SHOCK 2

SYOK

SHOCK

SYOK : Sirkulasi inadekwat Gagal perfusi jaringan Dapat menyebabkan gagal organ

• Aliran darah keorgan yg tidak adekwat • Hipotensi diikuti hipoperfusi • Ketidak seimbangan V02 & D02

.Shock can be result of -poor oxygen delivery -maldistribution of blood flow -the effect of cytokines on cell

function -a low perfusion pressure -or a combination of these factorsThe common denominator in all shock

states and the earliest manifestation of shock is reduced oxygen consumption (VO2)

.

FUNGSI MITOCHONDRIA

1. Pembentukan ATP2.Pengaturan ion Ca++ intraseluler3.Sensor oksigen4.Inisiatif awal program apoptosis dan

nekrosis sel5.Steroidogenesis dan sinyaling

.Cellular hypoxia can inciteSystemic Inflammatory Respon Syndrome

Two or more conditions *Temperature > 38o C or < 36o C *HR > 90x/min. *RR > 20 or PaCO2 < 32 torr *WBC > 12.000, <4.000 or<10% immature forms Multiple Organ Dysfunction Syndrome

The oxygen debt is caused by

*A low flow : in hypovolemic and cardiogenic shock

*A cellular or metabolic deficit : in septic shock

*A maldistribution of blood flow : in other types of shock

Shock states

Released various cytokines and interplay with various organ systems to cause end –organ damage or MODS.

Cytokines : NO-nitric oxide IL-2 TNF respiratory failure, capillary leak,

shunting, redistribution, depressed myocardial function, oxygen uncoupling, and cellular ischaemia

The mediator response in SIRS

1. Induction2. Triggering of cytokines synthesis

3. Evolution of cytokines cascade4. Elaboration of secondary mediators with ensuing cellular injury

Example :Endotoxin phagocytic cells (macrophag)

TNF-α activate complement coagulation cascades & induces endothelial cell activation

Hemodynamic profiles of shockType of shock PAOP C.O SVR----------------------------------------------------------- Cardiogenic ↑ ↓ ↑Hypovolemic ↓ ↓ ↑Distributive ↓ or N ↑ or N or ↓ ↓Obstructive ↑ or N or ↓ ↓ ↑

PAOP pulmonary artery occlusion pressureCO cardiac outputSVR systemic vascular resistance

EVALUATION OF SYMPTOMS

HISTORY In cardiogenic shock : cardiac disease,

poor cardiac function,CHF, myocardial isch., valvular heart disease.

In hypovolemic shock : blood loss, trauma, fluid losses, dehydration, third spacing or other fluid losses.

History

In distributive shock : infection or allergic agent, neurologic events or a reaction to various immunologic substance.

In obstructive shock : trauma cardiac tamponade, tension pneumothorax

In adult drop Systolic BP > 40 mmHg significant hypotension

General Symptoms of ShockCNS changes *Confusion, coma, combative behavior, agitation, stuporSkin changes *Cool, clammy, warm, diaphoresisCardiovascular *Increase or decrease heart rate, arrhythmia, angina, low high or

normal cardiac output, changes in pulmonary

pressure

General symptoms of shock

Pulmonary *Increased RR, increase or decrease in end- tidal CO2, decrease O2

saturation, increased pulmonary pressures, respiratory failure, decreased tidal

volume, decreased FRCRENAL *Decreased urine output, elevation in

BUN and creatinine levels, change in urine electrolyte levels

Common effects of shock on organs

Systemic : Capillary leak, formation of micro

vascular shunts, cytokine release

Cardiovascular : circulatory failure, depression of cardiovascular

function , arrhythmiaHaematologic : bone marrow suppression, coagulopathy, DIC, platelet dysfunction

.Hepatic : liver insufficiency, elevation of liver enzyme levels, coagulopathyNeuroendocrine : change in mental status, adrenal suppression, insulin resistance, thyroid dysfunctionRenal : renal insufficiency, change in urine electrolyte levels, elevation of BUN and creatinine levelsCellular : cell-to-cell dehiscence, cellular swelling, mitochondrial dysfunction, cellular leak

Hypovolemic shock

Cause : depletion of fluid in the intravascular space (hemorrhage, vomiting, diarrhea, dehydration, capillary leak or a combination)

SIRS capillary leakFindings : decreased CO, decreased

PCWP, increase SVREcho : decreased right-sided filling,

decreased stroke volume, increase aortic diameter

Perdarahan

Kehilangan akut darah dari sistim sirkulasi

Volume darah normal : * Dewasa : 7% BB ideal *Anak : 8-9% BB ideal

Perdarahan

Mulai segera resusitasi cairan agressifPengobatan disesuaikan dengan respon

pasien pada terapi awal

Tanda perdarahan Klas I -----------------------------------------------------------

