vasodilator and vasoconstrictor.pptx

vasodilator and vasoconstrictor, nursing, cardiovascular nursing

1. COLLEGE OF NURSING MADRAS MEDICAL COLLEGE, CHENNAI-03 MEDICAL SURGICAL NURSING-II vasodilators and vasoconstrictors BY EDWIN JOSE.L MSC(N) II YEAR, COLLEGE OF NURSING, MADRAS MEDICAL COLLEGE, CHENNAI

2. introduction Vasodilation can be produced with a variety of drugs. Some of these drugs act primarily on arterioles, some act primarily on veins, and some act on both types of vessels. The vasodilators are widely used, with indications ranging from hypertension to angina pectoris to heart failure They affect the muscles in the walls of the arteries and veins, preventing the muscles from tightening and the walls from narrowing. As a result, blood flows more easily through the vessels. The heart doesn't have to pump as hard, reducing blood pressure.

3. Meaning -vasodilator Vasodilators are a group of medicines that dilate (open) blood vessels, which allows blood to flow more easily. They affect the muscles in the walls of the arteries and veins, preventing the muscles from tightening and the walls from narrowing. As a result, blood flows more easily through the vessels. The heart doesn't have to pump as hard, reducing blood pressure. Some drugs used to treat hypertension, such as calcium channel blockers also dilate blood vessels. But the vasodilators that work directly on the vessel walls are hydralazine and minoxidil.

4. Classification of vasodilators According to the site of action Arterial dilators (mainly affect the arteries) Venous dilators (mainly affect the veins) Mixed dilators (affect veins and arteries) Another classification Directly acting vasodilators Indirectly acting vasodilators

5. Therapeutic classification Angiotensin converting enzyme inhibitors Angiotensin receptor blockers Nitrates Calcium channel blockers Beta blockers Minoxidil Hydralazine

6. EXAMPLES ACE INHIBITORS Benazepril (Lotensin) Captopril. Enalapril (Vasotec) Fosinopril . Lisinopril (Prinivil, Zestril) Moexipril . Perindopril. Quinapril (Accupril) ARBs Azilsartan ( Edarbi ) Candesartan ( Atacand ) Eprosartan . Irbesartan (Avapro) Losartan (Cozaar) Olmesartan (Benicar) Telmisartan ( Micardis ) Valsartan (Diovan)

7. NITRATES Nitroglycerin (such as Nitro-Dur, Nitrolingual , Nitrostat). Isosorbide (such as Dilatrate , Isordil ). Nitroprusside (such as Nitropress ). Amyl nitrite or amyl nitrate.  CALCIUM CHANNEL BLOCKERS Amlodipine (Norvasc) Diltiazem (Cardizem, Tiazac , others) Felodipine. Isradipine . Nicardipine. Nifedipine (Procardia) Nisoldipine ( Sular ) Verapamil ( Calan SR, Verelan )

8. BETA BLOCKERS Acebutolol. Atenolol (Tenormin) Bisoprolol ( Zebeta ) Metoprolol (Lopressor, Toprol XL) Nadolol ( Corgard ) Nebivolol (Bystolic) Propranolol (Inderal, InnoPran XL)

9. Arterial dilator used to treat  systemic  and  pulmonary  hypertension,  heart failure  and  angina . reduce arterial pressure by decreasing  systemic vascular resistance . in heart failure it acts by reducing the  afterload  on the left ventricle, which enhances stroke volume and cardiac output and leads to secondary decreases in ventricular  preload  and venous pressures. Anginal patients benefit from arterial dilators because by reducing afterload on the heart, vasodilators decrease the  oxygen demand  of the heart, and thereby improve the  oxygen supply/demand ratio . Eg. H ydralazine , calcium channel blockers, amlodipine

10. Venous dilator It reduces venous pressure, by reducing preload on the heart thereby decreasing cardiac output. This is useful in angina because it decreases the  oxygen demand  of the heart and thereby increases the  oxygen supply/demand ratio . Oxygen demand is reduced because decreasing preload leads to a reduction in  ventricular wall stress  by decreasing the size of the heart. Reducing venous pressure decreases proximal  capillary hydrostatic pressure , which reduces  capillary fluid filtration  and  edema  formation. Therefore, venous dilators are sometimes used in the treatment of heart failure along with other drugs because they help to reduce pulmonary and/or systemic edema that results from the heart failure.

