Cardiovascular Unit

By Pat Pence, RN, C, MSN

Heart

Located in mediastinum. Base (wider) is superior and under the 2nd

rib. Apex (narrow) is inferior and slightly to the

left between 5th and 6th ribs.

Heart wall

Composed of 3 layers. Pericardium: transparent, thin layer, lines

outside of heart, 2 layers that contain serous fluid to decrease friction.

Myocardium: middle, thickest and strongest, actual contracting muscle tissue.

Endocardium: innermost layer, thin layer of connective tissue.

4 Heart chambers

Right atrium: receives deoxygenated blood from superior vena cava, inferior vena cava and coronary sinus.

Right ventricle:pumps blood to lungs via pulmonary artery.

Left atrium: receives O2 rich blood from lungs via pulmonary veins.

Left ventricle: PMI, thickest, most muscular, pumps blood to all parts of body via aorta.

Separated by septum.

4 Heart valves

Heart functions as 2 separate pumps. Heart valves keep blood flowing forward

and prevent backflow (regurgitation). Tricuspid valve and mitral valve (AV

valves). Chordae tendineae and papillary muscles

connect valves to walls of heart and promote a tight seal to prevent backflow.

Semilunar valves

Pulmonary semilunar valve: between Rt ventricle and pulmonary artery.

Aortic semilunar valve: between left ventricle and aorta.

Coronary blood supply

Heart requires a constant supply of O2 rich blood and return of O2 poor blood from tissue to the lungs.

Rt./Lt. Coronary arteries. Coronary vein and coronary sinus. Collateral circulation.

Blood vessel pattern

Artery: largest, vessels that carry blood away from heart; thicker, elastic and muscle tissue.

Arteriole: smooth muscle, deliver blood to tissues; dilate or constrict in response to low O2/hi CO2, affect BP blood flow.

Capillary: endothelial cells, allow exchange of products; no muscle or elastic tissue.

Venules: small amounts of muscle and connective tissue.

Veins: larger veins have valves to prevent backflow of blood; carry blood back to heart; large diameter, thin walled.

Pulmonary circulation

Deoxygenated blood passes through pulmonary circulation to receive O2.

Right ventricle, pulmonary semilunar valve, pulmonary artery, pulmonary capillaries, pulmonary veins, left atrium, bicuspid valve, left ventricle, aortic semilunar valve, and aorta.

Systemic circulation

Refers to blood pumped from lt ventricle to all parts of body and then to rt atrium.

Aorta: largest artery, main trunk of systemic arterial circulation.

Vena cava: returns deoxygenated blood to rt atrium.

Superior vena cava: from head, neck, chest, and upper extremities.

Inferior vena cava: from parts of body below diaphragm.

Electrical conduction system

Automaticity: specialized ability to contract in rhythmic pattern.

Irritability: excitability or sensitivity. Hormones, ion concentration, changes in

body temp. affect the conduction system. Depolarization = contraction. Repolarization = relaxation (resting state).

Impulse pattern

Initiated in SA node in Rt. Atrium. “Pacemaker” of heart. Internodal pathways to atria.

AV node: Rt atrium, slows impulses to allow atrium to contract and ventricles to fill.

Bundle of His: group of conduction fibers in base of rt atrium.

Rt. and Lt. Bundle branches in septum. Perkinje’s fibers: surround ventricles.

Cardiac cycle: systole/diastole

Refers complete heartbeat. Systole: = contraction, blood is pumped out

of the ventricles. (depolarization). Atria relax to receive blood. (repolarization). AV valves close: S1: first heart sound. Ventricles contract in response to electrical

impulse having passed through.

Diastole

Diastole = relaxation, blood enters the relaxed chambers.

Ventricles fill. Semilunar valves close: S2: 2nd heart

sound. Atria contract in response to electrical

impulse.

Stroke volume/cardiac output

Stroke volume: volume of blood ejected (pumped) during each ventricular contraction (heartbeat).

Cardiac output: amount of blood ejected (pumped) by each ventricle per minute.

