1. The peripheral nervous system consists of the autonomic nervous system (ANS) and is concerned with involuntary regulation of cardiac muscles, smooth muscle, and glandular/visceral functions throughout the body. Visceral reflexes occur at the subconscious level. The ANS is composed of both sympathetic and parasympathetic fibers.

2. The somatic system is composed of a single neuron between the central nervous system (CNS) and the effector organ or sensory organ. The ANS has two neurons connecting the CNS to the effector organ. The first neuron (preganglionic) originates within the CNS and synapses in the ANS ganglion. The second neuron (postganglion) transmits signal to the effector organ. The preganglionic neuron is myelinated whereas the postganglionic neuron is unmyelinated.

3. The sympathetic nervous system (SNS) originates in the thoracolumbar spinal cord, the intermediolateral gray column of T1-12 and L1-3.

4. The T1-4/5 nerve roots constitute the superomedial cervical and cervicothoracic ganglia. The cervicothoracic ganglia are also called the stellate ganglia. These provide the sympathetic innervation of head, neck, upper extremities, heart, and lungs.

5. The fibers of the parasympathetic nervous system (PNS) originate in the pre- and postganglionic neurons in the brainstem (cranial nerves III, VII, IX, X, and XI) and sacral segments (S2, 3, and 4) of the spinal cord.

6. The vagus nerve accounts for 75% of PNS activity. It supplies PNS innervation to the heart, lungs, esophagus, stomach, small intestine, proximal half of the colon, liver, gallbladder, pancreas, and upper portion of the ureters.

The sacral fibers (S2, 3, and 4) form the pelvic visceral nerves (nervi erigentes). These supply the rest of the viscera not supplied by the vagus: descending colon, rectum, uterus, bladder, and lower portion of the ureters.

7. Norepinephrine (NE) is released by the postganglionic fibers of the SNS.

3. The postganglionic fibers release either acetylcholine (ACh) or NE.

4. Sympathetic stimulation

5. The PNS leaves the CNS through cranial nerves III, VII, IX, and X.

6. The PNS exits the spinal cord through sacral nerve fibers (S2, 3, and 4) (the nervi erigentes).

7. The vagus nerve contains the most parasympathetic nerve fibers.

8. The sacral parasympathetic nerves innervate the descending colon, rectum, uterus, lower ureters, bladder, and sexual reactions.

1. Tocolysis means inhibition of the uterine contractions of labor. The most commonly used drugs for tocolysis are opioids, magnesium sulfate, prostaglandin inhibitors, calcium channel blockers and beta-agonists. The side effects of beta tocolysis are tachycardia, hypotension, hypokalemia, hyperglycemia, cardiac dysrhythmias (including chest pain/ischemia), and pulmonary edema.

Contraindications to beta-tocolytic therapy include severe preeclampsia/eclampsia, intrauterine infection, maternal hyperthyroidism or cardiac disease, uncontrolled diabetes mellitus, significant vaginal bleeding, anemia, hypovolemia, and death in utero (DIU).

2. The mechanism of action of the xanthines is nonspecific inhibition of all three types of phosphodiesterases (PDEs), resulting in increased cyclic adenosine monophosphate and beta response. Xanthine drugs are theophylline, caffeine, aminophylline, and amrinone lactate (Inocor). Amrinone selectively inhibits PDE III → impeded breakdown of calcium (Ca) stores → increased inotropism. It also promotes lusitropism (diastolic relaxation) and ventricular filling.

3. Amrinone increases the cardiac index, left ventricular stroke index, and left ventricular ejection fraction, while decreasing left ventricular end-diastolic pressure, pulmonary capillary wedge pressure, pulmonary arterial pressure, right atrial pressure, and systemic vascular resistance (SVR). Heart rate (HR) and mean arterial pressure (MAP) are not affected.

Amrinone is started as a 0.75 μg/kg bolus over 2 to 3 minutes, followed by maintenance infusion of 5 to 10 μg/kg/min. Care must be taken not to give the bolus too quickly, otherwise severe hypotension may develop. Two other uncommon side effects include dose-related thrombocytopenia and centrilobar hepatic necrosis.

4. Digoxin blocks the sodium-potassium pump, facilitating calcium entry into myocardial cells. It is used mainly to treat congestive heart failure (CHF) and control supraventricular cardiac dysrhythmias. It may also benefit cardiomyopathies and cor pulmonale.

Indications for preoperative “digitalization” include previous CHF, increased heart size, coronary flow disturbances according to electrocardiogram (ECG), age >60, age >50 before lung surgery, anticipation of massive blood loss, atrial flutter, or atrial fibrillation, cardiovascular (CV) surgery, and rheumatic heart lesions.

