RN Expert Guides: Cardiovascular Care, 1st Edition (2008)

Chapter 4. Treatments

Many treatments are available for patients with cardiovascular disease. The dramatic ones, such as heart transplantation and artificial heart insertion, have received a lot of publicity. However, some more commonly used treatment measures include:

·

drug therapy

·

surgery

·

balloon catheter treatments

·

defibrillation

·

synchronized cardioversion

·

pacemaker insertion.

DRUG THERAPY

Types of drugs used to improve cardiovascular function include:

·

 

·

antiarrhythmics

·

antianginals

·

antihypertensives

·

 

·

adrenergics

·

beta-adrenergic receptor blockers

·

antilipemics.

Cardiac glycosides and PDE inhibitors

Cardiac glycosides and PDE inhibitors increase the force of the heart's contractions. Increasing the force of contractions is known as a positive inotropic effect, so these drugs are also called inotropic drugs (affecting the force or energy of muscular contractions). (See .)

UNDERSTANDING CARDIAC GLYCOSIDES AND PDE INHIBITORS

Cardiac glycosides and phosphodiesterase (PDE) inhibitors have a positive inotropic effect on the heart, meaning they increase the force of contraction. Use this table to learn about the indications, adverse reactions, and nursing considerations associated with these drugs.

DRUGS

INDICATIONS

REACTIONS

NURSING

CONSIDERATIONS

CARDIAC GLYCOSIDE

Digoxin (Lanoxin)

 

·

Digoxin toxicity (nausea, abdominal pain, headache, irritability, depression, insomnia, vision disturbances, arrhythmias)

·

Arrhythmias

·

Anorexia

·

If immediate effects are required (as with a supraventricular arrhythmia), a loading dose of digoxin is required.

·

Check apical pulse for 1 minute before administration; withhold drug and report pulse less than 60 beats/minute.

·

Therapeutic levels are 0.5 to 2 ng/ml.

PDE INHIBITORS

Inamrinone, milrinone (Primacor)

Heart failure refractory to digoxin, diuretics, and vasodilators

·

Arrhythmias

·

Nausea

·

Vomiting

·

Headache

·

Fever

·

Chest pain

·

Hypokalemia

·

Thrombocy-topenia

·

These drugs are contraindicated in patients in the acute phase of myocardial infarction (MI) and after an MI.

·

 

Cardiac glycosides, such as digoxin (Lanoxin), also slow the heart rate (called a negative chronotropic effect) and slow electrical impulse conduction through the atrioventricular (AV) node (called a negative dromotropic effect).

PDE inhibitors, such as inamrinone and milrinone (Primacor), are typically used for short-term management of heart failure or long-term management in patients awaiting heart transplant surgery. PDE inhibitors improve cardiac output by strengthening contractions. These drugs are thought to help move calcium into the cardiac cell or to increase calcium storage in the sarcoplasmic reticulum. By directly relaxing vascular smooth muscle, they also decrease peripheral vascular resistance (afterload) and the amount of blood returning to the heart (preload).

Antiarrhythmics

Antiarrhythmics are used to treat arrhythmias, which are disturbances of the normal heart rhythm. (See Understanding antiarrhythmics.)

Unfortunately, many antiarrhythmics can worsen or cause arrhythmias, too. In any case, the benefits of antiarrhythmic therapy need to be weighed against its risks.

Antiarrhythmics are categorized into four major classes: I (which includes IA, IB, and IC), II, III, and IV. The mechanisms of action of antiarrhythmics vary widely, and a few drugs exhibit properties common to more than one class. One drug, adenosine (Adenocard), doesn't fall into any of these classes.

CLASS I ANTIARRHYTHMICS

Class I antiarrhythmics are sodium channel blockers. This is the largest group of antiarrhythmic drugs. Class I drugs are commonly subdivided into classes IA, IB, and IC. With the development of many newer drugs, the use of this class of antiarrhythmics is decreasing.

Class IA antiarrhythmics

Class IA antiarrhythmics control arrhythmias by altering the myocardial cell membrane and interfering with autonomic nervous system control of pacemaker cells. Class IA antiarrhythmics include:

·

disopyramide (Norpace)

·

procainamide (Procanbid)

·

quinidine sulfate (Quinidex)

·

quinidine gluconate (Quinaglute).

Class IA antiarrhythmics also block parasympathetic stimulation of the sinoatrial (SA) and AV nodes. Because stimulation of the parasympathetic nervous system causes the heart rate to slow down, drugs that block the parasympathetic nervous system increase the AV node's conduction rate.

This increase in the conduction rate can produce dangerous increases in the ventricular heart rate if rapid atrial activity is present, as in a patient with atrial fibrillation. In turn, the increased ventricular heart rate can offset the ability of the antiarrhythmics to convert atrial arrhythmias to a regular rhythm.

UNDERSTANDING ANTIARRHYTHMICS

Antiarrhythmics are used to restore normal heart rhythm in patients with arrhythmias. Check this table for information about the indications, adverse reactions, and nursing considerations associated with these drugs.

DRUGS

INDICATIONS

ADVERSE

REACTIONS

NURSING

CONSIDERATIONS

CLASS IA ANTIARRHYTHMICS

Disopyramide (Norpace), procainamide (Pro-canbid), quinidine sulfate (Quinidex), quinidine gluconate (Quinaglute)

·

Ventricular tachycardia

·

Atrial fibrillation

·

Atrial flutter

·

Paroxysmal atrial tachycardia

·

Diarrhea

·

Nausea

·

Vomiting

·

Arrhythmias

·

Electrocardiogram (ECG) changes

·

Hepatotoxicity

·

Respiratory arrest

·

Check apical pulse rate before therapy. If you note extremes in pulse rate, hold the dose and notify the practitioner.

·

Use cautiously in patients with asthma.

CLASS IB ANTIARRHYTHMICS

Lidocaine (Xylocaine), mexiletine (Mexitil)

·

 

·

Drowsiness

·

Hypotension

·

Bradycardia

·

Arrhythmias

·

Widened QRS complex

·

IB antiarrhythmics may potentiate the effects of other antiarrhythmics.

·

Administer I.V. infusions using an infusion pump.

CLASS IC ANTIARRHYTHMICS

Flecainide (Tambocor), moricizine (Ethmozine), propafenone (Rythmol)

·

Ventricular tachycardia, ventricular fibrillation, supraventricular arrhythmias

·

New arrhythmias

·

Heart failure

·

Cardiac death

·

Correct electrolyte imbalances before giving.

·

Monitor the patient's ECG before and after dosage adjustments.

CLASS II ANTIARRHYTHMICS

Acebutolol (Sectral), esmolol (Brevibloc), propranolol (Inderal)

·

Atrial flutter, atrial fibrillation, paroxysmal atrial tachycardia

·

Ventricular arrhythmias

·

Arrhythmias

·

Bradycardia

·

Heart failure

·

Hypotension

·

Nausea and vomiting

·

Bronchospasm

·

Monitor apical heart rate and blood pressure.

·

Abruptly stopping these drugs can exacerbate angina and precipitate myocardial infarction.

CLASS III ANTIARRHYTHMICS

 

·

Life-threatening arrhythmias resistant to other antiarrhythmics

·

Aggravation of arrhythmias

·

Hypotension

·

Anorexia

·

Severe pulmonary toxicity (amiodarone)

·

Hepatic dysfunction

·

Amiodarone increases the risk of digoxin toxicity in patients also taking digoxin.

·

Monitor blood pressure and heart rate and rhythm for changes.

·

Monitor for signs of pulmonary toxicity (dyspnea, nonproductive cough, and pleuritic chest pain) in patient taking amiodarone.

CLASS IV ANTIARRHYTHMICS

Diltiazem (Cardizem), verapamil (Calan)

·

Supraventricular arrhythmias

·

Peripheral edema

·

Hypotension

·

Bradycardia

·

Atrioventricular block

·

Flushing (with diltiazem)

·

Heart failure

·

Pulmonary edema

·

Monitor heart rate and rhythm and blood pressure carefully when initiating therapy or increasing dose.

·

Calcium supplements may reduce effectiveness.

MISCELLANEOUS

Adenosine (Adenocard)

·

Paroxysmal supraventricular tachycardia

·

Facial flushing

·

Shortness of breath

·

Dyspnea

·

Chest discomfort

·

Adenosine must be given over 1 to 2 seconds, followed by a 20 ml flush of normal saline solution.

·

Record rhythm strip during administration.

Class IB antiarrhythmics

Lidocaine (Xylocaine), a class IB antiarrhythmic, is one of the antiarrhythmics commonly used in treating patients with acute ventricular arrhythmias. Other IB antiarrhythmics include mexiletine (Mexitil).

Class IB drugs work by blocking the rapid influx of sodium ions during the depolarization phase of the heart's depolarization-repolarization cycle, resulting in a decreased refractory period, which reduces the risk of arrhythmia.

Class IC antiarrhythmics

Class IC antiarrhythmics are used to treat patients with certain severe, refractory (resistant) ventricular arrhythmias. Class IC antiarrhythmics include flecainide (Tambocor), moricizine (Ethmozine), and propafenone (Rythmol).

Class IC antiarrhythmics primarily slow conduction along the heart's conduction system. Moricizine decreases the fast inward current of sodium ions of the action potential. This depresses the depolarization rate and effective refractory period.

CLASS II ANTIARRHYTHMICS

Class II antiarrhythmics include the beta-adrenergic antagonists, also known as beta-adrenergic receptor blockers. Beta-adrenergic receptor blockers used as antiarrhythmics include:

·

acebutolol (Sectral)

·

esmolol (Brevibloc)

·

propranolol (Inderal).

Class II antiarrhythmics block beta-adrenergic receptor sites in the heart's conduction system. As a result, the SA node's ability to fire spontaneously (automaticity) is slowed. The ability of the AV node and other cells to receive and conduct an electrical impulse to nearby cells (conductivity) is also reduced.

Class II antiarrhythmics also reduce the strength of the heart's contractions. When the heart beats less forcefully, it doesn't require as much oxygen to do its work.

CLASS III ANTIARRHYTHMICS

Class III antiarrhythmics are used to treat patients with ventricular arrhythmias. Amiodarone (Cordarone) is the most widely used class III antiarrhythmic.

Although the exact mechanism of action isn't known, class III antiarrhythmics are thought to suppress arrhythmias by converting a unidirectional block to a bidirectional block. They have little or no effect on depolarization.

CLASS IV ANTIARRHYTHMICS

The class IV antiarrhythmics include the calcium channel blockers. These drugs block the movement of calcium during phase 2 of the action potential and slow conduction and the refractory period of calcium-dependent tissues, including the AV node. The calcium channel blockers used to treat patients with arrhythmias are verapamil (Calan) and diltiazem (Cardizem).

ADENOSINE

Adenosine is an injectable antiarrhythmic drug indicated for acute treatment for paroxysmal supraventricular tachycardia. Adenosine depresses the pacemaker activity of the SA node, reducing the heart rate and the AV node's ability to conduct impulses for the atria to the ventricles.

Antianginals

When the heart's oxygen demand exceeds the amount of oxygen being supplied, areas of heart muscle become ischemic. When the heart muscle is ischemic, a person experiences chest pain. This condition is known as angina or angina pectoris.

correct angina by reducing myocardial oxygen demand (the amount of oxygen the heart needs to do its work, increasing the supply of oxygen to the heart, or both. (See How antianginals work.)

HOW ANTIANGINALS WORK

When the coronary arteries can't supply enough oxygen to the myocardium, angina occurs. This forces the heart to work harder, increasing heart rate, preload, afterload, and the force of myocardial contractility. Antianginals relieve angina by decreasing one or more of these four factors.

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The three classes of commonly used antianginals include:

·

nitrates (for acute angina)

·

beta-adrenergic receptor blockers (for long-term prevention of angina)

·

calcium channel blockers (used when other drugs fail to prevent angina). (See Understanding antianginals, pages 148 and 149.)

NITRATES

Nitrates are the drug of choice for relieving acute angina. Nitrates commonly prescribed to correct angina include:

·

isosorbide dinitrate (Isordil)

·

isosorbide mononitrate (Imdur)

·

nitroglycerin (Nitro-Bid).

·

When the veins dilate, less blood returns to the heart.

 

·

This, in turn, reduces the amount of blood in the ventricles at the end of diastole, when the ventricles are full. (This blood volume in the ventricles just before contraction is called preload).

·

By reducing preload, nitrates reduce ventricular size and ventricular wall tension so the left ventricle doesn't have to stretch as much to pump blood. This, in turn, reduces the heart's oxygen requirements.

·

As the coronary arteries dilate, more blood is delivered to the myocardium, improving oxygenation of the ischemic tissue.

UNDERSTANDING ANTIANGINALS

Antianginal drugs are effective in treating patients with angina because they reduce myocardial oxygen demand, increase the supply of oxygen to the heart, or both. Use this table to learn about the indications, adverse reactions, and nursing considerations associated with these drugs.

DRUGS

 

ADVERSE

REACTIONS

NURSING

CONSIDERATIONS

NITRATES

Isosorbide dinitrate (Isordil), isosorbide mononitrate (Imdur), nitroglycerin (Nitro-Bid)

·

Relief and prevention of angina

·

Headache

·

Hypotension

·

Dizziness

·

Increased heart rate

·

Only sublingual and translingual forms should be used to treat an acute angina attack.

·

Monitor the patient's blood pressure before and after administration.

·

Avoid giving nitrates to patients taking erectile dysfunction drugs because of the risk of severe hypotension.

BETA-ADRENERGIC RECEPTOR BLOCKERS

Atenolol (Tenormin), Carvedilol (Coreg), metoprolol (Lopressor), propranolol (Inderal)

·

 

·

First-line therapy for hypertension

·

Stable heart failure due to decreased left ventricle ejection fraction

·

Bradycardia

·

Fainting

·

Fluid retention

·

Heart failure

·

Arrhythmias

·

Nausea

·

Diarrhea

·

Atrioventricular blocks

·

Bronchospasm

·

Hypoglycemia

·

Monitor apical pulse rate before giving. Monitor blood pressure, electrocardiogram, and heart rate and rhythm frequently.

·

 

·

Monitor patients with a history of respiratory problems for breathing difficulty if using a nonselective beta-adrenergic receptor blocker.

CALCIUM CHANNEL BLOCKERS

Amlodipine (Norvasc), diltiazem (Cardizem), nifedipine (Adalat), verapamil (Calan)

·

Long-term prevention of angina (especially Prinzmetal's angina)

·

Hypertension

·

Orthostatic hypotension

·

Heart failure

·

Hypotension

·

Arrhythmias

·

Dizziness

·

Headache

·

Persistent peripheral edema

·

Pulmonary edema

·

Monitor cardiac rate and rhythm and blood pressure carefully when initiating therapy or increasing the dose.

·

Calcium supplementation may decrease the effects of calcium channel blockers.

The arterioles provide the most resistance to the blood pumped by the left ventricle (called peripheral vascular resistance). Nitrates decrease afterload by dilating the arterioles, reducing resistance, easing the heart's workload, and easing oxygen demand.

BETA-ADRENERGIC RECEPTOR BLOCKERS

Beta-adrenergic receptor blockers are used for long-term prevention of angina, and they're one of the main types of drugs used to treat hypertension. Beta-adrenergic receptor blockers include:

·

atenolol (Tenormin)

·

carvedilol (Coreg)

·

metoprolol tartrate (Lopressor)

·

propranolol (Inderal)

Beta-adrenergic receptor blockers decrease blood pressure and block beta-adrenergic receptor sites in the heart muscle and conduction system. Decreasing the heart rate and reducing the force of the heart's contractions result in a lower demand for oxygen.

CALCIUM CHANNEL BLOCKERS

Calcium channel blockers are commonly used to prevent angina that doesn't respond to drugs in either of the other antianginal classes. Some calcium channel blockers are also used as antiarrhythmics.

Calcium channel blockers include:

·

amlodipine (Norvasc)

·

diltiazem (Cardizem)

·

nifedipine (Adalat)

·

verapamil (Calan).

By preventing arterioles from constriction, calcium channel blockers also reduce afterload. In addition, decreasing afterload decreases the heart's oxygen demands.

Calcium channel blockers also reduce the heart rate by slowing conduction through the SA and AV nodes. A slower heart rate reduces the heart's need for oxygen.

Antihypertensives

Antihypertensives, which reduce blood pressure, are used in patients with hypertension, a disorder characterized by high systolic blood pressure, diastolic blood pressure, or both.

Treatment for hypertension begins with beta-adrenergic receptor blockers and diuretics. (See Treating hypertension.) If those drugs aren't effective, treatment continues with sympatholytic drugs (other than beta-adrenergic receptor blockers), vasodilators, angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), or a combination of drugs. (See Understanding antihypertensives, pages 152 and 153.)

Sympatholytics

The sympatholytics include several types of drugs but work by inhibiting or blocking the sympathetic nervous system, which causes dilation of the peripheral blood vessels or decreases cardiac output, thereby reducing blood pressure.

TREATING HYPERTENSION

Below is a flowchart for treating hypertension based on the recommendations of the Joint National Committee on the Detection, Evaluation, and Treatment of High Blood Pressure.

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UNDERSTANDING ANTIHYPERTENSIVES

Antihypertensives are prescribed to reduce blood pressure in patients with hypertension. Use this table to learn about the indications, adverse reactions, and nursing considerations associated with these drugs.

