NUR 239: Pharmacotherapeutics of CV Disorders

Mennonite College of Nursing @ Illinois State University

N 239: Pathphysiology and Pharmacotherapeutics I
Cardiovascular Study Guide II—CV Disorders

Hyperlipidemia and Atherosclerosis

See: Detailed Overview of Hyperlipidemia See: Update on Cholesterol and triglycerides

Elevated levels of blood lipidsàlead to atherosclerosis

Atherosclerosisàheart attack, stroke, and other cardiovascular events.

Lipids—cholesterol and triglycerides

Cholesterol: waxy, fatlike substance essential to growth and viability of body cells

Component of cell membranes
Used in synthesis of steroid hormones
About 7% circulates as blood serum and contribute to atherosclerotic plaques in arteries

Triglyerides: chemical form of most fats in food and in the body

Stored in adipose as energy source
Major component of VLDLs and chylomicrons

Lipids are encapsulated by lipoproteins–special fat-carrying proteins for transport in blood. (carry cholesterol and triglycerides)

HDL—high-density lipoprotein—carries cholesterol to liver
LDL—low-density lipoprotein—carries cholesterol back to liver or cholesterol dependent pathways (70%) and some to the nonreceptor dependent pathway (30%)
VLDL- very low density lipoprotein – carries cholesterol to blood vessels
Chylomicrons—carries triglycerides & cholesterol after ingestion/absorption from GI tract and carry to skeletal muscle for energy or fat for storage

2 sites of lipoprotein synthesis:

Liver—Synthesizes and releases VLDL & HDL; removes LDLs

Small intestine—synthesizes chylomicrons

Labs to know: fill in from ATP III guidelines

1. Total Blood cholesterol levels in adults:

Desirable: <200 mg/dl—low risk

Borderline-high: >240 mg/dl—risk doubles

High: >260 mg/dl—risk triples

2. HDL levels : “good guys”

Protective: >60 mg/dl

Increased risk: <35

Usually seen: 40-50

3. LDL levels: “bad guys”

Optimal: <100 or 130 mg/dl

Near-optimal: <100-129

Borderline high: 130-159

High: 160-189

4. Triglycerides:

Optimal: <150 mg/dl
high:

Hypercholesteremia:

Primary

elevated cholesterol levels that develops independent of other health problems or lifestyle behaviors.
May have a genetic basis (defective synthesis of apoproteins, lack of receptors, defective receptors). Familial hypercholesterolemia

NUR 239: Pharmacotherapeutics of CV Disorders

Secondary

associated with other health problems and behaviors.
Caused by obesity with high-caloric intake
Metabolic disorders such as diabetes mellitus.
blood cholesterol levels at least once every 5 years after age 20.

Atherosclerosis

Def: a type of arteriosclerosis or hardening of the arteries.
Characterized by formation of fibrofatty lesions in intimal lining of large and medium-sized arteries (coronaries most common); build-up of plaque in the lumen of arteries
Leading cause of cardiovascular disease and death among men/women in US
Development of lesions in arteries which gradually occlude them

Atherosclerotic lesions characterized by:

Accumulation of intracellular and extracellular lipids
Proliferation of vascular smooth muscle cells
Formation of scar tissue and connective tissue proteins.
Click here to see slides depicting varying degrees of atherosclerosis

Managing Hyperlipidemia— Report of ATPIII (Adult Treatment Panel) for Detection , Evaluation & Treatment of high blood cholesterol in adults

Patient ed website using these new guidelines: http://www.nhlbi.nih.gov/chd/

Prevention IS KEY

Step I—assess blood lipoprotein levels

Step 2—identify presence of atherosclerosis/ risk of coronary heart disease (CHD)

Step 3—identify major risk factors : cigarette smoking, hypertension, low HDL, premature CHD fam history, age

Step 4—If 2+ risk factors, determine 10 year risk of CHD

Step 5—Determine risk category

Step 6—Initiate therapeutic lifestyle changes (TLC)

TLC Diet–
Weight loss
Increased exercise

Step 7—add drug therapy—Work by affecting cholesterol production, increasing intravascular breakdown, or removing cholesterol from bloodstream.

