Chapter 30

*Cardiovascular disease is a generic term for disorders of the heart and blood
vessels.

Disorders of Myocardial Perfusion

-Coronary Heart Disease (CHD)- caused by impaired blood
flow to the myocardium; accumulation of atherosclerotic plaque in the
coronary arteries is the usual cause. May be asymptomatic or may lead to
angina pectoris, acute coronary syndrome, myocardial infarction,
dysrhythmias, heart failure, and sudden death.
-Pathophysiology: most common cause of reduced blood flow is
atherosclerosis.
*Atherosclerosis: progressive disease caused by plaque formation, which
affects the intimal and medial layers of the large and midsize arteries.
Lipoproteins and fibrous tissue accumulate in arterial wall; abnormal lipid
metabolism and injury to or inflammation of endothelial cells lining the artery
are key to development. Tends to develop where arteries branch. In addition
to obstructing blood flow it weakens arterial walls.
*Myocardial Ischemia: Oxygen supply is inadequate to meet metabolic
demands (critical for coronary perfusion and myocardial workload). Factors
contributing to myocardial ischemia include: Coronary Perfusion
(atherosclerosis, thrombosis, vasospasm, poor perfusion pressure);
Myocardial Workload (rapid heart rate; increased preload, afterload, or
contractility; increased metabolic demands); and Blood Oxygen Content
(reduced atmospheric oxygen pressure, impaired gas exchange, low red
blood cells and hemoglobin content).
-Incidence and Prevalence: mortality rate decreasing by 3.3 %;
leading cause of death for all ethnic groups except Asian females. Mostly
effect white males over the age of 45 and older, until women hit menopause
then risk is equal.

-Risk Factors: Nonmodifiable- Age (men >45, women >55);

gender, and genetics. Modifiable: Hypertension, diabetes, abnormal
blood lipids( ^ LDL and triglycerides, decreased HDL); cigarette smoking,
obesity, physical inactivity, diet, elevated homocysteine levels. Metabolic
syndrome (abdominal obesity, low HDL & high triglycerides, HTN, elevated
fasting glucose, clotting tendency, and inflammatory factors). Some specific
to woman include premature menopause, oral contraceptives, and hormone
replacement therapy.
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Interdisciplinary care: Care of patients with CHD focuses on

aggressive risk factor management to slow the atherosclerosis and maintain
myocardial perfusion.
Diagnostics:
Total serum cholesterol: is elevated in hyperlipidemia. Lipid Profile:
includes triglycerides, HDL, and LDL and enables calculation of the ration of
HDL to total cholesterol.
C-reactive Protein: serum protein associated with inflammatory process.
Ankle-Brachial Blood Pressure Index: inexpensive, noninvasive test for
PVD thats predictive of CHD; ABI <0.9 indicates peripheral arterial disease.
Exercise ECG: assess the cardiac response to increased workload induced
by exercise.
Electron Beam Computed Tomography: creates a 3D image of the heart
and coronary arteries that can reveal coronary artery calcification and other
abnormalities.
Myocardial Perfusion Imagining: evaluates myocardial blood flow and
perfusion, both at rest and during stress testing.
Medications: Cholesterol lowering medications including statins, bile acid
sequestrants, nicotinic acid, and fibrates. Low dose aspirin therapy and
Angiotensin-converting enzyme inhibitors or angiotensin receptor blockers.

Nursing Care: Nurses are instrumental in educating adults about their

risk for CHD, promoting participation in screening programs to identify that
risk, and teaching all patients measures to reduce their risk for CHD.
Assessment: Must focus on IDing risk factors. Health History: current s/s
such as chest pain or heaviness, SOB, weakness; current diet, exercise
patterns, and medications; smoking history and pattern of alcohol intake;
history of heart disease, HTN, or diabetes; family history of CHD or other
cardiac problems. Physical Exam: Current weight and appropriateness to
height; BMI; waist to hip ratio; blood pressure; strength and equality of
peripheral pulses.

