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MRCS Part B - Paul Edit > Critical Care Mo's Notes > Flashcards

Critical Care Mo's Notes Flashcards

1
Q

What is the pathophysiology of ARDS?

A
  1. Acute phase
    * exudate with neutrophils and cytokines causing destruction of the alveolar basementmembrane and capillary endothelim
  2. Chronic phase
    * fibroproliferation and organisation of the lung parenchyma, leads to scarring
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2
Q

What are the causes of ARDS?
VITAMIN

A

Vascular - TRALI, DIC
Infection - sepsis, diffuse pulmonary infections
Trauma - burns, pulonary contusions, fat embolism, drowning, smoke injury
Autoimmune - drugs,
Metabolic -
Idiopathic/iatrogenic - cardiopulmonary bypass
Neoplasia -

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3
Q

What is the Berlin criteria?

A

Classification of ARDS as mild moderate or severe accoding to PaO2/FiO2 (arterial oxygen to inspired oxygen)

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4
Q

What is the management of ARDS

A

Ventilation, Steroids, Fluids, Nutrition

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5
Q

What are two systems to calculate the % surface area of burns?

A

Wallace Rule of 9s
Lund and Browder

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6
Q

What is the normal value of ICP?

A

7 to 15mmHg

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7
Q

What is cushing’s triad?

A

hypertension
bradycardia
bradypnoea

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8
Q

MAP = ?

A

diastolic + 1/3 (systolic -diastolic)

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9
Q

What is a normal MAP?

A

50 - 150 mmHg

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10
Q

CPP = ?

A

MAP - ICP

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11
Q

How to manage raised ICP?

A

Sit up
Mannitol, furosemide
Avoid hyperthermia
Sedation
Hyperventilation
Burr hole/craniectomy

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12
Q

Describe the stages of shock

A
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13
Q

What is a normal intramuscular compartment pressure?

A

0 - 15mmHg

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14
Q

What is a pathological compartment pressure?

A

30 mmHg

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15
Q

Where to incise for faschiotomy of the leg?

A

2cm anterior and posterior to the tibial border

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16
Q

What is the pathogenesis of rhabdomyolysis?

A

myoglobin and other tissue breakdown products cause ATN and renal failure

17
Q

What are some causes of rhabdomyloysis?

A
  • Blunt trauma to skeletal muscle, e.g. crush injury
  • Massive burns
  • Hypothermia or hyperthermia
  • Ischemic reperfusion injury, e.g. clamp on an artery during surgery
  • Prolonged immobilization on a hard surface
  • Strenuous and prolonged spontaneous exercise, e.g. marathon running
  • Drugs, e.g. statins, fibrates, alcohol
18
Q

What bloods could be derranged in rhabodmyolosis?

A
  • Increased creatine kinase (CK) > 5 times the normal
  • Increased lactate, LDH, creatinine
  • Electrolyte disturbances:
    o Hyperkaliemia (and metabolic acidosis with an ↑ anion gap)
    o Hypocalcemia
    o Hyperphosphatasemia
    o Hyperuricemia
  • Myoglobinuria suggested by positive dipstick to blood in the absence of hemoglobinuria (red cells on microscopy)
19
Q

How to manage rhabdomyolysis?

A
  • ABC
  • Fluid resuscitation: ensure good hydration to support urine output >300 ml/h using IV crystalloid until myoglobinuria has ceased.
  • Diuretics, e.g. mannitol, may also be used
  • Alkalinization of urine: NaHCO3 to prevent renal damage
  • Treat electrolyte disturbances (hyperkalemia)
  • Monitor ECG, electrolytes, UOP, CK (6-12h), LDH, urine myoglobulin, compartment pressure.
20
Q

What is the mechanism of action of PPIs?

A

The PPI binds irreversibly to a hydrogen/potassium ATPase enzyme (proton pump) on gastric parietal cells and blocks the secretion of hydrogen ions, which combine with chloride ions in the stomach lumen to form HCL

21
Q

What are the functions of hydrogen chloride in the stomach/small intestine?

A
  • Activates pepsinogen to pepsin which help in proteolysis
  • Antimicrobial
  • Stimulates small intestinal mucosa to release CCK and secretin
  • Promotes absorption of calcium and iron in the small intestine
22
Q

What are the phases of gastric secretions?

A
  1. Cephalic phase (smell / taste of food)
    * 30% acid produced
    * Vagal cholinergic stimulation causing secretion of HCL and gastrin release from G cells
  2. Gastric phase (distension of stomach)
    * 60% acid produced
    * Stomach distension / low H+ / peptides causes Gastrin release
  3. Intestinal phase (food in duodenum)
    * 10% acid produced
    * High acidity / distension / hypertonic solutions in the duodenum inhibits gastric acid secretion via enterogastrones (CCK, secretin) and neural reflexes.
23
Q

What are the NCEPOD classifications of surgery?

