Hemodynamic Emergencies

Cardiogenic Shock

Overview

In everyday conversation, the word shock may describe emotional distress, but in emergency medicine it has a specific and potentially life-threatening meaning.
Shock occurs when the body cannot provide adequate blood flow and oxygen delivery to its tissues and vital organs.

Early recognition is essential because delayed treatment can lead to progressive organ dysfunction and death.

• Adequate tissue perfusion depends on three major components:
  • The pump — the heart.
  • The vessels — the circulatory system.
  • The fluid — circulating blood volume.
• Shock develops when one or more of these components fail.
• The four major categories of shock include:
  • Cardiogenic shock.
  • Hypovolemic shock.
  • Obstructive shock.
  • Distributive shock.
    • Anaphylactic shock.
    • Neurogenic shock.
    • Septic shock.

How Cardiogenic Shock Develops

Cardiogenic shock occurs when the heart cannot pump enough blood to maintain adequate circulation to the body’s tissues and organs.

• Several cardiac conditions may cause cardiogenic shock.
• Common causes include:
  • Severe left ventricular failure.
  • Acute myocardial infarction.
  • Advanced congestive heart failure.
  • Serious cardiac dysrhythmias.
  • Other conditions that significantly reduce myocardial pumping ability.
• When the heart’s pumping ability decreases:
  • Stroke volume falls.
  • Cardiac output decreases.
  • Blood pressure and tissue perfusion may decline.
  • Oxygen delivery to vital organs becomes inadequate.
  • The patient may eventually develop multiple-organ dysfunction or cardiac arrest.

Cardiac Output

• Cardiac output is the amount of blood pumped by the heart during one minute.
• It depends on:
  • Heart rate — the number of heartbeats per minute.
  • Stroke volume — the amount of blood ejected during each ventricular contraction.
• Cardiac output can be expressed as:
  • Cardiac Output = Heart Rate × Stroke Volume
• Cardiogenic shock develops when cardiac output falls enough that the body’s tissues can no longer be adequately perfused.

Recognizing Cardiogenic Shock

One of the most important steps in managing shock is early recognition and prompt activation of appropriate medical resources. This responsibility falls within the scope of every healthcare provider. The following clinical information can help identify patients who may be at risk for or already experiencing cardiogenic shock.

Clinical Signs: Evidence of poor perfusion, including pale or abnormal skin color, cool extremities, delayed capillary refill greater than 2 seconds, and hypotension; cyanosis; decreased oxygen saturation; abnormal lung sounds or pulmonary edema; cough that may or may not produce pink, frothy sputum; altered mental status or confusion; decreased level of consciousness; and possible cardiac arrest.

Reported Symptoms: Chest pain or discomfort, trouble breathing, shortness of breath, and dizziness.

Relevant Medical History: Coronary artery disease, previous myocardial infarction, heart failure, and hypertension.

Common Medications: Nitroglycerin, diuretics, beta blockers, calcium channel blockers, and ACE inhibitors.

The presence of pulmonary edema can be a helpful clinical finding when distinguishing cardiogenic shock from other forms of shock in the prehospital setting.

Prehospital Management

Basic prehospital care for a patient with cardiogenic shock is important, although treatment options may be limited. Assessment and management should continuously focus on Airway, Breathing, and Circulation.

When cardiogenic shock is strongly suspected, providers should be prepared to manage airway compromise caused by pulmonary edema and airway secretions, as well as hypoxia. Airway positioning and management, suctioning, supplemental oxygen, and positive-pressure ventilation may be required depending on the patient’s condition.

The patient should also be kept warm because decreased perfusion can interfere with the body’s ability to maintain normal temperature. Circulation may be significantly impaired because the heart is unable to pump effectively. Although the underlying pump failure cannot usually be corrected in the field, rapid recognition, early activation of ALS resources, and prompt transport to an appropriate hospital are essential.

Managing Common Causes of Cardiogenic Shock

Treating the suspected cause before severe hypoperfusion develops may improve the patient’s condition and outcome. Two of the most common conditions associated with cardiogenic shock are myocardial infarction and congestive heart failure.

Ischemic Chest Pain / Suspected Myocardial Infarction

• Recognize signs and symptoms as early as possible.
• Assess and manage the airway, breathing, and circulation.
• Administer 324 mg of chewable aspirin orally, when indicated.
• Assist the patient with prescribed sublingual nitroglycerin, when appropriate.
• Activate ALS and transport resources early.
• Provide rapid transport and notify a hospital with cardiac catheterization capabilities as soon as possible.

