Shock and Hemorrhage M. Alhashash MD, lecturer of general surgery,

Name: Shock and Hemorrhage M. Alhashash MD, lecturer of general surgery,
Uploaded: 2017-07-25T00:10:52+00:00
Duration: PTM34S31
Channel: Marilyn Butler
Description: Shock and Hemorrhage M. Alhashash MD, lecturer of general surgery,

Shock and Hemorrhage M. Alhashash MD, lecturer of general surgery,
hepatobiliary & liver transplant surgery.

Defining Shock Shock is best defined as inadequate tissue perfusion.
Can result from a variety of disease states and injuries. Can affect the entire organism, or it can occur at a tissue or cellular level.

Defining Shock (2 of 2) Shock is not adequately defined by: Pulse rate
Blood pressure Cardiac function Hypovolemia Loss of systemic vascular resistance

“Hypoperfusion can be present in the absence of significant hypotension.”

Definitions Hemorrhage Homeostasis Shock
Abnormal internal or external loss of blood Homeostasis Tendency of the body to maintain a steady and normal internal environment Shock INADEQUATE TISSUE PERFUSION Transition between homeostasis and death

Definitions O2 Delivery - volume of gaseous O2 delivered to the tissue/min. O2 Consumption - volume of gaseous O2 which is actually used by the tissue/min. O2 Demand - volume of O2 actually needed by the tissues to function in an aerobic manner Demand > consumption = anaerobic metabolism

Cardiovascular System Regulation to maintain volume and oxygen supply.
Neural hormonal

Cardiovascular System Regulation
Sympathetic Nervous System Increase Body activity Heart rate Strength of contractions Vascular constriction Bowel and digestive viscera Decreased urine production Bronchodilation Increases skeletal muscle perfusion

Baroreceptor Reflexes
High in the neck, each carotid artery divides into external and internal carotid arteries. At the bifurcation, the wall of the artery is thin and contains many vine-like nerve endings. The small portion of the artery is the carotid sinus. Nerve endings in this area are sensitive to stretch or distortion. Serve as pressure receptors or baroreceptors.

Carotid sinus

Similar area found in the arch of the aorta. Serves as a second important baroreceptor Large arteries, large veins, and the wall of the myocardium also contain less important baroreceptors. Baroreceptor reflexes help maintain blood pressure by two negative feedback mechanisms: By lowering blood pressure in response to increased arterial pressure By increasing blood pressure in response to decreased arterial pressure

Normal blood pressure partially stretches the arterial walls so that baroreceptors produce a constant, low-frequency stimulation. Impulses from the baroreceptors inhibit the vasoconstrictor center of the medulla and excite the vagal center when blood pressure increases. Results in vasodilation in the peripheral circulatory system and a decrease in the heart rate and force of contraction. Combined effect is a decrease in arterial pressure.

Baroreceptors adapt in 1 to 3 days to whatever pressure level they are exposed. Therefore, they do not change the average blood pressure on a long-term basis. This adaptation is common in people who have chronic hypertension.

When baroreceptor stimulation ceases due to a fall in arterial pressure, several cardiovascular responses are evoked: Vagal stimulation is reduced and sympathetic response is increased. The increase in sympathetic impulses results in increased peripheral resistance and an increase in heart rate and stroke volume. Sympathetic discharges also produce generalized arteriolar vasoconstriction, which decreases the container size.

Chemoreceptor Reflexes
Chemoreceptors Monitor level of CO2 in CSF Monitor level of O2 in blood

Carotid body

Chemoreceptor Physiology
Low arterial pressure leads to hypoxemia and/or acidosis. Hypoxemia/acidosis stimulate peripheral chemoreceptor cells within the carotid and aortic bodies. These bodies have an abundant blood supply. When oxygen or pH decreases, these cells stimulate the vasomotor center of the medulla. The rate and depth of ventilation are also increased to help eliminate excess carbon dioxide and maintain acid-base balance.

