Decrease in heart rate

Heart Blood vessels Increase in heart rate, heart muscle contractility, increase in speed of atrioventricular conduction P Decrease in heart rate, decrease in heart muscle contractility... 

Monitor the patient to determine whether the goal of ventricular rate control is met heart rate less than 100 bpm or decrease in heart rate of 20% from the pretreatment value. 

Parasympathetic stimulation causes a decrease in heart rate. Acetylcholine, which stimulates muscarinic receptors, increases the permeability to potassium. Enhanced K+ ion efflux has a twofold effect. First, the cells become hyperpolarized and therefore the membrane potential is farther away from threshold. Second, the rate of pacemaker depolarization is decreased because the outward movement of K+ ions opposes the effect of the inward movement of Na+ and Ca++ ions. The result of these two effects of potassium efflux is that it takes longer for the SA node to reach threshold and generate an action potential. If the heart beat is generated more slowly, then fewer beats per minute are elicited. 

Verapamil (Class IV antiarrhythmic drug) is an effective agent for atrial or supraventricular tachycardia. A Ca++ channel blocker, it is most potent in tissues where the action potentials depend on calcium currents, including slow-response tissues such as the SA node and the AV node. The effects of verapamil include a decrease in heart rate and in conduction velocity of the electrical impulse through the AV node. The resulting increase in duration of the AV nodal delay, which is illustrated by a lengthening of the PR segment in the ECG, reduces the number of impulses permitted to penetrate to the ventricles to cause contraction. 

Other outcomes include improvement in exercise tolerance and fatigue, decreased nocturia, and a decrease in heart rate. 

Clonidine, guanabenz, guanfacine, and methyldopa lower BP primarily by stimulating a2-adrenergic receptors in the brain, which reduces sympathetic outflow from the vasomotor center and increases vagal tone. Stimulation of presynaptic oq-receptors peripherally may contribute to the reduction in sympathetic tone. Consequently, there may be decreases in heart rate, cardiac output, total peripheral resistance, plasma renin activity, and baroreceptor reflexes. 

Physioiogicai There is an extensive literature that deals with the effects ginseng on CNS function, but effects are also seen in neuroendocrine function, carbohydrate and lipid metabolism, the immune system, and cardiovascular function (Gillis 1997). Ginsenosides induce a decrease in heart rate and have biphasic effects on blood pressure, with decreases preceded by a slight increase (Kaku et al. 1975). Ginsenoside Rgl had the most potent effects on blood pressure. Little or no effect is observed on respiration. 

In another study, decreases in heart rate and mean arterial blood pressure occurred in dogs following a single exposure to 0.5 mL/kg kerosene by aspiration, although these values returned to the control values within 60 minutes (Goodwin et al. 1988). The actual dose entering the lungs by aspiration cannot be determined. This study is limited, however, because only one dose was tested. 

Carbachol is a powerful cholinic ester that stimulates both muscarinic and nicotinic receptors, as well as exhibits all of the pharmacological properties of acetylcholine while in addition resulting in vasodilation, a decrease in heart rate, an increase in tone and con-tractability of smooth muscle, stimulation of salivary, ocular, and sweat glands as well as autonomic ganglia and skeletal muscle. For this reason, use of carbachol, like acetylcholine, is limited. The exception is that it is used in ophthalmological practice and post-operational intestines and bladder atony. Upon administration in the eye, the pupil constricts and the intraocular pressure is reduced. It is used for severe chronic glaucoma. Synonyms of this drag are doryl and miostat. 

Adverse reactions may include palpitations tachycardia elevation of blood pressure reflex decrease in heart rate arrhythmias (at larger doses) overstimulation restlessness dizziness insomnia dyskinesia euphoria dysphoria tremor headache changes in libido dry mouth unpleasant taste diarrhea constipation urticaria impotence. 