11. 3. Venous dilators reduce: Venous pressure and therefore cardiac preload Cardiac output Arterial pressure Myocardial oxygen demand Capillary fluid filtration and tissue edema Eg. Nitrates/ nitroglycerine –low dose, molsidomine

12. mixed dilators Organic nitrates and nitrites relax both arterial and venous vascular smooth muscle . At low concentrations, which are generally used clinically, venous dilation predominates, and net systemic vascular resistance is usually not affected. Pharmacologic effects occur rapidly. First-pass metabolism limits the use of these drugs to IV, sublingual, and topical (ointment) administration. Tolerance is a problem with sustained administration. Eg.Nitrglycerine – high dose, Nitropruside , Prazosin

13. Directly acting vasodilators  Direct-acting vasodilators are a class of antihypertensive medications that are used for severe  refractory   hypertension , malignant hypertension, and  hypertensive emergencies . These medications include  hydralazine , which can be administered orally,  intravenously , and intramuscularly;  minoxidil , which can be administered orally or topically; and  sodium nitroprusside , which is given intravenously. Once administered, direct acting vasodilators rapidly work on the vascular smooth muscle cells by preventing the increase of intracellular calcium concentration. As a result, direct acting vasodilators prevent vasoconstriction and promote vasodilation, leading to a reduction in the total peripheral resistance and  blood pressure . since direct acting vasodilators tend to work rapidly, they can result in sudden vasodilation and  hypotension . This may lead to side effects, including  dizziness , headache, reflex tachycardia, palpitations, and 

14.   Indirectly acting vasodilators  those that inhibit sympathetically mediated vasoconstriction. Drugs can inhibit sympathetic pathway at any point from the central nervous system to the peripheral nervous terminal. Prazosin a selective α 1   adrenergic antagonist reduces mean arterial pressure. those that inhibit rennin-angiotensin system Drugs that interfere with the sympathetic nervous system α1- blockers (Phentolamine, Phenoxybenzamine). α2 agonists ( clonidine) D1 receptor agonist : Fenoldopam

15. Usage of Vasodilators Systemic hypertension Heart failure Peripheral vascular disease Raynaud's disease Pulmonary hypertension.  angina Stroke chronic kidney disease preeclampsia hypertensive emergency

16. Mechanism of action In general, Vasodilators dilate or prevent constriction of the blood vessels, which allow greater blood flow to various organs in the body.  Many vasodilators bind to receptors on endothelial cells of the blood vessel, which stimulate calcium release. Calcium activates the enzyme nitric oxide synthase (NO synthase) and converts L-arginine into NO. It leaves the endothelial cell via diffusion and enters vascular smooth muscle cells. NO activates GTP and converts it into cGMP. cGMP then stimulates myosin-light chain phosphatase, which removes a single phosphate from myosin and actin filaments. The dephosphorylation of myosin and actin filaments allows vascular smooth muscle relaxation. 

17. ACE Inhibitors Prevent the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor.  

18. Angiotensin Receptor Blockers   Prevent angiotensin II from binding to its receptor

19. Nitrates Increase the amount of NO in vascular smooth muscle cells, causing vasodilation. Nitrates dilate veins more than arteries and decrease preload

20. Calcium Channel Blockers Block calcium channels in the cardiac and smooth muscles, causing decreased muscle contractility and vasodilation. There are two classes of CCBs: Dihydropyridines (act on the vascular smooth muscle), and non-dihydropyridines (act on the heart).

21. Minoxidil Directly relaxes arteriolar smooth muscle, with minimal effect on the vein. Cyclic AMP may mediate its effects

22. In hypertensive emergency following drugs are the first choice depending on systemic involvement.  Aortic dissection: intravenous esmolol, intravenous nitroprusside, or nitroglycerine Acute pulmonary edema : intravenous  nitroglycerine , nitroprusside, or clevidipine Acute myocardial infarction/unstable angina: intravenous esmolol or  nitroglycerine Acute renal failure: intravenous fenoldopam, clevidipine , or nicardipine Eclampsia: intravenous hydralazine, nicardipine, or labetalol Pheochromocytoma/hyperadrenergic state secondary to amphetamine or cocaine: intravenous clevidipine , phentolamine, or nicardipine

