9/18/17 Applying Your Data to Affect Your Care: Case Studies in Hemodynamics B. McLean, MN, RN, NP-BC, CCNS-BC, CCRN, FCCM 404-626-2843 Barbaramclean.com [email protected] Introduction Critical care is a concept, not a location, which frequently begins with ED intervention and culminates in ICU admission and continued management – Peter Safar Why the microcirculation is important in shock and why we MUST evaluate it! • where oxygen exchange takes place • plays a central role in the immune function • Plays a central role in insulin resistance • Plays a central role in maintaining vascular tone • During shock : first to go and last to recover 1 9/18/17 Cardiac Function • Function – Continuous propulsion of blood through arteries to capillaries to veins • Right heart circulation • Right heart fills from systemic veins (partially deoxygenated) • Right heart ejects to pulmonary artery (partially deoxygenated) • Left heart circulation • Left heart fills from pulmonary veins (maximally oxygenated) • Left heart ejects to aorta (maximally oxygenated) • Capillaries – microscopic vessels that allow for exchange of gases, nutrients and metabolic waste • Pulmonary capillaries perfuse alveoli, delivering CO2 and taking up Oxygen • Systemic capillaries perfuse tissues, delivering oxygen and taking up CO2 Capillaries • Capillaries – Smallest blood vessels connect arterial outflow and venous return – Microcirculation – flow from metarteriole through capillaries and into postcapillary venule – Exchange vessels – primary function is exchange between blood and interstitial fluid – Lack tunica media and tunica externa • Substances pass through just one layer of endothelial cells and basement membrane – Capillary beds – arise from single metarteriole • Vasomotion – intermittent contraction and relaxation • Throughfare channel – bypasses capillary bed Consider this….. • Patient 1 • Patient 2 – HR: 141 – HR 124 – SaO 92% 2 – SaO2 88% – ScvO 70% 2 – ScvO2 65% Are his tissues oxygenated Are her tissues oxygenated 2 9/18/17 TIME is the TISSUE ! From these two statements three things are obvious Early therapy before mitochondria gets damaged Macro circula7on should be op7mized first! Micro circula7on evaluated and op7mized Target! Preven7ng Mitochondrial injury Your questions????? • Is oxygen delivery adequate for the patient? • Is stroke volume adequate for oxygen consumption? • Is oxygen consumption adequate for oxygen demand? Circulatory shock • Decreased ability of blood flow to meet metabolic demands of the system • Tissue hypoperfusion is the common denominator in all forms of shock • Assuring blood flow and endpoints representing tissue perfusion are the cornerstones of hemodynamics 3 9/18/17 Understanding Tissue Oxygen • Tissue Oxygenation • The single MOST important critical care issue is tissue oxygenation • All physiologic components are designed to maintain balanced tissue oxygen consumption (demand) • Cardiac efficiency is ultimately measured by response to tissues in need of oxygen Oxygen Delivery to Tissues Ventilation O2 Return: Gas exchange Venous Alveoli ScvO2 O2 Delivery: Arterial ATP O2 consumption Cell Why Is Oxygen Important? • Used in cellular respiration – Needed for energy production by cells and tissues 2 ATP Glucose Oxygen KREB’S CYCLE GLYCOLYSIS Pyruvate + ELECTRON TRANSPORT 34 ATP 4 9/18/17 Why Is Oxygen Important? • Used in cellular respiration Da02 is not adequate – Needed for energy productionConsump:on too high by cells and tissues Cannot use it 2 ATP Glucose Oxygen Lactate KREB’S CYCLE GLYCOLYSIS Pyruvate + ELECTRON TRANSPORT 4 ATP Response to Decreased Oxygen Delivery or Increased Oxygen demands • Increased heart rate (compensatory) • Initially increased contractility (compensatory) • Vasoconstriction ( compensatory) • Increased respiratory rate (compensatory) • HGB offloads more oxygen (compensatory) “Hypoperfusion can be present in the absence of significant hypotension.” McLean, FCCS, 4th edition Understanding Tissue Oxygen • Tissue Oxygenation • The single MOST important issue is tissue oxygenation. • All physiologic components are designed to maintain balanced tissue oxygen consumption (demand). • What are the components affecting Oxygen Consumption? – Delivering Oxygen: heart rate x stroke volume (HgB content) – Metabolic demand at the cellular level (lactic acid) – Blood flow through the capillary ( SvO2) – Ability to dissociate oxygen from hemoglobin (SvO2) 5 9/18/17 Managing Tissue Oxygenation OxyHemoglobin ééé OXYGEN ééé Dissociation Delivery OXYGEN Consumpon Critical O2 Delivery The critical value is variable & dependent upon the patient, their disease, I and the metabolic 2 demands at the VO moment CANNOT be measured by S(c)v0 alone!!!! 