STUDY GUIDE
CRNA Intervie
Clinical Question & Answ
Study Guide
, www. CRNA School Prep Academy.com
CRNA SCHOOL CLINICAL INTERVIEW GU
4) What is the pathophysiology of ARDS (Acute Respiratory Dis
Syndrome)?
The pathophysiology of ARDS can be divided into three stages: exudative, proliferative,
Each stage reflects progressive changes in lung tissue and function.
Exudative Stage: The initial stage occurs within the first week of lung injury. It involves d
alveolar epithelium and vascular endothelium, leading to increased capillary permeability.
fluid, proteins, inflammatory cells, and red blood cells leak into the alveolar and interstitia
leakage results in the formation of hyaline membranes composed of fibrin and cellular deb
characteristic of ARDS. Damage to type I alveolar cells (which facilitate gas exchange) an
alveolar cells (which produce surfactant) leads to decreased surfactant production and inc
tension, causing alveolar collapse (atelectasis) and impaired gas exchange.
Proliferative Stage: This stage generally occurs 1 to 3 weeks after the initial lung injury.
II alveolar cells proliferate to repair and replace the damaged epithelium. There is also an
fibroblast activity leading to interstitial fibrosis, which can help in wound healing but may
to stiffening of the lung parenchyma. The regenerative processes attempt to restore lung
and function, but the proliferation of cells and extracellular matrix can lead to imperfect re
ongoing respiratory dysfunction.
Fibrotic Stage: The final stage can develop 3 weeks to months after the onset of ARDS a
characterized by extensive fibrosis and collagen deposition in the interstitial, alveolar, an
spaces. This extensive scarring can lead to significant reductions in lung compliance (the
lung to expand) and severe, permanent reductions in lung function. Microcysts may also f
destructive remodeling of lung tissue.
5) What are the optimal ventilator settings for ARDS?
In ARDS, the goal of mechanical ventilation is to support gas exchange while minimizing
injury. Key strategies include:
Low Tidal Volume Ventilation: Using low tidal volumes of 4-6 ml/kg of predicted body w
prevent volutrauma (damage due to overdistension of the lungs). This approach, supporte
like the ARDS Network trial, has been shown to reduce mortality in ARDS patients by limi
mechanical stress on the lungs.
Limiting Plateau Pressures: Maintaining plateau pressures (the pressure in the lungs at
inspiration during mechanical ventilation) below 30 cmH2O is critical to prevent barotraum
from high pressures). This approach helps to protect the lung tissue from pressure-induce
6) What are the symptoms of sepsis?
Sepsis is a life-threatening response to an infection that can lead to tissue damage, organ
death. Symptoms vary but typically include:
Signs of Infection: Presence of an infection that might have triggered the sepsis.
Tachycardia: Rapid heart rate as the body tries to maintain adequate blood flow desp
, www.CRNASchoolPrepAcademy.com
CRNA SCHOOL CLINICAL INTERVIEW GUI
7) Tell me the pathophysiology of sepsis
Molecular and Cellular Basis of Sepsis
Initial Trigger: Sepsis is triggered by an infection which may originate in any part of the bo
the lungs, urinary tract, skin, or abdomen. The presence of pathogens (bacteria, viruses, fu
parasites) activates the body's immune response. Pathogens release molecules known as p
associated molecular patterns (PAMPs), which are detected by the body's immune cells thr
recognition receptors (PRRs) like Toll-like receptors (TLRs).
Activation of Innate Immunity: Upon recognition of PAMPs, innate immune cells (such as
and neutrophils) are activated. These cells release a variety of signaling molecules includin
chemokines, and other mediators. Cytokines like interleukin-1 (IL-1), IL-6, and tumor necro
alpha (TNF-α) play pivotal roles in mediating the inflammatory response. These cytokines n
fighting the infection but also signal other immune cells to join the response.
Vascular Changes and Systemic Inflammation: The cytokines released during the innate
response induce vasodilation to increase blood flow to the affected area, facilitating the arr
immune cells. However, in sepsis, this response is exaggerated and uncontrolled, leading t
vasodilation, increased vascular permeability, and fluid leakage into tissues. This results in
and reduced tissue perfusion, which are hallmark symptoms of sepsis.
Excessive Cytokine Release and Cytokine Storm: In severe cases, the immune response
overly aggressive, leading to a cytokine storm. This refers to the massive and uncontrolled
cytokines into the bloodstream, which can cause widespread inflammation, tissue damage,
failure. The cytokine storm significantly contributes to the pathology of sepsis by disrupting
between pro-inflammatory and anti-inflammatory responses.
Activation of Coagulation Pathways: Sepsis also activates the coagulation cascade, whic
disseminated intravascular coagulation (DIC). This condition is characterized by the widesp
formation of blood clots in small vessels throughout the body, which can obstruct blood flow
further tissue damage and organ failure.
