What are the etiologies of hypotension?

Etiologies of Hypotension

Hypotension arises from four primary pathophysiologic mechanisms: decreased cardiac output (cardiogenic), reduced intravascular volume (hypovolemic), pathologic vasodilation (distributive), or mechanical obstruction to blood flow (obstructive), with each category distinguished by specific hemodynamic profiles and clinical presentations.

Cardiogenic Causes

Primary myocardial dysfunction leading to inadequate cardiac output characterizes this category, with cardiac index <2.2 L/min/m² and elevated systemic vascular resistance as compensatory vasoconstriction attempts to maintain perfusion pressure 1.

Acute Myocardial Infarction

• Occurs in 7-10% of AMI cases, representing the most common cause of cardiogenic shock with 30-day mortality rates of 40-45% despite contemporary treatment 1.
• Hemodynamic profile shows cardiac index <2.2 L/min/m², pulmonary capillary wedge pressure >15 mmHg, and elevated central venous pressure >15 mmHg 1.

Congestive Heart Failure

• Physical examination findings of pulmonary congestion (rales, tachypnea, pulmonary edema) and jugular venous distension indicate high risk of sudden death or early mortality 2.
• Patients with poor left ventricular function and cardiac syncope face greater risk of sudden death 2.

Mechanical Complications

• Valvular heart disease causing obstruction to flow (aortic stenosis, hypertrophic cardiomyopathy) may precipitate hypotension, particularly in young patients with family history of sudden death 2.

Hypovolemic Causes

Absolute or relative intravascular volume depletion produces hypotension through decreased venous return and preload, characterized by low cardiac index, elevated systemic vascular resistance, and decreased central venous pressure 1.

Hemorrhage and Blood Loss

• Acute blood loss represents the most immediately life-threatening hypovolemic cause, requiring rapid identification and source control 3.

Dehydration

• Volume depletion from inadequate fluid intake, excessive losses (vomiting, diarrhea), or third-spacing produces orthostatic hypotension defined as systolic blood pressure decline ≥20 mmHg or diastolic decline ≥10 mmHg within three minutes of standing 3, 4.
• Orthostatic hypotension is present in up to 40% of asymptomatic patients older than age 70 and 23% of those younger than age 60, making it a nonspecific finding 2.

Endocrine Causes

• Adrenal insufficiency from primary adrenal failure (Addison's disease, congenital 21-hydroxylase deficiency) or secondary central causes (hypopituitarism) produces hypotension with hyponatremia and hyperkalemia 5.
• Isolated hypoaldosteronism (primary with hyperreninism or secondary with hyporeninism from diabetes, renal failure, HIV) causes salt-wasting hypotension 5.
• Every acute hypotensive event should prompt consideration of adrenal crisis 5.

Distributive Causes

Pathologic vasodilation with decreased systemic vascular resistance characterizes this category, typically presenting with normal or increased cardiac output in early stages and normal or low central venous pressure 1.

Septic Shock

• Decreased systemic vascular resistance with warm extremities and increased lactate distinguishes septic from cardiogenic shock 1.
• Late-stage septic shock may develop myocardial depression but maintains the primary distributive pattern with decreased systemic vascular resistance 1.

Neurogenic Shock

• Spinal cord injury above T6 disrupts sympathetic outflow, producing vasodilation with decreased systemic vascular resistance and bradycardia 1.

Anaphylaxis

• Acute systemic vasodilation from mast cell degranulation produces rapid-onset hypotension with urticaria, angioedema, and bronchospasm 3.

Obstructive Causes

Mechanical impediment to venous return or cardiac output produces hypotension despite adequate intravascular volume and cardiac function.

