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Shock

and
Management Concept
Hardi Darmawan, MD, MPH&TM, FRSTM
Dept of Physiology ,Sriwijaya Medical School
RK Charitas Hospital
Palembang
What is shock?
SHOCK SYNDROME
Shock is a condition in which the
cardiovascular system fails to perfuse tissues
adequately
An impaired cardiac pump, circulatory
system, and/or volume can lead to
compromised blood flow to tissues
Inadequate tissue perfusion can result in:
generalized cellular hypoxia (starvation)
widespread impairment of cellular
metabolism
tissue damage organ failure
death
Definition
Inadequate peripheral perfusion
leading to failure of tissue oxygenation
may lead to anaerobic metabolism
Shock is a major critical illness that
involves almost every organ system. It is
not simply a problem of decreased blood
pressure. Rather, it is a problem of
inadequate tissue perfusion (Rice,1991)
Definisi
Hipotensi
Tekanan Darah Sistolik < 90 mmHg
Tekanan Darah Sistolik berkurang > 40
mmHg
Hipoperfusi
Perubahan status mental
Oliguria
Asidosis laktat
Diagnosis of Shock
MAP < 60
Clinical s/s of
hypoperfusion of
vital organs
PATHOPHYSIOLOGY OF SHOCK
SYNDROME
Impaired tissue perfusion occurs
when an imbalance develops between
cellular oxygen supply and cellular
oxygen demand.

All types of shock eventually result in
impaired tissue perfusion & the
development of acute circulatory
failure or shock syndrome.
Oxygen transport
and utilization
CARDIAC OUTPUT = HR X SV
Sympathetic n.
system
Catecholamine
release
Increase EDV via:
Venoconstriction
Arteriolar constriction
Renal reabsorption
Increased
contractility
Limited to 180 beats/min
before decreased CO
due to decreased
diastolic filling time
PATHOPHYSIOLOGY OF SHOCK
SYNDROME

Cells switch from aerobic to anaerobic metabolism


lactic acid production


Cell function ceases & swells


membrane becomes more permeable


electrolytes & fluids seep in & out of cell



Na+/K+ pump impaired

mitochondria damage

cell death



COMPENSATORY MECHANISMS:
Sympathetic Nervous System (SNS)-
Adrenal Response
SNS - Neurohormonal response
Stimulated by baroreceptors
Increased heart rate
Increased contractility
Vasoconstriction (SVR-Afterload)
Increased Preload
COMPENSATORY MECHANISMS:
Sympathetic Nervous System (SNS)-
Adrenal Response
SNS - Hormonal: Renin-angiotension system
Decrease renal perfusion
Releases renin angiotension I
angiotension II potent vasoconstriction &
releases aldosterone adrenal cortex
sodium & water retention
COMPENSATORY MECHANISMS:
Sympathetic Nervous System (SNS)-
Adrenal Response
SNS - Hormonal: Antidiuretic Hormone
Osmoreceptors in hypothalamus stimulated
ADH released by Posterior pituitary gland
Vasopressor effect to increase BP
Acts on renal tubules to retain water
COMPENSATORY MECHANISMS:
Sympathetic Nervous System (SNS)-
Adrenal Response
SNS - Hormonal: Adrenal Cortex
Anterior pituitary releases
adrenocorticotropic hormone (ACTH)
Stimulates adrenal Cx to release
glucorticoids
Blood sugar increases to meet
increased metabolic needs

Failure of Compensatory Response
Decreased blood flow to the tissues causes
cellular hypoxia
Anaerobic metabolism begins
Cell swelling, mitochondrial disruption, and
eventual cell death
If Low Perfusion States persists:

IRREVERSIBLE DEATH IMMINENT!!