CV System and Hormone Regulation
Catecholamines Epinephrine Norepinephrine

Role of Adrenal Medulla in Regulating

Antidiuretic Hormone (ADH)(water & pressure regulation) Release Posterior pituitary Drop in BP or increase in serum osmolarity Action Increase in peripheral vascular resistance Increase water retention by kidneys Decrease urine output Splenic vasoconstriction 200 mL of free blood to circulation

BPRenin-Angiotensin-Aldosterone Mechanism in Regulating BP

Angiotensin II Release Primary chemical from kidneys Lowered BP and decreased perfusion Action Converted from renin into angiotensin I Modified in lungs to angiotensin II 20-minute process Potent systemic vasoconstrictor 1-hour duration Causes release of ADH, aldosterone, and epinephrine

CV System and Hormone Aldosterone Release Action Adrenal cortex
Stimulated by angiotensin II Action Maintain kidney ion balance Retention of sodium and water Reduce insensible fluid loss

CV System and Hormone Glucagon Release Action Alpha cells of pancreas
Triggered by epinephrine Action Causes liver and skeletal muscles to convert glycogen into glucose Gluconeogenesis

Insulin Release Beta cells of pancreas Action Facilitates transport of glucose across cell membrane Erythropoietin Release Kidneys Hypoperfusion or hypoxia Action Increases production and maturation of RBCs in the bone marrow

Reabsorption of Tissue Fluids
Arterial hypotension, arteriolar constriction, and reduced venous pressure during hypovolemia lower the blood pressure in the capillaries (hydrostatic pressure). The decrease promotes reabsorption of interstitial fluid into the vascular compartment. Considerable quantities of fluid may be drawn into the circulation during hemorrhage.

Reabsorption of Tissue Fluids
Approximately 0.25 mL/min/kg of body weight (1 L/hr in the adult male) can be autotransfused from the interstitial spaces after acute blood loss.

Blood Blood Volume Average adult male has a blood volume of 7% of total body weight. Average adult female has a blood volume of 6.5% of body weight. Normal adult blood volume is 4.5–5 L. Remains fairly constant in the healthy body.

Blood Components Erythrocyte: 45% Miscellaneous blood products: <1%
Hemoglobin Hematocrit Miscellaneous blood products: <1% Platelets Leukocytes Monocytes, basophils, esonophils, neutrophils Plasma: 54%

Signs of Organ Hypoperfusion
Mental Status Changes Oliguria Lactic Acidosis

Categories of Shock HYPOVOLEMIC CARDIOGENIC DISTRIBUTIVE OBSTRUCTIVE

Stages of Shock Cellular Level

Four Stages Stage 1: Vasoconstriction
Stage 2: Capillary and venule opening Stage 3: Disseminated intravascular coagulation Stage 4: Multiple organ failure

Capillary-Cellular Relationship in Shock

Stage 1: Vasoconstriction (1 of 4)
< 15 % loss of blood volume. Vasoconstriction begins as minimal perfusion to capillaries continues. Oxygen and substrate delivery to the cells supplied by these capillaries decreases. Anaerobic metabolism replaces aerobic metabolism.

Production of lactate and hydrogen ions increases. The lining of the capillaries may begin to lose the ability to retain large molecular structures within its walls. Protein-containing fluid leaks into the interstitial spaces (leaky capillary syndrome).

Sympathetic stimulation produces: Pale, sweaty skin Rapid, thready pulse Elevated blood glucose levels The release of epinephrine dilates coronary, cerebral, and skeletal muscle arterioles and constricts other arterioles. Blood is shunted to the heart, brain, skeletal muscle, and capillary flow to the kidneys and abdominal viscera decreases.

If this stage of shock is not treated by prompt restoration of circulatory volume, shock progresses to the next stage.

Stage 2: Capillary and Venule Opening (1 of 5)
Stage 2 occurs with a 15% to 25% decrease in intravascular blood volume. Heart rate, respiratory rate, and capillary refill are increased, and pulse pressure is decreased at this stage. Blood pressure may still be normal.

As the syndrome continues, the precapillary sphincters relax with some expansion of the vascular space. Postcapillary sphincters resist local effects and remain closed, causing blood to pool or stagnate in the capillary system, producing capillary engorgement.

As increasing hypoxemia and acidosis lead to opening of additional venules and capillaries, the vascular space expands greatly. Even normal blood volume may be inadequate to fill the container. The capillary and venule capacity may become great enough to reduce the volume of available blood for the great veins and vena cava. Resulting in decreased venous return and a fall in cardiac output.

Low arterial blood pressure and many open capillaries result in stagnant capillary flow. Sluggish blood flow and the reduced delivery of oxygen result in increased anaerobic metabolism and the production of lactic acid. The respiratory system attempts to compensate for the acidosis by increasing ventilation to blow off carbon dioxide.

