Shock - Students PDF

SHOCK Asist. Univ. Dr. Tudor Borjog Sef Disciplina ATI Conf. Dr. Carmen Orban Definition Shock is a life-threatening condition of circulatory failure, causing inadequate oxygen delivery to meet cellular metabolic needs and oxygen consumption requirements, producing cellular and tissue h...

SHOCK Asist. Univ. Dr. Tudor Borjog Sef Disciplina ATI Conf. Dr. Carmen Orban Definition Shock is a life-threatening condition of circulatory failure, causing inadequate oxygen delivery to meet cellular metabolic needs and oxygen consumption requirements, producing cellular and tissue hypoxia. Shock is defined as a state of cellular and tissue hypoxia due to either reduced oxygen delivery, increased oxygen consumption, inadequate oxygen utilization, or a combination of these processes. This most commonly occurs when there is circulatory failure manifested as hypotension (ie, reduced tissue perfusion); however, it is crucial to recognize that a patient in shock can present hypertensive, normotensive, or hypotensive. Shock is initially reversible, but must be recognized and treated immediately to prevent progression to irreversible organ dysfunction. "Undifferentiated shock" refers to the situation where shock is recognized but the cause is unclear. Relevant physiology DO2 VO2 = CO x [(1.39 x Hb x SaO2) + (PaO2 x 0.003)] = CO x (CaO2 – ((SvO2 x 1,36 x Hb) + (0,0031 x PvO2)) arterial content of O2 venous content of O2 O2ER = VO2 / DO2 ( normaly arround 25% ) VO2 aprox. 250 ml/min DO2 aprox. 1000 ml/min Critical DO2 point = the point where maximum O2ER is reached. Beyond this point any increase in VO2 or decrease in DO2 leads to tissue hypoxia and anaerobic metabolism. Interpretation of O2ER High O2ER suggests Low O2ER suggests A. inadequate oxygen delivery A. increased oxygen delivery 1. oxygen (hypoxic hypoxia: low FiO2 gas or high altitude; lung hyperoxia, e.g high FiO2 gas, hyperbaric oxygen or ECMO disease) 2. anemia B. decreased oxygen consumption 3. altered cardiac contractility 1. decreased metabolic rate ( hypothyroidism, sedatives/ hypnotics, 4. Inadequate rate/ rhythm hypothermia ) 5. shock/ hypoperfusion due to other causes 2. decreased muscular activity ( sedation/analgesics, muscle paralysis, ventilatory support ) B. increased oxygen consumption (VO2) 3. antipyretics 1. fever and inflammatory states, e.g. sepsis, burns, trauma, surgery 4. Starvation/malnutrition 2. increased metabolic rate (hyperthyroidism, adrenergic drugs, hyperthermia, burns) 5. Sepsis due to shunting and histotoxic hypoxia 3. increased muscular activity (exercise, shivering, seizures, 6. Histotoxic hypoxia (cyanide poisoning) agitation/anxiety/pain, weaning from ventilation/ increased respiratory effort) Common point – Cardiac output CO = SV x HR PRELOAD AFTERLOAD CONTRACTILITY Myocardial sarcomere length just prior Is defined as the resistance to Is the change in peak isometric force to contraction. ventricular ejection - the "load" that (isovolumic pressure) at a given initial the heart must eject blood against fibre length (end diastolic volume) Determinants of preload A. Pressure filling the ventricle: 1. Intrathoracic pressure 2. Atrial pressure ( atrial contractility and rhythm, atrioventricular valve competence, ventricular end-systolic volume ) 3. Right atrial pressure 4. Mean systemic filling pressure 5. Total venous blood volume 6. Resistance to venous return 7. Venous vascular compliance B. Compliance of the ventricle: 1. Pericardial compliance: - Compliance of the pericardial walls - Compliance of the pericardial content Venous return = (Pmsf – RAP )/Rvr 2. Ventricular wall compliance - Duration of the ventricular diastole - Wall thickness - Relaxation proprieties of the muscle - End-systolic volume of the ventricle Determinants of afterload A. Wall stress defined by the law of Laplace Pxr/T P = the ventricular transmural pressure ( the difference T between the intrathoracic pressure and the ventricular cavity pressure r = the radius of the ventricle r T = the thickness of the ventricular wall P B. Input impedance – describes ventricular cavity pressure during systole and depend on: 1. Arterial compliance 2. Inertia of the blood column High transmural pressure ( negative intrathoracic 3. Ventricular outflow tract resistance pressure ) = high afterload 4. Arteriale resistance ( depends on the: length of the Low transmural pressure ( positive mechanical arterial tree, blood viscosity, vessel radius ) ventilation ) = low afterload Determinants of contractility 1. Preload - Increasing preload increases the force of contraction 2. Afterload ( Anrep effect ) - Increased afterload – increased end – systolic volume = increased sarcomere length = increased force of contraction 3. Heart rate ( Bowditch effect ) - at higher heart rates the heart does not have time to expel the intracellular calcium, so it accumulates leading to increase force of contraction. 