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 circulaon should be opmized first! Micro circulaon evaluated and opmized Target! Prevenng 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 productionConsumpon 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 shi 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: Shi 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 is on vasopressors – Patient requires CRRT • Oxyhemoglobin dissociation shifts to left: LATCHED on to HgB when LEFT: Lactic acid check • Cells cannot utilize what has been delivered

– êPaO2 available to provide to cells ( poor blood flow or cellular use failure)

– éSvO2 as less oxygen is released to dissolved state and used by the cells • Validate with arterial blood gas, lactic acid and absence of acidosis

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

Scv02 tells us about compensation, but acidosis measures (LA, BD, PvC02) tell us about adequacy!

12 9/18/17

Why Blood Gas…..

• ABG – Oxygenation – Ventilation – Acid-Base Status • VBG – Ventilation and Acid-Base Status – Cardiac Output (venous arterial PCO2 difference) – Endpoint of resuscitation (ScvO2 and ΔPCO2)

pH for the quick critical care

• If Base Deficit and pH less than perfect • ?patient breathing fast? • Big four questions? All answered from chemistry….. – Ketosis ( glucose) – Acute kidney injury (Cr) – Hyperchloremia (CL-) – Lactic acidosis (assumed)

Base Excess or Deficit

What does it mean? • Buffer/Base: A substance that can bind or release H+ ions in solution, thus keeping the pH of the solution relatively constant despite addition of large amounts of acid or base. • Calculated to reflect anions and cation relationship • Positive value, excess base, less H+, metabolic acidosis • Negative value, excess acid, less base, metabolic alkalosis • Metabolic component of acid-base status

• PCO2 independent

Read more about it Unmeasured anions idenfied by the Fencl-Stewart method predict mortality beer than base excess, anion gap, and lactate in paents in the pediatric intensive care unit. Balasubramanyan, Napa; MD, MRCPI; Havens, Peter; Hoffman, George

Crical Care Medicine. 27(8):1577-1581, August 1999.

13 9/18/17

Blood Gas Report(Arterial)

• pH (No Units) 7.35-7.45

• PaCO2 (mm Hg) 35-45

• PaO2 (mm Hg) 110 - 0.5(age) • HCO3- (mmol/L): calc 22-26 • B.E(mmol/L) -2 to 2

• O2 saturation: calc >90%

Blood Gas Report (mixed/central venous)

• pH 7.32-7.42

• PvCO2 40 - 50 (mm Hg)

• PvO2 36 - 42 (mm Hg) • Oxygen Saturation > 70% • Base Excess -2 to +2

Venous Arterial CO2 Difference

• Circulatory Failure – Associated with Tissue Hypercarbic Acidosis – Hypovolemia, sepsis, shock … • Cardiac Index = Endpoint of Resuscitation

14 9/18/17

Intensive Care Med (2008) 34:2218–2225 DOI 10.1007/s00134-008-1199-0 ORIGINAL

Fabrice Valle´e Benoit Vallet Central venous-to-arterial carbon dioxide Olivier Mathe difference: an additional target Jacqueline Parraguette Arnaud Mari for goal-directed therapy in septic shock? Stein Silva Kamran Samii Olivier Fourcade Miche`le Genestal

