DYSRHYTHMIAS - Use of Certain Drugs

o Beta-blockers (metropolol, propranolol)

DEFINITION o Calcium channel blockers
- Disorders of the formation or conduction (or o Antidysrhythmics
both) of the electrical impulse within the heart o Lithium
- These disorders can cause disturbances of the o Digoxin
heart rate, the heart rhythm, or both
- Dysrhythmias may initially be evidenced by the - Excessive parasympathetic tone or decreased
hemodynamic effect they cause sympathetic stimulation
- Dysrhythmias are diagnosed by analyzing the o Valsalva maneuver
electrocardiographic (ECG) waveform. Their o Deep relaxation
treatment is based on frequency and severity of o Sleep
symptoms produced o Vomiting
- Dysrhythmias are named according to the site of
origin of the impulse and the mechanism of - Noncardiac disorders
formation or conduction involved o Hypoxia
o Hypothermia
TYPES OF DYSRHYTHMIAS o Hyperkalemia
- Sinus o Stroke
- Atrial o Increased intracranial pressure
- Junctional o Hypothyroidism
- Ventricular o Glaucoma

SINUS DYSRHYTHMIA Treatment of Sinus Bradycardia

- Rhythyms originating from the Sinoatrial (SA) - Treatment will depend on the cause of the
Node dysrhythmia
o Stimulation of vagus nerve (bearing down
1. Normal Sinus Rhythms during defecation or vomiting) - attempts are
- During normal heart activity, SA node acts as made to prevent further vagal stimulation
the primary pacemaker o Medication (beta-blocker) - medication may
- NSR has a heart rate of 60 to100 BPM (in the be withheld
average adult) - Asymptomatic patients require no treatment but
should be monitored in case there is a progression
2. Sinus Bradycardia of the bradycardia
- Sinus bradycardia occurs when the sinus node - Atropine, 0.5 mg given rapidly as an intravenous
creates an impulse at a slower-than-normal (IV) bolus every 3 to 5 minutes to a maximum
rate. total dose of 3 mg, is the medication of choice in
- Has all the characteristics of NSR but the heart treating symptomatic sinus bradycardia.
rate is less than 60 BPM
3. Sinus Tachycardia
Causes of Sinus Bradycardia: - Occurs when the sinus node creates an
- Cardiac Diseases impulse at a faster-than-normal rate.
o SA node disease - Has same characteristics as NSR but has a rate
o Cardiomyopathy >100 BPM
o Myocarditis - It often occurs naturally as a means of
o Myocardial Ischemia increasing delivery of oxygen and nutrients
o Heart Block and removing waste products during times of
exertion, exercise or stress.
Causes of Sinus Tachycardia: - Described as a cycle of “slowing, then
- Cardiac Diseases: speeding up, then slowing again”
o Congestive heart failure
o Cardiogenic shock Causes of Sinus Dysrhythmia:
o Pericarditis - Cardiac Disorders:
o Inferior wall MI
- Use of certain drugs:
o Sympathomimetic drugs (epinephrine, - Use of Certain Drugs:
dopamine) o Digoxin
o Other stimulants o Morphine
o Amphetamine o Sedatives

- Increased sympathetic stimulation: - Autonomic Nervous System Stimulation:

o Strenuous exercise o Inhibition of reflex parasympathetic activity
o Pain (tone)
o Stress
o Fever - Other causes:
o Fear o Increased Intracranial pressure
o Anxiety o Multiple sclerosis
o Hypermetabolism
o Compensatory mechanism in shock Treatment of Sinus Dysrhythmia:
- Provided the patient is asymptomatic, usually no
- Other causes: treatment is needed
o Respiratory distress - If unrelated to respirations, consideration may be
o Hypoxia given to treating the underlying cause
o Pulmonary embolism
o Anemia ATRIAL DYSRHYTHMIA
o Sepsis - Originate in the atrial tissue or in the internodal
o Hyperthyroidism pathways
o Alcohol - Are among the most common types of
o Caffeine dysrhythmias, particularly in persons older than
o Nicotine 60 years of age
- Can diminish the strength of the atrial contraction
Treatment for Sinus Tachycardia: and affect ventricular filling time
- Asymptomatic patients require no treatment o This can lead to decreased cardiac output and
o However, patient should be encouraged to ultimately decreased tissue perfusion
abstain from triggers such as alcohol, caffeine, o The atrial contraction is called the atrial “kick”
and nicotine and normally supplies the ventricles with
- Treatment for symptomatic sinus tachycardia is about 30% of their blood.
directed at treating the cause
1. Premature Atrial Complexes (PACs)
4. Sinus Dysrhythmia - Early beats that originate outside the SA node
- Sinus arrhythmia occurs when the sinus node before it has a chance to depolarize
creates an impulse at an irregular rhythm; the - A premature atrial complex (PAC) is a single
rate usually increases with inspiration and ECG complex that occurs when an electrical
decreases with expiration. impulse starts in the atrium before the next
- Same as NSR except there is a patterned normal impulse of the sinus node.
irregularity - PACs are common in normal hearts. The
patient may say, “My heart skipped a beat.”
Causes of Premature Atrial Complexes o Conditions that enlarge atrial tissue and
- Cardiac diseases elevate atrial pressures
o Coronary Heart Disease o Following cardiac surgery
o Heart Failure o Mitral or tricuspid valve disease
o Valvular Heart Disease o Pericarditis/myocarditis

