Bleeding and Shock
Anatomy and physiology of the cardiovascular system
The cardiovascular system serves to provide the body with an adequate blood supply. This blood delivers oxygen and nutrients, hormones, and antibodies to the body’s tissues and removes waste products. Furthermore, the vascular system also helps to regulate body temperature, fluid balance, and blood pressure. The cardiovascular system consists of the heart, blood vessels, and blood.
The heart is a muscular organ with a single purpose - to pump blood to supply oxygen enriched red blood cells to the tissues of the body. The heart is divided down the middle into two sides (left and right) by a wall called the septum. Each side of the heart has an atrium (upper chamber), and a ventricle (lower chamber). Blood leaves each of the four chambers of the heart through a one-way valve. These valves keep the blood moving through the circulatory system in the proper direction. The largest valve is the aortic valve, lying between the left ventricle and the aorta. The aorta, the body's main artery, receives the blood ejected from the left ventricle and delivers it to all the other arteries so that they can carry oxygenated blood to the tissues of the body.
The right side of the heart receives deoxygenated blood from the veins of the body. Blood enters into the right atrium from the vena cavae, which then fill the right ventricle via the tricuspid valve. During contraction of the right ventricle, blood flows into the pulmonary artery via the pulmonic semilunar valve and the pulmonary circulation, where the blood is oxygenated. The left side of the heart receives oxygenated blood from the lungs through the pulmonary veins. Blood enters into the left atrium, and then passes into the left ventricle via the mitral or bicuspid valve. This ventricle of the heart is more muscular than the other because it must pump blood into the aorta and all the other arteries of the body.
The heart contains more than muscle tissue. The heart's electrical system, which is distributed throughout the entire heart, controls heart rate and enables the atria and ventricles to work together. Normal electrical impulses begin in the sinus node, just above the atria. The impulses travel across both atria, causing them to contract. Between the atria and the ventricles, the impulses cross over a bridge of special electrical tissue called the atrioventricular (AV) node. Here the signal is slowed down for about one tenth to two tenths of a second to allow blood time to pass from the atria to the ventricles. The impulses then exit the AV node and spread throughout both ventricles via the purkinje fibres and the bundle of his, causing the ventricular muscle cells to contract.
The systemic circulation is composed of arteries, veins, capillaries and blood. The blood vessels are a closed system of tubes through which blood flows. Arteries and arterioles take blood away from the heart. Arteries have three layers and are thicker and stronger than the other vessels in the body. The middle layer contains smooth muscle and a large amount of elastic fibers. The two most important properties of the arteries are elasticity (the ability to stretch) and contractility (the ability to constrict). The arterial walls become thicker, more muscular, and less elastic as the arteries branch into smaller vessels (arterioles). This smooth muscle in the wall of the artery allows for contraction and relaxation of the vessel; hence vasoconstriction (getting smaller) and vasodilation (getting larger). The arterial system is a high pressure system and contains about 20% of the systemic circulation.
The capillaries are distributors. The vessel walls are composed of a single layer of tissue. This thin wall serves to facilitate the exchange of gases, nutrients and wastes between the tissues and the blood supply. The blood flow at this level is slow which also serves to enhance exchange. Capillaries contain no smooth muscle and therefore lack the ability to actively vasodilate or vasoconstrict. At the origin of the capillary is a precapillary sphincter which acts as a stopcock to control the amount of blood entering the capillary. The capillaries contain about 5% of the systemic circulation.
The veins are similar to the arteries, in that they contain the same three layers as the arteries, but when compared to the arteries they have much thinner walls and fewer elastic fibers. Because of these characteristics the veins are very distensible. Their diameters change passively, in response to small changes in internal pressure. Hence, veins are able to receive large volumes of blood with minimal increases in pressure. The veins not only act as conduits to channel blood from the capillaries to the heart, they have the ability to adjust their total capacity to accommodate variations in the total blood volume. The venous system is a low pressure system.
About 75% of the blood volume is found in the venous system. Of this amount, the majority is found in the veins of the systemic organs (mostly areas like the skin and less essential organs). This reservoir is largely stored blood and is known as the peripheral venous pool. A second, similar reservoir is known as the central venous pool and is comprised of the great veins of the thorax and right atrium. When the peripheral veins constrict (due to stress or exertion) blood that has been stored in the peripheral venous pool is mobilized and enters the central venous pool returning to the heart. This serves to enhance cardiac filling. This system of distributing the blood volume has important implications for the body when it is in a shock situation.
