The goal of hemodynamic monitoring is to assess the cardiovascular state of the patient, define their reserve and monitor response to treatments and time.  Resuscitation efforts are essentially aimed at restoring and sustaining tissue wellness through maintaining an adequate amount of oxygenated blood flow to the metabolically active tissues. We need to monitor pressure, flow and function. To accomplish these goals one must be able to measure arterial pressure and all its components (i.e. waveforms), cardiac output and stroke volume as well as the adequacy of flow. Presently, there are several devices that can estimate the arterial pressure waveform from a finger plethysmographic device. They are very accurate until profound circulatory collapse makes peripheral pulse not representative of central pressures. These devices can also estimate stroke volume by intuiting the arterial pressure waveform in a fashion similar to that performed by the numerous minimally invasive hemodynamic monitoring devices we now have now. These non-invasive devices can quantify functional hemodynamic monitoring dynamic parameters. Also, pulse oximeter pleth density signals vary with pulse volume into the finger or skin and the pleth variability can also be used as a surrogate of pulse pressure variation. Furthermore, bioreactance can measure both cardiac output and intrathoracic fluid content through surface electrodes. Finally, end-tidal CO2 transiently varies with venous return, increasing if blood flow increases. So both eh bioreactance device and end-tidal CO2 can be used to identify cardiac output changes in response to a passive leg raising maneuver. Thus, one can measure arterial pressure waveforms and cardiac output continuously, assess volume responsiveness and monitor therapy. Finally, the dynamic changes in tissue O2 saturation (StO2) measured by near infrared spectroscopy of the thenar eminence during a vascular occlusion test defines peripheral circulatory insufficiency and local blood flow independent of arterial pressure.  Furthermore, heart rate variability decreases with increasing cardiovascular stress and can be readily measured in real time from the R-R intervals of the surface ECG signal.  Finally, the measure of urine output, skin temperature and sensorium all define effective tissue blood flow as reasonable end-points to resuscitation, if the patient is not overwhelmingly ill. When these measures are coupled to a treatment approach know to improve outcome, there is little reason to believe that such completely non-invasive approaches will be inferior to invasive ones in the management of the critically ill patient. 

1. Can We Be Intensive
and Non-invasive?
Michael R. Pinsky, MD, Dr hc
Department of Critical Care Medicine
University of Pittsburgh

2. Potential Conflicts of Interest
• Michael R. Pinsky, MD is the inventor of a US patent “Use of aortic pulse
pressure and flow in bedside hemodynamic management ” owned by the
University of Pittsburgh
• Michael R. Pinsky, MD is or was a medical advisor for:
– Abbott Corporation
– Arrow International
– Edwards LifeSciences
– LiDCO Ltd
– Hutchinson Medical
– väsamed
– Applied Physiology Ltd.
– Cheetah Medical
• Michael R. Pinsky, MD has received research funding in the past from:
– Deltex Ltd
– Pulsion Ltd
• Michael R. Pinsky, MD is receiving research funding as Principal
Investigator from the NHLBI
– K-24 HL67181-06, T32 HL07820-11 and R01 HL073198-04

3. Non-Invasive Hemodynamic Monitoring
• Electrocardiogram (ECG)
– rhythm analysis, heart rate variability
– stroke volume variation
• Arterial blood pressure
– automatic blood pressure monitoring (Dynamat )
– finger optical pulse pressure (Finapres )
• Pulse oximetry
– SpO2, heart rate
– plethysmographic pulse variation
• Transthoracic echocardiography
– fractional area of contraction, valve function, contraction
asynchrony
– LV volumes and contractility
• End-tidal CO2 and CO2 rebreathing
– physiological dead space, D gut lumen PCO2 (Tonocap )
– stroke volume & cardiac output: NICO2

• Impedance and Bioreactance Cardiography
– BioZ and NICOM 

4. Non-Invasive Hemodynamic Monitoring
• Electrocardiogram (ECG)
– rhythm analysis, heart rate variability
– stroke volume variation
• Arterial blood pressure
– automatic blood pressure monitoring (Dynamat )
– finger optical pulse pressure (Finapres )
• Pulse oximetry
– SpO2, heart rate
– plethysmographic pulse variation
• Transthoracic echocardiography
– fractional area of contraction, valve function, contraction
asynchrony
– LV volumes and contractility
• End-tidal CO2 and CO2 rebreathing
– physiological dead space, D gut lumen PCO2 (Tonocap )
– stroke volume & cardiac output: NICO2