- Certain use of drugs - Use of certain drugs

o Digitalis toxicity o Digitalis or quinidine toxicity
o Drugs that prolong the absolute refractory
period of the SA node (procainamide, - Noncardiac disorders
quinidine) o COPD
o Hypoxia
- Increased sympathetic tone o Hyperthyroidism
o Increased catecholamines o Pneumonia
o Pulmonary embolism
- Noncardiac disorders o Systemic arterial hypoxia
o Acute respiratory failure o Pulmonary hypertension
o Alcohol
o Anxiety Treatment of Atrial Flutter
o Caffeine - In patients experiencing an associated rapid
o Certain electrolyte imbalances ventricular rate who are symptomatic but stable,
o Nicotine treatment is directed at controlling the rate or
o Fatigue converting the rhythm to sinus rhythm
o Fever - Symptomatic patients (e.g., hypotension, signs of
o Hypothyroidism shock, or heart failure) should receive oxygen, an
o Hypoxia IV infusion of normal saline administered at a KVO
o Infectious disease rate, and prompt treatment
o COPD o MEDICATIONS:
 Beta-blockers
2. Atrial Flutter  Nondihydropyridine Calcium Channel
- Atrial flutter occurs because of a conduction Blockers
defect in the atrium and causes a rapid,  Digitalis
regular atrial rate, usually between 250 and - Synchronized cardioversion should be considered
400 times per minute. in unstable patients
- Results from circus reentry o Electrical Cardioversion
i. Impulse from SA node circles back through o Atrial Fibrillation
atria, returning to the SA node region and o If necessary, the energy may be increased
repeatedly restimulating the AV node over with subsequent shocks
and over at a rate of 250 to 350 BPM -
- Waves blend together in a saw-tooth or picket
fence pattern called flutter waves, or F waves 3. Atrial Fibrillation
i. Produces atrial waveforms that have a - Atrial fibrillation is an uncoordinated atrial
characteristic saw-tooth appearance called electrical activation that causes a rapid,
flutter waves (F waves) disorganized, and uncoordinated twitching of
atrial musculature.
Causes of Atrial Flutter: - Results for chaotic, asynchronous firing of
- Cardiac diseases: multiple areas within the atria
o MI - it is believed that atrial fibrillation stems from
o Cardiomyopathy the rapid firing of ectopic impulses (greater
 than 350 beats per minute) in circus reentry - Patients experiencing atrial fibrillation and an
pathways. associated rapid ventricular rate who are
symptomatic but stable, treatment is directed at
Causes of Atrial Fibrillation: controlling the rate or converting the rhythm to
- Cardiac diseases sinus rhythm
o MI - Symptomatic patients (e.g., hypotension, signs of
o Atrial septal defects shock, or heart failure) should receive oxygen, an
o CAD IV infusion of normal saline administered at a TKO
o Cardiomyopathy rate, and prompt synchronized cardioversion
o Congestive heart failure o If necessary, the energy level may be
o Congenital heart disease increased with subsequent shocks
o Ischemic heart disease
o Mitral regurgitation
o Mitral stenosis JUNCTIONAL DYSRHYTHMIA
o Pericarditis - Originate in AV junction (area around AV node
o Rheumatic heart disease and bundle of His)
o May also be caused by cardiac surgery - Can result from suppression or blockage of the SA
node, increased automaticity of the AV junction
- Use of certain drugs or a reentry mechanism
o Digitalis toxicity
o Aminophylline 1. Premature Junctional Complex (PJC)
- Premature junctional complex is an impulse
- Excessive sympathetic stimulation that starts in the AV nodal area before the
o Endogenous catecholamines released during next normal sinus impulse reaches the AV
exercise node.
- Single early electrical impulse that arises from
- Noncardiac disorders the AV junction
o Advanced age - Disrupt regularity of underlying rhythm
o COPD
o Diabetes Causes of PJCs
o Electrocution - Cardiac Diseases
o Hypoxia o Cardiomyopathy
o Hypokalemia o CAD
o Hypoglycemia o Congestive heart failure
o Hypertension o Congenital abnormalities
o Hyperthyroidism o Myocardial ischemia
o Pulmonary embolism o Pericarditis
o WPW syndrome o Rheumatic heart disease
o Idiopathic (no clear cause) o Swelling of the AV node after surgery
o May also occur in healthy people who use o Valvular heart disease
coffee, alcohol or nicotine to excess or who
are fatigued and under stress - Use of certain drugs
o Digitalis toxicity
o Cocaine
Treatment of Atrial Fibrillation o Excessive amphetamine intake
- If the rate of ventricular response is normal, the
dysrhythmia is usually well tolerated and requires - Noncardiac disorders
no immediate intervention o Acute respiratory failure
o Alcohol
 o Anxiety - Increased autonomic nervous system stimulation
o Caffeine o Increased vagal tone on the SA node
o Certain electrolyte imbalances
o COPD - Noncardiac disorder
o Fatigue o Hypoxia
o Fear or stress o Electrolyte imbalance
o Hyperthyroidism
o Hypoxia 3. Nonparoxysmal Junctional Tachycardia
o Nicotine - Junctional tachycardia is caused by enhanced
o Vigorous exercise automaticity in the junctional area, resulting
in a rhythm similar to junctional rhythm,
Treatment of PJC: except at a rate of 70 to 120.
- Generally do not require treatment - Fast ectopic rhythm that arises from bundle of
- PJCs caused by the use of caffeine, tobacco, or His at rate of 100 to 180 BPM
alcohol, or with anxiety, fatigue, or fever can be - Junctional Tachycardia is relatively rare but
controlled by eliminating the underlying cause when present may serious drop cardiac
output because of the very fast rate.
2. Junctional Rhythm
- Junctional Escape Rhythm or Junctional Causes of Junctional Tachycardia:
Rhythm occurs when the AV node, instead of - Cardiac diseases
