Every value a PAC produces is an expression of four things: how full the heart is (preload), how hard it must push (afterload), how strongly it squeezes (contractility), and how fast it beats (rate). Hold onto that framework and the numbers stop being a list and start telling a story.

Preload is the degree of stretch on the ventricular muscle at end-diastole — clinically approximated by filling pressures. Right-heart preload is estimated by the RA pressure / CVP; left-heart preload is estimated by the wedge pressure (PCWP), which reflects left atrial pressure when the balloon occludes flow in a PA branch.1 By the Frank–Starling relationship, more stretch increases stroke volume — up to a point, beyond which added filling stops helping.

Afterload is the resistance the ventricle pumps against. For the left ventricle this is estimated by systemic vascular resistance (SVR); for the right ventricle, by pulmonary vascular resistance (PVR). Both are calculated, not measured — the PAC provides the pressures and flow that feed the equations (see Calculators).

Contractility is the intrinsic force of contraction, independent of load. It's hard to measure directly at the bedside, but stroke volume, cardiac output, and cardiac power output all move with it. Cardiac output = heart rate × stroke volume; indexing to body surface area gives the cardiac index, which lets you compare patients of different sizes.4

A standard adult PAC is roughly 110 cm long, marked in 10 cm increments, and carries several lumens and a balloon within a single catheter body. Knowing which port is which is the difference between a clean measurement and a dangerous mistake.

• Distal (PA) lumen — opens at the tip in the pulmonary artery. Reads PA pressure, wedge pressure, and is where mixed venous samples are drawn. Never infuse into this port.
• Proximal (RA) lumen — opens ~30 cm from the tip in the right atrium. Reads CVP and is the injectate port for thermodilution cardiac output.
• Balloon inflation valve — inflates the tip balloon to float the catheter and to wedge. Standard adult balloons take up to ~1.5 mL of air; the original design used less in the smaller 5 Fr catheter.16
• Thermistor connector — a temperature sensor near the tip enables thermodilution cardiac output.2
• Additional infusion (VIP) ports — some catheters add a venous infusion port for fluids/medications.

The elegant idea behind the PAC is that you don't need to see it to know where it is — the pressure waveform tells you. As the balloon floats forward from a central vein, the trace changes character at each chamber.1

• Right atrium (~15–20 cm from IJ): low-amplitude trace with a, c, and v waves; mean 2–6 mmHg. Balloon is inflated here to begin floating.4
• Right ventricle (~30 cm): sudden tall systolic upstroke with a low diastolic pressure that sits near zero. Watch for ectopy here — the catheter irritates the RV.
• Pulmonary artery (~40 cm): systolic pressure stays similar to RV, but diastolic pressure rises and a dicrotic notch appears. That step-up in diastole is the signature of crossing the pulmonic valve.
• Wedge (~45–50 cm): with the balloon still inflated, the trace flattens into a low, atrial-appearing waveform — this is the occlusion (wedge) pressure, reflecting left atrial pressure. Deflate the balloon and the PA trace should return.

See the Waveforms tab for the annotated traces, and the Insertion Simulator to watch the transition in real time.

A pressure waveform is a story about one cardiac cycle. The atrial trace has three signature deflections, and knowing what each one means turns a wiggly line into diagnostic information.1

• a wave — atrial contraction (follows the P wave on ECG). Absent in atrial fibrillation; exaggerated ("cannon a waves") when the atrium contracts against a closed tricuspid valve, as in complete heart block or AV dissociation.
• c wave — bulging of the tricuspid valve into the atrium at the start of ventricular systole. Often subtle.
• v wave — passive atrial filling against a closed valve during ventricular systole. Giant v waves in the wedge trace are the classic sign of acute mitral regurgitation.

When PVR is normal, PA diastolic pressure closely approximates wedge — a useful surrogate that avoids repeated balloon inflation.

Overdamping (air bubbles, kinks, clot, or a loose connection) blunts the trace: the upstroke is slurred, the peak is falsely low, and the trough falsely high. Underdamping / "catheter whip" produces overshoot spikes and a falsely high systolic. Confirm with a square-wave (fast-flush) test before trusting any pressure.

See the Waveforms tab for the annotated normal traces.

Cardiac output is the volume of blood the heart pumps per minute (normal 4–8 L/min).4 The PAC's original breakthrough beyond pressure measurement was making this quantifiable at the bedside.2

A known volume of injectate (cooler than blood) is injected through the proximal (RA) port. The thermistor near the tip detects the resulting temperature dip downstream in the pulmonary artery. The area under that temperature–time curve is inversely proportional to cardiac output — a bigger, more prolonged dip means slower flow (low output); a small, brief dip means fast flow (high output).2

The reference method relates output to oxygen uptake: cardiac output = oxygen consumption (VO₂) ÷ arteriovenous oxygen content difference (CaO₂ − CvO₂). It ties cardiac output directly to the mixed venous saturation the PAC also measures (Module 7), and underlies why a falling SvO₂ often signals a falling output.

• Tricuspid regurgitation — recirculation distorts the curve, often falsely lowering the value.
• Intracardiac shunts — invalidate thermodilution entirely.
• Injectate problems — wrong volume or temperature, or slow/uneven injection.
• Rapid concurrent IV fluids and arrhythmias during the measurement.

Use the Calculators to turn a cardiac output into indexed and derived values.

