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FP-C / CCP-C
FP-C Hemodynamics & Vasopressor Review
Critical-care transport hemodynamics is a single equation wearing many disguises: MAP ≈ CO × SVR, with CO = HR × SV and stroke volume governed by preload, afterload and contractility. Every shock profile, every vasopressor question, and every 'why did the pressure crash on the vent' stem resolves to which variable broke and which agent or maneuver repairs it.
Doses and agent selection follow your protocols and the sending physician's plan; the exam tests class logic — which receptor does what — plus the transport-specific disciplines: lines labeled, pumps powered, waveforms zeroed and trended, and never bolusing through the pressor line.
Profiles: which variable broke
Hypovolemic/hemorrhagic: preload empty — low CO, compensatory high SVR (cold, clamped down), narrow pulse pressure. Fix the tank: volume/blood per protocol; pressors squeeze an empty pipe. Cardiogenic: pump failure — low CO, high SVR, congestion (crackles, JVD); fix contractility/afterload per protocol (inotropes; cautious fluids; treat the cause — reperfusion for MI). Distributive (septic/anaphylactic/neurogenic): pipes dilated — low SVR, often normal/high CO early (warm shock), wide pulse pressure; fix tone: vasopressors after/with volume (epinephrine and its receptor portfolio for anaphylaxis; norepinephrine-class alpha-dominant agents for sepsis per protocol; neurogenic adds bradycardia needing chronotropy). Obstructive: flow blocked — tension pneumothorax, tamponade, massive PE; no drug fixes a mechanical problem: decompress, recognize tamponade physiology (muffled tones, JVD, pulsus paradoxus), support and fly toward definitive care.
MAP = (SBP + 2×DBP)/3, the perfusion number for brain and kidneys — transport targets commonly quoted around ≥65 mmHg (higher for some neuro patients per the receiving plan). Trend it; single values lie. Shock index (HR/SBP) rising above ~0.9–1.0 flags decompensation earlier than either number alone — a favorite exam discriminator for 'which patient is sicker.'
Receptor classes, lines, and transport discipline
Receptor logic: alpha-1 → vasoconstriction (raises SVR/MAP; the workhorse for distributive shock); beta-1 → chronotropy + inotropy (raises CO; the workhorse for pump failure); beta-2 → bronchodilation + some vasodilation; vasopressin works via its own V1 receptors (catecholamine-independent squeeze); dopaminergic effects are historical exam trivia more than modern practice. Classify the big agents by dominant effect — norepinephrine (alpha-heavy with some beta-1: pressure with modest CO support), epinephrine (balanced alpha/beta: the anaphylaxis and arrest agent; inotropy plus squeeze), phenylephrine (pure alpha: pressure, with reflex bradycardia possible), dobutamine-class inotropes (beta-1 dominant: contractility, can drop SVR — pressure may dip as output rises) — and most exam questions become 'match the broken variable to the dominant receptor.'
Transport discipline: infusions on pumps with battery checked and spares; concentrations and lines labeled at every connection; never flush or push meds through the vasopressor line (a bolus of the dead-space pressor causes a hypertensive spike — and interrupting it causes collapse); know what happens at the pump's dead battery (and the aircraft's power inventory). Arterial lines: zero/level the transducer at the phlebostatic axis (re-level after every patient/altitude position change); overdamped traces (blunted, falsely low systolic) → check bubbles, kinks, clots, low bag pressure; underdamped/whip (falsely high systolic) → check tubing length/movement; when the art line and cuff disagree significantly, troubleshoot — and treat the patient, trending MAP, which both methods report most reliably.
Practice questions with answers & rationales
Q1. Two hypotensive patients: one cold, clamped, narrow pulse pressure after a GI bleed; one warm and flushed with a wide pulse pressure and fever. Same MAP — same treatment?
Answer: No. The first is hypovolemic: low CO with compensatory vasoconstriction — needs volume/blood; pressors alone squeeze an empty system and worsen tissue perfusion. The second is distributive (septic): dilated vasculature with low SVR — needs volume plus a vasoconstrictor (alpha-dominant agent per protocol) to restore tone. The exam point: MAP tells you perfusion pressure is inadequate; the skin, pulse pressure and history tell you which variable to fix.