• Impedance and Bioreactance Cardiography
– BioZ and NICOM 

5. Use of the electrocardiogram to assess
changes in LV stroke volume
• Ratio of R to T wave amplitude in stand lead
II in the supine position
– Changes in LV stroke volume directionally similar
to changes in the R/T ratio in dog: 100% specificity
– Pinsky et al. Appl Cardiopulm Pathophysiol 4:301-8, 1992
– Changes in LV volumes were linearly related to
changes in R/T ratio in humans: 100% sensitivity, r2
= 0.72 (group)
– Pinsky et al. Am J Cardiol 76:667-74, 1995

6. R/T ratio increases with
increasing LV stroke volume
Pinsky et al. Appl Cardiopulm Pathophysiol 4:301-8, 1992
200 ml NaCl infusion
R/T 4.98
R/T 7.99
SV 13.3 ml SV 18.9 ml
Closed chest anesthetized canine model

7. R/T ratio increases with
increasing LV stroke volume
Low ECG R/T 2.50High ECG R/T 2.89
High SV 10.6 ml Low SV 8.1 ml
Pulsus Alternans
is primarily a
Left-sided process
Pinsky et al. Appl Cardiopulm Pathophysiol 4:301-8, 1992

8. R/T ratio changes (DZ) predict directional
changes in LV stroke volume in the dog
Pinsky et al. Appl Cardiopulm Pathophysiol 4:301-8, 1992

9. R/T ratio changes
follow LV stroke
volume in humans
Pinsky et al. Am J Cardiol 76: 667-74, 1995
Beat-to-beat variation in R/T match
Beat-to-beat variation in LV SV

10. ECG R/T Ratio: Bottom Line
• Readily available from any ECG monitor
• Originally validated in 1985
– Feldman et al. Circulation 72:495-501, 1985
• Highly position sensitive
• Gives relative changes in EDV and SV
• Good trend monitor

11. Can Stroke Volume be Assessed
Non-invasively?
• Alternative methods of assessment of arterial
pulse pressure waveform
– Finger plethysmography analysis
– Finger pulse oximetry plethysmography signals
• Echocardiography
• Partial CO2 rebreathing
• Bioempedance and Bioreactance cardiography

12. Non-Invasive Hemodynamic Monitoring
• Electrocardiogram (ECG)
– rhythm analysis, heart rate variability
– stroke volume variation
• Arterial blood pressure
– automatic blood pressure monitoring (Dynamat )
– finger optical pulse pressure (Clearsight, CNAP)
• Pulse oximetry
– SpO2, heart rate
– plethysmographic pulse variation
• Transthoracic echocardiography
– fractional area of contraction, valve function, contraction
asynchrony
– LV volumes and contractility
• End-tidal CO2 and CO2 rebreathing
– physiological dead space, D gut lumen PCO2 (Tonocap )
– stroke volume & cardiac output: NICO2

• Impedance and Bioreactance Cardiography
– BioZ and NICOM 

13. 1st generation:
Fenapres
Stok et al. J Appl Physiol 74: 2687-93, 1993

14. Non-invasive measures of arterial pressure
Finepres®
Cohn et al. Hypertension 26:503-8, 1995
Non-invasive
Non-invasive
Non-invasive
Non-invasive
Invasive
Invasive
Invasive
Invasive

15. Non-invasive measure of stroke
volume from arterial pulse contour
Stok et al. J Appl Physiol 74: 2687-93, 1993
r = 0.96

16. Estimating Stroke Volume by Pulse Contour
Hamilton & Remington Formula
SV = K x Psa x (1 + Ts/Td)
Hamilton, Remington. Am J Physiol 148: 14-24, 1947

