiratory alklaosis
Excessive alveolar ventilation
- anxiety
- pain increasing RR
- hypoxia
- pulmonary embolism
- pneumothorax
- iatrogenic
50
Pathology og metabolic acidosis
1. Increased acid production or acid ingestion
| 2. Decreased acid excretion or rate of gastrointestinal and renal HCO3- loss
51
ABG characteristics metabolic acidosis
Low pH, low HCO3-, low BE
52
What is the anion gap?
Derived variable mainly for metabolic acidosis to determine the presence of unmeasured anions
53
What does the anion gap work out?
1. Work out whether metabolic acidosis is due to increased acid production or ingestion
2. Or, decreased acid excretion or loss of HCO3-
54
What is the anion gap formula?
Na+ - [Cl- + HCO3-]
55
What might cause an increase acid production or ingestion?
- Diabetic ketoacidosis [increased production]
- Lactic acidosis [increased production]
- Aspirin overdose [ingestion of acid]
56
What might cause a decrease anion gap?
- Gastrointestinal loss of HCO3- [e.g. diarrhoea, ileostomy, proximal colostomy]
- Renal tubular acidosis [retaining H+]
- Addison's disease [retaining H+]
57
Characteristics of metabolic alkalosis on ABG
Increased pH, increased HCO3-, increased BE
58
Causes of metabolic acidosis
- GI loss of H+ ions [e.g. vomiting, diarrhoea]
- Renal loss of H+ ions [e.g. loop diuretics, heart failure, nephrotic syndrome, cirrhosis, Conn's syndrome]
- Iatrogenic [e.g. addition of excess alkali such as milk-alkali syndrome]
59
What would mixed respriatory and metabolic acidosis/alkalosis look like?
Either:
- acidosis: low pH, high CO2, low HCO3- in cardiac arrest or multi-organ failure
- alkalosis: high pH, low CO2, high HCO3- in liver cirrhosis in addition to diuretic use, hyperemesis gravidarum, excessive ventilation in COPD
60
How does hyperventilation lead to perioral and peripheral parasthesia?
Hypocalcaemia
- As blood plasma becomes more alkalotic, the concentration of freely ionised calcium decreases
- Because both hydrogen ions and calcium are bound to serum albumin, when blood becomes alkalotic, the bound hydrogen ions dissociate from albumin, freeing up the albumin to bind with more alcium and thereby decreasing the freely ionised portion of total serum calcium leading to hypocalcaemia
- This hypocalcaemia related to alkalosis is responsible for the paraesthesia often seen with hyperventilation
61
2. Which of the following is a cause of T2 respiratory failure? PE, MND, or pulmonary oedema?
MND
- Reduced oxygen with increased CO2 due to alveolar hypoventilation
- Can occur due to number of reasons including increased resistance as a result of airway obstruction [e.g. COPD], reduced compliance of the lung tissue/chest wall [e.g. pneumonia/rib fractures/obesity], reduced strength of the respiratory muscles [e.g. GBS/MND], drugs acting on the respiratory centre reducing overall ventilation [e.g. opiates]
- Type 1 due to V/Q mismatch: reduced ventilation and normal perfusion seen in pulmonary oedema, bronchoconstriction, reduced perfusion with normal ventilation e.g. pulmonary embolism
62
You are called to see a 54 year old lady on the ward. She is three days post-cholecystectomy and has been complaining of shortness of breath. Her ABG is as follows:
```
pH: 7.49 (7.35-7.45)
pO2: 7.5 (10–14)
pCO2: 3.9 (4.5–6.0)
HCO3: 22 (22-26)
BE: -1 (-2 to +2)
Other values within normal range
```
1. What does ABG show?
2. DDx
1. T1 respiratory failure with accompanying alkalosis, likely due to patient high RR
2. PE, pneumonia, asthma, pulmonary oedema, severe atelectasis
63
A 75 year old gentleman living in the community is being assessed for home oxygen. His ABG is as follows:
```
pH: 7.36 (7.35-7.45)
pO2: 8.0 (10–14)
pCO2: 7.6 (4.5–6.0)
HCO3: 31 (22-26)
BE: +5 (-2 to +2)
Other values within normal range
```
1. ABG demonstrate?
2. What would you do?
1. This is a compensated respiratory acidosis.
This does not represent acute pathology.