5. Monoamine oxidase inhibitors (MAOIs) block the deoxidative deamination of endogenous catecholamines into inactive metabolites. They do not inhibit synthesis. This causes accumulation of NE, epinephrine, dopamine, and serotonin. Overdose symptoms include hyperactivity/agitation, hallucinations, hyperpyrexia, convulsions, hypertension (HTN), and hypotension. Ephedrine produces an exaggerated response due to release of stored catecholamines. Meperidine (Demerol) has been reported to cause hypertensive crisis, convulsions, and coma. The MAOIs also intensify depression caused by ethanol, analgesics, and general anesthesia.

Current recommendation is to stop MAOIs 2 weeks before surgery; few adverse effects have been reported in patients taking MAOIs who undergo regional or opioid anesthesia. Overdose is treated with alpha-blockers, ganglionic blockers, or direct-acting vasodilators.

6. TCAs block uptake of NE into adrenergic nerve endings. Side effects include tachycardia, dysrhythmias, hypotension, myocardial infarction, and CHF. Neuroleptic drugs, sedatives, atropine sulfate, ketamine (Ketalar), and sodium thiopental (STP) potentiate the effects of TCAs. Discontinuation of TCAs is not necessary before surgery, but possible drug interactions must be considered intraoperatively.

1. Dopamine receptors are presynaptic:

DA₁: vascular smooth muscle; vasodilation of renal/mesenteric vessels;

DA₂: vasodilation and inhibition of NE release.

Dopamine receptors have been found in the hypothalamus where they are involved in prolactin release and in the basal ganglia where they coordinate motor function. Dopamine also stimulates the chemoreceptor trigger zone of the medulla, producing nausea/vomiting.

Dopamine receptors have also been suggested in the GI tract: esophagus, stomach, and small intestine. (Metoclopramide [Reglan] promotes gastric emptying.)

2. There are two types of histamine receptors:

H₁: bronchoconstriction, intestinal contraction, coronary spasm, negative dromotropic effect (dromotropic: influence on conduction/excitation);

H₂: acid production by parietal cells of stomach, positive inotropic/chronotropic effects on myocardium that are not blocked by beta antagonism.

3. The beta-receptor has three components: receptor, two G proteins (which bind guanine and regulate the interaction of protein with adenyl cyclase), and catalytic moiety of adenyl cyclase. The receptor is a bifunctional protein that sits on the superficial surface of the plasma membrane and interacts with a chemical messenger (catecholamine). This activates the G protein, which in turn activates adenyl cyclase in a cascade fashion, increasing cyclic adenosine monophosphate and protein kinase A, and finally intracellular calcium. The final mediator of beta-receptor stimulation in cardiac muscle is calcium. In addition, activation of sarcolemmal calcium transport systems may occur directly by beta-receptor stimulation.

4. The receptor response to a catecholamine can be regulated by the following:

1. The Valsalva maneuver increases intrathoracic pressure by forced expiration against a closed glottis. Blood pressure (BP) momentarily increases as intrathoracic blood is forced into the heart (increased preload). Sustained pressure decreases venous return (VR) and therefore cardiac output (CO) and BP → reflex vasoconstriction and tachycardia.

Dysfunction of the SNS is implicated if exaggerated and prolonged hypotension develops during Valsalva (>50% decrease from resting MAP).

2. Bainbridge reflex is a venous baroreceptor reflex by which reduced venous pressure reduces the HR. (Reduced arterial pressures cause a reflex tachycardia.) The venous receptors are proposed to be more dominant in the moment-to-moment regulation of CO. HR, like CO, can be adjusted to the quantity of blood entering the heart.

There is characteristic, paradoxical slowing of the heart seen with spinal anesthesia. Blockade of the SNS levels of T1-4 ablates the efferent limb of the cardiac accelerator nerves. (Therefore, unopposed vagus → bradycardia.) The primary defect in the development of spinal hypotension is a decrease in VR → bradycardia. Reflex tachycardia is the usual response to hypotension or acidosis from other causes.

3. The drug of choice for bradycardia in the transplanted heart is isoproterenol, not atropine. Isoproterenol increases the discharge rate of the donor sinoatrial (SA) node by direct action (beta-adrenergic stimulation). There is no result from atropine in the denervated heart.

1. Ganglionic blockers interfere with neurotransmission at ANS ganglia. They produce their nicotinic effects by competing, mimicking, or interfering with ACh metabolism.

2. d–Tubocurarine (DTC) produces a competitive nondepolarizing block of both motor endplates and ANS ganglia (nicotinic cholinergic receptors).

3. DTC causes hypotension by the following: