SHOCK

Hasanul Arifin
Departemen Anestesiologi dan Reanimasi
Fakultas Kedokteran USU
27/03/2014 2
glucose oksigen
38 Mol ATP
glucose oksigen
2 Mol ATP
+
36 Mol Lactate
Definition of Shock
Reduced perfusion of vital organs leading to
inadequate oxygen and nutrients necessary
for normal tissue and cellular function.
DO
2
< VO
2

Cellular level:
Reduction of mitochondrial oxygen
Anaerobic glycolysis of ATP
Accumulation of pyruvate lactate Lactic Acidosis
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IT IS NOT LOW BLOOD PRESSURE !!!
IT IS HYPOPERFUSION..
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B1, nafas sesak, RR , cuping hidung
B2, HR , nadi halus cepat, TD. N/
Pulse-press , perfusi dingin, pucat, basah,
capill.refill > 2 det., lactic-acid
B3,
B4,
anxious, confused, lethargy
urine out-put , <0.5 ml/kg/jam, pekat
Hasanul, 2003
Shock in Trauma
Clinical differentiation
1. Hemorrhagic Shock
2. Non Hemorrhagic Shock
Cardiogenic
Tension pneumothorax
Neurogenic
Septic
Anaphylactic
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PRE-LOAD CONTRACTILITY AFTER-LOAD
STROKE VOLUME HEART-RATE
CARDIAC OUTPUT TOTAL PERIPHERAL
RESISTANCE
BLOOD PRESSURE
Hasanul, 2009
Tissue Perfusion
Pathophysiology
The human body responds to acute
hemorrhage by activating the following major
physiologic systems:
the hematologic,
cardiovascular,
renal, and
neuroendocrine systems.

The hematologic system
activating the coagulation cascade and
contracting the bleeding vessels (by means of
local thromboxane A
2
release).
platelets are activated (also by means of local
thromboxane A
2
release) and form an immature
clot on the bleeding source.
The damaged vessel exposes collagen, which
subsequently causes fibrin deposition and
stabilization of the clot.
Approximately 24 hours are needed for
complete clot fibrination and mature formation.

The cardiovascular system
initially responds to hypovolemic shock by increasing
the heart rate,
increasing myocardial contractility,
constricting peripheral blood vessels.
This response occurs secondary to an increased release of
norepinephrine and decreased baseline vagal tone
(regulated by the baroreceptors in the carotid arch, aortic
arch, left atrium, and pulmonary vessels).
The cardiovascular system also responds by
redistributing blood to the brain, heart, and kidneys
and away from skin, muscle, and GI tract.
The renal system
increase in renin secretion from the
juxtaglomerular apparatus.
Renin converts angiotensinogen to angiotensin I,
which subsequently is converted to angiotensin II
by the lungs and liver.
Angiotensin II has 2 main effects, both of which
help to reverse hemorrhagic shock :
vasoconstriction of arteriolar smooth muscle,
stimulation of aldosterone secretion by the adrenal
cortex. Aldosterone is responsible for active sodium
reabsorption and subsequent water conservation
The neuroendocrine system
increase in circulating antidiuretic hormone
(ADH).
ADH is released from the posterior pituitary gland
in response to :
decrease in BP (as detected by baroreceptors)
decrease in the sodium concentration (as detected by
osmoreceptors).
ADH indirectly leads to an increased reabsorption
of water and salt (NaCl) by the distal tubule, the
collecting ducts, and the loop of Henle.

HEMORRHAGE

HYPOVOLEMIA

Baroreceptor reflex (arterial & cardiopulmonary)
Circulating vasoconstrictors
Chemoreceptor reflexes
Renal reabsorption of Na+ and water
Cerebral ischemia


