Heart rate sympathetic nervous system effects

The cardiovascular effects of CR administered intravenously demonstrated a dose-dependent increase in blood pressure of short duration and an increased heart rate and arterial catecholamines. The cardiovascular effects of CR were postulated to be related to sympathetic nervous system effects as evidenced by the abolition of CR induced presser effects by phentolamine and 6-hydroxydopamine. 

Nitrous oxide produces respiratory depression (38,39). It has been shown to produce a direct myocardial depressant effect in dogs (40) and in humans breathing a 40% N2O/60% oxygen mixture (41) however, this may be offset by the activation of the sympathetic nervous system (42). The combination of nitrous oxide and opioids can produce decreases in myocardial contractiHty, heart rate, and blood pressure (43). 

Another mechanism to maintain CO when contractility is low is to increase heart rate. This is achieved through sympathetic nervous system (SNS) activation and the agonist effect of norepinephrine on P-adrenergic receptors in the heart. Sympathetic activation also enhances contractility by increasing cytosolic calcium concentrations. SV is relatively fixed in HF, thus HR becomes the major determinant of CO. Although this mechanism increases CO acutely, the chronotropic and inotropic responses to sympathetic activation increase myocardial oxygen demand, worsen underlying ischemia, contribute to proarrhythmia, and further impair both systolic and diastolic function. 

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.

Adrenaline is the main hormone released from the adrenal medulla. The glandular cells in this structure correspond to the second, postganglionic neuron of the sympathetic nervous system. Furthermore, adrenaline can be found in chromaffin cells in various tissues. For the better understanding of the function of noradrenaline it is important to realize that this substance, as a neuronal transmitter, affects only the innervated target structure, that is it acts mainly locally. Among these effects are the activation of the musculus dilatator to widen the pupillae in response to a reduced light intensity, an increase in heart rate as a response to a blood pressure drop due to a reduction of the peripheral resistance or constriction... 

The myocardial response to exercise includes an increase in heart rate and myocardial contractility. These effects are mediated in part by the sympathetic nervous system. Propranolol and other p-adrenoceptor blockers antagonize the actions of catecholamines on the heart... 

Unlike isoflurane, desflurane may stimulate the sympathetic nervous system at concentrations above 1 MAC. Sudden and unexpected increases in arterial blood pressure and heart rate have been reported in some patients, accompanied by increases in plasma catecholamine and vasopressin concentrations and increased plasma renin activity. These pressor effects may increase morbidity or mortality in susceptible patients. The mechanism of sympathetic activation is unclear but does not appear to be baroreceptor-mediated. Clonidine, esmolol, fentanyl and propofol partially block the response but lignocaine (lignocaine) is ineffective. 

Autonomic and hormonal control of cardiovascular function. Note that two feedback loops are present the autonomic nervous system loop and the hormonal loop. The sympathetic nervous system directly influences four major variables peripheral vascular resistance, heart rate, force, and venous tone. It also directly modulates renin production (not shown). The parasympathetic nervous system directly influences heart rate. In addition to its role in stimulating aldosterone secretion, angiotensin II directly increases peripheral vascular resistance and facilitates sympathetic effects (not shown). The net feedback effect of each loop is to compensate for changes in arterial blood pressure. Thus, decreased blood pressure due to blood loss would evoke increased sympathetic outflow and renin release. Conversely, elevated pressure due to the administration of a vasoconstrictor drug would cause reduced sympathetic outflow, reduced renin release, and increased parasympathetic (vagal) outflow. 

Drugs that block beta-1 receptors on the myocardium are one of the mainstays in arrhythmia treatment. Beta blockers are effective because they decrease the excitatory effects of the sympathetic nervous system and related catecholamines (norepinephrine and epinephrine) on the heart.5,28 This effect typically decreases cardiac automaticity and prolongs the effective refractory period, thus slowing heart rate.5 Beta blockers also slow down conduction through the myocardium, and are especially useful in controlling function of the atrioventricular node.21 Hence, these drugs are most effective in treating atrial tachycardias such as atrial fibrillation.23 Some ventricular arrhythmias may also respond to treatment with beta blockers. 

In addition to its effects on cardiac contractility, digitalis has a direct inhibitory effect on sympathetic nervous system activity.37,60 This effect is beneficial because it decreases stress on the failing heart by decreasing excessive sympathetic stimulation of the heart and peripheral vasculature2. Therapeutic levels of digitalis likewise stabilize heart rate and slow impulse conduc-... 

When injected intravenously, kinins produce a rapid fall in blood pressure that is due to their arteriolar vasodilator action. The hypotensive response to bradykinin is of very brief duration. Intravenous infusions of the peptide fail to produce a sustained decrease in blood pressure prolonged hypotension can only be produced by progressively increasing the rate of infusion. The rapid reversibility of the hypotensive response to kinins is due primarily to reflex increases in heart rate, myocardial contractility, and cardiac output. In some species, bradykinin produces a biphasic change in blood pressure—an initial hypotensive response followed by an increase above the preinjection level. The increase in blood pressure may be due to a reflex activation of the sympathetic nervous system, but under some conditions, bradykinin can directly release catecholamines from the adrenal medulla and stimulate sympathetic ganglia. Bradykinin also increases blood pressure when injected into the central nervous system, but the physiologic significance of this effect is not clear, since it is unlikely that kinins cross the blood-brain barrier. 

The sinoatrial (SA) node is innervated by both the sympathetic (beta and parasympathetic (vagus) nervous systems. Sympathetic activation increases the discharge rate of the SA pacemaker cells, and thereby increases heart rate (a positive chronotropic effect). Sympathetic nerves also innervate adrenergic receptors (betaj) on cardiac ventricular cells leading to an increase in stroke volume (a positive inotropic effect). Vagal activation, on the other hand, has the opposite effect and decreases heart rate and conduction velocity. In normal adults, cardiac vagal innervation is functionally predominant, so abolition of vagal activity results in a pronounced tachycardia (increased heart rate). 

Neural components that participate in the regulation of coronary blood flow include the sympathetic nervous system, the parasympathetic nervous system, coronary reflexes, and possibly, central control of coronary blood flow. Within the sympathetic system, stimulation of the stellate ganglion elicits coronary vasodilation, which is associated with tachycardia and enhanced contractility. This indirect coronary vasodilation is secondary to increased MVO2 related to increased heart rate, contractihty, and aortic pressure and occurs following stellate stimulation. The direct effect of the sympathetic system is a 1-mediated vasoconstriction at rest and during exercise. Other receptor types, 2 and have little influence on tone, whereas /32-stimulation produces a modest vasodUatory effect. Although coronary atherosclerosis may decrease blood flow secondary to obstruction, severe coronary atherosclerosis and obstruction also may increase the sensitivity of coronary arteries to the effects of aj-stimulation and vasoconstriction. 

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