Shock/Trauma/CPR/Ischemia

Question 1

According to Bucci et al. (2017), which two ultrasound-derived parameters predicted fluid responsiveness in anesthetized ventilated dogs?

Answer 1

Respiratory variation in aortic blood flow peak velocity (ΔVpeakAo) and caudal vena cava diameter (cCVC) predicted fluid responsiveness in anesthetized, mechanically ventilated dogs.

Question 2

What threshold of ΔVpeakAo did Bucci et al. (2017) identify as predictive of fluid responsiveness?

Answer 2

A ΔVpeakAo >16.5% predicted fluid responsiveness with sensitivity 92% and specificity 85%.

Question 3

According to Bucci et al. (2017), what physiologic mechanism underlies respiratory variation in aortic flow velocity?

Answer 3

Positive pressure ventilation causes changes in intrathoracic pressure that affect venous return and stroke volume, leading to measurable fluctuations in aortic velocity if the patient is preload-responsive.

Question 4

In Bucci et al. (2017), what is the significance of cCVC (collapsibility of caudal vena cava)?

Answer 4

cCVC assesses changes in CVC diameter during respiratory cycles; higher collapsibility suggests hypovolemia and preload responsiveness.

Question 5

According to Cecconi et al. (2014), how is shock defined?

Answer 5

Shock is defined as a life-threatening, generalized form of acute circulatory failure associated with inadequate oxygen utilization by cells.

Question 6

What are the four types of shock described by Cecconi et al. (2014)?

Answer 6

Hypovolemic, cardiogenic, obstructive, and distributive.

Question 7

According to Cecconi et al. (2014), what are key components of hemodynamic monitoring in shock?

Answer 7

Preload, contractility, afterload, heart rate/rhythm, and oxygen delivery/utilization metrics (e.g., ScvO2, lactate).

Question 8

What is the “gold standard” for cardiac output measurement as cited in Cecconi et al. (2014)?

Answer 8

Pulmonary artery catheter thermodilution remains the gold standard.

Question 9

According to Cannon (2018), what are the three classic phases of hemorrhagic shock?

Answer 9

Compensated (normotensive), decompensated (hypotensive), and irreversible (cellular injury leads to death despite resuscitation).

Question 10

According to Cannon (2018), how does permissive hypotension benefit hemorrhaging patients?

Answer 10

It limits rebleeding before definitive hemostasis by reducing arterial pressure and clot disruption.

Question 11

What is the major physiologic consequence of hemorrhagic shock described by Cannon (2018)?

Answer 11

Hypoperfusion leads to anaerobic metabolism, lactate accumulation, and systemic inflammation.

Question 12

According to McMurray et al. (2016), what is the utility of FAST in non-traumatized dogs and cats?

Answer 12

AFAST, TFAST, and Vet BLUE can detect free fluid, pericardial effusion, B-lines, and lung pathology in critical patients even without trauma.

Question 13

According to McMurray et al. (2016), how is abdominal fluid scoring performed in AFAST?

Answer 13

The number of quadrants with positive fluid scores is used to semi-quantify volume and guide fluid resuscitation.

Question 14

What cardiac output method did Shih et al. (2011) evaluate in dogs?

Answer 14

Ultrasound dilution technique using an extracorporeal arteriovenous loop (based on dye dilution principles).

Question 15

According to Shih et al. (2011), how accurate was ultrasound dilution cardiac output measurement during hypovolemia?

Answer 15

It provided accurate, reproducible CO measurements in normovolemic and hypovolemic states, making it a viable tool in critical care.

Question 16

What are the key domains evaluated in the RECOVER CPR evidence and knowledge gap analysis (2012)?

Answer 16

Preparedness, basic life support (BLS), advanced life support (ALS), post-cardiac arrest care, and monitoring.

Question 17

According to RECOVER 2012, what is the recommended chest compression rate and depth in dogs and cats?

Answer 17

100–120 compressions per minute, with a depth of 1/3–1/2 chest width.

