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Post Operative Management
1. Postoperative
Management
Jon N. Meliones, MD, MS, FCCM
Professor of Pediatrics
Medical Director Performance Improvement & Patient Safety
Medical Director PCICU
Duke University
3. Oxygen Delivery
• Definition
– Amount of oxygen being delivered to
the tissues
– DO2 = Oxygen Content x Cardiac
Output
DO2= CO * CaO2
= (HR x SV) [(Hgb*1.36*SaO2) + (.003*PaO2)]
8. Shock: Diagnosis
Noninvasive
• Vital signs
– HR, B.P. nl - , RR
• End organ function
– UOP
– Mental status changes
– Liver dysfunction correlates with outcome
9. Children’s Response
BP= CO x SVR
Heart rate
Systemic Vascular
% of Control
Resistance
100
Blood Pressure
Cardiac Output
25% 50%
% Blood Volume Loss
10. How to Measure CO?
• CO = Heart Rate x Stroke Volume
– SV determined by preload, afterload,
contractility
• Can we objective measure non-
invasive measures of CO?
11. Clinical Assessment of CO
• Exam:
– HR, BP, CVP
– pulses
– skin temperature, cap refill
– UOP
– Mental status
12. Clinical Assessment of CO
Surgeons
Tibby, SM “Clinicians’ abilities to estimate cardiac index in
ventilated children and infants” Arch Dis Child 1997
13. Clinical Assessment of CO
• Capillary Refill
– May be useful marker of hypovolemia
and myocardial function
– ? Correlates with CO and lactate
– Easy but… many confounding factors:
fever, room temp, vasoactive drugs…
careful!
• Core vs peripheral temp. difference
– >3 degrees associated with low output
14. Central vs Peripheral Temp
Metabolic Work
Sweat Amount
Core Temp
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17. Defining Low Cardiac output
Analysis of Arterial Wave Form
D D
P P
Dt
Dt
• Upstroke
– (Change Pressure (Dp)/(Change Time (Dt))
– Rapid = Good systolic function
– Area under curve = stroke volume
– FREE!!!!
18. Defining Low Cardiac
output
• Metabolic Markers
• Base deficit & pH
–Easy to obtain
–Poor correlation with outcome
–Many confounders
–Limitation - late
20. Mixed Venous Saturations
Amount of oxygen returning to heart
(NL > 65%)
Pulm Veins
Vena Cava
LA
RA 70 99
70 99 LV
RV
70 99
PA AO
Lactate = NL
21. Markers of O2 Delivery
• Mixed Venous saturation
– Fall in SVO2 may precede rise in
lactate
– Ideally sampled from PA
• Rarely occurs in Pediatrics
• SVC not too bad as reflects CNS
– Central vein may be adequate for
trends
22. Low Mixed Venous Saturations
Inadequate Oxygen delivery
(More oxygen extracted by tissues)
Pulm Veins
Vena Cava
LA
RA 50 99
50 99 LV
RV
50 99
PA AO
Lactate = High
23. High Mixed Venous Saturations
Inadequate Oxygen Extraction
(Tissues do not “see” oxygen)
Pulm Veins
Vena Cava
LA
RA 90 99
90 99 LV
RV
Great CO but,
AO Lactate = High
90 99
PA
24. Mixed Venous Saturations
Lactates
Mixed Lactate Intervent
Venous
Normal Normal None
Low (DO2 High Inc. CO
Low) Inc. CaO2
High (CO NL) High ????
31. Effects of Preload
• Preload is a major determinant of DO2
• Preload augmentation has limitations
(pressure effects may dominate)
– When is volume too much…when CVP with small
infusion (Overdistention just like lung)
– ed EDP may CBF (especially B.P.)
– ed Venous pressure
• ed LAP = Pulmonary edema
• ed CVP >15, Systemic edema
32. Effects of Contractility
• Contractility directly SV
– C.O. & DO2
• Inotropic agents have varying effects
• Neonatal myocardium
– Ca++ strong inotrope
– Less response to preload ( compliance)
– Mature alpha receptors
34. Neonatal vs Adult Heart
• Limited responsiveness to inotropes
– Beta receptors & NE (?? Inotropes)
– Less mature sympathetic system
– Underdeveloped iCA regulatory
mechanisms
– Muscle mass
• Greater dependence of CO on HR
and preload than contractility
35. Myocardial Contraction
• Contractility increases over 1st
months of life along with:
– #’s of sympathetic nerve fibers
within myocardium
– Total concentration of endogenous
norepinephrine
• There is a greater dependence of
CO on HR than contractility
during this time
36. Low Cardiac Output Syndrome
Decrease in CI in Newborns post ASO
Wessel DL. Managing LCOS after CHD surgery. Crit Care Med 2001; 29:s220-230.
