Shock - Emergency Approach -

1. Shock- Emergency Approach - First Part Assoc. Prof. Dr. Diana Cimpoesu

2. Shock - definition, epidemiology • Cardiovascular insufficiencythat creates an imbalance between tissue oxygen supply and oxygen demand • USA- over 1 milion casespresent to the ED/year • Precocious intervention at the non-traumatic patient – “the golden hour”

3. Shock –classification: 4 categories by etiology • Hypovolemic- due to inadequate circulating volume • Cardiogenic- due to inadequate cardiac pump function • Distributive- maldistribution of blood flow-septic, anaphylactic, neurogenic • Obstructive- extra-cardiac obstruction to blood flow :pulmonary embolism, cardiac tamponade, tension pneumothorax

5. Shock- physiopathology • SaO2=100%- normal 25% ofthe transported O2 linkedto Hb is consumedby the tissues – the venous blood will have a saturation of 75% • O2 supply is insufficient to meet demands- the first compensatory mechanism is the increase of CO (cardiac output) • If the increase of CO is insufficient – the amount of O2 extracted from Hb by tissues increses and SmVO2 decreases (O2saturationof the venous blood)

6. Shock-physiopathology • Demand>offer – anaerobic metabolism occurs- lactic acid • Lactic Acidosis : due to -the inadequate O2 delivery ( like in the cardiogenic shock) -Very high demand (consumptionof O2 increased) -Inadequate use of oxygen at the level of tissues (septic shock or post-resuscitation syndrome) • Lactic acid - marker of the disturbance demand/offer - usedin thepatient receiving department, diagnosis, treatment, prognosis • MBP=CO x peripheral vascular resistance, • COdecreases- the peripheral vascular resistanceincreases MBPis not an exact marker of the tissue hypo-perfusion

7. Shock- physiopathology Compensatory mechanisms: stimulationof carotid baro-receivers – sympathetic NS: • Arteriolar vessel constriction – circulation redistribution • HR increaseandmiocardial contractilities – increased DC • Constriction on the vessels of potentia • Release of vaso-active hormones (A,NA,D,C)-vasoconstriction • ADH release, activation of the renin-angiotension-retension system of Na and water-maintenance of the intravascular volume.

8. Hemorrhagic shock physiopathology • Compensatory mechanisms: sympathetic hyperactivity to maintain the effective circular volume • Vasoconstriction, circulation centralization, diuresis decrease • Straling forces modification by precapillar sphincter contraction: interstitial hydrostatic pressure increases, cell dehydration – “transcapillar refilling” • O2 tissular extraction increases (right deviation of HbO dissociation curve)

10. Hemorrhagic shock: decompensation mechanisms • Loss of precapillar sphincter vasoconstriction– vasodilatation, hypotension, myocardium and NCS ischemia, transudation of interstitial liquid • Increase of capillary permeability • Capillary blockage by leukokeratoses micro aggregates • Erythrocytic deformability decrease • Endothelian edema

11. Shock- physiopathology- cellular effects of O2 decrease • ATP depletion- membranous pump malfunction- Na inflow andK release • Cellular edema, cells no longer respond to stress hormones (insulin, cortisol, glucagon, catecholamines) • Intracellular destructions- cellular death • Hyper K, hypo Na, metabolic acidosis, hyperglicemia, lactic acidosis

12. Shock- symptoms • Symptoms suggesting the volume loss: bleeding, vomiting, diarrhea, polyuria, fever • Symptoms suggesting: acute coronary sdr., congestive acute heart failure, beta-blockers • Anaphylactic context • Neurologicaldisorders: vertigo, lipothymia, alteration of the mental status-coma • Trauma

14. Shock- physical examination • CV: distension of the throat veins, tachycardia, arrhythmia, decrease of the coronary perfusion pressure, decrease of the ventricle compliance, increase of the diastolic pressure in LV, pulmonary edema • Respiratory: tachypnea, increaseof RR, increase of the dead area, bronchospasm, hypocapnia, respiratory failure, acute respiratory distress sdr.

15. Shock- physical examination • Visceras: ileus, gastrointestinal bleeding, pancreatitis, alithiasiccholecystitis, mesenteric ischemia • Renal: decrease of the glomerulary filtering rate, redistribution of the renal flux, oliguria • Metabolism: respiratory alkalosis, then metabolic acidosis, hypo/hyperglycemia, hyperK.

17. Shock –clinical framework • Temperature • Hyperthermiaor hypothermia (endogenous=hypo metabolic shockor exogenous). • Cardiac frequency HR • Usuallyincreased; there can also be paroxistic bradycardiain hypovolemic shock, hypoglycemia, beta-blockers, pre-existent cardiac affections. • SBP • In the precocious phase it can be increased because it is a compensatory mechanism and increases DC and then, it decreases. • DBP • Increases at the debut by arterial vesselconstrictionand then it decreases.