Hypovolaemia and Shock
decreased blood volume
decreased cardiac output
decreased oxygen delivery
impaired macrocirculation
vasoconstriction
Inadequate perfusion
Erythrocyte aggregation
impaired micro circulation
tissue ischemia
organ failure
kidney
bowel
endotoxin
release
septic shock
Dampak Syok
Shock
Microcirculatory
Failure
Systemic
Inflammatory
Response
Translocation
Impaired Gut
Barrier Function
Compromised
Mucosal Integrity
Mucosal
Ischaemia
Reduced GI
Perfusion
Perfusi normal
Pompa jantung
Volume sirkulasi
Tahanan pembuluh darah perifer
Pathophysiological causes of shock.
Reduced Cardiac
Output
pump
problem
(Cardiogenic -
Ischaemic)

Reduced
Intravascular volume
fluid
problem
(Hypovolaemi
c)

Reduced Vascular
Resistance
pipe
problem
(Neurogenic -
Septic -
Anaphylactic)

After about an hour most patients will demonstrate a dysfunction of all
components and it may be difficult to identify the original cause.

CLASSIFICATIONS OF SHOCK

Cardiogenic
Hypovolemic
Distributive
sepsis,
anaphylaxis, and
neurogenic (spinal or epidural anaesthesia,
and spinal cord injury).
Obstructive
pulmonary embolism,
dissecting aortic aneurysm,
pericardial tamponade and
tension pneumothorax
Combined
Dissecting Throrecic
Aortic Aneurysm
Pulmonary Embolism
Pulmonary Emboli
Tamponade
Stages of Shock
Initial stage - tissues are under perfused, decreased CO,
increased anaerobic metabolism, lactic acid is building
g Compensatory stage - Reversible. SNS activated by low
CO, attempting to compensate for the decrease tissue
perfusion.
@ Progressive stage - Failing compensatory mechanisms:
profound vasoconstriction from the SNS ISCHEMIA
Lactic acid production is high metabolic acidosis
j Irreversible or refractory stage - Cellular necrosis
and Multiple Organ Dysfunction Syndrome may occur
DEATH IS IMMINENT!!!!
Pathophysiology Systemic
Level
Net results of cellular shock:
Osystemic lactic acidosis
Odecreased myocardial contractility
Odecreased vascular tone
Odecrease blood pressure, preload,
and cardiac output


Tanda dan gejala syok
Sistem Kardiovaskuler
Gangguan sirkulasi
Pucat, dingin, sianosis
Vena perifer kolaps
Nadi cepat dan halus
Tekanan darah rendah kurang bisa
jadi pegangan
Vena jugularis penting.
CVP

Sistem Respirasi
Nafas cepat dan dangkal
Sistem susunan saraf pusat
Perubahan mental / kesadaran
Sistem saluran cerna
Mual dan muntah
Sistem saluran kencing
Produksi urin < cc/kg/jam
Tanda dan gejala syok
Clinical Presentation:
Generalized Shock
Mental status: (LOC)
restless, irritable, apprehensive
unresponsive, painful stimuli only

Decreased Urine output

Shock Syndromes
Hypovolemic Shock
blood VOLUME problem
Cardiogenic Shock
blood PUMP problem
Distributive Shock
[septic;anaphylactic;neurogenic]
blood VESSEL problem
Hypovolemic Shock
Loss of circulating volume Empty
tank decrease tissue perfusion
general shock response
ETIOLOGY:
Internal or External fluid loss
Intracellular and extracellular compartments
Most common causes:
OHemorrhage
ODehydration
Hypovolemik Shock
A 25 year old woman was admitted in the ER
She had given birth 2 hours ago helped by dukun
Hypovolemic Shock:
External loss of fluid

Fluid loss: Dehydration
Nausea & vomiting, diarrhea, massive
diuresis, extensive burns

Blood loss:
trauma: blunt and penetrating
BLOOD YOU SEE
BLOOD YOU DONT SEE


BP 60, pulse just palpable,
over 160 per minute
Cold clammy skin, unconscious

Multiple iv line were inserted
and hemodilution started
Hypovolemic Shock:
Internal fluid loss