NURSING DIAGNOSIS: Imbalanced Nutrition: More than Body

Requirements; Ineffective Health Maintenance

The Patient with ANGINA PECTORIS

Angina Pectoris: chest pain resulting from reduced coronary blood flow,
which causes temporary imbalance between myocardial blood supply and
demand. Imbalance may be due to CHD, atherosclerosis, or vessel
constriction that impairs myocardial blood supply. Hypermetabolic conditions
such as exercise, thyrotoxicosis, stimulant abuse, hyperthyroidism, and
emotional stress an increase myocardial oxygen demand=angina. Anemia,
heart failure, ventricular hypertrophy, or pulmonary diseases may affect
blood and oxygen supplies=angina.
Patho:
Stable angina: most common and predictable; occurs with a predictable
amount of activity or stress and is a common manifestation of CHD; occurs
when the work of the heart is increased by physical exertion, exposure to
cold, or by stress; relieved by rest and nitrates.
Prinzmetals (variant) angina: atypical angina that occurs unpredictably and
often at night; caused by coronary artery spasm; may result from
hyperactive sympathetic nervous system responses, altered calcium flow in
smooth muscles, or reduced prostaglandins that promote vasodilation.
Unstable Angina: occurs with increasing frequency, severity, and duration;
pain is unpredictable and occurs with decreasing levels of activity or stress
and may occur at rest; risk for myocardial infarction.
Manifestations: Chest pain: substernal or precordial (across the chest wall),
may radiate to neck, arms, shoulders, or jaw. Quality: tight squeezing,
constricting, or heavy sensation, may also be described as burning, aching,
choking, dull, or constant. Associated Manifestations: Dyspnea, pallor,
tachycardia, anxiety, and fear. Atypical Manifestations: indigestion, nausea,
vomiting, upper back pain. Precipitating Factors: Exercise or activity, strong
emotion, stress, cold, heavy meal. Relieving factors: Rest, position change,
nitroglycerine.
Interdisciplinary Care: Management of stable angina focuses on
maintaining coronary blood flow and cardiac function; can often be managed
by medical therapy.
Diagnosis: based on past medical history and family history, a
comprehensive description of the chest pain, and physical assessment
findings.
ECG: may be normal, may show nonspecific changes in the ST segment and
T wave, or may show evidence of previous myocardial infarction;
characteristic ECG changes are seen during anginal episodes; during

ischemia ST segment is depressed or downsloping and the T wave may

flatten or invert; reverse when ischemia is relieved.
Stress ECG: monitor the cardiac response to an increased workload during
progressive exercise.
Radionuclide Testing: safe, noninvasive technique to evaluate myocardial
perfusion and left ventricular function; dye injected and heart scanned;
ischemic or infarcted cells do not take up the substance normally appearing
as a cold spot; if transient spots gradually fill in indicating reversibility;
severe ischemia or myocardial infarction, these areas remain void of
radioactivity.
Echocardiography: noninvasive test that uses ultrasound to evaluate cardiac
structure and function; evaluate movement of myocardial wall and assess for
possible ischemia or infarction.
Transesophageal echocardiography: uses ultrasound to identify abnormal
blood flow patterns as well as cardiac structures; probe is on the tip of an
endoscope and inserted into esophagus; avoids interference by breast, ribs,
or lungs.
Coronary Angiography: gold standard for evaluating the coronary arteries; a
catheter inserted into femoral or brachial artery is threaded into coronary
artery; dye is injected into each coronary opening allowing visualization of
the main coronary branches and any abnormalities.
Medications: may be used for acute and long term relief of angina. Goal of
drug treatment is to reduce oxygen demand and increase oxygen supply to
the myocardium. Three main classes of drugs are used to treat angina:
Nitrates, Beta Blockers, and Calcium Channel Blockers.
Nursing Care: reduce myocardial oxygen demand and improve oxygen
supply; usually treated in community settings; primary nursing focus is
education.
Assessment: Health History: chest pain including type, intensity, duration,
frequency, aggravating factors and relief measures; associated symptoms;
history of other CV disorders, PVD, or stroke; current medications and
treatment; usual diet, exercise, and alcohol intake patterns; smoking history;
use of other drugs. Physical Assessment: Vital Signs and heart sounds;
strength and equality or peripheral pulses; skin color and temp; physical
appearance during pain episode.

