DIAGNOSIS AND MANAGEMENT

OF SHOCK
Shock
 Always a symptom of primary cause
 Inadequate blood flow to meet tissue oxygen demand
 May be associated with hypotension
 Associated with signs of hypoperfusion: mental status change, oliguria, acidosis

Definisi
 Gangguan dari perfusi jaringan yang terjadi akibat adanya ketidakseimbangan
antara suplai oksigen ke sel dengan kebutuhan oksigen dari sel tersebut.
 Semua jenis shock mengakibatkan gangguan pada perfusi jaringan yang selanjutnya
berkembang menjadi gagal sirkulasi akut atau disebut juga sindroma shock
It’s not Low Blood Pressure!!
It’s Hypoperfusion!!

Shock Categories
Cardiogenic • Decreased contractility
• Increased filling pressures, decreased LV stroke work, decreased cardiac output
• Increased systemic vascular resistance à compensatory
Hypovolemic • Decreased cardiac output
• Decreased filling pressures
• Compensatory increase in systemic vascular resistance
Distributive • Normal or increased cardiac output
• Low systemic vascular resistance
• Low to normal filling pressures
• Sepsis, anaphylaxis, neurogenic, and acute adrenal insufficiency
Obstructive • Decreased cardiac output
• Increased systemic vascular resistance
• Variable filling pressures dependent on etiology
• Cardiac tamponade, tension pneumothorax, massive pulmonary embolus

CARDIOGENIC SHOCK MANAGEMENT

1. Treat arrhythmias
2. Diastolic dysfunction may require increased filling pressures
3. Vasodilators if not hypotensive
4. Inotrope administration
5. Vasopressor agent needed if hypotension present to raise aortic diastolic
pressure
6. Consultation for mechanical assist device
7. Preload and afterload reduction to improve hypoxemia if blood pressure
adequate

HYPOVOLEMIC SHOCK MANAGEMENT

1. Volume resuscitation : crystalloid, colloid
2. Initial crystalloid choices
a. Lactated Ringer’s solution
b. Normal saline (high chloride may produce hyperchloremic acidosis)
3. Match fluid given to fluid lost : Blood, crystalloid, colloid

DISTRIBUTIVE SHOCK MANAGEMENT

1. Restore intravascular volume
2. Hypotension despite volume therapy : Inotropes and/or vasopressors
3. Vasopressors for MAP < 60 mm Hg

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4. Adjunctive interventions dependent on etiology
5.
OBSTRUCTIVE SHOCK MANAGEMENT
1. Relieve obstruction
a. Pericardiocentesis
b. Tube thoracostomy
c. Treat pulmonary embolus
2. Temporary benefit from fluid or inotrope administration

Fluid Therapy
1. Crystalloids : Lactated Ringer’s solution, Normal saline
2. Colloids : Hetastarch, Albumin, Gelatins
3. Packed red blood cells
4. Infuse to physiologic endpoints
5. Correct hypotension first
6. Decrease heart rate
7. Correct hypoperfusion abnormalities
8. Monitor for deterioration of oxygenation

Inotropic/Vasopressor Agents
1. Dopamine
 Low dose (2-3 mg/kg/min) – mild inotrope plus renal effect
 Intermediate dose (4-10 mg/kg/min) – inotropic effect
 High dose ( >10 mg/kg/min) – vasoconstriction
 Chronotropic effect
2. Dobutamine
 5-20 mg/kg/min
 Inotropic and variable chronotropic effects
 Decrease in systemic vascular resistance
3. Norepinephrine
 0.05 mg/kg/min and titrate to effect
 Inotropic and vasopressor effects
 Potent vasopressor at high doses
4. Epinephrine
 Both a and b actions for inotropic and vasopressor effects
 0.1 mg/kg/min and titrate
 Increases myocardial O2 consumption

Therapeutic Goals in Shock

1. Increase O2 delivery
2. Optimize O2 content of blood
3. Improve cardiac output and blood pressure
4. Match systemic O2 needs with O2 delivery
5. Reverse/prevent organ hypoperfusion

