• IV Axis: Central Line, A line
• Labs: CBC, Urea/Cr, Na/K/Mg/Ca, Liver Enzymes
• Troponin I, CPK & MB
• Maintenance Fluids with/out K+
• Ventilation to take care of work of breathing
• Meds: Improve Cardiac Output
• To improve BP would you start Adrenaline ?
INOTROPES: OR ONE OF THESE ?
• Child started on:
• Dopamine & Dobutamine
• Both 7.5 mcg/kg/min
• Continous Infusion Vs Boluses
• Ist dose Bolus
• Ann Pharmacother. 2006 Oct;40(10):1797-803. Epub 2006 Sep 5.
Efficacy and safety of a furosemide continuous infusion following cardiac surgery.
• Intensive Care Med. 2001 Apr;27(4):711-5.
Continuous intravenous furosemide in haemodynamically unstable children after cardiac surgery.
BALANCE OF INOTROPY & VAODILATATION
• If BP permits: go up on the
• If Urine O/P not good: need
• If Extremities not warm; need
INOTROPES & VASODILATATION
• Once max required effect (not dose) of Inotropy &
• Once renal function has stabalised & urine o/p is good:
• Next step is to extubate the patient
• Cardiac Function improvement is not required for
• Cardiac Output improvement is essential
CLINICAL SCENARIO: DAY 4 ECHO
• Function has not changed but child now has:
• Come off ventilator
• And Inotropes are being weaned
• So, with same function: how come now child is better ?
• SYSTEMIC VASCULAR RESISTANCE
SYSTEMIC VASCULAR RESISTANCE
• Modulation of SVR changes Cardiac output
• Previously SVR was very high
• Now SVR has been brought down
• So, Cardiac function has not changed but
• Cardiac output has been increased
• Getting them on oral medications
• Inotropes: Digoxin
• Diuretics: oral furosemide
• Vasodilatation: Enalapril
represents a promising new drug candidate for potential use in the
treatment of human enteroviral infections.
MYOCARDITIS AND VACCINATION
• HISTORY NOTED
• UNRELATED TO VACCINATION, BUT
MYOCARDITIS AND VACCINATION
• Methyl mercury enhanced the immune damage and chronicity of coxsackie
B3 myocarditis in mice, compared with mice infected without prior mercury
• Ilback NG., Wesslen L., Fohlman Friman G. Effects of methyl mercury on cytokines,
inflammation and virus clearance in a common infection (Coxsackie B3 myocarditis) Toxicol.
Lett. 1996;89:19-28 22.
PERSONAL EXPERIENCE: MYOCARDITIS
• Complete heart Block
BETA BLOCKERS IN HEART FAILURE
• substantial reductions in sudden death and death
• Prevent progressive heart failure in patients
• MERIT & CIBIS II trials
• NYHA class II and III symptoms treated with blockers
• Advisable to consider blockers in IDC patients with mild to
moderate symptoms in spite of maximal treatment with ACE
• The Pediatric Randomized Carvedilol Trial in Children with Heart
• American College of Cardiology 55th Annual Scientific Session;
March 11-14, 2006; Atlanta, Georgia. Smaller Trial Late-Breaking
Clinical Trials II. Abstract 418-6.
• moderate to severe heart failure and contribute to sodium
retention, potassium loss, sympathetic activation, myocardial
fibrosis, and baroreceptor dysfunction
• major source of aldosterone is reduced hepatic clearance rather
than angiotensin dependent adrenal secretion
• with an ejection fraction < 35% and a history of NYHA class IV
heart failure is associated with a 30% reduction in the overall risk
of death RALES
• ANP is released from atrial myocytes in response to stretch, and
induces diuresis, naturesis, vasodilatation, and suppression of the
• ANP and brain natriuretic peptide are potent vasodilators and
Levosimendan for low cardiac output: a pediatric
Egan JR, et al
J Intensive Care Med 2006 July
Levosimendan was safely used in a small number of
pediatric patients with established low cardiac output
state who demonstrated improved hemodynamics and
tissue perfusion, with a tendency to reduced
conventional inotrope usage, and this warrants its
evaluation as an inotrope in the pediatric population.
• clinical effects prolonged due to active metabolite OR-1896
• Half life- 80hrs
• Potentiates hemodynamics after cessation of parent drug
• Dosing as indicated by clinical experience-
Loading dose of 6-24µg/kg followed by
infusion of < 0.4µg/kg/h
1. Enhances myocardial contractility by sensitizing myofilaments to
- binds to troponin C, stabilizes calcium-bound conformation
and prolongs the systolic actin-myosin interaction
2. Role of KATP channel activation
MITOCHONDRIAL KATP channels (mKATP)
SARCOLEMMAL MEMBRANE KATP
- potassium ion efflux and membrane hyperpolarisation
- inhibit inward L-type calcium current,
lower intracellular calcium current,
» vasodilatation in arteries, arterioles and veins
* acts as an vasodilator agent on systemic vasculature and
* Key role in maintaining basal tone of coronary vasculature
EFFECT ON LUSITROPHY
• Diastolic dysfunction –major component of heart failure, present in up to 50%
• Levosimendan does not appear to worsen lusitrophy due to its stabilizing
action of the calcium-troponin C complex
(and not increasing the binding affinity of calcium to troponin C)
CARDIOVASCULAR EFFECTS OF LEVOSIMENDAN:
-LV stroke volume
• Increase blood flow to renal medulla & small intestine
• Improved gastric mucosal oxygenation
Unlike other positive inotropic agents
(increase intracellular cAMP)
- not associated with increased incidence of arrhythmias leading to
ROLE IN ISCHAEMIA-REPERFUSION INJURY
(during ischaemia, acidosis decreases calcium sensitivity in the failing heart)
- levosimendan has potential to preserve contractile function
(unique myofilament action)
1. HEART FAILURE-
• beneficial effect on survival in acute decompensated failure compared to
dobutamine at 31 and 108 days
• positive inotropy +activation of KATP channels
- cardiogenic shock
- evolving myocardial infarction
- perioperative ischaemia
- emergence from CPB
• Judicious balance of
• Myocardial fx
• Afterload reduction
• Tweaking the SVR may be the most important
variable to change
• Most patients can be managed without
OUTPUT, RENAL OUTPUT
SECRET MANTRA TO IDEAL INOTROPY
NIRVANA TO GREAT CARDIAC OUTPUT
• CARDIAC FUNCTION
• AFTER LOAD
• CARDIAC RHYTHM
• Myocardial function
• Afterload (systemic vascular resistance)
• A combined or an individual effect of all these factors.