NURSING DIAGNOSIS: Ineffective Tissue Perfusion:

Cardiac; Risk for Ineffective Therapeutic Regimen
Management.

The Patient with Acute Coronary Syndrome:

Acute Coronary Syndrome (ACS): condition of unstable cardiac ischemia;
includes unstable angina and acute myocardial ischemia with or without
significant injury of myocardial tissues. Dynamic state in which coronary
blood flow is acutely reduced but not fully occluded; myocardial cells are
injured by the acute ischemia that results.
Manifestations: Cardinal manifestation is chest pain, usually substernal or
epigastric, radiating to the neck, left shoulder, and left arm; may occur at
rest and typically last longer than 10-20 minutes; prolonged and severe.
Dyspnea, diaphoresis, pallor, and cool skin may be present. Tachycardia,
hypotension, nausea, and light headedness.
Interdisciplinary Care: Patient usually presents to ER; pain may be
unrelieved by nitroglycerine or more severe and of longer intensity than
previous. ECG and blood levels of cardiac markers used to differentiate
between unstable angina and acute myocardial infarction. Coronary
Revascularization procedures may be performed within 48 hours if significant
CHD is identified.
Diagnosis: ECG and serum cardiac markers are primary test used to
establish Dx of ACS.
Cardiac Muscle Troponins (cardiac specific troponin T and cardiac specific
troponin 1: sensitive indicators of myocardial damage; may be elevated in
ACS or within normal limits if chest pain is due to unstable angina.
Creatinine Kinase (CK) and CK-MB: levels are likely to be within normal limits
or demonstrate transient elevation; returning to normal levels within 12-24
hours.
ECG: ST segment changes (elevation or depression) during chest pain that
resolve when the pain bates usually indicate acute myocardial ischemia and
severe underlying CHD.
Medications: include drugs to reduce myocardial ischemia and those to
reduce the risk for blood clotting. Fibrinolytic drugs; nitrates and beta
blockers; aspirin, other antiplatelets, and heparin.

Revascularization Procedures: used to restore blood flow and oxygen to

ischemic tissue. Nonsurgical techniques include transluminal coronary
angioplasty, laser angioplasty, coronary atherectomy, and intracoronary
stents.
Percutaneous Coronary Revascularization: procedures are used to restore
blood flow to ischemic myocardium in patients with CHD. Used to treat
patients with moderately severe, chronic stable angina unrelieved by medial
therapy, unstable angina, acute myocardial infarction, significant stenosis of
the left anterior descending coronary artery, and stenosis of a coronary
artery bypass. Catheter is introduced into arterial circulation and guided into
opening of narrowed coronary artery; guide wire is used to thread balloon,
stent, or therapeutic device into narrowed segment. COMPLICATIONS:
hematoma at the catheter site; pseudoanerurysm; embolism;
hypersensitivity to contrast dye; dysrhythmias; bleeding; vessel perforation;
and restenosis.
Coronary Artery Bypass Grafting: Involves using a section of a vein or an
artery to create a connection between the aorta and the coronary artery
beyond the obstruction; allows blood to perfuse the ischemia portion of the
heart; internal mammary artery in the chest and the saphenous vein from
the leg are the vessels most commonly used for CABG; safe and effective;
angina is totally relieved or significantly reduced in 90% of patients.

The Patient with Acute Myocardial Infarction

Acute Myocardial Infarction: necrosis of the myocardial cells; life
threatening. If circulation to the affected myocardium if not promptly
restored loss of functional myocardium affects the hearts ability to maintain
an affective cardiac output; may lead to cardiogenic shock and death.
Majority of deaths from MI occur during the initial period after symptoms
begin. Heightening public awareness of s/s of MI, importance of seeking
immediate medical assistance, and training in cardiopulmonary resuscitation
techniques are vital to decrease deaths.
MI rarely occurs without preexisting CHD. Risk factors include: age, gender,
heredity, race, smoking, obesity, hyperlipidemia, HTN, diabetes, sedentary
lifestyle, and diet.
Manifestations: Chest pain (substernal or precordial; may radiate to jaw,
neck, shoulder, or left arm); tachycardia, tachypnea; dyspnea, SOB; N/V;
anxiety and sense of impending doom; diaphoresis; cool mottled skin and