Perdarahan ml sampai 750Perdarahan (%BV) sampai 15%Nadi < 100Tensi NormalTek Nadi (mmHg) Normal atau

naikNafas 14 - 20Urine ml/jam > 30SSP/status mental sedikit Cemas Penggantian cairan Kristaloid (hukum 3:1)

Tanda perdarahan Klas II -----------------------------------------------------------Perdarahan ml 750-1500Perdarahan (%BV) 15-30%Nadi >100Tensi NormalTek Nadi (mmHg) TurunNafas 20-30Urine ml/jam 20-30SSP/status mental Cemas

sedangPenggantian cairan Kristaloid (hukum 3:1)

Tanda perdarahan Klas III -----------------------------------------------------------Perdarahan ml 1500-2000Perdarahan (%BV) 30-40%Nadi > 120Tensi TurunTek Nadi (mmHg) TurunNafas 30-40Urine ml/jam 5-15SSP/status mental Cemas

gelisah Penggantian cairan Kristaloid &

darah (hukum 3:1)

Tanda perdarahan Klas IV -----------------------------------------------------------Perdarahan ml >2000Perdarahan (%BV) >40%Nadi >140Tensi turunTek Nadi (mmHg) turunNafas >35Urine ml/jam tak adaSSP/status mental gelisah/letargiPenggantian cairan kristaloid & darah

(hukum 3:1)

Perdarahan bermakna

perlu konsultasi BEDAH

.

Keputusan Pengobatan

Respon pasien pada resusitasi cairan merupakan penentu terapi berikutnya

INGATBedakan antara “hemodinamik stabil” dan

“hemodinamik normal”

Keputusan Terapi

Respon cepat*< 20% perdarahan*Stabil : respon pada penggantian cairan*Lanjutkan monitor*Evaluasi dan konsultasi bedah

Keputusan Terapi

20-40% perdarahanTidak stabil : memburuk setelah terapi cairan

awalLanjutkan cairan dan darahEvaluasi dan konsultasi bedahPerdarahan berlanjut : operasi

Keputusan terapi

Tak ada respon (minimal)> 40% perdarahanTak ada respon pada terapi cairanSingkirkan kemungkinan shock

nonhemorrhagikOperasi segera

Diagnosis & pengobatan

Pitfalls*Tensi tidak sama dengan cardiac output*Umur*Atlit*Hipotermi*Pengobatan*Pacu-jantung

Distributive shock

Septic shockAnaphylactic shock, acute adrenal

insufficiency, neurogenic shock.Problem : shunts and capillary leakHaemodynamic : normal/increased CO, low

SVRLow-to-normal LVFPEcho : low SV, increase aortic diameter

Mitochondria pada sepsis

Terjadi gangguan morphologi (integritas membrane) mitochondria jantung setelah 24 jam sepsis Gram negative

(Circ shock 1992,26:452-560)Pembengkakan mitochondria otot rangka, setelah

18-48 shock endotoxin (Virchows arch 1994; 424:653-659)Fragmentasi dari membrane sel setelah 12-24

jam infeksi Escherichia Coli (shock 1996; 5:378-384)

Terganggu fungsi respirasi dari mitochondria hepar setelah 4 jam pemberian endotoxin

(Crit Care Med 2004; 32:478-488) Isi mitochondria diaphragma berkurang

sampai 50% (Am J Phys Endocrinol Metab 2006; 291 E. 1044-50)

Mekanisme Gangguan PadaMitochondria

Mitochondria pada Sepsis

Obstructive shock

Direct mechanical obstruction to cardiac filling

Case : cardiac tamponade, massive increase in intrathoracic pressure

Diagnostic testing

General laboratory : blood lactate, bicarbonate,

glucose, electrolyte Zn,Mg,Ca, BUN, creatinine, liver enzymes, ABG

analysisCoagulationHematologic parametersRenal parametersEchocardiography

Complications of shock

Low flow tissue perfusion activating factor of SIRS cytokines and vasoactives organ failure and MODS.

Sensitive organ : Lung (ARDS), kidney (ARF) If low flow state is not rapidly corrected

other organ dysfunctionMarker : metabolic acidosis or lactic acidosis prolonged increased morbidity and

mortality

Differential Diagnosis

Distributive shockHypovolemic shockObstructive shockCardiogenic shock

DD

Distributive shock :SepsisAnaphylaxisAnaphylactoid reactionsNeurogenic shockAdrenal gland dysfunctionTrauma, burns and pancreatitis

DD

Hypovolemic shockDehydration (low fluid intake, diarrhea, bowel

obstruction, sweating or diabetes insipidus)Diuresis (diuretics, hyperglycemia)Capillary leak and third spacing (burns,

sepsis, pancreatitis, surgical stress) Hemorrhage (trauma , GIT bleeding,

fractures, vascular injuries, ectopic pregnancy, etc)

Anemia

DD

Obstructive shockCardiac tamponade and restrictive

pericarditisPulmonary embolism Intrathoracic processes (pneumothorax,

pulmonary hypertension, diaphragmatic rupture)

DD

Cardiogenic shockAMISeptal infarctionsCardiomyopathies (viral, alcoholic, infectious)

Management and Therapy

The basic goal of shock therapy is the restoration of effective perfusion to vital organs and tissue before the onset of cellular injury.

