DRUGS USED IN CARDIOVASCULAR SYSTEM

Cardiac Glycosides (Digitalis)

DIGOXIN
❖ Digoxin is a medication used to help the heart pump more efficiently, and it is used for
many cardiac conditions specially heart failure.

❖ It’s part of the cardiac glycoside family.

• This family of drugs helps the heart pump more efficiently by affecting thesodium-
potassium pump in the cell membrane of the heart’s muscle fiber cells.

• This medication inhibits the normal function of the pump, which alters thestrength of
how the heart contracts.

• In addition, this drug alters how fast (rate) the heart contracts and the speed of
how electrical impulses are sent through the heart’s electrical conduction
system.
❖ So, in other words, this drug will alter the following actions in the heart:

• Inotropic action: strength of contractions

• Chronotropic action: rate the heart beats

• Dromotropic action: speed of how electrical impulses are sent through the heart

How does Digoxin affect these actions? In either a positive or negative way! (Hint:
remember this)

• Positive inotropic action causes the heart muscle to squeeze or contract

stronger

• Negative chronotropic action causes the heart to beat slower

• Negative dromotropic action slows down the impulses sent through the AV node

❖ When you combine these actions together it will create: a heart that squeezes blood
out more efficiently (hence, less back flowing of blood). This will increase stroke volume
(the amount of blood leaving the ventricle with each beat), which will increase cardiac
output (the amount of blood pumped by the heart each minute). When cardiac output
is increased, tissue perfusion also increases. So, more blood will reach vital tissues and
organs.
❖ Uses: Heart failure, cardiogenic shock, atrial fibrillation, atrial flutter
• In these conditions, there are issues with how the heart is pumping and emptying.

• This is either from failure of muscle fibers to contract (ex: heart failure or cardiogenic
shock) or the electrical contraction system is discharging electrical impulses too fast,
and this will affect how the heart pumps out blood (ex: atrial fibrillation or atrial flutter).

❖ Responsibilities of Nurse:
The nurse should be aware of how the drug works, why it is ordered, nursing
implications, signs, and symptoms of toxicity, and how to teach the patient how to take
the medication.

➢ Monitor for Digoxin Toxicity

 Therapeutic range: 0.5-2 ng/mL (greater than 2 ng/mL is toxic)

 Signs and Symptoms
• EARLY signs and symptoms are GI related (Nausea, vomiting, anorexia)

• Other signs and symptoms: vision changes with reports of yellow-greenish

vision or halos, blurred vision, and EKG changes…. (dysrhythmias)…tends to
be later.

 If you’re given a scenario and the patient is experiencing toxicity, what do you
do?
• Hold further doses and notify MD
• Be familiar with the antidote for Digoxin, which is Digibind.
 What are major causes of toxicity? ELECTROLYTE imbalances!
• Hypokalemia (low potassium level): <3.5 mEq/L

Note: Some patients will also be on diuretics that waste potassium (ex: loopdiuretics
like Furosemide) …must monitor potassium levels closely and the patient needs a
diet rich in potassium to maintain K+ levels (see more in theeducation section below).
• Hypercalcemia (high calcium level): >10.2 mg/dL
• Hypomagnesemia (low magnesium level): <1.5 mg/dL

 Who is at MOST risk for developing Digoxin Toxicity?

The elderly patient is due to a decreased in function of the renal and liver
systems. These are the main sites where the drug is removed. In addition, patients
who take calcium channel blockers CCBs) are at risk for digoxin toxicity too
(digoxin levels should be monitored regularly).

 Assess apical pulse for one full minute BEFORE administration of every
dose (Hint: remember the heart rate parameters)

HOLD Digoxin if HR
• Less than 60 bpm in ADULTS
• less than 70 bpm in CHILD
• less than 90-110 bpm in INFANTS
 Side effects:
Other side effects from the ones noted above: fatigue, headache, diarrhea,
thrombocytopenia
 Education for the patient:

• Teach patient about signs and symptoms of toxicity

• Importance of keeping appointments to have drug level, electrolytes, and
liver/renal function levels drawn.
• Consuming foods rich in potassium, if also taking drugs that waste
potassium(potatoes, pork, oranges, tomatoes, avocados, spinach, bananas).
• How to measure heart rate before taking the medication and when to call the MD.
Anticoagulants
 HEPARIN
❖ Family Name: Indirect thrombin inhibitors
• Enhances the activity of antithrombin III, which will inhibit thrombin and the
conversion of fibrinogen to fibrin.
• Work on intrinsic pathway of coagulation: this pathway is normally activated by
internal vascular trauma.

HEPARIN

Activates plasma Anti-Thrombin III

Heparin-AT III complex

Binds to clotting factors of intrinsic and common pathways

(Xa, IIa, IXa, Xia, XIIa and XIIIa) and inactivates them.
❖ Onset: Fast

❖ Duration: Short…stays in the system for hours

❖ Route of Administration:
• Injection (subcutaneous): administer 2 inches away from belly button, 1 inch
away from scars, rotate injection sites, Do NOT massage, or rub area
• Intravenous: if on a continuous IV drip, the patient will be on a Heparin drip
protocol, which will have very specific guidelines on how to titrate the drip to keep
the patient’s clotting levels therapeutic.
❖ Heparin Calculation:
It’s weight-based (always obtain a current and accurate weight for proper dosing).
❖ Monitor aPTT (activated partial thromboplastin time):
• Normal aPTT: 30-40 seconds