Question 18

According to RECOVER 2012, what is the recommended ventilation rate during CPR?

Answer 18

10 breaths per minute (1 breath every 6 seconds) during chest compressions.

Question 19

What are the three phases of CPR recognized by RECOVER 2012?

Answer 19

Basic life support (BLS), advanced life support (ALS), and post-cardiac arrest care.

Question 20

According to Rosenstein et al. (2018 Part 1), what are the primary sources of lactate?

Answer 20

Lactate is produced by glycolysis under anaerobic conditions, primarily by muscle, skin, brain, and erythrocytes.

Question 21

What are the three types of hyperlactatemia per Rosenstein et al. (2018 Part 1)?

Answer 21

Type A: hypoxia/hypoperfusion; Type B1: metabolic (e.g., liver disease, sepsis); Type B2: drug/toxin-induced (e.g., albuterol, metformin).

Question 22

According to Rosenstein et al. (2018 Part 2), what lactate trends are associated with improved survival?

Answer 22

A decrease in lactate ≥20% in the first 2–6 hours or normalization within 12–24 hours is associated with improved prognosis.

Question 23

What is lactate clearance, as discussed in Rosenstein et al. (2018 Part 2)?

Answer 23

The rate of lactate reduction over time, reflecting adequacy of perfusion and response to therapy.

Question 24

According to Hall & Drobatz (2021), what are the current trends in fluid resuscitation for hemorrhagic shock?

Answer 24

Use of balanced crystalloids, restrictive fluid strategies, early blood product administration, and avoidance of hemodilution.

Question 25

What was the historical approach to volume resuscitation in hemorrhagic shock discussed by Hall & Drobatz (2021)?

Answer 25

Large-volume isotonic crystalloid boluses aimed at normalizing BP, often leading to dilutional coagulopathy and edema.

Question 26

According to Fletcher & Boller (2021), what is the recommendation for fluid therapy during CPR?

Answer 26

Fluids are not routinely recommended unless the patient is hypovolemic; indiscriminate use may worsen outcomes.

Question 27

What pathophysiologic rationale supports fluid restriction during CPR in euvolemic patients (Fletcher & Boller, 2021)?

Answer 27

Excessive fluids may increase right atrial pressures, reduce coronary perfusion pressure, and impair venous return.

Question 28

What is coronary perfusion pressure (CPP) and why is it vital in CPR?

Answer 28

CPP = aortic diastolic pressure – right atrial pressure; it is the primary determinant of myocardial blood flow during CPR.

Question 29

What defines fluid responsiveness in veterinary ECC practice?

Answer 29

An increase in stroke volume or cardiac output ≥10–15% following a fluid bolus or maneuver (e.g., passive leg raise, mini-fluid challenge).

Question 30

What is an input sensor in hemodynamic monitoring?

Answer 30

A device or method that detects physiologic variables (e.g., pressure transducers, ultrasound for velocity or diameter).

Question 31

What is a controller algorithm in the context of critical care monitoring?

Answer 31

The logic or protocol guiding treatment decisions based on inputs (e.g., when to give fluids based on ΔVpeakAo >16%).

Question 32

Define actuator in fluid resuscitation.

Answer 32

The intervention used to modify the system state — e.g., administering fluids, vasopressors, or changing ventilation settings.

Question 33

What is the target setpoint in fluid therapy?

Answer 33

A physiologic goal (e.g., MAP ≥65 mmHg, lactate clearance ≥20%) that guides titration of therapy.

Question 34

Explain a feedback loop in shock management.

Answer 34

Ongoing reassessment of hemodynamic or metabolic markers (e.g., BP, lactate) that informs whether additional intervention is needed.

Question 35

According to Sheridan (2016), what are the three pathophysiologic components of inhalation injury?

Answer 35

1) Thermal injury to upper airways, 2) chemical injury from smoke toxins (e.g., acrolein, ammonia), and 3) systemic toxicity (e.g., CO, cyanide).

Question 36

What airway region is typically spared in direct thermal inhalation injury, according to Sheridan (2016)?

