Acute Coronary Syndrome (ACS)

 It occurs when ischemia is prolonged and not immediately

reversible.
 It encompasses the spectrum of unstable angina (UA), non-
ST-segment-elevation myocardial infarction (NSTEMI) and
ST-segment elevation myocardial infarction (STEMI).

Myocardial Infarction (MI)

 The formation of localized necrotic areas within the
myocardium. MI usually follows sudden coronary
occlusion and the abrupt cessation of blood and oxygen
flow to the heart muscle.

 Prolonged ischemia lasting more than 20 minutes

produces irreversible cellular damage and necrosis of the
myocardium. If ischemia persists, it takes approximately 4-
6 hours for the entire thickness of the heart muscle to
become necrosed.

 Ischemic Injury evolves over several hours toward

complete necrosis and infarction.

 Ischemia almost immediately alters the integrity and

permeability of the cell membrane to vital electrolytes,
thereby decreasing myocardial contractility.
 The autonomic nervous system attempts to compensate for
the depressed cardiac performance. This results to further
imbalance between myocardial oxygen supply and demand.

 MI almost always occurs in the left ventricle and often

significantly depresses left ventricular function. This is due
to occlusion of the LADA (left anterior descending artery).
This is referred to as anterior wall infarction.

 Alterations in function depend on the size and location of

an infarct.

 Contractile function in the necrotic area ceases

permanently.

 The 3 areas which develop in MI are as follows:

 Zone of infarction which records pathologic Q wave in

the ECG
 Zone of injury which gives rise to elevated ST
segment
 Zone of ischemia which produces inversion of T wave

 MI may be classified as follows:

 Transmural infarct, which extends from endocardium
to epicardium.
 Subendocardial infarct, which affects the endocardial
muscles.
  Intramural infarction, which is seen in patchy areas of
the myocardium and is usually associated with
longstanding angina pectoris.
 Healing requires formation of scar tissues that replace the
necrotic myocardial muscle; scar tissue inhibits
contractility.

Clinical Manifestations of Myocardial Infarction

 Pain
 Crushing, severe, prolonged, unrelieved by rest or
nitroglycerine; often radiating to one or both arms, the
neck and back.
 Characterized by “Levine’s sign” (chest hand-
clutching). This is the universal sign of distress in
angina pectoris and MI.
 Pathophysiologic Basis
 Cessation of blood supply to myocardium due to
thrombotic occlusion causes accumulation of
metabolites (e.g. lactic acid) within ischemic part
of myocardium. Lactic acid irritates nerve
endings, resulting to pain.

 Anxiety and Apprehension

 Feeling of “doom”, restlessness
 Pathophysiologic Basis:
  Severe pain of a heart attack is terrifying; most
clients are aware of the significance of a heart
attack; restlessness results from shock and pain.
 Shock
 This is manifested by systolic pressure below
80mmHg, gray facial color, lethargy, cold diaphoresis,
peripheral cyanosis, tachycardia/bradycardia, weak
pulse.
 Pathophysiologic Basis:
 This may be due to severe pain, severe reduction
in cardiac output and inadequate tissue perfusion,
thereby causing tissue hypoxia.
 Oliguria
 Urine flow of less than 30ml/hour.
 Pathophysiologic Basis:
 This indicates renal hypoxia due to inadequate
tissue perfusion.
 Fever
 Slight elevation of temperature occurs within 24 hours
and extends 3 to 7 days accompanied by leukocytosis
and elevated ESR.
 Pathophysiologic Basis
 Fever and leukocytosis result from destruction of
myocardial tissue and ensuing inflammatory
process.
 “Indigestion,” “Gas pains around the heart,” nausea
and vomiting.
 Pathophysiologic Basis:
  Client may prefer to believe that pain is cause by
“gas” or “indigestion” rather than by heart
disease; nausea and vomiting may result from
severe pain or from vasovagal reflexes conducted
from an area of damaged myocardium to
gastrointestinal tract.

 Acute Pulmonary Edema

 Sense of suffocation, dyspnea, orthopnea, gurgling/
bubbling respiration.
 Pathophysiologic Basis:
 Left ventricle becomes severely weakened in
pumping action owing to infarction; severe
pulmonary congestion results.
 ECG Changes
 MI causes elevation of ST segment, inversion of T
wave and enlargement of Q wave.
 Pathophysiologic Basis
 Pathologic Q wave develops from the area of
infarction; elevated ST segment results from the
area of injury; and inverted T wave originates
from the zone of ischemia.
 Elevation of ST segment heralds a pattern of
injury and usually occurs as an initial ECG
change in acute MI.

