Lecture 3 : Shock

Shock - Emergency Approach First Part

Shock - definition, epidemiology 

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Cardiovascular insufficiency which determines a disturbance/imbalance between the oxygen need and offer USA- one milion cases in ED/year Precocious intervention at the nontraumatic patient – “the golden hour”

Shock – classification 

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Hypovolemic- decrease of the circulant volume Cardiogenic- pump malfunction Distributive- maldistribution of the sanguine-septic, anaphylactic, neurogene flow Obstructive- obstruction of the sanguine flow because of extra-cardiac causes (pulmonary emboli, cardiac tamponade, pneumothorax under tension)

Shock: physiopathology 

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CaO2- O2 arterial = O2 linked to Hb plus a small quantity of O2 dissolved in plasma DO2- O2 release – it results from CaO2 and DC (CO) DO2 and VO2 (release and consumption of O2) is a sensitive balance between offer and demand

Shockphysiopathology 

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SaO2=100%- normal 25% of the transported O2 linked to Hb is consumed by tissues – the venous blood will have a saturation of 75% The offer of O2 insufficient- the first compensatory mechanism is the increase of CO If the increase of CO is insufficient – the percentage of O2 increases extracted by tissues from HbO2 and SmVO2 decreases (the saturation in O2of the venous blood)

Shock-physiopathology  

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Demand>offer – determination of se intră în anaerobiosis- lactic acid Lactic Acidosis : due to the inadequate release of O2 (just like in the cardiogenic shock) Very high demand (consumption of O2 = VO2 increased)status epilepticus 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 decreasesthe peripheral vascular resistance increases MBP is not an exact marker of the tissular bipo-perfusion

Shockphysiopathology 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 reninangiotension-retension system of Na and watermaintenance of the intravascular volume.

Shock- physiopathologycellular effects of O2 decrease  

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ATP depletion- membranous pump malfunctionNa 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 

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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

Shock- physical examination 

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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 RF, increase of the dead area, bronchospasm, hypocapnia, respiratory insufficiency, distress sdr. of the adult 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).

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Cardiac frequency

– Usually increased; there can also be paroxistic bradycardia in hypovolemic shock, hypoglycemia, beta-blockers, pre-existent cardiac affections.

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SBP

– In the precocious phase it can be increased because it is a compensatory mechanism and increases DC and then, it decreases.

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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.

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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.

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MBP = DBP + (MBP – DBP)/3

– Depends on DC 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

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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 

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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  

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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 DO2 – resolving of hyperandregenic 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 dynexs/cmp Contractility: DC 5 l/min, IC 2,5-4,5 l/min/mp HR 60-100/min PPC > 60 mmHg = DBP – PVC Tissular oxygenation: SmVO2 > 70 %, acid lactic < 2 mmoli/l

Hypovolemic shock: causes  

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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 

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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 physiopathology 

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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 

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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

Hemorrhagic shock: clinic and paraclinic Blood loss %

Class I

Class II

ClassIII

Class IV

< 15

15-30

30-40

40

800-1500

1500-2000

2000

- Volume ml 750 SBP

Unmodified

Normal

Reduced

Very low

DBP

Unmodified

Raised

Reduced

Very low (immeasurable)

HR

Easy tachycardia

100-120

120 (weak)

> 120 filiform

Capillary refilling

Normal

Delayed >2s

Delayed >2s

Undetectable

RF

Normal

Normal

Tachipnea > 20/min

Tachipnea > 20/min

Urinary output > 30

20-30

10-20

0-10

Extremities

Pale

Pale

Pale and cold

Anxious or aggressive

Anxious, aggressive or obnubilated

Obnubilated, confused or in a coma

Normal colour

Conscious state Alert

Hemorrhagic shock: Therapeutic objectives      

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Adequate lung oxygenation Hemorrhage control Loss replacements Monitoring therapy effects Myocardic contractibility support Acido-basic and electrolytic reequilibration Sustaining renal function

Hemorrhagic shock: treatment  

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ABC External hemorrhages control: raising the extremities, compressive bandage, surgery Loss replacement: peripheral and central venous approach, intravascular volume replacement, oxygen transport replacement, coagulation anomalies correction

Crystalline solutions 

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Isotones: SF, Ringer, dairy Ringer- replace the interstitial deficit also, rapid intra and extra vascular equilibration; it is administrated 3:1 compared to lost blood volume Hyper tones: 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 accessibility

Colloidal solutions 

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Big intravascular remenence, small volumes use for adequate volemic resuscitation, maintenance of intravascular colloidal smotic, useful in cardiac and renal insufficiency Albumen, dextran 40-70, HAES, Hemacel, plasma High price, anaphylactic reactions, antiplachetary effect and of faking direct compatibility result, histocitary system blockage, infection transmission

Blood transfusion and derivates     

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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) and of K, hypocalcaemia (1 g Ca glycolic iv for each 5U of transfused blood or plasma) Auto transfusion

Hemorrhagic shock: treatment Class I

2,5 l milky Ringer or physiological solution or 1 l colloid

Class II

1 l colloid + 1,5 l milky Ringer 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

Therapy efficiency       

Blood pressure HR, RF Urinary output CVP Consciousness state Skin coloring, capillary filling time Para clinic parameters (CO2, pH gastric mucous membrane, IC, SmVO2, lactic acid)

Anaphylactic shock 

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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: causes 

Medicines – – – –

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Foods and additives – – – – –

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Penicillin and other ABc aspirin trimetroprim AINS Sea fruits, fish Soy, nuts Flour, milk, eggs Monosodium glutamate, tartrasine Nitrates and nitrites

Others

– Hymenoptera stings – Insects – Contrast substances from radiology

Anaphylactic shockphysiopathology      

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

Anaphylactic shockclinic         

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   

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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.

Treatament   

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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.