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![Understanding of Shock
Physiology
The major physiologic determinants of tissue perfusion (and systemic blood
pressure [BP]) are
Cardiac output (CO) and
Systemic Vascular resistance (SVR)
BP = CO X SVR
CO is the product of heart rate (HR) and stroke volume (SV):
CO = HR X SV
Biologic processes that change any one of these physiologic parameters can result
in hypotension and shock.](https://image.slidesharecdn.com/shockdefinitiontypesandmanagement-converted-190705140718/85/Shock-Management-5-320.jpg)
![Anaphylactic Shock
Anaphylaxis is a Rapid, Generalized often unanticipated,
immunologically mediated events
that occur after exposure to certain foreign substance.
Causes:
Foods (Milk, soy, eggs, nuts, and shellfish)
Medications (Antibiotics [penicillin], NSAIDs, Anesthetics)
Venom (Hymenoptera stings)
Intravenous contrast materials, and latex.
Idiopathic-Up to 20%](https://image.slidesharecdn.com/shockdefinitiontypesandmanagement-converted-190705140718/85/Shock-Management-42-320.jpg)
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Shock Management
- 1. 05/07/2019 105/07/2019 1 (Definition,Types and Management) Presented by Ajas K Aliyar Intensive Care Outreach Nurse Al Mafraq Hospital Abu Dhabi
- 2. OBJECTIVES To develop anunderstanding of the definition and Pathophysiology and Stages of shock. To develop an understanding and overview of the different types of shock. To discuss Management of different Types of Shock.
- 3. What is shock? InadequateTissue Perfusion of Oxygenated Blood
- 4. Definition of Shock Oxygendelivery ≠ Oxygen Consumption (DO2 ≠ VO2) “A state of cellular and tissue hypoxia due to Reduced oxygen delivery and/or Increased oxygen consumption or Inadequate oxygen utilization” O2 Consumption O2 Delivery Empirical Criteria for Diagnosis of Circulatory Shock Systemic Arterial Hypotension (SBP <90 mm Hg/ MAP <65 mmHg associated tachycardia) Clinical Signs of Tissue Hypoperfusion (Cutaneous, Renal, Neurologic) Hyperlactatemia (Abnormal Cellular Oxygen Metabolism)
- 5. Understanding of Shock Physiology Themajor physiologic determinants of tissue perfusion (and systemic blood pressure [BP]) are Cardiac output (CO) and Systemic Vascular resistance (SVR) BP = CO X SVR CO is the product of heart rate (HR) and stroke volume (SV): CO = HR X SV Biologic processes that change any one of these physiologic parameters can result in hypotension and shock.
- 6. Understanding Shock-SVR SVR regulatedby Vessel length, Blood viscosity, blood vessel Diameter/tone. Dilatation opens blood vessels and increases volume to area but decreases return to heart Constriction decreases volume to area but increases return to heart
- 7. Understanding Shock-Stroke Volume Volumeof blood pumped by the heart in one Cycle What affect stroke volume ? Blood volume Rhythm problems Heart muscle problem Mechanical obstruction
- 8. Understanding of Shock Tissueperfusion is driven by Blood Pressure! So…. In other words When the blood flow (pressure) and O2 delivery to the cell are too low There will be shock!!!!
