Presentation on theme: "First Part Assoc. Prof. Dr. Diana Cimpoesu. Shock - definition, epidemiology Cardiovascular insufficiency that creates an imbalance between tissue oxygen."— Presentation transcript:
First Part Assoc. Prof. Dr. Diana Cimpoesu
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”
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
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)
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
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.
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.
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.
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.
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.
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
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
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%
Hemorrhagic shock: clinic and paraclinic Class I Class II ClassIII Class IV Blood loss % < Volume ml - Volume ml SBPUnmodifiedNormalReduced Very low DBPUnmodifiedRaisedReduced Very low (immeasurable) HR Easy tachycardia (weak) > 120 filiform Capillary refilling NormalDelayed > 2 s Delayed Undetectable RFNormalNormalTachipnea > 20/min Tachipnea Urinary output > Extremities Normal colour PalePale Pale and cold Conscious state Alert Anxious or aggressive Anxious, aggressive or obnubilated Obnubilated, confused or in a coma
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
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
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
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
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
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
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
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
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
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
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
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
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
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
Treatament Fluids i.v. 1-2 l or 20 ml/kg Corticosteroids: methylprednisolon 125 mg i.v. Blockings H1- diphenhydramine 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.