CO = SV X HR. Numerous factors affect CO.

Stroke volume factors

Preload: volume of blood within ventricles at end of diastole, comes from veins, before next contraction. Preload determines the amount of stretch placed on the myocardium.

Afterload: pressure that ventricles work against when they contract to eject blood from the heart. That pressure is located in arteries (peripheral resistance or arterial BP).

Normal heart overcomes afterload and maintains CO except when muscles have been damaged.

Contractility increased by norepinephrine and epinephrine.

Increased preload, afterload and contractility increase workload and O2 demand on heart.

Inotropic state

Inotropic state = strength of myocardial contraction unrelated to blood volume.

Affected by sympathetic stimulation, metabolic abnormality, hypoxemia, metabolic acidosis, drugs (epinephrine).

Starling’s law

To a point the heart will pump out all blood it receives within certain limits.

The more the fibers are stretched, the greater their force of contraction.

If stretched beyond capacity- blood will accumulate in ventricles and back up into pulmonary system.

Heart sounds

Produced by closure of valves. Lubb: (S1) long duration, low pitch, AV

valves close. Dubb: (S2) short duration, sharp sound,

semilunar valves close. Murmur: swishing sound, may be normal or

abnormal.

Cardiovascular assessment

Subjective data: past CV problems, health habits (smoking, diet, activity), current CV problems.

History: description of symptoms, when they occurred, course and duration, location, precipitating factors, relief measures.

Pain

Character, quality, radiation, associated symptoms.

Rated on pain scale. Location: *chest, radiated to jaw, left shoulder. Description: dull, sharp, pressure, squeezing,

crushing, viselike, grinding, radiating. Precipitating onset. Pain in extremities or lack of sensation.

Palpitations

Characterized by rapid, irregular, or pounding heartbeat.

Associated with dysrhythmias or ischemia.

Dyspnea

Exertional dyspnea is associated with decreased cardiac output.

DOE, DAR, PND, orthopnea.

Cough

Dry, productive, irritating, spasmodic. May be associated with dyspnea.

Fatigue

Exhaustion/ activity intolerance. Associated with decreased cardiac output. Depression may associated with fatigue.

Syncope

Fainting: brief lapse of consciousness. Caused by transient cerebral hypoxia. Sudden decrease in cardiac output to brain

resulting from dysrhythmia or decreased pumping action of heart.

Preceded by lightheadedness.

Objective data

Vital signs. LOC. Lung sounds. Bowel sounds. Sputum. Heart: Apical pulse, heart sounds, carotid arteries,

systemic with no bruit. Jugular veins not distended when sitting or

standing. Extremities: color, temp, moisture, edema, hair

distribution, capillary refill, clubbing, peripheral pulses, Homan’s sign, turgor.

Cyanosis

Caused by: excess of deoxygenated Hgb in blood.

Results from: decreased cardiac output and poor peripheral perfusion.

Diaphoresis

Profuse sweating associated with clamminess.

Result of decreased cardiac output and poor peripheral perfusion.

Edema

Wt. Gain of more than 3lb. In 24 hours. Inability of heart to pump efficiently or

accept venous return, causes backflow of blood and increased blood volume.

Increased hydrostatic pressure results and an increase in fluid to interstitial spaces.

Diagnostic Tests

CBC

Determination of RBCs, WBCs, platelets, Hgb, Hct.

Low Hgb = decreased O2 carrying capacity High WBC = infection or inflammation. High RBC = body compensating for

chronic hypoxemia by stimulating RBC production in bone marrow, leading to secondary polycythemia.

Cardiac enzymes

Elevated amounts of enzymes (proteins, cardiac “markers”) are released into blood during cardiac muscle cell damage.

These enzymes are helpful in determining the degree of myocardial damage and the timing of onset of damage.

Some enzymes are more specific to cardiac muscle tissue.

Creatine phosphokinase (CPK)

Enzyme found in brain, skeletal muscle, and myocardium.

Can be broken down into isoenzymes. CPK II (MB) is more specific to cardiac

tissue. Levels > 7.5 ng/ml associated c MI. Onset: 3-6 hours; peak 12-18 hours;

duration 3-4 days.