Medications to treat Hyperlipidemia

“Statins”: HMG-CoA reductase inhibitors à inhibit enzyme needed for hepatic synthesis of cholesterol so <LDL, VLDL trig. <inflamm

Prototype: Atorvastatin

Other key drugs:

Rosuvastatin, simvastatin

Name clue: “statin”

Actions:

Adverse Effects: nausea, constipation, diarrhea RARE myopathy, rhabdomylosis

Teteratogenic

Nursing Implications: give with food, teach pt to notify if has muscle aches

Bile acid-binding resins:

Prototype: Cholestyramine (Questran)

Other key drugs:

Name clue: “Chol”

Actions: binds bile acid in intestine so are lost in stool, liver breaks down cholesterol

Stays in intestine, not bloodstream

Adverse Effects: GI-constipation, bloating, flatulence

Nursing Implications: very safe; increase fluids, take 1 hour before or 4 hours after other meds, used with statins

Nicotinic acid

Prototype: Niacin

Other key drugs:

Name clue: “Ni”

Actions: prevents fatty acids from reaching liver, so < cholesterol and trig synthesis, increases HDLs

Adverse Effects: skin flushing, pruritus, GI irritation, hyperglycemia

Nursing Implications: take with food, take ASA 325mg 30 minutes before Niacin

Fibric acids

Prototype: Gemfibrozil (Lopid)

Other key drugs:

Name clue: “Fib”

Actions: increases oxidation of fatty acids in liver, lowers triglycerides and increases HDLs

Adverse Effects: GI upset, diarrhea; increase gallstones

Nursing Implications: Don’t use with statins-increases risk of rhabdomylosis (muscle dz)

Metabolic Syndrome (used to be called Syndrome X)—read more about it

Syndrome (cluster of symptoms and disorders) associated with high incidence of cardiac disease and stroke 2/2 hyperlipidemia, atherosclerosis
Caused by insulin resistance (inherited or due to obesity) and resultant hyperinsulinemia which leads to
- Activation of sympathetic nervous system, increasing cardiac output
- Increased peripheral vascular resistance and renal sodium retention à HTN
- Increased blood lipids and accelerated atherosclerosis
Diagnosed when a person has 3 or more of the following “metabolic risk factors” for heart disease:
- Hypertension (BP > 130/85)
- low HDLs (<40 mg/dl men; < 50 mg/dl,women)
- high triglycerides (>150 mg/dl)
- Truncal obesity (apple shape)
- Fasting blood sugar > 110 mg/dl
Can be treated with weight loss, exercise—if needed will add medications for hypertension & dyslipidemia

Hypertension (HTN; High blood pressure)

Primary HTN 90% of cases of HTN

chronic elevation in blood pressure occurring without evidence of other disease
Diagnosed when blood pressure exceeds 140/90
Also called Essential HTN
No specific identifiable cause

Secondary HTN— only 5-10% of cases (secondary to something else, may be something else causing it)

elevation of blood pressure resulting from some other disorder

Most common causes:

Renal disease

Most acute kidney disordersàdecreased urine formation, retention of salt/water, hypertension.
Reduced renal blood flowàaffected kidneys release excessive amounts of reninàincreasing circulating levels of angiotensin IIàarteriolar vasoconstriction

Disorders of Adrenocorticosteroid Hormones

These hormones facilitate salt and water retention by kidney
Salt-restricted diet reduces HTN

Pheochromocytoma

Very rare tumor of chromaffin tissue, which contains sympathetic nerve cells
Tumor commonly located in adrenal medulla.
Tumor cells produce and secrete epinephrine and norepinephrine.

