Pediatric Anesthesia considerations

'Kids are not small adults ' you will hear it many many times during your pediatric rotation nonetheless great care is needed when caring for young patients

1. Airway:
 Epiglottis  is floppy and is described as omega shaped, institutes routinely use straight blades(miller) to lift the epiglottis to help in intubation. I found it helpful to insert the blade move tongue to the left and elevate the epiglottis and to slowly  withdraw till one sees vocal cords.

Head is large relative to body size so in neonates one may have to put some blankets below the shoulders and only a small ring may be placed below head without elevating head the head is naturally placed in sniffing position

The ventilatory response to hypercapnia is blunted in infants
Hypoxia stimulates respiration
The tongue is large relative to oral cavity
Cricoid is the narrowest part of airway(subglottic) so even if a tube passes easily via vocal cords may get stuck at the level of cricoid so don't forced tube use small size tube
Be very gentle because mucosal edema will narrow the airway to a greater relative extent compared to adults
Tube size= 4+ age/4  reduce .5 size smaller if cuffed tube. Always keep .5 size smaller and .5 size larger.
If using cuffed tube inflate the cuff to ensure  the leak just disappears at 20 cm pressure.
Depth - nothing replaces careful auscultation ensuring bilateral breath sounds, however as a rough
guide after 2 year Depth = 12 + age/2


FRC is very close to closing capacity that combined with high oxygen requirement7cc/kg means infants desaturate rapidly

The ribs are horizontal compared  and accessory muscles of respiration are poorly developed with diaphragm being the main muscle.

Larynx is more cephalad @ C 3-4
Normal respiratory rate is 35 in neonate


2. Cardiac:  both ventricular walls are of same thickness opposed to adults where left ventricle is thicker than right
There is poor lusitrophy and ventricles are relatively stiff so cardiac output is greatly preload
dependent
The sympathetic system is less developed so spinal anesthesia does not produce as much hypotension. Parasympathetic stimulation is well developed so infants respond to noxious stimulation by bradycardia.
Normal heart rate in 120-160 in newborn, 105-135 by 1 yr of age 85-105 by 5 yr age
Systolic Bp is 60-65 in neonate,  90-100 by 1 yr age and and100 by 5 yr of age.
Blood volume is 85ml/kg in full term neonate and 80ml/kg in infants.
Hb at birth is 18-20 g/dl which decreases to 10 g/dl by 10 weeks of life in full term neonate
 EKG- at birth the thickness of right ventricle is same as left ventricle so in children EKG shows t wave inversion in leads V1-V3 with RBBB till 8 yr age
BOTH CARDIAC OUTPUT AND VENTILATION ARE RATE DEPENDENT(heart rate and respiratory rate respectively)
3.  CNS
Increases proportion of water in brain , blood brain barrier is immature
Increased MAC which is maximum in infants (3.5 for Sevoflorane)
Separation anxiety starts at 6 months

Physiological change in pregnancy

Remember most of changes are directed to prepare the mother to meet increased demands and progesterone is the harm alone responsible for many changes

1. GI- reduced lower GI tone , increased chances of reflux due to gravid uterus pressing on stomach- more pronounced after 12 weeks- so after 12 weeks it is better to do rapid sequence induction. Institutes routinely prescribe antacid prophylaxis to women presenting for surgery after 12 weeks if elective-po ranitidine, ranitidine takes around 60-90 minute for full action
Emergency - sodium citrate

The idea is that if the women aspirates during induction acidic contents will do more harm than neutral. Older notion was that upto 40 % parturients have more than 40 cc of gastric content with ph<2.5- this notion is being challenged but I would use antacid prophylaxis as the drugs are relatively benign.
Remember mortality is around 40 percent if one lobe is involved and upto  percent if more than one lobe is involved- it has improved in the age of  I phones

2. Hematological- RBC volume increases by 30 percent while plasma volume increases by around 45 percent so there is hemodilution so Hb concentration decreases. Clotting  factors 11 and 13 decrease, 2and 5 remain same all others increases.

