RNC NIC CORE EXAM TEST QUESTIONS AND SOLUTIONS
RATED A+
✔✔respiratory alkalosis - ✔✔- occurs when CO2 is excreted by the lungs in excess of
its production (blowing off too much CO2)
- characterized by increased pH, *decreased PaCO2*, normal bicarb
- **PaCO2 is the MOST sensitive indicator of ventilation**
✔✔causes of respiratory alkalosis - ✔✔- *mechanical ventilation* --> need to start
weaning the vent
- anxiety
- fever
- sepsis
- hypoxemia (pneumonia, atelectasis, pulmonary emboli, congestive heart failure,
asthma)
- central nervous syndrome disorders
- liver failure
- Reye's syndrome
- hyperthyroidism
- salicylate poisoning
✔✔peak inspiratory pressure (PIP) - ✔✔- how big the lungs open, like an accordion
- *decreases CO2 by increasing tidal volume*
- larger PIP = larger TV (lungs are expanding larger)
- too high causes barotrauma, especially in a very small baby (*wean this setting first*
unless the rate is excessively high)
- if PaCO2 is high (under-ventilating), go up on the PIP by 1-2
- if PaCO2 is low (over-ventilating), decrease the PIP by 1-2
✔✔rate on ventilator - ✔✔- vent setting used to "blow off" CO2
- usually okay if physiologic (40-60), otherwise wean
- if the PIP is already fairly low, then wean the rate
- if the PaCO2 is high (need to blow off more CO2), go up on the rate
- if the PaCO2 is low (blowing off too much CO2), go down on the rate
✔✔peak end expiratory pressure (PEEP) - ✔✔- sort of like CPAP
- keeps the lungs distended at the end of every breath
- like the functional residual capacity --> what is left in the lungs after you blow out as
much as possible
- 5 is physiologic
- going up on the PEEP will usually improve oxygenation, but your PaCO2 will also go
up (need to look at the difference between the PIP and PEEP)
✔✔mean airway pressure (MAP) - ✔✔- what the PIP and PEEP produce
- going up on this setting should improve ventilation and oxygenation
,✔✔high frequency oscillatory or jet ventilation - ✔✔- use very fast rates with relatively
low MAPs to achieve ventilatory goals
- HFOV has an active exhalation phase (prevents breath stacking), but jet does not
- indications: conventional vent failure (too high pressures/rates, max settings)
- delta P/amp = pressure
- Hz = rate (every Hz = rate of 60)
✔✔fetal circulation - ✔✔- 1) best oxygenated blood comes from the PLACENTA through
the UMBILICAL VEIN
- 2) UV --> ductus venosus (1st shunt) --> inferior vena cava
- 3) IVC --> right atrium --> most blood goes through the oval foramen (2nd shunt) -->
left atrium; about 1/3 of the blood goes from the RA to RV instead of through the PFO
- 3a) of the 1/3 blood going into the RV --> pulmonary artery --> most goes through the
ductus arteriosus (3rd shunt) instead of going to the lungs --> DA connects PA to aorta -
-> sends blood to lower body
- 4) RA --> LA --> LV --> aorta
- 5) aorta: blood goes to brain and upper body first
- deoxygenated blood goes back to the placenta through the umbilical arteries to get rid
of waste products
✔✔cardiovascular transition - ✔✔- fetal circulation is like a lazy river --> low resistance
circuit
- once the cord is clamped (cuts off the low-resistance placental circulation/lazy river) --
> systemic vascular resistance in the newborn INCREASES
- with lung expansion and increased oxygenation in transition compared to in-utero
values, the pulmonary vascular bed dilates and PVR DECREASES
- *90% of the RV output will now go through the pulmonary arteries instead of through
the PDA, like in utero*
✔✔how does the foramen ovale close? - ✔✔- in transition, increased SVR and
decreased PVR lead to *higher LA pressure and forced closure of the foramen ovale*
(left side of heart increases in pressure compared to the right)
- FO = between RA and LA
✔✔when does the ductus arteriosus close? - ✔✔- *begins to close immediately after
birth, but can remain open for several days*
- *within the first 12 hours after birth, there is functional closure of the DA*
- *anatomic closure of the DA can take up to one month*
- closure is mediated by oxygen and the loss of prostaglandin sensitivity
✔✔respiratory transition - ✔✔- 4 things must occur as the fetal lung changes from
secretion of fluid to absorption of fluid and functional residual capacity is established
(surfactant system):
1) fluid must be cleared from the airspaces
2) continuos breathing must be established
,3) PVR must fall below SVR
4) right-to-left shunting of venous blood returning to the heart must stop (i.e. foramen
ovale must close)
✔✔persistent pulmonary hypertension of the newborn (PPHN) - ✔✔- results from failure
to normally transition after birth
- combination of pulmonary hypertension (high pressure in the PA) with subsequent
right-to-left shunting through fetal channels (foramen ovale and ductus arteriosus) away
from the pulmonary vascular bed
- *if the PA pressure is higher than the systemic pressure (PA clamps down), blood will
flow the path of least resistance --> away from the lungs through the foramen ovale and
ductus arteriosus (RIGHT-TO-LEFT SHUNTING at the DUCTAL LEVEL)*
- the infant will become progressively hypoxemic and acidemic, which causes the PA to
clamp down even more --> once cycle starts, very difficult to break
✔✔*causes of PPHN* - ✔✔- stress
- sepsis
- hypoglycemia
- hypothermia
- respiratory distress syndrome
- meconium aspiration
- pneumonia
- asphyxia
- congenital diaphragmatic hernia
- hyperviscous blood
- anything!
