gas transport, control of ventilation and ABGS Flashcards
Gas transport
Oxygen
Bound to Hgb (SaO2)
Dissolved in plasma
Carbon dioxide
Bicarbonate
CO2 + H2O = H2CO3 = H+ + HCO3-
Bound to Hgb
Dissolved in plasma
control of ventilation
Mechanoreceptors: respond to stretch during inflation. A very large inflation can lead to a critical stretch of the lung parenchyma causing the Hering-Breuer reflex to which stops inspiration. These are found in the bronchial smooth muscle, trachea and visceral pleura.
Irritant receptors: respond to irritants such as cigarette smoke, dust, allergens or secretions. Cause a change in respiratory depth or frequency and induce a cough, sneeze or bronchospasm.
Chemoreceptors: most important of the sensors. Constantly sample arterial blood to maintain respiratory gases and pH within normal range located centrally (medulla) and peripherally (aortic arch and carotid body)
chemoreceptors
Centrally: in brain stem, increased H+ concentration in CSF
Peripherally: along major systemic arteries, principal stimulant is low pO2 in arterial blood. (Hypoxic drive)
hypoxic drive theory
If you give peole with COPD too much O2
Resp rate slows
Potential loss of consciousness
V/Q mismatch
Poorly ventilated alveoli will cause the body to reattribute blood flow: alveolar vasoconstriction
Administration of oxygen will cause vasodilation.
Alveoli are still poorly ventilated but are now better perfused= V/Q mismatch
Haldane effect
Where O2 concentration is lower CO2 carrying capacity of blood is increased. This is because O2 is realised from Hb to allow CO2 to bind
Administration of oxygen causes increased CO2 levels in the blood as it can not bind with Hb
Increased CO2 in the blood stream
Healthy people can increase minute ventilation to get rid of increased CO2 but COPD patients can not.
COPD and supplemental O2
Careful administration of O2 to COPD patients
Aim to maintain SpO2 of 88-92%
hypoxia and hypoxemia
Hypoxia: deficiency in the amount of oxygen reaching the tissues
Hypoxaemia: deficiency of oxygen in the arterial blood
causes of hypoxaemia
Alveolar hypoventilation Respiratory depression Respiratory muscle weakness Obstructive airways disease Diffusion Pulmonary oedema Acute respiratory distress syndrome V/Q mismatch Alveolar collapse Pneumothorax Obstructive airways disease
treatment of hypoxaemia
- Supplemental oxygen
- Physiotherapy
Positioning, mobilisation,
clearance of excess secretions,
use of adjuncts e.g. Flutter, Acapella - Non-Invasive Ventilation
Respiratory failure
May prevent mechanical ventilation
May facilitate earlier extubation
NIPPV; CPAP; BiPAP - Mechanical Ventilation
Pt. sedated, eliminates metabolic cost of breathing
Normal:<5% VO2. Critically ill: Up to 30% VO2
hypoxia clinical features
Dyspnoea Cyanosis Altered mental state Tachypnoea/hypoventilation Arrhythmias Peripheral vasodilation Systemic hypotension Coma
Arterial blood gases
A small sample of arterial blood is drawn from an artery to allow for analysis of oxygenation and acid-base balance of the patients blood and to guide treatment decisions.
Painful
ABG purpose
To evaluate acid-base status To evaluate oxygenation status To evaluate adequacy of ventilation To monitor patient To evaluate treatment
5 components of ABGs
pH 7.35 - 7.45 PaCO2 4.6 - 6 kPa PaO2 10.6 - 14.6 kPa HCO3- 22 – 26 mmol/L SaO2 95 - 100% 1kPa = 7.5 mmHg
hypoxaemia
PaO2 O2Saturation
Mild 8 - 10.5kPa 90-94%
Moderate 5.3 - 7.9kPa 75 – 89%
Severe < 5.3kPa < 75%
