Hypotension

Etiology

Blood pressure is primarily determined by cardiac output and total peripheral vascular resistance. Any condition that affects one or both of these factors can lead to hypotension.[5][6][7][8][9] Blood pressure refers to the force exerted by circulating blood on the walls of the arteries and is defined by the following equation:

• Blood pressure = Cardiac output × Total peripheral vascular resistance

SBP reflects the arterial pressure during cardiac contraction, whereas DBP represents the pressure during cardiac relaxation. MAP is the average blood pressure throughout one cardiac cycle and is primarily determined by DBP, as most of the cardiac cycle is spent in diastole. MAP is calculated using the following formula:

• Mean arterial pressure = (2/3 Diastolic blood pressure) + (1/3 Systolic blood pressure)

The heart functions as a pump to generate a pressure gradient that enables the distribution of blood throughout the body. This pumping capacity is referred to as cardiac output, which is calculated using the following equation:

• Cardiac output = Stroke volume × Heart rate

Total peripheral vascular resistance refers to the resistance encountered by blood as it flows through the terminal arterioles of various organs. This can be calculated using the following formula:

• Systemic vascular resistance = 80 × (Mean arterial pressure − Mean venous pressure) / Cardiac output

Alternatively, systemic vascular resistance can be calculated as:

• Systemic vascular resistance = (8 × L × η) / (π × [radius of a vessel]⁴)

Where L represents the length of the vessel, π is 3.14, and η is the blood viscosity.

As the length of vessels remains constant in the body and blood viscosity does not change rapidly, the primary modifiable factor is the vessel radius. A decrease in the diameter of arterioles increases resistance to blood flow, thereby raising blood pressure. Conversely, widening the diameter of terminal arterioles reduces resistance, which lowers blood pressure.

Total peripheral vascular resistance is primarily regulated by autonomic nervous system responses to fluctuations in blood pressure. The default state of arteriolar smooth muscle is relaxed or dilated. When autonomic input is impaired—often due to medications or disease—arterioles fail to constrict, potentially leading to hypotension. In orthostatic hypotension, a combination of autonomic nervous system dysfunction and mild hypovolemia, typically from dehydration, is the primary cause. While lying flat, fluid is evenly distributed throughout the body. However, upon standing, insufficient increases in heart rate and peripheral resistance result in a rapid, transient drop in blood pressure, leading to dizziness and, in some cases, syncope.

In healthy individuals, cardiac output and total peripheral vascular resistance function as compensatory feedback mechanisms. When cardiac output decreases, peripheral resistance compensates by constricting terminal arterioles to help maintain blood pressure. Conversely, when peripheral resistance decreases, cardiac output increases through an elevation in heart rate, thereby maintaining blood pressure. Disease states that affect stroke volume or heart rate can reduce cardiac output, impairing the body’s ability to generate adequate blood pressure.[10]

Medications can also contribute to hypotension. Calcium channel blockers and β-blockers are commonly used to lower heart rate in patients with tachydysrhythmias such as atrial fibrillation and supraventricular tachycardia.[11] However, excessive use of these agents may lead to toxicity, resulting in bradycardia and hypotension.[12] Diuretics can decrease stroke volume by reducing intravascular volume. In addition, various disease states, including arrhythmias, valvular regurgitation, valvular stenosis, heart failure (both diastolic and systolic), significant blood loss, and cardiac tamponade, can also cause hypotension.

Acute disease processes that can lead to hypotension are generally categorized into 4 broad groups—distributive shock, cardiogenic shock, hypovolemic shock, and obstructive shock. Distributive shock results from a loss of peripheral vascular resistance despite maintained cardiac function.[13][14] Conditions such as sepsis and anaphylaxis can cause this form of shock, characterized by widespread vasodilation that impairs perfusion of vital organs, even in the presence of normal or elevated cardiac output. In contrast, cardiogenic shock occurs when the heart fails to generate sufficient cardiac output despite the presence of maintained total peripheral resistance.[15] This type of shock is often seen in conditions such as acute myocardial infarction or severe heart failure, where the heart’s pumping ability is compromised.

