hemodyanamic monitoring in pediatric critical care, an overview

1. Hemodynamic monitoring
DR. TARUN CHANDRA
consultant PICU
Regency hospital kanpur

2. PEARLS

8. The Electrocardiogram
• Willem Einthoven in 1912
• 12 lead ECG
• 3 lead ECG
• Lead 2
• CM 5 configuration- ST segment changes

9. Hemodynamic Monitoring
A.Initial steps
1. Clinical assessment
2. Basic monitoring and assessment of global perfusion
3. Preload monitoring and fluid responsiveness
B.Advanced monitoring measures
1. Cardiac output monitoring
2. Assessment of cardiac contractility
3. Assessment of tissue perfusion.

10. Step 1: Clinical assessment
1. CRT: Capillary refill time
i. Pediatric Advanced Life Support Providers manual 2011
ii. The facility based IMNCI participants manual-2009
2. Urine Output
3. Sensorium
4. skin mottling.

11. Mottling Score

12. Step 2: Basic monitoring and assessment of global perfusion
Upstream & downstream markers:
1.Upstream markers-- systemic blood pressure, heart rate,
central venous pressure (CVP), pulmonary capillary wedge
pressure (PCWP), and cardiac output
2.downstream markers-- urine output, blood lactate, base
excess, tissue carbon dioxide levels, and mixed venous
oxygen and carbon dioxide levels.

13. A. Blood Pressure
Non– invasive BP Monitoring (NIBP):
The major limitations of NIBP are:
1)readings can be fallacious in
presence of hypoperfusion or
peripheral vasoconstriction
2) It gives intermittent readings
3)Accuracy of readings are dependent
on appropriate cuff size and
placement

14. Invasive hemodynamic monitoring
• William harvey– in 1600 observed that heart pumps blood in
continuous circuit
• Hales– 1733 statical essays containing haemostatics
• Van bergen & colleagues—mid 1950
compared invasive arterial measure-
ment & NIBP in healthy adults
• Cohn & luria

15. principles
1) Calibration
2) Zero setting
3) Levelling
4) Frequency response
5) impedence

17. How to check dampning?
• square wave test
Optimally damped - one to two oscillations before return to tracing
Underdamped -- more than 2 oscillations before returning to tracing
Overdamped -- less than 3 oscillations before returning to zero.

18. Check arterial waveform and interpret

19. • The farther into the periphery blood pressure is measured the waveform
appears narrower, systolic and pulse pressure increase and .the diastolic
pressure decrease. But MAP always remains same.
• Systolic blood pressure variations seen in hypovolemia
• Steep slope of upstroke suggests good contractility
• Position of dicrotic notch --low (low systemic vascular resistance) and high
(high afterload)
• Slope of decent -- steep (low systemic vascular resistance
Optimize natural frequency of system
• Use wide-bore, high-pressure tubing no longer than 122 cm (48 in)
• Avoid tubing extensions and minimize stopcocks
• Ensure that all connections are tightened
• Eliminate air from the flush fluid and air bubbles from the tubing system
• Keep continuous flush bag filled and keep external pressure cuff at 300
mm Hg pressure
• Keep cannulated extremity in a neutral or slightly extended position to
prevent catheter kinking

20. B. SpO2 monitoring
C. Lactate—downstream marker
normal value is approx. 1mmol/L
lactate metabolism
liver (50%), kidney(20%)
hyperlactaemeia(>5mmol/L)
TYPE A- faster production than removal-tissue hypoxia
TYPE B– B1-underlying disease
B2- drugs & toxins
B3- inborn errors of metabolism
Factors contributing hyperlactaemia:
• Increased production of lactate: tissue hypoxia
• Increased anaerobic glycolysis
• Inhibition of pyruvate dehydrogenase (in sepsis)
• Methanol/ethylene glycol/propofol toxicity
• Decreased clearance of lactate: liver dysfunction or failure, cardiopulmonary bypass
(minor reduction in clearance)
• Acute hyperventilation can elevate blood lactate levels, perhaps secondary to
increased splanchnic release of lactate during hyperventilation
• Lactate buffered solutions used in continuous veno-venous haemodiafiltration (CVVHDF)
• Medications (metformin, nucleosidic reverse transcriptase inhibitors, long-term linezolid use, intravenous
lorazepam, valproic acid)
• Haematologic malignancies.