diminished peripheral pulses; hypotension; palpitations and dysrhythmias;

s/s of left side heart failure; decreased LOC.
Complications: related to size and location
Dysrhythmias: disturbances or irregularities of heart rhythm are the most
frequent complication of MI.
Pump Failure: MI reduces myocardial contractility, ventricular wall motion,
and compliance.
Cardiogenic Shock: impaired tissue perfusion due to pimp failure, results
when functioning myocardial muscle mass decreases by more than 40%;
heart is unable to meet the needs of the body and maintain organ function;
low CO also impairs perfusion of coronary arteries and myocardium. Mortality
rate is 70%.
Infarct Extension: extension=increased myocardial necrosis from continued
blood flow impairment and ongoing injury. Expansion= permanent expansion
of the infarcted area from thinning and dilation of the muscles. Both cause
continuing chest pain, hemodynamic compromise, and worsening heart
failure.
Structural Defects: Necrotic muscle is replaced by scar tissue that is thinner
than the ventricular muscle mass; this can lead to ventricular aneurysm,
rupture of the interventricular septum or papillary muscle, and myocardial
rupture.
Pericarditis: inflammation of the pericardial tissue surrounding the heart;
causes chest pain that may be aching or sharp and stabbing; aggravated by
movement or deep breathing.
Interdisciplinary Care: Immediate treatment goals include: relieve chest
pain, reduce the extent of myocardial damage, maintain CV stability,
decrease cardiac workload, prevent complications.
Diagnosis: Serum cardiac markers are proteins released from necrotic heart
muscle; proteins most specific for MI are creatine kinase (CK, or creatine
phosphokinase, CPK) and cardiac specific troponins.
Serum levels of cardiac markers are ordered on admission and for 3
succeeding days. Serial blood levels help establish the diagnosis and
determine damage. Other lab test include:
Myoglobin: first cardiac markers to be detectable after an MI; lack of
specificity to cardiac muscle and rapid excretion limit its use.

CBC: show elevated WBC due to inflammation of injured myocardium; ESR

also rises due to inflammation.
ECG: reflects changes in conduction due to myocardial ischemia and
necrosis; changes include T wave inversion (ischemic changes); elevation of
ST segment (myocardial injury); and Q wave development (full thickness
infarction).
Echocardiography: evaluate cardiac wall motion and left ventricular function;
stunned/infarcted tissue does not contract effectively.
Radionuclide Imaging: evaluate myocardial perfusion; help ID specific area of
ischemia and damage.
Hemodynamic Monitoring: when MI significantly affects CO and
hemodynamic status.
Medications: Aspirin, Analgesia, Fibrinolytic Therapy, Antidysrhythmics.
Treatments: Monitored continuously; care provided in intensive coronary
care unit for the first 24 to 48 hours. IV line to allow rapid administration of
emergency medications.
Bed rest is prescribed for the first 12 hours to reduce cardiac workload;
bedside commode used. ADL gradually increased as tolerated. Quiet calm
environment with limited stimuli and visitors limited. Oxygen via nasal
cannula at 2-5 L/min to improve oxygenation.
Liquid diet to reduce gastric distention and myocardial work for first 4-12 hrs
followed by low fat, low cholesterol, reduced sodium diet. Small frequent
feedings recommended; caffeine and very hot/cold foods may be limited.
Revascularization Procedures: Immediate or early percutaneous coronary
revascularization which may follow or replace fibrinolytic therapy to restore
blood flow to ischemic myocardium, prompt PCR reduces hospital mortality.
CABG may also be performed.
Choice of procedure depends on patients age and immediate condition; time
elapsed from onset of s/s; and extent of myocardial disease and damage.
Patients with Large MIs and pump failure may use invasive devices
temporarily allowing the myocardium to heal. Intra-aortic balloon pump and
ventricular assist devises.
Intra-aortic Balloon Pump IABP: mechanical circulatory support device that
may be used after cardiac surgery or to treat cardiogenic shock following
AMI; temporarily supports cardiac function allowing the heart to gradually