23. administration Depending on the clinical setting, some routes of administration can be more beneficial than others. eg. in the setting of acute myocardial infarction (MI), patients will more likely benefit from sublingual nitroglycerin, as it is absorbed much faster by the sublingual route and allows the patient to feel more comfortable and often reduces the chest pain. Whereas for the patients who need to reduce their blood pressure in a non-emergent manner, the oral route is an acceptable route of administration.  Nitro vasodilators such as nitroprusside and nitroglycerin are frequently used in hypertensive emergencies. Sodium nitroprusside administration is via the intravenous route in such conditions. It starts blood pressure-lowering action within one minute or less, and these effects disappear within 10 minutes after discontinuation. Frequent clinical monitoring is necessary during the administration of this medication. 

24. Cont …. Similar to nitroprusside, nitroglycerin can be used intravenously in certain conditions. It has very similar kinetic, but it produces greater veno dilation compared to arteriolar dilation. Extended used is generally avoided due to concerns of tachyphylaxis. Severe hypertension during labor should be treated with intravenous labetalol/hydralazine or oral nifedipine to prevent intracranial hemorrhage or eclampsia.  Calcium channel blockers such as clevidipine and nicardipine can be used intravenously in hypertensive emergencies while amlodipine, nifedipine are oral formulations that are used in routine hypertension management.  Nebivolol and carvedilol are taken orally to treat hypertension.

25. Side effects ACE Inhibitors:   angioedema, dry cough (due to increased bradykinin levels), teratogenicity, hyperkalemia , and hypotension , acute pancreatitis. Examples : enalapril, lisinopril, captopril, ramipril.  Angiotensin Receptor Blockers:   hyperkalemia , hypotension, decrease GFR, teratogenicity. Examples : valsartan, losartan, candesartan. Calcium Channel Blockers:  gingival hyperplasia, dizziness, flushing, peripheral edema , AV block (with Non-dihydropyridines), constipation. Examples : Dihydropyridines: amlodipine, clevidipine , nicardipine, nifedipine; Non-dihydropyridines: diltiazem and verapamil   Nitrates:  reflex tachycardia, headache, flushing, and orthostatic hypotension. Examples : nitroglycerin , isosorbide mononitrate, isosorbide dinitrate. Cyanide toxicity does not occur with intravenous use, but methemoglobinemia can occur. 

26. Cont … Hydralazine:  compensatory tachycardia, headache, angina, SLE-like symptoms (in slow acetylators), fluid retention.  Nitroprusside:  Nitroprusside is metabolized to cyanide, and it can lead to cyanide toxicity. Toxicity can appear as little as four hours after initiation of infusion. Potential risk factors for the development of toxicity are underlying renal impairment, prolonged treatment period (over 48 hours), and the utilization of a higher dose. Minoxidil:  hypertrichosis, water retention, pericarditis that may progress to tamponade. Beta-Blockers:  bradycardia, dizziness, headaches, nausea, hypotension, metabolic abnormalities. Americal Heart Association/American Stroke Association recommends not reducing blood pressure during the initial 24 hours of ischemic stroke unless it is over 220/120 mm Hg to prevent the worsening of ischemic injury. In the patient with ischemic stroke, BP requires lowering to less than 180/110 mm Hg before administering alteplase with intravenous labetalol/nicardipine.

27. contraindications ACE Inhibitors:  pregnancy, previous history of angioedema, hereditary angioedema. ARBs:  ARBs are teratogens and should not be used in pregnant patients. Nitrates:  Nitrates decrease preload, so the administration of nitrates would be contraindicated in a person having an inferior MI (right ventricular infarction).  Calcium Channel Blocker : severe hypotension, hypersensitivity. Hydralazine:  CAD or angina (it can cause compensatory tachycardia), mitral valve rheumatic heart disease Beta-blockers:  Bradycardia, severe chronic obstructive pulmonary disease, hypotension, cardiogenic shock, and high degree of atrioventricular block.