A
  1. immediate - life of limbsaving - minutes - e.g. ruptured AAA, compartment syndrome
  2. urgent - deterioration of condition that could affect life - within hours e.g. bowel perf with peritonitis, critical limb ischaemia
  3. expediated - early intervention not a threat to life - within days e.g. tendon rupture
  4. elective - planned - as planned e.g. all others
24
Q

What are the constituents of bile?

A
  • Water.
  • Cholesterol.
  • Lecithin (a phospholipid)
  • Bile pigments (bilirubin & biliverdin)
  • Bile salts and bile acids (sodium glycocholate & sodium taurocholate)
  • Small amounts of copper and other excreted metals.
25
Q

What is a pancreatic pseudocyst?
when? where?

A

Collection of amylase-rich fluid enclosed in a wall of fibrous or granulation tissue
It requires 4 weeks or more from the onset of the attack

26
Q

What are the symptoms of a pancreatic pseudocyst?

A
  • Epigastric swelling
  • Dyspepsia
  • Vomiting
  • Mild fever
27
Q

What is the management of a fistula?
SNAP

A
  • Sepsis control
  • Nutritional support – a period of parenteral nutrition may be required
  • Anatomical assessment
  • Adequate fluid and electrolyte replacement
  • Protect skin to prevent excoriation
  • Planned surgery
28
Q

What is refeeding syndrome?

A

It is a metabolic disturbance which occur on feeding a person following a period of starvation. The metabolic consequences include:
* Hypophosphataemia
* Hypokalaemia
* Hypomagnesaemia
* Abnormal fluid balance

29
Q

Who is at risk of refeeding syndrome?

A

If one or more of the following:
* BMI < 16 kg/m2
* Unintentional weight loss >15% over 3-6 months * Little nutritional intake > 10 days
* Hypokalaemia, Hypophosphataemia or hypomagnesaemia prior to feeding (unless high)

If two or more of the following:
* BMI < 18.5 kg/m2 * Unintentional weight loss > 10% over 3-6 months
* Little nutritional intake > 5 days
* History of: alcohol abuse, drug therapy including insulin, chemotherapy, diuretics and antacids

30
Q

How to prevent re-feeding syndrome?

A
  • Start at up to 10 kcal/kg/day increasing to full needs over 4-7 days
  • Start immediately before and during feeding: oral thiamine 200-300mg/day, vitamin B co strong 1 tds and supplements
  • Give K+ (2-4 mmol/kg/day), phosphate (0.3-0.6 mmol/kg/day), magnesium (0.2-0.4 mmol/kg/day)
31
Q

When is TPN indicated?

A

General critical illness:
* Severe malnutrition (> 10 % weight loss)
* Multiple trauma
* Sepsis with MOF
* Severe burns
Gut problems:
* Short bowel syndrome (short gut)
* Enterocutaneous fistula
* Bowel obstruction
* IBD
* Radiation enteritis

32
Q

coronary artery perfusion pressure =

A

systemic diastolic arterial pressure - LVED pressure

33
Q

What are some complications of hypothermia?
Systems

A
  • Cardiovascular: decreased cardiac output (anaesthetized), arrhythmias, vasoconstriction, ECG abnormalities (increased PR interval, wide QRS complex)
  • Respiratory: increased pulmonary vascular resistance and V/Q mismatch, decreased ventilator drive. Increased gas solubility
  • Renal: decreased renal blood flow and glomerular filtration rate, cold diuresis.
  • Hematological: reduced platelet function and coagulation, increased fibrinolysis, increased hematocrit, left shift of oxygen dissociation curve.
  • Metabolic: reduced basal metabolic rate, metabolic acidosis, insulin resistance, hyperglycemia.
  • Gastrointestinal / hepatic: reduced gut motility.
  • Neurological: reduced cerebral blood flow, impaired conscious state leading to coma.
34
Q

What are the three stages of haemostatsis?

A
  1. Vasoconstriction: smooth muscle contraction by local reflexes, thromboxane A2, serotonin released from activated platelets
  2. Platelet activation: adherence, aggregation, plug
  3. Coagulation: intrinsic and extrinsic pathway → fibrinogen → fibrin
35
Q

How to insert a central line?

A
  • Anatomical landmarks: mastoid process, carotid pulse and the depression between the two heads of sternocleidomastoid immediately above the clavicle.
  • Locate:
    o Clavicle
    o 2 heads of sternomastoid
  • In the center of the triangle formed by the previous land marks, palpate the carotid artery and insert the needle lateral to it.
  • The needle is directed at 30ᵒ angle towards the patient in the coronal plane aiming towards the ipsilateral nipple
  • Aspirate as the needle advances, once the blood is aspirated, cannulate the vein with Seldinger technique
  • Suture the line in place
36
Q

What is the naloxone dose?

A

0.4 -2 mg IV initially and repeat every 2-3 min if no response, to a maximum of 10 mg

MRCS Part B - Paul Edit (29 decks)

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