Presentation on theme: "Shock Scott G. Sagraves, MD, FACS Assistant Professor Trauma & Surgical Critical Care Associate Director of Trauma UHS of Eastern Carolina."— Presentation transcript:
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.
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 + H 2 O ADP + P i + 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
INDICATIONS –volume status –cardiac status COMPLICATIONS –technical –anatomic –physiologic
West’s Lung Zones Zone I - P A > P a > P v Zone II - P a > P A > P v Zone III - P a > P v > P A P A = alveolar Pa = pulmonary artery Pv = pulmonary vein
Correct PA-C Position
Standard Parameters Measured –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 60 yo male 50 kg CO = 4.0 L/min BSA = 1.86 CI = 2.4 L/min/m 2 PATIENT B 60 yo male 150 kg CO = 4.0 L/min BSA = 2.64 CI = 1.5 L/min/m 2
PA Insertion 0 5 10 15 20 RA = 5RV = 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 Left ventricle systemic Right ventricle RVSWI PVRI LVSWI SVRI CVP MPAP PCWP MAP
Hemodynamic Calculations ParameterNormal 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 Vascular resistance = change in pressure/blood flow
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 O 2 Delivery - volume of gaseous O 2 delivered to the LV/min. O 2 Consumption - volume of gaseous O 2 which is actually used by the tissue/min. O 2 Demand - volume of O 2 actually needed by the tissues to function in an aerobic manner Demand > consumption = anaerobic metabolism
Rationale for Improving O 2 Delivery Insult Tissue Hypoxia Increased Delivery Increased Consumption Demands are met
Critical O 2 Delivery VO 2 I DO 2 I The critical value is variable & is dependent upon the patient, disease, and the metabolic demands of the patient.
Oxygen Calculations Arterial Oxygen Content (CaO 2 ) Venous Oxygen Content (CvO 2 ) Arteriovenous Oxygen Difference (avDO 2 ) Delivery (O 2 AVI) Consumption (VO 2 I) Efficiency of the oxygenation of blood and the rates of oxygen delivery and consumption
Arterial Oxygen Content CaO 2 = (1.34 x Hgb x SaO 2 ) + (PaO 2 x 0.0031) If low, check hemoglobin or pulmonary gas exchange
Arteriovenous Oxygen Difference avDO 2 = CaO 2 - CvO 2 Values > 5.6 suggests more complete tissue oxygen extraction, typically seen in shock
Oxygen Delivery (DO 2 I) O 2 AVI = CI x CaO 2 x 10 Normal values suggests that the heart & lungs are working efficiently to provide oxygen to the tissues. < 400 is bad sign
Oxygen Consumption VO 2 I = CI x (CaO 2 - CvO 2 ) If VO 2 I < 100 suggest tissues are not getting enough oxygen
SvO 2 SvO 2 =1- VO 2 DO 2
Resuscitation Goals CI = 4.5 L/min/m 2 DO 2 I = 600 mL/min/m 2 VO 2 I = 170 mL/min/m 2 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.
“Shock is a symptom of its cause.” -fccs course
Signs of Organ Hypoperfusion Mental Status Changes Oliguria Lactic Acidosis
Categories of Shock HYPOVOLEMIC CARDIOGENIC DISTRIBUTIVE OBSTRUCTIVE
Goals of Shock Resuscitation Restore blood pressure Normalize systemic perfusion Preserve organ function
Treatment - Hypovolemic Reverse hypovolemia vs. hemorrhage control Crystalloid vs. Colloid PASG role? Pressors?
Resuscitation Transport times 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 –defect in cardiac function Signs – 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
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?
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
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
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.
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?
Sepsis Fluids Correct the cause Antibiotics Debridement Vasopressors –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