Shock Overview

The word shock is used differently by the medical community and the general public. The connotation by the public is an intense emotional reaction to a stressful situation or bad news. The medical definition of shock is much different.

Medically, shock is defined as a condition where the tissues in the body don’t receive enough oxygen and nutrients to allow the cells to function. This ultimately leads to cellular death, progressing to organ failure, and finally, if untreated, whole body failure and death.

How the body works

Cells need two things to function: oxygen and glucose. This allows the cells to generate energy and do their specific jobs.

Oxygen in the air enters the body through the lungs; where oxygen molecules cross into the smallest blood vessels, the capillaries, and are picked up by red blood cells and attached to hemoglobin molecules. The red blood cells are pushed through the body by the actions of the pumping heart and deliver the oxygen to cells in all the tissues of the body. The hemoglobin then picks up carbon dioxide, the waste product of metabolism, where it is then taken back to the lungs and breathed out into the air, whereby the whole cycle begins again.

Glucose is generated in the body from the foods we eat. Glucose travels in the blood stream and uses an insulin molecule to “open the door,” where it then enters the cell to provide energy for cellular metabolism.

Shock Causes

When things go wrong

If cells are deprived of oxygen, instead of using aerobic (with oxygen) metabolism to function, the cells use the anaerobic (without oxygen) pathway to produce energy. Unfortunately, lactic acid is formed as a by product of anaerobic metabolism. This acid changes the acid-base balance in the blood, making it more acidic, and this leads to situation in which cells begin to leak toxic chemicals into the bloodstream, causing blood vessel walls to become damaged. The anaerobic process ultimately leads to the death of the cell. If enough cells die, organs start to fail, and the body starts to fail and death occurs.

Think of the cardiovascular system of the body as similar to the oil pump in your car. For efficient functioning, the electrical pump needs to work to pump the oil, there needs to be enough oil, and the oil lines need to be intact. If any of these components fail, oil pressure falls and the engine may be damaged. In the body, if the heart, blood vessels, or bloodstream (circulation) fail, then the body fails.

Where things go wrong

The oxygen delivery system to the body’s cells can fail in a variety of ways.

• The amount of oxygen in the air that is inhaled can be decreased.

• Examples include breathing at high altitude or carbon monoxide poisoning.

The lung may be injured and not be able to transfer oxygen to the blood stream. Examples of causes include:

• pneumonia (an infection of the lung),

• congestive heart failure (the lung fills with fluid or pulmonary edema), or

• trauma with collapse or bruising of the lung, or

• pulmonary embolism.

Fig. Effects of inadequate perfusion on cell function.

 

The heart may not be able to adequately pump the blood to the tissues of the body. Examples of causes examples include:

• Heart attack in which  muscle tissue is lost and the heart cannot beat as strong and pump blood throughout the body.

• A rhythm disturbance of the heart occurs when the heart can’t beat in a coordinated way.

• Inflammation of the sac around the heart (pericarditis) or inflammation of the heart muscle due to infections or other causes, in which the effective beating capabilities of the heart are lost.

There may not be enough red blood cells in the blood. If there aren’t enough red blood cells (anemia), theot enough oxygen can be delivered to the tissues with each heart beat. Examples of causes may include:

• acute or chronic bleeding,

• inability of the bone marrow to make red blood cells, or

• the increased destruction of red blood cells by the body (an example, sickle cell disease).

There may not be enough other fluids in the blood vessels. The blood stream contains the blood cells (red, white, and platelets), plasma (which is more than 90% water), and many important proteins and chemicals. Loss of body water or dehydration can cause shock.

The blood vessels may not be able to maintain enough pressure within their walls to allow blood to be pumped to the rest of the body. Normally, blood vessel walls have tension on them to allow blood to be pumped against gravity to areas above the level of the heart. This tension is under the control of the unconscious central nervous system, balanced between the action of two chemicals, adrenaline (epinephrine) and acetylcholine. If the adrenaline system fails, then the blood vessel walls dilate and blood pools in the parts of the body closest to the ground (lower extremities), and may have a difficult time returning to heart to be pumped around the body.

Since one of the steps in the cascade of events causing shock is damage to blood vessel walls, this loss of integrity can cause blood vessels to leak fluid, leading to dehydration which initiates a vicious circle of worsening shock.

Stages of shock

 

There are four stages of shock. As it is a complex and continuous condition there is no sudden transition from one stage to the next.

Initial

During this stage, the hypoperfusional state causes hypoxia, leading to the mitochondria being unable to produce adenosine triphosphate (ATP). Due to this lack of oxygen, the cell membranes become damaged, they become leaky to extra-cellular fluid, and the cells perform anaerobic respiration. This causes a build-up of lactic and pyruvic acid which results in systemic metabolic acidosis. The process of removing these compounds from the cells by the liver requires oxygen, which is absent.

Compensatory (Compensating)

This stage is characterised by the body employing physiological mechanisms, including neural, hormonal and bio-chemical mechanisms in an attempt to reverse the condition. As a result of the acidosis, the person will begin to hyperventilate in order to rid the body of carbon dioxide (CO2). CO2 indirectly acts to acidify the blood and by removing it the body is attempting to raise the pH of the blood. The baroreceptors in the arteries detect the resulting hypotension, and cause the release of adrenaline and noradrenaline.

Fig. Compensatory mecanisms

Noradrenaline causes predominately vasoconstriction with a mild increase in heart rate, whereas adrenaline predominately causes an increase in heart rate with a small effect on the vascular tone; the combined effect results in an increase in blood pressure. Renin-angiotensin axis is activated and arginine vasopressin is released to conserve fluid via the kidneys.

Fig. Compensatory mecanisms

Also, these hormones cause the vasoconstriction of the kidneys, gastrointestinal tract, and other organs to divert blood to the heart, lungs and brain. The lack of blood to the renal system causes the characteristic low urine production. However the effects of the Renin-angiotensin axis take time and are of little importance to the immediate homeostatic mediation of shock .

Progressive (Decompensating)

Fig. Compensatory mecanisms

 

Should the cause of the crisis not be successfully treated, the shock will proceed to the progressive stage and the compensatory mechanisms begin to fail. Due to the decreased perfusion of the cells, sodium ions build up within while potassium ions leak out. As anaerobic metabolism continues, increasing the body’s metabolic acidosis, the arteriolar smooth muscle and precapillary sphincters relax such that blood remains in the capillaries. Due to this, the hydrostatic pressure will increase and, combined with histamine release, this will lead to leakage of fluid and protein into the surrounding tissues. As this fluid is lost, the blood concentration and viscosity increase, causing sludging of the micro-circulation. The prolonged vasoconstriction will also cause the vital organs to be compromised due to reduced perfusion. If the bowel becomes sufficiently ischemic, bacteria may enter the blood stream, resulting in the increased complication of endotoxic shock.

Refractory (Irreversible)

At this stage, the vital organs have failed and the shock cao longer be reversed. Brain damage and cell death have occurred. Death will occur imminently.

Fig.  Effect of bood volume loss on arterial pressure

 

A medical emergency is an injury or illness that is acute and poses an immediate risk to a person’s life or long term health. These emergencies may require assistance from another person, who should ideally be suitably qualified to do so, although some of these emergencies can be dealt with by the victim themselves. Dependent on the severity of the emergency, and the quality of any treatment given, it may require the involvement of multiple levels of care, from a first aider to an emergency physician through to specialist surgeons.

 

Classification of shock

Shock is identified in most patients by hypotension and inadequate organ perfusion, which may be caused by either low cardiac output or low systemic vascular resistance. Circulatory shock can be subdivided into 4 distinct classes on the basis of underlying mechanism and characteristic hemodynamics, as follows:

• Hypovolemic shock

• Obstructive shock

• Distributive shock

• Cardiogenic shock

These classes of shock should be considered and systemically differentiated before establishing a definitive diagnosis of septic shock.

Hypovolemic shock results from the loss of blood volume caused by such conditions as gastrointestinal (GI) bleeding, extravasation of plasma, major surgery, trauma, and severe burns. The patient demonstrates tachycardia, cool clammy extremities, hypotension, dry skin and mucus membranes, and poor turgor.

Obstructive shock results from impedance of circulation by an intrinsic or extrinsic obstruction. Pulmonary embolism and pericardial tamponade both result in obstructive shock.

Distributive shock is caused by such conditions as direct arteriovenous shunting and is characterized by decreased resistance or increased venous capacity from the vasomotor dysfunction. These patients have high cardiac output, hypotension, large pulse pressure, a low diastolic pressure, and warm extremities with a good capillary refill. These findings on physical examination strongly suggest a working diagnosis of septic shock.

Cardiogenic shock is characterized by primary myocardial dysfunction, resulting in the inability of the heart to maintain adequate cardiac output. These patients demonstrate clinical signs of low cardiac output, while evidence exists of adequate intravascular volume. The patients have cool clammy extremities, poor capillary refill, tachycardia, narrow pulse pressure, and a low urine output.

Shock – Specific Types

Hypovolemic and Hemorrhagic Shock

Hypovolemic Shock

There needs to be enough red blood cells and water in the blood for the heart to push the fluids around within the blood vessels. When the body becomes dehydrated, there may be enough red blood cells, but the total volume of fluid is decreased, and pressure within the system decreases. Cardiac output is the amount of blood that the heart can pump out in one minute. It is calculated as the stroke volume (how much blood each heart beat can push out) multiplied by the heart rate (how fast the heart beats each minute). If there is less blood in the system to be pumped, the heart speeds up to try to keep its output steady.

Water makes up 90% of blood. If the body becomes dehydrated because water is lost or fluid intake is inadequate, the body tries to maintain cardiac output by making the heart beat faster. But as the fluid losses mount, the body’s compensation mechanisms fail, and shock may ensue.

Hypovolemic (hypo=low + volemic=volume) shock due to water loss can be the endpoint of many illnesses, but the common element is the lack of fluid within the body.

Gastroenteritis can cause significant water loss from vomiting and diarrhea, and is a common cause of death in third world countries. Heat exhaustion and heat stroke is caused by excessive water loss through sweating as the body tries to cool itself. Patients with infections can lose significant amounts of water from sweating. People with diabetes who have diabetic ketoacidosis lose significant water because of because of elevated blood sugar that cause excess water to be excreted in the urine.

Ultimately in hypovolemic shock, the patient cannot replace the amount of fluid that was lost by drinking enough water, and the body is unable to maintain blood pressure and cardiac output. In all shock states, when cells start to malfunction waste products build up, a downward spiral of cell death begins, increased acidosis occurs, and a worsening body environment leads to further cell death – and ultimately organ failure.

Hemorrhagic Shock

A subset of hypovolemic shock occurs when there is significant bleeding that occurs relatively quickly. Trauma is the most common example of bleeding or hemorrhage, but bleeding can occur from medical conditions such as:

• Bleeding from the gastrointestinal tract is common; examples include stomach or duodenal ulcers, colon cancers or diverticulitis.

• In women, excessive bleeding can occur from the uterus.

• People with cancers or leukemia have the potential to bleed spontaneously from a variety of sources if their bone marrow does not make enough clotting factors.

• Patients who are taking blood thinners (anticoagulant medications) can bleed excessively as well.

 

Hemorrhage classes

Class	Blood loss	Response	Treatment
I	<15 %(0.75 l)	min. fast heart rate, normal blood pressure	minimal
II	15-30 %(0.75-1.5 l)	fast heart rate, min. low blood pressure	intravenous fluids
III	30-40 %(1.5-2 l)	very fast heart rate, low blood pressure, confusion	fluids and packed RBCs
IV	>40 %(>2 l)	critical blood pressure and heart rate	aggressive interventions

 

Blood loss has two effects on the body. First, there is a loss of volume within blood vessels to be pumped (see hypovolemic shock) and second, a reduced oxygen carrying capacity occurs because of the loss of red blood cells. Otherwise healthy people can lose up to 10% of their blood volume (about the amount that a person donates at a blood drive) without becoming symptomatic with weakness, lightheadedness, or shortness of breath.