recover by decreasing myocardial workload and oxygen demand and

increasing perfusion of coronary arteries.
Ventricular Assist Devices: takes partial or complete control of cardiac
function; temporary or complete assist when there is a chance for recovery
of normal heart function after a period of cardiac rest. Nursing care includes
support, assessing hemodynamic function; pt is at risk for infection,
pneumonia. Mechanical failure is life threatening.
Cardiac Rehabilitation: long term program of medical evaluation, exercise,
risk factor modification, education, and counseling designed to limit the
physical and psychological effects of cardiac illness and improve the
patients quality of life.
Nursing Care: reducing cardiac work, identifying and treating complications
in a timely manner, and preparing the patient for rehab.
Assessment: must be timely and ongoing. Health History: Complaints of
chest pain including its location, intensity, character, radiation, and timing;
associated symptoms such as nausea, heartburn, SOB, and anxiety;
treatment measure taken since onset of pain; past medical history especially
cardiac related; chronic diseases; current medications and known allergies to
medications; smoking history and use recreational drugs and alcohol.
Physical Examination: General appearance including obvious signs of
distress; vital signs; peripheral pulses; skin color, temperature, and moisture;
LOC, heart and breath sounds; cardiac rhythm; bowel sounds, abdominal
tenderness.

NURSING DIAGNOSIS: Acute Pain, Ineffective Tissue

Perfusion, Ineffective Coping, and Fear.
**priorities include relieving chest pain, reducing cardiac work, and
promoting oxygenation.
Psychosocial support is especially important.

Cardiac Rhythm Disorders

Heart Muscle contracts in response to electrical stimulation. In the normal
heart, electrical stimulation produces a synchronized, rhythmic, heart muscle
contraction that propels blood into the vascular system. Changes in the
cardiac rhythm affects this synchronized activity and the hearts ability to
effectively pump blood to body tissues.

The Patient with a Cardiac Dysrhythmia

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Cardiac Dysrhythmia is a disturbance or irregularity in the electrical system

of the heart; may be benign or have lethal consequences. Prompt recognition
and quick action can be life saving.
Can develop for many reasons and not all are pathologic; such as in response
to exercise or fear. Regardless of cause; they can significantly affect CO;
patients response is key in determining the urgency and treatment needed.
Pathophysiology: arise through disruption of the properties that stimulate
and control the heartbeat: automaticity, excitability, conductivity, and
refractoriness.
Supraventricular Rhythms:
Normal Sinus Rhythm: NSR; normal heart rhythm in which impulses
originate in the SA node and travel through all normal conduction pathways
without delay; all waveforms are of normal configuration, look alike, and
have consistent durations. The rate is between 60 and 110 bpm.
Sinus Tachycardia: all of the characteristics of NSR except that the rate is
greater than 100 bpm; arises from enhanced automaticity in response to
changes in the internal environment. Sympathetic nervous system
stimulation or blocked vagal activity increases the heart rate; normal
response to any condition or event that increases the bodys demand for
oxygen and nutrients, such as exercise or hypoxia. May be an early sign of
cardiac dysfunction such as heart failure; detrimental in patients with cardiac
disease because it increase cardiac work and O2 use. Common causes:
exercise, excitement, anxiety, pain, fever, hypoxia, hypovolemia, anemia,
hyperthyroidism, myocardial infarction, heart failure, cardiogenic shock,
pulmonary embolism, caffeine intake, and certain drugs (atropine,
epinephrine, or isoproterenol). Manifestations: rapid pulse rate, heart racing,
SOB, dizziness.
Sinus Bradycardia: has all of the characteristics of NSR but the rate is less
than 60 bpm. May be due to increased vagal stimulation or depressed
automaticity due to injury or ischemia. Causes: pain, increased intracranial
pressure, sinus node disease, myocardial infarction, hypothermia, acidosis,
and certain drugs. Manifestations: may be asymptomatic; decreased cardiac
output, decreased LOC, syncope, hypotension.
Paroxysmal Supraventricular Tachycardia PSVT: Tachycardia of sudden
onset and termination; usually initiated by a reentry loop in or around the AV
node (an impulse reenters the same section of tissue over and over causing
repeated depolarizations). Affects ventricular filling and CO and decreases
coronary artery perfusion. Causes: Occurs more frequently in women.
Sympathetic stimulation and stressors such as fever, sepsis, and
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hyperthyroidism. May also be associated with CHD, MI, rheumatic heart

