CARDIAC CONDITIONS

Heart Failure Fluids limit

- adequacy of heart to pump throughout After lobe decrease
the body Test – digoxin level , abg , potassium level

Major cause S&S of worst HF

Left sided heart failure – Congestive heart - Rapid weight gain usually 3 pound per
failure week or 1-2 pounds within a night
- pulmonary congestion occurs when a - Decrease in exercise tolerance grasping 2
ventricle cannot fully pump out blood – 3 phase
throughout ventricle – Left ventricle pump - Cough that last 3 - 5 days
throughout circulation - Development of dyspnea or angina ( chest
- Ventricular Failure – pain ) at rest
- increase swelling in the 5th ankle and
Classification hands
Systolic HF ( contraction phase ) – reduce
ejection fraction – measurement of the Diagnostics
percentage giving to heart when - ANF ( atrial Nutri uretic factor )
contracting – Heart is unable to pump - BNP ( Brain natriuretic failure ) key
diagnosis of HR
Diastolic heart failure ( relaxation phase ) - Serum BUM and creatinine
- When left ventricle unable to relax during - Urinalysis
diastole - liver function test (asp , alp , direct
bilirubin, total bilirubin
Cause - ABG (for left sided HF )
Hypertension - ECG
Coronary heart disease - Hemodynamic monitoring – a screening
procedure either invasive or non invasive
Difference of Right HF and Left HF : (PAP, PWP)

Systemic congestion – right sided HF

AWHEAD Medical Management
Anorexia Basic lifestyle changes
Weight Gain ( restrict sodium intake )
Hepatomegaly (enlargement venous of - Avoid excessive alcohol intake , smoking ,
liver) and excessive fluid intake
Edema - weight reduction
Ascites - accumulation of fluid in abdominal - regular exercise
cavity
Distended neck Vein – Neck vain
engorgement Drug Therapy
- Anti hypertensive drugs ( ace inhibitors ,
beta blocker , Adrenergic blockers )
Pulmonary congestion – Left sided HF - Theoretics
UNLOADFATS - Digitalis
Upright position - Common for systolic HF ( ace - angiotensin
Nitrate administer converting enzyme - inhibitors ) promotes
Lasix vasodilation – reduces ejection to heart –
Oxygen promotes ventricular emptying
Ace Inhibitors - DRUGS THAT END TO PRIL –
Digoxin
 CARDIAC CONDITIONS
Nursing management for Ace inhibitor - Take note digitalis toxicity - Nausea and
- monitor for hypotension vomit, abdominal upset, HALO – Notify the
- monitor for hypovolemia Doctor

Side effect for Ace inhibitor Calcium Channel Blocker - promotes

- common – Dry persistent cough does that decrease contraction – common with
not respond to any cough medication tachycardia
Incase it arise – refer patient to doctor
- increases creatinine level / promote 3 generation of CCB
hyperkalemia ( excessive potassium ) 1st Drugs that ends with AMIL – DIPIN
Rifampin
* If incase patient cannot continue Ace Isoptin
inhibitor because dry persistent cough or Nifedipine – adalat – calciblock - immediate
creatinine increase , or potassium : Sub for : lowering of BP – round tablet ( blackish
gray plastic like , sublingual )
ARB ( angiotensin 2 receptor blockers ) Contraindicated with systolic disfunction
Action : drugs that ends WITH SARTAN
– Hydralazine (apresoline) Parenteral
Action : venous dilation – reduces amount Amlodipine
of blood that returns to heart Norvasc