The treatment of hemorrhagic shock depends on the cause. Finding and controlling the source of bleeding is of paramount importance. Intravenous fluids are used to help with resuscitation to increase the fluid volume within the blood vessel space, but blood transfusion is not always mandatory. If the bleeding is controlled and the patient becomes more stable, the bone marrow may be allowed to replenish the red blood cells that were lost.

If the red blood cell count in the blood decreases gradually over time, either because of bleeding or the inability of the body to make enough new red cells, the body can adjust to the lower levels to maintain adequate cell perfusion, but the individual’s exercise tolerance may decrease. This means that they may do well iormal daily activities but find that routine exercise or household activities bring on weakness or shortness of breath. The treatment depends on the underlying diagnosis, since it isn’t a total fluid problem as in hypovolemic shock.

Cardiogenic, Neurogenic, and Hypoglycemic Shock

Cardiogenic Shock

When the heart loses its ability to pump blood to the rest of the body, blood pressure decreases. Although there may be enough red blood cells and oxygen, they can’t get to the cells that need them.

Fig. Mechanisms of cardiogenic shock

 

The heart is a muscle itself and needs blood supply to work. When a heart attack occurs, the blood supply to part of the heart is lost, and that can stun and irritate the heart muscle so that it isn’t able to beat with an appropriate squeeze to push blood out to the rest of the body. This decreases stroke volume, and cardiac output falls.

Treatment includes trying to restore blood supply and the use of medications to support blood pressure. In more dire circumstances, machines can be used to assist the heart to support blood pressure.

Neurogenic Shock

There are involuntary muscles within blood vessel walls that maintain the squeeze so that the volume within the vessels stays constant even if the body changes position against gravity. As an analogy, is when you get up out of bed in the morning. If your blood vessels didn’t squeeze a little tighter, gravity would make the blood flow to your feet, the lowest part of your body, away from your brain, and you might pass out. The squeeze is maintained by signals from nerves in the sympathetic trunk, a long bundle of fibers running from the skull to the tailbone alongside the vertebral column.

In brain or spinal injury, the sympathetic trunk stops working and blood vessels dilate and result in blood pooling away from the heart. Since there isn’t enough blood returning to the heart, the heart has a hard time pumping blood through the body.

Treatment includes fluids and medications to increase the tone in the blood vessel walls.

Hypoglycemic Shock and Hyperglycemia

High or low blood sugars are almost always associated with diabetes. In people with diabetes, the body does not make enough insulin to permit glucose to enter the cells for aerobic metabolism. As treatment, insulieeds to be injected, or medicatioeeds to be taken to boost the body’s lower insulin production. There must be a balance between how much medication is taken and how much food is eaten.

If not enough food is ingested, then the blood sugar drops (hypoglycemia) and no glucose is available to enter the cells, even if there is enough insulin to permit glucose to enter the cells. The brain is very susceptible to low blood sugars, and coma has a very quick onset. Treatment is providing sugar. If the person is awake enough to swallow, a sugar solution by mouth is used, otherwise, intravenous fluids containing glucose are provided. If the lack of sugar was of short duration, the person will awaken almost immediately after treatment. If blood sugars remain low for prolonged periods of time, the brain’s ability to recover is potentially lost.

When blood sugar levels spiral high out of control, there is risk of significant dehydration and shock. If there is not enough insulin in the blood stream, cells cannot use the glucose that is present, and instead turn to an alternative anaerobic metabolism to generate energy. Since glucose can’t enter cells to be used, hyperglycemia (hyper= high + gly=sugar = emia) occurs as the glucose level builds up in the blood stream. The kidneys try to excrete excess sugar, but because of chemical concentration gradients between blood and urine, significant amounts of water also are lost. The body quickly becomes dehydrated and blood pressure drops, decreasing blood flow to cells. Cells which are now lacking glucose inside them are now starved of oxygen and turn to anaerobic metabolism, causing acid waste product build up. Excess acid in the body changes the metabolism for all organs, making it more difficult for oxygen to be used. Conditions will continue worsen until insulin and significant fluids are given to the patient.

Anaphylactic Shock

When the body develops an allergic reaction to some outside chemical or substance, it can activate its immune system to combat that substance. On occasion, there can be an excess response and multiple organ systems in the body can be affected and fail. This is known as anaphylaxis. Mast cells and basophils (a type of white blood cell) that contain histamine become unstable and leak their contents to affect the muscles of the lung, heart and blood vessels. These are smooth muscles that are part of the regulatory system of the body and are not under conscious control.

• The muscles that surround bronchial tubes go into spasm and cause wheezing and shortness of breath.

• The muscles that surround blood vessels dilate, causing blood pressure to drop.

• The histamine also causes flushing of the skin, urticaria (hives), vomiting and diarrhea.

• A variety of mechanisms cause the heart muscle to pump weakly and blood vessels to leak fluid.

The combination of these effects decrease blood flow and oxygen supply to cells in the body and can result in shock.

The most common causes of anaphylactic shock include allergic reactions to foods (especially peanuts), antibiotics, and bee and wasp stings. Children are often allergic to eggs, soy, and milk.

These allergens can cause the immune system to turn on the potential cascade to shock. Many patients have allergic reactions that are less severe and can just involve hives, but others can develop shortness of breath, wheezing, swelling of the tongue and mouth, and difficulty swallowing.

Medical interventions include injections of antihistamine like diphenhydramine (Benadryl), corticosteroids and adrenaline (epinephrine).

Patients with major allergic reactions must try to avoid the chemical trigger. They also often carry an Epipen (epinephrine injection kit) to inject themselves with epinephrine should an allergic reaction occur.

Shock Symptoms

Shock is defined as abnormal metabolism at the cellular level. Since it is not easy to directly measure cellular problems, the symptoms of shock are indirect measurements of cellular function. Shock is the end stage of all diseases, and symptoms will often be dependant on the underlying cause.

Vital signs

As the patient goes through the various stages of shock, vital signs change. In the early stages, the body tries to compensate by moving fluids around from within cells to the blood stream with an attempt to maintain blood pressure in a normal range. However, there may be a slight rise in the heart rate (tachycardia = tachy or fast + cardia or heart). For example, donating blood. A unit of blood (or about 10% of the bloods volume) is removed, yet the body compensates well, except for a little lightheadedness, which is often resolved by drinking fluids. Another example is exercising and forgetting to drink enough fluids and feeling a little tired at the end of the day.

As the body loses the ability to compensate, the breathing rate gets faster and the tachycardia increases as the body tries to pack as much oxygen onto the remaining red blood cells as possible and deliver them to the cells. Unfortunately, blood pressure starts to drop (hypotension=hypo or low + tension= pressure) as compensation mechanisms fail.

Body function

Cells don’t receive enough oxygen and the organs that they comprise begin to fail. All organs may be affected.

• As the brain is affected, the patient may become confused or lose consciousness (coma).

• There may be chest pain as the heart itself doesn’t get an adequate oxygen supply.

• Diarrhea may occur as the large intestine becomes irritated due to hypotension.

• Kidneys may fail and the body may stop producing urine.

• The skin becomes clammy and pale.

Shock Diagnosis

The approach to the patient in shock requires that treatment occur at the same time as the diagnosis occurs. The source of the underlying disease needs to be found. Sometimes it is obvious, for example, a trauma victim bleeding from a wound. Other times, the diagnosis is elusive. The type of tests will depend upon the underlying condition.

The diagnosis is most often found through the medical history. A thorough physical examination will be undertaken and the patients vital signs monitored.

• Patient vital signs monitored might include continual blood pressure and heart rate monitoring, and oxygen measurement. Special catheters may be inserted into the large veins in the neck, chest, arm, or groin and threaded near the heart or into the pulmonary artery, to measure pressures close to the heart, which may be a better indicator of the body’s fluid status. Other catheters may be inserted into arteries (arterial lines) to measure blood pressures more directly. Tubes may be placed in the bladder (Foley catheter) to measure urine output.

• Blood laboratory tests will be performed (the type dependent on the underlying disease or condition).

• Radiologic tests may be performed dependent on the underlying illness.

Differential diagnosis

Shock is a common end point of many medical conditions. It has been divided into four main types based on the underlying cause: hypovolemic, distributive, cardiogenic and obstructive. A few additional classifications are occasionally used including: endocrinologic shock.

Hypovolemic

This is the most common type of shock and is caused by insufficient circulating volume. Its primary cause is hemorrhage (internal and/or external), or loss of fluid from the circulation. Vomiting and diarrhea are the most common cause in children. With other causes including burns, environmental exposure and excess urine loss due to diabetic ketoacidosis and diabetes insipidus.

 Cardiogenic

This type of shock is caused by the failure of the heart to pump effectively. This can be due to damage to the heart muscle, most often from a large myocardial infarction. Other causes of cardiogenic shock include dysrhythmias, cardiomyopathy/myocarditis, congestive heart failure (CHF), contusio cordis, or cardiac valve problems.

Obstructive

Obstructive shock is due to obstruction of blood flow outside of the heart. Several conditions can result in this form of shock.

• Cardiac tamponade in which fluid in the pericardium prevents inflow of blood into the heart (venous return). Constrictive pericarditis, in which the pericardium shrinks and hardens, is similar in presentation.

• Tension pneumothorax Through increased intrathoracic pressure, bloodflow to the heart is prevented (venous return).

• Pulmonary embolism is the result of a thromboembolic incident in the blood vessels of the lungs and hinders the return of blood to the heart.

• Aortic stenosis hinders circulation by obstructing the ventricular outflow tract

Distributive

Distributive shock is due to impaired utilization of oxygen and thus production of energy by the cell. Examples of this form of shock are:

• Septic shock is the most common cause of distributive shock. Caused by an overwhelming systemic infection resulting in vasodilation leading to hypotension. Septic shock can be caused by Gram negative bacteria such as (among others) Escherichia coli, Proteus species, Klebsiella pneumoniae which release an endotoxin which produces adverse biochemical, immunological and occasionally neurological effects which are harmful to the body, and other Gram-positive cocci, such as pneumococci and streptococci, and certain fungi as well as Gram-positive bacterial toxins. Septic shock also includes some elements of cardiogenic shock. In 1992, the ACCP/SCCM Consensus Conference Committee defined septic shock: “. . .sepsis-induced hypotension (systolic blood pressure <90 mm Hg or a reduction of 40 mm Hg from baseline) despite adequate fluid resuscitation along with the presence of perfusion abnormalities that may include, but are not limited to, lactic acidosis, oliguria, or an acute alteration in mental status. Patients who are receiving inotropic or vasopressor agents may have a normalized blood pressure at the time that perfusion abnormalities are identified.”

• Anaphylactic shock Caused by a severe anaphylactic reaction to an allergen, antigen, drug or foreign protein causing the release of histamine which causes widespread vasodilation, leading to hypotension and increased capillary permeability.

• High spinal injuries may cause neurogenic shock. The classic symptoms include a slow heartrate due to loss of cardiac sympathetic tone and warm skin due to dilation of the peripheral blood vessels. (This term can be confused with spinal shock which is a recoverable loss of function of the spinal cord after injury and does not refer to the haemodynamic instability per se.)

Endocrine

Based on endocrine disturbances such as:

• Hypothyroidism (Can be considered a form of Cardiogenic shock) in critically ill patients, reduces cardiac output and can lead to hypotension and respiratory insufficiency.

• Thyrotoxicosis (Cardiogenic shock)

• may induce a reversible cardiomyopathy.

• Acute adrenal insufficiency (Distributive shock) is frequently the result of discontinuing corticosteroid treatment without tapering the dosage. However, surgery and intercurrent disease in patients on corticosteroid therapy without adjusting the dosage to accommodate for increased requirements may also result in this condition.