 Elevated CK-MB, elevated LDH, elevated AST

 Pathophysiolologic Basis
 These cardiac enzymes are produced in abnormally large
amounts because of cellular damage and death.
 CK-MB is the most cardiac-specific enzyme.
Elevated CK-MB in the presence of increased levels of LDH
strongly supports presence of MI.

 Elevated Troponin Levels. These are the most definitive

laboratory findings in MI.
 Troponin I 1.5ng/mL; Troponin T: above ng/ml

Interprofessional Collaborative Management for the

Patients with Myocardial Infarction

(1) Medications
 Analgesic
 For relief of pain. This is a priority.
 Morphine Sulfate, Lidocaine or Nitroglycerine are
administered intravenously. The drug of choice is Morphine.

 Thrombolytic Therapy
 To disintegrate blood clot by activating the fibrinolytic
processes.
 Streptokinase, urokinase and tissue plasminogen activator
(TPA) are currently used.
 Administration of thrombolytic is most crucial between 3 to 6
hours after the initial infarction has occurred.
 Detect for occult bleeding during and after thrombolytic
therapy.
 Assess neurologic status changes which may indicate G.I.
bleeding or cardiac tamponade.
 The effectiveness of the medication is evidenced by absence
of chest pain. Absence of blood clots improves blood flow
and oxygen supply to the myocardium.

 Anticoagulant and antiplatelet medications are

administered after thrombolytic therapy to maintain arterial
patency.
 Other medications: Beta-adrenergic blocking agents;
diazepam (Valium)

(2) Treatment

 Goals
 Prevention of further tissue injury and limitation of infarct
size.
 Maximize myocardial tissue perfusion and reduce myocardial
tissue demands.
 Supplemental oxygen by nasal cannula. This increases
oxygen supply. Nasal cannula does not intensify feeling of
suffocation in the client with MI.
 Cardiac monitoring to detect occurrence of dysrhythmias.
 Percutaneous transluminal coronary angioplasty (PTCA) may
be done to reopen an occluded artery.
 Diet: low-cholesterol, low-salt as prescribed.
 Activity: Bed rest is usually prescribed for 24 to 48 hours to
decrease oxygen demand. Progressive ambulation is
 implemented as soon as possible, unless complications
occurred.

(3) Nursing Interventions

 Promoting Oxygenation and Tissue Perfusion

 Instruct the patient to avoid overfatigue; stop activity
immediately in the presence of chest pain, dyspnea,
lightheadedness or faintness.
 Oxygen therapy by cannula for the first 24-48 hours or
longer if pain, hypotension, dyspnea or dysrhythmias
persist. Monitor VS changes, indicative of complications.
 Position the client in semi-Fowler’s position to allow greater
diaphragm expansion, thereby lung expansion and better
carbon dioxide-oxygen exchange.

 Promoting Adequate Cardiac Output

 Monitor the following parameters:
 Dysrhythmias on ECG changes
 VS (Vital Signs)
 Effects of daily activities on cardiac status
 Rate and rhythm of pulse

 Administer pharmacotherapy as prescribed.

 Promote rest and minimize unnecessary disturbances.

 Promoting Comfort
 Relieve pain. Administering Morphine sulfate as ordered.
This is to decrease sympathetic stimulation, which increases
 myocardial oxygen demand. In addition, this will prevent
shock which may result from severe pain.

 Providing rest
 The patient is usually placed on bed rest with commode
privileges for 24 to 48 hours.
 Administer diazepam (valium) as ordered.
 Explain that the purpose of CCU (Coronary Care Unit is for
continuous monitoring and safety during the recovery period.
 Provide psychosocial support to the client and his family.
Calmness and competency are extremely reassuring.

 Promoting Activity
 Gradual increase in activity is encouraged. After the first 24
to 48 hours, the client may be allowed to sit on a chair for
increasing periods of time and begins ambulation on the 4 th or
5th day.
 Monitor for signs of dysrhythmias, chest pain, and changes in
VS during activity.