Increased SVR and Cardiac Output
Shunting blood to vital organs

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Volume loss
Autonomic tone
Catecholamine release
Fluid shifts from
extracellular to
intravascular
Partial restoration of
intravascular volume
survival
Intervention / stabilization
Maintenance of perfusion
Continued volume loss
Blood flow shunted to vital
organs (heart,lung,brain)
Cellular hypoxia / anaerobic
metabolism
ATP production / lactic acidosis
Survival / delayed morbidity / mortality
Intervention / stabilization
Pathophysiology of Hypovolemic Shock
Venous capacitance
Heart rate
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ATP production / lactic acidosis
Survival / delayed morbidity /
mortality
Intervention / stabilization
Cellular function
impaired
Continued volume loss
Membrane porosity
Movement of fluid
from intravascular to
interstitial spaces
Lysozymal leakage
Cellular autodigestion
Irreversible
shock
intervention
DEATH
No. intervention
Cellular hypoxia /
anaerobic metabolism
PATHOPHYSIO, CONTN
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CELL MEMBRANE FAILURE:

DIRECT
Endotoxin
Complement
INDIRECT
Failure to maintain normal Na
+
, K
+
or Ca
2+
gradient
Decreased oxidative phosphorylation
OSMOTIC
GRADIENT
Water entry
into cell
CELLULAR
EDEMA
IMPAIRED
INTRACELLULAR
METABOLISM
EFEK SHOCK PADA TINGKATAN SEL
Na
+
entry
into cell
21
STAGES OF SHOCK
22
COMPENSATED SHOCK
Body defense mechanisms attempt to preserve
major organs
Precapillary sphincters close, blood is shunted
Increased heart rate and strength of contractions
Increased respiratory function, bronchodilation
23
COMPENSATED SHOCK
Will continue until problem solved or shock
progresses to next stage
Can be difficult to detect with subtle indicators
Tachycardia
Decreased skin perfusion
Alterations in mental status
Some medications such as propranolol can hide signs
and symptoms
24
UNCOMPENSATED SHOCK
Physiological response
Precapillary sphincters open, blood pressure falls
Cardiac output falls
Blood surges into tissue beds, blood flow
stagnates
Red cells stack up in rouleaux
25
UNCOMPENSATED SHOCK
Easier to detect than compensated shock
Prolonged capillary refill time
Marked increase in heart rate
Rapid thready pulse
Agitation, restlessness, confusion
26
IRREVERSIBLE SHOCK
Compensatory mechanisms fail, cell death begins,
vital organs falter
Patient may be resusitated but will die later of (ARDS,
renal and liver failure, sepsis)
Decompensation
Initial assessment
Airway , Breathing ok?

Circulation
HR within normal limit
Pulse pressure WNL
Warm, Pink, Dry
NO SHOCK
Initial assessment
Airway , Breathing ok?

Circulation
Tachycardia
Cutaneous vasoconstriction
Pulse pressure
Calmy
SHOCK
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Class I Class II Class III Class IV
Blood-Loss[ml] ->750 750-1500 1500-2000 >2000
Blood-loss [%BV] ->15% 15-30% 30-40% >40%
Pulse-Rate [x/min.] <100 >100 >120 >140
Blood-Pressure Normal Normal Decreased Decreased
Pulse-Pressure N or
increased
Decreased Decreased Decreased
Respiratory Rate 14-20 20-30 30-35 >35
Urine out-put
[ml/hour]
>30 20-30 5-15 Negligible
Mental status/CNS Slightly
anxious
Midly
anxious
Anxious
and
confused
Confused
and
lethargic
Estimated Fluid and Blood Losses Based on
Patients Initial Presentation
EBV = 70 ml/kg
Clinical differentiation
1. Hemorrhagic Shock
2. Non Hemorrhagic Shock
Cardiogenic
Tension pneumothorax
Neurogenic
Septic
Anaphylactic
Picture of isreali military or war
Non Hemorrhagic Shock
Cardiogenic Shock
Myocardial dysfunction
Blunt cardiac trauma
Cardiac tamponade
Air embolism
Valve rupture
ECG monitoring
Isoenzynme-CPK
Echocardiography
Tachycardia
Blowing heart sound
Venectasia regio colli
Hypotension
Ventil mechanism/flap-valve
Sesak nafas , RR >
Emphysema subcutan
Perkusi hypersonor
Suara paru menghilang pada ipsilateral
Trakhea terdorong kontralateral
Tachycardia
Hypotension