DRUGS

INDICATIONS

ADVERSE

REACTIONS

NURSING

SYMPATHOLYTIC DRUGS

Central-acting sympathetic nervous system inhibitors (such as clonidine [Catapres], guanabenz [Wytensin], guanfacine [Tenex], and methyldopa)

Alpha blockers (such as doxazosin [Cardura], phentolamine [Regitine], prazosin [Minipress], and terazosin [Hytrin])

Mixed alpha- and beta-adrenergic receptor blockers (such as labetalol [Normodyne])

Norepinephrine depletors (such as guanadrel [Hylorel])

·

Hypertension

·

Hypotension (alpha blockers)

·

Depression

·

Drowsiness

·

Edema

·

Vertigo (central-acting drugs)

·

Bradycardia

·

Hepatic necrosis

·

Arrhythmias

·

Monitor blood pressure and pulse before and after administration.

VASODILATORS

Diazoxide (Hyperstat I.V.), hydralazine (Apresoline), minoxidil, nitroprusside (Nitropress)

·

Used in combination with other drugs to treat moderate to severe hypertension

·

Hypertensive crisis

·

Tachycardia

·

 

·

Angina

·

Fatigue

·

Headache

·

Severe pericardial effusion

·

Hepatotoxicity

·

Nausea

·

Stevens-Johnson syndrome

·

Monitor blood pressure and pulse before and after administration.

·

Monitor patient receiving nitroprusside for signs of cyanide toxicity.

ANGIOTENSIN-CONVERTING ENZYME (ACE) INHIBITORS

Benazepril (Lotensin), captopril (Capoten), enalapril (Vasotec), lisinopril (Prinivil), quinapril (Accupril), ramipril (Altace)

·

Hypertension

·

Heart failure

·

Angioedema

·

Persistent cough

·

Rash

·

Renal insufficiency

·

Monitor blood pressure and pulse before and after administration.

ANGIOTENSIN II RECEPTOR BLOCKERS

Candesartan (Atacand), irbesartan (Avapro), losartan (Cozaar), olmesartan (Benicar), valsartan (Diovan)

·

Hypertension

·

Heart failure resistant to ACE inhibitors

·

Fatigue

·

 

·

Rash

·

Hypotension

·

Monitor blood pressure and pulse before and after administration.

The sympatholytic drugs are classified by their site or mechanisms of action and include:

·

central-acting sympathetic nervous system inhibitors, such as clonidine (Catapres), guanabenz (Wytensin), guanfacine (Tenex), and methyldopa (Aldomet)

·

alpha blockers, such as doxazosin (Cardura), phentolamine (Regitine), prazosin (Minipress), and terazosin (Hytrin)

·

mixed alpha- and beta-adrenergic receptor blockers such as labetalol (Normodyne)

·

norepinephrine depletors such as guanadrel (Hylorel).

Vasodilators

The two types of vasodilators include calcium channel blockers and direct vasodilators. Theses drugs decrease systolic and diastolic blood pressure.

Calcium channel blockers produce arteriolar relaxation by preventing the entry of calcium into the cells. This prevents the contraction of vascular smooth muscle.

Direct vasodilators act on arteries, veins, or both. They work by relaxing peripheral vascular smooth muscles, causing the blood vessels to dilate. This decreases blood pressure by increasing the diameter of the blood vessels, reducing total peripheral resistance.

The direct vasodilators include:

·

hydralazine (Apresoline)

·

minoxidil (Loniten)

·

diazoxide (Hyperstat I.V.)

·

nitroprusside (Nipride).

Hydralazine and minoxidil are usually used to treat patients with resistant and refractory hypertension. Diazoxide and nitroprusside are reserved for use in hypertensive crisis.

ACE inhibitors

ACE inhibitors reduce blood pressure by interrupting the renin-angiotensin-aldosterone system (RAAS). (See Antihypertensives and the RAAS.)

Commonly prescribed ACE inhibitors include:

·

benazepril (Lotensin)

·

captopril (Capoten)

·

enalapril (Vasotec)

·

lisinopril (Prinivil)

·

quinapril (Accupril)

·

ramipril (Altace).

Here's how the RAAS works:

ANTIHYPERTENSIVES AND THE RAAS

The renin-angiotensin-aldosterone system (RAAS) regulates the body's sodium and water levels and blood pressure.

·

Juxtaglomerular cells near the glomeruli in each kidney secrete the enzyme renin into the blood.

·

Renin circulates throughout the body and converts angiotensinogen, made in the liver, to angiotensin I.

·

In the lungs, angiotensin I is converted by hydrolysis to angiotensin II.

·

Angiotensin II acts on the adrenal cortex to stimulate production of the hormone aldosterone. Aldosterone acts on the juxtaglomerular cells to increase sodium and water retention and to stimulate or depress further renin secretion, completing the feedback system that automatically readjusts homeostasis.

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·

Normally, the kidneys maintain blood pressure by releasing the hormone renin.

·

Renin acts on the plasma protein angiotensinogen to form angiotensin I.

·

Angiotensin I is then converted to angiotensin II.

·

Angiotensin II, a potent vasoconstrictor, increases peripheral resistance and promotes the excretion of aldosterone.

·

Aldosterone, in turn, promotes the retention of sodium and water, increasing the volume of blood the heart needs to pump.

ACE inhibitors work by preventing the conversion of angiotensin I to angiotensin II. As angiotensin II is reduced, arterioles dilate, reducing peripheral vascular resistance.

By reducing aldosterone secretion, ACE inhibitors promote the excretion of sodium and water, reducing the amount of blood the heart needs to pump, resulting in a lowered blood pressure.

ANGIOTENSIN II RECEPTOR BLOCKERS

Unlike ACE inhibitors, which prevent production of angiotensin, ARBs inhibit the action of angiotensin II by attaching to tissue-binding receptor sites.

Commonly prescribed ARBs include:

·

candesartan (Atacand)

·

irbesartan (Avapro)

·

losartan (Cozaar)

·

olmesartan (Benicar)

·

valsartan (Diovan).

Diuretics are used to promote the excretion of water and electrolytes by the kidneys. By doing so, diuretics play a major role in treating hypertension and other cardiovascular conditions. (See Understanding diuretics.)

The major diuretics used as cardiovascular drugs include:

·

thiazide and thiazide-like diuretics

·

loop diuretics

·

potassium-sparing diuretics.

THIAZIDE AND THIAZIDE-LIKE DIURETICS

Thiazide and thiazide-like diuretics are sulfonamide derivatives. Thiazide diuretics include bendroflumethiazide (Naturetin), hydrochlorothiazide (HydroDIURIL), hydroflumethiazide (Saluron), and methyclothiazide (Enduron). Thiazide-like diuretics include chlorthalidone (Hygroton) and indapamide (Lozol).

UNDERSTANDING DIURETICS

Diuretics are used to treat patients with various cardiovascular conditions. They work by promoting the excretion of water and electrolytes by the kidneys. Use this table to learn about the indications, adverse reactions, and nursing considerations associated with these drugs.

DRUGS

INDICATIONS

ADVERSE

REACTIONS

NURSING

CONSIDERATIONS

THIAZIDE AND THIAZIDE-LIKE DIURETICS

Bendroflumethiazide (Naturetin), chlorthalidone (Hygroton), hydrochlorothiazide (HydroDIURIL), hydroflumethiazide (Saluron), indapamide (Lozol), methyclothiazide (Enduron)

·

Hypertension

·

Edema

·

Hypokalemia

·

Orthostatic hypotension

·

Hyponatremia

·

Dizziness

·

Nausea

·

Monitor potassium level.

·

Monitor intake and output.

·

Monitor glucose level in diabetic patients. Thiazide diuretics can cause hyperglycemia.

 

Bumetanide (Bumex), ethacrynic acid (Edecrin), furosemide (Lasix)

·

Hypertension

·

Heart failure

·

Edema

·

Dehydration

·

Orthostatic hypotension

·

Hyperuricemia

·

Hypokalemia

·

Hyponatremia

·

Dizziness

·

Muscle cramps

·

Rash

·

Monitor for signs of excess diuresis (hypotension, tachycardia, poor skin turgor, and excessive thirst).

·

Monitor blood pressure, heart rate, and intake and output.

·

Monitor electrolyte levels.

POTASSIUM-SPARING DIURETICS

Amiloride (Midamor), spironolactone (Aldactone), triamterene (Dyrenium)

·

Edema

·

Diuretic-induced hypokalemia in patients with heart failure

·

Cirrhosis

·

Nephrotic syndrome

·

Hypertension

·

Hyperkalemia

·

Headache

·

Nausea

·

Rash

·

Monitor electrocardiogram for arrhythmias.

·

Monitor potassium levels.

·

Monitor intake and output.

Thiazide and thiazide-like diuretics work by preventing sodium from being reabsorbed in the kidneys. As sodium is excreted, it pulls water along with it. Thiazide and thiazide-like diuretics also increase the excretion of chloride, potassium, and bicarbonate, which can result in electrolyte imbalances.

Initially, these drugs decrease circulating blood volume, leading to a reduced cardiac output. However, if the therapy is maintained, cardiac output stabilizes, but plasma fluid volume decreases.

LOOP DIURETICS

Loop (high-ceiling) diuretics are highly potent drugs. They include:

·

bumetanide (Bumex)

·

ethacrynic acid (Edecrin)

·

furosemide (Lasix).

The loop diuretics are the most potent diuretics available, producing the greatest volume of diuresis (urine production). They also have a high potential for causing severe adverse reactions.

Bumetanide is the shortest-acting diuretic. It's even 40 times more potent than another loop diuretic, furosemide.

Loop diuretics receive their name because they act primarily on the thick ascending loop of Henle (the part of the nephron responsible for concentrating urine) to increase the secretion of sodium, chloride, and water. These drugs may also inhibit sodium, chloride, and water reabsorption.

POTASSIUM-SPARING DIURETICS

Potassium-sparing diuretics have weaker diuretic and antihypertensive effects than other diuretics, but they have the advantage of conserving potassium.

·

amiloride (Midamor)

·

spironolactone (Aldactone)

·

triamterene (Dyrenium).

The direct action of the potassium-sparing diuretics on the distal tubule of the kidney produces:

·

increased urinary excretion of sodium and water

·

increased excretion of chloride and calcium ion

·

decreased excretion of potassium and hydrogen ion.

These effects lead to reduced blood pressure and increased serum potassium levels.

Spironolactone, one of the main potassium-sparing diuretics, is structurally similar to aldosterone and acts as an aldosterone antagonist.

Aldosterone promotes the retention of sodium and water and loss of potassium; spironolactone counteracts these effects by competing with aldosterone for receptor sites. As a result, sodium, chloride, and water are excreted, and potassium is retained.

Anticoagulants

Understanding anticoagulants, pages 160 and 161.) Major categories of anticoagulants include:

·

heparin

·

factor Xa inhibitors

·

oral anticoagulants

·

antiplatelet drugs.

HEPARIN

Heparin, prepared commercially from animal tissue, is used to prevent clot formation. Low-molecular-weight heparin, such as dalteparin (Fragmin) and enoxaparin (Lovenox), prevents deep vein thrombosis (a blood clot in the deep veins, usually of the legs) in surgical patients.

Because it doesn't affect the synthesis of clotting factors, heparin can't dissolve already formed clots. It does prevent the formation of new thrombi, though. Here's how it works:

·

 

 

·

Antithrombin III then inactivates factors IXa, Xa, XIa, and XIIa in the intrinsic and common pathways. The end result is prevention of a stable fibrin clot.

·

In low doses, heparin increases the activity of antithrombin III against factor Xa and thrombin and inhibits clot formation. Much larger doses are necessary to inhibit fibrin formation after a clot has formed. This relationship between dose and effect is the rationale for using low-dose heparin to prevent clotting.

·

Whole blood clotting time, thrombin time, and partial thromboplastin time are prolonged during heparin therapy. However, these times may be only slightly prolonged with low or ultra-low preventive doses.

UNDERSTANDING ANTICOAGULANTS

Anticoagulants reduce the blood's ability to clot and are included in the treatment plans for many patients with cardiovascular disorders. Use this table to learn about the indications, adverse reactions, and nursing considerations associated with these drugs.

DRUGS

INDICATIONS

ADVERSE

REACTIONS

NURSING

CONSIDERATIONS

HEPARINS

Heparin and low-molecular-weight heparins, such as dalteparin (Fragmin) and enoxaparin (Lovenox)

·

Deep vein thrombosis (prevention and treatment)

·

 

·

Disseminated intravascular coagulation (heparin)

·

Prevention of complications after myocardial infarction (MI)

·

Bleeding

·

Hemorrhage

·

Thrombocytopenia

·

Monitor thromboplastin time; the therapeutic range is 1½ to 2½ times the control.

·

Monitor the patient for signs of bleeding.

·

Concomitant administration with nonsteroidal anti-inflammatory drugs, iron dextran, or an antiplatelet drug increases the risk of bleeding.

·

Protamine sulfate reverses the effects of heparin.

FACTOR XA INHIBITORS

Fondaparinux (Arixtra)

·

Deep vein thrombosis (prevention and treatment)

·

acute pulmonary embolism

·

Hemorrhage

·

Thrombocytopenia

·

Nausea

·

Fever

·

Not interchangeable with heparin or low-dose heparins.

·

Monitor the patient for signs of bleeding.

·

Monitor complete blood count and platelet count.

·

Monitor anti-Xa levels. Goal for prophylaxis is 0.2 to 0.4 anti-Xa units/ml; goal for therapy is 0.5 anti-Xa units/ml.

ORAL ANTICOAGULANTS

Warfarin (Coumadin)

·

Deep vein thrombosis prophylaxis

·

Prevention of complications of prosthetic heart valves or diseased mitral valves

·

Atrial arrhythmias

·

Bleeding (may be severe)

·

Hepatitis

·

Diarrhea

·

Monitor prothrombin time and International Normalized Ratio.

·

Monitor the patient for signs of bleeding.

·

The effects of oral anticoagulants can be reversed with phytonadione (vitamin K).

ANTIPLATELET DRUGS

Aspirin (Ecotrin), dipyridamole (Persantine), ticlopidine (Ticlid), clopidogrel (Plavix)

·

Decreases the risk of death post-MI

·

Prevention of complications of prosthetic heart valves

·

Reduction of risk of MI after previous MI or in patients with unstable angina

·

Prevention of reocclusion in coronary revascularization procedures

·

GI distress

·

Bleeding

·

Thrombocytopenia

·

Angioedema

·

Monitor the patient for signs of bleeding.

·

Aspirin and ticlopidine should be taken with meals to prevent GI irritation.

·

Dipyridamole should be taken with a full glass of fluid at least 1 hour before meals.

Heparin can be used to prevent clotting when a patient's blood must circulate outside the body through a machine, such as a cardiopulmonary bypass machine or hemodialysis machine.

FACTOR XA INHIBITORS

Factor Xa inhibitors are a new class of anticoagulants. At this time, the only drug in this class is fondaparinux (Arixtra). Fondaparinux works by inhibiting only factor Xa. Factor Xa is the common point in the intrinsic and extrinsic clotting pathways. Inhibition of factor Xa prevents the formation of thrombin and the formation of a stable fibrin clot.

ORAL ANTICOAGULANTS

Oral anticoagulants alter the liver's ability to synthesize vitamin K-dependent clotting factors, including prothrombin and factors VII, IX, and X. Clotting factors already in the bloodstream continue to coagulate blood until they become depleted, so anticoagulation doesn't begin immediately. The major oral anticoagulant used in the United States is warfarin (Coumadin).

ANTIPLATELET DRUGS

Examples of antiplatelet drugs are:

·

aspirin (Ecotrin)

·

dipyridamole (Persantine)

·

ticlopidine (Ticlid)

·

clopidogrel (Plavix).

Antiplatelet drugs are used to prevent arterial thromboembolism, especially in patients at risk for myocardial infarction (MI), stroke, and arteriosclerosis (hardening of the arteries). They interfere with platelet activity in different drug-specific and dose-related ways.

Low dosages of aspirin (81 mg/day) appear to inhibit clot formation by blocking the synthesis of prostaglandins, which in turn prevents formation of the platelet-aggregating substance thromboxane A2. Dipyridamole and clopidogrel may inhibit platelet aggregation.

HOW THROMBOLYTICS DISSOLVE CLOTS

When a thrombus forms in an artery, it obstructs the blood supply, causing ischemia and necrosis. Thrombolytics can dissolve thrombi in the coronary and pulmonary arteries, restoring the blood supply to the area beyond the blockage.

Obstructed artery

A thrombus blocks blood flow through the artery, causing distal ischemia.

c4-tt4

Inside the thrombus

The thrombolytic enters the thrombus and binds to the fibrin-plasminogen complex, converting inactive plasminogen into active plasmin. Active plasmin digests fibrin, dissolving the thrombus. As the thrombus dissolves, blood flow resumes.

c4-tt5

Thrombolytics

Thrombolytics dissolve preexisting clots or thrombi, and they're commonly used in acute or emergency situations. They work by converting plasminogen to plasmin, which lyses (dissolves) thrombi, fibrinogen, and other plasma proteins. (See How thrombolytics dissolve clots. Also see Understanding thrombolytics, page 164.)

UNDERSTANDING THROMBOLYTICS

Sometimes called clot busters, thrombolytics are prescribed to dissolve a preexisting clot or thrombus. These drugs are typically used in acute or emergency situations. Use this table to learn about the indications, adverse reactions, and nursing considerations associated with these drugs.