 Promoting Nutrition and Elimination

 Provide small, frequent feedings.
 Provide low-calorie, low-cholesterol, low-sodium diet.
 Avoid stimulants.
 Avoid taking very hot or very cold foods. Vasovagal
stimulation may occur. This may lead to bradycardia and
cardiac arrest.
 Use of bedpan and straining at stool should be avoided.
Valsalva maneuver causes changes in blood pressure and
 heart rate, which may trigger ischemia, dysrhythmias,
pulmonary embolism or cardiac arrest.
 Use bedside commode.
 Administer stool softener as ordered, e.g. sodium doccusate
(Colace), senna (Senokot)

 Promoting Relief of Anxiety and Feeling of Well-Being

 Provide an opportunity for the client and family to explore
their concerns and to identify alternative methods of coping
as necessary.

 Facilitating Learning
 Teaching is started once the client is free of pain and
excessive anxiety.
 Promote a positive attitude and active participation of the
client and the family.

Cardiac Rehabilitation
 Is a process by which a person is restored to health and
maintains optimal physiologic, psychosocial, vocational and
recreational functions.
 It begins the moment a client is admitted to the hospital for
emergency care, it continues for months and even years after
the client is discharged from the health care facility.
 Goals of Rehabilitation
 To live as full, vital and productive a life as possible.
 Remain within the limits of the heart;s ability to respond to
activity and stress.
 Progressive Activity
 Activity progression is based on the metabolic equivalent of
the task (MET), the energy expenditure for various activities.
 In the hospital, exercise may be gradually implemented as
follows:
 Lying or sitting exercises (arms, legs and trunk) then
exercises progress to standing and slow walking in the hall.
(VS and heart rhythms are constantly monitored).
 An exercise is terminated if any of the following occurs:
cyanosis, cold sweats, faintness, extreme fatigue, severe
dyspnea, pallor, chest pain, PR more than 100 beats/min.,
dysrhythmias, BP greater than 160/95mmHg.
 Exercise must be done twice a day for about 20 minutes.
 Exercise provides the client a positive sign of progress and
recovery, a sense of control over their bodies, and tends to
decrease anxiety and depression during the recovery period.
 Home exercise program includes 2 to 12 week structured
walking program.
 Physical Activity Guidelines After Acute Coronary Syndrome
(F-I-T-T)
 Warm up/cool down
 Mild stretching for 3-5 minutes before the physical activity
and 5 minutes after the physical activity is important. Activity
shild not be started or stopped abruptly.
 F- Frequency
 The patient should perform physical activity 5 or more times
a week.
 I- ntensity
 Activity Intensity should be determined by the patient’s HR.
The person recovering from MI should not exceed 20
beats/min over the resting HR.

 T-ypes of Physical Activity

 Physical activity should be regular, rhythmic and repetitive,
using large muscles to build up endurance (walking, cycling,
swimming, rowing)
 T-ime
 Physical activity can be from 30 to 60 minutes. It is important
to begin slowly at personal tolerance (perhaps only 5 to 10
minutes) and build up to 30 minutes.

Teaching and Counseling

 Self-management Education Guide: Discharge after MI
 Discontinue smoking
 Control hypertension with continued medical supervision
 Eat a diet low in calories, saturated fats and cholesterol;
decrease in salt intake.
 Participate in weight reduction program.
 Progressive exercise based on discahrge MET level under
medical supervision
 Take prescribed medications at regular basis
 Resumption of sexual activity after 4 to 6 weeks from
discharge, if appropriate. Or when the client withn
uncomplicated MI (no dysrhythmias, shock or CHF) is
capable of walking one to flight of stair without difficulty.
 Stress Management techniques.
 Return to usual home activities, relationships and to work at
earliest opportunity would be beneficial.

 Teaching Guide on Resumption of Sexual Activity

 Assume less fatiguing position. Let the couple decide on their
less fatiguing position.
 The non-MI partner takes the active role.
 Perform sexual activity in a cool, familiar environment
 Take nitroglycerine before sexual activity.
 Refrain from sexual activity during a fatiguing day, after
eating a large meal, after drinking alcohol.
 If dyspnea, chest pain, dizziness or palpitations occur,
moderation should be observed; if symptoms persist, stop
sexual activity.
 Develop other means of sexual expression.

