shock doomsday

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SHOCKSHOCKDOOMSDAYDOOMSDAY

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http://upload.wikimedia.org/wikipedia/commons/1/19/Castle_Romeo.jpg


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Vicken Y. Totten

Shock lecture Thanks to David Cheng MD And all who taught me


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DefinitionDefinitionSHOCKSHOCK: :

inadequate organ inadequate organ perfusion to meet perfusion to meet

the tissue’s the tissue’s oxygenation oxygenation

demand demand


Slide 4PATHOPHYSIOLOGY OF SHOCK PATHOPHYSIOLOGY OF SHOCK SYNDROMESYNDROME

Cells switch from aerobic to anaerobic metabolism Cells switch from aerobic to anaerobic metabolism

lactic acid production lactic acid production

Cell function ceases & cells swellCell function ceases & cells swell

membranes becomes more permeablemembranes becomes more permeable

electrolytes & fluids seep in & out of cellelectrolytes & fluids seep in & out of cell

Cells Die in Many OrgansCells Die in Many Organs Death Death


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Stages of shockStages of shock Compensated /Early ShockCompensated /Early Shock

– Vasoconstriction Vasoconstriction (renin & carotid sinus baroceptor (renin & carotid sinus baroceptor – Increase in HR and RR <- sympthatic activation)Increase in HR and RR <- sympthatic activation)– Normotensive usually <- (aldosterone/ADH Na+/h20 Normotensive usually <- (aldosterone/ADH Na+/h20

retention)retention) Decompensated / late ShockDecompensated / late Shock

– Cool, clammy , hypotenisve. Cool, clammy , hypotenisve. – Vital organ preservationVital organ preservation– Worsening LOCWorsening LOC– Continued increase in HR and RR <-----(Chemreceptor Continued increase in HR and RR <-----(Chemreceptor

respose to metabolic acidosis) respose to metabolic acidosis) Irreversible-Irreversible-

– HR and RR dropHR and RR drop Multi Organ Failure Multi Organ Failure Impending death) Impending death)


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Symptoms of ShockSymptoms of Shock

AnxiousAnxious DizzinessDizziness WeaknessWeakness FaintnessFaintness ThirstyThirsty ““I am sick”I am sick”

Fevers / Rigors Fevers / Rigors (sepsis)(sepsis)

SSCP (cardiogenic)SSCP (cardiogenic) Wheezing Wheezing

(anaphylaxis)(anaphylaxis) Trauma pain Trauma pain

(hypovolemia)(hypovolemia)

General Symptoms Specific Symptoms


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Early Signs of Shock in Early Signs of Shock in Non Complicated Patients Non Complicated Patients

WARM EARLY STAGE / PRESHOCKWARM EARLY STAGE / PRESHOCK Need high index of suspicion b/c lack of signsNeed high index of suspicion b/c lack of signs

+/- tachycardia+/- tachycardia

+/- orthostatics (HR more sensitive than BP)+/- orthostatics (HR more sensitive than BP)

+/- pulse pressure narrowing+/- pulse pressure narrowing

+/-restless+/-restless


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““Hypoperfusion can be Hypoperfusion can be present in the absence of present in the absence of significant hypotension.”significant hypotension.”

(Don’t only relay on BP for (Don’t only relay on BP for diagnosisng shock)diagnosisng shock)

-fccs course-fccs course

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Signs of Late Shock Signs of Late Shock HypotensionHypotension

COLD LATE STAGECOLD LATE STAGE Cold, clammy and pale skin Cold, clammy and pale skin Rapid, weak, thready pulseRapid, weak, thready pulse Rapid breathing (blow off CO2 met acidosis)Rapid breathing (blow off CO2 met acidosis) CyanoticCyanotic AMS->ComaAMS->Coma AnuriaAnuria


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End Stage Clinical effectsEnd Stage Clinical effects

CardiovascularCardiovascular– Myocardial Myocardial

depression depression – Vasogenic effectsVasogenic effects

PulmonaryPulmonary– ARDSARDS

RenalRenal– ARFARF

GIGI– Ischemic bowelIschemic bowel

HepaticHepatic– Increased LFT’s, liver failureIncreased LFT’s, liver failure

HematologicHematologic– Neutropenia, Neutropenia,

ThrombocytopeniaThrombocytopenia– DIC (Gm- > Gm+)DIC (Gm- > Gm+)

CNSCNS– comacoma


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Multiple Organ Dysfunction Multiple Organ Dysfunction SyndromeSyndrome

Number of Number of OrgansOrgans

Mortality (%)Mortality (%)

00 0.80.811 6.86.822 26.226.233 48.548.544 68.868.855 83.383.3

*Adapted from Irwin and Rippe’s Critical Care Medicine 5th Edition, pg 1837


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CircumferentialSubendocardialInfarction dueto Shock


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ShockLung


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Acute congestion of liver due to shock


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Acute tubular necrosis of the kidney due to shock


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Intestinal mucosal hemorrhages due to shock


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Adrenal gland hemorrhage due to shock


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RememberRemember History and Physical often limited by patient’s History and Physical often limited by patient’s

conditioncondition

Patient presentation can be variable secondary Patient presentation can be variable secondary toto– Severity of the perfusion defectSeverity of the perfusion defect– Underlying causeUnderlying cause– Prior organ dysfunctionPrior organ dysfunction

Exam should be tailored to be performed Exam should be tailored to be performed quickly with highest yield for uncovering the quickly with highest yield for uncovering the cause of shock.cause of shock.


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Components (fluids, pump, Components (fluids, pump, pipes)pipes)


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Components:Components:– Blood (fluid)Blood (fluid)– Heart (pump)Heart (pump)– Blood Vessels Blood Vessels

(pipes)(pipes)


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Types of ShockTypes of Shock

Hypovolemic (fluids)Hypovolemic (fluids)

Cardiogenic (pump)Cardiogenic (pump)

Redistributive (pipes)Redistributive (pipes)(septic, neurogenic, anaphylactic)(septic, neurogenic, anaphylactic)


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Adequate circulating blood Adequate circulating blood volume depends on 3 volume depends on 3

components; components; A minor impairment in one A minor impairment in one can be compensated for by can be compensated for by

the other 2 for a limited time. the other 2 for a limited time. Prolonged or severe Prolonged or severe

impairments will lead to impairments will lead to SHOCK.SHOCK.