the sinus node, becomes the pacemaker of o Swelling of the AV junction after heart surgery
the heart o Damage to AV junction from inferior or
- Arises from AV junction at rate of 40 to 60 posterior wall MI or rheumatic fever
BPM
- Junctional Escape is potentially lethal because - Use of certain drugs
it indicates that the patient’s primary o Digoxin
pacemaker is not functioning. These patients o Theophylline
may require the placement of a pacemaker.
Furthermore, the slow rate may adversely - Noncardiac disorders
affect cardiac output. o Excessive cathecholamine administration
o Anxiety
CAUSES OF JUNCTIONAL RHYTHM o Hypoxia
- Cardiac diseases o Electrolyte imbalance (particularly
o Cardiomyopathy hypokalemia)
o Diseases of the SA node
o Heart failure 4. Atrioventricular Nodal Reentry Tachycardia
o Myocarditis - Atrioventricular nodal reentry tachycardia
o Postcardiac surgery (AVNRT) is a common dysrhythmia that occurs
o SA node ischemia when an impulse is conducted to an area in
o Rheumatic heart disease the AV node that causes the impulse to be
o Valvular heart disease rerouted back into the same area over and
over again at a very fast rate.
- Use of certain drugs
o Digoxin Causes of AVNRT
o Quinidine - Factors associated with the development of
o Beta-blockers AVNRT include caffeine, nicotine, hypoxemia, and
o Calcium channel blockers stress.
- Underlying pathologies include coronary artery
disease and cardiomyopathy; however, it occurs
 more often in females and not in association with - Use of certain drugs
underlying structural heart disease o Amphetamine intoxication
o Cocaine
VENTRICULAR DYSRHYTHMIA o Digoxin
- Premature ventricular complex (PVC) o Quinidine
- Ventricular escape complexes or rhythm o Phenothiazines
- Ventricular tachycardia o Tricyclic antidepressanta
- Ventricular fibrillation o Sympathomimetic drugs
- Asystole
- Autonomic nervous system stimulation
1. Premature Ventricular Complexes (PVCs) o Increased sympathetic stimulation
- A premature ventricular complex (PVC) is an o Exercise
impulse that starts in a ventricle and is o Emotional stress
conducted through the ventricles before the
next normal sinus impulse. - Noncardiac disorders
- Early ectopic beats that interrupt the normal o Stimulants (alcohol, caffeine, tobacco)
rhythm o Elecrtrolyte imbalance (hypokalemia,
- Originate from an irritable focus in the hyperkalemia, hypomagnesemia and
ventricular conduction system or muscle hypocalcemia)
tissue o Hypoxia
- PVCs can occur for no apparent reason in o Metabolic acidosis
individuals who have healthy hearts and are
usually of no significance. The incidence of Treatment of PVCs
PVCs increases with age and can occur during - Asymptomatic patients seldom require treatment
exercise or at rest. However, PVCs may also - Patients with myocardial ischemia, treatment of
be significant for two reasons. First, they can frequent PVCs includes:
precipitate more serious dysrhythmias such as o Administration of oxygen and placement of an
ventricular tachycardia or fibrillation. The IV line
danger is greater in patients experiencing o Identifying and correcting the underlying
myocardial ischemia and/or infarction. factor causing the PVCs
Second, PVCs can result in decreased cardiac  In some settings, administering lidocaine
output due to reduced diastolic filling time or other antidysrhythmics (e.g.,
and a loss of atrial kick. amiodarone) by IV push and a continued
- PVCs may produce a palpable pulse but they maintenance infusion
may also produce a diminished or o Administering potassium chloride
nonpalpable pulse (called a nonperfusing intravenously to correct hypokalemia or
PVC). Patients frequently experience the magnesium sulfate intravenously to correct
sensation of “skipped beats.” hypomagnesemia; adjusting drug therapy; or
correcting acidosis, hypothermia, and/or
Causes of PVC: hypoxia
- Cardiac Diseases:
o Myocardial ischemia and MI 2. Ventricular Tachycardia
o Congestive heart failure - VT is defined as three or more PVCs in a row,
o Irritation of ventricles by pacemaker or occurring at a rate exceeding 100 bpm.
electrodes or PA catheter - Fast dysrhythmia (100 to 250 BPM) that arises
o Enlargement of the ventricular chambers from the ventricles
o Mitral valve prolapse - Clinically, ventricular tachycardia is always
o Myocarditis significant. Even if the rhythm results in a
pulse, it should be considered as potentially
 unstable, as patients are likely to develop - Patients with pulseless VT should be treated as
worse rhythms and cardiac arrest. Usually VT though they are in VF
indicates significant underlying cardiovascular
disease. 3. Ventricular Fibrillation (VF)
- The most common dysrhythmia in patients
CAUSES OF VENTRICULAR TACHYCARDIA with cardiac arrest is ventricular fibrillation,
- Cardiac diseases: which is a rapid, disorganized ventricular
o Myocardial ischemia and MI rhythm that causes ineffective quivering of
o Coronary artery disease the ventricles. No atrial activity is seen on the
o Congestive heart failure ECG.
o Cardiomyopathy - Results from chaotic firing of multiple sites in
o Valvular heart disease the ventricles
o Pulmonary embolism - Causes heart muscle to quiver rather than
o Rheumatic heart disease contract efficiently, producing no effective
muscular contraction and no cardiac output
- Use of certain drugs - On the cardiac monitor, ventricular fibrillation
o Amphetamines appears like a wavy line, totally chaotic,
o Cocaine without any logic.
o Digoxin
o Quinidine CAUSES OF VENTRICULAR FIBRILLATION
o Sympathomimetic drugs (epinephrine) - Cardiac diseases
o Thyroid medications o Myocardial ischemia/infarction
o Theophylline drugs o Coronary artery disease

