Across the Lifespan Flashcards
how does pregnancy affect minute ventilation?
Progesterone is a respiratory stimulant. It increases minute ventilation up to 50%
- Vt increased by 40%
- RR increased by 10%
how does pregnancy affect the mother’s arterial blood gas?
Progesterone is a respiratory stimulant. It increases minute ventilation up to 50%. As a consequence, mom’s PaCO2 falls, and she develops respiratory alkalosis. Renal compensation eliminates bicarbonate to normalize blood pH. A small reduction in physiologic shunt explains the mild increase in PaO2. This increases the driving pressure of oxygen across the fetoplacental interface and improves fetal gas exchange.
- Arterial pH= no change
- PaO2 = increased (104-108 mmHg)
- PaCO2= Decreased (28-32 mmHg)
- HCO3= decreased ( 20mmol/L)
How does pregnancy affect the oxyhemoglobin dissociation curve?
Right shift (increase P50)-> facilitates O2 offloading to the fetus
How does pregnancy affect the lung volumes and capacities?
Functional residual capacity is reduced as a function of a decrease in expiratory reserve volume and residual volume (ERV decreases more than RV)
An increased oxygen consumption paired with a decreased FRC hastens the onset of hypoxemia. Failure to reverse hypoxemia results in brain death of the mother and the fetus
how does cardiac output change during pregnancy and delivery
How do blood pressure and systemic vascular resistance change during pregnancy?
Who is at risk for aortocaval compression, and how do you treat it?
In the supine position, the gravid uterus compresses both the vena cava and the aorta. This decreases venous return to the heart as well as arterial flow to the uterus and lower extremities. Decreased CO compromises fetal perfusion and can also cause the mother to lose consciousness.
By displacing the uterus away from the vena cava and aorta, we can reduce its compressive effects. We can accomplish this by elevating the mother’s right torso 15 degrees. It should be used for anyone in their 2nd (14-26 weeks) or 3rd trimester
How does the intravascular fluid volume change during pregnancy?
Intravascular fluid increases 35%
* plasma volume increases 45%
* erythrocyte volume increases 20%
What hematologic changes accompany pregnancy
- Clotting factors 1, 7, 8, 9, 10, 12 increase
- anticoagulants: Proteins S decreases and no change in protein C
- fibrin breakdown increases
- anti-fibrinolytic system: 11 & 13 decrease
How does MAC change during pregnancy?
MAC is decreased by 30-40%. This is probably due to increased progesterone.
How does pregnancy affect gastric pH and volume?
Pregnancy increases gastric volume and decreases gastric pH. This is due to increased gastrin.
How does pregnancy affect gastric emptying?
Before onset of labor = No change
After onset of labor = Slowed
How does pregnancy affect uterine blood flow?
Non-pregnant state = 100mL/min
Pregnancy at term = up to 700mL/min or 10% of the cardiac output (some texts say up to 800 or 900mL/min)
What conditions can reduce uterine blood flow?
uterine blood flow does NOT autoregulate- therefore, it is dependent on MAP, CO, and uterine vascular resistance (UVR).
Causes of reduced uterine blood flow:
* decreased perfusion: Maternal HoTN (sympathectomy, hemorrhage, aortocaval compression)
* increased resistance: Uterine contraction, HTN conditions that increase UVR
Uterine blood flow= (uterine artery pressure- uterine venous pressure)/ Uterine vascular resistance
Discuss the use of phenylephrine and ephedrine in the laboring pt.
Classic teaching states that phenylephrine increases uterine vascular resistance and reduces placental perfusion.
More recent evidence suggest that phenylephrine is as efficacious as ephedrine in maintaining placental perfusion and fetal pH in healthy mothers. In fact, mothers that received phenylephrine had higher fetal pH values (less fetal acidosis)
Which law determines which drugs will pass through the placenta?
The Fick principle determines which drugs can pass across the placenta.
Rate of diffusion (Diffusion coefficient x surface area x concentration gradient (between mom and fetus)/ membrane thickness
Drug characteristics that favor placental transfer:
* Low molecular weight < 500 Daltons (most anesthetic drugs and smaller than 500 Daltons)
* High lipid solubility
* nonionized
* nonpolar
Define the 3 stages of labor.
stage 1: beginning of regular contraction to full cervical dilation (10cm)
Stage 2: full cervical dilation to delivery of the fetus (pain in the perineum begins during stage 2)
Stage 3: Delivery of the placenta
How does uncontrolled labor pain affect the mother and the fetus?
May result in:
* increased maternal catecholamines -> HTN -> reduced uterine blood flow to the fetus
* maternal hyperventilation -> leftward shift of oxyhgb curve-> reduced delivery of O2 to the fetus
Compare and contrast the pain that results from the first and second stages of labor.
First stage:
* pain begins in the lower uterine segment and the cervix
* origin: T10-L1 posterior nerve roots
Second stage:
* Adds in pain impulses from the vagina, peritoneum, and pelvic floor.
* origins: S2-S4 posterior nerve roots
Compare and contrast the regional anesthetic technique that can be used for first and second stage labor pain.
Neuraxial techniques that provide analgesia to T10-L1 during the first stage of labor must be extended to cover S2-S4 during the second stage of labor
compare and contrast bupivicaine and ropivicaine for labor
discuss the use of 2-chloroprocaine for labor
- Useful for emergency C/S when epidural is already in place (very fast onset)
- metabolized by pseudocholinesterase in the plasma- minimal placental transfer
- antagonized opioid receptor (mu & kappa) and reduces the efficacy of epidural morphine
- risk of arachnoiditis when used for spinal anesthesia due to preservatives
- solutions without methylparaben and metabisulfite do not cause neurotoxicity
discuss the consequences of an epidural that is placed in the subdural space.
Although a rare and unpreventable event, It is possible to position the tip of the epidural catheter in the subdural space - between the dura and the arachnoid. Neither catheter aspiration nor a test dose will rule out subdural placement.
Within 10-25 minutes after the epidural is dosed, the patient will experience symptoms of an excessive cephalad spread of local anesthetic. Because the subdural space is a potential space, it holds a very low volume. For this reason, the block height for a given amount of local anesthetic will be much higher than if the same volume was administered in the epidural space.
What is the treatment for a total spinal?
A total spinal may result from:
* an epidural dose injected into the subarachnoid space
* an epidural dose injected into the subdural space
* a single shot spinal after a failed epidural block
Initial tx includes: vasopressors, IVF, left uterine displacement, elevation of the legs, and intubation if LOC
Discuss the fetal heart rate
The fetal heart rate is a surrogate measure of overall fetal wellbeing. it provides an indirect method to assess fetal hypoxia and acidosis. The use of this modality guides clinical decision-making so that we can minimize risk of fetal injury and demise
Fetal oxygenation is a function of uterine and placental blood flow. The fetus responds to stress with peripheral vasoconstriction, HTN, and a baroreceptor- mediated reduction in heart rate
Which fetal decelerations are unremarkable? which ones are cause for concern?
early decels do not present a risk of fetal hypoxemia, while late and variable decels require urgent assessment of fetal status
* variable decels: cord compression
* early decels: head compression
* Accelerations: OK or give O2
* Late Decels: placental insufficiency
VEAL CHOP
Define premature delivery, and list the potential complications from its occurance.
defined as delivery before 37 weeks gestation or less than 259 days from the last menstrual cycle. It is the leading cause of perinatal morbidity and mortality, and this risk is even higher for newborns weighing less than 1500g. This incidence of prematurity rises with multiple gestations and premature rupture of membranes.
Complications of premature delivery include:
* respiratory distress syndrome
* intraventricular hemorrhage
* NEC
* hypoglycemia
* hypocalcemia
* Hyperbilirubinemia
Discuss the use of steroids and tocolytic agents in the prevention of premature delivery.