Lactic dehydrogenase (LDH)

Found in many body tissues (cardiac, kidneys, RBCs, brain, stomach, skeletal muscle). Normal < 100 U/L.

Late indicator of damage. Rises in 24-72 hours; peaks in 3-4 days;

returns to normal levels in about 14 days. Not as specific as other enzymes.

Myoglobin

Small O2 binding protein found in cardiac and skeletal muscle.

Because it is smaller when compared to larger enzymes, it is detected earlier.

1-4 hours after onset. Peak 6-9 hrs. Must be done within 1st 18 hrs after onset. Normal < 92 men; < 76ng/ml women.

Troponin

Protein located on cardiac and skeletal muscle tissue.

3 forms. Troponin I is more specific; found exclusively in cardiac tissue.

Onset 3-6 hours; peaks 14-20 hours; returns to normal in 5-7 days.

Elevated levels of Troponin I is diagnostic of MI. Range 0 - 0.4ng/mL.

Serum Lipids

Cholesterol: fatty substance coated with 2 types of proteins. LDL or HDL.

Total cholesterol level is sum of all cholesterols. Level should be < 200mg/dl. (nonfasting test).

Associated with diet high in saturated fat, cholesterol and calories.

Hyperlipidemia: elevated levels of any or all of lipids in plasma.

Triglycerides: Mixture of fatty acids. Normal: 40-190 ng/dl.

HDL/LDL

HDL and LDL: need to fast 12 hrs. High-density lipoprotein: “good

cholesterol”. More protein than fat. Removes cholesterol from vessels and

transports to liver for removal. Higher the level = less risk of CAD. Desirable level = 35 or >.

LDL

Low-density lipoprotein: “bad cholesterol”. Promotes CAD.

Equal amount of fat and protein. Transports cholesterol from the liver to body

tissues, accumulating in vessel walls. Level < 160mg/dl (c no risk factors). Higher the

level = greater risk of CAD. Desired level for LDL depends on the risk factor profile of pt. More risks = a goal for a lower LDL level. (ex. 100mg/dl)

EKG

A graphic representation of the heart’s electrical activity reflected by changes in the electrical potential at the skin surface.

Recorded as a tracing on a strip of paper. “Resting” EKG over < one minute. Telemetry: continuous visualization on a

screen (monitor).

Purposes

Identify rhythm disturbances. Provides information about the position of

the heart in the chest and the size of the chambers.

Detects electrolyte imbalances. Monitors the effectiveness of pacemakers

and cardiotonic meds.

Holter monitor

“Ambulatory” EKG: a type of portable EKG which records 12- 48 hours of usual pt.’s activities with normal stress.

Pt keeps a diary of activities and symptoms. Purposes: determines exercise tolerance

post-MI. Provides more diagnostic information.

Inpatient or outpatient basis. Detects intermittent arrythmias c ADLs c

associated manifestations of dizziness, palpitations, chest pain.

Guages antiarrythmic meds. Instruct pt to update diary regularly and

note any symptoms; not to get monitor wet.

EKG waveforms

P wave: depolarization or contraction of the atria. SA node fires impulse, delay by AV node seen as space after P wave.

QRS complex: ventricles depolarize or contract, atria repolarize (relax), strong signal because of greater mass of ventricles.

T wave: ventricles repolarize or relax.

Intervals are the length of time it takes the impulse to travel from one area of heart to another.

Cardiac dysrhythmias result of abnormal pacemaker function.

Cardiac dysrhythmias (arrhythmia) Any cardiac rhythm that deviates from

normal sinus rhythm. The result of alteration in the formation of

impulses through the sinoatrial node. Results from irritability of myocardial cells

that generate impulses. S&S and treatment vary depending on type

and severity.

Classified according to origin (atrial or ventricular),

Mechanism: bradycardia, tachycardia, or both.

Normal sinus rhythm

Originates in SA node. Characterized by: Rate: 60-100 beats/min. P waves: precede each QRS complex.

