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A+E Flashcards

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1
Q

What are acid-base abnormalities?

A

Pathological changes in partial pressure of carbon dioxide or serum bicarbonate that typically produce abnormal arterial pH values.

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2
Q

What is defined as acidemia?

A

serum pH <7.35

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3
Q

What is defined as alkalaemia?

A

pH > 7.45

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4
Q

What is acidosis

A

Physiolocial processes that cause acid accumulation or alkali lossWh

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5
Q

What is alkalosis?

A

physiological processes that cause alkali accumulation or acid loss

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6
Q

What are the 4 categories of acid-base disorders?

A

Primary acid-base disturbances are defined as metabolic or respiratory based on clinical context and whether the primary change in pH is due to an alteration in serum HCO3− or in Pco2.

Metabolic acidosis = serum HCO3 > 26mmol/L
Metabolic alkalosis = serum HCO3 <22 mmol/L

Respiratory acidosis = Paco2 >6.0 kPa (hypercapnia)

Respiratory alkalosis = Paco2<4.6 kPa (hypocapnia)

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7
Q

What are some causes of metabolic acidosis?

A

Increased acid production
Acid ingestion
Decreased renal acid excretion
Gastrointestinal or renal HCO3- loss

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8
Q

What are some potential causes of metabolic alkalosis?

A

Acid loss (e.g. vomiting, diarrhoea)
HCO3- retention
(inability to excrete HCO3-)
- Renal loss of H+ ions (e.g. loop and thiazide diuretics, heart failure, nephrotic syndrome, cirrhosis, Conn’s syndrome)
- Iatrogenic (e.g. addition of excess alkali such as milk-alkali syndrome)

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9
Q

What are some potential causes of respiratory acidosis? x5

A

Decrease in minute ventilation (hypoventilation)
- CO2 accumulates in blood and so PaCO2 increases

  • Respiratory depression (opiates)
  • Guillain-Barre (paralysis leading to inadequate ventilation)
  • Asthma
  • COPD
  • Iatrogenic (incorrect mechanical ventilation settings)
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10
Q

What are some poential causes of respiratory alkalosis? x6

A

Increase in minute ventilation (hyperventilation)
- CO2 loss so PaCO2 decreases

  • anxiety
  • pain (resulting in increased resp rate)
  • hypoxia (resulting in increased alvelar ventilation in an attempt to compensate)
  • pulmonary embolism
  • pneumothorax
  • iatrogenic (e.g. excessive mechanical ventilation)
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11
Q

What is a simple versus a mixed acid/base disorder?

A

Simple acid/base disorder = single respiratory or metabolic problem

Mixed acid/base disorder = problem causing acidosis + problem causing alkalosis (may partially neutralise) OR 2+ problems causing acidosi OR 2+ problems causing alkalosis –> severe pH disturbance

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12
Q

How do the PCO2, HCO3- and pH levels differ in acute and chronic respiratory acidosis and alkalosis?

A

In acute respiratory acidosis there is no metabolic compensation initially so the bicarb is normal and the pH is very low.

In chronic respiratory acidosis metabolic compensation kicks in resulting in increased bicarb and less acidotic pH.

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13
Q

How is the pCO2 affected in metabolic acidosis and alkalosis?

A

In metabolic acidosis respiratory compensation kicks in immediately so pCO2 is reduced.

In metabolic alkalosis respiratory compensation kicks in immediately so there is increased pCO2.

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14
Q

What is the significance of high and low base excesses?

A

The base excess is another surrogate marker of metabolic acidosis or alkalosis.

High base excess (>+2mmol/L) indicates that there is an increased amount of HCO3- in the blood, which may be due to a primary metabolic alkalosis or a compensated respiratory acidosis.

Low base excess (<-2 mmol/L) indicates that there is a lower than normal amount of HCO3- in the blood, suggesting either a primary metabolic acidosis or a compensated respiratory alkalosis.

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15
Q

What is the anion gap and what is it used for? What is the formula?

