Presentation is loading. Please wait.

Presentation is loading. Please wait.

Mazen Kherallah, MD, FCCP King Faisal Specialist Hospital & Research Center Approach and Hemodynamic Evaluation of Shocks.

Similar presentations


Presentation on theme: "Mazen Kherallah, MD, FCCP King Faisal Specialist Hospital & Research Center Approach and Hemodynamic Evaluation of Shocks."— Presentation transcript:

1 Mazen Kherallah, MD, FCCP King Faisal Specialist Hospital & Research Center Approach and Hemodynamic Evaluation of Shocks

2 Shock Definition

3 Question #0 Which of the following is necessary in the definition of shock? (a) A drop in the systolic blood pressure of less than 90 mm Hg (b) A drop in the mean arterial pressure of less than 60 mm Hg (c) A drop in the SBP of 40 mm Hg or 20% from baseline (d) An elevated lactic acid of ≥ 4 mmoL/L (e) Any of the above

4 Question #1 Which of the following is necessary in the definition of shock? (a) Hypotension (b) Tissue hypoxia (c) Use of pressors (d) Multiple organ dysfunction

5 Shock Profound and widespread reduction in the effective delivery of oxygen leading to first to reversible, and then if prolonged, to irreversible cellular hypoxia and organ dysfunction” Kumar and Parrillo Leads to Multiple Organ Dysfunction Syndrome (MODS)

6 Pathophysiology

7 VO2 DO2 Oxygen delivery Oxygen uptake Oxygen extraction ratio

8 Mizock BA. Crit Care Med. 1992;20: Oxygen Consumption Oxygen Delivery Critical Delivery Threshold Lactic Acidosis Physiologic Oxygen Supply Dependency

9 sepsis Sepsis sepsis

10 Mizock BA. Crit Care Med. 1992;20: Oxygen Consumption Oxygen Delivery Pathologic Physiologic Pathologic Oxygen Supply Dependency

11 Pathophysiology Most forms of shock –Low cardiac output state –Supply-dependency of systemic VO 2 Septic shock –Systemic DO 2 and VO 2 are both supranormal, but an oxygen deficit remains –Peripheral oxygen extraction may be deranged and VO 2 is pathologically supply-dependent –Possible microvascular maldistribution of perfusion

12 Question #2 Which is not an important determinant of oxygen delivery? (a) Hemoglobin level (b) Cardiac output (c) pO 2 (d) SaO 2

13 Oxygen Delivery (DO 2 ) Cardiac Output x Oxygen Content CO x [(1.3 x Hgb x SaO 2 ) + (0.003 x PaO 2 )] –Hemoglobin concentration –SaO 2 –Cardiac output –PaO 2 (minimal)

14 Preload Contractility Cardiac Output Afterload

15 Preload Determined by end-diastolic volume Pressure and volume related by compliance of the ventricle

16 Left ventricular end-diastolic pressure versus left ventricular end-diastolic volume

17 Cardiac Output Sterling relationship Volume loading Cardiac output

18 Clinical Adaptation of the Sterling Myocardial Function Curves

19 Global Hemodynamic Relationships Preload Contractility Afterload

20 Question #3 Which can cause low preload? (a) High PEEP (b) Tension pneumothorax (c) Third spacing (d) Positive pressure ventilation (e) All of the above

21 Pathophysiology Inadequate/ineffective DO 2 leads to anaerobic metabolism Large/prolonged oxygen deficit causes decrease of high-energy phosphates stores Membrane depolarization, intracellular edema, loss of membrane integrity and ultimately cell death

22 Effects of Shock at Cellular Level

23

24 Common Histopathology Associated with Tissue Hypoperfusion and Shock?

25 Mitochondrial Dysfunction in Cell Injury Increased cytosolic Ca 2+, oxidative stress, lipid peroxidation Robbins & Cotran Pathologic Basis of Disease: 2005

26 Histopathology of Tissue Hypoperfusion Associated with Shock Coagulative necrosis Contraction bands Edema Neutrophil infiltrate Myocardium Diffuse alveolar damage Exudate, atelectasis Edema Hyaline membrane Lung Robbins & Cotran Pathologic Basis of Disease: 2005

27 Mucosal infarction Hemorrhagic mucosa Epithelium absent Small Intestine Liver Centrilobular hemorrhagic necrosis Nutmeg appearance Robbins & Cotran Pathologic Basis of Disease: 2005 Histopathology of Tissue Hypoperfusion Associated with Shock