17. 2nd Generation Clearsight

18. 2nd Generation Clearsight
Sen et al. West J Emerg Med 15:345, 2014

19. Non-invasive assessment of
arterial pressure variation
Bronzwaer et al. Front Physiol 5, 2014

20. Draeger Infinity CNAP

21. Draeger Infinity CNAP
Siebig et al. Int J Med Sci 6:37-42, 2009

22. Non-invasive measure of stroke
volume from arterial pulse contour
• Stok et al. J Appl Physiol 74: 2687-93, 1993
• Harms et al. Clin Sci 97:291-301, 1999
• Hirschl et al. Crit Care Med 25: 1909-14, 1997
• Remmen et al. Clin Sci 103:143-9, 2003
• Bogert & van Lieshout Experimental Physiol 90:437-46, 2005
• Imholz et al. Clin Autonomic Res 1:43-53, 2005
• Antonutto et al. Euro J Appl Physiol 69:183-8, 2005
• More than 15 others peer-reviewed references …

23. Finger Pressure Pleth:
Bottom Line
• Many basic science and clinical trials
showing accuracy of device in non-ICU
environments
• No studies assessing pulse pressure or
stroke volume variation
• Limited in hypotension and peripheral
vasoconstriction states
• No studies showing clinical utility

24. Non-Invasive Hemodynamic Monitoring
• Electrocardiogram (ECG)
– rhythm analysis, heart rate variability
– stroke volume variation
• Arterial blood pressure
– automatic blood pressure monitoring (Dynamat )
– finger optical pulse pressure (Clearsight , CNAP)
• Pulse oximetry
– SpO2, heart rate
– plethysmographic pulse variation
• Transthoracic echocardiography
– fractional area of contraction, valve function, contraction
asynchrony
– LV volumes and contractility
• End-tidal CO2 and CO2 rebreathing
– physiological dead space, D gut lumen PCO2 (Tonocap )
– stroke volume & cardiac output: NICO2

• Impedance and Bioreactance Cardiography
– BioZ and NICOM 

25. 0
50
100
150
ArterialPressure(mmHg)
-20
0
20
40
60
AorticFlow(L/min)
-10
0
10
20
30
40
EsophagealDopplerFlow
(L/min)
Arterial Pressure
Cineflo™ Aortic Flow Probe
Hemosonic™ Esophageal Doppler Calculated Flow
Pulse Oximetery Plethysmograph
0
50
100
150
200
250
Time (1 s)
PulseOximetryDensity
Effect of IVC Occlusion on Flow Measures in Man
Marquez et al. Crit Care Med 36:3001-7, 2008

26. Pleth Variability Index

27. Cut-off values:
DPP: 13%
DPpleth: 9%
Arterial signal
Plethysmographic signal
Natalini et al. Anesth Analg 103:1478-84, 2006
Arterial versus Plethysmographic Dynamic Indices to Predict
Volume Responsiveness in Hypotensive Patients

28. PPV %
DPOP%
Cannesson et al. Crit Care 9: R562-8, 2005
Relation between Respiratory Variations in Pulse Oximetry Plethysmographic
Waveform Amplitude and Arterial Pulse Pressure in Ventilated Patients
Alternative Use of Pulse Oximetry

29. Feissel et al. ISICEM 2005 (abstract)
Respiratory Variation of Plethysmographic Signal with Pulse Oximetry:
New Predictive Parameters of Fluid Responsiveness?
DPP predicts volume responsiveness

30. Using Pleth Variability Index
to Drive Resuscitation
Yu et al. J Clin Monit Comput 29:47-52, 2015
1h 2h 3h

31. Non-contact monitoring
mobile CVInsight

32. Pulse Plethysmographic Analysis:
Bottom Line
• Theoretical rationale for utility clear
• Technical aspects of signal analysis limited
– signal smoothing
– Reprocessing
– Rezeroing
• Limited in hypotension and peripheral
vasoconstriction states (norepinephrine)
• No outcomes studies
• Not yet ready for prime time

33. Non-Invasive Hemodynamic Monitoring
• Electrocardiogram (ECG)
– rhythm analysis, heart rate variability
– stroke volume variation
• Arterial blood pressure
– automatic blood pressure monitoring (Dynamat )
– finger optical pulse pressure (Finapres )
• Pulse oximetry
– SpO2, heart rate
– plethysmographic pulse variation
• Transthoracic echocardiography
– fractional area of contraction, valve function, contraction
asynchrony
– LV volumes and contractility
• End-tidal CO2 and CO2 rebreathing
– physiological dead space, D gut lumen PCO2 (Tonocap )
– stroke volume & cardiac output: NICO2