Pediatric Considerations
 BP not good indication of hypoperfusion
 Capillary refill, extremity temperature better signs of poor systemic
perfusion
 Epinephrine preferable to norepinephrine due to more chronotropic benefit
 Fluid boluses of 20 mL/kg titrated to BP or total 60 mL/kg, before
inotropes or vasopressors
 Neonates  consider congenital obstructive left heart syndrome as cause
of obstructive shock
 Oliguria
 <2 yrs old, urine volume <2 mL/kg/hr
 Older children, urine volume < 1 mL/kg/hr

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How Much Fluid To Give ?
1. Some measure of intravascular filling
a. Pressure (CVP or PAOP)
2. Some assessment of risk of pulmonary oedema and capillary leak
a. Pulmonary gas exchange (PaO2:FiO2)
b. Requirement for positive pressure (PEEP)
c. Chest X-ray
3. Some assessment of response to treatment
a. Changes in acid base balance, lactate
b. Measurement of cardiac output

What do you need to know when you resuscitate patients in Shock ?

 Arterial blood pressure
 Urine output
 Systemic acid–base balance (pH, SBE, lactate)
 Some clinical assessment of tissue perfusion
 “warm and well perfused” or “cold and shut down”
 Some measurement of global blood flow and tissue perfusion
 Cardiac output or cardiac index
 Arterial oxygen delivery, oxygen uptake index
 Mixed venous saturation and PvO2

Cardiogenic Shock Distributive Shock

Inotropes (Dop, Dob, Adr, Amr) Vasopreesor (NE, PE, Adr, Dop)

PUMP
Release tamponade, = Pipe = Vascular Blood Pressure
etc HEART

Cardiac Output x SVR

Obstructive
Shock

Volume = Blood

Fluids Hypovolemic Shock

Patofisiologi Respons Tubuh Terhadap Shock

 Respons Neuroendokrin
 Respons Hemodinamik
 Respons Metabolik

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RESPON NEUROENDOKRIN

FEAR NEUROENDOCRINE RESPONS

Stimulation of Limbic Area of Brain
increased
Hypothalamic, adrenomedullary, adrenocortical activity Adrenal Cortex
Cortisol
Release

R atrium
Low pressure Stretc Receptors

Renal
Renin Release

LOSS OF TONIC INHIBITION Pituitary Gland

OF CENTRAL AND ACTH, ADH, GH release
HYPOVOLEMIA SYMPATHETIC NERVOUS
Adrenal Gland
SYSTEM Epinephrine, NE release

Aorta/Carotids
High pressure baroreceptors

Angiotensin II

Decreased Renal Perfusion

Adrenal cortex
Aldosterone Release

RESPON HEMODINAMIK  mekanisme untuk memperbaiki keseimbangan kardiovaskular

 Redistribusi aliran darah
 Peningkatan Cardiac Output
 Memperbaiki Volume Intravaskular

RESPON HEMODINAMIK

Redistribusi Aliran Darah

HYPOTENSION

Stimulasi Neuroendokrin

Blood Flow Protected Blood Flow Decreased

Heart Skin
Brain Muscle
Adrenal/Pituitary Gland Splanchnic Circulation

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 Limited to 180 beats/min before decreased CO
due to decreased diastolic filling time

CARDIAC OUTPUT = Heart Rate x Stroke Volume

Increased contractility Increased EDV via :

Venoconstriction,
Sypathetic n. System Arteriolar constriction,
Cathecolamine release Renal reabsorbtion

MEMPERBAIKI VOLUME DARAH


 Transcapillary Refill Phase
1. Decreased capillary pressure caused by hypotension
2. Sympathetic increase in precapillary arteriolar constriction

Decrease capillary hydrostatic pressure promotes passage of fluid from interstitium to intravascular space
 Plasma Protein Restitution Phase
Increased plasma osmolarity due to mainly hepatic release of glucose, pyruvate, amino acids, etc.