39. Inotropes
• Dopamine myths
• Epinephrine myths
• What happened to Dobutamine?
• Milrinone is it the answer?
40. Low-Dose Dopamine: Renal Protective Effects.
Effects on Renal Fx Markers*
Criteria Dopamine (n=161) Placebo (n-163) Diff.
Peak SCr ( mMol/L ) 245 (144) 249 (147) NS
Peak BUN, 20 (10) 23 (12) NS
Change in SCr ( mMol/L ) 62 (107) 66 (108) NS
Change in BUN 6 (8) 7 (9) NS
# w/ SCr > 300 ( mMol/L ) 56 56 NS
Need for dialysis, 35 40 NS
Urine output (ml/hr)
Baseline 37 (40) 50 (59) NS
After 1 hour 71 (81) 72 (77) NS
After 24 hour 96 (101) 92 (72) NS
After 48 hour 99 (83) 109 (95) NS
* Mean (SD)
“Low dose DA did not confer any significant
protection from Renal Dysfunction.”
Renal dose Dopamine does not exist
(Bellomo R - Lancet 2000 )
41. Cardiac Output
#
#
900
#
800
700
C.O. 600
500
(L / min.) 400
300
200
100
0
Pre DA Pre DB Pre EP
DA DB EP
# = p < 0.05 vs. Pre drug
Mcgovern PCCM 2002
42. PVR
#
1600
1400 #
Rin 1200 #
1000
(d-s/cm) 800
600
400
200
0
Pre DA Pre DB Pre EP
DA DB EP
# = p < 0.05 vs. Pre EP
43. Inotropes
Dopamine:
< 7 mcg/kg/min
Highest correlation with JET
Epinephrine:
Dose not increase PVR/SVR
Dobutamine:
Yes! Early
44. Milrinone
Minimal ↑ HR
↑ CO
Diastolic
Relaxation
Minimal ↑ in
↓ SVR
O2 demand
↓ PVR
45. Milrinone
• PDE 3 inhibitor
• Inotropic- dilator
• Dosing:
-1
• Initial bolus: 25 to 100 μgkg
-1 -1
• Infusion: 0.25 to 1.00 μgkg min
• Half Life : 2-3 hr
• 80 % excreted unchanged
46. Primacorp Study: Results – LCOS/Death
Development of LCOS / Death in first 36 hours post-op. (n = 227)
Hoffman et al - Circulation 2003;107:996.)
47. Vasodilators
• Classified by site of action
• Venodilators: reduce preload -
Nitroglycerin
• Arteriolar dilators: reduce afterload
Minoxidil and Hydralazine
• Combined: act on both arterial and
venous beds and reduce both pre- and
afterload Sodium Nitroprusside
(Nipride)
50. Sodium Nitroprusside
• Direct NO donor
• Increases cGMP in Vascular Smooth
Muscle
• Balanced venous and arterial
dilatation
• Short duration of action of 1-2 min
-1 -1
• Dose: 0.25- 10 μgkg min
• Indication:
• Perioperative HTN
• Hypertensive Crisis
51. Sodium Nitroprusside
• Clinical Effects:
• Potent rapidly acting arterial and
venous dilator produces ↓↓↓SVR,
↓↓↓PVR and ↓↓↓ preload
• Reflex Tachycardia
• Coronary steal
• Inhibition of hypoxic pulmonary
vaso constriction promotes V/Q
mismatch and Hypoxia
52. Sodium Nitroprusside
• Side Effects
• Precipitous hypotension
• MI due to ↓ coronary perfusion
pressure
• Tachyphylaxis
• Cyanide Toxicity
• Hypoxia
53. NITROGLYCERINE
• Direct acting vasodilator requiring specific thiol
intermediates to generate NO
• Venodilation > arteriodilation
• Rapid onset
• Infusion: 0.5- to 10 mcg/kg/min, usual dose 1-3
mcg/kg/min
• ↓ Preload causes ↓LV wall tension,
↑subendocardial perfusion, ↓ myocardial O2
demand
• Superior Pulm. Vasodilator as compared to SNP
55. Pearls
• Heart rate, Core temp!
• Preload
– Optimize… if small infusions of volume
result in increases in CVP /LAP ...STOP!
• Contractility
– Calcium… important but bolusing is bad
– Dopamine…No data but consider up to 7
– Dobutamine…used in many institutions
– Epinephrine…Low < 0.1 PVR / SVR
– Milrinone…start at .75 but be careful in
ARF as accumulation will occur
