Surgery - Shock

SURGERY - SHOCK

DRA. LAHOZ HEMOSTASIS - REVIEW

BIOLOGY OF HEMOSTASIS

CAUSES OF BLEEDING 1. Congenital Factor Deficiencies  Coagulation Factor Deficiencies  Platelet Functional Defects 2. Acquired Hemostatic Defect  Platelet abnormalities - Quantitative Defects - Qualitative Defects  Acquired Hypofibrinogenemia  Myoloproliferative Diseases  Coagulopathy of Liver Diseases (Vit K)  Coagulopathy of Trauma  Acquired Coagulation Inhibitors  Anticoagulation & Bleeding (medication) EVALUATION OF HEMOSTASIS

4 MAJOR PHYSIOLOGIC EVENTS 1. Vascular Constriction 2. Platelet Plug Formation 3. Fibrin Formation/ Clot formation? Coagulation 4. Fibrinolysis

1. HISTORY  Bleeding tendencies – toothbrush, menses, dental extraction, spontaneous bruising  Transfusion  Medical Problems: Liver/ Renal  Family History of bleeding difficulties  Medications 2. PHYSICAL EXAMINATION  Bruises  Other illness – jaundice, wounds, renal 3. DIAGNOSTIC PROCEDURES  BLOOD TYPING  Platelet count  BT, PT, PTT TRANSFUSION - REVIEW 1. Whole Blood – fresh and banked FWB- provides greater coagulation activity than equal units of component therapy 2. Red blood Cell (PRBC) 3. Platelet Concentrate 4. Fresh Frozen Plasma 5. Tranexamic acid 6. Expanders – DEXTRAN 7. Human polymerized hemoglobin *AUTOTRANSFUSION TRANSFUSION INDICATIONS 1. Improvement in Oxygen-Carrying Capacity (RBC) 2. Treatment of anemia – Hb /= 30

20-30

5-15

Negligible

Slightly anxious Crystalloid

Mildly anxious Crystalloid

Anxious and confused Crystalloid + blood

Confused, lethargic Crystalloid + blood

Fluid replacement (3:1 rule)

Stage

I Compensated

II Mild

III moderate

IV Severe

Blood loss

3 seconds; Cold, mottled skin Absent(paralytic ileus, mucosal necrosis) None (anuria) Obtunded

SURGERY - SHOCK

DRA. LAHOZ

SHOCK

PHASES OF SHOCK

1.COMPENSATED PHASE

2.DECOMPENSATED PHASE 3.IRREVERSIBLE PHASE

PATHOPHYSIOLGY OF SHOCK

PHYSIOLOGIC RESPONSES HYPOVOLEMIC SHOCK CARDIOGENIC SHOCK VASOGENIC SHOCK (Septic shock) NEUROGENIC SHOCK

OBSTRUCTIVE SHOCK

TRAUMATIC

CLASSES OF SHOCK Loss of circulating blood volume Failure of heart as a pump Decreased resistance within capacitance vessels, usually in infections Form of vasogenic shock in which the spinal cord injury or spinal anesthesia causes vasodilation due to acute loss of vascular tone Form of cardiogenic shock due to mechanical impediment to circulation leading to depressed cardiac output rather than primary cardiac failure Injury leads to activation of inflammatory cells and release of circulation factors that modulate the immune system

A. Stretch receptors and Baroreceptors in the Heart and Vasculature B. Chemoreceptors C. Cerebral ischemia responses D. Release of endogenous vasoconstrictors E. Shifting of fluid into the intravascular space F. Renal reabsorption and conservation of salt and water PHYSIOLOGIC RESPONSES AFFERENT SIGNALS EFFERENT SIGNALS Baroreceptors (heart) Chemoreceptors (aorta & carotid bodies) (inflammatory mediators) Loss of Circulation Blood Volume Pain Hypoxemia/Hypercarbia Acidosis Infection Change in Temperature Emotional arousal Hypoglycemia

Cardiovascular response Hormonal response

SURGERY - SHOCK

DRA. LAHOZ HEMORRHAGE

SHOCK PITUITARY GLAND (Vasopressin/ADH)

DIMINISHED VENOUS RETURN DECREASED CARDIAC OUTPUT

CARDIOVASCULAR RESPONSE:  Increased Cardiac heart rate and contractility  Venous and arterial vasoconstriction  Redistribution of blood flow (selective vasoconstriction – less essential organs such as intestines, kidney, skin)  Brain & heart preserve blood flow

HEMORRHAGE SYMPATHETIC RESPONSE (CATHECHOLAMINE EFFECTS) EPINEPHRINE – ADRENAL MEDULLA NOREPINEPHRINE – SYNAPSES OF SYMPATHETIC NERVOUS SYSTEM  Hepatic glycogenolysis & Gluconeogenesis (Increased glucose availability to peripheral tissues)  Increased skeletal muscle glycogenolysis  Suppression of insulin release  Increase Glucagon release

HORMONAL RESPONSE STRESS

HPA AXIS Hypothalamus  Corticotropin releasing hormone Pituitary gland  Adrenocorticotropic Hormone (ACTH) Adrenal cortex  Cortisol CORTISOL: Acts with Epinephrine & Glucagon 1. Hyperglycemia - Gluconeogenesis - Insulin resistance 2. Muscle protein breakdown 3. Lipolysis 4. Retention of salt and water by nephrons

1 & 3  SUBSTRATE FOR HEPATIC GLUCONEOGENESIS SHOCK RAA SYSTEM Angiotensin II -Vasoconstrictor ( Splanchnic & Peripheral Vasc) -Secretion of Aldosterone -ACTH -Antidiuretic hormone Aldosterone – promotes reabsorption of sodium and water - Potassium & Hydrogen ions are lost

     

Increased water permeability Decreased water and Sodium loss Preserve Intravascular volume Potent Mesenteric vasoconstrictor Increased Hepatic Gluconeogenesis Increased Hepatic Glycolysis

SURGERY - SHOCK

DRA. LAHOZ

HEMORRHAGIC/HYPOVOLEMIC SHOCK

MANAGEMENT PRIORITIES  Secure Airway  Control Source of Blood Loss  Volume Resuscitation

SURGERY - SHOCK

DRA. LAHOZ

DAMAGE CONTROL RESUSCITATION

*BLOOD PRODUCTS (TRANSFUSSION) SEPTIC SHOCK SEPTIC SHOCK (VASODILATORY SHOCK) INFECTION + INFLAMMATION Fever Tachycardia Tachypnea Confusion Malaise Oliguria Hypotension

SURGERY - SHOCK

DRA. LAHOZ

TREATMENT PROTOCOLS Insulin Ventilatory Support Corticosteroids Immunoglobulin Modulation CARDIOGENIC SHOCK -Circulatory pump failure Hemodynamic Criteria  Sustained hypotension (SBP