Increased interstitial osmolarity

Increased interstitial volume and pressure

Transcapillary movement of albumin into intravascular space

HAEMODYNAMIC RESPONSES
Venoconstriction
Sympathetic n. system (SNS)
Catecholamines (CA) Reduced venous
Angiotensin II (ATII) capacitance
ADH

Arteriolar constriction
SNS, CA, ATII, ADH
Increased
ventricular filling
Decreased capillary P P

Fluid shift from interstitium into vascular

compartment Restoration of
blood volume
Increased distal tubular
reabsorption SV 
Aldosterone, ADH

Increased proximal tubular

reabsorption
SNS, CA, ATII CO 
Increased myocardial contractility
SNS, CA Increased ventricular
ejection fraction
BP 
Increased heart rate
SNS, CA

Increased SVR due to

SVR 
arteriolar construction
SNS, CA, ATII, ADH

RESPON METABOLIK
 Hyperglikemia
 Mobilisasi lemak

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  Katabolisme/pemecahan protein
 Peningkatan sintesis urea
 Peningkatan asam amino aromatik
 Penurunan sintesis reactan fase akut
 Peningkatan osmolalitas ekstrasel

RESPON METABOLIK
Release of:
Catecholamines
Cortisol Glycogen
Glucagon breakdown
Growth hormone

Conversion of
a.a. to glucose

HYPERGLYCEMIA

Impaired peripheral
glucose uptake
Breakdown of
skeletal muscle
into a.a.

Decreased Blood Volume


Decreased CO

Cellular hypoperfusion and hypoxia

Anaerobic Glycolisis
Pyruvat converted to lactic acid

METABOLIC ASCIDOSIS

Release of Cathecolamines, Cortisol, Glucagon


Lipolysis

Increase in Plasma Free Fatty Acids

Efek Shock Pada tingkatan Sel

Low-Flow, Poor Perfusion  Hypoxia  Anaerobic metabolism  Ascidosis  Decrease Cellular Energy Efficiency

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 Glucose breakdown. (A) Stage one, glycolysis, is anaerobic
(does not require oxygen). It yields pyruvic acid, with toxic by-
products such as lactic acid, and very little energy. (B) Stage
two is aerobic (requires oxygen). In a process called the Krebs
or citric acid cycle, pyruvic acid is degraded into carbon dioxide
and water, which produces a much higher yield of energy.

EFEK SHOCK PADA TINGKATAN SEL

CELL MEMBRANE FAILURE:
DIRECT
Endotoxin
Complement
INDIRECT
Failure to maintain normal Na+, K+ or Ca2+ gradient L
CELTH
Decreased oxidative phosphorylation DEA

OSMOTIC
GRADIENT

Na+ entry Water entry CELLULAR IMPAIRED

into cell into cell EDEMA INTRACELLULAR
METABOLISM

Efek Shock Pada Tingkatan Organ

 Kidney : Oliguric renal failure, High output renal failure
 Liver : Liver failure
 GI tract : Failure of intestinal barrier (sepsis, bleeding)
 Lung : Capillary leak associated with or caused by sepsis and infection
TENSION PNEUMOTHORAX

Prinsip Resusitasi
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1. Mempertahankan ventilasi
2. Meningkatkan perfusi
3. Terapi penyebab

MAINTAIN VENTILATION
Increased oxygen
Especially in: demand
Sepsis
Hypovolemia
Trauma
Hyperventilation

Diversi blood flow from vital organ

Respiratory fatigue

Organ injury
Respiratory failure
Respiratory acidosis, lethargy-coma, hypoxia

TREATMENT OF RESPIRATORY FAILURE

Hypovolemia (Blood Loss)

Decreased CO

Decreased Oxygen Delivery, Increased Oxygen Requirement

Metabolic ascidosis, hypoxemia  tachypnea

TREATMENT : Primary Resuscitation, Oxygen, Mechanical ventilation if needed

TREATMENT CONCEPT OF SHOCK

ENHANCING PERFUSION / OXYGEN DELIVERY

DO2 = CO x CaO2

Cardiac Arterial O2
output content

Oxygen delivery/DO2 = HR X SV X Hb X S02 X 1.34 + Hb X paO2

Inotropes Transfuse
Fluids Partially
dependent on
FIO2 and
pulmonary
status

Summary
 Shock is an altered state of tissue perfusion severe enough to induce
derangements in normal cellular function
 Neuroendocrine, hemodynamic and metabolic changes work together to restore
perfusion
 Shock has many causes and often may be diagnosed using simple clinical
indicators
 Treatment of shock is primarily focused on restoring tissue perfusion and oxygen
delivery while eliminating the cause

KAN-182 Mira Yulianti (01-107)