Pharmacology for Nurses · Introduction to the Cardiovascular System
Conduction of Electrical Impulses
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In 30 seconds
The heart does not wait for a signal from the brain — it generates its own electricity. A small group of specialized cells, the sinoatrial (SA) node, fires spontaneously roughly 60–100 times per minute, and the impulse spreads along a dedicated pathway: SA node The heart's primary pacemaker in the right atrium Full entry → → atria → atrioventricular (AV) node → bundle of His → bundle branches → Purkinje fibers Final relay cells spreading the impulse through the ventricles Full entry →, which carry the signal to the ventricular muscle. This orderly march of electricity coordinates the mechanical pumping described in the previous topic — electrical events always precede mechanical events. On the ECG A skin-surface recording of the heart's electrical activity Full entry →, the activity appears as the P wave (atrial Depolarization The rapid voltage change when ions rush into a cell Full entry →), the QRS complex (ventricular depolarization), and the T wave (ventricular Repolarization Return of the cell to its resting voltage Full entry →). Because most antidysrhythmic drugs act by altering ion channels in these cells, conduction is the bridge between normal heart function and the drug classes in Chapter 17.
Why this matters
Every dysrhythmia is, at bottom, a problem of electricity: an impulse that fires too fast, too slow, in the wrong place, or along a re-entrant loop. To understand why a drug is chosen — why lidocaine targets ventricular rhythms, why a beta blocker slows AV conduction in atrial fibrillation — you must know which structure generates the impulse and which channels conduct it. On the ECG, nurses see the electrical signature of conduction daily: a widened QRS suggests slowed ventricular conduction, a long PR interval suggests AV delay, and absent P waves point to a rhythm not driven by the SA node. Recognizing these patterns helps you anticipate which drug class a prescriber may order and detect drug toxicity (for example, excessive QRS widening) before it becomes dangerous.
The college version
Core Concepts
The conduction pathway: a relay race
The impulse starts in the SA node, the heart's natural pacemaker, located in the right atrium. It spreads across both atria, producing atrial contraction, then reaches the AV node Gateway between atria and ventricles that delays the impulse Full entry →, a gateway between atria and ventricles. The AV node deliberately slows the impulse — this "AV delay" gives the atria time to finish emptying before ventricular contraction begins. From the AV node the impulse shoots down the bundle of His, splits into right and left bundle branches running through the septum, and fans out through the Purkinje fibers in the ventricular walls, triggering coordinated, apex-first ventricular contraction. If the SA node fails, other cells can take over as escape pacemakers — but they fire more slowly, which is why SA node failure produces a slow rhythm rather than cardiac arrest.
Automaticity: cells that fire on their own
The defining property of pacemaker cells is Automaticity A cell's ability to fire on its own Full entry → — the ability to depolarize spontaneously. The SA node has the fastest intrinsic rate (60–100 beats/min at rest), the AV node the next fastest (40–60), and Purkinje fibers the slowest (20–40). This hierarchy matters clinically: when a faster pacemaker is suppressed (by disease or by drugs such as beta blockers), a slower one may take over, and the resulting rate tells you where the new pacemaker is. The intrinsic SA node rate is continuously adjusted up or down by the autonomic nervous system.
The action potential: ions moving across the membrane
Cardiac cells fire because charged ions move across the cell membrane through channels. The classic ventricular Action potential The sequence of ion movements that makes a cell fire Full entry → has five phases:
- Phase 0 (depolarization): sodium channels open, sodium rushes in, and the cell rapidly depolarizes. This phase produces the QRS complex on the ECG.
- Phase 1: sodium channels close; a brief repolarization begins.
- Phase 2 (plateau): calcium enters through L-type calcium channels, balancing potassium leaving, and the membrane stays depolarized. This long plateau is unique to cardiac muscle and is why cardiac contraction lasts much longer than a nerve impulse.
- Phase 3 (repolarization): calcium channels close, potassium continues to leave, and the cell returns to its resting voltage. This phase produces the T wave.
- Phase 4 (resting): pumps restore the ion gradients, and the cell is ready to fire again.
Pacemaker cells (SA and AV nodes) differ: their phase 4 is unstable and drifts upward, which is what makes them fire spontaneously. This is why the SA node is called a pacemaker — it has automaticity, not because it is told to beat.
Refractory periods: the heart can't be rushed
After firing, a cell cannot immediately fire again. During the absolute Refractory period Time after firing when a cell cannot (or can barely) fire again Full entry →, no stimulus can trigger a new action potential; during the relative refractory period, only a very strong stimulus can. Refractory periods protect the heart from sustained (tetanic) contraction and from re-entrant circuits — an impulse traveling a loop dies out when it meets tissue that is still refractory. Many antidysrhythmic drugs work precisely by lengthening refractory periods, which is how they break re-entry loops, a common mechanism of dangerous tachycardias.
The ECG: reading electricity from the skin
The ECG is a graph of the heart's net electrical activity measured at the body surface:
- P wave — atrial depolarization (before atrial contraction).
- PR interval — time from atrial depolarization to the start of ventricular depolarization, dominated by AV node delay.
- QRS complex — ventricular depolarization; its width reflects how fast the impulse travels through the ventricles.
- T wave — ventricular repolarization.
- QT interval — total time from ventricular depolarization through repolarization; prolonged QT raises the risk of torsades de pointes, a dangerous polymorphic ventricular tachycardia — the reason so many drugs carry QT-prolongation warnings.
