Apex Unit 1 Respiratory Flashcards
Match each intrinsic muscle of the larynx with its action on the vocal cords. Thyroarytenoi Cricothyroid Posterior cricoarytenoid Lateral cricoarytenoid
ABducts
ADducts
Elongates
Shortens
Thyroarytenoid + Shortens
Cricothyroid + Elongates
Posterior cricoarytenoid + ABducts
Lateral cricoarytenoid + ADducts
The superior laryngeal nerve innervates the
Underside of epiglottis
Cricothyroid muscles
Whenever you think about the innervation of the airway, there are 4 nerves that should come to mind:
- Trigeminal n.
- Glossopharyngeal n.
- Superior laryngeal n. (internal & external branch)
- Recurrent laryngeal n.
The question asked about the superior laryngeal nerve.
The SLN internal branch is a sensory nerve. It innervates the posterior side of the epiglottis to the top side of the vocal folds.
The SLN external branch is a motor nerve. It innervates the cricothyroid muscles.
Tensor palatine muscle relaxation will MOST likely cause airway obstruction at which level?
Soft palate
Soft palate: Relaxation of the tensor palatine muscle
Tongue: Relaxation of the genioglossus muscle
Epiglottis: Relaxation of the hyoid muscles
When compared to the trachea, which of the following is increased in the terminal bronchioles?
Cross-sectional area
The tracheobronchial tree is a branching network of airways that includes the trachea, bronchi, and bronchioles. This question asked about the anatomic and physiologic differences between the trachea and the terminal bronchioles.
A division is where an airway divides into two or more smaller airways. There are 23 – 25 divisions (or generations) in humans. At each division, the diameter of the new branches becomes smaller, however the total cross sectional area of all the airways in the division increases. This explains why airflow velocity slows as you move down the tracheobronchial tree.
The trachea contains cartilage (C-shaped rings) and goblet cells (mucus secretion), while the terminal bronchioles have neither.
Anatomic dead space begins in the mouth and ends in the:
Terminal bronchioles
The airway is functionally divided into 3 zones: conducting, respiratory, transitional.
The conducting zone is anatomic dead space. This region extends from the nares and mouth to the terminal bronchioles.
The respiratory zone is where gas exchange occurs. This region extends from the respiratory bronchioles to the alveoli.
What is the primary determinant of carbon dioxide elimination?
Alveolar ventilation
Alveolar ventilation (NOT minute ventilation) determines the rate of removal of carbon dioxide from the body. Let’s examine why…
Minute ventilation = Tidal volume x Respiratory rate
Alveolar ventilation = (Tidal volume – Dead space) x Respiratory rate
The key here is to recognize that dead space doesn’t contribute to gas exchange, so only the fraction of the tidal volume that reaches the respiratory zone contributes to gas exchange.
Which conditions will MOST likely increase the PaCO2 to EtCO2 gradient? (Select 3.)
Hypotension Endotracheal tube Laryngeal mask airway Neck flexion Positive pressure ventilation Atropine
Hypotension
Atropine
Positive pressure ventilation
Conditions that increase dead space tend to increase the volume of the conducting zone or reduce pulmonary blood flow.
Hypotension reduces pulmonary blood flow, which increases alveolar dead space.
Atropine is a bronchodilator, so it increases anatomic dead space by increasing the volume of the conducting zone.
Positive pressure ventilation increases alveolar pressure, which increases ventilation relative to perfusion. This is another way of saying that dead space increases.
Dead space is reduced by anything that reduces the volume of the conducting zone or increases pulmonary blood flow.
Examples include an endotracheal tube, LMA, or neck flexion.
A patient is in the sitting position. When compared to the apex of the lung, which of the following are higher in the base? (Select 2.)
Partial pressure of alveolar carbon dioxide
V/Q ratio
Partial pressure of alveolar oxygen
Blood flow
Partial pressure of alveolar carbon dioxide
Blood flow
The distribution of alveolar ventilation and perfusion is unequal throughout the lung.
The non-dependent region (apex in the sitting position) has a higher PAO2 and a higher V/Q ratio (V > Q).
The dependent region (base in the sitting position) has a higher PACO2 and has a lower V/Q ratio (V < Q).
Identify the statements that represent the MOST accurate understanding of V/Q mismatch. (Select 2.)
Hypoxic pulmonary vasoconstriction minimizes dead space.
Blood passing through underventilated alveoli tends to retain CO2.
The A-a gradient is usually small.
Bronchioles constrict to minimize zone 1.
Bronchioles constrict to minimize zone 1.