28 Brain Eosinophilia and shrinkage of neurons Neutrophil infiltration Bland infarct Punctate hemorrhages Brain Robbins & Cotran Pathologic Basis of Disease: 2005

29 Histopathology of Tissue Hypoperfusion Associated with Shock Kidney Tubular cells, necrotic Detached from basement membrane Swollen, vacuolated Pancreas Fat necrosis Parenchymal necrosis Robbins & Cotran Pathologic Basis of Disease: 2005

30 Incidence of Ischemic Histopathology in Patients Dying with Shock Hypovolemic n = 102 (%) Septic n = 93 (%) Cardiogenic n = 197 (%) Heart Lung Kidney Liver Intestine92616 Pancreas763 Brain634 McGovern VJ, Pathol Annu 1984;19:15

31 Shock Syndromes

32 Shock Cardiogenic shock - a major component of the the mortality associated with cardiovascular disease (the #1 cause of U.S. deaths) Hypovolemic shock - the major contributor to early mortality from trauma (the #1 cause of death in those < 45 years of age) Septic shock - the most common cause of death in American ICUs (the 13th leading cause of death overall in US)

33 PreloadAfterloadContractility Arterial pressure Cardiac output Peripheral resistance Heart rate Stroke volume Left ventricular size Myocardial fiber shortening Cardiac Performance

34 Compensatory Mechanisms

35 Case 1 34 year old involved in a motor vehicle accident arrived to emergency room with blood pressure of 70/30 and heart rate of 140/min

36 Question #5 Which is typical of hypovolemic shock? (a) High SVR (b) High cardiac output (c) High oxygen delivery (d) Normal wedge pressure

37 PreloadAfterloadContractility Arterial pressure Cardiac output Peripheral resistance Heart rate Stroke volume Left ventricular size Myocardial fiber shortening Hypovolemic Shock Compensatory Mechanism Adrenaline

38 CO SVR PWP EDV Hypovolemic Cardiogenic Obstructive afterload preload Distributive pre-resusc post-resusc Hypovolemic Shock Hemodynamics

39 Hemorrhagic Trauma Gastrointestinal Retroperitoneal Fluid depletion (nonhemorrhagic) External fluid loss -Dehydration -Vomiting -Diarrhea -Polyuria Interstitial fluid redistribution -Thermal injury -Trauma -Anaphylaxis Increased vascular capacitance (venodilatation) Sepsis Anaphylaxis Toxins/drugs Kumar and Parrillo, 2001 Hypovolemic Shock

40 Case 2 54 year old with acute onset chest pain arrived to emergency room with blood pressure of 70/30 and heart rate of 140/min

41 Question #5 Which is typical of cardiogenic shock? (a) Low SVR (b) High cardiac output (c) Low oxygen delivery (d) Low wedge pressure

42 PreloadAfterloadContractility Arterial pressure Cardiac output Peripheral resistance Heart rate Stroke volume Left ventricular size Myocardial fiber shortening Cardiogenic Shock Compensatory Mechanism Adrenaline

43 CO SVR PWP EDV Hypovolemic Cardiogenic Obstructive afterload preload Distributive pre-resusc post-resusc Cardiogenic Shock Hemodynamics

44 Kumar and Parrillo, 2001 Myopathic Myocardial infarction (hibernating myocardium) Left ventricle Right ventricle Myocardial contusion (trauma) Myocarditis Cardiomyopathy Post-ischemic myocardial stunning Septic myocardial depression Pharmacologic Anthracycline cardiotoxicity Calcium channel blockers Mechanical Valvular failure (stenotic or regurgitant) Hypertropic cardiomyopathy Ventricular septal defect Arrhythmic Bradycardia Tachycardia Cardiogenic Shock

45 Case 3 67 year old with fever, chills, SOB, and ugly looking abdominal wound arrived to emergency room with blood pressure of 70/30 and heart rate of 140/min

46 Question #6 Which is not typical of sepsis? (a) Low SVR (b) High cardiac output (c) Low oxygen delivery (d) Low wedge pressure

47 PreloadAfterloadContractility Arterial pressure Cardiac output Peripheral resistance Heart rate Stroke volume Left ventricular size Myocardial fiber shortening Distributive Shock Compensatory Mechanism Adrenaline