Impairment of the Adaptive Immune Response: While the innate immune response is imm
, www. CRNA School Prep Academy.com
CRNA SCHOOL CLINICAL INTERVIEW
1) What is the difference between SaO2 and PaO2?
SaO2 (Oxygen Saturation) refers to the percentage of hemoglobin binding sites in
that are occupied by oxygen. It provides an estimate of the oxygen levels in the b
measured noninvasively using a device called a pulse oximeter, which is typically
finger or an earlobe. Normal SaO2 values range from 90% to 100% in a healthy a
PaO2 (Partial Pressure of Oxygen) measures the pressure exerted by oxygen dis
arterial blood. Unlike SaO2, PaO2 requires an arterial blood sample, usually obta
an arterial blood gas (ABG) test. The PaO2 value is expressed in millimeters of m
(mmHg), with normal adult levels ranging from 80 to 100 mmHg.
A key difference is that SaO2 is an indirect measure of the amount of oxygen bo
hemoglobin, while PaO2 directly measures the amount of oxygen dissolved in the
Moreover, PaO2 is a more precise measurement but requires invasive methods to
whereas SaO2 offers a quicker and non-invasive means of estimation. It's also im
note that SaO2 can be affected by conditions such as carbon monoxide poisoning
cannot differentiate between oxygen and carbon monoxide, both of which bind to
2) What is MvO2?
MvO2 (Myocardial Oxygen Consumption) quantifies the oxygen used by the heart
crucial for understanding the metabolic demands of the heart and is influenced
such as heart rate, myocardial contractility, and the tension in the ventricular
calculation of MvO2 is typically done by considering the heart rate and systolic bl
but it can also involve more complex assessments such as the measurement of c
flow and the arterial-venous oxygen difference across the myocardium.
Understanding MvO2 is vital in clinical settings, especially in managing conditions
failure or coronary artery disease, where the oxygen demand and supply balance
3) What is the difference between hypoxia and hypoxemia?
Hypoxemia refers to low levels of oxygen in the blood and is specifically meas
parameters such as PaO2 in an arterial blood gas test. Normal PaO2 levels range
100 mmHg, and values below this range may indicate hypoxemia. This condition c
from various respiratory issues, such as asthma, pneumonia, or pulmonary embol
Hypoxia, on the other hand, occurs when there is an inadequate supply of oxyg
CRNA Intervie
Clinical Question & Answ
Study Guide
, www. CRNA School Prep Academy.com
CRNA SCHOOL CLINICAL INTERVIEW GU
4) What is the pathophysiology of ARDS (Acute Respiratory Dis
Syndrome)?
The pathophysiology of ARDS can be divided into three stages: exudative, proliferative,
Each stage reflects progressive changes in lung tissue and function.
Exudative Stage: The initial stage occurs within the first week of lung injury. It involves d
alveolar epithelium and vascular endothelium, leading to increased capillary permeability.
fluid, proteins, inflammatory cells, and red blood cells leak into the alveolar and interstitia
leakage results in the formation of hyaline membranes composed of fibrin and cellular deb
characteristic of ARDS. Damage to type I alveolar cells (which facilitate gas exchange) an
alveolar cells (which produce surfactant) leads to decreased surfactant production and inc
tension, causing alveolar collapse (atelectasis) and impaired gas exchange.
Proliferative Stage: This stage generally occurs 1 to 3 weeks after the initial lung injury.
II alveolar cells proliferate to repair and replace the damaged epithelium. There is also an
fibroblast activity leading to interstitial fibrosis, which can help in wound healing but may
to stiffening of the lung parenchyma. The regenerative processes attempt to restore lung
and function, but the proliferation of cells and extracellular matrix can lead to imperfect re
ongoing respiratory dysfunction.
Fibrotic Stage: The final stage can develop 3 weeks to months after the onset of ARDS a
characterized by extensive fibrosis and collagen deposition in the interstitial, alveolar, an
spaces. This extensive scarring can lead to significant reductions in lung compliance (the
lung to expand) and severe, permanent reductions in lung function. Microcysts may also f
destructive remodeling of lung tissue.
5) What are the optimal ventilator settings for ARDS?
In ARDS, the goal of mechanical ventilation is to support gas exchange while minimizing
injury. Key strategies include:
Low Tidal Volume Ventilation: Using low tidal volumes of 4-6 ml/kg of predicted body w
prevent volutrauma (damage due to overdistension of the lungs). This approach, supporte
like the ARDS Network trial, has been shown to reduce mortality in ARDS patients by limi
mechanical stress on the lungs.
Limiting Plateau Pressures: Maintaining plateau pressures (the pressure in the lungs at
inspiration during mechanical ventilation) below 30 cmH2O is critical to prevent barotraum
from high pressures). This approach helps to protect the lung tissue from pressure-induce
6) What are the symptoms of sepsis?