Always follow local protocols and verify that the patient has no allergy or contraindication before administering or assisting with any medication.

Prehospital treatment for a suspected myocardial infarction can help support the patient while definitive care is being arranged. Aspirin helps reduce further platelet aggregation and clot formation in the coronary arteries, while nitroglycerin may improve coronary blood flow and decrease the workload of the heart when appropriate.

These interventions may help reduce myocardial ischemia and support cardiac function, potentially decreasing the severity of systemic hypoperfusion associated with cardiogenic shock. Definitive treatment may require hospital-based procedures to restore blood flow through an obstructed coronary artery, so transport to a capable facility should not be unnecessarily delayed.

Congestive Heart Failure Management

Basic prehospital treatment of congestive heart failure (CHF) is relatively limited and often resembles the supportive treatment used for cardiogenic shock. Early recognition and intervention are important because they may help prevent progression to severe cardiogenic shock or respiratory arrest.

Patients should receive appropriate airway and breathing support based on their condition, and early activation of ALS resources can be especially important when the patient shows signs of worsening respiratory or circulatory compromise.

High Blood Pressure Emergencies

Overview

High blood pressure (hypertension or HTN) refers to blood pressure that is higher than the expected normal range. Hypertension is a major contributor to long-term cardiovascular disease and is associated with an increased risk of serious emergencies such as stroke and myocardial infarction.

In the prehospital environment, EMTs generally do not treat an elevated blood pressure reading by itself. Care should instead focus on identifying possible underlying causes, recognizing associated emergencies, and treating the patient’s symptoms according to local protocol.

Key Types and Concepts

Hypertension may be described as primary, secondary, systemic, or pulmonary.

Primary hypertension, also called essential hypertension, develops when elevated blood pressure itself is the main condition. It is the most common form and is usually what patients mean when they report a history of high blood pressure.

Secondary hypertension develops because of another medical condition or medication. The elevated blood pressure may improve when the underlying cause is identified and treated.

Systemic hypertension involves the blood vessels supplied by the left side of the heart. This is the type of blood pressure measured with a standard blood pressure cuff and is generally what is meant when the term hypertension is used without further description.

Pulmonary hypertension involves increased pressure within the pulmonary circulation supplied by the right ventricle. Evaluation may require more advanced testing. Possible causes include heart disease, lung disease, and pulmonary blood clots. Some patients may be prescribed pulmonary vasodilator medications such as sildenafil.

Blood Pressure Terminology

Systolic blood pressure (SBP) is the arterial pressure created when the ventricles contract. It is represented by the upper number in a blood pressure reading.

Diastolic blood pressure (DBP) is the arterial pressure present while the ventricles relax between contractions. It is represented by the lower number.

Blood pressure is influenced by multiple physiologic factors, including vascular resistance, circulating blood volume, and cardiac output.

Vascular tone depends on the contraction and relaxation of vascular smooth muscle. Vasoconstriction increases resistance and tends to raise blood pressure, while vasodilation decreases resistance and generally lowers blood pressure.

Circulating blood volume is regulated largely by the kidneys. Sodium balance, electrolyte regulation, and urine production all contribute to maintaining blood volume.

Cardiac output is influenced by preload, afterload, contractility, and heart rate.

• Preload refers to the amount of blood returning to and filling the heart before contraction.
  • Closely related to venous return.
  • Increased preload may increase cardiac output when the heart is functioning effectively.
• Afterload is the resistance the ventricle must overcome to eject blood.
  • Closely associated with arterial vascular resistance and blood pressure.
  • Excessive afterload can decrease cardiac output.
• Contractility describes the strength of myocardial contraction.
  • Greater contractility generally increases cardiac output and may increase blood pressure.
• Heart rate also affects cardiac output because it influences how often the heart pumps blood each minute.

Autonomic Regulation of Blood Pressure

• Sympathetic nervous system activity generally increases blood pressure.
  • Alpha-receptor stimulation in blood vessels causes vasoconstriction.
  • Beta-receptor stimulation in the heart can increase heart rate and contractility.
• Parasympathetic nervous system activity primarily affects heart rate.
  • It has relatively little direct effect on vascular tone or myocardial contractility.
  • Muscarinic receptor stimulation can decrease the heart rate.

Hypertension Associated With Cardiogenic Pulmonary Edema

• Severe systemic hypertension can markedly increase the afterload against which the left ventricle must pump.
• Increased afterload may reduce left ventricular cardiac output.
• Reduced cardiac output can contribute to or worsen pulmonary fluid congestion.
• Acute exacerbations of congestive heart failure may occur with significantly elevated blood pressure.