• Therapeutic level for patients on Heparin: 1.5 – 2.5 times the normal range
(about 60-80 seconds)
• Less than 60 seconds: NOT therapeutic…may need an increase in rate
and/or a bolus(depends on the Heparin protocol in place)
• Greater than 80 seconds: at risk for bleeding…decrease rate and may need
to turn offdrip for a period (again depends on the Heparin protocol in place)

❖ Antidote: protamine sulfate

❖ Used for the short term
❖ Can be used during pregnancy
❖ Watch for:
 Heparin-Induced Thrombocytopenia:
• HIT: occurs when antibodies develop against Heparin and platelet factor 4
complex.
• There will be a drop in platelets and new clots or worsening of current clots
can occur.
 Osteoporosis
• Occurs with long term/high doses of Heparin…. because Heparin increases
osteoclast activity and decreases osteoblast activity. Fall precaution is
important.
 Warfarin
❖ Family Name: Vitamin K antagonist

❖ Mechanism of Action
• Vitamin K helps make clotting factors in the liver.

• Since it’s a Vitamin K antagonist, it will work to inhibit clotting factors from using
Vitamin K.
• Works on extrinsic pathway of coagulation: this pathway is normally activated by
external trauma.

❖ Onset: Slow (takes about 3-5 days for patient to become therapeutic)

❖ Duration: Long…stays in the system for days

❖ Route of Administration:
• Orally via a pill: Give at SAME time every day.
• Missed dose?

o Take when remembered if SAME day

o If remembered next day, skip the forgotten dose, and take the regular
scheduled dose.

o Be sure to make a note of the missed dose and let MD know.

❖ Monitor PT/INR (prothrombin time/international normalized ratio)
• The INR is calculated from the PT.
• Normal INR: 0.75-1.25 in a patient who is NOT taking Warfarin
• Therapeutic INR level for patients on Warfarin: 2-3
• INR too low: not therapeutic…needs dose increased
• INR too high: at risk for bleeding…needs dose decreased

❖ Antidote: Vitamin K

❖ Used for the long term.

❖ Can NOT be used during pregnancy.

❖ Discourage foods high in vitamin K because they can decrease the INR level. This is
mainly green leafy vegetables. Example: spinach, kale, broccoli, etc.
❖ NO alcoholic beverage because this interferes with Warfarin.

❖ Warfarin and Heparin both are anticoagulants. They slow down the clotting process
but Do NOT break up an existing clot. A patient can be on both medications at the
same time until the patient’s INR level becomes therapeutic…. then the Heparin will
be discontinued.

❖ Education for both Heparin and Warfarin:

• No aspirin, NSAIDS or over-the-counter health supplements due to the risk of
bleeding…always speak with MD before taking any new medications.
• Signs and symptoms of bleeding: bleeding gums, blood in stool (dark/tarry), blood
in urine (red/pink urine), coffee ground emesis etc.
• No contact sports, use electric razors and soft bristle toothbrushes.
• No IM injections
 Antiplatelet Medications
❖ Description: Antiplatelet medications inhibit the aggregation of platelets in the
clotting process, thereby prolonging the bleeding time. Antiplatelet medications may
be used with anticoagulants.
❖ Uses: Used in the prophylaxis of long-term complications following myocardial
infarction, coronary revascularization, stents, and stroke. These medications are
contraindicated in those with bleeding disorders and known sensitivity.
❖ Side and adverse effects

• Bruising

• Hematuria

• Gastrointestinal bleeding

• Tarry stools

❖ Interventions

• Determine sensitivity before administration.

• Monitor vital signs.

• Instruct the client to take medication with food if gastrointestinal upset occurs.

• Monitor bleeding time.

• Instruct the client to monitor for side and adverse effects and in the measures to
prevent bleeding.

Thrombolytic Medications
(Alteplase, Tenecteplase)
❖ Mechanism of Action:
Thrombolytic medications activate plasminogen; plasminogen generates plasmin (the
enzyme that dissolves clots). Thrombolytic medications are used early during
myocardial infarction (within 4 to 6 hours of the onset of the infarct) to restore blood
flow, limit myocardial damage, preserve left ventricular function, and prevent death.

❖ Uses: Thrombolytics are also used in arterial thrombosis, deep vein thrombosis,
occluded shunts or catheters, and pulmonary emboli.

❖ Side and adverse effects

• Bleeding

• Dysrhythmias

• Allergic reactions
❖ Contraindications
• Active internal bleeding

• History of hemorrhagic stroke

• Intracranial problems, including trauma

• Intracranial or intraspinal surgery within the previous 2 months

• History of thoracic, pelvic, or abdominal surgery in the previous 10 days

• History of hepatic or renal disease

• Uncontrolled hypertension

• Recently required, prolonged cardiopulmonary resuscitation

• Known allergy to the specific product or any of its preservatives

❖ Interventions
• Determine aPTT, PT, fibrinogen level, hematocrit, and platelet count.

• Monitor vital signs.

• Assess pulses.

• Monitor for bleeding and check all excretions for occult blood.

• Monitor for neurological changes such as slurred speech, lethargy,

confusion, and hemiparesis.

• Monitor for hypotension and tachycardia.

• Avoid injections and unnecessary venipunctures if possible.

• Apply direct pressure over a puncture site for 20 to 30 minutes.

• Handle the client as little as possible when moving.

• Instruct the client to use an electric razor for shaving and to brush teeth gently.

• Withhold the medication if bleeding develops.

ANTI-HYPERTENSIVE DRUGS
DIURETICS
 Loop Diuretics
❖ Loop: These medications work on the Loop of Henle in the nephron (specifically the
thick ascending limb).