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An Approach to Shock – Know An Approach to Shock – Know this!this!

BP = SVR x COBP = SVR x COBP = blood pressureBP = blood pressure

CO = cardiac output (pump & fluids)CO = cardiac output (pump & fluids)SVR = systemic vascular resistance (pipes)SVR = systemic vascular resistance (pipes)


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An Approach to ShockAn Approach to Shock

If the blood pressure is low, then either the:If the blood pressure is low, then either the:CO is lowCO is low

ororSVR is lowSVR is low

ororBOTHBOTH


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Low SVRLow SVR

There are only a few causes of low SVR.There are only a few causes of low SVR.They ALL cause vasodilation:They ALL cause vasodilation:

•Septic shock•Neurogenic (spinal cord injury) shock•Anaphylaxis Shock•Vasodilator (antihypertensive)

Posioning


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How do you assess SVR?How do you assess SVR?

Look at and feel the patient!Look at and feel the patient!

Low SVR has the features:Low SVR has the features:• warm !!!warm !!!• pink pink • Bounding pulsesBounding pulses• hyperdynamic heart (fast and hyperdynamic heart (fast and

pounding)pounding)


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What if the SVR is high?What if the SVR is high?

• PalePale• Poor cap refill (>2 seconds)Poor cap refill (>2 seconds)• Cool arms/legs (>2 degree C difference)Cool arms/legs (>2 degree C difference)• Thready pulses (narrow pulse pressure (incr DBP))Thready pulses (narrow pulse pressure (incr DBP))

Cause of shock (low BP) is then:Cause of shock (low BP) is then:

low COlow CO


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What are factors of CO?What are factors of CO?

CO = HR x SVCO = HR x SV

CO = cardiac outputCO = cardiac outputHR = heart rateHR = heart rate

SV = stroke volumeSV = stroke volume


Slide 29

HR ProblemsHR Problems

• Heart Rate problems are easy to diagnoseHeart Rate problems are easy to diagnose

• Rate: bradycardia versus tachycardiaRate: bradycardia versus tachycardia


Slide 30 Low SV (stroke volume)Low SV (stroke volume)

Most difficult to diagnose Most difficult to diagnose and manageand manage


Slide 31

Stroke Volume depends on Stroke Volume depends on PreloadPreload--is the ventricle full?--is the ventricle full?

Hypovolemic ShockHypovolemic ShockObstructive Shock (ie Tension PTX, Tamponade)Obstructive Shock (ie Tension PTX, Tamponade)

Cardiac functionCardiac functionSqueezeSqueezeContractilityContractility–– can the ventricle contract?can the ventricle contract?Can blood get out? Can blood get out? Valve function: Valve function: normal?normal?regurgitation? regurgitation? stenosis?stenosis?


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BP = CO x SVRBP = CO x SVRCO = HR x SVCO = HR x SV

SV =SV =preload & cardiac contractility-valvepreload & cardiac contractility-valve

Perfusion (blood pressure) depends on:Perfusion (blood pressure) depends on:


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Components of BP summaryComponents of BP summary

Myocardial Contractility Stroke Volume Preload Cardiac Output Afterload Blood Pressure Heart Rate Systemic Vascular Resistance


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Why Monitor?Why Monitor?

Essential to understanding their diseaseEssential to understanding their disease

Describe the patient’s physiologic statusDescribe the patient’s physiologic status– Serial monitoringSerial monitoring

Facilitates diagnosis and treatment of shockFacilitates diagnosis and treatment of shock


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Monitoring clinical shock parameterMonitoring clinical shock parameterNoninvasiveNoninvasive ：： Blood pressure (SBP, MAP)Blood pressure (SBP, MAP) Urine outputUrine output Heart rateHeart rate Shock indexShock index

InvasiveInvasive ：： Pulmonary artery catheter: CVP, PAWP, CO, SVR, DOPulmonary artery catheter: CVP, PAWP, CO, SVR, DO22I, VOI, VO22I, I,

SvOSvO22 Arterial catheter: ABP, Serum lactate, Base deficitArterial catheter: ABP, Serum lactate, Base deficit


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Diagnosis of ShockDiagnosis of Shock

MAP < 60 or decrease MAP < 60 or decrease of 20 from baselineof 20 from baseline

systolic BP systolic BP 90 90 systolic BP > 40 mm systolic BP > 40 mm

Hg from the patient’s Hg from the patient’s baseline pressurebaseline pressure

Shock index (HR>SBP)Shock index (HR>SBP) Clinical s/s of Clinical s/s of

hypoperfusion of vital hypoperfusion of vital organsorgans


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Mean Arterial PressureMean Arterial Pressure

MAP is the mean perfusion pressure for the tissuesMAP is the mean perfusion pressure for the tissues– Most require a MAP of 60 or greater!Most require a MAP of 60 or greater!