• Impedance and Bioreactance Cardiography
– BioZ and NICOM 

34. Echocardiography to Non-Invasively
Assess LV Contractility
• Echocardiographic automated border detection
algorithms (acoustic quantification) accurately
measure LV volume throughout the cardiac cycle
allowing bedside estimates of LV end-systolic
pressure-volume relations (ESPVR)
– Accurately describes end-systolic pressure-volume
relations (ESPVR) and their change in response to positive
and negative inotropic agents in dogs
– Denault et al. Am J Physiol 272:H138-47, 1997
– Accurately describes ESPVR and their change following
heart surgery in humans
– Gorcsan et al. Anesthesiology 81:553-62, 1994

35. Echocardiographic Automated Border
Detection Algorithm Accurately Measures
LV Area
Gorcsan et al. Circulation 89:180-90, 1994

36. Echocardiographic Automated Border Detection LV
Area Accurately Tract LV Volume
Gorcsan et al J Am Soc Echocardiogr 6:482-9, 1993

37. Transesophageal Echocardiography-ABD and
LV Pressure
Gorcsan et al. Circulation 89:180-90, 1994

38. Transesophageal Echocardiography-ABD and
Arterial Pressure
Gorcsan et al. Anesthesiology 81:553-62, 1994

39. Gorcsan et al. Anesthesiology 81:553-62, 1994

40. Gorcsan et al. Anesthesiology 81:553-62, 1994

41. Arterial Pressure Wave Forms Can
Be Measured Non-Invasively
Gorcsan et al. (unpublished data)

42. LV Contractility Can Be
Non-Invasively Assessed
Gorcsan et al. (unpublished data)
End-systolic Elastance Estimated by Transthoracic echocardiography and Finepres

43. Dobutamine Does Not Increase LV
Contractility in Human Septic Shock
0
20
40
60
80
100
120
140
160
2 7 12
Severe Sepsis Sepsis +Dobutamine
0
20
40
60
80
100
120
140
160
2 7 12 17
Cariou et al. Intensive Care Med 34: 917-22, 2008

44. Depressed LV Contractility Persists in Most Septic
Patients following Withdrawal of Vasoactive Therapy
LV Area (cm2
)
0 5 10
DAY 1 DOBUTAMINE
LV Area (cm2
)
0 5 10
LV Area (cm2
)
0 5 10
ArterialPressure(mmHg)
0
40
80
120
160
200
DAY 1 BASELINE
LV Area (cm2
)
0 5 10
ArterialPressure(mmHg)
0
40
80
120
160
200
LV Area (cm2
)
0 5 10
DAY 4 BASELINE
LV Area (cm2
)
0 5 10
LV Area (cm2
)
0 5 10
DAY 4 DOBUTAMINE
LV Area (cm2
)
0 5 10
Cariou et al. Intensive Crit Care Med 34: 917-22, 2008

45. Ees during the Course of Human Septic Shock
60 yo, sepsis and pneumonia
0
20
40
60
80
100
120
140
160
180
0 5 10 15 20
LV Area (cm2)
ArterialPressure
(mmHg)
D1: Ees = 4
D5: Ees = 16
D8: Ees = 24
Cariou et al. Intensive Care Med 34: 917-22, 2008

46. LV Contractile Reserve in Sepsis
0
10
20
30
Day 1 Day 5 Day 9
Baseline
Dobutamine
E’es
*
P < 0.05
n = 12
Cariou et al. Intensive Care Med 34: 917-22, 2008

47. Echocardiographic Analysis of LV
Function: Bottom Line
• Established clinical utility
• Commonly used in Cardiology Outpatients
• Only one ICU study reporting its use
– Cariou et al. Intensive Care Med 34: 917-22, 2008
• Requires expert echocardiographer
– Inter-operator variability
• Limited imagining window (70% patients)
• Should be used more often to reduce
measurement errors

48. Ultrasonic Doppler
• Aortic root velocity
– Echocardiography
– Suprasternal notch ultrasound (USCOM)
• Descending aortic velocity
– Deltex velocity
– Hemosonic flow

49. Deltex CardioQ Velocity Probe Placement

50. (Mean Flow Velocity X Ejection Time) X Cross Sectional Area of Aorta
(Flow Velocity Integral)
Aortic Flow Velocity Integral
Cardiac Output = (Stroke Volume) X Heart Rate
Aorta
Doppler Determination of Cardiac Output