disease, myocarditis, pericarditis. Manifestations: palpitations and racing
heart, anxiety, dizziness, dyspnea, anginal pain, diaphoresis, extreme
fatigue, and polyuria.
Atrial Flutter: Rapid and regular atrial rhythm thought to result from intraatrial reentry mechanism. Two types: Type 1 has an atrial rate or 240-340
bpm and develops in the right atrium. Mechanism of type 2 is unidentified
with a rate or 350 bpm. Causes: sympathetic nervous system stimulation
due to anxiety, caffeine and alcohol intake, thyrotoxicosis, CHD or MI;
pulmonary embolism and abnormal conduction syndromes WPW or LGL
syndromes. Manifestations: palpitations or fluttering sensation in
chest/throat; if ventricular rate ^ decreased CO, decreased LOC,
hypotension, decreased urinary output, cool clammy skin.
Atrial Fibrillation: common dysrhythmia, disorganized atrial activity
without discrete atrial contractions. Multiple small reentry circuits develop in
the atria; atrial cells cannot repolarize in time to respond to the next
stimulus. Extremely rapid atrial impulses bombard the AV node, resulting in
an irregularly irregular ventricular response. A fib may occur suddenly and
recur, or it may be chronic. Commonly associated with heart failure,
rheumatic heart disease, CHD, HTN, and hyperthyroidism. Manifestations:
relate to rate of ventricular response; decreased CO such as hypotension,
SOB, fatigue, and angina; syncope or heart failure; peripheral pulses are
irregular and of variable amplitude.
Ventricular Dysrhythmias:
Premature Ventricular Contractions: are ectopic ventricular beats that
occur before the next expected beat of the underlying rhythm. Usually do not
reset the atrial rhythm and are followed by a full compensatory pause.
Frequent, recurrent, or multifold PVCs may be associated with an increased
risk for lethal dysrhythmias. Result from enhanced automaticity or reentry
phenomenon and may be triggered by anxiety or stress; tobacco, alcohol, or
caffeine; hypoxia; acidosis; and electrolyte imbalances; sympathomimetic
drugs; CHD; heart failure; mechanical stimulation of the heart; or reperfusion
after fibrinolytic therapy. Greatest incidence after MI.
Ventricular Tachycardia: rapid ventricular rhythm defined as three or more
consecutive PVCs; may occur in short burst or last more than 30 seconds.
The rate is greater than 100 bpm with regular rhythm. Reentry is responsible.
Myocardial ischemia and infarction are most common predisposing factors;
also associated with structural disorders such as valvular disease, rheumatic
disease, or cardiomyopathy. May occur with anorexia nervosa, metabolic
disorders, and drug toxicity. Manifestations: fluttering sensation in chest or
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palpitations and brief SOB; if sustained s/s of decreased CO and

hemodynamic instability including severe hypotension, a weak or
nonpalpable pulse, and loss of consciousness.
Ventricular Fibrillation: extremely rapid, chaotic ventricular depolarization
causing the ventricles to quiver and cease contracting; there is no cardiac
output. This is cardiac arrest and is a medical emergency and needs
immediate CPR. Death will follow the onset of VF within 4 min if not fixed.
Usually triggered by severe myocardial ischemia or infarction and occurs
without 50% of the time; terminal end of many disease processes. Other
causes include digitalis toxicity, reperfusion therapy, antidysrhythmic drugs,
hypo/hyperkalemia, hypothermia, metabolic acidosis, mechanical
stimulation, and electric shock. ECG show grossly irregular, bizarre
complexes with no discernable rate or rhythm.
Interdisciplinary Care: Recognizing lethal dysrhythmias is a matter of life
and death. Major goals of care include identifying the dysrhythmia,
evaluating its effect on physical and psychosocial well being, and treating
underlying cause. May involve correcting fluid and electrolyte or acid base
balance; treating hypoxia, pain, or anxiety; administering antidysrhytmic
medications; or mechanical and surgical interventions.
Diagnosis: ECG, cardiac monitoring, electrophysiology studies; Lab test:
serum electrolytes, drug levels, and arterial blood gases may be done to help
identify the cause of dysrhythmia.
ECG: 12-lead ECG may be required to accurately diagnosis a dysrhythmia;
provides information about underlying disease processes such as MI; may
monitor effects of treatment.
Cardiac Monitoring: Allows continuous observation of rhythm; used in
different circumstances. Continuous Cardiac Monitoring: provided by the
bedside and central monitoring stations; Electrodes placed on patients chest
attach to cables connected to monitor displaying rate and rhythm on a
bedside monitor connected to a central monitoring station which allows
monitoring of several patients at once. Telemetry may be used in acute care
settings when the patient is ambulatory; portable transmitter is worn around
the neck or waist. Home Monitoring: Used for patients who complain of
symptoms but are asymptomatic during evaluation; used to identify
intermittent dysrhythmias, silent ischemia, monitor effects of treatment, and
assess pacemaker or automatic cardioverter-defibrillator function.
Electrophysiology Studies: identify dysrhythmias and their causes; used to
analyze components of the conduction system, identify sites of ectopic
stimulation, and evaluate the effectiveness of treatment.