4. Other determinants: - Cathecolamines - ATP availability - Temperature - Hormones ( glucagon, thyroid ) - Calcium Cardiac ultrasound Clinical Diagnosis of Shock Neurologic: - altered mental status ( agitation, bradypsychic, bradylalia, coma ) Pulmonary: - tachypnea Cardiac: - hypotension ( MAP < 65 mmHg or a significant drop from baseline values - bradycardia - tachycardia : > 120 bpm is associated with profound bleeding in hemorrhagic shock shock index ( HR/BPs ) > 0.8 is suggestive of hemodynamic instability Renal: - low urine output ( usually less then 0.5 ml/kg/h ) Peripheral perfusion/temperture: - temperature is decreased in shock - warm peripheral skin temperature predicts septic shock - skin mottling Capillary refill time: - prolonged Types of shock CO SVR PRELOAD PUMP problem PIPES problem TANK problem Cardiogenic Obstructiv Distributiv Hypovolemic 1. Myocardial infarction 1. Pulmonary hypertension 1. Sepsis A. Hemorrhagic: 2. Cardiomyopathy 2. Pulmonary/air embolism 2. Anaphylaxis 1. Trauma 3. Arrythmias 3. Tension pneumothorax 3. Spinal cord injury 2. Gastric ulcers 4. Myocarditis 4. Tamponade 4. Adrenal insufficiency 3. Post-partum bleedings 5. Valvular dysfunction 5. Mediastinal tumors 5. Thyrotoxicosis B. Non – hemorrhagic: 6. Post-cardiopulmonary by-pass 6. Positive pressure ventilation 6. Hepatic insufficiency 1. Gastro-intestinal losses 7. Intrinsic depression ( SIRS 7. Dissection aneurysm 7. Inflammatory ( pancreatitis ) 2. Renal losses related ) 8. High spinal anesthesia 3. Burns  Cardiogenic Obstructiv Distributiv Hypovolemic HD ↑CVP, ↑PCWP, ↓CO, ↑SVR ↑CVP, ↑PCWP, ↓CO, ↑SVR var CVP, var PCWP, var CO, ↓SVR ↓CVP, ↓PCWP, ↑CO, ↑SVR Reduced contractility ± Reduced contractility ± RV RV dilation (PE) ± septal D sign (p/v Heart dilation Hyperdynamic Hyperdynamic overload) ± Wall motion abnormalities (hypodynamic in late sepsis) Pericardial effusion, RA collapse ± Valvulopathy (tamponade) IVC Plethoric IVC, reversal of flow in Plethoric IVC, reversal of flow in HV Variable IVC Small/collapsing IVC HV Lungs B-line pattern + pleural effusions Lack of lung sliding ± lung point (PTX) A line pattern A line pattern Other Pleural effusions (LV failure) DVT or clot in transit (PE) Evidence of infxn (cholecystitis, Blood or fluid in abdomen (FAST), Ectopic endocarditis, etc), cirrhosis, pregnancy, Aortic dissection, Skin Usually cool, Delayed cap refill Usually cool, Delayed cap refill Warm, flushed, Brisk cap refill Usually cool, Delayed cap refill Neck Increased JVP Increased JVP Variable Flat neck veins Weak pulses (narrow pulse pressure) Weak pulses (narrow pulse pressure) Other Weak pulses (narrow pulse pressure) Lung and heart sounds are unreliable Bounding pulses (wide pulse pressure) Evidence of blood (pallor) or volume loss indicators of tamponade or PTX. (axillary dryness) Cardiogenic Shock - Definition Cardiogenic Shock represents the final common pathway in which cardiovascular disease causes: 1. Circulatory failure 2. Hypoperfusion 3. End organ dysfunction Cardiogenic Shock – SCAI Shock Classification Cardiogenic Shock – Phenotypes & Severity Consider: - Different patterns of ventricular function - Filling pressures - Peripheral vascular tone - Cardiac output - Congestion End stage of cardiogenic shock: - Severe lactic acidosis ”hemometabolic” or - RV congestion “cardiometabolic” - Greater shock severity cardiogenic shock - Multiple organ failure Cardiogenic Shock – What are we monitoring? FOR ALL TYPES OF SHOCK BASICS: Clinical examination ECG Pulse oximetry Blood pressure Urine output Labs: ureea, creatinine, liver function tests (AST, ALT ) Acis -base status: lactat Cardiogenic Shock – What are we monitoring? FOR ALL TYPES OF SHOCK CARDIAC ULTRASOUND Cardiogenic Shock – What are we monitoring? FOR ALL TYPES OF SHOCK LUNG ULTRASOUND Cardiogenic