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

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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:

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

2 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

3 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.

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

5 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

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

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

8 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

9 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.

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

11 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.

12 Pulmonary Artery Catheter

13 INDICATIONS –volume status –cardiac status COMPLICATIONS –technical –anatomic –physiologic

14 PLACEMENT

15 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

16 Correct PA-C Position

17 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

18 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

19 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

20 PA Insertion 0 5 10 15 20 RA = 5RV = 22/4 PA 19/10 PAOP = 9

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

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

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

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

25 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

26 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

27 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

28 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

29 Too Many Numbers

30 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

31 Rationale for Improving O 2 Delivery Insult Tissue Hypoxia Increased Delivery Increased Consumption Demands are met

32 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.

33 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

34 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

35 Arteriovenous Oxygen Difference avDO 2 = CaO 2 - CvO 2 Values > 5.6 suggests more complete tissue oxygen extraction, typically seen in shock

36 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

37 Oxygen Consumption VO 2 I = CI x (CaO 2 - CvO 2 ) If VO 2 I < 100 suggest tissues are not getting enough oxygen

38 SvO 2 SvO 2 =1- VO 2 DO 2

39 Oxycalculations

40 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.

41 Break Time…

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

43 Signs of Organ Hypoperfusion Mental Status Changes Oliguria Lactic Acidosis

44 Components

45 Categories of Shock HYPOVOLEMIC CARDIOGENIC DISTRIBUTIVE OBSTRUCTIVE

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

47 In general, treat the cause...

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

49 Classes of Hypovolemic Shock

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

51 Resuscitation Transport times 100 minutes fluid was beneficial. Penetrating torso trauma benefited from limited resuscitation prior to bleeding control. Not applicable to BLUNT victims.

52 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

53 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

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

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

56 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

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

58 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

59 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?

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

61 Endpoints? ACS CoT ATLS - restoration of vital signs and evidence of end-organ perfusion Swan-guided resuscitation –C.I.  4.5, DO 2 I  670, VO 2 I  166 Lactic Acid clearance Gastric pH

62 Summary TypePAOPC.O.SVR HYPOVOLEMIC    CARDIOGENIC    DISTRIBUTIVE  or N varies  OBSTRUCTIVE   

63 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

64 Vasopressors & Inotropic Agents Dopamine Dobutamine Norepinephrine Epinephrine Amrinone

65 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

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

67 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.

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

69 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

70 Dilators + inotropes - inotropes Pressors

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

72 Case Studies

73 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.

74 Shotgun Blast

75 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?

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

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

78 ICU Course Intubated and monitored with PA-C PCWP = 22, CI = 3.5, SVRI = 2400, LVSWI = 39.8 HR = 120, BP = 110/56, SpO 2 = 91, UOP = 25 cc/hr What do you think...

79 HYPOVOLEMIA ADJUST YOUR WEDGE FOR THE PEEP

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

81 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

82

83

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

85 Sepsis Fluids Correct the cause Antibiotics Debridement Vasopressors –Phenylephrine –Levophed

86 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

87 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

88 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

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

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

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

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

93


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