(atrial depolarization) P-R interval: interval between atrial and

ventricular repolarization.

QRS: ventricular depolarization. T wave: ventricular repolarization. Rhythm: regular.

Sinus Tachycardia

A rapid regular rhythm. Originates in SA node. Rate: 100 or >. S&S: occasional palpitations, hypotension,

angina. Most are asymptomatic.

Sinus Bradycardia

A slow rhythm. Originates in SA node. Rate: <60. S&S: fatigue, lightheadedness, syncope. Some are asymptomatic.

Atrial fibrillation

A very rapid production of atrial impulses. Atria beat chaotically resulting in improper

contraction. Rate: 350-600. S&S: pulse deficit, palpitations, dyspnea,

angina, lightheadedness, pulmonary edema, decreased cardiac output.

May cause emboli or CHF.

Premature Ventricular Contractions PVCs: early ventricular beats that occur in

conjunction with regular rhythm. Originates in more than one location in

ventricles. S&S: depend on frequency of PVCs and

their effect on ability of heart to pump effectively.

Some are asymptomatic. Palpitations, weakness, lightheadedness,

decreased cardiac output. PVCs that last long enough to cause

ventricular tachycardia may lead to death.

Ventricular Tachycardia

A regular or slightly irregular rhythm in which 3 or more successive premature ventricular contractions occur.

Rate: 140-240. Life threatening. May lead to ventricular fibrillation and

death.

Ventricular fibrillation

Ventricular muscles are quivering. Characterized by rapid and disorganized

ventricular pulsation. *Medical emergency. S&S: are a result of no cardiac output. Loss of consciousness, lack of pulse, loss of

BP and respirations, possible seizures, and sudden death if untreated within 3 min.

Cardiac arrest

A sudden cessation of cardiac output and effective circulation.

Usually precipitated by ventricular fibrillation or ventricular asystole.

Asystole: a life threatening cardiac conduction characterized by absence of electrical and mechanical activity in heart. S&S: lack of pulse and breathing.

Atrial arrhythmias prevent proper filling of ventricles and decrease CO.

Ventricular arrhythmias prevent proper filling of ventricles, decrease or absent CO. Life-threatening.

V Tach is likely to result in V Fib and death.

Arteriogram

Series of radiographs taken after an injection of radiopaque dye into a coronary artery.

Diagnose vessel occlusion, pooling in chambers of heart, and congenital anomalies.

Stress Test

Exercise EKG. Types: Treadmill: walking, then increase

speed and incline until pt reaches a target HR, has chest pain, fatigue, extreme dyspnea, vertigo, or claudication (calf pain c walking, relieved c rest).

Stationary bicycle.

MUGA: (multigated acquistion scan) use of computers with EKG during scanning.

Persantine: pharmacological stress test. Vasodilator. No caffeine 12 hrs. prior.

Thallium: nuclear agent used during scan. Purpose: To evaluate CV fitness prior to an exercise

program, To diagnose exercise induced symptoms and

arrythmias, To evaluate the effectiveness of meds.

Nursing care: No eating, drinking, or smoking 2 hours prior.

Wear comfortable clothes. Continue all meds. Vitals, monitor. The earlier manifestations developed =

more serious the heart disease is.

Cardiac catheterization

Invasive procedure used to visualize heart chambers, valves, great vessels, and coronary arteries in order to determine the degree of blockage.

Catheter is inserted through a peripheral vessel and advanced to heart chambers.

Dye injected to assist in examining structure and motion of the heart.

Measure pressure within heart. Measure blood-volume relationship to

cardiac competence. Determine valvular defects, arterial

occlusion, or congenital anomalies. Blood samples obtained.

Nursing care

Check for allergy to iodine (used as contrast medium).

Consent. NPO. Give sedative as ordered. Instruct will feel warmth/fluttering sensation

as catheter is passed. Post-procedure: Pressure dressing and 5-

10lb. sandbag used to provide pressure over site to prevent hemorrhage.

Supine position 4- 8hrs. Then elevate HOB 30 degrees.

