Current Concepts in ICU Management

Barbara McLean, MN, RN, CCRN, CCNS-BC,NP-BC, FCCM Division of Critical Care
Grady Hospital System, Emory University

bamclean@mindspring.com www.barbaramclean.com

Check this patient!

Compromised Host Fever / hypotension Cultures obtained Antibiotics given Adequate volume resuscitation

3 L fluid given CI = 6 CVP= 17 HR 135 RR 31

ETC02 23 PaC02 24 Pa02 84 Fi02 1.0 ACMV

BP 70/30 SVV 19% pH 7.28

And now.
Patient is now hypotensive and tachycardic What do you do next?
Hetastarch Dobutamine Norepinephrine Amrinone PRBCS Dopamine

What is it.?
First - Recognize type of shock
CI = 6 Hb = 10.5 g/dL CVP = 17

Second find appropriate treatment

norepinephrine (not dopamine) through a central catheter as soon as available is the first-choice vasopressor agent to correct hypotension in septic shock
Critical Care Medicine: 2013 Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock: Update

Why identify patients at risk?

Easier management with simpler interventions an ounce of prevention. Prevent further deterioration Provide time for investigation and treatment

Determine your goals!

The Present and Future

Is the balance of oxygen delivery and oxyhemoglobin dissociation adequatetissue needs?
No

Global Venous O2 AG, Lactate

Is oxygen delivery sufficient?

SV Measurement Adequate oxygen carryng (HgB)
Not much

No

Are the individual tissues getting the oxygen they need?

Tissue O2 Microcirculation

Volume status-would it help to give fluid? What type?

SVV, PPV, SPV EVLWI

Volume response to treatment? Appropriate tissue oxygenation?

And in Sepsis? Using our language correctly

Definitions
The Continuum
SIRS Sepsis Severe Sepsis Septic Shock

SIRS- It All Starts Out So Innocent

Systemic Inflammatory Response Syndrome
Manifested by 2 or more of the following Clinical pressentations:
Temperature > 38C (100.4F) or < 36C (96.8F) Heart Rate > 90 per minute (contextual) RR > 20/min or PaCO2 < 32 mm Hg

And validated by 1 or more of the following lab results

WBC 12,000 or >10 % bands Increased PCT Members of the American College of Chest Physicians/Society of Crit Care Med Consensus Conference Committee: American College of Chest Physicians/Society Positive cultures
of Crit Care Med Consensus Conference: Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med 1992; 20: 864874

Definition - Sepsis
Sepsis
SIRS PLUS a documented infection
Positive CXR Positive U/A Cellulitis /Abscess Positive Blood Culture

Identifying Acute Organ Dysfunction as a Marker of Severe Sepsis

Respiratory
PaO2/FiO2 200 if lung only dysfunction/site of infection PaO2/FiO2 250 with other organ dysfunction/lung not site of infection

Cardiovascular
Tachycardia SBP<90mmHg MAP < 70mmHg (despite fluid) Need for Vasopressors

Renal
UO <0.5 ml/kg per hr (despite fluid)

Metabolic
Unexplained metabolic acidosis Lactate > 1.5 times upper normal

Hematologic
Platelets <80,000/mm3 Decline in platelet count of 50% over 3 days

Severe Sepsis: Defined

Severe Sepsis- Sepsis with evidence of organ dysfunction What is organ dysfunction?
Respiratory- PaO2/FiO2 Ratio < 300 Hepatic- Bilirubin > 4 Hematologic- INR >1.5 or Platelets <100 K Neurologic- GCS 10-12 Renal- Creatinine >2.0 Lactic Acid- Greater than 4

Definition Septic Shock

Septic Shock
Severe sepsis with persistent hypotension (refractory to fluid bolus) or: Acute circulatory failure in an infected patient not explained by another cause . Significant vasodilation is primary cause of hypotension .
Not fluid responsive May not respond to vasopressors

The Sepsis Continuum: FIRST, identify

SIRS Sepsis

Severe Sepsis

Septic Shock

A clinical response arising from a nonspecific insult, with 2 of the following: T >38oC or <36oC HR >90 beats/min RR >20/min WBC >12,000/mm3 or <4,000/mm3 or >10% bands

SIRS with a presumed or confirmed infectious process

Sepsis with organ failure

Refractory hypotension

Chest 1992;101:1644.

Therapy Across the Sepsis Continuum Severe Sepsis Septic Shock

SIRS

Sepsis

Early Goal Directed Therapy

Antibiotics, Source Control, VOLUME!!!!

Now what?
Xigris (hrAPC)
Steroids in vasopressor ??? resistant shcok

SIRS

Sepsis

Severe Sepsis

Septic Shock

Insulin and tight glucose control

???

Early Goal Directed Therapy

???

Antibiotics and Source Control

Surviving Sepsis Campaign 2013

Guidelines for Management of Severe Sepsis and Septic Shock

Dellinger RP, et al. Crit Care Med 2004; 32:858-873.

What to do..?
Single most important issue is failure to identify!
Guidelines, scoresheets, protocols NEVER take the place of clinical assessment, history and gut feeling

STAT.fluids, cultures, antibiotics and source control

Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. NEngl J Med 2001; 345:1368-1377 Kollef MH, Sherman G, Ward S, et al. Inadequate antimicrobial treatment of infections: a risk factor for hospital mortality among critically ill patients. Chest 1999; 115:462-474
18

The McLean-Piedmont Method

Question?
If we recognized Possible Sepsis Early, treated IMMEDIATELY with fluids, could we reduce mortality rate? Reduce Mortality by 20% system wide
Sepsis most frequent diagnosis associated with mortality system-wide.

McLean Model Sepsis: MEWS

What do these patients have in common?

Patient 1 HR 127 RR 34 Pa02 70 PaC02 23 Fi02 1.0 PEEP 12 Rate 20 ACMV BPS 80 BPD 55 Patient 2 133 28 91 PaC02 35 0.70 PEEP 15 Rate 15 SIMV BPS 80 BPD 40 Patient 3 113 18 100 PaC02 39 0.5 PEEP 20 Rate 10 SIMV BPS 100 BPD 60

Monitoring MEWS

EGDT

Sepsis resuscitation: 2013 guidelines

In the event of hypotension or lactate > 4 mmol/L (36 mg/dL)
a. Deliver an initial minimum of 30 mL/kg of crystalloid (or colloid equivalent) b. apply vasopressors for ongoing hypotension

In the event of persistent hypotension despite fluid resuscitation or lactate > 4 mmol/L (36 mg/dL)
a. achieve central venous pressure of > 8 mmHg b. consider dynamic fluid endpoints. !!!!! b. achieve central venous oxygen saturation of > 70% !!!!!!

