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C. Year 3: Clinical Foundations Course > Critical Care and the unwell patient post surgery > Flashcards

Critical Care and the unwell patient post surgery Flashcards

1
Q

What is the definition of shock?

1 - lack of respiratory drive
2 - failure of circulation to provide adequate perfusion of tissues
3 - increases tachycardia
4 - syncope

A

2 - failure of circulation to provide adequate

  • various classes ranging from I - IV
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2
Q

Acid-base disorders is a pathologic change in CO2 partial pressure (Pco2) or serum bicarbonate (HCO3−) that typically produce abnormal arterial pH values. What is the normal pH of blood?

1 - 7.30 - 7.45
2 - 7.20 - 7.45
3 - 7.35 - 7.45
4 - 7.34 - 7.65

A

3 - 7.35 - 7.45

<7.35 = acidosis
<7.45 = alkalosis

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3
Q

Acid-base disorders is a pathologic change in CO2 partial pressure (Pco2) or serum bicarbonate (HCO3−) that typically produce abnormal arterial pH values. If the PCO2 is >6.0 kPa (45mmHg) is this respiratory acidosis or alkalosis?

A
  • respiratory acidosis
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4
Q

Acid-base disorders is a pathologic change in CO2 partial pressure (Pco2) or serum bicarbonate (HCO3−) that typically produce abnormal arterial pH values. If the PO2 is <4.7 kPa (35mmHg) is this respiratory acidosis or alkalosis?

A
  • respiratory alkalosis
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5
Q

Bases are HCO3-
Acids are CO2

What is the normal range for a base excess?

1 - +1 to +2
2 - -1 to +2
3 - -2 to +2
4 - 0 to +2

A

3 - -2 to +2

  • normal we would expect, but the range can be - or +2
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6
Q

Acid-base disorders is a pathologic change in CO2 partial pressure (Pco2) or serum bicarbonate (HCO3−) that typically produce abnormal arterial pH values. If the HCO3- is <24mmol/l or a base excess (BE) < -2 is this metabolic acidosis or alkalosis?

A
  • metabolic acidosis
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7
Q

Acid-base disorders is a pathologic change in CO2 partial pressure (Pco2) or serum bicarbonate (HCO3−) that typically produce abnormal arterial pH values. If the HCO3- is >24mmol/l or a base excess (BE) > +2 is this metabolic acidosis or alkalosis?

A
  • metabolic alkalosis
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8
Q

Is a metabolic alkalosis or acidosis compensated for quickly by respiration or renal function?

A
  • respiratory is rapid response
  • changes in CO2 retention or expiration
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9
Q

Is a metabolic alkalosis or acidosis compensated for slowly by respiration or renal function?

A
  • renal function is slow
  • retains or excretes HCO3-
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10
Q

Which of the following does NOT typically cause respiratory alkalosis?

1 - PE
2 - pneumonia
3 - sepsis
4 - pain
5 - vomiting

A

5 - vomiting

  • all others cause respiratory alkalosis due to hyperventilation
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11
Q

Which of the following does NOT typically cause respiratory acidosis?

1 - severe pneumonia
2 - sedation/opioids
3 - ontubdation (drowsy)
4 - diarrhoea

A

4 - diarrhoea

  • all others reduce respiration and therefore retain CO2
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12
Q

Which of the following does NOT typically cause metabolic acidosis?

1 - hypoperfusion
2 - kidney failure
3 - vomiting
4 - gut dysfunction

A

3 - vomiting

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13
Q

Which of the following cause metabolic alkalosis?

1 - hypoperfusion
2 - kidney failure
3 - vomiting
4 - gut dysfunction

A

3 - vomiting

  • loss of HCL so too much HCO3-
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14
Q

The oxygen-hemoglobin dissociation curve shows the relationship between haemoglobin saturation with O2 (SO2) and partial pressure of O2 (PO2).

Partial pressure is a measurement of the individual components of a mixture of gas. Therefore if PO2 is high then there is more change for more O2 to bind with haemoglobin.

A

Haemoglobin absorbs different wavelengths of light depending on the degree of saturation. This is the basis of how pulse oximetry works.

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15
Q

Which of the following is the main driver of haemoglobin saturation?

1 - iron
2 - haematocrit
3 - PO2
4 - copper

A

3 - PO2

  • more O2 means more O2 to bind to haemoglobin
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16
Q

The oxygen-hemoglobin dissociation curve is plotted as a sigmoidal shape. What relevance does this have?

1 - less O2 affinity as O2 binds to haemoglobin
2 - increased O2 affinity as O2 binds to haemoglobin
3 - no relationship

A

2 - increased O2 affinity as O2 binds to haemoglobin

  • essentially easier to bind the 4th O2 molecule than the first O2 molecules
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17
Q

What is typically deemed an acceptable % saturation of O2 to haemoglobin that is sufficient to ensure adequate tissue perfusion?

1 - 90%
2 - 94%
3 - 75%
4 - 60%

A

2 - 94%

  • roughly = to 60mmHg
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18
Q

If a patient switches to anaerobic metabolism this can lead to an increase in what being released and diffusing into the blood?

