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Slide 1

SHOCKDOOMSDAY

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Slide 2

Vicken Y. Totten

Shock lecture

Thanks to David Cheng MD

And all who taught me

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Slide 3

Definition

SHOCK:inadequate organperfusion to meet

the tissuesoxygenationdemand

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Slide 4

PATHOPHYSIOLOGY OF SHOCKSYNDROME

Cells switch from aerobic to anaerobic metabolism

lactic acid production

Cell function ceases & cells swell

membranes becomes more permeable

electrolytes & fluids seep in & out of cell

Cells Die in Many Organs Death

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Slide 5

Stages of shock

Compensated /Early Shock

Vasoconstriction (renin & carotid sinus baroceptor Increase in HR and RR

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Slide 6

Symptoms of Shock

Anxious

Dizziness Weakness

Faintness

Thirsty

I am sick

Fevers / Rigors

(sepsis) SSCP (cardiogenic)

Wheezing

(anaphylaxis) Trauma pain

(hypovolemia)

General Symptoms Specific Symptoms

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Slide 7

Early Signs of Shock inNon Complicated Patients

WARM EARLY STAGE / PRESHOCK

Need high index of suspicion b/c lack of signs

+/- tachycardia

+/- orthostatics (HR more sensitive than BP)

+/- pulse pressure narrowing

+/-restless

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Hypoperfusion can bepresent in the absence of

significant hypotension.(Dont only relay on BP for

diagnosisng shock)

-fccs course

8

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Signs of Late ShockHypotension

COLD LATE STAGE

Cold, clammy and pale skin

Rapid, weak, thready pulse

Rapid breathing (blow off CO2 met acidosis)

Cyanotic AMS->Coma

Anuria

Slid 10

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Slide 10

End Stage Clinical effects

Cardiovascular Myocardial

depression

Vasogenic effects

Pulmonary ARDS

Renal ARF

GI Ischemic bowel

Hepatic Increased LFTs, liver failure

Hematologic Neutropenia,

Thrombocytopenia

DIC (Gm- > Gm+)

CNS

coma

Slid 11

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Slide 11

Multiple Organ Dysfunction Syndrome

Number ofOrgans

Mortality (%)

0 0.8

1 6.82 26.2

3 48.5

4 68.8

5 83.3

*Adapted from Irwin and Rippes Critical Care Medicine 5th

Edition, pg 1837

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CircumferentialSubendocardial

Infarction due

to Shock

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Shock

Lung

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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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Slide 18

Remember

History and Physical often limited by patientscondition

Patient presentation can be variable secondaryto Severity of the perfusion defect Underlying cause Prior organ dysfunction

Exam should be tailored to be performedquickly with highest yield for uncovering the

cause of shock.

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Slide 19

Components (fluids, pump,pipes)

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Slide 20

Components: Blood (fluid) Heart (pump)

Blood Vessels(pipes)

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Slide 21

Types of Shock

Hypovolemic (fluids)

Cardiogenic (pump)

Redistributive (pipes)

(septic, neurogenic, anaphylactic)

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Slide 22

Adequate circulating blood

volume depends on 3components;

A minor impairment in onecan be compensated for by

the other 2 for a limited time.

Prolonged or severeimpairments will lead toSHOCK.

22

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Slide 25

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Low SVR

There are only a few causes of low SVR.

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?

Look at and feel the patient!

Low SVR has the features:

warm !!!

pink

Bounding pulses

hyperdynamic heart (fast andpounding)

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What if the SVR is high?

Pale

Poor cap refill (>2 seconds)

Cool arms/legs (>2 degree C difference)

Thready pulses (narrow pulse pressure (incr DBP))

Cause of shock (low BP) is then:

low CO

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What are factors of CO?

CO = HR x SV

CO = cardiac outputHR = heart rate

SV = stroke volume

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HR Problems

Heart Rate problems are easy to diagnose

Rate: bradycardia versus tachycardia

Slide 30

Low SV (stroke volume)

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Low SV (stroke volume)

Most difficult to diagnoseand manage

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Stroke Volume depends on

Preload--is the ventricle full?

