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Cardinal Rules of Critical Care Medicine

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Advanced Review of Fundamental Critical Care Principles in the Treatment of Acute Illness ...

Advanced Review of Fundamental Critical Care Principles in the Treatment of Acute Illness
1. Time "Golden Hour"
2. Increase Oxygen Delivery
3. Reduce Oxygen Consumption
4. Restore Standard State Conditions "Resuscitation Endpoints"

Edward Omron MD, MPH, FCCP
Pulmonary and Critical Care Medicine
Morgan Hill, CA 95037
www.docomron.com

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  • Fourcardinal principles define the diagnostic and therapeutic boundaries of the discipline: First, outcome from acute illness is a function of time from diagnosis to initiation of goal directed therapy; and secondly, all current therapeutic endeavors attempt to contemporaneously improve oxygen delivery,minimize oxygen consumption, and restore standard state conditions. The Early Goal Directed paradigm facilitates the patient’s unique physiologic reserve and enhances the likelihood of recovery.
  • Stage 1: 15% blood loss (< 0.75L)Stage 2: 15 to 30% (0.75 to 1.5 L)Stage 3: 30 to 40%(1.5 to 2.0 L)Stage 4: > 40% (> 2 L)
  • The union army suffered 12,653 casualties (1,284 killed, 9,600 wounded, 1,769 captured/missing). This was a tragic union loss to the south however, there was a positive side..
  • Numerous studies havelooked at time to antimicrobial therapy in septic shock, and virtually all have founda reduction in mortality when antimicrobials were given in a timely fashion.Initiation of effective antimicrobial therapy within the first hour after onset of septicshock–related hypotension was associated with 79.9% survival to hospital dischargeFor every additional hour to effective antimicrobial initiation in the first 6 hours after onset of hypotension, survival dropped an average of 7.6%/hr.
  • Fig. 2. Mortality risk (expressed as adjusted odds ratio of death) with increasing delays ininitiation of effective antimicrobial therapy. Bars represent 95% CI. An increased risk ofdeath is already present by the second hour after hypotension onset (compared with thefirst hour after hypotension onset). The risk of death continues to increase up to morethan 36 hours after hypotension onset. (From Kumar A, Roberts D, Wood KE, et al. Durationof hypotension before initiation of effective antimicrobial therapy is the critical determinantof survival in human septic shock. Crit Care Med 2006;34:1589–96; with permission.)

Cardinal Rules of Critical Care Medicine Cardinal Rules of Critical Care Medicine Presentation Transcript

  • The Cardinal Rules of Critical Care Edward Omron MD, MPH, FCCP Pulmonary Critical Care Medicine edofiron@gmail.com
  • Cardinal Rules of Critical Care• Critical Care Medicine – A fusion of disparate medical specialties refined by applied bedside physiology whose ultimate goal is to improve overall morbidity and mortality in the acutely ill. – Interdisciplinary – Labor Intensive – Technically complex – Most expensive part of hospital care – ON THE EDGE OF CHAOS
  • Cardinal Rules of Critical Care1. Time “Golden Hour”2. Increase Oxygen Delivery3. Reduce Oxygen Consumption4. Restore Standard State Conditions• THIS IS EARLY GOAL DIRECTED THERAPY
