Professional Documents
Culture Documents
(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.
(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.
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.
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.
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
Dysrhythmias
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Decreased Cardiac Output
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Increased Cardiac Irritability
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Decreased Myocardial perfusion
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.
3. Cardioversion
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
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
Treatment
Oxygen Therapy
Digitalis, if uncontrolled fibrillation (rate is above 100 beats
per minute)
Quinidine
Beta adrenergic blockers
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 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
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
Antidysrhythmic Drugs
Class I
Fast (Sodium) Channel Blockers I
Disopyramide (Norpace)
Procainamide (Pronestyl)
Quinide Sulfate (Cardioquin)
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.
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.