A

An artifical measure that is caluculated by subtracting the toal number of anions (chloride + HCO3-) from the total number of cations (Na+). It is used to evaluate metabopic acidosis and determine the presence of unmeasured anions (e.g. albumin)

Formula = Na+ - (Cl- + HCO3-)

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16
Q

What are some potential causes of a high anion gap metabolic acidosis?

A

Typically relate to increased production/ingestion or reduced excretion of H+ by the kidneys.

  • diabetic ketoacidosis
  • lactic acidosis
  • toxins (e.g. aspirin, methanol, ethylene glycol)
  • renal failure
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17
Q

What are some causes of a normal anion gap mentabolic acidosis?

A

Typically due to loss of bicarbonate which is subsequently replaced nby chloride in the plasma, resulting in a stable overall anion concentration

  • GI loss of HCO3- (e.g. diarrhoea, ileostomy, proximal colostomy)
  • Renal tubular disease
  • Addison’s disease
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18
Q

What is acute bronchitis? How is it different to pneumonia?

A

Infection and inflammation in the bronchi and bronchioles

Pneumonia affects the alveolar space whereas bronchitis affects the bronchi and bronchioles - both are lower respiratory tracrt infections

Bronchitis is typically viral whereas pneumonia has a higher risk of being of bacterial origin

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19
Q
A
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20
Q

What is pneumonia?

A

infection of the lung tissue which causes inflammation of the lung tissue and sputum filing the airways and alveoli

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21
Q

What are the causes of pneumonia?

A

streptococcus pneumoniae (50%)
haemophilus influenzae (20%)
moraxella catarrhalis (in immunocompromised patients/pts with chronic disease)
pseudomonas aeruginosa (pts with CF or bronchiectasis)
staphylococcus aureus (pts with CF)

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22
Q

What are the risk factors for pneumonia? x10

A

Bronchiectasis
Asthma
Cystic fibrosis
COPD
Malnutrition
Diabetes
Heart failure
Sickle cell disease
Liver or kidney disease
Hospitalisation
Older age

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23
Q

What is the definition of hospital acquired pneumonia?

A

pneumonia which develops more than 48hrs after hospital admission

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24
Q

What are the key presentations of pneumonia? x7

A

Shortness Of breath
Cough (productive of sputum)
Fever
Haemoptysis (coughing up blood)
Pleuritic chest pain (sharp chest pain worse on inspiration)
Delirium (acute confusion associated with infection)
Feeling generally unwell