In a normal resting subject who is receiving no drugs, there is a moderate parasympathetic tone to the heart, and sympathetic activity is relatively low. The ventricular muscle receives little, if any, parasympathetic innervation. As the blood pressure rises in response to norepinephrine, the baroreceptor reflex is activated, parasympathetic impulses (which are inhibitory) to the heart increase in frequency, and what little sympathetic outflow there is may be reduced. Heart rate is slowed so much that the direct effect of norepinephrine to increase the rate is masked and there is a net decrease in rate. Under the conditions described, however, the impact of the reflex on the ventricles is very slight because there is no parasympathetic innervation and the preexisting level of sympathetic activity is already low. A further decrease in sympathetic activity therefore would have little further effect on contractility in this subject. Thus, a decrease in heart rate and an increase in stroke volume will occur, and cardiac output will change very little. 

This pattern differs from that seen following administration with either a conventional (3- or a-blocker. Acute administration of a (3-blocker produces a decrease in heart rate and cardiac output with little effect on blood pressure, while acute administration of an a-blocker leads to a decrease in peripheral vascular resistance and a reflexively initiated increase in cardiac rate and output. Thus, the pattern of cardiovascular responses observed after labetalol administration combines the features of (3- and a-blockade, that is, a decrease in peripheral vascular resistance (due to a-blockade and direct vascular effects) without an increase in cardiac rate and output (due to (3-blockade). 

Prolonged oral therapy with labetalol results in cardiovascular responses similar to those obtained following conventional (3-blocker administration, that is, decreases in peripheral vascular resistance, blood pressure, and heart rate. Generally, however, the decrease in heart rate is less pronounced than after administration of propranolol or other (3-blockers. 

Eor many years the prevailing view was that p-blockers are contraindicated in CHE. The physiological rationale for not using 3-blockers in heart failure was certainly well founded. Heart failure patients have a decrease in cardiac output. Since cardiac output is a function of stroke volume times heart rate (CO = SV xHR), an increased heart rate would be necessary to maintain an adequate cardiac output in the presence of the relatively fixed decrease in stroke volume observed in CHE. A rapid increase in heart rate does play an important role in the physiological response to acute hemorrhage. Thus, a decrease in heart rate, along with a depression in contractility produced by p-blockers, would be expected to precipitate catastrophic decompensation and this certainly can happen in the acute setting. 

Flecainide decreases the sinus cycle length but results in a clinically insignificant decrease in heart rate. 

Postmyocardial infarct patients show increased smwival if treated with a (5-adrenoceptor antagonist. The beneficial effect may be related to the decrease in heart rate and the antiischemic benefits of (5-adrenoceptor blockade. 

The hemodynamic effects of sotalol are related to its 3-adrenoceptor antagonist activity. Accordingly, decreases in resting heart rate and in exercise-induced tachycardia are seen in patients receiving sotalol. A modest reduction in systolic pressure and in cardiac output may occur. The reduction in cardiac output is a consequence of lowering the heart rate, since stroke volume is unaffected by sotalol treatment. In patients with normal ventricular function, cardiac output is maintained despite the decrease in heart rate because of the simultaneous increase in the stroke volume. 

Decreases in heart rate and cardiac output are the most obvious results of administration of p-blockers. Initially, blood pressure is not much affected, since peripheral vascular resistance will be reflexly elevated as a result of the drug-induced decrease in cardiac output. The reduction of blood pressure that occurs in chronic treatment correlates best with changes in peripheral vascular resistance rather than with a drug-induced variation in heart rate or cardiac output. 

The primary indication for clonidine use is in mild and moderate hypertension that has not responded adequately to treatment with a diuretic or a p-blocker. Since clonidine causes sodium and water retention and plasma volume expansion, it generally is administered in combination with a diuretic. A vasodilator can be added to the clonidine-diuretic regimen in the treatment of resistant forms of hypertension. Such drug combinations can be quite effective, since the reflex increases in heart rate and cardiac output that result from vasodilator administration are reduced or negated by clonidine-induced decreases in heart rate and cardiac output. 

