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Week7-11.22.01DrugstotreatCardiacConditions2.pptxMedications to treat Heart Failure, Angina & Hypertension
Pharmacology
NSG 220
Dr. Lopez
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Heart Failure AKA “congestive heart failure”
Progressive/chronic- cardiac output is decreased leading to decline in perfusion to the body and organs.
Heart can’t pump blood throughout the body to meet the body’s need for blood and oxygen
Causes: narrowed arteries (coronary heart disease), high blood pressure, birth defect (congenital heart disease), cardiomyopathy
S/S: shortness of breath, fatigue, edema(peripheral, abdomen) , tachycardia (depends on the side of heart failure), palpitations, dry hacking cough
Treatment Goal:
Improve quality of life and the ability to perform daily activities
Reduce symptoms
Permanent damage to the heart. Looses its tone- too stiff (fibrous/stiff) or too stretched(loss of elasticity)
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Heart Failure Drugs
Diuretics*- 1st line drug for all patients with s/s of volume overload or hx of volume overload.
RAAS inhibitors
Angiotensin-converting enzyme inhibitors
Angiotensin II receptor blockers
Aldosterone antagonists
Direct renin inhibitors
Beta blockers
Digoxin
Angiotensin II Receptor Blockers
Action
With careful control of dosage, can improve patient’s status
Protect from excessive sympathetic stimulation
Protect against dysrhythmias
Adverse effects
Fluid retention or worsening of HF
Fatigue
Hypotension*
Bradycardia or heart block
Renin-angiotensin-aldosterone system ( RAAS) inhibitors are a group of drugs that act by inhibiting the renin-angiotensin-aldosterone system
( RAAS) the system that regulates the blood pressure.
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Medications to treat Heart Failure
Class: Cardiac (Digitalis) Glycosides
Medication: Digoxin [Lanoxin, Lanoxicaps, Digitek]
Used to Treat: Congestive Heart Failure
MOA:
Slows down the heart rate
Increases myocardial contractility
Increased cardiac output
Increases force of ventricular contraction
Hemodynamic benefits
Increased cardiac output
Decreased sympathetic tone
Increased urine production
Decreased renin release
**It does not affect the blood pressure**
Adverse effects
Cardiac dysrhythmias, fatigue, anorexia, bradycardia, hypokalemia
Nursing Implications
Check heart rate (HR) & regularity for 1 full minute before administering
Hold for HR less than 60
Monitor digitalis & potassium levels to avoid toxicity
****Teach patients not to double up if they miss a dose.
***Narrow therapeutic range
Decreased sympathetic tone- reduces blood pressure, lowering heart rate, reduce CO, and stroke volume (via slowing down contractility, decreasing cardiact output, relaxing arteriols and reducing SVR (systemic vascular resistance)
Increased urine production- decreasing fluid volume- lowering water and NA, reducing volume, reducing the blood pressure
Decreased renin release- low renin reduces blood pressure (hypertension).
Peripheral vascular resistance (systemic vascular resistance, SVR) is the resistance in the circulatory system that is used to create blood pressure, the flow of blood and is also a component of cardiac function. When blood vessels constrict (vasoconstriction) this leads to an increase in SVR.
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Angina
Sudden pain beneath the sternum, that radiates to the left arm, shoulder and jaw.
Cause: blockage “atherosclerosis” of the coronary arteries reducing blood flow to the heart.
Drug therapy goal:
Prevent myocardial infarction
Prevent ischemia and anginal pain
Pharmacological Therapy
Organic Nitrate
Beta Blockers
Calcium Channel blockers
Drug therapy goal medications: cholesterol lowering (reduce plaque) & antiplatelet drugs to prevent (clots)
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Organic Nitrates
Medication: Nitroglycerin (IV, SL, Translingual spray, PO, Patches, topical ointment)
MOA: dilates the arteries and blood vessels to improve
Therapeutic Action*: Pain relief: Relieves pain by causing vasodilation.
Therapeutic Uses:
Acute Angina: sublingual tabs or translingual spray
Sustained Angina-transdermal patches, topical ointment and sustained-release oral capsules.
Nursing Implications:
*Onset: 2 min (SL); 3 min (PO); 30 min (topical)- can persist up to 1 hour.
Check blood pressure and pulse before each administration
Blood pressure can drop precipitously after a single dose.
Hold dose if systolic BP < 90 mm Hg or more than 30 mm Hg below baseline.
Do not discontinue NTG intravenous infusion abruptly–it may result in precipitous rebound hypertension, angina, or coronary artery vasospasms.