SDN ( isosorbide nitrate – tablet isordil ) IV infusion

Nesiritide ( Natrecor ) ( BMP )
Beta Blockers – antihypertensive drugs Premacore – delays release calcium
- Drugs that ends with OLOL – intracellular reservoir
Diuretics – removes extracellular fluids Dobutamine ( Dobutrex ) – administered
3 types with left ventricular defunction or with
Thiazide – inhibits reabsorption decrease cardiac activity
Loop Acting
- Frequent ECG monitoring , vitals sign
Potassium sparing diuretic ( spironolactone
specially BP
– Aldactone ) – inhibits absorption
Nursing management for Diuretics Risk factors in Cardiac conditions
- Monitor cerume creatinine and potassium
Modifiable risk factors
level
- Check first the blood pressure ( 90/60 – You can change or alter the factors
below stop med )
1. Stress
Side effect
2. Diet – High fat/sodium diet
- hypotension
3. Exercise – Regularly 3 to 5x a week
- hyperuricemia – increase uric acid in blood 4. Cigarette smoking
- ototoxicity – harmful to ear -Nicotine
-Tar
Digitalis ( digoxin – lanoxin ) – regulate the -Carbon monoxide
pressure to myocardial – Systolic HF 5. Alcohol drinking
6. Hx of diabetes
Nursing management 7. Excessive lipids in the blood or
- Monitor the pulse rate first before giving cholesterol
med – 60 below do not give the medicine 8. Obesity
- Cerume potassium should be monitored – 9. Personality/Behavioral type
Type A: Lives in Sedentary lifestyle
because it also increase potassium in blood
10. Use of oral contraceptive meds
 CARDIAC CONDITIONS
1. Unstable angina
2. NS temi
Non modifiable risk factors 3. Stemi
1. Age above 40 y/o
2. Gender M: Before 65, W: After 65 Cause: Fatty buildup in the walls of the
coronary arteries
3. Race – African American
4. Heredity – Fam hx of 1st degree
Determinant of the type of ACS:
family
1. Location of the blockage
2. Length of the time (Blockage)
3. Amount of damage. Clot occurs
Major s/sx of Cardiac Conditions
S/SX:
1. Chest pain/discomfort
-Chest pain/discomfort, chest tightness
-Seen in pt c angina pectoris
(naninikip), chest fullness (Mabigat)
-Acute coronary syndrome -Pain/discomfort
-Dysrrhythmias -Dyspnea
-Valvular heart disease
2. Dyspnea - Valvular heart disease Different DX:
Dyspnea on exertion – Physical -Blood test – diff. blood enzyme test
activity -ECG
Orthopnea – Lying down
PND – Paroxismal nocturnal dyspnea Risk factors: ALL
– occurs at night or in the middle of
your sleep – Pulmonary congestion UNSTABLE ANGINA (Angina Ischemia)
-Sit upright and feet should dangle -Change from stable to unstable
-Cause: Insufficient blood flow to the
Dyspnea even at rest
myocardium
3. Peripheral edema – HF (Right sided)
-Chest pain even at rest
4. Palpitations – Tachycardia, coffee, -Occurs more frequently and more severe
tea, energy drinks, chocolates and last longer
5. Fatigue – resulting from an activity -May progress into MI (Heart attack)
Early indication: in women
6. Dizziness – Syncope – Loss of Risk Factors: Coronary disease, DM, Aortic
consciousness within a seconds – insufficient, sclerosis
Decrease perfusion to the brain
7. Extremity pain – Intermittent Precipitating factors:
claudication – moderate to severe -Physical exertion
pain in legs or buttocks related to -Strong emotions
walking – reduce arterial perfusion -After sexual intercourse
-Chronic smoking
Ischemia – adequate blood flow
-Consumption of heavy meal
-REST AND LOWERING THE LEGS
-Exposure to extremely cold weather
8. Weight gain – sudden wt gain 2 .2
pounds (1L) of excess water – Clinical Manifestations:
accomulation of excessive fluid -Chest pain: Transient, temporary,
-First indicator of edema proxismal, substernal, precordial, heaviness
or tightness, radiates to one or both arms,
jaw, neck, back or even the stomach
ACUTE CORONARY SYNDROME (ACS) precipitated by physical exertion at relieve
-Umbrella term by rest and nitroglycerine
-Suddenly blocks
 CARDIAC CONDITIONS
TYPES: -Adv to carry atleast 3 tablets of NGT to
-Stable angina patients with angina pectoris
Less than 15 minutes -Stored in a cool, dry place, use air tight
Recurrence is less frequent cover
-Change the stock q 6 mos
-Unstable angina (Pre infarction angina, -Observe s/sx: Headache, faintness,
Intermittent coronary syndrome) dizziness, tachycardia occurs in first few
Last than more than 15 minutes doses – normal -don’t discontinue the doses
More frequent
Occurs at night Beta – Adrinergic blockers – Decrease
And pain increases when it came back Myocardial oxygen demand
NR: Monitor the PR, if the pt is bradycardic
-Prinzmetal angina – discontinue, eat before administration
Occurs at rest
Attack early hour in the morning and occur Antihypertensive drugs
at rest – Coronary artery spasm Vasodilation effects

