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A Free sample background from www.powerpointbackgrounds.com Slide 1 SHOCKDOOMSDAY 1.

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1 A Free sample background from www.powerpointbackgrounds.com Slide 1 SHOCKDOOMSDAY 1

2 A Free sample background from www.powerpointbackgrounds.com Slide 2 Vicken Y. Totten Shock lecture Thanks to David Cheng MD And all who taught me

3 A Free sample background from www.powerpointbackgrounds.com Slide 3 Definition SHOCK: inadequate organ perfusion to meet the tissue’s oxygenation demand

4 A Free sample background from www.powerpointbackgrounds.com Slide 4 PATHOPHYSIOLOGY OF SHOCK SYNDROME Cells switch from aerobic to anaerobic metabolism lactic acid production Cell function ceases & cells swell membranes becomes more permeable electrolytes & fluids seep in & out of cell Cells Die in Many Organs  Death Cells Die in Many Organs  Death

5 A Free sample background from www.powerpointbackgrounds.com Slide 5 Stages of shock Compensated /Early Shock Compensated /Early Shock –Vasoconstriction  (renin & carotid sinus baroceptor –Increase in HR and RR <- sympthatic activation) –Normotensive usually <- (aldosterone/ADH Na+/h20 retention) Decompensated / late Shock Decompensated / late Shock –Cool, clammy, hypotenisve. –Vital organ preservation –Worsening LOC –Continued increase in HR and RR <-----(Chemreceptor respose to metabolic acidosis) Irreversible- Irreversible- –HR and RR drop  Multi Organ Failure  Impending death)

6 A Free sample background from www.powerpointbackgrounds.com Slide 6 Symptoms of Shock Anxious Anxious Dizziness Dizziness Weakness Weakness Faintness Faintness Thirsty Thirsty “I am sick” “I am sick” Fevers / Rigors (sepsis) Fevers / Rigors (sepsis) SSCP (cardiogenic) SSCP (cardiogenic) Wheezing (anaphylaxis) Wheezing (anaphylaxis) Trauma pain (hypovolemia) Trauma pain (hypovolemia) General SymptomsSpecific Symptoms

7 A Free sample background from www.powerpointbackgrounds.com Slide 7 Early Signs of Shock in Non Complicated Patients WARM EARLY STAGE / PRESHOCK WARM EARLY STAGE / PRESHOCK Need high index of suspicion b/c lack of signs Need high index of suspicion b/c lack of signs +/- tachycardia +/- orthostatics (HR more sensitive than BP) +/- pulse pressure narrowing +/-restless

8 A Free sample background from www.powerpointbackgrounds.com Slide 8 “Hypoperfusion can be present in the absence of significant hypotension.” (Don’t only relay on BP for diagnosisng shock) -fccs course 8

9 A Free sample background from www.powerpointbackgrounds.com Slide 9 Signs of Late Shock Hypotension COLD LATE STAGE Cold, clammy and pale skin Cold, clammy and pale skin Rapid, weak, thready pulse Rapid, weak, thready pulse Rapid breathing (blow off CO2 met acidosis) Rapid breathing (blow off CO2 met acidosis) Cyanotic Cyanotic AMS->Coma AMS->Coma Anuria Anuria

10 A Free sample background from www.powerpointbackgrounds.com Slide 10 End Stage Clinical effects Cardiovascular Cardiovascular –Myocardial depression –Vasogenic effects Pulmonary Pulmonary –ARDS Renal Renal –ARF GI GI –Ischemic bowel Hepatic Hepatic –Increased LFT’s, liver failure Hematologic Hematologic –Neutropenia, Thrombocytopenia –DIC (Gm- > Gm+) CNS CNS –coma

11 A Free sample background from www.powerpointbackgrounds.com Slide 11 Multiple Organ Dysfunction Syndrome Number of Organs Mortality (%) 00.8 16.8 226.2 348.5 468.8 583.3 *Adapted from Irwin and Rippe’s Critical Care Medicine 5 th Edition, pg 1837

12 A Free sample background from www.powerpointbackgrounds.com Slide 12 Circumferential Subendocardial Infarction due to Shock

13 A Free sample background from www.powerpointbackgrounds.com Slide 13 Shock Lung

14 A Free sample background from www.powerpointbackgrounds.com Slide 14 Acute congestion of liver due to shock

15 A Free sample background from www.powerpointbackgrounds.com Slide 15 Acute tubular necrosis of the kidney due to shock

16 A Free sample background from www.powerpointbackgrounds.com Slide 16 Intestinal mucosal hemorrhages due to shock

17 A Free sample background from www.powerpointbackgrounds.com Slide 17 Adrenal gland hemorrhage due to shock

18 A Free sample background from www.powerpointbackgrounds.com Slide 18 Remember History and Physical often limited by patient’s condition History and Physical often limited by patient’s condition Patient presentation can be variable secondary to Patient presentation can be variable secondary to –Severity of the perfusion defect –Underlying cause –Prior organ dysfunction Exam should be tailored to be performed quickly with highest yield for uncovering the cause of shock. Exam should be tailored to be performed quickly with highest yield for uncovering the cause of shock.

