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First Part Assoc. Prof. Dr. Diana Cimpoesu. Shock - definition, epidemiology Cardiovascular insufficiency that creates an imbalance between tissue oxygen.

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Presentation on theme: "First Part Assoc. Prof. Dr. Diana Cimpoesu. Shock - definition, epidemiology Cardiovascular insufficiency that creates an imbalance between tissue oxygen."— Presentation transcript:

1 First Part Assoc. Prof. Dr. Diana Cimpoesu

2 Shock - definition, epidemiology Cardiovascular insufficiency that creates an imbalance between tissue oxygen supply and oxygen demand USA- over 1 milion cases present 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

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5 Shock- physiopathology SaO2=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)

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 (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, prognosis  MBP=CO x peripheral vascular resistance,  CO decreases- the peripheral vascular resistance increases MBP is not an exact marker of the tissue hypo-perfusion

7 Shock- physiopathology Compensatory mechanisms: stimulation of carotid baro- receivers – sympathetic NS: Arteriolar vessel constriction – circulation redistribution HR increase and miocardial 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)

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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 and K 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 Neurological disorders: vertigo, lipothymia, alteration of the mental status-coma Trauma

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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, increase of RR, increase of the dead area, bronchospasm, hypocapnia, respiratory failure, acute respiratory distress sdr.

15 Shock- physical examination Visceras: 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.

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17 Shock –clinical framework Temperature Hyperthermia or hypothermia (endogenous=hypo metabolic shock or exogenous). Cardiac frequency HR Usually increased; there can also be paroxistic bradycardia in 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 vessel constriction and 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 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 dyne x s/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 Class I Class II ClassIII Class IV Blood loss % < 15 15-3030-4040 - Volume ml - Volume ml750800-15001500-20002000 SBPUnmodifiedNormalReduced Very low DBPUnmodifiedRaisedReduced Very low (immeasurable) HR Easy tachycardia 100-120 120 (weak) > 120 filiform Capillary refilling NormalDelayed > 2 s Delayed Undetectable RFNormalNormalTachipnea > 20/min Tachipnea Urinary output > 30 20-3010-200-10 Extremities Normal colour PalePale Pale and cold Conscious state Alert Anxious or aggressive Anxious, aggressive or obnubilated Obnubilated, confused or in a coma

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, Hb pyridoxilated 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 Ca gluconate iv for each 5U of transfused blood or plasma) Auto transfusion

32 Hemorrhagic shock: treatment Class I 2,5 l Ringer lactate or physiological solution or 1 l colloid Class 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 mass Class IV 1 l Ringer or NaCl + 1 l colloid + 2 l integral blood or an equivalent volume of erythrocytic mass and colloid

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 IgE 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: mast cells and basophile degranulation

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.


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