• Relative adrenal insufficiency (Distributive shock) in critically ill patients where present hormone levels are insufficient to meet the higher demands

 

Shock Treatment

Shock Self-Care at Home

If you come upon a person in shock, the initial response should be to call 101 in Ukraine (911 in Usa) and activate the emergency response system. Self-care at home is not appropriate.

Lay the person down in a safe place and try to keep them warm and comfortable.

If the patient is not awake, is not breathing, and has no heartbeat, it is appropriate to start chest compressions following the American Heart Association guidelines. It is important to send someone to get an AED if one is available.

Shock Medical Treatment

• EMS personnel are well trained in the initial assessment of the patient in shock. The first course of action is to make certain that the ABCs have been assessed. The so-called ABCs are:

• Airway: assessment of whether the patient is awake enough to try to take their own breaths and/or if there is there anything blocking the mouth or nose.

• Breathing: assessment of the adequacy of breathing and whether it may need to be assisted with mouth-to-mouth resuscitation or more aggressive interventions like a bag and mask or intubation with an endotracheal tube and a ventilator.

• Circulation: assessment of the adequacy of the blood pressure adequate and determination of whether intravenous lines are needed for delivery of fluid or medications to support the blood pressure.

Fig. Shock resuscitation

 

• If there is bleeding that is obvious, attempts to control it with direct pressure will be attempted.

• A fingerstick blood sugar will be checked to make certain that hypoglycemia (low blood sugar) does not exist.

• In the emergency department, diagnosis and treatment will occur at the same time.

• Patients will be treated with oxygen supplementation through nasal cannulae, a face mask, or endotracheal intubation. The method and amount of oxygen will be titrated to make certain enough oxygen is available for the body to use. Again, the goal will be to pack each hemoglobin molecule with oxygen.

• Blood may be transfused if bleeding (hemorrhage) is the cause of the shock state. If bleeding is not the case, intravenous fluids will be given to bolster the volume of fluids within the blood vessels.

• Intravenous drugs can be used to try to maintain blood pressure (vasopressors). They work by stimulating the heart to beat stronger and by squeezing blood vessels to increase the flow within them.

Shock Prognosis

Shock is a culmination of multiple organ systems in the body that have failed or are in the process of failing. Even with the best of care, there is a significant risk of death. The mortality rate for shock depends upon the type and reason for the shock, and the age and underling health condition of the patient.

 

 

Hemorrhagic Shock

 

Background

Shock is a state of inadequate perfusion, which does not sustain the physiologic needs of organ tissues. Many conditions, including blood loss but also including nonhemorrhagic states such as dehydration, sepsis, impaired autoregulation, obstruction, decreased myocardial function, and loss of autonomic tone, may produce shock or shocklike states.

Pathophysiology

In hemorrhagic shock, blood loss exceeds the body’s ability to compensate and provide adequate tissue perfusion and oxygenation. This frequently is due to trauma, but it may be caused by spontaneous hemorrhage (eg, GI bleeding, childbirth), surgery, and other causes.

Most frequently, clinical hemorrhagic shock is caused by an acute bleeding episode with a discrete precipitating event. Less commonly, hemorrhagic shock may be seen in chronic conditions with subacute blood loss.

Fig. Classes of hemorragical shock

Physiologic compensation mechanisms for hemorrhage include initial peripheral and mesenteric vasoconstriction to shunt blood to the central circulation. This is then augmented by a progressive tachycardia. Invasive monitoring may reveal an increased cardiac index, increased oxygen delivery (ie, DO₂), and increased oxygen consumption (ie, VO₂) by tissues. Lactate levels, acid-base status, and other markers also may provide useful indicators of physiologic status. Age, medications, and comorbid factors all may affect a patient’s response to hemorrhagic shock.

Failure of compensatory mechanisms in hemorrhagic shock can lead to death. Without intervention, a classic trimodal distribution of deaths is seen in severe hemorrhagic shock. An initial peak of mortality occurs within minutes of hemorrhage due to immediate exsanguination. Another peak occurs after 1 to several hours due to progressive decompensation. A third peak occurs days to weeks later due to sepsis and organ failure.

Epidemiology

Frequency

United States

Accidental injuries remain the leading cause of death in individuals aged 1-44 years.Hemorrhagic shock is a leading cause of death among trauma patients.

History

History taking should address the following:

• Specific details of the mechanism of trauma or other cause of hemorrhage are essential.

• Inquire about a history of bleeding disorders and surgery.

• Prehospital interventions, especially the administration of fluids, and changes in vital signs should be determined. Emergency medical technicians or paramedics should share this information.

Physical

Findings at physical examination may include the following:

• Head, ears, eyes, nose, and throat

• Sources of hemorrhage usually are apparent.

• The blood supply of the scalp is rich and can produce significant hemorrhage.

• Intracranial hemorrhage usually is insufficient to produce shock, except possibly in very young individuals.

• Chest

• Hemorrhage into the thoracic cavities (pleural, mediastinal, pericardial) may be discerned at physical examination. Ancillary studies often are required for confirmation.

• Signs of hemothorax may include respiratory distress, decreased breath sounds, and dullness to percussion.

• Tension hemothorax, or hemothorax with cardiac and contralateral lung compression, produces jugular venous distention and hemodynamic and respiratory decompensation.

• With pericardial tamponade, the classic triad of muffled heart sounds, jugular venous distention, and hypotension often is present, but these signs may be difficult to appreciate in the setting of an acute resuscitation.

• Abdomen

• Injuries to the liver or spleen are common causes of hemorrhagic shock. Spontaneous rupture of abdominal aortic aneurysm (AAA) may also cause severe intra-abdominal hemorrhage and shock.

• Blood irritates the peritoneal cavity; diffuse tenderness and peritonitis are common when blood is present. However, the patient with altered mental status or multiple concomitant injuries may not have the classic signs and symptoms at physical examination.

• Progressive abdominal distention in hemorrhagic shock is highly suggestive of intra-abdominal hemorrhage.

• Pelvis

• Fractures can produce massive bleeding. Retroperitoneal bleeding must be suspected.

• Flank ecchymosis may indicate retroperitoneal hemorrhage.

• Extremities

• Hemorrhage from extremity injuries may be apparent, or tissues may obscure significant bleeding.

• Femoral fractures may produce significant blood loss.

• Nervous system

• Agitation and combativeness may be seen in the initial stages of hemorrhagic shock.

• These signs are followed by a progressive decline in level of consciousness due to cerebral hypoperfusion or concomitant head injury.

Differential Diagnoses

·        Abdominal Trauma, Blunt

·        Abdominal Trauma, Penetrating

·        Abortion, Complications

·        Anemia, Acute

·        Anemia, Chronic

·        Blast Injuries

·        Disseminated Intravascular Coagulation

·        Pneumothorax, Tension and Traumatic

·        Pregnancy, Ectopic

·        Pregnancy, Postpartum Hemorrhage

·        Pregnancy, Trauma

·        Shock, Cardiogenic

·        Shock, Hypovolemic

·        Shock, Septic

·        Spinal Cord Injuries

Laboratory Studies

• Laboratory studies are essential in management of many forms of hemorrhagic shock. Baseline levels are determined frequently, but these infrequently change the initial management after trauma. Serial evaluations of the following can help guide ongoing therapy.

• CBC

• Prothrombin time and/or activated partial thromboplastin time

• Urine output rate can help guide adequacy of perfusion.

• ABGs (Levels reflect acid-base and perfusion status.)

• Lactate and base deficit are used in some centers to indicate the degree of metabolic debt. Clearance of these markers over time can reflect the adequacy of resuscitation.

• Typed and crossmatched packed red blood cells should be ordered immediately based on clinical suspicion of hemorrhagic shock. Fresh frozen plasma and platelets also may be required to correct or prevent coagulopathies that develop in severe hemorrhagic shock.

Imaging Studies

Cervical spine, chest, and pelvis radiographs are the standard screening images for severe trauma. Other radiographs may be indicated for orthopedic injuries.

Computed tomography can be used to image the appropriate region of suspected injury. CT scanning frequently is the method of choice for evaluating possible intra-abdominal and/or retroperitoneal sources of hemorrhage in stable patients (see the image below). Oral contrast material may not increase the diagnostic yield of abdominal CT scanning in blunt trauma. Scanning should not be delayed to administer oral contrast material.

Fig. CT scan of a 26-year-old man after a motor vehicle crash shows a significant amount of intra-abdominal bleeding.

Bedside ultrasonography abdominal ultrasonography can be very useful for the rapid detection of AAA and free intra-abdominal fluid. Thoracic ultrasonographic findings can immediately confirm hemothorax or pericardial tamponade.

Directed angiography may be diagnostic and therapeutic. Interventional radiologists have had good success achieving hemostasis in hemorrhage caused by a variety of vessels and organs.

Other Tests

• An ECG can be useful for detecting dysrhythmias and cardiac sequelae of shock.

• Tissue oximetry using Near Infrared Spectroscopy (NIRS) shows promise for continuous noninvasive measurement of perfusion in hemorrhagic shock and other conditions.

Procedures

• Tube thoracostomy is necessary in significant hemothorax with or without pneumothorax.

• Central venous access facilitates fluid resuscitation and monitoring of central venous pressure and is necessary if peripheral intravenous access is inadequate or impossible to obtain.

• Diagnostic peritoneal lavage is used to detect intra-abdominal blood, fluid, and intestinal contents. It is sensitive but not specific for abdominal injury. It is not used to evaluate the retroperitoneum, which can hold significant hemorrhage, and does not identify the source of hemorrhage.

Prehospital Care

The standard care consists of rapid assessment and expeditious transport to an appropriate center for evaluation and definitive care.

Intravenous access and fluid resuscitation are standard. However, this practice has become controversial.

• For many years, aggressive fluid administration has been advocated to normalize hypotension associated with severe hemorrhagic shock. Recent studies of urban patients with penetrating trauma have shown that mortality increases with these interventions; these findings call these practices into question.

• Reversal of hypotension prior to the achievement of hemostasis may increase hemorrhage, dislodge partially formed clots, and dilute existing clotting factors. Findings from animal studies of uncontrolled hemorrhage support these postulates. These provocative results raise the possibility that moderate hypotension may be physiologically protective and should be permitted, if present, until hemorrhage is controlled.

• These findings should not yet be clinically extrapolated to other settings or etiologies of hemorrhage. The ramifications of permissive hypotension in humans remain speculative, and safety limits have not been established yet.

Emergency Department Care

Management of hemorrhagic shock should be directed toward optimizing perfusion of and oxygen delivery to vital organs.

Diagnosis and treatment of the underlying hemorrhage must be performed rapidly and concurrently with management of shock.

Supportive therapy, including oxygen administration, monitoring, and establishment of intravenous access (eg, 2 large-bore catheters in peripheral lines, central venous access), should be initiated.

• Intravascular volume and oxygen-carrying capacity should be optimized.

• In addition to crystalloids, some colloid solutions, hypertonic solutions, and oxygen-carrying solutions (eg, hemoglobin-based and perfluorocarbon emulsions) are used or being investigated for use in hemorrhagic shock.

• Blood products are often required in severe hemorrhagic shock. Replacement of lost components using red blood cells (RBCs), fresh frozen plasma (FFP), and platelets may be essential. The ideal ratio of RBCs to FFP remains undetermined. Recent combat experience has suggested that aggressive use of FFP may reduce coagulopathies and improve outcomes.

Determination of the site and etiology of hemorrhage is critical to guide further interventions and definitive care.

Control of hemorrhage may be achieved in the ED, or control may require consultations and special interventions.

Consultations

Consult a general or specialized surgeon, gastroenterologist, obstetrician-gynecologist, interventional radiologist, and others as required.

