Cari's story
Cari’s Story
A. How could an infection in Cari’s nasal passage and pharynx spread into her sinuses? The pharynx connects to the nasal meatuses, which can in turn cause an infection.
C. Which structures found in the terminal bronchioles and alveoli normally would protect Cari’s lungs from infectious pathogens and particulate matter? Macrophages in the terminal bronchioles and alveoli protect Cari’s lungs.
E. How would Cari’s lung compliance (the effort required to expand the lungs) be altered as her alveoli fill with fluid due to pneumonia? Her lung compliance will increase because of trying to force gases in and out of the alveoli. The lungs are filled with fluid due to pneumonia.
G. How does the elevation of Cari’s respiratory rate alter her minute ventilation? Her respiratory rate would rise due to shallow breaths.
H. Normal blood oxygen saturation levels are greater than 94 percent; Cari’s blood oxygen saturation level was 90 percent at the time of her exam and initial arterial blood gas analysis done when she was admitted to the hospital revealed her arterial PO2 was 55mmHG. How do these clinical findings relate to the internal respiration in Cari’s body? The arteries have too much oxygen. A normal resting level should be around 94% without any additional oxygen.
K. How would you have expected Cari’s decreased PCO2 and alkaline blood pH to have affected her breathing? Her rate of breathing would also decrease.
M. Which anatomical structures in Cari’s respiratory system were initially involved? Nasal cavity, external/internal nares, nasopharynx, pharynx, and sinuses.
O. Which damaging effects of tobacco smoke led to Cari’s impaired respiratory defense mechanisms? The cilia and villi begin to become hardened and die; they wouldn’t be able to filter particles through the nasal cavity, which would lead to the mucosal membrane drying out from the cigarette smoke. The lungs would then lose elasticity from over inflation of the lungs trying to supply
A. How could an infection in Cari’s nasal passage and pharynx spread into her sinuses? The pharynx connects to the nasal meatuses, which can in turn cause an infection.
C. Which structures found in the terminal bronchioles and alveoli normally would protect Cari’s lungs from infectious pathogens and particulate matter? Macrophages in the terminal bronchioles and alveoli protect Cari’s lungs.
E. How would Cari’s lung compliance (the effort required to expand the lungs) be altered as her alveoli fill with fluid due to pneumonia? Her lung compliance will increase because of trying to force gases in and out of the alveoli. The lungs are filled with fluid due to pneumonia.
G. How does the elevation of Cari’s respiratory rate alter her minute ventilation? Her respiratory rate would rise due to shallow breaths.
H. Normal blood oxygen saturation levels are greater than 94 percent; Cari’s blood oxygen saturation level was 90 percent at the time of her exam and initial arterial blood gas analysis done when she was admitted to the hospital revealed her arterial PO2 was 55mmHG. How do these clinical findings relate to the internal respiration in Cari’s body? The arteries have too much oxygen. A normal resting level should be around 94% without any additional oxygen.
K. How would you have expected Cari’s decreased PCO2 and alkaline blood pH to have affected her breathing? Her rate of breathing would also decrease.
M. Which anatomical structures in Cari’s respiratory system were initially involved? Nasal cavity, external/internal nares, nasopharynx, pharynx, and sinuses.
O. Which damaging effects of tobacco smoke led to Cari’s impaired respiratory defense mechanisms? The cilia and villi begin to become hardened and die; they wouldn’t be able to filter particles through the nasal cavity, which would lead to the mucosal membrane drying out from the cigarette smoke. The lungs would then lose elasticity from over inflation of the lungs trying to supply