shock various types and description of haemorrhagic shock
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Shock & Haemorrhagic shock
Shock Shock is the clinical syndrome that results from inadequate tissue perfusion which leads to hypoxia and ultimately cellular dysfunction. The cellular dysfunction is manifested as aerobic to anaerobic leading to lactic acidosis.
Principle mechanisms Not enough blood volume Pump failure Abnormalities of peripheral circulation (when all small blood vessels dilate) Mechanical blockage of outflow from the heart
Most common type of shock Insufficient circulating volume Primary cause = loss of blood or body fluids from an internal or external source Hemorrhage, severe burns, severe dehydration 4 Hypovolemic shock Scalp laceration 3 rd degree/full thickness burn
Failure of the heart to pump effectively Due to damage to the heart muscle Large myocardial infarction Arrhythmias (too fast or too slow) Cardiomyopathy Congestive heart failure (CHF) Cardiac valve problems 5 Cardiogenic Shock
Similar to hypovolemic shock - insufficient intravascular volume of blood or “relative" hypovolemia result of dilation of all blood vessels so the “tank” is much larger 6 Distributive shock Urticaria/anaphylaxis Meningococcic sepsis
Septic shock Overwhelming infection leading to profound systemic vasodilation Anaphylactic shock Severe reaction to an allergen, antigen, drug or foreign protein, releasing histamine causing widespread vasodilation, hypotension and increased capillary permeability Neurogenic shock Rarest form of shock. Trauma to spinal cord resulting in loss of autonomic and motor reflexes below injury level. Vessel walls relax uncontrolled, decreasing peripheral vascular resistance, result = vasodilation and hypotension 7 Distributive shock examples
Psychogenic shock Immediately follows sudden fright Eg bad news, severe pain( blow to the testes)
Haemorrhagic shock It is one of the commonest form of hypovolemic shock Hypovolemia leads to decreased preload which leads to increased sympathetic activity and vasoconstriction Vasoconstriction leads to decreased mean arterial pressure and ischemia which ultimately leads to multiorgan failure-ARDS,HEPATIC FAILURE,STRESS,GI BLEEDING.RENAL FAILURE . Ischemia leads to myocardial insufficiency and severe decrease in Systemic Vascular Resistance and finally death
Hemorrhage Classification
External Hemorrhage Results from soft tissue injury . Most soft tissue trauma is accompanied by mild hemorrhage and is not life threatening. Can carry significant risks of patient morbidity and disfigurement The seriousness of the injury is dependent on: Anatomical source of the hemorrhage (arterial, venous, capillary) Degree of vascular disruption Amount of blood loss that can be tolerated by the patient
Internal Hemorrhage Can result from: Blunt or penetrating trauma Acute or chronic medical illnesses Internal bleeding that can cause hemodynamic instability usually occurs in one of four body cavities: Chest Abdomen Pelvis Retroperitoneum
Internal Hemorrhage Signs and symptoms that may suggest significant internal hemorrhage include: Bright red blood from mouth, rectum, or other orifice Coffee-ground appearance of vomit Melena (black, tarry stools) Dizziness or syncope on sitting or standing Orthostatic hypotension Internal hemorrhage is associated with higher morbidity and mortality than external hemorrhage
Compensated shock 0-20% of blood loss Blood pressure is maintained via increased vascular tone and increased blood flow to vital organs
The Organs which well perfused : Brain Heart Kidneys Liver The Organs which are less perfused : Skin GI tract Skeletal Muscle
But why The body will make whatever adjustments it can to maintain…. Adequate Cardiac Output Brain and heart perfusions remain near normal while other less critical organ systems are, in proportion to the blood volume deficit, stressed by ischemia.
Uncompensated shock 20-40% loss of blood volume Decrease in BP Tachycardia
The body’s response Uncompensated shock The intravascular volume deficit exceeds the capacity of vasoconstrictive mechanisms to maintain systemic perfusion pressure. Increased cardiac output Increased respiration Sodium retention
Classification Class I Loss of up to 15% of total blood volume (0 to 750 ml in 70 kg person). Characterized by normal blood pressure, urine output, slight tachycardia, tachypnea, slight anxiety.
Class II Loss of 15 % to 30% of total blood volume (750 to 1,500 ml ) Characterized by normal blood pressure, tachycardia, mild tachypnea, decrease urine output and mild anxiety.
Class III Loss of 30% to 40% of total blood volume (1,500 to 2,ooo) Characterized by hypotension, tachycardia, tachypnea, decreased urine output , anxiety and confusion.
Class IV Loss of > 40% of total blood volume (>2,ooo) Characterized by severe hypotension and tachycardia, tachypnea, negligible urine output and lethargy
Class 4 Class 3 Class 2 Class 1 >2000 1500-2000 750-1500 <750 ml Blood loss (in ml) >40 30-40 15-30 <15 Blood volume (in%) >140 >120 >100 <100 Heart rate decreased Decreased mean arterial pressure<60 Normal (+tilt ) Normal or increased Blood pressure decreased Decrease Decreased Normal Pulse pressure Always delayed Usually delayed May be delayed Normal Capillary refill Always delayed Usually delayed Mildly delayed normal Respirations Essentially anuric 5-15 20-30 >30 Urinary output (ml/hr) Lethargic,obtunded confused Anxious Normal or anxious Mental status
Concomitant Factors Pre-existing condition eg Anaemia , HTN etc Rate of blood loss Patient Types Pregnant >50% greater blood volume than normal Fetal circulation impaired when mother compensating Athletes Greater fluid and cardiac capacity Obese CBV is based on IDEAL weight (less CBV)
Children CBV 8 – 9% of body weight Poor compensatory mechanisms TREAT AGGRESSIVELY! Elderly Decreased CBV Medications BP Anticoagulants
Hemorrhage Assessment Blood loss at the scene Mechanism of Injury/Nature of Illness Should only be used in conjunction with vital signs and other clinical signs of injury to determine the probability of injury Need for Additional Resources
Initial Assessment General Impression Obvious bleeding Mental Status Interventions Manage as you go O 2 Bleeding control Shock BLS before ALS!