51. Vpeakmin
∆Vpeak
Vpeakmax
∆Vpeak
(%)
before fluid
4
8
12
16
20
24
28
32
36
responders non responders

52. Hemosonic Esophageal Pulsed Doppler Probe Placement
Measures both velocity and
Aortic diameter to calculate
Flow giving a more accurate
estimate than velocity alone.
Monnet et al. Crit Care Med 35:477-82, 2007

53. Aortic
Blood
Flow
The PLR effects occur over a epoch of time
encompassing several cardiac and respiratory cycles
Prediction of Fluid Responsiveness
Spontaneous breathing and arrhythmias
PLR
Monnet et al. Crit Care Med 34:1402-7, 2006

54. 0
50
100
150
ArterialPressure(mmHg)
Arterial Pressure
Cineflo™ Aortic Flow Probe
-20
0
20
40
60
AorticFlow(L/min)
Hemosonic™ Esophageal Doppler Calculated Flow
-10
0
10
20
30
40
EsophagealDopplerFlow
(L/min)
Pulse Oximetery Plethysmograph
0
50
100
150
200
250
Time (1 s)
PulseOximetryDensity
Effect of IVC Occlusion on Flow Measures in Man
Marquez et al. Crit Care Med 36:3001-7, 2008

55. Comparison of Esophageal Doppler Monitor (Hemosonic™) to Aortic Flow Probe
(Cineflo™) Measures of Left Ventricular Stroke Volume during Venous Occlusion
OR2
y = 0.7836x - 13.454
R 2 = 0.8861
0
20
40
60
80
100
120
0 20 40 60 80 100 120
EsophagealDopplerStrokeVolume(ml)
OR7
y = 0.1946x + 19.24
R 2 = 0.087
0
20
40
60
80
100
120
0 20 40 60 80 100 120
OR4
y = 0.8023x + 0.66
R2= 0.9881
0
20
40
60
80
100
120
0 20 40 60 80 100 120
OR9
y = 0.5451x - 17.33
R 2 = 0.8605
0
20
40
60
80
100
120
0 20 40 60 80 100 120
OR3
y = -3.1023x + 171.39
R2 = 0.1749
0
20
40
60
80
100
120
0 20 40 60 80 100 120
OR8
y = 0.6621x - 5.6648
R2 = 0.9716
0
20
40
60
80
100
120
0 20 40 60 80 100 120
OR6
y = 0.7542x + 9.0652
R2 = 0.9666
0
20
40
60
80
100
120
0 20 40 60 80 100 120
Cineflo Stroke Volume (ml)
Cineflo Stroke Volume (ml) Cineflo Stroke Volume (ml) Cineflo Stroke Volume (ml)
Cineflo Stroke Volume (ml)Cineflo Stroke Volume (ml)Cineflo Stroke Volume (ml)
EsophagealDopplerStrokeVolume(ml)
EsophagealDopplerStrokeVolume(ml)
EsophagealDopplerStrokeVolume(ml)
EsophagealDopplerStrokeVolume(ml)
EsophagealDopplerStrokeVolume(ml)
EsophagealDopplerStrokeVolume(ml)
Marquez et al. Crit Care Med 36:3001-7, 2008

56. USCOM
Suprasternal notch positioning
Measures ascending aortic flow
Learning curve

57. USCOM
Tan et al. Br J Anaesth 94:287-29, 2005

58. Esophageal Doppler: Bottom Line
• Accurate measures of aortic flow velocity
• Operator-dependent
– Tight learning curve, results may vary with operator
and with probe mal-positioning
• When coupled with protocolized DO2
optimization improves outcome form critical
illness
• Limited to intubated patients
• Not the universal monitor because of discomfort

59. Non-Invasive Hemodynamic Monitoring
• Electrocardiogram (ECG)
– rhythm analysis, heart rate variability
– stroke volume variation
• Arterial blood pressure
– automatic blood pressure monitoring (Dynamat)
– finger optical pulse pressure (Clearsight , CNAP)
• Pulse oximetry
– SpO2, heart rate
– plethysmographic pulse variation
• Transthoracic echocardiography
– fractional area of contraction, valve function, contraction
asynchrony
– LV volumes and contractility
• End-tidal CO2 and CO2 rebreathing
– physiological dead space, D gut lumen PCO2 (Tonocap)
– stroke volume & cardiac output: NICO2