- Autonomic nervous system - Use of certain drugs

o Increased sympathetic stimulation o Digoxin (rarely)
o Exercise o Epinephrine
o Emotional stress o Procainamide
o Quinidine
- Noncardiac disorders
o Electrolyte imbalance (hypokalemia, acid-base - Noncardiac disorders
imbalance) o Acid-base imbalance
o Hypoxia o Drowning
o Trauma o Electric shock
o Ingestion of stimulants (alcohol, caffeine, o Severe hypothermia
tobacco) o Electrolyte imbalance (hypokalemia,
hyperkalemia, hypercalcemia)
TREATMENT OF VENTRICULAR TACHYCARDIA
- Maintain a patent airway, administer oxygen, and
place an IV line Death occurs if patient not promptly treated
- Stable patient can be treated with (defibrillation)
antidysrhythmics Unstable patients are managed
with immediate synchronized cardioversion (100J) Most common cause of prehospital cardiac arrest in
o Energy level may be increased if the adults
tachycardia does not convert with initial
treatments (100, 200, 300, 360 J or the
biphasic equivalent)
- Contributing causes should be considered and
treated
TREATMENT OF VENTRICULAR FIBRILLATION CAUSES OF IDIOVENTRICULAR RHYTHM
- Prompt delivery of CPR and defibrillation - Cardiac Diseases
- Organize ACLS actions around uninterrupted o MI
periods of CPR o Failure of all the heart’s higher pacemakers
- Initiate securing the airway and placing an IV line o Failure of supraventricular impulses to reach
in the course of treatment the ventricles due to a block in the conduction
- After one shock and a 2-minute period of CPR, system
administer epinephrine or vasopressin o Pacemaker failure
- Amiodarone may be considered when VF/VT is o 3rd degree AV block
unresponsive to CPR, defibrillation, and o Sick sinus syndrome
vasopressor therapy
o If amiodarone is unavailable, lidocaine may be - Use of certain drugs
considered if allowed by local protocol o Digoxin
- Continue CPR, stopping only to defibrillate and o Beta-blockers
reassess rhythm. o Calcium channel blockers
o Minimize interruptions in chest compressions o Tricyclic antidepressants
before and after shock; resume CPR beginning
with compressions immediately after each - Autononomic nervous system stimulation
shock o Increased vagal tone
- If the rhythm is successfully converted to an
effective electromechanical rhythm (with a pulse - Noncardiac disorders
and good perfusion): o Metabolic acidosis
o assess vital signs, support airway and o Hypoxia
breathing,
o provide medications to support blood TREATMENT OF IDIOVENTRICULAR RHYTHM
pressure, heart rate, and rhythm and to - For symptomatic patients:
prevent reoccurrence o Support the airway and breathing
o Deliver oxygen, perform an ECG, monitor the
blood pressure and pulse oximetry, and place
4. Idioventricular Rhythm
an IV infusion
- Idioventricular rhythm, also called ventricular
o Continually reassess the clinical status, and
escape rhythm, occurs when the impulse
correct any reversible conditions
starts in the conduction system below the AV
o Maintain a ventricular rate sufficient to
node.
produce adequate cardiac output
- Slow dysrhythmia (rate of 20 to 40 BPM) with
 Administer atropine or deliver
wide QRS complexes that arise from the
transcutaneous pacing
ventricles
 In unresolved idioventricular rhythm, the
- The decreased cardiac output associated with
atropine dose may be repeated
this dysrhythmia will likely cause the patient
o Lidocaine and amiodarone are
to be symptomatic (hypotension, syncope,
contraindicated
etc.). Patient assessment is essential because
- If there is no pulse, treat the dysrhythmia as if it is
the escape rhythm may be perfusing or
pulseless electrical activity (PEA)
nonperfusing.
- Idioventricular dysrhythmias are also common
5. Asystole
during cardiac arrest as they represent the
- Absence of any cardiac activity
final escape rhythm to be generated in an
- Appears as a flat (or nearly flat) line
attempt to perfuse the body.
- Complete cessation of cardiac output
- Terminal rhythm
- Chances of recovery extremely low
TREATMENT OF ASYSTOLE from the coronary circulation to meet its
- Promptly initiate CPR, deliver high-concentration continuous demands.
oxygen, place an IV line, and secure the airway - Increased demand. When there is an increase in
- Administer epinephrine, repeating its demand, flow through the coronary arteries
administration every 3 to 5 minutes needs to be increased.
o One dose of vasopressin may replace either - Ischemia. When there is blockage in a coronary
the first or second dose of epinephrine artery, flow cannot be increased, and ischemia
- Continue CPR throughout the resuscitation effort, results which may lead to necrosis or myocardial
stopping periodically to reassess for a change in infarction.
rhythm and to check for presence of a pulse
- Follow local protocols for terminating CAUSES
resuscitation efforts Several factors are associated with angina.
- Always verify the presence of asystole in two - Physical exertion. This can precipitate an attack
leads prior to initiating treatment by increasing myocardial oxygen demand.
o Misplacement of an ECG lead or a loose wire - Exposure to cold. This can cause vasoconstriction
can mimic asystole (or VF) on the monitor and elevated blood pressure, with increased
oxygen demand.
- Eating a heavy meal. A heavy meal increases the
ANGINA PECTORIS
blood flow to the mesenteric area for digestion,
- Angina pectoris is a clinical syndrome usually
thereby reducing the blood supply available to the
characterized by episodes or paroxysms of pain or
heart muscle; in a severely compromised heart,
pressure in the anterior chest.
shunting of the blood for digestion can be
- The cause is insufficient coronary blood flow,
sufficient to induce anginal pain.
resulting in a decreased oxygen supply when
- Stress. Stress causes the release of
there is increased myocardial demand for oxygen
catecholamines, which increased blood pressure,
in response to physical exertion or emotional
heart rate, and myocardial workload.
stress.

