Update on shock management Dr. Manal Al Maskati Oct, 2011 - Kuwait.

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Presentation transcript:

Update on shock management Dr. Manal Al Maskati Oct, Kuwait

Objectives  Briefing about pathophysiology of shock.  Initial steps of pt’s stabilization.  Work-up in A/E.  Some important procedures,which considered beneficial for shock management.  How ?When? and What ? medications are important to know to manage any type of shock.

Pathophysiology  Shock  inadequate delivery of substrates and oxygen to meet the metabolic needs of tissues.  Cell  anaerobic metabolic pathway  accumulation of lactic acid.  Hypoxic-ischemic injury  widespread cellular death  multiple system organ failure  death.

Pathophysiology  DO 2 (mL O 2 /min) = CaO 2 (mL O 2 /L blood) X CO (L/min)  DO 2 amount of oxygen delivered to body tissues/ min.  CaO 2 oxygen-carrying capacity depends on:  Hemoglobin (Hb) content  Arterial oxygen saturation (SaO 2 ).  CO cardiac output depends on:  stroke volume (SV)  heart rate (HR).  CO = HR (beats/min) X SV (mL/beat)  SV stroke volume depends on:  Preload  Afterload  Contractility  BP = CO X SVR

Treatment  ABC  Non-invasive monitors  Abx in septic shock with empiric coverage  Neonates : combination of ampicillin and gentamicin.  Older infants and children: third-generation cephalosporin,with vancomycin if indicated.  Baseline work-up

Treatment  Volume expansion Children with hypovolemic shock receive appropriate aggressive fluid resuscitation within the 1 st hr of resuscitation  optimal chance of survival and recovery.  Place 2 large-bore IV catheters or IO access.  Administer 20 mL/kg isotonic crystalloid infusion  re-evaluate  administer additional 20 mL/kg if needed.  If > 2-3 of 20-mL/kg volumes crystalloid given to patient at risk for hemorrhage  packed RBCs.  In study of survival in children with septic shock  children received an average 65 mL/kg of volume in 1 st hr had statistically increased chance of survival compared with other groups received < 40 mL/kg in 1 st hr.  Exception to repetitive volume resuscitation  cardiogenic shock.

Work-Up  CBC count  Hb oxygen-carrying capacity.  or white cell count septic shock.  Thrombocytopenia bleeding disorder or DIC.

 Acid-base status  Shock produces lactic acid metabolic acidosis with anion gap.  Diarrhea leads to direct bicarbonate loss.  Measurement of serum lactate level distinguish bicarbonate loss from lactic acidosis due to shock. Work-Up

 Complete metabolic panel  Hypernatremia intravascular volume contraction hypovolemic shock.  serum carbon dioxide metabolic acidosis.  Hypovolemia BUN and creatine levels.  liver enzymes hypoxic-ischemic damage to liver. Work-Up

 B-type natriuretic peptide  BNP : hormone produced by ventricular myocytes in response to myocardial wall stress.  Plasma BNP levels (adult and pediatric studies) in sepsis and congestive heart failure with cardiogenic shock.  Elevated levels of BNP myocardial stress, and improvement in cardiac function normalization of BNP levels. Work-Up

 Imaging Studies Never delay resuscitation of patient in shock CXR  Cardiomegaly in cardiogenic shock.  Small heart size in hypovolemic shock.  ARDS from pneumonia and sepsis. Work-Up

 Other Tests  Near-infrared spectroscopy (NIRS)  Values correlate with venous oxygen saturations noninvasive measurements of increased or decreased tissue oxygen saturation (adequate or inadequate DO 2 ).  Cardiac index  CO divided by body surface area (BSA)  Normal CI is L/min/m 2  Cardiac index invasive or noninvasive measurements (Doppler echocardiography, or classic pulmonary artery catheter). Work-Up

Procedures  Mixed Venous Oxygen Saturation (SvO 2 )  Blood gas from central venous catheter or Swan-Ganz catheter.  In patient with normal SaO 2 (90-100%)  SvO %.  Tissues extract 28-33% of oxygen delivered to them.  If oxygen extraction difference > 33%  poor tissue perfusion  state of shock.  If oxygen extraction difference < 25%  oxygenated blood shunting  distributive shock.

Procedures  Central venous pressure and pulmonary capillary wedge pressure  Low CVP or PCWP  inadequate intravascular volume.  Normal CVP  1-3 cm H 2 O.  Pressures > 10 cm H 2 O  volume overload or poor right-sided heart function  PCWP of cm H 2 o  good perfusion.

