HYPOVOLEMIC SHOCK

1. University of Medicine and Pharmacy, Iasi School of Medicine ANESTHESIA and INTENSIVE CARE Conf. Dr. Ioana Grigoras MEDICINE 4th year English Program Suport de curs HYPOVOLEMIC SHOCK

2. HYPOVOLEMIC SHOCK DEFINITION • syndrom characterized by decreased circulating blood volume (hypovolemia), which results in reduction of effective tissue perfusion pressureand generalized cellular dysfunctions. Forms: • Hemorrhagic shock • Non-hemorrhagic hypovolemic shock

3. HYPOVOLEMIC SHOCK CAUSES: • Hemorrhagic: • External blood loss (wounds) • Exteriorization of internal bleeding (hematemesis, melena, epistaxis, hemoptysis,etc.) • Internal bleeding (hemothorax, hemoperitoneum,etc. ) • Traumatic shock • Non-hemorrahagic: • Digestive losses (vomiting, diarrhea,nasogastric suction, billiary, digestive fistula, etc ) • Renal losses (diabetesmellitus, polyuriacaused by diuretics overdose,osmotic substances, polyuric phase of acute renal failure, etc.) • Skin losses (intense physical effort, overheated enviroment, burns, etc.) • Third space losses (peritonites, intestinal oclussion, pancreatits, ascitis pleural effusions, etc.)

4. PATHOPHYSIOLOGY Primary pathophysiological event (reduction of ventricular filling volumes and pressures) compensatory phenomena macrocirculatory reaction time decompensatory phenomena microcirculatory reaction

5. PATHOPHYSIOLOGY Hypodynamic shock: • Macrocirculatory reaction: • sympatho-adrenergic+ humoralreaction (ADH, cortizol, SRAA) • EFFECTS: centralisation of the circulation (compensatory effect) worsening of tisular hypoperfusion (decompensatory effect) • Microcirculatory reaction: • Alterations of capillary exchanges • EFFECTS: transcapilaryfilling (compensatory effect) capilary leak (decompensatory effect) • Maldistribution of blood flow • EFFECTS: preferential renal blood flowtowards medular region (cortical vasoconstriction) • Abnormal peripheral oxygen extraction • EFFECTS: early - increased (compensatory effect) late - decreased (decompensatory effect) • Rheologic changes • EFFECTS: ↑ blood viscosity,  blood flow, CID • Endhotelial modifications • EFFECTS: morpho-functional modifications proinflamatoryand procoagulatory status, altered permeability

6. HYPOVOLEMIC SHOCK CLINICAL SIGNS: • Intense thirst • Tachycardia • Tachypnea • Positive orthostatic test • Small pulse wave • hTA (blood hypotension) • Agitation, anxiety , confusion, coma • Oliguria • Cold extremities • Profuse sweating • Collapsed peripheral veins • Delayed return of color to the nail bed + History of hemorrhagic or non-hemorrhagic losses

7. CLASSIFICATIONOFHYPOVOLEMIC SHOCK

8. DIFFERENTIAL DIAGNOSISWITH OTHER FORMS OF SHOCK

9. ABBREVIATIONS: • HR – heart rate • BP – arterial blood pressure • CO – cardiac output • CVP –central venous pressure • PAOP – pulmonary artery occlusion pressure • SVR – systemic vascular resistance • Da-v O2 – oxygen arterial-venous difference • SvO2 – mixed venous blood oxygen saturation

10. HYPOVOLEMIC SHOCK TREATMENT PRINCIPLES • Initial treatment of shock states • Causative treatment – STOP losses • Volume repletion • Inotropic therapy • Vasomotor therapy

11. TREATMENT OF HYPOVOLEMICSHOCK • Causativetreatment – STOP losses • essential role • surgicaltreatment (when appropriate) • emergency surgery for ongoing hemorrhage

12. TREATMENT OF HYPOVOLEMICSHOCK • volume replacement • Vascular access site • Solutions forvolume replacement • Rhythm of administration