19 A Free sample background from www.powerpointbackgrounds.com Slide 19 Components (fluids, pump, pipes)

20 A Free sample background from www.powerpointbackgrounds.com Slide 20 Components: Components: –Blood (fluid) –Heart (pump) –Blood Vessels (pipes)

21 A Free sample background from www.powerpointbackgrounds.com Slide 21 Types of Shock Hypovolemic (fluids) Cardiogenic (pump) Redistributive (pipes) (septic, neurogenic, anaphylactic)

22 A Free sample background from www.powerpointbackgrounds.com Slide 22 Adequate circulating blood volume depends on 3 components; A minor impairment in one can be compensated for by the other 2 for a limited time. Prolonged or severe impairments will lead to SHOCK. 22

23 A Free sample background from www.powerpointbackgrounds.com Slide 23 An Approach to Shock – Know this! BP = SVR x CO BP = blood pressure CO = cardiac output (pump & fluids) SVR = systemic vascular resistance (pipes)

24 A Free sample background from www.powerpointbackgrounds.com Slide 24 An Approach to Shock If the blood pressure is low, then either the: CO is low or SVR is low orBOTH

25 A Free sample background from www.powerpointbackgrounds.com Slide 25 Low SVR There are only a few causes of low SVR. They ALL cause vasodilation: Septic shock Neurogenic (spinal cord injury) shock Anaphylaxis Shock Vasodilator (antihypertensive) Posioning

26 A Free sample background from www.powerpointbackgrounds.com Slide 26 How do you assess SVR? Look at and feel the patient! Low SVR has the features: warm !!! warm !!! pink pink Bounding pulses Bounding pulses hyperdynamic heart (fast and pounding) hyperdynamic heart (fast and pounding)

27 A Free sample background from www.powerpointbackgrounds.com Slide 27 What if the SVR is high? Pale Pale Poor cap refill (>2 seconds) Poor cap refill (>2 seconds) Cool arms/legs (>2 degree C difference) Cool arms/legs (>2 degree C difference) Thready pulses (narrow pulse pressure (incr DBP)) Thready pulses (narrow pulse pressure (incr DBP)) Cause of shock (low BP) is then: low CO

28 A Free sample background from www.powerpointbackgrounds.com Slide 28 What are factors of CO? CO = HR x SV CO = cardiac output HR = heart rate SV = stroke volume

29 A Free sample background from www.powerpointbackgrounds.com Slide 29 HR Problems Heart Rate problems are easy to diagnose Heart Rate problems are easy to diagnose Rate: bradycardia versus tachycardia Rate: bradycardia versus tachycardia

30 A Free sample background from www.powerpointbackgrounds.com Slide 30 Low SV (stroke volume) Most difficult to diagnose and manage

31 A Free sample background from www.powerpointbackgrounds.com Slide 31 Stroke Volume depends on Preload--is the ventricle full? Hypovolemic Shock Obstructive Shock (ie Tension PTX, Tamponade) Cardiac function Squeeze  Contractility – can the ventricle contract? Can blood get out?  Valve function: normal?regurgitation?stenosis?

32 A Free sample background from www.powerpointbackgrounds.com Slide 32 BP = CO x SVR CO = HR x SV SV =preload & cardiac contractility-valve Perfusion (blood pressure) depends on:

33 A Free sample background from www.powerpointbackgrounds.com Slide 33 Components of BP summary

34 A Free sample background from www.powerpointbackgrounds.com Slide 34 Why Monitor? Essential to understanding their disease Essential to understanding their disease Describe the patient’s physiologic status Describe the patient’s physiologic status –Serial monitoring Facilitates diagnosis and treatment of shock Facilitates diagnosis and treatment of shock

35 A Free sample background from www.powerpointbackgrounds.com Slide 35 Monitoring clinical shock parameter Noninvasive : Blood pressure (SBP, MAP) Blood pressure (SBP, MAP) Urine output Urine output Heart rate Heart rate Shock index Shock index Invasive : Pulmonary artery catheter: CVP, PAWP, CO, SVR, DO 2 I, VO 2 I, SvO 2 Pulmonary artery catheter: CVP, PAWP, CO, SVR, DO 2 I, VO 2 I, SvO 2 Arterial catheter: ABP, Serum lactate, Base deficit Arterial catheter: ABP, Serum lactate, Base deficit

36 A Free sample background from www.powerpointbackgrounds.com Slide 36 Diagnosis of Shock MAP < 60 or decrease of 20 from baseline MAP < 60 or decrease of 20 from baseline systolic BP  90 systolic BP  90  systolic BP > 40 mm Hg from the patient’s baseline pressure  systolic BP > 40 mm Hg from the patient’s baseline pressure Shock index (HR>SBP) Shock index (HR>SBP) Clinical s/s of hypoperfusion of vital organs Clinical s/s of hypoperfusion of vital organs

37 A Free sample background from www.powerpointbackgrounds.com Slide 37 Mean Arterial Pressure MAP is the mean perfusion pressure for the tissues MAP is the mean perfusion pressure for the tissues –Most require a MAP of 60 or greater! Dependent only on the elastic properties of the arterial walls and the mean blood volume in the arterial tree Dependent only on the elastic properties of the arterial walls and the mean blood volume in the arterial tree MAP = (2 x DBP) + SBP MAP = (2 x DBP) + SBP 3