Vasopressors: Target MAP of 65 mm Arterial catheter placement as soon as feasible . Norepinephrine

(Levophed) -1st choice Vasopressin 0.03u/min - 2nd choice or Epinephrine 2nd agent
Surviving Sepsis Campaign Management Guidelines Committee. Crit Care Med 2013

 Emerging data show that the choice, timing and amount of fluid therapy may affect clinical outcomes Early administration of fluid therapy in sepsis may improve survival Later fluid therapy in acute lung injury patients will increase the duration of ventilator dependence without achieving better survival

Why do we give volume

Volume expasion for hemodynamically unstable patients

Increase stroke volume (SV) and cardiac output (CO) Only 50% of patients respond to a fluid challenge Cumulative fluid balance may affect outcome Whether the patient is responsive to fluid or not? Optimal strategy of increasing CO and oxygen delivery

Perel et al. Critical Care 2013, 17:203

The administration of a fluid bolus is done frequently in the perioperative period to increase the cardiac output. Yet fluid loading fails to increase the cardiac output in more than 50% of critically ill and surgical patients.

Cheatham ML. Crit Care Med 2007; 35:1629-30

The Surviving Sepsis Campaign emphasizes the use of CVP as a resuscitation end-point, as suggested by the work of Rivers et al. Traditional CVP cannot be used to accurately direct resuscitation of the critically ill patients with elevations in IAP or ITP.

To do so places the patient at risk for underresuscitation with resultant organ dysfunction, failure, and increased mortality.

Cumulative fluid balance and mortality

Fluid resuscitation in septic shock: A positive fluid balance and elevated central venous pressure are associated with increased mortality. Crit Care Med 2011 Vol. 39, No. 2; John H. Boyd, Jason Forbes, MD; Taka-aki Nakada, Keith R. Walley,
James A. Russell,

retrospective review of the use of intravenous fluids during the first 4 days of care. Patients: The Vasopressin in Septic Shock Trial (VASST) study enrolled 778 patients who had septic shock and who were receiving a minimum of 5 ug of norepinephrine per minute.

A more positive fluid balance both early in resuscitation and cumulatively over 4 days is associated with an increased risk of mortality in septic shock.

Central venous pressure may be used to gauge fluid balance <12 hrs into septic shock but becomes an unreliable marker of fluid balance thereafter.

Why do we need dynamic fluid measures

Pulse Pressure Variation

Pulse pressure variation (PPV)
Calculated in the same manner as SVV, Also predict preload responsiveness well.

A 13% PPV predicts a 15% increase in CO for a 500mL volume bolus ANY signal that gives pulse density REQUIRED
Controlled variables
Ventilation Preisman S, Berkenstadt H, Perel A: Predicting fl uid responsiveness Kogan Heart S, rate
in patients undergoing cardiac surgery: functional haemodynamic parameters including the Respiratory Systolic Variation Test and static preload indicators. Br J Anaesth 2005, 95:746-755.

Pulse Pressure Variation

PPV = 32%

PPV = 5%

What I use for confirmation

Transducer which connects to existing A-line No calibration method required

How I use arterial based cardiac output

Unstable?

Volume resuscitation Vasopressors SV and arterial Cardiac output

Unstable on mechanical ventilation?

Assist-control

Fixed PR interval
P/F unstable

Patient unstable
SVV, SV and arterial based cardiac output

Hemodynamic Variables

*P < 0.05

Responder: SV increase of > 10% after fluid challenge Only MAP was different at baseline (higher in non-responders)

Lansdorp B, et al. Br J Anaesth. 2012;108(3):395-401.

Hemodynamic Variables

*P < 0.05

Lansdorp B, et al. Br J Anaesth. 2012;108(3):395-401.

Dynamic Variables
PPV SPV SVV

*P < 0.05

Responders and non-responders have different dynamic values at baseline Adjusting for TV improves predictive value of PPV, SPV, and SVV Passive leg raising test may be preferable with cardiac arrhythmia

Lansdorp B, et al. Br J Anaesth. 2012;108(3):395-401.

What do these patients have in common?

Patient 1 HR 127 RR 34 Pa02 70 PaC02 23 Fi02 1.0 PEEP 12 Rate 20 ACMV BPS 80 BPD 55 PP 25 SVV 16% Patient 2 133 28 91 PaC02 35 0.70 PEEP 15 Rate 15 SIMV BPS 80 BPD 40 PP 40 SVV 21% Patient 3 113 18 100 PaC02 39 0.5 PEEP 20 Rate 10 SIMV BPS 100 BPD 60 PP 40 SVV 15%

What are the Limitations of SVV?

Mechanical Ventilation
Currently, literature supports the use of SVV on patients who are 100% mechanically (control mode) ventilated with tidal volumes of more than 8cc/kg and fixed respiratory rates.

Lose their predictive value under conditions of

varying R-R intervals (atrial fibrillation), tidal volume varies from breath to breath (with assisted and spontaneous ventilation)

Spontaneous Ventilation
Currently, literature does not support the use of SVV with patients who are spontaneously breathing.

Arrhythmias
Arrhythmias can dramatically affect SVV. Thus, SVVs utility as a guide for volume resuscitation is greatest in absence of arrhythmias. Updated algorithms actually filter out beat to beat variability related to dysrhythmia (except sustained dysrhytmias for > 20 secs)

McLean Method Heart Rate

IOS
Volume
PPV SVV SV U/O ml/kg Echo SV (CV) 02 Oxyhemoglobin Dissociation P/F pPlat

Respiratory Rate

Cardiac
SV SVV PPV Systolic pressure Echo Oxyhemoglobin Dissociation P/F pPlat

Vascular Tone
PPV SVV PPV/SVV Diastolic pressure Echo Oxyhemoglobin Dissociation P/F pPlat

Tissue
Oxyhemoglobin Dissociation ,Anion Gap, Serum C02, Base, pH, Ketones

What about other information?

With a thermodilution, transpulmonary system, it is possible to calculate and index:
Intrathoracic blood volume Pulmonary vascular permeability index
Increased capillary permeability during the first 48 h in patients with sepsis was associated with a higher mortality rate during the intensive care unit (ICU) stay than those with decreased permeability 1, 2

1. Hotchkiss RS, Karl IE (2003) The pathophysiology and treatment of sepsis.N Engl J Med 348: 138150. 2. Abid O, Sun Q, Sugimoto K, Mercan D, Vincent JL (2001) Predictive value of microalbuminuria in medical ICU patients: results of a pilot study. Chest 120:19841988.

What about other information?

With a thermaldilution, transpulmonary system, it is possible to calculate and index:
Global end diastolic volume Extravascular lung water
Measurements of extravascular lung water (EVLW) correlate to the degree of pulmonary edema and have substantial prognostic information in critically ill patients. normal EVLW (defined as < 10mL/kg)
Martin GS, Eaton S, Mealer M, Moss M. Extravascular lung water in patients with severe sepsis: aprospective cohort study. Crit Care 2005;9:R74 R82. Kuzkov VV, Kirov MY, Sovershaev MA, et al. Extravascular lung water determined with single transpulmonary thermodilution correlates with the severity of sepsis-induced acute lung injury. CritCare Med 2006;34:16471653. [ Groeneveld AB, Verheij J. Extravascular lung water to blood volume ratios as measures of permeability in sepsis-induced ALI/ARDS. Intensive Care Med 2006;32:13151321. Patroniti N, Bellani G, Maggioni E, Manfio A, Marcora B, Pesenti A. Measurement of pulmonary edema in patients with acute respiratory distress syndrome. Crit Care Med 2005;33:25472554.

