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16 Cards in this Set
- Front
- Back
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Oxyhemoglobin Dissociation Curve
Factors |
pH
PCO2 Temperature Concentration of 2,3 DPG (component found in RBC) |
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Oxyhemoglobin Dissociation Curve
Right Shift |
R - Hgb has affinity for O2
More difficult for Hgb to pick up O2 R – O2 is more readily given up – tissues 2,3 DPG – Diphosphoglycerate Produced by erythrocytes Binds w/ Hgb & affinity of Hgb for O2 Fever, Acidosis,CO2 2,3 DPG Less oxygen being picked up because DPG is taking it’s place. At the tissue site o2 is readily given up, but there is not much so there may be hypoxia Rise in 2, 3 DP g H+ (acidosis, elevated H ions) temperature |
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Oxyhemoglobin Dissociation Curve
Left Shift |
L – Hgb has affinity for O2
Easier to pick up oxygen Hgb is more saturated for a given PaO2 L - O2 is less readily given up – tissues Tissue hypoxia temp, hypocapnia, Alkalosis, 2,3 DPG |
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Alveolar Shunt
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Atelectasis
Pulmonary edema Pneumonia Mucus plugs ARDS |
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Alveolar Dead Space
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Pulmonary emboli
Decreased CO Ventilation is greater than perfusion Alveolar PO2 rises Alveolar PCO2 falls |
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Acute Respiratory Failure
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Failure of pulmonary system to maintain adequate gas exchange in quantities sufficient to sustain life
Survival rate 75% Types Hypoxemic or Oxygenation failure Hypoxemic but normocapnic Hypercapnic or Ventilatory failure Hypoxemic & hypercapnic |
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Acute Respiratory Failure
Hypoxemic |
Oxygenation Failure
PaO2 < 60 on 60% O2 |
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Acute Respiratory Failure
Hypoxemic S/S |
Pneumonia
Pulmonary edema ARDS Pleural effusion VSD |
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Acute Respiratory Failure
Hypercapnic |
Ventilatory Failure
PaCO2 > 45, pH < 7.35 |
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Acute Respiratory Failure
Hypercapnic |
Neuromuscular D.
MS, MD, Mys Gravis Spinal cord injury Drug OD (anything that will decrease RR) Head injury Decreased Cardiac Output COPD |
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Acute Respiratory Distress Syndrome
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Noncardiac pulmonary edema & progressive refractory hypoxemia (giving o2 & continue to remain hypoxemic)
1st identified in 1967 AKA – shock lung, wet lung Severe form of acute respiratory failure Mortality rate – 50% Higher w/ septic shock (b/c of inflammatory process) Often fatal!!! |
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Acute Respiratory Distress Syndrome
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Systemic inflammatory response
Inflammation damages the alveolar capillary membrane Alveolar edema Proliferation of Type II cells decreased production of surfactant Hylaine membranes form Fibrotic Stage Collagen deposits Capillaries scarred Lungs stiffen Chronic/Recovery Gradual resolution of hypoxemia |
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Acute Respiratory Distress Syndrome
Newborn |
AKA – Hyaline Membrane Disease
Deficient of surfactant Deficient alveolar surface area Both affecting gas exchange Atelectasis occurs Leads to hypoxemia & hypercapnia Pulmonary vasoconstriction PVR impaired CO2 & O2 exchange |
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COPD
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Pathological changes expiratory air flow
Does not change markedly over time Does not show major reversibility in response to pharmacological agents Progressive Associated with abnormal & chronic inflammatory response of the lungs to noxious particles or gases Inflammation of all lung structures Airways, lung parenchyma & pulmonary vasculature |
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Chronic Bronchitis
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Mucous glands hypertrophy
In response to tobacco smoke Excessive mucous production in bronchial tree Excessive sputum production results Tobacco smoke damages cilia Cough occurs to clear excess sputum Chronic inflammation swelling of bronchial walls Excessive secretions can block airways Dx made: chronic cough & sputum production on daily basis Minimum of 3 months/year Not less than 2 consecutive years |
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Emphysema
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Irreversible enlargement of the gas-exchange airways and destruction of the alveolar walls
Classification r/t location of involvement Centriacinar (on bronchioles) /Centrilobular (on alveoli) Respiratory bronchioles & spread peripherally Associated w/ chronic smoking Affects upper ½ of lungs Panacinar/Panlobular Destroys entire alveolus Deficiency of Enzyme α1 - antitrypsin Affects lower lobes of lungs |