Blood is a viscous fluid which is heavier than water and constitutes about 8% of body weight. Average blood volume in an adult is between 4 and 6 litres. It serves to transport oxygen, carbon dioxide, nutrients, waste products, hormones and enzymes. It serves to regulate pH though buffer systems and protects against toxins and foreign microbes through special combat cells. Because of the large water content in the blood, it serves to regulate body temperature and control the water content of the cells. Finally blood prevents the loss of body fluids through clotting.
Differences between arterial, venous and capillary bleeding
Injuries and some illnesses can disrupt blood vessels and cause bleeding. Typically, bleeding from an open artery is bright red (high in oxygen) and spurts in time with the pulse. The pressure that causes the blood to spurt also makes this type of bleeding difficult to control. As the amount of blood circulating in the body drops so does the patient's blood pressure.
Blood from an open vein is much darker (low in oxygen) and flows steadily. Because it is under less pressure most venous blood does not spurt and is easier to manage. Bleeding from damaged capillary vessels is dark red and oozes from a wound steadily but slowly. It may clot spontaneously.
Components and function of blood:
Red Blood Cells (Erythrocytes)
White Blood Cells (Leukocytes)
Body Substance Isolation (Routine Practices)
For many years, guidelines have required medical personnel to take steps to protect themselves against diseases transmitted through blood. This is known as taking Universal Precautions. More recently the term Body Substance Isolation (BSI) has been used. BSI is an isolation strategy designed to prevent the transmission of potential pathogens between patients. BSI goes a step beyond Universal Precautions and assumes all body substances potentially infectious. For example, feces, nasal secretions, sputum, sweat, tears, urine and vomitus would also be considered infectious.
The current term used in Canada is Routine Practices. Routine Practices integrates the major features of Universal Precautions and BSI. This strategy applies to blood and all body fluids except sweat, regardless of whether or not they contain visible blood. Handwashing is recommended after glove removal regardless of whether or not hands are visibly soiled.
Methods of controlling external bleeding
During the primary survey, control any identified major bleeding by:
Application of a Tourniquet
Application of a tourniquet should only be considered as a last resort in the control of external bleeding.
· Tourniquets may only be used on extremities.
· Rapid transport to medical care should be immediately initiated.
· A commercial tourniquet, such as the SOF-TT, should be used if available.
· The tourniquet should be made from wide material such as a 7 to 10 centimeter (3-4 inch) wide cravat or a blood pressure cuff.
· Prior to application distal circulatory and neurological status must be assessed.
· The tourniquet should be applied as proximal to the injury site as possible.
· If the injury is anywhere below the knee, the tourniquet should be applied above the knee just enough to stop bleeding.
· If a blood pressure cuff is used it should be inflated to 30 mm Hg above the systolic pressure.
· Bleeding, distal circulation and neurological status must be re-evaluated after application of the tourniquet.
Tourniquets have, in the past, been released for three to five minutes every thirty minutes to allow distal circulation. Recent studies in the field and in hospital settings have discarded this as resultant blood loss only contributes to further complications of shock.
· If a tourniquet must be released prior to arrival at definitive care:
· The first release of the tourniquet may be done after the tourniquet has been in place for two hours and then every thirty minutes thereafter.
· Other methods of bleed control must be used while tourniquet is released (direct pressure, elevation, pressure points)
· Direct pressure, elevation, and pressure points should be used to control bleeding during the tourniquet release time.
· Time of tourniquet application, any release, and re-application must be documented. Health care staff at the receiving facility must be aware the patient has a tourniquet in place.
Internal Bleeding and Shock
Internal bleeding can be very serious, especially because you might not be aware that it is happening. Injury or damage to internal organs commonly results in extensive internal bleeding, which can cause hypovolemic shock before you realize the extent of blood loss. A person with a bleeding stomach ulcer may lose a large amount of blood very quickly. Similarly, a person who has a lacerated liver or a ruptured spleen may lose a considerable amount of blood within the abdomen. Yet, the patient has no outward signs of bleeding. Broken bones, especially broken ribs, also may cause serious internal blood loss.
Sometimes this bleeding extends into the chest cavity and the soft tissues of the chest wall. A broken femur can easily result in the loss of 1L or more of blood into the soft tissues of the thigh. Often, the only signs of such bleeding are local swelling and bruising due to the accumulation of blood around the ends of the broken bone.