1 - CO2
2 - O2
3 - Cl-
4 - K+

A

1 - CO2

  • causes increased PCO2
  • more CO2 binds to RBCs
  • carbonic anydrase converts H20 and CO2 into HCO3- and H+
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19
Q

If a patient switches to anaerobic metabolism this can lead to an increase in CO2 being released and diffusing into the blood. This is absorbed by RBCs, which create HCO3- and H+ due to carbonic anhydrase. What then happen to the pH?

1 - increases
2 - remains constant
3 - decreases

A

3 - decreases

20
Q

If we look at the oxygen-hemoglobin dissociation curve, it will shift to the right in times of stress due to increased CO2, reduce pH and increase temperatures What affect does this have on RBCs affinity for O2?

A
  • reduces
  • means O2 can be quickly offloaded where required
21
Q

2,3-diphosphoglycerate (2,3 DPG) acid present in RBCs and is a metabolic byproduct of glycolysis in RBCs. Does 2,3 GPG increase or decrease in times of stress or hypoxia?

A
  • increase production in RBCs
  • decreases where O2 levels are high, like near the lungs
22
Q

2,3-diphosphoglycerate (2,3 DPG) acid present in RBCs and is a metabolic byproduct of glycolysis in RBCs. 2,3 GPG increase during times of stress or hypoxia. Does 2,3 DPG increase or decrease haemoglobin affinity for O2?

A
  • decrease
  • good as it allows O2 to deposited where it is needed most
23
Q

In the oxygen-hemoglobin dissociation curve, it can shift to the right in the following:

  • increased CO2
  • increased temperature
  • increased 2,3 DPG
  • decreased pH

This causes an reduced affinity for O2 to RBCs. Does this mean a higher or lower partial pressure of O2 is required to saturate haemoglobin?

A
  • higher PO2 is required
24
Q

In the oxygen-hemoglobin dissociation curve, it can shift to the right in the following:

  • decreased CO2
  • decreased temperature
  • decreased 2,3 DPG
  • increased pH

This causes an increased affinity for O2 to RBCs. Does this mean a higher or lower partial pressure of O2 is required to saturate haemoglobin?

A
  • lower PO2 is required
25
Q

How much less should arterial PaO2 be than inspired O2 concentration?

1 - 50
2 - 25
3 - 10
4 - 1

A

3 - 10

  • O2 is diluted in alveolus with Co2 and H2O
  • if patient is given 30 or 50% O2 it will give a PaO2 of around 20 and 40kPa respectively
26
Q

If we know that oxygen is diluted by approximately 10 in the alveolus with CO2 and H2O and a patient is given 50% oxygen, but has a PaO2 of 15 kPa, what does that suggest?

1 - inspired O2 is not 50%
2 - patients mask is ill fitting
3 - patient has severe respiratory problems

A

3 - patient has severe respiratory problems

  • inability to oxygenate
27
Q

The VQ or ventilation/perfusion ratio can tell us about the lung function.

  • alveolar ventilation = O2 reaching alveolar (L/min)
  • perfusion = pulmonary blood flow reaching arteries and capillaries around alveolar (L/min)

What is the normal VQ in a patient who is healthy and stood upright?

1 - 0.5
2 - 0.8
3 - 1.2
4 - 2.0

A

2 - 0.8

normal V = 4L/min
normal Q = 5L/min
4/5 = 0.8

28
Q

The VQ or ventilation/perfusion ratio can tell us about the lung function.

  • alveolar ventilation = O2 reaching alveolar (L/min)
  • perfusion = pulmonary blood flow reaching arteries and capillaries around alveolar (L/min)

These can be caused by shunts, which is a perfused lung but no ventilation. Here blood is diverted away from the non-ventilated alveoli. Which of the following is NOT an example of this?

1 - COPD
2 - cystic fibrosis
3 - emphysema
4 - PE

A

4 - PE

  • the patient would have a normal Q but a low V
  • patient has a POOR response to O2
29
Q

The VQ or ventilation/perfusion ratio can tell us about the lung function.

  • alveolar ventilation = O2 reaching alveolar (L/min)
  • perfusion = pulmonary blood flow reaching arteries and capillaries around alveolar (L/min)

These can be caused by increased dead space. Here the lungs are being ventilated but there is less or no blood blood. Which of the following is NOT an example of this?

1 - gas embolism
2 - hypovolaemia
3 - emphysema
4 - PE

A

3 - emphysema

  • the patient would have a normal V but a low Q
  • patient has a GOOD response to O2
30
Q

If a patients has a pulmonary embolism this can block the pulmonary artery and create an acute increase in dead space (non-perfused lung tissue). Which of the following is NOT a symptom a patient is likely to present with if they have a PE?

1 - bradycardia
2 - dyspnoea (difficulty breathing)
3 - chest pain
4 - haemoptysis
5 - cough
6 - fever

A

1 - bradycardia

  • it would cause tachycardia
31
Q

What blood marker can be used to indicate deep vein thrombosis, which can lead to a PE?