21. D. Venous Oximetery :pulmonary artery: mixed venous oxygen
saturation (SVO2)
the level of the inferior vena cava, superior vena cava, or right atrium (RA):
central venous oxygen saturation (ScVO2).
Physiology of mixed venous oxygen saturation :4 compartments
1) Blood oxygen content
2) Oxygen delivery
3) Oxygen consumption from the microcirculation
4) Oxygen extraction ratio
Oxygen content (CaO2)
CaO2 = (0.003 x PaO2) + (1.34 x Hb x SaO2 )
Oxygen delivery (DO2)
DO2 = CaO2 x Q = (1.34 x Hb x SaO2 ) x Q
Oxygen consumption (VO2)
SvO2 = Oxygen Delivered - Oxygen Consumed
Oxygen Extraction ratio (O2 ER)
O2 ER = VO2/DO2 (normally 0.2-0.3 or 20-30%)

23. What is the relationship is between the (SvO2) and (ScvO2), and
can ScvO2 be substituted for SvO2?

24. Clinical utility of mixed venous saturation:
• The SCVO2 can be used in 2 ways
1. Relating the absolute ScVO2 value to the OER (eg, a low ScVO2 value [<
70%] accompanied by a high OER [> 0.25] could indicate relatively low CO)
2. Changes in ScVO2 might guide hemodynamic therapy, although it is
difficult in hyperdynamic conditions
Note: Occasionally, normal or increased SvO2 values are observed in a
patient, who, by all other criteria, demonstrates compromised tissue
oxygenation. Three etiologic mechanisms have been postulated for this
observation: arterial admixture, abnormalities in distribution of blood
flow, and histotoxic hypoxia

25. Step 3: Preload and fluid responsiveness
• Clinically RV preload-JVP or CVP
LV preload – pulmonary artery occlusion pr.
principle

27. Interpretation of central venous pressure
• The diastolic-pressure-volume relationship in cardiac muscle is not linear,
but rather curvilinear, with a progressively steeper slope at higher
volumes
• Ventricular compliance may change independent of end-diastolic volume
(eg, as a consequence of ischemia). The same effective preload may be
represented by two different CVP values if ventricular compliance changes
• CVP measurements are referenced to atmospheric pressure, but
physiologically, it is transmural pressure (the difference between
intracardiac and intrathoracic-extracardiac pressure) that determines
ventricular preload

28. Normal central venous pressure waveform morphology

29. Utility of CVP to Predict the Volume Responsive
• Dynamic Changes in CVP-- >1mm Hg
• ‘y’ descent– y descent greater than 4 mmHg– no response to fluid
• Hepatojugular reflux –sustained or not
• Pulmonary artery pressures– by swan ganz catheter
Limitations—lack of corelation b/w CVP & PAoP and diastolic response &
fluid responsiveness
levelling, measured at end exhalation(represented as highest point in
spontaneous breathing cycles & lowest point in PPV)
Conclusion– CVP and PAoP r not foolproof measure of preload

30. Dynamic indices for preload assessment
• Cavallaro proposition
– Group A SV related hemodynamic parameters determined by
mechanical ventilation induced cyclic variation in intrathoracic
pressure & include PPV- pulse pressure variation,its derivative & aortic
blood flow
– Group B- indices based on cyclic variation of non stroke volume
related hemodynamic parameters determined by mechanical
ventilation—includes vena cava diameter or ventricular pre-ejection
period
– Group C– indices based on preload redistribution maneuvers;
includes PLR & valsalva maneuvers