DRUGS

INDICATIONS

ADVERSE

REACTIONS

NURSING

CONSIDERATIONS

 

Alteplase (Activase), reteplase (Retavase), streptokinase (Streptase)

·

Acute myocardial infarction

·

Acute ischemic stroke

·

Pulmonary embolus

·

Catheter occlusion

·

Arterial thrombosis

·

Bleeding

·

Allergic reaction

·

Monitor partial thromboplastin time, prothrombin time, International Normalized Ratio, hemoglobin levels, and hematocrit before, during, and after administration.

·

Monitor vital signs frequently during and immediately after administration. Don't use an automatic blood pressure cuff to monitor blood pressure.

·

Monitor puncture sites for bleeding. Don't use a tourniquet when obtaining blood samples.

·

Monitor for signs of bleeding.

Some commonly used thrombolytics include:

·

alteplase (Activase)

·

reteplase (Retavase)

·

streptokinase (Streptase).

Adrenergics

Adrenergics are also called sympathomimetics because they produce effects similar to those produced by the sympathetic nervous system.

Adrenergics are classified based on their chemical structure: catecholamines (both naturally occurring and synthetic) and noncatecholamines (See Understanding adrenergics, pages 166 to 169.)

Therapeutic use of adrenergics depends on which receptors they stimulate and to what degree. Adrenergics can affect:

·

alpha-adrenergic receptors

·

beta-adrenergic receptors

·

dopamine receptors.

Most of the adrenergic drugs produce their effects by stimulating alpha- and beta-adrenergic receptors. These drugs mimic the action of norepinephrine or epinephrine.

Dopaminergic drugs act primarily on receptors in the sympathetic nervous system that are stimulated by dopamine.

CATECHOLAMINES

Because of their common basic chemical structure, catecholamines share certain properties. They stimulate the nervous system, constrict peripheral blood vessels, increase heart rate, and dilate the bronchi. They can be manufactured in the body or in a laboratory. Common catecholamines include:

·

dobutamine (Dobutrex)

·

dopamine (Intropin)

·

 

·

norepinephrine (Levophed)

Catecholamines are primarily direct-acting. When catecholamines combine with alpha or beta receptors, they cause either an excitatory or inhibitory effect. Typically, activation of alpha receptors generates an excitatory response except for intestinal relaxation. Activation of the beta receptors mostly produces an inhibitory response except in the cells of the heart, where norepinephrine produces excitatory effects. (See Learning about adrenergic receptor uses and effects, page 170.)

The effects of catecholamines depend on the dosage and the route of administration. Catecholamines are potent inotropes, meaning they make the heart contract more forcefully. As a result, the ventricles empty more completely with each heartbeat, increasing the heart's workload and the amount of oxygen it needs to do this harder work.

Catecholamines also produce a positive chronotropic effect, which means they cause the heart to beat faster. That's because the pacemaker cells in the heart's SA node depolarize at a faster rate. As catecholamines cause blood vessels to constrict and blood pressure to increase, the heart rate decreases as the body tries to prevent an excessive increase in blood pressure.

Catecholamines can cause the Purkinje fibers to fire spontaneously, possibly producing abnormal heart rhythms, such as premature

ventricular contractions and fibrillation. Epinephrine is likelier than norepinephrine to produce this spontaneous firing,

UNDERSTANDING ADRENERGICS

Adrenergic drugs produce effects similar to those produced by the sympathetic nervous system. Adrenergic drugs can affect alpha-adrenergic receptors, beta-adrenergic receptors, or dopamine receptors. However, most of the drugs stimulate the alpha and beta receptors, mimicking the effects of norepinephrine and epinephrine. Dopaminergic drugs act on receptors typically stimulated by dopamine.

Use this table to learn about the indications, adverse reactions, and nursing considerations associated with these drugs.

 

INDICATIONS

ADVERSE

REACTIONS

NURSING

CONSIDERATIONS

CATECHOLAMINES

Dobutamine (Dobutrex)

·

Increase cardiac output in short-term treatment of cardiac decompensation from depressed contractility

Headache, tingling sensation, bronchospasm, palpitations, tachycardia, cardiac arrhythmias (premature ventricular contractions), hypotension, hypertension and hypertensive crisis, angina, nausea, vomiting, tissue necrosis and sloughing (if catecholamine given I.V. leaks into surrounding tissue)

·

Correct hypovolemia before administering drug.

·

Incompatible with alkaline solution (sodium bicarbonate); don't mix or give through same line; don't mix with other drugs.

·

Administer continuous drip on infusion pump.

·

Give drug into a large vein to prevent irritation or extravasation at site.

·

Monitor cardiac rate and rhythm and blood pressure carefully when initiating therapy or increasing the dose.

Dopamine (Intropin)

·

Treat shock and correct hemodynamic imbalances

·

Increase cardiac output

·

Hypotension

Headache, bradycardia, palpitations, tachycardia, conduction disturbance, cardiac arrhythmias (ventricular), hypotension, hypertension and hypertensive crisis, azotemia, angina, nausea, vomiting, gangrene of extremities in high dose, tissue necrosis and sloughing (if catecholamine given I.V. leaks into surrounding tissue), bronchospasm

·

Correct hypovolemia before giving drug.

·

Administer continuous drip on infusion pump.

·

Give drug into a large vein to prevent extravasation; if extravasation occurs, stop infusion and treat site with phentolamine (Regitine) infiltrate to prevent tissue necrosis.

·

Monitor cardiac rate and rhythm and blood pressure carefully when initiating therapy or increasing the dose.

·

Monitor urine output during treatment, especially at high doses.

Epinephrine (Adrenalin)

·

Bronchospasm

·

 

·

Anaphylaxis

·

Restoration of cardiac rhythm in cardiac arrest

Restlessness, anxiety, dizziness, headache, tachycardia, palpitations, cardiac arrhythmias (ventricular fibrillation), hypertension, stroke, cerebral hemorrhage, angina, increased blood glucose levels, tissue necrosis and sloughing (if catecholamine given I.V. leaks into surrounding tissue)

·

Correct hypovolemia before giving drug.

·

Administer continuous drip on infusion pump.

·

Give drug into a large vein to prevent irritation or extravasation at site.

·

 

CATECHOLAMINES

Norepinephrine (Levophed)

·

Maintain blood pressure in acute hypotensive states

Anxiety, dizziness, headache, bradycardia, cardiac arrhythmias, hypotension, hypertension, tissue necrosis and sloughing (if catecholamine given I.V. leaks into surrounding tissue), fever, metabolic acidosis, increased blood glucose levels, dyspnea

·

Correct hypovolemia before giving drug.

·

Administer continuous drip on infusion pump.

·

Give drug into a large vein to prevent extravasation; if extravasation occurs, stop infusion, and treat site with phentolamine infiltrate to prevent tissue necrosis.

·

 

NONCATECHOLAMINES

Ephedrine

·

 

·

Treatment of orthostatic hypotension and bronchospasm

Anxiety, dizziness, headache, palpitations, hypotension, hypertension, nausea, vomiting

·

Correct hypovolemia before giving drug.

·

Give drug into a large vein to prevent irritation or extravasation at site.

·

Monitor cardiac rate and rhythm and blood pressure carefully when initiating therapy or increasing the dose.

Phenylephrine (Neo-Synephrine)

·

Maintain blood pressure in hypotensive states, especially hypotensive emergencies with spinal anesthesia

Restlessness, anxiety, dizziness, headache, palpitations, cardiac arrhythmias, hypertension, tissue necrosis and sloughing (if catecholamine given I.V. leaks into surrounding tissue)

·

Correct hypovolemia before giving drug.

·

Administer continuous drip on infusion pump.

·

Give drug into a large vein to prevent extravasation; if extravasation occurs, stop infusion, and treat site with phentolamine infiltrate to prevent tissue necrosis.

·

Monitor cardiac rate and rhythm and blood pressure carefully when starting therapy or increasing the dose.

NONCATECHOLAMINES

Noncatecholamine adrenergic drugs have various therapeutic uses because of the many effects these drugs can have on the body such as the local or systemic constriction of blood vessels by phenylephrine (Neo-Synephrine).

Direct-acting noncatecholamines that stimulate alpha activity include methoxamine (Vasoxyl) and phenylephrine.

Those that selectively exert beta2 activity include:

·

albuterol (Proventil)

·

isoetharine (Bronkosol)

·

metaproterenol (Alupent)

Dual-acting noncatecholamines combine both actions and include ephedrine.

Adrenergic blockers

Adrenergic blockers, also called sympatholytics, are used to disrupt sympathetic nervous system function. (See Understanding adrenergic blockers, page 171.)

These drugs work by blocking impulse transmission (and thus sympathetic nervous system stimulation) at adrenergic neurons or adrenergic receptor sites. The action of the drugs at these sites can be exerted by:

LEARNING ABOUT ADRENERGIC RECEPTOR USES AND EFFECTS

 

RECEPTOR

ACTIVATED

THERAPEUTIC

USES

ADVERSE

EFFECTS

 

Alpha1

·

Control topical superficial bleeding

·

Treat nasal decongestion

·

Elevate blood pressure

·

Delay absorption of local anesthetics

·

Decrease intraocular pressure

·

Hypertension

·

Necrosis with extravasation

·

Bradycardia

 

Alpha2

·

Treat glaucoma

·

Burning sensation

·

Ptosis

·

Redness and swelling of eyelid

 

Beta1

·

Treat heart failure, cardiac arrest, and shock

·

Tachycardia

·

Arrhythmias

·

Angina

 

Beta2

·

Produce bronchodilation

·

Delay preterm labor

·

Hyperglycemia

·

Tremors

 

Dopamine

·

Increase renal blood flow

·

Increase cardiac output

·

Elevate blood pressure

·

Ectopy

·

Nausea and vomiting

·

Tachycardia

·

Palpitations

·

interrupting the action of sympathomimetics (adrenergics)

         

·

reducing available norepinephrine

·

preventing the action of cholinergics.

Adrenergic-blocking drugs are classified according to their site of action as alpha-adrenergic receptor blockers or beta-adrenergic receptor blockers.

UNDERSTANDING ADRENERGIC BLOCKERS

Adrenergic blockers block impulse transmission at adrenergic receptor sites by interrupting the action of adrenergic drugs, reducing the amount of norepinephrine available, and blocking the action of cholinergics.

DRUGS

 

ADVERSE

REACTIONS

NURSING

CONSIDERATIONS

ALPHA-ADRENERGIC RECEPTOR BLOCKERS

Phentolamine (Regitine), prazosin (Minipress)

·

Hypertension

·

Pheochromocytoma

Orthostatic hypotension, bradycardia, tachycardia, edema, difficulty breathing, flushing, weakness, palpitations, shock

·

 

·

Instruct the patient to rise slowly to a standing position to avoid orthostatic hypotension.

BETA-ADRENERGIC RECEPTOR BLOCKERS

Nonselective Carvedilol (Coreg), labetalol (Normodyne), propranolol (Inderal), sotalol (Betapace), timolol (Blocadren)

Selective Acebutolol (Sectral), atenolol (Tenormin), esmolol (Brevibloc), metoprolol (Lopressor)

·

Prevention of complications after myocardial infarction, angina, hypertension, supraventricular arrhythmias, anxiety, essential tremor, cardiovascular symptoms associated with thyrotoxicosis, migraine headaches, pheochromocytoma

·

Hypotension, bradycardia, peripheral vascular insufficiency, bronchospasm (nonselective), sore throat, atrioventricular block, thrombocytopenia, hypoglycemia

·

Monitor vital signs and heart rhythm frequently.

·

Beta-adrenergic receptor blockers can alter the requirements for insulin and oral antidiabetics.

Alpha-adrenergic receptor blockers work by interrupting the actions of sympathomimetic drugs at alpha-adrenergic receptors. This results in:

·

relaxation of the smooth muscle in the blood vessels

·

 

·

decreased blood pressure.

Drugs in this class include phentolamine and prazosin.

Ergotamine (Ergomar) is a mixed alpha agonist and antagonist. At high dose, it acts as an alpha-adrenergic receptor blocker.

Alpha-adrenergic receptor blockers work in one of two ways:

·

They interfere with or block the synthesis, storage, release, and reuptake of norepinephrine by neurons.

·

They antagonize epinephrine, norepinephrine, or adrenergic (sympathomimetic) drugs at alpha-receptor sites.

Alpha-receptor sites are either alpha1 or alpha receptors. Alpha-adrenergic receptor blockers include drugs that block stimulation of alpha1 receptors and that may block alpha2

Alpha-adrenergic receptor blockers occupy alpha-receptor sites on the smooth muscle of blood vessels.

This prevents catecholamines from occupying and stimulating the receptor sites. As a result, blood vessels dilate, increasing local blood flow to the skin and other organs. The decreased peripheral vascular resistance helps to decrease blood pressure.

BETA-ADRENERGIC RECEPTOR BLOCKERS

Beta-adrenergic receptor blockers, the most widely used adrenergic blockers, prevent stimulation of the sympathetic nervous system by inhibiting the action of catecholamines and other sympathomimetic drugs at beta-adrenergic receptors.

Beta-adrenergic drugs are selective or nonselective. Nonselective beta-adrenergic drugs affect:

·

beta1-receptor sites (located mainly in the heart)

·

beta2-receptor sites (located in the bronchi, blood vessels, and the uterus).

Nonselective beta-adrenergic drugs include carvedilol, labetalol, propranolol, sotalol (Betapace), and timolol (Blocadren).

Selective beta-adrenergic receptor blockers primarily affect the beta1-adrenergic sites. They include acebutolol, atenolol, esmolol and metoprolol.

Some beta-adrenergic receptor blockers such as acebutolol have intrinsic sympathetic activity. This means that instead of attaching to beta receptors and blocking them, these beta-adrenergic receptor blockers attach to beta receptors and stimulate them. These drugs are sometimes classified as partial agonists.

Beta-adrenergic receptor blockers have widespread effects in the body because they produce their blocking action not only at the adrenergic nerve endings but also in the adrenal medulla. Effects on the heart include:

·

increased peripheral vascular resistance

·

decreased blood pressure

·

decreased force of contractions of the heart

·

decreased oxygen consumption of the heart

·

slowed conduction of impulses between the atria and ventricles

·

decreased cardiac output.

Some of the effects of beta-adrenergic receptor blockers depend on whether the drug is classified as selective or nonselective. Selective beta-adrenergic receptor blockers, which preferentially block beta1-receptor sites, reduce stimulation of the heart. They're commonly called cardioselective beta-adrenergic receptor blockers.

Nonselective beta-adrenergic receptor blockers, which block both beta1- and beta2

Antilipemics

Antilipemics are used to lower abnormally high blood levels of lipids, such as cholesterol, triglycerides, and phospholipids.

Examples of antilipemic drug classes include:

·

bile-sequestering drugs

·

fibric acid derivatives

·

HMG-CoA reductase inhibitors

·

cholesterol absorption inhibitors. (See Understanding antilipemics, pages 174 and 175.)

These drugs are used in combination with lifestyle changes, such as proper diet, weight loss, and exercise.

BILE-SEQUESTERING DRUGS

Bile-sequestering drugs help lower blood levels of low-density lipoproteins (LDLs). They combine with bile acids in the intestines to form an insoluble compound that's then excreted in the feces. The decreasing level of bile acid in the gallbladder triggers the liver to synthesize more bile acids from their precursor, cholesterol. As cholesterol leaves the bloodstream and other storage areas to replace the lost bile acids, blood cholesterol levels decrease.

UNDERSTANDING ANTILIPEMICS

Antilipemics are used to lower high blood levels of lipids by combining with bile acids, reducing cholesterol formation, inhibiting enzymes, and inhibiting cholesterol absorption.

Use this table to learn the indications, adverse reactions, and nursing considerations needed to safely give these drugs.

DRUGS

INDICATIONS

ADVERSE

REACTIONS

NURSING

CONSIDERATIONS

BILE-SEQUESTERING DRUGS

cholestyramine (Questran), colesevelam (Welchol), colestipol (Colestid)

·

Elevated cholesterol level

·

Constipation

·

Increased bleeding tendencies

·

Muscle and joint pain

·

Nausea, heartburn

·

Headache

·

Instruct patient that he'll need to return for periodic blood tests.

·

Give before meals.

·

Don't give the powder form dry; mix with fluid.

·

Give other drugs 1 hour before or 4 to 6 hours after these drugs.

FIBRIC ACID DERIVATIVES

fenofibrate (Tricor), gemfibrozil (Lopid)

·

Hypercholesterolemia

·

Hypertriglyceridemia

·

Rash, nausea, vomiting, diarrhea

·

Myalgia, flulike syndrome

·

Impotence

·

Dizziness, blurred vision

·

Abdominal pain, epigastric pain

·

Instruct the patient that he'll need to return for periodic blood tests.

·

Educate the patient on dietary and lifestyle changes to help lower cholesterol and triglyceride levels.

·

Give with meals.

HMG-COA REDUCTASE INHIBITORS

atorvastatin (Lipitor), fluvastatin (Lescol), lovastatin (Mevacor), pravastatin (Pravachol), simvastatin (Zocor), rosuvastatin (Crestor)

·

Elevated cholesterol, triglyceride, and low-density lipoprotein (LDL) levels

·

Prevention of cardiovascular disease in adults without clinically evident coronary disease but with multiple risk factors

·

Rhabdomyolysis with acute renal failure

·

Headache

·

Flatulence, abdominal pain, constipation, nausea

·

Instruct the patient that he'll need to return for periodic blood tests.