You must always be alert to the possibility of internal bleeding and assess the patient for related signs and symptoms, particularly if the mechanism of injury is severe. If you suspect that a patient is bleeding internally, you should promptly transport him or her to the hospital.
Mechanism of Injury
Internal bleeding is possible whenever the mechanism of injury suggests that severe forces affected the abdomen and/or the chest. These forces include rapid acceleration, rapid deceleration, shearing, or compression. Internal bleeding commonly occurs as a result of falls, blast injuries, and automobile or motorcycle crashes, whether the patient is a pedestrian, driver, or passenger.
As you assess a patient, look for signs of injury over the chest or abdomen, including contusions, abrasions, lacerations, or other signs of injury or deformity. You should always suspect internal bleeding in a patient who has a penetrating injury, such as a knife or gunshot wound.
Nature of Illness
Non-traumatic internal bleeding can lead to shock just as easily as bleeding caused by trauma. Internal bleeding can occur in the abdomen as a result of inflammatory bowel disease, an aneurysm, a ruptured ectopic pregnancy, or other medical conditions.
Abdominal pain and distention are common in these situations but are not always present. In older patients, dizziness, faintness, or weakness may be the first sign of non-traumatic internal bleeding. Ulcers or other gastrointestinal problems may cause vomiting of blood or bloody diarrhea.
It is not as important for you to know the specific organ or condition involved as it is to recognize that the patient is in shock and respond appropriately.
Signs and Symptoms
The most common symptom of internal abdominal bleeding is acute abdominal pain. Another common sign is bruising around the abdomen. This can occur with or without trauma. Bruising is also called contusion or ecchymosis. A hematoma, a mass of blood in the soft tissues beneath the skin, indicates bleeding into soft tissues and may be the result of either a minor or a severe injury.
Bleeding, however slight, from any body opening is serious. It usually indicates internal bleeding that is not easy to see or control. Bright red bleeding from the mouth, or rectum, or blood in the urine (hematuria) may suggest serious internal injury or disease. Non-menstrual vaginal bleeding is always significant.
Other signs and symptoms of internal bleeding in both trauma and medical patients include the following:
The following signs and symptoms may mean that a closed fracture is causing bleeding.
In addition to the previously listed signs and symptoms, the following may indicate a lacerated spleen or liver. Patients with an injury to either organ may have referred pain in the right shoulder (liver) or left shoulder (spleen). You should suspect internal abdominal bleeding in a patient with referred pain.
The first sign of hypovolemic shock (hypoperfusion) is a change in mental status, such as anxiety, restlessness, or combativeness. In non-trauma patients, weakness, faintness, or dizziness on standing is another early sign. Changes in skin color, or pallor, are seen often in both trauma and medical patients. Later signs of hypoperfusion suggesting internal bleeding include the following:
Casualties with these signs and symptoms are at risk. Some may be in danger. Even if their
bleeding stops, it could begin again at any moment. It could also be a sign their blood volume is too low to bleed anymore. Therefore, prompt transport is necessary.
Controlling internal bleeding or bleeding from the major organs usually requires surgery or other procedures that must be done in the hospital. The main responder role in these cases is to keep the patient still to promote clot formation and to provide high-flow oxygen and prompt transport. However, you can usually control internal bleeding of the extremities by splinting the extremity. You should never use a tourniquet to control the bleeding from closed, internal, soft-tissue injuries.
Follow these steps to care for casualties with possible internal bleeding:
Shock – An abnormal condition of inadequate blood flow to the body’s peripheral tissues associated with life threatening cellular dysfunction: also known as Hypoperfusion.
The Pathophysiological Progression of Shock
The shock state progresses through three stages.
The Compensatory Stage
In this stage cardiac output is decreased. To combat this and to restore cardiac output, the body activates compensatory mechanisms. These mechanisms are nervous, hormonal, and chemical.
Within seconds of detecting the loss of cardiac output, the brain activates the sympathetic branch of the autonomic nervous system. The heart is stimulated to beat faster and harder. Blood vessels to the essential organs i.e.; heart, brain etc. are vasodilated to increase their blood supply. Blood vessels going to non essential areas such as the skin, digestive tract, and kidneys are vasoconstricted to shunt blood to priority organs.
As a follow up to the activation of the sympathetic nervous system, the body releases potent chemicals in an attempt to restore cardiac output. The adrenal glands release epinephrine which causes potent vasoconstriction of both veins and arteries. This vasoconstriction increases blood pressure and facilitates venous return to the right side of the heart.