Sepsis is a life-threatening response to an infection that can lead to tissue damage, organ
death. Symptoms vary but typically include:
Signs of Infection: Presence of an infection that might have triggered the sepsis.
Tachycardia: Rapid heart rate as the body tries to maintain adequate blood flow desp
, www.CRNASchoolPrepAcademy.com
CRNA SCHOOL CLINICAL INTERVIEW GUI
7) Tell me the pathophysiology of sepsis
Molecular and Cellular Basis of Sepsis
Initial Trigger: Sepsis is triggered by an infection which may originate in any part of the bo
the lungs, urinary tract, skin, or abdomen. The presence of pathogens (bacteria, viruses, fu
parasites) activates the body's immune response. Pathogens release molecules known as p
associated molecular patterns (PAMPs), which are detected by the body's immune cells thr
recognition receptors (PRRs) like Toll-like receptors (TLRs).
Activation of Innate Immunity: Upon recognition of PAMPs, innate immune cells (such as
and neutrophils) are activated. These cells release a variety of signaling molecules includin
chemokines, and other mediators. Cytokines like interleukin-1 (IL-1), IL-6, and tumor necro
alpha (TNF-α) play pivotal roles in mediating the inflammatory response. These cytokines n
fighting the infection but also signal other immune cells to join the response.
Vascular Changes and Systemic Inflammation: The cytokines released during the innate
response induce vasodilation to increase blood flow to the affected area, facilitating the arr
immune cells. However, in sepsis, this response is exaggerated and uncontrolled, leading t
vasodilation, increased vascular permeability, and fluid leakage into tissues. This results in
and reduced tissue perfusion, which are hallmark symptoms of sepsis.
Excessive Cytokine Release and Cytokine Storm: In severe cases, the immune response
overly aggressive, leading to a cytokine storm. This refers to the massive and uncontrolled
cytokines into the bloodstream, which can cause widespread inflammation, tissue damage,
failure. The cytokine storm significantly contributes to the pathology of sepsis by disrupting
between pro-inflammatory and anti-inflammatory responses.
Activation of Coagulation Pathways: Sepsis also activates the coagulation cascade, whic
disseminated intravascular coagulation (DIC). This condition is characterized by the widesp
formation of blood clots in small vessels throughout the body, which can obstruct blood flow
further tissue damage and organ failure.
Impairment of the Adaptive Immune Response: While the innate immune response is imm
, www. CRNA School Prep Academy.com
CRNA SCHOOL CLINICAL INTERVIEW
1) What is the difference between SaO2 and PaO2?
SaO2 (Oxygen Saturation) refers to the percentage of hemoglobin binding sites in
that are occupied by oxygen. It provides an estimate of the oxygen levels in the b
measured noninvasively using a device called a pulse oximeter, which is typically
finger or an earlobe. Normal SaO2 values range from 90% to 100% in a healthy a
PaO2 (Partial Pressure of Oxygen) measures the pressure exerted by oxygen dis
arterial blood. Unlike SaO2, PaO2 requires an arterial blood sample, usually obta
an arterial blood gas (ABG) test. The PaO2 value is expressed in millimeters of m
(mmHg), with normal adult levels ranging from 80 to 100 mmHg.
A key difference is that SaO2 is an indirect measure of the amount of oxygen bo
hemoglobin, while PaO2 directly measures the amount of oxygen dissolved in the
Moreover, PaO2 is a more precise measurement but requires invasive methods to
whereas SaO2 offers a quicker and non-invasive means of estimation. It's also im
note that SaO2 can be affected by conditions such as carbon monoxide poisoning
cannot differentiate between oxygen and carbon monoxide, both of which bind to
2) What is MvO2?
MvO2 (Myocardial Oxygen Consumption) quantifies the oxygen used by the heart
crucial for understanding the metabolic demands of the heart and is influenced
such as heart rate, myocardial contractility, and the tension in the ventricular
calculation of MvO2 is typically done by considering the heart rate and systolic bl
but it can also involve more complex assessments such as the measurement of c
flow and the arterial-venous oxygen difference across the myocardium.
Understanding MvO2 is vital in clinical settings, especially in managing conditions
failure or coronary artery disease, where the oxygen demand and supply balance
3) What is the difference between hypoxia and hypoxemia?
Hypoxemia refers to low levels of oxygen in the blood and is specifically meas
parameters such as PaO2 in an arterial blood gas test. Normal PaO2 levels range
100 mmHg, and values below this range may indicate hypoxemia. This condition c
from various respiratory issues, such as asthma, pneumonia, or pulmonary embol
Hypoxia, on the other hand, occurs when there is an inadequate supply of oxyg
