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
failure
- pulmonary congestion occurs when a
ventricle cannot fully pump out blood
throughout ventricle – Left ventricle pump
throughout circulation
- Ventricular Failure –
Classification
Systolic HF ( contraction phase ) – reduce
ejection fraction – measurement of the
percentage giving to heart when
contracting – Heart is unable to pump
Diastolic heart failure ( relaxation phase )
- When left ventricle unable to relax during
diastole
Cause
Hypertension
Coronary heart disease
Difference of Right HF and Left HF :
- Rapid weight gain usually 3 pound per
week or 1-2 pounds within a night
- Decrease in exercise tolerance grasping 2
– 3 phase
- Cough that last 3 - 5 days
- Development of dyspnea or angina ( chest
pain ) at rest
- increase swelling in the 5th ankle and
hands
Diagnostics
- ANF ( atrial Nutri uretic factor )
- BNP ( Brain natriuretic failure ) key
diagnosis of HR
- Serum BUM and creatinine
- Urinalysis
- liver function test (asp , alp , direct
bilirubin, total bilirubin
- ABG (for left sided HF )
- ECG
- Hemodynamic monitoring – a screening
procedure either invasive or non invasive
(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
- monitor for hypotension
- monitor for hypovolemia
Side effect for Ace inhibitor
- common – Dry persistent cough does that
not respond to any cough medication
Incase it arise – refer patient to doctor
- increases creatinine level / promote
hyperkalemia ( excessive potassium )
* If incase patient cannot continue Ace
inhibitor because dry persistent cough or
creatinine increase , or potassium : Sub for :
ARB ( angiotensin 2 receptor blockers )
Action : drugs that ends WITH SARTAN
– Hydralazine (apresoline)
Action : venous dilation – reduces amount
of blood that returns to heart
SDN ( isosorbide nitrate – tablet isordil )
Beta Blockers – antihypertensive drugs
- Drugs that ends with OLOL –
Diuretics – removes extracellular fluids
3 types
Thiazide – inhibits reabsorption
Loop Acting
Potassium sparing diuretic ( spironolactone
– Aldactone ) – inhibits absorption
Nursing management for Diuretics
- Monitor cerume creatinine and potassium
level
- Check first the blood pressure ( 90/60 –
below stop med )
Side effect
- hypotension
- hyperuricemia – increase uric acid in blood
- ototoxicity – harmful to ear
Digitalis ( digoxin – lanoxin ) – regulate the
pressure to myocardial – Systolic HF
Nursing management
- Monitor the pulse rate first before giving
med – 60 below do not give the medicine
- Cerume potassium should be monitored –
because it also increase potassium in blood
- Take note digitalis toxicity - Nausea and
vomit, abdominal upset, HALO – Notify the
Doctor
Calcium Channel Blocker - promotes
decrease contraction – common with
tachycardia
3 generation of CCB
1st Drugs that ends with AMIL – DIPIN
Rifampin
Isoptin
Nifedipine – adalat – calciblock - immediate
lowering of BP – round tablet ( blackish
gray plastic like , sublingual )
Contraindicated with systolic disfunction
Parenteral
Amlodipine
Norvasc
IV infusion
Nesiritide ( Natrecor ) ( BMP )
Premacore – delays release calcium
intracellular reservoir
Dobutamine ( Dobutrex ) – administered
with left ventricular defunction or with
decrease cardiac activity
- Frequent ECG monitoring , vitals sign
specially BP
Risk factors in Cardiac conditions
Modifiable risk factors
You can change or alter the factors
1. Stress
2. Diet – High fat/sodium diet
3. Exercise – Regularly 3 to 5x a week
4. Cigarette smoking
-Nicotine
-Tar
-Carbon monoxide
5. Alcohol drinking
6. Hx of diabetes
7. Excessive lipids in the blood or
cholesterol
8. Obesity
9. Personality/Behavioral type
Type A: Lives in Sedentary lifestyle
10. Use of oral contraceptive meds
 CARDIAC CONDITIONS
Non modifiable risk factors
1. Age above 40 y/o
2. Gender M: Before 65, W: After 65
3. Race – African American
4. Heredity – Fam hx of 1st degree
family
Major s/sx of Cardiac Conditions
1. Chest pain/discomfort
-Seen in pt c angina pectoris
-Acute coronary syndrome
-Dysrrhythmias
-Valvular heart disease
2. Dyspnea - Valvular heart disease
Dyspnea on exertion – Physical
activity
Orthopnea – Lying down
PND – Paroxismal nocturnal dyspnea
– occurs at night or in the middle of
your sleep – Pulmonary congestion
-Sit upright and feet should dangle
Dyspnea even at rest
3. Peripheral edema – HF (Right sided)
4. Palpitations – Tachycardia, coffee,
