1. hypovolemia/shock 2. pulmonary embolism 3. acute myocardial infarction Ivan Čundrle, Pavel Suk, Jan Hruda ARK, FNUSA 2016 Shock in general Shock •Circulatory failure – supply ≠ demand • •1. cardiogenic – pump •2. obstructive – obstruction •3. hypovolemic – filling •4. distributive - shunts http://www.open.edu/openlearnworks/pluginfile.php/4862/mod_oucontent/oucontent/211/none/none/non_co m_session1_fig1.2.jpg 1. 2. 4. 3. Phases of Shock 1.Compensation 2.Decompensation 3.Refractory 4. •Inflammatory cascade induction and organ damage - „secondary-hit model“ • •Organ damage further increases inflammatory cascade induction – vicious circle • •Each type of shock differs at the beginning, however during the late phase all types of shock look similar (like distributive shock) • Pathophysiology •The main problem is cell hypoxia • • •Stress response –catecholamines, RAAS, cortisol, glucagon – •Systemic inflammatory response –Imunity, inflamatory mediators –Localy OK, but generalized response is harmful • Pathophysiology •1. Macrocirculation ¡„blood flow centralization“ ¡rarely „warm shock“ • •2. Microcirculation ¡Endothelium damage ¡Increased vascular leakage, leucocytes adherence ¡Main role in shock • •3. Coagulation ¡Intravascular coagulation ¡ •4. Metabolism ¡Increased gluconeogenesis, proteolysis ¡Lactate acidosis MODS •1. Circulation ¡Vasoplegia, cardiomyopathy • •2. Lungs ¡ARDS • •3. Kidney ¡AKI • • •4. Coagulation ¡DIC • •5. CNS ¡Altered consciousness • •6. GIT ¡Loss of barrier function • Signs/Symptoms •Nonspecific •Variable •Unreliable • •Hypotension, tachycardia: ¡SBP < 90 mmHg ¡MAP < 60 mm Hg ¡Tf > 100/min ¡Cave compensatory shock/BB • •Oliguria: ¡diuresis < 0,5 ml/kg/hr for 1 – 6hrs • •Tachypnea ¡> 30 breaths/min, dyspnea • •Skin: ¡Wet, cold ¡CRT(> 2 s) • •Mental state: ¡Confusion ¡Iritation ¡coma Diagnostics •1. Basic Lab ¡BC, coagulation (Q/INR, aPTT, fib) ¡ions, gly ¡urea, kreatin ¡CRP (sepsis?) ¡ •2. ABG ¡Ventilation/oxygenation ¡Lac, SvO2, ScvO2 • ABG •Lac •Product of anaerobic glycolysis •Non-toxic, serves also as a fuel •normal < 2 mmol/l •Mortality predictor •Early sign • •ScvO2 •O2ER = (SaO2 – SvO2) / SaO2, normaly 25% •normal SvO2 is 75% •SvO2 < 70% = O2supply impairment • Extended Hemodynamics http://image.slidesharecdn.com/4331304/95/shock-9-728.jpg?cb=1274963678 Initial resuscitation •Preload optimization – increasing CO, fluids „volume challenge“, PLR •Persistent hypotension – catechols (norepinephrine) •If CO does not rise with fluids, add inotropes (dobutamin) •Lowering of inadequately high afterload (hypertension crisis) • Causal treatment •1. Cardiogenic shock: ¡SCG - PCI ¡Arrhythmia treatment (AV block III., VT) • •2. Hypovolemic shock: ¡fluids ¡hemotherapy ¡damage control surgery/damage control resuscitation • •3. Obstructive shock: ¡thrombolysis ¡Pericardial effusion evacuation • 1. Hypovolemic Shock Most common Causes of Hypovolemia •Bleeding • •Loss of fluids (sweating, vomiting, diarrhea, ....) inadequate intake • •Burns • •3rd space losses –Ileus – •anafylaxis, sepsis (relativ hypovolemia) • Treatment 1.Initial resuscitation 2.Causal treatment • •Goal is to restore organ perfusion, O2 supply •Early initiation • •Secondary goal: restoration of O2 transportation capacity (ERY...) • Venous access •2-3 thick peripheral cannulas •Central venous access is secondary (good for catecholamine, not fluids) •Exception: thick central lines (Edwars AVA 9F) • http://www.wikiskripta.eu/images/math/7/c/c/7ccb10ea5c7f59cb8828fd956797a91d.png Arterial Catheter •Continuous blood pressure monitoration •accurate •PPV •Repeated blood draws • SPV / PPV https://upload.wikimedia.org/wikipedia/commons/7/7b/Pulse_pressure_variation.jpg