-Nocturnal Angina Anti platelet drugs – Aspirin

Occurs only at night Anticoagulants: Parenteral/oral administer
REM – Rapid eye movement concurrently (magkasabay)
Comadine or warfarin Sodium
-Angina Decubitus
Proxismal CP when sitting or standing Nursing Management in Heparin therapy:
Heparin prevents stable fibrin clot
-Intructable angina Effects is immediate - IV
Chronic and long duration Within 1 hour – SQ
Unresponsive to management Clotting time will return to normal
within 2 – 6hrs
-Post infarction angina
Occurs after MI, episodes of angina Nursing responsibility
Monitor of unexplained active bleeding,
hematuria, hematemesis, blood in the stool
-Give test dose of heparin, sensitivity
Angina Pectoris testing
DX: ECG, May reveal ST segment depression -Deep SQ: Do not massage/aspirate and
and T wave rotate to decrease irritation

Med management:
Night rates meds – Nitroglycerine NSTEMI
Vasodilators Non ST elevation MI
Typical ECG reading in MI patients
Nursing management NGT meds Blockage maybe partial or temporary
-pt should be sitting or supine position Damage is only small
-take a max of 3 doses at every 5 mins
interval, pag walang relief after 3 doses – STEMI
Stat intervention – MI ST elevation MI
-Gradual position change Block and prolonged blockage of blood
-Tingling sensation under the tounge supply
-effectiveness: 1 to 2 mins Causes changes in ECG and blood values
Sublingual NGT
-Offer sips of water before taking meds Causes
because it will dry the mouth - Fatty Build Up
-Avoid drinking alcohol Type of ACS
- Location
 CARDIAC CONDITIONS
- Length of time administered by IV – Thrombolitic therapy
- Amount of Damage that occurs (streptokinase) IV infusion or TPA
- administer within 3 – 6hrs after the initial
Signs and symptoms infarction
- assess for occult breathing
- Chest Pain/Discomfort/Tightness/Fullness
- Asses neurologic status of the patient
- Pain or discomfort
- Maintain patient position ( supine or flat on
- Dyspnea bed )
- administer after thrombolytic therapy and
Diagnostic test beta adrenergic blockers
- Blood Test - Cardiac monitoring
- ECG - PTCA
- Diet – Low salt and low cholesterol
- Pt should be in bed rest for first 48 hrs
- Progressive ambulation
Myocardial Infarction
Nursing management
Risk factors - Promote adequate cardiac output
- aterosclorosis - Ecg monitoring
- thrombus formation - Vital signs
- diabetes milletus - monitor effects of daily activity
- Promote rest and minimize unnecessary
Clinical manifestation disturbances without bathroom privelages
- Chest pain – Vice like (pinipiga) sudden onset - administer diazepam
and doesn’t relieve – often radiates – - Provide psychosocial support
characterized by levine sign - promote activity gradual increase after 48 hrs
- Anxiety and apprehension ( feeling of doom ) from bedrest to sitting up and dangling in bed
- Shock ( Systolic blood pressure of below observe then sit up in a chair then observe then
80mm and gray facial color ) stand up
- Lethargy - Promote comfort – Administer pain med
- Cold diapuresis - Promote elimination
- Peripheral cyanosis - Promote nutrtion – low calory
- Tachycardia or weak pulse - Avoid stimulants – very hot or cold foods
- Bradycardia - Food rich in caffeine