·

Monitor periodic liver function tests.

·

Give the drug at the same time each day; it doesn't need to be given with food.

·

Educate the patient on dietary and lifestyle changes to help lower cholesterol and triglyceride levels.

CHOLESTEROL ABSORPTION INHIBITORS

ezetimibe (Zetia)

·

Elevated cholesterol, triglyceride, and LDL levels

·

Given as adjunctive treatment with simvastatin

·

Cough

·

Myalgia, arthralgia

·

Headache, dizziness

·

Instruct the patient that he'll need to return for periodic blood tests.

·

Educate the patient on dietary and lifestyle changes to help lower cholesterol and triglyceride levels.

·

If giving with an HMG-CoA reductase inhibitor, give both drugs together.

Examples of bile-sequestering drugs include:

·

cholestyramine (Questran)

·

colesevelam (Welchol)

·

colestipol hydrochloride (Colestid).

Bile-sequestering drugs are the drugs of choice for treating a patient who can't reduce his LDL levels through dietary changes because of familial hypercholesterolemia.

FIBRIC ACID DERIVATIVES

Fibric acid derivatives reduce high triglyceride levels and, to a lesser extent, high LDL levels. It isn't known exactly how these drugs work, although it's thought that they:

·

reduce cholesterol production early in its formation

·

mobilize cholesterol from the tissues

·

increase cholesterol excretion

·

decrease synthesis and secretion of lipoproteins

 

·

decrease synthesis of triglycerides.

Fenofibrate (Tricor) and gemfibrozil (Lopid) are two commonly used fibric acid derivatives.

Fibric acid drugs are primarily used to reduce triglyceride levels and also reduce blood cholesterol levels. Gemfibrozil also increases the high-density lipoprotein (HDL) levels in the blood and increases the serum's capacity to dissolve additional cholesterol.

HMG-COA REDUCTASE INHIBITORS

HMG-CoA reductase inhibitors (also known as the statins) lower lipid levels by interfering with cholesterol synthesis. They inhibit the enzyme that's responsible for converting HMG-CoA to mevalonate, an early rate-limiting step in the biosynthesis of cholesterol.

Commonly prescribed HMG-CoA reductase inhibitors include:

·

atorvastatin (Lipitor)

·

fluvastatin (Lescol)

·

lovastatin (Mevacor)

·

pravastatin (Pravachol)

·

simvastatin (Zocor)

·

rosuvastatin (Crestor)

Statin drugs are used primarily to reduce LDLs and also reduce total blood cholesterol levels. They also produce a mild increase in HDLs. Because of their effect on LDL and total cholesterol, these drugs are used to not only treat hypercholesterolemia, but also for primary and secondary prevention of cardiovascular events.

CHOLESTEROL ABSORPTION INHIBITORS

As their name implies, cholesterol absorption inhibitors inhibit the absorption of cholesterol and related phytosterols from the intestine. At this time, ezetimibe (Zetia) is the only drug in the class.

Ezetimibe reduces blood cholesterol levels by inhibiting the absorption of cholesterol by the small intestine. This leads to a decrease in delivery of intestinal cholesterol to the liver, causing a reduction in hepatic cholesterol stores and an increase in clearance from the blood.

Ezetimibe may be used alone or with statins to help lower cholesterol. One drug currently on the market combines a statin (simvastatin) and ezetimibe to help decrease total cholesterol and LDLs, and increase HDL cholesterol.

SURGERY

Despite the drama of successful single- and multiple-organ transplants, treatment with improved immunosuppressants, and advances in ventricular assist devices (VADs), far more patients undergo conventional surgeries such as coronary artery bypass graft (CABG). Surgeries for the treatment of disorders of the cardiovascular system include:

·

CABG

·

minimally invasive direct coronary artery bypass (MIDCAB)

·

heart transplantation

·

vascular repair

·

valve surgery

·

VAD insertion.

Coronary artery bypass graft

A CABG circumvents an occluded coronary artery with an autogenous graft (usually a segment of the saphenous vein or internal mammary artery), thereby restoring blood flow to the myocardium.

The most common procedure, aortocoronary bypass, involves suturing one end of the autogenous graft to the ascending aorta and the other end to a coronary artery distal to the occlusion. (See Bypassing coronary occlusions, page 178.)

Other surgical techniques, such as the mini-CABG and direct coronary artery bypass, can reduce the risk of cerebral complications and accelerate recovery for patients requiring grafts of only one or two arteries.

Although the surgery relieves pain in about 90% of patients, its long-term effectiveness is unclear. Such problems as graft closure and development of atherosclerosis in other coronary arteries may make repeat surgery necessary. In addition, because a CABG doesn't resolve the underlying disease associated with arterial blockage, a CABG may not reduce the risk of MI recurrence. Patients most likely to benefit from a CABG include those with left main CAD, severe proximal left anterior descending CAD, three-vessel CAD with proximal stenoses or left ventricular dysfunction, and those with three-vessel CAD with normal left ventricular function at rest, but with inducible ischemia and poor exercise capacity.

BYPASSING CORONARY OCCLUSIONS

After the patient receives general anesthesia, surgery begins with graft harvesting. The surgeon makes a series of incisions in the patient's thigh or calf and removes a saphenous vein segment for grafting. Most surgeons prefer to use a segment of the internal mammarian artery.

Exposing the heart

Once the autografts are obtained, the surgeon performs a medial sternotomy to expose the heart and then initiates cardiopulmonary bypass.

To reduce myocardial oxygen demands during surgery and to protect the heart, the surgeon induces cardiac hypothermia and standstill by injecting a cold, cardioplegic solution (potassiumenriched saline solution) into the aortic root.

Securing the graft

After the patient is prepared, the surgeon sutures one end of the venous graft to the ascending aorta and the other end to a patent coronary artery that's distal to the occlusion. The graft is sutured in a reversed position to promote proper blood flow. The surgeon repeats this procedure for each occlusion to be bypassed.

In the example depicted below, saphenous vein segments bypass occlusions in three sections of the coronary artery.

Finishing the surgery

When the grafts are in place, the surgeon flushes the cardioplegic solution from the heart and discontinues cardiopulmonary bypass. He then implants epicardial pacing electrodes, inserts a chest tube, closes the incision, and applies a sterile dressing.

c4-tt6

During the procedure, the patient may be placed on cardiopulmonary bypass so the surgeon can work on a nonbeating heart. This is called an on-pump CABG. If cardiopulmonary bypass isn't used, the surgeon works on a beating heart, and this is known as an off-pump CABG. An off-pump CABG has several advantages over an on-pump CABG including decreased risk of complications and shorter hospital stay and recovery time.

PREPARING THE PATIENT

·

Reinforce the physician's explanation of the surgery.

·

Explain the complex equipment and procedures used on the intensive care unit (ICU) or postanesthesia care unit (PACU).

·

Explain that the patient awakens from surgery with an endotracheal (ET) tube in place, and he'll be connected to a mechanical ventilator. He'll also be connected to a cardiac monitor and may have in place a nasogastric (NG) tube, a chest tube, an indwelling urinary catheter, arterial lines, epicardial pacing wires and, possibly, a pulmonary artery (PA) catheter. Tell him that discomfort is minimal and that the equipment is removed as soon as possible.

·

Review incentive spirometry techniques and range-of-motion (ROM) exercises with the patient.

·

Make sure that the patient or a responsible family member has signed a consent form.

·

Before surgery, prepare the patient's skin.

·

Immediately before surgery, begin cardiac monitoring, and then assist with PA catheterization and insertion of arterial lines. Some facilities insert PA catheters and arterial lines in the operating room before surgery.

MONITORING AND AFTERCARE

·

After a CABG, look for signs of hemodynamic compromise, such as severe hypotension, decreased cardiac output, and shock.

·

 

·

 

·

Check and record vital signs and hemodynamic parameters every 5 to 15 minutes until the patient's condition stabilizes.

·

To ensure adequate myocardial perfusion, keep arterial pressure within the limits set by the physician. Usually, mean arterial pressure (MAP) less than 70 mm Hg results in inadequate tissue perfusion; pressure greater than 110 mm Hg can cause hemorrhage and

graft rupture. Monitor pulmonary artery pressure (PAP), central venous pressure (CVP), left atrial pressure, and cardiac output.

·

Be alert for changes in hemodynamics that indicate either hypervolemia or hypovolemia, especially an increase or decrease in CVP and PAP.

·

Give drugs as indicated and adjust according to the patient's response. Vasopressors may be used to help increase perfusion of the coronary arteries. Nitroglycerin may be administered to help minimize spasm of the newly grafted artery.

·

 

·

Monitor electrocardiograms (ECGs) continuously for disturbances in heart rate and rhythm. If you detect serious abnormalities, notify the physician and be prepared to assist with epicardial pacing or, if necessary, cardioversion or defibrillation.

·

Frequently evaluate the patient's peripheral pulses, capillary refill time, and skin temperature and color and auscultate for heart sounds; report abnormalities.

·

Evaluate tissue oxygenation by assessing breath sounds, chest excursion, and symmetry of chest expansion. Check arterial blood gas (ABG) results every 2 to 4 hours, and adjust ventilator settings to keep ABG values within ordered limits.

·

Maintain chest tube drainage at the ordered negative pressure (usually -10 to -40 cm), and assess regularly for hemorrhage, excessive drainage (greater than 200 ml/hour), and sudden decrease or cessation of drainage.

·

Monitor the patient's intake and output, and assess for electrolyte imbalance, especially hypokalemia and hypomagnesemia. Assess urine output at least hourly during the immediate postoperative period and then less frequently as the patient's condition stabilizes.

·

As the patient's incisional pain increases, give an analgesic or other drugs as indicated.

·

After weaning the patient from the ventilator and removing the ET tube, provide chest physiotherapy. Start with incentive spirometry, and encourage the patient to cough, turn frequently, and deep-breathe. Assist with ROM exercises to enhance peripheral circulation and prevent thrombus formation.

·

Explain that postpericardiotomy syndrome commonly develops after open-heart surgery. Instruct the patient about signs and symptoms, such as fever, muscle and joint pain, weakness, and chest discomfort.

 

·

Prepare the patient for the possibility of postoperative depression, which may not develop until weeks after discharge. Reassure him that this depression is normal and should pass quickly.

·

Maintain nothing-by-mouth status until bowel sounds return. Then begin the patient on clear liquids, and advance his diet as tolerated. Tell the patient to expect sodium and cholesterol restrictions, and explain that this diet can help reduce the risk of recurrent arterial occlusion.

·

 

·

Monitor for postoperative complications, such as stroke, pulmonary embolism, pneumonia, impaired renal perfusion, hypertension, MI, and infection.

·

Gradually allow the patient to increase activities as indicated. (See Using cardiac rehab.)

·

Provide support to the patient and his family to help them cope with recovery and lifestyle changes. (See Teaching the patient after a CABG, page 182.)

Cardiac rehab is an exercise program designed to monitor and improve cardiovascular status and help the patient learn how to manage heart disease.

Elements of cardiac rehab include:

·

individualized exercise program

·

diet, nutrition, and weight control

·

stress management

·

reduction of risk factors

·

lipid and cholesterol control.

Sessions are held weekly, based on patient need and tolerance. Heart rate, blood pressure, and symptoms are continuously monitored during the session. Education is provided based on the patient's individual needs.

Minimally invasive direct coronary artery bypass

Until recently, cardiac surgery required stopping the heart and using cardiopulmonary bypass to oxygenate and circulate blood. Now, a MIDCAB can be performed on a pumping heart through a small thoracotomy incision. The patient may receive only right lung ventilation along with drugs, such as beta-adrenergic receptor blockers, to slow the heart rate and reduce heart movement during surgery.

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT AFTER A CABG

Before discharge from the hospital, instruct the patient to:

·

watch for and immediately notify the practitioner of any signs of infection (redness, swelling, or drainage from the leg or chest incisions; fever; or sore throat) or possible arterial reocclusion (angina, dizziness, dyspnea, rapid or irregular pulse, or prolonged recovery time from exercise)

·

call the practitioner in the case of weight gain greater than 3 lb (1.4 kg) in 1 week

·

follow his prescribed diet, especially sodium and cholesterol restrictions

·

maintain a balance between activity and rest by trying to sleep at least 8 hours each night, scheduling a short rest period each afternoon, and resting frequently when engaging in tiring physical activity

·

participate in an exercise program or cardiac rehabilitation if prescribed

·

follow lifestyle modifications (no smoking, improved diet, and regular exercise) to reduce atherosclerotic progression

·

contact a local chapter of the Mended Hearts Club and the American Heart Association for information and support

·

make sure he understands the dose, frequency of administration, and adverse effects of prescribed drugs.

Advantages of MIDCAB include shorter hospital stays, use of shorter-acting anesthetic agents, fewer postoperative complications, earlier extubation, reduced cost, smaller incisions, and earlier return to work. Patients eligible for MIDCAB include those with proximal left anterior descending lesions and some lesions of the right coronary and circumflex arteries. (See Comparing types of CABGs.)

PREPARING THE PATIENT

·

Review the procedure with the patient, and answer his questions. Tell the patient that he'll be extubated in the operating room or within 2 to 4 hours after surgery.

·

 

·

 

·

Let the patient know that he should be able to walk with assistance the first postoperative day and be discharged within 48 hours.

·

Make sure that the patient or a responsible family member has signed a consent form.

COMPARING TYPES OF CABGS

FEATURES

ON-PUMP

CORONARY

ARTERY BYPASS

GRAFT (CABG)

OFF-PUMP

CABG

MINIMALLY

INVASIVE

DIRECT

CABG

Access site

·

Breastbone severed for heart access

·

Breastbone severed for heart access

·

Incision made between ribs for anterior heart access, no bones cut

Indications

·

Suitable for multivessel disease, any coronary artery

·

Suitable for multivessel disease, any coronary artery

·

Only used for one-vessel diseases in anterior portions of heart, such as left anterior descending artery, or some portions of the right coronary and circumflex arteries

Graft types

·

Combination of artery and vein grafts

·

Combination of artery and vein grafts

·

Arterial grafts (better long-term results)

Complications

·

Highest risk of postoperative complications

·

Reduced blood usage, fewer rhythm problems, less kidney dysfunction than on-pump CABG

·

Reduced blood usage, fewest complications, fastest recovery

Intubation

·

Up to 24 hours

·

Up to 24 hours

·

Usually for 2 to 4 hours

Incisions

·

Leg incisions for vein grafting, possibly arm incision for radial artery grafting

·

Leg incisions for vein grafting, possibly arm incision for radial artery grafting

·

No leg incisions, possibly arm incision for radial artery grafting

Heart and lung function

·

Heart and lung circulation bypassed mechanically, affecting blood cells

·

Drugs and special equipment used to slow heart and immobilize it; cardiopulmonary and systemic circulation still function

·

Drugs used to slow heart; cardiopulmonary and systemic circulation still function

MONITORING AND AFTERCARE

·

After a MIDCAB, look for signs of hemodynamic compromise, such as severe hypotension, decreased cardiac output, and shock.

·

Keep emergency resuscitative equipment immediately available.

·

Check and record vital signs and hemodynamic parameters every 5 to 15 minutes until the patient's condition stabilizes. Give drugs as indicated, and adjust according to the patient's response.

·

Monitor ECGs continuously for disturbances in heart rate and rhythm. If you detect serious abnormalities, notify the physician, and be prepared to assist with epicardial pacing or, if necessary, cardioversion or defibrillation.

·

To ensure adequate myocardial perfusion, keep arterial pressure within the limits set by the physician. Usually, MAP less than 70 mm Hg results in inadequate tissue perfusion; pressure greater than 110 mm Hg can cause hemorrhage and graft rupture. Monitor PAP, CVP, left atrial pressure, and cardiac output if a pulmonary artery (PA) catheter was inserted.

·

Frequently evaluate the patient's peripheral pulses, capillary refill time, and skin temperature and color and auscultate for heart sounds; report abnormalities.

·

Evaluate tissue oxygenation by assessing breath sounds, chest excursion, and symmetry of chest expansion.

 

·

Monitor the patient's intake and output, and assess for electrolyte imbalance, especially hypokalemia and hypomagnesemia. Assess urine output at least hourly during the immediate postoperative period and then less frequently as the patient's condition stabilizes.

·

Provide analgesia, or encourage the use of patient-controlled analgesia if appropriate.

·

Throughout the recovery period, assess for symptoms of stroke, pulmonary embolism, and impaired renal perfusion.

·

Provide chest physiotherapy and incentive spirometry, and encourage the patient to cough, turn frequently, and deep-breathe. Assist with ROM exercises to enhance peripheral circulation and prevent thrombus formation.

·

Explain that postpericardiotomy syndrome commonly develops after open-heart surgery. Instruct the patient about signs and symptoms, such as fever, muscle and joint pain, weakness, and chest discomfort.

·

 

·

Maintain nothing-by-mouth status until bowel sounds return. Then begin the patient on clear liquids, and advance his diet as tolerated. Tell the patient to expect sodium and cholesterol restrictions, and explain that this diet can help reduce the risk of recurrent arterial occlusion.

·

Gradually allow the patient to increase activities as indicated.

·

Monitor the incision site for signs of infection or drainage.

