Hypotension

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Hypotension

Definition

Hypotension is generally defined as a systolic blood pressure (SBP) < 90 mmHg, a diastolic BP < 60 mmHg, or a mean arterial pressure (MAP) < 65 mmHg. In hypertensive patients, a drop of ≥ 20–25% from baseline may be clinically significant even if absolute values remain above these thresholds.

Classification & Etiology

1. Absolute Hypotension (Systemic)

CategoryExamples
HypovolemicHemorrhage, dehydration, burns, GI losses, third-spacing
CardiogenicMI, heart failure, arrhythmias, cardiomyopathy, severe valvular disease
DistributiveSeptic shock, anaphylaxis, neurogenic shock, adrenal insufficiency
ObstructivePulmonary embolism, tension pneumothorax, cardiac tamponade, aortic stenosis
Iatrogenic / Drug-inducedAntihypertensives, diuretics, opioids, anesthetics, nitrates

2. Orthostatic (Postural) Hypotension

A drop of ≥ 20 mmHg systolic or ≥ 10 mmHg diastolic within 3 minutes of standing.
Causes:
  • 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

BP drop > 20 mmHg within 2 hours of a meal; common in elderly and autonomic neuropathy.

4. Postoperative Hypotension

(Bailey & Love, p. 341): Associated with adverse outcomes; often due to hypovolaemia, myocardial impairment, or vasodilation from neuraxial (subarachnoid/epidural) anaesthesia.

Pathophysiology

Blood pressure = Cardiac Output (CO) × Systemic Vascular Resistance (SVR)
CO = Heart Rate × Stroke Volume
Hypotension results from:
  • ↓ Preload (hypovolemia)
  • ↓ Contractility (cardiogenic)
  • ↓ SVR (distributive)
  • ↓ Venous return (obstructive)

Clinical Presentation

SeverityFeatures
MildLightheadedness, dizziness, fatigue
ModerateSyncope or presyncope, blurred vision, diaphoresis, pallor
Severe / ShockAltered consciousness, cold/clammy extremities, oliguria, cyanosis

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

TestPurpose
FBC, U&E, creatinineAnemia, renal impairment, electrolytes
Blood glucoseHypoglycemia-associated symptoms
LactateTissue perfusion / shock severity
ECGArrhythmia, myocardial ischemia
EchoCardiogenic cause, tamponade, valvular disease
CTPA / CXRPE, pneumothorax
Blood culturesSepsis
Cortisol / short synacthenAdrenal insufficiency
Autonomic function testsOrthostatic hypotension workup

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)

Step 1 — Remove reversible causes: withdraw or reduce vasoactive medications.
Step 2 — Non-pharmacologic interventions:
  • 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
Step 3 — Pharmacologic (if above fails):
  • 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

PopulationConsideration
ElderlyImpaired baroreflex; polypharmacy; higher fall risk
PregnantAortocaval compression in supine position; left lateral tilt required
Septic shockTarget MAP ≥ 65 mmHg; norepinephrine first-line (Surviving Sepsis Campaign)
Spinal cord injuryNeurogenic shock — loss of sympathetic tone; bradycardia + hypotension
PostoperativeHypovolemia, anesthetic agents, bleeding — must be rapidly identified (Bailey & Love, p. 341)

Sources: Harrison's Principles of Internal Medicine, 21st Ed. (p. 709) | Bailey & Love's Short Practice of Surgery, 28th Ed. (p. 341)

Septic shock

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Septic Shock

Definition (Sepsis-3 Criteria)

(Harrison's, p. 8257)
Sepsis = Suspected infection + acute organ dysfunction (SOFA score increase ≥ 2 points from baseline)
Septic shock = Sepsis plus all of the following despite adequate fluid resuscitation:
  • Vasopressor therapy required to maintain MAP ≥ 65 mmHg
  • Serum lactate > 2.0 mmol/L
This distinguishes septic shock from uncomplicated sepsis and identifies patients with the highest mortality (> 40%).
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