1 - troponin
2 - D-dimer
3 - atrial natriuretic peptide
4 - CRP

A

2 - D-dimer

  • a fibrin degradation product
32
Q

Aspiration pneumonia can occur post operatively. Is this dangerous?

A
  • yes
  • high rates of mortality
33
Q

While in hospital patients may develop hospital acquired pneumonia (HAP) within 72 hours following admission. Which strain of bacteria is most likely to cause this?

1 - E.coli
2 - staphylococcus
3 - streptococcus
4 - klebsiella

A

2 - staphylococcus

34
Q

While in hospital patients may develop hospital acquired pneumonia (HAP) within 72 hours following admission caused by staphylococcus. Which of the following is NOT a symptom of perioperative pneumonia?

1 - cough
2 - dyspnoea
3 - hypothermia
4 - lethargy
5 - green/yellow sputum

A

3 - hypothermia

  • would normally cause fever
34
Q

While in hospital patients may develop hospital acquired pneumonia (HAP) within 72 hours following admission caused by staphylococcus aureus
3 - streptococcus
4 - klebsiella

A
35
Q

Which of the following is NOT a sepsis 6?

1 - give fluids
2 - give analgesia
3 - give oxygen
4 - take urine count
5 - take blood lactate
6 - take 2 blood cultures

A

2 - give analgesia

  • we should give antibiotics
36
Q

If a patient has a haemorrhage, does their Hb drop immediately?

A
  • no
37
Q

If a patient needs blood, typically which blood is given?

1 - group A
2 - group B
3 - group AB
4 - group O

A

4 - group O

  • no antigens, so anyone can have it
  • people with O blood can ONLY receive O blood type though
38
Q

If a patient requires resuscitation fluids, how much and how quickly should it be given typically?

1 - crystalloid bolus of 500ml with Na+ (130-154mmol) over 15 mins
2 - crystalloid bolus of 250ml with Na+ (135-155mmol) over 15 mins
3 - crystalloid bolus of 500ml with Na+ (135-155mmol) over 30 mins
4 - crystalloid bolus of 150ml with Na+ (150-160mmol) over 15 mins

A

1 - crystalloid bolus of 500ml with Na+ (135-155mmol) over 15 mins

39
Q

If a patient requires maintenance fluids, how much and how quickly should it be given typically?

1 - 2.5 - 3ml/kg/day of water
2 - 2.5 - 30ml/kg/day of water
3 - 25 - 30ml/kg/day of water
4 - 25 - 3ml/kg/day of water

A

3 - 25 - 30ml/kg/day of water

  • 1mmol/kg/day of Na+. K+ and chloride
  • 50-100g glucose
40
Q

Top calculate mean arterial pressure (MAP), we use the formula:

MAP - central venous pressure (CVP), which is = to cardiac output x systemic vascular resistance. Why is MAP important?

1 - perfusion of the heart
2 - pressure around renal arteries
3 - perfusion pressure of organs

A

3 - perfusion pressure of organs

41
Q

How do we calculate mean arterial pressure (MAP) in a clinical setting?

1 - diastolic x 2 add systolic BP
2 - diastolic BP add systolic BP
3 - diastolic BP add 1/3 of systolic BP

A

3 - diastolic BP add 1/3 of systolic BP

42
Q

What is hypovolaemic shock?

1 - afterload reduction and possible bradycardia
2 - increased preload, decreased contractility and increased afterload
3 - preload reduced with compensatory increase in afterload
4 - afterload reduction due to vasodilation and increased HR

A

3 - preload reduced with compensatory increase in afterload

  • caused by blood loss, diarrhoea, burns or tissue oedema
43
Q

What is septic shock?

1 - afterload reduction and possible bradycardia
2 - increased preload, decreased contractility and increased afterload
3 - preload reduced with compensatory increase in afterload
4 - afterload reduction due to vasodilation and increased HR

A

4 - afterload reduction due to vasodilation and increased HR

  • caused by endotoxins or exotoxins and mediated by immune response
44
Q

What is cardiogenic shock?

1 - afterload reduction and possible bradycardia
2 - increased preload, decreased contractility and increased afterload
3 - preload reduced with compensatory increase in afterload
4 - afterload reduction due to vasodilation and increased HR

A

2 - increased preload, decreased contractility and increased afterload

  • myocardial injury
45
Q

What is spinal shock?

1 - afterload reduction and possible bradycardia
2 - increased preload, decreased contractility and increased afterload
3 - preload reduced with compensatory increase in afterload
4 - afterload reduction due to vasodilation and increased HR

A

1 - afterload reduction and possible bradycardia

  • sympathetic block
46
Q

What is obstructive shock?

1 - afterload reduction and possible bradycardia
2 - increased preload, decreased contractility and increased afterload
3 - preload reduced with compensatory increase in afterload
4 - decreased preload, distended neck veins, reduced contractility

A

4 - decreased preload, distended neck veins, reduced contractility

  • caused by cardiac tamponade or tension pneumothorax

C. Year 3: Clinical Foundations Course (8 decks)

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