Blood passing through underventilated alveoli tends to retain CO2.
What was wrong with the other answers?
V/Q mismatch usually increases (not decreases) the A-a gradient.
Hypoxic pulmonary vasoconstriction minimizes shunt (not dead space).
Variables described by the law of Laplace include all of the following EXCEPT:
radius.
tension.
pressure.
density.
Density
The law of Laplace states that as the radius of a sphere or cylinder becomes larger, the wall tension increases as well.
The variables in this equation include:
Tension Pressure Radius Density is not a variable in the law of Laplace.
Select the correct statements regarding the West zones of the lung. (Select 3.)
In zone 3 pulmonary blood flow is proportional to the arterial-to-venous pressure gradient.
In zone 1 there is no pulmonary blood flow.
In zone 3 alveolar pressure exceeds venous pressure.
In zone 1 alveolar pressure is higher than arterial pressure.
In zone 2 ventilation is greater than perfusion.
In zone 2 venous pressure is higher than alveolar pressure.
In zone 1 there is no pulmonary blood flow.
In zone 1 alveolar pressure is higher than arterial pressure.
In zone 3 pulmonary blood flow is proportional to the arterial-to venous pressure gradient.
Why were the other answers wrong?
In zone 2 ventilation is matched to perfusion (not V > Q).
In zone 2 arterial (not venous) pressure is higher than alveolar pressure.
In zone 3 venous pressure exceeds alveolar pressure (not the other way around).
A patient is breathing room air at sea level. The arterial blood gas reveals a PaO2 of 60 mmHg and a PaCO2 of 70 mmHg. Calculate the patient’s alveolar oxygen concentration.
(Enter your answer in mmHg and round to the nearest whole number)
62 mmHg
The alveolar gas equation tells us the partial pressure of oxygen in the alveolus. Imagine a patient that has a PaO2 of 100 mmHg. How do you know if this is good or bad? The alveolar gas equation provides the context to make this assessment.
Alveolar oxygen = FiO2 x (Pb - PH2O) - (PaCO2 / RQ)
0.21 x ( 760 - 47 ) - (70 / 0.8) = 62.23 ~ 62 mmHg
Causes of an increased A-a gradient include: (Select 2.)
hypoxic mixture.
V/Q mismatch.
hypoventilation.
diffusion limitation.
Diffusion limitation
V/Q mismatch
The A-a gradient is the difference between PAO2 and PaO2.
After we get a blood gas (PaO2) and calculate the alveolar gas equation (PAO2), we can use the A-a gradient to determine the cause of hypoxemia.
There are 5 causes of hypoxemia: hypoxic mixture, hypoventilation, diffusion limitation, V/Q mismatch, and shunt.
The A-a gradient is normal in hypoxic mixture and hypoventilation.
The A-a gradient is increased by diffusion limitation, V/Q mismatch, and shunt.
Which conditions reduce functional residual capacity? (Select 2.)
Pulmonary edema
COPD
Advanced age
Obesity
Pulmonary edema
Obesity
The FRC is the lung volume where the inward elastic recoil of the lungs is balanced by the outward elastic recoil of the chest wall (FRC = RV + ERV).
FRC is reduced by obesity and pulmonary edema.
Patients with COPD and advanced age have an increased FRC. Air trapping increases RV, and this increases FRC.
Closing capacity is the sum of closing volume and:
expiratory reserve volume.
tidal volume.
residual volume.
functional residual capacity.
Residual volume
Closing capacity is the lung volume above residual volume where the small airways begin to collapse during expiration. It is the sum of closing volume and residual volume.
Calculate the patient’s arterial oxygen content from the data set:
Hgb 9 g/dL Heart rate 100 bpm Stroke volume 70 mL SaO2 90% PaO2 60 mmHg
(Enter your answer as mL O2/dL blood and do not round your answer)
10.872 – 11.439
Oxygen content (CaO2) tells us how much oxygen is present in 1 deciliter of blood.
Most oxygen forms a reversible bond with hgb, while the remainder dissolves into the blood according to Henry’s law.
CaO2 = (1.34 x Hgb x SaO2) + (PaO2 x 0.003)
CaO2 = (1.34 x 9 g/dl x 0.90) + (60 x 0.003) = 11.034 mL O2/dL blood
Some books will use 1.32, 1.34, 1.36, or 1.39 as the constant, so we accepted a range of answers.
It’s easy to confuse CaO2 (O2 carrying capacity) and DO2 (O2 delivery). CaO2 equals how much O2 is in the blood, while DO2 equals how much O2 is delivered the tissues per minute.