Rather it reflects a compensation for a chronic respiratory acidosis secondary to chronic pulmonary disease.
Note this is an acidosis, not an acidaemia (pH normal, but only due to compensatory mechanisms: the high bicarbonate).
2. Nothing acutely as this man does not meet the criteria for long-term oxygen therapy (LTOT).
- Lifestyle advice and smoking cessation of necessary.
LTOT criteria are:
- PaO2 less than 7.3 kPa when stable.
- OR…
- PaO2 greater than 7.3 and less than 8.0 kPa when stable AND with any of:
- Secondary polycythaemia
- Peripheral oedema
- Nocturnal hypoxaemia
- Pulmonary hypertension
64
A 64 year old gentleman with a history of COPD presents with worsening shortness of breath and increased sputum production.
```
pH: 7.21 (7.35-7.45)
pO2: 7.2 (10–14)
pCO2: 8.5 (4.5–6.0)
HCO3: 29 (22-26)
BE: +4 (-2 to +2)
Other values within normal range
```
1. What does ABG show?
2. How much O2 would you give this man?
1. T2 respriatory failure with compensated acidosis
2. Oxygen administration in this group is a complicated issue. 100% oxygen makes subsets of COPD patients retain CO2, decreasing respiratory drive and worsening hypoxia and hypercapnia.
65
A 21 year-old woman presents feeling acutely lightheaded and short of breath. She has her final university exams next week.
```
pH: 7.48 (7.35-7.45)
pO2: 12.1 (10–14)
pCO2: 3.5 (4.5–6.0)
HCO3: 22 (22-26)
BE: +2 (-2 to +2)
Other values within normal range
```
1. ABG shwo and DDx?
2. Most likely Dx?
3. What to r/o
1. This is a respiratory alkalaemia
Differential diagnosis:
Pulmonary disease
Hypermetabolic states (e.g. infection or fever)
Pain
Anxiety hyperventilation
2/3. Anxiety
Based on the history, anxiety hyperventilation is the most likely cause here. However, it is very important to have considered the other options, in particular and to have ruled out a primary respiratory pathology or infection.
In the anxious patient who is short of breath and persistently tachycardic have you thought of PE?
66
A 32 year-old man presents to the emergency department having been found collapsed by his girlfriend.
```
pH: 7.25 (7.35-7.45)
pO2: 11.1 (10–14)
pCO2: 3.2 (4.5–6.0)
HCO3: 11 (22-26)
BE: -15 (-2 to +2)
Potassium: 4.5
Sodium: 135
Chloride: 100
Other values within normal range
```
1. ABG show
The anion gap is the difference between primary measured cations (sodium and potassium) and the primary measured anions(chloride and bicarbonate). It is calculated by subtracting the concentrations of chloride and bicarbonate (anions) from the concentrations of sodium and potassium (cations):
Anion gap = ([Na+] + [K+]) − ([Cl−] + [HCO3−])
Reference range usually 7–16 mEq/L (but varies between hospitals, some using 3-11)
Potassium is commonly left out of the equation as potassium concentrations, being very low, usually have little effect on the gap. This leaves the following equation:
Anion gap = [Na+] − ([Cl–] + [HCO3−])
Anion gap = ([Na+] + [K+]) − ([Cl−] + [HCO3−]) = 28.5
Normal range is 7 – 16.
N.B. Some analysers won’t include potassium in their calculations therefore for them >15 constitutes a raised anion gap.
Either way, this is a raised anion gap metabolic acidosis
The traditional mnemonic for the causes of a metabolic acidosis with raised anion gap is ‘MUDPILES’:
Methanol
Uraemia
Diabetic ketoacidosis (and alcoholic/starvation ketoacidosis)
Propylene glycol
Isoniazid
Lactate
Ethylene glycol
Salicylates
However, another way is to think about the mechanism of acidosis:
Excess production of acids
DKA, lactic acidosis (produced by poorly perfused tissues)
Ingestion of acids
Methanol, ethanol, ethylene glycol
Inability to clear acids
Renal failure
[/toggle title="What is the differential diagnosis for a metabolic acidosis with normal or decreased anion gap?" active="false"]
Loss of bicarbonate:
From the GI tract (diarrhoea or high-output stoma)
From the kidneys (renal tubular acidosis)
67
A 67 year-old man with a history of peptic ulcer disease presents with persistent vomiting.