Shock – What are we monitoring? FOR ALL TYPES OF SHOCK VExUS Cardiogenic Shock – What are we monitoring? FOR ALL TYPES OF SHOCK Arterial line Central venous line https://www.youtube.com/watch?v=QXsqFr-eGiM Cardiogenic Shock – What are we monitoring? FOR ALL TYPES OF SHOCK Cardiogenic Shock – Contemporary Standard Care Always treat the underlying etiology Volume alteration Acute volume overload (e.g., diuretic nonadherence, dietary indiscretion). Acute hypovolemia (e.g., over-diuresis, reduced oral intake, gastroenteritis). Acute reduction in LV ejection fraction Acute MI (the cause of ~75% of cardiogenic shock) Takotsubo cardiomyopathy Tachymyopathy. Peripartum cardiomyopathy. Myocarditis (e.g., viral, SLE, giant-cell, eosinophilic). Arrhythmia Bradyarrhythmia. Tachyarrhythmia (most often new-onset atrial fibrillation). Valvular dysfunction LV outflow tract obstruction (LVOTO). Prosthetic valve dysfunction (e.g., thrombosis). Native valve dysfunction (e.g., endocarditis, ruptured papillary muscle ). Other Thyroid disease. Medications: Toxicity (e.g. excess beta-blocker, digoxin toxicity). Medication nonadherence. Uncontrolled hypertension. Hypophosphatemia. Cardiogenic Shock – Contemporary Standard Care Respiratory stabilization Oxygen supplementation is recommended to keep arterial oxygen saturation above 90% 1. High flow oxygen therapy 2. Non-invasive mechanical ventilation with continuous positive airway pressure 3. Invasive mechanical ventilation - Reduces work of breathing - Improves LV loading conditions - Improves lung edema - Can worsen RV function Cardiogenic Shock – Contemporary Standard Care Hemodynamic stabilization – optimize MAP Hypertensive patient: Nitroglycerine is the first line agent The goal is to lower the afterload so that cardiac function improves and lung edema diminishes Hypotensive patient: 1. Norepinephrine is the first line agent 2. Epinephrine is an alternative for patients low LVEF 3. Vasopressin is usually reserved for RV predominant cardiogenic shock or mixed vasodilatatory – cardiogenic shock Once the arterial pressure has been restored or there is contractile dysfunction or pulmonary edema is refractory to mechanical ventilation or there are signs of hypoperfusion an inotropic agent is added: 1. Dobutamine 2. Milrinone 3. Levosimendan Cardiogenic Shock – Contemporary Standard Care Volume optimization Administer fluids only if: 1. The patient presents clear signs of volume responsiveness 2. There are no sign of pulmonary or systemic congestion 3. There are signs of inadequate organ perfusion If the patients present signs of pulmonary or systemic congestion volume removal is necessary. Cardiogenic Shock – Contemporary Standard Care Mechanical circulatory support Left ventricular assist device Cardiogenic Shock – Contemporary Standard Care Obstructive Shock – Cardiac tamponade. Pathophysiology The primary abnormality is compression of cardiac chambers due to increased pericardial pressure exceeding cardiac filling (diastolic) pressures Total venous return falls Cardiac chambers shrink Stroke volume declines Blood pressure drops Obstructive Shock – Cardiac tamponade. Causes Obstructive Shock – Cardiac tamponade. Diagnosis Diagnosis: Physical findings - Tachycardia and hypotension - Elevated jugular venous pressure ( Kussmaul sign ) - Pulsus paradoxus Echocardiography: 1. Pericardial effusion 2. Chamber collapse - Diastolic collapse of the right atrium - Diastolic collapse of the right ventricle - Left sided chamber collapse Obstructive Shock – Cardiac tamponade. Management Patients with cardiac tamponade require urgent pericardial fluid drainage to alleviate symptoms and prevent hemodynamic collapse. Pericardial fluid is most commonly drained via percutaneous pericardiocentesis. If percutaneous drainage is not appropriate or feasible, the pericardial fluid is drained via a surgical approach. Obstructive Shock – Cardiac tamponade. Approach algorithm Obstructive Shock – Pulmonary embolism. Pathophysiology Obstructive Shock – Pulmonary embolism. Echocardiography Obstructive Shock – Pulmonary embolism. CT scan Obstructive Shock – Pulmonary embolism. Pulmonary Index Severity index Obstructive Shock – Pulmonary embolism. Management Obstructive Shock – Pulmonary embolism. Management Obstructive Shock – Tension pneumothorax Obstructive Shock – Tension pneumothorax supine chest radiograph