---

Hypotension

Definition

---

Classification & Etiology

1. Absolute Hypotension (Systemic)

2. Orthostatic (Postural) Hypotension

• Autonomic dysfunction (Parkinson's disease, diabetes mellitus, pure autonomic failure, multiple system atrophy)
• Volume depletion
• Medications (alpha-blockers, diuretics, tricyclics, antipsychotics)
• Prolonged bed rest / deconditioning
• Aging (impaired baroreflex sensitivity)

3. Postprandial Hypotension

4. Postoperative Hypotension

---

Pathophysiology

• ↓ Preload (hypovolemia)
• ↓ Contractility (cardiogenic)
• ↓ SVR (distributive)
• ↓ Venous return (obstructive)

---

Clinical Presentation

---

Diagnosis

History

• Onset, triggers (posture, meals, medications)
• Volume status (fluid intake, bleeding, diarrhea)
• Comorbidities (cardiac disease, diabetes, Parkinson's)
• Full medication review

Examination

• Orthostatic vitals (supine, sitting, standing BP/HR)
• Skin: warm/flushed (distributive) vs. cold/clammy (cardiogenic/hypovolemic)
• Jugular venous pressure, heart sounds, lung auscultation
• Capillary refill, pulse volume

Investigations

---

Management

General / Acute

1. Position: Supine with legs elevated (Trendelenburg) if no contraindication
2. IV access + fluid resuscitation (crystalloids, colloids, blood products as indicated)
3. Treat the underlying cause (source control for sepsis, reperfusion for MI, pericardiocentesis for tamponade, decompression for pneumothorax)
4. Vasopressors (if MAP < 65 mmHg despite adequate fluid resuscitation):
   • Norepinephrine — first-line in septic shock
   • Dopamine — alternative (higher risk of arrhythmia)
   • Vasopressin — adjunct
   • Phenylephrine — neurogenic/anaphylactic shock
5. Inotropes (cardiogenic shock): dobutamine, milrinone

Orthostatic Hypotension (Harrison's, p. 709)

• Patient education on staged posture changes (supine → sitting → standing)
• Avoid large meals; avoid hot environments
• Isometric counterpressure maneuvers (leg crossing, squatting)
• Raise head of bed 10–20° to reduce supine hypertension and nocturnal diuresis
• Increase dietary fluid and salt intake
• Compression stockings / abdominal binders

• Fludrocortisone (mineralocorticoid; expands plasma volume)
• Midodrine (alpha-1 agonist vasoconstrictor)
• Droxidopa (L-DOPS) — norepinephrine prodrug; used in neurogenic orthostatic hypotension

---

Complications of Untreated Hypotension

• Syncope and falls (especially in elderly)
• Acute kidney injury (renal hypoperfusion)
• Myocardial ischemia
• Stroke / TIA
• Multi-organ dysfunction syndrome (shock)
• Death

---

Special Populations

---

---

Septic Shock

Definition (Sepsis-3 Criteria)

• Vasopressor therapy required to maintain MAP ≥ 65 mmHg
• Serum lactate > 2.0 mmol/L

qSOFA (quick SOFA) — bedside screening tool (does not require labs):

• Altered mental status (GCS < 15)
• Respiratory rate ≥ 22 breaths/min
• SBP ≤ 100 mmHg ≥ 2 of 3 = high suspicion for sepsis/poor outcome; prompt full SOFA assessment

---

Pathophysiology

1. Infection → systemic immune activation → release of PAMPs (e.g., LPS from gram-negatives, teichoic acid from gram-positives)
2. Cytokine storm (TNF-α, IL-1, IL-6) → endothelial dysfunction + widespread vasodilation
3. ↓ SVR → distributive shock → relative hypovolemia
4. Microvascular thrombosis + tissue hypoperfusion → cellular hypoxia → lactic acidosis
5. Myocardial depression (septic cardiomyopathy) — further reduces CO
6. Multi-organ dysfunction syndrome (MODS) — kidneys, liver, lungs (ARDS), coagulation (DIC)

---

Common Sources & Organisms

---

Clinical Presentation

---

SOFA Score (Organ Dysfunction Assessment)

---

Investigations

---

Management

The "Hour-1 Bundle" (initiate within 1 hour of recognition)

1. Measure lactate (re-measure if initial > 2 mmol/L)
2. Obtain blood cultures before antibiotics
3. Administer broad-spectrum antibiotics
4. Begin IV crystalloid 30 mL/kg for hypotension or lactate ≥ 4 mmol/L
5. Apply vasopressors if MAP < 65 mmHg despite fluids

---

1. Fluid Resuscitation

• IV crystalloid 30 mL/kg within first 3 hours
• Saline or balanced crystalloids (e.g., Hartmann's/lactated Ringer's) are acceptable
• Hydroxyethyl starches and gelatins are not recommended
• Further fluid guided by dynamic markers (pulse pressure variation, stroke volume variation, POCUS) and lactate clearance

2. Vasopressors

3. Antimicrobials

• Administer within 1 hour of septic shock recognition — mortality increases with each hour of delay
• Empiric broad-spectrum coverage based on likely source, local resistance patterns, and immune status:

• De-escalate once organism and sensitivities known
• Total duration typically 7–10 days (shorter if source controlled)

4. Source Control

• Drainage of abscesses, removal of infected devices/lines, surgical debridement
• Should be achieved as soon as medically feasible

5. Corticosteroids

• Consider hydrocortisone 200–300 mg/day IV (continuous infusion or intermittent dosing) if shock remains refractory despite adequate fluids and vasopressors
• Do not use dexamethasone or high-dose steroids

6. Supportive ICU Care

---

Monitoring Endpoints

---

Complications

• ARDS — most common cause of respiratory failure
• AKI — may require renal replacement therapy
• DIC — coagulopathy, bleeding, microvascular thrombosis
• Septic cardiomyopathy — reversible myocardial dysfunction
• Critical illness neuropathy/myopathy — prolonged weakness
• Secondary infections — fungal, C. difficile

---

Prognosis

• Septic shock carries in-hospital mortality of 40–60%
• Mortality correlates with: number of organs failing, lactate level, delay to antibiotics, source control adequacy
• Survivors face increased risk of long-term cognitive impairment, physical disability, and re-hospitalization (post-sepsis syndrome)

---