```
pH: 7.56 (7.35-7.45)
pO2: 10.7 (10–14)
pCO2: 5.0 (4.5–6.0)
HCO3: 31 (22-26)
BE: +5 (-2 to +2)
Other values within normal range
```
1. WHat does ABG show?
2. DDx
This is metabolic alkalaemia
[/toggle title="What' s the differential diagnosis of this ABG picture?" active="false"]
Differential diagnosis of a metabolic alkalosis or alkalaemia:
```
Persistent vomiting
E.g. gastric outlet obstruction (the classic example is pyloric stenosis in a baby)
Hyperaldosteronaemia
Diuretic use
Milk alkali syndrome
Massive transfusion
```
68
A seventeen year-old girl presents to the emergency department after an argument with her boyfriend. He says that she took lots of tablets. She denies this. You persuade her to let you do an ABG:
```
pH: 7.46 (7.35-7.45)
pO2: 12.5 (10–14)
pCO2: 3.5 (4.5–6.0)
HCO3: 22 (22-26)
BE: +1 (-2 to +2)
Other values within normal range
```
A few hours later she says she feels increasingly unwell and is complaining of ringing in her ears. A repeat gas shows:
```
pH: 7.15 (7.35-7.45)
pO2: 11.0 (10–14)
pCO2: 3.2 (4.5–6.0)
HCO3: 9 (22-26)
BE: -18 (-2 to +2)
Other values within normal range
```
1. Dx
2. Mx
1. This is the classic picture of aspirin overdose.
There is an initial respiratory alkalosis due to central respiratory centre stimulation causing increased respiratory drive.
In the later stages a metabolic acidosis develops along side the respiratory alkalosis as a result of direct effect of the metabolite salicylic acid and more complex disruption of normal cellular metabolism
2.Presentation of aspirin overdose
```
Hyperventilation
Sweating
Nausea & vomiting
Epigastric pain
Tinnitus
Deafness
ARDS (rare)
Hypoglycaemia (children in particular)
Investigations in aspirin overdose
```
Plasma salicylate concentration (initial and repeats)
Paracetamol levels (always check in any case of poisoning by anything)
ABG
Urea and electrolytes
Renal failure (rare) sometimes other electrolyte imbalances
Chest x-ray
If dropping sats or any suspicion of ARDS (non-cardiogenic pulmonary oedema)
Management of aspirin overdose
ABCDE and supportive care
Gastric lavage within 1h of ingestion (although no evidence for mortality reduction)
Activated charcoal
Correct electrolyte abnormalities
In mild/moderate cases (plasma concentration 500-700mg/l)
Alkalinise urine
Give 225ml of 8.4% bicarbonate solution over 1hr
Ensure urine pH over 7.5 (use indicator paper)
Bicarbonate will increase any pre-existing hypokalaemia – so don’t let it happen
Additional boluses of bicarbonate to maintain alkalinisation
N.B. Acidosis increases salicylate transfer across the blood brain barrier
Monitor U+Es regularly
In severe cases (plasma concentrations >700mg/l)
Haemodialysis
Prognosis in aspirin overdose
Generally good with treatment.
69
A normally fit and well 11 year-old boy presents with diarrhoea and vomiting. He is complaining of non-specific abdominal pain. A venous blood gas shows:
```
pH: 7.12 (7.35-7.45)
pO2: 11.5 (10–14)
pCO2: 3.2 (4.5–6.0)
HCO3: 9 (22-26)
BE: -17 (-2 to +2)
Lactate: 4.0
Potassium: 5.5
Glucose: 22
Other values within normal range
```
1. Dx
2. Mx
- DKA
Priorities for management include fluid resuscitation, insulin administration and careful management of potassium levels. Click here for a page detailing this, and click here for DKA questions
70
A 22 year-old lady with a known history of asthma presents to the emergency department with difficulty in breathing. Her initial ABG on 15 litres of oxygen shows:
```
pH: 7.54 (7.35-7.45)
pO2: 10.0 (10–14)
pCO2: 3.2 (4.5–6.0)
HCO3: 24 (22-26)
BE: +0 (-2 to +2)
Other values within normal range
```
After initial treatment the nurse in resus calls you to review the patient. The nurse says that although the patient’s respiratory rate has come down slightly she is looking more unwell. Her repeat gas shows:
```
pH: 7.36 (7.35-7.45)
pO2: 9.8 (10–14)
pCO2: 5.0 (4.5–6.0)
HCO3: 22 (22-26)
BE: -2 (-2 to +2)
```
1. Mx
This patient has asthma, ongoing difficulty in breathing and a rising CO2 (the fact that it is in the normal range is irrelevant) .
