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
underlying structural heart disease
VENTRICULAR DYSRHYTHMIA
- Premature ventricular complex (PVC)
- Ventricular escape complexes or rhythm
- Ventricular tachycardia
- Ventricular fibrillation
- Asystole
1. Premature Ventricular Complexes (PVCs)
- A premature ventricular complex (PVC) is an
impulse that starts in a ventricle and is
conducted through the ventricles before the
next normal sinus impulse.
- Early ectopic beats that interrupt the normal
rhythm
- Originate from an irritable focus in the
ventricular conduction system or muscle
tissue
- PVCs can occur for no apparent reason in
individuals who have healthy hearts and are
usually of no significance. The incidence of
PVCs increases with age and can occur during
exercise or at rest. However, PVCs may also
be significant for two reasons. First, they can
precipitate more serious dysrhythmias such as
ventricular tachycardia or fibrillation. The
danger is greater in patients experiencing
myocardial ischemia and/or infarction.
Second, PVCs can result in decreased cardiac
output due to reduced diastolic filling time
and a loss of atrial kick.
- PVCs may produce a palpable pulse but they
may also produce a diminished or
nonpalpable pulse (called a nonperfusing
PVC). Patients frequently experience the
sensation of “skipped beats.”
Causes of PVC:
- Cardiac Diseases:
o Myocardial ischemia and MI
o Congestive heart failure
o Irritation of ventricles by pacemaker or
electrodes or PA catheter
o Enlargement of the ventricular chambers
o Mitral valve prolapse
o Myocarditis
- Use of certain drugs
o Amphetamine intoxication
o Cocaine
o Digoxin
o Quinidine
o Phenothiazines
o Tricyclic antidepressanta
o Sympathomimetic drugs
- Autonomic nervous system stimulation
o Increased sympathetic stimulation
o Exercise
o Emotional stress
- Noncardiac disorders
o Stimulants (alcohol, caffeine, tobacco)
o Elecrtrolyte imbalance (hypokalemia,
hyperkalemia, hypomagnesemia and
hypocalcemia)
o Hypoxia
o Metabolic acidosis
Treatment of PVCs
- Asymptomatic patients seldom require treatment
- Patients with myocardial ischemia, treatment of
frequent PVCs includes:
o Administration of oxygen and placement of an
IV line
o Identifying and correcting the underlying
factor causing the PVCs
 In some settings, administering lidocaine
or other antidysrhythmics (e.g.,
amiodarone) by IV push and a continued
maintenance infusion
o Administering potassium chloride
intravenously to correct hypokalemia or
magnesium sulfate intravenously to correct
hypomagnesemia; adjusting drug therapy; or
correcting acidosis, hypothermia, and/or
hypoxia
2. Ventricular Tachycardia
- VT is defined as three or more PVCs in a row,
occurring at a rate exceeding 100 bpm.
- Fast dysrhythmia (100 to 250 BPM) that arises
from the ventricles
- Clinically, ventricular tachycardia is always
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
- Prompt delivery of CPR and defibrillation
- Organize ACLS actions around uninterrupted
periods of CPR
- Initiate securing the airway and placing an IV line
in the course of treatment
- After one shock and a 2-minute period of CPR,
administer epinephrine or vasopressin
- Amiodarone may be considered when VF/VT is
unresponsive to CPR, defibrillation, and
vasopressor therapy
o If amiodarone is unavailable, lidocaine may be
considered if allowed by local protocol
- Continue CPR, stopping only to defibrillate and
reassess rhythm.
o Minimize interruptions in chest compressions
before and after shock; resume CPR beginning
with compressions immediately after each
shock
- If the rhythm is successfully converted to an
effective electromechanical rhythm (with a pulse
and good perfusion):
o assess vital signs, support airway and
breathing,
o provide medications to support blood
pressure, heart rate, and rhythm and to
prevent reoccurrence
4. Idioventricular Rhythm
- Idioventricular rhythm, also called ventricular
escape rhythm, occurs when the impulse
starts in the conduction system below the AV
node.
- Slow dysrhythmia (rate of 20 to 40 BPM) with
wide QRS complexes that arise from the
ventricles
- The decreased cardiac output associated with
this dysrhythmia will likely cause the patient
to be symptomatic (hypotension, syncope,
etc.). Patient assessment is essential because
the escape rhythm may be perfusing or
nonperfusing.
