shock diagnosis & treatment

Shock Diagnosis & Treatment

Shock Diagnosis & Treatment

台大醫院 外科加護病房柯文哲 醫師

Three Tasks in SICU1 Shock ? resuscitation

2 underlying problems ? treatment

3 nutrition ? support

(metabolic support vs nutritional support)

Shock or Not?

70kg, adult male

HR BP CO

150/min80/min110/min

60/40120/80100/70

1.8L/min5.0Lmin3.4L/min

Shock

Inadequate tissue perfusion

1. What is the adequate tissue perfusion?

2. What is the optimal cardiac output for a patient at a specific time?

For example:

A patient with acute nercotizing pancreatitis?

Definition of ShockShock is a state of inadequate tissue perfusion

1 decreased tissue perfusion

2 inadequate tissue metabolism

Diagnosis of Shock• symptom & sign

• vital sign (BP, HR, RR)

• ABG

• urine output

• cardiac output

• SvO2 (mixed venous oxygen saturation)

• serum lactate

• tonometry

Symptom & Sign

Clinical finding:

color, temp., pulse, capillary refilling

conscious level

mental status:

clear even in very low C.O. state

but maybe confused in early sepsis

Vital organs: brain, heart, lung

棄車保帥 : divert blood flow to vital organs vessels in vital organs: no -receptors sympathetic tone blood vessel constriction except in vital organs

Symptom & Sign

Concept of vital organs: brain, heart, lung

Concept of compensation: sympathetic tone perfusion to vita organs

skin cool, pale GI paralysis, bleeding, “translocation” kidney oliguria

Symptom & sign

• Disadvantages:– Too late to be effective – Subjective– Not quantified– Unreliable in modern ICU

Vital Signs HR, BP, RR

Disadvantages:• large overlap between normal & abnormal

• when obvious (too late)

BP = CO × SVR

V = I × R

BP = CO × SVR

V = I × R

相信血壓 一定會倒楣

阿婆的故事

Vital Sign

• Advantages:– Quantified, objective number

– Automatic, computerized

– Continuous --> trend analysis,

not single value

Blood Gas Analysis

pH, BE

• intermittent measurement

• pH.: A real vital sign change only in decompensated state

Basic Model in Critical Care

stress => compensation

success

failure

survive

death

PH in ABG

Urine Output

• Advantages:– No instrument required (one Forley tube)– Simple and easy– Real time ( rapid reflection of renal perfusion)– Allow trend analysis

Urine Output

NTUH SICU routine:

U/O record q1h

Urine OutputNormal heart, kidney, endocrine, volume status

normal urine output

( p q q p )

• too many interfering factors:

renal diseases, diuretics, mannitol, glycerol, hyperglycemia, DI, ATN diuretic phases

• awkward in children

e.g. 3 cc/hr

• labor-intensive

Cardiac Output

Method:

1. Thermodilution (intermittent, continuous)

2. Pulse contour (PiCCO)

3. Bioimpedance

4. Indicator-thermodilution (COLD)

time

- T

CO =

Indicator - thermodilution

a b c d e

a

b

Noise, random, summation

c

d

Cardiac output

Intermittent Continuous

• Point observation • All times

• Contamination • Clean

• Labor intensive • Automatic

• inaccurate • Reliable

Cardiac Output• Intermittent: cold water injection

• continuous:

heating wire

pulse contour

impedance

Tissue Perfusion

demand supply

SvO2

(mixed venous oxygen saturation)

SvO2

(mixed venous oxygen saturation)

C.O.

Hb

SaO2

VO2

SvO2

Hepatic failure (Bil.: 16)

C.O.: 10 L/min

SvO2: 91%

Time

SvO2

CPR

SvO2

a. v.

shuntinability to use O2 (CN-, sepsis)

.c.

Serum Lactate Level

• Product of glycolysis

• A marker of anaerobic metabolism

Cori cycle

glucose

lactate

liver muscle

No glucose 6-phosphatase in muscle

Lactate

Disadvantage:

1. Global evaluation

2. Border zone

3. Skeletal muscle Vs liver

4. Quick upward, slowly downward

Lactate

SvO2 Lactate

Normal

Shunt or sepsisWell compensated low CO

Very bad

Anaerobic metabolism lactic acidHyperlactemia Vs lactic acidosis

Tonometry棄車保帥 :

1. Blood diverted to vital organs

GI tract is deprived of perfusion

2. 90% of total gut blood flow

mucosa & submucosa

CO2 + H2O H+ + HCO3-

Ka =

pHi = pKa + log

0.03PCO

]][HCO[H

2

3

0.03PiCO

][HCO

2

i3

Assume: [HCO3-]i = [HCO3

-]a

PiCO2 = PrCO2

Summary

1. Vital sign

2. U/O

3. C.O.

4. SvO2

5. Lactate

6. Tonometry

Estimation of the Previous Shock

• Amount of tissue damage:

CK, GOT

• result of tissue damage:

BUN, Cr, Bil

Treatment of Shock

以下那一個方法增加oxygen delivery 最多 ?

(1) PaO2: 100 200 mmHg

(2) CO: 4 5 L/min

(3) Hb: 7 11 g/dL

(4) PaCO2: 45 35 mmHg

( 5) HR: 100 150 /min

Oxygen Delivery

DO2 = CO Hb 1.39 SaO2

• C.O.

• O2 content of arterial blood

Hb

SaO2

Hb-O2 affinity (pH, PaCO2, temp, 2.3DPG)

27 mmHg PaO2

SaO2

50%

Shift to right :

pH , PaCO2 , temp , 2,3 DPG

How to increase DO2?

Hb SaO2 (PaO2) CO

Determining Factors of Cardiac Output

• Pre-load

• after-load

• contractility

• rhythm

• anatomic defects

Pre-load“effective circulation volume”

• hemorrhage (internal, external)

• dehydration (diarrhea, drain, burn, diuresis)

• vessel dilation

• fluid shift (edema, ascites, ileus, pleural effusion)

• cardiac tamponade, constrictive pericarditis

• tension pneumothorax

After-load• pulmonary embolism

• primary pulmonary hypertension

• atherosclerosis

• coarctation of aorta

• etc

Contractility• myocardial infarction

• cardiomyopathy

dilated

restrictive

hypertrophic

myocarditis

etc

Heart RhythmC.O. = HR S.V.

• bradycardia

• tachycardia

• arrhythmia

Anatomic Defects

• cardiac valvular diseases

• congenital heart diseases

• AV shunt

How to increase Cardiac output ?

1. Rhythm

2. Preload

3. Afterload

4. Contractility

D/D of ShockCVP BP CO SvO2

hyporolemiaobstructivecardiogenicsepsis (early) (late)

, N , N, T

, N

Treatment• How to increase oxygen delivery ?

Hb SaO2 (PaO2) CO

• how to increase C.O. ?

Rhythm pre-load after-load contractility

• How to increase metabolic efficiency ?

• How to decrease metabolic demand ?

Basic Model in Critical Care

stress => compensation

success

failure

survive

death