Complications of MI
 Dysrhythmias
 Cardiogenic shock
 Thromboembolism
 Pericarditis (Dressler’s Syndrome)
 Rupture of the myocardium
 Ventricular aneurysm
 Congestive Heart Failure

Dysrhythmias
 Abnormal cardiac rhythms which are due to the ff:
 Tissue ischemia
 Hypoxemia
 SNS and PNS influences
 Lactic Acidosis
 Hemodynamic abnormalities
 Drug toxicity
 Electrolyte imbalances

 These are due to abnormal automaticity, abnormal conduction

or both.
 The most common complication and most major cause of
death among clients with MI.
 The most common dysrhythmia in MI is premature
ventricular contraction (PVC’s)/ectopic beats
 PVC’s of 6 or more per minute is life threatening.

Pathophysiology of Premature Ventricular Contractions

Premature Ventricular Contractions

|
Ventricular Fibrillations
|
Cardiac Standstill/Arrest

Dysrhythmias
|
Decreased Cardiac Output
|
 Increased Cardiac Irritability
|
Decreased Myocardial perfusion

Common Dysrhythmias After MI

 Sinus
 Sinus Tachycardia
 Sinus Bradycardia
 Sinus Dysrhythmia
 Sick Sinus Syndrome

 Atrial
 Premature atrial contraction
 Paroxysmal atrial tachycardia
 Atrial flutter
 Atrial fibrillation

 Ventricular
 Premature ventricular contractions
 Ventricular bigeminy
 Ventricular fibrillation

 Conductive defects
 First degree AV block
 Second degree AV block
 Third degree block
Sinus Dysrhythmias
 Sinus tachycardia- is a dysrhythmia that where the heart rate
exceeds 100 beats per minute and regular.

 Etiology:
 The sympathetic fibers are stimulated thereb, speeding up
excitation of the SA node.
 Treatment
 Digitalis administration
 Treat underlying cause (fever, shock, electrolyte disturbances
etc.

 Supraventricular Tachycardia (SVT)

 Foci are above the ventricles
 Heart rate is above 150 beats/min.
 Treatment:
1. Vagal stimulation
2. Adenosine 6mg in 1 to 2 secs.; if no change, repeat 12
mg. in 1 to 3 secs.; then repeat 12 mg. again in 1 to 2 secs.
 It causes sinus pause/asystole then, the heart starts to beat

3. Cardioversion

Drug Alert: Adenosine (Adenocard)

- Observe patient for flushing, dizziness, chest pain or
palpitations
 Sinus bradycardia is a dysrhythmia where the heart rate
falls below 60 beats per minute.

 Etiology
 The parasympathetic fibers (vagal tone) are stimulated and
cause the sinus node to slow.
 Treatment
 Atropine to mg/ IV push to block vagal stimulation
 Isoproterenol 1mg/ 500ml D5W to stimulate sympathetic
response
 Pacemaker insertion

 Sinus arrythmia is a regular irregularity in rhythm which is

related to respiratory exchange. No treatment is necessary.

 Sick Sinus Syndrome is a dysrhythmia that is caused by a

diseased sinus node. The sinus node conducts at a slow rate
or may fail to conduct at all, producing sinus block or pauses.
There is related tachycardia, thus it is called “brady-
tachycardia syndrome”

 Treatment
 Treatment of ischemia due to arteriosclerotic heart disease,
MI
 Pacemaker insertion

Atrial Dysrhythmias
 Premature Atrial Contraction (PAC) is an ectopic beat that
originates in the atria and is discharged at a rate faster than
that of sinus node.

 Treatment
 Generally, PAC does not require treatment
 Quinidine or calcium-channel blocker may be prescribed if
PAC increases in frequency
 Paroxysmal Atrial Tachycardia (PAT) is a sudden onset of
an atrial tachycardia with rates that vary between 140 and 250
beats per minute.
 Treatment
 Valsalva maneuver to reduce the heart rate through vagal
stimulation
 Digitalis
 Beta adrenergic blockers (Propranolol)
 Calcium-channel blockers (Diltiazem)
 Cardioversion
 Morphine sulfate, Diazepam
*Avoid excess use of alcohol, cigarettes, caffeine

 Atrial Flutter is a dysrhythmia in which an ectopic atrial

focus captures the heart rhythm and discharges impulses at a
rate of between 200 and 400 times per minute. In ECg
complexes, the p-waves are saw-toothed.
 Treatment:
 Oxygen therapy
 Digitalis preparation
 Quinidine
 Beta-adrenergic blockers
 Cardioversion

 Atrial Fibrillation is a dysrhythmia that is caused by the

rapid and chaotic firing of atrial impulses by a multitude of
foci. In ECG complexes, there are no discernible p-waves.