Elevated Blood Pressure With Brain Injury

• Hypertension may occur as part of Cushing’s reflex, which can include increased blood pressure and reflex bradycardia.
• In this situation, increased sympathetic activity may be the body’s attempt to maintain adequate cerebral perfusion when intracranial pressure rises.

Hypertensive Disorders During Pregnancy

• Preeclampsia is a hypertensive disorder that develops during pregnancy.
  • It involves new-onset hypertension after approximately 20 weeks of gestation.
  • It may also be associated with proteinuria or evidence of organ dysfunction.
• Eclampsia is a life-threatening complication of preeclampsia.
  • It is characterized by new-onset seizures in a patient with preeclampsia.
  • Management may include magnesium sulfate and anticonvulsant therapy according to EMS scope and local protocol.

Understanding Blood Pressure Values

• A healthy adult blood pressure is often near 110/70 mmHg, although normal values vary from person to person.
• Traditionally, hypertension has commonly been recognized when systolic pressure is greater than 140 mmHg or diastolic pressure is greater than 90 mmHg.
• A patient’s normal baseline, medical history, symptoms, and overall clinical presentation should always be considered rather than relying on a single blood pressure value.

Identifying Hypertension in the Field

• Use the correct blood pressure cuff size for the patient.
• A cuff that is too large may produce an inaccurately low reading.
• A cuff that is too small may produce an inaccurately high reading.
• Consider obtaining a manual blood pressure when an automated reading appears inconsistent with the patient’s presentation.
• Compare blood pressure in both arms when clinically appropriate.
• Evaluate the patient for associated signs and symptoms.
  • Hypertension accompanied by symptoms may indicate a significant underlying condition.
    • Possible symptoms include headache, blurred vision, chest discomfort, shortness of breath, dizziness, neurologic changes, or other concerning findings.
  • A patient may also have elevated blood pressure without symptoms.
    • Determine whether the elevated pressure is contributing to the emergency or is simply an abnormal vital sign.
  • Elevated blood pressure without symptoms may occur for several reasons and should be interpreted in the context of the full assessment.
  • Remember that hypertension can be a sign of another serious condition rather than the primary emergency.

Medication History

• Review the patient’s medication list for drugs commonly used to manage hypertension.
  • ACE inhibitors often have names ending in -pril, such as lisinopril.
  • Angiotensin receptor blockers (ARBs) commonly end in -sartan, such as losartan.
  • Diuretics may include hydrochlorothiazide, spironolactone, or furosemide.
  • Beta blockers frequently end in -lol, such as metoprolol.
  • Alpha blockers may end in -zosin, such as doxazosin.
  • Calcium channel blockers include medications such as amlodipine.

Prehospital Care and Management

• Do not attempt to lower a patient’s blood pressure solely because the reading is elevated unless treatment is specifically authorized by protocol, medical direction, or another identified emergency requires intervention.
• Focus treatment on the patient’s presenting condition, signs, and symptoms.
  • Treat pain appropriately when pain may be contributing to elevated blood pressure.
  • Manage airway and breathing problems when present.
    • For cardiogenic pulmonary edema, positive airway pressure such as CPAP and medications such as nitrates may be considered when allowed by protocol and when no contraindications exist.
  • Manage preeclampsia or eclampsia according to local EMS guidelines.
• Patients with symptomatic hypertension or other concerning findings should generally be transported for further evaluation.
• Perform a complete assessment and remember that markedly elevated blood pressure may be associated with serious conditions such as stroke, acute coronary syndrome, heart failure, or other emergencies.

Low Blood Pressure and Shock

Introduction

Hypotension means blood pressure is lower than normal. Adequate blood pressure is essential for proper tissue perfusion because it helps deliver oxygen and other necessary nutrients throughout the body. When blood pressure becomes too low, organs and tissues may not receive enough oxygenated blood to function normally.

Core Concepts

Blood pressure plays a major role in maintaining adequate tissue perfusion. Sufficient pressure is needed to deliver oxygen and nutrients to vital organs. Blood pressure is influenced primarily by cardiac output and vascular resistance.

Cardiac output is the amount of blood pumped by the heart over a given period of time. Vascular resistance is created by the tone of the blood vessels, especially the contraction of smooth muscle within the peripheral circulation.