·

Provide support to the patient and his family to help them cope with recovery and lifestyle changes. (See Teaching the patient after a MIDCAB, page 186.)

Heart transplantation

Heart transplantation involves the replacement of a person's heart with a donor heart. It's the treatment of choice for patients with end-stage cardiac disease who have a poor prognosis, estimated survival of 6 to 12 months, and poor quality of life. A heart transplant candidate typically has uncontrolled symptoms and no other surgical options.

Transplantation doesn't guarantee a cure. Serious postoperative complications include infection and tissue rejection. Most patients experience one or both of these complications postoperatively.

Heart transplantation may be either orthotopic or heterotopic. Orthotopic is the most common type of heart transplantation. In this procedure, most of the patient's native heart is removed. The donor heart is then attached to the atrial cusps and the aorta and pulmonary artery are anastomosed. (See Quick guide to orthotopic heart transplantation.) Heterotopic heart transplantation is less commonly performed. In this procedure, the donor heart is grafted to the recipient heart, and the donor heart is used to help augment the native heart's pumping ability.

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT AFTER A MIDCAB

Before discharge from the facility following a minimally invasive direct coronary artery bypass (MIDCAB), instruct the patient to:

·

continue with the progressive exercise started in the facility

·

perform coughing and deep-breathing exercises (while splinting the incision with a pillow to reduce pain), and use the incentive spirometer to reduce pulmonary complications

·

avoid lifting objects that weigh more than 10 lb (4.5 kg) for the next 4 to 6 weeks

·

wait 2 to 4 weeks before resuming sexual activity

·

check the incision site daily, and immediately notify the practitioner of any signs of infection (redness, foul-smelling drainage, or swelling) or possible graft occlusion (slow, rapid, or irregular pulse; angina; dizziness; or dyspnea)

·

perform any necessary incision care

·

follow lifestyle modifications

·

take medications as prescribed, and report adverse effects to the practitioner

·

consider participation in a cardiac rehabilitation program.

Rejection typically occurs in the first 6 weeks after surgery, but it may still occur after this time. The patient is treated with monoclonal antibodies and potent immunosuppressants. The resulting immunosuppression places the patient at risk for life-threatening infection.

PREPARING THE PATIENT

·

Provide emotional support to the patient and his family. Begin to address their fears by discussing the procedure, possible complications, and the impact of transplantation and a prolonged recovery period on the patient's life.

·

Reinforce the physician's explanation of the surgery.

·

Discuss the immunosuppressant drugs that the patient will be taking. Remind the patient that these drugs increase his risk of infection

·

Explain the complex equipment and procedures used in the ICU and PACU.

 

·

Explain that the patient awakens from surgery with an ET tube in place and connected to a mechanical ventilator. He'll also be connected to a cardiac monitor and have in place an NG tube, a chest tube, an indwelling urinary catheter, arterial lines, epicardial pacing wires and, possibly, a PA catheter. Tell him that discomfort is minimal and that the equipment is removed as soon as possible.

·

Review incentive spirometry techniques and ROM exercises with the patient.

·

Make sure that the patient or a responsible family member has signed a consent form.

·

Before surgery, prepare the patient's skin.

·

Immediately before surgery, begin cardiac monitoring, and then assist with PA catheterization and insertion of arterial lines. Some facilities insert PA catheters and arterial lines in the operating room before surgery.

QUICK GUIDE TO ORTHOTOPIC HEART TRANSPLANTATION

The following illustrations show how a heart is transplanted.

The donor's heart

The donor's heart is removed after the surgeon cuts along these dissection lines.

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The recipient's heart

Before it can be removed, the recipient's heart is resected along these lines.

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The transplanted heart

The transplanted heart is sutured.

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MONITORING AND AFTERCARE

·

After surgery, maintain reverse isolation and strict infection control precautions.

·

Administer immunosuppressants, and monitor the patient closely for signs of infection. Transplant recipients may exhibit only subtle signs because immunosuppressants mask obvious signs.

·

Monitor vital signs every 15 minutes until stabilized, and assess the patient for signs of hemodynamic compromise, such as hypotension, decreased cardiac output, and shock.

·

If necessary, administer nitroprusside during the first 24 to 48 hours to control blood pressure. An infusion of dopamine can improve contractility and renal perfusion.

·

Volume replacement with normal saline, plasma expanders, or blood products may be necessary to maintain central venous pressure.

·

Patients with elevated PAP may receive prostaglandin E to produce pulmonary vasodilation and reduced right ventricular afterload.

·

Monitor ECGs for rhythm disturbances. Keep in mind that the transplanted heart's ECG waveform appears different from that of the patient's native heart. (See Effects of cardiac transplantation on an ECG waveform.)

·

Maintain the chest tube drainage system at the prescribed negative pressure. Regularly assess for hemorrhage or sudden stop of drainage.

 

·

Be prepared to help with a myocardial biopsy at about 7 days and 14 days postoperatively.

·

Keep in mind that the effects of denervated heart muscle or denervation (in which the vagus nerve is cut during heart transplant surgery) makes drugs such as edrophonium (Tensilon) and anticholinergics (such as atropine) ineffective. (See Teaching the patient after heart transplantation.)

ff2-b01382759RED FLAG

Be alert for signs suggestive of rejection, such as a cardiac index less than 2.2, hypotension, atrial or other arrhythmias, fever above 99.5° F (37.5° C), evidence of a third or fourth heart sound, peripheral edema, jugular vein distention, and crackles.

EFFECTS OF CARDIAC TRANSPLANTATION ON AN ECG WAVEFORM

An orthotopic heart transplantation (OHT) leads to characteristic findings on an electrocardiogram (ECG). Because the procedure provides the patient with a second functioning heart, the ECG shows two distinct cardiac rhythms—that of the native heart and that of the donor heart. These can be differentiated by analyzing the recipient's preoperative ECG. In addition, the donor heart's QRS complex usually has a higher amplitude. Remember that in OHT, the native heart's sinoatrial (SA) node remains intact. This accounts for the two P waves commonly seen on the posttransplant ECG. However, only the donor heart's SA node conducts through to the ventricles.

Initially, the atrial and ventricular rates are slow, requiring the use of a temporary pacemaker in the immediate postoperative period or therapy with such drugs as theophylline (Theo-Dur). The patient's native P waves will have a regular rhythm unrelated to the donor heart's QRS complexes. The donor atrial and ventricular rhythms are usually regular. Typically, two separate P waves are seen and the QRS complex may be widened secondary to ventricular conduction defects. Pacemaker activity should appear as long as the patient requires pacemaker support for chronotropic incompetence.

Orthotopic heart transplantation

This waveform shows two distinct types of P waves. P waves caused by the native heart's SA node are unrelated to the QRS complexes (first shaded area). P waves caused by the donor heart's SA node precede each QRS complex (second shaded area).

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Heterotopic heart transplantation

This waveform shows the ECG of the recipient's own heart (first shaded area) and the donor heart (second shaded area).

c4-tt11

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT AFTER HEART TRANSPLANTATION

Before discharge from the facility, instruct the patient to:

·

continue with the progressive exercise started in the facility

·

perform coughing and deep-breathing exercises (while splinting the incision with a pillow to reduce pain) and use the incentive spirometer to reduce pulmonary complications

·

avoid lifting objects that weigh more than 10 lb (4.5 kg) for the next 4 to 6 weeks

·

wait 2 to 4 weeks before resuming sexual activity

·

check the incision site daily and immediately notify the practitioner of any signs of infection (redness, foul-smelling drainage, or swelling)

·

perform any necessary incisional care

·

follow lifestyle modifications

·

take prescribed drugs (which will be lifelong), and report adverse effects to the practitioner

·

consider participation in a cardiac rehabilitation program as advised

·

immediately report any episodes of chest pain or shortness of breath

·

avoid crowds and anyone with an infectious illness

·

comply with follow-up visits as instructed.

Vascular repair

Vascular repair includes aneurysm resection, grafting, embolectomy, vena caval filtering, endarterectomy, and vein stripping. The specific surgery used depends on the type, location, and extent of vascular occlusion or damage. (See Types of vascular repair, pages 192 and 193.)

Vascular repair can be used to treat:

·

 

·

vascular obstructions that severely compromise circulation

·

vascular disease that doesn't respond to drug therapy or nonsurgical treatments such as balloon catheterization

·

life-threatening dissecting or ruptured aortic aneurysms

·

limb-threatening acute arterial occlusion.

All vascular surgeries carry a risk of vessel trauma, emboli, hemorrhage, infection, and other complications. Grafting carries added risks because the graft may occlude, narrow, dilate, or rupture.

PREPARING THE PATIENT

·

Make sure the patient and his family understand the physician's explanation of the surgery and its possible complications.

·

Make sure that the patient or a responsible family member has signed a consent form.

·

Tell the patient that he'll receive a general anesthetic and will awaken from the anesthetic in the ICU or PACU. Explain that he'll have an I.V. line in place, ECG electrodes for continuous cardiac monitoring, and possibly an arterial line or a PA catheter to provide continuous pressure monitoring. He may also have a urinary catheter in place to allow accurate output measurement. If appropriate, explain that he'll be intubated and placed on mechanical ventilation.

·

Before surgery, perform a complete vascular assessment. Take vital signs to provide a baseline. Evaluate the strength and sound of the blood flow and the symmetry of the pulses, and note bruits. Record the temperature of the extremities, their sensitivity to motor and sensory stimuli, and pallor, cyanosis, or redness. Rate peripheral pulse volume and strength on a scale of 0 to 4, and check capillary refill time by blanching the fingernail or toenail; normal refill time is less than 3 seconds.

·

Instruct the patient to restrict food and fluids for at least 8 hours before surgery.

ff2-b01382759RED FLAG

If the patient is awaiting surgery for aortic aneurysm repair, be on guard for signs and symptoms of acute dissection or rupture. Especially note sudden severe pain in the chest, abdomen, or lower back; severe weakness; diaphoresis; tachycardia; or a precipitous drop in blood pressure. If any of these occurs, notify the physician immediately.

MONITORING AND AFTERCARE

·

Check and record the patient's vital signs every 15 minutes until his condition stabilizes, then every 30 minutes for 1 hour, and hourly thereafter for 2 to 4 hours. Report hypotension and hypertension immediately.

·

Auscultate heart, breath, and bowel sounds, and report abnormal findings. Monitor the ECG for abnormalities in heart rate or rhythm. Also monitor other pressure readings, and carefully record intake and output.

·

Check the patient's dressing regularly for excessive bleeding.

 

·

 

·

Provide analgesics, as indciated, for incisional pain.

·

Frequently assess peripheral pulses, using Doppler ultrasonography if palpation is difficult. Check all extremities bilaterally for muscle strength and movement, color, temperature, and capillary refill time.

·

Change dressings and provide incision care as indicated. Position the patient to avoid pressure on grafts and to reduce edema. Give antithrombotics, as indciated, and monitor appropriate laboratory values to evaluate effectiveness.

·

Assess for complications, and immediately report relevant signs and symptoms. (See Complications of vascular repair, page 194.)

·

 

·

Assist the patient with ROM exercises to prevent thrombus formation. Assist with early ambulation to prevent complications of immobility.

·

Provide support to the patient and his family to help them cope with recovery and lifestyle changes. (See Teaching the patient after vascular repair.)

TYPES OF VASCULAR REPAIR

Several surgical options exist to repair damaged or diseased vessels. These options include aortic aneurysm repair, vena caval filter insertion, embolectomy, and bypass grafting.

Aortic aneurysm repair

Aortic aneurysm repair involves removing an aneurysmal segment of the aorta. The surgeon first makes an incision to expose the aneurysm site. If necessary, the patient is placed on a cardiopulmonary bypass machine. Next, the surgeon clamps the aorta, resects the aneurysm, and repairs the damaged portion of the aorta.

c4-tt12

Vena caval filter insertion

A vena caval filter traps emboli in the vena cava, preventing them from reaching the pulmonary vessels. Inserted transvenously by catheter, the vena caval filter, or umbrella, traps emboli but allows venous blood flow.

c4-tt13

Embolectomy

c4-tt14

c4-tt15

Bypass grafting

Bypass grafting serves to bypass an arterial obstruction resulting from arteriosclerosis. After exposing the affected artery, the surgeon anastomoses a synthetic or autogenous graft to divert blood flow around the occluded arterial segment. The autogenous graft may be a vein or artery harvested from elsewhere in the patient's body. This illustration shows a femoropopliteal bypass.

c4-tt16

P.194

COMPLICATIONS OF VASCULAR REPAIR

After a patient has undergone vascular repair surgery, monitor for these potential complications.

COMPLICATIONS

SIGNS AND SYMPTOMS

Pulmonary infection

·

Fever

·

Cough

·

Congestion

·

 

Infection

·

Redness

·

Warmth

·

Drainage

·

Pain

·

Fever

Renal dysfunction

·

Low urine output

·

Elevated blood urea nitrogen and serum creatinine levels

Occlusion

·

Reduced or absent peripheral pulses

·

Paresthesia

·

Severe pain

·

Cyanosis

Hemorrhage

·

Hypotension

·

Tachycardia

·

Restlessness and confusion

·

Shallow respirations

·

Abdominal pain

·

 

Valve surgery

To prevent heart failure, a patient with valvular stenosis or insufficiency accompanied by severe, unmanageable symptoms may require valve replacement (with a mechanical or prosthetic valve), valvular repair, or commissurotomy. (See Types of valve surgery, page 196.)

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT AFTER VASCULAR REPAIR

Before discharge from the facility, instruct the patient to:

·

 

·

continue with the progressive exercise started in the facility

·

perform coughing and deep-breathing exercises (while splinting the incision with a pillow to reduce pain) and use the incentive spirometer to reduce pulmonary complications

·

avoid lifting objects that weigh more than 10 lb (4.5 kg) for the next 4 to 6 weeks

·

check the incision site daily and immediately notify the practitioner of any signs and symptoms of infection

·

take medications as prescribed and report adverse effects to the practitioner

·

comply with the laboratory schedule for monitoring International Normalized Ratio if the patient is receiving warfarin (Coumadin).

Because of the high pressure generated by the left ventricle during contraction, stenosis and insufficiency most commonly affect the mitral and aortic valves. Other indications for valve surgery depend on the patient's symptoms and on the affected valve:

·

aortic insufficiency—valve replacement indicated after symptoms (palpitations, dizziness, dyspnea on exertion, angina, and murmurs) have developed or the chest X-ray and ECG reveal left ventricular hypertrophy

·

aortic stenosis—may not produce symptoms; valve replacement (or balloon valvuloplasty) recommended if cardiac catheterization reveals significant stenosis

·

mitral stenosis—valvuloplasty or commissurotomy indicated if the patient develops fatigue, dyspnea, hemoptysis, arrhythmias, pulmonary hypertension, or right ventricular hypertrophy

·

mitral insufficiency—valvuloplasty or valve replacement indicated when symptoms (dyspnea, fatigue, and palpitations) interfere with patient activities or in acute insufficiency (as in papillary muscle rupture).

Although valve surgery carries a low risk of mortality, it can cause serious complications. Hemorrhage, for instance, may result from unligated vessels, anticoagulant therapy, or coagulopathy resulting from cardiopulmonary bypass during surgery. Stroke may result from thrombus formation caused by turbulent blood flow through the prosthetic

valve or from poor cerebral perfusion during cardiopulmonary bypass. In valve replacement, bacterial endocarditis can develop within days of implantation or months later. Valve dysfunction or failure may occur as the prosthetic device wears out.

TYPES OF VALVE SURGERY

When a patient with valve disease develops severe symptoms, surgery may be necessary. Several surgical procedures are available.

Commissurotomy

During commissurotomy, the surgeon incises fused mitral valve leaflets and removes calcium deposits to improve valve mobility.

Valve repair

Valve repair includes resection or patching of valve leaflets, stretching or shortening of chordae tendineae, or placing a ring in a dilatated annulus (annuloplasty). Valve repair is done to avoid the complications associated with the use of prosthetic valves.

Valve replacement

Valve replacement involves replacement of the patient's diseased valve with a mechanical or biological valve.

In the Ross procedure, the patient's own pulmonic valve is excised and used to replace the diseased aortic valve. An allograft from a human cadaver is then used to replace the pulmonic valve. Advantages of this procedure include the potential for the pulmonary autograft to grow when used in children, anticoagulation isn't necessary, and increased durability.

Minimally invasive valve surgery

Minimally invasive valve surgery can be performed without a large median sternotomy incision to repair or replace aortic and mitral valves. Port access techniques may also be used for mitral valve surgery using endovascular cardiopulmonary bypass. Advantages of these types of surgery include a less invasive procedure, shorter hospital stays, fewer postoperative complications, reduced costs, and smaller incisions.

PREPARING THE PATIENT

·

 

·

Tell the patient that he'll awaken from surgery in an ICU or a PACU. Mention that he'll be connected to a cardiac monitor and have I.V. lines, an arterial line and, possibly, a PA or left atrial catheter in place.

·

Explain that he'll breathe through an ET tube connected to a mechanical ventilator and that he'll have a chest tube in place.

 

·

Make sure that the patient or a responsible family member has signed a consent form.

MONITORING AND AFTERCARE

·

 

·

Frequently assess heart sounds; report distant heart sounds or new murmurs, which may indicate prosthetic valve failure.

·

Take steps to maintain the patient's MAP between 70 and 100 mm Hg. Also, monitor PAP and left atrial pressure as indicated.