38 A Free sample background from www.powerpointbackgrounds.com Slide 38 Pulse Pressure=SBP-DBP The difference between the systolic (fxn of ejection fraction) and diastolic pressures (function of SVR and distensibility (elastic recoil) of the aorta Wide Wide –Normal 30-50 mmHg –Commonly seen with fever, anemia, exercise and hyperthyroidism –AR (aortic regurgitation) is also a cause Narrow Narrow –May indicate an increase in vascular resistance with decreased stroke volume (ie aortic stenosis or decreased intravascular volume)

39 A Free sample background from www.powerpointbackgrounds.com Slide 39 Invasive Markers Global Markers Global Markers –Base Deficit –Lactate Regional Markers Regional Markers –Gastric pH –Sublingual CO2

40 A Free sample background from www.powerpointbackgrounds.com Slide 40 Base Deficit Inadequate tissue perfusion leads to tissue acidosis Inadequate tissue perfusion leads to tissue acidosis Amount of base required to titrate 1 L of whole arterial blood to a pH of 7.4 Amount of base required to titrate 1 L of whole arterial blood to a pH of 7.4 Normal range +3 to –3 mmol per L Normal range +3 to –3 mmol per L Elevated base deficit correlates with the presence and severity of shock Elevated base deficit correlates with the presence and severity of shock

41 A Free sample background from www.powerpointbackgrounds.com Slide 41 Base Deficit Inadequate tissue perfusion leads to tissue acidosis Inadequate tissue perfusion leads to tissue acidosis Amount of base required to titrate 1 L of whole arterial blood to a pH of 7.4 Amount of base required to titrate 1 L of whole arterial blood to a pH of 7.4 Normal range +3 to –3 mmol per L Normal range +3 to –3 mmol per L Elevated base deficit correlates with the presence and severity of shock Elevated base deficit correlates with the presence and severity of shock

42 A Free sample background from www.powerpointbackgrounds.com Slide 42 Initial Lactate Weil and Afifi. (Circulation 1970)

43 A Free sample background from www.powerpointbackgrounds.com Slide 43 Lactate and Outcomes Adult Patients Demmers Ann Thorac Surg 70:2082-6:2000 A peak blood lactate level of >4.0 mmol/L was identified as a strong independent predictor of mortality and morbidity and suggests that tissue hypoperfusion

44 A Free sample background from www.powerpointbackgrounds.com Slide 44

45 A Free sample background from www.powerpointbackgrounds.com Slide 45 Gastric Intramucosal pH Blood flow is not uniformly distributed to all tissue beds Blood flow is not uniformly distributed to all tissue beds Regions with inadequate tissue perfusion may exist while global markers are ‘normal’ Regions with inadequate tissue perfusion may exist while global markers are ‘normal’ Gut mucosa among the first to be affected during shock and the last to be restored to normal Gut mucosa among the first to be affected during shock and the last to be restored to normal Intramucosal pH falls when perfusion becomes inadequate Intramucosal pH falls when perfusion becomes inadequate

46 A Free sample background from www.powerpointbackgrounds.com Slide 46 hypercarbia is a universal indicator of critically reduced tissue perfusion. Sublingual capnometry: A new noninvasive measurement for diagnosis and quantitation of severity of circulatory shock

47 A Free sample background from www.powerpointbackgrounds.com Slide 47 Sublingual CO2 Decrease gut perfusion Decrease gut perfusion –Gastric tissue = esophagus = sublingual tissue Non-invasive, hand held monitor Non-invasive, hand held monitor Rapid measurement Rapid measurement Sensitive marker of decreased blood flow Sensitive marker of decreased blood flow

48 A Free sample background from www.powerpointbackgrounds.com Slide 48 Sublingual capnometry: A new noninvasive measurement for diagnosis and quantitation of severity of circulatory shock P SL CO 2 provides a prompt indication of the reversal of tissue hypercarbia when circulatory shock is reversed

49 A Free sample background from www.powerpointbackgrounds.com Slide 49 Direct arterial pressure A-line

50 A Free sample background from www.powerpointbackgrounds.com Slide 50 Pulmonary Artery Catheter INDICATIONS INDICATIONS –volume status –cardiac status COMPLICATIONS COMPLICATIONS –technical –anatomic –physiologic

51 A Free sample background from www.powerpointbackgrounds.com Slide 51 Swan-Ganz Catheter

52 A Free sample background from www.powerpointbackgrounds.com Slide 52 PLACEMENT

53 A Free sample background from www.powerpointbackgrounds.com Slide 53 Correct PA-C Position From the RIJ approach, the RA is entered at approximately 25 cm, the RV at approximately 30 cm, and the PA at approximately 40 cm; the PCWP can be identified at approximately 45 cm. From the RIJ approach, the RA is entered at approximately 25 cm, the RV at approximately 30 cm, and the PA at approximately 40 cm; the PCWP can be identified at approximately 45 cm.