Medication Summary

Achievement of hemostasis, fluid resuscitation, and use of blood products are the mainstays of treatment. Pressor agents may be useful in some settings (eg, spinal shock), but these agents should not be substitutes for adequate volume resuscitation and blood product replacement.

Tranexamic acid (TXA) is an inexpensive antifibrinolytic drug that promotes blood clotting by preventing blood clots from breaking down. It has been shown to reduce mortality in trauma patients with uncontrolled hemorrhage. Further studies are planned to determine specific recommendations for TXA administration.

Vasopressors

Class Summary

These agents augment both coronary and cerebral blood flow during the low-flow state associated with shock.

 

Dopamine (Intropin)

 

Stimulates both adrenergic and dopaminergic receptors. Hemodynamic effect is dependent on the dose. Lower doses predominantly stimulate dopaminergic receptors that in turn produce renal and mesenteric vasodilation. Higher doses produce cardiac stimulation and renal vasodilation

Norepinephrine (Levophed)

 

Used in protracted hypotension following adequate fluid-volume replacement. Stimulates beta1-adrenergic and alpha-adrenergic receptors, which, in turn, increase cardiac muscle contractility and heart rate, as well as vasoconstriction; result is increased systemic BP and coronary blood flow.

 

Vasopressin (Pitressin)

 

Has vasopressor and ADH activity. Increases water resorption at distal renal tubular epithelium (ADH effect) and promotes smooth muscle contraction throughout the vascular bed of the renal tubular epithelium (vasopressor effects); however, vasoconstriction also is increased in splanchnic, portal, coronary, cerebral, peripheral, pulmonary, and intrahepatic vessels.

Epinephrine (Adrenalin, Bronitin)

 

Used for hypotension refractory to dopamine. Alpha-agonist effects include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta2-agonist effects include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects.

Further Inpatient Care

• Admit the patient to an ICU, surgical ICU, or pediatric ICU.

• Patients with hemorrhagic shock should be admitted to an intensive care or monitored setting appropriate for the underlying condition and physiologic state.

Transfer

• In hospitals without facilities to provide definitive care, patients should be stabilized as much as possible and transferred to a facility with a higher level of care.

Complications

• Coagulopathies may occur in severe hemorrhage. Fluid resuscitation, while necessary, may exacerbate coagulopathies.

• Sepsis and multiple organ system failure occur days after acute hemorrhagic shock.

• Death is a possible complication.

Hypovolemic Shock 

Hypovolemic shock refers to a medical or surgical condition in which rapid fluid loss results in multiple organ failure due to inadequate circulating volume and subsequent inadequate perfusion. Most often, hypovolemic shock is secondary to rapid blood loss (hemorrhagic shock).

Acute external blood loss secondary to penetrating trauma and severe GI bleeding disorders are 2 common causes of hemorrhagic shock. Hemorrhagic shock can also result from significant acute internal blood loss into the thoracic and abdominal cavities.

Two common causes of rapid internal blood loss are solid organ injury and rupture of an abdominal aortic aneurysm. Hypovolemic shock can result from significant fluid (other than blood) loss. Two examples of hypovolemic shock secondary to fluid loss include refractory gastroenteritis and extensive burns. The remainder of this article concentrates mainly on hypovolemic shock secondary to blood loss and the controversies surrounding the treatment of this condition. The reader is referred to other articles for discussions of the pathophysiology and treatment for hypovolemic shock resulting from losses of fluid other than blood.

The many life-threatening injuries experienced during the wars of the 1900s have significantly affected the development of the principles of hemorrhagic shock resuscitation. During World War I, W.B. Cannon recommended delaying fluid resuscitation until the cause of the hemorrhagic shock was repaired surgically. Crystalloids and blood were used extensively during World War II for the treatment of patients in unstable conditions. Experience from the Korean and Vietnam wars revealed that volume resuscitation and early surgical intervention were paramount for surviving traumatic injuries resulting in hemorrhagic shock. These and other principles helped in the development of present guidelines for the treatment of traumatic hemorrhagic shock. However, recent investigators have questioned these guidelines, and today, controversies exist concerning the optimal treatment of hemorrhagic shock.

For more information, see Medscape’s Trauma Resource Center.

Pathophysiology

The human body responds to acute hemorrhage by activating the following major physiologic systems: the hematologic, cardiovascular, renal, and neuroendocrine systems.

The hematologic system responds to an acute severe blood loss by activating the coagulation cascade and contracting the bleeding vessels (by means of local thromboxane A₂ release). In addition, platelets are activated (also by means of local thromboxane A₂ release) and form an immature clot on the bleeding source. The damaged vessel exposes collagen, which subsequently causes fibrin deposition and stabilization of the clot. Approximately 24 hours are needed for complete clot fibrination and mature formation.

The cardiovascular system initially responds to hypovolemic shock by increasing the heart rate, increasing myocardial contractility, and constricting peripheral blood vessels. This response occurs secondary to an increased release of norepinephrine and decreased baseline vagal tone (regulated by the baroreceptors in the carotid arch, aortic arch, left atrium, and pulmonary vessels). The cardiovascular system also responds by redistributing blood to the brain, heart, and kidneys and away from skin, muscle, and GI tract.

The renal system responds to hemorrhagic shock by stimulating an increase in renin secretion from the juxtaglomerular apparatus. Renin converts angiotensinogen to angiotensin I, which subsequently is converted to angiotensin II by the lungs and liver. Angiotensin II has 2 main effects, both of which help to reverse hemorrhagic shock, vasoconstriction of arteriolar smooth muscle, and stimulation of aldosterone secretion by the adrenal cortex. Aldosterone is responsible for active sodium reabsorption and subsequent water conservation.

The neuroendocrine system responds to hemorrhagic shock by causing an increase in circulating antidiuretic hormone (ADH). ADH is released from the posterior pituitary gland in response to a decrease in BP (as detected by baroreceptors) and a decrease in the sodium concentration (as detected by osmoreceptors). ADH indirectly leads to an increased reabsorption of water and salt (NaCl) by the distal tubule, the collecting ducts, and the loop of Henle.

The pathophysiology of hypovolemic shock is much more involved than what was just listed. To explore the pathophysiology in more detail, references for further reading are provided in the bibliography. These intricate mechanisms list above are effective in maintaining vital organ perfusion in severe blood loss. Without fluid and blood resuscitation and/or correction of the underlying pathology causing the hemorrhage, cardiac perfusion eventually diminishes, and multiple organ failure soon follows.

History

• In a patient with possible shock secondary to hypovolemia, the history is vital in determining the possible causes and in directing the workup. Hypovolemic shock secondary to external blood loss typically is obvious and easily diagnosed. Internal bleeding may not be as obvious as patients may complain only of weakness, lethargy, or a change in mental status.

• Symptoms of shock, such as weakness, lightheadedness, and confusion, should be assessed in all patients.

• In the patient with trauma, determine the mechanism of injury and any information that may heighten suspicion of certain injuries (eg, steering wheel damage or extensive passenger compartment intrusion in a motor vehicle accident).

• If conscious, the patient may be able to indicate the location of pain.

• Vital signs, prior to arrival in the ED, should also be noted.

• Chest, abdominal, or back pain may indicate a vascular disorder.

• The classic sign of a thoracic aneurysm is a tearing pain radiating to the back. Abdominal aortic aneurysms usually result in abdominal, back pain, or flank pain.

• In patients with GI bleeding, inquiry about hematemesis, melena, alcohol drinking history, excessive nonsteroidal anti-inflammatory drug use, and coagulopathies (iatrogenic or otherwise) is very important.

• The chronology of vomiting and hematemesis should be determined.

• The patient who presents with hematemesis after multiple episodes of forceful vomiting is more likely to have Boerhaave syndrome or a Mallory-Weiss tear, whereas a patient with a history of hematemesis from the start is more likely to have peptic ulcer disease or esophageal varices.

• If a gynecologic cause is being considered, gather information about the following: last menstrual period, risk factors for ectopic pregnancy, vaginal bleeding (including amount and duration), vaginal passage of products of conception, and pain. All women of childbearing age should undergo a pregnancy test, regardless of whether they believe that they are pregnant. A negative pregnancy test typically excludes ectopic pregnancy as a diagnosis.

Physical

The physical examination should always begin with an assessment of the airway, breathing, and circulation. Once these have been evaluated and stabilized, the circulatory system should be evaluated for signs and symptoms of shock.

Do not rely on systolic BP as the main indicator of shock; this practice results in delayed diagnosis. Compensatory mechanisms prevent a significant decrease in systolic BP until the patient has lost 30% of the blood volume. More attention should be paid to the pulse, respiratory rate, and skin perfusion. Also, patients taking beta-blockers may not present with tachycardia, regardless of the degree of shock.

Classes of hemorrhage have been defined, based on the percentage of blood volume loss. However, the distinction between these classes in the hypovolemic patient often is less apparent. Treatment should be aggressive and directed more by response to therapy than by initial classification.

• Class I hemorrhage (loss of 0-15%)

• In the absence of complications, only minimal tachycardia is seen.

• Usually, no changes in BP, pulse pressure, or respiratory rate occur.

• A delay in capillary refill of longer than 3 seconds corresponds to a volume loss of approximately 10%.

• Class II hemorrhage (loss of 15-30%)

• Clinical symptoms include tachycardia (rate >100 beats per minute), tachypnea, decrease in pulse pressure, cool clammy skin, delayed capillary refill, and slight anxiety.

• The decrease in pulse pressure is a result of increased catecholamine levels, which causes an increase in peripheral vascular resistance and a subsequent increase in the diastolic BP.

• Class III hemorrhage (loss of 30-40%)

• By this point, patients usually have marked tachypnea and tachycardia, decreased systolic BP, oliguria, and significant changes in mental status, such as confusion or agitation.

• In patients without other injuries or fluid losses, 30-40% is the smallest amount of blood loss that consistently causes a decrease in systolic BP.

• Most of these patients require blood transfusions, but the decision to administer blood should be based on the initial response to fluids.

• Class IV hemorrhage (loss of >40%)

• Symptoms include the following: marked tachycardia, decreased systolic BP, narrowed pulse pressure (or immeasurable diastolic pressure), markedly decreased (or no) urinary output, depressed mental status (or loss of consciousness), and cold and pale skin.

• This amount of hemorrhage is immediately life threatening.

• In the patient with trauma, hemorrhage usually is the presumed cause of shock. However, it must be distinguished from other causes of shock. These include cardiac tamponade (muffled heart tones, distended neck veins), tension pneumothorax (deviated trachea, unilaterally decreased breath sounds), and spinal cord injury (warm skin, lack of expected tachycardia, neurological deficits).

• The 4 areas in which life-threatening hemorrhage can occur are as follows: chest, abdomen, thighs, and outside the body.

• The chest should be auscultated for decreased breath sounds, because life-threatening hemorrhage can occur from myocardial, vessel, or lung laceration.

• The abdomen should be examined for tenderness or distension, which may indicate intraabdominal injury.

• The thighs should be checked for deformities or enlargement (signs of femoral fracture and bleeding into the thigh).

• The patient’s entire body should then be checked for other external bleeding.

• In the patient without trauma, the majority of the hemorrhage is in the abdomen. The abdomen should be examined for tenderness, distension, or bruits. Look for evidence of an aortic aneurysm, peptic ulcer disease, or liver congestion. Also check for other signs of bruising or bleeding.

• In the pregnant patient, perform a sterile speculum examination. However, with third-trimester bleeding, the examination should be performed as a “double set-up” in the operating room. Check for abdominal, uterine, or adnexal tenderness.

Causes

The causes of hemorrhagic shock are traumatic, vascular, GI, or pregnancy related.

• Traumatic causes can result from penetrating and blunt trauma. Common traumatic injuries that can result in hemorrhagic shock include the following: myocardial laceration and rupture, major vessel laceration, solid abdominal organ injury, pelvic and femoral fractures, and scalp lacerations.