- Idioventricular dysrhythmias are also common
during cardiac arrest as they represent the
final escape rhythm to be generated in an
attempt to perfuse the body.
CAUSES OF IDIOVENTRICULAR RHYTHM
- Cardiac Diseases
o MI
o Failure of all the heart’s higher pacemakers
o Failure of supraventricular impulses to reach
the ventricles due to a block in the conduction
system
o Pacemaker failure
o 3rd degree AV block
o Sick sinus syndrome
- Use of certain drugs
o Digoxin
o Beta-blockers
o Calcium channel blockers
o Tricyclic antidepressants
- Autononomic nervous system stimulation
o Increased vagal tone
- Noncardiac disorders
o Metabolic acidosis
o Hypoxia
TREATMENT OF IDIOVENTRICULAR RHYTHM
- For symptomatic patients:
o Support the airway and breathing
o Deliver oxygen, perform an ECG, monitor the
blood pressure and pulse oximetry, and place
an IV infusion
o Continually reassess the clinical status, and
correct any reversible conditions
o Maintain a ventricular rate sufficient to
produce adequate cardiac output
 Administer atropine or deliver
transcutaneous pacing
 In unresolved idioventricular rhythm, the
atropine dose may be repeated
o Lidocaine and amiodarone are
contraindicated
- If there is no pulse, treat the dysrhythmia as if it is
pulseless electrical activity (PEA)
5. Asystole
- Absence of any cardiac activity
- Appears as a flat (or nearly flat) line
- Complete cessation of cardiac output
- Terminal rhythm
- Chances of recovery extremely low
TREATMENT OF ASYSTOLE
- Promptly initiate CPR, deliver high-concentration
oxygen, place an IV line, and secure the airway
- Administer epinephrine, repeating its
administration every 3 to 5 minutes
o One dose of vasopressin may replace either
the first or second dose of epinephrine
- Continue CPR throughout the resuscitation effort,
stopping periodically to reassess for a change in
rhythm and to check for presence of a pulse
- Follow local protocols for terminating
resuscitation efforts
- Always verify the presence of asystole in two
leads prior to initiating treatment
o Misplacement of an ECG lead or a loose wire
can mimic asystole (or VF) on the monitor
ANGINA PECTORIS
- Angina pectoris is a clinical syndrome usually
characterized by episodes or paroxysms of pain or
pressure in the anterior chest.
- The cause is insufficient coronary blood flow,
resulting in a decreased oxygen supply when
there is increased myocardial demand for oxygen
in response to physical exertion or emotional
stress.
from the coronary circulation to meet its
continuous demands.
- Increased demand. When there is an increase in
demand, flow through the coronary arteries
needs to be increased.
- Ischemia. When there is blockage in a coronary
artery, flow cannot be increased, and ischemia
results which may lead to necrosis or myocardial
infarction.
CAUSES
Several factors are associated with angina.
- Physical exertion. This can precipitate an attack
by increasing myocardial oxygen demand.
- Exposure to cold. This can cause vasoconstriction
and elevated blood pressure, with increased
oxygen demand.
- Eating a heavy meal. A heavy meal increases the
blood flow to the mesenteric area for digestion,
thereby reducing the blood supply available to the
heart muscle; in a severely compromised heart,
shunting of the blood for digestion can be
sufficient to induce anginal pain.
- Stress. Stress causes the release of
catecholamines, which increased blood pressure,
heart rate, and myocardial workload.

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
patient to cardiogenic shock.
ASSESSMENT AND DIAGNOSTIC FINDINGS
The diagnosis of angina pectoris is determined
through:
- ECG: Often normal when patient at rest or when
pain-free; depression of the ST segment or T wave
inversion signifies ischemia. Dysrhythmias and
heart block may also be present. Significant Q
waves are consistent with a prior MI.
- 24-hour ECG monitoring (Holter): Done to see
whether pain episodes correlate with or change
during exercise or activity. ST depression without
pain is highly indicative of ischemia.
- Exercise or pharmacological stress
electrocardiography: Provides more diagnostic
information, such as duration and level of activity
attained before onset of angina. A markedly
positive test is indicative of severe CAD. Note:
Studies have shown stress echo studies to be
more accurate in some groups than exercise
stress testing alone.