When blood pressure falls, the body may attempt to maintain perfusion by increasing cardiac output, increasing vascular resistance, or using both mechanisms.

Hypotension is commonly associated with a blood pressure below approximately 90/60 mmHg. A systolic blood pressure below 90 mmHg is often considered hypotensive in adults. A mean arterial pressure (MAP) below approximately 65 mmHg may also suggest inadequate perfusion.

• Mean arterial pressure (MAP) represents the average arterial pressure during one complete cardiac cycle.
  • A commonly used formula is:
    MAP = DBP + 1/3 of the pulse pressure
    • Pulse pressure is the difference between systolic and diastolic pressure.
  • Example: for a blood pressure of 110/70 mmHg
    • Pulse pressure = 110 − 70 = 40
    • MAP = 70 + 1/3(40)
    • MAP ≈ 83 mmHg

In EMS, shock refers to inadequate tissue perfusion in which the body is unable to provide sufficient blood flow and oxygen to vital organs.

Four Major Forms of Shock

Hypovolemic Shock

Hypovolemic shock occurs when there is not enough circulating blood or fluid volume to adequately perfuse the body. Causes may include:

• Significant dehydration.
• Blood loss caused by trauma or another source of hemorrhage.

A useful way to remember hypovolemic shock is to think of it as a volume or fluid problem.

Cardiogenic Shock

Cardiogenic shock occurs when the heart cannot pump enough blood to meet the metabolic needs of the body. Possible causes and findings include:

• Severe heart failure.
• Acute myocardial infarction.
• Cool, pale, or dry extremities may be present because of poor peripheral perfusion.

This can be remembered as primarily a pump problem.

Distributive Shock

Distributive shock develops when vascular tone is lost and blood vessels become abnormally dilated. This decreases vascular resistance and can impair tissue perfusion.

Common causes include:

• Septic shock, in which widespread infection and the inflammatory response cause vasodilation.
• Neurogenic shock, which may occur when sympathetic nervous system activity is disrupted because of spinal cord or central nervous system injury.
• Anaphylactic shock, which is caused by a severe allergic reaction that produces widespread vasodilation and increased vascular permeability.
• Patients with distributive shock may have warm skin early in the process, especially with septic, neurogenic, or anaphylactic shock, although presentation varies depending on the cause and stage.

This type of shock can be remembered as a container or vascular-space problem.

Obstructive Shock

Obstructive shock occurs when a physical obstruction interferes with normal blood flow through the cardiovascular system.

Possible causes and findings include:

• Tension pneumothorax.
• Pulmonary embolism.
• Other conditions that mechanically restrict circulation.
• Findings may include jugular venous distention or signs of impaired cardiac output depending on the cause.

Early Findings of Shock

Initial signs and symptoms may include:

• Pale, cool, or diaphoretic skin.
• Warm extremities in certain distributive forms of shock.
• Delayed capillary refill.
• Anxiety, restlessness, or a feeling of impending doom.
• Tachycardia.

Compensated and Decompensated Shock

The stages of shock reflect whether the body is still able to maintain perfusion through compensatory mechanisms.

Compensated shock occurs when the body’s compensatory responses are still able to maintain blood pressure and perfusion despite an underlying problem. Findings may include tachycardia, vasoconstriction, cool skin, and delayed capillary refill while blood pressure remains relatively preserved.

Decompensated shock develops when compensation is no longer sufficient. Blood pressure falls, tissue perfusion worsens, and signs of organ dysfunction may begin to appear.

Irreversible shock is the advanced stage in which prolonged hypoperfusion causes severe cellular and organ damage that may no longer respond to treatment.

Autonomic Response to Shock

The body responds to hypoperfusion by activating the sympathetic nervous system.

• Sympathetic nervous system activation
  • Epinephrine and norepinephrine are released in response to poor perfusion.
  • Alpha-receptor stimulation increases vascular tone.
    • Blood vessels constrict.
    • Blood flow is redirected toward vital central organs.
  • Beta-receptor stimulation increases cardiac activity.
    • Heart rate increases.
    • Myocardial contractility increases.

Adequate Pressure Is Necessary for Vital Organs

Brain

• Inadequate cerebral perfusion may initially cause altered mental status, confusion, restlessness, or decreased responsiveness.
• Severe or prolonged hypoperfusion can lead to brain-cell injury and loss of normal neurologic function.

Heart

• The myocardium receives much of its blood supply during diastole.
• If coronary perfusion becomes inadequate, the heart may lose the oxygen and energy required to maintain effective cardiac output.

