Effects on heart rate

Verapamil (Table 1), the first slow channel calcium blocker synthesized to selectively inhibit the transmembrane influx of calcium ions into cells, lowers blood pressure in hypertensive patients having good organ perfusion particularly with increased renal blood flow. Sustained-release verapamil for once a day dosing is available for the treatment of hypertension. Constipation is a prominent side effect. Headache, dizziness, and edema are frequent and verapamil can sometimes cause AV conduction disturbances and AV block. Verapamil should not be used in combination with -adrenoceptor blockers because of the synergistic negative effects on heart rate and contractile force. 

True. Caffeine is a mild stimulant that in moderate dosage does little harm and provides a lift . When taken in excess it can have an adverse effect on heart rate. 

The second factor that exerts control on heart rate is the release of the catecholamines, epinephrine and norepinephrine, from the adrenal medulla. Circulating catecholamines have the same effect on heart rate as direct sympathetic stimulation, which is to increase heart rate. In fact, in the intact heart, the effect of the catecholamines serves to supplement this direct effect. In a denervated heart, circulating catecholamines serve to replace the effect of direct sympathetic stimulation. In this way, patients who have had a heart transplant may still increase their heart rate during exercise. 

In Phase I clinical trials with stable renal transplant patients, FTY720 led to a transient reduction in the number of circulating lymphocytes whilst being well-tolerated. Treatment was associated with a mild reduction in heart rate that was maximal 6 h after the first dose and returned to baseline with continuous treatment [52,53]. The mild effect on heart rate is believed to arise from SlPj and/or SlP3-mediated activation of G-protein-gated inwardly rectifying potassium (GIRK) channels in atrial myocytes [54-56]. 

Within a programme aimed at the development of thyroid hormone analogues as potentially useful plasma cholesterol-lowering agents, the pyrida-zinone derivative SK F L-94901 (98) has been prepared and investigated in the U.K. [419-422]. Whereas naturally occurring thyroid hormones cannot be employed for this purpose because of their undesirable effect on heart rate, (98) has been found to represent a potent thyromimetic which retains hepatic activity but lacks cardiac activity. Structural modifications and QSAR studies have been carried out [422]. 

Atropine Sulfate Dose Effects on Heart Rate... 

Atropine s peripheral effects on heart rate (Fig. 63) and blood pressure (not shown) are substantial and very rapid in onset, peaking at about 30-60 minutes. In this graph, baseline heart rate is shown as zero. Maximum heart rate at the ID50 is thus about 125 (60 + 65). It remains at this level for about 3 hours and returns to normal at about 9 hours. At the ID50, minor changes in the electrocardiogram were noted in a study by Hayes et al.. These changes rapidly revert to normal as HR declines. 

Cardiovasciilar system - in vitro systems for potential to prolong QT interval, effects on heart and blood vessels, anaesthetised and conscious (reflexes intact) animals with effects on heart rate, blood pressure, ECG... 

Cardiovascular effects Drugs that increase cholinergic activity may have vagotonic effects on heart rates (eg, bradycardia). The potential for this action may be particularly important in patients with sick sinus syndrome or other supraventricular cardiac conduction conditions. 

Cardiovascular disease Acute administration of 2 drops of apraclonidine has had minimal effect on heart rate or blood pressure however, observe caution in treating patients with severe cardiovascular disease, including hypertension. 

Sometimes a pharmacological effect is the sum of more than one drug effect. This may call for the combination of two or more models, as shown in Fig. 4 where both tachycardia and bradycardia are implied as drug effects. In this case, the model used consisted of two equations equal to Eq. (10), but with an opposite direction of effect on heart rate and different model parameter values. 

D. Nitroglycerin can reduce preload, which in turn reduces wall tension and increases subendocardial blood flow. Nitroglycerin also reduces afterload, but this is a small effect compared to the reduction in preload. Its effects on heart rate and contractility are minimal, and if anything reflex tachycardia and increase in contractility would be detrimental effects of too much nitroglycerin. 