Inspect site for bleeding and swelling. Monitor vital signs, heart and lung sounds,

peripheral pulses, color and sensation. Encourage fluids to eliminate dye. Monitor I&O, labs. Advise pt. to report chest pain.

Percutaneous transluminal coronary angioplasty (PTCA) Invasive surgical procedure performed in

cardiac cath lab. Consent required. Balloon tipped catheter is guided by

fluoroscopy from the femoral or brachial artery to the coronary arteries.

Balloon is inflated intermittently and opens narrowed vessel to improve blood flow.

1-2 hour procedure. Mild sedative is given. Post procedure: monitor catheter insertion

site for hemorrhage. Risk for complications.

Stent Placement

Used to treat abrupt or threatened vessel occlusion following PTCA.

Expandable, meshlike structures compress against vessel wall.

Potential for thrombus formation: must be on anticoagulants for 3 months.

Complications: hemorrhage, injury, dysrhythmias.

Risk factors for CV disease

Nonmodifiable: family history, Age: > with elderly. Sex: men > risk, but incidence increasing in

women. Race: African-American males (high BP,

CVA), Hispanics with diabetes, Caucasians have highest rate of CV disease, higher total cholesterol levels.

Modifiable factors

Smoking: 2-3 X > risk than nonsmokers. More Caucasian women smoke than other women.

Hyperlipidemia: diet, exercise, meds. Hypertension: BP > 140/90 mm Hg. Diabetes mellitus: related to elevated BS

levels, altered lipid metabolism c elevated cholesterol and triglycerides.

Obesity: increases workload. Increased obesity among Americans.

Sedentary lifestyle: exercise lowers BS levels, improves ratio of HDL to LDL, reduces Wt., BP, stress, and improves well-being.

Stress: releases catecholamines, results in vasoconstriction.

Oral contraceptives Psychosocial factors: Type A personality. Asthma: more prone to heart disease; meds

side effects or chronic lung inflammation damages arteries.

Homocysteine: elevated levels triple your risk; amino acid associate with folate deficiency.

Dietary Modifications

Total fat intake < 30 % of total calories. Saturated fats < 10 % of total calories. Sodium under 1g of sodium for every 1,000

calories consumed. Cholesterol < 300mg. (eggs, meat, butter,

whole milk) Alcohol moderation.

Polyunsaturated fats lower both LDL and HDL (corn oil).

Monounsaturated fats lower only LDL. (olive oil, canola oil).

Dietary supplements: Vitamin E, antioxidant.

Common cardiac drugs

Adrenergics Adrenergic blockers. Diuretics. Beta-blockers. Calcium channel blockers. ACE inhibitors. Vasodilators.

Adrenergics

Stimulate the sympathetic nervous system. Act on one or more of adrenergic receptor

sites. Alpha 1-receptor: increases force of

contraction of heart; vasoconstriction, increases BP.

Alpha 2-receptor: inhibits release of norepinephrine, vasodilator, decreases BP.

Beta1- receptor: increases HR/force of contraction, renin secretion and BP.

Beta 2- receptor: bronchodilation. Many of adrenergic drugs stimulate more

than one receptor site. Epinephrine: sc or IV, inhalation, topically.

Not po. Used in shock, cardiac arrest.

Dopamine: to correct hypotension. Ephedrine HCL: hypotension. (OTC meds). Norepinephrine bitartrate: shock, potent

vasoconstrictor. Side effects: hypertension, tachycardia,

palpitations, dysrhythmias, tremors, dizziness, difficulty urinating, nausea, vomiting.

Nursing implications

Monitor vitals and for side effects. Monitor urinary output for retention. Check IV site for tissue necrosis. Offer food to avoid N/V. Instruct pt. to read med labels.

Adrenergic Blockers

Stimulate alpha2 receptors , decrease sympathetic response, decrease epinephrine, norepinephrine and renin release, resulting in decreased peripheral vascular resistance.

(promote vasodilation to decrease BP) Minimal effect on CO and renal blood flow. Can cause Na/H2O retention. Given c

diuretic.