54 A Free sample background from www.powerpointbackgrounds.com Slide 54 Standard Parameters Measured Measured –Blood pressure –Pulmonary A. pressure –Heart rate –Cardiac Output –Stroke volume –Wedge pressure –CVP Calculated Calculated –Mean BP –Mean PAP –Cardiac Index –Stroke volume index –SVRI –LVSWI –BSA

55 A Free sample background from www.powerpointbackgrounds.com Slide 55 Why Index? Body habitus and size is individual Body habitus and size is individual “Indexing” to patient with BSA allows for reproducible standard “Indexing” to patient with BSA allows for reproducible standard PATIENT A 60 yo male 60 yo male 50 kg 50 kg CO = 4.0 L/min CO = 4.0 L/min BSA = 1.86 BSA = 1.86 CI = 2.4 L/min/m 2 PATIENT B 60 yo male 60 yo male 150 kg 150 kg CO = 4.0 L/min CO = 4.0 L/min BSA = 2.64 BSA = 2.64 CI = 1.5 L/min/m 2

56 A Free sample background from www.powerpointbackgrounds.com Slide 56

57 A Free sample background from www.powerpointbackgrounds.com Slide 57 PA Insertion 0 5 10 15 20 RA = 5RV = 22/4 PA 19/10 PAOP(wedge) = 9

58 A Free sample background from www.powerpointbackgrounds.com Slide 58 CVP CVP of SVC at level of right atrium CVP of SVC at level of right atrium pre-load “assessment” pre-load “assessment” normal 4 - 10 mm Hg normal 4 - 10 mm Hg

59 A Free sample background from www.powerpointbackgrounds.com Slide 59 PAOP (wedge) End expiration End expiration Wedge adjustment with positive pressure Wedge adjustment with positive pressure –Measured PAOP - ½ PEEP = “real PAOP”

60 A Free sample background from www.powerpointbackgrounds.com Slide 60 Vascular Resistance SYSTEMIC (SVR) MAP - CVP MAP - CVP C0 C0  SVR = vasoconstriction  SVR = vasodilation PULMONARY (PVR) MPAP - PAOP CO CO  PVR = constriction PE, hypoxia x 80 Vascular resistance = change in pressure/blood flow

61 A Free sample background from www.powerpointbackgrounds.com Slide 61 Cardiac Cycle pulmonary Left ventricle systemic Right ventricle RVSW PVR LVSW SVR CVP MPAP PCWP MAP

62 A Free sample background from www.powerpointbackgrounds.com Slide 62 Swan Ganz interpretation

63 A Free sample background from www.powerpointbackgrounds.com Slide 63 Too Many Numbers

64 A Free sample background from www.powerpointbackgrounds.com Slide 64 Definitions O 2 Delivery - volume of gaseous O 2 delivered to the LV/min. 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 Consumption - volume of gaseous O 2 which is actually used by the tissue/min. consumption > demand = anaerobic metabolism

65 A Free sample background from www.powerpointbackgrounds.com Slide 65 Mixed venous oxygen saturation Reflects difference between oxygen delivery and consumption Reflects difference between oxygen delivery and consumption Normal – 65-75% Normal – 65-75% Measurement taken from the distal port of a PA catheter Measurement taken from the distal port of a PA catheter

66 A Free sample background from www.powerpointbackgrounds.com Slide 66 SvO 2 : Low Values (< 60%)  CO/CI  CO/CI –  SV/SVI  Hgb  Hgb  SaO 2  SaO 2  O 2 consumption  O 2 consumption

67 A Free sample background from www.powerpointbackgrounds.com Slide 67 SvO 2 : High Values (> 75%) Sepsis Sepsis AV shunts/fistulae AV shunts/fistulae

68 A Free sample background from www.powerpointbackgrounds.com Slide 68 Oxycalculations

69 A Free sample background from www.powerpointbackgrounds.com Slide 69 Break Time…

70 A Free sample background from www.powerpointbackgrounds.com Slide 70 Goals of Shock Resuscitation Restore blood pressure Restore blood pressure Normalize systemic perfusion Normalize systemic perfusion Preserve organ function Preserve organ function

71 A Free sample background from www.powerpointbackgrounds.com Slide 71 Parameters of Adequate Resuscitation Urine output (0.5 - 1.0 ml/kg/hr) acceptable renal perfusion Reversal of lactic acidosis (nl. pH) improved perfusion Normal mental status adequate cerebral perfusion

72 A Free sample background from www.powerpointbackgrounds.com Slide 72 SHOCK: an EMERGENCY !!! Goal RAPIDLY RESTORE TISSUE PERFUSION Recognize it !!! Immediate stabilization: ABCImmediate stabilization: ABC ……. SHOTGUN approach ……. SHOTGUN approach Normalization of BP, pulse, UOP Hemodynamic parameters  Restoration of aerobic metabolism, elimination of tissue acidosis, repayment of O2 debt Treat the causeTreat the cause

73 A Free sample background from www.powerpointbackgrounds.com Slide 73 “Shock is a symptom of its cause.” -fccs course 73

74 A Free sample background from www.powerpointbackgrounds.com Slide 74 In general, treat the cause...

75 A Free sample background from www.powerpointbackgrounds.com Slide 75Management ABC’s ABC’s –Maintain airway –Decrease work of breathing & Optimize 02 –Circulation & Control Hemorrhage includes: Direct pressureDirect pressure Pressure pointsPressure points Fluids & DrugsFluids & Drugs Must address and treat: Must address and treat: –PRELOAD –AFTERLOAD –PUMP Re-assess every 5-15 minutes (the sicker the patient, the shorter the interval

76 A Free sample background from www.powerpointbackgrounds.com Slide 76 Management priorities in hypoperfused states BP potency: Dopamine...NE…Vasopressin/Phenylephrine When in doubt, try a little more volume

77 A Free sample background from www.powerpointbackgrounds.com Slide 77 Hypovolemia

78 A Free sample background from www.powerpointbackgrounds.com Slide 78 Time Outcomes of same vol. lost over diff. periods of time. Slow losses (III, IV) allow compensations to take effect. Rapid loss (I, II) of same vol. is fatal