Hypovolemic Shock

Obstructive Shock (ie Tension PTX, Tamponade)

Cardiac function

SqueezeContractilitycan the ventricle contract?Can blood get out? Valve function:

normal?

regurgitation?

stenosis?

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BP = CO x SVR

CO = HR x SVSV = preload & cardiac contractility-valve

Perfusion (blood pressure) depends on:

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Components of BP summary

MyocardialContractility

StrokeVolume Preload

CardiacOutput Afterload

Blood

Pressure Heart Rate

SystemicVascularResistance

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Why Monitor?

Essential to understanding their disease

Describe the patients physiologic status Serial monitoring

Facilitates diagnosis and treatment of shock

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Monitoring clinical shock parameter

Noninvasive

Blood pressure (SBP, MAP)

Urine output

Heart rate

Shock index

Invasive

Pulmonary artery catheter: CVP,PAWP, CO, SVR, DO2I, VO2I,SvO2

Arterial catheter: ABP, Serum

lactate, Base deficit

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Diagnosis of Shock

MAP < 60 or decreaseof 20 from baseline

systolic BP 90

systolic BP > 40 mmHg from the patientsbaseline pressure

Shock index (HR>SBP)

Clinical s/s of

hypoperfusion of vitalorgans

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Mean Arterial Pressure

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

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

MAP = (2 x DBP) + SBP3

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Pulse Pressure=SBP-DBP

The difference between the systolic (fxn ofejection fraction) and diastolic pressures (function ofSVR and distensibility (elastic recoil) of the aorta

Wide Normal 30-50 mmHg

Commonly seen with fever,anemia, exercise andhyperthyroidism

AR (aortic regurgitation) isalso a cause

Narrow May indicate an increase

in vascular resistance withdecreased stroke volume(ie aortic stenosis ordecreased intravascularvolume)

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Invasive Markers

Global Markers Base Deficit Lactate

Regional Markers Gastric pH Sublingual CO2

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Base Deficit

Inadequate tissue perfusion leads to tissueacidosis

Amount of base required to titrate 1 L of

whole arterial blood to a pH of 7.4 Normal range +3 to3 mmol per L

Elevated base deficit correlates with the

presence and severity of shock

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Base Deficit

Inadequate tissue perfusion leads to tissueacidosis

Amount of base required to titrate 1 L of

whole arterial blood to a pH of 7.4 Normal range +3 to3 mmol per L

Elevated base deficit correlates with the

presence and severity of shock

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Initial LactateWeil and Afifi. (Circulation 1970)

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Gastric Intramucosal pH

Blood flow is not uniformly distributed to all tissuebeds

Regions with inadequate tissue perfusion may existwhile global markers are normal

Gut mucosa among the first to be affected duringshock and the last to be restored to normal

Intramucosal pH falls when perfusion becomesinadequate

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Slide 47

bli l

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Sublingual CO2

Decrease gut perfusion Gastric tissue = esophagus = sublingual tissue

Non-invasive, hand held monitor

Rapid measurement Sensitive marker of decreased blood flow

Slide 48

Sublingual capnometry:

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Sublingual capnometry:

A new noninvasive measurement for diagnosis and

quantitation of severity of circulatory shock

P SLCO2

provides a

prompt

indication of the

reversal of

tissue

hypercarbia

whencirculatory

shock is

reversed

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Slide 50

Pulmonary Artery Catheter

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Pulmonary Artery Catheter

INDICATIONS volume status cardiac status

COMPLICATIONS technical anatomic physiologic

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Swan-Ganz Catheter

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PLACEMENT

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PLACEMENT

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C t PA C P iti

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Correct PA-C Position

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

Slide 54

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Standard Parameters

Measured Blood pressure Pulmonary A.

pressure Heart rate Cardiac Output Stroke volume Wedge pressure

CVP

Calculated Mean BP Mean PAP

Cardiac Index Stroke volume

index SVRI LVSWI

BSA

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Why Index?