Coarctation of Aorta

Narrowing of the aorta, reducing blood flow to lower parts of body and kidneys.

NUR 239: Pharmacotherapeutics of CV Disorders

Malignant Hypertension

Accelerated and potentially fatal form of disease
Characterized by sudden marked elevations in BP
May include intense arterial spasm of cerebral arteries
Injures walls of arterioles and may cause intravascular coagulation and fragmentation of RBC
Renal damage
needs immediate and rigorous medical treatment

Assessment & Treatment of HTN: EBP Approach: Guidelines from the Joint National Committee on Detection, Treatment and Prevention of Hypertension (JNC 7)

take BP: see JNC 7 Classification

Category	SBP	DBP
Normal	<120	<80
Pre-HTN	120-139	80-89
HTN, Stage 1	140-159	90-99
HTN, Stage 2	>160	>100

Identify risk/ contributing Factors:

Family hx
Age-related changes in BP
Race—HTN more prevalent/severe in African Americans than whites.
High salt intake
Obesity
Hyperinsulinemia: over secretion of insulin into the blood; happens before diabetes
Excess alcohol consumption
Low intake of Potassium, Calcium, and Magnesium
Stress—mostly causes transient alterations in BP
Oral contraceptive drugs
Diseases causing secondary HTN

3. Signs and Symptoms

-No early symptoms—“the silent killer”

-Later symptoms

Headache
Nocturia—indicating that kidneys are losing ability to concentrate urine

Target Organ Damage

Blood vessels: major risk for atherosclerosis:
Heart:

Atherosclerosisàheart failure, stroke, coronary artery disease, and peripheral artery disease.
HTN increases workload of left ventricle by increasing pressure against which heart must pump to eject blood into systemic circulationàleft ventricular hypertrophy.
Left ventricular hypertrophyàmajor risk factor for ischemic heart disease, cardiac dysrhythmias, sudden death, congestive heart failure.

Kidneys: nephrosclerosis, common cause of renal insufficiency.
Eyes: hypertensive retinopathyàbleeding, macular/optic nerve swelling, blindness

Treatment of HTN

Treatment Goal: BP <140/90 mmHg for everyone under 60, >60 years 150/90 mm/Hg
Majority of patients will require two medications to reach goal. (new guideline goal is relaxed)

Step 1: Lifestyle modifications

Weight reduction

Regular physical activity
Modification of alcohol intake
Smoking cessation
DASH diet: Increased intake of potassium, calcium, and magnesium (dietary, approach, stop, hypertension) more fruits and veggies and lowfat, lower sodium than TLC
Decreased sodium
Use of relaxation and biofeedback

Step 2: Initiate antihypertensive medications – see JNC 7 for choice of initial drugs

most common first-line drug categories are “ABCD” categories (see meds table)
- A = Angiotensin Converting Enzyme (ACE) inhibitors or Angiotensin II receptor blockers (ARBs)
- B = Beta Blockers (BB)
- C= calcium channel blockers (CCB)
- D = Diuretics
JNC suggests starting with “D” –Diuretics, specifically thiazide diuretics

Step 3: Adjust medications (change dosage, add medications from other categories) to achieve BP goal with minimal AEs. NUR 239: Pharmacotherapeutics of CV Disorders.

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Common Medications used to treat Hypertension

FIRST LINE MEDICATIONS:

ACE Inhibitors (ACE = angiotensin converting enzyme)

Prototype: Captopril (Capoten)

Other key drugs: Lisinopril (Zestril)
Name clue: “pril”

Actions: block angiotensin converting enzyme from converting angiotensin I to angiotensin II

Vasodilation (due to blocking angiotensin II)
Decreased sodium and water retention (due to blocking aldosterone)

Adverse Effects:

Dry cough in ~10-20%
Sometimes—hyperkalemia in pts with DM or renal disease who are taking NSAIDS, K supplements, spironolactone
Rare but serious: neutropenia, proteinuria, angioedema
Contraindicated in pregnancy