Corticosteroids: (betamethasone) hasten fetal lung maturity. These drugs begin to take effect within 18 hours, with a peak benefit at 48hrs
Tocolytic agents: stop labor around 24-48 hours. They provide a bridge that allows the corticosteroids time to work. Antibiotic prophylaxis for chorioamnionitis is also given at this time. Tocolytic agents or corticosteroids are seldom given after 33 weeks gestation
What are the side effects of beta-2 agonists when used for tocolysis?
Beta-2 agonists: Terbutaline, Ritodrine
Side effects:
* hypokalemia results from intracellular potassium shift.
* Beta-2 agonists cross the placenta and may increase FHR
* Hyperglycemia results from glycogenolysis in the liver
* the newborn of hyperglycemia mother is at risk of post-delivery hypoglycemia. The mother’s glucose supply is gone, but the insulin in the neonatal circulation remains
What are the effects of hypermagnesemia?
Side effects:
* Apnea
* HoTN
* Skeletal muscle weakness (synergism with nondepolarizers)
* CNS depression
* Reduced responsiveness to ephedrine and phenylephrine
What is the tx for hypermagnesemia?
- supportive measures
- Diuretics (to facilitate excretion of Mg)
- IV calcium (to antagonize Mg)
How can oxytocin be administered? What are potential side effects?
Oxytocin is synthesized in the supraoptic and paraventricular (primary) nuclei of the hypothalamus. It is released from the posterior pituitary gland.
You can give it IV (diluted in IVF), or the OB can inject it directly into the uterus.
Side effects:
* Water retention
* Hyponatremia
* reflex tachycardia
* Coronary vasoconstriction
how can methergine be administered?
Methergine is a ergot alkaloid. It can be given 0.2 mg IM (not IV)
IV administration can cause significant vasoconstriction, HTN, and cerebral hemorrhage
What are the pros and cons of general anesthesia for cesarean section?
Mortality is 17x higher with a general anesthetic
Failure to successfully manage the airway is the most common cause of maternal death
Benefits: Speed of onset, secured airway, greater hemodynamic stability
Drawbacks: Risk of difficult mask ventilation/laryngoscopy/intubation, risk of aspiration, Potential MH, absence of maternal awareness, Neonatal respiratory and CNS depression
Describe aspiration prophylaxis for the pt scheduled for cesarean section.
Triple prophylaxis against aspiration
* Sodium citrate to neutralize gastric acid
*H2 receptor antagonist (ranitidine) to reduce gastric acid secretion
*Gastrokinetic agent (metoclopramide) to hasten gastric emptying and increase LES tone
When is the pregnant pt who presents for non-obstetric surgery at risk for aspiration?
At app. 18-20 weeks gestation, pregnant pts are considered “full stomachs”. Therefore, they require RSI with aspiration prophylaxis (this may be needed earlier if the pt has symptoms of GERD). These recommendations also apply to the immediate postpartum period. (note: one text says to consider a “full stomach” at 12 weeks; consensus is 18-20)
secure the airway with a 6.0 -7.0 ETT
Aspiration precautions:
* non-particulate antacid (sodium citrate) 15-30 mL within 15-30 min of induction
* H2 antagonist (ranitidine) 1hr before induction
* Gastric prokinetic agent (reglan) 1hr before induction
Use left uterine displacement in the second and third trimester
What is the risk of NSAIDs when used in pregnant pts?
Avoid NSAIDs after the first trimester, as they may close the ductus arteriosus
Compare and contrast the diagnostic criteria for gestational HTN, preeclampsia, and eclampsia.
The classic triad of preeclampsia consists of HTN that develops after 20 wks gestation, proteinuria. Generalized edema is no longer a diagnostic requirement.
Discuss the balance of prostacyclin and thromboxane in the pt with preeclampsia
The healthy placenta produces thromboxane and prostacyclin in equal amts. However, the pt with preeclampsia produces up to 7x more thromboxane than prostacyclin.
Increased thromboxane favors vasoconstriction, platelet aggregation, and a reduced placental blood flow
compare and contrast mild and sever preeclampsia
Discuss the use of magnesium for preeclampsia
The presence of seizures differentiates between preeclampsia and eclampsia
Seizure prophylaxis with magnesium sulfate:
* load: 4g loading dose over 10 minutes
* infusion: 1-2 g/hr
* Tx for mg toxicity: 10mL of 10% calcium gluconate IV
Detail anesthetic management for the patient with preeclampsia.
Anesthetic management for preeclampsia:
* fluid management is balanced between a volume contracted patient and a “leaky” vasculature from endothelial dysfunction.
* Neuraxial anesthesia assists with blood pressure control and also provides better uteroplacental perfusion
* be sure to rule out thrombocytopenia (<100,000) before performing a neuraxial block
* due to airway swelling, these pts have a higher incidence of difficult intubation’
* These pts have an exaggerated response to sympathomimetics and methergine.
* if they are receiving magnesium therapy, they will exhibit an increased sensitivity to neuromuscular blockers
* Magnesium relaxes the uterus and increases the risk of postpartum hemorrhage
what is HELLP syndrome? what is the definitive tx?
HELLP syndrome stands for: hemolysis, elevated liver enzymes, and low platelet count. It develops in 5-10% of those with preeclampsia. The pts experience epigastric pain and upper abdominal tenderness.
Like preeclampsia, the definitive tx for HELLP syndrome is delivery of the fetus
discuss the anesthetic considerations for maternal cocaine abuse.
Cocaine is an ester-type local anesthetic that inhibits NE reuptake in the presynaptic SNS neuron. Flooding the synaptic cleft with NE increases SNS tone
- CV risks include tachycardia, dysrhythmias, and myocardial ischemia.
- Acute intoxication increases MAC
- Chronic use decreases MAC
- OB risks include spontaneous abortion, premature labor, placental abruption and low APGAR scores
- HTN is probably best treated with vasodilators
- Beta-blockers can cause heart failure if the SVR is significantly elevated
- HoTN May not respond to ephedrine in chronic cocaine abusers ( D/t catecholamine depletion). Phenylephrine is best option.
- Chronic cocaine abuse is associated with thrombocytopenia (check platelet count before neuraxial anesthesia)
What is the difference between placenta accreta, increta, and percreta? What is the major risk that these complications present?
The placenta normally implants into the decidua of the endometrium. There are three types of abnormal placental implantations:
* Accreta: Attaches to the surface of the myometrium
* Increta: Invades the myometrium
* Percreta: Extends beyond the uterus
Uterine contractility is impaired, and there is potential for tremendous blood loss. Though neuraxial anesthesia is safe, GA is preferred
what is placenta previa? how does it present?
Placenta previa occurs when the placenta attaches to the lower uterine segment.
- It partially or completely covers the cervical OS
- Associated with PAINLESS vaginal bleeding
- Potential for hemorrhage
What conditions increase the risk of placenta previa?
The risk of placenta previa is associated with previous cesarean sections and a history of multiple births
what are the risk factors for placental abruption? how does it present?
Partial or complete separation of the placenta from the uterine wall prior to delivery. It results in hemorrhage and fetal hypoxia.
Risk factors include:
* PIH (pregnancy induced HTN)
* Preeclampsia
* Chronic HTN
* Cocaine use
* Smoking
* Excessive alcohol use
it presents with painful vaginal bleeding. Pain may be so severe as to cause breakthrough when epidural is in place.
What is the most common cause of postpartum hemorrhage? what are the risk factors?
Uterine atony is the most common cause. The risk of uterine atony is increased by:
* Multiparity
* multiple gestations
* Polyhydramnios (too much amniotic fluid)
* Prolonged oxytocin infusion prior to surgery
A pt suffers from retained placental fragments. What IV medication can you give to help with the extraction?
IV nitroglycerine provides uterine relaxation for placental extraction
What are the tx options for uterine atony?
- uterine massage
- oxytocin
- Ergot Alkaloids
- Intrauterine Balloon
What does Apgar score mean?