CLINICAL MANIFESTATIONS
CLASSIFICATIONS
The severity of symptoms of angina is based on the
1. Stable angina. There is predictable and consistent
magnitude of the precipitating activity and its effect
pain that occurs on exertion and is relieved by
on activities of daily living.
rest and/or nitroglycerin.
- Chest pain. The pain is often felt deep in the chest
2. Unstable angina. The symptoms increase in
behind the sternum and may radiate to the neck,
frequency and severity and may not be relieved
jaw, and shoulders.
with rest or nitroglycerin.
- Numbness. A feeling of weakness or numbness in
3. Intractable or refractory angina. There is severe
the arms, wrists and hands.
incapacitating chest pain.
- Shortness of breath. An increase in oxygen
4. Variant angina. There is pain at rest, with
demand could cause shortness of breath.
reversible ST-segment elevation and thought to
- Pallor. Inadequate blood supply to peripheral
be caused by coronary artery vasospasm.
tissues cause pallor.
5. Silent ischemia. There is objective evidence of
ischemia but patient reports no pain.
COMPLICATIONS
- Myocardial infarction. Myocardial infarction is
PATHOPHYSIOLOGY
the end result of angina pectoris if left untreated.
Angina is usually caused by atherosclerotic disease.
- Cardiac arrest. The heart pumps more and more
- Almost invariably, angina is associated with a
blood to compensate the decreased oxygen
significant obstruction of at least one major
supply, and.the cardiac muscle would ultimately
coronary artery.
fail leading to cardiac arrest.
- Oxygen demands not met. Normally, the
myocardium extracts a large amount of oxygen
- Cardiogenic shock. MI also predisposes the familial heart disease who are experiencing chest
patient to cardiogenic shock. pain, and in patients with abnormal resting ECGs.
Abnormal results are present in valvular disease,
ASSESSMENT AND DIAGNOSTIC FINDINGS altered contractility, ventricular failure, and
The diagnosis of angina pectoris is determined circulatory abnormalities. Note: Ten percent of
through: patients with unstable angina have normal-
- ECG: Often normal when patient at rest or when appearing coronary arteries.
pain-free; depression of the ST segment or T wave - Ergonovine (Ergotrate) injection: On occasion,
inversion signifies ischemia. Dysrhythmias and may be used for patients who have angina at rest
heart block may also be present. Significant Q to demonstrate hyperspastic coronary vessels.
waves are consistent with a prior MI. (Patients with resting angina usually experience
- 24-hour ECG monitoring (Holter): Done to see chest pain, ST elevation, or depression and/or
whether pain episodes correlate with or change pronounced rise in left ventricular end-diastolic
during exercise or activity. ST depression without pressure [LVEDP], fall in systemic systolic
pain is highly indicative of ischemia. pressure, and/or high-grade coronary artery
- Exercise or pharmacological stress narrowing. Some patients may also have severe
electrocardiography: Provides more diagnostic ventricular dysrhythmias.)
information, such as duration and level of activity
attained before onset of angina. A markedly MEDICAL MANAGEMENT
positive test is indicative of severe CAD. Note: The objectives of the medical management of angina
Studies have shown stress echo studies to be are to increase the oxygen demand of the
more accurate in some groups than exercise myocardium and to increase the oxygen supply.
stress testing alone. - Oxygen therapy. Oxygen therapy is usually
- Cardiac enzymes (AST, CPK, CK and CK-MB; LDH initiated at the onset of chest pain in an attempt
and isoenzymes LD1, LD2): Usually within normal to increase the amount of oxygen delivered to the
limits (WNL); elevation indicates myocardial myocardium and reduce pain.
damage.
- Chest x-ray: Usually normal; however, infiltrates NURSING MANAGEMENT
may be present, reflecting cardiac - Treating angina. The nurse should instruct the
decompensation or pulmonary complications. patient to stop all activities and sit or rest in bed
- pCO2, potassium, and myocardial lactate: May in a semi-Fowler’s position when they experience
be elevated during anginal attack (all play a role in angina, and administer nitroglycerin sublingually.
myocardial ischemia and may perpetuate it). - Reducing anxiety. Exploring implications that the
- Serum lipids (total lipids, lipoprotein diagnosis has for the patient and providing
electrophoresis, and isoenzymes cholesterols information about the illness, its treatment, and
[HDL, LDL, VLDL]; triglycerides; phospholipids): methods of preventing its progression are
May be elevated (CAD risk factor). important nursing interventions.
- Echocardiogram: May reveal abnormal valvular - Preventing pain. The nurse reviews the
action as cause of chest pain. assessment findings, identifies the level of activity
- Nuclear imaging studies (rest or stress scan): that causes the patient’s pain, and plans the
Thallium-201: Ischemic regions appear as areas of patient’s activities accordingly.
decreased thallium uptake. - Decreasing oxygen demand. Balancing activity
- MUGA: Evaluates specific and general ventricle and rest is an important aspect of the educational
performance, regional wall motion, and ejection plan for the patient and family.
fraction.
- Cardiac catheterization with angiography:
Definitive test for CAD in patients with known MYOCARDIAL INFARCTION
ischemic disease with angina or incapacitating - Myocardial infarction (MI), is used synonymously
chest pain, in patients with cholesterolemia and with coronary occlusion and heart attack, yet MI
 is the most preferred term as myocardial ischemia - Catecholamine responses. The patient may
causes acute coronary syndrome (ACS) that can experience such as coolness in extremities,
result in myocardial death. perspiration, anxiety, and restlessness.
- In an MI, an area of the myocardium is - Fever. Unusually occurs at the onset of MI, but a
permanently destroyed because plaque rupture low-grade temperature elevation may develop
and subsequent thrombus formation result in during the next few days.
complete occlusion of the artery.
- The spectrum of ACS includes unstable angina, PREVENTION
non-ST-segment elevation MI, and ST-segment - Exercise. Exercising at least thrice a week could
elevation MI. help lower cholesterol levels that cause
vasoconstriction of the blood vessels.
PATHOPHYSIOLOGY - Balanced diet. Fruits, vegetables, meat and fish
- Unstable angina. There is reduced blood flow in a should be incorporated in the patient’s daily diet
coronary artery, often due to rupture of an to ensure that he or she gets the right amount of
atherosclerotic plaque, but the artery is not nutrients he or she needs.
completely occluded. - Smoking cessation. Nicotine causes
- Development of infarction. As the cells are vasoconstriction which can increase the pressure
deprived of oxygen, ischemia develops, cellular of the blood and result in MI.
injury occurs, and lack of oxygen leads to
infarction or death of the cells.