Kidneys

• The kidneys help regulate acid-base balance, remove waste products from the blood, and maintain proper electrolyte concentrations.
• Reduced renal perfusion can cause decreased urine production.
• Prolonged hypoperfusion may lead to accumulation of metabolic waste products, electrolyte abnormalities, and acid-base disturbances that further affect other organ systems.

Postural Hypotension

Orthostatic hypotension is a drop in blood pressure that occurs when a person changes position, particularly when moving from lying down or sitting to standing.

It is common in patients who are dehydrated or have decreased circulating blood volume. When the patient stands, blood can temporarily pool in the lower extremities. If the cardiovascular system cannot compensate quickly enough, cerebral perfusion decreases.

Orthostatic hypotension is commonly associated with dizziness, lightheadedness, weakness, or syncope.

Assessment and Recognition

• Begin with an assessment for evidence of impaired circulation.
  • Evaluate skin color, temperature, and moisture.
    • Pale, cool, or clammy skin may suggest poor perfusion.
  • Assess peripheral pulses.
    • A weak or absent radial pulse may indicate significant circulatory compromise.
    • However, the presence of a radial pulse does not guarantee that blood pressure or tissue perfusion is adequate.
  • Evaluate capillary refill when appropriate.
  • Assess the patient’s mental status.
• Obtain an accurate blood pressure using an appropriately sized cuff.
  • Consider obtaining a manual blood pressure when an automated reading appears unreliable or inconsistent with the patient’s presentation.

Prehospital Treatment and Management

Initial Care for Hypoperfusion

• Position the patient supine when clinically appropriate and when breathing or airway conditions do not require another position.
  • Routine Trendelenburg positioning is generally not recommended for the treatment of shock.
  • Routine elevation of the legs is also not considered a substitute for appropriate shock management.
• Provide oxygen when indicated based on the patient’s respiratory status and local protocol.
• Prevent heat loss and keep the patient warm, especially in patients experiencing hemorrhagic shock.
• Control significant external bleeding as early as possible.
• Request ALS resources when appropriate and available.
• Administer intramuscular epinephrine for anaphylaxis when indicated and according to EMS protocol.

Permissive Hypotension With Hemorrhage

• Some patients with uncontrolled hemorrhage may be managed using a strategy known as permissive hypotension, depending on EMS protocol and medical direction.
• This approach avoids unnecessarily raising blood pressure before bleeding is controlled and may involve limiting excessive crystalloid administration.
• The goal is to maintain enough perfusion for vital organs while reducing the possibility of worsening uncontrolled bleeding.
• Permissive hypotension is generally considered for selected hemorrhagic trauma patients and is not routinely applied to patients with suspected isolated traumatic brain injury or spinal cord injury.
• Continue searching for the underlying reason for hypotension and treat the specific cause whenever possible.

Always identify the underlying cause of low blood pressure and manage the condition according to the patient’s presentation, EMT scope of practice, local protocols, and medical direction.

Pericardial Tamponade Emergency

In prehospital care, EMTs must recognize conditions that are either common or immediately life-threatening. Cardiac tamponade is less common than many other cardiovascular emergencies, but it is a serious condition that can rapidly progress to obstructive shock and cardiac arrest. Because its findings may be subtle or confused with other illnesses or injuries, early recognition and rapid transport are especially important.

This section reviews the basic anatomy and causes of cardiac tamponade, common findings that may raise suspicion, assessment priorities, and supportive interventions appropriate for the EMT level.

Understanding Cardiac Tamponade

Cardiac tamponade develops when blood, fluid, or occasionally air accumulates within the pericardial space surrounding the heart.

Normally, a small amount of fluid exists between the layers of the pericardium to reduce friction as the heart contracts and relaxes. When an abnormal amount of material collects in this limited space, pressure begins to build around the heart.

As intrapericardial pressure increases, the heart—particularly the right-sided chambers—has increasing difficulty filling during diastole. Reduced ventricular filling decreases stroke volume and cardiac output. If the process continues, systemic perfusion falls and the patient may develop obstructive shock.

Untreated cardiac tamponade can become rapidly fatal.

Important: The material collecting in the pericardial space may include blood, serous fluid, inflammatory fluid, or, less commonly, air depending on the underlying cause.

Causes and Development

Cardiac tamponade may develop gradually or suddenly.

A slowly developing pericardial effusion may allow the pericardium some time to stretch, so a relatively large amount of fluid can accumulate before severe symptoms appear. In contrast, rapidly accumulating blood or fluid can produce life-threatening pressure even when the total volume is smaller.