Used to assess the newborn and guide resuscitative efforts. Five parameters are evaluated at 1 and 5 minutes after delivery. The score at 1 minute correlates with fetal acid-base status, while the 5 minute score may be predictive of neurologic outcome.
* Normal: 8-10
* Moderate distress: 4-7
* impending demise: 0-3
know how to calculate apgar score
what is the best indicator of ventilation during neonatal resuscitation?
resolution of bradycardia is the best indicator of adequate ventilation
How do you dose epi and fluids during neonatal resuscitation?
Epi: 1:10,000 , 10-30 mcg/kg IV or 0.05-0.1mg/kg intrathecal
Volume expander: PRBCs, NS, LR 10mL/kg over 5-10 minutes
what are the normal vital signs for a newborn? how do they trend as the child ages?
Why is the neonate’s minute ventilation higher than the adult?
Oxygen consumption and carbon monoxide production are twice those of adults. Therefore, the neonate must increase alveolar ventilation accordingly.
It is metabolically more efficient to increase respiratory rate than it is to increase tidal volume. This explains why newborns have a higher RR, yet tidal volume is the same as the adult on a per weight basis (6mL/kg)
What is the primary determinant of BP in the neonate?
Heart rate is the primary determinant of cardiac output and systolic BP
BP= HR x SV x SVR
The neonatal myocardium lacks the contractile elements to significantly adjust contractility or stroke volume; the ventricle is noncompliant. Furthermore, the Frank-starling relationship is underdeveloped (but not entirely absent) in the newborn. Therefore, the heart rate must be maintained to ensure adequate tissue perfusion and oxygen delivery
Describe the autonomic influence on the newborns heart
Autonomic regulation of the heart is immature at birth, with the SNS being less mature than the PNS. Stressful situations, such as laryngoscopy or suctioning of the airway may cause bradycardia. Atropine may be administered prior to induction to mitigate this response.
Additionally, the baroreceptor reflex is poorly developed, so the reflex fails to increase heart rate in the setting of hypovolemia
Contrast the breathing pattern in adults and infants
Adult= mouth or nose
infant= preferential nose breather up to 5 months of age
- most infants convert to oral breathing if the nasal passages are obstructed
- B/L choanal atresia may require emergency airway management if the infant is unable to mouth breathe
Contrast the relative size of the tongue in adults and infants
adult= small relative to oral volume
Infant= large relative to oral volume
- the tongue is closer to the soft palate, which makes it more likely to obstruct the upper airway
- More difficult to displace during laryngoscopy
contrast the relative neck length in adults and infants
adult= longer
infant=shorter
* more acute angle required to visualize the glottis
contrast the epiglottis shape in the adults and infants
adults= leaf (C shape), floppier, short
Infant= U (omega shape), stiffer, longer
* A stiff epiglottis makes it more difficult to displace during laryngoscopy
Contrast the vocal cord position in adults and infants
Adult= perpendicular to trachea
Infant= anterior slant
* Visualization and passage of the ETT may be more difficult
* ETT may get stuck in the anterior commissure
Contrast the laryngeal position in the adults and infants
Adult= C5-C6
Infant= C3-C4
* Larynx more superior/cephalad/rostral but NOT anterior. The only time the infant’s airway is more “anterior” is during neck flexion
* Same position as the adult in age 5-6 yrs
Contrast the narrowest point of the airway in adults and infants
Adult= glottis (vocal cords)
Infant= cricoid or glottis
* resistance to ett insertion beyond the vocal cords is likely at the cricoid ring.
* cricoid tissue is prone to inflammation and edema formation -> stridor or obstruction
* Poiseuille’s law- small changes in radius can significantly increase resistance to airflow (radius to the 4th power of laminar flow)
Contrast the orientation of the right mainstem bronchus in adults and infants
Adult: more vertical
Infant: less vertical
* up to age 3 year, both bronchi take off at 55 degrees.
* In the adult the right bronchus takes off at 25 degrees and the left at 45 degrees
Contrast the oxygen consumption, Alveolar ventilation, respiratory rate, tidal volume in the neonates and adults
Because the neonatal alveolar surface area is only 1/3 of the adult and oxygen consumption is twice that of the adult, the neonate must increase alveolar ventilation in order to sustain normal arterial gas tensions.
It is metabolically more efficient for the neonate to increase respiratory rate than it is to increase tidal volume.
Why do neonates desaturate faster than adults?
Neonates have a/an:
* Increased oxygen consumption to support metabolic demand
* Increase alveolar ventilation to increase oxygen supply.
* Slightly decreased FRC reflects a reduced oxygen reserve.
The net result is that the neonate has an increased ratio of alveolar ventilation relative to the size of its FRC. A faster gas turnover means that the 02 supply in the FRC is quickly exhausted during apnea.
Why is inhalation induction faster with neonates than with adults?
The increase ratio of alveolar ventilation relative to the size of the FRC explains a quicker inhalation induction for neonates.
A faster turn over of the FRC (fewer alveoli need to achieve steady state) allow a speedier development of anesthetic partial pressure inside the alveoli and consequently a more rapid change in the anesthetic partial pressure inside the brain and spinal cord.
What is the difference between fast and slow twitch muscle fibers? how does this relate to new natal pulmonary mechanics?
The diaphragm in intercostal muscles are composed of two types of muscle fiber:
* Type1= Slow-twitch muscle fibers are built for endurance-they are resistant to fatigue.
* Type2- fast-twitch Muscle fibers that are built for short bursts of heavy work-they tire easily.
A smaller number of type one, slow twitch and Durant’s muscle fibers within the diaphragm increases the neonates risk for respiratory fatigue and developing respiratory failure.
Compare and contrast neonates to adults in terms of FRC, VC, TLC, RV, CC, and VT.
How does the newborn’s ABG change from delivery to the 1st 24 hours of life?
How does hypoximia affect ventilation in the newborn?
Respiratory control doesn’t mature until 42-44 week.
* before maturation: hypoxemia depresses ventilation
* after maturation: hypoxemia stimulates ventilation
What is the P50 for fetal hemoglobin? Why is it important?
Fetal hemoglobin HGB F has a P50 of 19mmHg.
* hgb F shifts the curve to the left (latch)
* It benefits the fetus by creating an oxygen partial pressure gradient across the uteroplacental membrane that facilitates the passage of 02 from the mother to the fetus.
Why does Hgb F have a higher affinity for oxygen?
Adult hemoglobin hgb A consists of two alpha and two beta chains, While fetal hemoglobin has 2 alpha and 2 gamma chains.
We know that 2,3-DPG causes a right shift in the oxyhemaglobin dissociation curve, but you may not know that the binding site for 2,3-DPG is only on the Beta chain. Since hemaglobin F has 2 gamma instead of to Beta chains it does not bind 2,3-DPG. This shifts the curve to the left and explains why hemoglobin F has a higher affinity for oxygen.
What are indications for ffp transfusion in the new neonates?
The indications for transfusion of FFP mirror the recommendations set forth by the ASA guidelines. These include.
* Emergency reversal of warfarin
* Correction of coagulopathic bleeding with increased PT > 1.5 or increased PTT.
* Correction of coagulopathic bleeding if > 1 blood volume has been replaced and coagulation studies are not easily obtained.
FFP is NOT indicated for expansion of intravascular volume.
What is the dose for FFP transfusion in neonates?
Dose=10 - 20 ml/kilogram.
When is platelet transfusion indicated in the neonate? What is the dose?
Platelet transfusion is recommended for invasive procedures to maintain a platelet count above 50,000.
* dose if obtained from apheresis=5mL/kg
*Dose if pooled platelet concenteation = 1pack/10kg
Describe the physiologic changes that occur as a result of massive transfusion.
A massive transfusion is associated with:
* alkalosus-> Due to citrate metabolism to bicarbonate in the liver.
* hypothermia-> Due to transfusion of cold blood
* Hyperglycemia -> Due to dextrose additive to stored blood.
