Shock Scott G. Sagraves, MD, FACS Assistant Professor Trauma & Surgical Critical Care Associate Director of Trauma UHS of Eastern Carolina

Objectives Define & classify shock Outline management principles Discuss goals of fluid resuscitation Understand the concepts of oxygen supply and demand in managing shock. Describe the physiologic effects of vasopressors and inotropic agents

Goals Review hemodynamic techniques in the ICU Introduce the concept of the cardiac cycle Review of the pulmonary artery catheter parameters Utilize the presentation to analyze clinical cases and to feel comfortable with pa-c parameters.

“A momentary pause in the act of death.” -John Collins Warren, 1800s Shock: “A momentary pause in the act of death.” -John Collins Warren, 1800s

Hypotension In Adults: systolic BP  90 mm Hg mean arterial pressure  60 mm Hg  systolic BP > 40 mm Hg from the patient’s baseline pressure

Definition SHOCK: inadequate organ perfusion to meet the tissue’s oxygenation demand.

“Hypoperfusion can be present in the absence of significant hypotension.” -fccs course

Pathophysiology ATP + H2O  ADP + Pi + H+ + Energy Acidosis results from the accumulation of acid when during anaerobic metabolism the creation of ATP from ADP is slowed. H+ shift extracellularly and a metabolic acidosis develops

Pathophysiology ATP production fails, the Na+/K+ pump fails resulting in the inability to correct the cell electronic potential. Cell swelling occurs leading to rupture and death. Oxidative Phosphorylation stops & anaerobic metabolism begins leading to lactic acid production.

Why Monitor? Essential to understanding their disease Describe the patient’s physiologic status Facilitates diagnosis and treatment of shock

History 1960’s low BP = shock; MSOF resulted after BP restored 1970’s Swan & Ganz - flow-directed catheter thermistor  cardiac output 1980’s resuscitation based on oxygen delivery, consumption & oxygen transport balance.

Pulmonary Artery Catheter

Pulmonary Artery Catheter INDICATIONS volume status cardiac status COMPLICATIONS technical anatomic physiologic

PLACEMENT

West’s Lung Zones Zone I - PA > Pa > Pv Zone II - Pa > PA > Pv Zone III - Pa > Pv > PA PA = alveolar Pa = pulmonary artery Pv = pulmonary vein

Correct PA-C Position

Standard Parameters Measured Calculated Blood pressure Pulmonary A. pressure Heart rate Cardiac Output Stroke volume Wedge pressure CVP Calculated Mean BP Mean PAP Cardiac Index Stroke volume index SVRI LVSWI BSA

Why Index? Body habitus and size is individual Inter-patient variability does not allow “normal” ranges “Indexing” to patient with BSA allows for reproducible standard

Index Example PATIENT A PATIENT B CI = 2.4 L/min/m2 CI = 1.5 L/min/m2 60 yo male 50 kg CO = 4.0 L/min BSA = 1.86 CI = 2.4 L/min/m2 PATIENT B 60 yo male 150 kg CO = 4.0 L/min BSA = 2.64 CI = 1.5 L/min/m2

PA Insertion 20 15 10 5 RA = 5 RV = 22/4 PA 19/10 PAOP = 9

CVP CVP of SVC at level of right atrium pre-load “assessment” normal 4 - 10 mm Hg limited value

PAOP End expiration Reflection changes with positive pressure Waveforms change  every 20 cm

Waveform Analysis A wave - atrial systole C wave - tricuspid valve closure @ ventricular systole V wave - venous filling of right atrium

Cardiac Cycle pulmonary Right ventricle Left ventricle systemic MPAP PVRI MPAP pulmonary PCWP RVSWI Right ventricle Left ventricle LVSWI MAP CVP systemic SVRI

Hemodynamic Calculations Parameter Normal Cardiac Index (CI) 2.8 - 4.2 Stroke Volume Index (SVI) 30 - 65 Sys Vasc Resistance Index (SVRI) 1600 - 2400 Left Vent Stroke Work Index (LVSWI) 43 - 62

Cardiac Index C.I. = HR x SVI SVI measures the amount of blood ejected by the ventricle with each cardiac contraction. Total blood flow = beats per minute x blood volume ejected per beat

Vascular Resistance Index SYSTEMIC (SVRI) MAP - CVP CI  SVR = vasoconstriction  SVR = vasodilation PULMONARY (PVRI) MPAP - PAOP CI PVR = constriction PE, hypoxia x 80 x 80 Vascular resistance = change in pressure/blood flow

LVSWI = (MAP-PAOP) x SVI x 0.0136 Stroke Work LVSWI = (MAP-PAOP) x SVI x 0.0136 normal = 43 - 62 VSWI describe how well the ventricles are contracting and can be used to identify patients who have poor cardiac function. ventricular stroke work =  pressure x vol. ejected

Too Many Numbers

Definitions O2 Delivery - volume of gaseous O2 delivered to the LV/min. O2 Consumption - volume of gaseous O2 which is actually used by the tissue/min. O2 Demand - volume of O2 actually needed by the tissues to function in an aerobic manner Demand > consumption = anaerobic metabolism