Nursing Implications:

A key drug to treat HTN and HF with few AEs
First line drug to treat HTN in people w/ DM 2/2 slowing progression of renal impairment

ARBs—Angiotensin II receptor blockers

Prototype: Losartan (Cozaar)

Other key drugs : Telmisartan (Micardis)

Name clue: “sartan”
Actions: block angiotensin II receptor sites so block its action

Adverse Effects:

Contraindicated in pregnancy

Nursing Implications:

“cousins” to ACE inhibitors—same actions, fewer AEs (less cough, hyperkalemia)
Takes 3-6 weeks to reach maximal BP lowering effect

**IF HTN AND CHRONIC KIDNEY DISEASE ARB’S or ACE’S ARE USED**

Beta-blockers NOT FIRST LINE FOR HTN ANYMORE so SECOND LINE

Prototype: Propanolol (Inderol) (1^st gen)

Other key drugs: Atenolol (Tenormin) (2^nd gen)

Metoprolol (Lopressor /Toprol)

Name clue: “olol”
Actions: block b1 receptors in heart causing decrease HR and contractility
3 generations of BBs with different effects:

1^st gen: nonselective– block both b1 and b2 receptors so also causes bronchoconstriction
2^nd gen: cardioselective: block b1 receptors only so only act on the heart
3^rd gen: vasodilating: block b1 and a1 so also cause arterial dilation

Adverse Effects:

Bradycardia, bronchospasm (if 1^st gen, non-selective BB), orthostatic hypotension
Use cautiously with in clients with Asthma, COPD, DM (can lead to and mask symptoms of severe hypoglycemia)
DO not use in people with heart block
Do not stop abruptly if have CADà could lead to angina, MI

Nursing Implications

Key drug in HTN, HF, arrhythmias (also used for migraines, anxiety)
Take apical pulse and BP before administering: hold if P < 50-60 or BP < 90- 100 and notify prescriber

Calcium-Channel Blockers

Key drugs: Nifedipine (Procardia) (dilates arterioles)

Amlodipine (Norvasc) (dilates arterioles)

Diltiazem (Cardizem) (acts on arterioles and heart)

FOCUS ON PINE because others focus on arrhythmias

Actions: Block calcium ion channels in smooth muscle in peripheral & cardiac arterioles and in cardiac muscle, thus
slowing contraction and in SA and AV nodes slowing node firing

Adverse Effects:

Constipation
Flushing
Palpitations or bradycardia
Peripheral edema
Worsening HF

Nursing Implications:

Key drug in HTN, angina, arrhythmias

Diuretics

There are several classes of diuretics
All act on the kidney to increase urine output: this will decrease blood __________ and ___________
Used for: treatment of HTN, diuresis (removal of excess fluid volume), HF

Thiazide diuretics (safest because slow onset, fairly weak, and stop working when lose excess fluid)

Prototype: HCTZ (ie hydrochlorothiazide) (Hydrodiuril)

Actions: block Na and CL reabsorption in renal tubule, so increase loss of Na, CL, K, water in urine

Adverse Effects

Hypokalemia
Hypotension

Nursing Implications

Safest of the diuretics; slower onset, weaker diuretic– will not cause dehydration
Teach pt to increase dietary sources of potassium
Pts may need potassium supplements
Monitor fluid status: VS, daily weight, edema

Loop diuretics (much stronger, act on different places in kidnets, fast onset, don’t quit working àno ceiling effect)

Prototype: Furosemide (Lasix)

Actions:

block Na and CL reabsorption in Loop of Henle, so increase loss of Na, CL, K, water in urine
Very strong and very fast acting
Up to 10x greater diuresis than thiazides

Adverse Effects:

Hypokalemia-low potassium
Severe dehydration
Hypotension
Hearing loss (ototoxicity)