 Treatment
 Oxygen Therapy
 Digitalis, if uncontrolled fibrillation (rate is above 100 beats
per minute)
 Quinidine
 Beta adrenergic blockers

(Atrial Flutter and Atrial Fibrillation may cause

thromboembolism due to blood stasis in the chambers of the
heart)

Ventricular Dysrhythmias
 Premature Ventricular Contraction (PVC) is a
dysrhythmia that is produced by an ectopic beat originating in
a ventricle and being discharged at a rate faster than that of
the next normally occurring beat. PVC’s of 6/minute or
more is life threatening.

 Treatment
 Lidocaine/ IV push, drip
 Initial bolus dose: 75-100 mg then 50-100mg within 10-15
min. As needed
 Continuous IV drip in D5W 4:1 concentration
 Procainamide IV push, drip bolus dose: 300mg
 Bretylium continuous infusion if Lidocaine and
Procainamide are ineffective.

 Ventricular Bigeminy is a PVC where every other beat is a

ventricular complex.
 Treatment
Refer to PVC

 Ventricular Tachycardia
is a life threatening dysrhythmia that originates from an
irritable focus within the ventricle or more. A run of 3 PVC’s
occurs. It is an ineffective rhythm for maintaining cardiac
output. It is an emergency.

 Treatment
 Epinephrine 1mg/IV every 3 to 5 minutes or
Vasopressin 40 units/IV;
Amniodarone 300mg/IV push, then 150mg/IV push in 3 to
5 minutes
Lidocaine 1 to 1.5 mg/kg, then 0.5 to 0.75 mg/kg., total of
3mg/kg

 Defibrillation, if loss of consciousness occurs

 Cardioversion if conscious
 Sodium bicarbonate is admnistered to relieved lactic
acidosis.

 Ventricular Fibrillation is a dysrhythmia that is

characterized by the random and chaotic discharging of
impulses within the ventricle at rates that exceed 300 beats
per minute. It produces clinical death and must be reversed
immediately. It is an emergency.
 Treatment
 Immediate defibrillation; use 200-360 watt/sec (joules)
 Na Bicarbonate to relieve lactic acidosis, which causes
unsuccessful defibrillation
 Epinephrine. 1 mg/IV push (10ml) as bolus; repeat every 3
to 5 minutes in cardiac arrest as ordered.

Conduction Defects/Heart Blocks/AV Blocks

 Conduction is altered at the level of the AV node

1. First Degree AV block- the impulse is transmitted

normally, but it is delayed longer at the level of the AV
node.
2. Second Degree AV block- some, but not all of the
impulses are transmitted. The AV node becomes selective
about which impulses are conducted to the ventricles.
3. Third Degree AV block- no impulse from the SA node
is transmitted by the AV node

Treatment of AV Blocks
 First degree AV block requires no treatment
 Second degree AV block requires treatment if the ventricular
rate falls too low to maintain effective cardiac output.
 Third degree AV block requires treatment if cardiac output
is compromised.
*Treatment of choice: Ventricular Pacemaker

Summary of Therapeutic Modalities for Dysrhythmias

 Antidysrhythmic Drugs
 Artificial Cardiac Pacemaker
 Cardioversion/Defibrillation
 Cardiopulmonary Resuscitation

Antidysrhythmic Drugs
 Class I
 Fast (Sodium) Channel Blockers I
 Disopyramide (Norpace)
 Procainamide (Pronestyl)
 Quinide Sulfate (Cardioquin)

 Fast (Sodium) Channel Blockers II

 Lidocaine (Xylocaine)
 Mexilitine Hcl (Mexitil)

 Class II
 Beta-adrenergic Blockers
 Acebutolol HCL (Sectral)
 Propranolol (Inderal)

 Class III
 Prolong repolarization
 Adenosine (Adenocard)
 Amiodarone (Cardarone)
 Bretylium Tosylate (Bretylol)

 Class IV
 Calcium Channel Blockers
 Verapamil HCL (Calan)
 Diltiazem (Cardizem)

 Others
 Phenytoin (Dilantin)
 Digoxin (Lanoxin)

Cardiac Pacemaker
 Is an electronic device that delivers direct stimulation to the
heart, causing electrical depolarization and cardiac
contraction.
 The pacemaker initiates and maintains the heart rate when the
natural pacemakers of the heart are unable to do so.