❖ Diuretic: the goal is to increase urinary output by limiting how parts of the nephron
reabsorb sodium. Hence, if we don’t reabsorb much sodium back into the blood, it will
stay in the filtrate within the nephron, and this will keep more water in the filtrate
too…hence increasing urine production.

❖ Loops diuretics are the most powerful of all the types of diuretics when compared to
thiazides and potassium-sparing diuretics.

❖ Loop diuretic generic medication names end with NIDE or MIDE.

❖ Examples: Bumetanide, Furosemide, Torsemide except for Ethacrynic acid

❖ How these drugs work? They inhibit the Na-K-Cl (NKCC2) cotransporter protein
found in the thick ascending limb of the loop of Henle from transporting sodium,
potassium, and chloride into the cell for reabsorption. Therefore, by inhibiting this
transporter, it will prevent these ions (also called electrolytes) from being
reabsorbed into the blood.

❖ Uses:
Most of the time loop diuretics are ordered when a patient is experiencing fluid volume
overload in conditions like:
• Heart failure
• Liver impairment (ascites is present)
• Pulmonary edema
• Hypertension (not as effective as thiazides though)
• High calcium levels (hypercalcemia)
❖ Responsibilities of Nurse
• Patient will be losing fluid in the form of urine: watch for signs of dehydration
(removingtoo much fluid)

• Vitals (elevated heart rate and low blood pressure SBP <90)

• Monitor closely the patient’s intake and output: always strictly measure urine output
by having men urinate in a urinal and women to urinate in a toilet hat (some patients
may have a catheter).

• Daily weights (this is the best indicator of how much fluid the patient is losing). Weigh
the patient at the same time every day with the same scale.
❖ Monitor Labs:
• Assess for electrolytes imbalances and renal function. Most hospitalized patients
will have a daily BMP drawn.

• Monitor for electrolytes.

o Hypokalemia (normal level is 3.5-5 mEq/L): Many patients will experience low
potassium levels and will need potassium supplements while taking a loop
diuretic. Always check the potassium result before giving the next
dose…especially if the patient is taking Digoxin because hypokalemia
increases Digoxin Toxicity.

o Hypocalcemia

o Hyponatremia: If the patient is taking Lithium, monitor for Lithium toxicity

because low sodium levels in the blood can increase Lithium toxicity. A
normal Lithium level is 0.5-1.2 mmol/L.

o Hypomagnesemia
• Monitor for signs of gout due to high uric acid that can occur with this medication.

• Administer IV route very slowly (most used is Furosemide) due to the risk of
causing ototoxicity (damage to inner ear).

• Provide easy access to the bathroom (prevent falls) and avoid giving a dose right
before bedtime (these interrupts sleep and increases the risk of falling).

• Assess the effectiveness of the medication: decrease in edema, clearer lung fields,
decrease weight etc.

❖ Side effects
Hypokalemia, hypocalcemia, hypotension, increase urination, hyperuricemia,
hyponatremia, hypomagnesemia, ototoxicity

❖ Education

• Teach to be aware of signs and symptoms of dehydration (excessive thirst, fatigue,

no urination, hypotension), and how to measure blood pressure and heart rate at
home.
• Consuming a healthy diet that includes foods with potassium because this
medication can lower potassium levels.
• Changing positions slowly due to orthostatic hypotension that can occur because
of the change of fluid volume in the body.
• Monitoring weight daily (most patients taking a loop diuretic have heart failure so it
is important they measure their weight daily and contact their doctor if they gain 3
lbs. or more in 1 day…this could mean they are retaining fluid).
 Thiazides Diuretics
❖ Thiazides are not as powerful as loop diuretics, but get the job done for
providing diuresis effects.

❖ Example of thiazide diuretics: unfortunately, you can’t go by the ending of the

generic name like with other medications…but some do end with “thiazide”
• Hydrochlorothiazide (HCTZ)
• Indapamide
• Chlorothiazide
• Metolazone
• Chlorthalidone

❖ Uses
• Hypertension (usually prescribed first-line for primary hypertension…it helps
decrease sodium and water levels in the blood)

• Heart failure (sometimes used with antihypertensive like ACE Inhibitors)

• Renal calculi formed from calcium

❖ Responsibilities of Nurse
• Patient will be losing fluid in the form of urine: watch for signs of dehydration
(removing too much fluid)
• Vital Signs (elevated heart rate and low blood pressure SBP <90)
• Monitor closely the patient’s intake and output.
• Daily weight (this is the best indicator of how much fluid the patient is losing).
Weigh at the same time every day with the same scale.

❖ Monitor labs:
• Assess for electrolytes imbalances and renal function (BUN and creatinine).
Most hospitalized patients will have daily BMP drawn.
• Monitor:
o Hypokalemia (Normal level is 3.5-5 mEq/L): If patient is taking Digoxin, watch out for
Digoxin toxicity because a low potassium level can increase this… (normalDigoxin level:
0.5-2 ng/mL)
o Hyponatremia (normal level is 135-145 mEq/L): If patient is taking Lithium, watch
out for Lithium toxicity because low sodium levels in the blood can increase
this….(Normal Lithium level: 0.5-1.2 mmol/L)
o Hypercalcemia: Digoxin Toxicity
o Metabolic alkalosis
• Monitor for signs of gout due to high uric acid levels in the blood.
• Monitor glucose levels closely in diabetic patients for hyperglycemia…may
need a change insulin or oral diabetic medications as deemed by the
physician.
• Provide easy access to the bathroom (prevent falls) and avoid giving a dose right
before bedtime (these interrupts sleep and increases the risk of falling).
• Assess the effectiveness of the medication: decrease in edema, clearer lung
fields,decrease weight etc.

