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POEM > Circulation Part 2 - Critical Illnesses > Flashcards

Circulation Part 2 - Critical Illnesses Flashcards

1
Q

How does anaphylaxis present? (Easier if list by system)

A
  • Known exposure to allergen (or not)
  • Skin: pruritis/urticaria/erythema/angiodema
  • Oral: difficulty swallowing/oedema of lips, tongue, mouth
  • Laryngeal: hoarseness/stridor/change in voice/pruritis
  • Respiratory: cough/wheeze/chest tightness/cyanosis
  • GI: nause/vomiting/pain/diarrhoea
  • CV: tachycardia/palpitations/dizziness/syncope/chest pain/hypotension/shock (inc. in peripheral vasodilation and vascular permeability = drop in intravascular volume)
  • Neurological: anxiety/drop in GCS/change in behaviour/incontinence
  • Other: diaphoresis/sense of “impending doom”
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2
Q

Outline the definition of anaphylaxis.

A

Simple terms: anaphylaxis is a serious systemic hypersensitivity reaction that is rapid in onset and potentially life-threatening. There is life-threatening compromise of breathing and/or circulation (and may occur without typical skin features or circulatory shock being present.

NB/ you HAVE to mention respiratory or circulatory compromise when defining anaphylaxis!

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3
Q

Outline the pathophysiology of anaphylaxis.

A

Occurs in an individual after re-exposure to
an antigen to which they have produced IgE
antibodies to that recognize epitopes of the
allergen. These then bind to the high-affinity
IgE receptor (FcεRI) on the surface of mast
cells and basophils. Upon re-exposure, the
allergen may cross-link bound IgE resulting in
degranulation as well as de novo synthesis of
mediators. Histamine is thought to be the
primary mediator (pruritis, rhinorrhea,
tachycardia, and bronchospasm) but PGD2
and LTC4 contribute to bronchospasm and
vasodilation as well.

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4
Q

Outline the initial management of anaphylaxis.

A

ABCDE approach!

AIRWAY:

  • Secure airway (head tilt/chin left/airway adjuncts)
  • Administer adrenaline 0.5 mg IM (0.5ml of 1:1000) and repeat at 5 minute intervals

BREATHING:

  • Attach high-flow O2 15 L/min via NRBM
  • If wheeze (reflects bronchospasm) give salbutamol 5 mg O2 NEB (with addition of ipratropium bromide 500 mcg)

CIRCULATION:

  • Secure TWO wide-bore IV cannulas
  • IV fluids 500-100 mL 0.9% saline/Hartmann’s STAT
  • Hydrocortisone 200 mg IV
  • Chlorphenamine 10 mg IV
  • Apply 3-lead cardiac monitoring
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5
Q

What other short-term management considerations must you have?

A
  • No improvement - seek anaesthetist
  • Admit for observation (at least 6 hours post-adrenaline due to biphasic reactions)
  • Prednisolone 30-40 mg OD PO (3-5 day course)
  • Monitor ECG
  • Further IV fluids if required
  • Document event and allergy
  • Consider mast cell tryptase to confirm (must be done ASAP)
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6
Q

What is acute coronary syndrome?

A

ACS is a group of conditions due to reduced flow the coronary arteries such that muscle is unable to function properly or dies; Can be due to atherosclerosis, emboli,
vasculitis, cocaine use, severe anaemia, hyperthyroidism (increased demand).

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7
Q

Outline the types of acute coronary syndromes.

A
  1. STEMI: ST-elevation or new LBBB
  2. NSTEMI: ACS without ST-elevation/new LBBB but with raised troponin at 12 hours
  3. Unstable angina: ACS without ST-elevation/ new LBBB or raised troponin at 12 hours
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8
Q

How are acute coronary syndromes initially managed?

