Eggena 11-1 Flashcards
rhonchi
coarse, harsh sounds that change from one second to the next. They are produced by mucus flapping in the breeze of air moving in and out of the bronchi.
patient’s abnormal heart sounds
abnormal heart sound (S3 gallop)
second heart sound that is split into two on inspiration and expiration (fixed splitting of S2).
COPD is a mix of
emphysema
bronchitis
intrinsic asthma
the bronchitic component of COPD is due to
chronic irritation of respiratory passages, which causes goblet cells to multiply and submucosal glands to hypertrophy.
heavy cigarette smoking causes
loss of elastic support and turns small bronchioles into flabby cellophane like tubes.
why was the patient drowsy and weak?
patients tend to become drowsy when they retain excessive amounts of carbon dioxide.
Why did he have difficulty breathing?
high residual volume expands the chestwall to a point where its compliance is decreased and the msucles of inspiration are not in an optimal alignment.
in COPD, additional work is required to
overcome airway resistance. Resistance is increased on inspiration and expiration because airways are narrowed by excessive mucus, smooth muscle constriction and by a mucosal layer.
why was he cyanotic?
there is more than 5 g/dL of unoxygenated hemoglobin present in arterial blood.
hypoxemia was caused by
shunting of venous blood past poorly ventilated alveoli
a decrease in functional alveolar surface area (i.e. increase in physiologica dead space)
why were his feet swollen and his liver tender
excess interstitial fluid in these tissues was caused by an increased capillary hydrostatic pressure that upset the balance between filtration and reabsoprtion of water across the capillary wall in favor of filtration.
the increased capillary pressure resulted from increased venous pressure, and increased venous pressure resulted from failure of the right ventricle pump all the blood that was returned to it.
Why did his PaCO2 increase following oxygen administration?
The patient stopped breathing. His ventilation was being driven by the peripheral chemoreceptors in the carotid and aortic bodies. Oxygen sensitive cells were stimulated much more when the PaO2 was lower.
the central chemoreceptors became desensitized from chronic exposure to high levels of carbon dioxide.
autoregulation of blood flow
the price paid for decreased work of breathing was
increase in carbon dioxide in blood displaced oxygen
the increase in carbon dioxide in blood caused respiratory acidosis.
Why did correction of the PaCO2 to normal on the ventilator result in a metabolic acidosis?
The plasma bicarbonate levels were still high from his previous respiratory acidosis, and the excess bicarbonate takes hours to be excreted by the kidneys.
summary of the patient’s condition
hypoxic vasoconstriction increased the afterload of the right ventricle, leading to its hypertrophy and its diminished compliance, leading to the right atrium to hypertrophy.