- Oliguria Urine flow of less than 30 ml per hr – - Avoid stimulating activity like valsava
indicates renal hypoxia due to inadequate renal maneuver
perfusion - Identify methods of coping
- Fever within 24 hrs occurs 3 to 7 days - Facilitate Learning
- Indingestion – accompanied by nausea and - Enroll patient in cardiac rehabilitation
vomiting Sexual Health Teaching
- Acute pulmonary edema – sense of suffocation - Less fatigue positioning ( traditional position )
- presence of gargling or bubbling of respiration - Non MI partner should take the active role
- ECG- ST elevation , T wave elevation , changes - Cool Familiar place
enlargement of Q waves - Take nitroglicerin before sexual activity
- Refrain sexual activity in fatigue day or
3 waves consuming a lot of food or drinking alcohol
Zone of infarction - If chest pain stop activity
Zone of injury - Advice patient develop other means of sexual
Zone of Ischemia expression
LADA – anterio left infarction
- Blood test of cardiac enzymes – elevated of CK Complication
(cardiac damage) - LDH – AST (SGOT) normal - Ventivcular Dyrthmea – premature ventricular
value 70 – 40 contraction ( PVC ) of 6 or mor min is life
threatening – Most COMMON
Nursing Management - Cardiogenic shock
- Give analgesic for chest pain ( Morphine - Thromboembolism
sulfate ) take note of vital signs – ( Lidocane)
numbs a certain area – Nitroglicerin parenteral
 CARDIAC CONDITIONS
Cardiac Dysrhythmias
are disorders of the formation or conduction (or
both) of the electrical impulse within the heart. b. Sinus Bradycardia
These disorders can cause disturbances of the Stimulates parasympathetic fibers
heart rate, the heart rhythm, or both. Vagal stimulations: delivering electrical
impulses to the vagus nerve that causes the
Identifying dysrhythmias Sinus node to slow down
 Sites of Origin *Normal variations in athletes
Sinus (SA) node >Rate of below 60 bpm
Atria
Atrioventricular (AV) node or junction
Ventricles Clinical Manifestations:
>Below 60 bpm c regular rhythm
 Mechanisms of Formation or >P Wave: PQRS is in normal contour
Conduction >Everything in ECG is normal
Normal (idio) rhythm =but have slow rate
Bradycardia T
achycardia Management:
Dysrhythmia >Administer Atropine Sulfate
Flutter -0.5 to 1mg IV Push
Fibrillation -This is to block the vagal stimulations
Premature complexes
Blocks Risk factors:
>Myocardial Infarction
>Meningitis
SINUS NODE DYSRHYTHMIAS: >Hyperthyroidism
a. Sinus Tachycardia
Stimulates sympathetic fibers Incase the AP is not effective
>Rate of 100-160 bpm -Administer Atropine Sulfate +
>PR; QRS is in normal contour isoproterenol injection via IV
>Normal ECG
=But have fast rhythm If ineffective again,
Pacemaker is advised
Common Cause:
 Fever Atrial dysrhythmias
 ECG is above cardiac rate
 Taking stimulants such as: Coffee, teas 1. Premature Atrial
and energy drinks Contractions (PAC)
 Excessive physical activities -a single ECG complex that occurs when
 Medical conditions: an electrical impulse starts in the atrium
-Hyperthyroidism before the next normal impulse of the
-Mycocardial ischemia sinus node.
-Anemic -Ectopic beat discharged at the
-Taking drugs such as: Epi and rate faster than the Sinus node
Theophylline *Does not require treatment