P50 is reduced by: (Select 3.)
acidosis. hypocarbia. increased 2,3 DPG. carboxyhemoglobin. hgb F. hyperthermia.
Hgb F
Hypocarbia
Carboxyhemoglobin
The oxyhemoglobin dissociation curve plots hemoglobin saturation (SaO2) vs the oxygen tension in the blood (PaO2). P50 is the PaO2 where hemoglobin is 50% saturated with oxygen.
Decreased P50 (left shift):
Hgb has a stronger hold on oxygen.
Examples: Hgb F, hypocarbia, and carboxyhemoglobin
Increased P50 (right shift):
Hgb is more willing to release oxygen.
Examples: acidosis, hyperthermia, and increased 2,3 DPG
Identify the statement that BEST describes aerobic metabolism.
Pyruvic acid is converted to lactate.
1 molecule of glucose converts to 38 molecules ATP.
NADH is the final electron accepter during electron transport.
Electron transport occurs in the cytoplasm.
1 molecule of glucose converts to 38 molecules ATP.
You spend so much time thinking about how to get oxygen to the cells, however knowing the intracellular mechanism is nearly as important. While we won’t cover a semester of biochemistry here (thank goodness) we will provide a brief review of cellular energetics on the next page.
Which ion belongs in the box with the question mark?
hamburger shift
Chloride
CO2 is the by-product of aerobic respiration. It diffuses from the cells into the venous circulation and then diffuses into erythrocytes.
In the presence of carbonic anhydrase (inside the RBC), CO2 and H2O react to form H2CO3. Carbonic acid rapidly dissociates into H+ and HCO3-. The H+ is buffered by hemoglobin, and the HCO3- is transported to the plasma to function as a buffer.
Cl- is transported into the erythrocyte to maintain electroneutrality. This is known as the chloride or Hamburger shift.
The Haldane effect states that in the presence of deoxygenated hemoglobin, the carbon dioxide dissociation curve shifts:
to the right.
to the left.
up.
down.
To the left
The Haldane effect states that at a given PaCO2, deoxygenated hemoglobin can carry more CO2. This allows hemoglobin to load more carbon dioxide at the tissue level and release more CO2 in the lungs.
Deoxygenated hemoglobin causes the CO2 dissociation curve to shift to the left.
Consequences of hypercapnia include: (Select 2.)
increased oxygen carrying capacity.
hypokalemia.
hypoxemia.
increased myocardial oxygen demand.
Hypoxemia
Increased myocardial oxygen demand
Hypercarbia affects nearly all of the systems in the body. Consequences include:
Hypoxemia
Increased myocardial oxygen demand
Hyperkalemia (not hypokalemia)
Decreased oxygen carrying capacity (not increased)
All of this is explained in detail on the next page.
Which conditions increase minute ventilation for a given PaCO2? (Select 3.) Hypoxemia Carotid endarterectomy Respiratory alkalosis Sevoflurane Surgical stimulation Salicylates
Hypoxemia
Salicylates
Surgical stimulation
The CO2 response curve illustrates the minute ventilation for a given PaCO2.
A right shift means that the respiratory center is less sensitive to CO2.
Examples: sevoflurane, s/p carotid endarterectomy
A left shift means that the respiratory center is more sensitive to CO2.
Examples: hypoxemia, salicylates, and surgical stimulation
Respiratory alkalosis is a consequence (not a cause) of a left shift.
What is the pacemaker for normal breathing? Pneumotaxic center Ventral respiratory center Apneustic center Dorsal respiratory center
Dorsal respiratory center
The dorsal respiratory center is the respiratory pacemaker (dorsal = inspiration).
The ventral respiratory center is primarily responsible for expiration (ventral = expiration).
The pneumotaxic center inhibits the DRC (inhibits the pacemaker).
The apneustic center stimulates the DRC (stimulates the pacemaker).
The central chemoreceptor:
is stimulated by pH changes in the cerebrospinal fluid.
is unaffected by bicarbonate in the serum.
is located on the dorsal surface of the medulla.
responds to PaCO2 and PaO2.
Is stimulated by pH changes in the cerebrospinal fluid
The central chemoreceptor is located on the ventral surface of the medulla (not dorsal).
It responds to PaCO2 (not PaO2).
It is stimulated by the pH of the CSF.
Because HCO3- in the plasma does not freely diffuse across the blood-brain-barrier, it does not acutely affect the central chemoreceptor. If serum HCO3- rises, it takes hours or days for the CSF pH to equilibrate.