4.1 Physiologic Monitoring in the Cath Lab
Key Takeaways
- The CI technologist watches temperature, ECG, respiration, NIBP, intravascular pressure, pulse oximetry, capnography, and level of consciousness on every diagnostic cath, PCI, and moderate-sedation case.
- Selective RCA contrast commonly causes sinus bradycardia or AV block via the AV nodal artery; VT/VF and ST elevation or depression are ischemia or irritation until treated.
- Zero arterial transducers at the phlebostatic axis; overdamping underestimates systolic pressure (bubbles, kinks, loose connections), while underdamping overestimates it with a ringing waveform.
- SpO2 fails in poor perfusion, nail polish, and carbon monoxide exposure; a rising ETCO2 during sedation is hypoventilation, not a reassuring sign.
- Moderate sedation requires purposeful response to voice; response only to pain is too deep, and long cases need forced-air warming before hypothermia arrives.
Physiologic Monitoring in the Cath Lab
Outline Patient Care 1.C.1 is the watch list the cardiac-interventional technologist runs from first sheath to last hemostasis band: temperature, electrocardiogram (ECG), respiration, noninvasive blood pressure (NIBP), intravascular pressure, pulse oximetry, capnography, and level of consciousness (LOC). Diagnostic left-heart catheterization, percutaneous coronary intervention (PCI), and moderate sedation use the same streams. The tempo changes; the duty does not. A missed ST shift, a damped arterial line treated as cardiogenic shock, or a silent rise in end-tidal carbon dioxide (ETCO2) is how a “routine” diagnostic becomes an airway or arrest.
Quick Answer: Watch ST segments, rhythm, and the arterial waveform continuously. Zero the transducer at the phlebostatic axis. Treat a sluggish, rounded arterial tracing as overdamping. Treat rising ETCO2 during sedation as hypoventilation. A moderately sedated patient should still respond to voice.
Temperature
Typical adult core temperature is 36.5–37.5 °C. The suite is cold, the torso is exposed, contrast and flush are often room temperature, and chronic-total-occlusion or structural cases last hours. Hypothermia raises oxygen demand through shivering, worsens coagulopathy, and promotes arrhythmia. Apply forced-air warming to non-sterile surfaces early in a long case, not after the patient is already 35 °C. Large-volume room-temperature injectate deserves a fluid warmer when that is the plan. Report a downward trend; do not wait for a protocol floor. Hyperthermia is less common — stop a malfunctioning warmer, and consider infection or a drug reaction.
ECG: ST change, VT/VF, and the RCA injection
A continuous multi-lead display is not wallpaper. You are hunting ST elevation or depression in the territory being wired, ventricular tachycardia (VT) or ventricular fibrillation (VF), and atrioventricular (AV) block.
Right coronary artery (RCA) contrast is the classic teaching injection. In a right-dominant system the AV nodal artery arises from the RCA. A selective RCA injection commonly produces sinus bradycardia, PR prolongation, high-grade AV block, or a few seconds of asystole. Have atropine available and know the pacing plan before that injection, not after the rate hits 30. Announce the drop immediately. Most episodes resolve as contrast washes out; some do not.
Left coronary injections and balloon inflations more often produce ST elevation or depression — anterior leads for left-anterior-descending work, lateral leads for circumflex. New ST elevation during wiring is ischemia until the operator says otherwise. Closed-loop the finding with the arterial pressure: ST elevation plus a systolic pressure of 70 mmHg is a different sentence than ST elevation with a stable pressure.
VT and VF follow ischemia, reperfusion, catheter irritation in the left ventricle, coronary air, and thrombus. Recognition plus a charged defibrillator is the CI skill. Pulseless VT/VF is advanced cardiovascular life support (ACLS) while the operator withdraws from the coronary. Filter artifact: a flat ECG with a normal arterial waveform is a detached lead, not asystole.
Respiration
Look at the chest, the airway, and the capnograph together. Typical adult respiratory rate is 12–20 breaths/min. Tachypnea during PCI can be pain, pulmonary edema, contrast reaction, or embolism. Apnea after a sedation bolus is an airway emergency. Snoring or paradoxical chest motion is obstruction — jaw thrust and the sedation provider, not another milligram of midazolam.
NIBP versus intravascular pressure
NIBP is a cuff: intermittent, delayed, and unreliable in shock, marked arrhythmia, and intra-aortic balloon pump (IABP) support. Place the cuff on the arm opposite radial access so you do not cycle it over a sheath or a fresh arteriotomy.
Intravascular pressure from a sheath, diagnostic catheter, or arterial line is beat-to-beat. Trust it only after three checks:
-
Zero at the phlebostatic axis — fourth intercostal space, mid-axillary line, approximating the right atrium. A transducer on the floor reads falsely high; one on the drape above the chest reads low. Re-zero after table-height changes.
-
Confirm the labeled site and scale. A 120/10 tracing tagged “aortic” is a left-ventricular waveform in the wrong channel.