Body habitus and size is individual

Indexing to patient with BSA allows for

reproducible standard

PATIENT A

60 yo male

50 kg

CO = 4.0 L/min

BSA = 1.86

CI = 2.4 L/min/m2

PATIENT B

60 yo male

150 kg

CO = 4.0 L/min

BSA = 2.64

CI = 1.5 L/min/m2

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Slide 57

PA I ti

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PA Insertion

0

5

10

15

20

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

Slide 58

CVP

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CVP

CVP of SVC at level of right atrium

pre-load assessment

normal 4 - 10 mm Hg

Slide 59

PAOP ( d )

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PAOP (wedge)

End expiration

Wedge adjustment with positive pressure Measured PAOP - PEEP = real PAOP

Slide 60

V l R i t

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Vascular Resistance

SYSTEMIC (SVR)

MAP - CVP

C0

SVR = vasoconstriction

SVR = vasodilation

PULMONARY (PVR)

MPAP - PAOPCO

PVR = constrictionPE, hypoxia

x 80 x 80

Vascular resistance = change in pressure/blood flow

Slide 61

C di C l

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Cardiac Cycle

pulmonary

Left ventricle

systemic

Right ventricleRVSW

PVR

LVSW

SVR

CVP

MPAPPCWP

MAP

Slide 62

Swan Ganz interpretation

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Swan Ganz interpretation

Etiology CO PCWP SVR

cardiogenic decreased increased increased

hypovolemic decreased decreased increased

distributive increased decreased decreased

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T M N b

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Too Many Numbers

Slide 64

Definitions

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Definitions

O2Delivery- volume of gaseous O2delivered to the LV/min.

O2Consumption- volume of gaseous O2which is actually used by the tissue/min.

consumption > demand = anaerobic metabolism

Slide 65

Mixed venous oxygen saturation

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Mixed venous oxygen saturation

Reflects difference between oxygen deliveryand consumption

Normal65-75%

Measurement taken from the distal port of aPA catheter

Slide 66

SvO : Low Values (< 60%)

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SvO2: Low Values (< 60%)

CO/CISV/SVI

Hgb

SaO2

O2consumption

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Oxycalculations

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Oxycalculations

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B k Ti

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Break Time

Slide 70

G l f Sh k

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Goals of Shock

Resuscitation

Restore blood pressure

Normalize systemic perfusion

Preserve organ function

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Parameters of AdequateResuscitation

Urine output (0.5 - 1.0 ml/kg/hr)

acceptable renal perfusion

Reversal of lactic acidosis (nl. pH)improved perfusion

Normal mental status

adequate cerebral perfusion

Slide 72 SHOCK: an EMERGENCY !!!

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Goal RAPIDLY RESTORE TISSUE PERFUSION

Recognize it !!!

Immediate stabilization: ABC

. SHOTGUN approach

Normalization of BP, pulse, UOP

Hemodynamic parameters

Restoration of aerobic

metabolism, elimination of tissue

acidosis, repayment of O2 debt

Treat the cause

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Shock is a symptom of its

cause.

-fccs course

73

Slide 74

I l t t th

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In general, treat thecause...

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Slide 76

Management priorities

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Management prioritiesin hypoperfused states

Priority # Physiology to

improve

Intervention Parameter to target PAC

targets

Avoid

1 Volume Fluids CVP 10-15 DO2 Low Sao2

See CXR2 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...NEVasopressin/Phenylephrine

When in doubt, try a li ttle more volume

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Hypovolemia

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Hypovolemia

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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 Shock

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Classes of Hypovolemic Shock

Class I Class II Class III Class IV

Blood Loss < 750 750-1500 1500-2000 > 2000

% Blood Vol. < 15% 15 30% 30 40% > 40%

Pulse < 100 > 100 > 120 > 140

Blood Pressure Normal Normal Decreased Decreased

Pulse Pressure Normal Decreased Decreased Decreased

Resp. Rate 14 20 20 30 30 40 > 40

UOP > 30 20 30 5 15 negligible

Mental Status sl. Anxious mildly anx confused lethargic

Fluid crystalloid crystalloid blood blood

Slide 80

Clinical Signs of Acute

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Clinical Signs of AcuteHemorrhagic 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 Shock

