Cardiac depressants

Cardiac depressant Cardiac steroids Cardigin Car dilate Cardinal Clear Carding... 

A.ntiadrenergic and cardiac depressant bretyhum tosylate [61-75-6] C H yBrN vAS HyO S... 

CNS DEPRESSANT Substanccs, e.g. anaesthetics and narcotics, which depress the activity of the central nervous system. Symptoms following exposure include headache, dizziness, loss of consciousness, respiratory or cardiac depression, death. 

Komissarova finds that the total alkaloids of Magnolia fuscaia and magnolamine are cardiac depressants at 20 to 1,000 and 10 to 500 parts per million respectively. The differences between the two indicate that the total alkaloids include a component more potent than magnolamine. 

Does not reliably reverse respiratory or cardiac depression... 

Pentobarbital (Nembutal) 1 0-1 5 mg/kg Up to 50 mg/minute 10-20 mcg/mL (typically titrated to EEG) Hypotension, respiratory depression, cardiac depression, infection, ileus Requires mechanical intubation, pressors, hemodynamic monitoring... 

In the past, concentrations of 40,000 ppm were used clinically to produce anesthesia. Sudden and unforeseen fatalities from ethyl chloride anesthesia have been reported. Concentrations of 2 0,000 ppm or above have reportedly caused increased respiratory rate, cardiac depression, dizziness, eye irritation, and abdominal cramps. Exposure to 19,000ppm resulted in mild analgesia after 12 minutes, and 13,000ppm caused slight symptoms of inebriation. ... 

Amiodarone (16) has been the center of much interest because of its activity as a cardiac depressant useful in treating ventricular arrhythmia and many analogues have been prepared [4. I he originally patented procedure concludes simply by etherification of benzofuran-containing iodonated phenol 15 with 2-halodiethylaminoethane to give amiodarone (16) [5]. The synthesis t)f 15 is not detailed in the reference but the synthesis of benzbromarone contains closely analo-goii.s steps [6]. 

Propranolol is a prototype of this series of drugs and is the oldest and most widely used nonselective )3-adrenoblocker. It possesses antianginal, hypotensive, and antiarrhythmic action. Propranolol is a cardiac depressant that acts on the mechanic and electrophysio-logical properties of the myocardium. It can block atrioventricular conductivity and potential automatism of sinus nodes as well as adrenergic stimulation caused by catecholamines nevertheless, it lowers myocardial contractility, heart rate, blood pressure, and the myocardial requirement of oxygen. 

Potassium intoxication Do not infuse rapidly. High plasma concentrations of potassium may cause death through cardiac depression, arrhythmias, or arrest. Monitor potassium replacement therapy whenever possible by continuous or serial EGG. In addition to EGG effects, local pain, and phlebitis may result when a more than 40 mEg/L concentration is infused. 

Caution is advised when disopyramide is used in conjunction with other cardiac depressant drugs, such as... 

The toxicity associated with propranolol is for the most part related to its primary pharmacological action, inhibition of the cardiac (3-adrenoceptors. This topic is discussed in detail in Chapter 11. In addition, propranolol exerts direct cardiac depressant effects that become manifest when the drug is administered rapidly by the IV route. Glucagon immediately reverses all cardiac depressant effects of propranolol, and its use is associated with a minimum of side effects. The inotropic agents amrinone (Inocor) and milrinone (Primacor) provide alternative means of augmenting cardiac contractile function in the presence of -adrenoceptor blockade (see Chapter 15). Propranolol may also stimulate bron-chospasm in patients with asthma. 

N2O (commonly called laughing gas) produces its anesthetic effect without decreasing blood pressure or cardiac output. Although it directly depresses the myocardium, cardiac depression is offset by an N2O-mediated sympathetic stimulation. Likewise, respiration is maintained. Tidal volume falls, but minute ventilation is supported by a centrally mediated increase in respiratory rate. However, since the respiratory depressant effect of N2O are synergistic with drugs such as the opi-... 

Cardiac depressant activity. Tincture of the gland, administered by perfusion to rabbits, produced weak activity on the... 

Cardiac depressant activity. Hot water extract of the dried rhizome, at a concentration of 3 mg/mL, was active on the guinea... 

Bupropion was developed over 30 years ago in an attempt to synthesize a novel antidepressant. Researchers wanted the agent to be efficacious for the existing screening models, but be different structurally and biochemically from the tricyclics and MAOIs. The compound was to be devoid of sympathomimetic, anticholinergic, and cardiac depressant effects (Soroko and Maxwell, 1983). 

It also has anaesthetic, local irritant action. Quinine causes hypotension, cardiac depression (IV injection), stimulates myometrium and rapid IV injection causes hypoglycaemia. 

The earliest signs of CNS toxicity are circumoral and tongue numbness, tinnitus, tremor, and dizziness. These appear at plasma lidocaine (lignocaine) concentrations of about 5 pg-mL-1. The value for prilocaine is similar to lidocaine but bupivacaine toxicity appears at about half those of lidocaine. Further progression is evidenced by drowsiness, visual disturbances, or muscle twitching (plasma lidocaine of 5-10 pg-mL-1). Over 10 p-mL-1 grand mal convulsions, coma and respiratory arrest are likely. Serious CNS toxicity is indicative of imminent and potentially fatal cardiac toxicity since lidocaine is associated with direct cardiac depression at plasma concentrations in excess of 20 pg-mL-1. 