✔✔key points PPHN - ✔✔- *every newborn has an initially high PVR and is at risk for
developing PPHN*
- failure to successfully transition will lead to PPHN
✔✔type II pneumocytes - ✔✔- *principle cells responsible for surfactant production,
storage, secretion, and re-use*
- surfactant lowers surface tension within the alveolus (specifically at the air-liquid
interface)
✔✔transient tachypnea of the newborn (TTN) presentation - ✔✔- hx of maternal
sedation, *C-section delivery*, *precipitous vaginal delivery* (not enough squeezing)
- tachypnea, shallow respirations, grunting, retractions, nasal flaring, respiratory
acidosis, mild cyanosis/hypoxemia
- no evidence of shunting at FO or DA, normal lung volumes
✔✔apnea of prematurity (AOP) - ✔✔- most common respiratory problem in high-risk
neonatal population, not present within the first 24 hours of life
- *defined as periodic breathing with pathologic apnea in a premature infant; can be
classified as central, obstructive, or mixed*
, - diagnosis of exclusion because many disorders can cause apnea
- most episodes occur during REM sleep (preemies are in this most)
- clear lungs on CXR
✔✔apnea - ✔✔- *defined as cessation of respiratory air flow*
✔✔pathologic apnea - ✔✔- *defined as a pause in respirations for more than 20
seconds, or in the presence of cyanosis, bradycardia, pallor, or hypotonia*
✔✔periodic breathing - ✔✔- *consists of three or more respiratory pauses lasting 3
seconds, with less than 20 seconds of respirations between pauses*
✔✔central apnea - ✔✔- *includes complete cessation of breathing and is related to a
loss of diaphragmatic and other respiratory muscle function*
- no chest movement because the brain did not tell the baby to breathe
✔✔obstructive apnea - ✔✔- *characterized by respiratory efforts that are present but
without movement of air flow, occurring secondary to upper airway obstruction
anywhere from the nares to the larynx*
- chest movement with no air flow
✔✔mixed apnea - ✔✔- *combination of central and obstructive apnea, which accounts
for 50% of all apnea*
✔✔respiratory distress syndrome (RDS) - ✔✔- developmental disorder than results from
an inadequate amount of surface-active material to line the air spaces
- there is an inability to maintain a residual volume of air in the alveoli on expiration,
resulting in extensive atelectasis, ventilation/perfusion abnormalities, and the formation
of hyaline membranes
- r/t qualitative and quantitative abnormalities of the pulmonary surfactant system
✔✔*RDS predisposing factors* - ✔✔- prematurity
- male sex
- *maternal diabetes*
- perinatal asphyxia
- second-born twin
- familial predisposition
- C-section without labor
✔✔presentation of RDS - ✔✔- respiratory distress, usually within first 6 hours of life
- increased WOB, cyanosis, nasal flaring, lethargy, tachypnea, possibly apnea
✔✔TTN X-ray findings - ✔✔- *sunburst pattern with perihilar streakiness (right sided
common)*, classic finding of *fluid in the (interlobar) fissure*, mild pleural effusions with
blunting of costophrenic angles
RATED A+
✔✔respiratory alkalosis - ✔✔- occurs when CO2 is excreted by the lungs in excess of
its production (blowing off too much CO2)
- characterized by increased pH, *decreased PaCO2*, normal bicarb
- **PaCO2 is the MOST sensitive indicator of ventilation**
✔✔causes of respiratory alkalosis - ✔✔- *mechanical ventilation* --> need to start
weaning the vent
- anxiety
- fever
- sepsis
- hypoxemia (pneumonia, atelectasis, pulmonary emboli, congestive heart failure,
asthma)
- central nervous syndrome disorders
- liver failure
- Reye's syndrome
- hyperthyroidism
- salicylate poisoning
✔✔peak inspiratory pressure (PIP) - ✔✔- how big the lungs open, like an accordion
- *decreases CO2 by increasing tidal volume*
- larger PIP = larger TV (lungs are expanding larger)
- too high causes barotrauma, especially in a very small baby (*wean this setting first*
unless the rate is excessively high)
- if PaCO2 is high (under-ventilating), go up on the PIP by 1-2
- if PaCO2 is low (over-ventilating), decrease the PIP by 1-2
✔✔rate on ventilator - ✔✔- vent setting used to "blow off" CO2
- usually okay if physiologic (40-60), otherwise wean
