Beta blockers Adrenaline

This is not the end of the story about beta blockers. Subsequent research demonstrated that there are two subclasses of beta receptors, termed beta-1 and beta-2. Both are activated by adrenaline. Both are blocked by propranolol. Beta-1 receptors are found mostly in heart muscle but not much in the lungs, whereas beta-2 receptors are found mostly in the lungs but not much in the heart. These facts provided the opportunity for better drugs. Here is the argument. 

Beta-blockers. Beta-blocking agents (including atenolol [Tenormin] and metoprol [Lopressor]) are a class of drugs that block substances such as adrenaline (epinephrine), a key agent in the autonomic (involuntary) nervous system and in the activation of heart muscle. 

LIDOCAINE BETA-BLOCKERS 1. Risk of bradycardia (occasionally severe), l BP and heart failure with intravenous lidocaine 2. Risk of lidocaine toxicity due to T plasma concentrations of lidocaine, particularly with propranolol and nadolol 3. t plasma concentrations of propranolol and possibly some other beta-blockers 1. Additive negative inotropic and chronotropic effects 2. Uncertain, but possibly a combination of beta-blocker-induced 1 hepatic blood flow (due to 1 cardiac output) and inhibition of metabolism of lidocaine 3. Attributed to inhibition of metabolism by lidocaine 1. Monitor PR, BP and ECG closely watch for development of heart failure when intravenous lidocaine is administered to patients on beta-blockers 2. Watch for lidocaine toxicity 3. Be aware. Regional anaesthetics should be used cautiously in patients with bradycardia. Beta-blockers could cause dangerous hypertension due to stimulation of alpha-receptors if adrenaline is used with local anaesthetic... 

Co-administration of beta-blockers has been associated with an increased risk of severe allergic drug reactions and reduces the effect of adrenaline in the immediate treatment of anaphylactic shock. The mechanism involves changes in the regulation of anaphylactic mediators (281). 

Beta-blockers, by inhibiting the effect of adrenaline and noradrenaline on the heart, prevent the normal increase in heart rate, and are very effective in preventing exercise angina. Examples of beta-blockers used for this purpose include acebutolol, atenolol, metoprolol. nadolol, oxprenolol, pindolol, propranolol, sotalol and timolol. See ADRENOCEPTOR ANTAGONISTS. 

Beta-blockers, drugs that prevent the uptake of adrenaline by heart and chest cells, illustrate some of the promises and risks posed by long-term ther-... 

Adrenaline is contraindicated in cases of diabetes, hyperthyroidism, serious heart arrhythmias and coronary insufficiency or in combination with beta-blockers or monoamine oxidase (MAO) inhibitors. Lidocaine with adrenaline has a very rapid onset of action. Its duration of action is longer than that of lidocaine without adrenaline. However, inadvertent injection of a lidocaine-adrenaline solution into the vessels located near the nerve trunks increases the heart rate (immediate sinus tachycardia at over 130 beats per minute, spontaneously reversible in around 15 minutes) and increases ventricular excitability (risk of fibrillation). It can trigger angina attacks that may lead to a heart attack. It is therefore preferable not to use adrenaline before a full-face phenol peel. 

On the basis of these few reports, it cannot be said with certainty that an interaction occurs however, it is possible that ACE inhibitors could exacerbate the response to insect venom immunotherapy. Because of the potential severity of the reaction, extra caution should be taken in patients taking ACE inhibitors and undergoing desensitising treatment with Hy-menoptera (bee or wasp) venom. Some authors " and manufacturers advise temporarily withholding the ACE inhibitor before each desensitisation (24 hours was sufficient in one case), while others suggest temporary substitution of a different antihypertensive e.g. a calcium-channel blocker. Note that some evidence suggests that anaphylactic shock in patients taking beta blockers may be resistant to treatment with adrenaline (epinephrine), see Beta blockers + Inotropes and Vasopressors , p.848. Therefore beta bloekers are probably not a suitable alternative. 