Nursing Management: If treatment is badly needed,

>Treat underlying cause/condition >Calcium channel blockers: This is a
>If the pt is taking stimulants: hypertensive c antidysrhthmias action
-Advise to limit the intake of stimulants >Kynedine

Medications:
-Prescribed Digitalis administration
2. Paroxysmal Atrial
-Isoprenaline, or isoproterenol Tachycardia
-Propranolol -Sudden onset
>This is to slow down the heart rate -Episode of arrhythmia begins and ends
abruptly
 CARDIAC CONDITIONS
>Range of 140-250 bpm  PR interval – Not measurable
Management: (0.08 secs) – too long/short
>Valsalva maneuver  PRS: Generally normal
- breathing method that may slow Management:
your heart when it's beating too fast. To do -Prescribed Digitalis administration
it, you breathe out strongly through your -Beta adrenergic Blockers
mouth while holding your nose tightly -Propranolol
closed. This creates a forceful strain that can >If ineffective, Cardioversion
trigger your heart to react and go back into
normal rhythm. VENTRICULAR DYSRHYTHMIAS:
>Digitalis administration
- Monitor the PR, if below 60, don’t administer 1. Premature Ventricular
>Beta adrenergic blockers Contraction (PVC)
- Hypertensive with anti dsyrhythmias -Most common dysrhythmias
>If not effective, do a Cardioversion -Lifethreatening
-Impulse that starts in a ventricle and is
Advise patient to stop conducted through the ventricles
 Smoking before the next normal sinus impulse.
 Drinking >6 or more per/min
 Taking stimulants (Caffeine)
How to define PVC:
-Ectopic beat originate in the ventricle
3. Atrial Flutter and then discharged by a faster than
- Atrial flutter occurs in the atrium and that by an occurring beat.
creates impulses at an atrial rate >PVC in bigenemy – 2 PVC/min
between 250- 400 bpm >PVC in trigeminy – 3 PVC/min
- Dysrhythmias in which an ectopic >PVC in quadrgeminy – 4 PVC/min
atrial focuses in the heart rhythm and
discharge in the pulses Causes of PVC:
 Hypokalemia
Management:  Electrolyte imbalances
>Digitalis  Digitalis theraphy
>Calcium Channel Blockers  Stimulants SA: Coffee and teas
>If ineffective, Cardioversion  Hypoxia
 Hx of Congestive Heart Failure
4. Atrial Fibrillation Clinical Manifestations:
- It may start and stop suddenly.
-Rate varies depends upon the patients
-Ectopic focus cause rapid irregular
-Irregular P wave Is normal
contractions of the heart above the
-PR not measurable
atrium
-QRS usually 0.12 seconds wide
>Rate of atrium 350-600 bpm
 Lidocaine IV:
>Rate of ventricular 100-160 bpm
75 to 100 mg (1-4 mg/min)
=Rhythm is regular
 Procainamide
300 mg IV
Causes:
 Kynedine
 Prematic Heart Disease
 Preprylliuf- Continous infusion
 Mitral Stenosis (Valvular HD)
 Treat the underlying cause
 Cardiomyopathy
 Hypertensive Heart Disease
 Pericarditis 2. Ventricular Tachycardia
 Thyrotoxicosis - Ventricular tachycardia (VT) is defined
 Coronary Heart Disease as three or more PVCs in a row,
occurring at a rate exceeding 100 beats
Clinical manifestations: per minute.
 Rate is faster >Rate 60-100 bpm (Atrial)
 P wave: No definite >Rate of 110-210 bpm (Ventricular)
>Rhythm: Regular in ventricular,
irregular in atrial
 CARDIAC CONDITIONS
>P wave: QRS complex: Not visible (Epinephrine depends on the extent of
>PR interval: Not Measurable the reviving) MAX: 1 ampule in 5 mins
> QRS: greater tha 0.12 seconds wide
VT is an emergency because the patient is
usually (although not always) unresponsive and CONDUCTION DEFECTS:
pulseless.
Heart Blocks: Altered at the level of
Causes of VT: AV Node
 Myocardial Infarction AV blocks occur when the conduction of
 Digitalis toxicity the impulse through the AV nodal area
 Coronary Artery Disease is decreased or stopped.
 Hypokalemia
1. 1st Degree AV Block
Clinical Manifestations: First-degree heart block occurs
>Lidocaine IV when all the atrial impulses are
