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25 Cards in this Set
- Front
- Back
Summary of.
-respiratory acidosis -respiratory alkalosis -metabolic acidosis -metabolic alkalosis |
-respiratory acidosis: pH decreased, CO2 increased, HCO3 normal level, cause: hypoventilation (<12RR)
-respiratory alkalosis: pH increased, CO2 decreased, HCO3 normal level, cause hyperventilation (>20RR) -metabolic acidosis: pH decreased, CO2 normal level, HCO3 decreased, cause: diarrhea, starvation, renal failure -metabolic alkalosis: pH increased, CO2 normal level, HCO3 increased, cause: vomit, increased antacid use |
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Uncompensated (acute)
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-pH <7.35 of >7.45 = ABNORMAL
-CO2 or HCO3 = ABNORMAL -acute condition -ABNORMAL pH -ONE ABNORMAL value -one normal value (out running, stop running and it goes back to normal |
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Partially compensated (all 3 abnormal)
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-pH is still ABNORMAL, but it is more normal than before compensation took place
-CO2 AND HCO3 are ABNORMAL -all 3 levels are abnormal |
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Fully compensated (chronic) **COPD
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-pH is 7.35 to 7.45 is NORMAL
-CO2 and HCO3 are ABNORMAL -usually chronic condition -normal pH -2 abnormal values **7.35-7.4 = acidic **7.4-7.45 = alkaline |
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3 parts to respiration
-perfusion -ventilation -diffusion |
-perfusion: movement of blood between alveolar capillary membrane and body organs/tissues
-ventilation: movement of air between atmosphere and alveloi -diffusion: movement of gases between alveolar-capillary membrane (lungs to blood supply) |
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Ventilation
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amount of tidal volume (gas inspired and expired) x (times) RR (number of breaths/min) = minute volume
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Hyperventilation
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increase in depth and rate greater than demand = hypocapnia: decrease O2
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Hypoventilation
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reduced air entering = hypercapnia : increased CO2, decreased O2
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Anatomic dead space
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portion of the tidal volume remains in the conducting airways
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Alveolar dead space
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adequate ventilation but inadequate perfusion (pulmonary embolism) -->good gas, not good blood flow
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Three types of obstructive lung disease
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-asthma
-chronic bronchitis (COPD) -emphysema |
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What is the primary cause of obstructive lung disease?
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Cigarette smoking
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Asthma
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-inflammatory disease characterized by hypersponsiveness of the airways and episodic periods of bronchospasm
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VQ ratio
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ventilation/perfusion ratio. ratio of oxygen received in the pulmonary alveoli to the flow of blood through the alveolar capillaries.
-blood flow and ventilation are greater at bases of lung -normally perfusion exceeds ventilation * >1=good gas, poor blood flow * <.8=good blood flow, but poor gas exchange (asthma, CODP.) (lungs) |
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Asthma summary
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-affects smooth muscle
-reversible -often runs in the family -affects young and old people Causes: histamine-produces edema, leukotrines: smooth muscle constriction in airways |
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Patho of asthma
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-irritant, allergens, cold, stress, exercise
-release of inflammatory mediaters (Type 1 hypersensitivity. IgE) mast-cell in bronchial epithelium. Increase edema and vascular congestion -vascular permeability -edema formation from histamine -vascular congestion -production of thick mucous -decrease muco-ciliary function -thickening of airway walls AND contractile response -AIRWAY OBSTRUCTION -resistance to airflow and flow rates -OVERINFLATION: premature airway closure |
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Asthma attack
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-bronchospasm, airway edema, increase mucous production
-obstruction large/small airways, air trapping, respiratory acidosis, hypoxia |
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Causes of asthma (type 1 hypersensitivity reaction)
-extrinsic (allergic) -intrinsic (no known allergic cause) |
-Extrinsic (allergic): child or young adult, associated with hay fever, environmental factors, family history,IgE produced in response to exposure, mast cell degranulation, histamine= increase inflammation edema, leukotrines=smooth muscle constriction
-intrinsic (no known allergic cause): induced by respiratory track infection, chemicals, exercise, cold, emotion, spasm of airway |
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Manifestations of asthma
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-wheezing
-dyspnea -cough -use of accessory muscles -tachypnea (increase RR) -tachycardia (increase HR) -fatigue |
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Status Asthmaticus
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-really bad (they'll die soon)
-sever bronchospasm -silent chest (no audible air movement in lungs) -CO2>70 -hypoxemia -inhalers don't treat it |
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Chronic bronchitis
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-coupled with emphysema = COPD
-hypersecretion of mucous and chronic productive cough for 3 months duration for at lease 2 consecutive years |
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Patho of chronic bronchitis
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-tobacco smoke, air pollution
-continual bronchial irritation and inflammation -chronic bronchitis: bronchial edema, hypersecretion of mucous, chronic productive cough and bronchospasm, goblet cell hyperplasia in chronic bronchitis -airway obstruction, air trapping (collapse of bronchial wall), dyspnea, frequent infections -abnormal ventilation-perfusion ratio, hypoexemia, hypoventilation, right heart failure |
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Causes of chronic bronchitis
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-cigarette smoking (main cause)
-air pollution -inhaled irritants -aging (30-40 y/o onset) |
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What's the role of a goblet cell?
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-to produce mucous
-goblet cell hyperplasia in chronic bronchitis ** increase goblet cell=increase mucous production |
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Manifestation of chronic bronchitis
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-AM cough (due to buildup)
-sputum production -wheezing -frequent respiratory infections (due to mucous) -increased fremitus (put hand on chest, feel more vibration when talking) -headache (worse in AM)-->hypercapnia..increase in CO2 levels -Cor pulmonale (right side heart failure..edema and organ enlargement) -low O2 sat (normal=95-100%) -high CO2 -polycythemia: caused by hypoxia in which there is increased production of erythropoietin -"blue boater" related to CO2 retention-->blue=decreased gas exchange=cyanoic, bloater=edema, organ enlargement=right sided heart failure **Extra fluid |