13.5 Lecture Nervous Regulation of Circulation

Nervous Regulation of Circulation

• The autonomic nervous system regulates circulation via the sympathetic and parasympathetic systems.
• The sympathetic system is the more important of the two in regulating circulation.
• Sympathetic fibers exit the spinal cord through thoracic and lumbar spinal nerves, passing through the sympathetic chain to specific nerves or peripheral spinal nerves that supply the vasculature.
• Sympathetic innervation of arteries and arterioles increases resistance and decreases flow.
• Venous innervation and constriction decreases venous volume, which in turn increases preload.
• Parasympathetic innervation of the heart, via the vagus nerve, decreases heart rate, with minor effects on contractility.
• The parasympathetic nervous system plays a minor role in regulating vascular function.

Sympathetic Vasoconstriction

• Nerve fibers throughout the body continuously transmit impulses at a slow rate, maintaining partial constriction, which is evident during spinal anesthesia.
• Spinal anesthesia leads to a dramatic decrease in blood pressure, due to inhibiting the sympathetic system.
• The vasomotor center in the brain controls heart rate, contraction strength, and vascular tone.
• Sympathetic impulses are transmitted to both blood vessels and the adrenal medulla.
• The adrenal medulla secretes epinephrine and norepinephrine into the blood, which act directly on blood vessels.
• Nervous control rapidly increases arterial pressure through arterial constriction, venous constriction, and enhanced cardiac pumping.
• Arterial constriction increases peripheral resistance, thus increasing arterial pressure.
• Venous constriction displaces blood to the heart, increasing stretch and cardiac output.
• Enhanced cardiac pumping is achieved by elevating heart rate and contractility, greatly affecting cardiac output (cardiac output = stroke volume x heart rate).

Baroreceptors

• Baroreceptors, or stretch receptors, are located in the walls of large systemic arteries.
• Rising pressure causes stretch, which sends inhibitory signals to the CNS, decreasing autonomic nervous system stimulation.
• Aortic baroreceptors and carotid sinus baroreceptors (located prior to bifurcation) are key types.
• Baroreceptors respond rapidly to changing pressure, with impulses increasing as pressure increases, but they adapt to long-term stationary pressure.
• Rapid blood pressure changes induce activity, while slow adjustments may cause minimal response.
• Baroreceptor stimulation causes dilation of veins and arterioles, as well as decreased heart rate and contractility.
• Baroreceptors help maintain pressure upon standing by responding to decreased blood pressure with elevated blood pressure, and are considered a pressure buffer system.
• The effect of baroreceptors on long-term blood pressure regulation is controversial, potentially having a minimal effect through interaction with the kidneys.
• Baroreceptor stimulation during carotid endarterectomy can cause massive blood pressure swings.

Chemoreceptors

• Chemoreceptors are sensitive to low oxygen or elevated carbon dioxide and hydrogen levels.
• Diminished blood flow decreases oxygen while increasing CO2 and hydrogen levels.
• Chemoreceptors excite the vasomotor center.
• This chemoreceptor reflex is more important at lower blood pressures, as it's not powerful enough when arterial pressure is above 80.

Low Pressure Stress Receptors

• Atria and pulmonary arteries have low-pressure stress receptors in their walls, similar to baroreceptors.
• Atrial stretch reduces renal sympathetic nerve activity, causing dilation of arterioles and decreased tubular reabsorption.
• Stimulation is sent to the hypothalamus to decrease antidiuretic hormone secretion (ADH).
• Decreased afferent arterial resistance increases fluid filtration into the renal tubules.
• This, combined with decreased ADH, increases fluid loss by the kidneys.
• Atrial natriuretic peptide is released, causing further excretion of sodium and water.
• The Bainbridge reflex increases heart rate when blood volume is increased.

CNS Ischemic Response & Cushing Reaction

• When brain blood flow is insufficient to remove carbon dioxide from the brainstem vasomotor center, systemic pressure rises.
• Known as the CNS ischemic response, this can elevate arterial pressure to 250 for up to ten minutes.
• Sympathetic stimulation can be so great that peripheral vessels become occluded.
• This response is not a normal regulatory mechanism, but an emergency pressure control system for severe hypotension.
• The Cushing reaction results from increased CSF pressure in the cranial vault.
• Increased CSF pressure causes arterial compensation and closure.
• The Cushing reaction increases arterial pressure higher than CSF pressure for blood flow to continue.

Respiratory Effects on Arterial Pressure

• Arterial pressure rises and falls in a wave-like manner with respiration, caused by three factors:
  • Breathing signals spill over to the vasomotor center in the medulla.
  • Negative intrathoracic pressure causes blood vessels to expand, reducing venous blood return.
  • Atrial stretch receptors are influenced by intrathoracic pressure changes.
• Respiratory variation is significant in anesthesia, particularly with positive pressure ventilation, which alters intrathoracic pressure.