Parasympathetic nervous system, cardiac

Automaticity of cardiac fibers is controlled in part by activity of the sympathetic and parasympathetic nervous systems. Enhanced activity of the sympathetic nervous system may result in increased automaticity of the SA node or other automatic cardiac fibers. Enhanced activity of the parasympathetic nervous system tends to suppress automaticity conversely, inhibition of activity of the parasympathetic nervous system increases automaticity. Other factors may lead to abnormal increases in automaticity of extra-SA nodal tissues, including hypoxia, atrial or ventricular stretch [as might occur following long-standing hypertension or after the development of heart failure (HF)], and electrolyte abnormalities such as hypokalemia or hypomagnesemia. 

Figure 15.4 Effects of the autonomic nervous system on mean arterial pressure. The baroreceptors, chemoreceptors, and low-pressure receptors provide neural input to the vasomotor center in the brainstem. The vasomotor center integrates this input and determines the degree of discharge by the sympathetic and parasympathetic nervous systems to the cardiovascular system. Cardiac output and total peripheral resistance are adjusted so as to maintain mean arterial pressure within the normal range.

Figure 15.5 Effects of sympathetic and parasympathetic nervous activity on mean arterial pressure. The parasympathetic nervous system innervates the heart and therefore influences heart rate and cardiac output. The sympathetic nervous system innervates the heart and veins and thus influences cardiac output. This system also innervates the arterioles and therefore influences total peripheral resistance. The resulting changes in cardiac output and total peripheral resistance regulate mean arterial pressure.

Anatomically, the nervous system is divided into the central nervous system (CNS) consisting of the brain and the spinal cord and the peripheral nervous system comprised of neural cells forming a network throughout the body. The peripheral system is itself subdivided into two sections the somatic system, where control of skeletal muscles allows movement and breathing, and the autonomic system which controls the actions of smooth muscle, cardiac muscle and glandular tissues. Further subdivision of the autonomic system based on anatomical and biochemical factors creates the sympathetic and parasympathetic nervous systems. 

E. The effect of ganglionic blockade depends upon the predominant autonomic tone exerted within various organ systems. Since the activity of the parasympathetic nervous system predominates in the eye, the effect of ganglionic blockade is mydriasis, not miosis. Similarly, stimulation of the genital tract and urinary retention would be decreased. Since sympathetic nervous system activity predominates in blood vessels and the ventricles, vasodilation and a decreased cardiac output would follow ganglionic blockade. 

The basis for the antihypertensive activity of the ganglionic blockers lies in their ability to block transmission through autonomic ganglia (Fig. 20.2C). This action, which results in a decrease in the number of impulses passing down the postganglionic sympathetic (and parasympathetic) nerves, decreases vascular tone, cardiac output, and blood pressure. These drugs prevent the interaction of acetylcholine (the transmitter of the preganglionic autonomic nerves) with the nicotinic receptors on postsynaptic neuronal membranes of both the sympathetic and parasympathetic nervous systems. 

Cardiac effects include diminished contractility and, because the sinoatrial node is usually dominated by the parasympathetic nervous system, a moderate tachycardia. 

Recall that scopolamine, an ingredient in henbane, blocks muscarinic acetylcholine receptors. This blockade essentially removes the influence of the parasympathetic nervous system on the body. In the absence of this influence, the balance of forces is upset and the sympathetic nervous system gains the upper hand thus, your heart rate increases, your pupils dilate, salivation stops, your ability to urinate is impaired, and you become constipated overall, things get very uncomfortable. But none of this is directly lethal (unless the constipation makes one commit suicide). If you do die from an overdose of henbane, it is believed to result from either a complex series of events in your brain that lead to the loss of control of your diaphragm, causing death from asphyxiation, or from cardiac arrest. This is why the deadly nightshade is so deadly and how Shakespeare chose to kill King Hamlet with henbane. 

Correct choice = E. The parasympathetic nervous system is essential for life. Visceral motor (efferent) neurons innervate smooth muscle of the viscera, cardiac muscle, and the exocrine glands. 

In addition, through an effect in the central nervous system cardiac glycosides cause an increase in parasympathetic activity and therefore slow conduction through the AV node, hence their usefulness in atrial flutter and atrial fibrillation. 

What is the role of cardiac reflexes in the therapeutic use and efficacy of drugs that affect the parasympathetic nervous system ... 

Drugs that affect the parasympathetic nervous system tend to produce a high degree of baroreceptor-mediated responses under normal usage. Thus, their responses are typically limited in duration, irrespective of drug half-life. This may not apply when the drug is used under life threatening conditions (e.g.. the use of atropine in the resuscitation of cardiac failure), because the baroreceptor reflex is set at normal levels of tension. 

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. 

Dmgs can affect cardiac contraction by stimulating or inhibiting the heart. Contractions are also influenced by the autonomic nervous system (ANS). The sympathetic nervous system increases heart rate and the parasympathetic nervous system decreases heart rate. (See Chapter 15.)... 