Transpulmonary vs. Pulmonary Artery Thermodilution

Transpulmonary TD (EV 1000, PiCCO)

Pulmonary Artery TD (PAC)

Aorta

Pulmonary Circulation central venous bolus injection

Lungs

PA RA
PULSIOCATH
arterial thermodilution catheter

LA

Right Heart

Left heart

RV

LV

Body Circulation

In both procedures only part of the injected indicator passes the thermistor. Nonetheless the determination of CO is correct, as it is not the amount of the detected indicator but the difference in temperature over time that is relevant!

Why do we need EVLWI

Diagnosis Prognosis Goal to aggressive therapy Better guide to resuscitation in patients at risk for pulmonary edema (anyone with high permeability index)
Shock or severe sepsis ALI CHF

Monitoring of EVLW Pfeiffer UJ et al. Practical applications of fiberoptics in critical care monitoring. 1990, pp. 114-125 Boldt J. Crit Care Med 2002:6:52-59 Sakka SG et al. Intensive Care Med 2000;26:180-187

LPS

OA

Clinical examination, X-ray, CT, blood Gravimetry gases Thermodilution techniques:

thermo-dye dilution, single transpulmonary thermodilution

Fluid challenge is a technique in which large amounts of fluids are administered over a limited period of time under close monitoring to evaluate the patients response and avoid the development of pulmonary edema.

More than 50% of the patients with severe sepsis but without ARDS have increased EVLW, possibly representing sub-clinical lung injury.

Fluid and Hemodynamic Management

Starling Equation
- Kf capillary filtration coefficient - PIF interstitial hydrostatic pressure - pc capillary colloid osmotic pressure

Qf = Kf [(Pc- PIF) s(pc pIF)]

- Pc capillary hydrostatic pressure - s oncotic reflection coefficient - pIF interstitial colloid oncotic pressure

Pathophysiology:
Increases in capillary hydrostatic pressure Increased membrane permeability Diminished oncotic pressure gradient

Clinical implications:
Reductions in pulmonary capillary hydrostatic pressure/pulmonary artery occlusion pressure CVP Hemodynamic monitoring to avoid tissue hypoperfusion Fluid restriction/negative fluid balance Diuretics Combination therapy with colloids and furosemide?

Mortality as a function of EVLW. Patients were classified into four groups according to their highest EVLW value.

Sakka S G et al. Chest 2002;122:2080-2086

2002 by American College of Chest Physicians

Relationship between pulmonary hydrostatic pressure and lung edema formation under normal conditions and increased permeability.

Calfee C S , Matthay M A Chest 2007;131:913-920

2007 by American College of Chest Physicians

Cardiac Output Optimization Concept

EVLW Stroke Volume
Large increase in EVLW for small increase CO

OptimalPreload

Preload
0 0

Cardiac Ouput Maximization

EVLW as a quantifier of lung edema

ELWI = 19 ml/kg

Extravascular lung water index (ELWI) normal range: 3 7 ml/kg

ELWI = 7 ml/kg

ELWI = 14 ml/kg

ELWI = 8 ml/kg

Relevance of EVLW Assessment

The amount of extravascular lung water is a predictor for mortality in the intensive care patient
Mortality (%)
100 90 80 70 60 50 40 30

Mortality(% ) *p = 0.002 n = 373

n = 81
80 70 60 50 40 30

20
10 0 4 - 6 6 - 8 8 - 10 10 - 12 - 16 16 - 20 > 20 12 0 <7 0 n = 45 7 - 14 n = 174 14 - 21 n = 100 > 21 n = 54

20

ELWI (ml/kg)

Sturm J in: Lewis, Pfeiffer (eds): Practical Applications of Fiberoptics in Critical Care Monitoring, Springer Verlag Berlin - Heidelberg - NewYork 1990, pp 129-139

ELWI (ml/kg)
Sakka et al , Chest 2002

Relevance of EVLW Assessment

Volume management guided by EVLW can significantly reduce time on ventilation and ICU length of stay in critically ill patients, when compared to PCWP oriented therapy, Ventilation Days
n = 101 * p 0,05

Intensive Care days

* p 0,05

22 days PAC Group

9 days EVLW Group

15 days PAC Group

7 days EVLW Group

Mitchell et al, Am Rev Resp Dis 145: 990-998, 1992

Extravascular lung water in sepsis-associated acute respiratory distress syndrome: indexing with predicted body weight improves correlation with severity of illness and survival. Phillips CR; Chesnutt MS; Smith SM Critical Care Medicine. 36(1):69-73, 2008 Jan. Figure 3. Receiver operator characteristic curves for extravascular lung water indexed to predicted body weight (EVLWp), dead space-tidal volume fraction (Vd/Vt), extravascular lung water (EVLW), and Pao2/Fio2 for mortality with sensitivity vs. 1-specificity for identification of nonsurvivors. The areas under the curves were 0.988 +/- 0.019, 0.869 +/- 0.112, 0.851 +/0.113, and 0.643 +/- 0.137 for EVLWp, Vd/Vt, EVLW, and Pao2/Fio2, respectively.

2008 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins.

EVLW predicting mortality

Extravascular lung water indexed to predicted body weight is a novel predictor of intensive care unit mortality in patients with acute lung injury. Craig TR; Duffy MJ; Shyamsundar M; McDowell C; McLaughlin B; Elborn JS; McAuley DF Critical Care Medicine. 38(1):114-20, 2010 Jan. Figure 2. Receiver operator characteristic (ROC) curves for extravascular lung water indexed to predicted (EVLWp) and actual body weight (EVLWa) for mortality. The area under the curve (95% confidence interval [CI]) for EVLWp (0.8; CI, 0.6-0.9) was larger than for EVLWa (0.7; CI, 0.5-0.9), but there was no statistically significant difference between these two areas (p = .12).

2010 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins.

EVLW as Predictor

Extravascular lung water indexed to predicted body weight is a novel predictor of intensive care unit mortality in patients with acute lung injury. Craig TR; Duffy MJ; Shyamsundar M; McDowell C; McLaughlin B; Elborn JS; McAuley DF Critical Care Medicine. 38(1):114-20, 2010 Jan. Figure 1. A, Actual extravascular lung water (EVLWa) is increased in non-intensive care unit (ICU) survivors compared with ICU survivors. The median EVLWa was 16.4 (10.8-21.8) for non-ICU survivors and 10.5 (8.7-14.5) for ICU survivors *p = .0278 Mann-Whitney U test. B, predicted extravascular lung water (EVLWp) is increased in non-ICU survivors compared with ICU survivors. The median EVLWp was 17.5 (15.3-21.4) for non-ICU survivors and 10.6 (9.5-15.4) for ICU survivors. *p = .0029 Mann-Whitney U test.

2010 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins.

What am I looking for?

Indices of hypovolemia: SVV > 13% volume loading should decrease SVV. If not
Stop fluid administration Inotropic support initiated

Are the pulse analysis techniques as accurate as the PAC for monitoring CO?
Yes, (level of evidence, C) but it depends.
Not all monitors are the same. In stable patients they perform to a clinically acceptable level and have other advantages.
Continuous data Less invasive Offer other variables.

In shocked patients the evidence is less clear.