Medications: Goal of therapy is to suppress dysrhythmia formation; no drug

has been found to completely safe and effective; primarily used for acute
treatment. Over goal of therapy is to maintain an effective CO by stabilizing
cardiac rhythm. Antidysrhythmics classified by effects on cardiac action
potential: Class I fast sodium channel blockers; Class II beta blockers; Class
III block potassium channels; Class IV calcium channel blockers.
Sympathomimetics and anticholingeric agents may be used.
Countershock: used to interrupt cardiac rhythms that compromise cardiac
output and the patients welfare; direct current charge depolarizes all cells at
the same time and may stop tachydysrhythmia and allow sinus node to
recover control of impulse formation. Two types: synchronized cardioversion
and defibrillation.
Synchronized Cardioversion: direct electrical current synchronized with the
patients heart rhythm; usually done as an elective procedure to treat
supraventricular tachycardia, atrial fibrillation, atrial flutter, or
hemodynamically stable ventricular tachycardia. The nurse assist with
cardioversion by preparing the patient before the procedure; obtaining any
lab tests ordered; obtaining and documenting ECG strips prior to, during, and
after treatment; setting up the equipment; and monitoring the patients
response.
Defibrillation: emergency procedure that delivers direct current without
regard to the cardiac cycle. V fib is immediately treated as soon as the
dysrhythmia is recognized; early defib has been shown to improve survival in
patients experiencing VF.
Pacemaker Therapy: pulse generator used to provide an electrical stimulus
to the heart when the heart fails to generate or conduct its own at a rate that
maintains CO. Used to treat both acute and chronic conduction defects;
bradydysrhytmias, and tachydysrhythmias.
Temporary Pacemakers: use external pulse generator attached to a lead
threated IV into the r. ventricle, to temporary pacing wires implanted during
surgery or to external conductive pads placed on the chest wall for
emergency pacing.
Permanent Pacemaker: use internal pulse generator placed in a
subcutaneous pocket in the subclavian space or abdominal wall; generator
connects to leads sewn directly onto the heart or passed transvenously into
the heart.
Pacemakers are programmed to stimulate the atria or the ventricles (single
chamber pacing) or both (dual chamber pacing). The most commonly used