13. TREATMENT OF HYPOVOLEMICSHOCK • Volume replacement – SITE ofVASCULAR ACCESS • Peripheral vascular access • Multipleaccess (2-4 veins) • Large peripheral catheters • External jugular vein Advantages: • Short time of instalation • Requires basic knowledge and simple matherials • Minor complications (hematomas, cutaneous seroma, etc.) Disadvantages: • The diameter of peripheral catheter must be adapted for peripheral veins dimensions • Vascular access can be lost (restless patient, during transportation); must be changed at 24-48 hours; • no catecholamines administration (except in emergency for a short time period,until a central venous access is available) • Central venous access • After peripheral vascular access is established and volume replacement is initiated Advantages: • Reliable and long lasting venous access (7-10 days) • Allows CVP measuring and guiding of treatment • Allows the administration of catecholamines and hypertonic substances Disadvantages: • Riskof complication (at instalation – pneumothorax,cervical or mediastinal hematoma, cardiac dysrhytmias; during utilization – infection, gas embolism)

14. TREATMENT OF HYPOVOLEMICSHOCK • Volume replacement - Solutions for volume replacement • Isotonic crystalloid solutions • Hypertonic crystalloid solutions • Colloid solutions • Whole blood and red blood cells • Fresh-frozen plasma • Platelets

15. TREATMENT OF HYPOVOLEMICSHOCK Solutions for volume replacement -Isotonic crystalloid solutions • Normal saline (NaCl 0,9 %),Ringer solution,lactated Ringer solutions • Advantages: • easy available • cheap • reduced risks • Disadvantages: • Small volume effect (out of 1000ml infusedsolution – 250-300ml remains intravascullarly, the rest is distributed to the interstitial space) • short duration of volume effect • riskof interstitial edema, metabolic hyperchloremic acidosis -Hypertonic crystalloid solutions • hypertonic saline (NaCl 7,4%) • Advantages: • Efficient blood volume resuscitation with small solution volume (water is atracted from interstitial space ) • Avoidance of fluid overload and peripheral edema • Disadvantages: • may result in acute pulmonary edema

16. TREATMENT OF HYPOVOLEMICSHOCK Solutions for volume replacement Colloid sollutions • Dextrans: Dextran 70, Dextran 40 • Gelatines:Gelofusin, Haemacel, Eufusin • Hetastarch: Haes, Voluven, Refortan • Human albumin 5%, 20% • Advantages: • Good volume effect • Long duration of volume effect • Disadvantages: • expensive • risk for anaphylactic reactions • interfere with blood groups determination • can induce/ aggravate coagulation disorders

17. TREATMENT OF HYPOVOLEMICSHOCK Solution for volume replacement Blood and blood products are not volume solutions • Only isogroup isoRh blood • Only after restauration of intravascular volume with cristalloid /colloid solutions; • For correction of oxygen transport • In case of posthemorragic anemia (after volume replacement) or ongoing hemorrhage • In case of massive blood transfusion – add fresh-frozen plasma and platelet concentrate

18. TREATMENT OF HYPOVOLEMICSHOCK Volume replacement RHYTHM OF ADMINISTRATION • Rhytm of administration depends on: • Ongoing losses / stopped losses • Rhytm of losses – rapid (minutes, hours) or slow (days) instalation • For the patient with hypotension – normal saline (2000ml in the first 15-30 minutes) • after the first 15-30 minutes - volume replacement continues depending on the clinical and hymodinamic parameters (BP, HR, etc..)

19. TREATMENT OF HYPOVOLEMICSHOCK Volume replacement – MONITORING THE TREATMENT EFFICIENCY • Clinical parameters • normalisation of BP, HR, pulseamplitude, skin colour andtemperature, mental status, urinary output • Hemodynamic parameters • Normalization of CVP, PCPB, DC, RVS, so • Laboratory parameters • Normalization of acid-base balance, liver, renal tests, Hb şi Ht, so

20. TREATMENT OF HYPOVOLEMICSHOCK • Inotropic support • Only after volume replacement • Used to improve cardiac output • Dobutamine • inotropic positive support • peripheral arterial vasodilatation

21. TREATMENT OF HYPOVOLEMICSHOCK Vasopressor therapy • NOT RECOMMENDED (may aggravate peripheral hypoperfusionand metabolic acidosis) EXCEPTIONS • Only temporary • In case of ongoing hemorrhage, which outruns the possibilities of volume replacement • Only until surgical procedure stops the hemorrhage (emergency surgical treatment) • Noradrenaline, dopamine, adrenaline