48 CO SVR PWP EDV Hypovolemic Cardiogenic Obstructive afterload preload Distributive pre-resusc post-resusc Distributive Hemodynamics

49 Kumar and Parrillo, 2001 Septic (bacterial, fungal, viral, rickettsial) Toxic shock syndrome Anaphylactic, anaphylactoid Neurogenic (spinal shock) Endocrinologic Adrenal crisis Thyroid storm Toxic (e.g., nitroprusside, bretylium) Distributive Shock

50 PreloadAfterloadContractility Arterial pressure Cardiac output Peripheral resistance Heart rate Stroke volume Left ventricular size Myocardial fiber shortening Obstructive Shock Compensatory Mechanism Adrenaline

51 CO SVR PWP EDV Hypovolemic Cardiogenic Obstructive afterload preload Distributive pre-resusc post-resusc Obstructive Shock Hemodynamics

52 Kumar and Parrillo, 2001 Impaired diastolic filling (decreased ventricular preload ) Direct venous obstruction (vena cava) -I ntrathoracic obstructive tumors Increased intrathoracic pressure -Tension pneumothorax -Mechanical ventilation (with excessive pressure or volume depletion) -Asthma Decreased cardiac compliance -Constrictive pericarditis -Cardiac tamponade Impaired systolic contraction (increased ventricular afterload) Right ventricle -Pulmonary embolus (massive) -Acute pulmonary hypertension Left ventricle -Saddle embolus -Aortic dissection Extracardiac Obstructive Shock

53 Angio-oedema

54

55 Clinical Features

56 Symptoms of Shock Anxiety /Nervousness Dizziness Weakness Faintness Nausea & Vomiting Thirst Confusion Decreased UO Hx of Trauma / other illness Vomiting & Diarrhoea Chest Pain Fevers / Rigors SOB General SymptomsSpecific Symptoms

57 Signs of Shock Pale Cold & Clammy Sweating Cyanosis Tachycardia Tachypnoea Confused / Aggiatated Unconscious Hypotensive/Oliguric Stridor / SOB

58 Capillary Refill

59 Skin Mottling

60

61 Diagnosis and Evaluation Primary diagnosis - tachycardia, tachypnea, oliguria, encephalopathy (confusion), peripheral hypoperfusion (mottled, poor capillary refill vs. hyperemic and warm), hypotension Differential DX: –JVP - hypovolemic vs. cardiogenic –Left S3, S4, new murmurs – cardiogenic –Right heart failure - PE, tamponade –Pulsus paradoxus, Kussmaul’s sign – tamponade –Fever, rigors, infection focus - septic –Poor skin turgor and dry mucous membranes: hypovolemic

62 Tachycardia Greater than 160 in infant Greater than 140 in preschool age child Greater than 120 in school age child Greater than 100 in an adult

63 Unable to produce Tachycardia Limited cardiac response to catecholamine stimulation: elderly Autonomic dysfunction: DM Concurrent use of beta-adrenergic blocking agents The presence of a pacemaker

64 Severity of Hemorrhage Comparison of Adult vs Child

65 Classification of Hemorrhagic Shock

66

67

68 Shock Evaluation and Monitoring

69 Initial Therapeutic Steps A Clinical Approach to Shock Diagnosis and Management Admit to intensive care unit (ICU) Venous access (1 or 2 large-bore catheters) Central venous catheter Arterial catheter EKG monitoring Pulse oximetry Urine output monitoring Hemodynamic support (MAP < 60 mmHg) Fluid challenge Vasopressors for severe shock unresponsive to fluids

70 Diagnosis and Evaluation Hgb, WBC, platelets PT/PTT Electrolytes, arterial blood gases BUN, Cr Ca, Mg Serum lactate ECG Laboratory

71 A Clinical Approach to Shock Diagnosis and Management CXR Abdominal views* CT scan abdomen or chest* Echocardiogram* Pulmonary perfusion scan* * When indicated Initial Diagnostic Steps

72 Diagnosis Remains Undefined or Hemodynamic Status Requires Repeated Fluid Challenges or Vasopressors A Clinical Approach to Shock Diagnosis and Management Pulmonary Artery Catheterization Cardiac output Oxygen delivery –MVO2 –DO and VO Filling pressures Echocardiography Pericardial fluid Cardiac function Valve or shunt abnormalities

