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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