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Hypovolemic Shock

Causes hemorrhage vomiting

diarrhea dehydration third-space loss burns

Signscardiac outputPAOP/CVP

SVR

Slide 82

Treatment Hypovolemic

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Treatment - Hypovolemic

Reverse hypovolemia & hemorrhage control Crystalloid vs. Colloid

1 L crystalloid 250 ml colloid Watch for fluid overload by reassessing lung sounds

3:1 Rule (3cc crystalloid for 1cc bld loss)

Watch 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 bolus Colloids:(ex: albumin)

Will increase osmotic pressure, watch for pulm edema

Remain in vascular space longer (several hrs)

NOT increase survival

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

NOT FOR VOLUME

FFP for coagulopathy (all factors) Factor vii PLT for thrombocytopenia

Pressors?

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Slide 84

Role of PASG?

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Roleof PASG?

Higher mortality rate in penetrating thoracic, cardiactrauma

Role undefined in rural, blunt trauma

Splinting role

Slide 85

Cardiogenic Shock

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Cardiogenic Shock

Mech defect in cardiac function (lost > 40% Fxn)

Signs cardiac output PAOP/CVP SVR

left ventricular stroke work (LVSW)

Slide 86

Cardiogenic Shock

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Cardiogenic Shock

Myocardial failure (MI)

Severe Arrhythmia

Severe Valvular dysfunction

Reduction in cardiac output: >Decreased oxygen delivery

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Slide 89

Coronary Perfusion

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Coronary PerfusionPressure

Coronary PP = DBP - PAOP

coronary perfusion = P across coronary a.

GOAL - Coronary PP > 50 mm Hg

Slide 90

Treatment of CardiogenicSh k

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Shock

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

coronary arteries)

Maximize the cardiac output

Mntn normal rhythm (dysrhythmics, pacing,cardioversion)

Diastolic Vasopressors (dopamine, epi, norepi,vasopressin)

Improve myocardial contractility--Inotropes dobut and amrinone

Decrease the afterload (workload of the LV) IABP LVAD

Slide 91

The Failing Heart

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The Failing Heart

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

Fluids first, then cautious pressors

Remember aortic DIASTOLIC pressures drivescoronary perfusion (DBP-PAOP = CoronaryPerfusion Pressure)

If inotropes and vasopressors fail, intra-aorticballoon pump & LV assist devices

Slide 92

Intra-Aortic Balloon Pump

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Slide 93

Distributive Shock

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Distributive Shock

Types Sepsis Anaphylactic Acute adrenal insufficiency

Neurogenic

Signs cardiac output

PAOP SVR

Slide 94

Anaphylaxis

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Anaphylaxis

Slide 95

Anaphylactic Shock

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ap y act c S oc

Rapid onset

Diffuse vasodilation mechanism from

histamine & bradykinin

Edema from increased capillary permeability

Bronchoconstriction

Slide 96

Symptoms

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y pOnset within seconds and

progression to death in minutes Cutaneous manifestations

urticaria, erythema, pruritis,angioedema

Respiratory compromise stridor, wheezing, bronchorrhea, resp.

distress Circulatory collapse

tachycardia, vasodilation,hypotension

CNS

apprehension->ams->coma

Slide 97

Diagnosis

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g

History and physical alone make thediagnosis

Lab values serve no role

Histamine levels are elevated for about 30 min,tryptase for several hours.

Slide 98

Treatment

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Remove the antigen ABCs

IV Fluids, O2, cardiac monitor, pulse ox

First line Rx: Epinephrine

For severe bronchospasm, laryngeal edema, signsof upper airway obstruction, respiratory arrest orshock: IV epi

100 micrograms of 1:100,000 (place 0.1 mL of 1:1000 in10 mL of NS, give over 5-10 min)

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

Slide 99

Treatment

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2ndline: H1 blocker: Diphenhydramine 25-50 mg IV

H2 blocker: Ranitidine 50 mg or Famotidine 20 mg IV.)