tea, energy drinks, chocolates
5. Fatigue – resulting from an activity
Early indication: in women
6. Dizziness – Syncope – Loss of
consciousness within a seconds –
Decrease perfusion to the brain
7. Extremity pain – Intermittent
claudication – moderate to severe
pain in legs or buttocks related to
walking – reduce arterial perfusion
Ischemia – adequate blood flow
-REST AND LOWERING THE LEGS
8. Weight gain – sudden wt gain 2 .2
pounds (1L) of excess water –
accomulation of excessive fluid
-First indicator of edema
ACUTE CORONARY SYNDROME (ACS)
-Umbrella term
-Suddenly blocks
1. Unstable angina
2. NS temi
3. Stemi
Cause: Fatty buildup in the walls of the
coronary arteries
Determinant of the type of ACS:
1. Location of the blockage
2. Length of the time (Blockage)
3. Amount of damage. Clot occurs
S/SX:
-Chest pain/discomfort, chest tightness
(naninikip), chest fullness (Mabigat)
-Pain/discomfort
-Dyspnea
Different DX:
-Blood test – diff. blood enzyme test
-ECG
Risk factors: ALL
UNSTABLE ANGINA (Angina Ischemia)
-Change from stable to unstable
-Cause: Insufficient blood flow to the
myocardium
-Chest pain even at rest
-Occurs more frequently and more severe
and last longer
-May progress into MI (Heart attack)
Risk Factors: Coronary disease, DM, Aortic
insufficient, sclerosis
Precipitating factors:
-Physical exertion
-Strong emotions
-After sexual intercourse
-Chronic smoking
-Consumption of heavy meal
-Exposure to extremely cold weather
Clinical Manifestations:
-Chest pain: Transient, temporary,
proxismal, substernal, precordial, heaviness
or tightness, radiates to one or both arms,
jaw, neck, back or even the stomach
precipitated by physical exertion at relieve
by rest and nitroglycerine
 CARDIAC CONDITIONS
TYPES:
-Stable angina
Less than 15 minutes
Recurrence is less frequent
-Unstable angina (Pre infarction angina,
Intermittent coronary syndrome)
Last than more than 15 minutes
More frequent
Occurs at night
And pain increases when it came back
-Prinzmetal angina
Occurs at rest
Attack early hour in the morning and occur
at rest – Coronary artery spasm
-Nocturnal Angina
Occurs only at night
REM – Rapid eye movement
-Angina Decubitus
Proxismal CP when sitting or standing
-Intructable angina
Chronic and long duration
Unresponsive to management
-Post infarction angina
Occurs after MI, episodes of angina
Angina Pectoris
DX: ECG, May reveal ST segment depression
and T wave
Med management:
Night rates meds – Nitroglycerine
Vasodilators
Nursing management NGT meds
-pt should be sitting or supine position
-take a max of 3 doses at every 5 mins
interval, pag walang relief after 3 doses –
Stat intervention – MI
-Gradual position change
-Tingling sensation under the tounge
-effectiveness: 1 to 2 mins
Sublingual NGT
-Offer sips of water before taking meds
because it will dry the mouth
-Avoid drinking alcohol
-Adv to carry atleast 3 tablets of NGT to
patients with angina pectoris
-Stored in a cool, dry place, use air tight
cover
-Change the stock q 6 mos
-Observe s/sx: Headache, faintness,
dizziness, tachycardia occurs in first few
doses – normal -don’t discontinue the doses
Beta – Adrinergic blockers – Decrease
Myocardial oxygen demand
NR: Monitor the PR, if the pt is bradycardic
– discontinue, eat before administration
Antihypertensive drugs
Vasodilation effects
Anti platelet drugs – Aspirin
Anticoagulants: Parenteral/oral administer
concurrently (magkasabay)
Comadine or warfarin Sodium
Nursing Management in Heparin therapy:
Heparin prevents stable fibrin clot
Effects is immediate - IV
Within 1 hour – SQ
Clotting time will return to normal
within 2 – 6hrs
Nursing responsibility
Monitor of unexplained active bleeding,
hematuria, hematemesis, blood in the stool
-Give test dose of heparin, sensitivity
testing
-Deep SQ: Do not massage/aspirate and
rotate to decrease irritation
NSTEMI
Non ST elevation MI
Typical ECG reading in MI patients
Blockage maybe partial or temporary
Damage is only small
STEMI
ST elevation MI
Block and prolonged blockage of blood
supply
Causes changes in ECG and blood values
Causes
- Fatty Build Up
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
Management:
>Valsalva maneuver
- breathing method that may slow
your heart when it's beating too fast. To do
it, you breathe out strongly through your
mouth while holding your nose tightly
closed. This creates a forceful strain that can
trigger your heart to react and go back into
normal rhythm.