• Impedance and Bioreactance Cardiography
– BioZ and NICOM 

60. Partial Rebreathing CO2
Bottom Line
• System Requirements
– Stable VCO2
• Stable metabolic rate
• No worsening or recovering metabolic acidosis
– Stable CO
– Intubated patient or very cooperative one
• Practical uses
– Limited penetration through one of oldest methods
– Limited understanding of system requirements
– Not accurate in dynamically changing systems

61. Non-Invasive Hemodynamic Monitoring
• Electrocardiogram (ECG)
– rhythm analysis, heart rate variability
– stroke volume variation
• Arterial blood pressure
– automatic blood pressure monitoring (Dynamat)
– finger optical pulse pressure (ClearSight®, CNAP)
• Pulse oximetry
– SpO2, heart rate
– plethysmographic pulse variation
• Transthoracic echocardiography
– fractional area of contraction, valve function, contraction
asynchrony
– LV volumes and contractility
• End-tidal CO2 and CO2 rebreathing
– physiological dead space, D gut lumen PCO2 (Tonocap )
– stroke volume & cardiac output: NICO2

• Impedance and Bioreactance Cardiography
– BioZ and NICOM 

62. Use of ECG energy to measure CO
• Bio-impedance
–Bio-Z
• Bio-reactance
–NICOM

63. Noninvasive Hemodynamic Monitoring:
Impedance Cardiography (ICG)
• 4 dual sensors with 8 lead wires
placed on neck and chest
• Current transmitted by outer
electrodes and seeks path of least
resistance: blood filled aorta
• Baseline impedance (resistance) is
measured using inner electrodes
• With each heartbeat, blood volume
and velocity in the aorta change
• Corresponding change in impedance
is measured
• Baseline and changes in impedance
are used to measure and calculate
hemodynamic parameters
– from www.cardiodynamics.com

64. EKG
X(t)
DX
DV
DX’
dX/dt
VET
dX/dt max
SV = DV’
Global
Blood
volume
NICOM BioReactance

65. 0
Volts
Z = V / I
Io
Vo
Io
Vo
Ze = Re + jXe
q q
0
Amps

66. Zo = Vo / Io
DV = AM
Dwt or Dq = FM
0
Volts
Io
Vo
Io
Vo
DZe = Re + jDXe
0
Amps

67. Io
Io
V(t)
AM signal = DV(t)
DV
Vo
FM signal = Dw(t)
Dw
wo
Same shape
of signal

68. Bioimpedance Estimates of CO
Van De Water et al. Chest 2003;123:2028-33, 2003

69. Squara et al. Intensive Care Med 33:1432-8, 2007
Bioreactance
Noninvasive cardiac output monitoring (NICOM): a clinical validation

70. Keren et al. Am J Physiol 293:H583-9, 2007
Comparison of NICOM and CCOtd

71. Keren et al. Am J Physiol 293: H583-9, 2007
Evaluation of Non-invasive Continuous Cardiac Output
Monitoring System based on Thoracic Bioreactance

72. Comparison NICOM to PAC
Post op cardiac surgery patients
Lamia et al. J Clin Monitor Comput 32: 33-43, 2018

73. Bioimpedance and Bioreactance
Estimates of Cardiac Output:
Bottom Line
• FDA-approved to assess cardiac function
• Useful in many environments
– Outpatient
• Cardiovascular status
• Heart failure screening
• Bioimpedance: Inaccurate in acute care conditions
• Bio-reactance: Accurate and useful to guide therapy
– In patient
• ED, OR, ICU
• Reduced excess fluid infusion in non-responders

74. Non-Invasive Hemodynamic Monitoring
• Electrocardiogram (ECG)
– rhythm analysis, heart rate variability
– stroke volume variation
• Arterial blood pressure
– automatic blood pressure monitoring (Dynamat )
– finger optical pulse pressure (Finapres )
• Pulse oximetry
– SpO2, heart rate
– plethysmographic pulse variation
• Transthoracic echocardiography
– fractional area of contraction, valve function, contraction
asynchrony
– LV volumes and contractility
• End-tidal CO2 and CO2 rebreathing
– physiological dead space, D gut lumen PCO2 (Tonocap )
– stroke volume & cardiac output: NICO2

• Impedance and Bioreactance Cardiography
– BioZ and NICOM 

75. Thank You