Dependent only on the elastic properties of the Dependent only on the elastic properties of the arterial walls and the mean blood volume in the arterial walls and the mean blood volume in the arterial treearterial tree

MAP =MAP = (2 x DBP) + SBP (2 x DBP) + SBP 33


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Pulse Pressure=SBP-DBPPulse Pressure=SBP-DBPThe difference between the systolic (fxn of The difference between the systolic (fxn of

ejection fraction) and diastolic pressures (function ejection fraction) and diastolic pressures (function of SVR and distensibility (elastic recoil) of the aortaof SVR and distensibility (elastic recoil) of the aorta

WideWide– Normal 30-50 mmHg Normal 30-50 mmHg – Commonly seen with fever, Commonly seen with fever,

anemia, exercise and anemia, exercise and hyperthyroidismhyperthyroidism

– AR (aortic regurgitation) is AR (aortic regurgitation) is also a causealso a cause

NarrowNarrow– May indicate an increase May indicate an increase

in vascular resistance with in vascular resistance with decreased stroke volume decreased stroke volume (ie aortic stenosis or (ie aortic stenosis or decreased intravascular decreased intravascular volume)volume)


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Invasive MarkersInvasive Markers Global MarkersGlobal Markers

– Base DeficitBase Deficit– LactateLactate

Regional MarkersRegional Markers– Gastric pHGastric pH– Sublingual CO2Sublingual CO2


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Base DeficitBase Deficit Inadequate tissue perfusion leads to Inadequate tissue perfusion leads to

tissue acidosistissue acidosis Amount of base required to titrate 1 L Amount of base required to titrate 1 L

of whole arterial blood to a pH of 7.4of whole arterial blood to a pH of 7.4 Normal range +3 to –3 mmol per LNormal range +3 to –3 mmol per L Elevated base deficit correlates with Elevated base deficit correlates with

the presence and severity of shockthe presence and severity of shock


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Base DeficitBase Deficit Inadequate tissue perfusion leads to Inadequate tissue perfusion leads to

tissue acidosistissue acidosis Amount of base required to titrate 1 L Amount of base required to titrate 1 L

of whole arterial blood to a pH of 7.4of whole arterial blood to a pH of 7.4 Normal range +3 to –3 mmol per LNormal range +3 to –3 mmol per L Elevated base deficit correlates with Elevated base deficit correlates with

the presence and severity of shockthe presence and severity of shock


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Initial LactateInitial LactateWeil and Afifi. Weil and Afifi. (Circulation 1970)(Circulation 1970)


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Lactate and OutcomesLactate and OutcomesAdult PatientsAdult Patients

Demmers Ann Thorac Surg 70:2082-6:2000

A peak blood lactate level of >4.0 mmol/L was identified as a strong independent predictor of mortality and morbidity and suggests that tissue hypoperfusion


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Gastric Intramucosal pHGastric Intramucosal pH

Blood flow is not uniformly distributed to all Blood flow is not uniformly distributed to all tissue bedstissue beds

Regions with inadequate tissue perfusion Regions with inadequate tissue perfusion may exist while global markers are ‘normal’may exist while global markers are ‘normal’

Gut mucosa among the first to be affected Gut mucosa among the first to be affected during shock and the last to be restored to during shock and the last to be restored to normalnormal

Intramucosal pH falls when perfusion Intramucosal pH falls when perfusion becomes inadequatebecomes inadequate


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hypercarbia is a universal indicator of critically reduced tissue perfusion.

Sublingual capnometrySublingual capnometry: : A new noninvasive measurement for diagnosis and A new noninvasive measurement for diagnosis and

quantitation of severity of circulatory shockquantitation of severity of circulatory shock


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Sublingual CO2Sublingual CO2

Decrease gut perfusionDecrease gut perfusion– Gastric tissue = esophagus = sublingual Gastric tissue = esophagus = sublingual

tissuetissue Non-invasive, hand held monitorNon-invasive, hand held monitor Rapid measurementRapid measurement Sensitive marker of decreased blood Sensitive marker of decreased blood

flowflow


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Sublingual capnometrySublingual capnometry: : A new noninvasive measurement for diagnosis and A new noninvasive measurement for diagnosis and

quantitation of severity of circulatory shockquantitation of severity of circulatory shock

P P SLSL CO CO22 provides a provides a prompt prompt indication of the indication of the reversal of reversal of tissue tissue hypercarbia hypercarbia when when circulatory circulatory shock is shock is reversedreversed


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Direct arterial pressureDirect arterial pressureA-lineA-line


Slide 50 Pulmonary Artery CatheterPulmonary Artery Catheter

INDICATIONSINDICATIONS– volume statusvolume status– cardiac statuscardiac status

COMPLICATIONSCOMPLICATIONS– technicaltechnical– anatomicanatomic– physiologicphysiologic


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Swan-Ganz Catheter


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PLACEMENTPLACEMENT


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Correct PA-C PositionCorrect PA-C Position

From the RIJ approach, the RA is entered at From the RIJ approach, the RA is entered at approximately 25 cm, the RV at approximately approximately 25 cm, the RV at approximately 30 cm, and the PA at approximately 40 cm; the 30 cm, and the PA at approximately 40 cm; the PCWP can be identified at approximately 45 PCWP can be identified at approximately 45 cm. cm.


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Standard ParametersStandard Parameters

MeasuredMeasured– Blood pressureBlood pressure– Pulmonary A. Pulmonary A.

pressurepressure– Heart rateHeart rate– Cardiac OutputCardiac Output– Stroke volumeStroke volume– Wedge pressureWedge pressure– CVPCVP

CalculatedCalculated– Mean BPMean BP– Mean PAPMean PAP– Cardiac IndexCardiac Index– Stroke volume Stroke volume

indexindex– SVRISVRI– LVSWILVSWI– BSABSA


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Why Index?Why Index?