Answer This feature of bradycardia is typical of patients who take (3-blockers, which should be continued so they result ultimately in better anesthetic management. The drugs given could have been modified (i.e., etomidate instead of propofol, which does not raise or may cause a slower heart rate). The potent opioids in the fentanyl family all cause vagal transmitted bradycardia. The muscle relaxant vecuronium (norcuron) has no effect on heart rate and could have been replaced by pancuronium, which has a vagolytic effect and will counter bradycardia in the usual induction bolus doses. 

Tricyclic antidepressants have effects on heart rate (HR), blood pressure (BP), and three distinct measures of the electrocardiogram (EKG). The EKG parameters affected are (1) the PR interval, which represents depolarization of the aorta (2) the QRS duration, which represents intraventricular conduction time and (3) the QTc, which represents the depolarization and subsequent repolarization of the ventricles, corrected for cardiac rate. 

The direct slowing of sinoatrial rate and atrioventricular conduction that is produced by muscarinic agonists is often opposed by reflex sympathetic discharge, elicited by the decrease in blood pressure (see Figure 6-7). The resultant sympathetic-parasympathetic interaction is complex because muscarinic modulation of sympathetic influences occurs by inhibition of norepinephrine release and by postjunctional cellular effects. Muscarinic receptors that are present on postganglionic parasympathetic nerve terminals allow neurally released acetylcholine to inhibit its own secretion. The neuronal muscarinic receptors need not be the same subtype as found on effector cells. Therefore, the net effect on heart rate depends on local concentrations of the agonist in the heart and in the vessels and on the level of reflex responsiveness. 

Peter J-C et al Effects on heart rate of an anti-M2 acetylcholine receptor immune response in mice. FASEB J 2005 19 943. [PMID 15923404]... 

The effects of sympathomimetic drugs on blood pressure can be explained on the basis of their effects on heart rate, myocardial function, peripheral vascular resistance, and venous return (see Figure 6-7 and Table 9-4). The endogenous catecholamines, norepinephrine and epinephrine have complex cardiovascular effects because they activate both and 13 receptors. It is easier to understand these actions by first describing the cardiovascular effect of sympathomimetics that are selective for a given adrenoreceptor. 

Direct effects on the heart are determined largely by Bi receptors, although B2 and to a lesser extent a receptors are also involved, especially in heart failure. Beta-receptor activation results in increased calcium influx in cardiac cells. This has both electrical and mechanical consequences. Pacemaker activity—both normal (sinoatrial node) and abnormal (eg, Purkinje fibers)—is increased (positive chronotropic effect). Conduction velocity in the atrioventricular node is increased (positive dromotropic effect), and the refractory period is decreased. Intrinsic contractility is increased (positive inotropic effect), and relaxation is accelerated. As a result, the twitch response of isolated cardiac muscle is increased in tension but abbreviated in duration. In the intact heart, intraventricular pressure rises and falls more rapidly, and ejection time is decreased. These direct effects are easily demonstrated in the absence of reflexes evoked by changes in blood pressure, eg, in isolated myocardial preparations and in patients with ganglionic blockade. In the presence of normal reflex activity, the direct effects on heart rate may be dominated by a reflex response to blood pressure changes. Physiologic stimulation of the heart by catecholamines tends to increase coronary blood flow. 

Studies of the arrhythmogenic effects and the effects on heart rate of aconitine (14), X-desacetyl-lappaconitine (7), lappaconitine (6), lycoctonal (13), lycoctonine (12), lappaconine (15), avadharidine (9), lycaconitine (10), anthranoyl-lycoctonine (8), and cashmiradelphine (septentriodine) (11) were also reported.8 The alkaloids (6), (7), and (15) were found to be arrhythmogenic... 

The QT interval duration is heart rate dependent. The use of correction formulae derived from clinical data are not appropriate for use with dog ECGs. Algo-rhythms designed specifically for the dog are required and historical data from the dogs actually used in a given study is the preferred way to derive any QT correction (Meyners and Markert, 2004). Still better, if no drag-induced effect on heart rate is observed, no correction of the QT interval should be undertaken. 

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