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SHOCK

Clinical features and


pathophysiology

WIDODO

Sejarah syok
1960s
1960s
Sejak
Sejak 1905
1905 Sfignomanometer
Sfignomanometer
Syok
=
Hipotensi
Syok = Hipotensi
1970s
1970s
Swan
Swan &
& Ganz
Ganz
Syok
Syok == Hipovolemik,
Hipovolemik, cardiogenik,
cardiogenik, distributif
distributif
1980s
1980s
Teori
Teori supranormal
supranormal value
value (shoemaker),
(shoemaker),
Syok
=
hipoperfusion/
Decrease
Syok = hipoperfusion/ Decrease DO2
DO2 (oxygen
(oxygen delivery)
delivery)
2000s
2000s
SvO2
SvO2 (saturasi
(saturasi mixed
mixed vein),
vein), ditemukan
ditemukan sebagai
sebagai target
target endendpoint
resuscitation
pada
tissue
point resuscitation pada tissue
Syok
Syok == ketidakseimbangan
ketidakseimbangan antara
antara oksigen
oksigen delivery
delivery dan
dan
oksigen
konsumsi
dan
gangguan
pada
mikrosirkulasi
oksigen konsumsi dan gangguan pada mikrosirkulasi
2009-2011s
2009-2011s
Pada
Pada syok,
syok, selain
selain Terjadi
Terjadi hipoperfusi
hipoperfusi (( DO2),
DO2), juga
juga terjadi
terjadi
kerusakan
mitokondria
(seluler
level)
kerusakan mitokondria (seluler level)

Definition of Shock
Inadequate tissue perfusion
Decreased oxygen supply
Anaerobic metabolism
Accumulation metabolic waste

Shock
Life-threatening condition
Immediate or delayed mortality
Multiple aetiology

Recognition and Assessment


Physiological consequences of shock
clinical features
Document and report on progression

The Cardiovascular System

Pathogenic mechanisms of
shock
Hypovolemic
Hypovolemic
Capillary
leak

SVR
SVR
CO
CO
Microcirculation
Microcirculation
Maldistribution
Maldistribution

Distributive
Distributive

SVR
SVR
CO
CO

Extracardiac
Extracardiac
Obstructive
Obstructive

MAP
MAP

Myocardial
depressan

Inffective
perfusion

SHOCK
Cell Injury
MODS

Coronary
Coronary
perfusion
perfusion

Cardiogenic
Cardiogenic

Signs of Shock
Cold, clammy and pale skin
Rapid, weak, thready pulse
Shallow, rapid breathing
Oliguria
Reduction in MAP
Cyanosis
Loss of consciousness

Early Signs of Shock in Non


Complicated Patients
High index of suspicion
Minimum tachycardia
No measurable changes occur in blood
pressure
Pulse pressure is potentially very useful

Hypotension - a sign of cardiovascular


insufficiency
PUMP not working properly - cardiogenic
Not enough FLUID in the system- hypovolaemia
TUBING
:Distribution
network
is
malfunctioning- distributive
Normally, if one component malfunctions the
others compensate to return the blood pressure
to normal.
In shock, one element has malfunctioned and
the others have failed to adequately
compensate.

Level of Consciousness
Report and record

Alert
Verbal response to stimuli
Pain response to stimuli
Unresponsive to any stimuli

Causes of Shock
Severe or sudden blood loss
Large drop in body fluids
Myocardial infarction
Major infections
High spinal injuries
Anaphylaxis
Extreme heat or cold

Types of Shock
Hypovolemic Shock:
haemorrhagic
or non haemorrhagic

Other causes of shock


Cardiogenic Shock
Septic Shock
Neurogenic Shock
Anaphylactic Shock

Stages of shock
Compensated shock

Autotransfusion

Decompensated shock
Blood moves to more
vital organs

Irreversible shock
Multiple system / organ
damage
Even with treatment, death
is the result

Evaluation of Shock
Internal or external hemorrhage
Underlying cardiac problems
Sepsis
Trauma to spine cord
Contact with known allergic substance
Determine amount of blood loss
How long has casualty been bleeding?

Invasive monitoring
Essential in the definitive treatment
Direct arterial pressure
Central venous pressure
Cardiac output

Direct arterial pressure

CVP AND CIRCULATING VOLUME?