* hypocalcemia-> Due to the binding of calcium by citrate.
* hyperkalemia-> Due to the administration of older blood.
When RBC’s are stored, the cell membrane becomes dysfunctional, which allows potassium to leak into the supernatant. Administration of PRBC’s to neonates can lead to hyperkalemia and cardiac arrest. The risk is reduced by administering washed or fresh cells that are less than 7 days old.
What is the estimated blood volume in the premature neonate, term neonate, infant, child> one year?
A 3 kg term neonate requires emergency exploratory laparotomy for necrotizing enterocolitis. Her preoperative hematocrit is 50% .What is the maximum allowable blood loss to maintain a hematocrit of 40%?
Maximum ABL= EBV x (HCT starting- HCT Target)/ HCT starting
- EBV= 3kg x 80 to 100mL/kg (Premature vs neonate) = 240mL
- HCT-starting - HCT target = 50-40=10
- Mabl= 240 to 300mL x (50-40)/50= 48- 50mL
When do GFR And renal tubular function achieve full maturation?
Normal GFR is reached at 8 to 24 months of age.
* Before maturation, neonates do a poor job conserving water, so they are intolerant of fluid restriction. On the flip side, they are unable to excrete large volumes of water, so they do not do well with fluid overload either.
Normal tubular function is reached at 2 years of age.
In the 1st days of life, the neonate is an obligate sodium loser. After that, she is better able to retain sodium than excrete it. She also has a tendency to lose glucose to the urine.
Compare contrast the distribution of body water in the premature neonate, neonate, child and adult.
What signs suggest dehydration in the neonate?
Signs of dehydration:
Sunken anterior fontanel
Weight loss a 10% reduction in the 1st week is normal.
Irritability and lethargy.
Dry mucus membranes.
Absence of tears
Decrease skin turgor
Increased hematocrit in the absence of transfusion.
Describe the 4:2:1 rule of fluid management.
Step 1: 0-10kg-> begin with 4mL/kg/hr
Step2: 10-20kg-> add 2mL/kg/hr to previous total
Step3: >20kg -> add 1 mL/kg/hr to the previous total
If the pt is > 20kg, then you can uae the shortcut -> pts weight in kg+40
How should the NPO fluid deficit be replaced?
Multiply the patients hourly fluid maintenance rate by the number of hours of NPO time period replace this deficit over 3 hours.
1st hr: 50%
2nd hr: 25%
3rd hr: 25%
How should 3rd space losses be replaced in the neonates?
Replace fluid loss to third spacing and evaporation.
Minimal surgical trauma = 3-4 mL/kg/hr
Moderate surgical trauma = 5-6 mL/kg/hr
Major= 7-10mL/kg/hr
As a general rule, 3rd space loss is not included in the 1st hour of anesthesia.
What ratio should be used to replace blood loss with crystalloid, colloid, and blood?
Replace with crystallied at 3:1ratio.
Replace with colloid at 1:1 ratio
Replace with blood at 1:1ratio.
Which pediatric patient populations should receive an IVF that contains glucose?
Routine use of glucose containing solution is generally not recommended.
Instead these fluids should be reserved for infants and children at risk of developing hypoglycemia including:
* Prematurity
* Less than 48 hours of age.
* Small for gestational age.
* Newborns of diabetic mothers.
* Children with diabetes who received insulin on the day of surgery.
* Children who receive glucose based parental nutrition.
What is the cardiac output in the newborn? How does this affect pharmokinetics?
In the newborn, cardiac output is 200 ml/kg/min, which means that drugs are delivered to and removed from the rest of the body at a faster rate than the adult.
Discuss plasma protein binding in the neonate
Plasma protein should be thought of as a storage site or “sink” for drugs in the Plasma. A drug bound to a plasma protein cannot exert a physiologic effect.
- Before 6 months of age, there are lower concentrations of albumin and alpha-1 acid glycoprotein.
- Highly protein bound drugs will display higher free drug levels, which increases the risk of toxicity.
Discuss MAC in children. Does this rule apply to all volatile anesthetics?
MAC varies with age
* neonate (0-30 days) : MAC is lower than the infant
* Premature: MAC is lower than the neonate
* Infant 1-6 months: MAC is higher than the adult
* Infant 2-3 months: MAC peaks at its highest level
The MAC requirement pattern for sevo is different
* 0 to 6 months: MAC is higher (3.2%)
* 6months to 12 yrs: MAC is lower but still higher than the adult (2.5%)
How do you dose succinylcholine in the neonate?
Succ’s- 2mg/kg
* this is largely due to relatively higher ECF (Vd is higher)
How do you dose nondepolarizing neuromuscular blockers in the neonate? Why?
Dose= same as adult on mg/kg basis
* Although the ECF is larger, the NMJ is highly sensitive to the effects of nondepolarizers. These things cancel each other out, which explains why the doses the same as in adults.
What is the dose of IM succinylcholine? Which IM Site has the fastest onset of action?
The dose for neonates and infants is 5 mg/kg, while older children should receive 4 mg/kg.
Intralingual administration via the submental approach likely has the fastest onset.
What is the primary hemodynamic concern when a small child receives a second dose of succ’s?
In children less than 5 years of age succs may cause Bradycardia or asystole.
This can occur following the 1st dose but it is more likely after repeat administration intravenous atropine pretreatment 0.02 mg/kg will mitigate this response.
An infant that is susceptible to malignant hyperthermia develops a laryngospasm during induction of anesthesia. There is no IV in place. What is the best drug to give at this time?
Rocuronium is the only nondepolarizer that can be given via the IM route.
* if <1yr of age= 1mg/kg
* if >1r of age = 1.8 mg/kg
Describe the 5 types of tracheoesophageal atresia. which is the most common?
Esophageal atresia is the most common congenital defect of the esophagus, and most of these children also have a tracheoesophageal fistula.
Type C accounts for around 90% of all TEFs
In this configuration, the upper esophagus ends in a blind pouch, and the lower esophagus communicates with the distal trachea.
What prenatal findings suggest esophageal atresia?How is the diagnosis confirmed after birth?
Esophageal atresia prevents the fetus from swallowing amniotic fluid.(It can’t reach the stomach) The maternal polyhydramnios is a key diagnostic indicator for TEF.
Diagnosis is confirmed by the ability to pass a gastric tube into the stomach.Other symptoms include choking, coughing, and cyanosis during oral feeding.
what is the VACTERL association?
Approximately 25-50% of pts with TEF suffer from other congenital anomalies. Collectively these are known as VACTERL association. These pts require a thorough preoperative evaluation.
* V- Vertebral defects
* A- Imperforated Anus
* C- Cardiac Anomalies
* T- Tracheoesophageal fistula
* E- Esophageal atresia
* R- renal dysplasia
* L - limb anomalies
a patient with Type C TEF. Where should the tip of the ETT be positioned?
Place the ETT below the fistula but above the carina.
* if placed too high, respiratory gas is delivered to the stomach
* if placed too low, endobronchial intubation is likely
How should you induce anesthesia in a pt undergoing type C TEF repair?
Anesthetic management for TEF:
* Head up position and frequent suctioning minimize the risk of gastric aspiration
* Awake intubation or inhalation induction with spontaneous ventilation
* Positive-pressure ventilation -> gastric distention -> decreased thoracic compliance -> increased PIP required to ventilate-> downward spiral
*Placement of g-tube allows for gastric decompression. If the pt already has a g-tube, open it to atm before induction
* place the ETT below the fistula but above the carina.
* precordial stethoscope placed on the left chest will immediately detect a right mainstem intubation
* right lung compression during surgical repair is common. Right mainstem intubation will cause rapid desaturation.
Discuss the pathophysiology of respiratory distress syndrome?
Neonates who do not produce enough surfactant are at risk for respiratory distress syndrome (RDS)
* In the absence of adequate surfactant, the alveoli remain stiff and non-compliant.