50mg – 100mg (1-4mg/min) conducted through the AV node
>Procainamide IV into the ventricles at a rate slower
300 mg IV infusion than normal.
>If ineffective: >Pulse normally transmitted but
 Cardioversion may be the treatment of delayed in level of the AV node
choice, especially if the patient is >No treatment needed
 unstable. (Conscious)
 VT in a patient who is (unconscious) and
without a pulse is treated in the same
2. 2nd Degree AV Block
manner as ventricular fibrillation (VFIB): Some but not all of the impulses are
immediate defibrillation is the action of transmitted to the AV node
choice. >AV node – Conducted to the
ventriculation
This is a life threatening dysrhythmias >AV node: Selectively
-Emergency
Management:
-Requires treatment if ventricular
3. Ventricular Fibrillation rate becomes too low to maintain
-Most Severe effective cardiac output
-Dysrhythmias characterize by the
random chaotic discharging within
ventricular
3. 3rd Degree AV Block
-There is no atrial activity seen on the Third-degree heart block occurs
ECG. when no atrial impulse is conducted
through the AV node into the
Ventricular rate: Greater than 300/min ventricles.
Ventricular rhythm: Extremely irregular, >Cardiac output is compromised
without specific pattern >Administer Pacemaker
QRS shape and duration: Irregular,
undulating waves without recognizable
QRS complexes CARDIOVERSION &
Produces clinical death
DEFIBRILLATION
 Cardioversion (Conversion)
Clinical Manifestations - In cardioversion, the defibrillator is set to
>STAT Defib (200-400 joules/seconds) synchronize with the ECG on a cardiac
monitor so that the electrical impulse
Medications: discharges during ventricular depolarization
>Sodium Bicarbonate (QRS complex).
-This is to relieve lactic acidosis - Before cardioversion, the patient receives
>Before defib: intravenous sedation as well as an analgesic
-Push 0.1 of Epi medication or anesthesia.
To bring back the VS of the pt - The amount of voltage used varies from 25
to 150p joules, depending on the
 CARDIAC CONDITIONS
defibrillator’s technology and the type of time, ensure that you are not touching the
dysrhythmia patient, bed or equipment; as “Clear” is called
the second time, ensure that no one is touching
the bed, the patient, or equipment, including
 Defibrillation the endotracheal tube or adjuncts; and as
“Clear” is called the third time, perform a final
- used in emergency situations as the
visual check to ensure you and everyone else
treatment of choice for ventricular
are clear of the patient and anything touching
fibrillation and pulseless VT.
the patient.
- The electrical voltage required to
• Record the delivered energy and the results
defibrillate the heart is usually greater
(cardiac rhythm, pulse).
than that required for cardioversion. If
• After the event is complete, inspect the skin
three defibrillations of increasing
under the pads or paddles for burns; if any are
voltage have been unsuccessful,
detected, consult with the physician or a wound
cardiopulmonary resuscitation is
care nurse about treatment.
initiated and advanced life support
treatments are begun.
Nursing Management:
- The use of epinephrine or vasopressin
>Place patient in the flat firm surface
may make it easier to convert the
-Apply cardiac board on the patients bed
dysrhythmia to a normal rhythm with
-If none,place the pt to the floor
defibrillation. These drugs may also
>Apply interface material
increase cerebral and coronary artery
-Apply Lubricant to the paddles before
blood flow. After the medication is
Contacting the pt’s skin to prevent burning
administered and 1 minute of
The patient’s skin
cardiopulmonary resuscitation is
>Hold the handle of the paddle to prevent
performed, defibrillation is again
Electrocution
administered
>State clear, and make sure that all of the