  • Oxygen Demand, Consumption, and Delivery• Oxygen Demand – The amount of oxygen needed to satisfy the metabolic requirements of all body tissues. – In the resting basal state 250 mL O2 / min is demanded – Determined by body mass index (BMI), physiologic stress, infection, inflammation, temperature, trau ma, surgery, hemorrhage … – Coupled to cardiac output (HR x SV) and minute ventilation (RR x TV)
  • Oxygen Demand, Consumption, and Delivery• Oxygen Consumption – The total amount of oxygen used by all the different organ systems in the human body – In the resting basal state 250 mL/min of O2 is consumed – Equals the difference between the oxygen delivered by the arterial system and the amount of oxygen returned to the heart by the venous system – In Standard State Conditions: oxygen demand = oxygen consumption
  • Oxygen Demand, Consumption, and DeliverySvO2 73% SaO2 98% O2 demanded 250 mL/min O2 consumed 250 mL/min CaO2 – CvO2 = 5 mL/100 mLVenous O2 remaining Arterial O2 delivered750 mL/min 1000 mL/min
  • Oxygen Demand, Consumption, and Delivery in Shock PvO2 = 24% SvO2 = 24% SaO2 = 98% O2 demanded 800 mL/min O2 consumed 750 mL/min CaO2 = CaO2 – CvO2 = 15 mL/100 mL 20 mL /100 mLCvO2 = 5 mL/100 mL Venous O2 remaining Arterial O2 transferred 250 mL/min 1000 mL/min
  • Shock"a momentary pause in the act of death"• When oxygen demand exceeds consumption – Oxygen delivery is compromised – Global tissue hypoxia develops – Anaerobic metabolism with lactic acidosis – Cell injury followed by death – Organ system failure evolves to multisystem failure and death – Applicable to all forms of shock: • traumatic, septic, obstructive, hemorrhagic, hypovolem ic, cardiogenic, neurogenic, and anaphylactic
  • Cell Oxygenation
  • Anoxic Cell Death (Neuron) ACIDOSIS ANOXIA TIME
  • Stages of HemorrhageOXYGEN CONSUMPTION Critical Care 2004, 8: 373-381 OXYGEN DELIVERY
  • Cardinal Rules of Critical Care• Time or the Golden Hour – Outcome from acute illness is a function of time from diagnosis to initiation of goal directed therapy – The importance of time in acute illness was first codified in the American Civil War – Dr Jonathan Letterman, Medical Director of the Army 1862, organized health care delivery to improve survival and decrease extraction time from the battlefield arena.
  • Cardinal Rules of Critical Care• Battle of Fredericksburg Dec. 1862 – Triage was first codified – Ambulance Corps was developed to expedite treatment of traumatic battlefield injuries. – Aid stations positioned close to the battlefield and were integrated with Field Hospitals to coordinate care and reduce time for definitive treatment. – A civilian nurse corps presence began
  • Chatham House Field Hospital, Battle of Fredericksburg, Virginia 1862
  • Charles O’Leary, Medical Director, SixthCorps, Fredericksburg, Dec 13, 1862 “I had the opportunity of putting in operation the Field-Hospital organization … and witnessing its beneficialresults. Within a very few hours after the positions weredesignated for the Field Hospitals … the arrangementsnecessary for the proper care of the wounded were asthorough and complete as I have ever seen in a civilhospital. During the engagements of the 13th, theambulances being guided and governed with perfectcontrol and with a precision rare even in militaryorganizations, the wounded were brought without any delayor confusion to the hospitals of their respective divisions.”
