Postoperative

Management
Jon N. Meliones, MD, MS, FCCM
Professor of Pediatrics
Medical Director Performance Improvement & Patient Safety
Medical Director PCICU
Duke University
 Cardiogenic Shock
• Definition
–Diagnosis
–Effects of Shock
• Types of Shock
 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)]
 Determinants of Oxygen Delivery

Preload

Afterload Stroke Volume

Contractility
Cardiac Output
Heart Rate
O2 DELIVERY

Hemoglobin (O2 capacity)

Oxygen binding (SaO2) Oxygen Content
Oxygen Dissolved (PaO2)
Pathophysiology of Shock

O2 Supply < O2 Demand

 Shock
• Definition
– Inadequate DO2 to meet tissue needs
– Cellular oxygen deficiency
– Limitation or maldistribution of blood
flow
• Compensated
• Uncompensated
• Irreversible
– Organ failure & death
 LFTs,
MS ileus ARDS

SHOCK

BP UO
 Shock: Diagnosis
Noninvasive
• Vital signs
– HR, B.P. nl - ,  RR
• End organ function
–  UOP
– Mental status changes
– Liver dysfunction correlates with outcome
 Children’s Response
BP= CO x SVR
Heart rate

Systemic Vascular
% of Control

Resistance

100
Blood Pressure

Cardiac Output

25% 50%
% Blood Volume Loss
 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?
 Clinical Assessment of CO
• Exam:
– HR, BP, CVP
– pulses
– skin temperature, cap refill
– UOP
– Mental status
 Clinical Assessment of CO

Surgeons

Tibby, SM “Clinicians’ abilities to estimate cardiac index in

ventilated children and infants” Arch Dis Child 1997
 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
 Central vs Peripheral Temp
Metabolic Work

Sweat Amount

Mahmoud Hero Mahmoud Hero Core Temp Mahmoud Hero

Normal Function
Decreased Function
 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!!!!
 Defining Low Cardiac
output
• Metabolic Markers
• Base deficit & pH
–Easy to obtain
–Poor correlation with outcome
–Many confounders
–Limitation - late
 Metabolic Markers
• Lactate!!!!
– Elevation (> 2.0) indicates inadequate
tissue oxygen delivery
– Initial Lactate < 7, Maximum < 9, 4-6 hr
lactate < 4 predicts good outcome in
post-op CHD (Duke, Boston, CHOP)
– Rising Lactate = Bad outcome
• Lactate change > 0.75 / hr = poor outcome
 Mixed Venous Saturations
Amount of oxygen returning to heart
(NL > 65%)

Vena Cava Pulm Veins

RA LA
70 99

RV 70 99 LV

PA 70 99 AO
Lactate = NL
 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
 Low Mixed Venous Saturations
Inadequate Oxygen delivery
(More oxygen extracted by tissues)
Vena Cava Pulm Veins

RA LA
50 99

RV 50 99 LV

PA 50 99 AO
Lactate = High
High Mixed Venous Saturations
Inadequate Oxygen Extraction
(Tissues do not “see” oxygen)
Vena Cava Pulm Veins

RA LA
90 99

RV 90 99 LV
Great CO but,
PA 90 99 AO Lactate = High
 Mixed Venous Saturations
Lactates
Mixed Lactate Intervent
Venous
Normal Normal None

Low (DO2 High Inc. CO

Low) Inc. CaO2
High (CO NL) High ????
 Markers of O2 Delivery

• DO2 = VO2 x (arterio-venous difference)

• AVO2 Difference
– SaO2/ (SaO2 - SvO2)
– Ex. .95/(.95 - .75)= 4.75
– Ex. .95/(.95 - .55)= 2.38
– Ex. .95/(.95 - .35)= 1.58
– Ex. .80/(.80 - .65)= 5.3
– Ex. .75/(.75 - .35)= 1.88
 Markers of O2 Delivery
• Oxygen Extraction ratio
– (SaO2 - SvO2) / SaO2
– Ex. (.95 - .75)/.95 = .20
• 20% of arterial oxygen is extracted
– Ex. (.95 - .55)/.95 = .42 = 42%
– Ex. (.80 - .65)/.80 = .19 = 19%
– Ex. (.75 - .35)/.75 = .53 = 53%
– Ratio <0.3 or < 30% indicative of
adequate O2 delivery
Defining Low Cardiac
Output
• Adequate Oxygen Delivery
• O2 extraction < 0.3
• Lactate < 2.0
• Mixed venous
–PvO2 > 28
–SVO2 > 60
 Defining Low Cardiac
Output
• Marginal Oxygen Delivery
• O2 extraction 0.3 - 0.6
• Lactate < 2.0
• Mixed venous
–PvO2 > 28
–SVO2 > 55
 Defining Low Cardiac
Output
• Inadequate Oxygen Delivery
• O2 extraction >0.6
• Lactate >2.0
• Mixed venous
–PvO2 < 28
–SVO2 < 55
 Cardiogenic Shock:
Stagnant Hypoxia:  C.O.
• C.O. = Heart Rate x Stroke Volume
• Bradycardia
 C.O.
• Tachycardias
 C.O. by  SV
• Alterations in Stroke Volume
 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
 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
 Effects of Afterload

•  Afterload significantly  DO2

•  Afterload can dramatically  DO2
– Recent advancements Afterload
reduction
• Limitations of afterload reduction
– CBF - Excessive vasodilation
 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
 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
 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.
Low Cardiac Output Syndrome
Treatment for Systolic Dysfunction

• Inotropic Agents:Improve
Contractility
• Ca++, Glucose, pH
• Inotropes
• PDEI
• Vasodilators
 Inotropes

• Dopamine myths
• Epinephrine myths
• What happened to Dobutamine?
• Milrinone is it the answer?
 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 )
 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
 PVR
#
1600
1400 #
R in 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
 Inotropes
Dopamine:
 < 7 mcg/kg/min
 Highest correlation with JET
Epinephrine:
 Dose not increase PVR/SVR
Dobutamine:
 Yes! Early
 Milrinone

Minimal ↑ HR

↑ CO

Diastolic
Relaxation

Minimal ↑ in
O2 demand ↓ SVR
↓ PVR
 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
Primacorp Study: Results – LCOS/Death

Development of LCOS / Death in first 36 hours post-op. (n = 227)

Hoffman et al - Circulation 2003;107:996.)
 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)
Downloaded from: Drugs for the Heart (on 29 January 2006 10:14 PM)
© 2005 Elsevier
Downloaded from: Drugs for the Heart (on 29 January 2006 10:14 PM)
© 2005 Elsevier
 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
 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
 Sodium Nitroprusside
• Side Effects
• Precipitous hypotension
• MI due to ↓ coronary perfusion
pressure
• Tachyphylaxis
• Cyanide Toxicity
• Hypoxia
 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
Vasopressin
 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