pacemakers either sense activity in and pace the ventricles only or sense
activity in and pace both the atria and the ventricles.
A sharp spike is noted before the P wave with atrial pacing and bfore the QRS
complex with ventricular pacing. Pacing spikes are seen before both the P
wave and QRS complex in AV sequential pacing.
Implantable Cardioverter-Defibrillator: detects life threatening changes
in the cardiac rhythm and automatically delivers an electric shock to convert
the dysrhythmia back into a normal rhythm. ICDs are used for sudden death
survivors, patients with recurrent ventricular tachycardia, and patients with
demonstrated risk factors for sudden death. ICDs can deliver a shock as
needed, provide pacing on demand, and can store ECG records of
tachycardic episodes.
Cardiac Mapping: Used to locate and destroy ectopic focus and used to
identify the site of earliest impulse formation in the atria or the ventricles.
Catheter Ablation: destroys, removes, or isolates an ectopic focus; used to
treat supraventricular tachycardias, atrial fibrillation and flutter, and
paroxysmal ventricular tachycardia.
Vagal Maneuvers: stimulate the parasympathetic nervous system may be
used to slow the heart rate in supraventricular tachycardias called Carotid
Sinus Massage and Valsalva Maneuver(forced exhalation against a closed
glottis; increased intrathoracic pressure and vagal tone) both slow pulse
rate.
Nursing Care: Requires the ability to recognize, identify, and promptly treat
the dysrhythmia. Care focuses on maintaining CO, monitoring the response
to therapy, and teaching.
Assessment: Vital before treating any dysrhythmia. Health History:
complaints of palpitations; complaints of fluttering sensation or racing heart;
episodes of dizziness, lightheadedness, or syncope; timing; correlation with
food or beverage intake; activity; presence of chest pain, SOB, or other
associated symptoms; history of heart or endocrine diseases; current
medications. Physical Examination: LOC; vital signs including apical pulse for
a full minute; regularity and amplitude of peripheral pules; color; presence or
dyspnea, adventitious lung sounds; ECG rhythm analysis; O2 saturation
levels.

NURSING DIAGNOSIS AND INERVENTIONS: Decreased

Cardiac Output
The Patient with Sudden Cardiac Death
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Sudden Cardiac Death SCD: Defined as unexpected death occurring

within one hour of the onset of CV symptoms; usually caused by V fib and
cardiac arrest (sudden collapse, loss of consciousness, and cessation of
effective circulation that precedes biologic death)
Cardiac Causes: CHD; Reperfusion following ischemia; Myocardial
hypertrophy; Cardiomyopathy; Inflammatory myocardial disorders; Valve
disorders; Primary electrical disorders; Dissecting or rupturing aortic or
ventricular aneurysm; Cardiac drug toxicity.
Noncardiac Causes: Pulmonary embolism; Cerebral hemorrhage; Autonomic
dysfunction; Choking; Electrical Shock; Electrolyte and acid-base imbalances.
Manifestations: Severe chest pain, dyspnea, or orthopnea, and palpitations
or light headedness; abrupt with complete loss of consciousness and death
within minutes.
Interdisciplinary Care: The goal of are is to restore cardiac output and tissue
perfusion; treatment initiated as soon as clinical cardiac arrest is verified.
Life support must be instituted within 2-4 minutes to prevent permanent
neurologic damage and ischemic injury to other organs.
Basic Life Support: begins with ID of cardiac arrest and initiation of
emergency response. Patient is immediately shocked with AED and CPR is
immediately initiated. After five cycles of CPR rhythm is evaluated and
circulation checked. Analysis, shock, and CPR continued until ACLS protocols
initiated.
Advanced Life Support: provided by specially trained healthcare personnel.
Includes airway support to maintain the airway and oxygenation, use of IV
drugs following specific protocols, and additional interventions such as
repeated defibrillation procedures and cardiac pacing. Epinephrine,
vasopressin, sodium bicarb, and antidysrhythmic drugs are used to attempt
to restore and maintain an effective cardiac rhythm.
Postresuscitation Care: Patient is transferred to a coronary care unit and MI
treatment measures are instituted; antidysrhythmic continued for 24-48 hrs.
Recurrent risk is significant so extensive diagnostic testing and interventions
such angioplasty or surgical revascularization of the myocardium, ablation,
or an implantable cardioverter defribillator may be indicated.
Nursing Care: Treat the patient, not the monitor; recognize s/s of cardiac
compromise early. Activate emergency medial services system. Begin and
continue basic cardiac life support principles throughout the resuscitation
effort. Continually assess the effectiveness or emergency interventions.

Defibrillate pulseless VT or VF as soon as possible. Initiate ALS protocols

early.
Nursing Diagnosis: Ineffective Tissue Perfusion: Cerebral related to
ineffective cardiac output.
Impaired Spontaneous Ventilation related to cardiac arrest.
Spiritual Distress related to unexplained sudden cardiac death.
Disturbed Thought Processes related to compromised cerebral circulation.
Fear realted to risk for future episodes of sudden cardiac death.