Body habitus and size is individualBody habitus and size is individual

““Indexing” to patient with BSA allows for Indexing” to patient with BSA allows for reproducible standardreproducible standard

PATIENT APATIENT A 60 yo male60 yo male 50 kg50 kg CO = 4.0 L/minCO = 4.0 L/min BSA = 1.86BSA = 1.86

CI = 2.4 L/min/mCI = 2.4 L/min/m22

PATIENT BPATIENT B 60 yo male60 yo male 150 kg150 kg CO = 4.0 L/minCO = 4.0 L/min BSA = 2.64BSA = 2.64

CI = 1.5 L/min/mCI = 1.5 L/min/m22


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PA InsertionPA Insertion

0

5

10

15

20

RA = 5 RV = 22/4 PA 19/10 PAOP(wedge) = 9


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CVPCVP CVP of SVC at level of right atriumCVP of SVC at level of right atrium pre-load “assessment”pre-load “assessment” normal 4 - 10 mm Hgnormal 4 - 10 mm Hg


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PAOP (wedge)PAOP (wedge)

End expirationEnd expiration Wedge adjustment with positive pressureWedge adjustment with positive pressure

– Measured PAOP - ½ PEEP = “real PAOP”Measured PAOP - ½ PEEP = “real PAOP”


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Vascular Resistance Vascular Resistance

SYSTEMIC (SVR)SYSTEMIC (SVR)

MAP - CVP MAP - CVP C0C0

SVR = vasoconstrictionSVR = vasoconstriction SVR = vasodilationSVR = vasodilation

PULMONARY (PVR)PULMONARY (PVR)

MPAP - PAOPMPAP - PAOP COCO

PVR = constrictionPVR = constrictionPE, hypoxiaPE, hypoxia

x 80 x 80

Vascular resistance = change in pressure/blood flow


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Cardiac CycleCardiac Cycle

pulmonary

Left ventricle

systemic

Right ventricleRVSW

PVR

LVSW

SVR

CVP

MPAPPCWP

MAP


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Swan Ganz interpretationSwan Ganz interpretation

Etiology CO PCWP SVR cardiogenic decreased increased increased

hypovolemic decreased decreased increased

distributive increased decreased decreased


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Too Many NumbersToo Many Numbers


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DefinitionsDefinitions

OO22 Delivery Delivery - volume of gaseous O - volume of gaseous O2 2 delivered to the LV/min.delivered to the LV/min.

OO22 Consumption Consumption - volume of gaseous O - volume of gaseous O22 which is actually used by the tissue/min.which is actually used by the tissue/min.

consumption > demand = anaerobic metabolism


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Mixed venous oxygen saturationMixed venous oxygen saturation

Reflects difference between oxygen Reflects difference between oxygen delivery and consumptiondelivery and consumption

Normal – 65-75%Normal – 65-75% Measurement taken from the distal Measurement taken from the distal

port of a PA catheterport of a PA catheter


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SvOSvO22: Low Values (< 60%): Low Values (< 60%)

CO/CICO/CI SV/SVISV/SVI

HgbHgb

SaOSaO22

OO22 consumption consumption


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SvOSvO22: High Values (> 75%): High Values (> 75%) SepsisSepsis

AV shunts/fistulae AV shunts/fistulae


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OxycalculationsOxycalculations


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Break Time…Break Time…


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Goals of Shock Goals of Shock ResuscitationResuscitation

Restore blood pressureRestore blood pressure

Normalize systemic perfusionNormalize systemic perfusion

Preserve organ functionPreserve organ function


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Parameters of AdequateParameters of AdequateResuscitationResuscitation

Urine output (0.5 - 1.0 ml/kg/hr)Urine output (0.5 - 1.0 ml/kg/hr)acceptable renal perfusionacceptable renal perfusion

Reversal of lactic acidosis (nl. pH)Reversal of lactic acidosis (nl. pH)improved perfusionimproved perfusion

Normal mental statusNormal mental statusadequate cerebral perfusionadequate cerebral perfusion


Slide 72 SHOCK: an EMERGENCY !!!SHOCK: an EMERGENCY !!!Goal RAPIDLY RESTORE TISSUE PERFUSIONGoal RAPIDLY RESTORE TISSUE PERFUSION• Recognize it !!!Recognize it !!!

•Immediate stabilization: ABCImmediate stabilization: ABC

…… ……. SHOTGUN approach. SHOTGUN approach

Normalization of BP, pulse, Normalization of BP, pulse, UOPUOP

Hemodynamic Hemodynamic parametersparameters

Restoration of aerobic Restoration of aerobic metabolism, elimination of tissue metabolism, elimination of tissue acidosis, repayment of O2 debtacidosis, repayment of O2 debt

•Treat the causeTreat the cause


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““Shock is a symptom of its Shock is a symptom of its cause.”cause.”

-fccs course-fccs course

73


Slide 74

In general, treat the In general, treat the cause...cause...


Slide 75 ManagementManagement

ABC’sABC’s– Maintain airwayMaintain airway– Decrease work of breathing & Optimize 02Decrease work of breathing & Optimize 02– Circulation & Control Hemorrhage includes:Circulation & Control Hemorrhage includes:

• Direct pressureDirect pressure• Pressure pointsPressure points• Fluids & DrugsFluids & Drugs

Must address and treat:Must address and treat:– PRELOADPRELOAD– AFTERLOADAFTERLOAD– PUMPPUMP

Re-assess every 5-15 minutesRe-assess every 5-15 minutes(the sicker the patient, the shorter the interval(the sicker the patient, the shorter the interval


Slide 76

Management prioritiesManagement prioritiesin hypoperfused statesin hypoperfused states

Priority # Physiology to improve

Intervention Parameter to target PAC targets

Avoid

1 Volume Fluids CVP 10-15 DO2 Low Sao2 See CXR

2 Pressure Vasopressor SBP? 100 or within 20-25 torr MBP ? 80 of patient's Nl

Low SV, DO2 High HR, Resistances

3 Flow Inotrope Signs of perfusion DO2 Low BP, SV, Resistances

BP potency: Dopamine...NE…Vasopressin/Phenylephrine

When in doubt, try a little more volume


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HypovolemiaHypovolemia


Slide 78

Time

Outcomes of same vol. lost over diff. periods of time. Slow losses (III, IV)allow compensations to take effect. Rapid loss (I, II) of same vol. is fatal


Slide 79

Classes of Hypovolemic ShockClasses of Hypovolemic Shock


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Clinical Signs of Acute Clinical Signs of Acute Hemorrhagic ShockHemorrhagic Shock

% Blood loss Clinical Signs< 15 Slightly increased heart rate

15-30 Increased HR, increased DBP (narrow pp), prolonged capillary refill, flat neck veins