ASSESSMENT AND DIAGNOSTIC FINDINGS
CAUSES - Patient history. The patient history includes the
- Vasospasm. This is the sudden constriction or description of the presenting symptoms, the
narrowing of the coronary artery. history of previous cardiac and other illnesses,
- Decreased oxygen supply. The decrease in oxygen and the family history of heart diseases.
supply occurs from acute blood loss, anemia, or - ECG. ST elevation signifying ischemia; peaked
low blood pressure. upright or inverted T wave indicating injury;
- Increased demand for oxygen. A rapid heart rate, development of Q waves signifying prolonged
thyrotoxicosis, or ingestion of cocaine causes an ischemia or necrosis.
increase in the demand for oxygen. - Cardiac enzymes and isoenzymes. CPK-MB
(isoenzyme in cardiac muscle): Elevates within 4–
CLINICAL MANIFESTATIONS 8 hr, peaks in 12–20 hr, returns to normal in 48–
- Chest pain. This is the cardinal symptom of MI. 72 hr.
Persistent and crushing substernal pain that may - LDH. Elevates within 8–24 hr, peaks within 72–
radiate to the left arm, jaw, neck, or shoulder 144 hr, and may take as long as 14 days to return
blades. Pain is usually described as heavy, to normal. An LDH1 greater than LDH2 (flipped
squeezing, or crushing and may persist for 12 ratio) helps confirm/diagnose MI if not detected
hours or more. in acute phase.
- Shortness of breath. Because of increased oxygen - Troponins. Troponin I (cTnI) and troponin T
demand and a decrease in the supply of oxygen, (cTnT): Levels are elevated at 4–6 hr, peak at 14–
shortness of breath occurs. 18 hr, and return to baseline over 6–7 days. These
- Indigestion. Indigestion is present as a result of enzymes have increased specificity for necrosis
the stimulation of the sympathetic nervous and are therefore useful in diagnosing
system. postoperative MI when MB-CPK may be elevated
- Tachycardia and tachypnea. To compensate for related to skeletal trauma.
the decreased oxygen supply, the heart rate and - Myoglobin. A heme protein of small molecular
respiratory rate speed up. weight that is more rapidly released from
damaged muscle tissue with elevation within 2 hr
 after an acute MI, and peak levels occurring in 3– plaque formations, areas of necrosis/infarction,
15 hr. and blood clots.
- Electrolytes. Imbalances of sodium and potassium - Exercise stress test. Determines cardiovascular
can alter conduction and compromise response to activity (often done in conjunction
contractility. with thallium imaging in the recovery phase).
- WBC. Leukocytosis (10,000–20,000) usually
appears on the second day after MI because of IMMEDIATE TREATMENT FOR MI
the inflammatory process. MONA TASS
- ESR. Rises on second or third day after MI, - M: Morphine
indicating inflammatory response. o Analgesic drugs such as morphine are to
- Chemistry profiles. May be abnormal, depending reduce pain and anxiety, also has other
on acute/chronic abnormal organ beneficial effects as a vasodilator and
function/perfusion. decreases the workload of the heart by
- ABGs/pulse oximetry. May indicate hypoxia or reducing preload and afterload.
acute/chronic lung disease processes. - O: Oxygen
- Lipids (total lipids, HDL, LDL, VLDL, total o To provide and improve oxygenation of
cholesterol, triglycerides, phospholipids). ischemic myocardial tissue; enforced together
Elevations may reflect arteriosclerosis as a cause with bedrest to help reduce myocardial
for coronary narrowing or spasm. oxygen consumption. Given via nasal cannula
- Chest x-ray. May be normal or show an enlarged at 2 to 4 L/min.
cardiac shadow suggestive of HF or ventricular - N: Nitroglycerine
aneurysm. o First-line of treatment for angina pectoris and
- Two-dimensional echocardiogram. May be done acute MI; causes vasodilation and increases
to determine dimensions of chambers, blood flow to the myocardium.
septal/ventricular wall motion, ejection fraction - A: Aspirin
(blood flow), and valve configuration/function. o Aspirin prevents the formation of
- Nuclear imaging studies: Persantine or Thallium. thromboxane A2 which causes platelets to
Evaluates myocardial blood flow and status of aggregate and arteries to constrict. The earlier
myocardial cells, e.g., location/extent of the patient receives ASA after symptom
acute/previous MI. onset, the greater the potential benefit.
- Cardiac blood imaging/MUGA. Evaluates specific - T: Thrombolytics
and general ventricular performance, regional o To dissolve the thrombus in a coronary artery,
wall motion, and ejection fraction. allowing blood to flow through again,
- Technetium. Accumulates in ischemic cells, minimizing the size of the infarction and
outlining necrotic area(s). preserving ventricular function; given in some
- Coronary angiography. Visualizes patients with MI.
narrowing/occlusion of coronary arteries and is - A: Anticoagulants
usually done in conjunction with measurements o Given to prevent clots from becoming larger
of chamber pressures and assessment of left and block coronary arteries. They are usually
ventricular function (ejection fraction). Procedure given with other anticlotting medicines to
is not usually done in acute phase of MI unless help prevent or reduce heart muscle damage.
angioplasty or emergency heart surgery is - S: Stool Softeners
imminent. o Given to avoid intense straining that may
- Digital subtraction angiography (DSA). Technique trigger arrhythmias or another cardiac arrest.
used to visualize status of arterial bypass grafts - S: Sedatives
and to detect peripheral artery disease. o In order to limit the size of infarction and give
- Magnetic resonance imaging (MRI). Allows rest to the patient. Valium or an equivalent is
visualization of blood flow, cardiac chambers or usually given.
intraventricular septum, valves, vascular lesions,
NURSING MANAGEMENT - Anxiety may be a response to the symptoms;
- Administer oxygen along with medication therapy however, some patients report anxiety as the only
to assist with relief of symptoms. symptom.
- Encourage bed rest with the back rest elevated to
help decrease chest discomfort and dyspnea.
- Encourage changing of positions frequently to ASSESSMENT AND DIAGNOSTIC FINDINGS
help keep fluid from pooling in the bases of the - Physical Examination of the Heart. Reveals an
lungs. extra heart sound referred to as a mitral click. A
- Check skin temperature and peripheral pulses systolic click is an early sign that a valve leaflet is
frequently to monitor tissue perfusion. ballooning into the left atrium. In addition to the
- Provide information in an honest and supportive mitral click, a murmur of mitral regurgitation may
manner. be heard if progressive valve leaflet stretching and
- Monitor the patient closely for changes in cardiac regurgitation have occurred.
rate and rhythm, heart sounds, blood pressure, - Doppler Echocardiography. Used to diagnose and
chest pain, respiratory status, urinary output, monitor the progression of MVP.
changes in skin color, and laboratory values. MEDICAL MANAGEMENT