❖ Side effects
Electrolyte imbalances: hyponatremia, hypokalemia…. hypercalcemia,
hyperglycemia, hyperuricemia, metabolic alkalosis, dehydration, orthostatic
hypotension,

❖ Education
• Teach to be aware of signs and symptoms of dehydration (excessive thirst,
fatigue, no urination, hypotension), and how to monitor blood pressure and heart rate
at home.

• Consuming a healthy diet that includes foods that are high in potassium because
this medication can lower potassium levels.

• Changing positions slowly due to orthostatic hypotension that can occur

because of the change of fluid volume in the body.

• Monitoring weights daily.

• If diabetic, teach patient to monitor for hyperglycemia because this medication can
increase the blood glucose level.
 Potassium--Sparing Diuretics:
These medications don’t cause HYPOkalemia (like the other diuretics we’ve
discussed,such a loop diuretics and thiazide diuretics)

❖ They work on the distal parts of the nephron, specifically the last part of the distal
tubule and collecting duct. This is where they alter the sodium and potassium
exchange within the nephron.

❖ ***Potassium-sparing diuretics are relatively weak in their diuretic effects when

compared to the other families of diuretics. This is because of their limited effect on
how they alter sodium reabsorption. This why they are sometime prescribed with loop
or thiazide diuretics because by combining these diuretics it can help prevent
hypokalemia. Remember hypokalemia commonly occurs with loop and thiazide
diuretics.

❖ Uses
• Hypertension

• Edema/swelling due to heart failure, liver impairment, or nephrotic syndrome

• Hypokalemia because of diuretics that waste potassium
• Hyperaldosteronism (primary aldosteronism or Conn’s Syndrome) …mainly
Spironolactone
o This condition occurs when high amounts of aldosterone are produced by the
adrenal glands. This causes the body to keep sodium and lose potassium.
So, the patient will have hypokalemia and high blood pressure.
o Spironolactone will decrease the amount of aldosterone and help alleviate
signs and symptoms of this condition.
❖ Responsibilities as the Nurse:
• Patients will be losing fluid in the form of urine: watch for signs of dehydration
(removingtoo much fluid) and electrolyte imbalances (keeping too much potassium
in the blood)

• Vitals (elevated heart rate and low blood pressure SBP <90)

• Monitor closely the patient’s intake and output (especially urinary output…avoid in
patients with renal failure)
❖ Monitor Labs:
• Hyperkalemia: normal potassium is 3.5-5 mEq/L…watch levels >5 mEq/L

o Signs and symptoms of high potassium level: EKG changes tall, peaked T
waves, muscle weakness/cramps, difficulty breathing, nausea, vomiting,
diarrhea, mental status change, paresthesia etc.
o AVOID foods high in potassium or salt-substitutes (they contain potassium)
• Renal function: BUN and creatinine (contraindicated in patient with renal failure)
❖ Administer with a meal or right after to decrease GI side effects.

❖ Monitor CLOSELY if patient is taking:

• ACE Inhibitors, ARBs, or NSAIDs: these medications can increase
potassium levels…need to closely monitor potassium level.
• Lithium: potassium-sparing diuretics alter the way the nephron works so they can
reduce how well Lithium is cleared from the body, which can lead to lithium
toxicity. Normal Lithium level is 0.5-1.2 mmol/L
❖ Side effects
• Hyperkalemia, upset stomach

• Spironolactone: anti-androgen effects (gynecomastia, menstrual irregulars,

sexual dysfunction) …this is because spironolactone affects androgen and
progesterone receptors.

❖ Education Pieces for the Patient:

• Teach patient to be aware of signs and symptoms of dehydration (excessive thirst,
fatigue, no urination, hypotension), and hyperkalemia (nausea, vomiting, diarrhea,
muscle cramps/weakness, or tingling or paresthesia).
• Limiting foods high in potassium and avoid salt-substitutes:
o Potatoes (pork)
o Oranges
o Tomatoes
o Avocados
o Strawberries
o Spinach
o fIsh
o mUshrooms
o Musk Melons: cantaloupe
 Beta Blockers
❖ Beta blockers block the BETA receptors sites in the body so norepinephrine and
epinephrine can NOT bind to the receptor site and cannot elicit a sympathetic nervous
system response.

❖ Sympathetic nervous system: it’s the “fight or flight system” ….it works to save your
life from danger.

❖ When BETA receptors sites are stimulated by the SNS and have norepinephrine
and epinephrine bind to them, the person can experience (note these are just some
of the responses created by the sympathetic nervous system):

• Increase heart rate and blood pressure

This increases cardiac output and the workload on the heart, but it requires a lot of
oxygen demand by the myocardium.
• Increase strength of heart contractions
This helps to increase cardiac output.
• Bronchodilation
The bronchioles will dilate so breathing can be easier, and more oxygen can enter
the blood. Remember this oxygen is needed because the myocardium demands it
for this type of nervous system response.
• Increase blood sugar for energy via glycogenolysis in the liver.
Beta blockers will block many of these actions, and this can be helpful in certain
conditions when the workload of the heart needs to be decreased or the heart is
beatingtoo fast (dysrhythmias).
❖ It’s very important to know that there are different types of BETA RECEPTORS in the
body…. beta 1, beta 2, and beta 3.

• Beta 1 receptors are mainly located in the HEART and in the KIDNEYS (specifically
the juxtaglomerular cells that release renin).

• Beta 2 receptors are in the bronchioles of the LUNGS, GI system, vascular

smooth muscle and skeletal muscle, and ciliary body of the eye.

• Beta 3 receptors are in the fatty/adipose tissue of the body.