This is an extremely worrying sign as it shows that the patient is tiring.
This patient should be managed in a high dependency area and closely monitored for further deterioration.
The management of acute asthma will be found on the respiratory sections of this website.
71
A 62 year-old woman with a history of diabetes and a long smoking history presents to the emergency department with worsening shortness of breath. On auscultation of the chest there are widespread crackles and you notice moderate ankle oedema. ABG shows:
```
pH: 7.20 (7.35-7.45)
pO2: 8.9 (10–14)
pCO2: 6.3 (4.5–6.0)
HCO3: 17 (22-26)
BE: -8 (-2 to +2)
Other values within normal range
```
- Dx?
Note that despite the low pH the pCO2 is also high.
This is a picture of a mixed respiratory and metabolic acidosis.
Given the history of diabetes and ankle swelling, renal failure is a unifying diagnosis with pulmonary oedema contributing to a respiratory acidosis whilst the failure to clear acids causes a metabolic acidosis.
72
Which biochemical test would you want to know in the first few minutes after arrival of any unconscious or semi-unconscious patient? Why important?
- Blood glucose: see if patient hypoglycaemic
73
How to give glucose to hypoglycaemic patient in/out of hospital?
- 10% glucose 5ml/kg standard infusion
| - If out the hospital -> shove chocolate into mouth [paramedics can give glucagon, but it takes minutes to work]
74
Why is temperature an important observation in an unconscious patient?
See if hypothermic
75
Levels of hypothermia
Bellow 35 mild
Moderate below 32
Severe below 28
76
How to Tx hypothermic patients?
- Passively warming blankets, room etc.
- Actively warming fluids/oxygen warmed, can even give NG tube and warmed IV fluids
- Extracorporeal membrane oxygenation in extreme circumstances
77
Eye part of the GCS
Eyes
- 1 = open
- 2 = to voice
- 3 = to pain
- 4 = no response
78
Verbal part of GCS
Verbal
- 1 = no response
- 2 = moans/intelligible
- 3 = nonsensical speech
- 4 = disoriented
- 5 = orientated and alert
79
Motor part of GCS
```
6 = follows commands
5 = localizes pain
4 = withdraws form pain
3 = decorticate flexion
2 = decerebrate extension
1 = no response
```
80
Ways of applying painful stimulus
- Typically, trapezius squeeze
- Applying supraorbital or rubbing the sternum
- Mandibular pressure often favoured
81
List of diagnosis for coma patient
1. Neurological
- ischaemic stroke
- intracranial haemorrhage
- SdH
- Tumour
- CNS infection like meningitis, meningococcal virus
2. Metabolic
- glycaemias
- natraemias
- hhypercalcaemia
- Addisonian crisis
- hypothyroidism
- uraemia
3. Diffuse brain dysfunction
- seizures
- alcohol intoxication
opioid toxicity
drug OD
- poisoning
hypothermia
- neuroleptic malignant syndrome
- serotonin syndrome
4. Psychiatric
- psychiatric coma
- malingering
5. Head injuries
- skull fractures
- all the haemorrhages
82
normal range of potassium
- 3.5-5, less than 3 significant hypokalaemia
83
Danger if potassium over 5
cardiac arryhtmias and death [if over 6 particulrly]
84
How to treat hyperkalaemia
- Give calcium -> salbutamol -> insulin/dextrose
85
treating opioid overdose
Naloxone hydrochloride IV
- 400 mcg initially
[then 800mcg up to 2 doses at 1 minute intervals]
86
routes for naloxone
- Would do IV -> IM [but can take 15m] -> interosseous
87
Risk of treating someone with naloxone if Tx successful
- Risk of acute withdrawal -> headaches, changes BP, rapid HR, sweating, nausea, vomiting, tremors
- Can give 200mcg slowly can give in increments if patient okay -> so don’t get up really quickly
- Patient will likely be respiratory acidosis
88
Where is the common place for an extradural haemorrhage to occur?
