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Ch 6 · Hemodynamics

Intraoperative Hypotension & Hypertension

BP determinants, differential diagnoses, vasopressor/antihypertensive choice.

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Key Points

  • MAP = CO × SVR. CO = HR × SV. SV depends on preload, afterload, contractility.
  • Pulse pressure: narrow → AS, cardiac tamponade, low SV. Wide → AR, AVM, thyrotoxicosis.
  • First step in any hemodynamic change: confirm the measurement is real.
  • Phenylephrine is a pure α1 agonist — useful in hypotension with adequate HR. Avoid in low-CO states.
  • Norepinephrine is first-line for vasodilatory shock and increasingly used for routine intraoperative hypotension.

01Determinants of Blood Pressure

BP = the force exerted by circulating blood on the vessel walls. (MAP − CVP) = CO × SVR

Cardiac Output (CO) = HR × SV - Cardiac Index (CO/BSA) normal range 2.6–4.2 L/min/m² - Infants: SV relatively fixed → CO depends mainly on HR - Adults: SV plays a major role, especially when tachycardia is undesirable (CAD, HOCM, AS)

Stroke Volume (SV) depends on: 1. Preload — LVEDV 2. Afterload — SVR accounts for 95% of impedance to ejection 3. Contractility — EF is the most clinically useful index (normal LV EF ~60%)

02Components & Pulse Pressure

SBP, DBP, MAP Pulse Pressure (PP) = SBP − DBP - Normal ~40 mmHg at rest, up to ~100 with exertion - Narrow PP (< 25 mmHg): aortic stenosis, coarctation, tension pneumothorax, myocardial failure, shock, damping - Wide PP (> 40 mmHg): aortic regurgitation, PDA, atherosclerotic vessels, thyrotoxicosis, AVM, pregnancy, anxiety

03Intraoperative Hypertension — DDx

Always start with: "Is this measurement real?" (check cuff size, position, transducer level)

  • Light anesthesia — most common
  • Pain (sympathetic activation from surgical stimulation)
  • Chronic hypertension (uncontrolled or under-medicated)
  • Illicit drug use (cocaine, amphetamines)
  • Hypermetabolic state (MH, thyrotoxicosis, NMS, serotonin syndrome)
  • Elevated ICP — Cushing's triad: HTN + bradycardia + irregular respirations
  • Autonomic hyperreflexia (spinal cord lesion > T5)
  • Endocrine (pheochromocytoma, hyperaldosteronism)
  • Hypervolemia
  • Drug contamination (intentional — local with epi — or unintentional)
  • Hypercarbia

04Treatment of Hypertension

Temporize with fast-onset, short-acting drugs, then diagnose and treat the cause.

  • Deepen anesthesia: propofol bolus, ↑ volatile
  • Add analgesia: opioid (fentanyl 25–100 mcg)
  • Short-acting vasodilators:
  • Clevidipine — CCB in lipid emulsion (looks like propofol); 0.5–32 mg/h
  • Nitroglycerin — venous > arterial dilation
  • Nitroprusside — arterial > venous; cyanide toxicity risk; very expensive
  • Avoid NTG/NTP in intracerebral hemorrhage (cerebral vasodilator → ↑ ICP)
  • β-blockers:
  • Esmolol — affects HR >> BP
  • Labetalol — combined α + β, longer acting
  • Hydralazine — less predictable kinetics; longer acting

05Antihypertensive Comparison

DrugBolusOnsetPeakDurationInfusion
Clevidipine50–100 mcg1 min2–4 min5–15 min0.5–32 mg/h
Nitroglycerin10–50 mcg1 min1–3 min3–5 min0.1–1 mcg/kg/min
Nitroprusside10–50 mcg< 1 min1 min1–10 min0.1–1 mcg/kg/min
Labetalol5–10 mg2–5 min10–15 min45 min – 6 h
Esmolol10–20 mg1 min2 min10 min50–300 mcg/kg/min
Hydralazine5 mg5–20 min15–30 min2–6 h

06Intraoperative Hypotension — DDx

Start with measurement error: cuff size/position, transducer level, damping.

Then by mechanism: - Preload (hypovolemia): hemorrhage, evaporative loss, diuretics, prolonged NPO, vasodilation from anesthetics, positioning, PEEP, pneumoperitoneum, vena cava compression - Afterload (vasodilation): induction agents, volatiles, sepsis, anaphylaxis, sympathectomy from neuraxial block - Contractility: MI, cardiomyopathy, severe acidosis, hypocalcemia, β-blocker overdose - Obstruction: tension PTX, cardiac tamponade, PE, dynamic LVOT obstruction (HOCM), auto-PEEP - Rhythm: bradycardia, tachyarrhythmia, heart block

07Pressor Comparison

DrugReceptorsBolusInfusionNotes
Phenylephrineα150–200 mcg20–200 mcg/minReflex bradycardia; avoid in low-CO
EphedrineMixed α/β indirect5–10 mgTachyphylaxis; ↑ HR
Norepinephrineα1 + β10.02–1 mcg/kg/minFirst-line for vasodilatory shock
Epinephrineα + β (dose-dep)10–100 mcg0.02–0.2 mcg/kg/minArrest 1 mg; anaphylaxis 0.3 mg IM
VasopressinV11–2 U0.01–0.04 U/minCatecholamine-sparing
DopamineDA, β, α (dose)1–10 mcg/kg/minArrhythmogenic; falling out of favor
Dobutamineβ1 >> β22–20 mcg/kg/minInotrope; ↓ SVR; for low CO
MilrinonePDE-350 mcg/kg load0.125–0.5 mcg/kg/minInodilator; pulmonary vasodilator

References & Further Reading

  1. 1
    Textbook

    Gropper MA, Miller RD, Cohen NH, et al., eds. Miller's Anesthesia. 9th ed. Philadelphia: Elsevier; 2020.

  2. 2
    Textbook

    Flood P, Rathmell JP, Shafer S. Stoelting's Pharmacology and Physiology in Anesthetic Practice. 5th ed. Philadelphia: Wolters Kluwer; 2015.

  3. 3
    Textbook

    Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC, Ortega R, Sharar SR, Holt NF. Clinical Anesthesia. 8th ed. Philadelphia: Wolters Kluwer; 2017.

  4. 4
    Guideline

    Kinsella SM, Carvalho B, Dyer RA, et al. International consensus statement on the management of hypotension with vasopressors during cesarean section under spinal anaesthesia. Anaesthesia. 2018;73(1):71-92.

  5. 5
    Textbook

    Adriano A, Morris R, eds. 2021 CA-1 Tutorial Textbook (15th Ed.). Stanford University Medical Center, Department of Anesthesiology.

Citations are provided to direct further study. Always check the most current edition of guidelines and society recommendations — the information in this chapter is a teaching summary, not primary source material.