http://patentimages.storage.googleapis.com/WO2011094487A2/imgf000005_0001.png SPV / PPV https://upload.wikimedia.org/wikipedia/commons/thumb/0/01/Starling_RAP_combined.svg/2000px-Starling _RAP_combined.svg.png Witch fluid to use? žIons Na+ and K+ - ICT/ECT distribution • ž Oncotic pressure plasma/ECT distribution • • • •ICT 40% • ECT 20% •4% Glucose •Inadequate • •Absolute water deficit •Hypernatremia correction • • • • •ICT 40% • ECT 20% •4% • •Distribution volume Crystaloids •Fast leak into the ECT compartment •Substitution has to be 4x higher than the deficit (...recently questioned) → swellings • • • •ICT 40% • ECT 20% •4% • •Distribution volume Coloids •Do not leave the intravascular compartment •Equal the deficit •Adverse reactions, contraindication – sepsis – renal damage •Good for acute blood loss • • •ICT 40% • ECT 20% •4% • •Distribution volume Blood products •Only for blood loss corrections • •5% albumin – natural colloid –expensive • Fluid resuscitation goals •Blood pressure, heart rate •Centralization reversal •diuresis •Decrease of the PPV / SVV •Sc(v)O2 a lactate normalization • •Filling pressures(CVP, PAOP) not a good target • Acute bleeding •Blood loss •15% (750 ml) well compensated • •30% (1,5 l) – tachycardia, oliguria, normotension – however ↓ organ perfussion! • •More than 30%: hypotension, tachycardia, oligo-anuria, ... • •fractures •pelvis (5000ml) •femur (2000ml) •tibia (1000 ml) •humerus (800 ml) •radius (400ml) • Treatment •Basic approach ... ABCD •Stop the bleeding •Give i.v. Fluids + catecholamine •Blood type O- (4 immediately available), after 30 minutes type matched •Fresh frozen plasma 1:1 with erythrocytes •Target Hb 70-90 g/l, CNS trauma 100g/l •Thrombocytes 50 – 100 tis/ul •Fibrinogen 1,5 g/l •Prevent hypothermia, hypotension and acidosis • 2. Cardiogenic shock/ AIM AIM •Myocardial ischemia • •Causes 1.Increased demand – tachycardia 2.Low oxygen content – anemia, CO poisoning, hypotension, pulmonary disease 3.Low coronary artery blood flow • •90 % low coronary artery flow – coronary atherosclerosis • •Transmural ischemia – 3/4 of the myocardial wall (complete closure) •Laminar/subendomyocardial – 1/3 of the myocardial wall (partial closure + increased demand) Diagnostics 1.Patinet history/clinical evaluation 2.ECG a Lab 3.ECHO, SCG STEMI NSTEMI AP History Chest pain Chest pain Chest pain ECG ST elevation at least 2 mm in leads V1–V3 or at least 1 mm in V4–V6, I, aVL, II, III, aVF. ST elevation in at least two adjacent leads. New LBBB or (RBBB + LAH, RBBB + LPH). ST depression at least 1 mm and /or T wave inversion ST depression at least 1 mm and /or T wave inversion Lab Positive TNT Positive TNT Negative TNT Localization Anteroseptal V1-V4 Anterolateral V1-V6 Lateral I, aVL, V5, V6 Lower/diafragmatic II, III, aVF Treatment Continuous vital signs / ECG IV access Oxygen 4–8 l/min 12 lead ECG Blood draw – Lab /TNT Analgosedation - morphine ASA 500 mg i.v./200–400 mg p.o. heparin 5000 j i.v./enoxaparin 1 mg/kg s.c./i.v. clopidogrel 300 nebo 600 mg p.o. metoprolol i.v. If tachycardia Cardiogenic Shock •Severe, long-lasting arterial hypotension •Low CO •Increased filling pressure CVP/PAOP • •Alteration of consciousness, oliguria, cold periphery, sweat, cyanosis Treatment •Most important is to increase oxygen supply and lower oxygen consuption by myocardial muscle • •Preload optimalization: diuretics/fluids •Afterload optimalization: vasodilatation / cave coronary arthery perfussion •Inotropy – dobutamin • •Treatment of the cause – PCI/thrombolysis • Avoid •Tachycardia – short diastolic phase, increased work load (however, sometimes only chance how to increase CO) •Severe hypotension, hypovolemia, vasodilatation – low