2 Received: 26 October 2007 Abstract Objective: To test the 2.7 ± 0.8 l/min/m , P \ 0.0001) but Conclusion: Accepted: 6 June 2008 In hypothesis ICU- that, inresuscitated resuscitated septic not for ScvO2 paents, values (78 ± 5 vs. Published online: 8 July 2008 shock patients, central venous-to- 75 ± 5%, P = 0.07). From T0 to targeng Ó Springer-Verlag 2008 only ScvO2 arterial carbon may dioxide difference not be T12, thesufficient clearance of lactate was to Electronic supplementary material The [P(cv-a)CO2] may serve as a global significantly larger for the Low gap online version of this article index of tissue perfusion when the group than for the High gap group guide (doi:10.1007/s00134-008-1199-0 therapy) contains. central When venous oxygen the saturation 70% (P \ ScvO2 0.05) as well as the goal- decrease of supplementary material, which is available (ScvO ) goal value has already been SOFA score at T24 (P \ 0.01). At to authorized users. 2 reached. Design: Prospective T0, T6 and T12, CI and P(cv-a)CO2 values were inversely correlated value is reached, the presence of a P(cv-a)CO2 F. Valle´e O. Mathe J. Parraguette observational study. Setting: A A. Mari ÁS. Silva K.Á Samii Á 22-bed intensive care unit (ICU). (P \ 0.0001). Conclusion: In ICU- larger than 6 mmHg might be a useful tool to O. FourcadeÁ M. GenestalÁ Á Patients: After early resuscitation resuscitated patients, targeting only Poˆle d’AnestheÁ ´sie et Re´animation, in the emergency unit, 50 consecutive ScvO2 may not be sufficient to guide Unite´ de Re´animation Polyvalente de septic shock patients with therapy. When the 70% ScvO2 goal- Purpan, GRCB 48, Universite´ Paul Sabatier, ScvO2 [ 70% were included imme- value is reached, the presence of a idenfy paents who sll remain inadequately CHU de Toulouse, France diately after their admission into the P(cv-a)CO2 larger than 6 mmHg ICU (T0). Patients were separated in might be a useful tool to identify B. Vallet patients who still remain inadequately resuscitated. Poˆle d’Anesthe´sie et Re´animation, Low P(cv-a)CO2 group (Low gap; Hoˆpital Huriez, Universite´ Lille II, n = 26) and High P(cv-a)CO2 group resuscitated. CHU de Lille, France (High gap; n = 24) according to a threshold of 6 mmHg at T0. Mea- Keywords Venous CO2 ScvO2 Á Á F. Valle´e()) surements: Measurements were Lactate Septic shock Á Á Re´animation polyvalente adulte, performed every 6 h over 12 h (T0, Goal-directed therapy Cardiac index Hoˆpital Purpan, Place du Dr Baylac, TSA Á 40031, 31059 Toulouse Cedex 9, France T6, T12). Results: At T0, there was e-mail: [email protected] a significant difference between Low Tel.: +33-561-772288 gap patients and High gap patients for Fax: +33-561-772170 cardiac index (CI) (4.3 ± 1.6 vs.

Introduction ScvO2 appears to be a strong indicator of the balance between O2 demand and supply. In ICU-resuscitated The early haemodynamic management of septic shock patients however, ScvO2 or mixed venous oxygen satu- patients has recently been codified [1]. Rivers et al. show ration (SvO2)[3, 4], is often larger than 70% in spite of that an early optimisation (within the very first 6 h of evidence of abnormal tissue oxygenation. This oxygen treatment) targeting central venous oxygen saturation extraction defects might be related to severe microcircu- (ScvO2) and general haemodynamic parameters improved latory disorders [5] and/or mitochondrial damage and/or outcome in septic shock [2]. At the onset of septic shock, impairment of cellular respiration [6] resulting in most of

Comparison of rPCO2 and SvO2 • Key Points :

• SvO2 may reflect the metabolic rate and oxygen consumption

• rPCO2 and/or serial lactate levels and clearance may reflect the adequacy of tissue perfusion • AG, Bicarb, BASE reflect adequacy of tissue perfusion

Consider this…..

• Patient 1 • Patient 2 – HR: 141 – HR 124 – SaO 88% – SaO2 92% 2 – ScvO 65% – ScvO2 70% 2 – Base deficit -10 – Base deficit -2 – pH 7.30 – pH 7.39

Are his tissues oxygenated Are her tissues oxygenated

15 9/18/17

Lactate What does it mean? • LA levels represent balance between production and clearance • Increased production (anaerobic glycolysis) – Tissue hypoperfusion – Tissue dysoxia – Tissue dysmetabolism • Reduced metabolism – Hepatic and Renal • May be altered in critical illness • Increased glycolytic flux • Impaired pyruvate utilization • Absence of frank O2 deprivation • Clearance trend over time • Best predictor of anaerobiosis and hyperlactic acidemia is critical PvO2 of 27 mmHg

Lactate clearance as a target

Lactate clearance as a target

16 9/18/17

Laboratory Analysis

Chem Scene 1 Scene 3 Scene 5 Coag Scene 7 Scene 8 BUN 23 35 38 PTT 44.7 26.5 Cr 1.2 2.7 2.8 PT >80 35.9

C02 22 11 8 7.7 3.1 Bicarb calc INR Na 134 137 131 K+ 4.2 5.3 4.5 5.0 5.2

A/G 27 29 34 41

LA > 14 Ø 14 Ø 16 >20

BD - 4 - 8 -12 -15 -16

SCv02 60 45 20 78 81

Consider this…..