Rationale for Improving O2 Delivery Insult Tissue Hypoxia Demands are met Increased Delivery Increased Consumption

Critical O2 Delivery VO2I DO2I The critical value is variable & is dependent upon the patient, disease, and the metabolic demands of the patient. DO2I

Oxygen Calculations Arterial Oxygen Content (CaO2) Venous Oxygen Content (CvO2) Arteriovenous Oxygen Difference (avDO2) Delivery (O2AVI) Consumption (VO2I) Efficiency of the oxygenation of blood and the rates of oxygen delivery and consumption

Arterial Oxygen Content CaO2 = (1.34 x Hgb x SaO2) + (PaO2 x 0.0031) If low, check hemoglobin or pulmonary gas exchange

Arteriovenous Oxygen Difference avDO2 = CaO2 - CvO2 Values > 5.6 suggests more complete tissue oxygen extraction, typically seen in shock

Oxygen Delivery (DO2I) O2AVI = CI x CaO2 x 10 Normal values suggests that the heart & lungs are working efficiently to provide oxygen to the tissues. < 400 is bad sign

If VO2I < 100 suggest tissues are not getting enough oxygen Oxygen Consumption VO2I = CI x (CaO2 - CvO2) If VO2I < 100 suggest tissues are not getting enough oxygen

SvO2 VO2 SvO2 = 1- DO2

Oxycalculations

Resuscitation Goals CI = 4.5 L/min/m2 DO2I = 600 mL/min/m2 VO2I = 170 mL/min/m2 NOT ALL PATIENTS CAN ACHIEVE THESE GOALS Critically ill patients who can respond to their disease states by spontaneously or artificially meeting these goals do show a better survival.

Break Time…

“Shock is a symptom of its cause.” -fccs course

Signs of Organ Hypoperfusion Mental Status Changes Oliguria Lactic Acidosis

Components

Categories of Shock HYPOVOLEMIC CARDIOGENIC DISTRIBUTIVE OBSTRUCTIVE

Goals of Shock Resuscitation Restore blood pressure Normalize systemic perfusion Preserve organ function

In general, treat the cause...

Hypovolemic Shock Causes hemorrhage vomiting diarrhea dehydration third-space loss burns Signs  cardiac output  PAOP  SVR

Classes of Hypovolemic Shock

Treatment - Hypovolemic Reverse hypovolemia vs. hemorrhage control Crystalloid vs. Colloid PASG role? Pressors?

Resuscitation Transport times < 15 minutes showed pre-hospital fluids were ineffective, however, if transport time > 100 minutes fluid was beneficial. Penetrating torso trauma benefited from limited resuscitation prior to bleeding control. Not applicable to BLUNT victims.

Fluid Administration 1 L crystalloid  250 ml colloid crystalloids are cheaper blood must supplement either FFP for coagulopathy, NOT volume Watch for hyperchloremic metabolic acidosis when large volumes of NaCl are infused NO survival benefit with colloids

Role of PASG? Houston - Higher mortality rate in penetrating thoracic, cardiac trauma No benefit in penetrating cardiac trauma Role undefined in rural, blunt trauma Splinting role

Cardiogenic Shock Cause Signs defect in cardiac function  cardiac output  PAOP  SVR  left ventricular stroke work (LVSW)

Coronary Perfusion Pressure Coronary PP = DBP - PAOP coronary perfusion =  P across coronary a. GOAL - Coronary PP > 50 mm Hg

The Failing Heart Improve myocardial function, C.I. < 3.5 is a risk factor, 2.5 may be sufficient. Fluids first, then cautious pressors Remember aortic DIASTOLIC pressures drives coronary perfusion (DBP-PAOP = Coronary Perfusion Pressure) If inotropes and vasopressors fail, intra-aortic balloon pump

Distributive Shock Types Signs Sepsis Anaphylactic Acute adrenal insufficiency Neurogenic Signs ± cardiac output  PAOP SVR

SIRS - Distributive Shock Prompt volume replacement - fill the tank Early antibiotic administration - treat the cause Inotropes - first try Dopamine If MAP < 60 Dopamine = 2 - 3 g/kg/min Norepinephrine = titrate (1-100 g/min) R/O missed injury

Adrenal Crisis Distributive Shock Causes Autoimmune adrenalitis Adrenal apoplexy = B hemorrhage or infarct heparin may predispose Steroids may be lifesaving in the patient who is unresponsive to fluids, inotropic, and vasopressor support. Which one?