30-50 Above findings plus: hypotension, confusion, acidosis, decreased urine output

> 50 Refractory hypotension, refractory acidosis, death


Slide 81

Hypovolemic ShockHypovolemic Shock

CausesCauses– hemorrhagehemorrhage– vomitingvomiting– diarrheadiarrhea– dehydrationdehydration– third-space lossthird-space loss– burnsburns

SignsSigns cardiac outputcardiac output PAOP/CVPPAOP/CVP SVRSVR


Slide 82

Treatment - HypovolemicTreatment - Hypovolemic

Reverse hypovolemia & hemorrhage controlReverse hypovolemia & hemorrhage control Crystalloid vs. ColloidCrystalloid vs. Colloid

– 1 L crystalloid 1 L crystalloid 250 ml colloid 250 ml colloid• Watch for fluid overload by reassessing lung sounds Watch for fluid overload by reassessing lung sounds • 3:1 Rule (3cc crystalloid for 1cc bld loss)3:1 Rule (3cc crystalloid for 1cc bld loss)• Watch for hyperchloremic metabolic acidosis when large volumes of NaCl are infusedWatch for hyperchloremic metabolic acidosis when large volumes of NaCl are infused• Best to give in 250 mL boluses in CHF followed by reassessment for another 250 cc bolusBest to give in 250 mL boluses in CHF followed by reassessment for another 250 cc bolus

– Colloids:Colloids: (ex: albumin) (ex: albumin)• Will increase osmotic pressure, watch for pulm edemaWill increase osmotic pressure, watch for pulm edema• Remain in vascular space longer (several hrs)Remain in vascular space longer (several hrs)• NOT increase survivalNOT increase survival

prbc sooner than laterprbc sooner than later– 500 ml whole blood increases Hct 2-3%, 250ml PRBC’s increases Hct 3-4%500 ml whole blood increases Hct 2-3%, 250ml PRBC’s increases Hct 3-4%– Increases oxygen carrying capacityIncreases oxygen carrying capacity– Used with acute hemorrhaging (mntn Hct 24% and Hgb 8gUsed with acute hemorrhaging (mntn Hct 24% and Hgb 8g /dL)/dL)

NOT FOR VOLUMENOT FOR VOLUME– FFP for coagulopathy (all factors)FFP for coagulopathy (all factors)– Factor viiFactor vii– PLT for thrombocytopeniaPLT for thrombocytopenia

Pressors?Pressors?


Slide 83

ResuscitationResuscitation

Transport times < 15 minutes showed Transport times < 15 minutes showed pre-hospital fluids were ineffective, pre-hospital fluids were ineffective, however, if transport time > 100 minutes however, if transport time > 100 minutes fluid was beneficial.fluid was beneficial.

PenetratingPenetrating torso trauma benefited from torso trauma benefited from limited resuscitation prior to bleeding limited resuscitation prior to bleeding control. Not applicable to BLUNT control. Not applicable to BLUNT victims.victims.


Slide 84

RoleRole of PASG?of PASG?

Higher mortality rate in penetrating thoracic, cardiac Higher mortality rate in penetrating thoracic, cardiac traumatrauma

Role undefined in rural, blunt traumaRole undefined in rural, blunt trauma

Splinting roleSplinting role


Slide 85

Cardiogenic ShockCardiogenic Shock

MechMech– defect in cardiac function (lost > 40% Fxn)defect in cardiac function (lost > 40% Fxn)

SignsSigns cardiac outputcardiac output PAOP/CVPPAOP/CVP SVRSVR left ventricular stroke work (LVSW)left ventricular stroke work (LVSW)


Slide 86


Myocardial failure (MI)Myocardial failure (MI) Severe ArrhythmiaSevere Arrhythmia Severe Valvular dysfunctionSevere Valvular dysfunction

Reduction in cardiac output:Reduction in cardiac output:– >Decreased oxygen delivery>Decreased oxygen delivery


Slide 87

Symptoms of Cardiogenic Symptoms of Cardiogenic ShockShock

Skin: progressive peripheral vasoconstriction Skin: progressive peripheral vasoconstriction results in cool, moist, pale skin with mottlingresults in cool, moist, pale skin with mottling

CHF SxCHF Sx– JVD, HJR, APE, pedal edemaJVD, HJR, APE, pedal edema

Heart: Heart: – Sounds: d/t enlargement and congestion you can Sounds: d/t enlargement and congestion you can

hear murmurs or S3 or S4hear murmurs or S3 or S4– Pulse: rapid rate and thready/weak pulsePulse: rapid rate and thready/weak pulse

BP: decreased BP and MAPBP: decreased BP and MAP UO: decreases early d/t decreased renal UO: decreases early d/t decreased renal

perfusionperfusion


Slide 88


Assess for:Assess for:– Signs of heart failureSigns of heart failure – Signs of tamponadeSigns of tamponade– Cardiac dysrrhythmiaCardiac dysrrhythmia– Myocardial infarctionMyocardial infarction

– TachycardiaTachycardia– Muffled heart sounds or third heart soundMuffled heart sounds or third heart sound– Engorged neck veins with hypotensionEngorged neck veins with hypotension– DyspneaDyspnea– Edema in feet and anklesEdema in feet and ankles


Slide 89

Coronary Perfusion Coronary Perfusion PressurePressure

Coronary PP = DBP - PAOPCoronary PP = DBP - PAOP

coronary perfusion = coronary perfusion = P across coronary a. P across coronary a.