• Vascular disorders that can result in significant blood loss include aneurysms, dissections, and arteriovenous malformations.

• GI disorders that can result in hemorrhagic shock include the following: bleeding esophageal varices, bleeding peptic ulcers, Mallory-Weiss tears, and aortointestinal fistulas.

• Pregnancy-related disorders include ruptured ectopic pregnancy, placenta previa, and abruption of the placenta. Hypovolemic shock secondary to an ectopic pregnancy is common. Hypovolemic shock secondary to an ectopic pregnancy in a patient with a negative urine pregnancy test is rare but has been reported.

Differential Diagnoses

• Abruptio Placentae

• Aneurysm, Abdominal

• Aneurysm, Thoracic

• Fractures, Femur

• Fractures, Pelvic

• Gastritis and Peptic Ulcer Disease

• Placenta Previa

• Pregnancy, Ectopic

• Pregnancy, Postpartum Hemorrhage

• Pregnancy, Trauma

• Shock, Hemorrhagic

• Shock, Hypovolemic

• Toxicity, Iron

Laboratory Studies

• After the history is taken and the physical examination is performed, further workup depends on the probable cause of the hypovolemia, as well as on the stability of the patient’s condition.

• Initial laboratory studies should include analysis of the CBC, electrolyte levels (eg, Na, K, Cl, HCO₃, BUN, creatinine, glucose levels), prothrombin time, activated partial thromboplastin time, ABGs, urinalysis (in patients with trauma), and a urine pregnancy test. Blood should be typed and cross-matched.

Imaging Studies

• Patients with marked hypotension and/or unstable conditions must first be resuscitated adequately. This treatment takes precedence over imaging studies and may include immediate interventions and immediately taking the patient to the operating room.

• The workup for the patient with trauma and signs and symptoms of hypovolemia is directed toward finding the source of blood loss.

• The atraumatic patient with hypovolemic shock requires ultrasonographic examination in the ED if an abdominal aortic aneurysm is suspected. If GI bleeding is suspected, a nasogastric tube should be placed, and gastric lavage should be performed. An upright chest radiograph should be obtained if a perforated ulcer or Boerhaave syndrome is a possibility. Endoscopy can be performed (usually after the patient has been admitted) to further delineate the source of bleeding.

• A pregnancy test should be performed in all female patients of childbearing age. If the patient is pregnant and in shock, surgical consultation and the consideration of bedside pelvic ultrasonography should be immediately performed in the ED. Hypovolemic shock secondary to an ectopic pregnancy is common. Hypovolemic shock secondary to an ectopic pregnancy in a patient with a negative pregnancy test, although rare, has been reported.

• If thoracic dissection is suspected because of the mechanism and initial chest radiographic findings, the workup may include transesophageal echocardiography, aortography, or CT scanning of the chest.

• If a traumatic abdominal injury is suspected, a focused abdominal sonography for trauma (FAST) ultrasonography examination may be performed in the stable or unstable patient. Computed tomography (CT) scanning typically is performed in the stable patient.

• If long-bone fractures are suspected, radiographs should be obtained.

Prehospital Care

The treatment of patients with hypovolemic shock often begins at an accident scene or at home. The prehospital care team should work to prevent further injury, transport the patient to the hospital as rapidly as possible, and initiate appropriate treatment in the field. Direct pressure should be applied to external bleeding vessels to prevent further blood loss.

• Prevention of further injury applies mostly to the patient with trauma. The cervical spine must be immobilized, and the patient must be extricated, if applicable, and moved to a stretcher. Splinting of fractures can minimize further neurovascular injury and blood loss.

• Although in selected cases stabilization may be beneficial, rapid transport of sick patients to the hospital remains the most important aspect of prehospital care. Definitive care of the hypovolemic patient usually requires hospital, and sometimes surgical, intervention. Any delay in definitive care, eg, such as delayed transport, is potentially harmful.

• Most prehospital interventions involve immobilizing the patient (if trauma is involved), securing an adequate airway, ensuring ventilation, and maximizing circulation.

• In the setting of hypovolemic shock, positive-pressure ventilation may diminish venous return, diminish cardiac outcome, and worsen the shock state. While oxygenation and ventilation are necessary, excessive positive-pressure ventilation can be detrimental for a patient suffering hypovolemic shock.

• Appropriate treatment usually can be initiated without delaying transport. Some procedures, such as starting intravenous (IV) lines or splinting of extremities, can be performed while a patient is being extricated. However, procedures in the field that prolong transportation should be delayed. Benefits to giving IV fluids prior to departure from the scene are not clear; however, IV lines and fluid resuscitation should be started and continued once the patient is en route to definitive care.

• In recent years, there has been considerable debate regarding the use of military antishock trousers (MAST). MAST were introduced in the 1960s and, based mostly on anecdotal reports of success, their use became standard therapy in the prehospital treatment of hypovolemic shock in the late 1970s. By the 1980s, the American College of Surgeons Committee on Trauma included their use in the standard of care for all patients with trauma and signs or symptoms of shock. Since that time, studies have failed to show improved outcome with the use of MAST. The American College of Surgeons Committee on Trauma no longer recommends the use of MAST.

Emergency Department Care

Three goals exist in the emergency department treatment of the patient with hypovolemic shock as follows: (1) maximize oxygen delivery – completed by ensuring adequacy of ventilation, increasing oxygen saturation of the blood, and restoring blood flow, (2) control further blood loss, and (3) fluid resuscitation. Also, the patient’s disposition should be rapidly and appropriately determined.

Maximizing oxygen delivery

The patient’s airway should be assessed immediately upon arrival and stabilized if necessary. The depth and rate of respirations, as well as breath sounds, should be assessed. If pathology (eg, pneumothorax, hemothorax, flail chest) that interferes with breathing is found, it should be addressed immediately. High-flow supplemental oxygen should be administered to all patients, and ventilatory support should be given, if needed. Excessive positive-pressure ventilation can be detrimental for a patient suffering hypovolemic shock and should be avoided.

Two large-bore IV lines should be started. The Poiseuille law states that flow is inversely related to the length of the IV catheter and directly related to its radius to the fourth power. Thus, a short large-caliber IV catheter is ideal; the caliber is much more significant than the length. IV access may be obtained by means of percutaneous access in the antecubital veins, cutdown of saphenous or arm veins, or access in the central veins by using the Seldinger technique. If central lines are obtained, a large-bore single-lumen catheter should be used. Intraosseous access has and continues to be used for hypotensive children younger than 6 years. Intraosseous access has also been used in hypotensive adults. The most important factor in determining the route of access is the practitioner’s skill and experience.

Placement of an arterial line should be considered for patients with severe hemorrhage. For these patients, the arterial line will provide continuous blood pressure monitoring and also ease arterial blood gas testing.

Once IV access is obtained, initial fluid resuscitation is performed with an isotonic crystalloid, such as lactated Ringer solution or normal saline. An initial bolus of 1-2 L is given in an adult (20 mL/kg in a pediatric patient), and the patient’s response is assessed.

If vital signs return to normal, the patient may be monitored to ensure stability, and blood should be sent for typed and cross-matched. If vital signs transiently improve, crystalloid infusion should continue and type-specific blood obtained. If little or no improvement is seen, crystalloid infusion should continue, and type O blood should be given (type O Rh-negative blood should be given to female patients of childbearing age to prevent sensitization and future complications).

If a patient is moribund and markedly hypotensive (class IV shock), both crystalloid and type O blood should be started initially. These guidelines for crystalloid and blood infusion are not rules; therapy should be based on the condition of the patient.

The position of the patient can be used to improve circulation; one example is raising the hypotensive patient’s legs while fluid is being given. Another example of useful positioning is rolling a hypotensive gravid patient with trauma onto her left side, which displaces the fetus from the inferior vena cava and increases circulation. The Trendelenburg position is no longer recommended for hypotensive patients, as the patient is predisposed to aspiration. In addition, the Trendelenburg position does not improve cardiopulmonary performance and may worsen gas exchange.

Autotransfusion may be a possibility in some patients with trauma. Several devices that allow for the sterile collection, anticoagulation, filtration, and retransfusion of blood are available. In the trauma setting, this blood almost always is from a hemothorax collected by means of tube thoracostomy.

Controlling further blood loss

Control of further hemorrhage depends on the source of bleeding and often requires surgical intervention. In the patient with trauma, external bleeding should be controlled with direct pressure; internal bleeding requires surgical intervention. Long-bone fractures should be treated with traction to decrease blood loss.

In the patient whose pulse is lost in the ED or just prior to arrival, an emergency thoracotomy with cross-clamping of the aorta may be indicated to preserve blood flow to the brain. This procedure is palliative at best and requires immediate transfer to the operating room.

In the patient with GI bleeding, intravenous vasopressin and H₂ blockers have been used. Vasopressin commonly is associated with adverse reactions, such as hypertension, arrhythmias, gangrene, and myocardial or splanchnic ischemia. Therefore, it should be considered secondary to more definitive measures. H₂ blockers are relatively safe but have no proven benefit.

Somatostatin and octreotide infusions have been shown to reduce gastrointestinal bleeding from varices and peptic ulcer disease. These agents possess the advantages of vasopressin without the significant side effects.

In patients with variceal bleeding, use of a Sengstaken-Blakemore tube can be considered. These devices have a gastric balloon and an esophageal balloon. The gastric one is inflated first, and then the esophageal one is inflated if bleeding continues. The use of this tube has been associated with severe adverse reactions, such as esophageal rupture, asphyxiation, aspiration and mucosal ulceration. For this reason, its use should be considered only as a temporary measure in extreme circumstances.

Virtually all causes of acute gynecological bleeding that cause hypovolemia (eg, ectopic pregnancy, placenta previa, abruptio placenta, ruptured cyst, miscarriage) require surgical intervention.

Early consultation and definitive care are the keys. The goal in the ED is to stabilize the hypovolemic patient, determine the cause of bleeding, and provide definitive care as quickly as possible. If transfer to another hospital is necessary, resources should be mobilized early.

In patients with trauma, if the emergency medical services personnel indicate potential serious injury, the surgeon (or trauma team) should be notified prior to the patient’s arrival. In a 55-year-old patient with abdominal pain, for example, emergency ultrasonography of the abdomen may be necessary to identify an abdominal aortic aneurysm before the vascular surgeon is notified. Every patient should be individually evaluated, because delaying definitive care can increase morbidity and mortality.

Resuscitation

Whether crystalloids or colloids are best for resuscitation continues to be a matter for discussion and research. Many fluids have been studied for use in resuscitation; these include isotonic sodium chloride solution, lactated Ringer solution, hypertonic saline, albumin, purified protein fraction, fresh frozen plasma, hetastarch, pentastarch, and dextran 70.

Proponents of colloid resuscitation argue that the increased oncotic pressure produced with these substances decreases pulmonary edema. However, the pulmonary vasculature allows considerable flow of material, including proteins, between the intravascular space and interstitium. Maintenance of the pulmonary hydrostatic pressure at less than 15 mm Hg appears to be a more important factor in preventing pulmonary edema.

Another argument is that less colloid is needed to increase the intravascular volume. Studies have shown this to be true. However, they still have not demonstrated any difference in outcome with colloids compared with crystalloids.

Synthetic colloid solutions, such as hetastarch, pentastarch, and dextran 70, have some advantages compared with natural colloids such as purified protein fraction, fresh frozen plasma, and albumin. They have the same volume-expanding properties, but because of their structures and high molecular weights, they remain mostly in the intravascular space, reducing the occurrence of interstitial edema. Although theoretic advantages exist, studies have failed to show a difference in ventilatory parameters, pulmonary function test results, days using a ventilator, total hospital days, or survival.