Focused History & Physical examination Rapid Trauma Assessment Full head to toe Consider air medical if stage 2+ blood loss Focused Physical Exam Guided by c/c Vitals, SAMPLE, and OPQRST Additional Assessment Orthostatic hypotension Tilt test: 20 BP or P from supine to sitting
Fractures and Blood Loss Pelvic fracture: Femur fracture: Tibia/fibula fracture: Hematomas and contusions: 2,000 mL 1,500 mL 500 – 750 mL 500 mL
Ongoing Assessment Reassess vitals and mental status: Q 5 min: UNSTABLE patients Q 15 min: STABLE patients Reassess interventions: Oxygen ET IV Medication actions Trending: improvement vs. deterioration Pulse oximetry End-tidal CO 2 levels
Management C-ABCs of trauma Control hemorrhage (splint the limb!!) Obtain IV access and resuscitate with fluids and blood 2 liters crystalloid for adults 20 cc/kg crystalloid x 2 for kids Blood vs. Crystalloid?? Long term critical care management
Management goals AFTER securing the ABCs: stop the bleeding! restore volume! correct any electrolyte/acid-base disturbances!
Apply direct pressure : with gloved hand, sterile dressing(s). Bleeding stopped ? Yes No Elevate extremity : above victim’s heart, continue direct pressure Locate pressure point, apply pressure : maintain direct pressure over wound Treat for shock : care for wound, seek definitive care Bleeding stopped? Bleeding stopped? No Bleeding from extremity? No Apply tourniquet (last resort) Yes No Definitive therapy
Apply pressure directly to wound site: Gloved hand, dressing If dressing soaks thru, add more gauze on top and press harder 37 Direct pressure Apply direct pressure : with gloved hand, sterile dressing(s). Bleeding stopped? Yes No Elevate extremity : above victim’s heart, continue direct pressure Locate pressure point, apply pressure : maintain direct pressure over wound Treat for shock : care for wound, seek definitive care Bleeding stopped? Bleeding stopped? No Bleeding from extremity? No Apply tourniquet (last resort) Yes No Definitive therapy
If possible, raise wound site above level of victim’s heart 38 Elevate wound site Apply direct pressure : with gloved hand, sterile dressing(s). Bleeding stopped? Yes No Elevate extremity : above victim’s heart, continue direct pressure Locate pressure point, apply pressure : maintain direct pressure over wound Treat for shock : care for wound, seek definitive care Bleeding stopped? Bleeding stopped? No Bleeding from extremity? No Apply tourniquet (last resort) Yes No Definitive therapy
Find proximal “pressure point” and press on it (radial, ulnar , brachial, axillary , femoral arteries—not carotid) Apply direct pressure to site 39 Pressure points Apply direct pressure : with gloved hand, sterile dressing(s). Bleeding stopped? Yes No Elevate extremity : above victim’s heart, continue direct pressure Locate pressure point, apply pressure : maintain direct pressure over wound Treat for shock : care for wound, seek definitive care Bleeding stopped? Bleeding stopped? No Bleeding from extremity? No Apply tourniquet (last resort) Yes No Definitive therapy
Apply band above injury site, tighten to stop bleeding: Last resort—risky Note time of application Reassess frequently 40 Tourniquet Apply direct pressure : with gloved hand, sterile dressing(s). Bleeding stopped? Yes No Elevate extremity : above victim’s heart, continue direct pressure Locate pressure point, apply pressure : maintain direct pressure over wound Treat for shock : care for wound, seek definitive care Bleeding stopped? Bleeding stopped? No Bleeding from extremity? No Apply tourniquet (last resort) Yes No Definitive therapy
Volume Resuscitation Rapid Responder Give 500cc-1 Liter crystalloid rapid improvement of BP/HR/Urine output < 20% blood loss Transient Responder Give 500cc-1 Liter crystalloid improves briefly then deteriorates 20-40% blood loss Continue crystalloid infusion +/- Blood
Non Responder Give 2 Liters crystalloid/ 2 units Blood no response > 40% blood loss
Correction of any electrolyte/acid-base disturbances Normalization of acidosis and oxygen consumption are the best current indicators of adequate resuscitation Base deficit and lactate level are good indications of tissue perfusion
Bicarbonate HCO 3 combined with hydrogen ion to form water and carbon dioxide CO 2 diffuses into cells and worsens intracellular acidosis It is not indicated for lactic acidosis from HS Best treatment of acidosis from HS is restoring perfusion to ischemic tissue.
Complications Multi organ dysfunction Coagulopathy
Multiple organ failure pt who survive HS but die in the hospital later usually die of MOF or sepsis MOF results from systemic inflammatory response Duration and severity of HS correlate with incidence of MOF Patients who get > 6 units of packed RBCs in the first 12 hours of HS resusitation have higher risk of MOF
Coagulopathy Hypothermia Most common cause of coagulopathy in HS Significant coagulopathy begins at 34 o c Undetectable on lab tests of coagulation ,blood warmed to 37 c before testing Note that Treat with warmed fluids and external rewarming
Platelet dysfunction and deficiency Second most common cause Hypothermia cause plt dysfunction Thrombocytopenia is common is massive HS Degree of thrombocytopenia not correlated directly with volume of blood loss Platelets transfusion