At temples:
| - middle meningeal artery
89
What typical presentation is seen in patients with an EdH?
Lucid interval
90
Tx for EdH and SdH
```
EdH = cranioplasty with a vein clamped etc.
SdH = burr hole
```
91
Risk for patients with SdH
Can cone if on anticoagulatns
92
Why are doctors concerned if patient has a Laport sctructure?
Patient difficult to intubate
93
What is subluxation?
o Subluxation -> quadriplegia -> driving without seatbelt. Can be breathing problem at C3/4. Christopher Reeve.
94
Sign of a basal skull fracture
```
o Blood and CSF leak
o Ear
o Nose
o Panda eyes
o Battle sign bleeding middle cranial fossa
```
95
NICE guidelines for a head CT with 1 hour
GCS < 13, GCS <15 at 2 hours after injury, susecpted skull fracture, sign basal skull fracure, post-traumatic seizure, focal neurological deficit, more than one episode of vomiting since head injury
96
NICE guidance for head CT within 8 hours
No risk factors present and on current anticoagulant Tx
97
Which area of the typically herniates through the brain?
Uncal area of the temporal lobe herniates through the tentorium -> dilated pupils
98
particular precaution to take for patient with a head injury
Full cervical spine immobilization should be attempted for people who have sustained a head injury and any risk factors for cervical spinal injury for example:
• Glasgow Coma Scale (GCS) less than 15 on initial assessment.
• Neck pain or tenderness.
• Focal neurological deficit.
• Paraesthesia in the extremities
99
How to prevent patient from aspirating in the CT scanner
- Using a suction device to remove vomit from airway
- Log roll patient in the CT scanner
- Further aspiration can be prevented by intubating patient
100
What are the indications for intubation
- Deterioration LOC
- Facial injuries: bleeding into airways
- Ventilationary insuffienacy [O2 below 10, CO2 6]
- Multiple fits
- agitation
101
Organs affected by paracetamol toxicity
- Liver is the principal organ affected
- Brain scan also be affected with confusion and disorientation [encephalopathy]
- Also, kidneys can be affected with reduction in urine, and kidney failure can occur
102
How long does it take for patients to be symptomatic with paracetamol poisoning?
After 24 hours
- nausea
- vomiting
- abdominal pain
- encephalopathy
103
poisonous metabolite generated from having paraetamol?
N-acetyl-p-benzoquinoneimine [NAPQI]
104
What can the body produce to nullify NAPQI?
Glutathione
105
how does NAC work?
Glutathione donor preventing NAPQI accumulation
106
RFs for low glutathione
Anorexics, alcoholics, P450 inducing drugs
107
How long does it take for paracetamol to buildup in the body?
Starts at 4 hours, peak at 8 hours
108
All patients should have which blood tests?
Serum paracetamol concentration
ALT/AST
Coagulation and INR
109
Examplee NAC drug
N-actyl cysteine
| - Parvolex
110
What should be given to patient if under 2 hours of having the OD?
Activated charcoal
111
If over 8 hours or staggered dose of paracetamol?
Acetylcystine infusion
112
What sad persons score?
Socring system to help evaluate risk or self-harm
- Sex
- Age
- Depression
- Previous suicide attemps
- Excessive alcohol
- Rational thinking loss
- Single
- Organised attempt
- No social support
- Stated future intent
113
What to do if patient if flushed and vomited after NAC infusion?
- Anaphylactoid reactions occur anywhere between 10-50% and are more likely to occur in patients with lower paracetamol ingestions (NAPQI appears to be protective). Typically, this reaction occurs after the first bag of NAC.
o Stop the infusion
o Treat with loratadine 10mg (2.5mg <12kg, 5mg <30kg) PO or promethazine 12.5 mg IV (0.25mg/kg)
o The NAC can then be recommenced once symptoms settle at half rate for 30 minutes and then recommenced as per normal protocol.
