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Shock Shock Presentation Transcript

  • Dr. BALBIR SINGHDNB PEDIATRICSJ.L.N. HOSPITAL & RESEARCH CENTREBHILAI
  • DEFINITION• Shock is an acute syndrome that occurs because of cardio vascular dysfunction and inability of circulatory system to provide adequate oxygen and nutrients to meet the metabolic demand of vital organ. OrAcute circulatory failure with inadequate tissue perfusion resulting in generalized cellular hypoxia. If untreated leads to metabolic acidosis, organ dysfunction and death.
  • CATEGORISATION OF SHOCK1. On the basis of type Hypovolemic Cardiogenic Distributive Obstructive Dissociative2. On the basis of Severity Compensated Decompensated Irreversible
  • REGULATORY SYSTEM• Baroreceptors / Chemoreceptors in carotid body . Aortic Arch.• Volume receptors – In rt Atrium and pulmonary bed.• Adrenal medulla through catecholamine.• Renin Angiotensin Aldosterone System .• Hypothalemic pituitary response through ACTH and Vasopressin
  • PRE-DISPOSING FACTOR- Asphyxia- Prematurity- Sepsis- Blood loss- Metabolic Derrangement (i) Hypoglycemia (ii) Hypocalcemia
  • ETIOLOGY OF SHOCKHYPOVOLEMIC Blood Loss - Fetomaternal - Twin to twin transfusion - Birth Trauma - DIC Fluid Loss - Excessive insensible loss in preterm - Poor fluid intake - Vommiting - DiarrheaCARDIOGENIC - CHD - Congenital myocarditis - Cardiomyopathy - Arrhythmias - Hypoglycemia - Acidosis and sepsis
  • DISTRIBUTIVE - Septicemia - Adrenal Insufficiency - Neurogenic - HIE - Administration of vasodilatorsOBSTRUCTIVE - Congenital Diaphragmatic Hernia - Tension Pneumothorax - Interstitial Emphysema - Cardiac TamponadeDISSOCIATIVE - Severe anaemia - Methaemoglobinemia
  • COMPENSATEDBlood Pressure NormalDecreased tissue perfusion - Cold, pale,Ashen grey skin -Tachycardia - Normal / Mild Tachypnoea -CFT- prolonged -U/O- Adequate -BP- Normal - Normal /Wide pulse pressure - Bounding Peripheral pulses - Vomiting and Ileus - Irritable - Peripheral to core temperature diff. >2 F.
  • DECOMPENSATED STAGE• Anaerobic metabolism sets decreased tissue perfusion- lactic acidosis-depresses myocardium.• Characterized by hypotension and exxag signs of decreased tissue perfusion• Marked tachycardia• Tachypnoea / acidotic breathing• Marked decreased in CFT• Mottling• Hypotension• Oliguria• Lethargic• Temperature difference b/n p/c > 5° F.
  • IRREVERSIBLE STAGE• Characterised by severe damage to vitals organs- Death occurs inspite of restoration of circulation• Bradycardia• Acidotic breathing and apnea• Cold and Cyanotic periphery• Anuria• Gross hypotension• Coma
  • PRINCIPLES OF MANAGEMENT1) Rapid recognition and resuscitation2) Correction of secondary consequences of Shock3) Maintain vital organ function4) Identification and correction of aggravating factors5) VIP approach should be used. V= Ventilation I= Infusion P= Pumping or Cardiovascular stability
  • THERAPEUTIC ENDPOINTS• Normal pulses(no differential b/w peripheral & central)• CRT< 2sec• Warm extremities• Normal mental status• Normal BP• Urine output > 1ml/kg/hr• ↓Serum Lactate• ↓ Base deficit• Svo2 >70%
  • Positioning & O₂ Administration• Place a hypotensive child in the Trendlenburg position as long as breathing is not compromised• Allow a stable child to remain in most comfortable position• High flow O₂ in all children with shock• Ventillatory support may be needed
  • Vascular Access• For fluid resuscitation & administration of medication• Compensated Shock- Peripheral access is preffered• Hypotensive Shock- Intraosseous or Central
  • FLUID RESUSCITATION• Give isotonic crystalloid in a 20 ml/kg bolus over 5-20 min.• Repeat 20 ml/kg boluses to restore blood pressure and tissue perfusion.• Repeat fluid bolus based on clinical signs like HR,CRT,level of consciousness & urine output.• Suspected cardiogenic shock-large fluid boluses not recommended.• Monitor for pulmonary oedema or worsening tissue perfusion during infusion.• FLUID REFRACTORY SHOCK – not responding to >60ml/kg fluid.
