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 CategoriesCardiogenic • Decreased contractility

• Increased filling pressures, decreased LV stroke work, decreased cardiac output

• Increased systemic vascular resistance à compensatoryHypovolemic • 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 MANAGEMENT1. Treat arrhythmias 2. Diastolic dysfunction may require increased filling pressures 3. Vasodilators if not hypotensive4. Inotrope administration5. Vasopressor agent needed if hypotension present to raise aortic diastolic

pressure 6. Consultation for mechanical assist device7. Preload and afterload reduction to improve hypoxemia if blood pressure

adequate

HYPOVOLEMIC SHOCK MANAGEMENT1. Volume resuscitation : crystalloid, colloid2. Initial crystalloid choices

a. Lactated Ringer’s solutionb. Normal saline (high chloride may produce hyperchloremic acidosis)

3. Match fluid given to fluid lost : Blood, crystalloid, colloid

DISTRIBUTIVE SHOCK MANAGEMENT1. Restore intravascular volume

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2. Hypotension despite volume therapy : Inotropes and/or vasopressors3. Vasopressors for MAP < 60 mm Hg4. Adjunctive interventions dependent on etiologyOBSTRUCTIVE SHOCK MANAGEMENT1. Relieve obstruction

a. Pericardiocentesis b. Tube thoracostomy c. Treat pulmonary embolus

2. Temporary benefit from fluid or inotrope administration

Fluid Therapy1. Crystalloids : Lactated Ringer’s solution, Normal saline2. Colloids : Hetastarch, Albumin, Gelatins3. Packed red blood cells4. Infuse to physiologic endpoints5. Correct hypotension first6. Decrease heart rate7. Correct hypoperfusion abnormalities8. Monitor for deterioration of oxygenation

Inotropic/Vasopressor Agents1. 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 Shock1. Increase O2 delivery2. Optimize O2 content of blood3. Improve cardiac output and blood pressure4. Match systemic O2 needs with O2 delivery5. 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 à 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

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 leakKAN-182 Mira Yulianti (01-107)

a. Pulmonary gas exchange (PaO2:FiO2)b. Requirement for positive pressure (PEEP)c. Chest X-ray

3. Some assessment of response to treatmenta. Changes in acid base balance, lactateb. 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

Patofisiologi Respons Tubuh Terhadap Shock Respons Neuroendokrin Respons Hemodinamik Respons Metabolik

RESPON NEUROENDOKRIN

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Cardiogenic Shock

PUMP=

HEARTPipe =

Vascular

Volume = Blood

Blood Pressure

Cardiac Output x SVRObstructive

Shock

Inotropes (Dop, Dob, Adr, Amr)

Vasopreesor (NE, PE, Adr, Dop)

Release tamponade, etc

Hypovolemic Shock

Fluids

Distributive Shock

RESPON HEMODINAMIK à mekanisme untuk memperbaiki keseimbangan kardiovaskular Redistribusi aliran darah Peningkatan Cardiac Output Memperbaiki Volume Intravaskular

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FEARStimulation of Limbic Area of Brain

increasedHypothalamic, adrenomedullary,

adrenocortical activity

NEUROENDOCRINE RESPONS

Adrenal CortexCortisol Release

RenalRenin Release

Pituitary GlandACTH, ADH, GH release

Adrenal GlandEpinephrine, NE release

Angiotensin II

Adrenal cortexAldosterone

Release

HYPOVOLEMIA

LOSS OF TONIC INHIBITION OF CENTRAL

AND SYMPATHETIC NERVOUS SYSTEM

Aorta/CarotidsHigh pressure baroreceptors

Decreased Renal Perfusion

R atriumLow pressure Stretc

Receptors

Redistribusi Aliran Darah

RESPON HEMODINAMIK

HYPOTENSION

Stimulasi Neuroendokrin

Blood Flow ProtectedHeartBrain

Adrenal/Pituitary Gland

Blood Flow DecreasedSkin

MuscleSplanchnic Circulation

Transcapillary Refill Phase

1. Decreased capillary pressure caused by hypotension2. 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 RESPONSESVenoconstriction

Sympathetic n. system (SNS)Catecholamines (CA)Angiotensin II (ATII)

ADH

Reduced venous capacitance

Arteriolar constrictionSNS, CA, ATII, ADH

Decreased capillary P

Fluid shift from interstitiuminto vascular compartment

Increased distal tubular reabsorption

Aldosterone, ADH

Increased proximal tubular reabsorption

SNS, CA, ATII

Increased myocardial contractilitySNS, CA

Restoration of blood volume

Increased ventricular filling

P

Increased ventricular ejection fraction

SV

CO

BP Increased heart rate

SNS, CA

Increased SVR due to arteriolar constructionSNS, CA, ATII, ADH

SVR

RESPON METABOLIK Hyperglikemia

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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

Sypathetic n. SystemCathecolamine release

Increased contractility

Increased EDV via :Venoconstriction,

Arteriolar constriction, Renal

reabsorbtion

MEMPERBAIKI VOLUME DARAH

Mobilisasi lemak Katabolisme/pemecahan protein

Peningkatan sintesis urea Peningkatan asam amino aromatik

Penurunan sintesis reactan fase akut Peningkatan osmolalitas ekstrasel

RESPON METABOLIKRESPON METABOLIK

Breakdown of skeletal muscle

into a.a.

Conversion of a.a. to glucose

Release of:CatecholaminesCortisolGlucagonGrowth hormone

Impaired peripheral glucose uptake

HYPERGLYCEMIAHYPERGLYCEMIA

Glycogen breakdown

Decreased Blood Volume

Decreased CO

Cellular hypoperfusion and hypoxia

Anaerobic GlycolisisPyruvat converted to lactic acid

METABOLIC ASCIDOSIS

Release of Cathecolamines, Cortisol, Glucagon

Lipolysis

Increase in Plasma Free Fatty Acids

Efek Shock Pada tingkatan SelLow-Flow, Poor Perfusion Hypoxia Anaerobic metabolism Ascidosis Decrease Cellular Energy Efficiency

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CELL MEMBRANE FAILURE:

DIRECT EndotoxinComplementINDIRECTFailure to maintain normal Na+, K+or Ca2+gradientDecreased oxidative phosphorylation

OSMOTIC GRADIENT

Water entry into cell

CELLULAR EDEMA

IMPAIRED INTRACELLULAR

METABOLISM

CELL DEATH

Na+entry into cell

EFEK SHOCK PADA TINGKATAN SEL

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 ResusitasiKAN-182 Mira Yulianti (01-107)

1. Mempertahankan ventilasi2. Meningkatkan perfusi3. Terapi penyebab

MAINTAIN VENTILATIONMAINTAIN VENTILATIONIncreased oxygen

demand

Hyperventilation

Respiratory failureRespiratory acidosis, lethargy-coma, hypoxia

Especially in:Sepsis

HypovolemiaTrauma

Respiratory fatigue Diversi blood flow from vital organ

Organ injury

TREATMENT OF RESPIRATORY FAILUREHypovolemia (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 SHOCKENHANCING PERFUSION / OXYGEN DELIVERY

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

Cardiac output

Arterial O2content

Fluids Transfuse Partially dependent on

FIO2 and pulmonary

status

Inotropes

DO2 = CO x CaO2

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

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