General Review Set 2 Flashcards

1
Q

What is the purpose of the Anion Gap?

A

Assess origin of metabolic acidosis by differentiating between gain in acid or loss of buffer

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2
Q

What are the general principles that would explain the abnormal conditions that would lead to a metabolic acidosis? (2)

A
  1. Net gain of fixed acids (increased production or decreased removal aka renal failure or disease)
  2. Reduction of buffer base (loss of bicarb via diarrhea)
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3
Q

How is the anion gap measured?

A

Comparing the difference between major measured cations (Na+) and major measured anions (Cl- + HCO3-) showing the amount of unmeasured anions

  • Na - (cl + HCO3)
  • Normal = 9-14 mmol/L
  • A balance would have a net neutral charge
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4
Q

Why does a normal anion gap metabolic acidosis cause fluid shifting?

A

When excessive bicarb is lost, an anion is lost (loss of negative charge) resulting in a chloride shift from intracellular to extra cellular spaces to maintain electroneutrality

  • Hyperchlormic imbalance causes fluid shifting (NAGMA)
  • recall the law of electroneutrality; they will shift to ensure balance.
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5
Q

What is the formula to calculate PaCO2 to compensate for metabolic acidosis?

A

PaCO2 = ([1.5xHCO3] + 8) +/- 2

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6
Q

what happens with a High Anion Gap Metabolic Acidosis (HAGMA)?

A
  1. Excessive fixed acids are produced (or ingested), the fixed acids dissipate in the blood into an acid (+ charge) and base (- charge) pair
  2. The acid is buffered by bicarb while the base remain = high anion gap with decreased bicarb (balances out with lower values)
  • just focus on the bolded bit
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7
Q

What factors may be helpful in recognizing a Myocardial Infarction (MI)?

A

Cardiac markers; there are more factors but these are good indicators from a blood gas

  1. Troponin I
  2. Creatine Kinase (CK)
  3. Myoglobin
  4. B-type Natriuertic peptide (NMB)
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8
Q

What cations and anions would be in the intracellular fluid?

A
  1. Cations = K+ and Mg++
  2. HPO4 and SO4
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9
Q

What cations and anions would be in the extracellular fluid?

A
  1. Cations = Na, K, Ca, Mg
  2. Cl, HCO3, Lactate
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10
Q

What is Diabetic Ketoacidosis (DKA)

A

In the absence of sufficient insulin, particularly in type 1 diabetes, the body breaks down fat for energy, producing ketones and leading to DKA, a potentially life-threatening condition

  • A complication of diabetes, type 1 is more common than type 2
  • Occurs when there is a culmination of keytones as a resulting in metabolic acidosis
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11
Q

What are keytones

A

Keytones are a byproduct of the use of fat as an energy source (rather than glucose and ATP); they are formally produced but the liver.

  • Culmination of keytones can result in metabolic acidosis
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12
Q

How does Diabetic Ketoacidosis differ between type 1 and 2 diabetes?

A
  • Type 1 is primarily due to insulin deficiency
  • Type 2 is often triggered by severe metabolic stress or relative insulin deficiency
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13
Q

Without insulin, would a body become hyperglycaemic or hypoglycaemic.

A

Hyperglycaemia would occur because glucose can’t enter the cells for energy without insulin.

  • Insulin promotes uptake of glucose into cells, especially muscle and adipose tissue.
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14
Q

What is type 1 diabetes?

A

An autoimmune condition where the pancreas produces little to no insulin.

  • leads to high blood sugar
  • requires insulin admin
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15
Q

What is type 2 diabetes

A

Insulin resistance and relative insulin deficiency

  • lifestyle choices are the cause and management involves lifestyle changes, oral meds, and insulin therapy in some cases
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16
Q

What are the primary functions of insulin

A

Regulation of blood glucose levels by:

  • Facilitating uptake of glucose into cells (and storage) which lowers it
  • Enhances utilization by converting by glycosides (glucose to ATP) for energy
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17
Q

Management of anaphylactic shock?

A

Early Intubation (Airways) and Epinephrine

  • Bronchodilators (Ventolin does not fix though)
  • Antihistamines
  • Corticosteroids
  • Fluid resuscitation
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18
Q

Management of neurogenic shock?

A

Fluid management + sympathomimetic agents (Vasoconstrictiing + Inotropic drugs)

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19
Q

Two mechanisms causing loss of vessel tone in distributive shock?