28. monitoring Vasodilators can be monitored by checking the blood levels of certain drugs. Microvascular monitoring is another way to detect therapeutic levels in patients who are taking vasodilators. Microvascular monitoring is the subject of many clinical trials and targets patients before and after vasodilator therapy as a way to detect hemodynamic coherence.  After initiation of vasodilators, blood pressure (both standing and sitting/supine), heart rate should be monitored. If the patient is on hydralazine and develops lupus-like symptoms, check antinuclear antibody (ANA) titers and anti-histone antibody levels. Clinicians should also check renal function values after 2 to 3 weeks after initiation of ACE Inhibitors and ARBs. Signs/symptoms of pericardial effusion should require monitoring while patients are on minoxidil. 

29. toxicity ACE Inhibitors:  There are few documented cases of ACE inhibitor overdose. One case report stated that treating a patient who overdosed on lisinopril with hemodialysis worked. In general, supportive care should be established in every case (IV fluids, vasopressors in case of severe hypotension).  ARBs:  Very few cases of ARB overdoses have been reported. Treating overdose of this medication like any other drug intoxication is recommended.  Calcium Channel Blocker : There is not much evidence on reversing the toxicity of CCBs. One study showed that high-dose insulin and life support were most effective in reversing toxicity. Nitroprusside:  Sodium thiosulfate is indicated in the patient who has cyanide toxicity. It provides sulfur, which converts cyanide into thiocyanate and prevents further adverse effects.   Hydralazine, Nitrates:  Very few reported cases of overdose exist to date. Recommendations are to treat these overdoses like any other drug overdose. Beta-Blockers:  Glucagon, sodium bicarbonate, and or magnesium may be used.

30. NURSING MANAGEMENT Check for the contraindications mentioned above to this drug (e.g., drug allergy, CAD, cerebral insufficiency, and such) to avoid potential side effects. Emphasize to the patient the significance of complete adherence to pharmacological therapy to guarantee optimum therapeutic benefits. Educate the patient on the necessity of good lifestyle choices like regular exercise, weight loss, smoking cessation, and a low-sodium diet to enhance the benefit of vasodilator therapy

31. NURSING DIAGNOSIS Acute pain (e.g., headache or migraine) related to the side effect of the drug Impaired Skin Integrity related to the side effects on the skin of the vasodilators Risk for decreased output related to increased fluid volume excretion as a side effect of vasodilators Risk for Imbalanced Fluid Volume related to patient response to drug therapy Risk for Injury related to side effect of drug therapy Deficient Knowledge related to drug action and side effect

32. Nursing interventions Assess the patient for signs and symptoms of stroke or heart failure, such as hypertension and chest pain. Check the patient’s allergy status. Assess if the patient is pregnant or lactating Check medical history for renal impairment or persistent hypotension. Assess the patient’s mental status while on vasodilator treatment. Check for the status of peripheral veins prior to cannulation and administration of intravenous vasodilators

33. Cont ….. Administer vasodilators on empty stomach. Educate the patient about the action, indication, common side effects, and adverse reactions to note when taking vasodilators. Instruct the patient on how to self administer oral vasodilators. Start stool charting if the patient develops loose stools Advise the patient to immediately report any signs of dizziness or severe headaches. Encourage checking blood pressure levels at the same time of the day, on a daily basis at home Perform routine blood tests to check for the patient’s renal function as ordered by the physician. Monitor the patient’s response to vasodilators.

34. Nurses responsibilities-ACE inhibitors The initial dose of ACE has a risk of first-dose hypotension, therefore patients should be advised to sit or lie down for 2-4 hours after this.  In patients taking diuretics, close supervision is needed when commencing treatment Advise patients to avoid driving and other hazardous Avoid excess intake of alcohol since this can enhance hypotensive effect. This medication should not be stopped without medical consultation. Advise patients to rise slowly in order to avoid postural hypotension.