Steroids (Methylprednisolone 125 mg IV or Prednisone

40-60 mg po)

Albuterol

For patients taking Beta-blockers with refractoryhypotension, think about glucagon

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Slide 101

SEPSIS

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SEPSIS

Systemic Inflammatory Response (SIRS)manifested by two or > of following: Temp > 38 or < 36 centigrade

HR > 90 RR > 20 or PaCO2 < 32 WBC > 12,000/cu mm or > 10% Bands (immature

wbc)

Slide 102

Risk factors of Sepsis

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p

Extreme age: 65 years

Surgical / invasive procedures

Malnutrition

Chronic illness DM, CRF, Hepatitis

Compromised immune status AIDS, immunosuppressives, EtOH, malignancies

Drug resistant organisms

Slide 103

What is Sepsis?

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SIRS Sepsis Severe Sepsis Septic

Shock Sepsis is the combination of the Systemic

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

Severe Sepsis: SIRS criteria, source of infection andinfection-induced organ dysfunction or hypoperfusionabnormalities (sepsis + lacticacidosis/oliguria/AMS/etc.)

Septic Shock: SIRS criteria, source of infection, andhypotens ionnot reversed with fluid resuscitation andassociated with organ dysfunction or hypoperfusionabnormalities

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Slide 107

Neurogenic shock

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Slide 108

Neurogenic 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

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g

Essential derangement:paralysis of thesympathetic chain whichcontrols vascular tone from

injury to thoracic orcervical level spinal cordinjury.

Produces decreased SVR

from loss of vascular toneand bradycardia fromunopposedparasympathetic input toSA node.

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Slide 110

Treatment of NeurogenicShock

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Shock

Increase vascular tone and improve CO Increase preload with fluids CVP

PAWP

Increase vascular tone

Vasopressors Maintain heart rate

Treat bradycardia if symptomatic

Maintain adequate oxygenation Watch with SCI because of the disruption of O2to the medulla

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

Steroids (Methylprednisolone 30mg/kg over 15 min in first hour, then5.4 mg/kg/hr x 23 hours)

There are contradicting studies, all of which have flaw

The symptoms of neurogenic shock typically last 1-3 weeks

Slide 111

Obstructive Shock

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Obstructive Shock

Causes Cardiac Tamponade Tension Pneumothorax Massive Pulmonary Embolus

Signs cardiac output PAOP/CVP SVR

TreatmentNeedle decompressionEmbolectomy / TPA

Slide 112

Adrenal CrisisDi ib i Sh k

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Distributive Shock

Causes Autoimmune adrenalitis Adrenal apoplexy = B hemorrhage or infarct

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

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

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

Slide 113

Vasopressor Agents?

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g

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

Risk tachycardia and increased myocardial oxygen

consumption if used too soon

Rationale, increased C.I. improves global perfusion

Slide 114

Vasopressors & Inotropic

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Vasopressors & InotropicAgents

Dopamine

Dobutamine

Norepinephrine

Epinephrine

Amrinone

Slide 115

Dopamine

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p

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

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

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

SIDE EFFECTS tachycardia > 20 g/kg/min to norepinephrine

Slide 116

Dobutamine

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-agonist

5 - 20 g/kg/min

potent inotrope, variable chronotrope

caution in hypotension (inadequate volume)

may precipitate tachycardia or worsenhypotension

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Slide 118

Epinephrine

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- and -adrenergic effects

potent inotrope and chronotrope

dose 1 - 10 g/min

increases myocardial oxygen consumption

particularly in coronary heart disease

Slide 119

Amrinone

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Phosphodiesterase inhibitor, positive inotropicand vasodilatory effects

increased cardiac stroke output without anincrease in cardiac stroke work

most often added with dobutamine as a secondagent

load dose = 0.75 -1.5 mg/kg5 - 10 g/kg/mindrip

main side-effect - thrombocytopenia

Slide 120

vasopressin

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V1vascular smooth muscle receptorvasoconstriction

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

hyponatremia, skin necrosis

Slide 121

Calcium Sensitisation by

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yLevosimendan

Enhanced contractility of myocardial cellby amplifying trigger for contraction with

no change in total intracellular Ca2+

Clinical trials status

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Slide 123

Dont forget...

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-Samuel D. Gross, 1872

Shock: rude unhinging of the

machinery of life.

123

Slide 124

??????????? For the humanspeaker

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speaker

Shock VT

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