test 2 fb Flashcards
Volume controlled ventilation is being used, what needs to be monitored?
PIP, Pplat, and static compliance
Pressured controlled ventilation is being used, what needs to be monitored?
exhaled tidal volume
Inconsistent tidal volume is being administered so it’s best to measure with how much the patient breaths out.
Pressure regulated volume control (PRVC) mode of ventilation uses a combination of volume and pressure. How does this mode of ventilation accomplish this?
Volume-targeted
Pressure-targeted
Pressure-targeted, pressure regulated
Pressure-regulated, volume targeted
Pressure-regulated, volume targeted
The proper depth of endotracheal tube (ETT) for pediatric over 1 years old?
Determine tube depth after watching it go through the cords is 3x the ETT size.
When comparing EtCO2 and PaCO2, which statement is true?
PaCO2 > EtCO2
EtCO2 will always be less than the PaCO2. This relationship is vital to understand and allows the clinician to gauge the approximate PaCO2 value. The standard gradient between the EtCO2 and PaCO2 is 3-5 mmHg, with the PaCO2 always the higher number.
Oxygen delivery (DO2) is a product of what?
SaO2, Hgb, cardiac output (Q)
What would be the anticipated findings in the early stages of septic shock?
Increased CO/CI, increased SVR, increased SvO2
Increased CO/CI, decreased SVR, increased SvO2
Decreased CO/CI, decreased SVR, decreased SvO2
Decreased CO/CI, increased SVR, decreased SvO2
Increased CO/CI, decreased SVR, increased SvO2
In the early stages of septic shock, the cardiac output (CO) and cardiac index (CI) are increased, SVR is decreased, and SvO2 is increased. Mediators causing vasodilation are present in early stages of septic shock, whereas vasoconstriction appears in the later stages of septic shock. The SvO2 is increased in the early stages of septic shock because the tissues are incapable of extracting oxygen from the blood, so the venous blood is more saturated with oxygen when it returns to the lungs for reoxygenation.
You are transporting a 4 kg, 3-day-old neonate in severe sepsis and metabolic acidosis who is intubated and sedated. Before intubation, the patient’s initial respiratory rate was 44, with a corresponding EtCO2 of 22. What would be the most appropriate vent settings for this patient?
SIMV 30, PC 14, Vte 20-30 mL, PEEP 5, FiO2 1.0
SIMV 30, PC 10, Vte 30-40 mL, PEEP 5, FiO2 0.30
SIMV 40, PC 10, Vte 24-32 mL, PEEP 5, FiO2 0.30-0.50
SIMV 40, PC 12, Vte 15-30 mL, PEEP 5, FiO2 0.50
SIMV 40, PC 10, Vte 24-32 mL, PEEP 5, FiO2 0.30-0.50
With metabolic acidosis, always allow the patient to compensate. If the patient is paralyzed, then match their respiratory rate and EtCO2 reading to that which it was before intubation to continue blowing off excess acid (CO2). Removing excess acid will help prevent the pH from decreasing and prevent a potential lethal acidemia. Remember - for every 10 mmHg of change in PaCO2, there will be an inverse change in pH by 0.08.
A neonate has an order for continuous prostaglandin administration. What is the starting dose?
0.05-0.1 mcg/kg/min
Pediatric patients will not demonstrate hypotension secondary to hemorrhage, until approximately ________ loss of blood volume.
25%
Neonates and pediatric patients compensate well. Decompensation usually does not occur until approximately 25% blood loss. That may only be 10-20 milliliters of blood loss in a neonate. Normal circulating blood supply is 75-80 mL/kg.
The second stage of labor ends with:
Delivery of the fetus
The first stage of labor begins with the onset of labor and ends with full cervical dilation (10cm) and 100% effacement. The second stage of labor starts when the cervix is fully dilated and ends with delivery of the fetus. The third stage begins after the birth of the fetus and ends with delivery of the placenta.
The team is transporting a 5-day-old neonate. On arrival, the report states that the baby is suffering from Tetralogy of Fallot (TOF). What is the long-term treatment to correct this heart defect?
Prostaglandin (PGE1) administration to ensure patency of the vessels
Jatene procedure to perform an arterial switch
Catheterize and dilate the pulmonary artery (PA) and patch the ventricular septal defect (VSD)
Indomethacin for patent ductus arteriosus (PDA) closure and placement of a patch to prevent shunting of blood
Catheterize and dilate the pulmonary artery (PA) and patch the ventricular septal defect (VSD)
Patients that suffer from Tetralogy of Fallot have multiple issues. Most often, they suffer from a VSD, stenotic pulmonic valve, RV hypertrophy, and a pulmonary artery outflow obstruction. Patency of the ductus arteriosus is essential short-term and accomplished with the administration of prostaglandin (PGE1). Administration of oxygen needs to be minimal. While PGE1 administration is essential short-term, the question is in regards to the long-term treatment of this defect. Long-term treatment is dilation of the pulmonary artery to alleviate the PA outflow obstruction and surgical repair of the VSD.
A patient was recently admitted for an inferior myocardial infarction. There is now a new systolic murmur upon cardiac auscultation. What is the most common cause of this?
Mitral valve stenosis
Pulmonic valve regurgitation
Mitral valve regurgitation
Aortic valve stenosis
Mitral valve regurgitation
Acute mitral valve regurgitation can occur after an MI secondary to rupture of the papillary muscle, which results in a mitral leaflet flail. Acute mitral valve regurgitation occurs more commonly with an inferior MI, and results in a decrease in cardiac output, leading to CHF and cardiogenic shock. Pulmonic valve regurgitation and mitral valve stenosis both present as diastolic murmurs. Aortic valve stenosis presents as a systolic murmur but not a new onset finding after recent MI.
A patient is suffering from right heart failure. What hemodynamic change would NOT be expected?
Decreased pulmonary capillary wedge pressure (PCWP)
Decreased central venous pressure (CVP)
Decreased pulmonary artery pressure (PAP)
Increased systemic vascular resistance (SVR)
Decreased central venous pressure (CVP)
Inadvertant migration of the intra-aortic balloon may cause all of the following EXCEPT:
Loss of renal perfusion
Loss of flow to the carotid artery
Loss of blood flow to the renal arteries
Loss of flow to the subclavian artery
Loss of flow to the carotid artery
Migration of the intra-aortic balloon will cause a loss of blood flow to the renal arteries, decreased renal perfusion, loss of blood flow to the subclavian arteries and loss of circulation to the left arm via the radial artery.