As acidosis increases and pH falls, the RBCs may cluster together (rouleaux formation). Halts perfusion Affects nutritional flow and prevents removal of cellular metabolites Clotting mechanisms are also affected, leading to hypercoagulability. This stage of shock often progresses to the third stage if fluid resuscitation is inadequate or delayed, or if the shock state is complicated by trauma or sepsis.

Stage 3: Disseminated Intravascular Coagulation (DIC) (1 of 4)
Time of onset will depend on degree of shock, patient age, and pre-existing medical conditions. Stage 3 occurs with 25% to 35% decrease in intravascular blood volume. At this stage, hypotension occurs. This stage of shock usually requires blood replacement.

Stage 3 is resistant to treatment (refractory shock), but is still reversible. Blood begins to coagulate in the microcirculation, clogging capillaries. Capillaries become occluded by clumps of RBCs. Decreases capillary perfusion and prevents removal of metabolites Distal tissue cells use anaerobic metabolism, and lactic acid production increases.

Lactic acid accumulates around the cell. Cell membranes no longer have the energy needed to maintain homeostasis. Water and sodium leak in, potassium leaks out, and the cells swell and die.

Pulmonary capillaries become permeable, leading to pulmonary edema. Decreases the absorption of oxygen and results in possible alterations in carbon dioxide elimination May lead to acute respiratory failure or adult respiratory distress syndrome (ARDS) If shock and disseminated intravascular coagulation (DIC) continue, the patient progresses to multiple organ failure.

Stage 4: Multiple Organ Failure (1 of 2)
The amount of cellular necrosis required to produce organ failure varies with each organ and the underlying condition of the organ. Usually hepatic failure occurs, followed by renal failure, and then heart failure. If capillary occlusion persists for more than 1 to 2 hours, the cells nourished by that capillary undergo changes that rapidly become irreversible. In this stage, blood pressure falls dramatically (to levels of 60 mmHg or less). Cells can no longer use oxygen, and metabolism stops.

Stage 4: Multiple Organ Failure (2 of 2)
If a critical amount of the vital organ is damaged by cellular necrosis, the organ soon fails. Failure of the liver is common and often presents early. Capillary blockage may cause heart failure. GI bleeding and sepsis may result from GI mucosal necrosis. Pancreatic necrosis may lead to further clotting disorders and severe pancreatitis. Pulmonary thrombosis may produce hemorrhage and fluid loss into the alveoli. Leading to death from respiratory failure.

Goals of Shock Resuscitation
Restore blood pressure Normalize systemic perfusion Preserve organ function

Hypovolemic Shock Causes hemorrhage vomiting diarrhea dehydration
third-space loss burns Signs  cardiac output  PAOP  SVR

Hypovolemic Shock Hemorrhagic Shock Parameter I II III IV
Blood loss (ml) <750 750–1500 1500–2000 >2000 Blood loss (%) <15% 15–30% 30–40% >40% Pulse rate (beats/min) <100 >100 >120 >140 Blood pressure Normal Decreased Respiratory rate (bpm) 14–20 20–30 30–40 >35 Urine output (ml/hour) >30 5–15 Negligible CNS symptoms Anxious Confused Lethargic

Cardiogenic Shock Results from pump failure Etiologic categories
Decreased systolic function Resultant decreased cardiac output Etiologic categories Myopathic Arrhythmic Mechanical Extracardiac (obstructive)

Obstructive Shock Causes Signs Cardiac Tamponade Tension Pneumothorax
Massive Pulmonary Embolus Signs  cardiac output  PAOP  SVR

Distributive Shock Types Signs Sepsis Anaphylactic
Acute adrenal insufficiency Neurogenic Signs ± cardiac output  PAOP(pulmonary artery occlusive pressure) SVR

Summary Type PAOP C.O. SVR HYPOVOLEMIC    CARDIOGENIC   
DISTRIBUTIVE  or N varies  OBSTRUCTIVE   

Clinical Presentation
Clinical presentation varies with type and cause, but there are features in common Hypotension (SBP<90 or Delta>40) Cool, clammy skin (exceptions – early distributive, terminal shock) Oliguria Change in mental status Metabolic acidosis