Nursing Implications

No ceiling effect—will continue working (causing diuresis even to the point of severe dehydration)
Carefully monitor fluid status: I & O, VS, daily weight, edema
Teach pt to increase dietary sources of potassium
Pts may need potassium supplements

Potassium-sparing diuretics:

Prototype: Spironolactone (Aldactone )

Other key drugs: triamterene

Actions: blocks aldosterone (spironolactone) or acts directly on renal tubule to increase loss of Na (and water) in urine,
and retain K

Adverse Effects:

hyperkalemia

Nursing Implications

Weak diuretics; Usually used in combination with thiazide or loop diuretic to prevent excessive K loss
- (triamterene is a component of many combination diuretics such as Dyazide (HCTZ +
  triamterene)
Teach pts to avoid dietary sources of potassium and potassium supplements
Don’t use in patients with renal disease

SECOND LINE MEDS

Alpha-Blockers

name clue:

Prazosin (Minipress) Doxazosin-Cardura

Block a receptors in arteries à vasodilation; 1^st dose phenomenon; take at HS

Centrally acting

Alpha Agonist Clonidine-Catapres

Block norepinephrine realease in brain à decreases HR and contractility

Direct Vasodilators

Hydralazine-Apresoline Nitroglycerin-NitroBid (IV)

Do not stop abruptly à high BP

General Nursing Implications of antihypertensives:

AEs more likely in elders, those with renal disease and/or DM, and with multiple or large doses of HTN meds
Teach pts to:
- take at same time each day and not skip doses
- Monitor BP, P and weight
- Watch for orthostatic hypotension
- Don’t stop suddenly

See interactive informational website aimed at consumers: http://www.nhlbi.nih.gov/hbp/index.html

NUR 239: Pharmacotherapeutics of CV Disorders

Heart Failure:

Insufficient CO for demand
Inability of heart to supply sufficient blood to meet metabolic demand (O2 need of tissues)
Impaired pumping ability of heart
Accompanied by congestion of body fluids
Not a disease, but a syndrome

Cardiac output: amount of blood heart pumps each minute or volume of blood ejected by ventricle into the circulation per minute

CO=stroke volume * heart rate. CO = SV x HR

–Ave. adult = 3.5 – 8.0 L/min.

Either > HR or > SV or both will > Cardiac Output

Cardiac reserve: Ability of the normal heart to > CO up to 5 times the resting level to meet increased demands = 5 (4 – 8 LPM)

In Heart Failure, there is little if any cardiac reserve…cannot >CO more

Low CO triggers Compensatory Mechanisms:

Most rapid response (minutes) : Sympathetic Nervous System Stimulation:
- Increases heart rate (b1)
- Increases contractiltiy (b1)
- Increases venous return through vasoconstriction (> preload)

Renal Retention of Fluid (days):

stimulation of renin-angiotensin-aldosterone system
angiotensin II –> vasoconstriction
Aldosterone –> kidneys save Na & water
happens within days

Cardiac remodeling (months):

Ventricular dilation: > length of myofibrils (due to chronic stretch) and > heart chambers
Ventricular hypertrophy:> size (diameter) of myofibrils so >muscle mass of LV

Short-term effects: all increase CO

Long-term effects: weaken heart

Heart Failure

Pumping ability of heart impaired –> low perfusion of organs/ tissues
Often accompanied by congestion of body tissues –> edema, pulmonary congestion

Overviews—heart failure online AHA site aimed at consumer education: http://www.americanheart.org/presenter.jhtml?identifier=1486

From the NIH: http://www.nhlbi.nih.gov/health/dci/Diseases/Hf/HF_WhatIs.html

Causes of HF: Pathophysiology	examples
Myocardial Diseases	Heart attack, when damages heart muscle
Valvular Heart diseases	Mitral valve prolapse
Congenital heart defects	Born with it
Constrictive Pericarditis	Swelling, squeezes heart
Excessive work demands

Types or Classifications of Heart Failure

High-Output vs. Low-Output Failure

High—uncommon type caused by excessive need for cardiac output.