>Digitalis administration
- Monitor the PR, if below 60, don’t administer
>Beta adrenergic blockers
- Hypertensive with anti dsyrhythmias
>If not effective, do a Cardioversion
Advise patient to stop
 Smoking
 Drinking
 Taking stimulants (Caffeine)
3. Atrial Flutter
- Atrial flutter occurs in the atrium and
creates impulses at an atrial rate
between 250- 400 bpm
- Dysrhythmias in which an ectopic
atrial focuses in the heart rhythm and
discharge in the pulses
Management:
>Digitalis
>Calcium Channel Blockers
>If ineffective, Cardioversion
4. Atrial Fibrillation
- It may start and stop suddenly.
-Ectopic focus cause rapid irregular
contractions of the heart above the
atrium
>Rate of atrium 350-600 bpm
>Rate of ventricular 100-160 bpm
=Rhythm is regular
Causes:
 Prematic Heart Disease
 Mitral Stenosis (Valvular HD)
 Cardiomyopathy
 Hypertensive Heart Disease
 Pericarditis
 Thyrotoxicosis
 Coronary Heart Disease
Clinical manifestations:
 Rate is faster
 P wave: No definite
 PR interval – Not measurable
(0.08 secs) – too long/short
 PRS: Generally normal
Management:
-Prescribed Digitalis administration
-Beta adrenergic Blockers
-Propranolol
>If ineffective, Cardioversion
VENTRICULAR DYSRHYTHMIAS:
1. Premature Ventricular
Contraction (PVC)
-Most common dysrhythmias
-Lifethreatening
-Impulse that starts in a ventricle and is
conducted through the ventricles
before the next normal sinus impulse.
>6 or more per/min
How to define PVC:
-Ectopic beat originate in the ventricle
and then discharged by a faster than
that by an occurring beat.
>PVC in bigenemy – 2 PVC/min
>PVC in trigeminy – 3 PVC/min
>PVC in quadrgeminy – 4 PVC/min
Causes of PVC:
 Hypokalemia
 Electrolyte imbalances
 Digitalis theraphy
 Stimulants SA: Coffee and teas
 Hypoxia
 Hx of Congestive Heart Failure
Clinical Manifestations:
-Rate varies depends upon the patients
-Irregular P wave Is normal
-PR not measurable
-QRS usually 0.12 seconds wide
 Lidocaine IV:
75 to 100 mg (1-4 mg/min)
 Procainamide
300 mg IV
 Kynedine
 Preprylliuf- Continous infusion
 Treat the underlying cause
2. Ventricular Tachycardia
- Ventricular tachycardia (VT) is defined
as three or more PVCs in a row,
occurring at a rate exceeding 100 beats
per minute.
>Rate 60-100 bpm (Atrial)
>Rate of 110-210 bpm (Ventricular)
>Rhythm: Regular in ventricular,
irregular in atrial
 CARDIAC CONDITIONS
>P wave: QRS complex: Not visible
>PR interval: Not Measurable
> QRS: greater tha 0.12 seconds wide
VT is an emergency because the patient is
usually (although not always) unresponsive and
pulseless.
Causes of VT:
 Myocardial Infarction
 Digitalis toxicity
 Coronary Artery Disease
 Hypokalemia
Clinical Manifestations:
>Lidocaine IV
50mg – 100mg (1-4mg/min)
>Procainamide IV
300 mg IV infusion
>If ineffective:
 Cardioversion may be the treatment of
choice, especially if the patient is
 unstable. (Conscious)
 VT in a patient who is (unconscious) and
without a pulse is treated in the same
manner as ventricular fibrillation (VFIB):
immediate defibrillation is the action of
choice.
This is a life threatening dysrhythmias
-Emergency
3. Ventricular Fibrillation
-Most Severe
-Dysrhythmias characterize by the
random chaotic discharging within
ventricular
-There is no atrial activity seen on the
ECG.
Ventricular rate: Greater than 300/min
Ventricular rhythm: Extremely irregular,
without specific pattern
QRS shape and duration: Irregular,
undulating waves without recognizable
QRS complexes
Produces clinical death
Clinical Manifestations
>STAT Defib (200-400 joules/seconds)
Medications:
>Sodium Bicarbonate
-This is to relieve lactic acidosis
>Before defib:
-Push 0.1 of Epi
To bring back the VS of the pt
(Epinephrine depends on the extent of
the reviving) MAX: 1 ampule in 5 mins
CONDUCTION DEFECTS:
Heart Blocks: Altered at the level of
AV Node
AV blocks occur when the conduction of
the impulse through the AV nodal area
is decreased or stopped.