79 A Free sample background from www.powerpointbackgrounds.com Slide 79 Classes of Hypovolemic Shock

80 A Free sample background from www.powerpointbackgrounds.com Slide 80 Clinical Signs of Acute Hemorrhagic Shock % Blood lossClinical Signs < 15Slightly increased heart rate 15-30Increased HR, increased DBP (narrow pp), prolonged capillary refill, flat neck veins 30-50Above findings plus: hypotension, confusion, acidosis, decreased urine output > 50Refractory hypotension, refractory acidosis, death

81 A Free sample background from www.powerpointbackgrounds.com Slide 81 Hypovolemic Shock Causes Causes –hemorrhage –vomiting –diarrhea –dehydration –third-space loss –burns Signs Signs –  cardiac output –  PAOP/CVP –  SVR

82 A Free sample background from www.powerpointbackgrounds.com Slide 82 Treatment - Hypovolemic Reverse hypovolemia & hemorrhage control Reverse hypovolemia & hemorrhage control Crystalloid vs. Colloid Crystalloid vs. Colloid –1 L crystalloid  250 ml colloid Watch for fluid overload by reassessing lung soundsWatch for fluid overload by reassessing lung sounds 3:1 Rule (3cc crystalloid for 1cc bld loss)3:1 Rule (3cc crystalloid for 1cc bld loss) Watch for hyperchloremic metabolic acidosis when large volumes of NaCl are infusedWatch for hyperchloremic metabolic acidosis when large volumes of NaCl are infused Best to give in 250 mL boluses in CHF followed by reassessment for another 250 cc bolusBest to give in 250 mL boluses in CHF followed by reassessment for another 250 cc bolus –Colloids: (ex: albumin) Will increase osmotic pressure, watch for pulm edemaWill increase osmotic pressure, watch for pulm edema Remain in vascular space longer (several hrs)Remain in vascular space longer (several hrs) NOT increase survivalNOT increase survival prbc sooner than later prbc sooner than later –500 ml whole blood increases Hct 2-3%, 250ml PRBC’s increases Hct 3-4% –Increases oxygen carrying capacity –Used with acute hemorrhaging (mntn Hct 24% and Hgb 8g /dL) NOT FOR VOLUME –FFP for coagulopathy (all factors) –Factor vii –PLT for thrombocytopenia Pressors? Pressors?

83 A Free sample background from www.powerpointbackgrounds.com Slide 83 Resuscitation Transport times 100 minutes fluid was beneficial. Transport times 100 minutes fluid was beneficial. Penetrating torso trauma benefited from limited resuscitation prior to bleeding control. Not applicable to BLUNT victims. Penetrating torso trauma benefited from limited resuscitation prior to bleeding control. Not applicable to BLUNT victims.

84 A Free sample background from www.powerpointbackgrounds.com Slide 84 Role of PASG? Higher mortality rate in penetrating thoracic, cardiac trauma Higher mortality rate in penetrating thoracic, cardiac trauma Role undefined in rural, blunt trauma Role undefined in rural, blunt trauma Splinting role Splinting role

85 A Free sample background from www.powerpointbackgrounds.com Slide 85 Cardiogenic Shock Mech Mech –defect in cardiac function (lost > 40% Fxn) Signs Signs –  cardiac output –  PAOP/CVP –  SVR –  left ventricular stroke work (LVSW)

86 A Free sample background from www.powerpointbackgrounds.com Slide 86 Cardiogenic Shock Myocardial failure (MI) Myocardial failure (MI) Severe Arrhythmia Severe Arrhythmia Severe Valvular dysfunction Severe Valvular dysfunction Reduction in cardiac output: Reduction in cardiac output: –>Decreased oxygen delivery

87 A Free sample background from www.powerpointbackgrounds.com Slide 87 Symptoms of Cardiogenic Shock Skin: progressive peripheral vasoconstriction results in cool, moist, pale skin with mottling Skin: progressive peripheral vasoconstriction results in cool, moist, pale skin with mottling CHF Sx CHF Sx –JVD, HJR, APE, pedal edema Heart: Heart: –Sounds: d/t enlargement and congestion you can hear murmurs or S3 or S4 –Pulse: rapid rate and thready/weak pulse BP: decreased BP and MAP BP: decreased BP and MAP UO: decreases early d/t decreased renal perfusion UO: decreases early d/t decreased renal perfusion

88 A Free sample background from www.powerpointbackgrounds.com Slide 88 Cardiogenic Shock Assess for: Assess for: –Signs of heart failure –Signs of tamponade –Cardiac dysrrhythmia –Myocardial infarction –Tachycardia –Muffled heart sounds or third heart sound –Engorged neck veins with hypotension –Dyspnea –Edema in feet and ankles

89 A Free sample background from www.powerpointbackgrounds.com Slide 89 Coronary Perfusion Pressure Coronary PP = DBP - PAOP coronary perfusion =  P across coronary a. GOAL - Coronary PP > 50 mm Hg