- Directed at controlling the symptoms

- Eliminate caffeine and alcohol from the diet and
MITRAL VALVE PROLAPSE to stop smoking
- Most patients do not require any medications
It is a deformity that usually produces no symptoms.
although antiarrhythmic medications may be
Rarely, it progresses and can result in sudden death.
prescribed.
- Mitral valve repair or replacement may be
necessary in the advance stages of the disease.
PATHOPHYSIOLOGY

- A portion of one or both mitral valve leaflets

balloons back into the atrium during systole. NURSING MANAGEMENT
- The ballooning stretches the leaflet to the point
- Health Teaching
that the valve does not remain closed during
o Educate the patient about the diagnosis and
systole (i.e., ventricular contraction).
the possibility that the condition is hereditary
- Blood then regurgitates from the left ventricle
o Patient may be at risk for infectious
back into the left atrium.
endocarditis. Teach patient on how to
- About 15% of patients who develop murmurs
minimize the risk.
eventually experience heart enlargement, atrial
o Patient should inform the health care
fibrillation, pulmonary hypertension, or heart
provider id symptoms develop
failure.
o Caffeine and alcohol should be avoided
o Read product labels of over-the-counter
products such as cough medicines because it
CLINICAL MANIFESTATIONS may contain alcohol, caffeine, ephedrine and
- Most are asymptomatic epinephrine.
- Fatigue may occur regardless of activity level and
amount of rest or sleep.
- Shortness of breath is not correlated with activity MITRAL REGURGITATION
levels or pulmonary function.
- Involves blood flowing back from the left ventricle
- Atrial or ventricular dysrhythmias may produce
into the left atrium during systole.
the sensation of palpitations, but palpitations
- Often the edges of the mitral valve leaflets do not
have been reported while the heart has been
close during systole. The leaflets cannot close
beating normally.
completely because the leaflets and chordae
- Chest pain, which is often localized to the chest, is
tendineae have thickened and fibrosed, resulting
not correlated with activity and may last for days.
in their contraction.
PATHOPHYSIOLOGY