Medications  Dextrose administration often necessary  If glucose level low g/kg IV Dextrose.  Shock with documented hypocalcemia, or caused by arrhythmias (hyperkalemia, hypermagnesemia, or calcium channel blocker toxicity) calcium therapy.  Recommended dose is mg/kg ( mL/kg of calcium chloride 10%) IV at infusion rate 100 mg/min.

 Sodium bicarbonate use in treatment of shock is controversial.  No better effect on  Ability to defibrillate  DO 2  Survival rates in shock and cardiac arrest Medications

 In patients with persistent shock or ongoing bicarbonate loss (eg, severe diarrhea) careful replacement of bicarbonate. HCO 3 - (mEq) = Base deficit X patient's weight (in kg) X 0.3  Half of calculated bicarbonate deficit administered initially. OR  mEq/kg/dose IV infused over 1-2 minutes. Medications

 Vasopressors/inotropic agents  Increase myocardial contractility + variable effects on peripheral vascular resistance  Dopamine o 1st inotrope fluid-refractory septic shock. o Low dose (2-5 mcg/kg/min IV) vasodilatory effect on end-organ perfusion. o Intermediate dose (5-10 mcg/kg/min IV) improves myocardial contractility + CO + enhancing conduction. o Higher dose (10-20 mcg/kg/min IV ) increases peripheral vasoconstriction + BP. Medications

 Dobutamine o Good for cardiogenic shock. o Increases cardiac contractility + peripheral vasodilation (afterload and improve tissue perfusion). o Less likely to precipitate ventricular dysrhythmias than epinephrine. o Dose begins with 5 mcg/kg/min IV, gradually increased to 20 mcg/kg/min IV. Medications

 Epinephrine o For fluid refractory dopamine resistant, non- vasodilatory (cold) shock. o Increases myocardial contractility + peripheral vasoconstriction. o Risk of ventricular dysrhythmias + extremities ischemia o Dose : 0.1 mcg/kg/min IV, titrated upward according to effect and adverse effects. o Severe cases 2-3 mcg/kg/min IV or higher. Medications

 Norepinephrine o For fluid-refractory, dopamine-resistant vasodilatory (warm) shock. o Increases peripheral vasoconstriction BP. o Best pressor agent increases BP in shock persists after adequate fluid replacement. o Dose : 0.1 mcg/kg/min IV,titrated upward according to effect and adverse effects. Medications

 Phosphodiesterase Enzyme Inhibitor  Inamrinone + milrinone o Useful for shock with adequate intravascular volume, but need increased cardiac contractility and better peripheral perfusion ( compensated shock with poor peripheral perfusion). o Improve cardiac inotropy + peripheral vasodilation. o Phosphodiesterase inhibitor used together with catecholamines increase myocardial contractility + reducing systemic vascular resistance and afterload. Medications

 Inamrinone + milrinone o Inamrinone : loading dose of 0.75 mg/kg IV over 2-3 minutes followed by continuous IV infusion of 5-10 mcg/kg/min. o Milrinone : loading dose of mcg/kg over 10 minutes, followed by continuous IV infusion of mcg/kg/min. o Adverse effects: arrhythmias + thrombocytopenia Medications

 Prostaglandin E1 o Neonates with shock (large liver, enlarged cardiac silhouette, or heart murmur) obstructive shock(PDA closure). o PDA allow sufficient systemic blood flow to bypass obstructive lesion. o PGE1 maintains patency of PDA. o Dose mcg/kg/min IV as continuous infusion. o Adverse effects : fever, apnea, or hypotension due to vasodilation. Medications

 Corticosteroid o Use of corticosteroids in septic shock controversial o Adrenocortical failure or infarction (Waterhouse- Friderichsen syndrome) cardiovascular failure + hyporesponsiveness to catecholamines. o Initiation of stress-dose hydrocortisone ( mg/m 2 /d IV), may be lifesaving. o A serum cortisol level drawn prior to first dose of corticosteroids serum cortisol level low replacement doses. Medications

 Corticosteroid o Study of adult patients with septic shock survived 48 hours,dependent on inotropic agents showed some benefit when treated with supraphysiologic doses of corticosteroids. o Patients developed adrenal insufficiency 1-2 mg/kg hydrocortisone IV every 6 hours OR 50 mg/kg bolus followed by same amount infused over 24 hours. o Therapy continued for patients absolute baseline cortisol level < 20 mcg/dL. Medications

 Initial steps of stabilization make tremendous difference in pts survival.  In non-cardiogenic shock fluid fluid fluid.  Early Abx improved survival in septic shock.  Arrange for ICU bed.  Don’t forget the Team-Work management. Take Home Message

Thank you Discussion