gagal sirkulasi inggris---
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Circulation Failure
(Shock)
PEDIATRIC EMERGENCY DEPARTMENT
MEDICAL FACULTY
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SHOCK
Acute syndrome that occurs because of cardiovascular
dysfunction and the inability of the circulatory system to
provide adequate oxygen and nutrients to meet themetabolic demands of vital organs
Cardiac Output = Heart rate x Stroke Volume
CO = HR x SV
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Shock phase
1. Compensated
- Early homeostatic mechanism will maintain vitalorgan function
- Blood pressure, urine output & cardiac functionis still normal
2. Uncompensated- Circulation failure
- Toxic material released
- Vital organ disturbance
3. Irreversible
- Cell damage cell death
- Multi organ system dysfunction
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Shock Clinical Manifestation
Clinical signs Compensated UncompensatedIrreversibleBlood loss (%) < 25 25-40 > 40
Heart rate tachycardia + tachycardia ++ tachycardia/ bradicardia
Systolic BP normal normal/ falling plummeting
Pulse volume normal/ reduce reduced + reduced ++
Capillary refill normal/ increase increase + increase ++
Skin cool, pale cold, mottled cold, deathly pale
Respiratory rate tachypnoea + tachypnoea ++ sighing respiration
Mental state mild agitation lethargic/ uncooperative reacts only to pain/
unresponsive
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Typesof Shock
1. HYPOVOLEMIC
decreased circulating blood volume
2. DISTRIBUTIVE
misdistribution of normal intravascular volume
3. CARDIOGENIC
cardiac pump failure
4. OBSTRUCTIVE
obstruction of cardiac filling/out flow
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ETIOLOGI
1. Hypovolemic
Dehydration, Hemorrhage, Capillary leaks
2. DistributiveVasodilatation venous pooling decrease preload
Anaphylaxis, sepsis, drug intoxication, trauma, spinal cordinjury
3. CardiogenicCongenital heart disease, myocarditis, dysritmia
4. Obstructive Cardiactamponade, tension pneumothorax, pulmonary
embolus
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PATHOPHYSIOLOGY OF SHOCK
COMPENSATED
HIPOVOLEMIC SHOCK
PRELOAD
CARDIACOUTPUT BLOOD PRESSURE
SYMPHATETIC DISCHARGE
VASOCONSTRICTIONHR
CONTRACTILITY
UNCOMPENSATED
MYOCARDIAL PERFUSION
MYOCARDIAL O2CONSUMPTION
TISSUE ISCHEMIA
CARDIACOUTPUT
Loss of auto regulation
MEDIATOR RELEASE of microcirculation
CELL FUNCTION
CELL DEATH
DEATHOF ORGANISM
Diadaptasi dari : White MK, Hill JH, Blumer JL : Shock in the pediatric patient,
Adv Pediatr 34:139-174, 1987
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Diagnosis
History Etiology ? Most caused : hypovolemia(dehydration, hemorrhagic), sepsis and congenital
hearth disease, respectively
Physical examination - Cardiovascular status : heart rate, polls, capillary
refill, blood pressure
- Other vital organs : respiration rate & type,consciousness, skin perfusion (pale, mottled,
cyanosis), temperature, urine output
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Laboratory Data
routine blood (Hb , Ht , thrombocytopenia, leucocytosis,
neutropenia), renal function test (BUN, creatinine ), liver
function test, electrolyte, hypoglycemia, arterial blood gas, blood
culture, routine urine
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TREATMENT& MONITORING
A. InitialResuscitation
- Ventilation
- Oxygenation(FiO2 100%)
- Vascularaccess(60-90 second
not successful intra osseous)
20 ml/ kgbw (
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InitialMonitoring
1. Monitoringcardiovascular/ vitalsigns and peripheral
perfusionafterfluid challenge (loading)
2. Urine Catheter > 1 ml/ kgbw/ hour
3. Laboratory analysis: urine & blood, blood gas analysis,
glucose & electrolyte, culture
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B. NextResuscitation
1. Ifnotrespond after 2-3 xfluid challenge intubations & ventilation support
2. Evaluation blood gas analysis, and corrected : -
metabolic acidosis (pH < 7,15) natrium bicarbonate
8,4% 1 meq /kgbw (ventilation adequate)- respiratory acidosis ventilator pulse ox meter for
perfusion monitoring -
hypocalcaemia, hypoglycemia and electrolyte
3. If hypotension (+) and polls (-) catheter central venous andgive fluid according CVP
4. Inotropic drugs
5. Blood Transfusion ifHb < 5 g/dl ( 10 ml/ kgbw)
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INOTROPIC DRUGS
DRUG DOSE EFFECT
Dopamine 1-4 ug/kg/mnt Vasodilator splanchivic5-10 ug/kg/mnt Contractility
>10-15 ug/kg/mnt Vasoconstriction Isoproterenol
0,1-1,0 ug/kg/mnt Contractility
Vasodilator peripheral Dobutamine
1-15 ug/kg/mnt Contractility Epinephrine0,1-0,2 ug/kg/mnt Contractility
resistance
systemic vascular
0,5-1,5 ug/kg/mnt resistance systemicvascular
Bolus 10-20 ug/kg/mnt contractility
resistance
systemic vascular
Ca-chloride 10-20 mg/kg contractility
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ResuscitationMonitoring
- Whatstheetiology ?
Consultstootherdivision
- Evaluationand treatmentforotherorgans
: renal, liver, heart, lung, CNS
- Laboratory, ECG and x-ray photo
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FluidResuscitation
1. Crystalloid
- Normalsaline(NaCl0,9%)
- Isotonic fluid: * Ringerslactate
* Ringersacetate
* Normosol, Plasma-lyte, etc
* Bloodvolume
* Changelossextracellular fluid
* Inducteddiuresis* Cheap
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2. Colloid
- Blood* Whole blood* Low titer - O negative (donor universal)
* Cross matched
* Washed erythrocyte
- Plasma and its component
* Plasma (Fresh frozen)
* Albumin* Plasmanate
- Molecule weight >> capillary wall
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- Benefit :
* A little colloid volume intravascular >>
* Colloid osmotic pressure lung edema rare
- Side effect :
* Anaphylactic reaction
* Affected clothing time
* Expensive
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Thank you
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