A. Rhodes , personal communication ESICM 2010

What is the arterial tone? Hypotension Relationship between PPV/SVV Better relationship of elastance /vascular tone than SVR No assumption regarding volume distribution Physics calculation
PP reflects variance SV more regarding EF

PP/SV normal 1.2-2

What is the arterial tone? Hypotension, volume responsiveness PP/SV normal 1.2- 1.5
< 0.9 indicates vasoconstriction, SVV > 13%
Volume

< 0.9 indicates vasoconstriction, SVV<13%

Inotrope /vasodilator Volume

> 1.5 indicates vasodilation, SVV>13%

Volume vasopressor

Pinsky, personal communication ESICM 2011

Variation from Ventilation

SVV, PPV, and SPV are created by tidal volumeinduced changes in venous return. presumes a constant R-R interval and are measured from diastole to systole + pressure ventilation causes changes in venous return, which is accentuated in hypovolemic patients take advantage of the swings in venous return in order to determine the fluid responsiveness of hypotensive patients

Perfusion Index
Perfusion Index, or PI, is a relative assessment of the pulse strength at the monitoring site. PI display ranges from .02% (very weak pulse strength) to 20% (very strong pulse strength). Perfusion Index is a numerical value that indicates the strength of the IR (infrared) signal return- ing from the monitoring site.

Crit Care Med. 2002 Jun;30(6):1210-3. Use of a peripheral perfusion index derived from the pulse oximetry signal as a noninvasive indicator of perfusion.

..the variation of the peripheral perfusion index in healthy adults and related it to the central-to-toe temperature difference and capillary refill time in critically ill patients after changes in clinical signs of peripheral perfusion. Poor peripheral perfusion was defined as a capillary refill time >2 secs and central-to-toe temperature difference > or = 7 degrees C. Peripheral perfusion index and arterial oxygen saturation were measured by using the Philips Medical Systems Viridia/56S monitor. The distribution of the peripheral perfusion index was skewed and values ranged from 0.3 to 10.0, median 1.4 (inner quartile range, 0.7-3.0).

Crit Care Med. 2002 Jun;30(6):1210-3. Use of a peripheral perfusion index derived from the pulse oximetry signal as a noninvasive indicator of perfusion.

A cutoff peripheral perfusion index value of 1.4 best reflected the presence of poor peripheral perfusion in critically ill patient Changes in peripheral perfusion index and changes in core-to-toe temperature difference correlated significantly (R =.52, p <.001).

Use of a peripheral perfusion index derived from the pulse oximetry signal as a noninvasive indicator of perfusion Alexandre Pinto Lima, MD; Peter Beelen, RN; Jan Bakker, MD, PhD

Changes in the peripheral perfusion index reflect changes in the core-to-toe temperature difference. Therefore, peripheral perfusion index measurements can be used to monitor peripheral perfusion in critically ill patients. (Crit Care Med 2002; 30:1210 1213)

Perfusion Index
Saturation

Infrared Red

What is a Normal PI ?
108 healthy, 37 critically ill adults (finger sensors) PI range: 0.3% to 10%, median 1.4% ROC used to determine the cutoff value 1.4% PI best discriminated normal from abnormal

Lima, et al. CCM 2002

Clinical Uses for PI

Normals have been suggested to be:
>1.4% adults, >1.27% neonates

Site selection (varies between patients and sites) Chorioamnionitis (placental membrane/amniotic fluid infection) Effectiveness of Servoflorane anesthesia Monitor onset/effectiveness of epidural anesthesia Predict illness severity scores (good correlation) Monitor/quantify peripheral perfusion Detect shock states PI trend may best reflect changes in condition

Clinical Uses for PI

Below 1.4, PI indicates poor perfusion The PI is unique for each patient and the trend is what is important!

EGDT

SVV PI PLR

Sepsis resuscitation: 2013 guidelines

Serum lactate measured Blood cultures obtained before antibiotics administered Improve time to broad-spectrum antibiotics 45 mins Initial empiric therapy include 1 or more drugs with activity against ALL likely pathogens (bacterial and or fungal or viral) Reassessed daily to optimize activity, prevent development of resistance, reduce toxicity, and reduce costs

Surviving Sepsis Campaign Management Guidelines Committee. Crit Care Med 2013

Diagnosis
Before the initiation of antimicrobial therapy, at least two blood cultures should be obtained
At least one drawn percutaneously At least one drawn through each vascular access device if inserted longer than 48 hours

Other cultures such as urine, cerebrospinal fluid, wounds, respiratory secretions or other body fluids should be obtained as the clinical situation dictates Other diagnostic studies such as imaging and sampling should be performed promptly to determine the source and causative organism of the infection Weinstein MP. Rev Infect Dis 1983;5:35-53
may be limited by patient stability
Blot F. J Clin Microbiol 1999; 36: 105-109.

Therapeutic Strategies in Sepsis

Optimize Organ Perfusion
Expand effective blood volume. Hemodynamic monitoring. Early goal-directed therapy.
16% reduction in absolute risk of in-house mortality. 39% reduction in relative risk of in-house mortality. Decreased 28 day and 60 day mortality. Less fluid volume, less blood transfusion, less vasopressor support, less hospital length of stay.

2013 Guideline: Small Changes

Early antibiotics Aggressive fluids
Colloids and crystalloids

Levophed, Epinephrine and vasopressin Glucose control at BS 190 x 2 Corticosteroids 200-300 continuously Use of dynamic measures for fluid resuscitation Dobutamine moves up the ladder

What about this one.?

64 year old with severe sepsis (not septic shock) Infection
Acute onset fever, chills, cough RML and RLL infiltrates

SIRS Criteria
Tachycardia, tachypnea, leukocytosis with shift

Organ dysfunction
Renal, pulmonary

Hypotension
NOT refractory to fluid bolus (yet)

What next?
In addition to continuing fluids and antibiotics, which of the following will you recommend now?
Methylprednisolone in supraphysiologic doses Hydrocortisone in physiologic doses Hydrocortisone and fludrocortisone in physiologic doses No corticosteroids

Corticosteroids in Sepsis: refractory hpotension **first measure the serum lactate

Look for cryptic shock

Physiologic doses
Replacement Stress dose

Pharmacologic doses
Anti-inflammatory

Why do we need ScV02?

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 of Oxygen Consumption?
Oxygen delivery Metabolic demand at the cellular level Blood flow through the capillary Ability to dissociate oxygen from hemoglobin

Understanding Tissue Oxygen

Tissue Oxygenation There are two mechanisms designed to meet oxygen consumption (demand)
Increase oxygen delivery Increase the release (dissociation) of oxygen from hemoglobin

In the best of critical situations, both delivery and dissociation increase to maintain cells failure of one mechanism will be supported by compensation by the other

Managing Tissue Oxygenation

OxyHemoglobin
Dissociation

OXYGEN Delivery

OXYGEN Consumption

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.