❖ Types of Beta Blockers

All generic beta blockers names end in “LOL”.

 Selective beta blockers are selective to only beta 1 receptors. Atenolol, Esmolol,
Metoprolol etc.
These medications are sometimes referred to as cardio selective because they
mainly target the heart since it’s mainly made up of beta 1 receptors.
 Nonselective beta blockers block BOTH beta 1 and beta 2 receptors. Propranolol,
Sotalol, Timolol etc.
They’re not selective to one certain type of beta receptor. Therefore, they will target the
heart and kidneys too, but will also target the GI system, LUNGS, vascular smooth
muscle etc. These medications have more of a peripheral effect than the selective beta
blockers.
 ***It’s important to remember what patient populations cannot take the nonselective
betablockers and side effects they may cause for exams. ***
❖ Mechanism of Action of Beta Blockers (how they affect the body)

 Slow heart rate (both selective and nonselective)

• Beta receptors (mainly beta 1) are in the cardiac nodal tissue and conduction
system of the heart. These areas control our heart rate. Beta blockers slow down
how they work, so they’re helpful with dysrhythmias like supraventricular tachycardia.

• Monitor for AV blocks like 2 or 3 degree and severe bradycardia(contraindicated)

• Mask tachycardia during hypoglycemic episodes in diabetics because these

medications keep the heart rate from increasing (remember they slow down the heart
rate).

 Decrease the strength of contractions (both selective and

nonselective)

• Beta receptors (mainly beta 1) are in the cardiac myocytes that control the strength
of the heart’s contractions. Beta blockers cause a negative inotropic effect
because they make the contractions weaker. This helps ease the workload on the
heart and decrease oxygen consumption by the myocardium (great for treating
stable angina due to coronary artery disease).
• Watch for the development or worsening of heart failure…not to be used in patient
with uncompensated heart failure or cardiogenic shock.
 Lowers blood pressure (both selective and nonselective)

• Beta receptors (mainly beta 1) are in the juxtaglomerular cells of the kidneys.
Beta blockers will prevent angiotensin II from being created in the RAAS
because it inhibits the release of RENIN by the juxtaglomerular cells.
Remember angiotensin II normally causes vasoconstrictor, but there will be
vasodilation instead and the influence of aldosterone will be decreased (so
less water is reabsorbed by the kidneys), and this will decrease blood volume and
in turn decrease the blood pressure.
• Watch for hypotension.
 Decrease intraocular pressure (only nonselective)

The ciliary body of eye has beta 2 receptors. The ciliary body of the eye is
responsible for the production of aqueous humor. In patients with glaucoma, the high
eye pressure is high due to a high amount of aqueous humor collecting in the eye.
Nonselective beta blockers (example eye drops like Timolol) will decrease the
production of aqueous humor and help decrease intraocular pressure.
 Bronchoconstriction (only nonselective)

Nonselective affect beta 2 receptors which are found in the bronchioles of the lungs.
These medications should NOT be used in patients with asthma or COPD due to the
risk of bronchoconstriction.

 Hypo/hyperglycemia (only nonselective)

Educate the diabetic patient to monitor glucose closely.

 Peripheral vasoconstriction (only nonselective)

Avoid in patients with peripheral vascular disease. These medications may cause
cold feet and hands and erectile dysfunction.

❖ Uses
Hypertension, stable angina (CAD), dysrhythmias (example SVT), compensated
heart failure, migraines, glaucoma (example: Timolol), tremors, anxiety

❖ Side Effects, Responsibilities, Education:“Beta Block”

• Bradycardia and blocks….2- or 3-degree heart blocks. Monitor EKG and teach
patient to monitor heart rate at home for bradycardia
• Exacerbate heart failure due to negative inotropic effect. Monitor for pulmonary
edema, swelling in extremities, jugular venous distention, weight gain, I and O’s, daily
weights…TEACH patient to monitor self at home
• Taper off (beta blockers are typically tapered off over 2 weeks or so) … TEACH
patient to NEVER just stop taking because the body will have withdrawal issues
like rebound hypertension, ischemia that leads to angina etc.

• Asthma & COPD patients can’t have nonselective beta blockers

due to bronchoconstriction… Propranolol, Sotalol, Timolol etc.

• Blood glucose monitored closely in diabetes (TEACH). They need to

monitor for hypo/hyperglycemic AND the masking of hypoglycemia due to
NO TACHYcardia experienced with blood glucose drops.

• Low blood pressure (hypotension)…TEACH patient to monitor blood pressure at

home.

• Orthostatic hypotension: monitor and teach…. slowly changes positions when

going from a sitting to lying position to standing.

• Circulation impaired due to peripheral vasoconstriction (NONselective). Peripheral

circulation is circulation to the vessel to the hands, legs, feet, and arms.

• Erectile dysfunction, cold feet and hands, leg cramps…NOT for patient with
peripheral vascular disease.

• Know overdose signs and symptoms: Bradycardia, heart blocks, low blood pressure,
mental status changes: very lethargic or fainting, difficulty breathing due to
bronchospasm, heart block… TEACH patient to monitor for these as well.
 CALCIUM CHANNEL BLOCKERS

❖ Calcium channel blockers work to block L-Type the calcium channels in the:
• Vascular smooth muscle cells: coronary arteries and peripheral arteries
• Cardiac myocytes: cells that control the strength of the heart’s contractions
• Cardiac nodal tissue: cells that are responsible for the electrical conductionof the
heart (specifically the cells in the SA and AV nodes)

❖ What’s the big deal about blocking calcium channels?