  • Cardinal Rules of Critical Care• Golden Hour concept from World War I• An appreciation of time between wounding and shock treatment. If the patient was treated within 1 hour, mortality was 10%; after 8 hours the mortality was 75%.• Time from injury Mortality• 1 hr 10 %• 3 hr 12 %• 5 hr 36 %• 8 hr 75 %• 10 hr 75 %Bull Med Soc Chir 1918; 44:205
  • Cardinal Rules of Critical Care• Golden Hour concept since World War II Survival Time To Treatment• Vietnam War 97.5% 1 hours• Korean War 95.5% 5 hours• World War 2 95.5% 10 hours• Regarding penetrating torso injuries• Medical success was attributed to helicopter evacuation, whole blood, medical teams, and forward hospitals• Not really a “Golden Hour” but a term used to indicate urgency of care and the crucial importance of timeAnn Emerg Med 1981; 10: 659-661Acad Emerg Med 2001; 8: 758-760
  • Cardinal Rules of Critical Care• R Adams Cowley, M.D. – "There is a Golden Hour between life and death. If you are critically injured you have less than 60 minutes to survive. You might not die right then; it may be three days or two weeks later -- but something has happened in your body that is irreparable.“ – Surgeon in the Vietnam War, applied military paradigm of expedited extraction and treatment to the civilian sector – Initiated the first EMS and Air Evac system for Trauma in the State of Maryland
  • Cardinal Rules of Critical Care• Rivers, Emmanuel M.D. – NEJM 2001; 345: 1368-1377 – Early goal-directed therapy in severe sepsis and septic shock during the first 6 Golden Hours after presentation – Significant reductions in mortality, morbidity in experimental group that optimized oxygen delivery and consumption variables
  • SEPTIC SHOCK PRESENT Fluid bolus 20 ml/kg SBP < 90 mmHg, orSBP ≤ 90 mmHg or MAP ≤ 65 mmHg (.9 NaCl or LR) MAP < 65 mmHg, or OR PLUS Lactate > 4 mmol/L Lactate ≥ 4 mmol/L Vasopressors if MAP is PLUS judged to be critically low Clinical Picture c/w Infection YES Boluses crystalloid CVP < 8 mmHg Asses or colloid equivalent s until Insert ScvO2 CVP > 8 mmHg CVP Catheter < 70% MAP ≥ 65 Dobutamine or RBCs depending Check Achiev on HCT MAP e ALL Goals? Resuscitation complete. Establish re-evaluation intervals.
  • Cardinal Rules of Critical Care• Shoemaker, WC M.D. – Chest 1988;94:1176-1186 – Prospective trial of early goal-directed therapy in high risk surgical patients • Shock, Trauma, Hemmorrhage, – Marked improvement in mortality in experimental groups that received early pre- operative and perioperative optimization of oxygen transport variables
  • Initiation of effective antimicrobial therapy after septic-shock hypotensionCrit Care Med 2006;34:1589–96 Fraction of total patients Time from hypotension onset (Hrs)
  • Mortality risk with increasing delays ininitiation of effective antimicrobialtherapy (Crit Care Med 2006;34:1589–96) Odds Ratio of Death Time (hrs)
  • Cardinal Rules of Critical Care• Maximize Oxygen Delivery – Improve Cardiac Performance • Preload Augmentation (crystalloid/colloid/PRBC) • Inotropes (Dobutamine/norepinephrine) • Peripheral vasoconstrictors (vasopressin/Neosynephrine) • Afterload reduction (Nitroglycerin/Nicardipine) – Transfuse Packed Red Blood Cells – Assume control of ventilation/oxygenation – FIO2 factors
  • Cardinal Rules of Critical Care• Components of Oxygen Delivery – DO2 (oxygen delivery in mL O2/min) – DO2 = CO x CaO2 x10 – DO2 = (HR x SV) x CaO2 x10 – DO2=(HR x SV)x(1.34 x Hb x SaO2)x10 – DO2 = 1000 mL/min Standard State Conditions