Is cardiac output responsive to intravascular fluid loading? Assumes that venous return and LV preload are the primary determinants of cardiac output (Starlings Law of the Heart) Assumes low LV end-diastolic volume (EDV) equals preload-responsiveness Attempts to assess EDV through surrogate measures
CVP, Ppao, LV end-diastolic area, RV EDV, intrathoracic blood volume

Sepsis management: 2013

Dobutamine
patients with cardiac dysfunction (filling pressures, cardiac output OR clinical signs of hypoperfusion after restoration of BP with volume resuscitation Do NOT use strategy to increase Cardiac index to predetermined supranormal level

Surviving Sepsis Campaign Management Guidelines Committee. Crit Care Med 2013

Aortic pulse wave

Systolic pressure

Pressure [mmHg]

120

100

Average pressure

80

1 second

Diastolic pressure

Pulse pressure = systolic pressure - diastolic pressure

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

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

Venous Oxygenation Patterns

Sv02 Scv02

Pv02

Oxygenation Patterns with Normal Function

Alveoli

Sv02 :0.6 0.8

RV

LA LV Cell Sa02 :0.95 1.0

RA

Scv02 :0.65- 0.85

Managing Tissue Oxygenation

OxyHemoglobin
Dissociation

OXYGEN Delivery

OXYGEN Consumption

Compensation in attempts to sustain Tissue Oxygen

OXYGEN release
COMPENSATION: Shift to the right Release oxygen to save the cells MEASURE: Scv02 Always Compensatory Always an EMERGENCY

PROBLEM Oxygen delivery inadequate for oxygen demand Primary failure

OXYGEN Delivery
OXYGEN Demand & Consumption

Compensation Oxygenation

Sv02 Scv02 Low Pv02

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 (in the presence of LA)

OXYGEN Delivery

OXYGEN release OXYGEN Demand & Consumption

COMPENSATION: Cardiac output increases Despite increase, tissue hypoperfusion persists (LA)

Targeting Mixed Venous Saturation few studies have specifically targeted resuscitation to a mixed venous saturation of >70% prospective, randomized trial in adults:
treatment to a mixed venous saturation >70% did not reduce mortality compared with therapy targeting a normal CI (Gattinoni et al NEJM 1995)

Measuring Oxygen
mixed venous oxygen saturation (SvO2) balance between systemic oxygen delivery and consumption during treatment of critically ill patients central venous oxygen saturation (ScvO2) reflects degree of oxygen extraction from brain and upper part of body beneficial effects on patient outcome by continuous measurement
Rivers et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. NEJM 2001; 345:13681377

Monitoring Venous Oxygenation

ScvO2 is usually less than SvO2 by about 23% but two change in parallel In septic shock ScvO2 often exceeds SvO2 by about 8% -correlation between these two parameters may worsen ScvO2/SvO2 should not be used alone in assessment of cardiocirculatory system

But
Sa02 is pre-cell reservoir: 95-100% Sv02 is global post cell left over: 60-80% Scv02 is partial (upper extremities) post cell left over: 65-85%

Tissue Oxygenation
overwhelmed compensatory mechanisms and low SvO2 tissue hypoxia and lactate ----Vincent JL, De
Backer D. Oxygen transport the oxygen delivery controversy. Intensive Care Med 2004; 30:19901996

drop in SvO2 or ScvO2 does not necessarily mean tissue hypoxia occurs!

What do these patients have in common?

Patient 1 HR 127 RR 34 Pa02 70 PaC02 23 Fi02 1.0 PEEP 12 Rate 20 ACMV BPS 80 BPD 55 Sv02 45% AG 34 LA 6.1 PP 25 SVV 16% Patient 2 133 28 91 PaC02 35 0.70 PEEP 15 Rate 15 SIMV BPS 80 BPD 40 Sv02 70% AG 41 LA 7.2 PP 40 SVV 21% Patient 3 113 18 100 PaC02 39 0.5 PEEP 20 Rate 10 SIMV BPS 100 BPD 60 Sv02 65 AG 13 LA 2.8 PP 40 SVV 15%

Case Demonstration
57 male, underline DM Conscious disturbance, fever RR 32 PR 123 BT 38.7 BP 70/40 mmHg One touch: high pH 7.1; HCO3- :12 WBC 8900, Band 22%, CRP: 9 Hb 10.4 Lactate > 12

 CVP : 7 cm H2O

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

What do these patients have in common?

Patient 1 Patient 2 Patient 3

HR 127
RR 34 Pa02 70 PaC02 23 Fi02 1.0 PEEP 12 Rate 20 ACMV BPS 80 BPD 55 PI 0.6 (1.5) Sv02 45%

133
28 91 PaC02 35 0.70 PEEP 15 Rate 15 SIMV BPS 80 BPD 40 PI 1.2 (3.4) Sv02 70%

113
18 100 PaC02 39 0.5 PEEP 20 Rate 10 SIMV BPS 100 BPD 60 P! 2.2 (6.3) Sv02 65

EGDT

SVV PI PLR

Scv02 tells us about compensation, but acidosis measures tell us about adequacy!

The Oxygenation Profile

Acid-Base Disturbances Are common in critical patients May be complex or mixed Are often confusing Requires accurate analysis to facilitate appropriate treatment

Focus on Metabolic Acidosis

The Oxygenation Profile

Chemistry Profile Overview Facilitates evaluation of tissue metabolism or renal failure
Total serum C02 (direct measure of reserve serum buffer and is used to calculate bicarbonate) Serum blood glucose Serum ketones Lactic acid : chemistry special laboratory

Facilitates evaluation of problem and compensation

The Oxygenation Profile

Cells: Producer
Produces acid during metabolism: acid transported as carbonic acid Tissue acids increase in insulin deficiency states Tissue acids increase in tissue hypoxia states Acidosis: acid (H+) uptake in exchange for potassium release provides buffer effect and promotes intracellular hypokalemia Alkalosis: acid (H+) release in exchange for potassium uptake provides buffer effect and promotes intracellular hyperkalemia

Kidney: Regulator Major volume and electrolyte regulator Acid regulator Base regulator

Cells: Regulate pH

Lung: Acid regulator Rate and depth of breaths depends on the carbonic acid and therefore the pH

The Oxygenation Profile Direct Effects from Acid : Presence or Absence pH: directly reflects acid
When acid goes up, pH goes down Acids are formed as end products of protein, carbohydrate, and fat metabolism. To maintain the bodys normal pH (7.35-7.45), the H2C03 must be controlled:
H+ must be neutralized (buffer and cells) or excreted (requires renal function) C02 must be regulated via ventilation
115

The Oxygenation Profile

Components of the ABG and Chemistry Panel that are indicators in acid-base balance/imbalance. pH | pCO2 | pO2 | O2 Sat| (H+)HC03| Base| Total CO2

Direct measure of acid Inversely reflects acid (estimates one of the major buffers)

Response to increase in acid H+ and related acid pH

H+ pH C02

mL/DL

Acid content

mmHg

Response to increase in acid H+ and related acid pH

H+ pH

C02

mL/DL

Acid content

mmHg

Response to increase in acid H+ and related acid pH

H+ pH C02

mL/DL

Acid content

mmHg

Response to increase in acid H+ and related acid pH

H+ pH

C02

mL/DL

Acid content

mmHg

Compensation in attempts to sustain Tissue Oxygen

Sv02 Normal to High With Persistent Lactic Acidosis

Cells do not need it! OR Cells need it but cannot get it!

