Heart rate increase

FIGURE 9.15 In vivo effec ts o f P-adreno cep tor partial agonis ts o f differing in trinsic efficacy. Changes in heart rate (increases in beats/min) shown in anesthetized cats. Chloralose/pento barbital anesthesia (filled circles) yield low basal heart rates, while urethane/pen to barbital anaesthesia (open circles) yields high basal heart rates. Responses to (in order of descending relative intrinsic efficacy) (a) pirbuterol, (b) prenalterol, and (c) pindolol. Redrawn from [50],... 

Headache, nausea, increased heart rate, increase in systolic blood pressure, palpitations, anginal and nonspecific chest pain Nausea, vomiting, ectopic beats, tachycardia, anginal pain, palpitations, hypotension, dyspnea Anxiety, insomnia, tenseness, restlessness, headache, light-headedness, dizziness, nausea, dysuria, pallor... 

Vasoconstriction of peripheral blood vessels Regulates release of neurotransmitters decreases tone, motility, and secretions of gastrointestinal tract Increased heart rate, increased force of myocardial contraction... 

Dobutamine is a P-adrenergic inotropic agent that can be utilized for improvement of cardiac output and oxygen delivery. Doses of 2 to 20 mcg/kg per minute increase cardiac index however, heart rate increases significantly. Dobutamine should be considered in septic patients with adequate filling... 

Figure 1.2 Negative feedback. These types of responses are employed throughout the body in order to maintain homeostasis. In this example, any change in blood pressure, which is monitored within the circulatory system and processed within the CNS, will cause reflex changes in heart rate. The change in heart rate will be in the opposite direction of the change in blood pressure if blood pressure increases, then heart rate decreases if blood pressure decreases, then heart rate increases. In this way, blood pressure is adjusted back to its normal value.

Heart Pi/ P2 Increased heart rate Increased contractility Decreased heart rate... 

Changes in heart rate also affect the contractility of the heart. As heart rate increases, so does ventricular contractility. The mechanism of this effect involves the gradual increase of intracellular calcium. When the electrical impulse stimulates the myocardial cell, permeability to calcium is increased and calcium enters the cell, allowing it to contract. Between beats, the calcium is removed from the intracellular fluid and the muscle relaxes. When heart rate is increased, periods of calcium influx occur more frequently and time for calcium removal is reduced. The net effect is an increase in intracellular calcium, an increased number of crossbridges cycling, and an increase in tension development. 

At rest, the MAP is closer to the diastolic pressure because the diastolic phase of the cardiac cycle lasts almost twice as long as the systolic phase. During exercise when heart rate increases and the length of diastole decreases, systolic pressure contributes more to the MAP. 

The benefits result from blockade of //j receptors in the myocardium, which reduces heart rate, myocardial contractility, and BP, thereby decreasing myocardial oxygen demand. The reduced heart rate increases diastolic time, thus improving ventricular filling and coronary artery perfusion. 

Physical effects of high doses of ketamine include decreased respiration and heart rate, increased blood pressure, and the possibility of vomiting and convulsions. These can lead to cardiac and respiratory arrest, coma, and death. The risk of ketamine overdose is much greater when it is mixed with other drugs such as alcohol, Ecstasy, caffeine, or cocaine. Overdoses of ketamine have been reported when people boost the drug (take another dose before the first dose wears off) to prolong its psychedelic effects. 

Activation of the parasympathetic branch causes pupillary dilation, increases salivation, constricts lung bronchi, decelerates heart rate, increases digestion, and stimulates conversion of glycose to glycogen. Whereas the parasympathetic branch is involved in physiological sexual arousal, the sympathetic branch is involved in the physiological aspect of orgasm. 

Heart rate increase was not very great (Fig. 48), even at and above the ID 50 (calculated to be about 12 mcg/kg, based on inspection of the NF results shown above). This signifies a high central/peripheral ratio, which is obviously preferable from a toxicity standpoint, especially in a hot climate. 

The side effects of methylphenidate are very similar to the amphetamines, but because it is somewhat less potent they may be a little milder. The common side effects of methylphenidate are appetite loss, weight loss, insomnia, and nausea. Taking methylphenidate with meals and no later than 6 PM can control most of these. On rare occasions, methylphenidate can cause headache, dizziness, nervousness, increased heart rate, increased blood pressure, tics, and, in extremely rare cases, paranoia. 

Propranolol slows heart rate, increases the effective refractory period of atrioventricular ganglia, suppresses automatism of heart cells, and reduces excitability and contractibihty of the myocardium. It is used for supraventricular and ventricular arrhythmias. Synonyms of this drug are anaprilin, detensiel, inderal, novapranol, and others. 

