5.2 Vasoactives, Sedation & Emergency Medications

Vasoactives, Sedation, and Emergency Medications in the Cardiac Lab

ARRT Patient Care 1.E.1.c is vasoactives (constrictors, dilators). 1.E.1.d is emergency medications. The rest of 1.E.1.e is analgesics, antiemetics, antihypertensives, antiarrhythmics, and moderate sedation. These drugs share one exam logic: they change blood pressure, rhythm, or consciousness in seconds, and the R.T.(CI) is the person watching the arterial line, the electrocardiogram, and the crash cart while the operator is looking at a coronary.

Advanced cardiovascular life support (ACLS) is required for CI clinical experience. This section teaches recognition and the technologist's role. It does not replace an ACLS card, and it does not invent milligram tables as if ARRT published them. Typical teaching doses below are labeled as such.

Quick Answer: Nitroglycerin (SL/IV/IC) treats spasm and ischemia but drops blood pressure and is cautioned in right-ventricular (RV) infarct. Pressors are not interchangeable: phenylephrine is pure alpha-1, norepinephrine is a common shock pressor, epinephrine is for arrest and anaphylaxis. Atropine treats vagal bradycardia. Adenosine is for SVT and for fractional flow reserve (FFR) hyperemia. Amiodarone or lidocaine treat VT/VF. Moderate sedation is midazolam plus fentanyl; flumazenil can seize. Sodium bicarbonate is not a routine arrest drug.

Dilators: nitroglycerin and nitroprusside

Nitroglycerin (NTG) is the everyday dilator. Sublingual tablets or spray treat ischemic chest pain before or during a case. Intravenous infusion treats ongoing ischemia or hypertensive urgency in the lab. Intracoronary boluses treat catheter-induced spasm, ostial spasm, and are a first move in slow flow or no-reflow when the operator asks. The action is venodilation (preload down) plus coronary dilation. Hypotension is the reaction you must catch — look at the arterial line before you hand the syringe.

RV infarct, usually an inferior STEMI with right-ventricular involvement, is the classic caution. These patients are preload-dependent. NTG can drop blood pressure precipitously. If the operator is wiring a right coronary and the systolic pressure is already 80 mm Hg, do not independently push sublingual NTG because the patient reports chest pressure.

Nitroprusside is a potent arterial dilator used for afterload reduction (hypertensive crisis, acute heart-failure afterload dump) and sometimes intracoronary for no-reflow. Cyanide toxicity is a prolonged-infusion issue, not a single intracoronary dose issue. Immediate hypotension is the intra-case risk. Have a pressor plan before a nitroprusside infusion runs away.

Constrictors: phenylephrine, norepinephrine, epinephrine, dopamine, vasopressin

Match the drug to the physiology; do not treat “pressor” as one bottle.

Phenylephrine is a pure alpha-1 agonist. It raises systemic vascular resistance. It is useful for vasodilatory hypotension (sedation-related, NTG-related) when contractility is intact. Reflex bradycardia can appear. Typical teaching is a dilute intravenous bolus the circulating registered nurse draws; you keep the arterial waveform visible.

Norepinephrine combines alpha constriction with some beta-1 support. It is a common first-line vasopressor for shock with low vascular resistance. It produces less reflex bradycardia than phenylephrine. Extravasation can injure tissue — know the IV site.

Epinephrine is alpha plus beta. Use it for cardiac arrest, anaphylaxis, and profound hypotension. It raises heart rate and contractility as well as vascular resistance. In the lab it also appears as intracoronary epinephrine in some no-reflow algorithms — that is a physician-directed decision, not a circulating guess.

Dopamine is historically taught as dose-dependent (low “renal,” medium inotropic, high vasopressor). Modern shock algorithms have de-emphasized it; ARRT may still list it. Higher teaching doses are constricting and arrhythmogenic.

Vasopressin appears in arrest algorithms conceptually as a non-adrenergic vasopressor. Know that it lives on the crash cart and that it is not a coronary dilator. Do not reach for vasopressin to treat catheter spasm.

Emergency and antiarrhythmic core: atropine, adenosine, amiodarone, lidocaine

Atropine treats vagal reactions and symptomatic bradycardia — sheath insertion, contrast into the right coronary, or a full bladder. Typical ACLS teaching is 0.5–1 mg IV, repeatable to the algorithm ceiling. Atropine will not fix a wide, dying rhythm that needs pacing or epinephrine. Announce the rate and the arterial pressure when you call for it.