18. Shock –clinical outview • Pulse pressure • SBP-DBP, depends on the aorta rigidity and on the diastolic volume: it increases precociously in shock and then decreases before SBP. • Paradoxical pulse • The modification of SBP with breath. The increase and decrease of intratoracic pressure affects the cardiac output. • It is met in asthma, cardiac tamponade and decompensate cardiac insufficiency. • MBP = DBP + (MBP – DBP)/3 • Depends on CO şi RP, assures adequate tissular perfusion, decreases in shock.

19. Shock – Clinical Framework • Shock index = HR/SBP = 0,5-0,7 (n) • Depends on the effort of the LV in acute circulatory insufficiency • CNS: agitation, delirium, confusion, torpor, coma – decrease of pressure of cerebral perfusion • Skin: cold, wet, sweated, cyanosis • CV, respiratory, visceral organs, renal, metabolism – see above

20. Shock – paraclinic exams • Base evaluation: HLG, electrolytes, glycemia, urea, creatinine, TQ, IQ, aPTT, urine summary, ecg, thoracic Rx. • Secondary evaluation: arterial blood gases, lactic acid, PDF, hepatic function • Non invasive monitoring: CO2-end tidal, DC calculated, echocardiogram • Invasive monitoring: capillary filling pressure, PVC, DC, SmVO2, vascular resistance, DO2, VO2 • For etiology and complications: cultures, cranial CT, pelvis, abdominal, lumbar puncter, cortizol level, pelvian and abdominal echography

21. Shock - treatment • A – IOT, mechanic ventilation, tracheal aspiration • B – decrease of respiratory labor, sedation, mechanic ventilation, decrease of oxygen demand, SaO2 > 93 %, PaCO2 < 35-40 mmHg, pH > 7,3 • C – fluid reanimation (crystalline capsule, colloid), peripheral and central venal access, vasopressin for MBP > 60 mmHg and SBP > 90 mmHg • Decrease O2 demand – resolving of hyperandrenergic status (analgesic, relaxation, warmth, tranquilizers), Hb > 10 g%

22. Shock-vasoactive agents • Dopamina:0-25mcg/kg/min, alfa,beta,D • Noradrenaline:0,01-0,5mcg/kgc/min, alfa1,beta1 • Phenyleffrine:0,15-0,75mcg/kgc/min (alfa) • Adrenaline:0,01-0,75 mcg/kcg/min • Dobutamine:2-20mcg/kgc/min,beta1,2, alfa 1 • Isoproterenol:0,01-0,02 mcg/kgc/min, beta 1,2

23. Shock– therapy evaluation parameters • Traditional: BP normalization, HR, urinary output, circulator volume (intra/extra cellular) • CVP 10-12 mmHg, PAOP 12-18 mmHg • MBP 90-100 mmHg, RVP 800-1400 dynexs/cmp • Contractility: DC 5 l/min, IC 2,5-4,5 l/min/mp • HR 60-100/min • Tissular oxygenation: SmVO2 > 70 %, acid lactic < 2 mmoli/l

24. Hypovolemic shock: causes • Hemorrhagic shock • Absolute hypovolemia: diarrhea, vomiting, fever, polyuria, diuretics, burns etc. • Relative hypovolemia: losses in III space – intestinal occlusion, pancreatitis, entero mesenteric attack, edema • Traumatic shock (hemorrhagic shock, spinal shock, obstructive shock)

25. Hemorrhagic shock: causes • Trauma: lesions of parenchymal organs, lungs, myocardium, big vessels, retroperitoneal hemorrhage, big bones and pelvis fractures, scalp hemorrhages, epitasis • Gastrointestinal: esophageal varices, hemorrhagic ulcer, gastritis, esophagitis, Mallory-Weiss syndrome, tumors, mesenteric ischemia • Genitourinary: vaginal bleeding, neoplasm, abortion, metrorrhagia, placental presentation, placental retention, uterine rupture, ectopic pregnancy • Vascular: aneurisms, aorta dissection, ateriovenous malformation

26. Hemorrhagic shock: clinic and paraclinic

27. Hemorrhagic shock: Therapeutic objectives • Adequate lung oxygenation • Hemorrhage control • Loss replacements • Monitoring therapy effects • Myocardic contractibility support • Acido-basic and electrolytic reequilibration • Sustaining renal function

28. Hemorrhagic shock: treatment • ABC • External hemorrhages control: raising the extremities, compressive bandage, surgery • Loss replacement: peripheral and central venous acces, intravascular volume replacement, oxygen transport replacement, coagulation anomalies correction