- Cardiac enzymes (AST, CPK, CK and CK-MB; LDH
and isoenzymes LD1, LD2): Usually within normal
limits (WNL); elevation indicates myocardial
damage.
- Chest x-ray: Usually normal; however, infiltrates
may be present, reflecting cardiac
decompensation or pulmonary complications.
- pCO2, potassium, and myocardial lactate: May
be elevated during anginal attack (all play a role in
myocardial ischemia and may perpetuate it).
- Serum lipids (total lipids, lipoprotein
electrophoresis, and isoenzymes cholesterols
[HDL, LDL, VLDL]; triglycerides; phospholipids):
May be elevated (CAD risk factor).
- Echocardiogram: May reveal abnormal valvular
action as cause of chest pain.
- Nuclear imaging studies (rest or stress scan):
Thallium-201: Ischemic regions appear as areas of
decreased thallium uptake.
- MUGA: Evaluates specific and general ventricle
performance, regional wall motion, and ejection
fraction.
- Cardiac catheterization with angiography:
Definitive test for CAD in patients with known
ischemic disease with angina or incapacitating
chest pain, in patients with cholesterolemia and
familial heart disease who are experiencing chest
pain, and in patients with abnormal resting ECGs.
Abnormal results are present in valvular disease,
altered contractility, ventricular failure, and
circulatory abnormalities. Note: Ten percent of
patients with unstable angina have normal-
appearing coronary arteries.
- Ergonovine (Ergotrate) injection: On occasion,
may be used for patients who have angina at rest
to demonstrate hyperspastic coronary vessels.
(Patients with resting angina usually experience
chest pain, ST elevation, or depression and/or
pronounced rise in left ventricular end-diastolic
pressure [LVEDP], fall in systemic systolic
pressure, and/or high-grade coronary artery
narrowing. Some patients may also have severe
ventricular dysrhythmias.)
MEDICAL MANAGEMENT
The objectives of the medical management of angina
are to increase the oxygen demand of the
myocardium and to increase the oxygen supply.
- Oxygen therapy. Oxygen therapy is usually
initiated at the onset of chest pain in an attempt
to increase the amount of oxygen delivered to the
myocardium and reduce pain.
NURSING MANAGEMENT
- Treating angina. The nurse should instruct the
patient to stop all activities and sit or rest in bed
in a semi-Fowler’s position when they experience
angina, and administer nitroglycerin sublingually.
- Reducing anxiety. Exploring implications that the
diagnosis has for the patient and providing
information about the illness, its treatment, and
methods of preventing its progression are
important nursing interventions.
- Preventing pain. The nurse reviews the
assessment findings, identifies the level of activity
that causes the patient’s pain, and plans the
patient’s activities accordingly.
- Decreasing oxygen demand. Balancing activity
and rest is an important aspect of the educational
plan for the patient and family.
MYOCARDIAL INFARCTION
- Myocardial infarction (MI), is used synonymously
with coronary occlusion and heart attack, yet MI
 is the most preferred term as myocardial ischemia
causes acute coronary syndrome (ACS) that can
result in myocardial death.
- In an MI, an area of the myocardium is
permanently destroyed because plaque rupture
and subsequent thrombus formation result in
complete occlusion of the artery.
- The spectrum of ACS includes unstable angina,
non-ST-segment elevation MI, and ST-segment
elevation MI.
PATHOPHYSIOLOGY
- Unstable angina. There is reduced blood flow in a
coronary artery, often due to rupture of an
atherosclerotic plaque, but the artery is not
completely occluded.
- Development of infarction. As the cells are
deprived of oxygen, ischemia develops, cellular
injury occurs, and lack of oxygen leads to
infarction or death of the cells.
CAUSES
- Vasospasm. This is the sudden constriction or
narrowing of the coronary artery.
- Decreased oxygen supply. The decrease in oxygen
supply occurs from acute blood loss, anemia, or
low blood pressure.
- Increased demand for oxygen. A rapid heart rate,
thyrotoxicosis, or ingestion of cocaine causes an
increase in the demand for oxygen.
CLINICAL MANIFESTATIONS
- Chest pain. This is the cardinal symptom of MI.