Side effects: orthostatic hypotension, tachycardia, bradycardia, dry mouth, drowsiness and dizziness.

Not used as frequently. Methyldopa (Aldomet) one of 1st drugs

widely used in controlling hypertension. Clonidine: 7 day transdermal patch.

Alpha adrenergic blockers

Block alpha adrenergic receptors to promote vasodilation and decrease BP.

Benefits: do not affect BS, lipids, or respiratory function.

Prazosin HCL (Minipress): selective Diuretic added to reduce edema. Side effects: hypotension, tachycardia, wt.

Gain, nausea, drowsiness, nasal congestion.

If taken with NTG can cause syncope. If taken with other hypertensive drugs or

alcohol can cause hypotension. Monitor for fluid retention. Encourage pt to decrease salt intake. Therapeutic effect takes 4 weeks.

Beta-adrenergic blockers: decrease HR, BP, CO, and force of contractions.

Inderal: nonselective (beta1 and 2): many side effects- bronchoconstriction.

Metaprolol (Lopressor) cardioselective. Uses: cardiac dysrhythmias, hypertension,

tachycardia, and angina.

Side effects

Beta-adrenergic blockers: bradycardia, dizziness, hypotension, HA, mood changes.

Nursing: Monitor vital signs, assess lung sounds, instruct to avoid stopping med and to avoid orthostatic hypotension.

Alpha/beta blockers

Causes vasodilation, decreased HR and contractility of heart.

Large doses increase airway resistance- decreased dosage necessary in asthma pts.

Labetalol HCL (Trandate, Normadyne). May cause orthostatic hypotension,

palpitation and syncope.

Diuretics

Thiazides Loop diuretics Osmotic diuretics Carbonic anhydrase inhibitors Potassium-sparing diuretics

Diuretics

Purpose: to decrease BP and edema. Single or combination therapy. Produce diuresis by inhibiting Na and H2O

reabsorption in one or more segments of the renal tubules.

Diuretics that act closest to the glomeruli have the greatest effect on Na loss.

Potassium-wasting or sparing.

Combination diuretics may promote both K+ wasting and sparing.

5 categories: thiazide/thiazide-like loop osmotic carbonic anhydrase inhibitor potassium-sparing

Thiazides

Act on the distal convoluted tubule to promote Na and H2O excretion and cause vasodilation to decrease BP.

Used in pts. c normal renal function. Not for immediate treatment. Increases BS. Monitor BS.

Should be taken in am (long half-life) to avoid nocturia.

Can elevate lipids and uric acid. Can cause hypokalemia and hypocalcemia

(potential for digitalis toxicity). HCTZ is usually 1st one in this group

ordered. Inexpensive/ well tolerated.

Nursing implications

Assess vital signs, wt., urine output, labs, BS, edema.

Advise to take in am and c food. Instruct to include foods rich in K+ or may

need K+ supplement. Instruct pt. regarding potential for postural

hypotension.

Loop diuretics

Potent drugs that act on ascending loop of Henle by inhibiting Cl transport of Na into circulation.

No effect on BS. Edecrin is most potent and rarely used. Bumex is more potent than Lasix. Can be used in pts.c renal disease.

Main side effects: fluid and electrolyte imbalances, high uric acid, elevated lipids.

Digitalis toxicity can result due to loss of K+.

Lasix: PO: onset of action 30-60”; IV- 5”.

Osmotic diuretics

Act by increasing concentration of plasma and fluid in renal tubules, Na, Cl, K+, and H2O loss.

Used: to prevent kidney failure, decrease ICP and IOP.

Mannitol: IV potent K+ wasting diuretic used in emergency.

Uses: to prevent acute renal failure decrease cerebral edema reduce IOP in narrow-angle glaucoma promoted diuresis in chemotherapy pts.

Carbonic anhydrase inhibitors

Act by blocking the action of enzyme carbonic anhydrase which causes increased Na, K+, and bicarbonate excretion.

Potential for metabolic acidosis; high BS, uric acid, and Ca levels.