- 9. Why should youcare Shock? High mortality 20%-90% O2 Deprivation and Build Up of waste products Could be fatal without timely management Rapidly become Irreversible>>>Multiorgan failure (MOF)>>>Death The early stages of shock are more amenable to therapy and are more likely to be reversible Early , timely and appropriate management -Deterioration can be prevented -Signs of impending deterioration can be reversed -Reduces mortality
- 10. Pathophysiology and Stagesof shock
- 11. Stages Of Shock Non-Progressive(Decompensated) •Stage Of “Pre shock” • Compensatory Response to decreased Perfusion • Decreased CO is maintained by Increase in HR and SVR • Comp. Tachycardia • MAP Maintained • Cool Extremities (Vasoconstriction) • Mildly Elevated lactate • Adequate UOP • Cerebral Perfusion Intact • Reversible Progressive(Compensated) • Stage of “Shock” • Compensatory Mechanism Fails • Dyspnea • Symptomatic Tachycardia • MAP drops more than 15 MMHG • Cool, clammy skin • Cerebral Perfusion low- Decreased LOC/Restless • Oliguria • Metabolic acidosis- Worsens • Reversible If Recognized and treated appropriately Irreversible(Refractory) • Stage of “End-organ dysfunction” • Irreversible organ damage, multiorgan failure (MOF), and Death • Severe drops in MAP/Refractory • Aneuric, AKI • Acidemia- Depress CO • Hyperlactatemia often worsens • Profound Decrease in Cerebral Perfusion/Obtundation/Co ma • Irreversible • Death
- 12. • Blood Volume ProblemHypovolemic Shock •Blood Pump ProblemCardiogenic Shock • Blood Vessel ProblemDistributive shock • Extra-cardiac Pump Failure Problem Obstructive shock TYPES OF SHOCK
- 13. Types and Etiologyof Shock • Pulmonary vascular • Mechanical • Septic Shock • Non-septic • Cardiomyopathic • Arrythmogenic • Mechanical • Hemorrhagic • Non-Hemorrhagic Hypovolemic Shock Cardiogenic Shock Obstructive Shock Distributive Shock COMBINED SHOCK Example: Sepsis/Pancreatiti s + Hypovolemic + Cardiogenic shock Severe Traumatic Injury>>Hypovole mic + Distributive
- 14. Epidemiology of Shock 62% 16% 16% 4%2% In a Trial of 1600 Patients in ICU Distributive(Septic) 62% Hypovolemic 16% Cardiogenic 16% Obstructive 4% Other Distributive Shock 2% 34% 34% 30% 2% Study of 103 Patients in a busy Urban ED Septic Shock 33% Hypovolemic 33% Cardiogenic 29% Other forms of Shock 2%
- 15. EVALUATIONS OF SHOCK Resuscitationshould be started even while investigation of the cause is ongoing Once identified, the cause must be corrected rapidly Undifferentiated Shock!!!! Medical History Physical Examination-ABCDEFG,SAMPLE Clinical Investigations
- 17. Initial Treatment Approachto Shock Key Principles in the Treatment of Shock 1. Recognize shock early 2. Assess for type of shock present 3. Initiate therapy simultaneous with the evaluation into the etiology of shock 4. Restoration of oxygen delivery is the aim of therapy 5. Identify etiologies of shock which require additional lifesaving interventions
- 18. Initial Approach toall types of Shock ❑ Early, adequate hemodynamic support of patients in shock is crucial ❑ The initial management of shock is problem-oriented, and the goals are therefore the same, regardless of the cause Important components of resuscitation is The VIP rule VENTILATE INFUSE PUMP • O2 Administration • Fluids Administration • Vasoactive Drug administration
- 19. The Initial managementof shock A • Establish A Patent Airway • Basic Airway Manure • Intubation/MV B • Administration of oxygen • To increase oxygen delivery and prevent pulmonary hypertension C • Fluids Resuscitation(Type, Rate and Objective of Fluids) • Vasoactive Agents (Vasopressors, Inotropic Agents, Vasodilators) • Mechanical Support (IABP,ECMO) TYPE OF FLUID>> CRYSTALLOIDS, COLLOIDS RATE OF FLUID>>300-500ML OVER 20-30 MINS OBJECTIVE OF FLUID ADMINISTRATION>>INCREASE SYSTEMIC ART PRESSURE>>HR>>UOP
- 20. Prognosis Sepsis and septicshock Are associated with long-term morbidity and mortality Requiring placement into long-term acute care facilities or post-acute care centers. Septic shock has a mortality rate between 40% and 50%. Cardiogenic shock Mortality rate ranging from 50% to 75%, an improvement over prior mortality rates. Hypovolemic and obstructive shock Generally have much lower mortality and respond better to timely treatment.
- 21. 68 Years ofMale with History of HTN and Duodenal Ulcer presents to the ER with epigastric abdominal pain with radiation to his back and dizziness. The patient is hypotensive, tachycardic, Afebrile, and with cool and clammy skin What type of Shock is this?