Common Confusions
| Do Not Confuse | With | Difference |
|---|---|---|
| Depolarization | Contraction | Depolarization is the electrical event; contraction is the mechanical result — electricity always comes first |
| P wave | QRS complex | P wave is atrial depolarization; QRS is ventricular depolarization (larger, since ventricles have more muscle) |
| PR interval | QT interval | PR measures AV delay; QT measures total ventricular depolarization + repolarization |
| SA node failure | Cardiac arrest | If the SA node stops, slower escape pacemakers take over — a slow rhythm, not no rhythm |
| AV node block | Bundle branch block | AV block delays/prevents the impulse reaching the ventricles; bundle branch block slows spread within the ventricles (widened QRS) |
| Pacemaker cell automaticity | Neuronal firing | Pacemaker cells drift spontaneously toward threshold; neurons must be stimulated — this is why the heart self-fires |
Eli explains
The same idea, in plain words
Explain it like I’m 10
Your heart has its own tiny battery and wiring. The SA node sends an electrical "go" signal about once a second, like a coach blowing a whistle, and it travels down special wires to the bottom of the heart, telling the muscle when to squeeze. Backup whistles further down the wires keep the heart beating even if the main one stops — just more slowly. An ECG machine photographs that electricity so we can see if the signal comes from the right place at the right speed.
Worked example
Follow one heartbeat through the system as a patient lies on a monitor:
- The SA node fires. A P wave appears as the atria depolarize, and the atria contract (atrial systole).
- The impulse reaches the AV node, which slows it briefly. On the ECG this shows as the PR interval — a normal finding; a prolonged PR interval (first-degree AV block) means the delay is excessive, sometimes because of a drug or disease.
- The impulse races down the bundle of His and bundle branches into the Purkinje fibers. The QRS complex appears as the ventricles depolarize, and ventricular systole follows immediately — this is the heartbeat you feel at the wrist, delayed a few milliseconds after the QRS on the monitor.
- The ventricles repolarize, producing the T wave, and the cycle resets. The time from one P wave to the next gives the rate; the rhythm is "normal sinus rhythm" only if each P wave is followed by a QRS at a regular, appropriate interval.
Now imagine a drug that blocks sodium channels (a Class I antidysrhythmic). Its expected electrical effect is slower phase 0 depolarization, which widens the QRS — you would watch QRS width on the monitor for exactly this reason. That is mechanism-based monitoring: predict the electrical change, then look for it.
Key takeaways
- Electrical conduction order: SA node → atria → AV node → bundle of His → bundle branches → Purkinje fibers.
- The AV node is the only normal electrical connection between atria and ventricles; its delay lets atrial contraction finish before ventricular contraction begins.
- Automaticity hierarchy: SA node 60–100, AV node 40–60, Purkinje fibers 20–40 beats/min — the fastest pacemaker normally drives the heart.
- Ventricular action potential: phase 0 sodium influx (depolarization), phase 2 calcium plateau (contraction), phase 3 potassium efflux (repolarization).
- ECG landmarks: P = atrial depolarization, QRS = ventricular depolarization, T = ventricular repolarization, PR = AV delay, QT = total ventricular electrical activity.
- Refractory periods prevent sustained contraction and normally stop re-entry circuits; many antidysrhythmic drugs lengthen them.
- Drug classes target specific phases: Class I blocks sodium channels (phase 0), Classes II and IV slow the SA/AV nodes, Class III prolongs repolarization (phase 3). Details in Chapter 17.
- ECG interpretation, rhythm identification, and drug administration follow scope-of-practice rules that vary by jurisdiction and facility — verify against your institution's policies.
Check yourself
5 review questions from the chapter. Try each one, then open the answer.
List the conduction pathway in order, from the primary pacemaker to the ventricular muscle.
Show answer
SA node → atrial muscle → AV node → bundle of His → right/left bundle branches → Purkinje fibers → ventricular muscle.
Why does the AV node deliberately slow the impulse, and what ECG interval reflects that delay?
Show answer
The AV delay gives the atria time to finish ejecting blood into the ventricles before the ventricles contract. It is reflected in the PR interval.
A patient's monitor shows no P waves but a regular, narrow QRS at about 50 beats/min. What does the absence of P waves suggest about where the impulse is originating?
Show answer
The rhythm is not being driven by the SA node (which produces P waves). The rate of about 50 beats/min is consistent with the AV node taking over as pacemaker (an escape rhythm at the AV node's intrinsic rate of 40–60).
Which ion is responsible for the rapid depolarization (phase 0) of ventricular muscle cells, and which drug class blocks that channel?
Show answer
Sodium (Na⁺) influx drives phase 0. Class I antidysrhythmic drugs block sodium channels (see Chapter 17, Topic 2).
A drug prolongs the QT interval. In which phase of the action potential is it acting, and what dysrhythmia risk should the nurse be alert to?
Show answer
A prolonged QT interval indicates slowed repolarization (phase 3, potassium efflux). The associated risk is torsades de pointes, a polymorphic ventricular tachycardia; this is why QT-prolonging drugs require careful monitoring and why electrolyte abnormalities (especially low potassium and magnesium) matter.
Study tools & related lessonsKey vocabulary · Related
Key vocabulary
- SA node
- The heart's primary pacemaker in the right atrium
- AV node
- Gateway between atria and ventricles that delays the impulse
- Automaticity
- A cell's ability to fire on its own
- Action potential
- The sequence of ion movements that makes a cell fire
- Depolarization
- The rapid voltage change when ions rush into a cell
- Repolarization
- Return of the cell to its resting voltage
- Refractory period
- Time after firing when a cell cannot (or can barely) fire again
- Purkinje fibers
- Final relay cells spreading the impulse through the ventricles
- ECG
- A skin-surface recording of the heart's electrical activity
Sources & references
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