• A decrease in preload, decrease in myocardial function and an
increase in afterload allcause a decrease in renal perfusion.
• The art is in assessing which of these is affecting the renal blood
Renal output is dependent on
COMPENSATION, BP, MYOCARDIAL DYSFUNCTION
• The myocardial function and SVR are clinically assessed by
• the peripheral pulse being good and
• the extremities being warm.
• It is a misconception that myocardial function being poor would
be reflected in the blood pressure of the child.
• The body compensates for the decreased myocardial function
(resulting in decreased cardiac output) by vasoconstriction (increase
in SVR) and maintains the blood pressure.
• At the cost of the splanchnic circulation (renal is part of it).
• The preload is assessed by several mechanisms. One of
the more reliable indicator in the ICU of the preload status
is echocardiographic assessment of the IVC status. Serial
assessment of respiratory variation and diameter of IVC
are reliable indicators of fluid status of a child.
• So, lack of respiratory variability and dilated IVC would
indicate good or maximized preload status.
Short of echocardiography, the most reliable clinical sign of assessing if
the preload will bring down the heart rate and improve the BP is a gentle
sustained pressure by hand on the liver. If the myocardium cannot handle the
preload the pressure would go up temporarily only and heart rate would not
come down but not come down.
If the patient truly has occult or true volume depletion, the blood pressure
would go up and heart rate come down. This response will be sustained till the
hand is on the liver. This test must be performed with great
caution in children with EF low
• One has to be sure of lack of occult or true hypovolemia
• If one is aware that the preload is adequate then one should
initiate afterload reduction.
• This is best achieved using Milrinone.
• Dobutamine and Levosimendan are additional drugs which work in
a similar fashion.
• In cardiac patients, myocardial function is likely to be
compromised if the patient is post op and inotropy without
vasoconstriction should be used.
CLINICAL THUMB RULES
• 1. SVR is clinically assessed by the warmth of the extremity
• 2. Cardiac output (a complex final endpoint of several factors) is assessed by
• peripheral pulse volume.
• 3. Need for Volume can be assessed by assessing serial IVC status
• 4. Afterload reducing agents are heart friendly
• 5. Vasoconstricting agents are not heart friendly (increase load on heart)
• 6. Inotropes with vasodilating agents are best used because usually the
etiology is multifactorial
• 7. Prior to afterload reduction make sure occult hypovolemia is ruled out.
• H/o blood loss
• Excess urine output
• Check clinically-
• Take help of ECHO
• Correct accordingly
Drugs Chrono Ionotro Vasodila Vasocon Dose
Epi ++ + Low dose High dose 0.03-0.3
NorEpi + - - All dose 0.05-0.3
Dopa + + Low dose High dose
Dobu - + Low dose High dose 0.5 to 5-10
Milrinone - + ++ - 0.03- 0.8
CLINICAL CONDITIONS INTREPRETATION STEPS/DECISSION
poor pulse vol,
LOW CO Start Ionotropic drugs-
poor pulse vol
LOW CO Add Diuretics
Better pulse volume
Better urine output,
BP-normal to high
High after load Need MILRINONE
Good pulse vol
BP- normal or lower
Due to vasodilation
Good pulse vol
BP- normal to high
↑ Afterload Milrinone
Low vol pulse
Hypovolemia Fluid boluses
Good vol pulse
Optimized CO Maitain same
Plan weaning off the
Good vol pulse
Fall in CO Increase ionotropic
Good vol pulse
HOW TO TAPER IONOTROPES
• Add Digoxin- slow digitalization
• Once digitalization done- taper Dopamine by
0.1mcg/kg/min in every 1-2 hrs till reached 5
mcg/kg/min. Patient to be monitored
• by ABG, specifically by LACTATE.
• Then taper Dobutamine same way upto 5
HOW TO TAPER IONOTROPES
• Once Dopamine and Dobutamine reached 5 mcg/kg/min add oral
vasodilators- ENALAPRIL – give test dose 0.1mg/kg, look for
• Effect of occult hypovolemia
• Increase in serum urea
• Decrease in urine out put.
• Milrinone reduced to 1/2 dose after first test dose and if no hypotension, no
increase in urea and no drop in urine output give 2nd dose.
• If hemodynamics stable then taper dopa and dobuta gradually alternately.
• Patient to be monitored by serum lactate level
RHYTHM AS THE 4TH