Hypovolemic shock is characterized by a significant loss of total blood volume, leading to hypotension. Although cardiac output and peripheral resistance may usually be preserved, the reduced blood volume leads to insufficient perfusion. Common causes include fluid loss due to diuretics, gastrointestinal illness, or blood loss through trauma or gastrointestinal bleeding. Additionally, conditions such as cortisol deficiency in Addison disease can lead to fluid loss through the urine and relative cortisol insufficiency. Sheehan syndrome, a form of postpartum pituitary necrosis resulting from shock or hemorrhage, can also cause hypotension due to a deficiency of pituitary hormones.

Obstructive shock occurs when conditions obstruct blood flow, such as pulmonary embolism, tension pneumothorax, cardiac tamponade, constrictive pericarditis, and restrictive cardiomyopathies. These conditions reduce cardiac output, leading to hypotension. In some cases, hypotensive shock may result from a combination of these conditions. An example is Waterhouse-Friderichsen syndrome, which involves adrenal gland failure due to hemorrhage, often caused by a Neisseria bacterial infection. This condition impairs the adrenal glands' ability to produce essential hormones, resulting in hypotension and shock.

Epidemiology

The prevalence of hypotension varies significantly depending on the underlying cause. Nontraumatic, symptomatic episodes are more common in older adults. In contrast, physically active and otherwise healthy individuals often have lower resting blood pressures, which are typically not clinically concerning.

Pathophysiology

The autonomic nervous system regulates blood pressure through a balance between sympathetic and parasympathetic activity. The sympathetic branch increases blood pressure by elevating heart rate and constricting arterioles. In contrast, the parasympathetic branch lowers blood pressure by reducing heart rate and dilating arterioles, which increases vessel diameter. Disruption of these pathways, whether due to acute illness or pharmacological intervention, impairs compensation and contributes to hypotension.

History and Physical

Hypotension is often asymptomatic. When symptoms do occur, lightheadedness or dizziness is the most common. Syncope may result if blood pressure drops significantly. Persistent hypotension can lead to changes in mental status, such as decreased responsiveness, confusion, or focal neurological signs such as weakness or difficulty speaking.[16]

Associated symptoms can offer important clues to the underlying cause of hypotension. Acute myocardial infarction may present with chest pain, diaphoresis, and nausea or vomiting. Pulmonary embolism often presents with dyspnea and hypoxia. Fever may suggest an infectious process. Other accompanying symptoms may include an irregular heartbeat, headache, stiff neck, severe upper back pain, productive cough, diarrhea, vomiting, dysuria, allergic reactions, fatigue, and visual disturbances.

Physical examination findings can aid in diagnosing the underlying cause of hypotension. Warm skin, edema, increased secretions, and tachycardia may suggest septic or anaphylactic shock. In contrast, cardiogenic shock typically presents with cool, dry extremities and bradycardia. Obstructive shock may be indicated by jugular venous distention, peripheral edema, pulmonary crackles, distant heart sounds, and pulsus paradoxus. Indicators of hypovolemia include delayed capillary refill, dry mucous membranes, and reduced skin turgor..

Evaluation

Evaluation should be guided by the suspected underlying cause. Initial laboratory tests typically include a complete blood count with differential, basic metabolic panel, thyroid-stimulating hormone, and free thyroxine. An elevated white blood cell count, increased lactate levels, or signs of infection in tests such as urinalysis or chest radiography may indicate septic shock. A reduced hemoglobin concentration could suggest significant blood loss. Markedly elevated thyroid-stimulating hormone or low free thyroxine levels may suggest myxedema coma as the underlying cause. Electrocardiography, along with serum troponin and B-type natriuretic peptide levels, may assist in identifying cardiac etiologies.

