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.

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)

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

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

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

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, failure, bronchospasm, hypocapnia, respiratory 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 < 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%

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

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

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)

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

Hemorrhagic shock: clinic and paraclinic

Class I Class II ClassIII Class IV Blood loss % - Volume ml SBP DBP HR Easy tachycardia Capillary refilling Normal RF Urinary output Extremities Conscious state < 15 750 Unmodified Unmodified Normal > 30 Normal colour Alert 15-30 800-1500 Normal Raised 100-120 Delayed > 2 s Normal 20-30 Pale Anxious or aggressive 30-40 1500-2000 Reduced Reduced 120 (weak) Delayed > 2 s Tachipnea > 20/min 10-20 Pale Anxious, aggressive or obnubilated 40 2000 Very low Very low (immeasurable) > 120 filiform Undetectable Tachipnea > 20/min 0-10 Pale and cold 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 Class IV 1 l Ringer or NaCl + 0,5 l colloid + 1-1,5 l integral blood or an equivalent volume of erythrocytic mass 1 l Ringer or NaCl + 1 l colloid + 2 l integral blood or an equivalent volume of erythrocytic mass and colloid

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

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

Ag

IgE mast cells and basophile mast cells and basophile degranulation 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:

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 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.