Low—caused by disorders that impair pumping ability of heart.

Systolic vs. Diastolic Failure

Systolic Failure—Impaired ejection of blood during systole

Involves a decrease in cardiac contractility and ejection fraction
Commonly results from condition that impair contractile performance or hemodynamic conditions producing volume overload or pressure overload
Ejection fraction = normal ventricle ejects 50-65% of blood in ventricle during contraction
Ejection fraction declines progressively during systolic heart failure.

Diastolic Failure—impaired filling of heart during diastole

Characterized by smaller ventricular chamber size, ventricular hypertrophy, and poor ventricular compliance (ability to stretch during filling)
Causes include those that restrict diastolic filling, those that increase ventricular wall thickness and reduce chamber size and those that delay diastolic relaxation.

Right-Sided vs. Left-Sided Failure

Right and left ventricles must maintain equal output to function effectively
Long-term heart failure usually involves both sides

Right-Sided Failure—cor pulmonale

Caused by conditions that restrict blood flow from Rt. Ventricle into lungs—ex. stenosis or regurgitation of tricuspid or pulmonic valves and Pulmonary diseases

Results in:

Decreased pumping of deoxygenated blood from systemic circulation into pulmonic circulation
Accumulation / congestion / back up of blood in venous system leading to fluid retention and edema in peripheral tissues and abdominal organs
Left-Sided Failure

Caused by heart muscle or heart valves problems – most common: acute myocardial infarction and cardiomyopathy
Results in:

decreased cardiac output—less oxygenated blood pumped into systemic circulation
increased left atrial and ventricular end-diastolic pressures [preload]
Accumulation / congestion / back up of blood in pulmonary circulation leads to fluid accumulation in the lungs

Clinical Manifestations of CHF:

Fluid retention and edema (due to congestion from right-sided failure)

Weight gain

. Pitting edema

. Ascites—fluid accumulation in the abdomen

Congestion of hepatic veins that drain into inferior vena cava

à impaired liver function and hepatic cell death

à Congestion of GI tract may interfere with digestion and nutrient absorption

Jugular vein distention [JVD]
Nocturia—nightly increase in urine output

Respiratory manifestations (due to congestion from left-sided failure)

SOB
Exertional dyspnea—related to increase in activity
Orthopnea—SOB occurring when person is supine
Paroxysmal nocturnal dyspnea—occurs during sleep
Chronic dry, nonproductive cough
Cardiac asthma—bronchospasm due to congestion of bronchial mucosa causing wheezing and breathing difficulty
Cheyne-Stokes respiration (periodic breathing)—Slow waxing and waning of respiration

Fatigue and weakness
Cyanosis

Diagnostic Methods

Electrocardiograph—indicate atrial or ventricular hypertrophy, underlying disorder of cardiac rhythm, or conduction abnormalities
Chest radiographs—size and shape of heart and pulmonary vessels, pulmonary edema
Echocardiograph—reveal size and function of cardiac valves and size and motion of both ventricles
Radionuclide angiography and cardiac catheterization—describe underlying causes
Invasive hemodynamic monitoring

Central venous pressure (CVP)—reflects amount of blood returning to heart
Pulmonary capillary wedge pressure (PCWP)—monitors pulmonary capillary pressures in direct communication with pressures from left heart

NUR 239: Pharmacotherapeutics of CV Disorders

Blood tests: BNP: B type natriuretic hormone (or brain naturetic hormone)

a cardiac hormone secreted by ventricles due to pressure or volume overload
is a marker for heart failure– used for diagnosis and monitoring
BNP levels go up with uncompensated HF; are normal with no HF
<100 pg/mL = no heart failure
100 – 200 = compensated HF (Class II ~ 200)
200 – 400 = moderate HF (Class III)
> 400 = severe HF

7. Two classification systems

NY Heart Association Functional Classification of Patients with Heart Disease
—based on how patient feels and limitations with physical activity