To summarize, in the compensatory stage of shock, the body recognizes it has a problem and initiates compensatory sympathetic mechanisms in an attempt to maintain cardiac output.
Clinical Findings in Compensatory Shock
Blood Pressure - the blood pressure may be normal with possibly an elevated diastolic reading due to systemic arteriolar vasoconstriction (systolic may also be increased in end stage compensatory shock).
Heart Rate - the heart rate is increased because of sympathetic stimulation. A sinus tachycardia occurs. Depending on the degree of shock and compensatory mechanisms a heart rate of 100 to 150 could be expected.
Skin - the skin is cool, pale, and clammy as a result of peripheral vasoconstriction and increased sweat gland activity.
Level of Consciousness - as the patient enters into the compensatory phase the patient may be restless and anxious. In the latter phase of the compensatory stage the level of consciousness may decrease due to decreased blood supply to the brain. The patient may present as confused and lethargic.
Respirations - may be rapid and shallow with a rate up to two times the normal.
Pupils - may be dilated, but will react to light.
The Decompensated (Progressive) Stage
If the shock is not reversed during the compensatory phase the mechanisms initiated during the compensatory stage to restore the cardiac output begin to have detrimental effects on the patient. This is due to the fact that prolonged and severe vasoconstriction has adverse effects on cellular function, capillary dynamics and specific organ systems.
Because of arteriolar vasoconstriction capillary blood flow is decreased, and oxygen delivery to the cells is reduced. This results in build up and eventual release of toxins from the cells into the tissue. With these toxic changes in the tissue environment, the precapillary sphincters open causing a fluid shift from the vascular compartment into the cellular beds. The end result is a loss of circulating blood volume that results in decreased venous return and reduced cardiac output. The patient further deteriorates, but no significant permanent damage is done if treated promptly and reversed.
Clinical Findings in Decompensated Shock
Blood Pressure - the blood pressure begins to plummet. The pulse pressure (the difference between the diastolic and systolic pressures) decreases (<30 mmHg is significant warning).
Heart Rate - the heart rate continues to increase and may exceed 150 beats per minute. Peripheral pulses will be rapid and thready and may in fact be absent.
Skin - the skin will be cold and clammy and in specific areas (lips, ear lobes, and nail beds) it may be cyanotic.
Level of Consciousness - the level of consciousness is severely altered. The patient may present with bizarre, inappropriate behavior or may be lethargic and unresponsive.
Respirations - the patient will be obviously short of breath and the respirations will be shallow.
Pupils - the pupils will be dilated and sluggish to react.
The Irreversible Stage
The irreversible stage is often referred to as the refractory or end stage shock. In this phase the patient has failed to respond to any form of therapy and is pre-cardiac arrest. Cells have begun to die and downward spiral begins. Cell death = organ death = organ failure = system failure = death. Once a patient reaches this stage of shock, permanent damage and most likely death occurs.
Clinical Findings of Irreversible Shock
Blood Pressure - except for brief periods the patient will not sustain any blood pressure.
Heart Rate - patient will have no peripheral pulses and the rate could be fast, slow, or irregular.
Skin - will be cold, cyanosed, or mottled.
Level of Consciousness - patient will be unconscious and unresponsive
Respirations - may be slow, deep, rapid and shallow, irregular or even absent.
Pupils - will be fixed and dilated.
General Management for Shock
Assessments and management of shock uses the following guidelines. Special considerations are included in the specific classification of shock.
General Signs of Shock
The Classification of Shock
There are many classifications models for shock. For the purpose of this discussion we will identify five.
Hypovolemic shock is an emergent condition in which severe blood and/or fluid loss makes the heart unable to present enough blood to the body. It develops when the intravascular blood volume is decreased in relation to the size of the intravascular compartment (ie: veins and arteries). Hypovolemic shock is usually associated with volume deficits in excess of 15%. Losses of blood volume can either be internal or external. Internal losses may be associated with such events as G.I. bleeds, AAA’s, or internal hemorrhages secondary to trauma.
External losses are associated with blood loss (most common), in the case of trauma and bleeding disorders; plasma, in the case of burns; body fluid, in the case of excessive perspiration, vomiting, and diarrhea. The pathophysiology of hypovolemic shock is that when the intravascular volume is reduced, venous return is reduced, cardiac output decreases, and the blood pressure drops. The end result is poor tissue perfusion which can lead to organ failure.
