Diapozitivul 1

Shock- Emergency Approach -First PartAssoc. Prof. Dr. Diana CimpoesuShock - definition, epidemiologyCardiovascular insufficiency that creates an imbalance between tissue oxygen supply and oxygen demandUSA- over 1 milion cases present to the ED/yearPrecocious intervention at the non-traumatic patient the golden hour Shock classification: 4 categories by etiologyHypovolemic- due to inadequate circulating volume Cardiogenic- due to inadequate cardiac pump functionDistributive- maldistribution of blood flow-septic, anaphylactic, neurogenic Obstructive- extra-cardiac obstruction to blood flow :pulmonary embolism, cardiac tamponade, tension pneumothorax

Shock- physiopathologySaO2=100%- normal 25% of the transported O2 linked to Hb is consumed by 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 (O2 saturation of the venous blood)

Shock-physiopathologyDemand>offer anaerobic metabolism occurs- lactic acid Lactic Acidosis : due to-the inadequate O2 delivery ( like in the cardiogenic shock)-Very high demand (consumption of 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 - used in the patient receiving department, diagnosis, treatment, prognosisMBP=CO x peripheral vascular resistance, CO decreases- the peripheral vascular resistance increasesMBP is not an exact marker of the tissue hypo-perfusionShock- physiopathologyCompensatory mechanisms: stimulation of carotid baro-receivers sympathetic NS:Arteriolar vessel constriction circulation redistribution HR increase and miocardial contractilities increased DCConstriction on the vessels of potentiaRelease of vaso-active hormones (A,NA,D,C)-vasoconstrictionADH release, activation of the renin-angiotension-retension system of Na and water-maintenance of the intravascular volume.Hemorrhagic shock physiopathologyCompensatory mechanisms: sympathetic hyperactivity to maintain the effective circular volumeVasoconstriction, circulation centralization, diuresis decreaseStraling forces modification by precapillar sphincter contraction: interstitial hydrostatic pressure increases, cell dehydration transcapillar refilling O2 tissular extraction increases (right deviation of HbO dissociation curve)

Hemorrhagic shock: decompensation mechanismsLoss of precapillar sphincter vasoconstriction vasodilatation, hypotension, myocardium and NCS ischemia, transudation of interstitial liquidIncrease of capillary permeabilityCapillary blockage by leukokeratoses micro aggregatesErythrocytic deformability decreaseEndothelian edemaShock- physiopathology- cellular effects of O2 decreaseATP depletion- membranous pump malfunction- Na inflow and K releaseCellular edema, cells no longer respond to stress hormones (insulin, cortisol, glucagon, catecholamines)Intracellular destructions- cellular deathHyper K, hypo Na, metabolic acidosis, hyperglicemia, lactic acidosisShock- symptomsSymptoms suggesting the volume loss: bleeding, vomiting, diarrhea, polyuria, feverSymptoms suggesting: acute coronary sdr., congestive acute heart failure, beta-blockersAnaphylactic contextNeurological disorders: vertigo, lipothymia, alteration of the mental status-comaTrauma

Shock- physical examinationCV: 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 edemaRespiratory: tachypnea, increase of RR, increase of the dead area, bronchospasm, hypocapnia, respiratory failure, acute respiratory distress sdr. Shock- physical examinationVisceras: ileus, gastrointestinal bleeding, pancreatitis, alithiasic cholecystitis, mesenteric ischemia

Renal: decrease of the glomerulary filtering rate, redistribution of the renal flux, oliguria

Metabolism: respiratory alkalosis, then metabolic acidosis, hypo/hyperglycemia, hyperK.

Shock clinical frameworkTemperatureHyperthermia or hypothermia (endogenous=hypo metabolic shock or exogenous).Cardiac frequency HRUsually increased; there can also be paroxistic bradycardia in hypovolemic shock, hypoglycemia, beta-blockers, pre-existent cardiac affections. SBPIn the precocious phase it can be increased because it is a compensatory mechanism and increases DC and then, it decreases. DBPIncreases at the debut by arterial vessel constriction and then it decreases.

Shock clinical outviewPulse pressureSBP-DBP, depends on the aorta rigidity and on the diastolic volume: it increases precociously in shock and then decreases before SBP.Paradoxical pulseThe 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)/3Depends on CO i RP, assures adequate tissular perfusion, decreases in shock.Shock Clinical FrameworkShock index = HR/SBP = 0,5-0,7 (n)Depends on the effort of the LV in acute circulatory insufficiencyCNS: agitation, delirium, confusion, torpor, coma decrease of pressure of cerebral perfusionSkin: cold, wet, sweated, cyanosisCV, respiratory, visceral organs, renal, metabolism see above

