shock diagnosis & treatment
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Shock Diagnosis & Treatment. 台大醫院 外科加護病房 柯文哲 醫師. Three Tasks in SICU. Shock ? resuscitation 2 underlying problems ? treatment 3 nutrition ? support (metabolic support vs nutritional support). Shock or Not?. Shock. Inadequate tissue perfusion. - PowerPoint PPT PresentationTRANSCRIPT
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