A

ABCDE approach + MONAT:

  1. Morphine: 10 mg in 10 mL slow IV - titrate to pain (+ 10 mg metoclopramide IV)
  2. Oxygen: if saturations <90% (maintain at 90-94%)
  3. Nitrates: sublingual GTN if not hypotensive (then PRN)
  4. Aspirin 300 mg PO loading dose (if not already given pre-hospital - then 75 mg OD)
  5. Ticagrelor 180 mg or clopidogrel 300 mg PO (depending on local guidelines) then 75 mg OD
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9
Q

What investigations should be performed during initial assessment?

A
  1. 12-lead ECG (then continuous cardiac monitoring)
  2. Bloods: FBC, U&E, LFTs, CRP, glucose plus cardiac enzymes (STAT then again at 10-12 hours post-pain onset), magnesium, phosphate, lipid profile
  3. CXR (LVF signs, alternative cause of chest pain)
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10
Q

List risk factors for myocardial infarction.

A
  • Smoking
  • Hypertension
  • Old age
  • Male sex
  • Diabetes
  • Hyperlipidaemia
  • Family history
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11
Q

Discuss the pathophysiology of myocardial infarction.

A
  • Typically affects LV
  • Results from sudden occlusion of a coronary artery or branch thereof by thrombosis over an existing atheromatous plaque
  • May also occur from vasculitic processes e.g. GCA/Kawazaki disease
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12
Q

Outline the criteria for diagnosis acute myocardial infarction.

A

Two of following three features:

  • History of cardiac-type ischaemic chest pain
  • Evolutionary changes on serial ECGs
  • A rise in serum cardiac markers
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13
Q

Outline the presentation of a STEMI.

A

Classic presentation:

  • Sudden onset
  • Severe
  • Constant central chest pain
  • Radiates to arms, neck, or jaw
  • Similar to previous angina pectoris episodes but greater severity and unrelieved by GTN
  • One or more associated symptoms: sweating, nausea, vomiting, SOB

Atypical presentation:

  • New onset ‘dyspeptic’ pain - indigestion-like
  • No chest pain (particularly history of T2DM/HF
  • LVF
  • Collapse/syncope
  • Confusion
  • Stroke
  • Incidental ECG finding at later date
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14
Q

What are some important elements to enquire about in a history in suspected STEMI?

A
  • IHD
  • HTN
  • T2DM
  • Hyperlipidaemia
  • Contraindications to thrombolysis
  • Drug history, including drugs of abuse (especially cocaine)
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15
Q

What is the appropriate investigation of a suspected STEMI?

A
  • Relies on history and ECG changes
  • Record ECG ASAP - within minutes of arrival
  • Review old notes and previous ECGs
  • Ensure continuous cardiac monitoring and pulse oximetry
  • Monitor BP and RR
  • Obtain IV access and send blood for cardiac markers, U&E, glucose, FBC, and lipids
  • Obtain CXR if suspicion of LVF or aortic dissection
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16
Q

Outline acute ECG changes seen in STEMI.

A
  • ST-elevation: most important. Significant if elevated > 1 mm in two limb leads or > 2 mm in two adjacent chest leads.
  • Reciprocal ST-depression may occur in ‘opposite’ side of heart.
  • Pathological Q-waves: electrically inert necrotic myocardium.
  • T-wave inversion: deeply inverted, symmetrical, and pointed
  • Conduction problems: LBBB.
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17
Q

Outline chronic ECG changes seen in STEMI.

A
  • Months following MI
  • ECG changes usually resolve - ST-segments become isoelectric again unless ventricular aneurysm develops
  • T-waves gradually become +ve again
  • Q-waves usually remain indicating an old MI.
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18
Q

ECG changes in different leads allow us to localise a myocardial infarct. Match the leads to the location of the infarct.

A
  • V1-3 = anteroseptal
  • V5-6, aVL = anterolateral
  • V2-V4 = anterior
  • I, II, aVL, V6 = lateral
  • II, III, aVF = Inferior
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19
Q

Outline coronary artery blood supply and dominance.

A
  • LAD = anterior/septal
  • LCX = antero-lateral
  • RCA = inferior, RV, and ventricular septum (most people also SA node)
  • 15% of people inferior wall supplied by LCX (left dominance)
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20
Q

How is STEMI managed?