Total  Plasma protein concentration decreases  , albumin decreases and globulin and fibrinogen increases so edema is normal finding in pregnancy.


Pseudocholinesterase levels reduce by 20-25% though effect of scolding is not clinically increased.
Remember maternal hemorrhage is the most common cause of maternal mortality worldwide nature acts by hemodiluting blood and increasing coagulatability. On the other hand increased coagulability have increase chances of PE in pregnancy
WCC increases and increases to 15000 during labor.

3. Cardiac- cardiac output increases to 50  % mainly due to increase in stroke volume (30 %) and increase in HR(20-25%)
In pregnant patients worrying bradycardia is HR less than 60 opposed to 40 in non pregnant
C.O = HR times Stroke Volume
 Reduced SVR due to progesterone , reduced  systolic and diastolic bp
Remember cardiac output increases in left lateral position to about 14%

 EKG- left axis deviation, st depression, T wave inversion in lead III,LVH is common

Grade 1-2 mid systolic murmur is common due to tricuspid regurgitation

Aortocaval compression- compression of aorta and inferior vena cava in supine position can cause hypotension after 18 weeks so wedge is applied during cesarean section to tilt the uterus to left.

4. Respiratory - increased tidal volume, MV increases by 50 % so hyperventilation produces
Respiratory alkalosis with mild hypocapnia with increased PO2
Reduced FRC 30 %combined with increased oxygen demands warrant meticulous  per oxygenation
prior to GA.

Capillary engorgement of airway with airway edema due to increased plasma volume and reduced plasma protein increase the incidence of difficult airway in pregnancy and they bleed more on repeated attempts do laryngoscopy.


5. Renal- increased GFR reduced the amount of urea and creatinine in pregnant patients.

6. Nervous system
MAC reduces by 35-40 percent but ensure sufficient anesthesia
Engorgement of epidural veins reduce the dose of epidural or spinal drugs.
Increased sympathetic nervous system activity which is maximal at term so epidural or spinal anesthesia By producing sympathetic block produce more pronounced hypotension.

7. Endocrine: increased TBG require increased dose of levo thyroxine in hypothyroid patients,
Insulin resistance due to increased levels of HPL , prolactin .

Cardio tocography Decelerations during fetal monitoring

1. Early decelerations: due to fetal head compression during uterine contractions leading to fetal vagal stimulation leading to fetal bradycardia ( with fetal hr staying above 100bpm).

Lowest fetal heart rate- at peak of uterine contractions


2.

Late decelerations: due to dip in fetal heart rate due to fetal hypoxia during uterine contractions sign of uteroplacental  insufficiency .

Lowest fetal HR- after peak of uterine contractions


3. Variable deceleration:  poorly related to uterine contractions sign of umbilical cord compression- most serious

Lowest fetal hr- unrelated to uterine contractions

------------------------------------------
 Normal baseline variability- changes in heart rate <5bpm are normal
Loss of normal variability- drugs, fetal hypoxia

How to manage worrying decelerations- late, variable
1. Left lateral position of mother
2. Give mother supplemental oxygen
3. Tocolytic medications- terbutaline, magnesium, nitroglycerin

Digoxin and Anesthesia

Legend says that there was a merchant with rebellious heart who was thirsty and he drank water from a pond in which there were many leaves and flowers of Foxglove plants (Digitalis purpura) floating and on drinking water his rebellious heart  inproved.

Old drug used extensively , narrow therauptic index ,still used you need to know every bit of it as it is like uranium which when used properly lights the houses but if used in wrong way blows houses.

Mechanism of action: Increased intracellular calcium by inhibiting Sodium potassium ATPase pump

Onset: IV  - 5 minutes
Stays in body for 72 hours in patients with normal kidney function(So be cautious in patients with Renal failure as 60 % excreted unchanged in urine)


Is a positive inotrope and depresses conduction via AV node.