S-A node Decrease in heart rate Vagal arrest P Increase in heart rate... 

CVS In hypnotic dose, hypotension and decrease in heart rate occurs. In toxic dose, there is a severe decrease in blood pressure due to ganglionic blockade. 

Heart rate In CHF patients, the heart rate is decreased. Digitalis produce a decrease in heart rate by stimulation of vagus. The vagal effect is probably evoked by sensitization of carotid baroreceptors, and by direct stimulation of vagal centre. The vagal action can be blocked by atropine but after full digitalising dose the effect can not be blocked by atropine and it is due to its direct cardiac action. In CHF patients, the sympathetic activity is increased as a compensatory phenomenon which leads to tachycardia. Digitalis decreases the... 

Sevoflurane, in common with all volatile agents, reduces cardiac output and systemic blood pressure. It does so mainly through a reduction in peripheral vascular resistance. Although it is a systemic vasodilator it does not appear to produce significant dilatation of small coronary vessels and there is no possibility of coronary steal as hypothesised for isoflurane. A small increase in heart rate may be observed. This is less pronounced than with isoflurane and desflurane and is almost certainly the result of reflex activity secondary to the reduction in peripheral vascular resistance. Sevoflurane is associated with a stable heart rhythm and does not predispose the heart to sensitisation by catecholamines. In children, halothane causes a greater decrease in heart rate, myocardial contractility and cardiac output than sevoflurane at all concentrations. For these reasons sevoflurane is advocated for use in outpatient dental anaesthesia, especially in children. 

Atracurium causes minimal cardiovascular effects except those associated with some histamine release if the drug is given rapidly or in high doses. As with vecuronium, it produces little increase in heart rate in fact, decreases in heart rate have been reported. This is once again thought to be due to the effects of other agents, such as the opiates, or as a result of vagal stimulation. The incidence of histamine release with atracurium is about one-third of that observed after tubocurarine administration. 

Effects of autonomic blockade on the response to phenylephrine (Phe) in a human subject. Left The cardiovascular effect of the selective K-agonist phenylephrine when given as an intravenous bolus to a subject with intact autonomic baroreflex function. Note that the increase in blood pressure (BP) is associated with a baroreflex-mediated compensatory decrease in heart rate (HR). Right The response in the same subject after autonomic reflexes were abolished by the ganglionic blocker trimethaphan. Note that resting blood pressure is decreased and heart rate is increased by trimethaphan because of sympathetic and parasympathetic withdrawal. In the absence of baroreflex buffering, approximately a tenfold lower dose of phenylephrine is required to produce a similar increase in blood pressure. Note also the lack of compensatory decrease in heart rate. 

Serotonin directly causes the contraction of vascular smooth muscle, mainly through 5-HT2 receptors. In humans, serotonin is a powerful vasoconstrictor except in skeletal muscle and heart, where it dilates blood vessels. At least part of this 5-HT-induced vasodilation requires the presence of vascular endothelial cells. When the endothelium is damaged, coronary vessels constrict. As noted previously, serotonin can also elicit reflex bradycardia by activation of 5-HT3 receptors on chemoreceptor nerve endings. A triphasic blood pressure response is often seen following injection of serotonin in experimental animals. Initially, there is a decrease in heart rate, cardiac output, and blood pressure caused by the chemoreceptor response. After this decrease, blood pressure increases as a result of vasoconstriction. The third phase is again a decrease in blood pressure attributed to vasodilation in vessels supplying skeletal muscle. Pulmonary and renal vessels seem especially sensitive to the vasoconstrictor action of serotonin. 

Physical effects also accompanied the experience. There was an intoxication that produced dizziness and a lack of coordination on trying to move about. The recording of the second session revealed slurred speech and awkward sentence patterns. Diaz had a decrease in heart rate accompanied by a chill. Both subjects had a normal pupillary response to a light shined into their eyes. 

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