SHK 1 ® Diagnosis and Management of Shock SHK 1 ®

SHK 2 ® Objectives Identify the major types of shock and principles of management Review fluid resuscitation and use of vasopressor and inotropic agents Understand concepts of O 2 supply and demand Discuss the differential diagnosis of oliguria Identify the major types of shock and principles of management Review fluid resuscitation and use of vasopressor and inotropic agents Understand concepts of O 2 supply and demand Discuss the differential diagnosis of oliguria SHK 2 ®

It is all about tissue oxygen!!!!

SHK 4 ® 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 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 SHK 4 ®

Focusing On Blood Flow Dynamics Oxygenation –CO/CI –HgB –Sa02 –Cardiac output response relating to Volume load Pressure load –Tissue demand for oxygen –Tissue extraction of oxygen Blood Flow Dynamics Oxygenation –CO/CI –HgB –Sa02 –Cardiac output response relating to Volume load Pressure load –Tissue demand for oxygen –Tissue extraction of oxygen

Focusing On Does the patient have volume Where is it Are they tachycardic Are they hypoxic at the cells ASSUME tissue hypoxia –Tachypnea or hyperventilation –Metabolic acidosis in absence of renal failure or ketosis –+ lactic acid Does the patient have volume Where is it Are they tachycardic Are they hypoxic at the cells ASSUME tissue hypoxia –Tachypnea or hyperventilation –Metabolic acidosis in absence of renal failure or ketosis –+ lactic acid

Focusing On Problems with delivery –Cardiac output –Volume –Contractility –Valves –Rhythm Proportional Use –Capillary flow –Oxyhemoglobin disassociation –Tissue demand Problems with delivery –Cardiac output –Volume –Contractility –Valves –Rhythm Proportional Use –Capillary flow –Oxyhemoglobin disassociation –Tissue demand

Diagnosing SHOCK Blood Pressure –BP = CO x SVR SVR= (MAP-CVP)80/CO –N: dynes Cardiac Output –CO = SV X HR – N: 4-6 MAP, CVP, PaOP Vascular Tone (SVR) –N: 2-8, 2-12 Blood Pressure –BP = CO x SVR SVR= (MAP-CVP)80/CO –N: dynes Cardiac Output –CO = SV X HR – N: 4-6 MAP, CVP, PaOP Vascular Tone (SVR) –N: 2-8, 2-12

Hemo measures RAP: 2-8 mm Hg RVP: Systolic mmHg/Diastolic < RAP PAP: Systole mmHg/Diastolic 5-15 PaOP: < PAD, 2-12 CO 4-6 L/min Sv02: 65-75% RAP: 2-8 mm Hg RVP: Systolic mmHg/Diastolic < RAP PAP: Systole mmHg/Diastolic 5-15 PaOP: < PAD, 2-12 CO 4-6 L/min Sv02: 65-75% Always read and perform on EXPIRATION!!!!!!!!!

Stroke Volume Stroke Volume Contractility Rhythm Afterload Cardiac output Preload Heart Rate

CVP:2-8 VOLUME PCW: LV Function 2-12 book, THINK 8-12 PCW: LV Function 2-12 book, THINK 8-12 Sv02: 65-75% Sa02: % CO: 4-6 EJECTION SVR RESISTANCE SVR RESISTANCE

SHK 12 ® Shock Categories SHK 12 Cardiogenic Hypovolemic Distributive Obstructive Cardiogenic Hypovolemic Distributive Obstructive ®

SHK 13 ® Cardiogenic Shock: A noncompliant heart cannot increase SV Decreased contractility Increased filling pressures, decreased LV stroke work, decreased cardiac output Increased systemic vascular resistance – compensatory Decreased contractility Increased filling pressures, decreased LV stroke work, decreased cardiac output Increased systemic vascular resistance – compensatory