Maintenance dosage 20 to 40 mg/day. Titrate, depending on blood pressure and heart rate. Increases to a maximum of 60 mg/day divided into 2 doses may be necessary. There should be an interval of at least 7 days between dosage increases. 

In the cardiovascular system the effect on the heart rate is prominent. The depressive influence of the nervus vagus on the pacemaking activity in the heart is concentration dependently reduced and thereby the heart rate increases. This can be therapeutically useful in various forms of bardycardia, especially if they are caused by a vagus overstimulation, for example in the carotis-sinus syndrom. There is hardly any effect on the vasculature except a vasodilatation in the thoracic region after very high doses of atropine. 

The 3-blockers significantly reduce the peripheral manifestations of hyperthyroidism, particularly elevated heart rate, increased cardiac output, and muscle tremors. Although the 3-blockers can improve the clinical status of the hyperthyroid patient, the patient remains biochemically hyperthyroid. The 3-blockers should not be used as the sole form of therapy in hyperthyroidism. They are most logically employed in the management of hyperthyroid crisis, in the preoperative preparation for thyroidectomy, and during the initial period of administration of specific antithyroid drugs (see Chapter 65). 

Skin temperature and heart rate increased slightly. Vertigo, ataxia,... 

The effects on the heart (Hj response) are minor, but the heart rate increases. 

A teenage boy is seen at the office of a dental surgeon for extraction of an impacted wisdom tooth. He is so nervous that the dentist decides to administer a sedative to calm the boy. After intravenous administration of the sedative (promethazine), the boy relaxes and the extraction is accomplished with no complications. However, when the boy stands up from the dental chair, he turns very pale and faints. Lying on the floor, he rapidly regains consciousness, but has a rapid heart rate of 120 bpm and a blood pressure of only 110/70 mm Hg. When he sits up, his heart rate increases to 140 bpm, his pressure drops to 80/40 mm Hg, and he complains of faintness. He is helped to a couch in the reception area, where he rests for 30 minutes. At the end of this time the boy is able to sit up without symptoms and, after an additional 15 minutes, is able to stand without difficulty. What autonomic effects might promethazine have that would explain the patient s signs and symptoms Why did his heart rate increase when his blood pressure dropped ... 

Third, in REM sleep, at least, it is a well-established fact that the tonic increases in heart rate and blood pressure are associated with brain stem mediated activation and that the dramatic phasic blood pressure and heart rate increases are correlated with the clusters of eye movement that periodically punctuate each REM period, whereas heart rate pauses occur in the inter-REM intervals. 

NOS3 (eNOS) Hypertension and decreased heart rate Increased plasma renin activity Lack of response to ACh and calcium ionophore Increased sensivity to phenylephrine, serotonin, and nitroglycerine Shesely et al. (1996 ) Kojda et al. (1999)... 

A 14-year-old boy received an intravenous dose of methylprednisolone 30 mg/kg for progressive glomerulonephritis. After 5 hours, his heart rate had fallen to 50/minute and an electrocardiogram showed sinus bradycardia. His heart rate then fell to 40/minutes and a temporary transvenous pacemaker was inserted and methylprednisolone was withdrawn. His heart rate increased to 80/minutes over 3 days. After a further 3 days, he was treated with oral methylprednisolone 60 mg/m2/day and his heart rate fell to 40/minutes in 5 days. Oral methylprednisolone was stopped on day 8 of treatment and his heart rate normalized. 

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. 

Nicotinic Muscarinic Autonomic ganglia All parasympathetic effector cells Visceral and bronchiole smooth muscle Cardiac muscle Exocrine glands (salivary, intestinal, lacrimal] Sweat glands Mediate transmission to postganglionic neuron Contraction (generally] Decreased heart rate Increased secretion Increased secretion... 

Sibutramine (Meridia), a weight-loss drug introduced in 1998, inhibits the reuptake of the brain chemicals norepinephrine, dopamine, and serotonin, but does not promote monoamine release like the amphetamines. Yet the drug has been linked to serious side effects, including rapid heart rate, increased blood pressure, heart disease, stroke, seizure, and mental impairments. In March 2002, Italy s Health Ministry announced that it was immediately withdrawing all sibutramine products from the market due to health-related problems. Also, Meridia was the subject of a class action lawsuit filed in the United States. 

As an anesthetic, ketamine increases sympathetic nervous activity, which results in an increased heart rate, increased blood pressure, some dilation of bronchial tubes, pupil dilation, and related secondary effects. 

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