GOAL - Coronary PP > 50 mm Hg


Slide 90 Treatment of Cardiogenic Treatment of Cardiogenic ShockShock

Increase oxygen supply to the heartIncrease oxygen supply to the heart– Decrease O2 consumption (pain meds/sedation)Decrease O2 consumption (pain meds/sedation)– Increase O2 delivery (Mech vent, reperfusion of the Increase O2 delivery (Mech vent, reperfusion of the

coronary arteries)coronary arteries) Maximize the cardiac outputMaximize the cardiac output

– Mntn normal rhythm (dysrhythmics, pacing, Mntn normal rhythm (dysrhythmics, pacing, cardioversion)cardioversion)

– Diastolic Vasopressors (dopamine, epi, norepi, Diastolic Vasopressors (dopamine, epi, norepi, vasopressin)vasopressin)

– Improve myocardial contractility--InotropesImprove myocardial contractility--Inotropes• dobut and amrinonedobut and amrinone

Decrease the afterload (workload of the LV)Decrease the afterload (workload of the LV)– IABPIABP– LVADLVAD


Slide 91

The Failing HeartThe Failing Heart

Improve myocardial function, C.I. < 3.5 is a risk Improve myocardial function, C.I. < 3.5 is a risk factor, 2.5 may be sufficient.factor, 2.5 may be sufficient.

Fluids first, then cautious pressorsFluids first, then cautious pressors

Remember aortic DIASTOLIC pressures drives Remember aortic DIASTOLIC pressures drives coronary perfusion (DBP-PAOP = Coronary coronary perfusion (DBP-PAOP = Coronary Perfusion Pressure)Perfusion Pressure)

If inotropes and vasopressors fail, intra-aortic If inotropes and vasopressors fail, intra-aortic balloon pump & LV assist devicesballoon pump & LV assist devices


Slide 92

Intra-Aortic Balloon Pump


Slide 93

Distributive ShockDistributive Shock

TypesTypes– SepsisSepsis– AnaphylacticAnaphylactic– Acute adrenal insufficiencyAcute adrenal insufficiency– NeurogenicNeurogenic

SignsSigns– ± cardiac output± cardiac output PAOPPAOP SVRSVR


Slide 94

AnaphylaxisAnaphylaxis


Slide 95

Anaphylactic ShockAnaphylactic Shock

Rapid onsetRapid onset Diffuse vasodilation mechanism from Diffuse vasodilation mechanism from

histamine & bradykinin histamine & bradykinin Edema from increased capillary permeabilityEdema from increased capillary permeability

BronchoconstrictionBronchoconstriction


Slide 96

SymptomsSymptoms Onset within seconds and Onset within seconds and

progression to death in minutesprogression to death in minutes Cutaneous manifestationsCutaneous manifestations

– urticaria, erythema, pruritis, angioedemaurticaria, erythema, pruritis, angioedema Respiratory compromiseRespiratory compromise

– stridor, wheezing, bronchorrhea, resp. stridor, wheezing, bronchorrhea, resp. distressdistress

Circulatory collapseCirculatory collapse– tachycardia, vasodilation, hypotensiontachycardia, vasodilation, hypotension

CNS CNS – apprehension->ams->comaapprehension->ams->coma


Slide 97

DiagnosisDiagnosis

History and physical alone make the History and physical alone make the diagnosisdiagnosis

Lab values serve no roleLab values serve no role– Histamine levels are elevated for about 30 min, Histamine levels are elevated for about 30 min,

tryptase for several hours.tryptase for several hours.


Slide 98

TreatmentTreatment

Remove the antigenRemove the antigen ABC’sABC’s IV Fluids, O2, cardiac monitor, pulse oxIV Fluids, O2, cardiac monitor, pulse ox First line Rx:First line Rx:

– EpinephrineEpinephrine– For severe bronchospasm, laryngeal edema, signs For severe bronchospasm, laryngeal edema, signs

of upper airway obstruction, respiratory arrest or of upper airway obstruction, respiratory arrest or shock: IV epishock: IV epi

• 100 micrograms of 1:100,000 (place 0.1 mL of 1:1000 in 100 micrograms of 1:100,000 (place 0.1 mL of 1:1000 in 10 mL of NS, give over 5-10 min)10 mL of NS, give over 5-10 min)

– If less severe, can give 0.3-0.5 mL 1:1000 SCIf less severe, can give 0.3-0.5 mL 1:1000 SC


Slide 99

TreatmentTreatment

22ndnd line: line:– H1 blocker: Diphenhydramine 25-50 mg IVH1 blocker: Diphenhydramine 25-50 mg IV– H2 blocker: Ranitidine 50 mg or Famotidine 20 mg IV.)H2 blocker: Ranitidine 50 mg or Famotidine 20 mg IV.)– Steroids (Methylprednisolone 125 mg IV or Prednisone Steroids (Methylprednisolone 125 mg IV or Prednisone

40-60 mg po)40-60 mg po)– AlbuterolAlbuterol– For patients taking Beta-blockers with refractory For patients taking Beta-blockers with refractory

hypotension, think about glucagonhypotension, think about glucagon


Slide 100

Septic ShockSeptic Shock

http://srs.dl.ac.uk/Annual_Reports/AnRep99_00/Meningitis_Figure_1.jpg


Slide 101

SEPSISSEPSIS

Systemic Inflammatory Response (SIRS) Systemic Inflammatory Response (SIRS) manifested by two or > of following:manifested by two or > of following:– Temp > 38 or < 36 centigradeTemp > 38 or < 36 centigrade– HR > 90HR > 90– RR > 20 or PaCO2 < 32RR > 20 or PaCO2 < 32– WBC > 12,000/cu mm or > 10% Bands (immature WBC > 12,000/cu mm or > 10% Bands (immature

wbc) wbc)


Slide 102

Risk factors of SepsisRisk factors of Sepsis

Extreme age: <1 and >65 yearsExtreme age: <1 and >65 years Surgical / invasive proceduresSurgical / invasive procedures MalnutritionMalnutrition Chronic illnessChronic illness

– DM, CRF, HepatitisDM, CRF, Hepatitis Compromised immune statusCompromised immune status

– AIDS, immunosuppressives, EtOH, malignanciesAIDS, immunosuppressives, EtOH, malignancies Drug resistant organismsDrug resistant organisms


Slide 103

What is Sepsis?What is Sepsis? SIRS SIRS Sepsis Sepsis Severe Sepsis Severe Sepsis Septic Septic

ShockShock Sepsis is the combination of the Systemic Sepsis is the combination of the Systemic

Inflammatory Response Syndrome (SIRS) & a Inflammatory Response Syndrome (SIRS) & a confirmed or presumed infectious etiology.confirmed or presumed infectious etiology.