  • • Fluid resuscitation may consist of natural or artificial colloids or crystalloids.• Crystalloids are less expensive.• Fluid resuscitation initially target a CVP of >8mmHg.• More rapid & greater amount may be needed in pt. with sepsis induced tissue hypoperfusion
  • TYPE OF SHOCK: FLUID BOLUSES / RATE OF DELIVERYType of shock Volume of Rate of delivery fluidHypovolemic shock (non- 20 ml/kg bolus (repeat Deliver rapidlyDKA) PRN) (over 5-10 min)Distribute shockObstructive shockCardiogenic shock 5-10 ml/kg bolus Deliver more slowly(Non poisonings) (repeat PRN) (over 10-20 min)
  • MONITORING To assess effectiveness of fluid resuscitation & pharmacological support• Spo₂• Heart rate• Blood pressure & pulse pressure• Mental status• Temprature• Urine output
  • FREQUENT ASSESSMENT Frequently reassess child’s respiratory,cardiovascular & neurologic status to• Evaluate trends in child’s condition• Determine response to therapy• Plan the next treatment interventions At any point child’s condition could deteriorate,requiring life saving interventions such as Endotracheal intubation or Needle thoracotomy.
  • Indication for Blood Products• Hypovolemic neonate due to blood loss with inadequate perfusion despite 2-3 boluses of 20 ml/kg of isotonic crystalloid• Packed RBCs 10 ml/kg• Warm blood should be used• Complications- hypothermia,myocardial dysfunction,hypocalcemia
  • PHARMACOLOGIC SUPPORT• Vasoactive agents used because they affect -Myocardial contractility -Heart rate -Vascular smooth muscle tone• Choice of agent depend on child’s physiologic state• Indicated when shock persist after adequate volume resuscitation to optimize preload
  • (1) Ionotropes -Dopamine,Dobutamine,Epinephrine• ↑ Cardiac contractility,↑ HR• Variable effect on SVR(2) Phosphodiesterase inhibitors -Milrinone,amrilinone• ↓ Afterload• Improve coronary artery blood flow & contractility(3)Vasodilators – Nitroglycerine,Nitroprusside• ↓ Afterload,↓ Venous return(4)Vasopressors(Vasoconstrictors) – Epinephrine,NE,Dopamine,Vasopressin• ↑ SVR• NE has ionotropic effects whereas Vasopressin is a pure vasoconstrictor
  • CHOICE OF VASOACTIVE AGENT DEPENDS ON UNDERLYING PATHOPHYSIOLOGY Normal BP Low BP First line Second line First line Second lineCardiogenic shock Dobutamine Milrinone Adrenaline Low dose(myocardial dysfunction milrinone+increase SVR)Warm septic shock(decrease NA(preferred) or dopamine NA + VasopressinSVR+ - myocardial with aggressive fluid dobutamine/ (never alone,dysfunction) rususcitation. Add dopamine add to NA) dobutamibe if shock not reversedCold septic shock (myocardial Dobutamine milrinone Adrenaline/D Add NA ifdysfunction SVR increase) opamine MAP remains low.