Tension Pneumothorax
Neurogenic Shock,
Spinal Shock
Cedera tulang belakang
Cedera medulla spinalis
Sympathetic denervasi
Vasodilatasi, gambaran hypovolemia
No tachycardia,
No vasokonstriksi
Septic Shock
Jarang terjadi segera setelah trauma
Dapat terjadi pada kasus trauma yang
terlantar
Luka tembus abdomen, perforasi
Shock septik pada periode awal :
Tachycardia
Perifer hangat
Systolik bisa normal
Pulse pressure lebar
27/03/2014 40 Hasanul, 2009
Pneumothorax
Hematothorax
Cardiac Tamponade
Spinal Shock
Myocardial
Contussion
Hemorrhagic Shock
Perdarahan ( Hemorrhage)


Kehilangan akut volume sirkulasi darah
( hilang volume, hilang RBC )
Volume Darah
(EBV, Estimated Blood Volume)
Dewasa : 70 mL/kg
Anak anak : 80 90 mL/kg



Resusistasi cairan harus segera dimulai bila
tanda tanda dan gejala kehilangan darah
tampak atau diduga, JANGAN menunggu s/d
tanda tanda shock jelas.


Perdarahan kelas I
( s/d 15 % EBV)
Klinis minimal
Pada penderita sehat, tidak perlu diganti
Dalam 24 jam akan ada kompensasi
Bila ada kehilangan cairan tubuh oleh sebab
lain, ganti kehilangan cairan primer
Perdarahan kelas II
( 15 s/d 30% EBV)
tachycardia
tachypnoe
Pulse pressure menyempit ( diastolik naik, ok
katekolamine )
Gelisah ringan
Hampir selalu membutuhkan transfusi
Perdarahan kelas III
( 30 s/d 40% EBV)
tanda perfusi inadekwat
tachycardia
tachypnoe
Pulse pressure menyempit ( diastolik naik, ok
katekolamine )
Systolik menurun
Produksi urine menurun, pekat
Gelisah dan cofuse
Perdarahan kelas IV
( >40% EBV)
tanda perfusi inadekwat sangat jelas
tachycardia
tachypnoe
Pulse pressure sanagt menyempit atau diastolik
yang tdk terukur
Produksi urine sangat menurun s/d negatif, pekat
Penurunan kesadaran
Kulit dingin , pucat, basah
Memerlukan transfusi dan tindakan bedah segera
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Class I Class II Class III Class IV
Blood-Loss[ml] ->750 750-1500 1500-2000 >2000
Blood-loss [%BV] ->15% 15-30% 30-40% >40%
Pulse-Rate [x/min.] <100 >100 >120 >140
Blood-Pressure Normal Normal Decreased Decreased
Pulse-Pressure N or
increased
Decreased Decreased Decreased
Respiratory Rate 14-20 20-30 30-35 >35
Urine out-put
[ml/hour]
>30 20-30 5-15 Negligible
Mental status/CNS Slightly
anxious
Midly
anxious
Anxious
and
confused
Confused
and
lethargic
Estimated Fluid and Blood Losses Based on
Patients Initial Presentation
EBV = 70 ml/kg


PBW = Predictive Body Weight
lk = 50 + 2.3 ( Ht inches 60)
pr = 45.5 + 2.3 ( Ht inches 60)
Kegunaan Klinis
Tabel Prakiraan Kehilangan Darah
Dengan menyesuaikan tanda dan gejala dari penderita pada
tabel, dapat diperkirakan berapa kehilangan darah yang sdh
terjadi.
Kemudian kita dapat memperhitungkan berapa jumlah cairan
yang harus diberikan untuk resusitasi
Bila post resisitasi belum ada tanda perbaikan, maka
kemungkinan :
Ongoing loss
Prakiraan ada kesalahan (BB tidak sesuai, kurang jeli menilai tanda dan
gejala
Ada tambahan kehilangan cairan lain selain perdarahan
Shock bukan ok. perdarahan

Sources of Hemorrhage
Femur fracture ( 1500 mL)
Chest
Abdomen (liver, spleen)
Retroperitoneal ( 2-4 L)
Muscle compartments

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