Severe Sepsis: SIRS criteria, source of infection and Severe Sepsis: SIRS criteria, source of infection and infection-induced organ dysfunction or hypoperfusion infection-induced organ dysfunction or hypoperfusion abnormalities abnormalities (sepsis + lactic (sepsis + lactic acidosis/oliguria/AMS/etc.)acidosis/oliguria/AMS/etc.)

Septic Shock: SIRS criteria, source of infection, andSeptic Shock: SIRS criteria, source of infection, and hypotensionhypotension not reversed with fluid resuscitation and not reversed with fluid resuscitation and associated with organ dysfunction or hypoperfusion associated with organ dysfunction or hypoperfusion abnormalitiesabnormalities


Slide 104

Septic ShockSeptic Shock

Bacterial, viral, fungal infectionBacterial, viral, fungal infection

““Warm shockWarm shock” is early stage” is early stage– Fever, tachycardia, tachypnoea, Fever, tachycardia, tachypnoea,

leucocytosis, leucocytosis, – inadequate oxygen extraction (High inadequate oxygen extraction (High

SvOSvO22, Metabolic acidosis) in infected , Metabolic acidosis) in infected tissuestissues

““Cold shockCold shock” is late stage” is late stage


Slide 105 Septic/Inflammatory ShockSeptic/Inflammatory ShockSigns: Signs: EarlyEarly– warm w/ vasodilation, often adequate urine – warm w/ vasodilation, often adequate urine output, febrile, tachypneic.output, febrile, tachypneic. LateLate-- vasoconstriction, hypotension, oliguria, -- vasoconstriction, hypotension, oliguria, altered mental status.altered mental status.

Monitor/findings: Monitor/findings: EarlyEarly—hyperglycemia, respiratory—hyperglycemia, respiratory alkylosis, hemoconcentration, alkylosis, hemoconcentration, WBC typically normal or low.WBC typically normal or low. LateLate – Leukocytosis, lactic acidosis – Leukocytosis, lactic acidosis Very LateVery Late– Disseminated Intravascular – Disseminated Intravascular Coagulation & Multi-Organ Coagulation & Multi-Organ System Failure. System Failure.


Slide 106

Septic Shock TXSeptic Shock TX

Prompt volume replacement - fill the tankPrompt volume replacement - fill the tank

Early antibiotic administration - treat the causeEarly antibiotic administration - treat the cause

If MAP < 60If MAP < 60– Dopamine = 2 - 3 Dopamine = 2 - 3 g/kg/ming/kg/min– Norepinephrine = titrate (1-100 Norepinephrine = titrate (1-100 g/min)g/min)


Slide 107 Neurogenic shockNeurogenic shock

http://images.google.com/imgres?imgurl=http://www.bronsonhealth.com/heart_prevention/images/hdr1.jpg&imgrefurl=http://www.bronsonhealth.com/content_long.asp?menu=Nm&h=76&w=324&sz=10&hl=en&start=28&tbnid=o2fQkRt_Ks5BRM:&tbnh=28&tbnw=118&prev=/images?q=bradycardia+ekg&start=20&ndsp=20&svnum=10&hl=en&lr=&sa=N


Slide 108

Neurogenic ShockNeurogenic Shock

Essential derangement: Essential derangement: paralysis of the paralysis of the sympathetic chain which sympathetic chain which controls vascular tone from controls vascular tone from injury to thoracic or injury to thoracic or cervical level spinal cord cervical level spinal cord injury.injury.

Produces decreased SVR Produces decreased SVR from loss of vascular tone from loss of vascular tone and bradycardia from and bradycardia from unopposed unopposed parasympathetic input to parasympathetic input to SA node.SA node.


Slide 109

Neurogenic (Vasogenic) ShockNeurogenic (Vasogenic) Shock

Caused byCaused by::– Spinal cord injury loss of SNS Spinal cord injury loss of SNS

Massive venous pooling & arteriolar dilatationMassive venous pooling & arteriolar dilatation Signs and SymptomsSigns and Symptoms::

– Hypotension without tachycardiaHypotension without tachycardia– Warm pink skin from cutaneous vasodilationWarm pink skin from cutaneous vasodilation– Low BP w/ minimal response to fluidsLow BP w/ minimal response to fluids– Accompanying Neurologic deficitAccompanying Neurologic deficit

Spinal shock is not Neurogenic shockSpinal shock is not Neurogenic shock– Spinal Shock: the temporary loss of spinal reflex activity Spinal Shock: the temporary loss of spinal reflex activity

that occurs below a total or near total spinal cord injurythat occurs below a total or near total spinal cord injury


Slide 110

Treatment of Neurogenic Treatment of Neurogenic ShockShock

Increase vascular tone and improve COIncrease vascular tone and improve CO– Increase preload with fluidsIncrease preload with fluids

• CVPCVP• PAWPPAWP

– Increase vascular toneIncrease vascular tone• VasopressorsVasopressors

– Maintain heart rateMaintain heart rate• Treat bradycardia if symptomaticTreat bradycardia if symptomatic

– Maintain adequate oxygenationMaintain adequate oxygenation• Watch with SCI because of the disruption of OWatch with SCI because of the disruption of O22 to the medulla to the medulla

– Initiate therapy to prevent DVT Initiate therapy to prevent DVT • Sluggish venous flow will increase risk factorsSluggish venous flow will increase risk factors

– Steroids (Methylprednisolone 30mg/kg over 15 min in first hour, then 5.4 Steroids (Methylprednisolone 30mg/kg over 15 min in first hour, then 5.4 mg/kg/hr x 23 hours)mg/kg/hr x 23 hours)