SHK 14 ® Hypovolemic Shock: An empty heart cannot eject well Decreased cardiac output Decreased filling pressures Compensatory increase in systemic vascular resistance Decreased cardiac output Decreased filling pressures Compensatory increase in systemic vascular resistance SHK 14 ®

SHK 15 ® Distributive Shock Normal or increased cardiac output Low systemic vascular resistance Low to normal filling pressures Sepsis, anaphylaxis, neurogenic, and acute adrenal insufficiency Normal or increased cardiac output Low systemic vascular resistance Low to normal filling pressures Sepsis, anaphylaxis, neurogenic, and acute adrenal insufficiency SHK 15 ®

Severe Sepsis and Septic Shock Increased cardiac output Decreased systemic vascular resistance Hypotension: refractory to volume Sv02 Consumption of clotting components due to hyperinflammation, hypercoagulation PLATELETS!!!!!! Increased cardiac output Decreased systemic vascular resistance Hypotension: refractory to volume Sv02 Consumption of clotting components due to hyperinflammation, hypercoagulation PLATELETS!!!!!!

Severe Sepsis Pathophysiology Microvascular dysfunction  Inflammation  Coagulation  Fibrinolysis Hypoperfusion/hypoxia Microvascular thrombosis Endothelial dysfunction Organ dysfunction Global tissue hypoxia Direct tissue damage  

SHK 18 ® Obstructive Shock: Block the outflow Decreased cardiac output Increased systemic vascular resistance Variable filling pressures dependent on etiology Cardiac tamponade, tension pneumothorax, massive pulmonary embolus Decreased cardiac output Increased systemic vascular resistance Variable filling pressures dependent on etiology Cardiac tamponade, tension pneumothorax, massive pulmonary embolus

Shock states variable Hemorrhage CardiacHypo Distribute Comp Sepsis Decomp Sepsis CI Hgb Sv02 LA N OR BD N OR

Shock states variable Hemorrhage CardiacHypo Distribute Comp Sepsis Decomp Sepsis CI BP FP HR UO

SHK 21 ® Shock Therapies SHK 21 Lots of concepts in a short time! Focus on the MOST vital tools for resolution Treat the problem Lots of concepts in a short time! Focus on the MOST vital tools for resolution Treat the problem ®

SHK 22 ® Therapeutic Goals in Shock Increase O 2 delivery Optimize O 2 content of blood Improve cardiac output and blood pressure Match systemic O 2 needs with O 2 delivery Reverse/prevent organ hypoperfusion Increase O 2 delivery Optimize O 2 content of blood Improve cardiac output and blood pressure Match systemic O 2 needs with O 2 delivery Reverse/prevent organ hypoperfusion

SHK 23 ® Cardiogenic Shock Management Treat arrhythmias Diastolic dysfunction may require increased filling pressures Vasodilators if not hypotensive Inotrope administration Treat arrhythmias Diastolic dysfunction may require increased filling pressures Vasodilators if not hypotensive Inotrope administration

SHK 24 ® Cardiogenic Shock Management Vasopressor agent needed if hypotension present to raise aortic diastolic pressure Consultation for mechanical assist device Preload and afterload reduction to improve hypoxemia if blood pressure adequate Vasopressor agent needed if hypotension present to raise aortic diastolic pressure Consultation for mechanical assist device Preload and afterload reduction to improve hypoxemia if blood pressure adequate

SHK 25 ® Hypovolemic Shock Management Volume resuscitation – crystalloid, colloid Initial crystalloid choices –Lactated Ringer’s solution –Normal saline (high chloride may produce hyperchloremic acidosis) Match fluid given to fluid lost –Blood, crystalloid, colloid Volume resuscitation – crystalloid, colloid Initial crystalloid choices –Lactated Ringer’s solution –Normal saline (high chloride may produce hyperchloremic acidosis) Match fluid given to fluid lost –Blood, crystalloid, colloid SHK 25 ®