A
  1. ABCDE + MONAT
  2. Cath lab for PCI if <12 hour from symptom onset
  3. If PCI cannot be performed in 90 minutes assess risk of bleeding offer thrombolysis as per protocol
21
Q

What are the indications for PCI/thrombolysis?

A
  1. ST-elevation of >1 mm in 2 limb leads, or
  2. ST-elevation of >= 2 mm in two or more contiguous chest leads, or
  3. LBBB in the presence of a typical history of acute MI (note: LBBB does not have to be new)
22
Q

List absolute contraindications for thrombolysis?

A
  • Stroke in past 3 months; neurosurgery in past 6 months; intracranial bleed within the past year
  • Cerebral tumour or metastases
  • GI, GUT, retropertioneal, or intraocular bleeding within the last month
  • Coagulopathy (e.g. haemophilia), anticoagulation (warfrain, DOACs, LMWH)
  • Thrombocytopaenia (platelets <50 x 10^9 L)
  • Severe hypertension: sBP >200 mmHg, diastolic BP >120 mmHg
  • Major surgery within the last 2 weeks
23
Q

Outline long-term management of ACS.

A
  • Beta-blocker (reduce myocardial demand)
  • ACEi (prevents adverse cardiac remodelling)
  • GTN spray PRN if required
  • Aldosterone antagonist if LV function <40%
  • Cardiovascular RF reduction: aspirin/statin/BP control/smoking cessation/cardiac rehab
24
Q

What is diabetic ketoacidosis (DKA)?

A
  • Relative lack of insulin resulting in hyperglycaemia as cells unable to take up glucose - ‘starvation in the midst of plenty’
  • Causes cells to switch to beta-oxidation of fats for metabolism
  • Production of acidic ketones

Easy way to remember:

  • Diabetic = glucose > 11 mmol/L
  • Keto = capillary ketones > 3 mmol/L or ++ urinary
  • Acidosis = pH < 7.3 or HCO3- <15
25
Q

How does DKA present?

A
  • Nausea and vomiting
  • Polydipsia
  • Polyuria
  • Abdominal pain (may be severe)
  • Kussmaul breathing
  • Confusion
  • Drop in GCS
  • Coma
26
Q

What may be seen on examination in DKA?

A
  • Evidence of dehydration (prolonged cap. refill; reduced skin turgor; dry mouth)
  • Decreased circulation volume reflected by rapid HR; and hypotension
  • Increased respiratory rate
  • Ketotic breath odour
27
Q

How is DKA managed?

A
  1. ABCDE
  2. Confirm diagnosis: perform VBG, capillary/urine ketones, and glucose measurement
    - Glucose > 11 mmol/L or known diabetes
    - pH < 7.3 or HCO3- <15
    - Ketones > 3 mmol/L or ++ urinary ketones
  3. Intravenous fluids (dehydration more lethal than hyperglycaemia)
    - 1 L saline over 1 hour (faster if hypotensive) - without potassium
    - 1 L saline over 2 hours
    - 1 L saline over 2 hours
    - 1 L saline over 4 hours
    - 1 L saline over 4 hours
    - 1 L saline over 6 hours
    - 1 L saline over 6 hours
    * review VBG K+ results for K+ replacement
  4. Fixed rate insulin infusion:
    - IV insulin infusion 0.1 unit/kg/hour from 50 units Actrapid in 50 mL 0.9% saline (max rate 15 units per hour)
    - When capillary glucose < 14 mmol/L, give 10% IV glucose at 125 ml/hour in addition to the 0.9% saline (glucose given to drive glucose into cells to reduce ketosis and acid production)
  5. Investigate cause:
    - History
    - Top to tail examination
    - Bloods (FBC, glucose, U&Es, LFTs, osmolality, CRP)
    - Blood culture
    - MSU
    - CXR
28
Q

How do upper GI bleeds normally present?