Cardiac Tamponade

• Beck's triad of hypotension, elevated jugular venous pressure, and muffled heart sounds establishes the diagnosis 6.
• Raised jugular venous pressure reflects elevated right-sided filling pressures as blood cannot enter the compressed chambers, distinguishing tamponade from hypovolemic shock 6.
• Echocardiographic findings include pericardial fluid collection, right atrial and ventricular diastolic collapse, and respiratory variation in ventricular filling 6.
• Mortality reaches 80-90% in trauma-related tamponade if not promptly recognized and treated with immediate pericardiocentesis 6.

Massive Pulmonary Embolism

• Acute right ventricular failure from elevated pulmonary vascular resistance produces hypotension with elevated jugular venous pressure but clear lung fields 1.

Tension Pneumothorax

• Mediastinal shift and vena cava compression reduce venous return, producing hypotension with absent breath sounds and hyperresonance on the affected side 3.

Medication-Induced Hypotension

Iatrogenic causes represent a common and reversible etiology, particularly in elderly patients taking multiple medications 2.

Antihypertensive Agents

• Vasodilators, calcium channel blockers, ACE inhibitors, and angiotensin receptor blockers directly reduce systemic vascular resistance 2.
• Diuretics produce volume depletion and orthostatic hypotension 2.

Cardiovascular Drugs

• Beta-blockers reduce cardiac output through negative chronotropic and inotropic effects 2.
• Nitrates used for angina cause venodilation and preload reduction 2.

Central Nervous System Agents

• Sedatives, antipsychotics, and antidepressants impair autonomic reflexes and may prolong QT interval, predisposing to life-threatening arrhythmias 2.

Anesthetic Agents

• Propofol-induced vasodilation during induction commonly produces hypotension requiring vasopressor support with phenylephrine or norepinephrine 7.

Autonomic Dysfunction

Impaired autonomic nervous system responses to postural changes produce orthostatic hypotension through failure of compensatory vasoconstriction and heart rate increase 3.

Diabetic Autonomic Neuropathy

• Progressive autonomic nerve damage in long-standing diabetes impairs baroreceptor reflexes and produces orthostatic and postprandial hypotension 5, 8.

Primary Autonomic Failure

• Bradbury-Eggleston syndrome (pure autonomic failure) causes peripheral autonomic impairment with orthostatic hypotension 8.
• Shy-Drager syndrome (multiple system atrophy) produces central autonomic impairment with orthostatic hypotension and parkinsonian features 8.

Dopamine-Beta-Hydroxylase Deficiency

• Rare genetic defect causing absence of norepinephrine with dopamine accumulation produces severe orthostatic hypotension 8.

Baroreceptor Dysfunction

• Causes wide blood pressure swings unrelated to posture, distinguishing it from typical orthostatic hypotension 8.

Reflex-Mediated Hypotension

Paroxysmal parasympathetic activation produces transient hypotension and bradycardia through specific triggers 2.

Vasovagal Syncope

• Patients with suspected reflex-mediated or vasovagal syncope should be considered at low risk of adverse outcome 2.
• Recurrence of symptoms such as lightheadedness or syncope on standing is more significant than numeric blood pressure changes 2.

Situational Syncope

• Cough, micturition, defecation, or carotid sinus pressure may precipitate hypotension through vagal stimulation 8.

Critical Pitfalls in Diagnosis

• Do not assume orthostatic hypotension indicates volume depletion alone, as it is common in patients with cardiac disease and other documented diagnoses, detected in most patients within 2 minutes of standing 2.
• Avoid delaying vasopressor treatment while waiting for fluid resuscitation if mean arterial pressure <60-65 mmHg, as prolonged hypotension >15 minutes causes organ injury 7.
• Recognize that hypotension may serve as a biomarker for other pathologic processes rather than the primary cause of organ injury, particularly when it persists despite intervention 2.
• Consider pheochromocytoma as a rare cause of hypotension, especially during surgical removal without adequate preoperative alpha-blockade 5.
• Evaluate for carcinoid crisis in any patient presenting with flushing and hypotension, which responds to subcutaneous somatostatin analogs 5.