Respiratory Control and Arterial Blood Gases Flashcards

1
Q

What are Central Pattern Generators?

A
  • neuronal circuits that can produce rhythmic motor patterns, for breathing

Various inputs that can modify this rhythm

  • Emotional inputs from the cerebral cortex
  • Lung mechanoreceptors
  • Chemoreceptors (central/peripheral)
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2
Q

What is Minute Ventilation (VE)?

A
  • Respiratory Rate x Tidal Volume
  • RR x TT
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3
Q

What is the Pleuritic Chest Pain?

A
  • pain caused by inflammation of the parietal pleura, most pronounced with deep breathing, coughing, sneezing or laughing
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4
Q

What is a Pleural Rub?

A
  • abnormal lung sounds caused by layers of pleura rubbing together during breathing
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5
Q

What are the inspiratory muscles and their innervation?

A
  • Diaphragm: Phrenic nerves from C3-C5
  • External Intercostal Muscles: Thoracic nerve T1-T11

Accessory muscles

  • Sternocleidomastoid: XI cranial Nerve
  • Scalene muscles: C3-C8
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6
Q

What are the expiratory muscles and their innervation?

A
  • Abdominal wall: T5-T12
  • External intercostal muscles: T1-T12
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7
Q

Pons and DRG

Explain the Respiratory Centre

A
  • Cerebrum –> Pons –> Medulla Oblongata

Pons

  • contains two nuclei
  • not essential for respiration but exerts fine control over medullary neurons

Medulla Oblongata

  • Dorsal Respiratory Group of Neurons: trigger inspiratory impulses
  • Ventral Respiratory Group: trigger inspiratory and expiratory impulses, during exercise and other times of active exhalation
  • Central chemoreceptors: detect H+ in the CSF, reflects the amount of CO2 in the blood
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8
Q

What are lug stretch receptors?

A
  • mechanoreceptors in the lungs, in the vagal nerve afferent fibers
  • they sense lung stretching, and terminate the breath to prevent over-stretching
  • Sense abnormal changes in airway mechanical properties
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9
Q

What are irritants and particulate receptors?

A
  • mechanoreceptors, that are part of the vagal afferent fibers
  • C-fiber neurons: activated by oedema and molecules such as bradykinin
  • Irritant receptors: respond to punctate mechanical stimuli
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10
Q

What is involved in sensing peripheral PO2 and CO2 ?

A
  • The Carotid body: a bundle of cells outside the bifurcation of the carotid arteries.
  • they do the bulk of the sensing
  • carotid bodies also sense pH
  • The Aortic Body: a bundle of cells within the aortic arch
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11
Q

What is the ventilatory response of peripheral chemoreceptors to PCO2

A
  • the body is very sensitive to changes in PCO2 and the VE (minute ventilation) can be changed to compensate for this
  • this effect is reduced when opioids are ingested: this is the most common cause of hypercarbic respiratory failure
  • if there is hypercarbia, the body is more sensitive to hypoxaemia
  • the body is more sensitive to CO2
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12
Q

What are the two types acidosis?

A
  • Respiratory acidosis: High PCO2
  • Metabolic acidosis: Low HCO3-
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13
Q

What types of alkalemia are there?

A
  • Respiratory alkalosis: low PCO2
  • Metabolic alkalosis: high HCO3-
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14
Q

What can cause Metabolic Acidosis?

A
  • *Renal Tubular acidosis (RTA)**
  • types I-III
  • all show loss in urinary bicarbonate and hyperchloremic acidosis

GI Losses

Acetazolamide

Excessive chloride administration (intravenous fluids with NaCl)

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15
Q

What is the anion gap?

A

the uncounted anions- the uncounted cations

  • this consists mainly of albumin, phosphate, sulfate, etc..
  • should 12mEq/L
  • main cations = K+, Na+
  • main anions= Cl-. HCO3-
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16
Q

What is Anion Gap Metabolic Acidosis?

A
  • an increase in the number of anions in the blood sue to metabolic processes
  • anion gap is > 12mEq/L
17
Q

GOLD MARK

What are the causes of Anion Gap Metabolic Acidosis?

A
  • Glycols (ethylene and propylene)
  • Oxoproline
  • L-lactate
  • D-lactate
  • Methanol
  • Aspirin
  • Renal failure
  • Ketoacidosis
18
Q

What are the compensatory mechanisms for both types of acidosis?

A
  • Respiratory acidosis: retain HCO3 through metabolic mechanisms, can take days
  • Metabolic acidosis: reduce CO2: increase respiratory rate
19
Q

What are the compensatory mechanisms for both types of alkalosis?

A
  • Respiratory alkalosis: reduce HCO3 in the body, increased excretion through the kidneys
  • Metabolic alkalosis: retain CO2, reduced BR/ hypoventilation
20
Q

What is Base Excess/Deficit?

A
  • Base Excess: the dose of acid that would be needed to return blood to normal under standard conditions
  • Base Deficit: the dose of alkali needed to return blood to normal pH
21
Q

What is the cause of metabolic alkalosis?

A
  • increased aldosterone
  • vomiting
22
Q

What care causes of respiratory acidosis?

A
  • increased dead space e.g emphysema
  • weakness; depression of respiratory centre
23
Q

What causes respiratory alkalosis?

A
  • hyperventilation due to pain or anxiety
  • pregnancy
  • hypoxaemia
24
Q

VE= minute ventilation

What is the definition of hypoventilation with regards to the VE?

A
  • when ventilation is insufficient to maintain a normal PaCO2 and acid-base status
  • low ventilation
25
Q

What can cause respiratory depression?

A
  • Opiates/ narcotics (heroin, legal prescription narcotics)
  • Alcohol
  • Anaesthesia and other sedatives
  • Cerebral diseases
26
Q

What can be seen in this CXR?

A
  • a saddle embolism
  • straddles the bifurcation of the pulmonary trunk
27
Q

What is HAPE?

A
  • High Altitude Pulmonary Oedema
  • non-cardiogenic pulmonary oedema
28
Q

What are the signs and symptoms of a PE?

A
  • Hypoxaemia
  • Dyspnoea
  • Cough
  • Pleuritic Chest pain
  • Pleural Rub
  • Syncope
  • Tachycardia
29
Q

Symptoms of a DVT

A
  • Calf pain
  • Leg swelling
30
Q

What diagnostic testing can be done for a PE or DVT?

A
  • Blood D-dimer level: screen for a possible clot, D-dimers are present in crosslinked fibrin mess ( a clot) –> not specific to PE
  • V/Q Scan for a PE
  • CT pulmonary angiography for a PE
  • Duplex ultrasound for a DVT