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25
What are the signs of pneumonia?
Tachypnoea Tachycardia Hypoxia Hypotension Fever Confusion
26
What are the characteristic chest signs of pneumonia?
Bronchial breath sounds = harsh breath sounds equally loud on expiration and inspiration caused by consolidation of the lung tissue around the airway Focal coarse crackles = air passing through sputum in the airways Dullness to percussion due to lung tissue collapse and/or consolidation
27
What are the investigations for pneumonia?
CURB 65, CXR, FBC, U+Es, CRP Sputum cultures, blood cultures, legionella and pneumococcal urinary antigens
28
What is the management for pneumonia?
Mild CAP = 5 day course of oral antibiotics (amoxicillin or macrolide) Moderate - severe CAP = 7-10 day course of dual antibiotics (amoxicillin and macrolide)
29
What are the potential complications of pneumonia?
sepsis, pleural effusion, empyema, lung abscess, bronchiectasis, death
30
What is CURB-65?
An algorithm for assessment of pneumonia severity C - confusion (new disorientation in person, place or time) U - urea >7 R - respiratory rate ≥ 30 B - blood pressure <90 systolic or ≤ 60 diastolic 65 - age ≥ 65
31
What is pleuritic chest pain?
pain on deep inspiration (feels like sandpaper on lungs during breathing)
32
What are the mortality percentages for CURB 65 scores?
0=0.7% 1=2.1% 3=9.2% 4-5=15-40%
33
What are the implications of CURB 65 scores 0-5?
0-1 = mild, only admit if social circumstances or single worrying feature 2 = moderate, admit to hospital 3-5 = severe, admit and monitor closely 4-5 = consider admission to critical care unit
34
What are the top 2 causes of typical bacterial pneumonia>
Strep pneumoniae Haemophilus influenzae
35
What are some pf the causes of atypical pneumonia and what is a key diagnostic sign for each? x5
Legionella - recent holiday and can cause SIADH Mycoplasma - erythema multiforme rash (target lesions) Chlamydia pneumoniae- common in school-age children Coxiella burnetii (Q fever) - farmer with flu-like illness Chlamydia psittaci - contracted from infected birds (Legions of Psittaci MCQs)
36
What is an abdominal aortic aneurysm (AAA)?
Dilatin of the abdominal aorta with a diameter of more than 3cm
37
What are the risk factors for AAA?
- Men are affected significantly more often and at a younger age than women - increased age - smoking - hypertension - family history - existing cardiovascular disease
38
What is the current UK screening programme for AAAs?
All men in england are offered a screening USS at age 65 to detect asymptomatic AAA Women are not routinely offered screening, as they are much lower risk
39
How do AAAs usually present? x4
- Most commonly asymptomatic and present on rupture - Non-specific abdo pain - Pulsatile and exapnsive mass in the abdomen when palpated with both hands - Incidental finding on abdo x-ray, USS or CT scan
40
How are AAAs classified?
By severity depending on size Normal: less than 3cm Small aneurysm: 3 – 4.4cm Medium aneurysm: 4.5 – 5.4cm Large aneurysm: above 5.5cm
41
How are AAAs managed?
1. Treating reversible risk factors - stop smoking - healthy diet and exercise - optimising management of hypertension, diabetes and hyperlipidaemia 2. screening and surveillance - yearly for patient with aneurysms 3-4.4cm - 3 monthly for patients with aneurysms 4.5-5.4cm 3. Elective repair for patients who are symptomatic, the diameter is growing more than 1cm per year or the diameter is greater than 5.5cm - open repair via laparotomy - endovascular aneurysm repair using a stent inserted via the femoral arteries
42
What are the DVLA rules for patients with AAA?
- Inform the DVLA if they have an aneurysm greater than 6cm - Stop driving if it is above 6.5cm - Stricter rules for heavy vehicle drivers
43
How does a ruptured AAA present? x5
Severe abdominal pain that may radiate to the back or groin Haemodynamic instability (hypotension and tachycardia) Pulsatile and expansile mass in the abdomen Collapse Loss of consciousness SURGICAL EMERGENCY
44
What is the management for a ruptured AAA>
SURGICAL EMERGENCY - senior support required - fluid resuscitation aiming for permissive hypotension (attempt to minimise blood loss) - direct transfer to theatre for haemodynamically unstable patients - CT angiogram to diagnose or exclude ruptured AAA in stable patients
45
What causes arrhythmias?
Interruption to the normal electrical signals which coordinate the contraction of the heart muscle
46
What are the shockable rhythms in a pulseless patient (cardiac arrest)? x2
Shockable: - ventricular tachycardia - ventricular fibrillation
47
What are the non-shockable rhythms in a pulseless patient (cardiac arrest)? x2