 Toxicity: Increased in Hypokalemia, Hypercalcemia, hypomagnesemia, many drugs including Amiodarone, Diuretics

Should I hold am dose on day of surgery: Practice varies but if one is taking for heart failure or resistant arrhythmia it is better to continue on am of surgery with sip of water anesthetizing a patient with controlled heart failure and arrhythmia is easier than one with uncontrolled.

Anesthetic considerations of patients with Mitral regurgitation

The whole idea is to maintain forward stroke volume to maintain coronary and vital organ perfusion. So

1. Minimize SVR: Avoid direct alpha one agonists which increases SVR , Increased SVR will move blood into LA rather than to forward flow.

2. Maintain Preload

3. Maintain HR towards high normal side as high heart rate decreases diastolic time and reduces regurgitation cach.

4.In patients with coexisting pulmonary hypertension avoid increases in airway pressures.

5. Co existing AF is common so the patient may be on oral coagulants prior to surgery.

So use Ephedrine over phenylephrine for hypotension with normal heart rate
Prefer Inotropes with predominantly B1 action like epinephrine as they will maintain heart rate without increasing SVR. Milrinone, Levosimendan are good choices.

Myocardial Stunning, Hebernation, Ischaemic preconditioning

You will hear these 3 terms multiple times in your career let me simplify them.

1. Myocardial Stunning: Think of a situation as if you are working in the OR as a resident suddenly your attending comes and hits you what will happen to you- You will be stunned and will stop working, stop thinking  for some time and  at that time you will need  support to function properly

similarly if the heart is hit by a reversible insult(ischemia, pressure) it stops working for some time and wont function unless support is provided - Inotropes, Pacing, Baloon pump , ECMO


2. Myocardial Hibernation:(Smart Heart)

Think of Polar bears who hibernate
When the food supply is low polar bear goes sleeping to survive to on low resources and if you happen to go to its cave you will see polar bear not moving at all and from a distance it will look as if he/she is dead. How will you differentiate whether the polar bear is dead or hibernating- challenge it.(Have reliable shoes to help you run before you do that)


similarly when there is chronic low oxygen supply to a wall/walls of heart  due to stenosis of the corresponding coronary artery the corresponding wall becomes hypokinetic and on normal echo it will look as if dead. How will you differentiate- try challenging with perfusion scans.



3. Ischaemic preconditioning:(What does not Kill you makes you stronger)

Short periods of ischemia will make the heart stronger to subsequent longer periods of ischemia.
Think of a situation when you are asking your buddy about a tough rotation you are about to start- your buddy tells the horror stories and you will become upset for some time but you will be better able to withstand that rotation

Remember Inhalational anesthetics mimic the effect of Ischemic preconditioning via activating ATP sensitive potassium channels and depleting intracellular calcium so that the heart is better able to withstand periods of ischemia- So may provide better protection from ischemia.
 

Blood Supply of HEART

Blood to the heart is supplied by two coronary arteries (right and left) in majority of patients, variations include (a) may have 3 coronary arteries, Right, Left and posterior. (b) may have only one coronary artery which supplies entire heart

Right coronary artery:  Divides into Right marginal and PDA (aka posterior interventricular artery)Right atrium, Right Ventricle , Posterior wall of left ventricle(near posterior IV groove) and posterior 1/3 rd of interventricular septum

Left coronary artery:  divides into Circumflex and LAD (aka anterior interventricular artery)

Circumflex: supplies  LA and  lateral part of Left ventricle

LAD: supplies anterior 2/3 rd of interventricular septum and anterior walls of both ventricles

Dominance : Whosoever gives rise to PDA is dominant, The dominant one supplies the AV node

85%  RCA gives rise to PDA so Right dominant
15% LCA gives rise to PDA so Left dominant.

So if you are left dominant and occlude your LCA you will infarct in the Anterior, Lateral AND POSTERIOR or INFERIOR (PDA) walls of Left Ventricle as opposed to  only anterior and lateral.

SA node 60% of cases by RCA 40% by LCA