A
  1. Haematemesis = vomiting fresh blood; “coffee-grounds” –> haemoglobin converted to methaemoglobin by stomach acid.
  2. Malaena = passage of black, tarry, malodorous stools. Oxidation of haem by intestinal bacterial enzymes.
29
Q

List the differential diagnoses for a UGI bleed.

A
  1. Peptic ulcer (gastric/duodenal)
  2. Gastritis/erosions
  3. Oesophagitis
  4. Mallory-Weiss tear
  5. Oesophageal varices
  6. Portal hypertensive gastropathy
  7. Malignancy
30
Q

How should one assess a suspected UGI bleed?

A
  1. ABCDE approach + senior help
    - IV fluid resuscitation (aim for sBP 100)
    - in massive blood loss transfuse blood, FFP and platelets as per local massive haemorrhage protocol
    - blood transfusion if Hb <7 g/L in variceal bleed or <8 g/L in non-variceal bleed
    - patient MUST be haemodynamically stable before OGD
  2. Examination: signs of common causes (e.g. decompensated/chronic liver disease) and do a PR examination for melaena
  3. Bloods: G&S/crossmatch, FBC (blood loss), U&Es (inc. urea in GI bleeds), LFTs (varices risk), clotting (coagulopathy in liver disease), glucose
  4. Catheterise (monitor UO)
  5. CXR and AXR (once stable)
  6. OGD
  7. Observations: check regularly
  8. Keep ALL patients NBM
31
Q

Outline the Glasgow-Blatchford score in suspected UGI bleeds.

A
  • Pre-endoscopy
  • Assesses likelihood of patient needing intervention
  • 0 = manage as OP
  • > =1 = manage as IP
32
Q

Outline the Rockall score in suspected UGI bleeds.

A
  • Post-endoscopy
  • Mortality risk assessment
  • <= 2 = good prognosis
  • > = 8 = high mortality risk
33
Q

What is sepsis?

A

Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. If not identified and managed promptly, it can lead to septic shock, multiple organ failure, and death.

34
Q

Describe the diagnosis of sepsis?

A

Step 1: Are the SIRS criteria met?

SIRS Criteria: (4 of the criteria based on observations, 1 based on Point Of Care glucose and 1 based on Laboratory results)

Any 2 of:

  • New onset of Confusion or Altered Mental State
  • Temperature >38.3 or <36 ⁰C, Heart Rate >90 beats / minute
  • Respiratory Rate (counted over 60 seconds) >20 breaths / minute
  • Blood Glucose > 7.7mmol/L (in the absence of known Diabetes) - Finger prick capillary blood.
  • Laboratory- WCC > 12 x 10^9/L OR < 4x10^9/L

Step 2 : Is Sepsis/infection likely based on symptoms/signs/ past history? (based on history/clinical examination) or any confirmed/proven infection ?

If SIRS criteria met (any 2) and Step 2 is positive then Sepsis diagnosis

35
Q

How is severe sepsis diagnosed?

A
  • Evidence of end organ dysfunction
  • Main red flag indicators: HR > 130, RR > 25 or U on the
    AVPU scale
  • useful for identifying severe sepsis while waiting
    confirmatory laboratory or imaging test results,
    avoiding unnecessary treatment delays. The
    presence of any one of these indicates “red flag
    sepsis” and treatment should be started promptly
  • Lactate of > 2mmol/l is indicative of severe sepsis
36
Q

Outline the management of sepsis (sepsis six).

A
  1. Apply supplemental oxygen, keep oxygen sats> 94%; 88-92% if COPD
  2. Intravenous access, prepare to take bloods (FBC, U&E, CRP, LFTs, coagulation, VBG) and start intravenous fluids
    If Hypotensive/lactate >2mmol/litre- give 500 mL STAT
    Many be repeated if clinically indicated - do not exceed 30 mL/kg = 2100 mL, in 70kg person
  3. Venous blood gas result to determine Lactate (If Lactate > 4, then septic shock)
  4. Blood Cultures- at least one peripheral set using ANNT
  5. Intravenous antibiotics within 1 hour, use local guidelines but examples include gentamicin for Urinary, amoxicillin for chest, tazocin for intra-abdominal sepsis. Know the doses and beware of antibiotic allergies.
  6. Monitor urinary output hourly - consider urinary catheterisation if patient non-ambulant
37
Q

What is the significance of lactate in sepsis?

