This document discusses vasodilators and vasoconstrictors. It begins by defining vasodilators as drugs that dilate blood vessels, allowing blood to flow more easily. It then classifies vasodilators based on their site of action (arterial, venous, or mixed) and mechanism (direct or indirect acting). Examples of different classes of vasodilators are provided, along with their mechanisms, uses, administration routes, side effects, and monitoring considerations. The document provides a comprehensive overview of vasodilator drugs.

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. Hydralazine, 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 α1 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.

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

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

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

21. 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).

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

23. 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

24. 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.

25. 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.

26. 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.

27. 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.

28. 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.

29. 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.

30. 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.

31. 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

32. 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

33. 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

34. 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.

35. 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.

36. NURSES RESPONSIBILITIES-ARBs
 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)

37. 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

38. 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.

39. Vaso constrictor

40. 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.

41. 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.

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

43. Cont……
Based on clinical classification
1. Vassopressor eg. Nor adrenaline, dopamine
2. Cardiac stimulants eg. Adrenaline
3. CNS stimulants eg.amphetamines
4. Bronchodilators eg. Adrenaline, salbutamol
5. Nasal decongestants eg. Ephedrine
6. Uterine relaxants eg. Terbutaline
7. Appetite suppressants eg. fenfluamine

44. Another classification
 sympathomimetic drugs
 Non-sympathomimetics

45. 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.

46. Adrenergic Agonists

47. 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.

48. 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.

49. 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.

50. 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.

51. Pharmacokinetics

52. 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.

53. 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.

54. 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.

55. 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.

56. 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.

57. 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.

58. 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.

59. Indications
Alpha-agonists are indicated for the following medical conditions:
 Phenylephrine is a potent vasoconstrictor and alpha1-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 alpha1-adrenergic receptors, leading
to peripheral vasoconstriction and an increase in vascular tone and blood pressure.
 Clonidine specifically stimulates alpha2-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

60. Pharmacokinetics

61. 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

62. 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.

63. 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

64. 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.

65. 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

66. 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.

67. 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.

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

69. 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

70. 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

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

72. 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.

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

74. 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.

75. 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.

76. thakyou