• Patient 1 • Patient 2 – HR: 141 – HR 124

– SaO2 92% – SaO2 88%

– ScvO2 70% – ScvO2 65% – Base deficit -10 – Base deficit -2 – LA 4.1 – pH 7.39 – pH 7.30 – Do you even need a lactate?

Are his tissues oxygenated Are her tissues oxygenated

Goal of shock resuscitation

• Reverse of hypotension (macro) • Clinically well perfused • Adequate tissue perfusion and oxygenation (micro) • NO MATTER WHAT, no-one and nothing stops you from investigating what your patient presents with!

17 9/18/17

Consider this…..

• Patient 3 • Patient 4 – HR: 141 – HR: 124 – CVP: 14 – CVP: 18 – U/O 0.2 ml/kg/ for 4 hours – U/O 0.1 ml/kg/ for 4 hours – AP: 102/41/ MaP 61 – AP: 98/65/ MaP76

Does he have volume? Does she have volume?

So what should we do?

• Focus on stroke volume • A means to an end • Always about tissue oxygenation

Our goal is to….

Heart Cardiac Stroke rate Output volume

beats L/ ml/ /min min beat

18 9/18/17

Stroke Volume (SV) and Stroke Volume Index: • Stroke Volume – Volume of blood that is ejected during systole – SV = end diastolic volume (EDV) – end systolic volume (ESV) – Normal: 60 to 100 ml/beat – Max SV: 120 to 200 ml/beat, depending on size, heredity, and conditioning • Stroke Volume Index – Stroke index is defined as the amount of blood ejected per beat indexed to BSA • Normal: 25 to 35 ml/m2

55

What do you think? 1

What do you think 2?

19 9/18/17

Even with your favs….

SvO2 can overpredict…..

20 9/18/17

Questions

• A 50- year-old male with myocardial ischemia presents with the following: – HR 141 BPM – CO 6 .2 L/min – SV 43 ml SV 43 – BP 128/68 MAP 88 mmHg SVO2 51% – SVO2 51% – BD: –10 – LA: 4.1 Is the stroke volume – pH; 7.28 adequate? – CVP 10 mmHg – PAWP 16 – SaO2 94% • Is the cardiac output for his tissue is adequate ?

Questions

• Question 5 – Same patient after treatment with fluid 30 ml/kg his numbers are as follow: – HR 100 BPM – CO 5.1L/min – MAP 84 mmHg – PAWP 13 mmHg

– SVO2 61% (reduction in metabolic acidosis) – BD -5 SV 51 – CVP 7 mmHg – SaO2 95% SVO2 61% Is the stroke volume • Is he better or worse ? adequate?

Resuscitation end points

Macro circulation Micro circulation • Lactate < 2 mmol/L • CVP 8–12 mm Hg: • SCVO2 > 70% in the absence • (MAP) >=65 mm Hg despite normal vital sign Tissue of signs or symptoms of acidosis • Urine output >=to 0.5 mL/kg/hr • normal Gap

• SCVO2(superior vena cava) hypoperfusion >=70% • SV >40 ml/beat • CO to supply tissue oxygenation can persist can persist

21 9/18/17

Even with the ‘best’ parameters it is not always easy to make the right decision.………

“The First Concern”

“the first concern in any life-threatening illness is to maintain an adequate supply of oxygen to sustain oxidative metabolism”

[Marino 4th edition)

Hemodynamic Profiles M Pinsky. Functional hemodynamic Monitoring. Current Opinion Critical Care 2007;13:318