demonstrates an atypical right basal pneumothorax in a patient on mechanical ventilation Distributive Shock – Septic Shock. Definition Sepsis is defined as a life-threatening organ dysfunction caused by a dysregulated host response to infection. Septic shock should be considered a subset of sepsis in which underlying circulatory, cellular, and metabolic abnormalities contribute to a greater risk of mortality than that posed by sepsis alone. Distributive Shock – Septic Shock. Definition Sepsis is defined as a suspected or documented infection coupled with a SOFA score of more then 2 points. Septic Shock is defined as the presence of sepsis coupled with by vasopressor requirement to maintain mean arterial pressure of 65 mmHg or above AND a blood lactate of more than 2 mmol/l, in the absence of hypovolemia. Distributive Shock – Septic Shock. Definition qSofa score Glasgow coma scale < 15 Respiratory > 22 frequency Systolic blood < 100 pressure Distributive Shock – Septic Shock. Distributive Shock – Septic Shock. Volume Resuscitation Consider a personalized approach Distributive Shock – Septic Shock. Volume Resuscitation Distributive Shock – Septic Shock. Vasopressors Distributive Shock – Septic Shock. Antimicrobial therapy Distributive Shock – Septic Shock. Rational approach and management Distributive Shock – Septic Shock. One more remark Distributive Shock – Anaphylactic Shock - World Allergy Organization criteria Criterion 1 — Acute onset of an illness (minutes to several hours) with simultaneous involvement of the skin, mucosal tissue, or both (eg, generalized hives, pruritus or flushing, swollen lips-tongue-uvula) and at least one of the following: - respiratory compromise (eg, dyspnea, wheeze-bronchospasm, stridor, reduced peak expiratory flow, hypoxemia). - circulatory compromise: Reduced BP or associated symptoms of end-organ dysfunction (eg, hypotonia, collapse, syncope, incontinence). - Severe gastrointestinal symptoms (eg, severe crampy abdominal pain, repetitive vomiting), especially after exposure to non-food allergens. Criterion 2 — Acute onset of hypotension or bronchospasm or laryngeal involvement (eg, stridor, vocal changes, odynophagia) after exposure to a known or highly probable allergen for that patient (minutes to several hours), even in the absence of typical skin involvement. Distributive Shock – Anaphylactic Shock Anaphylactic Shock is characterized by a profound reduction in venous tone, and has features of hypovolemic shock also, with fluid extravasation causing reduced venous return, as well as depressed myocardial function. Distributive Shock – Anaphylactic Shock - pathophysiology Cardiac effects - myocardial ischemia, probably due to coronary vasospasm, and if it severe enough can cause myocardial infarctionas well as - conduction defects, including atrial and ventricular arrhythmias - stress cardiomyopathy (Takotsubo syndrome), which predominantly affects post-menopausal women, may also occur in anaphylaxis Distributive Shock – Anaphylactic Shock - pathophysiology Upper airway symptoms : Respiratory effects - sneezing, rhinorrhea, dysphonia, laryngeal edema, - laryngeal obstruction - oropharyngeal angioedema. Lower airway manifestations of anaphylaxis include - cough, wheeze, - -pulmonary hyperinflation, edema, - hemorrhage, - respiratory failure, or respiratory arrest Distributive Shock – Anaphylactic Shock - pathophysiology Responses to fluid shifts - Massive fluid shifts occur during anaphylaxis due to increased vascular permeability ( 35 percent of intravascular volume can shift to the extravascular space within 10 minutes during anaphylaxis ) - Compensatory responses include release of endogenous catecholamines, angiotensin II, and endothelins. - Some patients, however, experience abnormal elevations of peripheral vascular resistance (maximal vasoconstriction), yet shock persists due to reduced intravascular volume - Others have decreased systemic vascular resistance despite elevated levels of catecholamines. Distributive Shock – Anaphylactic Shock - Management 1. Epinephrine - im 0.3 – 0.5 mg every 5 – 15 minutes ( or more often ) - start iv infusion at 0.1 micrograms/kg/min 2. Normal saline bolus – rapid infusion of 1 – 2 liters - repeat as needed 3. Oxigenation and/or imediat intubation 4. Salbutamol - 2.5 – 5 mg in 3 ml saline via nebulizer or - 2 – 3 puffs by metered