2.3 Autonomic modulation & the cardiac cycle

Autonomic control of the heart

Although the SA node can beat on its own, the autonomic nervous system constantly adjusts heart rate, conduction, and force of contraction to meet the body's needs. Two opposing branches do this work, and the CRAT exam expects you to know their transmitters, receptors, and effects.

Sympathetic (adrenergic) branch

The sympathetic nerves release norepinephrine onto beta-1 (B1) receptors found throughout the SA node, AV node, and working myocardium, and circulating epinephrine from the adrenal medulla adds to the effect. The results, the "fight or flight" response, are:

• Positive chronotropy (faster rate): B1 stimulation increases the funny current and calcium current, steepening the SA node's phase 4 slope so it reaches threshold sooner.
• Positive dromotropy (faster conduction): the AV node conducts more quickly, shortening the PR interval.
• Positive inotropy (stronger contraction) and positive lusitropy (faster relaxation), largely by increasing the calcium available to the contractile machinery.

Parasympathetic (cholinergic) branch

The parasympathetic supply travels in the vagus nerve (cranial nerve X) and releases acetylcholine onto M2 muscarinic receptors concentrated in the SA and AV nodes, with little innervation of the ventricles. Its effects, "rest and digest," oppose the sympathetics:

• Negative chronotropy: acetylcholine opens potassium channels and reduces the funny and calcium currents, flattening the phase 4 slope and slowing SA firing.
• Negative dromotropy: AV conduction slows, lengthening the PR interval and, with strong vagal tone, producing AV block.

Because vagal fibers barely reach ventricular muscle, the parasympathetic system has little direct effect on contractility. At rest, vagal tone dominates: the intrinsic SA rate is near 100, yet the resting heart rate sits around 70 because ongoing vagal braking holds it down. Useful vocabulary: chronotropy is rate, dromotropy is conduction velocity, inotropy is contractility, and lusitropy is relaxation.

The two branches are coordinated by the baroreceptor reflex. Stretch receptors in the carotid sinus and aortic arch sense blood pressure: a rise in pressure increases vagal output and withdraws sympathetic tone to slow the heart, while a fall does the opposite to speed it up and maintain perfusion. This reflex is why clinical vagal maneuvers, such as carotid sinus massage or the Valsalva maneuver, can slow AV conduction enough to terminate or unmask a supraventricular tachycardia, a fact worth remembering when a strip suddenly slows during such a maneuver.

The cardiac cycle

The cardiac cycle is the sequence of mechanical events in one heartbeat, divided into systole (ventricular contraction and ejection) and diastole (relaxation and filling). A crucial principle for rhythm analysis is that electrical events precede and trigger the mechanical events:

• The P wave (atrial depolarization) precedes atrial contraction, which delivers the "atrial kick," the final 20-30% of ventricular filling.
• The QRS complex (ventricular depolarization) precedes ventricular contraction; the ventricles begin isovolumetric contraction and then eject blood.
• The T wave (ventricular repolarization) precedes ventricular relaxation and diastolic filling.

Mechanically, each cycle runs through isovolumetric contraction, ejection, isovolumetric relaxation, and filling. Valve closure produces the heart sounds: S1 as the AV valves close at the start of systole, and S2 as the semilunar valves close at the start of diastole. Diastole is normally longer than systole and is when the coronary arteries fill, which matters clinically because very fast rates shorten diastole and cut both ventricular filling and coronary perfusion. During ejection the left ventricle develops systemic pressures around 120 mmHg while the right ventricle generates only about 25 mmHg, each matching the resistance of its circuit. The fraction of end-diastolic volume ejected with each beat is the ejection fraction, normally 55-70%, and it is a key bedside measure of pump function.

Cardiac output

The purpose of all this electrical and mechanical activity is to move blood, quantified as cardiac output (CO):

CO = heart rate (HR) x stroke volume (SV)

Normal cardiac output is roughly 4-8 L/min, with a typical stroke volume near 70 mL. Stroke volume itself depends on preload (the Frank-Starling relationship, in which more filling stretches the muscle and yields a stronger beat), afterload (the resistance the ventricle pumps against), and contractility (set by the inotropic state). Higher preload and greater contractility raise stroke volume, while excessive afterload lowers it. Raising heart rate increases output up to a point, but if the rate climbs so high that diastolic filling time collapses, stroke volume falls and cardiac output can actually decrease, an important idea when evaluating tachyarrhythmias. The same logic applies at the other extreme: in a profound bradycardia, stroke volume may be normal or even large, yet the slow rate can leave cardiac output too low to sustain blood pressure, which is why both very fast and very slow rhythms can compromise a patient.

How autonomic tone appears on the ECG

Because the two branches act on the nodes, changes in autonomic balance are visible on the rhythm strip. Rising sympathetic tone produces a faster sinus rate with a shorter PR and QT interval. Rising vagal tone produces a slower sinus rate with a longer PR interval, and may generate sinus bradycardia, sinus arrhythmia (the normal beat-to-beat rate variation with breathing, faster on inspiration and slower on expiration), or transient vagally mediated AV block. Recognizing these patterns lets the technician distinguish benign autonomic effects from true conduction disease.