SourceCommon Pathogens
Lung (pneumonia)S. pneumoniae, Klebsiella, Pseudomonas
Urinary tractE. coli, Klebsiella, Enterococcus
Abdomen (peritonitis)Mixed gram-negatives, Bacteroides, Enterococcus
Skin / soft tissueS. aureus (MRSA), Group A Streptococcus
Bloodstream (catheter)Staph. epidermidis, Candida, S. aureus
CNS (meningitis)N. meningitidis, S. pneumoniae

Clinical Presentation

SystemFeatures
CardiovascularHypotension, tachycardia, warm/flushed skin (early); cold/clammy (late)
RespiratoryTachypnea, hypoxia, ARDS
NeurologicalConfusion, agitation, obtundation
RenalOliguria, rising creatinine
GI/HepaticIleus, jaundice, elevated transaminases
HaematologicalThrombocytopenia, DIC, leukocytosis or leukopenia
MetabolicElevated lactate, metabolic acidosis, hyperglycemia

SOFA Score (Organ Dysfunction Assessment)

Organ SystemParameters Scored
RespiratoryPaO₂/FiO₂ ratio
CoagulationPlatelets
LiverBilirubin
CardiovascularMAP / vasopressor requirement
CNSGlasgow Coma Scale
RenalCreatinine / urine output
Score 0–24; higher = greater dysfunction; score ≥ 2 above baseline = sepsis-defining organ failure.

Investigations

TestPurpose
Blood cultures (×2)Identify organism — obtain before antibiotics
FBC, CRP, procalcitoninInfection severity, monitoring
Serum lactateTissue hypoperfusion; guides resuscitation
ABGAcid-base status, PaO₂/FiO₂
U&E, creatinine, LFTsOrgan dysfunction
Coagulation screen (INR, APTT, fibrinogen, D-dimer)DIC
Urine culture, CXR, CT abdomen/pelvisSource identification
Focused cardiac ultrasound (POCUS)Volume status, cardiac function, tamponade

Management

(Harrison's, p. 8273 | Surviving Sepsis Campaign Guidelines)

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

(Harrison's, p. 8273)
AgentRole
NorepinephrineFirst-line — alpha + beta adrenergic; titrate to MAP ≥ 65 mmHg
VasopressinAdd-on to norepinephrine to reduce its dose (0.03–0.04 units/min)
EpinephrineSecond-line; added if MAP target not achieved
DopamineAvoid except in bradycardic patients at low risk of tachyarrhythmias
DobutamineFor myocardial dysfunction / low CO despite adequate filling pressures

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:
Suspected SourceEmpiric Regimen (example)
Community pneumoniaBeta-lactam + macrolide or fluoroquinolone
HAP/VAPAntipseudomonal beta-lactam ± aminoglycoside
Urosepsis3rd-gen cephalosporin or piperacillin-tazobactam
AbdominalPiperacillin-tazobactam or carbapenem + metronidazole
Unknown sourceBroad gram-positive + gram-negative + anaerobe coverage
MRSA riskAdd vancomycin or linezolid
ImmunocompromisedAdd antifungal (e.g., echinocandin)
  • 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

InterventionTarget / Details
Mechanical ventilation (ARDS)Lung-protective: TV 6 mL/kg IBW, plateau pressure < 30 cmH₂O
Glucose controlTarget 7.8–10 mmol/L (140–180 mg/dL); avoid hypoglycemia
Renal replacement therapyFor AKI with fluid overload, severe acidosis, or hyperkalemia
DVT prophylaxisLMWH (unless bleeding risk)
Stress ulcer prophylaxisPPI or H₂ blocker in high-risk patients
NutritionEarly enteral nutrition preferred; avoid prolonged NPO
TransfusionRBC transfusion if Hb < 70 g/L (< 90 g/L in myocardial ischemia)

Monitoring Endpoints

ParameterTarget
MAP≥ 65 mmHg
Urine output≥ 0.5 mL/kg/hr
Lactate clearance≥ 10% reduction per 2 hours; normalize to < 2 mmol/L
CVP (if used)8–12 mmHg (less reliable alone)
ScvO₂≥ 70%

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)

Sources: Harrison's Principles of Internal Medicine, 21st Ed. (pp. 8257, 8273) | Surviving Sepsis Campaign International Guidelines
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