90 A Free sample background from www.powerpointbackgrounds.com Slide 90 Treatment of Cardiogenic Shock Increase oxygen supply to the heart Increase oxygen supply to the heart –Decrease O2 consumption (pain meds/sedation) –Increase O2 delivery (Mech vent, reperfusion of the coronary arteries) Maximize the cardiac output Maximize the cardiac output –Mntn normal rhythm (dysrhythmics, pacing, cardioversion) –Diastolic Vasopressors (dopamine, epi, norepi, vasopressin) –Improve myocardial contractility--Inotropes dobut and amrinonedobut and amrinone Decrease the afterload (workload of the LV) Decrease the afterload (workload of the LV) –IABP –LVAD

91 A Free sample background from www.powerpointbackgrounds.com Slide 91 The Failing Heart Improve myocardial function, C.I. < 3.5 is a risk factor, 2.5 may be sufficient. Improve myocardial function, C.I. < 3.5 is a risk factor, 2.5 may be sufficient. Fluids first, then cautious pressors Fluids first, then cautious pressors Remember aortic DIASTOLIC pressures drives coronary perfusion (DBP-PAOP = Coronary Perfusion Pressure) Remember aortic DIASTOLIC pressures drives coronary perfusion (DBP-PAOP = Coronary Perfusion Pressure) If inotropes and vasopressors fail, intra-aortic balloon pump & LV assist devices If inotropes and vasopressors fail, intra-aortic balloon pump & LV assist devices

92 A Free sample background from www.powerpointbackgrounds.com Slide 92 Intra-Aortic Balloon Pump

93 A Free sample background from www.powerpointbackgrounds.com Slide 93 Distributive Shock Types Types –Sepsis –Anaphylactic –Acute adrenal insufficiency –Neurogenic Signs Signs –± cardiac output –  PAOP –  SVR

94 A Free sample background from www.powerpointbackgrounds.com Slide 94 Anaphylaxis

95 A Free sample background from www.powerpointbackgrounds.com Slide 95 Anaphylactic Shock Rapid onset Rapid onset Diffuse vasodilation mechanism from histamine & bradykinin Diffuse vasodilation mechanism from histamine & bradykinin Edema from increased capillary permeability Edema from increased capillary permeability Bronchoconstriction Bronchoconstriction

96 A Free sample background from www.powerpointbackgrounds.com Slide 96 Symptoms Onset within seconds and progression to death in minutes Cutaneous manifestations Cutaneous manifestations –urticaria, erythema, pruritis, angioedema Respiratory compromise Respiratory compromise –stridor, wheezing, bronchorrhea, resp. distress Circulatory collapse Circulatory collapse –tachycardia, vasodilation, hypotension CNS CNS –apprehension->ams->coma

97 A Free sample background from www.powerpointbackgrounds.com Slide 97 Diagnosis History and physical alone make the diagnosis History and physical alone make the diagnosis Lab values serve no role Lab values serve no role –Histamine levels are elevated for about 30 min, tryptase for several hours.

98 A Free sample background from www.powerpointbackgrounds.com Slide 98 Treatment Remove the antigen Remove the antigen ABC’s ABC’s IV Fluids, O2, cardiac monitor, pulse ox IV Fluids, O2, cardiac monitor, pulse ox First line Rx: First line Rx: –Epinephrine –For severe bronchospasm, laryngeal edema, signs of upper airway obstruction, respiratory arrest or shock: IV epi 100 micrograms of 1:100,000 (place 0.1 mL of 1:1000 in 10 mL of NS, give over 5-10 min)100 micrograms of 1:100,000 (place 0.1 mL of 1:1000 in 10 mL of NS, give over 5-10 min) –If less severe, can give 0.3-0.5 mL 1:1000 SC

99 A Free sample background from www.powerpointbackgrounds.com Slide 99 Treatment 2 nd line: 2 nd line: –H1 blocker: Diphenhydramine 25-50 mg IV –H2 blocker: Ranitidine 50 mg or Famotidine 20 mg IV.) –Steroids (Methylprednisolone 125 mg IV or Prednisone 40-60 mg po) –Albuterol –For patients taking Beta-blockers with refractory hypotension, think about glucagon

100 A Free sample background from www.powerpointbackgrounds.com Slide 100 Septic Shock

101 A Free sample background from www.powerpointbackgrounds.com Slide 101 SEPSIS Systemic Inflammatory Response (SIRS) manifested by two or > of following: Systemic Inflammatory Response (SIRS) manifested by two or > of following: –Temp > 38 or 38 or < 36 centigrade –HR > 90 –RR > 20 or PaCO2 20 or PaCO2 < 32 –WBC > 12,000/cu mm or > 10% Bands (immature wbc)

102 A Free sample background from www.powerpointbackgrounds.com Slide 102 Risk factors of Sepsis Extreme age: 65 years Extreme age: 65 years Surgical / invasive procedures Surgical / invasive procedures Malnutrition Malnutrition Chronic illness Chronic illness –DM, CRF, Hepatitis Compromised immune status Compromised immune status –AIDS, immunosuppressives, EtOH, malignancies Drug resistant organisms Drug resistant organisms