Loss of Intravascular integrity

Increased capillary membrane
permeability

Decreased Colloidal Osmotic Pressure
(third spacing)
Pathophysiology of
Hypovolemic Shock
Decreased intravascular volume leads to.
Decreased venous return (Preload, RAP) leads to...
Decreased ventricular filling (Preload, PAWP) leads
to.
Decreased stroke volume (HR, Preload, &
Afterload) leads to ..
Decreased CO leads to...(Compensatory
mechanisms)
Inadequate tissue perfusion!!!!
Assessment & Management
S/S vary depending on severity of fluid
loss:
15%[750ml]- compensatory mechanism
maintains CO
15-30% [750-1500ml- Hypoxemia, decreased
BP & UOP
30-40% [1500-2000ml] -Impaired
compensation & profound shock along with
severe acidosis
40-50% - refactory stage:
loss of volume= death

On arrival
After infusion
Guidelines for the clinical use of
red cell transfusions
British Journal of Hematology 2001, 113, p24-31
15% loss (750 ml)
crystalloids, no transfusion
15-30% loss (800-1500 ml)
crystalloids, colloids, no transfusions
30-40% loss (1500-2000 ml)
crystalloids, colloids, probably transfusion
> 40% loss (> 2000 ml)
crystalloids, colloids, requires transfusion
Clinical Presentation
Hypovolemic Shock
Tachycardia and tachypnea
Weak, thready pulses
Hypotension
Skin cool & clammy
Mental status changes
Decreased urine output: dark &
concentrated

Hypovolemic Shock:
Hemodynamic Changes
Correlate with volume loss
Low CO
Decreased RAP ( Preload)
Decreased PAD, PAWP
Increased SVR (Afterload)

Initial Management Hypovolemic
Shock
Management goal: Restore circulating
volume, tissue perfusion, & correct
cause:
Early Recognition- Do not relay on BP!
(30% fld loss)
Control hemorrhage
Restore circulating volume
Optimize oxygen delivery
Vasoconstrictor if BP still low after volume
loading
Penanganan Syok Hipovolemik
Mengembalikan volume intravaskuler
Tekanan Darah
Nadi
Perfusi organ
Pilihan cairan
Kristaloid
Koloid
PRC
American Soc of Anesthesiologists 1996



2
1
Hemorrhage

1. Loss of IVF
1. Poor sluggish perfusion
2. Increasing pulse rate
3. Decreasing BP
2. Partially compensated by
ISF (transcapillary refill)
2
1
Crystalloids for
hemorrhage

1. Rapid Infusion to
normalize IVF
2. After IVF stabilized,
infusion is intended for
ISF
3. Volume required thus
2-4x initially lost IVF
1
2
Ringer Lactate
Ringer Acetate
NaCl 0.9%
Pulmonary Edema Neurogenic
Treatment
Impaired perfusion secondary to
reduced volume
restore volume
Restoration of circulating volume can
be achieved by the infusion of 3 mL of
balanced electrolyte solution for each
milliliter of blood lost.
Fluids are infused through two large-
bore intravenous lines
Treatment
Administration of supplemental
oxygen
Control bleeding
Foley catheter to monitor renal
function
establishment of urine output at
approximately 50 cc/hr for the
adult
Pasang jalur IV satu/lebih no. 18 / 16
Infus cepat Kristaloid / kombinasi+ koloid
Bila perdarahan, ambil contoh darah
Bila vena sudah terisi, peningkatan isi
nadi dan tekanan darah, infus lambatkan
Jangan kelebihan cairan
Penanganan Syok Hipovolemik
Cardiogenic Shock

DEFINISI
Simply stated, cardiogenic shock is lack of
perfusion from pump failure.
Cardiogenic shock is related to the
inability of the myocardium to produce
sufficient flow and/or pressure to
maintain adequate tissue perfusion.