- 22. Hypovolemic Shock Due toreduced intravascular volume (i.e., reduced preload), which, in turn, reduces CO Non-hemorrhagic Hemorrhagic
- 23. Hypovolemic Shock-Causes Non-hemorrhagic Gastrointestinal losses Skinlosses Renal losses Third space losses into the extra vascular space Hemorrhagic Trauma Gastrointestinal bleeding Intraoperative and postoperative bleeding Retroperitoneal bleeding Tumor or abscess erosion into major vessels Ruptured ectopic pregnancy, postpartum hemorrhage, uterine or vaginal hemorrhage
- 24. CLASSIFICATION OF HEMORRHAGICSHOCK In a normal Adult, a tachycardia after blood loss indicates at least a 15% loss of blood volume(<750 MLs) CLASS PULSE B.P CNS STATUS URINE OUTPUT BLOOD LOSS FLUID REPLACEMEN T CLASS I <100 BPM NORMAL SLIGHTLY ANXIOUS >30ML/HR <15% 750CC CRYSTALLOID S CLASS II >100 BPM NORMAL MILDLY ANXIOUS 15-20ML/HR 15%-30% 750-1500 CC CRYSTALLOID S CLASS III >120 BPM DECREASED CONFUSED 5-15 ML/HR 30%-40% 1500-2500 CC CRYSTALLOID S+BLOOD CLASS IV >140 BPM DECREASED LETHARGIC NIL 40% >2500 CC CRYSTALLOID S+BLOOD
- 25. Hypovolemic Shock-Management Maximize oxygendelivery Control further blood loss Fluid resuscitation Adequate Ventilation, Increase O2 saturation of Blood and Restoring Blood Flow -Assess Airway and Breathing -High Flow O2/ Ventilatory Support -IPPV -Two large-bore IV lines/EJV/CVC/IO -Arterial line (ABP,ABG) -Initial fluid resuscitation -Crystalloids-RL/NS (1-2 L) -Type O blood -Position Both crystalloid and type O blood (Marked Hypotension, Class IV Bleed) Trauma External bleeding should be controlled with direct pressure Internal bleeding-surgical Long-bone fractures -Traction to decrease blood loss. GI Bleed PPI Vasopressin/ Octriotide infusion Endoscopy, Sengstaken-Blakemore tube Gynecological bleeding Surgical intervention. Crystalloids Vs colloids (?? Best for resuscitation)
- 26. A 55 YO/Mwith HTN,DM presents in ED with “Crushing” substernal chest pain, diaphoresis, hypotension, tachycardia and cool, clammy extremities. What Type of Shock is This?
- 27. Cardiogenic Shock Clinical Definitionof Cardiogenic Shock is “Decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume”
- 28. Persistent (>30 minutes)Hypotension with systolic arterial pressure <90mm Hg Signs and symptoms of end organ hypoperfusion (Restlessness, Confusion, cold cyanotic extremities, oliguria<30ml/hr) Reduction in cardiac index <2.2 litres /min/m2 Presence of elevated left ventricle filling pressure(PCWP>18 mm Hg) Cardiogenic Shock criteria
- 29. Cardiogenic Shock-Causes …. Cardiomyopathic MechanicalArrythmogenic Myocardial infarction Severe valvular insufficiency Tachyarrhythmia Severe right ventricle infarction Acute valvular rupture Bradyarrhythmia Myocarditis, Myocardial contusion Acute or severe ventricular septal wall defect Acute exacerbation of severe heart failure from dilated cardiomyopathy , Ruptured ventricular wall aneurysm
- 30. Cardiogenic Shock-Investigation ECG Chest X-ray Echocardiography ABG,Lactate, Electrolytes, Cardiac enzymes, Renal parameters Right heart catheter (to measure cardiac output, central venous, pulmonary artery and wedge pressures and mixed venous blood) Urinary catheter(measure hourly urine output)
- 31. Cardiogenic Shock-Management 1.LIFE SAVINGINTERVENTIONS Emergency revascularization: either PCI (if coronary anatomy amenable) or CABG (if coronary anatomy not amenable to PCI) in MI Peri-interventional antiplatelet and antithrombotic medication CS due to mechanical complications: Urgent Interventional surgical Closure CS due to Arrythmogenic: Correct Arrhythmia 2.PHARMACOLOGIC CIRCULATORY SUPPORT Fluid administration Vasoactive agents (Vasopressors and Inotropic support)
- 32. Cardiogenic Shock-Management 3.MECHANICAL CIRCULATORYSUPPORT (MCS) Percutaneous short-term MCS devices (IABP, TandemHeart and Impella CP,ECMO) Surgical mechanical circulatory support devices and heart transplantation
- 35. DISTRIBUTIVE SHOCK Vasodialatory shock“ Causedby Loss of Vasomotor Control resulting in arteriolar/venular dilation. Characterized by severe peripheral vasodilation and low SVR Systemic vasodilation leads to decreased blood flow to the brain, heart, and kidneys causing damage to vital organs
- 36. 81 Y/F presentsin ED with Chest infection and altered mental status. She is febrile to 39.4, hypotensive with a widened pulse pressure, tachycardic and with warm extremities. What Type of Shock is This?