31. Stroke Volume Variation
• Diff. b/w insp. & exp. Phases of ventilation--- by PiCCO(pulsion
medical systems germany), LiDCO (LiDco group PLC england) & FloTrac
(edwards lifesciences, USA) – pulse contour analysis to measure cardiac
output & SVV. Variaton of >10% -- sensitive predictor of fluid resposiveness
Systolic Pressure Variation
• Diff. b/w the max. & min. systolic pr. Over single resp. cycle:
SPmax - SPmin or as a SPV(%) = 100 X (SPmax - SPmin)/ [(SPmax + SPmin)/2])
sensitivity of 82%, specificity of 86% & AUC ROC of 0.92 using a threshhold of
8.5mmHg
dUp = SPmax – Spref
dDown = SPref – Spmin
The large Ddown and total systolic pressure variation of nearly 30 mm Hg
suggests the diagnosis of hypovolemia

32. Pulse Pressure Variation
• Comparison of the pulse pressure during inspiration with pulse pressure
during expiration demonstrates the degree to which the pulse pressure is
preload limited.
• prerequisites: sinus rhythm, -nce of spontaneous ventilatory effort, -
nce of right heart failure, tidal volume of >8ml/kg
• PPV(%) = 100X (PPmax - PPmin)/[(PPmax + PPmin)/2].
• A PPV of •13% has been shown to be a specific and sensitive indicator of
preload responsiveness
•

33. Respiratory variability of the SVC and IVC
• Distensibility index---dIVC =(Dmax - Dmin)/Dmin
• dIVC above 18% was predictive of an increase in cardiac index of at least
15% with fluid loading
• sensitivity of 90% and a specificity of 90%
• Caveats:
1) PPV, no spontaneous efforts
2) no arrythmia ( sinus rhythm)
3) no single value is reliable
4) further investigation of these techniques in setting of vasoactive drugs
5) how extremes of ventilation

34. Passive Leg Raising
• Can b used in spontaneously breathing & in arrhythmias
• International consensus guidelines for shock
• Monnet- Used esophageal Doppler measurements of aortic blood flow as
a surrogate of cardiac output-inc. in aortic flow by 10 % predict volume
responsiveness with sensitivity of 97% & specificity of 94%
• Thiel & colleagues:

35. • Respiratory Systolic Variation Test
• End-expiratory occlusion test (EEOT)
• Conclusion:
dynamic indices r superior to static
preload responsiveness does not equate to needing more preload

36. Step 4: Cardiac output monitoring

37. Basic principles of thermodilution and indicator dilution
methods

38. The Direct Fick Method
Flow (volume/time) = indicator added (mass/time)/
change in indicator concentration (mass/volume)
Vulnerable to many errors , invasive,most technically
challenging.

39. Continuous cardiac output measurement: Minimal/Non-
invasive:
• Arterial pressure waveform analysis
PiCCO– analyses systolic portion of art. Waveform
LiDCO– analyses waveforms with pulse power analysis
Flotrac/vigileo– analyses waveform 100 times/sec over 20 sec

40. Echocardiography and Doppler technology to measure cardiac
output
• 2D echocardiography TTE or TOE technique
• Doppler technology
• CO2 rebreathing
• Bioimpedance and bioreactance
• Volume clamp method

41. Step 5: Assessment of cardiac contractility
• Echocardiography
EF (%) = {(EDV- ESV)/ EDV} x 100
assessment of preload, ventricular or valvular pathologies, pulmonary
embolism, or congenital shunt defects

42. Step 6: Assessment of microcirculation / regional tissue
perfusion
• issues need to be addressed
• 1. The reliability and reproducibility of the measurement
• 2. The identification of the most relevant microcirculatory parameters
which need to be determined;
• 3. The prognostic value of these parameters in guiding therapy
A. Orthogonal polarisation spectral (OPS) and sidestream dark
eld (SDF) imaging devices:

43. B. NIRS (Near-infrared spectroscopy)
uses beers law
signal is limited to vessels that have a diameter less than 1 mm (arterioles,
capillaries, and venules
tissue O2 saturation (StO2)
total tissue hemoglobin (HbT)
absolute tissue hemoglobin index (THI)
StO2 represents the balance between O2 delivery and O2 consumption,
does not measure microcirculatory blood flow
not suitable in conditions of heterogeneous blood flow.
influenced by adipose tissue thickness as well as the presence of edema