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25 Cards in this Set

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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
Uncompensated (acute)
-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
Partially compensated (all 3 abnormal)
-pH is still ABNORMAL, but it is more normal than before compensation took place
-CO2 AND HCO3 are ABNORMAL
-all 3 levels are abnormal
Fully compensated (chronic) **COPD
-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
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)
Ventilation
amount of tidal volume (gas inspired and expired) x (times) RR (number of breaths/min) = minute volume
Hyperventilation
increase in depth and rate greater than demand = hypocapnia: decrease O2
Hypoventilation
reduced air entering = hypercapnia : increased CO2, decreased O2
Anatomic dead space
portion of the tidal volume remains in the conducting airways
Alveolar dead space
adequate ventilation but inadequate perfusion (pulmonary embolism) -->good gas, not good blood flow
Three types of obstructive lung disease
-asthma
-chronic bronchitis (COPD)
-emphysema
What is the primary cause of obstructive lung disease?
Cigarette smoking
Asthma
-inflammatory disease characterized by hypersponsiveness of the airways and episodic periods of bronchospasm
VQ ratio
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)
Asthma summary
-affects smooth muscle
-reversible
-often runs in the family
-affects young and old people

Causes: histamine-produces edema, leukotrines: smooth muscle constriction in airways
Patho of asthma
-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
Asthma attack
-bronchospasm, airway edema, increase mucous production
-obstruction large/small airways, air trapping, respiratory acidosis, hypoxia
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
Manifestations of asthma
-wheezing
-dyspnea
-cough
-use of accessory muscles
-tachypnea (increase RR)
-tachycardia (increase HR)
-fatigue
Status Asthmaticus
-really bad (they'll die soon)
-sever bronchospasm
-silent chest (no audible air movement in lungs)
-CO2>70
-hypoxemia
-inhalers don't treat it
Chronic bronchitis
-coupled with emphysema = COPD
-hypersecretion of mucous and chronic productive cough for 3 months duration for at lease 2 consecutive years
Patho of chronic bronchitis
-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
Causes of chronic bronchitis
-cigarette smoking (main cause)
-air pollution
-inhaled irritants
-aging (30-40 y/o onset)
What's the role of a goblet cell?
-to produce mucous
-goblet cell hyperplasia in chronic bronchitis

** increase goblet cell=increase mucous production
Manifestation of chronic bronchitis
-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