Calcium plays a HUGE role in cell contraction. Therefore, if cell contraction can be
decreased or inhibited it will cause cell relaxation. In some cases, such as
hypertension, angina, and certain types ofdysrhythmias, it’s advantageous for the cell
to relax rather than contract.
This will cause:

• Vasodilation: When peripheral arteries relax (hence vasodilate) this will decrease
arterial blood pressure.

o This leads to a decrease in systemic vascular resistance (SVR) which

decreases cardiac afterload:

Remember cardiac afterload is the amount of resistance the left ventricle must
overcome to pump out blood. If we decrease that resistance (hence the SVR), it
will ease the workload on the heart and decrease the oxygen consumption by
the myocardium.

• Dilation of coronary arteries: the cardiac muscle will benefit from this because it
will allow more blood to flow (hence oxygen) to the cardiac muscle. In addition, the
dilation can help prevent a spasm of the coronary arteries because their relaxed.
❖ Actions of CCB:
• If calcium channels are blocked in the SA (sinoatrial) node, this will DECREASE
the heart rate (remember the SA node is the pacemaker). This produces a
negative chronotropic effect.

• If calcium channels are blocked in the AV (atrioventricular) node, it will

DECREASE the speed of conduction of the electrical impulses (remember
the AV node is the gatekeeper and relays the electrical impulses by slowing down
the impulse it received from the SA node). This produces a negative
dromotropic effect.
Therefore, some CCBs are great at treating dysrhythmias like supraventricular
tachycardia and atrial fibrillation. These dysrhythmias result in a fast, abnormal
heartbeat that usually starts in the AV node.
❖ Types of Calcium Channel Blockers

➢ Dihydropyridines: end with “pine” (Amlodipine, Felodipine, Nifedipine)

• More vascular smooth muscle selective
• Mainly for hypertension and angina

➢ Non-dihydropyridines: more myocardium selective (Phenylalkylamines:

Verapamil, Benzothiazepines: Diltiazem)
• Antiarrhythmic (helpful with supraventricular tachycardia and atrialfibrillation),
hypertension, angina)
❖ Uses
• Hypertension,
• Angina (especially variant angina “prinzmetal angina”. Prinzmetal angina are chest
pain that occurs at rest due to a vasospasm of the coronary arteries. CCBs will
keep them relaxed)
• Supraventricular tachycardia
• A-fib
• Raynaud’s disease(decreased circulation issues)
• Spasms of vessels (cerebral)
• Migraines, etc.

❖ Responsibilities as the Nurse, Side effects, and Patient Education:

• Monitor vital signs, especially heart rate (bradycardia) and blood pressure
(hypotension). Teach patient how to do this as well and to record it and report to
the doctor if heart rate or blood is too low.
• Risk for reflex tachycardia due to hypotension (this occurs when the blood
pressure drops, and the heart rate increases to compensate for the decrease in
blood pressure).
• Teach about orthostatic hypotension and that the patient needs to change
positions slowly (this helps when there is a decrease in blood pressure when
going from a sitting or lying position to a standing position). Teach: Go SLOW

• Monitor EKG closely for arrhythmias: 1st degree AV block is a side effect due
to the decrease in the speed of conduction by the AV node.

• These medications are contraindicated in patients with 2 or 3rd degree heart block.
• Monitor for signs and symptoms of heart failure…WHY? Remember these
medications (especially the non-dihydropyridines) alter how the heart pumps
(creates a negative inotropic effect) and this weakens the heart’s
contractions. Signs and symptoms of heart failure: crackles, edema, dyspnea,
weightgain…monitor intake and output, daily weights, lung sounds etc.
• Teach patient to avoid taking CCBs with grapefruit juice….it will increase the
drug level of the calcium channel blocker.
• Encourage a high fiber diet due to constipation with Verapamil or Diltiazem
(these medications can slow down GI motility).
• Watch out for gingival hyperplasia: enlargement of gums…. teach patient about
good oral hygiene and regular dental visits (mainly with dihydropyridines ex:
amlodipine)
• Taking Digoxin too? Digoxin levels must be monitored because CCBs can
increase digoxin levels. Watch out for Digoxin toxicity…. signs and symptoms
include (teach these signs and symptoms to the patient too).
 ANGIOTENSIN II RECEPTOR BLOCKERS VS. ACE INHIBITORS
To help you from confusing these medications, remember this about the generic name:

❖ ACE Inhibitors will end with “pril” …example: Lisinopril, Benazepril, Captopril,
Fosinopril, Enalapril, Lisinopril, Moexipril, Perindopril, Quinapril, Ramipril

❖ ARBs will end with “sartan” …example: Losartan, Candesartan, Eprosartan, Irbesartan,
Losartan, Olmesartan, Telmisartan

❖ Both mediations affect the renin-angiotensin-aldosterone system (RAAS) BUT in

DIFFERENT ways. However, they both achieve the SAME results.

❖ What is RAAS? This system manages the blood pressure, especially when it drops
too low.
Here is a quick review on how the renin-angiotensin-aldosterone system works:

Blood pressure drops => Kidney releases Renin => this activates Angiotensinogen in the
Liver => it turns into Angiotensin I => ACE (angiotensin=converting enzyme) converts it to
=> Angiotensin II => this active vasoconstrictor will act on receptors, specifically
Angiotensin II receptor Type I => constrict vessels and triggers the adrenal cortex to
release aldosterone to help increase blood volume (kidneys will keep sodium and water
but excrete potassium.
❖ How do these medications work to affect RAAS?
Both medications target Angiotensin II so it won’t be able to act as a
vasoconstrictor, but in different ways.