35. NURSES RESPONSIBILITIES-ARB s Assess blood pressure and pulse routinely (watch for hypotension…SBP less than 90, especially if the patient is also taking diuretics or other cardiac medications or if they are hypovolemic/dehydrated). Monitor Potassium level Monitor increased liver enzyme - watch in patient at risk for liver failure Monitor for Angioedema (very rare for it to occur with an ARB compared to an ACE Inhibitor)

36. NURSES RESPONSIBILITIES-nitrates Store tablet form in its original container. Sit or lie down upon first indication of oncoming anginal pain. Spit out the rest of the sublingual tablet as soon as pain is completely relieved,  Report blurred vision or dry mouth. Both warrant withdrawal of drug. Change position slowly and avoid prolonged standing. Dizziness, light-headedness, and syncope (due to postural hypotension) occur most frequently in older adults. Do not drink alcohol too soon after taking nitroglycerin. It may cause severe postural hypotension (sharp drop in BP), vertigo, flushing, or pallor if you drink alcohol too soon after taking nitroglycerin. Report any increase in frequency, duration, or severity of anginal attack

37. NURSES RESPONSIBILITIES-calcium channel blockers Monitor BP carefully during titration period. Patient may become severely hypotensive, especially if also taking other drugs known to lower BP. Monitor blood sugar in diabetic patients. Nifedipine has diabetogenic properties. Monitor for gingival hyperplasia and report promptly. Keep a record of nitroglycerin use and promptly report any changes in previous pattern. Occasionally, people develop increased frequency, duration, and severity of angina when they start treatment with this drug or when dosage is increased. Be aware that withdrawal symptoms may occur with abrupt discontinuation of the drug (chest pain, increase in anginal episodes, MI, dysrhythmias). Inspect gums visually every day. Changes in gingivae may be gradual, and bleeding may be exhibited only with probing.

38. Vaso constrictor

39. introduction The  autonomic  nervous system  (ANS)  works to keep the body’s  homeostasis  against internal and external changes in the environment which alter the body’s internal functions (e.g.,  blood  pressure regulation, urinary excretion, water balance, and digestive functions). A  vasoconstrictor , also  vasopressor  or simply  pressor , is any substance that acts to cause vasoconstriction (narrowing of the  lumena  of  blood vessels ) and usually results in an increase of the  blood pressure . The opposite process,  vasodilation , is the opening of blood vessels. Vasoconstrictors are used in medicine to treat  hypotension . Many vasoconstrictors act on specific receptors, such as  vasopressin  receptors or  adrenoreceptors . Vasoconstrictors are also used clinically to increase  blood pressure  or to reduce local blood flow. Exposure to moderately high levels of  stress  also induces vasoconstriction.

40. Meaning- vasoconstrictor Vasoconstrictor drugs are drugs which contract the smooth muscle in blood vessels which causes the vessal to constrict which increases systemic vascular resistance leading to increase in blood pressure.

41. Classification of Vasoconstrictors Based on catechol nucleus Catecholamines eg. Adrenaline, nor adrenaline Non catecholamines eg. Epiderine , amphetamine Based on mode of action Directly acting vasoconstrictor Indirectly acting vasoconstrictor Mixed amines

42. Cont …… Based on clinical classification Vassopressor eg. Nor adrenaline, dopamine Cardiac stimulants eg. Adrenaline CNS stimulants eg.amphetamines Bronchodilators eg. Adrenaline, salbutamol Nasal decongestants eg. Ephedrine Uterine relaxants eg. Terbutaline Appetite suppressants eg. fenfluamine

43. Another classification sympathomimetic   drugs  Non-sympathomimetics

44. sympathomimetic   drugs Adrenergic agonists( sympathomimetic drugs)  are autonomic nervous system drugs that stimulate the adrenergic receptors of the sympathetic nervous system (SNS), either directly (by reacting with receptor sites) or indirectly (by increasing norepinephrine levels). An adrenergic agonist is also called a  sympathomimetic  because it stimulates the effects of SNS. Adrenergic agonists  are further classified into three: alpha- and beta-adrenergic agonists, alpha-specific adrenergic agonists, beta-specific adrenergic agonists .

45. Adrenergic Agonists

46. indications These agents are commonly used for treatment of glaucoma,  asthma , and shock or shock-like conditions. Glaucoma  is an  eye  condition characterized by increased in intraocular pressure. Alpha adrenergic agonists help dilate the pupils, decrease the secretion of aqueous humor, and increase the uveoscleral outflow. This mechanisms relieve the eyes of too much pressure. Shock  is a complication most commonly caused by acute blood loss that can significantly alter the functions of the organs and tissues. The effects of these agents to  cardiovascular system  include pressure increase, vasoconstriction, and increase blood flow to the muscles. Asthma   is a hypersensitivity reaction to specific triggers characterized by inflammatory reactions and bronchospasm.  Beta agonists  are usually used for treatment of bronchospasm and other obstructive respiratory conditions.