Pulseless electrical activity (all electrical activity expect VF/VT, including sinus rhythm without a pulse) Asystole (no significant electrical activity)
48
What is narrow complex tachycardia?
A fast heart rate with a QRS complex duration of less than 0.12 seconds (3 small squares)
49
What are the 4 main differentials for narrow complex tachycardia? How is each treated?
Sinus tachycardia - treatment focuses on underlying cause Supraventricular tachycardia - treated with vagal manoeuvres and adenosine Atrial fibrillation - treated with rate or rhythm control Atrial flutter - rate or control or rhythm control
50
What is SVT?
Supraventricular tachycardia is where there is a QRS complex directly followed by a T wave and then a QRS complex. There are P waves byt they are often buried in the T waves so unseen. SVT is characterised by sudden onset and a regular rhythm. Can appear with no apparent cause
51
How is atrial fibrillaiton identified on ECG?
Absent P waves Irregularly irregular ventricualr rhythm
52
What is the pathophysiology of atrial flutter./
A re-entrant rhythm occurs in either atrium meaning that rather than just passing through the atria once and stimulating a contraction, the electrical signal re-circualtes in a loop due to an extra electrical pathway in the atria. The signal goes round and round the atrium without interruption causing the flutter.
53
What is the treatment for atrial flutter?
similar to Atrial fibrillation - anticoagulation based on the CHA2DS2-VASc score - radiofrequency ablation of the re-entrant rhythm can be a permanent solution
54
What are the distinguishing features of atrial flutter on ECG?
Rate around 300 bpm Saw-tooth pattern QRS complex at regular intervals Often 2 atrial contraction for every one ventricular contraction
55
What is broad complex tachycardia?
A fast heart rate with a QRS complex duration of more than 0.12 seconds (3 small squares)
56
What are the 4 types of broad complex tachycardia? WHat is the treatment for each?
Ventricular tachycardia - treated with IV amiodarone Polymorphic ventricular tachycardia e.g. torsades de pointes - treated with IV magnesium Atrial fibrillation + bundle branch block - treated as AF Supraventricualr tachycardia + BBB - treated as SVT
57
What are the life-threatening features of arrhythmias/
Loss of consciousness (syncope) Heart muscle ischaemia (e.g. chest pain) Shock Severe heart failure
58
How are life-threatening arrhythmias treated?
Synchronised DC cardioversion under sedation or GA IV amiodarone is added if initial schoks unsuccessful
59
What is the definition of a prolonged QT interval ? (men/women)
>440 milliseconds in men (12 small squares) >460 milliseconds in women (11.5 small squares)
60
What does a prolonged QT interval signify?
It represents prolonged repolarisation of the heart muscle cells (myocytes) after a contraciton.
61
What are some causes of prolonged QT?
Long QT syndrome (inherited) Medications e.g. antipsychotics, citalopram, fleicanide, sotalol, amiodarone and macrolide antibiotics Electrolyte imbalances e.g. hypokalaemia, hypomagnesaemia and hypocalcaemia
62
What is the management for prolonged QT intervals?
Stop meds causing the prolonged QT Correct electrolyte disturbances Beta blockers Pacemakers or implantable cardioverter defibrillators
63
What is torsades de pointes?
A type of polymorphic ventricualr tachycardia where the height of the QRS complexes get progressively smaller, then larger and then smaller. Translated as twisting of the spikes as seen in the ECG
64
What is the acute management for torsades de pointes? x3
correcting the underlying cause e.g. electrolyte disturbances or medications magnesium infusion defibrillation if ventricular tachycardia occurs
65
What are ventricualr ectopics?
Premature ventricular beats caused by random electrical discharges outside of the atrial They are relatively common at all ages and in healthy patients but there is increased likelihood in patients with pre-existing heart condtions
66
WHat is bigeminy?
When every other beat is a ventricualr ectopic.
67
What is first degree heart block? What is the defining sign on ECG ?
When there is delayed conduction through the atrioventricular node but every p wave is followed by a QRS complex. On ECG the PR interval is greater than 0.2 seconds (1 big square)
68
What is second-degree heart block? What are the 2 types?
When some atrial impulses don't make it through the atriventricular node to the ventricles so there are instances where p waves are not follwed by QRS complexes. 2 types: Mobitz 1 (Wenckebach) Mobitz 2
69
What is mobitz type 1 heart block?
Where the conduction through the AV node takes progressively longer until it finally fails, after which it resets, and the cycle restarts. On ECG the PR interval increases until a P wave is not followed by a QRS complex and then it returns to normal and the cycle repeats itself.