Gradual or Subacute Causes

Conditions that may slowly produce a pericardial effusion include:

• Pericarditis or inflammation of the pericardium.
• Malignancy.
• Advanced renal disease.
• Severe hypothyroidism.
• Autoimmune or inflammatory disease.

Sudden or Acute Causes

Acute cardiac tamponade may occur because of:

• Myocardial rupture associated with an acute myocardial infarction.
• Penetrating or blunt trauma to the chest.
• Injury associated with invasive cardiac procedures or surgery.
• Complications involving cardiac or vascular structures.

The speed of fluid accumulation is often as important as the total amount of fluid present. A slow internal bleed may initially produce less obvious findings than a rapidly expanding hemorrhage.

Clinical Findings

Cardiac tamponade does not always present with every classic finding. EMTs should consider the overall clinical picture, mechanism of injury, medical history, vital signs, and evidence of poor perfusion.

Possible Signs

• Evidence of penetrating or blunt chest trauma.
• Recent cardiac surgery or an invasive cardiac procedure.
• Signs of an underlying infection or inflammatory illness.
• Jugular venous distention.
• Muffled or distant heart sounds.
• Narrowing pulse pressure.
• Hypotension as the condition progresses.
• Tachycardia.
• Tachypnea.
• Weak peripheral pulses.
• Pale, cool, or clammy skin.
• Cyanosis in severe cases.
• Altered mental status.
• Syncope or loss of consciousness.
• Other findings of poor systemic perfusion.

Beck’s Triad

The traditional Beck’s triad associated with cardiac tamponade consists of:

• Hypotension.
• Jugular venous distention.
• Muffled heart sounds.

The complete triad may not be present, particularly early in the condition, so its absence does not rule out cardiac tamponade.

Pulsus Paradoxus

Pulsus paradoxus refers to an exaggerated decrease in systolic blood pressure during inspiration, generally greater than about 10 mmHg.

Although this finding can occur with cardiac tamponade, identifying it accurately in the field may be difficult and should not delay treatment or transportation.

Possible Symptoms

Patients may report:

• Chest pain or chest pressure.
• Shortness of breath.
• Difficulty breathing when lying flat.
• Lightheadedness or dizziness.
• Generalized weakness.
• Nausea.
• Fainting or near-fainting.

The quality and severity of symptoms depend greatly on the underlying cause and the speed at which tamponade develops.

Patients may also show findings related to the original problem, such as traumatic injury, myocardial infarction, infection, or another cardiovascular emergency.

Assessment

Begin with the standard assessment of Airway, Breathing, and Circulation, while identifying and treating immediate life threats.

Cardiac tamponade should be considered when a patient has a compatible mechanism, medical history, or combination of circulatory findings. Particular concern is warranted when poor perfusion occurs after penetrating chest trauma or when hypotension is accompanied by jugular venous distention.

Assessment should include the patient’s overall appearance, mental status, respiratory effort, skin condition, pulse quality, blood pressure, and evidence of trauma or underlying cardiac disease.

When cardiac tamponade is suspected, attempt to determine what may have caused it without delaying transportation. Information about recent trauma, cardiac procedures, surgery, myocardial infarction, renal disease, infection, or other illnesses may help receiving providers prepare for definitive treatment.

Prehospital Management

Definitive treatment for cardiac tamponade requires removal of pressure from around the heart, usually through pericardial drainage or surgical intervention. These procedures are beyond the EMT scope in routine prehospital care.

For the EMT, treatment is primarily supportive while arranging rapid transportation to an appropriate facility.

• Maintain and protect the airway as needed.
• Assess breathing and provide ventilatory assistance when necessary.
• Administer supplemental oxygen when indicated by hypoxemia, respiratory distress, or local protocol.
• Continuously reassess circulation and signs of shock.
• Control external bleeding and manage associated traumatic injuries.
• Keep the patient warm and minimize unnecessary movement.
• Request ALS assistance early when appropriate.
• Minimize scene time when tamponade or significant obstructive shock is suspected.
• Transport rapidly to a facility capable of providing definitive cardiovascular or trauma care.
• Be prepared for deterioration and cardiac arrest.

Ventilation Considerations

Positive-pressure ventilation may be necessary when the patient cannot ventilate adequately or is in respiratory or cardiac arrest. However, increasing intrathoracic pressure can further reduce venous return in a patient with severely impaired cardiac filling.

