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MyNICaS Hemodynamic Presentation for Clinicians
- 3. Standard laptop Medical Carts 2-in-1 Tablet My Non Invasive Cardiac System (MyNICaS) System Components JGF Cleland et al; Non invasive measurements of Cardiac Output and Cardiac Power Index by whole body bio impedance in patients with Heart Failure; European Journal of Heart Failure 2012; 11 3 ICG Disposable Sensors MyNICaS ModuleICG Cable ECG Cable
- 4. ∆R: Change of elect’ resistance B: Aortic valve open X: Aortic valve close ∆R ECG Elec’ resistance / Volume changes of the arterial sys. B X Sys. phase Dia. phase Whole Body (Regional) Impedance Technology 4 - Proprietary - Sensors Placement ♥ Imperceptible electrical signal is transmitted through the blood in the arterial system by using two sensors arranged in a wrist-to-ankle configuration. ♥ With each heart beat, the volume of blood in the arterial system changes and this results in a change in the body electrical resistance. ♥ Cardiac Output as well as other hemodynamic and fluids parameters are calculated by proprietary algorithms.
- 5. Cardiac output measurement Comparison of Whole-body bio impedance w Pulse Contour Analysis 5 - Proprietary - ∆R (Volume ) α β NICaS CO = HR x x x Factor Factor = f (gender, body size, fluid content, blood elec’ resistivity) (α+β)∆R R β Whole body bio-impedance utilized by MyNICaS directly and continuously measures volume changes of the arterial system and calculate stroke volume and cardiac output Pulse contour analysis measure pressure and estimate volume under the assumption of constant SVR and aortic compliance; Calibration with the thermodilution is required as SVR or aortic compliance may be changed
- 6. ♥ “Agreement between NICaS CO and Thermodilution CO is within the boundaries of the FDA guidelines of bio-equivalence. NICaS CO is applicable for non-invasive assessment of cardiac function” O. L. Paredes et al, Impedance Cardiography for Cardiac Output Estimation. Circulation Journal 2006; 70:1164-1168 MyNICaS Validation About 800 Correlations to Thermodilution 6 - Proprietary - ♥ "The differences of the hemodynamic responses to vasodilation therapy may be better depicted by the MyNICaS when compared with thermodilution" G. Cotter et al, Accurate, Noninvasive Continuous Monitoring of Cardiac Output by Whole-Body Electrical Bio-impedance. Chest 2004; 125: 1431-1440 ♥ "The results of the present study suggest that MyNICaS might be more accurate then thermodilution for CO determination due to the tendency of thermodilution to under estimate CO when high and over estimate it when low" Guillermo Torre-Amiot et al, Whole-Body Bioimpedance is accurate in Non Invasive Determination of CO: A TD Prospective, Double Blinded Evaluation. Eur J of HF, June 2004 r = 0.90 Bias = -0.114 Precision = 0.982 P < 0.001 1.0 3.0 5.0 7.0 9.0 11.0 13.0 TD-CO (l/min) 13.0 11.0 9.0 7.0 5.0 3.0 1.0 NICaS-CO (l/min) 0.0 2.0 4.0 6.0 8.0 Average ( TD-CO, NICaS-CO) NICaS-CO –TD-CO 3.0 2.0 1.0 0.0 -1.0 -2.0 -3.0
- 7. Whole-Body Impedance* Validation during Hemodialysis Stroke Volume correlation to Echo Doppler 7 § No. of patients = 17 § No. of measurements = 64 (33 during first h and 31 during last h of HD treatment in 2 treatments at the same week) § Overall Pearson correlation, r = 0.92, P<0.001 § First hour Pearson correlation, r = 0.93. P<0.001 ; Last hour Pearson correlation, r = 0.92. P<0.001 § Mean (95% CI) TFR [ml] at the time of measurements during first and last hours = 1001 (609, 1392) and 2142 (1523, 2762) respectively § Bias = 1.3 ml ; Limits of agreement (95% CI) = (-11.6, 14.1) ml * NI Medical, Israel 50 60 70 80 90 100 110 45 50 55 60 65 70 Mean Arterial Pressure (mmHg) Stroke Volume (ml) NICaS Echo Subgroup 1: SV decrease (N=14) Subgroup 2: SV increase (N=11) Michael Germain, MD, Prof. Y. Chait, Prof. Nathan W. Levin