47. Alpha- and Beta-Adrenergic Agonists Alpha- and beta- agonists  are drugs that are generally sympathomimetic. These agonists stimulate all of the adrenergic receptors so they affect both alpha- and beta-receptors. Eg.dopamine , dobutamine, and epinephrine.

48. Therapeutic Action The desired and beneficial actions of alpha- and beta-agonists are as follows: Acting on the adrenergic receptors of the target organs, (i.e., increased heart rate and myocardial contractility with the heart, bronchodilation with lungs, decrease intraocular pressure with eyes). Other effects include: sweating, pupil dilation, increase in rate and depth of respirations Facilitating the breakdown of  glucose  stores ( glycogenolysis)  so it can be used as energy.

49. Indications Sympathomimetic of choice for shock is  dopamine , a naturally occurring catecholamine .  Aside from stimulating the heart to increase the rate and force of its contractions, it also causes dilation of the renal and splanchnic arterioles increasing blood flow to the kidneys. This way, renal shutdown is prevented. Dobutamine  and  ephedrine  are synthetic catecholamines indicated for treatment of  heart failure . They increase cardiac contractility without causing increase in oxygen demand. Ephedrine  stimulates release of norepinephrine from nerve endings. Its use is declining because of availability of drugs with more predictable onset and action. Many OTC cold products contain this.

50. Pharmacokinetics

51. Contraindications and Cautions Allergy to any component of the drug.  To prevent hypersensitivity reactions. Pheochromocytoma.  Systemic overload of catecholamines could be fatal. Pulmonary  hypertension .  Exacerbated by the effect of the drug. Tachyarrhythmias and ventricular fibrillation.  Increased heart rate and oxygen consumption caused by drugs can exacerbate these conditions. Hypovolemia .  Fluid replacement is the preferred treatment associated with  hypotension . Halogenated hydrocarbon  general anesthetics .  This sensitizes the myocardium to catecholamines and could cause serious cardiac effects. Peripheral cardiovascular disease.  Caution should be used as this can be exacerbated by systemic vasoconstriction effect of the drug.

52. Adverse Effects Related to sympathetic stimulation: headache, sweating, feelings of tension or  anxiety , piloerection CV: arrhythmias,  hypertension , palpitations,  angina , dyspnea GI:  nausea ,  vomiting ,  constipation Because of vasoconstrictive effects, care must be taken to avoid  extravasation  of any infused drugs. The vasoconstriction in the area of extravasation can lead to necrosis and cell death in that area.

53. Interactions Tricyclic antidepressant (TCA) and monoamine oxidase inhibitors ( MAOI ).  Increased effects of these drugs related to increased norepinephrine levels or increased receptor stimulation that occurs with both drugs. TCAs increase sympathomimetic effects with phenylephrine but decreased antihypertensive effects with clonidine. Ma huang , guarana, caffeine.  Increased risk of hypertension especially with alpha agonists. Propranolol . Paradoxical hypertension with clonidine Any other adrenergic antagonist.  Loss of effectiveness of drugs.

54. Nursing Assessment Assess for contraindications or cautions (e.g. history of allergy, pheochromocytoma, fatal arrhythmias, etc.) to avoid adverse effects. Establish baseline physical assessment to monitor for any potential adverse effects. Assess vital signs, especially pulse and blood pressure to monitor for possible excess stimulation of the cardiac system. Note respiratory rate and auscultate lungs for adventitious sounds to evaluate effects on  bronchi  and respirations. Monitor urine output to evaluate perfusion of the kidneys and therapeutic effects. Monitor laboratory test results (e.g. liver and renal function tests) to determine need for possible dose adjustment, and serum electrolyte levels to evaluate fluid loss and appropriateness of therapy.