For this reason, EMTs should provide ventilation when clinically required while avoiding unnecessary or excessive ventilation and following local protocol.

Trauma Considerations

For suspected traumatic tamponade:

• Identify and manage other immediately life-threatening chest injuries.
• Control accessible external hemorrhage.
• Provide spinal motion restriction only when indicated by the mechanism and patient assessment according to current protocol.
• Avoid delaying transport for nonessential interventions.

Rapid Transport Is Critical

A patient with cardiac tamponade may progress from compensated shock to severe hypotension and cardiac arrest. Prehospital care cannot correct the pressure surrounding the heart, making early recognition, supportive care, ALS activation when appropriate, and rapid transport the primary EMT priorities.

Continue reassessing the patient throughout transport and be prepared to begin CPR and other resuscitative measures if cardiac arrest occurs.

Key NREMT concept: Cardiac tamponade is a form of obstructive shock in which pressure surrounding the heart prevents adequate ventricular filling, reducing cardiac output and tissue perfusion.

Aortic Aneurysm Emergencies

Aortic aneurysms are not among the most frequently encountered prehospital emergencies, but they can become rapidly life-threatening. Because the condition may be overlooked or mistaken for other illnesses, EMTs should recognize important risk factors, warning signs, and symptoms that may suggest an aneurysm, dissection, or rupture.

This study section reviews the major types of aortic aneurysms, possible complications, common risk factors, clinical findings, and basic EMT-level management.

Overview of the Aorta and Aneurysms

The aorta is the body’s largest artery. It carries oxygenated blood from the left ventricle to the major organs and peripheral tissues.

• The aorta begins at the heart as the ascending aorta.
  • The ascending aorta is part of the thoracic portion of the aorta.
• The vessel then forms the aortic arch and continues downward through the chest as the descending thoracic aorta.
• After passing through the diaphragm, it becomes the abdominal aorta.
  • The abdominal aorta eventually divides into the iliac arteries.

An aneurysm develops when part of an arterial wall becomes weakened and expands beyond its normal diameter. This creates an abnormal balloon-like enlargement that may become increasingly fragile as it grows.

The two major locations are:

• Thoracic aortic aneurysm (TAA), which occurs within the chest.
  • An ascending aortic aneurysm is considered a type of thoracic aneurysm.
• Abdominal aortic aneurysm (AAA), which occurs below the diaphragm within the abdomen.
  • AAA is the more commonly encountered type.

Study Tip: The abbreviation AAA means abdominal aortic aneurysm, not ascending aortic aneurysm.

Major Complications

Weakening of the aortic wall creates the potential for dissection or rupture.

• Aortic dissection occurs when a tear develops in the inner lining of the aorta and blood enters between layers of the vessel wall, creating a false channel or lumen.
• Aortic rupture occurs when the damaged vessel wall tears completely and blood escapes from the aorta.
• Larger aneurysms generally carry a greater risk of dissection or rupture.
  • As aneurysm size increases, the chance of serious complications usually increases.
• Both dissection and rupture can be rapidly fatal without definitive hospital treatment.

Risk Factors

Recognizing risk factors can increase an EMT’s suspicion when evaluating a patient with unexplained chest, back, abdominal, or neurologic symptoms.

Common risk factors include:

• Atherosclerosis.
• Long-term hypertension.
• History of tobacco use.
• Family history of aortic aneurysm.
• Previous aneurysm.
• Increasing age.
• Male sex, particularly for abdominal aortic aneurysm.
• Connective-tissue disorders such as Marfan syndrome.
• Loeys-Dietz syndrome.
• Abnormalities involving the aortic valve.
• Certain inherited vascular disorders.
• Pregnancy in selected patients with underlying vascular risk.

Potential Causes

Some aortic aneurysms develop without a clearly identifiable cause. Others are associated with conditions that weaken or damage the aortic wall.

Possible causes or contributing conditions include:

• Atherosclerotic disease.
• Chronic hypertension.
• Marfan syndrome.
• Loeys-Dietz syndrome.
• Inflammation or infection involving blood vessels.
• Aortic valve abnormalities.
• Traumatic injury.
• Inherited abnormalities of connective tissue or the vascular wall.

Recognizing an Aortic Aneurysm

Patients with an aortic aneurysm may have no symptoms until the aneurysm becomes large, dissects, or ruptures. Findings vary depending on the location of the aneurysm and whether a complication has occurred.

A thoracic aneurysm may sometimes produce chest discomfort or tenderness. An abdominal aneurysm may occasionally produce a noticeable or pulsatile sensation in the abdomen.