Signs and symptoms of hypovolemic shock may include:
It may be triggered by events other than the loss of blood and may be due to other fluid or plasma loss.
It may also develop from blood loss not visible to external assessment. Examples of this hidden blood loss may include:
Mechanisms of injury and thorough history assessment may provide information on the development of hidden hemorrhagic shock.
Cardiogenic shock is due to the impaired ability of the heart to pump the blood. Cardiogenic shock is usually the result of severe left ventricular failure, secondary to acute myocardial infarction or congestive heart failure. The hypotension that accompanies this form of shock aggravates the situation by decreasing coronary perfusion. With decreased coronary perfusion, the heart muscle becomes even more damaged, thus establishing a vicious cycle that ultimately results in complete pump failure.
Other causes of cardiogenic shock are:
During cardiogenic shock, the activation of compensatory mechanisms can actually worsen the situation. When the peripheral resistance increases in an attempt to maintain blood pressure, the myocardial workload increases. This, in turn, increases the myocardial oxygen demand, further aggravating myocardial ischemia and infarction. Cardiac output is further depressed.
While the most common cause of cardiogenic shock is severe left ventricular failure, a number of other factors can have the same clinical manifestation. These include chronic progressive heart disease, such as cardiomyopathy, rupture of the papillary heart muscles or interventricular septum, and end-stage valvular disease (mitral stenosis or aortic regurgitation). Most patients who experience cardiogenic shock will have normal blood volume. However, some casualties will be hypovolemic from an excessive use of prescribed diuretics or the severe diaphoresis that accompanies some acute cardiac events. Casualties may also experience relative hypovolemia (neurogenic shock) from the vasodilatory (blood vessel dilation) effects of drugs such as nitroglycerin.
Signs and symptoms of cardiogenic shock may include:
Neurogenic shock may be described as inadequate peripheral resistance due to widespread vasodilation. With this inappropriate vasodilation, a disproportionate amount of blood collects in the capillary bed. This reduces venous return, cardiac output, and arterial blood pressure.
Neurogenic shock is most commonly due to an injury that results in severe spinal cord injury or total transection of the cord. Other causes of neurogenic shock include: central nervous system injury, septicemia from bacterial infection, anaphylactic reaction, insulin overdose, and Addisonian crisis (a disorder of the adrenal glands). In neurogenic shock there is an absence of the sympathetic response. Always suspect neurogenic shock with spinal injuries.
This condition is a type of shock that accompanies a bacterial infection and is often due to the release of endotoxins (poisons) by the bacteria or infected tissues. The toxins are carried by the blood to non-infected areas until the whole body is affected. The toxins then damage the vessel walls throughout the body, causing them to become leaky and unable to constrict well.
Widespread dilation of vessels, in combination with the loss of plasma through the injured vessel walls, results in shock. Septic shock is a complex problem. First, there is an insufficient volume of fluid in the container, because much of the blood has leaked out of the vascular system into the interstitial spaces (hypovolemia). Second, the fluid that has leaked out often collects in the respiratory system, interfering with ventilation. Third, there is a larger-than-normal vascular bed (due to systemic vasodilation) to contain the smaller-than-normal volume of intravascular fluid. Septic shock is almost always a complication of some very serious illness, injury or surgery.
Signs and symptoms include:
Anaphylaxis, or anaphylactic shock, occurs when a person reacts violently to a substance to which he or she has been sensitized. Sensitization means becoming sensitive to a substance that did not initially cause a reaction. Do not be misled by a patient who reports no history of allergic reaction to a substance on first or second exposure. Each subsequent exposure after sensitization tends to produce a more severe reaction. Anaphylaxis is a true medical, life-threatening emergency.
Instances that cause severe allergic reactions commonly fall into the following four categories:
Anaphylactic reactions can develop in minutes or even seconds after contact with the substance to which the patient is allergic. The signs of such allergic reactions are very distinct and not seen with other forms of shock. In anaphylactic shock, there is no loss of blood, no vascular damage, and only a slight possibility of direct cardiac muscular injury. Instead, there is widespread vascular dilation. The combination of poor oxygenation and poor perfusion in anaphylactic shock may easily prove fatal.
Signs and symptoms:
Anaphylactic shock is a true emergency. If the casualty has an epinephrine autoinjector, assist them to use it. High concentrations of oxygen should be delivered to the casualty if you are trained. Be prepared to support respiratory and circulatory functions.