·

Frequently assess the patient's peripheral pulses, capillary refill time, and skin temperature and color, and auscultate for heart sounds. Evaluate tissue oxygenation by assessing breath sounds, chest excursion, and symmetry of chest expansion. Report any abnormalities.

·

Check ABG values every 2 to 4 hours, and adjust ventilator settings as needed.

·

Maintain chest tube drainage at the prescribed negative pressure (usually -10 to -40 cm H2O for adults). Assess chest tubes frequently for signs of hemorrhage, excessive drainage (greater than 200 ml/hour), and a sudden decrease or cessation of drainage.

·

As indicated, give analgesic, anticoagulant, antibiotic, antiarrhythmic, inotropic, and pressor drugs as well as I.V. fluids and blood products. Monitor intake and output, and assess for electrolyte imbalances, especially hypokalemia. When anticoagulant therapy begins, evaluate its effectiveness by monitoring prothrombin time and International Normalized Ratio daily.

·

After weaning from the ventilator and removing the ET tube, promote chest physiotherapy. Start the patient on incentive spirometry, and encourage him to cough, turn frequently, and deep-breathe.

·

Throughout the patient's recovery period, observe him carefully for complications. (See Teaching the patient after valve surgery, page 198.)

ff2-b01382759RED FLAG

Monitor the ECG continuously for disturbances in heart rate and rhythm, such as bradycardia, ventricular tachycardia, and heart block. Such disturbances may signal injury of the conduction system, which may occur during valve replacement from proximity of the atrial and mitral valves to the atrioventricular node. Arrhythmias may also result from myocardial irritability or ischemia, fluid and electrolyte imbalance, hypoxemia, or hypothermia. If you detect serious abnormalities, notify the practitioner, and be prepared to assist with temporary epicardial pacing.

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT AFTER VALVE SURGERY

·

 

·

immediately notify the practitioner if signs or symptoms of heart failure (weight gain, dyspnea, or edema) develop

·

notify the practitioner if signs or symptoms of postpericardiotomy syndrome (fever, muscle and joint pain, weakness, or chest discomfort) develop

·

follow the prescribed medication regimen and report adverse effects

·

follow his prescribed diet, especially sodium and fat restrictions

·

maintain a balance between activity and rest

·

follow his exercise or rehabilitation program if prescribed

·

inform his dentist and other practitioners of his prosthetic valve before undergoing surgery or dental work and to take prophylactic antibiotics before such procedures.

Ventricular assist device insertion

A VAD is a device that's implanted to support a failing heart. A VAD consists of a blood pump, cannulas, and a pneumatic or electrical drive console.

VADs are designed to decrease the heart's workload and increase cardiac output in patients with ventricular failure.

A VAD is commonly used while a patient waits for a heart transplant. In a surgical procedure, blood is diverted from a ventricle to an artificial pump. This pump is synchronized to the patient's ECG and then functions as the ventricle. (See Ventricular assist device: Help for the failing heart.) VADs are also indicated for use in patients with cardiogenic shock that doesn't respond to maximal pharmacologic therapy or with an inability to be weaned from cardiopulmonary bypass.

A VAD is used to provide systemic or pulmonary support, or both:

·

A right VAD provides pulmonary support by diverting blood from the failing right ventricle to the VAD, which then pumps the blood to the pulmonary circulation by way of the VAD connection to the pulmonary artery.

·

With a left VAD, blood flows from the left ventricle to the VAD, which then pumps blood back to the body by way of the VAD connection to the aorta.

 

·

When biventricular support is needed, both may be used. (See A closer look at VADs, page 200.)

VENTRICULAR ASSIST DEVICE: HELP FOR THE FAILING HEART

A ventricular assist device (VAD) functions like an artificial heart. The major difference is that the VAD assists the heart instead of replacing it. The VAD can aid one or both ventricles. The pumping chambers themselves aren't usually implanted in the patient.

A permanent VAD is implanted in the patient's chest cavity, although it still provides only temporary support. The device receives power through the skin by a belt of electrical transformer coils (worn externally as a portable battery pack). It can also operate off an implanted, rechargeable battery for up to 1 hour at a time.

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PREPARING THE PATIENT

·

Prepare the patient and his family for VAD insertion; be sure to explain how the device works, what its purpose is, and what to expect after insertion.

·

 

·

Continue close patient monitoring, including continuous ECG monitoring, pulmonary artery and hemodynamic status monitoring, and intake and output monitoring.

A CLOSER LOOK AT VADS

There are three types of ventricular assist devices (VADs).

·

A right VAD provides pulmonary support by diverting blood from the failing right ventricle to the VAD, which then pumps the blood to the pulmonary circulation via the VAD connection to the left pulmonary artery.

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·

With a left VAD, blood flows from the left ventricle to the VAD, which then pumps blood back to the body via the VAD connection to the aorta.

·

When a right and left VAD are used, it's referred to as a biventricular VAD.

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MONITORING AND AFTERCARE

Assess the patient's cardiovascular status at least every 15 minutes until stable, and then hourly. Monitor blood pressure and hemodynamic parameters, including cardiac output and cardiac index, ECG, and peripheral pulses.

·

Inspect the incision and dressing at least every hour initially, and then every 2 to 4 hours as indicated by the patient's condition.

·

Monitor urine output hourly, and maintain I.V. fluid therapy as indicated. Watch for signs of fluid overload or decreasing urine output.

·

Assess chest tube drainage and function frequently. Notify the physician if drainage is greater than 150 ml over 2 hours. Auscultate lungs for evidence of abnormal breath sounds. Evaluate oxygen

saturation or mixed venous oxygen saturation levels, and administer oxygen as indicated.

·

Obtain hemoglobin levels, hematocrit, and coagulation studies as indicated. Administer blood component therapy as indicated.

·

Assess the incision and the cannula insertion site for signs of infection. Monitor the white blood cell count and differential daily, and take rectal or core temperatures every 4 hours.

·

Use sterile technique in dressing changes. Change the dressing site over the cannula sites daily or according to facility policy.

·

Assess for signs and symptoms of bleeding.

·

Turn the patient every 2 hours, and begin ROM exercises when he's stable.

·

Administer antibiotics prophylactically if ordered. (See Teaching the patient after VAD insertion.)

DISCHARGE TEACHING

ff3-b01382759

Before discharge following the insertion of a ventricular assist device (VAD), instruct the patient to:

·

immediately report redness, swelling, or drainage at the incision site; chest pain; or fever

·

 

·

follow his prescribed medication regimen and report adverse effects

·

follow his prescribed diet, especially sodium and fat restrictions

·

maintain a balance between activity and rest

·

follow his exercise or rehabilitation program (if prescribed)

·

comply with the laboratory schedule for monitoring International Normalized Ratio if the patient is receiving warfarin (Coumadin).

Balloon catheter treatments

Balloon catheter treatments for cardiovascular disorders include percutaneous balloon valvuloplasty, percutaneous transluminal coronary angioplasty (PTCA) and intra-aortic balloon pump (IABP) counterpulsation.

PERCUTANEOUS BALLOON VALVULOPLASTY

Percutaneous balloon valvuloplasty can be performed in the cardiac catheterization laboratory. It's intended to improve valvular function by enlarging the orifice of a stenotic heart valve caused by congenital defect, calcification, rheumatic fever, or aging. A small balloon valvuloplasty catheter is introduced through the skin at the femoral vein. (See Percutaneous balloon valvuloplasty

PERCUTANEOUS BALLOON VALVULOPLASTY

In balloon valvuloplasty, the physician inserts a balloon-tipped catheter through the femoral vein or artery and threads it into the heart. After locating the stenotic valve, he inflates the balloon, increasing the size of the valve opening.

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Although valve surgery remains the treatment of choice for valvular heart disease, percutaneous balloon valvuloplasty offers an alternative for individuals who are considered poor candidates for surgery.

ff1-b01382759AGE AWARE

Elderly patients with aortic disease commonly experience restenosis 1 to 2 years after undergoing valvuloplasty.

Despite the decreased risks associated with more invasive procedures, balloon valvuloplasty can lead to complications, including:

·

worsening valvular insufficiency by misshaping the valve so that it doesn't close completely

·

pieces breaking off of the calcified valve, which may travel to the brain or lungs and cause embolism (rare)

·

severely damaging delicate valve leaflets, requiring immediate surgery to replace the valve (rare)

·

bleeding and hematoma at the arterial puncture site

 

·

MI (rare), arrhythmias, myocardial ischemia, and circulatory defects distal to the catheter entry site.

PREPARING THE PATIENT

·

Describe the procedure to the patient and his family, and tell them that it takes 1 to 4 hours to complete.

·

Explain that a catheter will be inserted into an artery or a vein in the patient's groin and that he may feel pressure as the catheter moves along the vessel.

·

Reassure the patient that although he'll be awake during the procedure, he'll be given a sedative. Instruct him to report any angina during the procedure.

·

Check the patient's history for allergies; if he has had allergic reactions to shellfish, iodine, or contrast media, notify the physician.

·

Make sure that the patient or a responsible family member has signed a consent form.

·

Restrict food and fluids for at least 6 hours before the procedure.

·

Make sure that the results of coagulation studies, complete blood count (CBC), serum electrolyte studies, blood typing and crossmatching, blood urea nitrogen (BUN) levels, and serum creatinine levels are available.

·

Obtain baseline vital signs and assess peripheral pulses.

·

Apply ECG electrodes and insert an I.V. line if not already in place.

·

Administer oxygen through a nasal cannula.

·

Perform skin preparation according to your facility's policy.

·

Give the patient a sedative as indicated.

MONITORING AND AFTERCARE

·

Assess the patient's vital signs and oxygen saturation every 15 minutes for the first hour and then every 30 minutes for 4 hours, unless his condition warrants more frequent checking.

·

Monitor I.V. infusions, such as heparin or nitroglycerin, as indicated.

·

Assess peripheral pulses distal to the catheter insertion site as well as the affected extremity's color, sensation, temperature, and capillary refill time.

·

Monitor cardiac rhythm continuously, and assess hemodynamic parameters closely for changes.

·

 

·

Instruct the patient to remain in bed for 8 hours and to keep the affected extremity straight. Maintain sandbags in position, if used to apply pressure to the catheter site. Elevate the head of the bed 15

to 30 degrees. If a hemostatic device was used to close the catheter insertion site, anticipate that the patient may be allowed out of bed in only a few hours.

·

Assess the catheter site for hematoma, ecchymosis, and hemorrhage. If an expanding ecchymotic area appears, mark the area to help determine the pace of expansion. If bleeding occurs, locate the artery and apply manual pressure; then notify the physician.

·

 

·

Document the patient's tolerance of the procedure and status after it, including vital signs, hemodynamic parameters, appearance of the catheter site, ECG findings, condition of the extremity distal to the insertion site, complications, and necessary interventions. (See Teaching the patient after percutaneous balloon valvuloplasty.)

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT AFTER PERCUTANEOUS BALLOON VALVULOPLASTY

Before discharge from the facility, instruct the patient to:

·

resume normal activity

·

notify the practitioner if he experiences bleeding or increased bruising at the puncture site or recurrence of symptoms of valvular insufficiency, such as breathlessness or decreased exercise tolerance

·

comply with regular follow-up visits.

Percutaneous transluminal coronary angioplasty

PTCA offers a nonsurgical alternative to coronary artery bypass surgery. The physician uses a balloon-tipped catheter to dilate a coronary artery that has become narrowed because of atherosclerotic plaque. (See Looking at PTCA.)

Performed in the cardiac catheterization laboratory under local anesthesia, PTCA doesn't involve a sternotomy, so it's less costly and requires shorter hospitalization. Patients can usually walk the next day and return to work in 2 weeks.

PTCA works best when lesions are readily accessible, noncalcified, less than 10 mm, concentric, discrete, and smoothly tapered. Patients with a history of less than 1 year of disabling angina make good candidates because their lesions tend to be softer and more compressible.

LOOKING AT PTCA

Percutaneous transluminal coronary angioplasty (PTCA) can open an occluded coronary artery without opening the chest. This procedure is outlined in the steps below.

First, the cardiologist must thread the catheter into the artery. The illustration below shows the entrance of a guide catheter into the coronary artery.

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When angiography shows the guide catheter positioned at the occlusion site, the cardiologist carefully inserts a smaller double-lumen balloon catheter through the guide catheter and directs the balloon through the occlusion.

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The cardiologist then inflates the balloon, causing arterial stretching and plaque fracture as shown below. The balloon may need to be inflated or deflated several times until successful arterial dilatation occurs.

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Complications of PTCA are acute vessel closure and late restenosis. To prevent restenosis, such procedures as stenting, atherectomy, and laser angioplasty may be performed. Also, vascular brachytherapy and drug-eluting stents have been found to decrease the incidence of restenosis. (See Preventing restenosis.)

PREVENTING RESTENOSIS

Standard angioplasty is performed to remove the plaque blockage in the coronary artery. However, restenosis of the vessel is a frequent complication that occurs from scar tissue formation rather than plaque buildup.

Vascular brachytherapy

Coronary drug-eluting stents

Stents are used to open arteries that feed the heart, thereby improving circulation to myocardial tissue. One complication of stents is restenosis of the vessel. Drug-eluting stents open the artery and also release a drug to the implantation site that helps reduce restenosis. The drug works by blocking smooth-muscle proliferation.

Placement of drug-eluting stents during a cardiac catheterization or angioplasty procedure is the same as for regular stents. Postprocedural care is also the same.

·

Describe the procedure to the patient and his family, and tell them that it takes 1 to 4 hours to complete.

·

Explain that a catheter will be inserted into an artery or a vein in the patient's groin and that he may feel pressure as the catheter moves along the vessel.

·

Reassure the patient that although he'll be awake during the procedure, he'll be given a sedative. Instruct him to report any angina during the procedure.

·

Explain that the physician injects a contrast medium to outline the lesion's location. Warn the patient that he may feel a hot, flushing sensation or transient nausea during the injection.

·

Check the patient's history for allergies; if he has had allergic reactions to shellfish, iodine, or contrast media, notify the practitioner.

·

Make sure that the patient or a responsible family member has signed a consent form.

·

Locate, mark, and record the amplitude of bilateral distal pulses.

 

·

Restrict food and fluids for at least 6 hours before the procedure.

·

Make sure that the results of coagulation studies, CBC, serum electrolyte studies, blood typing and crossmatching, BUN levels, and serum creatinine levels are available.

·

Obtain baseline vital signs and assess peripheral pulses.

·

Apply ECG electrodes and insert an I.V. line if not already in place.

·

Administer oxygen through a nasal cannula.

·

Perform skin preparation according to your facility's policy.

·

Instruct the patient to tell the surgical team immediately if he has breathing difficulties, sweating, numbness, itching, nausea, vomiting, chills, or heart palpitations during the procedure.

·

Give the patient a sedative as indicated.

MONITORING AND AFTERCARE

·

Assess the patient's vital signs and oxygen saturation every 15 minutes for the first hour and then every 30 minutes for 4 hours, unless his condition warrants more frequent checking.

·

 

·

Assess peripheral pulses distal to the catheter insertion site as well as the affected extremity's color, sensation, temperature, and capillary refill time.

·

Monitor cardiac rhythm continuously, and assess hemodynamic parameters closely for changes.

·

Monitor the 12-lead ECG results, particularly changes in ST segments indicating ischemia or infarction.

·

Instruct the patient to remain in bed for 8 hours and to keep the affected extremity straight. Maintain sandbags in position, if used to apply pressure to the catheter site.

·

Elevate the head of the bed 15 to 30 degrees. If a hemostatic device was used to close the catheter insertion site, anticipate that the patient may be allowed out of bed in only a few hours.

·

Administer I.V. fluids as indicated (usually 100 ml/hour) to promote excretion of the contrast medium. Be sure to assess for signs of fluid overload.

·

Assess the catheter site for hematoma, ecchymosis, and hemorrhage. If bleeding occurs, locate the artery and apply manual pressure; then notify the physician.

 

·

After the physician removes the catheter, apply direct pressure for at least 10 minutes, and monitor the site often.

·

Document the patient's tolerance of the procedure and status afterward, including vital signs, hemodynamic parameters, appearance of the catheter site, ECG findings, condition of the extremity distal to the insertion site, complications, and necessary interventions. (See Teaching the patient after PTCA.)

ff2-b01382759RED FLAG

Immediately report signs and symptoms of angina (including chest pain), fluid overload (tachycardia, dyspnea, edema), and abrupt arterial reclosure (chest pain, ECG changes)

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT AFTER PTCA

If the patient doesn't experience complications from percutaneous transluminal coronary angioplasty (PTCA), he may go home in 6 to 12 hours. Before discharge, instruct the patient to:

·

call his practitioner if he experiences bleeding or bruising at the arterial puncture site

·

return for a stress thallium imaging test and follow-up angiography as recommended by his practitioner

·

report chest pain to the practitioner because restenosis can occur after PTCA.

Intra-aortic balloon pump counterpulsation

IABP counterpulsation temporarily reduces left ventricular workload and improves coronary perfusion. (See Understanding a balloon pump.)

A 34-, 40-, or 50-cc balloon-tipped catheter is placed in the descending aorta between the left subclavian artery and the renal artery. The balloon is attached to a console that contains the gas for inflation (usually helium) and displays the waveforms. (See Parts of an IABP, page 210.)

IABP counterpulsation may benefit patients with:

·

cardiogenic shock due to acute MI

·

septic shock

·

intractable angina before surgery

·

intractable ventricular arrhythmias

·

ventricular septal or papillary muscle ruptures.