* Small alveoli tend to collapse
* Larger alveoli become over distended (they accept the gas from the collapsed alveoli)
* this promotes atelectasis, reduces the surface area where gas exchange can take place, creating a V/Q mismatch
* Hypoxemia leads to acidosis and possibly the return to fetal circulation (more on this later)
Discuss the Use of pre and post-ductal SP02 monitoring in the newborn.
A pre ductal Pulse oximeter is placed on the right extremity, while the post-ductal monitor is usually placed on the lower extremity (either side)
A difference between the pre and post-ductal values suggest.
* pulm htn
* right to left cardiac shunt
*return to fetal circulation via the PDA
The patient has a hernia at the foramen of Bochdalek. Which congenital condition does this patient have?
Congenital diaphragmatic hernia is a diaphragmatic defect that allows the abdominal contents to enter the thoracic cavity.
*The foramen a Bochdalek is the most common sight of herniation (usually on the left side).
* Other sites herniation include the foramen of Morgagni and around the esophagus.
What signs and symptoms suggest a congenital diaphragmatic hernia?
CDH is usually diagnosed at birth. The newborn will have a scaphoid abdomen (sunken in) and likely experience respiratory distress.
other findings include:
* barrel chest
* Cardiac displacement
* fluid-filled gastrointestinal segments in the thorax
Describe the ventilatory management of the pt with a congenital diaphragmatic hernia.
The mass effect of the abdominal contents within the chest impairs lung development, leading to pulmonary hypoplasia. One or both lungs can be affected (increased PVR and decreased compliance)
- Keep PIP <25-30 cmH2O to minimize barotrauma and the risk of pneumothorax of the “good” lung. This may require permissive hypercapnia. While it will increase PVR, it’s the lesser of two evils in this situation.
- Avoid other conditions that increase PVR (Hypoxia, acidosis, hypothermia)
- Abdominal closure may increase PIP. The surgeon can create a temporary ventral hernia to increase the abdominal volume.
- a pulse oximeter placed on a lower extremity can warn of increased intra-abdominal pressure.
Compare and contrast omphalocele and gastroschisis
Describe the anesthetic concerns for a pt with omphalocele or gastroschisis.
Anesthetic management:
* If gastroschisis, abdominal contents are placed in a bag after delivery. This minimizes water and heat loss.
* Monitor peak airway pressure. If PIP >25-30cmH2O, then surgical closure of the abdomen may require staging.
* Closure may increase intra-abdominal pressure: P-abd -> decreased venous return -> decreased cardiac output-> decreased systemic perfusion
* Measure SpO2 on the lower extremity to monitor for impaired venous return
* Nitrous oxide distends the bowel and may impair surgical closure
* Expect major fluid and electrolyte shifts.
How and when does pyloric stenosis present?
Pyloric stenosis occurs when hypertrophy of the pyloric muscle creates a mechanical obstruction at the gastric outlet (between the stomach and the duodenum). An olive- shaped mass can be palpated just below the xiphoid process
* the infant presents with non-bilious projectile vomiting.
* It occurs in the first 2-12 weeks of life
* it is more common in males
Describe the pathophysiology of pyloric stenosis.
Vomiting depletes water and causes hyponatremia, hypokalemia, hypochloremia, and metabolic alkalosis.
- the lungs compensate with respiratory acidosis
- the kidneys try to correct metabolic alkalosis by excreting bicarbonate
As dehydration continues, aldosterone increases (Na+ and water retention). To maintain electroneutrality, the kidneys lose hydrogen in the urine. This causes paradoxical acidification of the urine.
If dehydration is not corrected, impaired tissue perfusion increases lactate production and produces metabolic acidosis. This is a late complication!
Describe the anesthetic management of the pt with pyloric stenosis.
- pyloric stenosis is a medical (not surgical) emergency. Surgical correction (pyloromyotomy) should be postponed until the fluid, electrolyte, and acid-base status are optimized
- Anticipate a full stomach, so empty the stomach before induction, intubated with awake or with RSI, and extubate awake.
- Place an oro- or nasogastric tube after induction. You can use it to assess the pylorus for an air leak following surgical repair. An air leak suggests mucosal perforation.
- Liberal hydration to correct dehydration. May require glucose supplementation
- Postoperative apnea is common. This is possibly due to the fact that CSF pH remains alkalotic even after serum acid-base status is normalized
What is necrotizing enterocolitis, and who is at risk?
NEC is necrosis of the bowel, usually the terminal ileum and proximal colon. Although the pathophysiology is incompletely understood, NEC is likely the result of early feeding. Impaired absorption by the gut leads to stasis, bacterial overgrowth, and infection. This increases the risk of bowel perforation.
Babies at risk:
* Prematurity (<32 weeks)
* Low birth weight (<1500 grams)
Discuss the management of NEC pts
Babies with NEC are managed medically, however, bowel perforation necessitates bowel resection and usually colostomy. These pts often have a metabolic acidosis and require substantial fluid replacement.
Bowel resection early in life can lead to short gut syndrome (nutrient malabsorption) as the pt ages
What is retinopathy of prematurity?
Vasculogenesis occurs 16-44 weeks post conception. This process begins at the macula then continues outwards towards the edges of the developing retina over time.
ROP is defined by two phases:
* Phase 1= inhibited growth of retinal vessels
* Phase 2 = overgrowth of abnormal vessels with fibrous bands that extend to the vitreous gel which can precipitate retinal detachment
What are the risk factors for ROP?
Key risk factors for ROP:
* prematurity
* low birth weight
* hyperoxia
* Mechanical ventilation
* Blood transfusion
* intraventricular hemorrhage
* Sepsis
* Vitamin E deficiency
Discuss the relationship between FiO2 and ROP
Until retinal maturation is complete (up to 44 wks post-conception), FiO2 should be titrated to SpO2 89-94%
what is apoptosis?
the process of programmed cell death. While this is a healthy response during normal development, there are concerns that commonly used anesthetic agents can kill neurons, potentially causing neurocognitive delays later in life.
Which anesthetic agents have been implicated in apoptosis?
Agents that have been implicated in apoptosis tend to antagonize the NMDA receptor, stimulate the GABA receptor, or both.
Drugs associated: Halogenated agents, nitrous oxide, propofol, ketamine, etomidate, barbiturates, benzos
Unknown effect: precedex, opioids, xenon
Give the name, location and function of the 3 fetal shunts.
Ductus Venosus: Function- allows umbilical blood to bypass the liver, Location- umbilical vein-> inferior vena cava
Foramen Ovale: Function- shunts blood from the RA to LA to bypass the lungs to perfuse the upper body (heart and brain), Location -RA-> LA
Ductus arteriosus: Function- Shunts blood from the pulmonary trunk (artery) to the aorta to perfuse the lower body, Location- Pulmonary artery -> proximal descending aorta
when does each fetal shunt close? what is the adult remnant of each?
Ductus venosus: Closes- clamping of umcilical cord, Remnant- Ligamentum venosus
Foramen ovale: Closes- 3 days, remnant- fossa ovalis
Ductus arteriosus: Closes- several weeks after birth, Remnant- ligamentum arteriosum
List 6 ways the fetal circulation is different from the adult circulation.
- The placenta is the organ of respiration (Adult=lungs)
- the circulation if arranged in parallel (adult= series)
- Right-to-left shunting occurs across the foramen ovale and ductus arteriosus.
- PVR is high- the lungs are collapsed and filled with fluid, so there is very little pulmonary blood flow.
- SVR is low - the placenta provides a large, low resistance vascular bed
- there’s minimal pulmonary blood flow, and left atrial pressure is low
Describe the circulatory changes that occur during the transition to extrauterine life.
brings forth several changes required for survival:
* First breath -> lung expansion -> increased PaO2 & decreased PaCO2 -> decreased PVR
* the placenta separates from the uterine wall (or cord clamp) -> increased SVR
* decreased PVR + increased SVR-> LA pressure > RA pressure -> the flap valve of the foramen ovale closes
* decreased PVR -> reversal of blood flow through the ductus arteriosus -> exposes the DA to increased PO2 -> DA closure
* decreased circulating PGE1 (released from the placenta) -> DA closure
What is the risk of a patent foramen ovale?