73 Hemodynamic Monitoring Measurement of PCWP

74

75 Components of the Atrial Waves

76 The difference between CVP and PCWP waves

77 The mean of the A wave approximates ventricular end-diastolic pressure

78 Reading CVP V A c

79 Reading PCWP A V V A

80 Differences in CVP and PCWP EKG correlation

81 Reading the mean of an A wave 22+10/2=16

82 Question #7 Which is true about the “wedge”? (a) Measures LVEDV (b) Falsely elevated by PEEP (c) Increased in pulmonary HTN (d) Accurately measured in mitral stenosis

83 Wedge Pressure Correlates well with LA and LVEDP if normal anatomy Reliable measure of preload (volume) only with normal/stable ventricular compliance Falsely elevated by PEEP (and auto-PEEP)

84 Shock Management

85 Management Treatment of underlying cause Volume Vasopressors

86 A Clinical Approach to Shock Diagnosis and Management Identify source of blood or fluid loss in hypovolemic shock Intra-aortic balloon pump (IABP), cardiac angiography, and revascularization for LV infarction Echocardiography, cardiac cath and corrective surgery for mechanical abnormality Pericardiocentesis surgical drainage for pericardial tamponade Thrombolytic therapy, embolectomy for pulmonary embolism Source control and early broad antibiotics for septic shock

87 Perfusion Goals in Patients with Septic Shock HEMODYNAMCS MAP > 60 mm Hg PAOP = mmHg Cardiac Index > 2.2 L/min/m2 ORGAN PERFUSION CNS - improved sensorium Skin - warm, well perfused Renal - UOP > 0.5 cc/kg/hr Decreasing lactate (<2.2 mM/L) Improved renal, liver fucntion O2 DELIVERY ADEQUACY Arterial Hgb SpO2 > 92% Hgb concentration > 9 gm/dL SVO2 > 65% Blood Lactate Conc < 2 mM/L

88 Volume Therapy Crystalloids Lactated Ringer’s solution Normal saline Colloids Hetastarch Albumin Packed red blood cells Infuse to physiologic endpoints

89 Rivers E, Nguyen B, Havstad S, et al 2001;345: Early Goal Directed Therapy 89

90

91 49.2% 33.3% Standard Therapy N=133 EGDT N=130 P = 0.01* *Key difference was in sudden CV collapse, not MODS Early Goal-Directed Therapy Results: 28 Day Mortality Vascular Collapse 21% vs 10% p=0.02 MODS 22% vs 16% P=0.27 NEJM 2001;345: Mortality %

92 Rivers E, Nguyen B, Havstad S, et al. 2001;345: In-hospital mortality (all patients) Standard therapy EGDT 28-day mortality 60-day mortality NNT to prevent 1 event (death) = Mortality (%) The Importance of Early Goal-Directed Therapy for Sepsis-induced Hypoperfusion 92

93 SepsisSIRSSevere SepsisSeptic ShockInfection Early Goal Directed Therapy Early Goal-Directed Therapy (EGDT): involves adjustments of cardiac preload, afterload, and contractility to balance O 2 delivery with O 2 demand: Fluids, Blood, and Inotropes Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. NEJM 2001;345:1368.  CVP > 8-12 mm Hg  MAP > 65 mm Hg  Urine Output > 0.5 ml/kg/hr  ScvO 2 > 70%  SaO 2 > 93%  Hct > 30% * Therapies Across The Sepsis Continuum

94 Type of Fluids

95 Therapy: Resuscitation Fluids Crystalloid vs. colloid Optimal PWP vs mm Hg mL/kg fluid challenge in hypovolemic or septic shock with Re-challenges of mL/kg mL challenges in cardiogenic

96 Vasoactive Agent Receptor Activity Agent a1 a2b1 b2Dopa Dobutamine Dopamine++/+++ ? Epinephrine Norepinephrine / Phenylephrine++/+++ + ? 0 0

97 0 Vasopressors/Inotrops

98

99

100

101 Dopamine Norepinephrine

102 Intra-Aortic Balloon Pump

103 Take Home Points Shock is defined by inadequate tissue oxygenation, not hypotension Oxygen delivery depends primarily on CO, Hgb and SaO 2 (not pO 2 ) Volume expand with crystalloids and blood, if indicated; then add vasoactive drugs to improve vital organ perfusion Early treatment of shock is critical

104 Thank You


Download ppt "Mazen Kherallah, MD, FCCP King Faisal Specialist Hospital & Research Center Approach and Hemodynamic Evaluation of Shocks."

Similar presentations


Ads by Google