Obstructive Shock Causes Signs Cardiac Tamponade Tension Pneumothorax Massive Pulmonary Embolus Signs  cardiac output  PAOP  SVR

Endpoints? ACS CoT ATLS - restoration of vital signs and evidence of end-organ perfusion Swan-guided resuscitation C.I.  4.5, DO2I  670, VO2I  166 Lactic Acid clearance Gastric pH

Summary Type PAOP C.O. SVR HYPOVOLEMIC    CARDIOGENIC    DISTRIBUTIVE  or N varies  OBSTRUCTIVE   

Vasopressor Agents? Augments contractility, after preload established, thus improving cardiac output. Risk tachycardia and increased myocardial oxygen consumption if used too soon Rationale, increased C.I. improves global perfusion

Vasopressors & Inotropic Agents Dopamine Dobutamine Norepinephrine Epinephrine Amrinone

Dopamine Low dose (0.5 - 2 g/kg/min) = dopaminergic Moderate dose (3-10 g/kg/min) = -effects High dose (> 10 g/kg/min) = -effects SIDE EFFECTS tachycardia > 20 g/kg/min  to norepinephrine

Dobutamine -agonist 5 - 20 g/kg/min potent inotrope, variable chronotrope caution in hypotension (inadequate volume) may precipitate tachycardia or worsen hypotension

Norepinephrine Potent -adrenergic vasopressor Some -adrenergic, inotropic, chronotropic Dose 1 - 100 g/min Unproven effect with low-dose dopamine to protect renal and mesenteric flow.

Epinephrine - and -adrenergic effects potent inotrope and chronotrope dose 1 - 10 g/min increases myocardial oxygen consumption particularly in coronary heart disease

Amrinone Phosphodiesterase inhibitor, positive inotropic and vasodilatory effects increased cardiac stroke output without an increase in cardiac stroke work most often added with dobutamine as a second agent load dose = 0.75 -1.5 mg/kg  5 - 10 g/kg/min drip main side-effect - thrombocytopenia

Dilators - inotropes + inotropes Pressors

Summary `pressors & inotropes dilator Dobutamine Milrinone/Amrinone Labetalol Ca+2 blocker ACE inhibitor hydralazine nitroglycerine Nipride -dopamine Isuprel Digoxin Calcium -blocker - inotrope + inotrope epinephrine -dopamine norepinephrine pressor neosynephrine

Case Studies

GSW 24 year old male victim of a shotgun blast to his right lower quadrant/groin at close range. Hemodynamically unstable in the field and his right lower extremity was cool and pulseless upon arrival to the trauma resuscitation area.

Shotgun Blast

Post-op Patient received 12 L crystalloid, 15 units of blood, 6 units of FFP, and 2 6 packs of platelets. HR 130, BP 96/48, T 34.7° C PAWP 8, CVP 6, CI 4.2, SVRI 2700, LVSWI 42. Diagnosis? Treatment?

SHOCK/HYPOVOLEMIA FLUIDS… FLUIDS… FLUIDS… BLOOD & PRODUCTS TRANSFUSION CORRECT ACIDOSIS COAGULOPATHY HYPOTHERMIA

MVC 38 year old female restrained driver who was involved in a high speed MVC. She sustained a pulmonary contusion and fractured pelvis.

ICU Course Intubated and monitored with PA-C PCWP = 22, CI = 3.5, SVRI = 2400, LVSWI = 39.8 HR = 120, BP = 110/56, SpO2 = 91, UOP = 25 cc/hr What do you think...

ADJUST YOUR WEDGE FOR THE PEEP HYPOVOLEMIA ADJUST YOUR WEDGE FOR THE PEEP

Wedge Adjustment Measured PAOP - ½ PEEP = “real PAOP” PEEP = 28, therefore “real wedge” = 8

Auto-Pedestrian Crash Thrown from the rear bed of pick up truck during a MVC at 60 mph. Hemodynamically unstable Pain to palpation of the pelvis Hematuria with Foley® insertion

ICU Course Pelvis “closed” QID Dressings, intubated, PA-C inserted PCWP = 20, CI = 5.2, SVRI = 280, LVSWI = 24.5, PEEP = 8 Diagnosis? Treatment?

Sepsis Fluids Correct the cause Vasopressors Antibiotics Debridement Phenylephrine Levophed

Initial Resuscitation CVP: 8- 12 mm Hg MAP  65 mm Hg UOP  0.5 cc/kg/hr Mixed venous Oxygen Sat  70% Consider: Transfusion to Hgb  10 Dobutamine up to 20 g/kg/min

Vasopressors Assure adequate fluid volume Administer via CVL Do not use dopamine for renal protection Requires arterial line placement Vasopressin: Refractory shock Infusion rate 0.01 – 0.04 Units/min

Steroid Use in Sepsis Refractory shock 200-300 mg/day of hydrocortisone in divided doses for 7 days ACTH test Once septic shock resolves, taper dose Add fludrocortisone 50 g po q day

Geriatric Trauma 70 year old female MVC while talking on her cell phone ruptured diaphragm and spleen s/p OR Intubated and PA-C

ICU Course PCWP = 28, CI = 1.8, SVRI = 3150, LVSWI = 20.7 Diagnosis? Treatment?

Cardiogenic Shock Preload augmentation - Consider Fluids Contractility dopamine dobutamine phosphodiesterase inhibitor Afterload reduction nitroglycerin

Shock: “rude unhinging of the machinery of life.” Don’t forget... Shock: “rude unhinging of the machinery of life.” -Samuel D. Gross, 1872