29. Crystalline solutions • Isotones: NS, Ringer, Ringer lactate - replace the interstitial deficit also rapid intra and extra vascular equilibration; it is administrated 3:1 compared to lost volume of blood • Hypertonic fluids: NaCl hypertonic solution- perfusion reduced volume for a satisfactory volemic recovery, positive intropic effect, peripheral vasodilatator; hypernatremia danger, extreme cerebral dehydration (Na >170 mEq/l) • Economic reason - accessibility

30. Colloidal solutions • Important intravascular remanence time, small volumes use for adequate volemic resuscitation, maintenance of intravascular colloidal osmotic, useful in cardiac and renal insufficiency • Albumen, dextran 40-70, HAES, Haemacel, plasma • High price, anaphylactic reactions, antiplachetary effect and of faking direct compatibility result, histocitary system blockage, infection transmission

31. Blood transfusion and derivates • O2 transport capacity increase • Homologous isogroup blood, izoRh, integral, eritrocitary mass, washed erytocytes • Artificial blood: perflorocarbonic emulsions, Hbpyridoxilated polymer • Coagulation dysfunction corrections, CID treatment: frozen fresh plasma, heparin therapy • Contribution of citric acid (from preserved blood) and of K, could induce hypocalcaemia ( necessitate 1 g Cagluconateiv for each 5U of transfused blood or plasma) • Auto transfusion

32. Hemorrhagic shock: treatment

33. Therapy efficiency • Blood pressure MBP 90-100 mmHg • HR, RR • Urinary output • CVP 10-12 mmHg • Consciousness state • Skin coloring, capillary refil time<2 sec • Paraclinic parameters : CO2, pH gastric mucous membrane, IC, SmVO2, lactic acid < 2 mm/l

34. Anaphylactic shock • Anaphylaxis – a systemic, severe reaction of hypersensitivity accompanied by low blood pressure and by compromising the airways with vital risk, determined by anaphylaxis mediators release (IgE from mast cells) • Anaphylactic syndrome- the same reaction without IgE • Incidence: in the USA varies between 5/1000 and 2/10000

35. Anaphylactic shock-physiopathology • Hypersensitivity reaction type I-IgE • Mast cells digranulation • Mediators issue • Complement activation • Metabolism modulation arachidonic acid • But also hypersensitivity reaction of type II and III

36. mast cells and basophile degranulation Ag Release of mediators from mast cells and basophiles in an IgE dependent fashion: bradikinine, histamin, serotonin. Complement Activation Modularea metab. ac.arahi- donic,Leucotriene,PG,Tx: IgE mast cells and basophile

37. Anaphylactic shock: causes • Medicines • Penicillin and other • aspirin • trimetroprim • AINS • Foods and additives • Sea fruits, fish • Soy, nuts • Flour, milk, eggs • Monosodium glutamate, tartrasine • Nitrates and nitrites • Others • Hymenoptera stings • Insects • Contrast substances from radiology

38. Anaphylactic shock-clinic • Urticaria • Angioedema • Non systematic abdominal pains • Nausea, vomiting, diarrhea • Bronchospasm • Rhinorrhea • Conjunctivitis • Lipothymia or palpitations • Anaphylaxis= any combinations of these signs and low blood pressure or compromising of air way

39. Clinic signs evolution • Pruritus • Erythema • Urticaria • Dyspnea, anxiety, lipothymia, syncope • Apparition within 60 minutes from the exposure- gravity sign – death risk • Symptoms recurrence - biphasic phenomenon - 20% of patients

40. Positive and differential diagnosis Positive = historic and physical exam Differential: • Vague vessel reactions • Myocardium ischemia • Status astmaticus • Convulsions • Epiglottises • Congenital angioedema • Obstruction of air ways by foreign bodies • Laboratory: histamine, high tryptase

41. Treatament • A- angioedema, air ways release • B- IOT or oxygen therapy • C- i.v. access, monitorising, pulse oxymetry • Adrenaline- treats the bronchospasm, laryngeal edema, laringospasm, respiratory stop, shock: i.v. bolus 100 mcg (1:100000) • Perfusion 1-4 mcg/min • I.m- 0,5 mg • S.c- 0,3-0,5 ml of 1:1000

42. Treatament • Fluids i.v. 1-2 l or 20 ml/kg • Corticosteroids: methylprednisolon 125 mg i.v. • Blockings H1- diphenhydramine 25-50 mg i.v., i.m., p.o. • Blockings H2- ranitidine 50 mg i.v. • Nebulised albuterol 2,5 mg or 5 mg/kg i.v. • Glucagon 1 mg i.v. la 5 min. then 5-15 mcg/min • Aminophyline 5-6 mg/kg i.v.