The European Society of Intensive Care Medicine (ESICM) advises against the use of colloids-hydroxyethyl starches (HES) in patients with severe sepsis or risk of acute kidney injury. Physicians should also avoid using colloids in patients with head injury and refrain from administering gelatins and HES in organ donors

The combination of hypertonic saline and dextran also has been studied because of previous evidence that it may improve cardiac contractility and circulation. Studies in the US and Japan have failed to show any difference when this combination was compared with isotonic sodium chloride solution or lactated Ringer solution. Thus, despite the many available resuscitation fluids, current recommendations still advocate the use of normal saline or lactated Ringer solution. In the US, one reason for the predominant use of crystalloids over the other resuscitative fluids is cost.

Recent literature suggests that the early administration of FFP and platelets improves survival and decreases overall PRBC need in patients undergoing a massive transfusion

Restoring normal circulating volume and BP prior to definitive control of bleeding

Although some data indicate that a systolic BP of 80-90 mm Hg may be adequate in penetrating truncal trauma without head injury, further studies are needed.

Current recommendations are for aggressive fluid resuscitation with lactated Ringer solution or normal saline in all patients with signs and symptoms of shock, regardless of underlying cause.

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Antisecretory agents

Class Summary

These agents have vasoconstrictive properties and can reduce blood flow to portal systems.

Somatostatin (Zecnil)

 

Naturally occurring tetradecapeptide isolated from the hypothalamus and pancreatic and enteric epithelial cells. Diminishes blood flow to portal system because of vasoconstriction. Has similar effects as vasopressin but does not cause coronary vasoconstriction. Rapidly cleared from the circulation, with an initial half-life of 1-3 min.

Octreotide (Sandostatin)

 

Synthetic octapeptide. Compared to somatostatin, has similar pharmacological actions with greater potency and longer duration of action.

Used as adjunct to nonoperative management of secreting cutaneous fistulas of the stomach, duodenum, small intestine (jejunum and ileum), or pancreas.

Complications

• Neurologic sequelae

• Death

Prognosis

• The prognosis is dependent on the degree of volume loss.

 

Cardiogenic Shock

 

Background

Cardiogenic shock is a physiologic state in which inadequate tissue perfusion results from cardiac dysfunction, most often systolic. It is a major, and frequently fatal, complication of a variety of acute and chronic disorders, occurring most commonly following acute myocardial infarction (MI). (See Pathophysiology, Etiology, and Prognosis.)

Although ST-segment elevation MI (STEMI, previously termed Q-wave MI) is encountered in most patients, cardiogenic shock may also develop in patients with non ̶ ST-segment elevation acute coronary syndrome (NSTEMI, NSTACS, or unstable angina). (See the images below.)

 

 

 

Patient with an acute anterolateral myocardial infarction who developed cardiogenic shock. Coronary angiography images showed severe stenosis of the left anterior descending coronary artery, which was dilated by percutaneous transluminal coronary angioplasty.

 

 

 

 

Echocardiogram image from a patient with cardiogenic shock shows enlarged cardiac chambers; the motion study showed poor left ventricular function. Courtesy of R. Hoeschen, MD.

The clinical definition of cardiogenic shock is decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume. Hemodynamic criteria for cardiogenic shock are sustained hypotension (systolic blood pressure < 90 mm Hg for at least 30 min) and a reduced cardiac index (< 2.2 L/min/m²) in the presence of elevated pulmonary capillary wedge pressure (>15 mm Hg). (See DDx, Workup.)

The diagnosis of cardiogenic shock can sometimes be made at the bedside by observing hypotension, absence of hypovomeia, and clinical signs of poor tissue perfusion, which include oliguria, cyanosis, cool extremities, and altered mentation. These signs usually persist after attempts have been made to correct hypovolemia, arrhythmia, hypoxia, and acidosis. (See Presentation, DDx.)

Pathophysiology

Cardiogenic shock is recognized as a low cardiac output state secondary to extensive left ventricular infarction, development of a mechanical defect (eg, ventricular septal defect or papillary muscle rupture), or right ventricular infarction.

Disorders that can result in the acute deterioration of cardiac function and lead to cardiogenic shock include myocardial infarction (MI) or myocardial ischemia, acute myocarditis, sustained arrhythmia, severe valvular dysfunction, and decompensation of end-stage cardiomyopathy from multiple etiologies. Autopsy studies show that cardiogenic shock is generally associated with the loss of more than 40% of the left ventricular myocardial muscle.

Myocardial pathology

Cardiogenic shock is characterized by systolic and diastolic dysfunction. Patients who develop cardiogenic shock from acute MI consistently have evidence of progressive myocardial necrosis with infarct extension. Decreased coronary perfusion pressure and increased myocardial oxygen demand play a role in the vicious cycle that leads to cardiogenic shock.

Patients suffering from cardiogenic shock often have multivessel coronary artery disease with limited coronary blood flow reserve. Ischemia remote from the infarcted zone is an important contributor to shock. Myocardial diastolic function is also impaired, because ischemia causes decreased myocardial compliance, thereby increasing left ventricular filling pressure, which may lead to pulmonary edema and hypoxemia.

Cellular pathology

Tissue hypoperfusion, with consequent cellular hypoxia, causes anaerobic glycolysis, the accumulation of lactic acid, and intracellular acidosis. Also, myocyte membrane transport pumps fail, which decreases transmembrane potential and causes intracellular accumulation of sodium and calcium, resulting in myocyte swelling.

If ischemia is severe and prolonged, myocardial cellular injury becomes irreversible and leads to myonecrosis, which includes mitochondrial swelling, the accumulation of denatured proteins and chromatin, and lysosomal breakdown. These events induce fracture of the mitochondria, nuclear envelopes, and plasma membranes.

Additionally, apoptosis (programmed cell death) may occur in peri-infarcted areas and may contribute to myocyte loss. Activation of inflammatory cascades, oxidative stress, and stretching of the myocytes produces mediators that overpower inhibitors of apoptosis, thus activating the apoptosis.

Reversible myocardial dysfunction

Large areas of myocardium that are dysfunctional but still viable can contribute to the development of cardiogenic shock in patients with MI. This potentially reversible dysfunction is often described as myocardial stunning or as hibernating myocardium. Although hibernation is considered a different physiologic process than myocardial stunning, the conditions are difficult to distinguish in the clinical setting and they often coexist.

Myocardial stunning represents postischemic dysfunction that persists despite restoration of normal blood flow. By definition, myocardial dysfunction from stunning eventually resolves completely. The mechanism of myocardial stunning involves a combination of oxidative stress, abnormalities of calcium homeostasis, and circulating myocardial depressant substances.

Hibernating myocardium is a state of persistently impaired myocardial function at rest, which occurs because of the severely reduced coronary blood flow. Hibernation appears to be an adaptive response to hypoperfusion that may minimize the potential for further ischemia or necrosis. Revascularization of the hibernating (and/or stunned) myocardium generally leads to improved myocardial function.

 

 

Cardiovascular mechanics of cardiogenic shock

The main mechanical defect in cardiogenic shock is a shift to the right for the left ventricular end-systolic pressure-volume curve, because of a marked reduction in contractility. As a result, at a similar or even lower systolic pressure, the ventricle is able to eject less blood volume per beat. Therefore, the end-systolic volume is usually greatly increased in persons with cardiogenic shock.

The stroke volume is decreased, and to compensate for this, the curvilinear diastolic pressure-volume curve also shifts to the right, with a decrease in diastolic compliance. This leads to increased diastolic filling, which is associated with an increase in end-diastolic pressure. The attempt to enhance cardiac output by this mechanism comes at the cost of having a higher left ventricular diastolic filling pressure, which ultimately increases myocardial oxygen demand and causes pulmonary edema.

As a result of decreased contractility, the patient develops elevated left and right ventricular filling pressures and low cardiac output. Mixed venous oxygen saturation falls because of the increased tissue oxygen extraction, which is due to the low cardiac output. This, combined with the intrapulmonary shunting that is often present, contributes to substantial arterial oxygen desaturation.

Systemic effects

When a critical mass of left ventricular myocardium becomes ischemic and fails to pump effectively, stroke volume and cardiac output are curtailed. Myocardial ischemia is further exacerbated by compromised myocardial perfusion due to hypotension and tachycardia.

The pump failure increases ventricular diastolic pressures concomitantly, causing additional wall stress and thereby elevating myocardial oxygen requirements. Systemic perfusion is compromised by decreased cardiac output, with tissue hypoperfusion intensifying anaerobic metabolism and instigating the formation of lactic acid, which further deteriorates the systolic performance of the myocardium.

Depressed myocardial function also leads to the activation of several physiologic compensatory mechanisms. These include sympathetic stimulation, which increases the heart rate and cardiac contractility and causes renal fluid retention, hence augmenting the left ventricular preload. The raised heart rate and contractility increases myocardial oxygen demand, further worsening myocardial ischemia.

Fluid retention and impaired left ventricular diastolic filling triggered by tachycardia and ischemia contribute to pulmonary venous congestion and hypoxemia. Sympathetically mediated vasoconstriction to maintain systemic blood pressure amplifies myocardial afterload, which additionally impairs cardiac performance. Finally, excessive myocardial oxygen demand with simultaneous inadequate myocardial perfusion worsens myocardial ischemia, initiating a vicious cycle that ultimately ends in death, if uninterrupted.

Usually, a combination of systolic and diastolic myocardial dysfunction is present in patients with cardiogenic shock. Metabolic derangements that impair myocardial contractility further compromise systolic ventricular function. Myocardial ischemia decreases myocardial compliance, thereby elevating left ventricular filling pressure at a given end-diastolic volume (diastolic dysfunction), which leads to pulmonary congestion and congestive heart failure.

Shock state

Shock state, irrespective of the etiology, is described as a syndrome initiated by acute systemic hypoperfusion that leads to tissue hypoxia and vital organ dysfunction. All forms of shock are characterized by inadequate perfusion to meet the metabolic demands of the tissues. A maldistribution of blood flow to end organs begets cellular hypoxia and end organ damage, the well-described multisystem organ dysfunction syndrome. The organs of vital importance are the brain, heart, and kidneys.

A decline in higher cortical function may indicate diminished perfusion of the brain, which leads to an altered mental status ranging from confusion and agitation to flaccid coma. The heart plays a central role in propagating shock. Depressed coronary perfusion leads to worsening cardiac dysfunction and a cycle of self-perpetuating progression of global hypoperfusion. Renal compensation for reduced perfusion results in diminished glomerular filtration, causing oliguria and subsequent renal failure.

Etiology

Cardiogenic shock can result from the following types of cardiac dysfunction:

• Systolic dysfunction

• Diastolic dysfunction

• Valvular dysfunction

• Cardiac arrhythmias

• Coronary artery disease

• Mechanical complications

The vast majority of cases of cardiogenic shock in adults are due to acute myocardial ischemia. Indeed, cardiogenic shock is generally associated with the loss of more than 40% of the left ventricular myocardium, although in patients with previously compromised left ventricular function, even a small infarction may precipitate shock. Cardiogenic shock is more likely to develop in people who are elderly or diabetic or in persons who have had a previous inferior myocardial infarction (MI).

Complications of acute MI, such as acute mitral regurgitation, large right ventricular infarction, and rupture of the interventricular septum or left ventricular free wall, can result in cardiogenic shock. Conduction abnormalities (eg, atrioventricular blocks, sinus bradycardia) are also risk factors.

Many cases of cardiogenic shock occurring after acute coronary syndromes may be due to medication administration. The use of beta blockers and angiotensin-converting enzyme (ACE) inhibitors in acute coronary syndromes must be carefully timed and monitored.

In children, preceding viral infection may cause myocarditis. In addition, children and infants may have unrecognized congenital structural heart defects that are well compensated until there is a stressor. These etiologies plus toxic ingestions make up the 3 primary causes of cardiogenic shock in children.