103 A Free sample background from www.powerpointbackgrounds.com Slide 103 What is Sepsis? SIRS  Sepsis  Severe Sepsis  Septic Shock SIRS  Sepsis  Severe Sepsis  Septic Shock Sepsis is the combination of the Systemic Inflammatory Response Syndrome (SIRS) & a confirmed or presumed infectious etiology. Sepsis is the combination of the Systemic Inflammatory Response Syndrome (SIRS) & a confirmed or presumed infectious etiology. Severe Sepsis: SIRS criteria, source of infection and infection-induced organ dysfunction or hypoperfusion abnormalities (sepsis + lactic acidosis/oliguria/AMS/etc.) Severe Sepsis: SIRS criteria, source of infection and infection-induced organ dysfunction or hypoperfusion abnormalities (sepsis + lactic acidosis/oliguria/AMS/etc.) Septic Shock: SIRS criteria, source of infection, and hypotension not reversed with fluid resuscitation and associated with organ dysfunction or hypoperfusion abnormalities Septic Shock: SIRS criteria, source of infection, and hypotension not reversed with fluid resuscitation and associated with organ dysfunction or hypoperfusion abnormalities

104 A Free sample background from www.powerpointbackgrounds.com Slide 104 Septic Shock Bacterial, viral, fungal infection Bacterial, viral, fungal infection “Warm shock” is early stage “Warm shock” is early stage –Fever, tachycardia, tachypnoea, leucocytosis, –inadequate oxygen extraction (High SvO 2, Metabolic acidosis) in infected tissues “Cold shock” is late stage “Cold shock” is late stage

105 A Free sample background from www.powerpointbackgrounds.com Slide 105 Septic/Inflammatory Shock Signs: Early– warm w/ vasodilation, often adequate urine output, febrile, tachypneic. output, febrile, tachypneic. Late-- vasoconstriction, hypotension, oliguria, Late-- vasoconstriction, hypotension, oliguria, altered mental status. altered mental status. Monitor/findings: Early—hyperglycemia, respiratory alkylosis, hemoconcentration, alkylosis, hemoconcentration, WBC typically normal or low. WBC typically normal or low. Late – Leukocytosis, lactic acidosis Late – Leukocytosis, lactic acidosis Very Late– Disseminated Intravascular Very Late– Disseminated Intravascular Coagulation & Multi-Organ Coagulation & Multi-Organ System Failure. System Failure.

106 A Free sample background from www.powerpointbackgrounds.com Slide 106 Septic Shock TX Prompt volume replacement - fill the tank Prompt volume replacement - fill the tank Early antibiotic administration - treat the cause Early antibiotic administration - treat the cause If MAP < 60 If MAP < 60 –Dopamine = 2 - 3  g/kg/min –Norepinephrine = titrate (1-100  g/min)

107 A Free sample background from www.powerpointbackgrounds.com Slide 107 Neurogenic shock

108 A Free sample background from www.powerpointbackgrounds.com Slide 108 Neurogenic Shock Essential derangement: paralysis of the sympathetic chain which controls vascular tone from injury to thoracic or cervical level spinal cord injury. Essential derangement: paralysis of the sympathetic chain which controls vascular tone from injury to thoracic or cervical level spinal cord injury. Produces decreased SVR from loss of vascular tone and bradycardia from unopposed parasympathetic input to SA node. Produces decreased SVR from loss of vascular tone and bradycardia from unopposed parasympathetic input to SA node.

109 A Free sample background from www.powerpointbackgrounds.com Slide 109 Neurogenic (Vasogenic) Shock Caused by: Caused by: –Spinal cord injury loss of SNS Massive venous pooling & arteriolar dilatation Massive venous pooling & arteriolar dilatation Signs and Symptoms: Signs and Symptoms: –Hypotension without tachycardia –Warm pink skin from cutaneous vasodilation –Low BP w/ minimal response to fluids –Accompanying Neurologic deficit Spinal shock is not Neurogenic shock Spinal shock is not Neurogenic shock –Spinal Shock: the temporary loss of spinal reflex activity that occurs below a total or near total spinal cord injury

110 A Free sample background from www.powerpointbackgrounds.com Slide 110 Treatment of Neurogenic Shock Increase vascular tone and improve CO Increase vascular tone and improve CO –Increase preload with fluids CVPCVP PAWPPAWP –Increase vascular tone VasopressorsVasopressors –Maintain heart rate Treat bradycardia if symptomaticTreat bradycardia if symptomatic –Maintain adequate oxygenation Watch with SCI because of the disruption of O 2 to the medullaWatch with SCI because of the disruption of O 2 to the medulla –Initiate therapy to prevent DVT Sluggish venous flow will increase risk factorsSluggish venous flow will increase risk factors –Steroids (Methylprednisolone 30mg/kg over 15 min in first hour, then 5.4 mg/kg/hr x 23 hours) There are contradicting studies, all of which have flawThere are contradicting studies, all of which have flaw The symptoms of neurogenic shock typically last 1-3 weeks The symptoms of neurogenic shock typically last 1-3 weeks

111 A Free sample background from www.powerpointbackgrounds.com Slide 111 Obstructive Shock Causes Causes –Cardiac Tamponade –Tension Pneumothorax –Massive Pulmonary Embolus Signs Signs –  cardiac output –  PAOP/CVP –  SVR Treatment Treatment Needle decompression Embolectomy / TPA Embolectomy / TPA