The PFO increases the risk of paradoxical embolism (embolus goes to the brain instead of the lungs)
* 30% of the adult population has a patent foramen ovale
what drugs can be used to close the ductus arteriosus? which can be used to open it?
Closed with indomethacin
Opened with prostaglandin E1
What is an intracardiac shunt?
Describes an abnormal blood flow pattern from an abnormal communication between the pulmonary and systemic circulations
Central to your understanding of shunt lesions is a solid foundation about the balance between PVR and SVR. Blood follows the path of least resistance!
what conditions affect PVR and SVR? how?
successful management of shunt lesions necessitates a solid understanding of the factors that affect PVR and SVR. know this table!
what is a cyanotic shunt? list 5 examples.
also called a right-to-left shunt. It describes a situation where venous blood bypasses the lungs. Since this blood is not exposed to oxygen in the lungs, it dilutes the final PO2 of the blood ejected by the left ventricle.
Examples (remember the 5 T’s)
1. Tetralogy of Fallot (most common)
2. Transposition of the great arteries
3. Tricuspid valve abnormality (ebstein’s anomaly)
4. Truncus arteriosus
5. Total anomalous pulmonary venous connection
What are the hemodynamic goals for the pt with a right to left shunt?
Pathophysiology: Decreased pulmonary blood flow- hypoxemia, LV volume overload, LV dysfunction
Hemodynamic goals: Maintain SVR, decrease PVR: hyperoxia, hyperventilation, avoid lung hypoventilation
what is an acyanotic shunt? list 4 examples
left to right shunt. It describes a situation where blood in the left side of the heart recirculates through the lungs instead of perfusing to the body
Examples:
* Ventricular septal defect (most common)
* Atrial septal defect
* patent ductus arteriosus
* coarctation of the aorta
what are the hemodynamic goals for the pt with a left to right shunt?
Pathophysiology: Decreased Systemic blood flow- low cardiac output, HoTN
Increased Pulmonary blood flow- Pulmonary HTN, RVH
Hemodynamic goals: avoid increased SVR, avoid decreased PVR by avoiding alkalosis, hypocapnia, High FiO2, Vasodilators
How do intracardiac shunts affect an inhalation or IV induction?
Inhalation induction time:
* Right to left shunt = slower induction
* Left to right= minimal effect
IV induction
* right to left shunt- faster induction
* left to right shunt- slower induction (most likely)
What is eisenmenger syndrome?
can occur when a pt with a left to right shunt develops pulmonary HTN. This reverses the flow through the shunt, which causes a right to left shunt, hypoxemia, and cyanosis
What are the 4 defects associated with tetralogy of Fallot?
- right ventricular outflow tract obstruction
- right ventricular hypertrophy due to high-pressure load from the RV obstruction
- Ventricular septal defect due to septal malalignment
- an overriding aorta that receives blood from both ventricles
The ratio of PVR to SVR determines how much blood travels to the lungs and the systemic circulation
How does a “tet-spell” present? What situations increase the risk of tet spells?
A tet spell is precipitated by increased sympathetic activity such as crying, agitation, pain, defecation, fright or trauma. This increases myocardial contractility, Which can cause spasm of the infra-valvular region of the RVOT. The net effect is increased right to left shunting causing hypoxemia.
Only children with unrepaired tetralogy of fallot can experience tet spells. When a tet spell begins, the child will hyperventilate with the onset of hypoxemia. Additionally, the child will assume a squatting position. This increases intraabdominal pressure and compresses the abdominal arteries, Which increases RV preload, SVR, and blood flow through the RVOT. This restores pulmonary blood flow, reduces the magnitude of right to left shunt, and improves oxygenation.
What is the treatment for a “tet spell” that occurs during the perioperative period?
- FiO2 100%
- Intravascular volume expansion
- increase SVR with phenylephrine to augment PVR to SVR ration.
- reduce SNS stimulation to improve dynamic RVOT obstruction- deepen anesthesia, beta-blockade with short-acting agent (esmolol)
- inotropes worsen RVOT obstruction and are best avoided
- avoid excessive airway pressure
- An infant may be placed in a knee-chest position to mimic squatting
What are the hemodyanmic goals for tetralogy of Fallot?
What is the best IV induction agent for the pt with tetralogy of Fallot?
Ketamine (1-2 mg IV or 3-4 mg IM) is the best induction agent. It increases SVR and reduces shunting.
Even though it increases contractility, this effect is minor compared to the benefit of increasing SVR
What is the most common congenital cardiac anomaly in infants and children? How about adults?
Infants and children= Ventricular septal defect (VSD). Many of these close by 2 year s of age.
Adults: Bicuspid aortic valve
What is the coarctation of the aorta? which syndrome is highly associated with this anomaly?
Coarctation of the aorta is the narrowing of the thoracic aorta in the vicinity of the ductus arteriosus. It typically occurs just before of after the ductus arteriosus, but in rare instances, it occurs proximal to the left subclavian artery.
Turner syndrome is highly associated with coarctation of the aorta
How is blood pressure affected in the pt with coarctation of the aorta?
As a general rule:
* SBP is elevated in the upper extremities.
* SBP is reduced in the lower extremities.
Discuss Ebstein’s anomaly.
Ebsteins anomaly is the most common congenital defect of the tricuspid valve. There is usually an ASD or PFO.
This condition is characterized by downward displacement of the tricuspid valve and atrialization of the right ventricle (d/t the ASD or PFO)
- tricuspid regurgitation can be severe
- Right to left shunting occurs at the level of the atria
- supraventricular tachycardia is common
Discuss the anesthetic management of the patient who has previously undergone Fontan completion.
This pt has a single ventricle that pumps blood into the systemic circulation.
There is no ventricle to pump blood into the pulmonary circulation, so…
* Blood flow into the lungs is completely dependent on negative intrathoracic pressure during spontaneous breathing
* positive- pressure ventilation disrupts this arrangement and should be avoided/minimized
* these pts are preload dependent - do not let them get dry!
What is truncus arteriosus?
Truncus arteriosus is characterized by a single artery that gives rise to the pulmonary, systemic, and coronary circulations. With only one artery, there is no specific pathway for blood to enter the pulmonary circulation before being pumped into the systemic circulation. There is usually a VSD as well.
Decreasing PVR or increasing pulmonary blood flow steals blood from the systemic and coronary circulations
Discuss the typical ages affected and speed of onset for epiglottitis (Supraglottits) and croup (laryngotracheobronchitis) .
Contrast the regions affected by epiglottitis and croup. How do these present on a lateral neck x-ray
Epiglottis: Region affected- supraglottic structures
Lateral neck x-ray- swollen epiglottis (thumb sign)
Croup: region affects: laryngeal structures
Lateral neck x-ray: subglottic narrowing (steeple sign)
Discuss the clinical presentation and treatment of epiglottis.
Clinical presentation:
* high fever
* Tripod position helps breathing
* 4 D’s: drooling, dysphonia, dyspnea, dysphagia
Tx:
* O2
* Urgent airway management - tracheal intubation or tracheostomy
* Abx (if bacterial)
* induction with spontaneous ventilation (CPAP 10 -15 cmH2O minimizes airway collapse)
* ENT surgeon must be present
* Post-op ICU care
Discuss the clinical presentation and tx of croup.