Shock states & haemodynamic manifestations


Type

HR

SV

CVP

PCWP

CO/CI

PR

Spinal Shock

Anaphylaxis

Sepsis

Heart Block

Pump Failure

Relatively
low

Relatively
low

Vol Overload

Inflow obstruction

Outflow obstruction

Hypovolemic
Distributive

Cardiogenic

Treatment of Shock
Increase tissue perfusion and
oxygenation status
Maintain airway
Control bleeding
Baseline vital signs
Level of consciousness

Apakah
Oxygen Delivery
(DO2) ?

6 langkah perjalanan oksigen dari


udara ke sel
Uptake in the Lung

Oxygenation PaO2

Carrying capacity

CaO2

SaO2
Haemoglobin
Flow rate
Cardiac Output

Delivery

OXYGEN DELIVERY
(DO2)
Cardiac Output
(CO)

Heart Rate
(HR)

Preload

(SaO2 or SpO2)

Stroke Volume
(SV)

Afterload

Contractility

Hemoglobin
(Hgb)

DO2

Oxygen Delivery
DO2
=
Q (L/min/m2) x
CaO2
(L/min/m2)
DO2 = 3 x (1.34 x Hb x SaO2) x 10
DO2 = 3 x (1.34 x 14 x 0.98) x 10
DO2 = 551 ml/min
(10 dL/L adalah Faktor koreksi, sebab CI dalam L/min/m2 sedangkan CaO 2
in ml/dl)

Normal Range (CO):


ml/min
Normal Range (CI) :
ml/min/m2

800

520

1000

720

6 langkah perjalanan oksigen dari


udara ke sel
Uptake in the Lung
Carrying capacity
Delivery
Organ distribution
Diffusion

Cellular use

Oxygenation PaO2

CaO2
DO2

SaO2
Haemoglobin
Flow rate
Cardiac Output
Autoregulation
Distance

Mikrosirkulas
i

Mitochondria

ATP = energy

VO2

Oxygen
consumption/uptake

The Fick Equation:


Oxygen Uptake adalah produk perkalian dari
Cardiac Output dan perbedaan antara Oxygen
Content arteri dengan vena:

VO2 = Q x [(CaO2 - CvO2)]

Oxygen
consumption/uptake
The Fick Equation:

VO2 = Q x (CaO2 - CvO2)


VO2 = Q x [(1.34 x Hb) x (SaO2 - SvO2) x
10]
VO2 = 3 x [ (1.34 x 14) x (.98 - .73) x 10 ]
VO2 = 3 x [ 46 ]
VO2 = 140 ml/min/m2

Normal VO2: 110 - 160 ml/min/m2

Extraction Ratio O2ER


adalah fraksi oksigen yang diambil dari kapiler
(capillary bed)

O2ER: berasal dari rasio dari Oxygen Uptake


terhadap Oxygen Delivery
O2ER = VO2 / DO2 x 100
Normal Extraction
25 %
atau 1-SvO2 = if SvO2 75% --> O2ER = 25%

Mixed Venous Oxygen


(SvO2)
Apakah Mixed Venous
Oxygen Saturation (SvO2),
dan bagaimana
mengukurnya?

Treatment of Shock
Positioning
ABCD approach
Fluid therapy
Drug therapy
Keep patient at normal temperature
Prevent hypothermia
Minimize effect of shock

On-going assessment - every 10-15 minutes

Specific measures
Hypovolaemia: Blood transfusion
Electrolyte/acid base imbalance
Sepsis: Antibiotics, ?steroids
Neurogenic: Steroids
Anaphylactic: Adrenalin

Algorithm for Investigation and Treatment of


Shock

Hypovolaemic Shock
Haemorrhage: Overt or occult
Reduction in circulating volume
Reduction in venous return and CO
O2 supply-demand imbalance
Lactic acidosis
Reduction in venous oxygen saturation
Non haemorrhagic hypovolaemia
Severe burns, vomiting and diarrhoea

Changes in CO and MAP in haemorrhage

Clinical Signs of Acute


Hemorrhagic Shock
% Blood loss
< 15
15-30

Clinical Signs
Slightly increased heart rate, local
swelling, bleeding
Increased heart rate, increased diastolic
blood pressure, prolonged capillary refill