Cardiogenic Shock
The impaired ability of the
heart to pump blood
Pump failure of the right or
left ventricle
Most common cause is LV
MI (Anterior)
Occurs when > 40% of
ventricular mass damage
Mortality rate of 80 % or >

Etiologies of Cardiogenic Shock
I. Ischemic heart disease
A. Acute myocardial infarction, usually
anteroseptal
B. Ventricular septal defect
C. Papillary muscle rupture
D. Ventricular aneurysm
II. Valvular heart disease
A. Acute mitral or aortic insufficiency
B. Severe aortic stenosis

Etiologies of Cardiogenic Shock
III. Arrhythmias
A. Supraventricular
B. Ventricular
IV.Trauma
A. Tension pneumothorax
B. Pericardial tamponade, may
include nontraumatic causes
C. Cardiac contusion
Cardiogenic Shock:
Pathophysiology
Impaired pumping ability of LV leads
to
Decreased stroke volume leads to..
Decreased CO leads to ..
Decreased BP leads to..
Compensatory mechanism which may lead
to
Decreased tissue perfusion !!!!
Cardiogenic Shock:
Pathophysiology
Impaired pumping ability of LV leads
to
Inadequate systolic emptying leads to ...
q Left ventricular filling pressures (preload)
leads to...
q Left atrial pressures leads to .
q Pulmonary capillary pressure leads to
Pulmonary interstitial & intraalveolar
edema !!!!
Diagnosa Syok Kardiogenik
Cardiac Output berkurang
LV filling pressure meningkat
SVR meningkat
Clinical Presentation
Cardiogenic Shock
Similar catecholamine compensation
changes in generalized shock &
hypovolemic shock
May not show typical tachycardic
response if on Beta blockers, in heart
block, or if bradycardic in response to
nodal tissue ischemia
Mean arterial pressure below 70 mmHg
compromises coronary perfusion
(MAP = SBP + (2) DBP/3)
Cardiogenic Shock:
Clinical Presentation
Abnormal heart sounds

Murmurs
Pathologic S3 (ventricular gallop)
Pathologic S4 (atrial gallop)
Clinical Presentation
Cardiogenic Shock
Pericardial tamponade
muffled heart tones, elevated neck
veins
Tension pneumothorax
JVD, tracheal deviation, decreased or
absent unilateral breath sounds, and
chest hyperresonance on affected
side
CLINICAL ASSESSMENT
Pulmonary &
Peripheral Edema
JVD
CO
Hypotension
Tachypnea,
Crackles

PaO2
UOP
LOC
Hemodynamic changes:

PCWP,PAP,RAP &
SVR
COLLABORATIVE MANAGEMENT
Goal of management
Treat Reversible Causes
Protect ischemic myocardium
Improve tissue perfusion
Treatment is aimed at
Early assessment &
treatment!!!
Optimizing pump by:
Increasing myocardial O2
delivery
Maximizing CO
Decreasing LV workload
(Afterload)
COLLABORATIVE MANAGEMENT
Limiting/reducing myocardial damage
during Myocardial Infarction:
Increased pumping action & decrease
workload of the heart
Inotropic agents
Vasoactive drugs
Intra-aortic balloon pump
Cautious administration of fluids
Transplantation
Consider thrombolytics, angioplasty in specific
cases

Management Cardiogenic
Shock
OPTIMIZING PUMP FUNCTION:
Pulmonary artery monitoring is a
necessity !!
Aggressive airway management: Mechanical
Ventilation
Judicious fluid management
Vasoactive agents
Dobutamine
Dopamine
Management Cardiogenic
Shock
OPTIMIZING PUMP FUNCTION (CONT.):
Morphine as needed (Decreases preload,
anxiety)
Cautious use of diuretics in CHF
Vasodilators as needed for afterload
reduction
Short acting beta blocker, esmolol, for
refractory tachycardia

Hemodynamic Goals of
Cardiogenic Shock
Optimized Cardiac function involves cautious
use of combined fluids, diuretics, inotropes,
vasopressors, and vasodilators to :
Maintain adequate filling pressures (LVEDP
14 to 18 mmHg)
Decrease Afterload (SVR 800-1400)
Increase contractility
Optimize CO/CI
Treatment of
Cardiogenic Shock
Determinants of Myocardial
Oxygen Consumption
I. Heart rate
II. Contractility
III. Wall tension, preload
IV. Afterload
Treatment
Cardiogenic shock cannot be managed
appropriately without the ability to
measure right and left ventricular filling
pressures, cardiac index, and arterial blood
pressure or the ability to calculate oxygen
delivery, oxygen consumption, and
pulmonary and systemic vascular
resistance. The pulmonary artery
catheter,therefore, is mandatory.