SHK 26 ® Distributive Shock Therapy Restore intravascular volume Hypotension despite volume therapy –Inotropes and/or vasopressors Vasopressors for MAP < 60 mm Hg Adjunctive interventions dependent on etiology Restore intravascular volume Hypotension despite volume therapy –Inotropes and/or vasopressors Vasopressors for MAP < 60 mm Hg Adjunctive interventions dependent on etiology SHK 26 ®

SHK 27 ® Obstructive Shock Treatment Relieve obstruction –Pericardiocentesis –Tube thoracostomy –Treat pulmonary embolus Temporary benefit from fluid or inotrope administration Relieve obstruction –Pericardiocentesis –Tube thoracostomy –Treat pulmonary embolus Temporary benefit from fluid or inotrope administration

SHK 28 ® Fluid Therapy Crystalloids –Lactated Ringer’s solution –Normal saline Colloids –Hetastarch –Albumin –Gelatins Packed red blood cells Infuse to physiologic endpoints Crystalloids –Lactated Ringer’s solution –Normal saline Colloids –Hetastarch –Albumin –Gelatins Packed red blood cells Infuse to physiologic endpoints SHK 28 ®

SHK 29 ® Fluid Therapy Correct hypotension first Decrease heart rate Correct hypoperfusion abnormalities Monitor for deterioration of oxygenation Correct hypotension first Decrease heart rate Correct hypoperfusion abnormalities Monitor for deterioration of oxygenation SHK 29 ®

SHK 30 ® Inotropic / Vasopressor Agents Dopamine –Low dose (2-3  g/kg/min) – mild inotrope plus renal effect –Intermediate dose (4-10  g/kg/min) – inotropic effect –High dose ( >10  g/kg/min) –  vasoconstriction –Chronotropic effect Dopamine –Low dose (2-3  g/kg/min) – mild inotrope plus renal effect –Intermediate dose (4-10  g/kg/min) – inotropic effect –High dose ( >10  g/kg/min) –  vasoconstriction –Chronotropic effect SHK 30 ®

SHK 31 ® Inotropic Agents Dobutamine –5-20  g/kg/min –Inotropic and variable chronotropic effects –Decrease in systemic vascular resistance Dobutamine –5-20  g/kg/min –Inotropic and variable chronotropic effects –Decrease in systemic vascular resistance SHK 31 ®

SHK 32 ® Inotropic / Vasopressor Agents Norepinephrine –0.05  g/kg/min and titrate to effect –Inotropic and vasopressor effects –Potent vasopressor at high doses Norepinephrine –0.05  g/kg/min and titrate to effect –Inotropic and vasopressor effects –Potent vasopressor at high doses SHK 32 ®

SHK 33 ® Inotropic / Vasopressor Agents Epinephrine –Both  and  actions for inotropic and vasopressor effects –0.1  g/kg/min and titrate –Increases myocardial O 2 consumption Epinephrine –Both  and  actions for inotropic and vasopressor effects –0.1  g/kg/min and titrate –Increases myocardial O 2 consumption SHK 33 ®

SHK 34 ® Oliguria Marker of hypoperfusion Urine output in adults 2 hrs Etiologies –Prerenal –Renal –Postrenal Marker of hypoperfusion Urine output in adults 2 hrs Etiologies –Prerenal –Renal –Postrenal SHK 34 ®

SHK 35 ® Evaluation of Oliguria History and physical examination Laboratory evaluation –Urine sodium –Urine osmolality or specific gravity –BUN, creatinine History and physical examination Laboratory evaluation –Urine sodium –Urine osmolality or specific gravity –BUN, creatinine SHK 35 ®

SHK 36 ® Evaluation of Oliguria Laboratory TestPrerenal ATN Blood Urea Nitrogen/>2010–20 Creatinine Ratio Urine Specific Gravity>1.020<1.010 Urine Osmolality (mOsm/L)>500<350 Urinary Sodium (mEq/L) 40 Fractional Excretion of Sodium (%) 2