Propranolol reduces the clearance of bupivacaine and so theoretically the toxicity of bupivacaine may be increased. There has been a single report of enhanced bupivacaine cardiotoxicity in a patient also receiving metoproioi and digoxin. The coronary vasoconstriction caused by cocaine is increased by propranolol. Beta blockers may interact with adrenaline (epinephrine)-containing local anaesthetics. 

Note that local anaesthetic preparations of lidocaine often contain adrenaline (epinephrine), which may interact with beta blockers, see Beta blockers -I- Inotropes and Vasopressors , p.848. 

One of the normal physiological responses to a fall in blood sugar levels is the mobilisation of glucose from the liver under the stimulation of adrenaline from the adrenals. This sugar mobilisation is blocked by non-selective beta blockers (such as propranolol) so that recovery from hypoglycaemia is delayed and may even proceed into a full-scale episode in a hypoglycaemia-prone diabetic. Normally the adrenaline would also increase the heart rate, but with the beta-receptors in the heart already blocked this fails to occur. A rise in blood pressure occurs because the stimulant effects of adrenaline on the beta-2 receptors (vasodilation) are blocked leaving the alpha (vasoconstriction) effects unopposed. 

Effects on blood pressure and heart rate The hypertensive effects of adrenaline (epinephrine) can be markedly increased in patients taking non-selective beta blockers such as propranolol. A severe and potentially life-threatening hypertensive reaction and/or marked bradycardia can develop. Cardioselective beta blockers such as atenolol and metoprolol interact minimally. An isolated report describes a fatal hypertensive reaction in a patient given propranolol and phenylephrine, but concurrent use normally seems to be uneventful Paradoxically, marked hypotension occurred in one patient given low-dose carvedilol and dobutamine. Anaphylaxis Some evidence su ests that anaphylactic shock in... 

Adrenaline (epinephrine) stimulates alpha- and beta-receptors of the cardiovascular system, the former results in vasoconstriction (mainly alphaj) and the latter in both vasodilatation (mainly beta2) and stimulation of the heart (mainly betaj). The net result is usually a modest increase in heart rate and a small rise in blood pressure. However, if the heta-reeeptors are blocked by a non-selective beta blocker, such as propranolol or nadolol (see Table 22.1 , (p.833) for a list), the unopposed alpha vasoeonstrietion causes a marked rise in blood pressure, followed by reflex bradyeardia. Cardioselective beta blockers such as atenolol and metoprolol, whieh are more selective for betaj receptors, do not prevent the vasodilator aetion of adrenaline at beta2 receptors to the same extent, and therefore the effect of any interaction is relatively small. Consequently, adrenaline has been used to assess the degree of beta blockade produced by propranolol and other beta blockers.Phenylephrine is largely an alpha stimulator, therefore beta blockers should have a minimal effect on its action. 

Caffeine causes the release of catecholamines, such as adrenaline, into the blood, which could account for the increases in heart rate and blood pressure that are seen. The blood pressure rise may be exaggerated in the presence of non-selective beta blockers, which block vasodilatation leaving the alpha (vasoconstrictor) effects of adrenaline unopposed. This will also oppose the actions of the beta blockers. 

When anaphylactic reactions do occur in patients taking beta blockers, it may be preferable to use a beta-agonist bronchodilator such as isoprena-line rather than adrenaline (epinephrine). Glucagon, which has inotropic and chronotropic actions that are only minimally antagonised by beta blockers, may also be effective in reversing anaphylactoid shock in patients taking beta blockers. ... 

Adrenaline, which turns on both receptors, increases heart rate via the beta-1 receptor and dilates airways by the beta-2 receptors. Propranolol, which is a nonspecihc blocker of both beta-1 and beta-2 receptors, decreases heart rate and lowers blood pressure, beta-1 receptor action, but can constrict airways in the lung, beta-2 receptor action, and that is not so good. 

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