- 8. MyNICaS Parameters - Proprietary -8 Parameter Definition Normal Range Derivation/Formula Heart Rate HR Number of heart beats each minute 60 - 90 bpm (beats per minute) Measurement of the R-R interval on the ECG Stroke Volume SV Amount of blood pumped by the left ventricle each heartbeat 60 - 130 ml SV ~ ∆R / R Stroke Index SI Stroke volume normalized for body surface area 35 - 65 ml/m 2 SI = SV/ BSA Cardiac Output CO Amount of blood pumped by the left ventricle each minute 4.0 – 8.0 l/min CO = HR x SV / 1000 Cardiac Index CI Cardiac Output normalized for body surface area 2.5 - 4.0 l/min/m 2 CI = CO / BSA Cardiac Power Index CPI An indicator of myocardial contractility 0.45 – 0.85 w/m 2 CPI = CI x MAP x 0.0022 Total Peripheral Resistance TPR The resistance to the flow of blood in the arterial system Afterload 770 - 1500 dynes x sec /cm5 TPR = MAP / CO x 80 Total Peripheral Resistance Index TPRI The resistance to the flow of blood in the arterial system normalized for body surface area 1600 - 3000 dynes x sec /cm5 x m 2 TPRI = MAP / CI x 80 Total Body Water TBW The amount of fluids as a % of body weight Individually calculated as per gender and BMI TBW ~ Ht 2 / R Respiration Rate RR Number of breaths each minute 8 – 24 breaths / minute Ø Ø
- 11. Preload TBW Total Body Water Contractility CP Cardiac Power Afterload TPR Total Peripheral Resist. Determined by vasodilation and fluid respond as trended by NICaS TPRI, CPI and TBW SV Stroke Volume HR Heart Rate X 11 - Proprietary - = X XCO Cardiac Output SaO2 Oxygen Saturation Hgb Hemoglobin DO2 Oxygen Delivery Oximeter Blood Test Basic Physiology – O2 Delivery MyNICaS Guided determination of Preload, Contractility and Afterload Contractility Power of contraction PRELOAD, CONTRACTILITY, AFTERLOAD
- 13. 13 Hypertension - Proprietary - 1. Merai R, Siegel C, Rakotz M, Basch P, Wright J, Wong B; DHSc., Thorpe P. CDC Grand Rounds: A Public Health Approach to Detect and Control Hypertension. MMWR Morb Mortal Wkly Rep. 2016 Nov 18;65(45):1261-1264 The Problem: § About 1 of 3 U.S. adults - or about 75 million people - have high blood pressure1 § Only about half (54%) of these people have their high blood pressure under control1 § Hypertension control is based on a trial and error process as it is not clear which medication is the most appropriate to start with (JNC8 protocol) § Low patient compliance Our solution § Treat hypertension as per each patient’s hemodynamic profile (Vasoconstricted, Hyperdynamic or Mixed hemodynamic) Expected results: ü Improve hypertension control to >90% ü Improve cardiac output while controlling BP ü Use less medications
- 14. NICaS reveals: Normal HR Hypertension (stage II) Patient is Vasoconstricted Low cardiac output Normal Cardiac power High Afterload Normal TBW 14 Case Study 1 – Hypertension Control - Proprietary - Treatment: ACEI (after 2 weeks)
- 15. 15 Case Study 2, 3: Hypertension Control - Vasoconstricted Baseline: Patient is vasoconstricted: High BP (163/88), low CI (2.3), no medications After 3 days of treatment with Enaladex 2x10 mg Normal BP (127/76) and CI (3.2) - Proprietary - Baseline: Patient is vasoconstricted: High BP (159/86), Good CI (2.9), no medications After treatment with Diuretics Normal BP (135/81) but CI reduced to (2.1)