SHK 37 ® Therapy in Acute Renal Insufficiency Correct underlying cause Monitor urine output Assure euvolemia Diuretics not therapeutic Low-dose dopamine may  urine flow Adjust dosages of other drugs Monitor electrolytes, BUN, creatinine Consider dialysis or hemofiltration Correct underlying cause Monitor urine output Assure euvolemia Diuretics not therapeutic Low-dose dopamine may  urine flow Adjust dosages of other drugs Monitor electrolytes, BUN, creatinine Consider dialysis or hemofiltration SHK 37 ®

Case 1 CO/ CI : 11.4/7.2 90/55 MAP 62 PAM 45 FP: 28/26 HR 158 SVR –(62-28/11.4 ) 80 =238 UO < 0.3 cc/kg CO/ CI : 11.4/7.2 90/55 MAP 62 PAM 45 FP: 28/26 HR 158 SVR –(62-28/11.4 ) 80 =238 UO < 0.3 cc/kg What are your concerns? –CO? –CI? –SVR? –BP? –U/O

Case 2 CO/ CI : 3.1/1.8 MAP 69 PAM 35 FP: 21/25 HR 138 SVR –(69 -25/3.5) 80 = 1135 UO < 0.3 cc/kg CO/ CI : 3.1/1.8 MAP 69 PAM 35 FP: 21/25 HR 138 SVR –(69 -25/3.5) 80 = 1135 UO < 0.3 cc/kg What are your concerns? –CO? –CI? –SVR? –BP? –U/O

Case 3 CO/ CI : 3.8/ /50 MAP 62 CVP: 4 HR 143 UO < 0.3 cc/kg CO/ CI : 3.8/ /50 MAP 62 CVP: 4 HR 143 UO < 0.3 cc/kg What are your concerns? –CO? –CI? –BP? –U/O

Therapeutic Goals in Shock Increase O 2 delivery –Cardiac output Volume, Inotropes Optimize O 2 content of blood –HgB and Sa0 2 PRBC and 0 2 therapy Improve cardiac output and blood pressure –Inotropes, Volume and Vasoactive therapies Match systemic O 2 needs with O 2 delivery –Goal directed therapy Increase O 2 delivery –Cardiac output Volume, Inotropes Optimize O 2 content of blood –HgB and Sa0 2 PRBC and 0 2 therapy Improve cardiac output and blood pressure –Inotropes, Volume and Vasoactive therapies Match systemic O 2 needs with O 2 delivery –Goal directed therapy Reverse/prevent organ hypoperfusion

Case 1 CO/ CI : 11.4/7.2 90/55 MAP 62 PAM 45 FP: 28/26 HR 158 SVR –(62-28/11.4 ) 80 =238 UO < 0.3 cc/kg CO/ CI : 11.4/7.2 90/55 MAP 62 PAM 45 FP: 28/26 HR 158 SVR –(62-28/11.4 ) 80 =238 UO < 0.3 cc/kg Diagnosis –Severe Sepsis Sepsis Guidelines

Case 2 CO/ CI : 3.1/1.8 MAP 69 PAM 35 FP: 21/25 HR 138 SVR –(69 -25/3.5) 80 = 1135 UO < 0.3 cc/kg CO/ CI : 3.1/1.8 MAP 69 PAM 35 FP: 21/25 HR 138 SVR –(69 -25/3.5) 80 = 1135 UO < 0.3 cc/kg Diagnosis –Cardiogenic Shock Inotropic

Case 3 CO/ CI : 3.8/ /50 MAP 62 CVP: 4 HR 143 UO < 0.3 cc/kg CO/ CI : 3.8/ /50 MAP 62 CVP: 4 HR 143 UO < 0.3 cc/kg Diagnosis: Hypovolemia Volume loading Assess for hemorrhage

SHK 45 ® 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 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 SHK 45 ®

SHK 46 ® Pediatric Considerations Neonates – 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 Neonates – 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 SHK 46 ®

SHK 47 ® Key Points