Pv02

Anion Gap
If Metabolic acidosis is present, is anion gap wide (> 20)?
Calculate the anion gap (AG). If the anion gap is 20, there is a primary metabolic acidosis regardless of pH or serum bicarbonate concentration. The acidosis is due to increased H+ Gap is generally wide only with metabolic ACID production ( Lactic Acid/ Ketoacid)

Principle: The body does not generate a wide anion gap as a compensatory mechanism for a primary disorder. With a wide AG, metabolic acidosis is ALWAYS the primary disorder!

Anion Gap
Anion gap is a concept used to estimate electrolyte (anions & cation) levels in the serum and {measures or estimates the , sic} conditions that influence them (Tabers Cyclopedic Medical Dictionary, 2005). Normal Anion Gap = (Na+) - (Cl- + HCO3-) = 12 (+/- 2) Positive charged ions and negative charged ions are relatively equal in normal physiology. In vivo physiology all equal! The measured ions (lab analysis) are represented by Na+, Cl- and HC03- (or total serum C02), the external measured gap of 12 (+/- 2) is considered acceptable

Na+

(Cl - + HCO3 -)

Anion Gap
Anion Gap = (Na+) - (Cl- + HCO3-)

When there is an increase in unmeasured ions, there will be a gap between the + and measures A gap of > 20 implies a metabolic increase in acid production. Lactic Acid and Ketoacid donate H+ . H+ binds to HC03 and/or Cl changing the charge HC03 and/or Cl The gap between + and gets wide
(Cl - + HCO3 -) : light on the negatives

(Lactic acid or ketones donated H+) heavy on the positives Na+ constant

Anion Gap
Used to confirm type of metabolic acidosis with ABG Used to diagnose metabolic acidosis without ABG Affected by:
albumin (for each 1 gm decrease in albumin , add three points to gap) hyperchloremia (usually from fluid resuscitation)
High Cl- causes decrease in available HC03 High Cl- binds to H+ HCl Cannot compensate because is not a compound that can be blown off Metabolic acidosis with normal gap: non-gap acidosis most commonly occurs in hyperchloremia

EGDT

SVV PI PLR

Base Bicarb AG

So what about lactate?

Lactate Levels
The other acid: Lactate Levels Lactic acid is a product of carbohydrate metabolism.
It is normal to produce 15 to 20 mmol/kg of lactic acid per day. The normal plasma level is 0.5 to 1.5 meq/L
Hyperlactatemia is considered to be present if the level exceeds 4 to 5 meq/L. Lactic acidosis is considered to be present if the elevated lactate level is in conjunction with a gap >20 in the absence of elevated glucose /ketosis.

Lactic acid is rapidly buffered by extracellular bicarbonate resulting in lactate. The liver and kidneys convert lactate back to pyruvate which is then converted to CO2 & H2O or glucose.

Lactate Levels
Is serum Lactate a good marker of adequacy of perfusion?
Type A lactic acidosis primarily results from an imbalance between tissue oxygen demand, delivery and use. The blood lactate level in type A lactic acidosis is related to the total oxygen debt and the magnitude of tissue hypoperfusion.

Elevated blood lactate levels associated with metabolic acidosis are common among critically ill patients with systemic hypoperfusion, tissue hypoxia and metabolic dysfunction. Blood lactate levels also increase with clearance failure , i.e., kidney or liver dysfunction

Lactate Levels
Utility of a single high initial lactate have been debated
poor sensitivity and specificity

Lactate clearance is a better predictor of mortality

Lac-time: time it takes to clear 10% of lactate Time to clear < 24 hours , improves survival in Severe sepsis Lac-time also directly correlated with number of organ failures

One lactate (lactic acid ) level is not as predictive or evaluative as a series over 24 hours ( i.e., Q6H)
1. 2. Bakker, J., Coffernils, M., Leon, M., Vincent, J.L. (1991). Blood lactate levels are superior to oxygen-derived variables in predicting outcomes in human patient shock. Chest, 99, 956-962. Bakker, J., Gris, P., Coffernils, M., Kahn R.J., Vincent, J.L. (1996). Serial blood lactate levels can predict the development of multiple organ failure following septic shock. Am J Surg, 171(2), 221-226. Nguyen, H.B., Rivers, E.P., Knoblich, B.P., et al. (2004). Early lactate clearance is associated with improved outcome in severe sepsis and septic shock. Crit Care Med, 32(8), 1637-1642.

3.

LACTIC ACID TABLE

What do these patients have in common?

Patient 1
HR 127 RR 34 Pa02 70 PaC02 23 Fi02 1.0 PEEP 12 Rate 20 ACMV BPS 80 BPD 55 Sv02 45% AG 34 LA 6.1

Patient 2
133 28 91 PaC02 35 0.70 PEEP 15 Rate 15 SIMV BPS 80 BPD 40 Sv02 70% AG 41 LA 7.2

Patient 3
113 18 100 PaC02 39 0.5 PEEP 20 Rate 10 SIMV BPS 100 BPD 60 Sv02 65 AG 13 LA 2.8

EGDT

SVV PI PLR

Base Bicarb AG LA

A-V PCO2 Gradient (DPCO2)

Can the PCO2 gradient between arterial and venous blood gas samples (DPCO2) represent adequacy of perfusion?

A-V PCO2 Gradient (PCO2)

PCO2 = PvCO2 PaCO2 The PCO2 is an index to identify the critical oxygen delivery point (VO2/DO2). The critical oxygen delivery point is when consumption (VO2) is dependent on delivery (DO2)

A-V PCO2 Gradient (PCO2)

critical oxygen delivery point is associated with an abrupt increase of blood lactate levels and a significant widening in PCO2 Since CO2 is 20x more soluble in aqueous solutions than O2, it is logical that PCO2 may serve as an excellent measurement of adequacy of perfusion.

Comparison of PCO2 and SvO2

Key Points : SvO2 may reflect the metabolic rate and oxygen consumption PCO2 and/or serial lactate levels and clearance may reflect the adequacy of tissue perfusion

Definitions of ETC02
Capnometry is the measurement of expired CO2 and provides a numeric display of CO2 tension in mm Hg or % CO2 Capnograph is the measuring instrument Capnography is the graphic representation of expired CO2 over time Capnography End-tidal CO2 concentration is close to arterial PaCO2 levels Inversely Indicates the adequacy of alveolar ventilation Capnogram is the waveform displayed by the capnograph

PaCO2 vs. PeTCO2

PaCO2= Partial Pressure of Carbon Dioxide in arterial blood gases The PaCO2 is measured by drawing the ABGs, which also measure the arterial pH

If ventilation and perfusion are stable PaCO2

should correlate to PetCO2

Capnograms Normal
Zero baseline Rapid, sharp uprise Alveolar plateau Well-defined end-tidal point Rapid, sharp downstroke
A B B C C D D DE Deadspace Dead space and alveolar gas Mostly alveolar gas End-tidal point Inhalation

Interpretation of ETCO2
Excellent correlation between ETCO2 and cardiac output when cardiac output is low. When cardiac output is near normal, then ETCO2 correlates with minute volume. Only need to ventilate as often as a load of CO2 molecules are delivered to the lungs and exchanged for 02 molecules.