55. Nursing intervention Use extreme caution in calculating and preparing doses of these drugs because even small errors could have serious effects. Use proper, aseptic technique when administering ophthalmic or nasal agents (alpha- and beta- adrenergic agonists) to prevent injection and assure the therapeutic effectiveness of the drug. Monitor patient response closely (vital signs, ECG, urine output) to ensure the most benefit with the least amount of toxicity. Maintain  phentolamine  on standby in case extravasation occurs. Save the area by infiltrating 10 mL of saline containing 5-10 mg of phentolamine. Provide comfort measures (e.g. light control, encouragement to void, monitoring bowel functions, support and relaxation measures) to help patient cope with the sympathomimetic effects of the drug. Provide patient education about drug effects and warning signs to report.

56. Alpha-Specific Adrenergic Agonists Alpha-specific adrenergic agonists  or  alpha-agonists  are drugs that bind primarily to alpha-receptors rather than to beta-receptors. eg. clonidine, midodrine, and phenylephrine.

57. Therapeutic Action The desired and beneficial action of alpha-agonists is: Acting as a powerful postsynaptic alpha-adrenergic receptor stimulant causing  vasoconstriction  and  raising systolic and diastolic blood pressure  with little effect on the beta-receptors of the heart.

58. Indications Alpha-agonists are indicated for the following medical conditions: Phenylephrine  is a potent vasoconstrictor and alpha 1 -agonist with little or no effect on the heart or bronchi and is used in many combination cold and allergy products. Parenterally, it is used in the following medical conditions: shock or shock-like states and  paroxysmal supraventricular tachycardia. It is also used to prolong local  anesthesia  and to maintain blood pressure during spinal anesthesia. Topically, it used for treatment of  allergic rhinitis  and symptoms of  otitis media . Midodrine  is an oral drugs used to treat orthostatic  hypotension  in patients who do not respond to traditional therapy. It activates alpha 1 -adrenergic receptors, leading to peripheral vasoconstriction and an increase in vascular tone and blood pressure. Clonidine  specifically stimulates alpha 2 -receptors of the CNS leading to decreased CNS outflow of norepinephrine. Orally and transdermally , it is used to control hypertension and as an injection, it is for epidural infusion for controlling  cancer  pain

59. Pharmacokinetics

60. Contraindications and Cautions Allergy to any component of the drug.  To prevent hypersensitivity reactions. Severe hypertension or tachycardia.  Possible additive effects. Narrow-angle glaucoma.  Can be exacerbated by arterial constriction. Pregnancy and lactation.  No adequate studies on the effects so use is reserved for situations in which the benefit to the mother outweighs any potential risk to the fetus or neonate. CV disease and vasospasm.  Caution is used because these conditions could be aggravate by the vascular effects of the drug Thyrotoxicosis and  diabetes .  Sympathetic stimulation has thyroid-stimulating and glucose-elevating effects Renal or hepatic impairment.  Can interfere with metabolism and excretion of the drug

61. Adverse Effects Use of alpha-agonists may result to these adverse effects: CNS: anxiety, restlessness,  depression ,  fatigue , strange dreams, personality changes Sympathetic stimulation: blurred vision, photosensitivity CV: arrhythmias, ECG changes, blood pressure changes, peripheral vascular problem GI: nausea, vomiting,  anorexia GU: decreased urinary output, difficulty urinating,  dysuria , changes in sexual function Sudden  withdrawal  can lead to: tachycardia, hypertension, arrhythmias, flushing, and even death. Taper drugs over 2-4 days.

62. Interactions The following are drug-drug interactions involved in the use of alpha-agonists: MAOIs: severe hypertension, headache, and hyperpyrexia with phenylephrine TCA: increased sympathomimetic effects with phenylephrine; decreased antihypertensive effects with clonidine Digoxin , beta-blockers,  antipsychotics : increased drug effects with midodrine Adrenergic antagonists: loss of effectiveness of adrenergic agonists

63. Nursing Assessment Assess for contraindications or cautions (e.g., history of allergy, CV diseases, thyrotoxicosis or  diabetes , etc.) to avoid adverse effects. Establish baseline physical assessment to monitor for any potential adverse effects. Assess level of orientation, affect, reflexes, and vision to monitor for CNS changes related to drug therapy. Monitor blood pressure and pulse, assess peripheral perfusion, and obtain electrocardiogram, if indicated, to determine drug effectiveness and evaluate for adverse CV effects. Monitor urine output to evaluate perfusion of the kidneys and therapeutic effects. Evaluate patient for nausea and constipation to assess adverse effects of the drug and establish appropriate interventions. Monitor laboratory test results (e.g., liver and renal function tests) to determine need for possible dose adjustment.