A
  1. Loss of sympathetic control (neurogenic)
  2. Presence of vasodilator substances in blood (anaphlaytic)
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20
Q

Effect of blood loss on hemoglobin and hematocrit

A

Decreased hemoglobin and hematocrit

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21
Q

Effect of fluid loss on hemoglobin and hematocrit?

A

Increased hemoglobin and hematocrit

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22
Q

what drugs would be given for a allergic reaction?

A

Epinephrine and vasodilators (initially) for severe reactions.

  • Prednisone or dexamethasone would be given if the reaction is not severe or an emergency.
  • Prednisone and dexamethasone would be continued after the incident to prevent a flare up.
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23
Q

Epinephrine Nebulized dosage?

A

1mg/ml (1:1000) or 3-5mls

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24
Q

what flow rate is required for Aersolization of medications with a SVN?

A

6-8 lpm for svn

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25
Q

Management strategy for VCD?

A

Call speech therapist if you can, but the following can be done:

  1. 3 sniffs followed by shhh sound
  2. Give a bento (lorazepam)
  • The goal with step 1 is to interrupt autonomic function with higher brain function actions
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26
Q

Why is a FLo2Max special?

A

Unlike a NRB, the flow can go down to 2lpm.

  • Recall that 6lpm is a minimum flow rate for masks to create CO2 washout
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27
Q

How to take HR and RR?

A
  1. Count for a full minute
  2. Count for 30 and x2
  3. Count for 15 and x4
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28
Q

How to take HR and RR?

A
  1. Count for a full minute
  2. Count for 30 and x2
  3. Count for 15 and x4
29
Q

What assessment and maintaince is typically required of an ETT during a routine ICU assessment?

A
  • Size/type
  • Depth, CxR to confirm
  • Position at the teeth
  • Cuff pressure
  • Inspection of the tube and site or site of necrosis or irritation/oral care and repositioning of the tube/section
30
Q

What assessment and maintaince is typically required of an ETT during a routine ICU assessment?

A
  • Size/type
  • Depth, CxR to confirm
  • Position at the teeth
  • Cuff pressure
  • Inspection of the tube and site or site of necrosis or irritation/oral care and repositioning of the tube/section
31
Q

What assessment and maintaince is typically required of an trach during a routine ICU assessment?

A
  • Size/type
  • CxR position
  • Cuff/Cuff pressure (is cuff up or down)
  • Stoma site inspection for discharge, dryness, bleeding, signs of infection
  • Tracheostomy care with suction if indicated
  • Weaning considerations
32
Q

How does PPV ventilation impact V/Q matching

A

Can increase V/Q mismatchin.

  • Can lower perfusion to the lungs
33
Q

How does PPV affect venous return and CO?

A

PPV decreases venous return (increased intrathoracic positive pressure) which causes decreased CO

34
Q

Which arrhythmias would receive cardio version?

A
  • Atrial fibrillation
  • Atrial flutter
  • Ventricular tachycardia
35
Q

What types of arrhythmias would require a pacemaker?

A

Bradycardia and heart blocks

36
Q

Why do consolidations occur with pneumonia?

A

Lung tissue becomes solid due to infection or inflammation

36
Q

What can be expected with dull percussion?

A

Fluid or solid tissue is present

  • Pleural effusion
  • Consolidation
  • Tumors
  • Atelectasis
37
Q

What can be expected with hyperresonant percussion?

A

Increased air content = enhances vibration of underlying tissues so…

  • pneumothorax
  • emphysema (hyperinflated)
  • Asthma (air trapping)
38
Q

What is obstructive (resorptive) atelectasis

A

When obstructions block an airway leading to the absorption of air from the alveoli distal to the blockage causing the alveoli to collapse

  • Can be caused by mucus plug, foreign body, tumor
  • common post op and chronic bronchitis
39
Q

What is compression atelectasis

A

External pressure on the lungs causing them to collapse.

  • usually occurs with pleural effusions, hemothorax’s, and pneumothoraxes
40
Q

What is the purpose of sigh breaths?

A

Recruit collapsed alveoli to improve gas exchange and oxygenation by:

  • Increasing FRC
  • Enhancing surfactant distribution
  • Maintaining lung compliance
41
Q

What are sigh breaths?