It's also used for patients who suffer pump failure before or after cardiac surgery.

The physician may perform balloon catheter insertion at the patient's bedside as an emergency procedure or in the operating room.

UNDERSTANDING A BALLOON PUMP

An intra-aortic balloon pump consists of a polyurethane balloon attached to an external pump console by means of a large-lumen catheter. It's inserted percutaneously through the femoral artery and positioned in the descending aorta just distal to the left subclavian artery and above the renal arteries.

Inflation

This external pump works in precise counterpoint to the left ventricle, inflating the balloon with helium early in diastole and deflating it just before systole. As the balloon inflates, it forces blood toward the aortic valve, thereby raising pressure in the aortic root and augmenting diastolic pressure to improve coronary perfusion. It also improves peripheral circulation by forcing blood through the brachiocephalic, common carotid, and subclavian arteries arising from the aortic trunk.

c4-tt24

Deflation

The balloon deflates rapidly at the end of diastole, creating a vacuum in the aorta. This reduces aortic volume and pressure, thereby decreasing the resistance to left ventricular ejection (afterload). This decreased workload, in turn, reduces the heart's oxygen requirements and, combined with the improved myocardial perfusion, helps prevent or diminish myocardial ischemia.

c4-tt25

PREPARING THE PATIENT

·

Explain to the patient that the physician is going to place a catheter in the aorta to help his heart pump more easily. Tell him that, while the catheter is in place, he can't sit up, bend his knee, or flex his hip more than 30 degrees.

 

·

Attach the patient to a continuous ECG monitor, and make sure he has an arterial line, a PA catheter, and a peripheral I.V. line in place.

·

Gather a surgical tray for percutaneous catheter insertion, heparin, normal saline solution, the IABP catheter, and the pump console. Connect the ECG monitor to the pump console.

·

If possible, make sure the patient or a responsible family member has signed a consent form.

PARTS OF AN IABP

The following illustrations show a balloon pump and a close up of the controls and screen.

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c4-tt27

MONITORING AND AFTERCARE

·

After the IABP catheter is inserted, select either the ECG or the arterial waveform to regulate inflation and deflation of the balloon. With the ECG waveform, the pump inflates the balloon in the middle of the T wave (diastole) and deflates with the R wave (before systole). With the arterial waveform, the upstroke of the arterial wave triggers balloon inflation. (See Interpreting intra-aortic balloon waveforms, pages 212 to 214.)

·

Frequently assess the insertion site. Don't elevate the head of the bed more than 30 degrees, to prevent upward migration of the catheter and occlusion of the left subclavian artery. If the balloon occludes the artery, you may see a diminished left radial pulse, and the patient may report dizziness. Incorrect balloon placement may also cause flank pain or a sudden decrease in urine output.

·

Asses the patient's cardiovascular and respiratory status at least every 4 hours. If possible, place the IABP on standby to eliminate extraneous sounds.

·

 

·

Assess distal pulses, color, temperature, and capillary refill of the patient's extremities every 15 minutes for the first 4 hours after insertion. After 4 hours, assess hourly for the duration of IABP therapy.

·

Watch for signs of thrombus formation, such as a sudden weakening of pedal pulses, pain, and motor or sensory loss.

·

 

·

Encourage active ROM exercises every 2 hours for the arms, the unaffected leg, and the affected ankle.

·

Maintain adequate hydration to help prevent thrombus formation.

·

If bleeding occurs at the catheter insertion site, apply direct pressure and notify the physician.

·

An alarm on the console may indicate a gas leak from a damaged catheter or ruptured balloon. If the alarm sounds or you see blood in the catheter, shut down the pump console, and immediately

place the patient in Trendelenburg's position to prevent an embolus from reaching the brain. Then notify the physician. (See Troubleshooting an IABP.)

·

After the patient's signs and symptoms of left-sided heart failure diminish, only minimal drug support is required, and the physician begins weaning the patient from IABP counterpulsation by reducing the frequency of pumping or decreasing the balloon volume. A minimum volume or pumping ratio must be maintained to prevent thrombus formation. Most consoles have a flutter function that moves the balloon to prevent clot formation. Use the flutter function when the patient has been weaned from counterpulsation but the catheter hasn't yet been removed.

·

To discontinue the IABP, the physician deflates the balloon, clips the sutures, removes the catheter, and allows the site to bleed for 5 seconds to expel clots.

·

After the physician discontinues the IABP, apply direct pressure for 30 minutes, and then apply a pressure dressing. Evaluate the site for bleeding and hematoma formation hourly for the next 4 hours. (See Teaching the patient after IABP treatment, page 218.)

INTERPRETING INTRA-AORTIC BALLOON WAVEFORMS

During intra-aortic balloon counterpulsation, you can use electrocardiogram and arterial pressure waveforms to determine whether the balloon pump is functioning properly.

Normal inflation-deflation timing

Balloon inflation occurs after aortic valve closure; deflation, during isovolumetric contraction, occurs just before the aortic valve opens. In a properly timed waveform such as the one shown below, the inflation point lies at or slightly above the dicrotic notch. Both inflation and deflation cause a sharp V. Peak diastolic pressure exceeds peak systolic pressure; peak systolic pressure exceeds assisted peak systolic pressure.

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Early inflation

With early inflation, the inflation point lies before the dicrotic notch. Early inflation dangerously increases myocardial stress and decreases cardiac output.

c4-tt29

Early deflation

With early deflation, a U shape appears, and peak systolic pressure is less than or equal to assisted peak systolic pressure. This won't decrease afterload or myocardial oxygen consumption.

c4-tt30

Late inflation

With late inflation, the dicrotic notch precedes the inflation point, and the notch and the inflation point create a W shape. This can lead to a reduction in peak diastolic pressure, coronary and systemic perfusion augmentation time, and augmented coronary perfusion pressure.

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Late deflation

With late deflation, peak systolic pressure exceeds assisted peak systolic pressure. This threatens the patient by increasing afterload, myocardial oxygen consumption, cardiac workload, and preload. It occurs when the balloon has been inflated for too long.

c4-tt32

TROUBLESHOOTING AN IABP

 

PROBLEM

POSSIBLE

CAUSES

INTERVENTIONS

High gas leak (automatic mode only)

 

·

Check for blood in the tubing.

·

Stop pumping.

·

Notify the physician to remove the balloon.

Condensation in extension tubing, volume limiter disk, or both

·

Remove condensate from the tubing and volume limiter disk.

·

Refill, autopurge, and resume pumping.

Kink in balloon catheter or tubing

·

Check the catheter and tubing for kinks and loose connections; straighten and tighten any found.

·

Refill and resume pumping.

Tachycardia

·

Change wean control to 1:2 or operate on “manual” mode.

·

 

Malfunctioning or loose volume limiter disk

·

Replace or tighten the disk.

·

Refill, autopurge, and resume pumping.

System leak

·

Perform a leak test.

Balloon line block (in automatic mode only)

Kink in balloon or catheter

·

Check the catheter and tubing for kinks and loose connections; straighten and tighten any found.

·

Refill and resume pumping.

Balloon catheter not unfurled; sheath or balloon positioned too high

·

Notify the physician immediately to verify placement.

·

Anticipate the need for repositioning or manual inflation of the balloon.

Condensation in tubing, volume limiter disk, or both

·

Remove condensate from the tubing and volume limiter disk.

·

Refill, autopurge, and resume pumping.

Balloon too large for aorta

·

Decrease volume control percentage by one notch.

Malfunctioning volume limiter disk or incorrect volume limiter disk size

·

Replace the volume limiter disk.

·

Refill, autopurge, and resume pumping.

No electrocardiogram (ECG) trigger

 

·

Adjust ECG gain, and change the lead or trigger mode.

Lead disconnected

·

Replace the lead.

Improper ECG input mode (skin or monitor) selected

·

Adjust ECG input to appropriate mode (skin or monitor).

No atrial pressure trigger

Arterial line damped

·

Flush the line.

Arterial line open to atmosphere

·

Check connections on the arterial pressure line.

Trigger mode change

Trigger mode changed while pumping

·

Resume pumping.

Irregular heart rhythm

Patient experiencing arrhythmia, such as atrial fibrillation or ectopic beats

·

Change to R or QRS sense (if necessary to accommodate irregular rhythm).

·

Notify the physician of arrhythmia.

Erratic atrioventricular (AV) pacing

Demand for paced rhythm occurring when in AV sequential trigger mode

·

Change to pacer reject trigger or QRS sense.

Noisy ECG signal

Malfunctioning leads

·

Replace the leads.

·

Check the ECG cable.

Electrocautery in use

·

 
   

·

Select an alternative trigger if the patient has a heartbeat or rhythm.

·

Keep in mind that the internal trigger is used only during cardiopulmonary bypass or cardiac arrest.

Purge incomplete

OFF button pressed during autopurge; interrupted purge cycle

·

Initiate autopurging again or initiate pumping.

High fill pressure

Malfunctioning volume limiter disk

·

Replace the volume limiter disk.

·

Refill, autopurge, and resume pumping.

Occluded vent line or valve

·

Attempt to resume pumping.

·

If unsuccessful, notify the physician and contact the manufacturer.

No balloon drive

No volume limiter disk

·

Insert the volume limiter disk, and lock it securely in place.

Tubing disconnected

·

Reconnect the tubing.

·

 

Incorrect timing

INFLATE and DEFLATE controls set incorrectly

·

Place the INFLATE and DEFLATE controls at set midpoints.

·

Reassess timing and readjust.

Low volume percentage

 

·

Assess the cause of decreased volume, and reset if necessary.

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT AFTER IABP TREATMENT

Before discharge from the facility, instruct the patient to:

·

call his practitioner if he experiences bleeding or bruising at the insertion site

·

return for follow-up testing as recommended by his practitioner

·

report chest pain to the practitioner.

CARDIOVASCULAR RESYNCHRONIZATION TECHNIQUES

When the electrical conduction of the heart is disrupted, cardiac output is diminished, and perfusion of blood and oxygen to all body tissues is affected. Treatment to restore the heart's conduction needs to begin quickly. Some treatments include defibrillation, an implantable cardioverter-defibrillator (ICD), synchronized cardioversion, and pacemaker insertion.

Defibrillation

In defibrillation, electrode paddles are used to direct an electric current through the patient's heart. The current causes the myocardium to depolarize, which in turn encourages the SA node to resume control of the heart's electrical activity. (See Biphasic defibrillators.)

BIPHASIC DEFIBRILLATORS

Many hospital defibrillators are monophasic, delivering a single electric current that travels in one direction between the two pads or paddles on the patient's chest. A large amount of electric current is required for effective monophasic defibrillation.

Differences between monophasic and biphasic defibrillators

Energy usage

The biphasic defibrillator delivers two electric currents and lowers the heart muscle's defibrillation threshold, making it possible to successfully defibrillate ventricular fibrillation with smaller amounts of energy. Instead of using 200 joules, an initial shock of 150 joules is usually effective.

Number of shocks needed

The biphasic defibrillator can adjust for differences in impedance (the resistance of the current through the chest). This reduces the number of shocks needed to terminate ventricular fibrillation.

Benefits of biphasic defibrillation

Because the biphasic defibrillator requires lower energy levels and fewer shocks, damage to the myocardial muscle is reduced. Biphasic defibrillators used at the appropriate energy level may be used for defibrillation and, in the synchronized mode, for synchronized cardioversion.

The electrode paddles delivering the current may be placed on the patient's chest or, during cardiac surgery, directly on the myocardium.

Because some arrhythmias, such as ventricular fibrillation, can cause death if not corrected, the success of defibrillation depends on early recognition and quick treatment.

In addition to treating ventricular fibrillation, defibrillation may also be used to treat ventricular tachycardia that doesn't produce a pulse, or polymorphic ventricular tachycardia with a pulse.

Automated external defibrillators

An automated external defibrillator (AED) has a cardiac rhythm analysis system. The AED interprets the patient's cardiac rhythm and gives the operator step-by-step directions on how to proceed if defibrillation is indicated. Most AEDs have a “quick-look” feature that allows visualization of the rhythm with the paddles before electrodes are connected.

DEFIBRILLATOR PADDLE PLACEMENT

Here's a guide to correct paddle placement for defibrillation.

For anterolateral placement, place one paddle to the right of the upper sternum, just below the right clavicle, and the other over the fifth or sixth intercostal space at the left anterior axillary line.

c4-tt33

Anteroposterior placement

For anteroposterior placement, place the anterior paddle directly over the heart at the precordium, to the left of the lower sternal border. Place the flat posterior paddle under the patient's body beneath the heart and immediately below the scapulae.

c4-tt34

The AED is equipped with a microcomputer that analyzes a patient's heart rhythm at the push of a button. It then audibly or visually prompts you to deliver a shock.

PATIENT PREPARATION

·

Assess the patient to determine if he lacks a pulse. Call for help, and perform cardiopulmonary resuscitation (CPR) until the defibrillator and other emergency equipment arrive.

·

Connect the monitoring leads of the defibrillator to the patient, and assess his cardiac rhythm in two leads.

·

Expose the patient's chest, and apply conductive pads at the paddle placement positions. (See Defibrillator paddle placement.)

MONITORING AND AFTERCARE

·

Turn on the defibrillator and, if performing external defibrillation, set the energy level at 360 joules (J) for an adult.

 

·

Charge the paddles by pressing the charge buttons, which are located on either the machine or the paddles.

·

Place the paddles over the conductive pads, and press firmly against the patient's chest, using 25 lb (11.3 kg) of pressure.

·

Reassess the patient's cardiac rhythm in two leads.

·

If the patient remains in a shockable rhythm, instruct all personnel to stand clear of the patient and the bed. Also, make a visual check to make sure everyone is clear of the patient and the bed.

·

Discharge the current by pressing both paddle discharge buttons simultaneously.

·

Reassess the patient's pulse, and give 2 minutes of CPR. Reassess his cardiac rhythm.

·

If necessary, prepare to defibrillate a second time at 360 J. Announce that you're preparing to defibrillate, and follow the procedure described above.

·

 

·

If the patient still has no pulse after the first two cycles of defibrillation and CPR, give supplemental oxygen, and begin administering appropriate medications such as epinephrine. Also, consider possible causes for failure of the patient's rhythm to convert, such as acidosis and hypoxia.

·

If defibrillation restores a normal rhythm, assess the patient. Obtain baseline ABG levels and a 12-lead ECG. Provide supplemental oxygen, ventilation, and medications as needed. Prepare the defibrillator for immediate reuse.

·

Document the procedure, including the patient's ECG rhythms before and after defibrillation; the number of times defibrillation was performed; the voltage used during each attempt; whether a pulse returned; the dosage, route, and time of any drugs administered; whether CPR was used; how the airway was maintained; and the patient's outcome. (See Teaching the patient after defibrillation.)

Implantable cardioverter-defibrillator

An ICD has a programmable pulse generator and lead system that monitors the heart's activity, detects ventricular bradyarrhythmias and tachyarrhythmias, and responds with appropriate therapies. It's used for antitachycardia and bradycardia pacing, cardioversion, and defibrillation. (See Types of ICD therapy, page 222.) Some defibrillators also have the ability to pace the atrium and the ventricle. ICDs store information, and ECGs allow the information to be retrieved to revaluate the device's function.

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT AFTER DEFIBRILLATION

Before discharge:

·

instruct the patient to report any episodes of chest pain to the practitioner

·

encourage the family to learn cardiopulmonary resuscitation as well as how to use an automated external defibrillator

·

instruct the patient to consider an implantable cardioverter-defibrillator, if recommended by his practitioner.

TYPES OF ICD THERAPY

Implantable cardioverter-defibrillators (ICDs) can deliver a range of therapies, depending on the arrhythmia detected and how the device is programmed. Therapies include antitachycardia pacing, cardioversion, defibrillation, and bradycardia pacing. Some ICDs can also provide biventricular pacing.

THERAPY

DESCRIPTION

Antitachycardia pacing

A series of small, rapid electrical pacing pulses used to interrupt atrial arrhythmias or ventricular tachycardia and return the heart to its normal rhythm. Antitachycardia pacing isn't appropriate for all patients; it's initiated by the practitioner after appropriate evaluation of electrophysiology studies.

Cardioversion

A low- or high-energy shock (up to 34 joules) that's timed to the R wave to terminate atrial fibrillation or ventricular tachycardia and return the heart to its normal rhythm.

 

A high-energy shock (up to 34 joules) to the heart to terminate atrial fibrillation or ventricular fibrillation and return the heart to its normal rhythm.

Bradycardia pacing

Electrical pacing pulses used when the natural electrical signals are too slow. ICD systems can pace one chamber (VVI pacing) of the heart at a preset rate or sense and pace both chambers (DDD pacing).

INSERTING AN ICD

To insert an implantable cardioverter-defibrillator (ICD), the cardiologist makes a small incision near the collarbone and accesses the subclavian vein. The leadwires are inserted through the subclavian vein, threaded into the heart, and placed in contact with the endocardium.

The leads are connected to the pulse generator, which is placed under the skin in a specially prepared pocket in the right or left upper chest. (Placement is similar to that used for a pacemaker.) The cardiologist then closes the incision and programs the device.

c4-tt35

To implant an ICD, the cardiologist positions the lead (or leads) transvenously in the endocardium of the right ventricle (and the right atrium, if both chambers require pacing). The lead connects to a generator box, which is implanted in the right or left upper chest near the clavicle. (See Inserting an ICD.)