Initial Assessment Airway Breathing Circulation Disability
Expose body surfaces

Treatment Manage the emergency Determine the underlying cause
Definitive management or support

Definitive Management
Hypovolemic – Fluid resuscitate (blood or crystalloid) and control ongoing loss Cardiogenic - Restore blood pressure (chemical and mechanical) and prevent ongoing cardiac death Distributive – Fluid resuscitate, pressors for maintenance, immediate abx/surgical control for infection, steroids for adrenocortical insufficiency

Vasopressors & Inotropic Agents
Dopamine Dobutamine Norepinephrine Epinephrine Amrinone

Differential Shock Assessment Findings
Assumed to be hypovolemic until proven otherwise Cardiogenic shock Differentiate from hypovolemic shock by: Chief complaint Chest pain Dyspnea Tachycardia Heart rate Signs of congestive heart failure Dysrhythmias

Distributive shock Differentiate from hypovolemic shock by: Mechanism suggesting vasodilation Spinal cord injury Drug overdose Sepsis Anaphylaxis Warm, flushed skin Lack of tachycardia response (not reliable)

Obstructive shock Differentiate from hypovolemic shock by signs and symptoms of: Cardiac tamponade Tension pneumothorax Pulmonary embolism

Detailed Physical Examination
Vital signs Pulse Blood pressure Orthostatic vital signs Evaluate patient’s ECG

Crystalloids Solutions with dissolved crystals in water
Less osmotic pressure than colloids Can equilibrate more quickly between vascular and extravascular spaces 2/3 of crystalloid fluid leaves vascular space < 1 hr 3 mL of crystalloid replaces 1 mL of blood

Hypertonic and Hypotonic Solutions
Hypertonic solutions Higher osmotic pressure than body cells 7.5% saline Hypotonic solutions Lower osmotic pressure than body cells Distilled water 0.45% sodium chloride (0.45% NaCl)

Isotonic Solutions Lactated Ringer's solution Normal saline
Glucose-containing solutions (e.g., D5W)

Colloids Solutions that contain molecules too large to pass through capillary membrane Remain within blood vessels longer Examples Whole blood Plasma Packed red blood cells dextran

Cardiogenic Shock Improve pumping action of heart and manage dysrhythmias Fluid replacement Drug therapy (if needed) Cardiogenic shock due to myocardial ischemia or infarction requires: Reperfusion strategies Possible circulatory support Manage tension pneumothorax and cardiac tamponade

Neurogenic Shock Treatment similar to hypovolemia
Avoid circulatory overload Monitor lung sounds for pulmonary congestion Vasopressors may be indicated

Anaphylactic Shock Subcutaneous epinephrine in acute anaphylactic reactions Other therapy Oral, IV, or IM antihistamines Bronchodilators Steroids reduce inflammatory response Crystalloid volume replacement Airway management

Septic Shock Treatment
Management of hypovolemia (if present) Correction of metabolic acid-base imbalance Antibiotics in one hour.

Hemorrhage

ETIOLOGY OF HAEMORRHAGE CAUSES OF HAEMORRHAGE
INJURY /TRAUMA [+ operations]-It commonly results in tearing or cutting of a blood-vessel-integrity of wall breached Trivial OR Major DISEASES that alter coagulation Congenital –platelet defects Coagulation factor defects Acquired scurvy Sepsis DIC

TYPES OF HAEMORRHAGE AMOUNT OF LOSS --MINOR/MAJOR ACUTE/CHRONIC
ARTERIAL/VENOUS/CAPILLARY/MIXED LOCALIZED/DIFFUSE EXTERNAL/ INTERNAL OVERT/OCCULT

TYPES OF HAEMORRHAGE SPECIFIC TYPES Bruise or ecchymosis .
Extravasation of blood /pouring out of blood into the areolar tissues, which become boggy Haematemesis and melena Haemoptysis . Haematuria Epistaxis

TYPES OF HAEMORRHAGE (operative)
CLASSIFICATION OF SURGICAL HAEMORRHAGE 1-Primary, occurring at the time of the injury 2-Reactionary, or within twenty-four hours of the accident, during the stage of reaction 3-Secondary, occurring at a later period and caused by faulty application of a ligature or septic condition of the wound . In severe haemorrhage, as from the division of a large artery, the patient may collapse and death ensue from syncope . 4-Tertiery : infection

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 (1 of 2)
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 (2 of 2)
Signs and symptoms that may suggest significant internal hemorrhage include: Bright red blood from mouth, rectum, or other orifice Coffee-ground appearance of vomitus 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.