A systemic inflammatory response syndrome–type mechanism has also been implicated in the etiology of cardiogenic shock. Elevated levels of white blood cells, body temperature, complement, interleukins, and C-reactive protein are often seen in large myocardial infarctions. Similarly, inflammatory nitric oxide synthetase (iNOS) is also released in high levels during myocardial stress. Nitric oxide production induced by iNOS may uncouple calcium metabolism in the myocardium resulting in a stunned myocardium. Additionally, iNOS leads to the expression of interleukins, which may themselves cause hypotension.

Left ventricular failure

Systolic dysfunction

The primary abnormality in systolic dysfunction is abated myocardial contractility. Acute MI or ischemia is the most common cause; cardiogenic shock is more likely to be associated with anterior MI. The causes of systolic dysfunction leading to cardiogenic shock can be summarized as follows:

• Ischemia/MI

• Global hypoxemia

• Valvular disease

• Myocardial depressant drugs – Eg, beta blockers, calcium channel blockers, and antiarrhythmics

• Myocardial contusion

• Respiratory acidosis

• Metabolic derangements – Eg, acidosis, hypophosphatemia, and hypocalcemia

• Severe myocarditis

• End-stage cardiomyopathy – Including valvular causes

• Prolonged cardiopulmonary bypass.

• Cardiotoxic drugs – Eg, doxorubicin (Adriamycin)

Diastolic dysfunction

Increased left ventricular diastolic chamber stiffness contributes to cardiogenic shock during cardiac ischemia, as well as in the late stages of hypovolemic shock and septic shock. Increased diastolic dysfunction is particularly detrimental when systolic contractility is also depressed. The causes of cardiogenic shock due primarily to diastolic dysfunction can be summarized as follows:

• Ischemia

• Ventricular hypertrophy

• Restrictive cardiomyopathy

• Prolonged hypovolemic or septic shock

• Ventricular interdependence

• External compression by pericardial tamponade

Greatly increased afterload

Increased afterload, which can impair cardiac function, can be caused by the following:

• Aortic stenosis

• Hypertrophic cardiomyopathy

• Dynamic aortic outflow tract obstruction

• Coarctation of the aorta

• Malignant hypertension

Valvular and structural abnormality

Valvular dysfunction may immediately lead to cardiogenic shock or may aggravate other etiologies of shock. Acute mitral regurgitation secondary to papillary muscle rupture or dysfunction is caused by ischemic injury. Rarely, acute obstruction of the mitral valve by a left atrial thrombus may result in cardiogenic shock by means of severely decreased cardiac output. Aortic and mitral regurgitation reduce forward flow, raise end-diastolic pressure, and aggravate shock associated with other etiologies.

Valvular and structural abnormalities associated with cardiogenic shock include the following:

• Mitral stenosis

• Endocarditis

• Mitral aortic regurgitation

• Obstruction due to atrial myxoma or thrombus

• Papillary muscle dysfunction or rupture

• Ruptured septum or free wall arrhythmias

• Tamponade

Decreased contractility

Reduced myocardial contractility can result from the following:

• Right ventricular infarction

• Ischemia

• Hypoxia

• Acidosis

Right ventricular failure

Greatly increased afterload

Afterload increase associated with right ventricular failure can result from the following:

• Pulmonary embolism

• Pulmonary vascular disease – Eg, pulmonary arterial hypertension and veno-occlusive disease

• Hypoxic pulmonary vasoconstriction

• Peak end-expiratory pressure

• High alveolar pressure

• Acute respiratory distress syndrome

• Pulmonary fibrosis

• Sleep disordered breathing

• Chronic obstructive pulmonary disease

Arrhythmias

Ventricular tachyarrhythmias are often associated with cardiogenic shock. Furthermore, bradyarrhythmias may cause or aggravate shock due to another etiology. Sinus tachycardia and atrial tachyarrhythmias contribute to hypoperfusion and aggravate shock.

Epidemiology

International occurrence

Several multicenter thrombolytic trials in Europe reported a prevalence rate of cardiogenic shock following MI of approximately 7%.

Race-, sex-, and age-related demographics

Race-stratified mortality rates from cardiogenic shock are as follows (race-based mortality differences disappear with revascularization):

• Hispanics – 74%

• African Americans – 65%

• Whites – 56%

• Asians/others – 41%

The overall incidence of cardiogenic shock is higher in men than in women, with females accounting for 42% of patients with cardiogenic shock. This difference results from the increased prevalence of coronary artery disease in males. However, a higher percentage of female patients with MI develop cardiogenic shock than do males with MI.

Median age for cardiogenic shock mirrors the bimodal distribution of disease. For adults, the median age ranges from 65-66 years. For children, cardiogenic shock presents as a consequence of fulminant myocarditis or congenital heart disease.

Prognosis

Cardiogenic shock is the leading cause of death in acute myocardial infarction (MI). In the absence of aggressive, highly experienced technical care, mortality rates among patients with cardiogenic shock are exceedingly high (up to 70-90%). The key to achieving a good outcome is rapid diagnosis, prompt supportive therapy, and expeditious coronary artery revascularization in patients with myocardial ischemia and infarction.

Morbidity and mortality

Complications of cardiogenic shock may include the following:

• Cardiopulmonary arrest

• Dysrhythmia

• Renal failure

• Multisystem organ failure

• Ventricular aneurysm

• Thromboembolic sequelae

• Stroke

• Death

The following predictors of mortality were identified from the Global Utilization of Streptokinase and Tissue-Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I) trial :

• Increasing age

• Prior MI

• Altered sensorium

• Cold, clammy skin

• Oliguria

Echocardiographic findings such as left ventricular ejection fraction and mitral regurgitation are independent predictors of mortality. An ejection fraction of less than 28% is associated with a survival rate of 24% at 1 year, compared with a survival rate of 56% with a higher ejection fraction. Moderate or severe mitral regurgitation was found to be associated with a 1-year survival rate of 31%, compared with a survival rate of 58% in patients with no regurgitation.

Outcomes in cardiogenic shock significantly improve only when rapid revascularization can be achieved. The SHOCK (Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock?) trial demonstrated that overall mortality when revascularization occurs is 38%.When rapid revascularization is not attempted, mortality rates approach 70%. Rates vary depending on the procedure (eg, percutaneous transluminal coronary angioplasty, stent placement, thrombolytic therapy).

Physical Examination

Characteristics of patients with cardiogenic shock include the following:

• Patients in shock usually appear ashen or cyanotic and have cool skin and mottled extremities

• Peripheral pulses are rapid and faint and may be irregular if arrhythmias are present

• Jugular venous distention and crackles in the lungs are usually (but not always) present; peripheral edema also may be present.

• Heart sounds are usually distant, and third and fourth heart sounds may be present

• The pulse pressure may be low, and patients are usually tachycardic

• Patients show signs of hypoperfusion, such as altered mental status and decreased urine output

A systolic murmur is generally heard in patients with acute mitral regurgitation or ventricular septal rupture. The associated parasternal thrill indicates the presence of a ventricular septal defect, whereas the murmur of mitral regurgitation may be limited to early systole.

The systolic murmur, which becomes louder upon Valsalva and prompt standing, suggests hypertrophic obstructive cardiomyopathy (idiopathic hypertropic subaortic stenosis).

Diagnostic Considerations

Conditions to consider in the differential diagnosis of cardiogenic shock include the following:

• Systemic inflammatory response syndrome

• Acute coronary syndrome

• Aortic regurgitation

• Dilated cardiomyopathy

• Restrictive cardiomyopathy

• Congestive heart failure and pulmonary edema

• Mitral regurgitation

• Pericarditis and cardiac tamponade

• Hypovolemic shock

• Papillary muscle rupture

• Acute valvular dysfunction

Right ventricular infarction

Right ventricular infarction occurs in up to 30% of patients with inferior myocardial infarction (MI) and becomes hemodynamically unstable in 10% of these patients. The diagnosis is made by identifying an ST-segment elevation in the right precordial leads (V₃ or V₄ R) and/or typical hemodynamic findings after right heart catheterization. These are elevated right atrial and right ventricular end-diastolic pressures with normal to low pulmonary artery wedge pressure and low cardiac output.

Echocardiography findings can also be very helpful in the diagnosis of right ventricular infarction. Patients with cardiogenic shock due to this condition have a better prognosis than do patients when compared to those with cardiogenic shock due to left ventricular systolic failure.

Regarding the management of cardiogenic shock due to right ventricular infarction, supportive therapy begins with the restoration and maintenance of right ventricular preload with fluid administration. However, excessive fluid resuscitation may compromise left ventricular filling by introducing an interventricular septal shift.

Inotropic therapy with dobutamine may be effective in increasing cardiac output in patients with right ventricular infarction. Maintenance of systemic arterial pressure in order to maintain adequate coronary artery perfusion may require vasoconstricting agents, such as norepinephrine. In unstable patients, an intra-aortic balloon pump (IABP) may be useful for ensuring adequate blood supply to the already compromised right ventricle.

Revascularization of the occluded coronary artery, preferably by percutaneous transluminal coronary angioplasty (PTCA), is crucial for management and has shown to dramatically improve outcome.

Acute mitral regurgitation

Acute mitral regurgitation is usually associated with inferior MI due to ischemia or infarction of the papillary muscle. It occurs in approximately 1% of MIs, and posteromedial papillary muscle is involved more frequently than anterolateral muscle. Acute mitral regurgitation usually happens 2-7 days following acute MI and manifests with an abrupt onset of pulmonary edema, hypotension, and cardiogenic shock.

Echocardiography findings are extremely useful in making a diagnosis. The 2-dimensional (2-D) echocardiographic image shows the malfunctioning mitral valve, and findings from a Doppler study can be used to document the severity of mitral regurgitation. Right heart catheterization is often required for stabilizing the patient. Tall V waves identified on pulmonary arterial and wedge pressure waveforms indicate acute mitral regurgitation. However, the diagnosis must be confirmed based on echocardiography or left ventriculography findings before definitive therapy or surgery is initiated.

Hemodynamic stabilization by reducing afterload, either with nitroprusside or an IABP, is often instituted. Definitive therapy requires revascularization, if ischemia is present, and/or surgical valve repair or replacement, if a structural valvular lesion is present. The mortality rate in the presurgical era was 50% in the first 24 hours, with a 2-month survival rate of 6%.

Cardiac rupture

Rupture of the free wall of the left ventricle occurs within 2 weeks of the MI and may occur within the first 24 hours. The rupture may involve the anterior, posterior, or lateral wall of the ventricle.

Cardiac rupture often presents as sudden cardiac death. Premortem symptoms include chest pain, agitation, tachycardia, and hypotension. This diagnosis should be considered in patients with electromechanical dissociation who have a history of anginal pain. Patients rarely, if ever, survive cardiac rupture.

Ventricular septal rupture

Approximately 1-3% of acute MIs are associated with ventricular septal rupture. Most septal ruptures occur within the week following MI. Patients with acute ventricular septal rupture develop acute heart failure and/or cardiogenic shock, with physical findings of a harsh holosystolic murmur and left parasternal thrill.

A left-to-right intracardiac shunt, as demonstrated by a step-up (>5% increase in oxygen saturation) between the right atrium and right ventricle, confirms the diagnosis. Alternatively, 2-D and Doppler echocardiographic findings can be used to identify the location and severity of the left-to-right shunt.

Rapid stabilization using an IABP and pharmacologic measures, followed by emergent surgical repair, is lifesaving. The timing of surgical intervention is controversial, but most experts suggest operative repair within 48 hours of the rupture.

Ventricular septal rupture portends a poor prognosis unless management is aggressive. Immediate surgical repair of patients with ventricular septal rupture is reported to be associated with survival rates of 42-75%; therefore, prompt surgical therapy is imperative as soon as possible after the diagnosis of ventricular septal rupture is confirmed.