  • Components of O2 Delivery DO2 = 1000 mL/min
  • Components of O2 Delivery• Oxygen Content (CaO2) – CaO2 = Hb x SaO2 x 1.34 + PaO2 x 0.003 – Hb or Hemoglobin – SaO2 or Arterial Saturation – Dissolved Oxygen or PaO2 – CaO2 = 20 mL O2/ 100 mL blood (Standard State)• The greatest contributor to oxygen content is the patient’s hemoglobin level!• The least important is the PaO2
  • Oxyhemoglobin Disassociation Curve
  • Components of Oxygen Delivery• Cardiac Output (HR x SV) – Stroke Volume – Heart Rate (Autoregulated and not manipulated) – Greatest overall effect on DO2• Stroke Volume – Preload (preload augmentation) – Afterload Reduction – Contractility (inotropes)
  • Effects of PaO2, Hemoglobin, cardiac output on DO2 (oxygen delivery) FiO2 PaO2 SaO2 Hb (g/dL) C.O. (l/min) DO2(ml/min) %• 0.21 70 96% 13 5.3 900 0• 0.21 45 75% 7 4 288 -68• 0.60 350 98% 7 4 384 +25• 0.60 350 98% 10.5 4 568 +48• 0.60 350 98% 10.5 6 852 +50Increasing cardiac output has the greatest overall effect on DO2
  • Components of Oxygen DeliveryDO2 =[(PaO2 x 0.003 + [Hb x SaO2 x 1.34]) x CO x 10] • Increasing CO has a greater effect because of multiplier effect • Increasing CO is the most effective method of increasing DO2! • Increasing Hb is good but less multiplier effect • PaO2 small effect because of 0.003
  • Components of Oxygen Delivery• Preload Augmentation of Stroke Volume – DO2 (oxygen delivery in mL O2/min) – DO2 = CO x CaO2 x 10 – DO2 = HR x SV x CaO2 x 10 – DO2 = HR x SV x Hb x SaO2 x 13.8
  • Starling Curve Volume Unresponsive preload-independenceStroke Volume Volume Responsive preload-dependence Preload or Left Ventricular End Diastolic Volume (LVEDV)
  • Preload Augmentation s/p fluid bolus Preload RESPONSIVE NormalStroke Volume Abnormal (Cardiogenic or septic shock) 50 mL 100 mL 150 mL 200 mL Preload or LVEDV
  • Preload Augmentation s/p fluid bolus Preload UNRESPONSIVEStroke NormalVolume Abnormal (Cardiogenic or septic shock) 50 mL 100 mL 150 mL 200 mL Preload or LVEDV
  • Starling Curve normal heartStroke volume preload-dependence failing heartHow do you know? preload-independenceLeg RaisePP Variation PCO2TTESVO2CCICardiac US . Preload or LVEDV
  • Cardinal Rules of Critical Care• Myocardial Oxygen Delivery – Coronary blood flow is greatest during diastole – Coronary blood flow is least during systole – Coronary Perfusion Pressure = – Aortic Diastolic Pressure – LVEDP (PCWP) – 80 -12 mm Hg or 68 mm Hg Standard State – Imperatives: increase ADP or Decrease PCWP to improve O2 delivery (i.e. CPR) – SaO2 and SvO2 Factors
  • Cardinal Rules of Critical Care• Minimize oxygen consumption – Sedation analgesia strategy (RASS Score) – Hypothermia, Normothermia and rarely neuromuscular blockade – Work of breathing • Ventilator, NIV, Bronchodilators, Diuresis, Pulmonary toilet, steroids, antibiotics… – Myocardial Oxygen Consumption (Special Case) • Heart Rate, Preload, Afterload, Contractility, Metabolic factors.
  • Cardinal Rules of Critical Care• What is VO2 or Oxygen Consumption? – VO2 = Arterial O2 delivery – Venous O2 delivery – The difference represents the amount of oxygen consumed by the tissues – Normal = 250 mL/min or 5 mL/100 mL blood – Oxygen Utilization Coefficient = 0.25 • SaO2 – SvO2 25%
  • Oxygen Consumption SaO2 = 97%SvO2 = 72%
  • Fick Equation for Oxygen Consumption• VO2= Oxygen Consumption (250 mL/min)• VO2 = 10*C.O.*(CaO2 –CvO2)• VO2 = 10 * C.O. * (1.34*Hgn*SaO2 -1.34*Hgn*SvO2)• VO2 = 1.34*Hgn*10*C.O.*(SaO2 –SvO2)• Solve for SvO2? Or the mixed venous saturation?