Uses: decrease IOP, for edema, seizures. Diamox PO or IV.

Potassium-sparing diuretics

Mild diuretic that is weaker than thiazides and loop diuretics.

K+ supplements should NOT be used. Act in collecting tubules and interfere c

NaK+ pump controlled by aldosterone. More effective if used c K+ wasting diuretic

(Aldactone and HCTZ).

Nursing implications

Side effects: hyperkalemia. Should not be taken c ACE inhibitor

because both spare K+. Instruct pt. to avoid foods rich in K+. Monitor for hyperkalemia: labs, EKG, vital

signs, nausea, diarrhea, ABD cramps.

Vasodilators

Potent antihypertensive drugs that cause vasodilation.

Peripheral edema results due to Na/H2O retention: given c diuretic.

Reflex tachycardia results due to vasodilation: given c beta blocker.

Diazoxide (Hyperstat) and Sodium nitroprusside (Nipride, Nitropress) used in hypertensive emergency.

Hydralazine HCL (Apresoline) used for hypertension.

ACE Inhibitors

Act by inhibiting angiotensin-converting enzyme,

Inhibits formation of angiotensin II (prevents vasoconstriction)

Blocks release of aldosterone (Na retaining hormone) resulting in Na and H2O excretion.

Used to treat hypertension or CHF.

African-Americans and elderly need a diuretic added to achieve therapeutic response.

10 different drugs in this category. 1st drug Captopril (Capoten). Most drugs end in “pril”.

Side effects: hypotension and hyperkalemia. Nursing implications: Should not be given c

Potassium-sparing diuretics or salt substitutes containing potassium.

Captopril is given 20” to 1 hr ac.

Angiotensin II blockers

New drugs similar to ACE inhibitors. Block angiotensin II from receptors. Cause vasodilation and decreased

peripheral resistance. Losartan (Cozaar). Can cause angioedema. Not as effective c African-Americans.

Calcium channel blockers

Decrease calcium levels and promote vasodilation = decreased BP.

Better BP response in African-Americans. Verapamil (Calan), Diltiazem (Cardizem),

Nifedipine (Procardia). Side effects: dizziness, bradycardia,

hypotension, HA.

Cardiac glycosides

3 effect on heart: 1. Positive inotropic action (increases

myocardial contraction, CO). 2. Negative chronotropic action (decreases

HR). 3. Negative dromotropic action (decreases

conduction of heart cells).

Used to treat CHF, atrial flutter or atrial fibrillation.

Nursing: Check apical pulse for 1”. HOLD if <60.

Potassium-wasting diuretics and cortisone c digoxin can result in hypokalemia and digoxin toxicity.

Digitoxin (potent cardiac glycoside c long half-life) vs Digoxin.

Ensure that correct drug is given. Check serum digoxin levels. Normal level = 0.5- 2.0 ng/mL. Check serum K+ levels.

Instruct pt. to eat foods rich in K+. Monitor for signs of digoxin toxicity:

anorexia, nausea, vomiting, bradycardia, cardiac dysrhythmias, visual disturbances.

Monitor response to med: decreased HR, decreased rales.

Teach pt to take pulse and when to call MD.

Antianginal drugs

Nitrates Beta blockers Calcium channel blockers

Increase blood flow by increasing O2 flow or decreasing O2 demand.

Nitrates: relax coronary arteries and dilates veins. Beta blockers: decreases HR/contractility to

decrease O2 demand. Calcium channel blockers: relax coronary

arteries, dilates arterioles, decrease HR/contractility.

Nitrates

Nitroglycerin (NTG): 1st drug to treat angina. Must be given SL, ointment, patch, IV. Give NTG 1 tab (0.4mg or gr1/150) SL q 5”

up to 3 doses until chest pain relieved. Call MD if pain not relieved by the 3rd dose.

Monitor BP and pulse. May have stinging/biting sensation.

Side effects: HA (most common), dizziness or faintness.

Nitrobid ointment not used as much due to effect lasts only 6-8hrs.

