Resistance peripheral vascular

Class II drugs are classical (3-adrenoceptor antagonists such as propranolol, atenolol, metoprolol or the short-acting substance esmolol. These drugs reduce sinus rate, exert negative inotropic effects and slow atrioventricular conduction. Automaticity, membrane responsiveness and effective refractory period of Purkinje fibres are also reduced. The typical extracardiac side effects are due to (3-adrenoceptor blockade in other organs and include bronchospasm, hypoglycemia, increase in peripheral vascular resistance, depressions, nausea and impotence. 

DHPs are potent arterial vasodilators. They act on resistance vessels and therefore reduce peripheral vascular resistance, lower arterial blood pressure, and antagonize vasospasms in coronary or peripheral arteries. By reducing afterload, DHPs also reduce cardiac oxygen demand. Together with their vascular spasmolytic effect, this explains most of the beneficial actions of DHPs in angina pectoris. Most DHPs are only licensed for the therapy of hypertension, some of them also for the treatment of angina pectoris and vasospastic (Prinzmetal) angina. 

Monitoring the patient in shock requires vigilance on the part of the nurse The patient s heart rate, blood pressure, and ECG are monitored continuously. The urinary output is measured often (usually hourly), and an accurate intake and output is taken. Monitoring of central venous pressure via a central venous catheter will provide an estimation of the patient s fluid status. Sometimes additional hemodynamic monitoring is necessary with a pulmonary artery catheter. The use of a pulmonary artery catheter allows the nurse to monitor a number of parameters, such as cardiac output and peripheral vascular resistance The nurse adjusts therapy according to the primary health care provider s instructions. 

PC After meals (post cibum) PVR Peripheral vascular resistance... 

The answer is d. (Hardman, pp 212—213.) Only isoproterenol will lower mean blood pressure, decrease peripheral vascular resistance, and increase heart rate. Methacholine decreases heart rate as does propranolol. Atropine has no action on peripheral resistance. Norepinephrine causes intense vasoconstriction and raises the mean blood pressure. 

A high sodium intake and increased circulating natriuretic hormone inhibition of intracellular sodium transport, resulting in increased vascular reactivity and a rise in BP and / Increased intracellular concentration of calcium, leading to altered vascular smooth muscle function and increased peripheral vascular resistance. 

Acutely, diuretics lower BP by causing diuresis. The reduction in plasma volume and stroke volume associated with diuresis decreases cardiac output and, consequently, BP. The initial drop in cardiac output causes a compensatory increase in peripheral vascular resistance. With chronic diuretic therapy, the extracellular fluid volume and plasma volume return almost to pretreatment levels, and peripheral vascular resistance falls below its pretreatment baseline. The reduction in peripheral vascular resistance is responsible for the long-term hypotensive effects. Thiazides lower BP by mobilizing sodium and water from arteriolar walls, which may contribute to decreased peripheral vascular resistance. 

Reserpine depletes norepinephrine from sympathetic nerve endings and blocks the transport of norepinephrine into its storage granules. When the nerve is stimulated, less than the usual amount of norepinephrine is released into the synapse. This reduces sympathetic tone, decreasing peripheral vascular resistance and BP. 

Guanethidine and guanadrel deplete norepinephrine from postganglionic sympathetic nerve terminals and inhibit the release of norepinephrine in response to sympathetic nerve stimulation. This reduces cardiac output and peripheral vascular resistance. 

With advancing age, the patient with essential hypertension progressively changes his hemodynamic pattern into one of normal cardiac output with increased peripheral arteriolar constriction and, finally, later in the natural course of the disease into one of lower cardiac output and further increase in peripheral vascular resistance ). 

If the hemodynamic defect in essential hypertension is peripheral arteriolar vasoconstriction with increased total peripheral vascular resistance, peripheral vasodilators would appear an ideal therapeutic approach. 

Cardiovascular effects Harmala alkaloids have cardiovascular effects (Aarons et al. 1977). Harmine, harmaline, and harmalol decrease heart rate, but increase pulse pressure, peak aortic flow, and myocardial contractile force in dogs. Harmine reduces systemic arterial blood pressure and peripheral vascular resistance. Vascular resistance effects are not mediated by jS-adrenergic or histamine HI receptors. 

Adrenal medulla. On the one hand, release of epinephrine elicits cardiovascular effects, such as increases in heart rate und peripheral vascular resistance. On the other, it evokes metabolic responses, such as glycogenolysis and li-polysis, that generate energy-rich substrates. The sensation of hunger is suppressed. The metabolic state corresponds to that associated with physical exercise - silent stress . 

Clonidine is a selective o -adrenergic agonist. Clonidine has expressed hypotensive action, which is associated with a reduction of general peripheral vascular resistance, reduced frequency of cardiac beats, and a reduction of cardiac output. The mechanism of action of clonidine is caused by stimulation of o -adrenoreceptors of the inhibitory structures of the brain as well as a reduction of sympathetic impulses to the blood vessels and brain. 

It is believed that, like diuretics, using j3-adrenoblockers leads to a reduction of cardiac output. Heart rate and overall peripheral vascular resistance declines. 

