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MRCS PART B > cRIT CARE > Flashcards

cRIT CARE Flashcards

1
Q

What is pulse pressure?

A

Difference between systolic and diastolic
Represents force of the heart

Low - reduced stroke volume as preload decreased

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2
Q

Compartment syndrome

A

increased pressure within a closed osteofascial compartment, resulting in impaired local circulation and necrosis of muscle

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3
Q

Rhabdo tx

A
  • 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.
  • Alkalinisation : Sodium bicarbonate infusion has been used to limit myoglobin- induced
    tubular injury in the presence of acidic urine. It alkalinises the urine >
    6.5 pH.
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4
Q

Preload

A

End diastolic volume of the ventricles

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5
Q

Regulation of BP

A

Short term - Baroreceptors (sensors located in the carotid sinus or aortic arch), sensing blood pressure via stretch .

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6
Q

Angiotensin II

A

Vasocontrictor
increases sodium reabsorption

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7
Q

Fasciotomy

A

Anterolateral - 15-20cm incision anterior to shaft of fibula. LM -TT - careful of SPN

Posteriomedial - 15-20cm incision, MM- TT

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8
Q

Pancreatitis station - management

A

I will resuscitate this patient by giving him a fluid bolus and providing analgesia!!

Nutrition
fluid

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9
Q

Cause of retroperitoneal bleeding

A

AAA, pancreatitis

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10
Q

Which factors stimulate pancreatic secreation

A

Vagal, secretin, CCK, gastrin

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11
Q

Pathogenesis of pancreatitis

A

Duct obstruction -> premature activation of pancreatic digestive enzymes -> autodigestion -> trypsin -> increase in vascular permeability

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12
Q

Why NJ tube feeding in pancreatitis

A

Passes duodenojejunal flexure - prevents CCK being released

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13
Q

Transmission of pain

A

1st order - Nociceptors -> alpha fast, delta slow
2nd order - spinal cord - spinotholamic tract
3rd order - primary somatosensory cortex - thalamus

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14
Q

ADH

A

released due to increase serum osmalirity and decreases in volume

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15
Q

Afterload

A

Pressure heart must work during systole

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16
Q

Signs of As

A

Ejection systolic murmur
Pardoxical splitting of S2
narrowed pulse pressure

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17
Q

CPP

A

Systemic diastolic arterial pressure - LVED Pressure

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18
Q

Hypocalcemia signs

A

Paraesthesia, tetany, larygospasm, seizure, confusion

QT prolongation, bradycardia, dilated cardiomyopathy

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19
Q

Hypercalcemia ECG

A

Short QT, Wide T, ST elevation, prominent U

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20
Q

How is CO2 carried in the blood

A

Bicarbonate
carboxyheamoglobin
dissolved

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21
Q

ABG - resp acidois compensation

A
  1. cellular bicarb - small amount
  2. renal - takes 3-5 days
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22
Q

Clinical markers of cardiac index

A

Pulse rate, systolic BP, CRT, Temp, urine output

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23
Q

what are the different types of pelvic fractures

A

Young Burgess
- Lateral compression
-Anteroposterior compression
- Vertical shear

24
Q

What is inside a neutrophil

A

lysomal granuals

25
Q

How do neutrophils bind

A

Margination - adhesion - transmigration - migration

26
Q

What is cerebral perfusion pressure?

A

Net pressure gradient causing blood flow to the brain

CPP = MAP - ICPSV

27
Q

Why does dilation occur in raised ICP?

A

Uncus of the temporal lobe of brain herniates through the tentorium cerebelli
occulomotor nerve compresed
parasympathetic paralysis
unopposed sympathetic - mydriasis

28
Q

Burns:
How do you assess adequacy of fluid?

A
  1. Clinical measures of cardiac index
  2. Central venous pressure - reflection of right heart
  3. Hemotocrit
29
Q

Types of burns

A

Superficial
- Dry, red, no blisters, pain , brisk CRT

Superficial partial thickness
- moist, red/pink, blisters, sluggish

Superfical deep
-moist, blotchy, pain, no CRT

Full thickness
- dry, black, no pain, no CRT,

30
Q

Why no colloids in burns

A

Burns can lead to capillary leak
colloids leak into extravascular space, exerts oncotic pressure and triggers third space loss

31
Q

What is cushings response?

A

physiological nervous system response (mixed vagal and sympathetic stimulation) to an elevated ICP that results in cushing’s triad.

Increased sytolic bP and widened PP
Bradycarida
irregular bretahing

32
Q

Raised ICP clinical picture

A

Headache
N+V
Papiloedema
Dilated pupil - occulomotor
Lateral gaze - abducens

33
Q

What are the effects of raised ICP?