Reversible myocardial dysfunction

Other causes of severe, reversible myocardial dysfunction are sepsis-associated myocardial depression, myocardial depression following cardiopulmonary bypass, and inflammatory myocarditis. In older literature, this presentation is often referred to as cold septic shock. In these situations, myocardial dysfunction occurs from the effects of inflammatory cytokines, such as tumor necrosis factor and interleukin 1.

Myocardial dysfunction may vary from mild to severe and may lead to cardiogenic shock. For patients in cardiogenic shock, cardiovascular support with inotropic agents may be required until recovery, which generally occurs after the underlying disease process resolves.

Differential Diagnoses

• Myocardial Infarction

• Myocardial Ischemia

• Myocardial Rupture

• Myocarditis

• Pulmonary Edema, Cardiogenic

• Pulmonary Embolism

• Sepsis, Bacterial

• Septic Shock

• Shock, Distributive

• Shock, Hemorrhagic

Resuscitation, Ventilation, and Pharmacologic Intervention

Initial management includes fluid resuscitation to correct hypovolemia and hypotension, unless pulmonary edema is present. Central venous and arterial lines are often required. Swan-Ganz catheterization and continuous percutaneous oximetry are routine.

Oxygenation and airway protection are critical; intubation and mechanical ventilation are commonly required. However, although positive pressure ventilation may improve oxygenation, it may also compromise venous return, preload, to the heart. In any event, the patient should be treated with high-flow oxygen. Studies in patients with acute cardiogenic pulmonary edema have showoninvasive ventilation to improve hemodynamics and reduce the intubation rate. Mortality is, however, unaffected.

A study by Shin et al suggested that patients who receive extracorporeal cardiopulmonary resuscitation (CPR) versus conventional CPR for longer than 10 minutes following in-hospital arrest have a greater chance of survival.^[12]

Pharmacologic therapy

Patients with myocardial infarction (MI) or acute coronary syndrome are given aspirin and heparin. Both of these medications have been shown to be effective in reducing mortality in separate studies. Before initiating therapy, however, care should be taken to ensure that the patient does not have a myocardial wall rupture that is amenable to surgery.

The glycoprotein IIb/IIIa inhibitors improve the outcome of patients with non–ST-segment elevation acute coronary syndrome (NSTACS). They have been found to reduce recurrent MI following percutaneous coronary intervention (PCI) and in cardiogenic shock.

Hemodynamic Support

Dopamine, norepinephrine, and epinephrine are vasoconstricting drugs that help to maintain adequate blood pressure during life-threatening hypotension and help to preserve perfusion pressure for optimizing flow in various organs. The mean blood pressure required for adequate splanchnic and renal perfusion (mean arterial pressure [MAP] of 60 or 65 mm Hg) is based on clinical indices of organ function.

In patients with inadequate tissue perfusion and adequate intravascular volume, initiation of inotropic and/or vasopressor drug therapy may be necessary. Dopamine increases myocardial contractility and supports the blood pressure; however, it may increase myocardial oxygen demand. Dobutamine may be preferable if the systolic blood pressure is higher than 80 mm Hg; it has the advantage of not affecting myocardial oxygen demand as much as dopamine does. However, the resulting tachycardia may preclude the use of this inotropic agent in some patients.

Dopamine is usually initiated at a rate of 5-10 mcg/kg/min intravenously, and the infusion rate is adjusted according to the blood pressure and other hemodynamic parameters. Often, patients may require high doses of dopamine (as much as 20 mcg/kg/min).

If the patient remains hypotensive despite moderate doses of dopamine, a direct vasoconstrictor (eg, norepinephrine) should be started at a dose of 0.5 mcg/kg/min and titrated to maintain an MAP of 60 mm Hg. The potent vasoconstrictors (eg, norepinephrine) have traditionally been avoided because of their adverse effects on cardiac output and renal perfusion.

Vasopressor supportive therapy

Dopamine

At doses of approximately 10 mcg/kg/min, alpha-adrenergic effects lead to arterial vasoconstriction and an elevation in blood pressure. The blood pressure increases primarily as a result of the inotropic effect. The undesirable effects are tachycardia and increased pulmonary shunting, as well as the potential for decreased splanchnic perfusion and increased pulmonary arterial wedge pressure.

Norepinephrine

The dose of norepinephrine may vary from 0.2-1.5 mcg/kg/min, and large doses, as high as 3.3 mcg/kg/min, have been used because of the alpha-receptor down-regulation in persons with sepsis.

Epinephrine

Administration of this agent is associated with an increase in systemic and regional lactate concentrations. The use of epinephrine is recommended only in patients who are unresponsive to traditional agents. The undesirable effects are an increase in lactate concentration, a potential to produce myocardial ischemia, the development of arrhythmias, and a reduction in splanchnic flow.

 

Inotropic supportive therapy

Dobutamine

In the setting of acute myocardial infarction (MI), dobutamine use could increase the size of the infarct because of the increase in myocardial oxygen consumption that may ensue. In general, avoid dobutamine in patients with moderate or severe hypotension (eg, systolic blood pressure < 80 mm Hg) because of the peripheral vasodilation.

Phosphodiesterase inhibitors

Phosphodiesterase inhibitors (PDIs), which include inamrinone (formerly amrinone) and milrinone, are inotropic agents with vasodilating properties and long half-lives. The hemodynamic properties of PDIs are (1) a positive inotropic effect on the myocardium and peripheral vasodilation (decreased afterload) and (2) a reduction in pulmonary vascular resistance (decreased preload).

PDIs are beneficial in persons with cardiac pump failure, but they may require concomitant vasopressor administration. Unlike catecholamine inotropes, these drugs are not dependent on adrenoreceptor activity; therefore, patients are less likely to develop tolerance to these medications.

 

Thrombolytic Therapy

Although thrombolytic therapy (TT) reduces mortality rates in patients with acute myocardial infarction (MI), its benefits for patients with cardiogenic shock secondary to MI are disappointing. When used early in the course of MI, TT reduces the likelihood of subsequent development of cardiogenic shock after the initial event.

In the Gruppo Italiano Per lo Studio Della Streptokinase Nell’Infarto Miocardio trial, 30-day mortality rates were 69.9% in patients with cardiogenic shock who received streptokinase, compared to 70.1% in patients who received a placebo.

Similarly, other studies employing a tissue plasminogen activator did not show reductions in mortality rates from cardiogenic shock. Lower rates of reperfusion of the infarct-related artery in patients with cardiogenic shock may help to explain the disappointing results from TT. Other reasons for the decreased efficacy of TT are the existence of hemodynamic, mechanical, and metabolic causes of cardiogenic shock that are unaffected by TT.

Intra-Aortic Balloon Pump

The use of the IABP reduces systolic left ventricular afterload and augments diastolic coronary perfusion pressure, thereby increasing cardiac output and improving coronary artery blood flow. The IABP is effective for the initial stabilization of patients with cardiogenic shock. However, an IABP is not definitive therapy; the IABP stabilizes patients so that definitive diagnostic and therapeutic interventions can be performed.^{[18, 19]}

The IABP also may be a useful adjunct to thrombolysis for initial stabilization and transfer of patients to a tertiary care facility. Some studies have shown lower mortality rates in patients with myocardial infarction (MI) and cardiogenic shock treated with an IABP and subsequent revascularization, as previously mentioned.

Complications may be documented in up to 30% of patients who undergo IABP therapy; these relate primarily to local vascular problems, embolism, infection, and hemolysis.

The impact of treatment with an IABP on long-term survival is controversial and depends on the patient’s hemodynamic status and the etiology of the cardiogenic shock. Patient selection is the key issue; inserting the IABP early, rather than waiting until full-blown cardiogenic shock has developed, may result in clinical benefit.

Ramanathan et al found that rapid and complete reversal of systemic hypoperfusion with IABP counterpulsation in the SHOCK trial and SHOCK registry was independently associated with improved inhospital, 30-day, and 1-year survival, regardless of early revascularization. This suggests that complete reversal of systemic hypoperfusion with IABP counterpulsation is an important early prognostic feature.

In the IABP-SHOCK II study, 600 patients with cardiogenic shock complicating acute myocardial infarction were randomized to intraaortic balloon counterpulsation or no intraaortic balloon counterpulsation. All patients were expected to undergo early revascularization. Use of intraaortic balloon counterpulsation did not significantly reduce 30-day mortality in these patients.

Ventricular Assist Devices

In recent years, left ventricular assist devices (LVADs) capable of providing complete short-term hemodynamic support have been developed. The application of LVAD during reperfusion, after acute coronary occlusion, causes reduction of the left ventricular preload, increases regional myocardial blood flow and lactate extraction, and improves general cardiac function. The LVAD makes it possible to maintain the collateral blood flow as a result of maintaining the cardiac output and aortic pressure, keeping wall tension low and reducing the extent of microvascular reperfusion injury.

A pooled analysis from 17 studies showed that the mean age of this group of patients with LVADs was 59.5 ± 4.5 years and that mean support duration was 146.2 ± 60.2 hours. In 78.5% of patients (range, 53.8-100%), adjunctive reperfusion therapy, mainly percutaneous transluminal coronary angioplasty (PTCA), was used. Mean weaning and survival rates were 58.5% (range, 46-75%) and 40% (range, 29-58%), respectively.

In any case, comparing studies is difficult because important data are usually missing, mean age of patients were different, and time to treatment is not standardized. Hemodynamic presentation seems to be worse compared with data reported in the SHOCK trial, with lower cardiac index, lower systolic aortic pressure, and higher serum lactates. Taking these considerations into account, LVAD support seems to give no survival improvement in patients with cardiogenic shock complicating acute myocardial infarction (MI), compared with early reperfusion alone or in combination with IABP.

However, LVADs as a bridging option for patients with cardiogenic shock must be considered cautiously and must be avoided in patients who are unlikely to survive or are not likely to be transplant candidates. Further investigations are required to better define indications, support modalities, and outcomes.

The indications for insertion of a ventricular assist device are controversial. Such an aggressive approach to support the circulatory system in cardiogenic shock is appropriate (1) after the failure of medical treatment and an IABP, (2) when the cause of cardiogenic shock is potentially reversible, or (3) if the device can be used as a bridging option.

Percutaneous Transluminal Coronary Angioplasty

The retrospective and prospective data favor aggressive mechanical revascularization in patients with cardiogenic shock secondary to myocardial infarction (MI).

Reestablishing blood flow in the infarct-related artery may improve left ventricular function and survival following MI. In acute MI, studies show that percutaneous transluminal coronary angioplasty (PTCA) can achieve adequate flow in 80-90% of patients, compared with 50-60% of patients after thrombolytic therapy (TT).

Several retrospective clinical trials have shown that patients with cardiogenic shock due to myocardial ischemia benefitted (reduction in 30d mortality rates) when treated with angioplasty. A study of direct (primary) PTCA in patients with cardiogenic shock reported lower mortality rates in patients treated with angioplasty combined with the use of stents than in patients treat with medical therapy.

Coronary Artery Bypass Grafting

Critical left main artery disease and 3-vessel coronary artery disease are common findings in patients who develop cardiogenic shock. The potential contribution of ischemia in the noninfarcted zone contributes to the deterioration of already compromised myocardial function.

Coronary artery bypass grafting (CABG) in the setting of cardiogenic shock is generally associated with high surgical morbidity and mortality rates. Because the results of percutaneous interventions can be favorable, routine bypass surgery is often discouraged for these patients.

 

 

 

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26.                      http://reference.medscape.com/drug/intropin-dopamine-342435

27.                      http://reference.medscape.com/drug/levarterenol-levophed-norepinephrine-342443

28.                      http://reference.medscape.com/drug/adh-pitressin-vasopressin-342073

29.                      http://reference.medscape.com/drug/epipen-jr-epinephrine-342437

30.                      http://emedicine.medscape.com/article/152191-medication

 

 

 

Підготував Доброродній А.В.