Persistent and crushing substernal pain that may
radiate to the left arm, jaw, neck, or shoulder
blades. Pain is usually described as heavy,
squeezing, or crushing and may persist for 12
hours or more.
- Shortness of breath. Because of increased oxygen
demand and a decrease in the supply of oxygen,
shortness of breath occurs.
- Indigestion. Indigestion is present as a result of
the stimulation of the sympathetic nervous
system.
- Tachycardia and tachypnea. To compensate for
the decreased oxygen supply, the heart rate and
respiratory rate speed up.
- Catecholamine responses. The patient may
experience such as coolness in extremities,
perspiration, anxiety, and restlessness.
- Fever. Unusually occurs at the onset of MI, but a
low-grade temperature elevation may develop
during the next few days.
PREVENTION
- Exercise. Exercising at least thrice a week could
help lower cholesterol levels that cause
vasoconstriction of the blood vessels.
- Balanced diet. Fruits, vegetables, meat and fish
should be incorporated in the patient’s daily diet
to ensure that he or she gets the right amount of
nutrients he or she needs.
- Smoking cessation. Nicotine causes
vasoconstriction which can increase the pressure
of the blood and result in MI.
ASSESSMENT AND DIAGNOSTIC FINDINGS
- Patient history. The patient history includes the
description of the presenting symptoms, the
history of previous cardiac and other illnesses,
and the family history of heart diseases.
- ECG. ST elevation signifying ischemia; peaked
upright or inverted T wave indicating injury;
development of Q waves signifying prolonged
ischemia or necrosis.
- Cardiac enzymes and isoenzymes. CPK-MB
(isoenzyme in cardiac muscle): Elevates within 4–
8 hr, peaks in 12–20 hr, returns to normal in 48–
72 hr.
- LDH. Elevates within 8–24 hr, peaks within 72–
144 hr, and may take as long as 14 days to return
to normal. An LDH1 greater than LDH2 (flipped
ratio) helps confirm/diagnose MI if not detected
in acute phase.
- Troponins. Troponin I (cTnI) and troponin T
(cTnT): Levels are elevated at 4–6 hr, peak at 14–
18 hr, and return to baseline over 6–7 days. These
enzymes have increased specificity for necrosis
and are therefore useful in diagnosing
postoperative MI when MB-CPK may be elevated
related to skeletal trauma.
- Myoglobin. A heme protein of small molecular
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–
15 hr.
- Electrolytes. Imbalances of sodium and potassium
can alter conduction and compromise
contractility.
- WBC. Leukocytosis (10,000–20,000) usually
appears on the second day after MI because of
the inflammatory process.
- ESR. Rises on second or third day after MI,
indicating inflammatory response.
- Chemistry profiles. May be abnormal, depending
on acute/chronic abnormal organ
function/perfusion.
- ABGs/pulse oximetry. May indicate hypoxia or
acute/chronic lung disease processes.
- Lipids (total lipids, HDL, LDL, VLDL, total
cholesterol, triglycerides, phospholipids).
Elevations may reflect arteriosclerosis as a cause
for coronary narrowing or spasm.
- Chest x-ray. May be normal or show an enlarged
cardiac shadow suggestive of HF or ventricular
aneurysm.
- Two-dimensional echocardiogram. May be done
to determine dimensions of chambers,
septal/ventricular wall motion, ejection fraction
(blood flow), and valve configuration/function.
- Nuclear imaging studies: Persantine or Thallium.
Evaluates myocardial blood flow and status of
myocardial cells, e.g., location/extent of
acute/previous MI.
- Cardiac blood imaging/MUGA. Evaluates specific
and general ventricular performance, regional
wall motion, and ejection fraction.
- Technetium. Accumulates in ischemic cells,
outlining necrotic area(s).
- Coronary angiography. Visualizes
narrowing/occlusion of coronary arteries and is
usually done in conjunction with measurements
of chamber pressures and assessment of left
ventricular function (ejection fraction). Procedure
is not usually done in acute phase of MI unless
angioplasty or emergency heart surgery is
imminent.
- Digital subtraction angiography (DSA). Technique
used to visualize status of arterial bypass grafts
and to detect peripheral artery disease.