–person can go back and forth between categories based on symptoms

I	No symptoms and no limitation in ordinary physical activity	BNP ~ 100
II	Mild symptoms and slight limitation during ordinary activity. Comfortable at rest	BNP ~ 200
III	Marked limitation in activity due to symptoms, even during less-than-ordinary activity. Comfortable only at rest.	BNP ~ 350
IV	Severe limitations. Experiences symptoms even while at rest	BNP ~ 1000
	http://www.clinlabnavigator.com/Tests/Flash/BTypeNatriureticPeptide.swf

AAC/AHA Heart Failure Guidelines and Classification System—see diagram posted in module –classification based on progressive nature of HF—can’t go back to lower level
–includes recommendations for treatment

NUR 239: Pharmacotherapeutics of CV Disorders

Medications used to treat Heart Failure

First line drugs:

Key drugs in this class used in HF

Key Points

ACE Inhibitors or ARBs: block RAA–

block angiotensin II production
–vasodilation arterioles
–vasodilation venules

block aldosterone production
–less Na and H20 retention in kidney

favorable impact on cardiac remodeling

ACE:

Captopril (Capoten)
Enalapril (Vasotec)
Lisinopirl (Zestril)

ARB:

Losartan (Cozaar)
Vlasartan (Diovan)

All pts with HF should take ACE inhibitors

Reduce symptoms, improve functioning and prolong life

ARBs can be used instead if pt has difficulty with AEs of cough and/or angioedema

see AEs, nursing implications in HTN notes

Beta-blockers

–lower heart rate and decrease cardiac workload

–3^rd generation BBs also cause vasodilation

only cardioselective B-Blockers:

carvedilol (Coreg)– 3rd gen
bisoprolol (Zebeta) –2nd gen
sustained release metoprolol (Toprol XL)

Most pts with HF should take BBs

improve cardiac function, reduce symptoms, prolong survival

protect heart from excessive SNS stimulation

need to start with low dose and monitor closely

see AEs, nursing implications in HTN notes

Diuretics

increase urine output, thus decrease fluid overload

Thiazides for most (HCTZ)

Loop– furosemide (Lasix) for more severe edema

Diuretics used in pts with congestive symptoms–

fluid volume excess–edema, JVD, crackles, dyspnea, orthopnea, etc

see AEs, nursing implications in HTN notes

Second line drugs: Add these drugs in Stage C or D as needed

Cardiac Glycosides (Digitalis):

Digoxin (Lanoxin)

positive inotropic effect: increases contractility

negative chronotropic effect: slows SA and AV node impulses

-improves CO, reduces symptoms but does not prolong life

very dangerous drug:!!

long 1/2 life
very narrow therapeutic window– small difference between therapeutic and toxic dose
optimal therapeutic blood level:0.5-0.8ng/dl
if have hypokalemia, can develop toxicity at normal blood level
early toxicity S&S: anorexia, nausea & vomiting
later toxicity S&S: vision changes– halos, blurry, yellow tint, fatigue, CV arrythmias– can vary from bradycardia (AV block) to ventricular fibrillation
drug interactions with lots of other meds

nursing implications:

monitor K– if on diuretic, should be on K supplements
assess apical pulse before admin– hold if <60 or >120 or a change from pts normal and call provider

Vasodilator drugs

produce relaxation of vascular smooth muscle
reduce afterload (through arterial dilation)
reduce preload (though venous dilation)

nitrate: isosorbide dinitrate (venous dilation)

hydralazine (Apresaline) (arteriolar dilation)

often are combined

orthostatic hypotension and reflex tachycardia

aldosterone antagonists

· block actions of aldosterone

spironolactone (Aldactone)

promotes cardiac remodeling, reduces symptoms and prolongs life

see AEs, nursing implications in HTN notes

NUR 239: Pharmacotherapeutics of CV Disorders