A
  • Sepsis = under-perfusion of tissues, de-oxygenation, and anaerobic metabolism causing lactate production to increase
  • Lactate > 2 is indicative of severe sepsis
  • Lactate > 5 is indicative of septic shock
  • Lactate level is highly predictive of death/poor outcomes
38
Q

Outline the common presentation of ectopic pregnancy.

A
  • Abdominal pain
  • Pelvic pain
  • Amenorrhoea or missed period
  • Vaginal bleeding
  • Shoulder tip pain
  • Cervical motion tenderness (Chandelier’s)
  • Dizziness, fainting, and syncope
  • Breast tenderness
39
Q

Outline signs of ectopic pregnancy.

A
  • Pelvic or abdominal tenderness
  • Adnexal tenderness
  • Abdominal distension
  • Enlarged uterus
  • Rebound tenderness
  • Risk of rupture on palpation - avoid internal examination if suspected
40
Q

How is ectopic pregnancy investigated?

A
  • Pregnancy test
  • Refer immediately to OBGYN if:
    Positive pregnancy test + any of: pelvic, cervical motion, and abdominal tenderness.
  • Once referred: transvaginal USS
41
Q

How is ectopic pregnancy managed?

A

If ectopic pregnancy detected, offer treatment based on hCG level:

  • < 1,500 IU/L = methotrexate
  • 1,500-5,000 IU/L = either
  • > 5,000 IU/L = surgical removal by laparoscopic salpingectomy (if fertility issues - salpingotomy)
  • For those undergoing surgical treatment, anti-D is required.
  • Repeat hCG once a week until negative result.
42
Q

Outline the presentation of abdominal aortic aneurysms.

A
  1. Asymptomatic = none.
  2. Symptomatic = abdominal pain radiating to back or groin; intermittent claudication
  3. Rupture = abdominal pain radiating to back or groin; collapse
43
Q

Outline the signs of abdominal aortic aneurysm.

A
  1. Asymptomatic = non-tender epigastric mass (+/- bruit); pulsatile and expansile
  2. Symptomatic = tender epigastric mass; limb ischaemia; retroperitoneal fibrosis
  3. Rupture = acute surgical abdomen; lumbar haematoma; shock and loss of consciousness
44
Q

How are abdominal aortic aneurysms investigated?

A
  1. Surveillance with USS abdomen
    - 3-4.4 cm (every 12 months)
    - 4.5-5.4 cm (every 3 months)
    - > 5.5 cm (consider treatment)
  2. ESR/CRP (exclude inflammatory cause)
  3. ECG
  4. CXR
  5. CT - can show mural thrombus; ‘crescent sign’ - blood within thrombus - imminent rupture?
  6. MRI angiography
45
Q

How is abdominal aortic aneurysm managed?

A
  1. Endovascular aneurysm repair (EVAR)

2. Open surgical repair

46
Q

What are the symptoms of meningitis and meningococcal disease?

A
  • headache
  • fever
  • nausea/vomiting
  • photophobia
  • drowsiness
  • seizures
47
Q

What are signs of meningoccal disease?

A
  • neck stiffness

- purpuric rash (particularly with invasive meningococcal disease)

48
Q

How is meningitis investigated?

A

Investigations suggested by NICE

    full blood count
    CRP
    coagulation screen
    blood culture
    whole-blood PCR
    blood glucose
    blood gas

*Lumbar puncture if no signs of raised intracranial pressure

49
Q

How is meningitis managed?

A
  • Pre-hospital: IM benzylpenicillin
  • Initial empirical therapy aged 3 months - 50 years Intravenous cefotaxime (or ceftriaxone)
  • Meningococcal meningitis = Intravenous benzylpenicillin or cefotaxime (or ceftriaxone)

POEM (11 decks)

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