Point-of-care ultrasonography (POCUS) is a valuable tool for evaluating and managing shock, especially in emergency settings. Commonly used protocols include the Focused Assessment with Sonography in Trauma (FAST) exam and the Rapid Ultrasound in Shock and Hypotension (RUSH) protocol.[17] Ultrasonography can aid in the early detection of critical conditions such as internal hemorrhage, pneumothorax, pleural effusion, pericardial effusion, and major vascular pathologies, including aortic dissection or aneurysm. Evaluation of the inferior vena cava can help assess fluid responsiveness.[18] Significant variability in inferior vena cava diameter suggests a high likelihood of fluid responsiveness, whereas minimal variability may support the early initiation of vasopressor therapy. When clinically indicated, advanced imaging modalities such as computed tomography (CT) and magnetic resonance imaging (MRI) should be pursued, particularly when acute surgical conditions are suspected. Please see StatPearls' companion resource, "Diagnostic Ultrasound Use in Undifferentiated Hypotension," for more information.

Treatment / Management

Asymptomatic hypotension generally does not require aggressive intervention. However, management should focus on identifying and addressing the underlying cause if the patient is symptomatic. Initial treatment typically begins with the administration of isotonic crystalloid. Obtaining blood cultures and initiating broad-spectrum antibiotics are essential if sepsis is suspected.[19]

Patients with confirmed surgical pathology should undergo prompt surgical evaluation, followed by appropriate intervention. In cases of acute hemorrhage, transfusion of blood products is warranted, and the source of bleeding must be identified and addressed. Definitive management may require consultation with a surgeon, interventional radiologist, or gastroenterologist.

Appropriate treatment should be initiated when cardiac etiologies, such as dysrhythmias or cardiogenic shock, are identified, often with input from a cardiologist. For patients presenting after an overdose of medications such as β-adrenergic antagonists or calcium channel blockers, early consultation with a poison control center or medical toxicologist is recommended. In cases of suspected anaphylactic shock, intramuscular epinephrine is the first-line treatment. Adjunctive therapies may include corticosteroids and antihistamines. Intravenous epinephrine can be considered for refractory cases.[20]

Patients who remain hypotensive despite initial management may require vasopressor support. Common agents include norepinephrine, vasopressin, and epinephrine. An MAP target greater than 65 mm Hg is commonly used as a treatment goal.[21] Please see StatPearls' companion resource, "Refractory Shock," for more information.(A1)

Differential Diagnosis

The differential diagnosis of hypotension is broad, and etiologies can be categorized into several major clinical groups based on underlying mechanisms.[22] While not exhaustive, the following list outlines common causes to consider. Management should be guided by the patient's history, physical examination, and diagnostic workup:

• Benign or asymptomatic hypotension.
• Orthostatic hypotension.
• Distributive shock: This includes septic shock, medication effects or overdose, and anaphylactic and neurogenic shock (eg, acute spinal cord injury).
• Cardiogenic shock: This may result from decompensated heart failure, medication effects or overdose, acute myocarditis, acute myocardial infarction, high-degree atrioventricular block, atrial fibrillation with rapid ventricular response, or ventricular dysrhythmias.
• Hypovolemic shock: This is caused by hemorrhagic causes (eg, trauma, gastrointestinal bleeding, and aortic rupture), dehydration, diabetic ketoacidosis, and hyperosmolar hyperglycemic state.
• Obstructive shock: This includes massive pulmonary and cardiac embolism, tension pneumothorax, cardiac tamponade, and decompensated pulmonary hypertension.
• Combined-type hypotensive shock.

Prompt identification of the underlying etiology is essential to guide effective treatment. Delays in diagnosis may result in avoidable complications and poorer clinical outcomes.

Prognosis

The prognosis of benign hypotension is typically very favorable. In contrast, symptomatic hypotension has a variable prognosis, depending on the underlying etiology and the severity of the condition. Early recognition and treatment of the underlying etiology are crucial for improving outcomes.

Complications

If left untreated, hypotension can result in inadequate perfusion of vital organs, leading to end-organ damage and, if not addressed, potentially death. Treatment should focus on identifying and managing the underlying cause to prevent these serious complications. Possible complications of untreated hypotension include decreased responsiveness, acute renal failure, cardiac dysrhythmias, bowel ischemia, cerebrovascular accidents, respiratory failure, coma, and, ultimately, death. Prompt intervention is essential to mitigate these risks and preserve organ function.