The intrinsic spontaneous rate of the SA node depolarization is 90 to 100 beats/min and is modulated by autonomic nerve inputs. The parasympathetic nervous system (PNS) normally is dominant. The right vagus nerve, with acetylcholine as its neurotransmitter, innervates the SA node. Acetylcholine slows SA node depolarization and therefore lowers heart rate. The left vagus nerve innervates the AV node, at which the neurotransmitter acetylcholine decreases the velocity of impulse transmission. Nodal areas have high acetylcholinesterase activity, so they rapidly clear acetylcholine.

Cardiac sympathetic nerves (SNS) originate from spinal nerves C-7 to T-6, pass to the stellate ganglion, then to the epicardial plexus. The right epicardial plexus, with norepinephrine as the neurotransmitter, innervates the SA node. Norepinephrine increases heart rate. Elevated temperature and stretch also can act directly on the SA node to increase heart rate. The left epicardial plexus innervates the AV node, at which norepinephrine increases conduction velocity.

The external environment of the heart also influences myocardial performance. Endocrine agents with cardiac actions include the adrenal catecholamines epinephrine and norepinephrine, whose actions mimic those of the cardiac sympathetic nerve; thyroid hormone and growth hormone, which play a nutritive role and set the basal tone of the cardiovascular system; and insulin and glucagon, which both have a direct positive inotropic effect.

Blood gases can directly and indirectly alter cardiac function. Severe hypoxia directly depresses myocardial function. Very high CO2 directly depresses myocardial function, and acidosis decreases Ca++ release from SR and consequently decreases contractility. Indirectly, moderate hypoxia causes activation of the sympathetic nervous system, and increases heart rate, contractility, and therefore cardiac output. Moderate hypercapnia also causes a sympathetic activation and increases heart rate, contractility, and therefore cardiac output.

Cardiac Output

The cardiac output is the volume of blood pumped by the heart each minute. It can be calculated as stroke volume times heart rate. Factors that alter stroke volume or heart rate will change cardiac output. Normally it is about 5 L/min (70 mL/beat x 72 beats/min). Cardiac index is defined as cardiac output/body surface area, and it allows comparisons of cardiac function between individuals of different sizes.

Cardiac output measurements are direct or indirect. Direct determination uses a type of flowmeter. A Doppler flowmeter actually measures velocity, which is converted to an estimation of flow based on the vessel cross-sectional area. Indirect measurement often involves the Fick principle.

Cardiac Output = O2 consumed per minute / Pulmonary venous O2 − pulmonary arterial O2

An indicator dilution technique involves injection of a known amount of dye and measurement of the consequent concentration change downstream. However, dye can accumulate if multiple measurements are taken. Thermal dilution involves injection of cold saline and measurement of the resultant change in temperature downstream. This approach can be performed with a Swan-Ganz catheter and is suitable for multiple determinations.

Improved ventricular imaging techniques allow accurate measurement of ventricular end-diastolic and ventricular end-systolic volumes. Consequently, imaging combined with electrocardiographic measurement of heart rate allows noninvasive measurement of cardiac output and ejection fraction.