64. Nursing Diagnosis Decreased cardiac output related to blood pressure changes, arrhythmias, or vasoconstriction Disturbed sensory perception related to CNS effects Risk for  injury  related to CNS or CV effects

65. Implementation  Do not discontinue abruptly to prevent rebound hypertension. Monitor blood pressure, orthostatic blood pressure, pulse, rhythm, and cardiac output regularly to adjust dose or discontinue the drug of CV effects are severe. Maintain phentolamine on standby when administering phenylephrne in case extravasation occurs. Save the area by infiltrating 10 mL of saline containing 5-10 mg of phentolamine within 12 hours after extravasation to preserve tissue. Provide comfort measures (e.g., rest and environmental control) to help patient cope with the drug effects. Provide patient education about drug effects and warning signs to report to promote understanding and compliance.

66. Beta-Specific Adrenergic Agonists Beta-specific adrenergic agonists  or  beta-agonists  are drugs that bind primarily to beta-receptors rather than to alpha-receptors. Popular examples of drugs under this class include albuterol, salmeterol, and terbutaline. Therapeutic Action The desired and beneficial action of beta-agonists is: Acting on beta-adrenergic receptors to produce increased heart rate, positive inotropic effect, bronchodilation, and vasodilation.

67. Indications Beta-agonists are indicated for the following medical conditions: Treatment of bronchial spasm,  asthma , and other obstructive pulmonary conditions. Pharmacokinetics

68. Contraindications and Cautions Allergy to any component of the drug.  To prevent hypersensitivity reactions. Pulmonary hypertension.  Can be exacerbated by drug effects Anesthesia with halogenated hydrocarbons.  Can sensitize the myocardium to catecholamines and could cause a severe reaction Eclampsia, uterine  hemorrhage , and intrauterine death.  Can be complicated by uterine relaxation or increased blood pressure Thyrotoxicosis and diabetes.  Sympathetic stimulation has thyroid-stimulating and glucose-elevating effects Severe renal impairment.  Can alter drug excretion

69. Adverse Effects Use of beta-agonists may result to these adverse effects: CNS: anxiety, restlessness, fatigue,  fear , tremor, headache CV: tachycardia, angina,  myocardial infarction , palpitations Respiratory: difficulty of breathing, bronchospasm, severe pulmonary edema GI: nausea, vomiting, anorexia, GI upset Others: sweating, pupil dilation, rash,  muscle  cramps

70. Interactions Other sympathomimetic drugs: increased sympathomimetic effects Beta-blockers: decreased therapeutic effects

71. Nursing Assessment Assess for contraindications or cautions (e.g., history of allergy, uterine hemorrhage, thyrotoxicosis or diabetes, etc.) to avoid adverse effects. Establish baseline physical assessment to monitor for any potential adverse effects. Assess CV status (pulse rate and blood pressure) to evaluate for any CV effects associated with SNS stimulation. Assess respiratory status to monitor drug effects and assess for respiratory adverse effects. Monitor urine output to evaluate perfusion of the kidneys and therapeutic effects. Monitor laboratory test results (e.g., liver and renal function tests) to determine need for possible dose adjustment.

72. Nursing Diagnosis Acute pain  related to CV and systemic effects Decreased cardiac output related to CV effects Ineffective tissue perfusion  related to CV effects

73. interventions Monitor pulse and blood pressure carefully during administration to arrange to discontinue the drug at any sign of toxicity. Ensure that a beta-blocker is readily available when giving parenteral isoproterenol in case severe reaction occurs. Use minimal doses of isoproterenol needed to achieve desired effects to prevent adverse effects and maintain patient safety. Provide comfort measures to help patient cope with the drug effects. Provide patient education about drug effects and warning signs to report to promote understanding and compliance.

74. Nurses responsibilities-vasoconstrictors Monitor constantly while patient is receiving vasoconstrictor. Adjust flow rate to maintain blood pressure at low normal. Observe carefully and record mental status. Monitor intake and output chart. Be alert to patient complaints of headache ,vomiting, palpitation, arrhythmias, chest pain. Continue to monitor vital signs.

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