112 A Free sample background from www.powerpointbackgrounds.com Slide 112 Adrenal Crisis Distributive Shock Causes Causes –Autoimmune adrenalitis –Adrenal apoplexy = B hemorrhage or infarct This is suspected when patient is non- responsive to fluids, vasopressors and antibiotics. This is suspected when patient is non- responsive to fluids, vasopressors and antibiotics. Electrolytes may reveal hypoNa+ & hyperK+ Electrolytes may reveal hypoNa+ & hyperK+ Steroids may be lifesaving in patient who is unresponsive to fluids-inotropic-vasopressor (hydrocortisone 100mg IV) Steroids may be lifesaving in patient who is unresponsive to fluids-inotropic-vasopressor (hydrocortisone 100mg IV)

113 A Free sample background from www.powerpointbackgrounds.com Slide 113 Vasopressor Agents? Augments contractility, after preload established, thus improving cardiac output. Augments contractility, after preload established, thus improving cardiac output. Risk tachycardia and increased myocardial oxygen consumption if used too soon Risk tachycardia and increased myocardial oxygen consumption if used too soon Rationale, increased C.I. improves global perfusion Rationale, increased C.I. improves global perfusion

114 A Free sample background from www.powerpointbackgrounds.com Slide 114 Vasopressors & Inotropic Agents Dopamine Dopamine Dobutamine Dobutamine Norepinephrine Norepinephrine Epinephrine Epinephrine Amrinone Amrinone

115 A Free sample background from www.powerpointbackgrounds.com Slide 115 Dopamine Low dose (0.5 - 2  g/kg/min) = dopaminergic Low dose (0.5 - 2  g/kg/min) = dopaminergic Moderate dose (3-10  g/kg/min) =  -effects Moderate dose (3-10  g/kg/min) =  -effects High dose (> 10  g/kg/min) =  -effects High dose (> 10  g/kg/min) =  -effects SIDE EFFECTS SIDE EFFECTS –tachycardia –> 20  g/kg/min  to norepinephrine

116 A Free sample background from www.powerpointbackgrounds.com Slide 116 Dobutamine  -agonist  -agonist 5 - 20  g/kg/min 5 - 20  g/kg/min potent inotrope, variable chronotrope potent inotrope, variable chronotrope caution in hypotension (inadequate volume) may precipitate tachycardia or worsen hypotension caution in hypotension (inadequate volume) may precipitate tachycardia or worsen hypotension

117 A Free sample background from www.powerpointbackgrounds.com Slide 117 Norepinephrine Potent  -adrenergic vasopressor Potent  -adrenergic vasopressor Some  -adrenergic, inotropic, chronotropic Some  -adrenergic, inotropic, chronotropic Dose 1 - 100  g/min Dose 1 - 100  g/min Unproven effect with low-dose dopamine to protect renal and mesenteric flow. Unproven effect with low-dose dopamine to protect renal and mesenteric flow.

118 A Free sample background from www.powerpointbackgrounds.com Slide 118 Epinephrine  - and  -adrenergic effects  - and  -adrenergic effects potent inotrope and chronotrope potent inotrope and chronotrope dose 1 - 10  g/min dose 1 - 10  g/min increases myocardial oxygen consumption particularly in coronary heart disease increases myocardial oxygen consumption particularly in coronary heart disease

119 A Free sample background from www.powerpointbackgrounds.com Slide 119 Amrinone Phosphodiesterase inhibitor, positive inotropic and vasodilatory effects Phosphodiesterase inhibitor, positive inotropic and vasodilatory effects increased cardiac stroke output without an increase in cardiac stroke work increased cardiac stroke output without an increase in cardiac stroke work most often added with dobutamine as a second agent most often added with dobutamine as a second agent load dose = 0.75 -1.5 mg/kg  5 - 10  g/kg/min drip load dose = 0.75 -1.5 mg/kg  5 - 10  g/kg/min drip main side-effect - thrombocytopenia main side-effect - thrombocytopenia

120 A Free sample background from www.powerpointbackgrounds.com Slide 120 vasopressin V1 vascular smooth muscle receptor vasoconstriction V1 vascular smooth muscle receptor vasoconstriction 0.01-0.04 units/min 0.01-0.04 units/min Risk: coronary, mesenteric ischemia, hyponatremia, skin necrosis Risk: coronary, mesenteric ischemia, hyponatremia, skin necrosis

121 A Free sample background from www.powerpointbackgrounds.com Slide 121 Calcium Sensitisation by Levosimendan Enhanced contractility of myocardial cell by amplifying trigger for contraction with no change in total intracellular Ca 2+ Enhanced contractility of myocardial cell by amplifying trigger for contraction with no change in total intracellular Ca 2+ Clinical trials status Clinical trials status Enhanced contractility of myocardial cell by amplifying trigger for contraction with no change in total intracellular Ca 2+ Enhanced contractility of myocardial cell by amplifying trigger for contraction with no change in total intracellular Ca 2+ Clinical trials status Clinical trials status

122 A Free sample background from www.powerpointbackgrounds.com Slide 122 Endpoints? ACS / ATLS - restoration of vital signs and evidence of end-organ perfusion ACS / ATLS - restoration of vital signs and evidence of end-organ perfusion Swan-guided resuscitation Swan-guided resuscitation –C.I.  4.5, DO 2 I  670, VO 2 I  166 Lactic Acid clearance Lactic Acid clearance Gastric pH Gastric pH

123 A Free sample background from www.powerpointbackgrounds.com Slide 123 Don’t forget... -Samuel D. Gross, 1872 Shock: “rude unhinging of the machinery of life.” 123

124 A Free sample background from www.powerpointbackgrounds.com Slide 124 ??????????? For the human speaker


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