A/E:
*Hypotension, headache, reflexive tachycardia, flushing
Reflexive Tachycardia- If blood pressure decreases, the heart beats faster in an attempt to raise it. This is called reflex tachycardia. This can happen in response to a decrease in blood volume (through dehydration or bleeding), or an unexpected change in blood flow.
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Nitrates
Medications: Isosorbide Mononitrate (SR, IR)- po only, Isosorbide Dinitrate (IR, SR)- PO & SL
MOA: Dilates (widens) blood vessels, making it easier for blood to flow through them and easier for the heart to pump.
Therapeutic Use:
prevent angina attacks (chest pain)
Will not treat an angina attack that has already begun.
Instruct the patient to:
Take this medicine by mouth with a glass of water.
Follow the directions on the prescription label.
Take this medicine on an empty stomach, at least 30 minutes before or 2 hours after food. Do not take with food.
****Long-acting preparations (transdermal patches, topical ointment, sustained-release oral tablets or capsules) should be discontinued slowly. If they are withdrawn abruptly, vasospasm may result"
*sustained-released- Time-release drugs use a special technology to release small amounts of the medication into a person's system over a long period of time. This is also referred to as sustained release, extended release, or controlled release. These tend to come in pill form and are simply made to be more potent but dissolve slowly
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Beta Blockers
Medications: Propranolol, metoprolol (PO, IV)
MOA: Blocks stimulation of beta and bet 2 adrenergic receptor sites, reducing certain
Therapeutic Uses: HTN, HF, MI, Stable and Unstable Angina
*Therapeutic effects on pain: Prevent pain of stable angina primarily by decreasing heart rate and contractility, which reduces cardiac oxygen demand.
Adverse Effects: Bradycardia, orthostatic hypotension, impotence
Nursing Implications:
Take with food to increase absorption
Obtain baseline vital signs
Do not discontinue abruptly
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Calcium Channel Blockers
MOA: Prevents calcium from entering the smooth muscle cells of the heart and arteries.
When calcium enters these cells, it causes a stronger and harder contraction, so by decreasing the calcium, the hearts' contraction is not as forceful. Calcium channel blockers relax and dilate narrowed blood vessels, reduces heart rate and lowers blood pressure
Medications: amlodipine besylate, bepridil, diltiazem, nicardipine
Therapeutic Uses: HTN, variant angina
A/E: Palpitations, Headache, Dizziness, fatigue, nervousness, bradycardia, flushing, hypotension*, syncope, peripheral edema
Nursing Implications
Check blood pressure, heart rate, and cardiac monitor prior to administering diltiazem.
Assess baseline renal (BUN, Cr) and liver function (AST, ALT) lab tests.
Monitor for signs of heart failure (e.g., pulmonary edema, weakness, dyspnea).
Provide analgesic for headache.
Use caution during position changes to prevent orthostatic hypotension.
*hypotension- sign of toxicity
Calcium causes the heart and arteries to contract more strongly. By blocking calcium, calcium channel blockers allow blood vessels to relax and open.
Decrease systemic vascular resistance- decrease afterload.
Syncope is a temporary loss of consciousness usually related to insufficient blood flow to the brain “fainting or passing out”
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Hypertension
Primary “Essential”
No identifiable cause
Chronic and progressive
Lifelong condition (treated but not cured)
Secondary
Less than 10% have
There is an identifiable cause
Can be cured (removing the cause or managed by drugs used for primary HTN
Blood pressure Facts
BP categories
Normal
Systolic BP below 120 mm Hg and diastolic BP below 80 mm Hg
Prehypertension
Systolic BP of 120 to 139 mm Hg or diastolic BP of 80 to 89 mm Hg
Hypertension
Systolic BP above 140 mm Hg or diastolic BP above 90 mm Hg
Stage 2 hypertension: Systolic BP and diastolic BP in different categories (e.g., 160/92 mm Hg)
Consequences of uncontrolled or untreated
Heart disease
Myocardial infarction (MI)
Heart failure
Angina pectoris
Kidney disease
Stroke
Medications to treat HTN (cont.)
Diuretics
MOA: Help the body get rid of excess sodium (salt) and water and help control blood pressure. They are often used in combination with additional prescription therapies.
Medications:
Thiazide- Chlorthalidone, chlorothiazide, hydrochlorothiazide, indapamide.