1. 1st Degree AV Block
First-degree heart block occurs
when all the atrial impulses are
conducted through the AV node
into the ventricles at a rate slower
than normal.
>Pulse normally transmitted but
delayed in level of the AV node
>No treatment needed
2. 2nd Degree AV Block
Some but not all of the impulses are
transmitted to the AV node
>AV node – Conducted to the
ventriculation
>AV node: Selectively
Management:
-Requires treatment if ventricular
rate becomes too low to maintain
effective cardiac output
3. 3rd Degree AV Block
Third-degree heart block occurs
when no atrial impulse is conducted
through the AV node into the
ventricles.
>Cardiac output is compromised
>Administer Pacemaker
CARDIOVERSION &
DEFIBRILLATION
 Cardioversion (Conversion)
- In cardioversion, the defibrillator is set to
synchronize with the ECG on a cardiac
monitor so that the electrical impulse
discharges during ventricular depolarization
(QRS complex).
- Before cardioversion, the patient receives
intravenous sedation as well as an analgesic
medication or anesthesia.
- The amount of voltage used varies from 25
to 150p joules, depending on the
 CARDIAC CONDITIONS
defibrillator’s technology and the type of
dysrhythmia
 Defibrillation
- used in emergency situations as the
treatment of choice for ventricular
fibrillation and pulseless VT.
- The electrical voltage required to
defibrillate the heart is usually greater
than that required for cardioversion. If
three defibrillations of increasing
voltage have been unsuccessful,
cardiopulmonary resuscitation is
initiated and advanced life support
treatments are begun.
- The use of epinephrine or vasopressin
may make it easier to convert the
dysrhythmia to a normal rhythm with
defibrillation. These drugs may also
increase cerebral and coronary artery
blood flow. After the medication is
administered and 1 minute of
cardiopulmonary resuscitation is
performed, defibrillation is again
administered
- This treatment continues until a stable
rhythm resumes or until it is
determined that the patient cannot be
revived.
- -200-360 joules/sec
When performing defibrillation or
cardioversion, the nurse should remember
these key points:
• Use multifunction conductor pads or paddles
with a conducting agent between the paddles
and the skin (the conducting agent is available
as a sheet, gel, or paste).
• Place paddles or pads so that they do not
touch the patient’s clothing or bed linen and are
not near medication patches or direct oxygen
flow.
• If cardioverting, ensure that the monitor leads
are attached to the patient and that the
defibrillator is in sync mode. If defibrillating,
ensure that the defibrillator is not in sync mode
(most machines default to the “not-sync”
mode).
• Do not charge the device until ready to shock;
then keep thumbs and fingers off the discharge
buttons until paddles or pads are on the chest
and ready to deliver the electrical charge.
• Exert 20 to 25 pounds of pressure on the
paddles to ensure good skin contact.
• Before pressing the discharge button, call
“Clear!” three times: As “Clear” is called the first
time, ensure that you are not touching the
patient, bed or equipment; as “Clear” is called
the second time, ensure that no one is touching
the bed, the patient, or equipment, including
the endotracheal tube or adjuncts; and as
“Clear” is called the third time, perform a final
visual check to ensure you and everyone else
are clear of the patient and anything touching
the patient.
• Record the delivered energy and the results
(cardiac rhythm, pulse).
• After the event is complete, inspect the skin
under the pads or paddles for burns; if any are
detected, consult with the physician or a wound
care nurse about treatment.
Nursing Management:
>Place patient in the flat firm surface
-Apply cardiac board on the patients bed
-If none,place the pt to the floor
>Apply interface material
-Apply Lubricant to the paddles before
Contacting the pt’s skin to prevent burning
The patient’s skin
>Hold the handle of the paddle to prevent
Electrocution
>State clear, and make sure that all of the
people in the room are going to distance
themselves at the patient’s bed
>Position the paddle:
-Right of the sternum (3rd ICS)
-Left mid axillary (5th ICS)
Cardiopulmonary Resuscitation
-Usually perform in cardiopulmonary arrest
-Clinical death
-Pulselessness
-Breathlessness
>Within 4-6 minutes after the onset of the
arrest – more than 6 mins indicates brain dead
Basic Life Support (BLS)
-Use of hands and mouth
-Sincere desire of giving the patient a 2 nd
chance of life
Advanced Cardiac Life Support (ACLS)
-Requires BLS
-Use of advanced equipment
-Emergency drug
-fluids
>To stabilize the patient
CPR performs ABCD:
Airway
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