Q2. Why does norepinephrine suit septic shock while dobutamine-class inotropes suit cardiogenic shock?
Answer: Match dominant receptor to broken variable. Sepsis breaks SVR (vasodilation): norepinephrine's strong alpha-1 restores vascular tone with enough beta-1 to support output. Cardiogenic shock breaks contractility: beta-1-dominant inotropes raise stroke volume — but their beta-2 vasodilation can lower SVR, so pressure may need a co-running vasopressor. Giving a pure squeezer to a failing pump raises afterload against a weak ventricle; giving a pure inotrope to a vasoplegic patient drops their remaining tone — both are tested mismatches.
Q3. Your art line shows 84/62 while the cuff reads 108/70. The waveform looks blunted and rounded. Which do you believe?
Answer: Suspect an overdamped arterial line: bubbles, clot, kink, or low flush-bag pressure blunt the waveform and under-read systolic. Troubleshoot — inspect/flush per protocol, check the bag, re-level and re-zero the transducer. Note MAP is least distorted by damping, and the two methods' MAPs often agree even when systolics diverge. The credited behavior: fix the measurement before treating a number, and trend MAP rather than chasing systolic.
Q4. Mid-flight, the patient's MAP falls from 72 to 54 right after your partner flushes a medication through 'the closest port.' What likely happened?
Answer: Two classic possibilities: the flush went through the vasopressor line — first bolusing dead-space pressor (transient spike you may have missed) and then effectively interrupting the continuous infusion as the line refilled, collapsing pressure; or an incompatible drug was pushed into the pressor line. Recovery: confirm the pressor is actually infusing (pump running, line patent, connections), support pressure per protocol, and re-establish the rule: pressor lines are dedicated — label them, and never flush or piggyback through them.
Q5. What does a rising shock index tell you that the individual vitals don't?
Answer: Shock index = HR/SBP; normal runs roughly 0.5–0.7. A climbing index (heart rate rising toward or past systolic pressure, e.g., 0.9–1.0+) reveals decompensation while both numbers still look individually 'acceptable' — the compensation machinery consuming itself. It's especially valuable in young, healthy-compensating patients and in trending during transport: a 118/78 patient with HR 122 is sicker than vitals-glancing suggests, and the exam loves making you say why.
Q6. Your neurogenic-shock patient (C5 injury) is hypotensive at 78/44 with a heart rate of 52. Why won't volume alone fix this, and what class of support is needed?
Answer: The cord injury severed sympathetic outflow: the vasculature can't constrict (low SVR) and the heart can't compensate with tachycardia — a distributive shock with bradycardia. Volume helps fill the dilated space but doesn't restore tone or rate: this patient typically needs an agent with both alpha (tone) and beta-1 (chronotropy/inotropy) activity per protocol, plus temperature management (they also can't thermoregulate below the lesion). Spotting 'hypotension + bradycardia + trauma' as neurogenic is the tested recognition.
Q7. Before lifting with three infusions running, what's your pump-and-power checklist?
Answer: Confirm each drug, concentration and rate against the orders; label lines at the pump and the patient ends; check pump battery levels and bring spares/spare pump; know the aircraft's inverter/outlet situation; ensure carrier-compatible fluids and enough volume of each drip for the transport plus margin (calculate time-to-empty bag); set lines untangled with the pressor line identified and protected; and brief your partner on which infusion never pauses. Infusion interruptions at altitude — battery, kink, empty bag — are operational failures the exam assigns directly to the crew.
Common mistakes to avoid
- Starting pressors on an empty tank — distributive logic applied to hemorrhage.
- Mismatching receptor class to broken variable (pure alpha into a failing pump; pure inotrope into vasoplegia).
- Chasing systolic values from a damped or whipping art line instead of troubleshooting and trending MAP.
- Flushing or piggybacking through a dedicated vasopressor line.
- Missing neurogenic shock's bradycardia signature and treating it like hemorrhage.
- Boarding without the drip math: battery, bag volume, and time-to-empty calculated for every infusion.