30-50

Above findings plus: hypotension,


confusion, acidosis, decreased urine output

> 50

Refractory hypotension, refractory


acidosis, death

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

Non-Haemorrhagic Shock
Cardiogenic Shock
Septic Shock
Neurogenic Shock
Anaphylactic Shock

Cardiogenic Shock
Primary myocardial failure
Arrhythmia
Tamponade
Contusion
Pump failure
Reduction in cardiac output:
Decreased blood supply
Decreased oxygen delivery

Cardiogenic Shock
Assess for:
Signs of heart failure
Signs of tamponade
Cardiac dysrrhythmia
Myocardial infarction
Tachycardia
Muffled heart sounds or third heart sound
Engorged neck veins with hypotension
Dyspnoea
Oedema in feet and ankles

COLLABORATIVE
MANAGEMENT
Treatment is aimed at :

Goal of management : Early assessment &


Treat Reversible Causes
Protect ischemic
myocardium
Improve tissue perfusion

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

Septic Shock
Bacterial, viral, fungal infection
Gram negative and gram positive bacteria
High output failure: warm shock
Fever, tachycardia, tachypnoea, leucocytosis

Inadequate oxygen extraction


High SvO2, Metabolic acidosis

Cold shock
Atypical presentation in immuno-compromised
patients
Diabetes, Cirrhosis, immunosuppression

Severe Sepsis

Stimulation of inflammatory cascades


Cardiovascular derangement
Vasoplegia & hypotension
Relative hypovolaemia
Widespread dysfunction of microcirculation:
capillary leak
Simultaneous activation of coagulation cascades
Formation of intravascular thrombus
Tissue injury & multi-organ dysfunction

Septic shock multi-organ failure


CNS : confusion
Heart: reduced diastolic BP -> fall in myocardial O2
supply. Reversible biventricular dilatation
myocardial depressant substance.
Lungs: V/Q mismatch. ARDS
Kidneys: failure of autoregulation. ARF from fluid
redistribution, circulating nephrotoxins (cell injury)
Liver: cholestasis & hyperbilirubinaemia
Splanchnic circulation: hypotension leads to superficial
mucosal injury. Bacterial translocation.

Septic shock multi-organ failure


Metabolic & Endocrine:
Hyperglycaemia: circulating catecholamines,
lactic acidosis, catabolic state
Adrenal insufficiency

Septic Shock in trauma


patients
Develops 2 - 5 days after injury occurs
Carries a poor prognosis
Assess for:
Penetrating abdominal injuries
Signs of infection
Warm pink skin and dry elevated body
temperature
Tachycardia
Wide pulse pressures

Neurogenic Shock
Caused by:
Spinal cord injury
Certain drugs
Brain stem, spinal or torso trauma

Venous pooling and arteriolar dilatation


Signs and Symptoms:
Hypotension without tachycardia
Warm pink skin
Low blood pressure & minimal response to fluids

Anaphylactic shock

Anafilaksis

Suatu sindrom klinik yang terjadi

akibat suatu reaksi alergis (reaksi


imunologis) bersifat sistemik yg
cepat
mengenai beberapa organ,
Respirasi
meliputi
:
Sirkulasi
Pencernaan
Kulit dan lain-lain
Jika sindrom tsb menyebabkan syok
disebut syok Anafilaksis, yg kalau
tidak dikelola dgn cepat dan tepat
dpt KEMATIAN

Anafilaktoid
(anaphylactoid)
Non immunologic
reaction
Merupakan reaksi anafilaksiis yg tdk

disebabkan oleh reaksi imunologis


Mekanisme belum diketahui dgn
jelas
Gejala sama dgn reaksi imunologis,
tapi sedikit lebih ringan
Lebih banyak ditemukan dibanding
reaksi imunologis.

REAKSI
Anafilaksis

Anafilaktoid

Imunologis

Non Imunologis

Lepasnya
Mediators

GEJALANYA SAMA
KEDUANYA KEMATIAN

Anaphylactic Shock
Rapid onset
Primary systems:
Cardiovascular, Respiratory
Skin, Gastrointestinal, coagulation
Face, pharynx and laryngeal oedema
Adrenaline is life saving

Anaphylactic Shock
Diffuse vasodilatation
Increase size of vascular bed
Blood is trapped in small vessels and viscera
Temporary loss in total circulatory volume
Sudden severe allergic reaction to:
Drugs, Toxins, Foods, Plants