• ACE Inhibitors inhibit ACE from converting angiotensin I to angiotensin II….so no

angiotensin II.

• Angiotensin II receptor blockers (ARBs) inactivate the receptors that readily

accept angiotensin II called Angiotensin II Receptors Type 1….so angiotensin II
can’t bind to it receptors to do its job.

❖ What effects do these medication cause?

They both will lead to vasodilation of vessels, which will decrease the systemic
vascular resistance and blood pressure. In addition, it will decrease the release
of aldosterone, which will cause the kidneys to excrete sodium and water but
keep potassium…. watch for hyperkalemia with these medications.
❖ Uses
They both treat the same conditions as:
• Hypertension
• Heart failure
• Post myocardial infarction
• Diabetic Nephropathy in Type 2 Diabetics (helps slow down the progression of the
disease): these medications will decrease the blood pressure, which will help
decrease the amount of protein in the urine…hence slowing down the progression
of renal disease associated to diabetes.
❖ Side Effects
• One of the main concepts we need to take away from these two medications is
that ACE Inhibitors can cause a dry, nagging cough in SOME patients along
with angioedema (this is deep swelling of the tissues and is a medical
emergency).
• These side effects are less likely with ARBs. In fact, some patients who do
experience the cough while taking an ACE Inhibitor may be switched to an ARB
to help alleviate it.

 WHY a cough with ACE Inhibitors and not ARBs?

ACE is a substance that not only converts Angiotensin I to Angiotensin II, but it
breakdowns and inactivates an inflammatory substance called bradykinin.
However, if ACE is inhibited it can’t do this and bradykinin will increase and it can
lead to a dry, nagging cough in SOME patients.This doesn’t occur with ARBs because
ACE will not be inhibited.
❖ Nursing Considerations and Patient Education
• Monitor potassium levels for hyperkalemia (normal potassium is 3.5-5 mEq/L).
Educate to avoid salt substitutes with potassium and eating an excessive intake of
foods high in potassium like potatoes, avocadoes, bananas etc.
• Monitor renal function (elevated BUN and Creatinine, less than 30 cc/hr
urinaryoutput, swelling). Patients who are at risk for renal failure are those who
are dependent on the RAAS to maintain cardiac output….example: patients
with severe heart failure
• Monitor liver function
• Assess for hypotension (SBP less than 90) and educate the patient to monitor
their blood pressure at home (daily) and to record the measurements to show the
physician during follow-up appointments.
• Preventing rebound hypertension (blood pressure becomes extremely
elevated and it is hard to bring down) …. teach the patient to NEVER abruptly
quit taking themedication because it can lead to this condition.
• Stress the importance of lifestyle changes because antihypertensive meds
do NOT cure high pressure…. needs to eat healthy, exercise, and quit
smoking.
• Both medications are contraindicated in pregnancy.
Adrenergic Blockers
• Centrally acting sympatholytic stimulate α-receptors in the central nervous
system to inhibit vasoconstriction, thus reducing peripheral resistance.

• These medications decrease sympathetic vasoconstriction by reducing the

effects of norepinephrine at peripheral nerve endings, resulting in vasodilation
and decreased BP.

• These medications are used to maintain renal blood flow.

• Examples: Doxazosin, Prazosin, Terazosin

❖ Uses: Hypertension, Heart Failure, BPH

❖ Contraindicated: Impaired liver function.

❖ Side and adverse effects
• Sodium and water retention
• Edema
• Drowsiness, dizziness
• Dry mouth
• Hypotension
• Bradycardia, Reflex tachycardia
• Impotence
• Depression
• Weight gain
• Gastrointestinal disturbances
• Nasal congestion

❖ Interventions
• Monitor vital signs.
• Monitor liver function tests.
• Monitor for fluid retention and edema.
• Instruct the client to change positions slowly to prevent orthostatic hypotension.
• Instruct the client in how to monitor the BP.
• Instruct the client to monitor for edema.
• Instruct the client to decrease salt intake.
• Instruct the client to avoid over-the-counter medications.
• Instruct the client not to discontinue medication because abrupt withdrawal can
cause severe rebound hypertension.
Antianginal drugs
 NITROGLYCERIN
It is part of the drug family of nitrates and because of this it causes vasodilation
of blood vessels. This will lead to an increase in blood supply going to the
heart, which will help with decreasing its workload. It used to relieve or prevent
chest pain.

❖ As the nurse what can expect to see in your patient after they’ve received this
medication?
• Facial flushing
• Burning or tingling under tongue
• Headache
• Dizzy
• Hypotension
❖ When a patient is having chest pain nurse must:
• Notify MD
• Follow orders: Most facilities have standing orders for when a patient starts
to have chest pain. These are sometimes called chest pain protocols. They
typically include:
o Administering nitroglycerin and other drugs like morphine etc.
o Placing patient on oxygen via nasal cannula to keep oxygen saturation within
normal limits
o Obtaining a 12-lead EKG
o Drawing cardiac enzymes etc.
❖ Things to Consider BEFORE Giving Nitro:
• Confirm the patient has no known allergy to nitroglycerin.
• Confirm the patient has NOT recently taken a phosphodiesterase inhibitor
like Sildenafil (Viagra) or Tadalafil (Cialis)…this can lead to severe
hypotension or even death.
• Contraindicated for patients with increased intracranial pressure.

• When giving nitroglycerin (sublingual or as oral spray) have the patient sit
down because this medication causes dizziness.
• Then, confirm patient’s vital signs (especially blood pressure). Remember this
medication will lower blood pressure. It is important to make sure the patient’s
SBP (systolic blood pressure) is within parameters. Most hospital’s protocols
require the SBP to be greater than 90…if not contact the MD for further orders.