Treatment
Broadly based on four methods
(a) increasing contractility
(b) altering preload and afterload
(c) providing mechanical support
(d) controlling arrhythmias.
Treatment
Increasing Contractility
The three drugs commonly used to increase
cardiac contractility are dobutamine,
dopamine, noradrenalin and isoproterenol.
Reducing Preload and Afterload
Diuretics may be used as an adjuvant in the
treatment of cardiogenic shock but not as a
primary agent.
vasodilator therapy may be added to reduce
preload and afterload, thereby enhancing
cardiac output and reducing myocardial
oxygen needs
Treatment
Mechanical Interventions
tension pneumothorax, relief of
tension in the chest cavity
pericardiocentesis in the case of
pericardial tamponade
intraaortic balloon pump
Treatment
Common Drugs for Arrhythmias
Supraventricular
tachycardia
Digitalis
Verapamil
Propanolol
Procainamide
Quinidine
Ventricular ectopy
Lidocaine
Procainamide
Bretylium
Quinidine
DISTRIBUTIVE SHOCK
Maldistribution of blood to the tissues.
Acute vasodilation without concommitant
increase in intravascular volume.
Inadequate tissue perfusion.
This type of shock is seen in :
sepsis,
anaphylaxis, and
neurogenic (spinal or epidural
anaesthesia, and spinal cord injury).
Mechanism of distributive
shock
http://content.nejm.org/cgi/reprint/345/8/588.pdf
Sepsis
Anaphylaxis
Neurogenic

Septic Shock

DEFINISI
Result of the systemic effects of infection,
primarily with bacterial or fungal
organisms
inadequate oxygen delivery
supernormal oxygen demand by the
increased metabolism of septic cells
metabolic derangement of cellular
metabolism such that cells cannot
utilize oxygen
Pathophysiology
Early Septic Shock (Warm Shock)
low systolic blood pressure
a relative normal pulse pressure and
stroke volume
normal or high cardiac output
Because these patients tend to be
vasodilated and have a low systemic
vascular resistance, the skin is usually
warm (or even flushed) and dry. (a
"relative" hypovolemia)

Pathophysiology
Early Septic Shock (Warm Shock)
Tachycardia and tachypnea
Arterial blood gases usually reveal a
moderate respiratory alkalosis
Lactate levels are usually normal or
only mildly increased initially
Pathophysiology
Late Septic Shock (Cold Shock)
Impaired organ function
intravascular fluid retention
depletion of the functional
extracellular fluid volume
Cardiac index usually falls below
normal
Lactate levels begin to rise rapidly
bicarbonate levels fall

Pathophysiology
Late Septic Shock (Cold Shock)
pH becomes increasingly acidotic
The skin becomes cold, clammy,
mottled, and cyanotic
Oliguria and depressed mental
status are common
accompaniments of severe sepsis.
Diagnosa Syok Distributif
Cardiac Output normal atau meningkat
LV filling pressure normal atau rendah
SVR berkurang

Gambaran Hemodinamik Syok
Jenis Syok PAOP
Cardiac
Output
SVR
Kardiogenik
Hipovolemik
Distributif / nl / nl /
Obstruktif
Tamponade
Jantung
Emboli Paru



/ nl






Hipotensi
Biasanya (tidak selalu) cardiac output
berkurang, kecuali Sepsis berat
Tidak selalu berarti syok
Hipertensi bisa CO rendah dan
hipoperfusi organ (Gagal Jantung)
Penting pemeriksaan fisik

PRINCIPLES OF MANAGEMENT
identify cause
establish adequate ventilation and
oxygenation
restore optimum intravascular
volume
maintain adequate cardiac output
and renal perfusion
maintain optimum internal
metabolic environment