Clinical applications
Endotracheal intubation Etiologies of hypocapnea/hypercapnea Cardiopulmonary resuscitation Respiratory problems V/Q mismatch

Capnography & Pulse Oximetry

CO2:
Relects ventilation Detects apnea and hypoventilation immediately Should be used with pulse oximetry

O2 Saturation:
Reflects oxygenation 30 to 60 second lag in detecting apnea or hypoventilation Should be used with capnography

ACLS: Waveform Capnography

After intubation, exhaled carbon dioxide is detected, confirming tracheal tube placement. Highest value at end-expiration.

2010 American Heart Association. All rights reserved.

ETCO2 & Cardiac Resuscitation

Non-survivors
Average ETCO2: 4-10 mmHg

Survivors (to discharge)

Average ETCO2: >30 mmHg

ETCO2 & Cardiac Resuscitation

If patient is intubated and pulmonary ventilation is consistent with bagging, ETCO2 will directly reflect cardiac output Flat waveform can establish PEA
Increasing ETCO2 can alert to return of spontaneous circulation

Configuration of waveform will change with obstruction

Capnograms Normal
Zero baseline Rapid, sharp uprise Alveolar plateau Well-defined end-tidal point Rapid, sharp downstroke
A B Deadspace BCDead space and alveolar gas C D Mostly alveolar gas D End-tidal point DE Inhalation of CO2 free gas

Physiology
Relationship between CO2 and RR
RR CO2 RR CO2 Hyperventilation Hypoventilation

What is this?

What is this?

ABNORMALITIES
Gradual Hyperventilation Decreasing temp Gradual in volume Sudden increase in ETCO2 Sodium bicarb administration Release of limb tourniquet Gradual increase Fever Hypoventilation Increased baseline Rebreathing Exhausted CO2 absorber

USES
Metabolic
Assess energy expenditure

Cardiovascular
Monitor trend in cardiac output Can use as an indirect Fick method, but actual numbers are hard to quantify Measure of effectiveness in CPR Diagnosis of pulmonary embolism: measure gradient

PULMONARY USES
Effectiveness of therapy in bronchospasm
Monitor PaCO2-PetCO2 gradient Worsening indicated by rising Phase III without plateau

Find optimal PEEP by following the gradient. Should be lowest at optimal PEEP. Can predict successful extubation.
Dead space ratio to tidal volume ratio of >0.6 predicts failure. Normal is 0.33-0.45

Limited usefulness in weaning the vent when patient is unstable from cardiovascular or pulmonary standpoint Confirm ET tube placement

Circulation and Metabolism Capnography Is A Direct Measurement Of Ventilation Indirectly Measures Metabolism And Circulation Increased Metabolism : Increase The Production Of Carbon Dioxide: Increasing The PetC02 Decrease In Cardiac Output Lowers Pulmonary Perfusion: Decrease Delivery Of Carbon Dioxide To The Pulmonary Capillaries: Results In Decrease The PetC02

V/Q Mismatch If ventilation or perfusion are unstable, a Ventilation/Perfusion (V/Q) mismatch can occur Alters the correlation between PaC02 and PetCO2 V/Q mismatch can be caused by blood shunting
atelectasis (perfusing unventilated lung area) dead PE or Hypovolemia

PetCO2 Values Ventilation

Normal 30 45 mmHg
(PaC02 within 10 mmHg)

HypoPerfusion
ETC02 is significantly lower than PaC02 PaC02 high

Hypoventilation > 45 mmHg Hyperventilation < 35 mmHg Pay close attention!

Ventilation Perfusion Match

Critically ill patients often have rapidly changing dead space and V/Q mismatch Higher rates and smaller TV can increase the amount of dead space ventilation High mean airway pressures and PEEP restrict alveolar perfusion, leading to falsely decreased readings Low cardiac output will decrease the reading
MUST compare blood and exhaled C02

CO2 Physiology a-ADCO2

Normally 2-3mmHg. Adults < 10 mmHg Widened if
Incomplete alveolar emptying Poor sampling High VQ abnormalities (normal 0.8), seen with PE, hypovolemia, arrest, lateral decubitus

Decreased with shunt

a-ADCO2 small Causes:
Atelectasis, mucus plug, right mainstem ETT

PaCO2-PetCO2 gradient
PetCO2 is usually less Difference depends on the number of underperfused alveoli Decreased cardiac output will increase the gradient The gradient can be negative when healthy lungs are ventilated with high TV and low rate

Case in point PetC02 = 20 mmHg Hypoventilation is assumed PaC02 is 76 mmHg What is the gradient? Is ventilation the problem? Is perfusion the problem?

The conventional view serves to protect us from the painful job of thinking.

John Kenneth Galbraith (1908-2006)

Limited Role of Pulse Oximetry in Assessing Ventilation

Normal SaO2 determined by PaO2 If patient hypoventilates, PaCO2 increases and will drive PaO2 downward in direct proportion to PaCO2 increase
If PaCO2 increases by 10, PaO2 will decrease by 10 If PaO2 is 90, will decrease to 80 mm Hg
SaO2 will decrease from 98 to 97.

Oximeter is not sensitive to rises in PaCO2 When oxygen therapy is added or increased, rise in PaCO2 is completely obscured

Capnography & Pulse Oximetry

CO2:
Relects ventilation Detects apnea and hypoventilation immediately Should be used with pulse oximetry

O2 Saturation:
Reflects oxygenation 30 to 60 second lag in detecting apnea or hypoventilation Should be used with capnography

Why Capnography versus Pulse Oximetry? Capnography provides an immediate picture of patient condition (EWS) Pulse oximetry is delayed Capnography will show immediate apnea, while pulse oximetry continue measuring a saturation for several minutes

Case Example of Limited Role of Oximetry in Hypoventilation

PaO2
SpO2 FIO2 PetCO2 pH

95
.98 RA 39 7.38

80
.96 RA 54 7.25

99
.98 .30 60 7.23

A 56 year old man admitted to the outpatient procedure area for a follow-up colonoscopy. The patient had a colonoscopy 3 years earlier where a pre cancerous polyp was removed. During this procedure, the physician elects to use Propofol instead of Midazolam due to its more rapid elimination and shorter recovery time. Twenty minutes into the procedure, you note the PetCO2 listed below. What would your actions be based on this information?
P RR BP SpO2 PetCO2

Admission

72

12

132/72

100

37

5 minutes into procedure

76

10

128/70

100

42

20 minutes into procedure

73

10

134/78

100

48

A 76 year old female is being weaned from mechanical ventilation. He has a mainstream CO2 analyzer in his ventilator circuit. Fifteen minutes into the weaning attempt, the following information is available. Based on this information, what would you do?

P
0730 (weaning initiated) 0745 71

RR
15

BP
130/86

SpO2
98

PetCO2

35

82

19

128/88

97

51

A 73 year old man is on your unit with the diagnosis of CHF and COPD. He has been improving and is expected to be discharged tomorrow. He is on oxygen therapy at 4 LPM and is simultaneously be monitored by capnography via the nasal cannula, sidestream method. At 0300, you hear the CO2 alarm and go into investigate. He is difficult to arouse. The following information is available to you. What would your actions be based on this information?