Assessment Caution: Avoid repeatedly or aggressively palpating a suspected abdominal aneurysm. Your priority is recognition, supportive care, and transport rather than attempting to define the aneurysm manually.

Possible Findings With a Thoracic Aortic Aneurysm

Symptoms may include:

• Sudden or sharp chest pain.
• Back pain.
• Shortness of breath.
• Difficulty breathing.
• Difficulty swallowing.
• Pressure or discomfort within the chest.

Possible Findings With an Abdominal Aortic Aneurysm

Symptoms may include:

• Deep abdominal pain.
• Throbbing or pulsating discomfort.
• Lower back or flank pain.
• Pain extending toward the groin, buttocks, or legs.
• A sensation of pulsation within the abdomen.

Findings Associated With Aortic Dissection

Aortic dissection can cause symptoms that resemble myocardial infarction, stroke, or other cardiovascular emergencies.

Possible signs include:

• Hypertension, particularly early in the event.
• Hypotension when severe circulatory compromise or rupture occurs.
• Significant difference between blood pressure readings in the two arms.
• Unequal or absent peripheral pulses.
• Weakness in an arm or leg.
• Altered mental status.
• Syncope.
• Neurologic deficits that resemble a stroke.
• Signs of myocardial ischemia or infarction.
• Signs of poor perfusion.
• Muffled heart sounds if the dissection produces cardiac tamponade.

Possible symptoms include:

• Sudden, severe chest, back, or neck pain.
• Pain that changes location as the dissection progresses.
• Severe pain radiating from the chest toward the back.
• Pain involving an arm or leg.
• Paresthesia, numbness, or tingling.
• Extremity weakness.
• Stroke-like complaints.
• Symptoms resembling an acute coronary syndrome.
• Abdominal or pelvic discomfort in some patients.

A combination of sudden severe chest pain and new neurologic deficits should increase suspicion for aortic dissection.

Findings Associated With Aortic Rupture

Rupture can result in massive internal hemorrhage and rapid development of hypovolemic shock.

Possible signs include:

• Sudden evidence of shock or severe hypoperfusion.
• Hypotension.
• Pale, cool, or clammy skin.
• Weak or absent peripheral pulses.
• Altered mental status.
• Syncope or sudden loss of consciousness.
• Rapid deterioration.
• Muffled heart sounds if bleeding results in cardiac tamponade.
• Hemoptysis in selected thoracic ruptures.
• Cardiac arrest.

Possible symptoms include:

• Severe chest pain.
• Severe back pain.
• Severe abdominal pain.
• Shortness of breath.
• Difficulty swallowing.
• Sudden weakness or lightheadedness.
• A strong sensation or urge to have a bowel movement in some abdominal presentations.

Important: A dissection may progress to rupture. Therefore, findings of dissection may appear before signs of catastrophic internal bleeding develop.

Prehospital Treatment and Transport

Definitive treatment depends on the location, size, and stability of the aneurysm. Small, stable aneurysms may be monitored medically, while symptomatic aneurysms, dissections, or ruptures may require emergency vascular or cardiothoracic surgery.

For the EMT, care is primarily supportive while arranging prompt transport.

Basic Interventions

• Recognize high-risk presentations early.
• Maintain the airway.
• Assess and support breathing.
• Continuously evaluate circulation and perfusion.
• Place the patient in a position of comfort when appropriate.
• Limit unnecessary physical activity or exertion.
• Provide supplemental oxygen when indicated by hypoxemia, respiratory distress, or protocol.
• Assist ventilation when the patient cannot ventilate adequately.
• Treat signs of shock according to local EMS protocol.
• Keep the patient warm.
• Reassess mental status, pulse, blood pressure, and respiratory status frequently.
• Request ALS resources early when appropriate.

Transport Considerations

• Minimize unnecessary scene time in patients with suspected dissection or rupture.
• Transport to an appropriate receiving facility capable of providing definitive cardiovascular or vascular care when feasible.
• Consider local transport capabilities, distance, and available ground or air medical resources.
• Provide early hospital notification when the patient’s condition is critical or aortic rupture/dissection is strongly suspected.

Key NREMT concept: An aortic aneurysm is a weakened, enlarged section of the aorta. Dissection involves separation of the vessel wall layers, while rupture causes major internal bleeding. Sudden severe chest, back, or abdominal pain with signs of poor perfusion, pulse differences, neurologic findings, or shock should raise concern for a life-threatening aortic emergency.