• There are contradicting studies, all of which have flawThere are contradicting studies, all of which have flaw The symptoms of neurogenic shock typically last 1-3 weeksThe symptoms of neurogenic shock typically last 1-3 weeks


Slide 111

Obstructive ShockObstructive Shock CausesCauses

– Cardiac TamponadeCardiac Tamponade– Tension PneumothoraxTension Pneumothorax– Massive Pulmonary EmbolusMassive Pulmonary Embolus

SignsSigns cardiac outputcardiac output PAOP/CVPPAOP/CVP SVRSVR

TreatmentTreatmentNeedle decompressionNeedle decompression

Embolectomy / TPAEmbolectomy / TPA


Slide 112

Adrenal Crisis Adrenal Crisis Distributive Shock Distributive Shock

CausesCauses– Autoimmune adrenalitisAutoimmune adrenalitis– Adrenal apoplexy = B hemorrhage or infarctAdrenal apoplexy = B hemorrhage or infarct

This is suspected when patient is non-This is suspected when patient is non-responsive to fluids, vasopressors and responsive to fluids, vasopressors and antibiotics.antibiotics.

Electrolytes may reveal hypoNa+ & hyperK+Electrolytes may reveal hypoNa+ & hyperK+ Steroids may be lifesaving in patient who is Steroids may be lifesaving in patient who is

unresponsive to fluids-inotropic-vasopressor unresponsive to fluids-inotropic-vasopressor (hydrocortisone 100mg IV)(hydrocortisone 100mg IV)


Slide 113

Vasopressor Agents?Vasopressor Agents?

Augments contractility, after preload established, Augments contractility, after preload established, thus improving cardiac output.thus improving cardiac output.

Risk tachycardia and increased myocardial oxygen Risk tachycardia and increased myocardial oxygen consumption if used too soonconsumption if used too soon

Rationale, increased C.I. improves global perfusionRationale, increased C.I. improves global perfusion


Slide 114

Vasopressors & Inotropic Vasopressors & Inotropic AgentsAgents

DopamineDopamine

DobutamineDobutamine

NorepinephrineNorepinephrine

EpinephrineEpinephrine

AmrinoneAmrinone


Slide 115

DopamineDopamine Low dose (0.5 - 2 Low dose (0.5 - 2 g/kg/min) = dopaminergicg/kg/min) = dopaminergic

Moderate dose (3-10 Moderate dose (3-10 g/kg/min) = g/kg/min) = -effects-effects

High dose (> 10 High dose (> 10 g/kg/min) = g/kg/min) = -effects-effects

SIDE EFFECTSSIDE EFFECTS– tachycardiatachycardia– > 20 > 20 g/kg/min g/kg/min to norepinephrine to norepinephrine


Slide 116

DobutamineDobutamine

-agonist-agonist

5 - 20 5 - 20 g/kg/ming/kg/min

potent inotrope, variable chronotropepotent inotrope, variable chronotrope

caution in hypotension (inadequate volume) caution in hypotension (inadequate volume) may precipitate tachycardia or worsen may precipitate tachycardia or worsen hypotensionhypotension


Slide 117

NorepinephrineNorepinephrine

Potent Potent -adrenergic vasopressor-adrenergic vasopressor

Some Some -adrenergic, inotropic, chronotropic-adrenergic, inotropic, chronotropic

Dose 1 - 100 Dose 1 - 100 g/ming/min

Unproven effect with low-dose dopamine to protect Unproven effect with low-dose dopamine to protect renal and mesenteric flow.renal and mesenteric flow.


Slide 118

EpinephrineEpinephrine

- and - and -adrenergic effects-adrenergic effects

potent inotrope and chronotropepotent inotrope and chronotrope

dose 1 - 10 dose 1 - 10 g/ming/min

increases myocardial oxygen consumption increases myocardial oxygen consumption particularly in coronary heart diseaseparticularly in coronary heart disease


Slide 119

AmrinoneAmrinone Phosphodiesterase inhibitor, positive inotropic Phosphodiesterase inhibitor, positive inotropic

and vasodilatory effectsand vasodilatory effects

increased cardiac stroke output without an increased cardiac stroke output without an increase in cardiac stroke workincrease in cardiac stroke work

most often added with dobutamine as a second most often added with dobutamine as a second agentagent

load dose = 0.75 -1.5 mg/kg load dose = 0.75 -1.5 mg/kg 5 - 10 5 - 10 g/kg/min g/kg/min dripdrip

main side-effect - thrombocytopeniamain side-effect - thrombocytopenia


Slide 120

vasopressinvasopressin

V1V1 vascular smooth muscle receptor vascular smooth muscle receptor vasoconstrictionvasoconstriction

0.01-0.04 units/min 0.01-0.04 units/min Risk: coronary, mesenteric ischemia, Risk: coronary, mesenteric ischemia,

hyponatremia, skin necrosis hyponatremia, skin necrosis


Slide 121

Calcium Sensitisation by Calcium Sensitisation by LevosimendanLevosimendan

Enhanced contractility of myocardial cell Enhanced contractility of myocardial cell by amplifying trigger for contraction with by amplifying trigger for contraction with no change in total intracellular Cano change in total intracellular Ca2+2+

Clinical trialsClinical trials status status


Slide 122

Endpoints?Endpoints?

ACS / ATLS - restoration of vital signs and ACS / ATLS - restoration of vital signs and evidence of end-organ perfusionevidence of end-organ perfusion

Swan-guided resuscitationSwan-guided resuscitation– C.I. C.I. 4.5, DO 4.5, DO22I I 670, VO 670, VO22I I 166 166

Lactic Acid clearanceLactic Acid clearance

Gastric pHGastric pH


Slide 123

Don’t forget...Don’t forget...

-Samuel D. Gross, 1872-Samuel D. Gross, 1872

Shock: “rude unhinging of the machinery of life.”

123


Slide 124

??????????? For the human ??????????? For the human speakerspeaker

shock doomsday

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