• Also, if possible, place the patient on a cardiac monitor to monitor for ST

segment abnormalities like ST segment elevation or depression.

❖ Preparations of Nitroglycerin
• Tablet

• Spray

• Paste

❖ Method of Administration:

➢ Nitroglycerin Tablet

The vial that contains the nitro tablets is dark brown. WHY? Nitroglycerin is
very sensitive to heat, light, or moisture. Therefore, be sure to protect the
medication. In addition, once the vial is opened the tablets are good for 3
months.
 • Perform hand hygiene and don gloves.
• Perform the patient’s rights.
• Place one tablet under the tongue. Inform the patient NOT to swallow or
chew the tablet, but let it dissolve under the tongue. In addition, have the
patient NOT eat or drink anything for 10-15 minutes after administration.

• After administration of the first dose, monitor the patient’s blood pressure
very closely and their chest pain rating. Contact the physician for further
orders. Is it decrease or increasing?

• If chest pain is still present and blood pressure is within parameters, after 5
minutes administer a 2nd dose.
• Again, monitor the patient’s blood pressure very closely and chest pain rating.
If chest pain is still present and blood pressure is within parameters, after 5
minutes you may administer a 3rd dose.
• No more than 3 doses are given.
➢ Nitroglycerin Oral Spray

The vial is dark brown for the same reason as stated above. Never shake the
bottle of spray and always keep it in an upright position. In addition, if we are
using a new bottle of oral spray ALWAYS prime the bottle by spraying 5-8
sprays.
**Always prime the bottle away from your face and others. **
 • Perform hand hygiene and don gloves.
• Perform the patient’s rights.
• Spray 1 spray under the tongue. Inform the patient to slightly hold their
breath and not breathe in the medication while we are spraying it and tell
the patient to NOT rinse the mouth or eat/drink anything for 10 minutes.

➢ Nitroglycerin Ointment
It is a vasodilator, and it is used to prevent chest pain (angina) in patients with
coronaryartery disease. Nitroglycerin ointment is absorbed through the skin and
enters the bloodstream. This will cause the coronary arteries on the heart to
dilate, so more blood flows to the heart muscle, and this will prevent ischemia.

Nitro ointment is prescribed by the physician in inches. For instances, a

doctor may order a patient to receive 1 inch of Nitropaste ointment. As the nurse
we will be responsible for administering and teaching the patient how to
measure out the prescribed about of nitro ointment. We will do this by using
the application papers that are included with the medication.

❖ Tips for nurses:

• ALWAYS wear gloves when removing the old application paper and while
administering a new dose (if you come into contact with the ointment, we may
experience side effects).

• Measure the ointment on the side of the application paper that is NOT
PRINTED. Why? When the nitroglycerin meets the print on the application
paper, it will cause the print to leak into the medication.

• Rotate sites: chest, upper arm/legs, back

• Always use a site where the skin is completely intact and free from hair
(trim the hair, if needed…NEVER shave it).

• Tape the application paper down with tape and cover with a plastic type
dressing (nitro stains clothes).
 • Always date, time, and initial the application papers and this will be done
on the PRINTED side. Don’t do this over the scale because you will need to
see the scalewhen you measure it out on the opposite side.

• Always assess the patient’s vital signs prior to administering a new dose.
Make sure the patient is NOT hypotensive.

➢ Nitropaste Patch

First, remove the old application paper. Remember use gloves!!!

• Perform hand hygiene and don gloves.

• Find the application paper.
• Gently remove the applicator paper.
• Clean the skin with a cloth to remove the excessive amount of medication
leftbehind.
• Doff gloves and perform hand hygiene.
Then apply the new dose (remember performing the patient’s five rights):

• Write the date, time, and your initials on the new application paper. Remember
do this on the PRINTED side.
• Don gloves.

• Flip the application paper over, so you will be measuring the ointment on the
non-PRINTED side. We will be able to see the scale through the paper
because the application paper is thin.

• Measure out the prescribed amount using the scale.

• Select a NEW site to place the application paper.

• Take the application paper with the ointment side facing the patient’s
skin and lightly spread the ointment on the skin (Do NOT rub or massage
it) and keep the application paper on the skin.

• Then cover it with a plastic type wrapping (tegaderm etc.) and tape it down.
 Positive Inotropic and Cardiotonic Medication

❖ Description
• These medications stimulate myocardial contractility and produce a
positive inotropic effect.

• These medications are used for short-term management of advanced

heart failure; the increase in myocardial contractility improves cardiac,
peripheral, and kidney function by increasing cardiac output, decreasing
preload, improving blood flow to the periphery and kidneys, decreasing
edema, and increasing fluid excretion. As a result, fluid retention in the
lungs and extremities is decreased.

❖ Side and adverse effects

• Dysrhythmias

• Hypotension

• Thrombocytopenia

• Hepatotoxicity manifested by elevated liver enzyme levels

• Hypersensitivity manifested by wheezing, shortness of breath, pruritus,

urticaria, clammy skin, and flushing.
❖ Interventions
• Positive inotropic and cardiotonic medications are used for intravenous (IV)
administration.

• Monitor the apical pulse and BP.

• Monitor for hypersensitivity.

• Assess lung sounds for wheezing and crackles.

• Monitor for edema.

• Monitor for relief of heart failure as noted by reduction in edema and lessening
of dyspnea, orthopnea, and fatigue.

• Monitor electrolyte and liver enzyme levels, platelet count, and renal function
studies; the medications may decrease potassium and increase liver enzyme
levels; continuous electrographic monitoring is done during administration.