-
Judge damping. A fast-flush square-wave test that rings excessively is underdamped: systolic pressure is overestimated, diastolic underestimated, overshoot visible. Long whippy tubing and some air contribute. An overdamped waveform is sluggish and rounded with a narrowed pulse pressure: air bubbles, loose connections, kinks, clot at the tip, or a stopcock not fully open. Systolic pressure is underestimated. Flush, tighten, unkink, and re-zero before anyone treats “hypotension” that is really a bubble.
Typical adult aortic pressure tracks a reasonable NIBP, on the order of 90–140/60–90 mmHg, with many labs treating mean arterial pressure (MAP) <65 mmHg as a call-out unless the physician set another floor. Left-ventricular end-diastolic pressure (LVEDP) is commonly 6–12 mmHg; a climbing LVEDP with falling SpO2 is congestion.
Pulse oximetry
A common adult target is SpO2 ≥94% on room air (labs set floors, often 92%). Two-wavelength pulse oximetry estimates saturation, not oxygen content. It lies when:
- Perfusion is poor — shock, vasoconstriction, hypothermia, or a finger on the radial-access side.
- Nail polish, gel nails, or a dirty probe block the light path.
- Carbon monoxide is present: carboxyhemoglobin is read like oxyhemoglobin, so SpO2 can look near-normal while the patient is hypoxemic. Use co-oximetry, not the finger probe, in CO exposure.
- Motion, cautery, and methemoglobin also distort the number.
Move the probe to an ear or forehead, correlate with the waveform, and treat the patient.
Capnography
Adult ETCO2 is typically 35–45 mmHg. During moderate sedation, a rising ETCO2 is hypoventilation — the patient is retaining CO2. Stimulate, support the airway, and stop stacking narcotic or midazolam. A sudden loss of ETCO2 is apnea, a disconnected sample line, or, with an advanced airway, esophageal intubation or circuit disconnect. Falling ETCO2 with a preserved waveform can mean hyperventilation, falling cardiac output, or embolism. Capnography catches oversedation before SpO2 crashes.
Level of consciousness
Moderate sedation should leave a patient who responds purposefully to voice or light touch. Response only to pain, or no response, is too deep — notify the sedation provider and support ventilation. Document a simple scale the lab actually uses (voice / pain / unresponsive, Ramsay, or Richmond Agitation-Sedation Scale (RASS)). Agitation is a finding too: ischemia, hypoxia, full bladder, or paradoxical sedation.
Parameter / typical adult values / CI action
| Parameter | Typical adult values | CI action |
|---|---|---|
| Temperature | 36.5–37.5 °C | Forced-air warming on long cases; report shivering or a falling trend |
| ECG | Sinus 60–100/min; watch ST, PR, QRS | RCA injection: bradycardia/AV block; VT/VF: defibrillate per ACLS |
| Respiration | 12–20/min, unlabored | Tachypnea = pain, congestion, reaction; apnea/snoring = airway |
| NIBP | About 90–140/60–90 mmHg | Opposite the access arm; do not trust it in shock or IABP |
| Intravascular pressure | Zero at phlebostatic axis; MAP often ≥65 mmHg | Treat damping; re-zero after table-height changes |
| SpO2 | Often ≥94% on room air | Distrust poor perfusion, nail polish, and carbon monoxide |
| ETCO2 | 35–45 mmHg | Rise = hypoventilation; sudden loss = apnea or disconnect |
| LOC | Purposeful response to voice in moderate sedation | Pain-only or unresponsive = too deep; call the sedation provider |
Worked case
During an RCA injection the rate falls to 38 with new 2:1 AV block, the NIBP cuff fails to cycle, the arterial line looks rounded after a table raise, and ETCO2 has climbed from 38 to 52 mmHg while the patient no longer answers to name. Four problems, four actions: announce the AV block and have atropine and pacing ready; re-zero at the phlebostatic axis and flush the line (the rounded tracing is overdamping after a height change, not automatically cardiogenic shock); stimulate and support ventilation for hypoventilation; tell the sedation provider the patient is no longer responding to voice.
Exam traps
- NIBP and arterial-line systolic pressure are not interchangeable when the waveform is damped.
- An SpO2 of 99% does not exclude carbon monoxide exposure.
- Rising ETCO2 is not “the patient is waking up.”
- RCA bradycardia is common enough to prepare for, not rare enough to ignore.
A CI technologist is preparing for a selective right-coronary injection in a right-dominant patient. Which monitoring finding is MOST characteristic of this injection, and what is the BEST preparation?
After a table-height change, the arterial waveform becomes rounded and sluggish with a narrowed pulse pressure, and the displayed systolic value is much lower than the last NIBP. The MOST likely explanation is:
During moderate sedation for elective PCI, ETCO2 rises from 36 to 54 mmHg, respiratory rate falls, and the patient no longer answers to name but withdraws from a sternal rub. What do these findings indicate?