PATIENT PREPARATION

·

Reinforce the cardiologist's instructions to the patient and his family, answering any questions they may have.

·

Be sure to emphasize the need for the device, the potential complications, and ICD terminology.

·

Restrict food and fluid for 12 hours before the procedure.

·

 

·

Make sure that the patient or a responsible family member has signed a consent form.

ff3-b01382759TEACHING THE PATIENT AFTER ICD IMPLANTATION

Before discharge from the facility, instruct the patient to:

·

avoid placing excessive pressure over the insertion site or moving or jerking the area until the postoperative visit

·

check the incision site daily and immediately notify the practitioner of any signs and symptoms of infection

·

wear medical alert identification and carry information regarding his implantable cardioverter-defibrillator (ICD) at all times

·

 

·

take drugs as prescribed and report adverse effects to the practitioner.

MONITORING AND AFTERCARE

·

The patient will be monitored on a telemetry unit.

·

Monitor for arrhythmias and proper device functioning.

·

Gradually allow the patient to increase activities.

·

Monitor the incision site for signs of infection or drainage.

·

Maintain the occlusive dressing for the first 24 hours.

·

If the patient experiences cardiac arrest, initiate CPR and advanced cardiac life support.

·

Provide support to the patient and his family to help them cope with recovery and lifestyle changes.

·

Encourage family members to learn CPR. (See Teaching the patient after ICD implantation.)

ff2-b01382759

Monitor for signs and symptoms of a perforated ventricle with resultant cardiac tamponade, distant heart sounds, pulsus paradoxus, hypotension accompanied by narrowed pulse pressure, bulging neck veins, increased venous pressure, cyanosis, decreased urine output, restlessness, and complaints of fullness in the chest. Notify the practitioner immediately, and prepare the patient for emergency surgery.

ff2-b01382759RED FLAG

For external defibrillation, use anteroposterior paddle placement; don't place paddles directly over the pulse generator.

Synchronized cardioversion

Cardioversion (synchronized countershock) is an elective or emergency procedure used to correct tachyarrhythmias (such as atrial tachycardia, atrial flutter, atrial fibrillation, and symptomatic ventricular tachycardia). It's also the treatment of choice for patients with arrhythmias that don't respond to drug therapy.

In synchronized cardioversion, an electric current is delivered to the heart to correct an arrhythmia. Compared with defibrillation, it uses much lower energy levels and is synchronized to deliver an electric charge to the myocardium at the peak R wave.

The procedure causes immediate depolarization, interrupting reentry circuits (abnormal impulse conduction that occurs when cardiac tissue is activated two or more times, causing reentry arrhythmias) and allowing the SA node to resume control.

Synchronizing the electric charge with the R wave ensures that the current won't be delivered on the vulnerable T wave and disrupt repolarization. Thus, it reduces the risk that the current will strike during the relative refractory period of a cardiac cycle and induce ventricular fibrillation.

PREPARING THE PATIENT

·

Describe the procedure to the patient.

·

If possible, make sure that the patient or a responsible family member has signed a consent form.

·

Withhold all food and fluids for 6 to 12 hours before the procedure. If cardioversion is urgent, withhold food beginning as soon as possible.

·

Obtain a baseline 12-lead ECG.

·

Connect the patient to a pulse oximeter and blood pressure cuff.

·

If the patient is awake, give a sedative.

·

Place the leads on the patient's chest, and assess his cardiac rhythm.

·

Apply conductive gel to the paddles or attach defibrillation pads to the chest wall; position the pads so that one pad is to the right of the sternum, just below the clavicle, and the other is at the fifth or sixth intercostal space in the left anterior axillary line.

MONITORING AND AFTERCARE

·

Turn on the defibrillator, and select the ordered energy level, usually between 50 and 100 J. (See Choosing the correct cardioversion energy level, page 226.)

·

Activate the synchronized mode by depressing the synchronizer switch.

·

Check that the machine is sensing the R wave correctly.

·

Place the paddles on the chest, and apply firm pressure.

·

Charge the paddles.

·

Instruct other personnel to stand clear of the patient and the bed to avoid the risk of an electric shock.

·

Discharge the current by pushing both paddles' discharge buttons simultaneously.

 

·

If cardioversion is unsuccessful, repeat the procedure two or three times as indicated, gradually increasing the energy with each additional countershock.

·

If normal rhythm is restored, continue to monitor the patient, and provide supplemental ventilation as long as needed.

·

If the patient's cardiac rhythm changes to ventricular fibrillation, switch the mode from synchronized to defibrillate, and defibrillate the patient immediately after charging the machine.

·

When using handheld paddles, continue to hold the paddles on the patient's chest until the energy is delivered.

·

Remember to reset the sync mode on the defibrillator after each synchronized cardioversion. Resetting this switch is necessary because most defibrillators automatically reset to an unsynchronized mode.

·

Document the use of synchronized cardioversion, the rhythm before and after cardioversion, the amperage used, and how the patient tolerated the procedure. (SeeTeaching the patient after synchronized cardioversion.)

CHOOSING THE CORRECT CARDIOVERSION ENERGY LEVEL

When choosing an energy level for cardioversion, try the lowest energy level first. If the arrhythmia isn't corrected, repeat the procedure using the next energy level. Repeat this procedure until the arrhythmia is corrected or until the highest energy level is reached. The monophasic energy doses (or equivalent biphasic energy dose) used for cardioversion are:

·

100, 200, 300, 360 joules (J) for unstable monomorphic ventricular tachycardia with a pulse

·

50, 100, 200, 300, 360 J for unstable paroxysmal supraventricular tachycardia

·

100, 200, 300, 360 J for unstable atrial fibrillation with a rapid ventricular response

·

50, 100, 200, 300, 360 J for unstable atrial flutter with a rapid ventricular response.

Permanent pacemaker insertion

A permanent pacemaker is a self-contained device that's surgically implanted in a pocket under the patient's skin. This implantation is usually performed in an operating room or a cardiac catheterization laboratory.

Permanent pacemakers function in the demand mode, allowing the patient's heart to beat on its own but preventing it from falling below a preset rate.

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT AFTER SYNCHRONIZED CARDIOVERSION

Before discharge:

·

 

·

encourage family members to learn cardiopulmonary resuscitation and use of an automated external defibrillator

·

instruct the patient to take drugs and attend follow-up visits with the practitioner as recommended.

Permanent pacemakers are indicated for patients with:

·

persistent brady-arrhythmia

·

complete heart block

·

congenital or degenerative heart disease

·

 

·

Wolff-Parkinson-White syndrome

·

sick sinus syndrome.

Pacing electrodes can be placed in the atria, the ventricles, or both chambers (atrioventricular sequential or dual chamber). Biventricular pacemakers are also available for cardiac resynchronization therapy in some patients with heart failure. (See Understanding pacemaker codes, pages 228.)

The most common pacing codes are VVI for single-chamber pacing and DDD for dual-chamber pacing. To keep the patient healthy and active, some pacemakers are designed to increase the heart rate with exercise. (See Biventricular pacemaker, page 229.)

PREPARING THE PATIENT

·

 

·

Before pacemaker insertion, clip the hair on the patient's chest from the axilla to the midline and from the clavicle to the nipple line on the side selected by the physician.

·

Establish an I.V. line.

·

Obtain baseline vital signs and a baseline 12-lead ECG.

·

Make sure that the patient or a responsible family member has signed a consent form.

·

Give sedation as indciated.

MONITORING AND AFTERCARE

·

Monitor the patient's ECG to check for arrhythmias and to ensure correct pacemaker functioning.

 

·

Check the dressing for signs of bleeding and infection.

·

Change the dressing according to your facility's policy.

·

Check vital signs and level of consciousness (LOC) every 15 minutes for the first hour, every hour for the next 4 hours, and then every 4 hours.

·

Provide the patient with an identification card that lists the pacemaker type and manufacturer, serial number, pacemaker rate setting, date implanted, and the physician's name. (See Teaching the patient after permanent pacemaker insertion, page 230.)

UNDERSTANDING PACEMAKER CODES

The capabilities of pacemakers are described by a five-letter coding system, although typically only the first three letters are used.

First letter

The first letter identifies which heart chambers are paced. Here are the letters used to signify these options:

·

V—Ventricle

·

A—Atrium

·

D—Dual (ventricle and atrium)

·

O—None.

Second letter

The second letter signifies the heart chamber where the pacemaker senses the intrinsic activity:

·

V—Ventricle

·

A—Atrium

·

D—Dual

·

O—None.

Third letter

·

T—Triggers pacing

·

 

·

D—Dual; can be triggered or inhibited depending on the mode and where intrinsic activity occurs

·

O—None; the pacemaker doesn't change its mode in response to sensed activity.

Fourth letter

The fourth letter denotes the pacemaker's programmability; it tells whether the pacemaker can be modified by an external programming device:

·

P—Basic functions programmable

·

M—Multiprogrammable parameters

·

C—Communicating functions such as telemetry

·

R—Rate responsiveness (rate adjusts to fit the patient's metabolic needs and achieve normal hemodynamic status)

·

O—None.

Fifth letter

The fifth letter denotes the pacemaker's response to a tachyarrhythmia:

·

P—Pacing ability—pacemaker's rapid burst paces the heart at a rate above its intrinsic rate to override the tachycardia source

·

S—Shock—an implantable cardioverter-defibrillator identifies ventricular tachycardia and delivers a shock to stop the arrhythmia

·

D—Dual ability to shock and pace

·

O—None.

BIVENTRICULAR PACEMAKER

How it works

It works by sending tiny electrical signals to the left and right ventricles at the same time, ultimately causing the walls of the left ventricle to pump together. The result is more efficient pumping of the heart, improved circulation, and decreased fluid backup in the heart muscle and lungs.

How it's placed

Insertion is similar to a regular pacemaker. However, in addition to the two leads that are used in most pacemakers, a third lead is placed into a cardiac vein and paces the left ventricle.

c4-tt36

Temporary pacemaker insertion

A temporary pacemaker is typically used in an emergency. The device consists of an external, battery-powered pulse generator and a lead or electrode system.

Temporary pacemakers usually come in three types:

·

transcutaneous

·

transvenous

·

epicardial.

In a life-threatening situation, a transcutaneous pacemaker is the best choice. This device works by sending an electrical impulse from the pulse generator to the patient's heart by way of two electrodes, which are placed on the front and back of the patient's chest.

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT AFTER PERMANENT PACEMAKER INSERTION

Before discharge from the facility, instruct the patient to:

·

report any chest pain or palpitations to his practitioner

·

carry information regarding his pacemaker with him at all times

·

 

·

follow instructions from his practitioner regarding checkups on pacemaker function.

Transcutaneous pacing is quick and effective, but it's used only until the physician can institute transvenous or permanent pacing.

In addition to being more comfortable for the patient, a transvenous pacemaker is more reliable than a transcutaneous pacemaker.

Transvenous pacing involves threading an electrode catheter through a vein into the patient's right atrium or right ventricle. The electrode is attached to an external pulse generator that can provide an electrical stimulus directly to the endocardium.

Indications for a temporary transvenous pacemaker include:

·

management of bradycardia

·

presence of tachyarrhythmias

·

other conduction system disturbances.

The purposes of temporary transvenous pacemaker insertion are:

·

to maintain circulatory integrity by providing for standby pacing in case of sudden complete heart block

·

to increase heart rate during periods of symptomatic bradycardia

·

occasionally, to control sustained supraventricular or ventricular tachycardia.

Among the contraindications to pacemaker therapy are electro-mechanical dissociation and ventricular fibrillation.

Epicardial pacing is used during cardiac surgery, when the surgeon may insert electrodes through the epicardium of the right ventricle and, if he wants to institute AV sequential pacing, the right atrium. From there, the electrodes pass through the chest wall, where they remain available if temporary pacing becomes necessary.

PREPARING THE PATIENT

·

Teach measures to prevent microshock; warn the patient not to use any electrical equipment that isn't grounded.

 

·

When using a transcutaneous pacemaker, don't place the electrodes over a bony area because bone conducts current poorly. With a female patient, place the anterior electrode under the patient's breast but not over her diaphragm.

·

If the physician inserts the transvenous pacer wire through the brachial or femoral vein, immobilize the patient's arm or leg to avoid putting stress on the pacing wires.

MONITORING AND AFTERCARE

·

After instituting use of any temporary pacemaker, assess the patient's vital signs, skin color, LOC, and peripheral pulses to determine the effectiveness of the paced rhythm. Perform a 12-lead ECG to serve as a baseline, and then perform additional ECGs daily or with clinical changes. Also, if possible, obtain a rhythm strip before, during, and after pacemaker placement; any time the pacemaker settings are changed; and whenever the patient receives treatment because of a complication due to the pacemaker.

·

Continuously monitor the ECG reading, noting capture, sensing, rate, intrinsic beats, and competition of paced and intrinsic rhythms. If the pacemaker is sensing correctly, the sense indicator on the pulse generator should flash with each beat.

·

Record the date and time of pacemaker insertion, the type of pacemaker, the reason for insertion, and the patient's response. Note the pacemaker settings. Document complications and the measures taken to resolve them.

·

If the patient has epicardial pacing wires in place, clean the insertion site and change the dressing daily. At the same time, monitor the site for signs of infection. Always keep the pulse generator nearby in case pacing becomes necessary.

·

Prepare the patient for permanent pacemaker surgery as appropriate.

Radiofrequency ablation

Radiofrequency ablation is a procedure that destroys the heart's tissue in order to treat a heartbeat that originates outside the SA node. (See Types of cardiac ablation, pages 232 and 233.) It's most commonly used for atrial fibrillation, atrial flutter, and supraventricular tachycardias, including AV nodal reentry and Wolff-Parkinson-White syndrome, and certain types of ventricular tachycardia.

PREPARING THE PATIENT

·

Explain the treatment and preparation to the patient and his family.

·

Make sure the patient or a responsible family member has signed a consent form.

 

·

Obtain a 12-lead ECG and laboratory studies, and make sure other tests (such as an echocardiogram and cardiac catheterization) have been completed.

·

Withhold food and fluids for 8 hours before the procedure

TYPES OF CARDIAC ABLATION

Cardiac ablation therapy depends on the specific ablative method and type of medical procedure required. Here's a list of common types of cardiac ablation:

·

Surgical ablation:

·

Minimally invasive ablation: Although this term can be used as above, it generally means a procedure where peripheral access (femoral, brachial, subclavian) to a vein is obtained followed by placement of several specialized catheters that provide intracardiac rhythm monitoring and a source of energy for ablation of the cardiac tissue. This procedure generally takes place in the electrophysiology laboratory instead of the operating suite.

·

The maze or Cox-Maze III procedure: The gold standard for arrhythmia treatment, including atrial fibrillation, this procedure was originally only done during open heart surgery with cardiopulmonary bypass. The procedure can now be done in some patients via minimally invasive access to the beating heart through a smaller chest incision where endoscopes guide the surgical treatment. However, not all arrhythmias can be treated with this more limited access.

The surgeon makes several small, specifically located cuts in the heart muscle where abnormal impulses are originating based on intracardiac monitoring leads, leaving the normal conduction pathways open. The cut areas form scar tissue that prevents the abnormal impulses from being conducted through the heart.

·

Radiofrequency ablation: Instead of surgical incisions, radio waves are directed to the ectopic foci in the heart muscle, obliterating small portions of abnormal tissue by heat. These areas also scar, permanently blocking abnormal conduction. Newer radiofrequency ablation equipment comes with the capacity to direct cooled saline to the area to reduce excessive heat production, making the procedure safer and more comfortable. Most of these procedures are carried out with minimally invasive techniques through peripheral access sites, but they can be done during other cardiac surgery as well.

·

Microwave and ultrasound techniques:

·

Laser ablation: The increased technology of laser use has made delicate procedures, such as cardiac ablation, possible with small, very focused laser beams. The essential goals of the procedure remain the same. There's hope that this technique will be particularly useful for atrial fibrillation by reducing the risk

of pulmonary vein stenosis. The procedure can be done by peripheral access or during cardiac surgery.

·

Cryoablation: This technique uses a special, extremely cold catheter tip to freeze and destroy tiny amounts of abnormally conducting cardiac tissue. Still being studied extensively, preliminary results show equal results compared with the Maze procedure, and equal complication rates. Cryoablation has been done by peripheral access and during other cardiac surgical procedures.

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT AFTER RADIOFREQUENCY ABLATION

Before discharge from the facility, instruct the patient to:

·

call the practitioner if redness, welling, or drainage at the incision site occurs

·

report signs and symptoms that his arrhythmia is recurring

·

take his pulse and keep a record for the practitioner

·

remember that he may be on antibiotics for up to 12 weeks after the procedure.

ff2-b01382759RED FLAG

Left atrial ablation and ablation for persistent atrial flutter are contraindicated if an atrial thrombus is present. Left ventricular ablation is contraindicated if a left ventricular thrombus is found. Ablation catheters usually aren't inserted through a mechanical prosthetic heart.

MONITORING AND AFTERCARE

·

Enforce bed rest for 1 to 6 hours with the operative leg extended during this time.

·

Monitor the patient's ECG for the onset of new arrhythmias.

·

Initiate aspirin therapy to prevent thromboembolic aftereffects.

·

Review any medication changes with the patient. (See Teaching the patient after radiofrequency ablation.)