Penanggulangan Syok
Prinsip dasar
Meningkatkan O
2
delivery
Cara
resusitasi cairan
meningkatkan kontraktilitas jantung
meningkatkan SVR
Memperbaiki kelainan irama
Optimalisasi O
2
content darah
Pasang kateter urin
The goal of all treatment is to maintain adequate
tissue perfusion and treat the underlying cause
Penanganan Syok Distributif
Syok Septik
I. Correct primary process
A. Antibiotics
B. Drainage
II. Resuscitation
A. Ventilatory support and 02, as
needed
B. Fluids
C. Inotropes
D. Vasodilators or vasopressors
Resuscitation
increase vascular volume
crystalloid solutions are preferred for raising
intravascular volume
severe acidosis may impair cardiac function if the
arterial pH is < 7. 1, bicarbonate may be required.
Dopamine in doses of 5 to 15 ug/kg/min seems
ideal for improving myocardial contractility and
cardiac output in hypotensive vasodilated
patients.

Syok Anafilaktik
Epinephrine SQ
Resusitasi cairan
Epinephrine IV
Penanganan Syok Distributif
Terapi Cairan
Mengganti volume intravaskuler
Menentukan status volume cairan
pasien
Vena leher
Auskultasi paru
CVP
Resusitasi Cairan
Koreksi hipotensi
Turunkan HR
Koreksi hipoperfusi
Oliguria
Perubahan status mental
Asidosis laktat
Pantau perburukkan oksigenasi
Prioritas dalam Terapi Cairan
EMERJENSI :
VOLUME INTRAVASKULAR
CURAH JANTUNG
PERFUSI ORGAN VITAL
SUB-EMERJENSI :
INTERSTITIAL
INTRASEL
TANDA-TANDA VITAL
PROD. URIN

Jenis Cairan
Kristaloid
Ringer Asetat / Ringer Laktat
Normal Saline
Koloid
Hetastarch
Albumin 5%
PRC
Meningkatkan kapasitas angkutan O
2
Fresh-frozen plasma
Tidak diindikasikan untuk mengganti volume





TERAPI CAIRAN
ASERING
RINGER LAKTAT
NORMAL SALINE

RESUSITASI

KRISTALOID

KOLOID

ELEKTROLIT

NUTRISI
MENGGANTIKAN KEHILANGAN AKUT CAIRAN
DEXTRAN- 40
MEMENUHI KEBUTUHAN HARIAN
ELEKTROLIT DAN NUTRISI
KA-EN 1B
KA-EN 3A
KA-EN 3B
KA-EN 4A
KA-EN 4B

AMIPAREN
AMINOVEL- 600
PAN- AMIN G
KA-EN MG 3
Martos -10
TRIPAREN I
TRIPAREN II






RUMATAN
KONSEP MEDIS

KOREKSI
- NaCl 3 %
- MgSO
4
20 %
- Mannitol 20 %

TREATMENT CONCEPT OF SHOCK

ENHANCING PERFUSION / OXYGEN DELIVERY
Oxygen delivery/DO
2
= HR X SV X Hb X S0
2
X 1.34 + Hb X paO
2
Cardiac
output
Arterial O
2

content
Fluids
Transfuse
Partially
dependent on
FIO
2
and
pulmonary
status
Inotropes
DO
2
= CO x CaO
2
Cardiac Output x SVR
Pipe = Vascular
Pump =
Heart
Volume =
Blood
Hypovolemic
Shock
Cardiogenic
Shock
Distributive
Shock
Inotropes
(Dob,Dop,Adr,Amr)
Vasopressor ( NE,PE,ADR,Dop)
Fluids
Obstructive
Shock
Release
tamponade,etc
Blood Pressure
John Collin Warren (1800s)

momentary pause
in the act of
death.

Samuel D. Gross
(late 19
th
century)
rude unhinging of
the machinery of
life.

Arthur C. Guyton