- 37. Septic Shock Sepsis Two ormore of SIRS criteria • Temp > 38 or < 36 C • HR > 90 • RR > 20 • WBC > 12,000 or < 4,000 • Plus the presumed existence of infection • Blood pressure can be normal! Sepsis,Severe Sepsis and Septic Shock • Sepsis: Systemic host response to infection with SIRS • Severe Sepsis: Sepsis plus end-organ dysfunction or hypo perfusion • Septic Shock: Sepsis with hypotension, despite fluid resuscitation; evidence of inadequate tissue perfusion
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- 40. Septic Shock-Treatment Antibiotics- Survivalcorrelates with how quickly the correct drug was given Cover gram positive and gram negative bacteria Add additional coverage as indicated Pseudomonas- Gentamicin or Cefepime MRSA- Vancomycin Intra-abdominal or head/neck anaerobic infections- Clindamycin or Metronidazole Asplenic- Ceftriaxone for N. meningitidis, H. infuenzae Neutropenic – Cefepime or Imipenem
- 41. A 34 YO/Fpresents to ER after dining at a restaurant,where shortly after eating the first few bites of her meal, became anxious, diaphoretic, began wheezing, noted diffuse pruritic rash, nausea, and a sensation of her “throat closing off”. She is currently hypotensive, tachycardic and ill appearing with Dyspnea. What Type of Shock is This?
- 42. Anaphylactic Shock Anaphylaxis isa Rapid, Generalized often unanticipated, immunologically mediated events that occur after exposure to certain foreign substance. Causes: Foods (Milk, soy, eggs, nuts, and shellfish) Medications (Antibiotics [penicillin], NSAIDs, Anesthetics) Venom (Hymenoptera stings) Intravenous contrast materials, and latex. Idiopathic-Up to 20%
- 43. Anaphylactic Shock-Symptoms First>>Pruritus, flushing Urticariaappear Next>>Throat fullness, Anxiety Chest tightness, SOB Lightheadedness Finally>>Altered mental status Respiratory distress a Circulatory collapse
- 44.
- 45. Anaphylactic Shock-Diagnosis Clinical diagnosis Definedby Airway compromise, Hypotension, or involvement of Cutaneous, Respiratory, or GI systems Look for exposure to drug, food, or insect bite Labs have no role
- 46. Anaphylactic Shock-Treatments Airway BreathingCirculation Disability Exposure ECG, Cardiac /Hemodynamic Monitoring, Pulse Oxymetry, IV Cannulations Establish Patent Airway High Flow O2, IV Fluids Challenge Medications Consider Early Intubation/Surgical Airway Consider Epinephrine Infusion if Shock
- 47. Anaphylactic Shock-Treatments Epinephrine 0.3 mgIM of 1:1000 (Epi-pen) Anterolateral Thigh Repeat every 5-15 min as needed Caution with patients taking beta blockers IV Fluid Challenge 1-2 L in First Hour
- 48. Anaphylactic Shock-Treatments Corticosteroids Methylprednisolone 1-2mg /KG IV /Prednisone 0.5-1 mg/KG PO Antihistamines H1 blocker- Diphenhydramine 25-50 mg IV/IM/PO H2 blocker- Ranitidine 50 mg IV/IM,150MG PO Severe Wheeze/Dyspnea Sabutamol 5 MG X 3 Doses in an hour Atrovent nebulizer Magnesium sulfate 2 g IV over 20 minutes
- 49. A 41 YO/MPresents to ER after a car accident, Complaining of decreased sensation below his waist and is now hypotensive, bradycardic, with warm extremities What Type of Shock is This?