- if the PIP is already fairly low, then wean the rate
- if the PaCO2 is high (need to blow off more CO2), go up on the rate
- if the PaCO2 is low (blowing off too much CO2), go down on the rate
✔✔peak end expiratory pressure (PEEP) - ✔✔- sort of like CPAP
- keeps the lungs distended at the end of every breath
- like the functional residual capacity --> what is left in the lungs after you blow out as
much as possible
- 5 is physiologic
- going up on the PEEP will usually improve oxygenation, but your PaCO2 will also go
up (need to look at the difference between the PIP and PEEP)
✔✔mean airway pressure (MAP) - ✔✔- what the PIP and PEEP produce
- going up on this setting should improve ventilation and oxygenation
,✔✔high frequency oscillatory or jet ventilation - ✔✔- use very fast rates with relatively
low MAPs to achieve ventilatory goals
- HFOV has an active exhalation phase (prevents breath stacking), but jet does not
- indications: conventional vent failure (too high pressures/rates, max settings)
- delta P/amp = pressure
- Hz = rate (every Hz = rate of 60)
✔✔fetal circulation - ✔✔- 1) best oxygenated blood comes from the PLACENTA through
the UMBILICAL VEIN
- 2) UV --> ductus venosus (1st shunt) --> inferior vena cava
- 3) IVC --> right atrium --> most blood goes through the oval foramen (2nd shunt) -->
left atrium; about 1/3 of the blood goes from the RA to RV instead of through the PFO
- 3a) of the 1/3 blood going into the RV --> pulmonary artery --> most goes through the
ductus arteriosus (3rd shunt) instead of going to the lungs --> DA connects PA to aorta -
-> sends blood to lower body
- 4) RA --> LA --> LV --> aorta
- 5) aorta: blood goes to brain and upper body first
- deoxygenated blood goes back to the placenta through the umbilical arteries to get rid
of waste products
✔✔cardiovascular transition - ✔✔- fetal circulation is like a lazy river --> low resistance
circuit
- once the cord is clamped (cuts off the low-resistance placental circulation/lazy river) --
> systemic vascular resistance in the newborn INCREASES
- with lung expansion and increased oxygenation in transition compared to in-utero
values, the pulmonary vascular bed dilates and PVR DECREASES
- *90% of the RV output will now go through the pulmonary arteries instead of through
the PDA, like in utero*
✔✔how does the foramen ovale close? - ✔✔- in transition, increased SVR and
decreased PVR lead to *higher LA pressure and forced closure of the foramen ovale*
(left side of heart increases in pressure compared to the right)
- FO = between RA and LA
✔✔when does the ductus arteriosus close? - ✔✔- *begins to close immediately after
birth, but can remain open for several days*
- *within the first 12 hours after birth, there is functional closure of the DA*
- *anatomic closure of the DA can take up to one month*
- closure is mediated by oxygen and the loss of prostaglandin sensitivity
✔✔respiratory transition - ✔✔- 4 things must occur as the fetal lung changes from
secretion of fluid to absorption of fluid and functional residual capacity is established
(surfactant system):
1) fluid must be cleared from the airspaces
2) continuos breathing must be established
,3) PVR must fall below SVR
4) right-to-left shunting of venous blood returning to the heart must stop (i.e. foramen
ovale must close)
✔✔persistent pulmonary hypertension of the newborn (PPHN) - ✔✔- results from failure
to normally transition after birth
- combination of pulmonary hypertension (high pressure in the PA) with subsequent
right-to-left shunting through fetal channels (foramen ovale and ductus arteriosus) away
from the pulmonary vascular bed
- *if the PA pressure is higher than the systemic pressure (PA clamps down), blood will
flow the path of least resistance --> away from the lungs through the foramen ovale and
ductus arteriosus (RIGHT-TO-LEFT SHUNTING at the DUCTAL LEVEL)*
- the infant will become progressively hypoxemic and acidemic, which causes the PA to
clamp down even more --> once cycle starts, very difficult to break
✔✔*causes of PPHN* - ✔✔- stress
- sepsis
- hypoglycemia
- hypothermia
- respiratory distress syndrome
- meconium aspiration
- pneumonia
- asphyxia
- congenital diaphragmatic hernia
- hyperviscous blood
- anything!