A

Decreased CPP - ischemia
Midline shift - ventricular outflow obstruction
Herniation - occulomotor damage
compression of medulla - ventilation

34
Q

Difference between neurogenic and spinal shock?

A

Neuorgenic is a form of distbutive shock - autonimic dysfucntion - lack of sympathetic
This leads to hypotension, bradycardia and vasodilation

spinal shock - transient
Loss of sensormotor
physiological repsonse - can improve
lack of reflexes and muscle
some featurres of neuor shock - bradyacraida and hypotension

35
Q

Function of potassium

A

Fluid balance
nerve impulse function
muscles function
cardiac muscle function

36
Q

Homeostasis of potassium

A

Potassium = intracellular
Na/k pump - insulin
Na/k - DCT- Aldosterone
Acid base stasis of blood

37
Q

hyperkalemia on heart

A

Depolirasation of resting membrane -> BRADYCARDIA -> Cardiac arrest, decrease action potential

38
Q

High urine output post AKI

A

Initially reduced GFR, then recovers, distal tubules do not recover - plasma filtered at glomerulus is not reabsorbed - extreme polyuria

39
Q

Chronic renal failure and anaemia

A

Reduced production of EPO
Circulating bone marrow toxins -> bone marrow supression
ureamia increases cell wall fragidity

40
Q

What leads to an increase in Aldosterone

A

Increased angiotensin ii
reduced sodium
Increased potassium

41
Q

Counter current

A

Thick ascending limb imperable to water -

42
Q

Stages of wound healing

A
  1. Heamostasis - vasoconstriction, platelets, activation of cascade
  2. inflammation - neutrophils
  3. inflammation - macrophages
  4. proliferative - fibroblasts , epitherlisation
  5. maturation, remnodelling
43
Q

How does vascular surgery interfere with heamostasis?

A

Easier platelet activation, higher fibrinogen, shutdown of fibrinolysis

44
Q

What is DIC

A

Pathological consumpative coagulopathy due to activation of the coagulation and fibrolynitc system. This leads to formation fo mico thrombi and consumption of clotting factors and fibronogen.

45
Q

Signs of DIC

A
  1. Widespread heamorrhage
  2. Thombocytopenia , decreased fibrinogen and increased FDP
46
Q

What is necrotising facsitis

A

Necrotising fasciitis is a life-threatening rapidly-progressing infection that spreads along the fascial planes and subcutaneous tissue.

47
Q

fever

A

pyogenes -> IL1 and TNF alphas -> prostaglandin in hypothamus -> fever

48
Q

Crystalloids

A

Water soulable moleulces

49
Q

Colloids

A

Contain larger insoluable molecules

50
Q

Why no colloids in trauma

A

in SIRS - Endothelial dysfunction - capillary leak.
colloids can seap through and pull out water

51
Q

What is MAP?

A

Average arterial pressure mainatined throughout a cardiac cycle

52
Q

Compents of TPN

A

Water, carbohydrates (50%), lipids (30%), proteins, vitamins, nitrogen, trace elements

53
Q

Negatives of complete carbohydrate feed

A

glucose intolerance: as part of the stress response, critically unwell patients are often in a state of
hyperglycemia and glucose intolerance.

  • Fatty liver: the excess glucose occurring as a consequence of the above is converted to lipid in the liver
  • Respiratory failure: the extra CO2 released upon oxidation of the glucose may lead to respiratory failure and increased ventilatory requirements
  • Relying solely on glucose may lead to a deficiency of the essential fatty acids.
54
Q

How would you manage hypovalemic shock

A
  1. Fluids and bloods
  2. Control bleeding - pelvic binder, stabilising fractures, laparotomy
55
Q

Pathophysiology of ARDS

A
  • An acute phase, characterized by
    1) Widespread destruction of the capillary endothelium, extravasation of protein-rich fluid and interstitial
    edema
    2) Migration of neutrophils and extensive release of cytokines
    3) The alveolar basement membrane is also damaged, and fluid seeps into the airspaces, stiffening the
    lungs and causing ventilation/perfusion mismatch.
  • A later reparative phase, characterized by
    4) Fibroproliferation, and organization of lung tissue.
    5) If resolution does not occur, disordered collagen deposition occurs leading to extensive lung scarring.
56
Q

Portal HTN

A

Cirrhosis resulting from chronic liver disease and is characterized by liver cell damage, fibrosis and nodular
regeneration.

The fibrosis obstructs portal venous return and portal hypertension develops.
* Arteriovenous shunts within the liver also contribute to the hypertension

MRCS PART B (10 decks)

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