- Magnetic resonance imaging (MRI). Allows
visualization of blood flow, cardiac chambers or
intraventricular septum, valves, vascular lesions,
plaque formations, areas of necrosis/infarction,
and blood clots.
- Exercise stress test. Determines cardiovascular
response to activity (often done in conjunction
with thallium imaging in the recovery phase).
IMMEDIATE TREATMENT FOR MI
MONA TASS
- M: Morphine
o Analgesic drugs such as morphine are to
reduce pain and anxiety, also has other
beneficial effects as a vasodilator and
decreases the workload of the heart by
reducing preload and afterload.
- O: Oxygen
o To provide and improve oxygenation of
ischemic myocardial tissue; enforced together
with bedrest to help reduce myocardial
oxygen consumption. Given via nasal cannula
at 2 to 4 L/min.
- N: Nitroglycerine
o First-line of treatment for angina pectoris and
acute MI; causes vasodilation and increases
blood flow to the myocardium.
- A: Aspirin
o Aspirin prevents the formation of
thromboxane A2 which causes platelets to
aggregate and arteries to constrict. The earlier
the patient receives ASA after symptom
onset, the greater the potential benefit.
- T: Thrombolytics
o To dissolve the thrombus in a coronary artery,
allowing blood to flow through again,
minimizing the size of the infarction and
preserving ventricular function; given in some
patients with MI.
- A: Anticoagulants
o Given to prevent clots from becoming larger
and block coronary arteries. They are usually
given with other anticlotting medicines to
help prevent or reduce heart muscle damage.
- S: Stool Softeners
o Given to avoid intense straining that may
trigger arrhythmias or another cardiac arrest.
- S: Sedatives
o In order to limit the size of infarction and give
rest to the patient. Valium or an equivalent is
usually given.
NURSING MANAGEMENT
- Administer oxygen along with medication therapy
to assist with relief of symptoms.
- Encourage bed rest with the back rest elevated to
help decrease chest discomfort and dyspnea.
- Encourage changing of positions frequently to
help keep fluid from pooling in the bases of the
lungs.
- Check skin temperature and peripheral pulses
frequently to monitor tissue perfusion.
- Provide information in an honest and supportive
manner.
- Monitor the patient closely for changes in cardiac
rate and rhythm, heart sounds, blood pressure,
chest pain, respiratory status, urinary output,
changes in skin color, and laboratory values.
MITRAL VALVE PROLAPSE
It is a deformity that usually produces no symptoms.
Rarely, it progresses and can result in sudden death.
PATHOPHYSIOLOGY
- A portion of one or both mitral valve leaflets
balloons back into the atrium during systole.
- The ballooning stretches the leaflet to the point
that the valve does not remain closed during
systole (i.e., ventricular contraction).
- Blood then regurgitates from the left ventricle
back into the left atrium.
- About 15% of patients who develop murmurs
eventually experience heart enlargement, atrial
fibrillation, pulmonary hypertension, or heart
failure.
CLINICAL MANIFESTATIONS
- Most are asymptomatic
- Fatigue may occur regardless of activity level and
amount of rest or sleep.
- Shortness of breath is not correlated with activity
levels or pulmonary function.
- Atrial or ventricular dysrhythmias may produce
the sensation of palpitations, but palpitations
have been reported while the heart has been
beating normally.
- Chest pain, which is often localized to the chest, is
not correlated with activity and may last for days.
- Anxiety may be a response to the symptoms;
however, some patients report anxiety as the only
symptom.
ASSESSMENT AND DIAGNOSTIC FINDINGS
- Physical Examination of the Heart. Reveals an
extra heart sound referred to as a mitral click. A
systolic click is an early sign that a valve leaflet is
ballooning into the left atrium. In addition to the
mitral click, a murmur of mitral regurgitation may
be heard if progressive valve leaflet stretching and
regurgitation have occurred.
- Doppler Echocardiography. Used to diagnose and
monitor the progression of MVP.
MEDICAL MANAGEMENT
- Directed at controlling the symptoms
- Eliminate caffeine and alcohol from the diet and
to stop smoking
- Most patients do not require any medications
although antiarrhythmic medications may be
prescribed.
- Mitral valve repair or replacement may be
necessary in the advance stages of the disease.