  • Dopamine Dobutamine Norepinephrine EpinephrineLow dose ↑ C.O. ↑ TPR ↑ cardiac contraction2-5 µg/kg/min ↑ stroke volume ↑ SBP ↑DBP ↑ H.R.vasodilatation ↑ renal without marked ↑perfusion in H.R.Moderate dose No/ minor effect C.O. unchanged BP rise → dose on5-10 µg/kg/min on BP and PVR Especially useful in rapid I.V. inj.↑ myocardial contraction children with low BP SBP> DBP↑ C.O.High dose > 15 µg/kg/min Dose 3-20 µg/kg Dose 0.1- 1 µg/kg/min Vasodilataion at smallVasoconstriction /min dose↑ SBP Vasoconstriction at↑ pulse pressure higher dose Dose 0.01-2µg/kg/minDrip calculation – Drip calculation – Drip calculation – Drip calculation –6 x b.w.(kg) =mg in 6 x b.w.(kg) =mg 0.6 x b.w.(kg) =mg in 0.6 x b.w.(kg) =mg in100ml;1 ml / hr = 1 mcg/ in 100ml;1 ml / hr 100ml;1 ml / hr = 0.1 100ml;1 ml / hr = 0.1kg / min = 1 mcg/ kg / min mcg/ kg / min mcg/ kg / min
  • ASSESSMENT OF RESPONSE TO IONOTROPES1. Improvement in blood pressures2. Improvement in thermoregulation3. Increased urine output4. Increased oxygenation5. Decreased base deficit and lactate6. Shift of mixed venous concentration towards normal7. The core- peripheral temperature gradient narrows8. Cardiac output returns to normal9. Patient looks better.
  • STEROID THERAPY• Hydrocortisone therapy be reserved for use in children –with catecholamine resistance - suspected or proven Adrenal insufficiency• Patient at risk for Adrenal insufficiency - children with severe septic shock & purpura - with pituitary or adrenal abnormalities• Children who have clear risk factor should be treated with stress dose steroid (Hydrocortisone 50mg/m²/24hrs)
  • Extracorporeal Membrane Oxygenation(ECMO)• Use of ECMO be limited to refractory pediatric septic shock and/or respiratory failure that can’t be supported by conventional therapies
  • Stepwise management of hemodynamic support in neonates Recognize decrease mental status and perfusion, maintain airway and establish access according to PALS guidelines Push 20 cc/kg isotonic saline or colloid boluses up & over 60 cc/kg Correct hypoglycemia & hypocalcemia Administer antibiotics Fluid responsive Fluid refractory shock Observe in PICU Establish Central Venous access, begin dopamine or dobutamine therapy and establish arterial monitoring Fluid refractory - dopamine / dobutamine resistant shock
  • FLUID REFRACTORY - DOPAMINE / DOBUTAMINE RESISTANT SHOCK Titrate epinephrine for cold shock, norepinephrine for warm shock to normal clinical endpoints & ScvO2 saturation > 70% Catcholamine - resistant shock Begin Hydrocortisone if at risk of absolute adrenal insufficiency Normal BP Low BP Low BP Cold shock Cold shock Warm shock ScvO2 < 70% ScvO2 < 70% ScvO2 > 70% Add vasodilator Titrate volume or type III Titrate volume & norepinephrine Phosphodiesterase inhibitor & epinephrine with volume loading Persistent Catcholamine - resistant shock
  • Persistent Catcholamine - resistant shock Start cardiac output measurement & direct fluid, inotrop, vasopressor,vasodilator and hormonal therapy to attain CI > 3.3 and < 6.0 L/min/M2 Refractory shock Consider ECMO Persistent Catcholamine - resistant shock
  • REFERENCES• PALS Provider Manual – 2010, American Academy of Pediatrics,American Heart Association,Indian Academy of Pediatrics.• Surviving Sepsis Campaign (SSC): International Guidelines for Management of Severe Sepsis and Septic Shock : 2008- Critical Care Medicine 2008 Vol. 36,No.1.• Analysis of the evidence for the lower limit of systolic & mean arterial pressure in children: Krarn U. Haque, MD, FAAP; Arno L Zaritsky, MD, FAAP, FCCM:Pediatr Crit Care Med 2007 Vol. 8, No. 2.• Behrman R E, Kleigman RM,Jenson HB, Nelson Text Book of Pediatrics, 18th edition,2007.• Ionotropic Therapy:The Intensivist:Newsletter of Pediatric Intensive Care Chapter:IAP- Jan.2007;3-13