- 18. 18 Heart Failure management in the community - Proprietary - The Problem: § Heart Failure patients are normally discharged from hospital with diuretics and Beta blockers but not enough afterload reduction § Physicians in the community tend not to change medications prescribed at the hospital § At a certain point of time patient’s intravascular volume will be reduced resulting in decompensation and fluid accumulation § High hospital readmission (about 20-22% within 30 days and 50% within 6 month) Our solution § Adjust medications (Diuretics, Afterload reduction, Beta Blockers) as patient’s hemodynamics changes over time (Vasoconstriction and volume status) Expected results: ü Significant reduction of hospital’s readmission (by > then 50%)
- 19. NICaS reveals: Normal HR Normal BP No edema, patient fill good Normal TBW Patient is not OK and needs Medical Attention Low Contractility High Afterload 19 Case Study 5 – CHF in the community - Proprietary - Treatment: ACE Inhibitor + low salt diet (after 10 weeks)
- 22. 22 Heart Failure management in the community Conclusions ü “The ICG technology will identify residents with impending heart failure before they decompensate allowing time to make necessary adjustments that will prevent the decompensation” Prof. Arman T. Askari, Cleveland Clinic - Proprietary - ü “The results of the program were quite impressive. There were no readmissions to the hospital from either site for heart failure in over 6 months. The majority of residents could be optimally titrated on medications for heart failure and taken off medications that were not addressing the pathophysiology of the resident as suggested by the NICaS ICG analysis” Matthew Wayne MD, CMD; Chief Medical Officer, Communicare Family of Companies (40 residents with history of heart failure) ü “I have found MyNICaS to be very useful in making better informed decisions about adjustments to multiple cardio active medications in patients with advanced heart failure – particularly when it is not clear whether a more aggressive diuresis or vasodilatation is required” Prof. Martin R. Cowie MD MSc FRCP FESC, Imperial College London (Royal Brompton Hospital)
- 24. 24 Heart Failure management in the CCU/ICU Fluids/ Vasodilators Optimization 1. High TPRI § CPI increases as a respond to vasodilators - Primary diagnosis is Afterload (Vasoconstriction) § CPI decreases as a respond to vasodilators - Primary diagnosis is Preload/ Contractility 2. Normal TPRI § CPI increases as a respond to fluid challenge - Primary diagnosis is Preload § CPI decreases as a respond to fluid challenge - Primary diagnosis is Contractility 12 3 4 3. Low TPRI § CPI increases as a respond to vasopressors - Primary diagnosis is Afterload (Vasodilatation) § CPI decreases as a respond to vasopressors - Primary diagnosis is Preload/ Contractility 1 2 3