Shock paraclinic examsBase evaluation: HLG, electrolytes, glycemia, urea, creatinine, TQ, IQ, aPTT, urine summary, ecg, thoracic Rx. Secondary evaluation: arterial blood gases, lactic acid, PDF, hepatic functionNon invasive monitoring: CO2-end tidal, DC calculated, echocardiogramInvasive monitoring: capillary filling pressure, PVC, DC, SmVO2, vascular resistance, DO2, VO2For etiology and complications: cultures, cranial CT, pelvis, abdominal, lumbar puncter, cortizol level, pelvian and abdominal echographyShock - treatmentA IOT, mechanic ventilation, tracheal aspirationB decrease of respiratory labor, sedation, mechanic ventilation, decrease of oxygen demand, SaO2 > 93 %, PaCO2 < 35-40 mmHg, pH > 7,3C fluid reanimation (crystalline capsule, colloid), peripheral and central venal access, vasopressin for MBP > 60 mmHg and SBP > 90 mmHgDecrease O2 demand resolving of hyperandrenergic status (analgesic, relaxation, warmth, tranquilizers), Hb > 10 g%

Shock-vasoactive agentsDopamina:0-25mcg/kg/min, alfa,beta,DNoradrenaline:0,01-0,5mcg/kgc/min, alfa1,beta1Phenyleffrine:0,15-0,75mcg/kgc/min (alfa)Adrenaline:0,01-0,75 mcg/kcg/minDobutamine:2-20mcg/kgc/min,beta1,2, alfa 1 Isoproterenol:0,01-0,02 mcg/kgc/min, beta 1,2Shock therapy evaluation parametersTraditional: BP normalization, HR, urinary output, circulator volume (intra/extra cellular)CVP 10-12 mmHg, PAOP 12-18 mmHgMBP 90-100 mmHg, RVP 800-1400 dynexs/cmpContractility: DC 5 l/min, IC 2,5-4,5 l/min/mp HR 60-100/minTissular oxygenation: SmVO2 > 70 %, acid lactic < 2 mmoli/lHypovolemic shock: causesHemorrhagic shockAbsolute hypovolemia: diarrhea, vomiting, fever, polyuria, diuretics, burns etc.Relative hypovolemia: losses in III space intestinal occlusion, pancreatitis, entero mesenteric attack, edemaTraumatic shock (hemorrhagic shock, spinal shock, obstructive shock)Hemorrhagic shock: causesTrauma: lesions of parenchymal organs, lungs, myocardium, big vessels, retroperitoneal hemorrhage, big bones and pelvis fractures, scalp hemorrhages, epitasisGastrointestinal: esophageal varices, hemorrhagic ulcer, gastritis, esophagitis, Mallory-Weiss syndrome, tumors, mesenteric ischemiaGenitourinary: vaginal bleeding, neoplasm, abortion, metrorrhagia, placental presentation, placental retention, uterine rupture, ectopic pregnancyVascular: aneurisms, aorta dissection, ateriovenous malformationHemorrhagic shock: clinic and paraclinicClass IClass IIClassIIIClass IVBlood loss %< 1515-3030-4040 - Volume ml750800-15001500-20002000SBPUnmodifiedNormalReducedVery lowDBPUnmodifiedRaisedReducedVery low (immeasurable)HR Easy tachycardia100-120120 (weak)> 120 filiformCapillary refillingNormalDelayed> 2 sDelayed > 2 sUndetectableRFNormal

Normal

Tachipnea > 20/minTachipnea > 20/minUrinary output> 3020-3010-200-10ExtremitiesNormal colourPalePalePale and coldConscious stateAlertAnxious or aggressiveAnxious, aggressive or obnubilatedObnubilated, confused or in a comaHemorrhagic shock: Therapeutic objectivesAdequate lung oxygenationHemorrhage controlLoss replacementsMonitoring therapy effectsMyocardic contractibility supportAcido-basic and electrolytic reequilibrationSustaining renal functionHemorrhagic shock: treatment ABCExternal hemorrhages control: raising the extremities, compressive bandage, surgeryLoss replacement: peripheral and central venous acces, intravascular volume replacement, oxygen transport replacement, coagulation anomalies correction

Crystalline solutionsIsotones: 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 bloodHypertonic 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

Colloidal solutionsImportant intravascular remanence time, small volumes use for adequate volemic resuscitation, maintenance of intravascular colloidal osmotic, useful in cardiac and renal insufficiencyAlbumen, dextran 40-70, HAES, Haemacel, plasmaHigh price, anaphylactic reactions, antiplachetary effect and of faking direct compatibility result, histocitary system blockage, infection transmissionBlood transfusion and derivatesO2 transport capacity increaseHomologous isogroup blood, izoRh, integral, eritrocitary mass, washed erytocytesArtificial blood: perflorocarbonic emulsions, Hb pyridoxilated polymerCoagulation dysfunction corrections, CID treatment: frozen fresh plasma, heparin therapyContribution of citric acid (from preserved blood) and of K, could induce hypocalcaemia ( necessitate 1 g Ca gluconate iv for each 5U of transfused blood or plasma) Auto transfusionHemorrhagic shock: treatmentClass I2,5 l Ringer lactate or physiological solution or 1 l colloidClass II

1 l colloid + 1,5 l Ringer lactate or physiological solution Class III

1 l Ringer or NaCl + 0,5 l colloid + 1-1,5 l integral blood or an equivalent volume of erythrocytic massClass IV

1 l Ringer or NaCl + 1 l colloid + 2 l integral blood or an equivalent volume of erythrocytic mass and colloidTherapy efficiencyBlood pressure MBP 90-100 mmHgHR, RRUrinary outputCVP 10-12 mmHgConsciousness stateSkin coloring, capillary refil time