✔✔key points PPHN - ✔✔- *every newborn has an initially high PVR and is at risk for
developing PPHN*
- failure to successfully transition will lead to PPHN
✔✔type II pneumocytes - ✔✔- *principle cells responsible for surfactant production,
storage, secretion, and re-use*
- surfactant lowers surface tension within the alveolus (specifically at the air-liquid
interface)
✔✔transient tachypnea of the newborn (TTN) presentation - ✔✔- hx of maternal
sedation, *C-section delivery*, *precipitous vaginal delivery* (not enough squeezing)
- tachypnea, shallow respirations, grunting, retractions, nasal flaring, respiratory
acidosis, mild cyanosis/hypoxemia
- no evidence of shunting at FO or DA, normal lung volumes
✔✔apnea of prematurity (AOP) - ✔✔- most common respiratory problem in high-risk
neonatal population, not present within the first 24 hours of life
- *defined as periodic breathing with pathologic apnea in a premature infant; can be
classified as central, obstructive, or mixed*
, - diagnosis of exclusion because many disorders can cause apnea
- most episodes occur during REM sleep (preemies are in this most)
- clear lungs on CXR
✔✔apnea - ✔✔- *defined as cessation of respiratory air flow*
✔✔pathologic apnea - ✔✔- *defined as a pause in respirations for more than 20
seconds, or in the presence of cyanosis, bradycardia, pallor, or hypotonia*
✔✔periodic breathing - ✔✔- *consists of three or more respiratory pauses lasting 3
seconds, with less than 20 seconds of respirations between pauses*
✔✔central apnea - ✔✔- *includes complete cessation of breathing and is related to a
loss of diaphragmatic and other respiratory muscle function*
- no chest movement because the brain did not tell the baby to breathe
✔✔obstructive apnea - ✔✔- *characterized by respiratory efforts that are present but
without movement of air flow, occurring secondary to upper airway obstruction
anywhere from the nares to the larynx*
- chest movement with no air flow
✔✔mixed apnea - ✔✔- *combination of central and obstructive apnea, which accounts
for 50% of all apnea*
✔✔respiratory distress syndrome (RDS) - ✔✔- developmental disorder than results from
an inadequate amount of surface-active material to line the air spaces
- there is an inability to maintain a residual volume of air in the alveoli on expiration,
resulting in extensive atelectasis, ventilation/perfusion abnormalities, and the formation
of hyaline membranes
- r/t qualitative and quantitative abnormalities of the pulmonary surfactant system
✔✔*RDS predisposing factors* - ✔✔- prematurity
- male sex
- *maternal diabetes*
- perinatal asphyxia
- second-born twin
- familial predisposition
- C-section without labor
✔✔presentation of RDS - ✔✔- respiratory distress, usually within first 6 hours of life
- increased WOB, cyanosis, nasal flaring, lethargy, tachypnea, possibly apnea
✔✔TTN X-ray findings - ✔✔- *sunburst pattern with perihilar streakiness (right sided
common)*, classic finding of *fluid in the (interlobar) fissure*, mild pleural effusions with
blunting of costophrenic angles