Cardiac depressant effects may occur when verapamil or diltiazem is combined with a (p-adrenoceptor antagonoist or a cardiac glycoside. Nifedipine and verapamil are metabolised by cytochrome P-450 3A4. Inhibitors of this enzyme, e.g. HIV-protease inhibitors, cimetidine, fluoxetine, ketoconazole, erythromycin, will increase plasma levels and the dose should be carefully monitored. Conversely, enzyme inducers, e.g. carbamazepine, rifampicin, phenytoin, will decrease their plasma concentrations. 

The most important toxic effects reported for calcium channel blockers are direct extensions of their therapeutic action. Excessive inhibition of calcium influx can cause serious cardiac depression, including cardiac arrest, bradycardia, atrioventricular block, and heart failure. These effects have been rare in clinical use. 

Propranolol Nonselective competitive antagonist at adrenoceptors Decreased heart rate, cardiac output, and blood pressure decreases myocardial oxygen demand Prophylaxis of angina for other applications, see Chapters 10, 11, and 13 Oral and parenteral, 4-6 h duration of action Toxicity Asthma, atrioventricular block, acute heart failure, sedation Interactions Additive with all cardiac depressants... 

Verapamil, diltiazem Nonselective block of L-type calcium channels in vessels and heart Reduced vascular resistance, cardiac rate, and cardiac force results in decreased oxygen demand Prophylaxis of angina, hypertension, others Oral, IV, duration 4-8 h Toxicity Atrioventricular block, acute heart failure constipation, edema Interactions Additive with other cardiac depressants and hypotensive drugs... 

Propranolol 13- Adrenoceptor blockade Direct membrane effects (sodium channel block) and prolongation of action potential duration slows SA node automaticity and AV nodal conduction velocity Atrial arrhythmias and prevention of recurrent infarction and sudden death Oral, parenteral duration 4-6 h Toxicity Asthma, AV blockade, acute heart failure Interactions With other cardiac depressants and hypotensive drugs... 

In vitro, U-II is a potent constrictor of vascular smooth muscle its activity depends on the type of blood vessel and the species from which it was obtained. Vasoconstriction occurs primarily in arterial vessels, where U-II can be more potent than endothelin 1, making it the most potent known vasoconstrictor. However, under some conditions, U-II may cause vasodilation. In vivo, U-II has complex hemodynamic effects, the most prominent being regional vasoconstriction and cardiac depression. In some ways, these effects resemble those produced by ET-1. Nevertheless, the role of the peptide in the normal regulation of vascular tone and blood pressure in humans appears to be minor. 

N.A. Quassinoids, ailanthone, quassin, alkaloids, flavonols, tannins." Antimalarial, against cancerous cells, counter worms, excessive vaginal discharge, gonorrhea, malaria, antispasmodic, cardiac depressant. 

Isolated heart not explored Hypoxia-induced cardiac depression cardioprotection Akagi et al., 1995... 

Beta blockers that bind to both beta-1 and beta-2 receptors (nonselective agents, see Table 20-2) may induce bronchoconstriction in patients with asthma or similar respiratory problems. These patients should be given one of the more cardioselective beta antagonists, such as atenolol (Tenormin) or metoprolol (Lopressor, others). Beta blockers may also produce excessive cardiac depression in individuals with certain types of cardiac disease. Beta blockers are generally well tolerated in most patients, however, and major problems are infrequent. 

Mistletoe has hypotensive, cardiac-depressant, and sedative properties. Traditionally, it is used for high blood pressure, arteriosclerosis, nervous tachycardia, hypertensive headache, chorea, and hysteria. 

Local anesthetics block the sodium channels, are cardiac depressants, and bring about a ventricular conduction defect and block that may progress to cardiac and ventilatory arrest if toxic doses are given. In addition, these agents produce arteriolar dilation. Circulatory failure may be treated with vasopressors such as ephedrine, metaraminol (Aramine), or mephentermine (Wyamine). Artificial respiration and cardiac massage may also become necessary. Among the local anesthetics, only cocaine blocks the uptake of norepinephrine, causes vasoconstriction, and may precipitate cardiac arrhythmias. 

The pressor response to ephedrine is due in part to peripheral constriction and in part to myocardial stimulation. Vasoconstriction can be demonstrated by intra-arterial injection, but compared to epinephrine, ephedrine is only about one thousandth as active. This would imply that the cardiac effect is predominant in increasing the arterial pressure. This, however, is difficult to demonstrate. In perfused hearts, ephedrine produces only minor stimulation and cardiac depression appears if the drug is repeated. 

Reserpine (Serpasil) depletes the store of catecholamine peripherally and centrally and attenuates, but does not abolish, sympathetic reflexes. Reserpine is useful in the management of mild to moderate hypertension. Its onset of action is very slow (2 to 3 weeks) when given orally. The side effects of reserpine are manifested by cholinergic hyperactivity such as diarrhea, bradycardia, and nasal stuffiness. Reserpine can activate a peptic ulcer (cholinergic dominance) and cause depression (depletes norepinephrine stores). Reserpine and propranolol have potential cardiac depressant activity and should not be used together. 

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