Shock and Hemorrhage

M. Alhashash MD,lecturer of general surgery,

hepatobiliary & liver transplant surgery.malhashash@gmail.com 01093368234

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– 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

Baroreceptor Reflexes• 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

Baroreceptor Reflexes

• 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.

Baroreceptor Reflexes

• 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.

Baroreceptor Reflexes

• 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

CV System and Hormone Regulation

• 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

CV System and Hormone Regulation

• 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

• 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

• Alpha cells of pancreas• Triggered by epinephrine

– Action• Causes liver and skeletal muscles to convert glycogen

into glucose• Gluconeogenesis

CV System and Hormone Regulation

• 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%– 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 ShockCellular 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.

Stage 1: Vasoconstriction (2 of 4)

• 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).

Stage 1: Vasoconstriction (3 of 4)

• 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.

Stage 1: Vasoconstriction (4 of 4)

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.

Stage 2: Capillary and Venule Opening (2 of 5)

• 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.

Stage 2: Capillary and Venule Opening (3 of 5)

• 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.

Stage 2: Capillary and Venule Opening (4 of 5)

• 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.

Stage 2: Capillary and Venule Opening (5 of 5)

• 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: Disseminated Intravascular Coagulation (DIC) (2 of 4)

• 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.

Stage 3: Disseminated Intravascular Coagulation (DIC) (3 of 4)

• 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.

Stage 3: Disseminated Intravascular Coagulation (DIC) (4 of 4)

• 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 Decreased Decreased

Respiratory rate (bpm) 14–20 20–30 30–40 >35

Urine output (ml/hour) >30 20–30 5–15 Negligible

CNS symptoms Normal Anxious Confused Lethargic

Cardiogenic Shock

• Results from pump failure– Decreased systolic function– Resultant decreased cardiac output

• Etiologic categories– Myopathic– Arrhythmic– Mechanical– Extracardiac (obstructive)

Obstructive Shock

• Causes– Cardiac Tamponade– Tension Pneumothorax– Massive Pulmonary Embolus

• Signs– cardiac output– PAOP– SVR

Distributive Shock

• Types– 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

Differential Shock Assessment Findings

• 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)

Differential Shock Assessment Findings

• 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 HAEMORRHAGECAUSES 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 HAEMORRHAGEDepend 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

PlateletAggregation

PlateletActivation

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

Surgical treatment of haemorrhage

• Diathermy• Sutures• Harmonic devices

SURGICAL HAEMOSTASISINTERNAL HAEMORRHAGE

/WOUNDS

Causes• Penetrating wounds chest,abdomen,neck,limbs• Upper GI haemorrhage BleedingUlcers• Lower GI haemorrhage Diverticulosis Haemorrhoids Carcinomas

SURGICAL HAEMOSTASISINTERNAL HAEMORRHAGE /WOUNDSPrinciples of managementTreat the primary causeAvoid irreversible shockFluid & electrolytesBlood 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