0100 0200

87 79

14 10

138/82 134/84

95 97

31 33

0300

83

10

138/78

95

59

Final Case.
Case 4 A 44 yr old male admitted to MICU with unknown fever, SOB, hypoxemia. pH 7.34, PaCO2 38, PaO2 44, SpO2 .78. He is intubated, IMV 12/44. Extubates himself, is reintubated. Sedation is increased. RR decreases to 12. .What is the effect of sedation on ventilation?
Pulse Pre extubation Extubated 114 102 RR 44 38 NIBP 132/64 138/60 SpO2 98 97 PetCO 2 34 33 Meds 2 mg Midazolam, 50 mcg/Fentanyl 5 mg bolus Gtt to 4 mg Midazolam, Gtt to 100 mcg/Fentanyl

Post 76 reintubation and sedation

12

128/88

99

47

Now a case.

ARDSnet
ARDSNet ventilation
RR 35, Vt = 5ml/kg PBW plateau pressure ~ 33
PaO2/FiO2 62 with 18 PEEP 100% O2

APRV
PaO2/FiO2 86

Vitals..
Fluid balance Blood Pressure
HR + 3.7 liters 135/80 95 128 10 mmHg 82/38

CVP
FiO2 Urine output

1.0
60ml/hr 0ml

PaO2/FiO2

82

Hypotension, tachycardia, high normal CVP, hypoxemia, fluid long

What would you do? Fluid load, decreased urine output, high normal CVP in shock Vasopressors? Inotropes? Fluids?

Transpulmonary thermodilution measurements

CI SVRI GEDVI SVV EVLWI 2.7 L/min/m2 825 dyne.cm.sec-5/m2 550 ml/m2(800-1000) 18-20% (13%) 19 ml/kg

= = = = =

Septic, dry but with severe pulmonary edema

Gave 500 ml bolus of NS

MAP = 55 mmHg CVP = 10mmHg CI = 3.2 L/min/m2 SVRI = 950 dyne.cm.sec-5/m2 GEDVI = 625 ml/m2(800-1000) SVV = 16% (13%) EVLWI = 19 ml/kg No change in lung water so given 2 additional boluses

Next..
MAP = 58 mmHg CVP = 11mmHg CI = 4.1 L/min/m2 SVRI = 985 dyne.cm.sec-5/m2 GEDVI = 825 ml/m2(800-1000) PPV = 12- 13% (13%) EVLWI = 21 ml/kg
At the time fluid was stopped and low dose norepinephrine was started.

12 hours later on norepinephrine

MAP = 76 mmHg CI = 4.1 L/min/m2 SVRI = 1250 dyne.cm.sec-5/m2 Fluid balance + additional 3.2 liters in ARF GEDVI = 1100 ml/m2(800-1000) PPV = 9% (<13%) EVLWI = 22 ml/kg PBW

Diuresis was started with furosemide

EVLW

CO

Large decrease in EVLW for small decrease preload

Preload

The Case for Measuring EVLW in ARDS Can drown with only 200-300 ml extra lung water Want to know precisely what is happening to lung water with resuscitative and therapeutic interventions CXR, oxygen need, severity of injury LIS, are imprecise determinates of the amount of pulmonary edema No correlation to PaOP, CVP or fluid balance with lung water

The case for measuring EVLW EVLW predicts mortality in ARDS EVLW predicts progression to ALI in patients at risk EVLW driven protocols only approach shown to improve mortality

Patient 2 Patient 3 What do these patients have in common? Patient 1 HR 127 RR 34 133 28 123 21

Pa02 70 PaC02 23 Fi02 1.0 PEEP 12 Rate 20 ACMV

BPS 80 BPD 55 Sv02 45% AG 34 LA 6.1 SVV 16% EVLWI 11% / SV 62 Would you give fluid? What type Post fluid EVLWI 13%/ SV 75/ SVV 12%

91 PaC02 35 0.70 PEEP 15 Rate 15 SIMV

BPS 80 BPD 40 Sv02 70% ( levo 10 mgms) AG 41 LA 7.2 SVV 21% EVLWI 15% /41 Would you give fluid? What type Post fluid EVLWI 16%/64/SVV 16%

100 PaC02 39 0.5 PEEP 20 Rate 10 SIMV

BPS 80 BPD 60 Sv02 58 AG 23 LA 4.8 SVV 15% EVLWI 17%/ 41 Would you give fluid? What type? Post fluid 22%/ 40/SVV 14%

How I use arterial based cardiac output

Volume resuscitation Vasopressors SV and arterial Cardiac output

Assist-control

Unstable and P/F decreasing +/- ACS

Unstable?

Unstable on mechanical ventilation?

Fixed PR interval
P/F unstable Patient unstable SVV, SV and arterial based cardiac output

Central line, femoral arterial line with sensor Continuous arterial based cardiac output

Intemittent Iced injectate for EVLW

The Present and Future

Is the balance of oxygen delivery and oxyhemoglobin dissociation adequatetissue needs?
No

Global Venous O2 AG, Lactate

Is oxygen delivery sufficient?

SV Measurement Adequate oxygen carryng (HgB)
Not much

No

Are the individual tissues getting the oxygen they need?

Tissue O2 Microcirculation

Volume status-would it help to give fluid? What type?

SVV, PPV, SPV EVLWI

Volume response to treatment? Appropriate tissue oxygenation?

Physiological Truth
There is no such thing as a Normal Cardiac Output Cardiac output is either
Adequate to meet the metabolic demands Inadequate to meet metabolic demands

Absolute values can only be used as minimal levels below which some tissue beds are under perfused

Conclusions Regarding Different Monitors Hemodynamic monitoring becomes more effective at predicting cardiovascular function when measured using performance parameters
CVP and arterial pulse pressure (PP) variations predict preload responsiveness ScvO2, SvO2 predict the adequacy of oxygen transport

Summary and Key Points

EVLW as a valid measure for the extravascular water content of the lungs is the only parameter for quantifying lung edema available at the bedside. Blood gas analysis and chest x-ray do not reliably detect and measure lung edema CVP and PaOP do not predict who will respond to fluid and when enough is enough ScV02 reveals depth of compensation, LA and AG reflect adequacy It all adds up to better management!

Case Presentation 2 ScV02: 54%, HR 128, RR 26 22% SVV what now? PP/SV 0.8 . Vasoconsticted or dilated? Next?

Volume responsive!

Case Presentation 2 SVV 15% PP/SV 1.8 Sv02 50% Next?

Vasopressor

Case Presentation 2 SVV 20% PP/SV 0.8 Sv02 80% Next?

Volume inotrope dilator

Goals for cardiocirculatory therapy

ScvO2 >70% or SvO2 >65% MAP (mean arterial pressure) >65 mmHg Cardiac Index >2.0 l/min/m2 CVP 815 mmHg (dependent on ventilation mode) SVV < 13 % PAOP 1215 mmHg Diuresis >0.5 ml/kgBW/h Lactate <3 mmol/l

GMS German Medical Science 2010, Vol. 8, pp 1-25 Carl,M. Alms,A. et al

Before I came here I was confused about this subject. Having listened to your lecture I am still confused. But on a higher level. -Enrico Fermi