Cardiac reflexes

Smatresk, N.J. 1986. Ventilatory and cardiac reflex responses to hypoxia and NaCN in Lepisosteus osseus, an air-breathing fish. Physiol. Zool. 59 385-397. 

The effects of norepinephrine on cardiac function are complex because of the dynamic interaction of the direct effects of norepinephrine on the heart and the initiation of powerful cardiac reflexes. The baroreceptor reflexes are discussed in detail in Chapter 9. 

Discuss the role of cardiac reflexes in the therapeutic use and efficacy of drugs that... 

Use of a muscarinic antagonist blocks the actions of the parasympathetic nervous system in a dose-dependent manner, leaving the actions of the sympathetic nervous system relatively unopposed by cardiac reflexes. Administration of a parasympathetic (muscarinic) antagonist will result in sympathetic effects (e.g.. tachycardia, increased cardiac output). Normally, this would precipitate an increase in parasympathetic activity, due to baroreceptor reflexes. The level of ACh secretion may increase, however, because receptors are blocked and physiologic actions normally seen with an increase in ACh are blocked in a dose-dependent manner, leaving the actions of the sympathetic system dominant. Tachycardia and increased cardiac output are seen, and peripheral resistance remains increased. 

Which classes of autonomic drugs are less likely be affected by cardiac reflexes ... 

At lower doses, a paradoxical decrease in heart rate and cardiac output is seen, due in part to cardiac reflexes. 

Questions 13 to 46 using the blood pressure trace (see Figure below), answer each question. Consider cardiac reflexes in your answer. Each letter represents the administration of a drug, allowing sufficient time for recovery. The drugs used are propranolol, hydralazine, clonidine, and prazosin. 

The correct choice is "C. All of the other drugs listed as potential choices elicit cardiac reflexes, which would decrease the effect of the drug. The effects of clonidine would be more sustained, because baroreceptor-mediated compensatory reflexes are blocked at the NTS level, due to the 2 agonist activity of clonidine. 

A is propranolol. Propranolol decreases cardiac output but has little effect on peripheral resistance. Thus, initial hypotensive effects are somewhat lower than those of an a,-antagonist, and a significant proportion of the effects are attenuated by cardiac reflexes. Reflex sympathetic activity causes vasoconstriction, which raises systemic pressure. However, due to the blockade of beta receptors by the drug, such activity does not cause increased cardiac output. Thus, initial hypotensive effects are somewhat attenuated, to a greater extent than with the other drugs presented, but not as attenuated as with a vasodilator. 

This drug produces significant reduction in pressure with little attenuation by cardiac reflexes. Of the drugs presented, an a, antagonist would be the most likely candidate, as vascular diameter is increased, causing a significant decrease in pressure. Compensatory reflex sympathetic activity is blocked at the alpha-receptor level, leaving an increase in cardiac output as the major compensatory factor. 

The significant factor here is that a direct vasodilator provides little or no compensation for cardiac reflexes. The initial result is a significant lowering of pressure with arterial vasodilatation. 

However, this is quickly compensated for by increased sympathetic activity. Because the drug blocks none of the sympathetic receptors, the effects of cardiac reflexes are pronounced and the effects attenuated. The other drugs presented all affect sympathetic receptors. 

What are the cardiac reflex actions induced by quinidine ... 

Use preoperatively to decrease secretions and block cardiac reflexes 0 Common drug examples ... 

In this hypothetical mechanistic scheme, it is postulated that electrocardiographic alterations produced by exposure to air pollutants will result partly from central nervous system (CNS)-mediated changes in cardiac autonomic tone. This supposition is based on the fact that the main cytokines that are released in response to air pollution can alter CNS activity. Also subjecting the lungs to noxious stimuli may elicit powerful cardiac reflexes that can alter sympathetic and parasympathetic activity. This is a critical consideration, because it is well established that both divisions of the autonomic nervous system exert a profound influence on the repolarization properties of the heart. These potential changes may play a vital role in the culminative response of inhaled particles on the cardiopulmonary system. 