Clonidine is a selective Oj-adrenergic agonist that exhibits pronounced hypotensive action that is associated with a reduction of overall peripheral vascular resistance, decline in frequency of cardiac contraction, and reduced cardiac output. Clonidine is the drug of choice for treating various degrees of hypertension when used in combination with oral diuretics. 

Methyldopa is an a-methoxylated derivative of levodopa that exhibits hypotensive action by reducing overall peripheral vascular resistance and reducing heart work. Antihypertensive action of methyldopa consists of the biotransformation of methyldopa into methylnoradrenaline (methylnorepinephrine), which acts as a pseudo neurotransmitter. The current, universally accepted point of view is that the action of methyldopa is carried out through the CNS, where methylnorepinephrine, a powerful stimulant of a-adrenergic receptors of the medulla, inhibits the vasomotor center. 

Verapamil possesses antiarrhythmic, antianginal, and hypotensive activity. It reduces the myocardial need for oxygen by reducing contractility of the myocardium and slowing the frequency of cardiac contractions. It causes dilation of coronary arteries and increased coronary blood flow. It reduces tonicity of smooth musculature, peripheral arteries, and overall peripheral vascular resistance. It provides antiarrhythmic action in supraventricular arrhythmia. 

Carvedilol also (1) attenuates the pressor effects of phenylephrine, (2) causes vasodilation, and (3) reduces peripheral vascular resistance. These effects contribute to the reduction of blood pressure and usually are seen within 30 minutes of drug administration. 

Hydralazine and dihydralazine are predominantly arterial vasodilators which cause a reduction in peripheral vascular resistance but also reflex tachycardia and fluid retention. They were used in the treatment of hypertension, in combination with a -blocker and a diuretic. Long-term use of these compounds may cause a condition resembling lupus erythematodes with arthrosis, dermatitis and LE-cells in the blood. This risk is enhanced in women and in patients with a slow acetylator pattern. When combined with the venous vasodilator isosorbide (an organic nitrate) hydralazine was shown to be mildly beneficial in patients with congestive heart failure (V-HEFT I Study). Hydralazine and dihydralazine have been replaced by other therapeutics, both in hypertension treatment and in the management of heart failure. 

Reduction of peripheral vascular resistance and cardiac afterload, probably because the enhanced loss of the sodium ions leads to a blunted vasoconstrictor response to endogenous catecholamines. This effect is relevant in the long-term treatment of essential hypertension with thiazide diuretics. 

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. 

Hemodynamic effects Decreased peripheral vascular resistance and blood pressure Venodilation is prominent Cardiac stimulation occurs because of cardiovascular reflexes and enhanced release of norepinephrine Similar to phenoxybenzamine Decreased peripheral vascular resistance and blood pressure Veins seem to be less susceptible to antagonism than arteries thus, postural hypotension is less of a problem Cardiac stimulation is less because release of norepinephrine is not enhanced... 

The actions of p-blockers on blood pressure are complex. After acute administration, blood pressure is only slightly altered. This is because of the compensatory reflex increase in peripheral vascular resistance that results from a (3-blocker-induced decrease in cardiac output. Vasoconstriction is mediated by a-receptors, and a-receptors are not antagonized by (3-receptor blocking agents. Chronic administration of (3-blockers, however, results in a reduction of blood pressure, and this is the reason for their use in primary hypertension (see Chapter 20). The mechanism of this effect is not well understood, but it may include such actions as a reduction in renin release, antagonism of (3-receptors in the central nervous system, or antagonism of presynaptic facilita-tory (3-receptors on sympathetic nerves. 

The most common hemodynamic effect of acutely administered labetalol in humans is a decrease in peripheral vascular resistance and blood pressure without an appreciable alteration in heart rate or cardiac output. 

This pattern differs from that seen following administration with either a conventional (3- or a-blocker. Acute administration of a (3-blocker produces a decrease in heart rate and cardiac output with little effect on blood pressure, while acute administration of an a-blocker leads to a decrease in peripheral vascular resistance and a reflexively initiated increase in cardiac rate and output. Thus, the pattern of cardiovascular responses observed after labetalol administration combines the features of (3- and a-blockade, that is, a decrease in peripheral vascular resistance (due to a-blockade and direct vascular effects) without an increase in cardiac rate and output (due to (3-blockade). 

Prolonged oral therapy with labetalol results in cardiovascular responses similar to those obtained following conventional (3-blocker administration, that is, decreases in peripheral vascular resistance, blood pressure, and heart rate. Generally, however, the decrease in heart rate is less pronounced than after administration of propranolol or other (3-blockers. 

Usual IV doses of verapamil are not associated with marked alterations in arterial blood pressure, peripheral vascular resistance, heart rate, left ventricular end-diastolic pressure, or contractility. 

At higher concentrations, nitroglycerin also relaxes arteriolar smooth muscle, which leads to a decrease in both peripheral vascular resistance and aortic impedance to left ventricular ejection (decreased afterload). The decreased resistance to ventricular ejection may also reduce myocardial wall tension and oxygen requirements. 

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