- Mitral regurgitation may result from problems

with one or more of the leaflets, the chordae
MITRAL STENOSIS
tendineae, the annulus, or the papillary muscles.
- Regardless of the cause, blood regurgitates into - It is an obstruction of blood flowing from the left
the atrium during systole. atrium into the left ventricle.
- With each beat of the left ventricle, some of the - The leaflets often fuse together. Eventually, the
blood is forced back into the left atrium, adding to mitral valve orifice narrows and progressively
the blood flowing in from the lungs. obstructs blood flow into the ventricle.
- This causes the left atrium to stretch and
eventually hypertrophy and dilate
- The backward flow of blood from the ventricle PATHOPHYSIOLOGY
diminishes the volume of blood flowing into the
atrium from the lungs. As a result, the lungs - The left atrium has great difficulty moving blood
become congested, eventually adding extra strain into the ventricle because of the increased
on the right ventricle. resistance of the narrowed orifice.
- Poor left ventricular filling can cause decreased
cardiac output.
CLINICAL MANIFESTATIONS - The increased blood volume in the left atrium
causes it to dilate and hypertrophy.
- Chronic mitral regurgitation is often - Because there is no valve to protect the
asymptomatic pulmonary veins from the backward flow of blood
- Acute mitral regurgitation (e.g. that resulting from from the atrium, the pulmonary circulation
a myocardial infarction) usually manifests as becomes congested.
severe congestive heart failure - As a result, the right ventricle must contract
- Dyspnea against an abnormally high pulmonary arterial
- Fatigue pressure and is subjected to excessive strain.
- Weakness Eventually, the right ventricle fails.
- Palpitations
- Shortness of breath on exertion
- Cough from pulmonary congestion CLINICAL MANIFESTATIONS

- Dyspnea on exertion as a result of pulmonary

ASSESSMENT AND DIAGNOSTIC FINDINGS venous hypertension.
- Symptoms usually develop after the valve opening
- Doppler Echocardiography. To diagnose and is reduced by one-third to one-half its usual size.
monitor the progression of mitral regurgitation. - Fatigue as a result of low cardiac output.
- Transesophageal Echocardiography. Provides the - Dry cough or wheezing. Due to the enlarged left
best images of the mitral valve. atrium may create pressure on the left bronchial
tree.
- Patients may expectorate blood (ie, hemoptysis)
MEDICAL MANAGEMENT - Experience palpitations
- Orthopnea
- angiotensin-converting enzyme (ACE) inhibitors
- Paroxysmal nocturnal dyspnea (PND)
- angiotensin receptor blockers (ARBs)
- Repeated respiratory infections.
- beta-blockers
- Once symptoms of heart failure develop, the
patient needs to restrict his or her activity level to
ASSESSMENT AND DIAGNOSTIC FINDINGS
minimize symptoms.
- Surgical intervention consists of mitral - Doppler echocardiography is used to diagnose
valvuloplasty (ie, surgical repair of the valve) or mitral stenosis.
valve replacement
- Electrocardiography (ECG) and cardiac in diastole for myocardial perfusion, and the
catheterization with angiography may be used to decreased blood flow into the coronary arteries.
help determine the severity of the mitral stenosis. - Blood pressure is usually normal but may be low.
Pulse pressure may be low (30 mm Hg or less)
because of diminished blood flow.
MEDICAL MANAGEMENT

- Anticoagulants. To decrease the risk for

ASSESSMENT AND DIAGNOSTIC FINDINGS
developing atrial thrombus and May also require
treatment for anemia. - Physical Examination
- Avoid strenuous activities and competitive - Doppler echocardiography
sports, both of which increase the heart rate.
- Surgical intervention:
o Valvuloplasty, usually a commissurotomy to MEDICAL MANAGEMENT
open or rupture the fused commissures of the
mitral valve. - Medications are prescribed to treat dysrhythmia
o Percutaneous transluminal valvuloplasty or - Definitive treatment for aortic stenosis is surgical
mitral valve replacement may be performed. replacement of the aortic valve.
- Patients who are symptomatic and are not
surgical candidates may benefit from one-balloon
or two-balloon percutaneous valvuloplasty
AORTIC STENOSIS
procedures.
- Narrowing of the orifice between the left ventricle
and the aorta.

PATHOPHYSIOLOGY

- Progressive narrowing of the valve orifice occurs,

usually over several years to several decades.
- The left ventricle overcomes the obstruction to
circulation by contracting more slowly but with
greater energy than normal, forcibly squeezing
the blood through the smaller orifice.
- The obstruction to left ventricular outflow
increases pressure on the left ventricle, and the
ventricular wall thickens, or hypertrophies. When
these compensatory mechanisms of the heart
begin to fail, clinical signs and symptoms develop.

CLINICAL MANIFESTATIONS

- Mostly asymptomatic
- Exertional dyspnea. caused by increased
pulmonary venous pressure due to left ventricular
failure.
- Orthopnea, PND, and pulmonary edema may also
occur, along with dizziness and syncope because
of reduced blood flow to the brain.
- Angina pectoris is a frequent symptom; it results
from the increased oxygen demands of the
hypertrophied left ventricle, the decreased time