EFFECTS OF HAEMORRHAGE
Depend upon following: Acute loss vs Chronic loss The amount of loss The compensatory mechanisms General state of health

Physiological Response to Hemorrhage
The body’s initial response to hemorrhage is to stop bleeding by chemical means (hemostasis). This vascular reaction involves: Local vasoconstriction Formation of a platelet plug Coagulation Growth of tissue into the blood clot that permanently closes and seals the injured vessel

Haemostasis overview:
BV Injury Platelet Aggregation Activation Blood Vessel Constriction Coagulation Cascade Stable Hemostatic Plug Fibrin formation Reduced Blood flow Contact/ Tissue Factor Primary hemostatic plug Neural

MANAGEMENT OF HAEMORRHAGE
Prevention Precautions during surgery Operative method of control of haemorrhage Blood Transfusion

Hemorrhage Control External Hemorrhage
Direct pressure and pressure dressing General management Direct pressure Elevation Ice Pressure points Constricting band Tourniquet May use a BP cuff by inflating the cuff 20–30 mmHg above the SBP Release may send toxins to heart Lactic acid and electrolytes

Tourniquets are ONLY used as a last resort!

Specific Wound Considerations (1 of 2)
Head Wounds Presentation Severe bleeding Skull fracture Management Gentle direct pressure Fluid drainage from ears and nose DO NOT pack Cover and bandage loosely Neck Wounds Presentation Large vessel can entrap air Management Consider direct digital pressure Occlusive dressing

Specific Wound Considerations (2 of 2)
Gaping Wounds Presentation Multiple sites Gaping prevents uniform pressure Management Bulky dressing Trauma dressing Sterile, non-adherent surface to wound Compression dressing Crush Injury Presentation Difficult to locate source of bleeding Normal hemorrhage control mechanism nonfunctional Management Consider an air-splint and pressure dressing Consider tourniquet

NB Fit Individuals may have more effective compensatory mechanisms before experiencing cardiovascular collapse. Elderly patients or those with chronic medical conditions may have less tolerance to blood loss, less ability to compensate, and may take medications such as betablockers that can potentially blunt the cardiovascular response

SURGICAL HAEMOSTASIS Surgical treatment of haemorrhage DIRECT PRESSURE
In small blood-vessels pressure will be sufficient to arrest haemorrhage permanently . LIGATURE In large vessels with a reef-knot main artery of the limb exposed by dissection at the most accessible point .

SURGICAL HAEMOSTASIS Diathermy Sutures Harmonic devices
Surgical treatment of haemorrhage Diathermy Sutures Harmonic devices

SURGICAL HAEMOSTASIS INTERNAL HAEMORRHAGE /WOUNDS
Causes Penetrating wounds chest,abdomen,neck,limbs Upper GI haemorrhage BleedingUlcers Lower GI haemorrhage Diverticulosis Haemorrhoids Carcinomas

SURGICAL HAEMOSTASIS INTERNAL HAEMORRHAGE /WOUNDS
Principles of management Treat the primary cause Avoid irreversible shock Fluid & electrolytes Blood and blood products

TRANSFUSION MANAGEMENT
Early recognition of significant blood loss it is commoner to see patients who have been under-transfused than over-transfused. It is essential to pay attention to and act on recordings of pulse rate and blood pressure. In a fit patient without cardiac disease, persistent tachycardia − even if blood pressure is maintained − is likely to indicate continuing blood loss.

Transfusion management
All patients require large-bore intravenous cannulas. Central venous pressure monitoring is valuable in major haemorrhage or if there is cardio-respiratory disease. Haemoglobin concentration − interpretation The haemoglobin can underestimate the extent of blood loss in cases of acute haemorrhage before haemodilution has occurred, or can overestimate it if the patient is already anaemic from chronic blood loss.

Concluding Remarks Know how to distinguish different types of shock and treat accordingly Look for early signs of shock SHOCK = hypotension

Shock and Hemorrhage M. Alhashash MD, lecturer of general surgery,

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Shock and Hemorrhage M. Alhashash MD, lecturer of general surgery,

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