- 25. 25 Navigation Pathway for CCU/ICU - Proprietary - Hypertension Vasoconstricted (high BP, low CI, high TPRI) - Increase dose/add: ACEI, ARB or other Vasodilator - Consider reduce: BB - Target: BP<140/90, TPRI<3,650 Pulmonary Edema (elevated BP, low CI, high TPRI, SpO2<90%, severe respiratory disorder) - Increase dose/add: Isosorbide dinitrate - Increase does/add: diuretic (e.g. Furosemide/ Lasix) – make sure SI not reduced - Target: lower TPRI until SBP reduces by 25% Exacerbated HF (normal BP, low CI, high TPRI - Increase dose/add: vasodilation (e.g. ACEI, ARB, if not effective add Hydralazine) - Consider increase dose/ add: Positive Inotropic Agents, Aldospirone - Target: CPI>0.30, TPRI<3,650 Low perfusion (Cardiogenic Shock) (low BP, low CI, low CPI) - Exclude RV dysfunction by Echo cardiography - Exclude dehydration or hemorrhage - Increase dose/add: positive Inotropic Agent (e.g. Cardiac Glycoside) - Add fluid if TBW low or normal+edema +SI<30 - Consider mech. support if no response to drugs - Target: CPI>0.30, MAP>65 Hypertension Hyperdynamic (High BP, Normal TPRI, High CPI) - High SI: increase dose/add: CCB w negative inotropic Effect (e.g. Verapamil) - High HR: increase dose/add: Beta Blocker - Consider diuretic (e.g. Aldospirone, Furosemide/ Lasix). If TBW low – avoid diuretics - Target: BP<140/90, CPI<1.00 Hyperdynamic Circulation (Low TPRI, High CPI) - Identify cause and treat accordingly (Stress, withdrawal state, sever pain, hepato-syndrom, early sepsis, sever allergic reaction, anemia, large arteriovenous fistula, multiple small arteriovenous shunts, hyperthyroidism, beriberi, paget disease etc.) - Target: CI<4.5 Distributive Shock (Low TPRI, High CI) - Identify cause and treat accordingly (Septic, anaphylactic, adrenal insufficiency, neurogenic) - Add fluids if fluids responsiveness (PLR) - Add vasopressors (Norepinephrine, Epinephrine, Vasopressin) to maintain MAP>65 COLD-WET WARM-WET WARM-DRYCOLD-DRY
- 26. 26 Hemodynamic trends during dialysis treatment Intradialytic Hypotension (IDH) Subgroups IDH due to Cardiac Power (CPI) reduction: CPI is reduced due to preload reduction CI reduced, no significant change in TPRI IDH due to TPRI reduction( Vasodilation): TPRI reduces, CI increase, No significant change in CPI IDH due to Mixed Hemodynamic: Both CPI & TPRI reduces No significant change in CO CI – Cardiac Output Index; CPI- Cardiac Power Index; TPRI – Total Peripheral Resistance Index 40 50 60 70 80 90 100 110 120 130 140 150 160 0.5 1.0 1.5 2.0 2.5 3.0 3.5 4.0 4.5 5.0 5.5 6.0 Cardiac Output Index [l/mim/m2] IDH - CPI REDUCTION (35 out of 99, 35.4%) Blood Pressure [mmHg] 40 50 60 70 80 90 100 110 120 130 140 150 160 0.5 1.0 1.5 2.0 2.5 3.0 3.5 4.0 4.5 5.0 5.5 6.0 Cardiac Output Index [l/mim/m2] IDH - TPRI DECREASED (37 out of 99, 37.4%) Blood Pressure [mmHg] 40 50 60 70 80 90 100 110 120 130 140 150 160 0.5 1.0 1.5 2.0 2.5 3.0 3.5 4.0 4.5 5.0 5.5 6.0 Cardiac Output Index [l/mim/m2] IDH - COMBINED HEMODYNAMIC (27 out of 99, 27.3%) Blood Pressure [mmHg]
- 27. 27 Hemodynamic trends during dialysis treatment Intradialytic Hypertension (IH) Subgroups CI – Cardiac Output Index; CPI- Cardiac Power Index; TPRI – Total Peripheral Resistance Index IH due to Vasoconstriction: TPRI increases, CI decrease, no significant change in CPI IDH due to Hyperdynamic state CPI increases, CI increase, No significant change in TPRI IDH due to Mixed Hemodynamic: Both CPI & TPRI increase No significant change in CI
- 28. 28 Summary ü Hemodynamic management of patients in the critical care setting and of chronic patients is a great challenge ü Blood pressure is an important vital sign but does not provide the full information needed for an effecting hemodynamic management ü Clinicians ability to estimate cardiac output is limited ü Non-invasive hemodynamic monitoring and graphically trending of Total Peripheral Resistance and Cardiac power provides a good hemodynamic understanding www.mynicas.com