coronary artery perfusion pressure (Ao pressure – EDP LV) •Increased preload/afterload – increase of wall tension, work • Treatment •Oxygen – increase O2 supply •NIV, invasive ventilation – oxygenation, decreases preload/afterload •Diuretics/fluids – decrease preload, in later phase optimization of preload (fluid challenge/PLR) •Catecholamine – norepinephrine for blood pressure, dobutamin (milrinon, levosimendan) for inotropy •Vasodilatancia – nitrates, coronary artery, but also systemic vasculature ( increased blood pooling, preload lowering; arterial – afterload lowering) •Morphine – improves dyspnea • • 3. Obstructive shock/ PE Pulmonary Embolism •Sudden obstruction of pulmonary vasculature with emboli (blood cloth, fat, tumor, air/gas, foreign body, ...) • •Etiology: •85% low extremity/pelvic DVT Risc Factors •Virchov trias - venostasis, hypercoagulation, vessel wall damage • •Major surgery •Lower extremity fractures •Hypercoagulation (Leiden ...) •Heart Failure (blood stasis) •Sepsis (coagulation activation) •High age (70 years) •Immobilization •Obesity •Pregnancy •Economy class syndrome •corticoids, diuretics, HAC Diagnosis •History •Sudden dyspnea, chest pain, tachypnea, cough, syncope, hemoptysis • •Clinical evaluation •tachypnea, cyanosis, hypotension, shock, tachycardia, neck veins distension • •Lab •ABG - hypoxia, hypocapnea, Ralc •DD- negative – practically excludes PE •DD- positive – tumors, inflammation, post-surgery, sepsis ... • EKG http://www.ipej.org/0905/baranchuk1.jpg Chest X-ray http://2.bp.blogspot.com/-NathXTYJckY/TgqqizYrLYI/AAAAAAAAAD8/VLSlOko1sTA/s1600/pulmonary+infarctio n.jpg http://images.radiopaedia.org/images/157210/332aa0c67cb2e035e372c7cb3ceca2_jumbo.jpg Excludes other reasons for dyspnea Fleischman sign- atelectasis Westerman sign – decreased pulmonary vascularization ECHO http://www.teachingmedicine.com/Media/module_t/im1008_38.png http://simbionix.com/wp-content/uploads/2014/08/McConnells-Sign-in-Pulmonary-Embolism-TN.jpg RV dilatation, paradoxical septum movements, pulmonary hypertension, Tri regurgitation CT - AG http://openi.nlm.nih.gov/imgs/rescaled512/3152729_kcj-41-356-g007.png Other •Vein US – femoral, popliteal •TEE – thrombus in pulmonary artery •Swan-Ganz - precapillary PH, high CVP, high RV pressure, increase PAP, •Ventilation/perfusion scan – low specificity • Managment •Clinical probability, DD, echo and CT angio Signs of DVT 3 Clinical probability: -low 0-1 (3,4%) -moderate 2-6 (20%) -high 7 (63%) - -0-4 PE less probable -More than 4 - PE highly probable Other dg improbable 1,5 Tachycardia 100 1,5 Immobilization more than 3 days, surgery within 4 weeks 1,5 DVT, PE in history 1,5 hemoptysis 1 malignancy 1 1. High risk PE (shock, hypotension) • •CT angio or ECHO, if CT unavailable/impermissible for the patient • •CT/ECHO positive - trombolysis 2. Low risk PE (without shock/hypotension) • •High clinical suspicion – CT angio •Low clinical suspicion – DD • •Negative DD nearly completely exclude PE • •TNT, NT pro BNP, RV dysfunction – thrombolysis/heparinization Massive PE – unstable or RV dysfunction, TNT, NTproBNP • •Thrombolysis – optimally within 48 hrs alteplasis (0,9mg/kg)—10 mg bolus iv. + 90 mg cont. iv. for 2 hrs •+ heparin for min 72 hrs - UHF 80 IU/kg bolus + 18 IU/kg/hr • • Thrombolysis contraindications http://3.bp.blogspot.com/-GgIJk5RUo78/UiWcL0GNykI/AAAAAAAAAv0/Zz6BE_ADO1s/s1600/Thrombolysis+Contra indications.jpg Small PE •UF heparin – bolus 80IU/kg + 18IU/kg/hr—aPTT 1,5-2,5 times norm •At least 6-10 days, than warfarin • •LMWH- as effective as UHF, s.c. every 12 hrs •At least 6-10 days, than warfarin •Cave – renal dysfunction, antiXa (terap. 0,6-1,0 U/ml) 3 hrs after administration