  • Four Determinants of Mixed Venous OximetrySvO2 = SaO2 - (VO2 / C.O. x Hgb x 1.34) SvO2 = Mixed venous saturation (%) SaO2 = Arterial oxygen saturation (%) VO2 = Oxygen consumption mL (O2/min) Hgb = Hemoglobin concentration (g/dL) Cardiac Output (C.O.) = dL/min
  • Mixed Venous Saturation• Percentage of hemoglobin saturated with oxygen in mixed venous blood• Flow weight average of the venous saturations from all perfused vascular beds• Four Determinants: – SaO2, VO2, Cardiac Output, and Hb• Physiologic oxygen reserve in times of stress
  • Cardinal Rules of Critical Care
  • Why measure SvO2?• A decrease in SvO2 is an early indicator of a threat to tissue oxygenation• Earlier information results in earlier diagnosis with interventions• Normal range of SvO2 = 60-80%• Critical component of EGDT algorithm
  • PaO2 vs PvO2 in Cardiogenic Shock Arterial Venous Saturation Difference SHOCK
  • Master EquationScvO2 SvO2 = SaO2 - (VO2 / C.O. x Hgb x 1.34)• Acute Illness or Post-op Surgery – SaO2, VO2, Cardiac Output, and Hb are dynamically changing concurrently – Optimize each parameter then recheck ScvO2 to assess response to intervention – Transfusion is critical in EGDT to increase O2 delivery and secondary increase in SvO2
  • Cardinal Rules of Critical Care• Restore Standard State Conditions or Resuscitation Endpoints• What are standard state conditions? – pH = 7.400, PCO2 = 40 mm Hg, [HCO3] = 24.5 mmol/L, SBE = 0 mEq/L, and SID = 39.8 mEq/L – SvO2 > 60%, Lactate < 4 mmol/L – Oxygen DEMAND = Oxygen CONSUMPTION – Multi-organ system recovery
  • Cardinal Rules of Critical Care• Is oxygen consumption adequate for demand? – Lactic acid level > 4 mmol/L and SvO2 < 60% – Increase DO2 and minimize VO2 – Effective endpoints of resuscitation • Continuous Cardiac Index • SvO2 or ScvO2 • Serum lactate (Tissue hypoxia) • Venous – arterial PCO2 – Directly correlates with cardiac index • Metabolic acid-base status (SBE) • Cardiac US
  • Cardinal Rules of Critical Care• Endpoints of Resuscitation – 50% of critically ill patients who present in shock who were resuscitated to normal vital signs continued to have increased lactate and low SvO2 and ScvO2
  • Endpoints of Resuscitation• Conventional Endpoints are lagging indicators of inadequate oxygen delivery – Blood Pressure – Heart Rate – Urine Output – Mental Status Changes – Central Venous Pressure (poor surrogate of filling pressures)
  • More Effective Resuscitation Endpoints • Continuous Cardiac Index – Pulse pressure variation – Systolic pressure variation • SvO2 or ScvO2 • Serum lactate (Tissue hypoxia) • Venous – arterial PCO2 – Directly correlates with cardiac index • Metabolic acid-base status (SBE) • Real time cardiac ultrasound
  • Systolic Pressure Variation
  • Resuscitation Endpoints• A single set of data points is useless – C.I., SvO2, PaCO2-PvCO2, SBE, Lactate• Construct multiple data points to assess trends and response to interventions!• REAL time bedside interventions• Resuscitate each organ system – CNS, Lungs, Heart, GI tract, Skin …
  • Real Time Critical Care US
  • Subxiphoid View:Pulmonary Embolism with dilatedRight ventricleAfter TPA administraton
  • IVC Caliper Measurement as anIndex of preload responsivenessOnly valid in sedated, mechanicallyventilated patientsPreload responsiveness:IVC Caliber change with respirationMechanical ventilation: Inspiratory caliper increases secondary to positive thoracic pressure Expiratory caliper is constantIVC caliper increases in right heartfailure, hypervolemia, or could benormalIVC caliper decreases in hypovolemia
  • REFERENCESCrit Care Clin 26 (2010) 239–253Crit Care Med 2013; 41:580–637Crit Care Clin 27 (2011) 53–76Civetta, Taylor and Kirbys Critical Care, 4thEdition, 2009:Chapter 19, Chapter 26.