Transderm Nitro patch applied daily. Rotate sites.

Tylenol can be given for HA. Taper dose of ointment and patch.

Other nitrates

Isosorbide dinitrate (Isordil): PO, SL, chewable, SR forms. Flushing may occur.

Isosorbide mononitrate (Imdur): PO, SR. Tolerance to nitrates may develop. SR

Imdur form provides continued delivery and decreases tolerance.

Nursing implications.

Have pt sit or lie down when giving initial dose and when giving NTG.

Monitor vital signs. Give sip of water prior to NTG to enhance

absorption. Instruct pt when to call MD.

Drugs for Circulatory disorders

Anticoagulants/antiplatelets Thrombolytics Antilipemics Peripheral vasodilators

Anticoagulants

Used to inhibit new clot formation in veins. Do NOT dissolve clots already formed. Heparin: binds c antithrombin III,

inactivates thrombin, inhibits conversion of fibrinogen to fibrin.

Must be given subcut for prophylaxis, IV to treat acute thrombosis.

Monitor PTT. Monitor for bleeding. Protamine sulfate IV is antidote. Side effects: itching and burning.

Low molecular weight heparins

Lower risk of bleeding. Protamine sulfate is antidote.

More stable response. Can be started inpt. and taught to give injections at home.

PTT not needed. Binds to antithrombin III. Enoxaparin (Lovenox), dalteparin (Fragmin).

Given subcut BID in ABD. Prefilled syringes. Instruct pt not to take other antiplatelet

drugs (ASA).

Coumadin

Long term oral anticoagulant. Inhibit hepatic synthesis of Vit K and

affecting clotting factors. Warfarin (Coumadin) most commonly used

form. Monitor PT/INR. (INR 2-3) Monitor for bleeding. (Vit K/blood or

platelets are given as antidote).

Antiplatelets

Prevents thrombosis in arteries by suppressing platelet aggregation.

Used to prevent MI or CVA. ASA, dipyridamole (Persantine), ticlopidine

(Ticlid). DC ASA one week prior to any surgery.

Thrombolytics

Used to dissolve clots by converting plasminogen to plasma.

Reduces tissue necrosis caused by blocked artery.

Used to treat coronary artery thrombi, DVT, pulmonary embolism.

5 drugs: ex. Streptokinase.

Must by given IV and within 4-6 hrs. Side effects: hemorrhage, allergic reaction. Contraindications: recent bleeding (CVA,

trauma, taking anticoagulants or ASA) and severe hypertension.

Antidote: aminocaproic acid (Amicar). Labs: CBC, PT, EKG. Monitor vitals and for

signs of bleeding.

Antilipemics

Lower abnormal lipid blood levels when diet, exercise and smoking cessation are ineffective.

Resins: bind c bile acids in intestine. Cholestyramine (Questran); Colestipol (Colestid). Powder mixed c water or juice. Side effects: constipation, peptic ulcer.

Fibric acid derivatives: gemfibrozil (Lopid).

Nicotinic acid (Niacin, Vit B2): very effective but has many side effects (flushing, GI). Requires large doses. Careful monitoring.

Statins: inhibit enzyme HMG CoA reductase in cholesterol synthesis in liver.

Reduces cholesterol within 2 weeks. Names end in “statin”.

Ex: Lovastatin (Mevacor), atorvastatin (Lipitor), simvastatin (Zocor), pravastatin (Pravachol).

Statins are contraindicated in liver disease. Nursing implications for all antilipemics: Give c water/meals. Monitor liver enzymes, lipid

levels, vital signs. Instruct pt. drug therapy is lifetime commitment. Not a replacement for diet/exercise.

Peripheral vasodilators

Increase blood flow to extremities and promote vasodilation.

Used in peripheral vascular disease. Ex. Vasodilan. Side effects: tachycardia, hypotension,

flushing, HA dizziness, GI.

Nursing implications

Assess vital signs and circulation to extremities.

Instruct pt. not to smoke, drink alcohol, or use ASA like drugs without MD approval.

Take med with meals.