Symptoms

Apprehension and flushing


Wheezing or shortness of breath & cough
Rapid, weak pulse
Cyanosis
Generalized itching or burning
Watering and itching of the eyes
Hypotension
Coma

Algoritma
penanganan syok
anafilaksis

Baringkan dalam posisi syok, alas keras


Bebaskan jalan nafas
Tentukan penyebab dan lokasi masuknya
(ringan)
Jika masuk lewat ekstremitas pasang turniket
Adrenalin 1 : 1000 0,25 ml (0,25 mg) subkutan
Monitor pernapasan dan hemodinamik
Suplemen oksigen
Adrenalin 1 : 1000 0,25 ml(0,25 mg) intramuskuler (sedang)
atau 1:10000 2,5 5 ml(0,25-0,5) intravena (berat)
Berikan sublingual atau trans tracheal bila vena kollaps

Terapi
syokdrug
Adrenalin
merupakan
of choice
dari syok
anafilaksis
anafilaksis.
Hal ini disebabkan 3 faktor
yaitu :

1. Adrenalin merupakan bronkodilator yang


kuat
2. Adrenalin merupakan vasokonstriktor
pembuluh darah dan inotropik yang kuat
3. Adrenalin merupakan histamin bloker,
melalui peningkatan produksi cyclic AMP

Adminsitration Guidelines
for Epinephrine
Mild reactions:

0.3-0.5 mL 1: 1000 (0.3-0.5 mg) SC


May repeat q5-10 min
Consider 0.1-0.2 mL (0.1-0.2 mg) at site
of sting or entry

Moderate to severe reactions:


Slow IV infusion of 0.1-0.2 mL 1:1000 in
10 mL NS or 1-2 mL of 1:10,000 in 10 mL NS
(1:100,000)
For persistent hypotension consider:
Continous infusion of 1-2 mg in 250 mL
D5W or NS (4-8 g/mL) at 2+ g/min
SC = subcutanneously; IV = intravenously;
NS = normal saline; D5W= 5% dextrose in

Shock Key Points

Blood Pressure is Cardiac Output multiplied by Peripheral


Resistance.

Cardiac Output is Heart Rate times Stroke Volume.

Hypotension is caused by either inadequate Cardiac Output or


inadequate Peripheral Resistance

Heart Rate, Stroke Volume and Total Peripheral Resistance


exist in dynamic equilibrium: these interactions maintain blood
pressure. If one of the three becomes abnormal, the other two
compensate. This represents the cardiovascular physiologic
reserve.

Hypotension is an indication of 1) an abnormality of Heart


Rate, Stroke Volume or Peripheral Resistance, & 2) failure of
the others to compensate

Shock Key Points

Shock is acute circulatory failure leading to inadequate tissue perfusion


and end organ injury: it classified as being due to malfunction of 1) the
Pump (cardiogenic), 2 ) the Tubing (distributive), or 3) the Fluid
(hypovolemic).

The heart rate is a fundamental element of hypotension both in terms of


cause (tachyarrhythmias / bradyarrhythmias) and compensation
hypotension should be accompanied by a tachycardia.

Low Stroke volume is caused by a problem with reception or a problem


with ejection.

Problems with reception are: inadequate venous return or cardiac


inflow obstruction.

Fluid loss is caused by either absolute hypovolemia (e.g. blood loss) or


relative hypovolemia (third spacing).

Shock Key Points

Cardiac inflow obstruction is caused by a pericardial (tamponade) or


intrathoracic process (PEEP), or a lesion within the heart itself (mitral
stenosis).

Problems with ejection include pump failure (ischaemia, overload,


contusion, inflammation) and outflow obstruction (embolism, aortic
stenosis, aortic cross clamps).

Shock caused by low peripheral vascular resistance is caused by loss of


tonic vasoconstriction (vasoplegia), due to sympathectomy, anaphylaxis
or sepsis, leading to relative hypovolemia.

Vasodilation associated with septic shock occurs due to increased


synthesis of nitric oxide, activation of ATP-sensitive potassium channels
in vascular smooth muscle, and deficiency of vasopressin.

Summary
Life threatening: Early goal directed therapy and regular
monitoring by trained staff will change outcome.

Early detection : DONT RELY ON BP


High index of suspicion
Monitor casualties susceptible to shock

TERIMA
KASIH

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