Potassium-sparing- amiloride hydrochloride, spironolactone, triamterene
Loop diuretics- furosemide, bumetanide
Direct Acting vasodilators
Cause the muscle in the walls of the blood vessels (mainly arterioles) to relax, allowing the vessel to dilate ultimately allowing improvement in blood flow.
Medications:
Hydralazine
Headaches, heart palpitations, body aches and joint pain (temporary symptoms)
Minoxidil – side effect- hair growth, fluid retention
Medications to treat HTN
Beta-blockers -End in “olol”
Medication: Carvedilol, Labetalol, metoprolol tartrate, atenolol, propranolol hydrochloride
MOA: (lower blood pressure/and HR)
reduce the heart rate, the heart's workload and the heart's output of blood ultimately lowering blood pressure.
A/E:
Bradycardia
AV heart block,
Asthma*
Postural hypotension
Usually only hold these medications for low blood pressure
ACE inhibitors- “pril”
Medications: captopril, lisinopril, fosinopril sodium, enalapril maleate
MOA: Lower BP by preventing the formation of angiotensin II and thereby preventing angiotensin II–mediated vasoconstriction and aldosterone-mediated volume expansion. (Stop angiotensin I from converting to angiotensin II allowing the blood vessels to relax)
**Less effective in African Americans (often see angioedema). Usually not 1st of choice prescribed
*A/E:
Persistent dry, hacking cough* (3.9% and 35% among patients )
First-dose hypotension
Angioedema*
hyperkalemia
Angiotensin is a chemical that causes the arteries to become narrow, especially in the kidneys but also throughout the body. ACE stands for Angiotensin-converting enzyme. ACE inhibitors help the body produce less angiotensin, which helps the blood vessels relax and open up, which, in turn, lowers blood pressure.
*Non-selective beta-blockers cause asthma symptoms in people with asthma. They cause the airways to narrow and become more sensitive.
(first dose to months later) The mechanism of ACE-I-induced cough is still unclear. The possible mediators that play a role in the development of cough are bradykinin and substance P, which are destroyed by ACE. Thus, bradykinin and substance P accumulate in the upper and lower respiratory tracts by inhibition of this enzyme by ACE-I.
Dry cough- avoid in patients with sleep apnea
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ARBS (angiotensin II receptor blockers) end in “tan”
Medications: Losartan, Valsartan, Irbesartan
MOA: Inhibits angiotensin converting enzyme from producing angiotensin 2 (the major vasoconstrictor), which narrows the blood vessels causing your heart to work harder. They block angiotensin II from binding to the receptors on the blood vessels. It also triggers the release of aldosterone.
Used treat:
Lowers blood pressure
Heart failure
Diabetic Nephropathy- (DM II)- slow down progression of the disease, decrease blood pressure, decrease proteinuria
Nursing:
Assess the blood pressure and heart rate
Monitor potassium levels
Monitor kidney function (labs)- BUN (5-20), Creatinine (0.6-1.2 mg) & urine output (30 cc/hr).
Teach patients: Monitor blood (hypotension), avoid salt substitutes with Potassium, avoid potassium sparing (Arbs can increase medication), never stop the medication on their own. Do not take a missed dose.
RAAS- (system manages the blood pressure)- increases blood pressure when needed. Increase blood volume.
Angio-tension converting enzyme is found in the lungs, heart, arteries, kidneys and intestines.
ACE inhibitors and ARBs work on the same biochemical pathway in the body to stop high blood pressure, but at different spots.
ACE inhibitors block a natural substance in the body called angiotensin I from being converted to angiotensin II. Angiotensin II constricts the blood vessels, causing blood pressure to increase. Stopping the conversion of angiotensin I to angiotensin II results in blood vessel relaxation and a decrease in blood pressure.
ARBs also target the angiotensin pathway, but they work by blocking angiotensin II from binding to receptors on the blood vessels that affect blood vessel constriction. In the end, this also results in blood vessel relaxation and a decrease in blood pressure.
Kidney disease- high blood pressure, forces more protein into the urine- lowering bp, reduces the proteinuria
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Treatment for HTN
Lifestyle Modifications
Sodium restriction
DASH (Dietary Approaches to Stop Hypertension) eating plan
Alcohol restriction
Aerobic exercise
Smoking cessation
Weight Loss
Maintenance of potassium and calcium intake (important for cardiac function)
Pharmacologic Therapy
Diuretics
Direct-acting vasodilators: hydralazine and minoxidil
Beta-Adrenergic Blockers
ACE Inhibitors
Calcium Channel blockers
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Questions?