Answer 36

The lower airways (below the vocal cords) are typically spared due to efficient heat dissipation in the upper airway.

Question 37

According to Sheridan (2016), how do chemical irritants in smoke contribute to lung injury?

Answer 37

They disrupt epithelial integrity, increase vascular permeability, promote neutrophilic inflammation, and impair mucociliary clearance, leading to bronchospasm and edema.

Question 38

What systemic toxins are most commonly implicated in fire-related inhalation injury (Sheridan, 2016)?

Answer 38

Carbon monoxide (CO) and hydrogen cyanide (HCN).

Question 39

How does carbon monoxide toxicity impair oxygen delivery (Sheridan, 2016)?

Answer 39

CO binds hemoglobin with 200x the affinity of oxygen, forming carboxyhemoglobin (COHb) and causing a leftward shift in the oxyhemoglobin dissociation curve, reducing tissue O₂ release.

Question 40

What is the treatment of choice for carbon monoxide poisoning (Sheridan, 2016)?

Answer 40

100% oxygen to reduce COHb half-life; hyperbaric oxygen may be used in severe cases.

Question 41

What clinical signs might suggest cyanide toxicity in smoke-inhalation patients (Sheridan, 2016)?

Answer 41

Lactic acidosis, seizures, cardiac arrest, and high central venous O₂ saturation due to impaired cellular O₂ utilization.

Question 42

How does hydrogen cyanide disrupt cellular respiration (Sheridan, 2016)?

Answer 42

HCN inhibits cytochrome c oxidase in the mitochondrial electron transport chain, leading to cytotoxic hypoxia and lactic acidosis.

Question 43

According to Pigott & Rudloff (2021), what is the primary goal of fluid therapy in TBI patients?

Answer 43

To maintain adequate cerebral perfusion pressure (CPP) while avoiding exacerbation of intracranial hypertension.

Question 44

What fluids are contraindicated in TBI due to potential to worsen cerebral edema (Pigott & Rudloff, 2021)?

Answer 44

Hypotonic fluids (e.g., 5% dextrose, sterile water) and large volumes of isotonic crystalloids without osmotic properties.

Question 45

According to Pigott & Rudloff (2021), what fluids may reduce intracranial pressure in TBI?

Answer 45

Hyperosmolar agents such as hypertonic saline (HTS) and mannitol.

Question 46

What are the typical doses for hypertonic saline and mannitol in veterinary TBI (Pigott & Rudloff, 2021)?

Answer 46

- HTS: 3–5 mL/kg of 7.2%–7.5% over 5–10 minutes. - Mannitol: 0.5–1.0 g/kg over 15–20 minutes.

Question 47

What is the risk of using mannitol repeatedly or in hypovolemic patients (Pigott & Rudloff, 2021)?

Answer 47

Osmotic diuresis can lead to hypovolemia and hypotension, which may reduce cerebral perfusion pressure (CPP).

Question 48

What fluid choice is preferred in hypovolemic TBI patients, according to Pigott & Rudloff (2021)?

Answer 48

Hypertonic saline is preferred due to volume-sparing effects and ability to restore CPP without causing cerebral edema.

Question 49

What is cerebral perfusion pressure (CPP) and how is it calculated?

Answer 49

CPP = MAP – ICP; it represents the pressure gradient driving cerebral blood flow.

Question 50

What is the minimum CPP target in TBI patients (Pigott & Rudloff, 2021)?

Answer 50

CPP should be maintained ≥ 60–70 mmHg in most patients to ensure adequate brain perfusion.

Question 51

What is the role of colloids in TBI, per Pigott & Rudloff (2021)?

Answer 51

Their role is controversial; some evidence suggests increased mortality in humans, and use should be cautious in veterinary patients.

Question 52

Define osmotherapy.

Answer 52

The therapeutic use of hyperosmolar agents (e.g., mannitol, HTS) to reduce intracranial pressure by drawing water out of brain tissue into the vascular space.

Question 53

What pathophysiologic process underlies cerebral edema in TBI?