Adenosine has two lab jobs, and mixing them up is an exam trap. (1) Supraventricular tachycardia (SVT) — brief AV nodal block; typical teaching 6 mg rapid IV then 12 mg, with a flush, crash cart nearby. A few seconds of asystole or pause can be expected. (2) FFR hyperemia — typically an intravenous infusion (common teaching 140 mcg/kg/min) or operator-directed intracoronary boluses so the coronary is maximally dilated. Warn the patient about chest pressure and flushing. FFR adenosine is not “the patient is in SVT.”

Amiodarone and lidocaine treat ventricular tachycardia / ventricular fibrillation per ACLS. Amiodarone is a common antiarrhythmic after defibrillation and epinephrine in a shockable arrest; lidocaine is an acceptable alternative. Both can cause hypotension (amiodarone especially if pushed fast). Pads should already be on before you need them.

Beta blockers, calcium-channel blockers, antihypertensives

Beta blockers (metoprolol, esmolol) are anti-ischemic, rate-controlling, and antihypertensive. Contraindications in teaching lists: decompensated heart failure, marked bradycardia, high-grade AV block, active severe bronchospasm, and shock. Esmolol's short half-life is useful when you might need the effect to vanish.

Diltiazem and verapamil slow AV conduction for atrial fibrillation or flutter with rapid ventricular response and for some SVTs. They are negative inotropes — avoid in decompensated reduced-ejection-fraction failure and in irregular wide-complex rhythms that might be pre-excited. Intracoronary nicardipine or verapamil (sometimes diltiazem) treat coronary spasm and no-reflow. Watch the arterial pressure; intracoronary calcium-channel blockers can drop systemic pressure.

Other intravenous antihypertensives in the lab include nicardipine infusions, hydralazine, and the nitrates already named. Treat the number in context: a systolic of 90 mm Hg during right-coronary ischemia is not hypertension to treat, and a systolic of 210 mm Hg before large-bore access is.

Moderate sedation, analgesics, antiemetics, reversal

Most labs use midazolam (benzodiazepine) plus fentanyl (opioid) for moderate sedation. The CI technologist does not independently “give more sedation.” You watch respiratory rate, pulse oximetry, capnography if used, blood pressure, and whether the patient still responds. Fentanyl causes respiratory depression and, in overdose, rigidity. Midazolam causes respiratory depression and amnesia.

Naloxone reverses opioids. The patient may wake in pain with a catecholamine surge. Re-sedation can occur because naloxone may wear off first. Flumazenil reverses benzodiazepines. The exam trap is seizure risk, especially in chronic benzodiazepine users or mixed overdoses. Flumazenil is not a routine wake-up button after every uneventful case.

Ondansetron is the common antiemetic. It can prolong QT; it is still widely used. Vomiting under a sterile drape is an aspiration risk and a field-contamination event. Have a basin and suction ready before the first contrast run in a nauseated patient.

Sodium bicarbonate is not routine in undifferentiated arrest. Teaching indications that still appear: severe metabolic acidosis, hyperkalemia, and certain sodium-channel-blocker poisonings. Do not push amp after amp because the code is long.

ACLS in the cath lab: recognition and the tech's role

CI clinicals require ACLS. The exam still wants the technologist's job description:

1. Recognize — loss of the arterial waveform, ventricular fibrillation on the monitor, sudden unresponsiveness, agonal breathing.
2. Call it — loud, closed-loop: “No arterial waveform, VF on the monitor.”
3. Bring the crash cart, attach the defibrillator, and get pads on (or follow the sterile defibrillation plan your lab uses).
4. Defibrillate as directed; clear the table; know how the fluoro table locks and how the C-arm parks so compressions and shocks can happen.
5. Document drugs, joules, times, and rhythms.

If a stem asks who runs the ACLS algorithm, the ACLS-trained team does. If it asks who gets the pads and the cart, that is the CI technologist. Do not invent sequences that contradict a current ACLS card.

Pressor versus dilator versus antiarrhythmic

Scenario

During right-coronary PCI the patient yawns, the arterial line falls to 62/40, and the rate is 38. This is a vagal picture until proven otherwise. Atropine as ordered, fluids, legs up if the table allows, stop NTG, and tell the operator. It is not an epinephrine arrest yet, and it is not a reason to give more fentanyl. If the same patient had a clear RV infarct and a systolic of 80 mm Hg, NTG would be the wrong “chest-pain” reflex.

Exam traps

• NTG in RV infarct.
• Adenosine for FFR is hyperemia, not an SVT rescue by default.
• Flumazenil and seizures.
• Bicarbonate is not a routine arrest drug.
• Phenylephrine is a constrictor; NTG is a dilator — they are not interchangeable “cardiac meds.”