NURSING MANAGEMENT
- Health Teaching
o Educate the patient about the diagnosis and
the possibility that the condition is hereditary
o Patient may be at risk for infectious
endocarditis. Teach patient on how to
minimize the risk.
o Patient should inform the health care
provider id symptoms develop
o Caffeine and alcohol should be avoided
o Read product labels of over-the-counter
products such as cough medicines because it
may contain alcohol, caffeine, ephedrine and
epinephrine.
MITRAL REGURGITATION
- Involves blood flowing back from the left ventricle
into the left atrium during systole.
- Often the edges of the mitral valve leaflets do not
close during systole. The leaflets cannot close
completely because the leaflets and chordae
tendineae have thickened and fibrosed, resulting
in their contraction.
PATHOPHYSIOLOGY
- Mitral regurgitation may result from problems
with one or more of the leaflets, the chordae
tendineae, the annulus, or the papillary muscles.
- Regardless of the cause, blood regurgitates into
the atrium during systole.
- With each beat of the left ventricle, some of the
blood is forced back into the left atrium, adding to
the blood flowing in from the lungs.
- This causes the left atrium to stretch and
eventually hypertrophy and dilate
- The backward flow of blood from the ventricle
diminishes the volume of blood flowing into the
atrium from the lungs. As a result, the lungs
become congested, eventually adding extra strain
on the right ventricle.
CLINICAL MANIFESTATIONS
- Chronic mitral regurgitation is often
asymptomatic
- Acute mitral regurgitation (e.g. that resulting from
a myocardial infarction) usually manifests as
severe congestive heart failure
- Dyspnea
- Fatigue
- Weakness
- Palpitations
- Shortness of breath on exertion
- Cough from pulmonary congestion
ASSESSMENT AND DIAGNOSTIC FINDINGS
- Doppler Echocardiography. To diagnose and
monitor the progression of mitral regurgitation.
- Transesophageal Echocardiography. Provides the
best images of the mitral valve.
MEDICAL MANAGEMENT
- angiotensin-converting enzyme (ACE) inhibitors
- angiotensin receptor blockers (ARBs)
- beta-blockers
- Once symptoms of heart failure develop, the
patient needs to restrict his or her activity level to
minimize symptoms.
- Surgical intervention consists of mitral
valvuloplasty (ie, surgical repair of the valve) or
valve replacement
MITRAL STENOSIS
- It is an obstruction of blood flowing from the left
atrium into the left ventricle.
- The leaflets often fuse together. Eventually, the
mitral valve orifice narrows and progressively
obstructs blood flow into the ventricle.
PATHOPHYSIOLOGY
- The left atrium has great difficulty moving blood
into the ventricle because of the increased
resistance of the narrowed orifice.
- Poor left ventricular filling can cause decreased
cardiac output.
- The increased blood volume in the left atrium
causes it to dilate and hypertrophy.
- Because there is no valve to protect the
pulmonary veins from the backward flow of blood
from the atrium, the pulmonary circulation
becomes congested.
- As a result, the right ventricle must contract
against an abnormally high pulmonary arterial
pressure and is subjected to excessive strain.
Eventually, the right ventricle fails.
CLINICAL MANIFESTATIONS
- Dyspnea on exertion as a result of pulmonary
venous hypertension.
- Symptoms usually develop after the valve opening
is reduced by one-third to one-half its usual size.
- Fatigue as a result of low cardiac output.
- Dry cough or wheezing. Due to the enlarged left
atrium may create pressure on the left bronchial
tree.
- Patients may expectorate blood (ie, hemoptysis)
- Experience palpitations
- Orthopnea
- Paroxysmal nocturnal dyspnea (PND)
- Repeated respiratory infections.
ASSESSMENT AND DIAGNOSTIC FINDINGS
- Doppler echocardiography is used to diagnose
mitral stenosis.
- Electrocardiography (ECG) and cardiac
catheterization with angiography may be used to
help determine the severity of the mitral stenosis.
MEDICAL MANAGEMENT
in diastole for myocardial perfusion, and the
decreased blood flow into the coronary arteries.
- Blood pressure is usually normal but may be low.
Pulse pressure may be low (30 mm Hg or less)
because of diminished blood flow.

- Anticoagulants. To decrease the risk for

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

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