Rapid diagnosis of LVF in ED

Rapid diagnosis of LVF in ED

• 1.
  Rapid diagnosis ofLVF in ED by non-invasive measurement of inotropy. Brendan E. Smith1,2 and Veronica M. Madigan1 1 School of Biomedical Science, Charles Sturt University, Bathurst, NSW, Australia. 2 Specialist in Anaesthesia and Intensive Care, Bathurst Base Hospital, Bathurst, NSW, Australia.
• 2.
  Introduction. Inotropy (myocardial contractility)as a concept is well known to all clinicians but not as a discrete quantity. Depressed inotropy is an important feature of many ED presentations – 1o Cardiac Conditions – AMI, LVF, Cardiomyopathy 2o Myocardial Depression – Septicaemia, Pancreatitis, Pneumonia, DKA, Burns, Hypoxia, Crush Injury, Hypovolaemia, Anaemia, Thyroid Disorders, Hyper + Hypothermia, Poisoning, Evenomation, Iatrogenic e.g. Antihypertensives, Chemotherapy, Electrolyte Disorders, Steroids, ……
• 3.
  Why is inotropyso important? BP = SVR x HR x SV : SV x HR = CO. Preload Inotropy Afterload Fluid loading Blood Pressure Power of the heart
• 4.
  How do weassess inotropy? - We use surrogates of global cardiac function - BP, HR, urine output, skin perfusion, capillary refill, skin temperature, bowel sounds, sweating, granny’s seaweed….. - All of these are notoriously unreliable indicators of cardiac function even in the hands of senior clinicians.
• 5.
  When should weuse inotropes? In >95% of cases this is done by clinical judgment alone! Which inotrope and how much? What are our therapeutic targets? How do we know we’ve reached them? If only we could measure inotropy!!
• 6.
  But how canwe measure inotropy in the ED? First, we developed a formula based on haemodynamic theory to calculate the maximum external energy output of the heart which could be derived from clinical data which could be easily acquired in the ED. The basis of the formula is that the energy developed by the heart during contraction due to it’s inotropy must appear as some other form of energy in the circulation. N.B. The heart follows the “all or nothing rule” – when it contracts it gives it all it’s got at that moment and that depends on its inotropy!
• 7.
  Conservation of Energy Theenergy produced by cardiac contraction must be converted to either Potential Energy (PE) in the form of blood pressure or Kinetic Energy (KE) in the form of blood flow. But could we measure PE & KE? Would the measurement be reliable? How long would it take? Could we monitor Rx with it?
• 8.
  Potential Energy PE developedby the heart appears in the form of the energy needed to raise the stroke volume up to arterial pressure in a given systolic time, the Flow Time. Work Done = ΔP x ΔV PE = ΔP x SV Flow Time ΔP = Mean Arterial Pressure - CVP / JVP, SV and Flow Time are measured directly using CW Doppler. (Uscom Ltd., Sydney, Australia)
• 9.
  Potential Energy PE = BPm x SV x 10-3 7.5 x FT 7.5 and 10-3 are required to convert BP in mmHg to kPa and SV in ml to m3 to conform with SI units. The unit for PE is therefore Joules/second, or Watts.
• 10.
  Kinetic Energy The KE of any moving mass is given by – KE = ½mV2 The mass of blood ejected per Stroke Volume is - SV(ml) x 10-6 x Density of blood, ρ (1,055 kg/m3) The KE developed by the heart in a given flow time is – KE = 1 x SV x 10-6 x ρ x Vm2 2 x Flow Time (Vm is measured by CW Doppler)
• 11.
  Total Inotropy =PE + KE ( = blood pressure + blood flow) Inotropy = BPm x SV x 10-3 + 1 x SV x 10-6 x ρ x V2 7.5 x FT 2 x FT (The Smith-Madigan Formula) The SI unit of inotropy is therefore the Watt.
• 12.
  Inotropy Index But howdo we judge inotropy in patients of varying size, e.g. large and small adults, children, infants?
• 13.
  Inotropy Index By analogy to cardiac index which is – Cardiac Index = Cardiac Output Body Surface Area Smith-Madigan Inotropy Index = Inotropy BSA The SI unit of SMII is therefore W/m2
• 14.
  Part 1 -Validation of SMII We studied 250 normal patients undergoing preoperative anaesthetic assessments 5 - 17 days prior to minor day case surgery, who were normotensive and free of any CVS disease or medication. (i.e. ASA1) Age range - 3 to 74 years Weight range - 13.5 to 104 kg 136 Female, 114 Male. CW-Doppler studies carried out on the aortic valve, via the suprasternal notch to measure SV and V.
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  Results 1. Mean Inotropy Index was 1.78 W/m2 (Range 1.35 – 2.24, SD = 0.16) 2. Inotropy index decreased almost linearly with age:- Mean SMII for subjects < 35 years = 1.87 W/m2 (Range 1.83 – 2.27, SD = 0.08) Mean SMII in patients > 50 years = 1.68 W/m2 (Range 1.56 – 2.25, SD = 0.14) (p = 0.038) 3. There was no significant sex difference. Normal SMII therefore defined as 1.6 – 2.2 W/m2 (mean +/- 2SD which encompassed 240 patients, 96%)
• 16.
  Part 2 –LVF Patients 83 ED patients diagnosed by Cardiologist as LVF (NYHA criteria) +/- Echocardiography Inotropy measured prior to any therapeutic intervention. Data collected by U/S examination, BP & Hb estimation. Data entered into bespoke computer program to derive inotropy index from the S-M formula.
• 17.
  Results 1. Mean SMII was 0.73 W/m2 (0.43 – 0.97, SD 0.13) 2. Mean time to obtain SMII = 3.9 minutes (1.5 – 7.6, SD 1.4) 3. No patient in the LVF group had an SMII above 0.97 v the lowest SMII in the control group = 1.35 (p < 0.001)
• 18.
  >2.4 60-75 8 12 14 0.62 0.97 1.13 1.38 (1.6 - 2.2) <90 800-1200
• 19.
  Treatment Diagnosis Ist SMII Treatment Final SMII AMI 0.67 Dobutamine 1.53 Septicaemia 0.75 Fluids + Noradrenaline 1.54 Septicaemia 1.08 Fluids + Noradrenaline 1.62 Cardiomyopathy 0.72 Dobutamine 1.46 Hypovolaemia 1.21 Fluids 1.54 Hypovolaemia 1.26 Fluids 1.68 Pancreatitis 0.86 Fluids + Noradrenaline 1.58 SMII > 1.2 responded to fluids only. SMII < 1.1 required an inotrope to restore normal haemodynamics Recent work (n = 41) confirms SMII ~ 1.15 as cut-off point.
• 20.
  Conclusions. • Measurement ofInotropy Index in ED is entirely feasible. • Measurement typically takes less than 4 minutes. • Inotropy Index in LVF is significantly lower than normal controls (p < 0.001) • Inotropy Index may aid diagnosis of LVF and guide therapy with inotropic agents in ED.
• 24.
  Questions?