2 DO2I Oxygen Consumption: At the TISSUES • Balance between delivery and dissociation: availability • Goal: O2 availability > O2 consumption • Adequate O2 delivery may become insufficient if tissue O2 consumption increases! – Fever increases O2 consumption 10% per degree – Agitation can increase O2 consumption by 40% 6 9/18/17 Understanding Tissue Oxygen • Components of Oxygen Delivery • 1. Cardiac Output = Heart rate x stroke volume • 2. Total hemoglobin (02 carrying capacity) • 3. Saturation of hemoglobin • First line compensatory mechanism ( patient) – Increase the heart rate and stroke volume to increase delivery when cells are hyper metabolic and/or when oxygen is not functionally dissociating from its’ transporter, hemoglobin. Understanding Tissue Oxygen • The amount of oxygen required by the cells changes every second – When demand/consumption increases, hemoglobin releases oxygen more rapidly • Shift to the right: release – When demand/consumption decreases, hemoglobin decreases release or latches on to oxygen • Shift to the left: latched on • Second compensatory mechanism: – hemoglobin more aggressively releases oxygen to dissolve in the blood (partial pressure) to be used by the cells Hemoglobin affinity for oxygen is not static + le shi ↓ H Summary ↓ CO2 Hold on ↓ temperature ↓ 2,3 BPG At any PO2 more O2 bound. right shiA ssues At any PO2 less O2 bound. Source Undetermined 7 9/18/17 Understanding Tissue Oxygen • Oxygen dissociation as a compensatory response • Shifts in the bound oxygen mean that there is a change in the way oxygen is – Taken up by the hemoglobin molecule at the alveolar level (Sa02) • Depends on the partial pressure of alveolar gas (PA02) – Released related to the partial pressure of capillary oxygen (Pa02, Pcap02) • Capillary oxygen depends on the tissue oxygen (Pti02) • Tissue oxygen goes down when cells are hypermetabolic and/ or the delivery is inadequate Dissociating Oxygen: rapid shift to right Example Oxygenation Measures SvO2 0.60 -0.80 PA Alveoli ScvO2 LV RV 0.65 -0.85 Systemic Key Point: arteries cell Difference between saturation of arterial versus venous is how much oxygen the cells use. SaO2 0.95 – 1.00 24 8 9/18/17 Central Venous and Mixed Venous O2 Saturation • ScvO2 on CVP monitor • SvO2 on PA catheter • SvO2 is a sensitive but non-specific measure of cardiovascular instability • Although ScvO2 tracked SvO2, 7 ± 4 % higher Targeting Mixed/Central Venous Saturation • normally 70-75% • may be elevated in sepsis – maldistribution of blood flow but – Increasing LA • reduced venous saturation with normal arterial saturation→ increase in O2 extraction – imbalance between VO2 and DO2 – improve supply Targeted ScvO2 • ScvO2 > 70 % reflected adequate oxyhemoglobin BUT not adequate perfusion unless tissue acidosis is absent! • Do not keep ScvO2 too high • Immediate ScvO2 level will be used for the endpoint if it is on lower side • require additional parameters to assess perfusion state 9 9/18/17 The DO2 - VO2 Curve Compensation in attempts to sustain Tissue Oxygen PROBLEM Oxygen delivery inadequate for OXYGEN oxygen demand Primary failure release COMPENSATION: ShiP to the right OXYGEN Release oxygen to save the Delivery cells OXYGEN MEASURE: Demand & Scv02 ↓↓↓↓ Always Compensatory Consumpon Always an EMERGENCY Compensation in attempts to sustain Tissue Oxygen PROBLEM Scv02 normal to ↑↑↑↑ in the face of suspicion (HR↑, RR↑ persistent acidosis (LA)) MUST BE considered as failure to release OXYGEN oxygen (in the presence of ↑↑LA) or to flow the blood Delivery OXYGEN COMPENSATION: Cardiac output increases release Despite increase, :ssue OXYGEN hypoperfusion persists (↑↑LA) Demand & Consumpon 10 9/18/17 Oxycalculations When delivery is inadequate: look to the tissues • Shift to right of oxyhemoglobin dissociation curve: doesn’t matter what Cardiac Output you have measured: – Demand is high – Cardiac Output is poor (relative to demand) – Content of oxygen is low • Oxyhemoglobin dissociation shifts to right: RISK when RELEASE to RIGHT • Cell demands more (éconsumer of oxygen) • éPaO2 needed to provide to cells • êSvO2 to as more oxygen is released to dissolved stae and used When delivery is adequate and cells can utilize oxygen • Shift to left – Demand may be normal – Cardiac Output is adequate (relative to demand) – Content of oxygen is adequate • Oxyhemoglobin dissociation shifts to left: LATCHED on to HgB when LEFT: Lactic acid check • Cell demands less – êPaO2 needed to provide to cells – éSvO2 as less oxygen is released to dissolved state and used by the cells – represents less is needed at cells • Validate with arterial blood gas and absence of acidosis when condition warrants it 11 9/18/17 When delivery appears adequate and cells cannot utilize oxygen • Shift to left – All appears adequate EXCEPT – Patient has acidosis – Patient