Capillary Arterial Stroke flow constricti Volume on

LOW total volume, LOW flow Hypovolemic

High venous volume, Cardiogenic LOW flow

High arterial volume, High flow Septic Occlusion to perfusion Compensated Septic High venous volume, Decompensate LOW flow d

22 9/18/17

Case 1 4 months PTA Cardiac Catheterization • LV mildly dilated • LA severely dilated • Aortic valve mildly regurgitant • Mitral severely regurgitant and mildly stenotic • Tricuspid valve mildly regurgitant • Pulmonary venous volume and pressure overload (pulmonary HTN) • EF 55 to 60% • Recommendation: valvular replacement

Case 1 4 months PTA Cardiac Catheterization • Procedure – Mechanical valve replacement of both aortic and mitral valve – TEE performed – Enlarged the aortic arch (expanded with dacron patch) – Transferred to the SICU

Case 1 4 months PTA Cardiac Catheterization Wound Check status post Valve repair • Patient: – C/O Feels sick, coughing with frothy sputum – DIB – Mid-sternal chest pressure – Bilateral leg swelling, abdominal swelling • Physician – INR : 2.4 – Wounds good – Volume overloaded – RUQ pain – Atrial fibrillation vs atrial flutter, RVR 137 • Admit to telemetry for cardioversion

23 9/18/17

Case 1

Time/ Scene 1 Date

BPS 110

BPD 83

MaP 94

HR 135

RR 22

Temp undoc

Sa02 94%

12 Lead ECG Afib, Pre-Cardioversion

Patient 3, Scene 2 12 Lead ECG Afib, Post-Cardioversion

24 9/18/17

Patient 3, scene 3

• Progressively deteriorating • Requiring fluids and vasopressors from RRT

Case 1

Time/ Scene 2 Date Progressively deteriorang

BPS 81 Requiring fluids and vasopressors from RRT

BPD 52 What do you need? MaP 60 What do you think? Why can’t we assess her SaO2? HR 62

RR 29

Temp 35.6

Sa02 Unable to assess

Unaware……

• nurse note 744 AM • Hypovolemic ? – Physician notified regarding HR and BP – Patient confused • Cardiogenic ? – Cold extremities appears to be in shock • Septic ? – Request made for ICU bed • physician note 0910 AM • Distributive ? – Cardiogenic shock • Cold, BP 80/50 • Minimal UOP – Our ? Dehydration vs renal • Obstructive ? failure • Patient acidotic and Cr trending up – Patient will likely require inotropes

25 9/18/17

Prior to downfall: cont • Consider vasodilation but BP is 80/50 – ? Volume status • Echocardiogram shows EF 15% (down from 55 to 60%) • Class IV cardiogenic shock noted • ICU, STAT!

Admission to MICU

• Immediate transfer to MICU – Unable to obtain BP, could not feel pulse – Right central line (Scv02, CVP) placed – placed within 15 minutes – Femoral arterial line placed shortly after – Treatment based on the pressure monitored (venous with abnormal waves: severe TR)

ECG gets better or worse…?

26 9/18/17

Vital Signs Scene/ Scene 5 Scene 6 Scene 7 Scene8 measure BPS 80 93 161 82 BPD 59 66 86 57 BPM 64 71 104 64 HR 82 99 100 142 RR 22 30 35 38 Temp 38.1 cold Sa02 .99 1.0 1.0 .84 Scv02 40% 58% 70% 30%

CVP 10 12 21 19

Simulated Central Venous Waveform in Tricuspid Regurgitation: Large V wave

27 9/18/17

Case 1

• Nurse adds FloTrac transducer • Discusses therapy with physician • ABG results – 78 – 54 – 7.12 – BD -10 – LA 6.1

The tale of pressure: times are estimate 2/21 1330 1400 1430 1500- 1630 2050 2/22 1530 0726 dopamine ------15 max 20mcgm mcgms

levophed 30 mgm/ 30 mgm/ cont ----- max 30 mgm/ kg/min kg/min kg/min peripher al epinephrine 1 mgm 10 max 10 mcgms/ mcgms/ min min vasopressin 0.04 0.04 units/min units/min

phenylephrine 200 max 400 mcms/ min Bicarbonate 150 mls 150 drip per hour

dobutamine 10 mcgm/ kg/min milrinone 0.375 mcg/ ------0.503 kg/min

FFP 4 units

Signs of Organ Hypoperfusion

• Base Deficit • Wide anion gap • Low, normal or high Sv02 • Lactic Acidosis • Mental Status Changes • Oliguria