Basic resuscitation :1.Rapid placement of a large- bore i.v line or a

high-flow central line as a route for fluid resuscitation

2. Secure the airway and high-flow oxygenation oxygen saturation > 92%. Put on mechanical ventilation if necessary

3.Foley catheter

General goals for support of shock patients

Hemodynamic supportMAP > 60-65 mmHgPCWP= 15-18 mmHgCardiac index > 2.1 L/min per m2 of body

surface area for cardiogenic and obstructive shock

Cardiac index > 4.0 L/min per m2 body surface area for septic, traumatic, or hemorrhagic shock

General goals

Optimization of oxygen deliveryHb level > 10 g/dlArterial oxygen saturation > 92%

Reversal of organ system dysfunctionMaintain urine output > 0.5 ml/kg per hour

Therapy

Fluid management Crystalloid, koloid and blood componentVasoactive drugsMonoclonal antibodies

Shock in children

CO = SV x HR In children : the cardiac output is primarily

maintained by changes in heart rate.Hypovolemia or decreased SVR

compensate with dramatic increase in the heart rate.

HR 160-200 x/min impending circulatory failure

CO falls by 25% rapid decompensationBradycardia & hypotension

uncompensated shock rapidly irreversible shock.

Signs of Shock Early Late-------------------------------------------------------

Narrowed pulse pressure Decreased systolic pressure

Orthostatic changes Decreased diastolic pressure

(older patients) Cold, pale skinDelayed capillary filling Altered mental statusTachycardia Confusion and lethargyHyperventilation Diaphoresis Decreased urine output

Classification and Etiologies of ShockTYPE OF SHOCK ETIOLOGYHypovolemic: Trauma (hemorrhage) Pump is empty Dehydration

(Vomiting etc) Metabolic disease

(DM) Excessive sweating

(infant)Cardiogenic: Weak/sick Rhytm disturbances pump Congestive heart

failure Cardiomyopathy Post-resuscitation

Classification and Etiologies of ShockTYPE OF SHOCK ETIOLOGY -------------------------------------------------------------Distributive: Sepsis Fluid distribution Anaphylaxis Spinal cord injury Third spacing of

fluidsObstructive: Obstruction Tension

pneumothorax of outflow Cardiac tamponade Pulmonary embolism

Therapy of shock in childrenPositionOxygen Intravenous accessFluidReassess Inotropes- Epinephrine, Dobutamine,

DopamineCardiogenic shock – SVT: Adenosine or synchronized

cardioversion VF: defibrillation

Note

The most common error in treating shock is underestimating the severity of the condition.

If there are signs of compensated shock, treat early and aggressively to prevent a bad outcome.

All patients require an IV, oxygen therapy, and cardiopulmonary monitoring.

Summary

Resuscitation of shock is based on close monitoring and hemodynamic support and replacement of intravascular volume.

Kelainan Elektrolit

Harus dilihat secara menyeluruh adanya kelainan yang lain

Osmolarity = 2Na + glucose + BUN + ETOH

18 2.8 4.6

mosmol/Liter

Hyponatremia < 135 meq/L

Manifestasi klinik bila Na < 120 abdominal pain, headache, agitations, hallucinations, cramps, confusion, lethargy, seizures

Kausa hiponatremia

Hypotonic Hypovolemic -- Extra renal Renal losses EuvolemicHypervolemic Isotonic (pseudo)Hypertonic

Hipernatremia Na > 150

Gejala bila osmolarity > 350 Irritability, ataxia Lethargy, coma, seizure

Kausa hipernatremia

Loss of water Reduced water intake Water loss in excess of sodiumGain of sodium

Hipokalemia K < 3.5

Bila K < 2.5 CNS -weakness, cramps, hiporefleksia GIT – ileus CVS – disritmia, worsening of digoxin toxicity hipotensi/hipertensi U waves, ST depression, prolonged

QT Renal –metabolic alkalosis worsening hepatic

encephalopathy Glucose intolerance

Kausa hipokalemia

Shift into the cellReduced intake Increased loss Renal loss MiscellaneousGI loss (vomiting, diarrhea, fistulas)

Hiperkalemia K > 5.5

Cardiac arrestECG : peak T wave, prolonged PR intervalVF, blockNeromuscular: weakness, paralysisGIT : vomiting, colic, diarrhea

Kausa hiperkalaemia

FactitiousMetabolic acidemia (acute) Increased intake into the plasmaOliguric RF Impaired renin-aldosterone axisPrimary renal tubular potassium secretory

defect Inhibition of renal tubular secretion of KAbnormal K distribution