- 50. Neurogenic Shock “Vasogenic shock” ▪Associated with cervical and high thoracic spine injury ▪ Primary spinal cord SCI occurs within minutes and Secondary SCI occurs hours to days after the initial insult ▪ A Combination of both primary and secondary injury that lead to loss of sympathetic tone and thus unopposed parasympathetic response driven by the Vagus nerve ▪ Leads to decreased tissue perfusion and initiation of the shock response. Hypotension, Brady arrhythmia, and Temperature dysregulation/flushed warm skin
- 51. Neurogenic Shock/Treatment A,B,C ---RememberC-spine precautions Fluid resuscitation ❑ The first-line treatment for hypotension is intravenous fluid resuscitation ❑ If hypotension persists despite euvolemia, vasopressors and inotropes are the Second lines. ❑ Proffered agent Norepinephrine (Hypotension and Bradycardia) ❑ Recommend MAP at 85–90 mmHg for the first 7 days(Improve spinal cord perfusion) ❑ For Bradycardia: Atropine, Pacemaker ❑ Methylprednisolone is controversial & given early and in high doses ❑ Initial c-spine immobilization is important to prevent further spinal cord injury. (Miami J/Philadelphia collar) ❑ Surgical intervention may be required for decompression of spinal injury
- 52. Obstructive Shock Obstructive shockis mostly due to extracardiac causes of cardiac pump failure and often associated with poor right ventricle output. Associated with a physical Obstruction/blockage of Great Vessels or something interfering with filling/ Emptying of heart The causes can be divided into two categories 1.Pulmonary vascular 2.Mechanical Most Common Causes Cardiac Tamponade Pulmonary Embolism Tension Pneumothorax
- 53. Obstructive Shock/Cardiac Tamponade AClinical syndrome caused by the accumulation of fluid in the pericardial space Prevents venous return to and contraction of heart Reduced Ventricular filling and Cardiac Compromise “Clinical diagnosis” , Large Heart CXR, 2D-Echo, “Beck’s Triad” Classic Symptoms “Definitive Therapy” Emergency subxiphoid percutaneous drainage Pericardiocentesis (with or without echocardiography guidance)
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- 55. Obstructive Shock/Pulmonary Embolism ThrombusVs Embolus “Sudden lodgment of a blood clot in a Pulmonary Artery With subsequent obstruction of blood supply to the Lung parenchyma” Unable to generate enough pressure to overcome the high pulmonary vascular resistance with PE Right Ventricular Failure
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- 57. PE-Signs and Symptoms ClassicSymptoms Sudden, unexplained Dyspnea(SOB) Dull Chest Pain (Pleuritic, worse with a deep breath) Cough. Classic Signs Tachycardia, Tachypnea, Decreased breath sounds over a portion of a lung Rales/Crackles Hypotension Elevated Pressure in the Neck veins, suggesting an obstruction in the pulmonary artery Swelling /tenderness over the thigh or calf
- 58. PE - Diagnosis ABG-SevereHypoxemia Unstable>>>CT Chest PE Stable>>>Well’s Criteria, D-Dimer Well’s Score ≤4>>>D-Dimer(+)>>>CT PE Well’s Score 5/6>>>CT PE/VQ Scan Well’s Score ≥ 7>>> Begin anticoagulation without delay Rx: Heparin, Consider Thrombolytics
- 59. Tension Pneumothorax Air trappedin pleural space with 1-way Valve Air/pressure builds up Mediastinum shifted Obstructs venous return to Heart No Tests!!!! Classic Symptoms Hypotension Jugular Vein Distention Diminished or Absent Breath Sounds Tracheal Deviation
- 60. Tension pneumothorax Clinical diagnosiswith no time for investigation!!!!
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- 62. Pearls Shock is aclinical manifestation of Circulatory failure Associated with High morbidity and Mortality. Four types of shock: Distributive, Cardiogenic, Hypovolemic, and Obstructive. Requires a good understanding of underlying Pathophysiology, clinical, biochemical, and hemodynamic manifestations of the different types of shock. Serum lactate level is a useful risk stratification tool in managing undifferentiated shock. Timely diagnosis and initiation of appropriate therapy are of paramount importance. (Prevent Progression to Irreversible MOF and Death) Treatment includes Hemodynamic stabilization and Correction of underlying etiology of shock.
- 63. Pearls Prognosis andPatient Education Patient Education is important about What is Shock? What are the Symptoms of Shock? Should I see a Doctor or Nurse? Will I Need Tests? How is Shock Treated?
- 64. References 1.National Center forBiotechnology Information (NCBI) www.ncbi.nlm.nih.gov/books/NBK531492/ 2.Wolters Kluwer Health- UpToDate for Clinicians and Medical Students www.uptodate.com/contents/definition-classification-etiology-and- Pathophysiology-of-shock-in-adults? 3.Jean-Louis Vincent, M.D.,Ph.D and Daniel De Backer, M.D., PhD, New England Journal of Medicine, https://www.nejm.org/doi/full/10.1056/nejmra1208943 4. European Heart Journal, Volume 36, Issue 20, 21 May 2015, Pages 1223– 1230,https://doi.org/10.1093/eurheartj/ehv051