28 9/18/17

Case 2

• 57 male, underline DM • Conscious disturbance, fever • RR 32 HR 123 BT 38.7 BP 70/40 mmHg • pH 7.1; HCO3- :12 • WBC 8900, Band 22% • Hb 10.4 • Lactate > 12

Case 2

SCVO2 : 49% • CVP 8 cm H2O • SBP 73 mmHg • Lactate > 12 • Glucose 950

2 hours later

29 9/18/17

4 hours

• BP 93/40 mmHg • Glucose 280

• SCvO2 62 • Lactate 5 • CVP 11

• Keep fluid/ vasopressor/ insulin

6 hours

• BP 92/60 mmHg • Glucose 180

• SCvO2 72 • Lactate 1.8 • CVP 13 • Goal achieved • Survive at 30 days

When a problem comes along….

640-730 1140

wbc 14.8 neutrophils 91% PT 17.4 13.4 INR 1.7 1.3 HgB 8.8 10.2 platelets 205 169 fibrinogen 157 192

30 9/18/17

You must fix it….

640-730 1400

Na 140 141 K 4.2 4.5

C02 6 14 glu 60 168 BUN 15 17 Cr 1.99 2.24 Albumin 2.5 2.9 Anion Gap 34 30 Ca 6.7 6.8

4/25 530a 7-8

4/25 530a 7-8 4/25Sa02 530a 7-8 964/25 530a 7-8

Pa02 90 61 75Sv02 67 35 8044 CI / 3.2 PaC02 56 62 F 63 73 50 Volume pH 6.68 6.89 7.24 Dopa 13 14 Lactate 17.2 16.4

Levo 80 70 HC03 8 10 12 12 15 21 Rally pack/ 360 BE/BD -29 -23 -23Bicarb -21 -18 -7 HFOV .9 HgB 8.2 35 5 Sa02 83 91BPS 88 79 48 7989

Sv02 60 78BPD 74 42 42 4074

CI 4.7 6.4HR 5.7 1704.9 1104.2

7-8 a 8-9 9-10 11-12 12-1 5 6 7p

Sa02 98 88 93 83 88 75 43 89

Sv02 88 84 74 60 72 --- 31 72

CI / 4.4 5.3 4.7 6 --- 4.9 4.5

Volume 2100 2200 2300 230 2400 300 350

Dopa 10 14 15 15 15 13 13 13

Levo 45 45 45 Epi 4 6 off Bicarb

FFP Endo 3600 HFOV 1.0 tool BPS 98 100 110 118 105 105 110 130

BPD 47 49 55 50 58 70 60 64

HR 88 92 95 100 98 118 122 125

31 9/18/17

The Biggest Issue is Oxygen

• Validate with Sv02 • Validate with venous to arterial C02 • Validate with GAP! – > 20

• Validate with total serum C02 • Validate with ABG/base deficit • Validate with serial lactic acid levels – Lac-time

32 9/18/17

Fix it good….The Goal of Hemodynamic Monitoring • Tissue perfusion – Blood flow – Cardiac funtion – Cellular measures – ScV02, SV02, regional oxygen measures • Assure adequate volume and stretch • KNOW your endpoints, define them clearly and strive to achieve! “Excellence is to do a common thing in an uncommon way.” Booker T. Washington

Key Points: Stroke Volume is just the beginning! • Watch the gap

• Observe serum C02 • Arterial blood gas • Monitor lactate clearance • Be aware it is a late measure, not immediate

• Immediate measure Sv02 • Marry LA and AG

Thank you…for all you do!

B. McLean, MN, RN, NP-BC, CCNS-BC, CCRN, FCCM https://ekc.box.com/v/cookeville 404-626-2843 barbaramclean.com [email protected]

33