A multivariate approach of analyzing the psychophysiological measures obtained from heart period has been proposed as a method for obtaining cardiac autonomic information (Backs, 1995,1998). The multivariate approach attempts to improve the sensitivity and diagnosticity of heart rate by identifying the neurogenic activity of the sympathetic and parasympathetic nervous systems responsible for the observed heart rate in a task. Principal components analysis (PCA) was used in the present study to extract information about the sympathetic and parasympathetic nervous systems common to RSA, low-frequency HRV, residual heart period, and heart period. Details of how the components were derived are presented in the Method section. 

PCA of the measures results in two components that are used to compute autonomic component scores that may reveal the activity of the sympathetic and parasympathetic nervous systems within the "doctrine of autonomic space" (Bemtson et al., 1991). However, the use of PCA to extract cardiac autonomic information can only be validated through examination of the extent to which the PCA method is consistent with better methods of obtaining the same information. 

Cardiac autonomic (parasympathetic) nervous system function respiratory variation in heart rate (R-R interval) measured in ECG recordings (12 standard leads) in supine position during normal, deep breathing... 

Cardiac variability-vagal tone Changes in heart rate as a function of stimulation are related to changes in respiratory sinus arrhythmia that reflect changes in the parasympathetic nervous system (Posner, 2001)... 

The cardiac system also has vagus afferent sensory nerves that duplicate the transmission of nociceptive information but it bypasses the gating mechanism in the spinal cord. This feedback circuit carries information directly to vagal motor neurons that regulate sinoatrial and atrioventricular nodal firing rates. This can functionally override the inherent cardiac rhythm generators. It is clear that there is a complex interaction between the sympathetic and parasympathetic nervous system. 

Although blood pressure control follows Ohm s law and seems to be simple, it underlies a complex circuit of interrelated systems. Hence, numerous physiologic systems that have pleiotropic effects and interact in complex fashion have been found to modulate blood pressure. Because of their number and complexity it is beyond the scope of the current account to cover all mechanisms and feedback circuits involved in blood pressure control. Rather, an overview of the clinically most relevant ones is presented. These systems include the heart, the blood vessels, the extracellular volume, the kidneys, the nervous system, a variety of humoral factors, and molecular events at the cellular level. They are intertwined to maintain adequate tissue perfusion and nutrition. Normal blood pressure control can be related to cardiac output and the total peripheral resistance. The stroke volume and the heart rate determine cardiac output. Each cycle of cardiac contraction propels a bolus of about 70 ml blood into the systemic arterial system. As one example of the interaction of these multiple systems, the stroke volume is dependent in part on intravascular volume regulated by the kidneys as well as on myocardial contractility. The latter is, in turn, a complex function involving sympathetic and parasympathetic control of heart rate intrinsic activity of the cardiac conduction system complex membrane transport and cellular events requiring influx of calcium, which lead to myocardial fibre shortening and relaxation and affects the humoral substances (e.g., catecholamines) in stimulation heart rate and myocardial fibre tension. 

Because cardiac muscle is myogenic, nervous stimulation is not necessary to elicit the heart beat. However, the heart rate is modulated by input from the autonomic nervous system. The sympathetic and parasympathetic systems innervate the SA node. Sympathetic stimulation causes an increase in heart rate or an increased number of beats/min. Norepinephrine, which stimulates ( -adrenergic receptors, increases the rate of pacemaker depolarization by increasing the permeability to Na+ and Ca++ ions. If the heart beat is generated more rapidly, then the result is more beats per minute. 

Muscarinic receptors are responsible for postganglionic parasympathetic neurotransmission and thus for control of a wide range of smooth muscle, cardiac muscle and secretory responses. Some responses originating in the sympathetic division of the autonomic nervous system, such as sweating and piloerection, also are mediated through muscarinic receptors. 

Neurohumoral (extrinsic) compensation involves two major mechanisms (previously presented in Figure 6-7)—the sympathetic nervous system and the renin-angiotensin-aldosterone hormonal response—plus several others. Some of the pathologic as well as beneficial features of these compensatory responses are illustrated in Figure 13-2. The baroreceptor reflex appears to be reset, with a lower sensitivity to arterial pressure, in patients with heart failure. As a result, baroreceptor sensory input to the vasomotor center is reduced even at normal pressures sympathetic outflow is increased, and parasympathetic outflow is decreased. Increased sympathetic outflow causes tachycardia, increased cardiac contractility, and increased vascular tone. Vascular tone is further increased by angiotensin II and endothelin, a potent vasoconstrictor released by vascular endothelial cells. The result is a vicious cycle that is characteristic of heart failure (Figure 13-3). Vasoconstriction increases afterload, which further reduces ejection fraction and cardiac output. Neurohumoral antagonists and vasodilators... 

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