Clinical presentation:
* mild fever
* inspiratory stridor
* Barking cough
Tx
* O2
* Racemic epi
* corticosteroids
* humidification
* fluids
* intubation rarely required
Discuss the pathophysiology and presentation of postintubation laryngeal edema
AKA post-intubation croup, post intubation laryngeal edema is a complication of ETT or rigid bronchoscopy
The tracheal mucosa perfusion pressure is 25cmH2O. Using an ETT that is too large or injecting excessive amount of air into the cuff reduces tracheal perfusion -> edema -> decreased subglottic airway diameter -> increased WOB
the pt present with hoarseness, a barky cough, and/or stridor. It typically occurs within 30-60 minutes following extubation
*What are the risk factors for postintubation laryngeal edema?
Risk factors (all are from a small airway or airway trauma)
* Age <4
* ETT is too large
* ETT cuff volume is too high (too much air was injected or N2O was used during the procedure)
* Traumatic or multiple intubation attempts (one reason not to use an uncuffed tube)
* Prolonged intubation
* Coughing (cuff rubs against the tracheal mucosa)
* head or neck surgery
* head repositioning during surgery
* hx of infectious or post-intubation croup
* trisomy 21
* Upper respiratory tract infection?
What is the best way to minimize the risk of postintubation laryngeal edema?
The best treatment is prevention!
Post-intubation laryngeal edema can occur with cuffed or uncuffed ETT’s, but the key point is maintaining an air leak <25cmH2O. If you are using a cuffed ETT, then you should use a manometer to intermittently measure cuff pressure.
What is the tx for postintubation laryngeal edema?
Tx aims to reduce swelling and improve airflow:
* cool and humidified O2
* Nebulized racemic epi 0.5 mL of 2.25% solution in 2.5mL of 0.9% sodium chloride
* Dexamethasone 0.25-0.5 mg/kg IV (maximum effect requires 4-6 hrs)
* Heliox is a helium + O2 mixture that improves laminar airflow by reducing Reynold’s number
Unlike laryngotracheobronchitis (infectious croup), post-intubation croup is not infectious. Therefore, antibiotics are not indicated
The pt should be observed for a minimum of 4 hours after the racemic epi treatment is complete
A pt with a respiratory infection presents for a tonsillectomy. Which signs and symptoms favor postponing procedure?
How can you reduce the risk of airway complications while anesthetizing a child with an upper resp infection?
- Avoid mechanical irritation of the airway: Facemask >LMA»>ETT
- Mechanical irritation (ETT use) Increases the risk of bronchospasm 10-fold
- If an ETT must be used, then use a smaller size than normal because these children are at higher risk of postintubation croup
- Dexamethasone 0.25-0.5 mg/kg will reduce the risk of post-intubation croup
- ensure deep plane of anesthesia before instrumenting the airway
- Propofol attenuates airway reactivity and may reduce the risk of bronchospasm
- Sevo is the best volatile agent because it is non-pungent
- pretreatment with an inhaled bronchodilator (albuterol or ipratropium) or glycopyrrolate does not provide a clear benefit
Describe the presentation of the child who presents with foreign body aspiration.
Over 60% of children with foreign body aspiration present with the classic triad of cough, wheezing, and decreased breath sounds on the affected side (usually right)
Airway obstruction significant enough to impair gas exchange can quickly progress to hypoxemia, cyanosis, altered mental status, cardiac arrest, and death
- Supraglottic obstruction ->stridor
- Subglottic obstruction-> wheezing
what are the complications of rigid bronchoscopy?
rigid bronchoscopy is the “gold standard” procedure to retrieve the foreign body.
Complications of rigid bronchoscopy:
* laryngospasm
* bradycardia during scope insertion
* Post-intubation croup
* Pneumothorax
Which syndromes are associated with difficult airway management?
describe the airway in the pt with trisomy 21.
Trisomy 21 pt is at risk for difficult ventilation and intubation:
* Small mouth
* large tongue
* palate is narrow with a high arch
* Midface hypoplasia
* atlantoaxial instability (C1 & C2 subluxation - avoid neck flexion)
* Subglottic stenosis (use smaller EtT)
* OSA
* Chronic pulmonary infections
What is the CHARGE Association?
C- Coloboma (a hole in one of the eye structures)
H- heart defects
A- Choanal atresia (back of nasal passage is obstructed)
R- Retardation of growth and development
G- Genitourinary problems
E- Ear anomalies
What is CATCH 22?
also called DiGeorge syndrome of 22q11.2 gene deletion syndrome
C- Cardiac defects
A- abnormal face
T- Thymic hypoplasia
C- Cleft palate
H- Hypocalcemia (due to hypoparathyroidism)
22- 22q11.2 gene deletion (the cause of the syndrome)
what are the unique anesthetic considerations for the pt with DiGeorge syndrome?
Hypocalcemia is common (remember hyperventilation, albumin, and citrated blood products lower free Ca2+ in the blood)
If the thymus is absent, the child is at high risk for infection. Tx consists of thymus transplant or mature T cell infusion. Transfusion of leukocyte-depleted irradiated blood is best
What activities correspond with 1, 4 , and 10 Metabolic equivalents?
1 MET= Poor functional capacity- Self-care activities, working on computer, walking 2 blocks slowly
4 MET= good functional capacity- Climbing a flight of stairs without stopping, walking up a hill (>1-2 blocks), Light housework, raking leaves, gardening
10 METs or more= Outstanding functional capacity - strenuous sports (running, swimming, basketball)
How does Minute Ventilation change in the elderly?
Minute ventilation increases
* increased Vd necessitates an increased Ve to maintain a normal PaCO2
How does lung elasticity change in the elderly?
Lung elasticity decreases. This collapses the small airways and causes the lung to become overfilled with gas. Consequences include:
- Increased Vd
- decreased alveolar surface area
- V/Q mismatch
- Increased A-a gradient
- Decreased PaO2
How does chest wall compliance change in the elderly?
Chest wall compliance decreases. The chest is stiffer and more difficult to expand. This is caused by:
- calcification of joints
- diaphragmatic flattening
- increased A:P diameter
- Decreased intervertebral disc height
- Decreased respiratory muscle strength
- Decreased lung elastic recoil
why does residual volume increase in the elderly? what are the consequences of this?
The aged lung has a reduced elastic recoil, which causes it to become overfilled with gas. This process increases residual volume, which explains why the FRC increases as we age.
- closing capacity surpasses FRC at around 45 years old in the supine position and around 65 years old when standing.
*when CC> FRC, the small airways collapse during tidal breathing. This contributes to V/Q mismatch, increased anatomic dead space, and a reduction in PaO2
How does arterial compliance change in the elderly?
decreases as a function of loss of elastin and increased collagen.
- Increased SVR-> Increased BP
- Increased Pulse pressure
- increased myocardial wall tension to overcome higher afterload
- Increased myocardial hypertrophy
How does myocardial compliance change in the elderly?
Myocardial compliance decreases:
* Impaired relaxation may cause diastolic dysfunction
* atrial kick becomes more important for ventricular priming and maintenance of cardiac output
How does the cardiac conduction system change in the elderly?
there is fibrosis of the conduction system and loss of SA node tissue. These changes increase the incidence of dysrhythmias
How do the blood pressure and pulse pressure change in the elderly?
BP increases as a function of reduced arterial compliance (Increased SVR)
Pulse pressure is also increased for this reason
How do systolic and diastolic function change in the elderly?
Systolic function- no change
Diastolic function decreases as a function of reduced compliance and increased wall stiffness that impairs myocardial relaxation
How do hear rate, SV, and CO change in the elderly?
They all decrease
Describe the autonomic changes that occur in the elderly
- Decreased adrenergic receptor density
- Decreased response to catecholamines
- Increased circulating catecholamines as partial compensation
- Reduced ability to increase HR during HoTN ( Decreased baroreceptor function)
- Impaired thermoregulation increases the risk of hypothermia
How does MAC change in the elderly?
MAC decreases 6% each decade of life after age 40
Contrast the onset of postoperative delirium and postoperative cognitive dysfunction
Postop delirium: early postop period
POCD: weeks to months after surgery
Contrast the treatment of postoperative delirium and postoperative cognitive dysfunction.