The PAC's real power is combining pressure and flow into values that localize the problem: is the heart under-filled, pumping weakly, or fighting too much resistance? These are all calculated from the measured inputs.4

• Cardiac index (CI) = CO / BSA — output scaled to body size (normal 2.5–4 L/min/m²).
• Stroke volume / index (SV, SVI) — volume per beat; falls with poor preload or contractility.
• SVR = 80·(MAP − CVP)/CO — left-sided afterload (normal 800–1200). High in hypovolemic and cardiogenic shock; low in distributive shock.
• PVR = 80·(MPAP − PCWP)/CO — right-sided afterload; elevated in pulmonary hypertension.
• Cardiac power output (CPO) = MAP·CO/451 — the product of pressure and flow. A commonly cited threshold of <0.6 W flags severe dysfunction and is associated with poor outcomes in shock.17

Compute all of these in the Calculators tab.

Forrester and colleagues mapped acute MI patients onto a simple grid using cardiac index (cutoff ~2.2 L/min/m²) and wedge pressure (cutoff ~18 mmHg).3 The same two axes — perfusion and congestion — still frame bedside thinking today (the clinical "warm/cold, wet/dry" profiles):

Blood sampled from the distal (PA) port is true mixed venous blood — the pooled return from the whole body after the tissues have taken what they need. Its saturation, SvO₂ (normal ~60–80%), is a real-time readout of the balance between oxygen delivery and oxygen consumption.19

The tissues are extracting more oxygen than usual. Causes fall into two buckets:

• Reduced delivery — low cardiac output, anemia (low hemoglobin), or low arterial saturation.
• Increased consumption — fever, shivering, pain, agitation, or seizures.

Counter-intuitively, a high value can accompany very sick patients. Causes include distributive/septic shock (microcirculatory shunting), cyanide toxicity, severe liver disease, hypothermia, deep sedation or paralysis, and left-to-right shunts — or simply a wedged or contaminated sample.

Central venous saturation (ScvO₂), drawn from an ordinary central line in the SVC, is a convenient surrogate that trends with SvO₂ but is not identical — the two can diverge by several points, and the relationship shifts in shock.19 Use trends rather than treating a single number as absolute.

Most complications are related to insertion and to catheter residence. Serious events are uncommon but can be lethal, which is why the PAC is reserved for patients whose management genuinely depends on it.14

• Arrhythmias — transient RV ectopy is common as the tip crosses the ventricle; usually resolves as it advances. Transient right bundle branch block can occur.
• Access complications — pneumothorax, arterial puncture, and the usual central-line risks.

• Pulmonary artery rupture — rare (estimated 0.03–0.2%) but carries a high mortality (estimated 41–70%). Risk rises with pulmonary hypertension, distal tip migration, balloon over-inflation, and anticoagulation.14
• Pulmonary infarction — from a persistently wedged or distally migrated tip. Keep the balloon deflated between wedge measurements and watch the PA trace for spontaneous wedging.
• Thrombosis, valvular injury, and knotting — associated with prolonged dwell time.
• Infection — catheter-related bloodstream infection; PAC-associated bacteremia has been reported around 1.3–2.3%.19

• Damped trace → fast-flush; check for air, kinks, clot, or a loose transducer connection.
• Can't wedge / no resistance → suspect balloon rupture; stop inflating and never aspirate forcefully.
• Spontaneous wedge → pull the catheter back until the PA trace returns.
• Continuous rise on wedging (overwedge) → deflate immediately.

The PAC earns its place when it distinguishes shock states that look similar at the bedside but need opposite treatments. The pattern of filling pressures, output, resistance, and SvO₂ points to the cause.

*Early/warm septic shock is typically high-output; output can fall late. In tamponade, look for equalization of diastolic pressures (RA ≈ RV diastolic ≈ PA diastolic ≈ wedge).

Cardiogenic shock is now staged A through E — from "at risk" (A) through "beginning" (B), "classic" (C), "deteriorating" (D), and "extremis" (E).1617 This is where the PAC has seen a resurgence: contemporary registry data associate complete hemodynamic profiling with a PAC with lower in-hospital mortality in cardiogenic shock, particularly when done early.18

Remove the catheter once it is no longer changing management and the patient is hemodynamically stable. Withdraw with the balloon fully deflated, ideally during expiration, watching the ECG for ectopy as the tip crosses the RV. Confirm no bleeding at the site and document.

More bad hemodynamic numbers come from setup than from misreading a correct trace. A beautifully interpreted wrong value is still wrong. Four habits protect you: level, zero, check the dynamic response, and read at end-expiration.5

Position the transducer's air–fluid interface (the stopcock you open to air) at the phlebostatic axis — the 4th intercostal space at the mid-anteroposterior chest. This is the reference point for the heart's chambers.5

Open the transducer to atmosphere and zero the monitor so it treats atmospheric pressure as 0 mmHg. Zero at setup, per your unit protocol, and any time a reading looks implausible. Leveling sets where you measure from; zeroing sets the baseline — you need both.

Pull the flush device and watch how the trace responds — this checks the system's dynamic response before you trust any pressure.

• Optimal: a sharp square that drops and returns with 1–2 quick oscillations. Trust the numbers.
• Overdamped: a slurred return with no oscillations — falsely low systolic, falsely high diastolic. Causes: air bubbles, kinks, clots, loose connections, or a low flush-bag pressure. Fix the line.
• Underdamped: many oscillations / ringing — falsely high systolic, falsely low diastolic ("catheter whip"). Causes: stiff or long tubing, excessive stopcocks.

See the annotated over- and underdamped traces in the Waveform Interpreter.

Intrathoracic pressure is closest to atmospheric at end-expiration, so read CVP, PA, and wedge pressures there in both spontaneously breathing and ventilated patients. Respiratory swings move the trace up and down; picking the wrong point is a common error. Read from the graphic waveform, not just the monitor's digital number, which averages across the respiratory cycle.4