A

Deeper than normal breathes to help reopen collapsed alveoli preventing/reducing atelectasis

42
Q

Signs of reduced sympathetic nervous system function

A
  • Hypotension
  • Arrhythmias
  • bradycardia
  • no cough or gag
  • bronchial hyperreactivity.
43
Q
A
44
Q

Where should the ETT sit on a chest x ray?

A

2-5cm above the carina

  • the carina rests around the 5-7th rib
45
Q

Why does the diffusion rate increase when the pressure gradient and the surface area increases?

A

A larger pressure gradient increases the driving force for gas movement, and a greater surface area increases the available space for diffusion, both of which lead to an increased diffusion rate.

46
Q

What does henry’s law describe?

A

How o2 therapy works: the greater the pressure the greater the diffusion

  • gas diffusion is directly proportional to the gas partial pressure
47
Q

What can you expect for a v/q in the apical region of the lungs?

A

To have increased deadspace because perfusion is gravity dependent

48
Q

What can you expect for a Basal region v/q ratio

A

Lower v/q ratio: less deadspace more shunt

49
Q

What tissue layer attaches to the lung surface?

A

The visceral pleura, it is often what is felt for during a chest tube insertion

  • (make sure they aren’t touching the walls)
  • no pain fibres
50
Q

What tissue layer attaches to the inner chest wall?

A

The parietal pleura, has pain receptors

51
Q

What space lays between the parietal and visceral pleura?

A

The pleural space

52
Q

What space lays between the parietal and visceral pleura?

A

The pleural space

53
Q

How does Carboxyhemoglobin (HbCO) affect the oxyhemoglobin curve?

A

Shifts the curve to the left; Hb has 210x more affinity for CO than O.

54
Q

Why does Methemoglobin form? (MetHb)

A

Occurs when furious iron (Fe++) oxidizes to ferric (Fe+++) which cannot bind oxygen and is caused by nitrate posoning or toxic reaction to oxidant drugs

55
Q

What are traits of neurogenic shock?

A

Loss of sympathetic tone and vasodilation

  • loss of ability to sweat
  • low hemodynamic (parasympathetic reaction)
  • Occurs >T6
56
Q

Reduction of sympathetic nervous system signs?

A
  • Hypotension
  • Arrhythmias
  • bradycardia
  • no cough or gag
  • bronchial hyperreactivity.
57
Q

why is prednisone used for acute spinal cord injuries

A

Reduce inflammation in the body while also slowing the activity of the immune system

  • Can help your body by limiting the effects of inflammation, which can affect mobility or irritate nerves.
58
Q

Sympathetic vs parasympathetic?

A

Both are parts of the autonomic system (rest and digest). Both work together to maintain balance (homeostasis) in the body.

  • Parasympathetic promotes calm and recovery
  • Sympathetic system prepares the body for action and stress.
59
Q

What inotropes would be used to address spinal shock?

A

Norepinephrine is the preferred inotrope due to its strong vasoconstrictive and moderate inotropic effects.

  • Dopamine, epinephrine, and phenylephrine can also be used depending on the patient’s specific hemodynamic needs.
60
Q

What injury is associated with the following:

  • Injury is above T6 vertebrae and blunts the ability to sweat?
A

Neurogenic shock

61
Q

4 Cardinal signs of airway obstruciton

A
  • Hot potato voice
  • Stridor
  • Sensation of dyspnea
  • Drooling (difficulty of swallowing secretions)
62
Q

Why does HFNC work well with Bronchiolitis treatment?

A

Deadspace washout and improves WOB

  • Success is indicated by improved R R and HR
  • Assessment should be done within the first hour
63
Q

Why do you keep lower PEEPs on hypotensive patients?

A

Preserving venous return; lower peep reduces intrathoracic pressure which helps maintain better venous return to the heart, in turn maintains CO which helps stabilize BP

64
Q

why does increased intrathoracic pressure decrease cardiac output and heart rate?

  • hint think Frank starling curve
A

Heart can’t stretch as much, HR will initially increase to compensate than decrease (decompensate)

65
Q

In BiPAP what would you max IPAP setting be and why?

A

Generally 25, but can go up to 28 depending on patient.

  • the big concern is gastric distension
  • EPAP is based on need, so play it by the patient
66
Q

Aside from CHF, why would there be increased vascularization on an x-ray?

A

The body is compensating to improve v/q, the apices are better ventilated so it disperses to improve v/q

67
Q

What does mottled skin indicate?

A
  • Poor skin perfusion
  • Decreased CO
  • Cold stress
68
Q
A