Reflex bradycardia

Phenylephrine. Phenylephrine hydrochloride is an a -adrenoceptor agonist. Phenylephrine produces powerful vasoconstrictor and hypertensive responses. This results in baroreceptor activation of a reflex bradycardia and thus is useful in the treatment of supraventricular tachyarrhythmias. Unlike epinephrine [51-43-4] the actions of which are relatively transient, phenylephrine responses are more sustained (20 min after iv dosing and 50 min after subcutaneous dosing) (86). 

Phase 1 During phase 1, the increased thoracoabdominal pressure transiently increases venous return, thereby raising BP and reflexly lowering heart rate. Phase 2 During phase 2, the sustained rise in intrathoracic pressure reduces venous return VR and so BP falls until a compensatory tachycardia restores it. Phase 3 The release of pressure in phase 3 creates a large empty venous reservoir, causing BP to fall. Show that the heart rate remains elevated. Phase 4 The last phase shows how the raised heart rate then initially leads to a raised BP as venous return is restored. This is followed by a reflex bradycardia before both parameters eventually return to normal. 

The clinical uses of these drugs are associated with their potent vasoconstrictor action. They are used to restore or maintain blood pressure during spinal anesthesia and certain other hypotensive states. The reflex bradycardia induced by their rapid intravenous injection has been used to terminate attacks of paroxysmal atrial tachycardia. Phenylephrine is commonly used as a nasal decongestant, although occasional nasal mucosal... 

B. Phenylephrine is an aj-selective agonist. It causes an increase in peripheral vascular resistance. The major cardiovascular response to this drug is a rise in blood pressure associated with reflex bradycardia. The slowing of the heart rate is blocked by atropine. 

The administration of angiotensin II to an animal with intact baroreceptor reflexes results in reflex bradycardia in response to the marked vasoconstriction. When baroreceptor reflexes are depressed (barbiturate anesthesia) or if vagal tone is inhibited (atropine or vagotomy), angiotensin directly induces cardiac acceleration. 

Angiotensin II stimulates the influx of Ca" " into cardiac muscle cells and can exert a direct inotropic effect at cardiac muscle. In addition, angiotensin II can stimulate the sympathoadrenal system and thereby increase myocardial contractility. In contrast to its effects on vascular smooth muscle, the ability of angiotensin to increase the contractile force of the heart is far less potent. Therefore, in spite of the positive chronotropic and inotropic effects produced by angiotensin II, cardiac output is rarely increased. In fact, angiotensin II may decrease cardiac output through reflex bradycardia induced by the rise in peripheral resistance that it causes. In contrast, centrally administered angiotensin II increases both blood pressure and cardiac output. 

Mechanism of Action An alpha-adrenergic receptor agonist that causes vasoconstriction, reflex bradycardia, inhibits GI smooth muscle and vascular smooth muscle supplying skeletal muscle and increases heart rate and force of heart muscle contraction. Therapeutic Effect Increases both systolic and diastolic pressure. 

Systemic Headache, reflex bradycardia, excitability, restlessness, and rarely arrhythmias. 

It is a vasopressor agent with some structural similarity to adrenaline and has a powerful alpha receptor stimulant action. The pressor response is accompanied by reflex bradycardia. It is used as a nasal decongestant and mydriatic agent and also in the treatment of paroxysmal supraventricular tachycardia. 

It is a potent alpha-adrenergic blocking agent and only haloalkylamine used clinically. It effectively prevents the responses mediated by alpha receptors and diastolic blood pressure tends to decrease. It interferes with the reflex adjustment of blood pressure and produces postural hypotension. It increases the cardiac output and decreases the total peripheral resistance. It also antagonizes cardiac arrhythmias provoked by catecholamines. Apart from these effects, phenoxybenzamine has other actions also e.g. antagonism of acetylcholine, histamine, 5-hydroxytryptamine (serotonin). However, the vasodilatation produced by phenoxybenzamine is because of alpha blockage. Adverse reactions are miosis, dryness of mouth, inhibition of ejaculation, palpitation, nasal stuffiness and in higher doses, postural hypotension and reflex bradycardia. 

The drug is given into a central vein at a rate of 2-10 pg-min-1. Its effects are very transitory and disappear rapidly if the infusion stops. Infusions up to 0.05 pg kg-l-min-1 increase myocardial contractility and heart rate as the result of 31 stimulation. At doses of 0.1-0.3 pg kg-l min-1 vasocon-striction (a stimulation) accompanied by a reflex bradycardia predominates. 

Phenylephrine is used to increase peripheral vascular resistance when cardiac output is maintained. It increases arterial blood pressure and this often results in reflex bradycardia. It is mainly used to correct anaesthesia-induced hypotension. It is also used to dilate the pupil (mydriasis) and as a nasal decongestant. 

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. 

The primary side effects associated with alpha-1-specific agonists are caused by excessive stimulation of alpha-adrenergic responses. Some of the more frequent side effects include increased blood pressure, headache, and an abnormally slow heart rate (because of reflex bradycardia). Some patients also report chest pain, difficulty breathing, and feelings of nervousness. These side effects are quite variable and are usually dose-related (i.e., they occur more frequently at higher doses). 

A 68-year-old man was given 0.5% bupivacaine 4 ml or spinal anesthesia, and 5 minutes later complained of nausea and developed hypotension, loss of consciousness, and a tonic-clonic seizure. He had first-degree heart block 4 minutes after subarachnoid injection, followed 1 minute later by third-degree heart block, and then asystole. He was successfully resuscitated. Proposed theories included a reflex bradycardia resulting from reduced venous return and/or unopposed... 

Total intravenous anesthesia with propofol resulted in a reduced heart rate and a higher frequency of oculocardiac reflex bradycardia than thiopental/isoflurane anesthesia, with a higher sensitivity of children younger than 6 years in all groups (11). 

Viscum contain lectins that are cytotoxic by inhibiting protein synthesis on the ribosomal level in a manner similar to the toxalbumins ricin and abrin. Viscotoxin and phoratoxin are cardiac toxins and vasoconstrictors. Both produced reflex bradycardia, negative inotropic effects, and, in high doses, vasoconstriction of skin and skeletal muscle vessels in animals. 

Cardiovascular Status. Persons exposed to aerosols, smokes, or solutions of PCSI materials may have transient increases in SBP and DBP, often with reflex bradycardia. This could be compounded because of the emotional experience of being involved in a civil disturbance. Those with a history of cardiovascular disease may require hospital admission and further investigation. 

Baroreceptor reflexes can be blocked at the ganglionic synapse with Nn receptor antagonists. Alternatively, a reflex bradycardia can be blocked with muscarinic antagonists a reflex tachycardia can be blocked with fl, antagonists. 

Example Hexamethonium will block the reflex bradycardia that occurs when phenylephrine (an alpha-adrenoceptor agonist) causes vasoconstriction, but it will not block a bradycardia that results from the direct activation by ACh of M receptors in the heart. 

Given systemically, they increase mean blood pressure (BP) via vasoconstriction, with minimal effects on pulse pressure (PP). The increase in BP elicits a reflex bradycardia. Cardiac output (CO) may be decreased but can be offset by an increase in venous return, which may increase stroke volume (SV). 

Norepinephrine (NE) has little effect on p2 receptors. It increases TPR and both diastolic and systolic BP. Positive inotropic action of NE causes a small to moderate increase in pulse pressure (PP). Compensatory vagal reflexes tend to overcome the direct positive chronotropic effects of NE (reflex bradycardia may ensue), but the positive inotropic effects are maintained. 

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