The cardiac effects of the calcium antagonists, ie, slowed rate (negative chronotropy) and decreased contractile force (negative inotropy), are prominent in isolated cardiac preparations. However, in the intact circulation, these effects may be masked by reflex compensatory adjustments to the hypotension that these agents produce. The negative inotropic activity of the calcium antagonists may be a problem in patients having heart failure, where contractility is already depressed, or in patients on concomitant -adrenoceptor blockers where reflex compensatory mechanisms are reduced. 

Ipecac is prepared from the dried roots and rhizomes of Cephaelis ipecacuanha (Brot.) A. Rich, and contains the alkaloids emetine [483-18-1] (17) and cephaeJine [483-17-0] (18) in a ratio between 2 1 and 4 1. It has been used extensively in cough preparations and is beheved to act by gastric reflex stimulation. Toxic effects include vomiting, irritation of the gastrointestinal tract, and cardiac arrhythmias (19). Ipecac symp is available over-the-counter in the United States only in 30-mL containers for use as an emetic in treating poisonings. 

Death from overdose of barbiturates may occur and is more likely when more than 10 times the hypnotic dose is ingested. The barbiturates with high lipid solubility and short half-lives are the most toxic. Thus the lethal dose of phenobarbital is 6—10 g, whereas that of secobarbital, pentobarbital, or amo-barbital is 2-3 g. Symptoms of barbiturate poisoning include CNS depression, coma, depressed reflex activity, a positive Babinski reflex, contracted pupils (with hypoxia there may be paralytic dilation), altered respiration, hypothermia, depressed cardiac function, hypotension, shock, pulmonary complications, and renal failure. 

The fluid and protein shift into the abdomen (called third-spacing) may be so dramatic that circulating blood volume is decreased, which causes decreased cardiac output and hypovolemic shock. Accompanying fever, vomiting, or diarrhea may worsen the fluid imbalance. A reflex sympathetic response, manifested by sweating, tachycardia, and vasoconstriction, may be evident. With an inflamed peritoneum, bacteria and endotoxins are absorbed easily into the bloodstream (translocation), and this may result in septic shock. Other foreign substances present in the peritoneal cavity potentiate peritonitis, notably feces, dead tissues, barium, mucus, bile, and blood. 

Autonomic reflexes control cardiac muscle, smooth muscle and glands. 

Loss of plasma volume leads to a decrease in MAP. Baroreceptors located in the aortic and carotid sinuses detect this fall in MAP and elicit reflex responses that include an increase in the overall activity of the sympathetic nervous system. Sympathetic stimulation of the heart and blood vessels leads to an increase in cardiac output (CO) and increased total peripheral resistance (TPR). These adjustments, which increase MAP, are responsible for the short-term regulation of blood pressure. Although increases in CO and TPR are effective in temporary maintenance of MAP and blood flow to the vital organs, these activities cannot persist indefinitely. Ultimately, plasma volume must be returned to normal (see Table 19.1). 

A decrease in plasma volume leads to decreased MAP, which is detected by baroreceptors in the carotid sinuses and the arch of the aorta. By way of the vasomotor center, the baroreceptor reflex results in an overall increase in sympathetic nervous activity. This includes stimulation of the heart and vascular smooth muscle, which causes an increase in cardiac output and total peripheral resistance. These changes are responsible for the short-term regulation of blood pressure, which temporarily increases MAP toward normal. 

In the periphery, 5-HT4 receptor mRNA is found in vascular smooth muscle. Newly developed drugs that activate 5-HT4 receptors are of interest for their potential in treating cardiac arrhythmia. The 5-HT4 receptor is also located on neurons of the alimentary tract, for example the myenteric plexus of the ileum, and on smooth muscle cells and secretory cells of the gastrointestinal tract, where they evoke secretions and the peristaltic reflex. 5-HT4 receptor agonists (e.g. cisapride, prucalopride, tegaserod) are used therapeutically in the treatment of constipation-predominant irritable bowel syndrome and in functional motility disorders of the upper gastrointestinal tract. 

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