Postop delirium:
* Treat underlying cause
* antipsychotics- haldol
* minimize polypharmacy
POCD:
* No specific treatment
* most cases are mild and tend to resolve around 3 months
to minimize the risk of either/both conditions, it’s best to use rapidly metabolized drugs
How does sensitivity to local anesthetics change in the elderly?
Sensitivity to local anesthetics increase:
* Decreased number of myelinated nerves
* decreased diameter of myelinated nerves
* decreased conduction velocity
Do the elderly require a dosage adjustment for intrathecal or epidural anesthesia? why?
They require a dosage adjustment for both
* Intrathecal - CSF volume is reduced -> greater spread of local anesthetics
* Epidural- volume of epidural space is reduced -> greater spread of local anesthetics
Why is it more difficult to place a neuraxial block in the elderly?
Anatomic changes make it more difficult to place a neuraxial block in the elderly:
* Less space between the posterior spinous processes
* Decreased intravertebral disc height
* Narrow intervertebral foramen
* calcification of joints
How does the glomerular filtration rate change in the elderly?
The GFR decreases:
* GFR is 125 mL/min in the adult male
* GFR decreases by 1mL/min/year after the age 40
Consequences include:
* Risk of fluid overload (less plasma delivered to the nephrons per unit time)
* Impaired drug elimination (consider dosage adjustments if age >60)
How do serum creatinine and creatinine clearance change in the elderly?
Serum creatinine does not change.
- GFR decreases with age. In theory, this should increase serum creatinine
- Muscle mass also declines with age, so less creatinine is produced.
- These 2 processes cancel each other out, so the net effect is that serum creatinine is unchanged
Creatinine clearance, however, is decreased. This is the most sensitive indicator of glomerular function in the elderly.
How does the production of plasma proteins change in the elderly?
Alpha-1 glycoprotein: increases ( large reservoir for basic drugs = decreased free fraction)
Albumin- production decreases (smaller reservoir for acidic drugs = increased free fraction)
Pseudocholinesterase: production decreases (succ’s duration increases in men> women)
how does circulation time change in the elderly?
Circulation time increases. Reduced CO prolongs the time of drug delivery from the site of administration to the site of action
- Slower IV induction (decreased CO prolongs drug delivery from site of administration to site of action)
- Faster inhalation induction (decreased CO favors faster equilibration between FA and FI)
how does lean body mass change in the elderly? why is it important?
Lean body mass decreases as a function of reduced muscle mass. This causes:
- Decreased Basal metabolic rate
- Decreased total body water
- Decreased blood volume
- Decreased plasma volume
- Decreased Vd for hydrophilic drugs (higher than expected Cp for a given dose)
- Decreased neuromuscular reserve
- Hypothermia sets in faster
Causes of postop delirium in elderly.
Mnemonic DELIRIUM
Drug use (what new drugs have been introduced)
Electrolyte imbalance
Lack of drugs (withdrawal)
Infection (UTI and respiratory)
Reduced sensory input
Intracranial dysfunction
Urinary retention and fecal impaction
Myocardial event, male gender
OB: what hormones contribute to vascular engorgement and hyperemia in pregnancy?
- Progesterone
- Estrogen
- Relaxin
OB: What type of laryngoscope handle is recommended for large breasted women?
A short-handled laryngoscope (Datta handle)
OB: When does the latent phase of labor end?
When the cervix dilates to 2-3cm
When does the active phase of labor occur?
In Stage 1 when the cervix is 3-10cm dilated (after the latent phase)
OB: When should oxytocin be administered during a C-section?
After the delivery of the placenta
OB: What can happen if you administer oxytocin too quickly?
Cardiovascular collapse
OB: What is the second-line drug for stimulating uterine contractions?
Methergine
What route should methergine be administered?
Methergine (an ergot alkaloid) should be given IM because IV administration can cause significant vasoconstriction, HTN, and cerebral hemorrhage)
What are the side effects of prostaglandin F2?
(hemabate/Carboprost)
* N/V
* Diarrhea
* Hypotension or HTN
* Bronchospasm
What position is best for intubating for c-section?
HELP (head elevated laryngoscopy position)
there should be a line connecting the sternal notch and the external auditor meatus: the head and neck should be above the chest
OB: what drug can cause the closure of the ductus arteriosus for the fetus if given to the mother?
Ketorolac (NSAIDs)
OB: when is optimal time for the pregnant pt to have surgery?
2-6 weeks post delivery, but second trimester if she must during pregnancy
the highest risk for teratogenicity in the pregnant patient is during:
organogensis (day 13-60)
OB: what are the roles of thromboxane in the pt with preeclampsia?
- Increase platelet aggregation
- Increases vasoconstriction
- Increases uterine activity
- Decreases uteroplacental blood flow
Treatment for acute HTN in the preeclamptic patient includes:
- Labetolol 20mg IV followed by 40-80 mg q 10 min up to a max of 22mg
- Hydralazine 5mg IV q20 min up to a max dose of 20 mg
- Nifedipine 10mg PO q20 min up to a max does of 50 mg
- Nicardipine infusion started at 5mg/hr and titrated by 2.5mg/hr q 5 min up to a max dose of 15 mg/hr
OB: chronic cocaine abuse is associated with what blood dyscrasia?
Thrombocytopenia. Check the platelet count before neuraxial anesthesia
What are the most significant concerns regarding abnormal placental implantation?
Impaired uterine contractility and the potential for tremendous blood loss during labor and delivery.
List 3 causes of DIC that occurs during labor and delivery
- amniotic fluid embolism
- placenta abruption
- intrauterine fetal demise
OB: how long does it take for a neonates oxygen to rise to 90%
after delivery, the normal SpO2 is 60%. It should rise to 90% after 10 minutes
At what post-conceptual week does surfactant production begin?
22-26 weeks
Neonates: what are 6 risk factors for respiratory distress syndrome?
- Low birth weight
- Low gestational age
- Barotrauma from positive pressure ventilation
- Oxygen toxicity
- Endotracheal intubation
- Maternal diabetes
After congenital diaphragmatic hernia is diagnosed, how long is repair normally delayed?
5-15 days
List 3 physiologic conditions to avoid in a neonate with CDH.
Avoid conditions that increase PVR
1. Hypoxia
2. Acidosis
3. Hypothermia
When is pyloric stenosis most commonly diagnosed?
First 2-12 week of life
Excessive vomiting leads to what 5 metabolic abnormalities?
- Dehydration
- Hyponatremia
- Hypokalemia
- Hypochloremia
- Metabolic alkalosis & compensated respiratory acidosis (early)
how does pyloric stenosis impact urinary pH?
Early-stage- Alkalotic urine secondary to bicarbonate excretion
Late-state- Acidic urine secondary to hydrogen excretion (due to aldosterone)
Is pyloric stenosis a medical or surgical emergency?
Medical. The pt should be optimized before surgery
In the infant with pyloric stenosis, severe dehydration should be treated with a bolus of:
20 mL/kg of 0.9% NS
NEC affects what region of the bowel?
Terminal ileum and proximal colon
Is NEC a medial or surgical emergency?
Medical- BUT if bowel perforation occurs, immediate surgery is indicated
What action (if taken too early) can cause NEC in a premature baby?
Early feeding. Impaired absorption by the gut leads to stasis, bacterial overgrowth, and infection. This increases the risk of bowel perforation.
In the pt at risk for ROP, supplemental oxygen should be minimized to maintain SpO2 between:
89-94%
Where should you place the pulse ox on a child with ROP?
RUE. Preductal is preferred because it correlates with the O2 sat in the retinal vessels
Neonate: What is kernicterus?
Fetal encephalopathy. Increases in serum bilirubin can lead to kernicterus
risk factors: Prematurity, low plasma protein concentration, and acidosis
tx: phototherapy and exchange transfusion