dose inhaler Hypovolemic Shock – Hemorrhagic Shock “ A person dies from injury nearly every 3 minutes, and 40% of these deaths are due to major hemorrhage or its consequences.” Death from hemorrhage is early, with 60% of deaths occurring within the first 3 hours. Hypovolemic Shock – Hemorrhagic Shock. Classification Class I Class II Class III Class IV blood < 15% 15 – 30% 30 – 40% > 40% volume loss blood normal minimal hypotension hypotension pressure changes heart rate normal tachycardia tachycardia tachycardia respiratory normal tachypnea tachypnea tachypnea rate pulse normal decreased decreased decreased pressure capillary normal prolonged prolonged pronged refill time urine output normal normal diminished anuric Hypovolemic Shock – Hemorrhagic Shock. Causes The four main causes of major hemorrhage : 1. Trauma 2. Surgery 3. Obstetric a. antepartum: placental abruption, placenta previa, uterine rupture b. postpartum – 4Ts: tone ( uterine atony ), trauma, tissue ( retained placenta ), thrombin ( coagulopathy ) 4. Medical a. gastrointestinal: - Non – variceal ( peptic ulcer disease, gastritis, esophagitis ) - Esophageal varices b. medical ( anticoagulants ) Hypovolemic Shock – Hemorrhagic Shock. Management Principles 1. Control source of bleeding 2. Minimize the use of intravenous ( fluids in the resuscitation of trauma patients. 3. Transfuse blood products as soon as the need is recognized. 4. Rapidly mobilize all needed resources (eg, surgery, anaesthesia, blood bank, transfer to trauma center). 5. Use thromboelastography, or comparable rapid point-of-care assessment of coagulation, to guide trauma resuscitation whenever possible. Hypovolemic Shock – Hemorrhagic Shock. Management And 2 short, large - bore ( minimum 16G ) intravenous lines. Hypovolemic Shock – Hemorrhagic Shock. Management – iv fluids Why minimize the use of intravenous fluids ? Increases the risk of coagulopathy by: 1. Diluting the clothing factors 2. Diluting the platelets 3. Hypothermia Hypovolemic Shock – Hemorrhagic Shock. Management - blood products Blood products should be given as soon as the need for transfusion is recognized. To limit the adverse systemic effects of injury (eg, coagulopathy) and minimize the risks associated with large-scale transfusion, blood products : red blood cells : plasma : platelets – are best given in a ratio of 1:1:1. 1. Red blood cells - target hemoglobin concentration > 7 – 9 g/dl - group O can be given until group and crossmatch are available - group O Rhesus negative is reserved for pregnant patients - should be transfused through a warming device and rapid infuser Hypovolemic Shock – Hemorrhagic Shock. Management – blood products 2. Fresh frozen plasma - provides a balanced source of pro – and anticoagulant factors - contains acute phase reactants, immunoglobulin and albumin - it can be used as a volume expander - dose: 15 – 20 ml/kg 3. Platelets - maintain a platelet count above 50x109/l in most situation, and above 100x109/l in traumatic brain injury. Hypovolemic Shock – Hemorrhagic Shock. Management – What else can we give? 4. Fibrinogen supplementation - target: a fibrinogen concentration above 150 mg/dl in most situation, and above 200 mg/dl in obstetric hemorrhage - initial dose is 3 – 4 g of fibrinogen concentrate or 15 – 20 units of cryoprecipitate 5. Prothrombin complex concentrate - a plasma derived concentrate containing the vitamin K – dependent coagulation factors ( II, VII, IX, X ) - usually used for reversal of anti-vitamin K anticoagulants Hypovolemic Shock – Hemorrhagic Shock. Management – What else can we give? 6. Tranexamic acid - antifibrinolytic agent - initial dose is 1 g iv immediately, followed by 1 g infused in 8 h ( over a period of 24 h ) 7. Calcium - Ca2+ is a cofactor in the activation of factors II, VII, IX and X along with protein C and S - Ca2+ contributes to the platelet adhesion at the site of vessel injury - hypocalcemia results from the citrate chelation of serum Ca2+ - monitoring of ionized form of calcium is important – target is above 0.9 mmol/l - 3 – 6 g of Calcium gluconate to every 6 UI or red blood cells Hypovolemic Shock – Hemorrhagic Shock. Management – trombelastography Hypovolemic Shock – Hemorrhagic Shock. Management – Avoid !!! Coagulopathy Hypothermia - Reduces enzymatic activity of coagulation Acidosis factors - Impaires platelet function Thank you !