- This treatment continues until a stable
people in the room are going to distance
rhythm resumes or until it is
themselves at the patient’s bed
determined that the patient cannot be
>Position the paddle:
revived.
-Right of the sternum (3rd ICS)
- -200-360 joules/sec
-Left mid axillary (5th ICS)
When performing defibrillation or
cardioversion, the nurse should remember Cardiopulmonary Resuscitation
these key points: -Usually perform in cardiopulmonary arrest
-Clinical death
• Use multifunction conductor pads or paddles -Pulselessness
with a conducting agent between the paddles -Breathlessness
and the skin (the conducting agent is available
as a sheet, gel, or paste). >Within 4-6 minutes after the onset of the
• Place paddles or pads so that they do not arrest – more than 6 mins indicates brain dead
touch the patient’s clothing or bed linen and are
not near medication patches or direct oxygen Basic Life Support (BLS)
flow. -Use of hands and mouth
• If cardioverting, ensure that the monitor leads -Sincere desire of giving the patient a 2 nd
are attached to the patient and that the chance of life
defibrillator is in sync mode. If defibrillating,
ensure that the defibrillator is not in sync mode Advanced Cardiac Life Support (ACLS)
(most machines default to the “not-sync” -Requires BLS
mode). -Use of advanced equipment
• Do not charge the device until ready to shock; -Emergency drug
then keep thumbs and fingers off the discharge -fluids
buttons until paddles or pads are on the chest >To stabilize the patient
and ready to deliver the electrical charge.
• Exert 20 to 25 pounds of pressure on the CPR performs ABCD:
paddles to ensure good skin contact.
• Before pressing the discharge button, call Airway
“Clear!” three times: As “Clear” is called the first Breathing
 CARDIAC CONDITIONS
Circulation  Provide psychosocial support
Definitive drugs -Concerns of the patient
-Coping mechanism
-Ensures pt’s comfort
When to stop CPR?  Maintain a positive body image
 When the client is revived  Provide health teaching:
 When EMS (Emergency Medical -Advise patient to take his/her pulse
Services) activated/arrived upon awakening for full minute
 If the rescuer/responder is exhausted -Report for any sudden change in the
 When the client is dead Pulse Rate, Any increasing indicates
malfunctions
-Report S/SX: Palpitations, Dizziness,
Pacemaker Insertion Chest pain, Dyspnea, prolong hiccups
-Advise to use Electrical device
- Electronic device that provides electrical
-If dizziness occurs, stops the device
stimuli to the heart muscle.
- Battery operated generator, time electric
Sources of Electromagnetic Inferences that
signals to trigger contractions of the heart
may effect the pulse generator:
muscle and controlling heart rate
 High energy radar
- Pacemakers can be permanent or temporary.
 Radiotransmitters
 Electrodevices
Temporary:
 Airport screening device
 CPR
 Antidepth device
 Open heart surgery
 Microwaves
 Sinus Arrest
 Complete heart block
*Distance yourself for about 5-10 feet
 Symptomatic sinus bradycardia
 Myocardial Infarction

Permanent:
 Irreversible complete heart block

2 techniques:

1. Transvenous (Endocardial)
-Cephalic vein (Along arm) or
externaljugular vein (Around neck)
-Endocardial transvenous technology
peripheral end is connected to the
pulse generator, implanted to the skin
to the R/L pectoral region
-Size of the box of cigarette

2. Transthoracic
-Surrounding the heart
-Open (Anterior chest) to the surface of
The R/L ventricle or atrium then
Treaded subcutaneous on the
abdominal wall above or below the
ambilitus (waist)

Nursing Management:
 Monitor the ECG and VS
 Observe the pacemaker malfunction: Pt
c dizziness, Chest pain, dyspnea,
prolong hiccups
 Practice sterile technique when
cleaning the incisions dressing to
prevent infection