Clinical Indications
 Symptomatic bradyarrhythmias
 Sinoatrial bradyarrhythmias
 Sinoatrial arrest
 Sick sinus syndrome
 Heart block
 Second degree heart block
 Complete heart block

 Prophylaxis
 Following acute MI; arrhythmias and conduction defects
 Before or following cardiac surgery
 During coronary arteriography
 Before permanent pacing

 Tachyarrythmias
 Supraventricular
 Ventricular

Pace Modes
 Demand rate (synchronous; non-competitive)
atrial/ventricular
 It triggers electrical firings only when the heart rate goes
slow.
 It does not compete with the heart’s basic rhythm.
 If the client’s heart rate falls below a predetermined escape
interval (programmed into pulse generator), an electrical
stimulus is delivered to the heart.

 Fixed rate (asynchronous, competitive) atrial/ventricular

 It delivers an electrical stimulus at a preset constant rate that
is independent of the patient’s own rhythm.
 Does not allow atrial contribution to the cardiac output. May
be valuable in complete heart block.

 Synchronous Atrial/Ventricular (Dual chamber pacemaker)

 A demand form of pacing which is able to increase heart rate
to accompany the physiological demands of the body.
 An actual electrode senses the patient’s atrial depolarization,
waits for a preset interval (simulated PR interval) and triggers
firing of ventricular pacer.
 If rapid atrial rhythm occurs, the ventricular pacemaker
stimulates the ventricle at a fixed rate independent of atrial
activity.

Temporary Pacemakers
 Temporary pacing of the heart is usually done as an
emergency procedure that allows observation of the effects of
pacing on heart function before a permanent pacemaker is
implanted.
 Transvenous approach to position the electorde in the apex of
right ventricle is done.
 The external pulse generator is attached to the patient.

Permanent Pacemakers
 Permanent pacing of the heart may be implanted through the
following techniques:

 Transvenous (endocardial)
 The electrode is threaded through cephalic or external jugular
vein into the right ventricle. This is done under local
anesthesia.
 The peripheral end of the electrode is connected to the pulse
generator which is implanted underneath the skin below the
right or left pectoral region.

 Transthoracic (Epicardial)
 Anterior chest is open and electrodes are sutured to the
surface of the right or left ventricle or atrium, then threaded
subcutaneously to the abdominal wall either above or below
waist.

*Note: Paced beats are characterized by sharp spikes that

preceed each ECG complex.

Nursing Interventions for clients with Artificial Cardiac

Pacemakers

 Monitor ECG following implantation of pacemaker,

including VS
 Observe for indications of pacemaker malfunction like
dizziness, faintness, lightheadedness, chest pain, shortness of
breath, prolonged hiccups.
 Make sure all equipment in the client’s unit are grounded, to
prevent ventricular fibrillation. (use 3-pronged plugs).
 Practice sterile technique for dressing changes to prevent
wound infection.
 Provide psychosocial support:
 Explore concerns of the client
 Encourage to utilize coping mechanisms
 Ensure client comfort
 Maintain a positive body image
 Provide client education which includes the following:
 Take daily pulse for one full minute.
 Report any sudden slowing of pulse greater than 4 to 5 beats
per minute or any increase in pulse rate
 The best time to take the daily pulse is in the morning upon
awakening.
 Report signs and symptoms of dizziness, fainting,
palpitations, prolonged hiccups and chest pain to the
physician (indicative of pacemaker failure)
 May use electrical devices with caution.
 If dizziness occurs, stop using the device.
 Sources of electromagnetic inference (EMI) that may affect
some pulse generators as follows:
*High-energy radar
*TV and radio transmitters
* Electrocautery machines
*airport screening devices
*antitheft devices (inform the security guard on
presence of pacemaker)
 Move 5 to 10 feet away from the source of EMI if dizziness
occurs.