Answer 53

Blood–brain barrier disruption, ionic shifts, and cytotoxic or vasogenic edema contribute to increased intracranial pressure.

Question 54

What is the risk of overaggressive fluid therapy in TBI?

Answer 54

Exacerbation of cerebral edema, increased ICP, hemodilution, and reduced oxygen-carrying capacity.

Question 55

What is the role of the mitochondrial electron transport chain in cellular respiration and how is it disrupted by cyanide?

Answer 55

Cyanide inhibits cytochrome c oxidase (Complex IV), halting electron transfer and ATP production, leading to anaerobic metabolism and lactic acidosis.

Question 56

How does hydrogen cyanide toxicity affect venous oxygen saturation?

Answer 56

SvO₂ and ScvO₂ may appear falsely elevated because tissues cannot extract oxygen, leading to high oxygen content in venous blood.

Question 57

What is the half-life of carboxyhemoglobin (COHb) in room air, 100% oxygen, and hyperbaric conditions?

Answer 57

- Room air: ~4–6 hours - 100% O₂: ~60–90 minutes - Hyperbaric O₂: ~20–30 minutes

Question 58

How does hyperbaric oxygen therapy benefit CO poisoning beyond displacing CO from hemoglobin?

Answer 58

Increases dissolved oxygen in plasma, promotes mitochondrial recovery, reduces lipid peroxidation, and limits delayed neurologic sequelae.

Question 59

What are the RECOVER 2012 guidelines for neurologic post-ROSC care in dogs and cats?

Answer 59

Maintain normothermia, treat seizures promptly, avoid hypoxia and hypotension, consider hyperosmolar therapy for cerebral edema, and monitor neurologic function frequently.

Question 60

What are the two main types of cerebral edema relevant to TBI pathophysiology?

Answer 60

- Cytotoxic edema: intracellular swelling from energy failure (early) - Vasogenic edema: BBB disruption leading to extracellular fluid accumulation (later or with inflammation).

Question 61

How does mannitol reduce ICP in TBI?

Answer 61

Osmotically draws water from brain tissue into vasculature and improves blood rheology by decreasing endothelial swelling.

Question 62

How does hypertonic saline reduce ICP differently from mannitol?

Answer 62

Raises serum osmolality and reduces endothelial swelling without diuretic effect; also increases blood pressure and improves CPP more rapidly.

Question 63

What effect does rapid hypotonic fluid administration have in TBI?

Answer 63

Promotes water movement into brain cells, worsening cerebral edema and increasing ICP.

Question 64

How does systemic inflammation worsen outcomes after inhalation injury?

Answer 64

Neutrophilic infiltration and cytokine release exacerbate lung capillary leak, leading to ARDS-like changes and impaired oxygenation.

Question 65

What board-relevant differential diagnosis should always be considered with lactic acidosis and elevated ScvO₂?

Answer 65

Cyanide toxicity, sepsis-induced mitochondrial dysfunction, and severe anemia with tissue dysoxia.

Question 66

What respiratory pattern may develop in CO or cyanide toxicity prior to collapse?

Answer 66

Tachypnea progressing to dyspnea and apnea due to metabolic acidosis, CNS dysfunction, or respiratory muscle fatigue.

Question 67

What is the main determinant of cerebral blood flow and how is it affected by PaCO₂?

Answer 67

Cerebral blood flow is directly proportional to PaCO₂: hypercapnia causes vasodilation and ↑ ICP; hypocapnia causes vasoconstriction and ↓ ICP.

Question 68

Why is controlled ventilation important in managing TBI?

Answer 68

Prevents hypoventilation (hypercapnia → ↑ ICP) or overventilation (hypocapnia → cerebral ischemia). Target PaCO₂ = 35–38 mmHg.

Question 69

How does a left-shift in the oxyhemoglobin dissociation curve (as in CO poisoning) impair oxygen delivery?

Answer 69

Hemoglobin holds onto oxygen more tightly, decreasing its release to tissues despite adequate saturation.