70
WHat is mobitz type 2 heart block?
When there is intermittent failure of conduction through the AV node, with an absence of QRS complexes following P waves. The PR interval remains normal.
71
What is 3rd degree/complete heart block?
Where there is no observable relationship between P waves and QRS complexes.
72
What arrhythmias put patients at increased risk of asystole? x4
Mobitz type 2 3rd degree heart block Previous asystole Ventricular pauses longer than 3 seconds
73
What is the management for patients with arrhythmias who are unstable and at risk of arrhythmias?
1. IV atropine (antimuscarinic which inhibits the parasympathetic nervous system) 2. Inotropes e.g. isoprenaline or adrenaline 3. Temporary cardiac pacing (transcutaneous or transvenous) 4. Permanent implantable pacemaker
74
What are some examples of when IV fuids may be required? x3
Nil by mouth pateints (e.g. bowel obstruction, ileus, pre-operatively) Vomiting/severe diarrhoea Hypovolaemia
75
What are the 2 major types of IV fluids and what's the difference? Which one is used more frequently and why?
Crystalloids - solutions of sall molecules in water (e.g. sodium chhlordie, Hartmann's, dextrose) Colloids - solutions of larger organic molecules (e.g. albumin) Crystalloids are used more frequently because they have been shown to be more effective in initial fluid resus and colloids carry a risk of anaphylaxis.
76
Give some examples of common fluids prescribed, their tonicity and what they are used for? x4
NaCl 0.9% (normal saline) - isotonic, used for resus/maintenance Hartmann's solution - isotonic, used for resus/maintenance NaCl 0.18%/Glucose 4% - hypotonic, used for maintenance 5% dextrose - hypotonic, used for maintenance
77
What are the 5 R's of IV fluid prescribing?
Resuscitation Routine management Replacement Redistribution Reassessment
78
What are some key causes of fluid loss that may lead to fluid requirement? x6
vomiting (or NG tube loss) diarrhoea polyuria fever hyperventilation increased darin output (e.g. biliary drain, pancreatic drain)
79
What are some clinical signs suggestive of hypervoleaemia? x7
increased respiratory rate (>20 breaths per min) decreased O2 sats bilateral crackles on auscultation hypertension elevated JVP increased urine output abdo distension postivie fluid balance weight gain
80
What are some clinical findings suggestive of hypovolaemia? x8
increased heart rate (>90bpm) hypotension (systolic BP <100 mmHg) prolonged capillary refill time non-visible JVP decreased GCS (severe fluid depletion) increased output from wounds and drains decreased urine output (<30mls/hr) negative fluid balance weight loss other sources of fluid loss
81
What do you give as an initial fluid bolus for resuscitation fluids?
250-500ml of a crystalloid solution (e.g. NaCl 0.9%/Hartmann's) over less than 15 mins
82
Up to what volume can you repeat resuscitation fluid boluses for ongoing hypovolaemia?
2000ml fluid
83
Why are maintenance fluids given?
If patients are unable to meet their fluit and/or electrolyte needs orally/enterally
84
What are the NICE guidelines for daily maintenance fluid requirements? (H2O, electrolytes, glucose)
25-30ml/kg/day of water 〰️ 1mmol/kg/day of K+, Na+ and Cl- 〰️ 50-100g/day of glucose to limit starvation ketosis (not fulfilling nutritional needs)
85
What is the adjustment needed when prescribibng maintenance fluids for obese patients?
adjust the prescription to their IDEAL weight not the actual weight
86
In which patient groups is extra consideration needed when prescribing fluids?
Obese Elderly Renally impaired or cardiac failure Malnourished at risk of refeeding syndrome
87
What conditions/issues can cause problems with fluid distribution?
Gross oedema Severe sepsis Hypernatraemia/hyponatraemia Renal, liver and/or cardiac impairment Post-operative fluid retention and redistribution Malnourishment and refeeding issues
88
Why does vomiting cause significant potassium loss? What does this mean in terms of fluid prescribing for patients who are vomiting?
Vomiting causes direct loss of stomach acid (HCl) which leads to a build up of bicarbonate in the blood --> metabolic acidosis. To compensate for this the kidneys excrete more bicarbonate and potassium is often the counter ion for bicarbonate resulting in loss of potassium as well. This means that for vomiting patients, Hartmann's solution is preferred over normal saline as it contains extra potassium
89
What are potential complications of fluid prescribing?
acute pulmonary oedema fluid overload hypo/hypernatraemia hypo/hyperkalaemia
90
What are some immediate treatments for A-E problems? x4
Airway manoeuvres Oxygen Fluid bolus Glucose
91
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